Paleodiet List 1997 2005

PALEOLITHIC DIET SYMPOSIUM LIST(1997-2005)
The PALEODIET list is a semi-private, semi-moderated symposium for researchers with interest in and knowledge of primitive diets
and their relevance to modern life. Our primary audience is biologists, paleontologists, anthropologists, physiologists, and health care
professionals, though laymen are not necessarily excluded.
The discussions include the latest scientific research, review of existing research, analysis of practical applications, and general
knowledge exchange on all aspects of the paleolithic nutrition and exercise, including consideration of how modern diet may cause
certain health problems and what changes may ameliorate these conditions.
PALEODIET Archives
Subject: Celiac Ass'n Speech
From: Dean Esmay
Date: Fri, 21 Mar 1997 12:18:49 -0500
I had the pleasure of contributing a few suggestions and helping to edit copy on the following speech, which
was written by Ron Hoggan and presented at the Annual General Meeting of the Calgary Chapter of the
Canadian Celiac Association on March 15, 1997.
Hoggan is a noted writer on celiac disease whose work has appeared in numerous places, including at least
one paper published in MEDICAL HYPOTHESES.
Hoggan is also member of this mailing list, but agreed to let me post this as the first official message for this
list. Comments or questions on the following speech are invited.
Dean Esmay
Gluten is a Dubious Luxury of Non-Celiacs, by Ron Hoggan
(Note: In this paper I use the term "gluten" generically, as we celiacs use it, to refer to all proteins peculiar to
cereal grains.)
One must wonder why, in spite of increasing lifespans in the advanced industrialized nations, modern
medicine has failed to clearly identify the cause of many neurological, autoimmune and malignant diseases.
The gluten-free diet is only recommended where there is a clear indication of advanced, gluten-induced
disease, but is this the best advice?
We may sometimes feel disadvantaged by the strict gluten-free diet we have to follow. It is costly and
inconvenient. But perhaps it is those who continue to consume glutinous foods who should be concerned.
Gluten, while dangerous to celiacs, has never been investigated for deleterious effects on the general
population. Yet we have studies that show that hunter-gatherers following traditional life-ways do not
develop the neurological, auto-immune and malignant diseases that people living in the industrialized world
experience, and these people rarely eat gluten-rich foods (1, 2). There is already compelling evidence
connecting the advent of agriculture to bone and joint disease (3), and humankind has only been cultivating
cereal grains for approximately 10, 000 years (2, 4), which is but a brief moment in evolutionary terms.
Remember too, it is only a small population located in the Near East, that has had that length of exposure to
cereal grains (4); most of the world has had agriculture for an even shorter period of time. Neurological and
auto-immune diseases, as well as malignancies, are over-represented among celiacs (5), suggesting that
glutens/gliadins may be a major environmental contributor to such diseases. Yet this area of investigation
appears to have been avoided in research on these health problems. One must wonder at the cause of this
neglect of such an important possibility.
There is abundant evidence connecting the advent of agriculture with retardation of long bone growth, dental
enamel hypoplasia, iron deficiency anemia (indicated by porotic hyperostosis), juvenile osteoporosis, and
joint disease (18). Do these conditions sound familiar? Many are the commonest signs of celiac disease, and
they were apparently the rule, not the exception, in cultures adapting to agriculture.
We know, from paleontologists' study of human remains from the ancient past, that when a culture begins to
cultivate cereal grains they experience substantial reductions in height, which is variously reported as 5" and
6"(2, 4). Clearly, the reduction is substantial and significant. We know, too, that these remains demonstrate
weaker bone structure (through reductions in peak bone-mass) and evidence of articular damage(3).
Additionally, ancient Egyptians, who consumed a diet that would be considered very "heart-healthy" in our
culture, have left behind mummies which clearly demonstrate atherosclerosis (7). While the evidence from
the ancients is compelling, there can always be counter-arguments and debates when we are reaching back as
far as 10, 000 years into the past. Yet a few marginal pockets of scientific enquiry have explored a few
elements of modern implications of this issue.
Paleolithic Diet Symposium List
1/298 (1997)
W.J.Lutz (4) has offered an alternative perspective on the "French Paradox." (The "French Paradox" is the
unusually low rate of death by myocardial infarction among the French despite quite high per-capita rates of
fat consumption.) Dr. Lutz has studied the spread of agriculture through Europe. He presents a picture
whereby the spread of agriculture, and thus the period of time a culture has been exposed to cereal grains, is
inversely related to the incidence of cardiovascular disease. The underlying assumption, of course, is that the
longer the exposure, the greater the likelihood that those who were intolerant to these grains were trimmed
from the gene pool of such cultures; it seems that the less time a culture has been exposed to gluten, the
greater the portion of the population that continues to develop cancers and cardiovascular disease. (Lutz also
provides similarly compelling data on the rates of breast cancer mortality.)
This work is confirmed by Simmoon's observation that there is a negative correlation between the frequency
of antigen HLA-B8 and the length of time wheat farming has been practised in various parts of Europe (19).
Another interesting study done in China produced what the investigators found to be rather surprising
results(8). In this investigation, the researchers plotted the diets of more than 3500 rural Chinese women, and
measured their levels of SHBG (sex-hormone binding globulins). They were very surprised to find that
wheat consumption, and perhaps reduced fish consumption, were the strongest predictors of levels of SHBG,
which would indicate an increased risk of cardiovascular disease.
Another study has connected gluten with neurological illness (9). This group of researchers tested 53 patients
with neurological illness of unknown origin for antibodies against gliadin. More than half of them (30
people) demonstrated these antibodies. Nine of those folks proved to have celiac disease, but the other 21
only demonstrated an immune response to gluten, of a type that is often dismissed as meaningless. This study
has some far-reaching implications for neurological research.
Yet another indication that celiacs are not the only segment of the population to suffer from the adverse
effects of gluten is a study that was carried out on a very small group of siblings of celiacs(10). When
subjected to rectal gluten challenge, half of the siblings showed an immune response to gluten, but these
results did not correlate with the hereditary predictors of celiac disease.
As for the connection between autoimmunity and cereal grains, it is clear and compelling. The theoretical
perspective of molecular mimicry suggests that gliadin-derived peptides may activate the immune system
against collagenous tissues, and since intestinal permeability (not celiac disease) is all that is required to
allow the passage of these peptides into the bloodstream, a significant number of many types of autoimmune
diseases seem likely to benefit from a gluten-free diet (11).
In total, then, there are several studies which demonstrate (often coincidentally) that a much larger group
than those with celiac disease are mounting an immune response against gluten, and that this response is
causing or contributing to serious illness. Phytic acid in whole cereal grains binds to minerals, including
calcium. This chemical bond is not broken in the GI tract. The net result is the binding and wasting of muchneeded dietary calcium, even among those whose immune systems can tolerate gluten, and these grains may
be implicated in osteoporosis (12).
I would now like to draw your attention back to the issue of malignancy. _Medical Hypotheses_ will soon
publish a paper I have written which suggests (among other things) that gluten may be implicated in a great
many cases of lymphoma (14). Gluten has been demonstrated to interfere with the celiac patient's ability to
mount an immune response to malignancies (15, 16, 17). In my paper, I have postulated a dynamic whereby
gluten may have a similar effect in others who are simply sensitive to gluten, or who have a sub-clinical form
of this disease.
Ray Audette, a populist writer, has said that Stanislaw Tanchou "....gave the first formula for predicting
cancer risk. It was based on grain consumption and was found to accurately calculate cancer rates in major
European cities. The more grain consumed, the greater the rate of cancer." Tanchou's paper was delivered to
the Paris Medical Society in 1843(20).
We hear all the time about pollution in the industrial world being the source for modern man's high incidence
of cancer. It is the chemical additives, we are told, in the food we eat, that causes much of the problem.
Perhaps.
I would like to suggest that the evidence from antiquity, the pattern of the spread of agriculture in Europe
coinciding with the patterns of civilizatory illnesses, the levels of SBHG associated with wheat consumption,
the high incidence of gliadin antibodies among those with neurological illnesses of unknown origin, the
sensitivity to gluten among siblings of celiacs in spite of the absence of genetic indicators associated with
celiac disease, and my own investigation of the literature regarding lymphoma, all point to the strong
possibility that gluten is a dangerous substance to many more people than just celiacs.
Sources:
2/298 (1997)
1. Eaton B, Konner M, Shostak M, " Stone Agers in the Fast Lane: Chronic Degenerative Diseases in
Evolutionary Perspective" _The American Journal of Medicine_ 1988; 84:739-749
2. Eaton S, Konner M, "Paleolithic Nutrition" _NEJM_ 1985; 312(5): 283-289
3. Eaton S, Nelson D, "Calcium in evolutionary perspective" _Am. J. Clin. Nutr._1991; 54: 281S - 287S
4. Lutz W J, "The Colonisation of Europe and Our Western Diseases" _Medical Hypotheses_ 1995; 45: 115120
5. Lindeberg S, et al. "Cardiovascular risk factors in a Melanesian population apparently free from stroke and
ischaemic heart disease: the Kitava study" _J Intern Med_ 1994 Sep.
6. Lewin R, "A Revolution of Ideas in Agricultural Origins" _Science_ 1988; 240: 984-986
7. Zimmerman M, "The paleopathology of the cardiovascular system" _Tex Heart Inst J_ 1993; 20(4): 252257
8. Gates et. al. "Association of dietary factors and selected plasma variables with sex hormone-binding
globulin in rural Chinese women" Am J Clin Nutr 1996; 63: 22-31.
9. Hadjivassiliou M, Gibson A, Davies-Jones G, Lobo A, Stephenson T, Milford-Ward A, "Does cryptic
gluten sensitivity play a part in neurological illness?" _Lancet_ 1996; 347: 369-371
10. Troncone R, Greco L, Mayer M, Mazzarella G, Maiuri L, Congia M, Frau F, deVirgilis S, Auricchio S,
"In Siblings of Celiac Children, Rectal Gluten Challenge Reveals Gluten Sensitization Not Restricted to
Celiac HLA" _Gastroenterology_ 1996; 111: 318-324
11. Ostenstad B, Dybwad A, Lea T, Forre O, Vinje O, Sioud M, "Evidence for monoclonal expansion of
synovial T cells bearing V Alpha 2.1/V beta 5.5 gene segments and recognizing a syntehtic peptide that
shares homology with a number of putative autoantigens"
12. Lindeberg, Staffan, personal correspondence Feb, 1997
14. Hoggan R, "Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens" _Medical
Hypotheses_ In Press 1997.
15. Maclaurin B, Cooke W, Ling N, "Impaired lymphocyte reactivity against tumour cells in patients with
coeliac disease" _Gut_ 1971; 12: 794-800
16. Egan L, Walsh S, Stevens F, Connolly C, Egan E, McCarthy C, "Celiac-Associated Lymphoma"
_Journal of Clinical Gastroenterology_ 1995; 21(2): 123-129
17. Swinson C, Slavin G, Coles E, Booth C, "Coeliac Disease and Malignancy" _Lancet_ 1983; Jan 15: 111115
18. Armelagos G, Van Gerven D, Martin D, Huss-Ashmore R, "Effects of Nutritional Change on the Skeletal
Biology of Northeast African (Sudanese Nubian) Populations" _From Hunters to Farmers The Causes and
Consequences of Food Production in Africa_ Clark & Brandt (eds.) 1984; II: 37-146
19. Simoons F, "Celiac disease as a geographic problem" _Food, Nutrition and Evolution_ 1981; eds.
Walcher D, and Kretchmer N, Masson Publishing, New York
20. Audette R, lowcarb listserv at:, March 11, 1997 from: Vilhjalmur Stefansson's book _Cancer Disease of
Civilization_ 1960; Hill and Wang, New York, NY.
Background Sources:
21. Davis D, "Paleolithic Diet, Evolution, and Carcinogens" _Science_ 1987; 238: 1633-1634
22. Carpenter K, "Protein requirements of adults from an evolutionary perspective" _Am J Clin Nutr_1992;
55: 913-917
23. Eaton S, "Humans, Lipids and Evolution" _LIPIDS_ 1992; 27(10): 814-819
24. Troncone R, Greco L, Mayer M, Mazzarella G, Maiuri L, Congia M, Frau F, deVirgilis S, Auricchio S,
"In Siblings of Celiac Children, Rectal Gluten Challenge Reveals Gluten Sensitization Not Restricted to
Celiac HLA" _Gastroenterology_ 1996; 111: 318-324
25. Marsh M, "Bone Disease and Gluten Sensitivity: Time to Act, to Treat, and to Prevent" _The American
Journal of Gastroenterology_ 1994; 89(12): 2105-2107
26. Young T, Hochman R, Scopelliti J, "Celiac Disease and Arthropathy: Case Report and Literature
Review" _The Guthrie Journal_ 1993; 62(3): 99-104
27. Lindh E, Ljunghall S, Larsson K, Lavo B, " Screening for antibodies against gliadin in patients with
osteoporosis" _Journal of Internal Medicine_ 1992; 231: 403-406
28. de Boer W, Maas M, Tytgat G, "Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Diet
in Celiac Sprue" _Journal of Clinical Gastroenterology_ 1993; 16(4): 317-319
29. Mathus-Vliegen E, Halteren H, Tytgat G, "Malignant lymphoma in coeliac disease: various
manifestations with distinct symptomatology and prognosis?" _Journal of Internal Medicine_ 1994; 236: 4349
3/298 (1997)
30. Rosenberg S, "The Low-Grade Non-Hodgkin's Lymphomas: Challenges and Opportunities" _Journal of
Clinical Oncology" 1985; 3(3): 299-310
28. Swinson C, Coles E, Slavin G, Booth C, "Coeliac Disease and Malignancy" _Lancet_ 1983; Jan 15: 111115
31. Wright D, Jones D, Clark H, Mead G, Hodges E, Howell W, "Is adult-onset coeliac disease due to a lowgrade lymphoma of intraepithelial T lymphocytes?" _Lancet_ 1991; 337: 1373-1374
32. Gouldie R, Lee F, "Coeliac disease and lymphoma" _Lancet_ 1991; 338: 570
33. Freeman H, Weinstein W, Shnitka T, Piercey J, Wensel R, " Pirmary abdominal Lymphoma" _The
American Journal of Medicine_ 1977; 63: 585-594
34. Holmes G, Piror P, Lane M, Pope D, Allan R, "Malignancy in coeliac disease-effect of a gluten free diet"
_Gut_ 1989; 30: 333-338
35. Sturgess R, Ciclitira P, "Coeliac disease and lymphoma" _Lancet_ 1991; 338: 318-319
36. Egan L, Walsh S, Stevens F, Connolly C, Egan E, McCarthy C, _Journal of Clinical Gastroenterology_
1995; 21(20: 123-129
37. Lopes P, Morris D, Galbraith P, Lillicrap D, Pross H, "Lymphoproliferative Disease of "Lak Cell"
precursor Large Granular Lymphocytes in Association with Celiac Disease" _American Journal of
Hematology_ 1993; 43: 116-122
38. Black, Paul "Psychoneuroimmunology: Brain and Immunology" _Scientific American: SCIENCE &
MEDICINE_ 1995; 2(6): 16-25
39. Kapur A, Isaacs P, Kelsey P, "Linear IgA dermatosis, coeliac disease, and extralinear B cell lymphoma"
_Gut_ 1995; 37: 731-733
40. Ilyas M, Niedobitek G, Agathanggelou A, Barry R, Read A, Tierney R, Young L, Rooney N, "NONHODGKIN'S LYMPHOMA, COELIAC DISEASE, AND EPSTIEN-BARR VIRUS: A STUDY OF 13
CASES OF ENTEROPATHY-ASSOCIATED T- AND B-CELL LYMPHOMA" _Journal of Pathology_
1995; 177: 115-122
41. Cooke W, Holmes G, _Coeliac Disease_ 1984; Churchill Livingstone, NY
PALEODIET Archives
Subject: Re: Celiac Ass'n Speech
From: Bob Avery
Date: Sat, 22 Mar 1997 05:08:57 EST
Dean and Ron,
It was unclear to me from reading the recent Paleoposts whether the grain indictment referred only to (1)
wheat, (2) wheat plus other glutenous cereals (if so, please enumerate), or (c) all cereals, glutenous and nonglutenous alike. In some parts it appeared that only gluten was being indicted, but in others the word
"cereals" was used with no distinctions being made as to their type. Or do all cereals, including rice, contain
gluten? Could you clarify?
Bob Avery
PALEODIET Archives
Subject: Glutenous Grains
From: Ron Hoggan
Date: Sat, 22 Mar 1997 16:46:34 -0700
Hi Bob,
I began the post with:
"Note: In this paper I use the term "gluten" generically, as we celiacs use it, to refer to all toxic proteins in
cereal grains."
I did so because I knew that the original audience would understand what I was saying. Of course, I forgot to
alter it for the list, and I apologize for that cognitive lapse.
I was using the term gluten to refer to the protein fractions of wheat, rye, barley and oats. Technically the
other cereal grains also contain gluten, but there is a dissonance between the jargon of the celiac patient, and
scientific terminology.
I hope that clarifies the issue, and I'm sorry for any confusion.
4/298 (1997)
Best Wishes, Ron Hoggan Calgary, Alberta, Canada
PALEODIET Archives
Subject: Clear communication
From: Ward Nicholson
Date: Sat, 22 Mar 1997 18:49:25 -0600
Bob Avery writes:
> It was unclear to me from from reading the recent Paleoposts whether the grain indictment referred
> only to (1) wheat, (2) wheat plus other glutenous cereals (if so, please enumerate), or (c) all
> cereals, glutenous and non-glutenous alike. In some parts it appeared that only gluten was being
> indicted, but in others the word "cereals" was used with no distinctions being made as to their
> type. Or do all cereals, including rice, contain gluten? Could you clarify?
I would like to add a related request here to the researchers on this list who are posting to try if at all possible
to translate your findings and communications into plain English.
As a lay person with a very keen interest in Paleodiet, I have spent many hours at the local university library
digging up references, and my number-one complaint by far is feeling like I am reading language from
another planet. In having written up some of the research myself for other lay people interested in the
subject, I found most of my time was spent simply trying to decipher what I found in the research journals
and put it into a form I felt people of intelligence but without the specialized training or understanding of all
the jargon could understand.
If Paleodiet research is not to seep out and have a widespread influence on the public until long after it is
past-due to be heard, I believe those communicating the research need to make a concerted effort to write in
terms others can understand. I have discussed privately with a couple of others interested in the field why
Paleodiet research is lagging in getting out to the public and has not had the influence on the nutrition field
that it should have yet, and in my opinion, the complicated research lingo amounting to a communication gap
is the reason.
Also there is fact that researchers generally tend to keep in their own world and do not make concerted
efforts to publish popularly, but primarily in obscure journals. Then, too, there is the question of the research
being scattered all over the place in these obscure journals, making it exceedingly difficult to find even if you
are keenly interested in it like I have been.
Aside from Eaton, Shostak and Konner's "Paleolithic Prescription" which seemingly went mostly unnoticed
in the bookstores when it was first published in 1988 (although it seemed to have made some inroads and in
the medical community's thinking) little attempt to present the scientific research (complete with references
not only for credibility but for those who want to pursue the material further) in a unified, coherent, all-inone-place fashion has been made by the Paleodiet community. I personally think it would behoove
researchers to follow the lead of people like Stephen Jay Gould in publishing for the popular science press,
who has shown you can write popularly with rigor and need not fear sullying your scientific reputation, but
in fact, perhaps, increase it.
So to summarize, one thing I would like to see discussed on this list besides just the research are ways to see
that Paleodiet is better publicized and communicated to the nutritional world at large which seems largely
ignorant of it so far. And hopefully we can begin breaking down the communication gap by beginning to
address it first right here on this list itself. Thanks,
--Ward Nicholson
Wichita, KS
PALEODIET Archives
Subject: Questions on terminology
Date: Sat, 22 Mar 1997 23:47:39 -0600
I enjoyed reading Ron Hoggan's recap of the celiac disease/gluten connection. However, there are several
points I am unclear on due to undefined terminology. Ron, would you be so kind as to fill in the blanks for
those of us without the extensive background you have in the field? Specifically here are the words and
concepts I am unclear on:
5/298 (1997)
> Neurological and auto-immune diseases, as well as malignancies, are over-represented among celiacs
> (5), suggesting that glutens/gliadins may be a major environmental contributor to such diseases.
The word gliadins here seems to slip in without any definition--only some sort of unclear similarity (in my
mind) to glutens due to the context. What exactly are gliadins and why are they distinguished here from
glutens rather than simply lumped in together under the catchall term "gluten" that you are using as a catchall
for many other proteins also found in cereal grains?
> There is abundant evidence connecting the advent of agriculture with retardation of long bone
> growth, dental enamel hypoplasia, iron deficiency anemia (indicated by porotic hyperostosis),
> juvenile osteoporosis, and joint disease (18). Do these conditions sound familiar?
All but two. I would like to know in plain terms what "dental enamel hypoplasia" is, as well as "porotic
hyperostosis." I know from past study in the research that the latter is some kind of bone disease, but I can't
remember exactly what kind. Please fill me in.
> We know, from palenotologists' study of human remains from the ancient past, that when a culture
> begins to cultivate cereal grains they experience substantial reductions in height, which is
> variously reported as 5" and 6"(2, 4). Clearly, the reduction is substantial and significant. We
> know, too, that these remains demonstrate weaker bone structure (through reductions in peak
> bone-mass) and evidence of articular damage(3).
I am not sure I know what "articular damage" refers to. Could you please explain? (Maybe just a technical
term of good ole "arthritis"? :-\)
> W.J.Lutz (4) has offered an alternative perspective on the "French Paradox." (The "French Paradox"
> is the unusually low rate of death by myocardial infarction among the French despite quite high
> per-capita rates of fat consumption.)
I know this may be being a bit picky about the language here, but is there any reason "myocardial infarct"
could not more simply be rendered as "heart attack" so it would be more clear to more people, or is there
some reason "heart attack" is just not considered an accurate-enough term, and therefore it is mandatory to
use "myocardial infarct" instead?
Further on...
> This work is confirmed by Simmoon's observation that there is a negative correlation between the
> frequency of antigen HLA-B8 and the length of time wheat farming has been practised in various
> parts of Europe (19).
What is "antigen HLA-B8, " is this negative correlation good or bad, and what does it do in the body? It
doesn't tell me a whole lot that there is a negative correlation when I don't even know what HLA-B8 is in the
first place. I thought an antigen was a foreign protein the body reacted to by producing antibodies. The above
statement--in my mind--seems to suggest that somehow a substance the body does not produce somehow
varies with the consumption of wheat. That doesn't seem to make sense to me. Either that, or I am just not
getting something here. Please explain.
> Another interesting study done in China produced what the investigators found to be rather
> surprising results(8). In this investigation, the researchers plotted the diets of more than 3500
> rural Chinese women, and measured their levels of SHBG (sex-hormone binding globulins). They
> were very surprised to find that wheat consumption, and perhaps reduced fish consumption, were the
> strongest predictors of levels of SHBG, which would indicate an increased risk of cardiovascular
> disease.
I cannot figure out from the above whether the levels of SHBG went up or down in relation to wheat and fish
consumption, only that there is some sort of correlation. Does SHBG go up when wheat and fish
consumption go up, or is it the reverse? Furthermore, it is not clear to me from the above whether *higher*
or *lower* levels of SHBG result in an increased or decreased risk of cardiovascular disease. It only seems
to say that there is some sort of correlation, but what that correlation is is unclear to me here. Beyond this,
what the heck do sex-hormone binding globulins (SHBG) do in the body in the first place, and why would it
be good or bad if their levels went up or down?
> Another study has connected gluten with neurological illness (9). This group of researchers tested
> 53 patients with neurological illness of unknown origin for antibodies against gliadin. More than
> half of them (30 people) demonstrated these antibodies. Nine of those folks proved to have celiac
> disease, but the other 21 only demonstrated an immune response to gluten, of a type that is often
> dismissed as meaningless. This study has some far-reaching implications for neurological research.
This seems clear enough--that an immune response to gluten might still be problematic even if the person
does not have classic hereditary markers for celiac disease.
> Yet another indication that celiacs are not the only segment of the population to suffer from the
6/298 (1997)
> adverse effects of gluten is a study that was carried out on a very small group of siblings of
> celiacs(10). When subjected to rectal gluten challenge, half of the siblings showed an immune
> response to gluten, but these results did not correlate with the hereditary predictors of celiac
> disease.
I am not sure I understand the underlying assumptions here you are basing your statements on. Are you
saying that certain immune responses somehow are used as "markers" for certain hereditary characteristics
(which perhaps cannot be directly determined except through these markers) that may predict for celiac
disease? And that there are additional immune responses that you are postulating may also predict for it, but
conventional scientific wisdom does not yet acknowledge them?
> As for the connection between autoimmunity and cereal grains, it is clear and compelling. The
> theoretical perspective of molecular mimicry suggests that gliadin-derived peptides may activate
> the immune system against collagenous tissues, and since intestinal permeability (not celiac
> disease) is all that is required to allow the passage of these peptides into the bloodstream, a
> significant number of many types of autoimmune diseases seem likely to benefit from a gluten-free
> diet (11).
This seems clear enough except for the part about collagen. According to my dictionary, collagen is a
"fibrous protein constituent of bone, cartilage, tendon, and other connective tissue." So what? What is the
point about collagen here? I would guess there is perhaps sp, e postulation being made here that the immune
system's action against collagen could be the mechanism behind bone deterioration seen in Neolithic farming
communities, but this is a leap I am simply guessing at. Is this is fact what is being suggested, or am I
completely off base? I am unclear.
> In total, then, there are several studies which demonstrate (often coincidentally) that a much
> larger group than those with celiac disease are mounting an immune response against gluten, and
> that this response is causing or contributing to serious illness. Phytic acid in whole cereal
> grains binds to minerals, including calcium. This chemical bond is not broken in the GI tract. The
> net result is the binding and wasting of much-needed dietary calcium, even among those whose
> immune systems can tolerate gluten, and these grains may be implicated in osteoporosis (12).
Okay, clear enough.
> I would now like to draw your attention back to the issue of malignancy. _Medical Hypotheses_ will
> soon publish a paper I have written which suggests (among other things) that gluten may be
> implicated in a great many cases of lymphoma (14). Gluten has been demonstrated to interfere with
> the celiac patient's ability to mount an immune response to malignancies (15, 16, 17). In my paper,
> I have postulated a dynamic whereby gluten may have a similar effect in others who are simply
> sensitive to gluten, or who have a sub-clinical form of this disease.
This is clear language--thanks.
> I would like to suggest that the evidence from antiquity, the pattern of the spread of agriculture
> in Europe coinciding with the patterns of civilizatory illnesses, the levels of SBHG associated
> with wheat consumption, the high incidence of gliadin antibodies among those with neurological
> illnesses of unknown origin, the sensitivity to gluten among siblings of celiacs in spite of the
> absence of genetic indicators associated with celiac disease, and my own investigation of the
> literature regarding lymphoma, all point to the strong possibility that gluten is a dangerous
> substance to many more people than just celiacs.
Several questions here. Again, please explain what gliadin is and why antibodies against it would be
something that might lead to neurological illness. What are the possible mechanisms you would postulate?
And again, what do SBHGs do in the body, and are their correlated levels with increased wheat consumption
ones of increase or decrease, and is more or less SBHG good or bad? I don't have the background in
physiology or pathology to have a clue about any of this.
Thanks, Ron. I know it may seem tedious to you to explain these things, but remember, not all of us have the
background you do. I take Discover magazine, Science News, and read several issues of Scientific American
a year, and I like to think I am science-literate for a lay person, but I am really struggling here with some of
this.
--Ward Nicholson
Wichita, KS
PALEODIET Archives
Subject: Re: Questions on terminology
7/298 (1997)
From: (Ron Hoggan)

Date: Sun, 23 Mar 1997 01:22:05 -0700 (MST)
Hi Ward, Your demands for excellence are certainly apparent in your writing and in the questions you are
asking here. I will try for the same level of clarity in my responses. :=)
> Specifically here are the words and concepts I am unclear on: Neurological and auto-immune
> diseases, as well as malignancies, are over-represented among celiacs (5), suggesting that
> glutens/gliadins may be a major environmental contributor to such diseases. The word gliadins here
> seems to slip in without any definition--only some sort of unclear similarity (in my mind) to
> glutens due to the context. What exactly are gliadins
They are a sub-group of alcohol soluble proteins
> and why are they distinguished here from glutens Due to my sloppy writing. I should have stuck
> with the term gluten. rather than simply lumped in together under the catchall term "gluten" that
> you are using as a catchall for many other proteins also found in cereal grains?
Yes, that is what I should have done.
> There is abundant evidence connecting the advent of agriculture with retardation of long bone
> growth, dental enamel hypoplasia, iron deficiency anemia (indicated by porotic hyperostosis),
> juvenile osteoporosis, and joint disease (18). Do these conditions sound familiar? All but two. I
> would like to know in plain terms what "dental enamel hypoplasia"
holes in dental enamel, usually horizontal, and usually due to a period or periods of malnutrition
> is, as well as "porotic hyperostosis." I know from past study in the research that the latter is
> some kind of bone disease, but I can't remember exactly what kind. Please fill me in.
It is a condition where the outer layer of the bone becomes enlarged. It indicates a condition of iron
deficiency anemia.
> We know, from palenotologists' study of human remains from the ancient past, that when a culture
> begins to cultivate cereal grains they experience substantial reductions in height, which is
> variously reported as 5" and 6"(2, 4). Clearly, the reduction is substantial and significant. We
> know, too, that these remains demonstrate weaker bone structure (through reductions in peak
> bone-mass) and evidence of articular damage(3). I am not sure I know what "articular damage"
> refers to. Could you please explain? (Maybe just a technical term of good ole "arthritis"? :-\)
Sorry, I don't agree with you here. Articular damage is joint damage. I'm pretty convinced that it would be
due to arthritis, but I think I would have a fight on my hands trying to defend my position against some of the
practitioners who specialize in that area. You wouldn't believe how I've been trashed on alt.support.arthritis
on that very point. :=)
> W.J.Lutz (4) has offered an alternative perspective on the "French Paradox." (The "French Paradox"
> is the unusually low rate of death by myocardial infarction among the French despite quite high
> per-capita rates of fat consumption.) I know this may be being a bit picky about the languare
> here, but is there any reason "myocardial infarct" could not more simply be rendered as "heart
> attack" so it would be more clear to more people, or is there some reason "heart attack" is just
> not considered an accurate-enough term, and therefore it is mandatory to use "myocardial infarct"
> instead?
Nope, just sloppy writing. I tell my students to write what they mean, and don't use specialized words unless
they are necessary for clarity and precision..... then I have to admit to the same error today. Don't tell my
students, okay?
> Further on... This work is confirmed by Simmoon's observation that there is a negative correlation
> between the frequency of antigen HLA-B8 and the length of time wheat farming has been practised
> in various parts of Europe (19). What is "antigen HLA-B8, " is this negative correlation good or bad,
> and what does it do in the body?
Sorry that presumes familiarity with celiac disease. It is a gene. It indicates a predisposition for celiac
disease. Although it is present in 20% to 30% of the population, only a small fraction of those who have it
develop celiac disease. A huge majority of celiacs have this gene.
> It doesn't tell me a whole lot that there is a negative correlation when I don't even know what
> HLA-B8 is in the first place. I thought an antigen was a foreign protein the body reacted to by
> producing antibodies. The above statement--in my mind--seems to suggest that somehow a substance
> the body does not produce somehow varies with the consumption of wheat. That doesn't seem to
> make sense to me. Either that, or I am just not getting something here. Please explain.
8/298 (1997)
I was saying (although not clearly) that the incidence of this gene is reduced with an increased duration of
wheat consumption. This suggests to me that perhaps some of the other people with autoimmune diseases,
and gluten sensitivity, associated with HLA-B8 are suffering from gluten consumption. It must have been
serious enough, and the onset early enough (prior to reproduction) to reduce this gene's representation in the
gene pool.
> Another interesting study done in China produced what the investigators found to be rather
> surprising results(8). In this investigation, the researchers plotted the diets of more than 3500
> rural Chinese women, and measured their levels of SHBG (sex-hormone binding globulins). They
> were very surprised to find that wheat consumption, and perhaps reduced fish consumption, were the
> strongest predictors of levels of SHBG, which would indicate an increased risk of cardiovascular
> disease. I cannot figure out from the above whether the levels of SHBG went up or down in relation
> to wheat and fish consumption, only that there is some sort of correlation. Does SHBG go up when
> wheat and fish consumption go up, or is it the reverse?
It is the reverse, although I'm not clear about why. The SHBG correlate positively with HDLs, which
bespeaks a reduced risk of atherosclerosis. That means that wheat consumption is associated with reductions
in SHBG, and therefore, with an increased risk.
> Furthermore, it is not clear to me from the above whether *higher* or *lower* levels of SHBG
> result in an increased or decreased risk of cardiovascular disease. It only seems to say that
> there is some sort of correlation, but what that correlation is is unclear to me here. Beyond
> this, what the heck do sex-hormone binding globulins (SHBG) do in the body in the first place, and
> why would it be good or bad if their levels went up or down?
As near as I can tell, they bind to sex hormones in the blood, presumably for wasting, but I'm not at all sure
of that. Why do you ask such difficult questions?
> Another study has connected gluten with neurological illness (9). This group of researchers tested
> 53 patients with neurological illness of unknown origin for antibodies against gliadin. More than
> half of them (30 people) demonstrated these antibodies. Nine of those folks proved to have celiac
> disease, but the other 21 only demonstrated an immune response to gluten, of a type that is often
> dismissed as meaningless. This study has some far-reaching implications for neurological research.
> This seems clear enough--that an immune response to gluten might still be problematic even if the
> person does not have classic hereditary markers for celiac disease.
Hey! That's one point for me!
> Yet another indication that celiacs are not the only segment of the population to suffer from the
> adverse effects of gluten is a study that was carried out on a very small group of siblings of
> celiacs(10). When subjected to rectal gluten challenge, half of the siblings showed an immune
> response to gluten, but these results did not correlate with the hereditary predictors of celiac
> disease. I am not sure I understand the underlying assumptions here you are basing your statements
> on. Are you saying that certain immune responses somehow are used as "markers" for certain
> hereditary characteristics (which perhaps cannot be directly determined except through these
> markers) that may predict for celiac disease? And that there are additional immune responses that
> you are postulating may also predict for it, but conventional scientific wisdom does not yet
> acknowledge them?
I'm saying that 1/2 of the siblings tested with a rectal gluten challenge showed an immune response (either
elevated levels of a specific type of lymphocytes, or damage to the intestinal villi). This gluten sensitivity did
not correlate with the genetic markers we associate with gluten sensitivity and celiac disease. That is,
somehow another (probably genetic) factor also seems to be at work in gluten sensitivity.
> As for the connection between autoimmunity and cereal grains, it is clear and compelling. The
> theoretical perspective of molecular mimicry suggests that gliadin-derived peptides may activate
> the immune system against collagenous tissues, and since intestinal permeability (not celiac
> disease) is all that is required to allow the passage of these peptides into the bloodstream, a
> significant number of many types of autoimmune diseases seem likely to benefit from a gluten-free
> diet (11). This seems clear enough except for the part about collagen. According to my
> dictionary, collagen is a "fibrous protein constituent of bone, cartilage, tendon, and other
> connective tissue." So what? What is the point about collagen here? I would guess there is perhaps
> sp, e postulation being made here that the immune system's action against collagen could be the
> mechanism behind bone deterioration seen in Neolithic farming communities, but this is a leap I am
> simply guessing at.
9/298 (1997)
No, my point is that in many autoimmune diseases, such as some types of arthritis, celiac disease, some types
of nephropathy, etc., there is damage to the collagen.
> Is this is fact what is being suggested, or am I completely off base? I am unclear.
I think that gluten will eventually be revealed as one of the primary causes of autoimmune diseases which
are now thought to have multiple interacting causes.
> In total, then, there are several studies which demonstrate (often coincidentally) that a much
> larger group than those with celiac disease are mounting an immune response against gluten, and
> that this response is causing or contributing to serious illness. Phytic acid in whole cereal
> grains binds to minerals, including calcium. This chemical bond is not broken in the GI tract. The
> net result is the binding and wasting of much-needed dietary calcium, even among those whose
> immune systems can tolerate gluten, and these grains may be implicated in osteoporosis (12). Okay,
> clear enough.
> I would now like to draw your attention back to the issue of malignancy. _Medical Hypotheses_ will
> soon publish a paper I have written which suggests (among other things) that gluten may be
> implicated in a great many cases of lymphoma (14). Gluten has been demonstrated to interfere with
> the celiac patient's ability to mount an immune response to malignancies (15, 16, 17). In my paper,
> I have postulated a dynamic whereby gluten may have a similar effect in others who are simply
> sensitive to gluten, or who have a sub-clinical form of this disease. This is clear language--thanks.
> I would like to suggest that the evidence from antiquity, the pattern of the spread of agriculture
> in Europe coinciding with the patterns of civilizatory illnesses, the levels of SBHG associated
> with wheat consumption, the high incidence of gliadin antibodies among those with neurological
> illnesses of unknown origin, the sensitivity to gluten among siblings of celiacs in spite of the
> absence of genetic indicators associated with celiac disease, and my own investigation of the
> literature regarding lymphoma, all point to the strong possibility that gluten is a dangerous
> substance to many more people than just celiacs.
> Several questions here. Again, please explain what gliadin is and why antibodies against it would
> be something that might lead to neurological illness. What are the possible mechanisms you would
> postulate? And again, what do SBHGs do in the body, and are their correlated levels with increased
> wheat consumption ones of increase or decrease, and is more or less SBHG good or bad? I don't have
> the background in physiology or pathology to have a clue about any of this.
> Thanks, Ron. I know it may seem tedious to you to explain these things, but remember, not all of
> us have the background you do. I take Discover magazine, Science News, and read several issues of
> Scientific American a year, and I like to think I am science-literate for a layperson, but I am
> really struggling here with some of this.
Yes, this was written for a group of people who have celiac disease. Most of us know that most celiacs have
HLA-B8. We may not be too clear on what that is, but we know it is in most celiacs, but only in a minority
of the general population. I guess I should have altered it for the list.
I was also under some time constraints. I had promised the organizer that I would keep the talk under 15
minutes. (She knows me.) You might not believe this, but I do get a little carried away, at times, and she
didn't want me going on and on for hours.
Thanks for your comments, Ward.
Best Wishes, Ron
PALEODIET Archives
Subject: Re: Celiac Ass'n Speech
From: Dean Esmay
Date: Sun, 23 Mar 1997 05:31:43 -0500
I take no credit for Ron's paper except that I made some small content suggestions and suggested some
alternate phrasing in some spots. I have never seen anyone explicitly put forth the suggestion that glutens are
a primary culprit in modern disease processes (although Ray Audette does refer generically to "foreign
proteins" in grains, beans, and dairy), but the idea seems to have merit. Certainly hunter/gatherers never eat
the stuff, and apparently some fairly healthy horticulturists do not either.
10/298 (1997)
I had told Ron he'd better put something at the top explaining to people that "gluten" is a phrase celiacs
commonly use to refer to all proteins peculiar to cereal grains, but perhaps that wasn't sufficient. (Ron refers
to them as "toxic proteins" but I'm less willing to use that phrasing.) But that is the short answer; "gluten"
refers generically proteins peculiar to all forms of cereal grains. (All grains contain glutens, although the
amount varies. Wheat is quite high in it, whereas if I'm not mistaken brown rice is relatively low.)
The paper in question was delivered to a specialized audience of people with celiac disease (a potentially
deadly condition brought about by intolerance to glutens) and health professionals who treat them. My
forwarding it here was because it raises interesting issues that touch on the concept of paleolithic nutrition.
One of the beliefs of some in the paleolithic nutrition field is that excessive carbohydrate consumption
causes many of the diseases of civilization, especially hypertension, atherosclerosis, and diabetes. Grains and
grain products are post-agricultural humanity's primary source for carbohydrate; hunter/gatherers, who of
course would rarely eat grains, seem to average only about 30% carbohydrate intake, with most of it very
high in fibre and quite low on the glycemic index, with animal and nut protein frequently making up a
majority of the calories.
However, it seems quite possible that dietary carbohydrate might be a red herring, or a smaller ingredient
than it is sometimes regarded as. The first thing to make me realize this was Staffan Lindeberg's studies on
the Kitava (and Lindeberg is also a member of this listserv, BTW). The Kitava are not hunter/gatherers, but
are not exactly agriculturalists either; they would best be defined as primitive horticulturists, as they mostly
cultivate wild plants and do not grow or consume cereal grains (and if I'm not mistaken, do not eat dairy
either). Their diet is relatively high in carbohydrate and somewhat low in fat, although saturated fat intake is
fairly high. About 80% of them smoke cigarettes on a daily basis, and while they are physically active, they
are only somewhat more so than most Westerners. Yet their rates of obesity, diabetes, stroke, and heart
attacks are vanishingly small. (I don't know if Lindeberg and his team ever looked for rheumatoid arthritis or
cancer, two common autoimmune diseases typical to civilization. Perhaps he can tell us that himself.)
Genetics does not seem to be the explanation, either. For a very good summary of Lindeberg's work written
by Lindeberg himself, with a bibliography of his complete papers as published in peer-reviewed journals, see
http://www.panix.com/~donwiss/paleodiet/sl1.shtml.
In _The Paleolithic Prescription_, Eaton, Shostak, and Konner stated that while grains and grain products
were unnatural to humans in the wild, they were "too valuable" to suggest giving up their use, although he
never explained exactly what he thought was valuable about them. I wonder at times whether Eaton has
rethought that matter.
PALEODIET Archives
Subject: More on glutens
From: Dean Esmay
Date: Sun, 23 Mar 1997 06:28:41 -0500
To give some examples of what I'm talking about, Arthur De Vany, who's currently writing a book which he
has excerpted at http://www.socsci.uci.edu/econ/personnel/devany/Essay.html, makes the following
statement:
> "The only universal characteristic of ancestral and living hunter gatherer diets is the almost
> complete absence of simple carbohydrates. There were no simple carbohydrates like sugar and pasta.
> Fruits were tough and fibrous, not the refined, sweet stuff we have today. The closest thing to a
> simple carb was honey, rare and guarded by wild bees. There were no grain or cereal sources of
> carbs in the ancestral diet." (From "Evolutionary Fitness: What Evolution Teaches Us About How to
> Live and Stay Healthy Copyright 1995 by Arthur De Vany, Ph.D. and excerpted at the above URL.)
I don't want to pick on De Vany, who is far from alone in making this kind of claim. But this somewhat
common belief appears to be false. There's more to cereal grains than that they are high in simple
carbohydrate; they also contain forms of protein (which can be generically referred to as glutens) which are
completely foreign to the human animal, and which have been shown to cause serious disease in at least
some individuals. Allergies to cereal grains seem to be among the most common of food allergies, too. As
Hoggan mentions, there is at least some evidence that the proteins in grains may be implicated in far more
serious autoimmune responses than just food allergies. Ray Audette has often suggested that obesity is an
autoimmune disorder, and has also suggested that what he calls "foreign proteins" in grains and beans may
be a primary culprit in a number of diseases that hunter/gatherers never suffer from.
11/298 (1997)
One might also wonder about dairy. I know of no evidence that the ancestral human diet would ever include
dairy. In fact, although I eat dairy products myself, you could argue that the consumption of dairy is just
about the most bizarre thing that modern humans do. Dairy products contain lactose, and compellingly, about
75% of the world population is lactose-intolerant. But lactose isn't the only foreign substance; casein is also
in all dairy products, and is another substance which would be foreign to the human digestive tract, and
which appears to cause at least some individuals problems. I know of no rigorous evidence that casein is a
major danger, but it does seem logical to posit that substances unique to foods that would never have been
eaten by humans in nature should be looked at with suspicion.
PALEODIET Archives
Subject: Thanks, and another question or three :-)
Date: Sun, 23 Mar 1997 10:57:59 -0600
Hi Ron, thanks for your great reply to my response to your gluten paper--I think you answered every single
nitpicking question I had. :-) Sorry if I sounded a bit peeved here and there in asking all those questions. At
the time, I just thought, "Oh no! Here we go again with another scientific paper that makes me feel like an
idiot!" :-) (Any smart-aleck comments from anyone on the possible truth of that supposition will be met with
a rap on the knuckles with a No. 2 pencil. :-))
I have another question on gluten, and then another couple of generic questions about Paleodiet for anybody
here. First, Ron, based on wide reading in the field, I have had suspicions about the problematic role of
grains for some time, although I wasn't really sure, so it is great to see all the research you are doing going
into the whys and wherefores. So due to your and others' influences, I have been trying to cut back on grain
products recently, but I have a problem in that I am a distance runner, and I can't seem to get the oomph I
need without eating a certain amount of grains. I don't do what the running community calls "carbo-load"
(that is, stuff yourself with carbohydrates for fuel prior to tough workouts or races), but I *have* seemed to
find that my energy has better staying power during my runs if I eat some kind of bread at the meal prior to
my runs. Potatoes and such--another kind of carb--don't seem to do the trick as well. Also, too much fruit and
my blood-sugar reacts by getting pumped up but then nosediving. (I have pretty sensitive blood sugar due to
a past history of over-indulgence.)
My question is this: The breads I have been eating are all "sprouted"-type breads. I.e., either the very
moist/heavy "Manna"-brand breads (round loaves), or the types of sprouted bread like "Ezekiel bread" or
Shiloh Farms "7-grain" breads you can find in the health-food store. At first I was under the impression that
when they were sprouted, grains became gluten-free, but I have recently learned (I think) that this is an
illusion. Is it true that sprouted breads are just as problematic as those made from regularly processed and
milled grains?
Assuming the answer to that question is yes, or at least a qualified yes--well, then, what to do for someone
like me who has been dependent on them for energy? Perhaps I just need to experiment more, or commit to a
longer-term program of getting myself off grains, and maybe my energy for running wold eventually return
to normal levels. But just wondered if anybody here who is an endurance athlete had any practical
suggestions or examples from your own life specifically about how you made the transition.
Question number two: Recently I was talking privately with a Paleodiet researcher (who may or may not be
on this list yet, I don't know), who said the often-cited estimate of a ratio of 65% plant/35% animal foods for
humans during Paleolithic times has turned out to have been based on mistabulated ethnographic data. (As
far as I can tell, "ethnographic data" apparently meant that a database of modern hunter-gatherers
plant/animal-food eating patterns had been amassed, and was the basis for projecting back into the past what
the ratio may have been in prehistory, but I may be wrong in that interpretation.)
Anyway, with a corrected retabulation of the data, it is looking like the ratio of animal foods in Paleolithic
times would have been more like 50%, possible as high as 65%, ever since homo erectus 1.7 million years
ago. Also, the researcher said that muscle meats would have been the very *last* part of the animal to be
eaten, with the brains, organs, and bone marrow being far more highly prized.
12/298 (1997)
I found this a bit mind-boggling, mainly because of the practical implications for people trying to
approximate a Paleodiet today. Due to the way food animals are processed and put on sale today, you can't
even find brains or bone marrow, and precious few organs for the eating. This means--according to what I
understand--that in focusing mainly on muscle meats today, we are eating the lowest-grade portion of the
animal. And beyond that, there is the factor of cost: It would be cost-prohibitive for most people even in fully
economically developed countries to afford to eat 50% or 65% of their diet as meat--let alone be able to feed
the whole world this way. Even if the ratio were the lower 35% animal food, it would still be a tough row to
hoe for most people other than the economically well-off getting that much in our modern diets.
This obviously means we have to make some compromises--or at least intelligent substitutions--in trying to
achieve the nutrient profile obtainable from a truly Paleolithic diet. I have developed quite a taste for meat as
I have changed my diet to be somewhat more in conformity with what is known of the Paleolithic norm, but I
know it's nowhere close to what it could be. So my question is: what do those of you in the Paleodiet
research community do about your own diets, assuming you are trying to put into practice what you have
learned in your research? Is it really necessary to eat as high as 50-65% animal products for optimal health,
or is there perhaps a *range* of say 10 or 20% to 60% that for all practical purposes might get close to the
same results? And/or if not, are there other foods or supplements that might wisely be used to bridge the
gap?
Third question: The "caloric restriction" research community studying longevity in lower animals (and more
recently in primates) has found lifespans can be greatly increased in lower animals by restricting food intake
so as to lower the rate of metabolic wear-and-tear on the body. From what I know about it--which is not very
much--in addition to volume of food intake, the caloric restriction researchers have also seemingly
implicated protein, and specifically animal protein, as a factor that accelerates aging, and so they advise
minimizing its intake to the lowest prudent level. (To what they call "CRAN" or "CRON, " meaning
respectively, "caloric restriction with adequate nutrition" or "caloric restriction with optimal nutrition.") This
would seem to be at direct odds with current dietary advice in the Paleodiet community.
My question about this point is: Is focusing strictly on longevity inevitably at cross-purposes with fully
robust Paleolithic nutrition? Are there cost/benefits to the level of protein intake--or to anything for that
matter--so that it is folly to think you can have your cake and eat it too? That you have to weigh the pluses
and minuses and settle with the particular compromise that pleases you the most?
An example: From reports of people practicing caloric restriction, it seems that among other things one
experiences drastically reduced sex drive as well as muscularity--you get extremely skinny and--apparently, I
am surmising this--probably don't have very high sex hormone levels in view of the reduced sex drive many
seem to experience. (These just seem to be the actual results that people doing it experience.)
Anyway, let's assume caloric restriction in a modern protected lab environment might theoretically result in
increased longevity. Looking at the other side of the coin, would the characteristics of reduced sex drive and
decreased muscularity and physical prowess not have been counter-survival for the species in a rough-andtumble Paleolithic environment? I am myself not interested in doing caloric restriction, because I simply
don't feel my best nor enjoy life in the present without certain amounts of food and certain levels of animal
protein, but I do wonder if I might be sacrificing a bit of longevity. It's something I don't at all worry about,
but nevertheless it is an interesting question, I think.
Any comments from the researchers or anybody else on the list about any of this?
--Ward Nicholson
Wichita, KS
PALEODIET Archives
Subject: Stanislas Tanchou
From: Ray Audette
Date: Sun, 23 Mar 1997 21:57:51 -0800
Tanchou was the doctor who first recognized auto-immune diseases as a unique type of disorder. One of the
characteristics he listed for recoginizing such a "disease of civilization" was that they never appeared in wild
animal populations or in hunter-gatherers. This characteristic is shared by obesity, diabetes, cancer, etc.
The resulting 100 year search for auto-immune diseases among hunter-gatherers was documented by
Vilhjalmur Stefansson in his book "Cancer Disease of Civilization"(New York, Hill & Wang, 1960).
Stefansson is considered by many as the father of Paleolithic Nutrition. He adopted the Inuit diet in 1906 and
almost never ate vegetables again. He died in 1962 after writing his autobiography "Discovery".
13/298 (1997)
Perhaps the best synopsis of Stefansson's nutritional work is found in his 3 part article in Harpers Magazine
in the 1930s. Dean has a copy, perhaps he would post it.
Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition" http://www.sofdesign.com/neander
PALEODIET Archives
Subject: Staffan Lindeberg series in Harper's Monthly
From: Dean Esmay
Date: Mon, 24 Mar 1997 02:39:31 -0500
Indeed, the 3-part "Adventures in Diet" article by Stefansson is one of the treasures of my (very) modest
library. I would be happy to digitize it and run it through OCR software, but since the articles were published
in 1960 I believe they would still be covered under copyright law. I believe I would need permission from
either Harper's or Stefansson's estate to reprint it electronically. I've been meaning for some time to contact
Harper's, but I lack any kind of address for them.
PALEODIET Archives
Subject: Grains and primates
From: Ray Audette
Date: Tue, 25 Mar 1997 00:03:41 -0800
As pointed out in many sources, grains are not edible to any species of primate without technological
intervention. After all raw grain is essentially flour, water and fiber (in French - paper mache) and will cause
a bowel obstruction in any primate if eaten in sufficient quantities. As humans have only been eating grains
for about 350 generations, our primate immune systems recognize grain proteins as "foreign" and will
therefore mount a response to them. Auto-immune diseases such as cancer have shown a mathematical
correlation to grain consumption and indeed OSHA lists all grains as potential work place carcinogens.
Grains also inhibit digestion in primates by absorbing and eliminating many vitamins necessary to
metabolize natural foods. A good example of this is Pelegra, a vitamin deficiency disease caused by eating
corn - even though corn contains the very vitamin (nicotenic acid) whose deficiency causes the disease.
A good account of the effects of grain in ancient times can be found in Eades' "Protein Power" in the chapter
Curse of the Mummies. This tells of the thousands of autopsies performed on ancient Egyptians, who in spite
of eating what the "Battle Creek" nutritionalists would consider ideal, had higher obesity rates, heart disease
rates, and probability higher cancer rates given their short lifespans.
Ray Audette Author "NeanderThin: A Caveman's Guide to Nutrition" http://www.sofdesign.com/neander
PALEODIET Archives
Subject: Carbs and Proteins
From: Art De Vany
Date: Mon, 24 Mar 1997 17:02:00 -0800
I do agree with Dean Esmay's point regarding the excerpt from my in-progress book. Alas, simplification is
inevitable when one excerpts material from more lengthy and complex content. In emphasizing the relatively
low carbohydrate content of hunter-gatherer diets, and particularly the seemingly low glycemic indices of
their foods, I was mounting an attack on a good deal of modern diet advice and not giving the whole story.
The book will contain a discussion of the role of altered and foreign substances in the diet and their
connection to the Western Diseases, to the extent there is credible research on these subjects. Certain large
proteins do seem to be implicated in immune responses because they make their way to the lower intestine
where such responses are elicited.
I should like to put forth a proposition that seems to generalize and contain the key points of the many
models of Paleolithic living and modern living. It is this:
14/298 (1997)
The paleolithic pattern is multidimensional; it encompasses diet and activity, and it is not a steady state
pattern, but one of adaptation and novelty that accommodates variety of eating and activity patterns. Diet and
activity cannot be understood adequately unless they are part of an integrated model and analyses based on
averages are misleading. Averages are but one moment of the whole distribution on a single axis in the
multidimensional space and are falsely predicated on normal or bell-shaped distributions which living
organisms fail to follow [they follow power laws]. Averages and steady-state analyses can be highly
misleading in understanding a far-from-equilibrium living system. A multidimensional, dynamic model is
essential for understanding the complex, self-organized processes that are at work here.
Here is the maladaptation hypothesis within the dynamic framework. The paleolithic pattern is an attractor in
a multidimensional dynamic space and this attractor lies some distance from the modern pattern. The
distance between these two attractors is a measure of the degree to which paleolithic humans are maladapted
to modern life.
The implications of this view are far-reaching. The fat axis, protein locii, carb dimensions and so on are but a
few subspaces of this large dynamic pattern. Projecting complex patterns onto these simpler subspaces is
useful, but also can be highly misleading. Three or four macronutrient component models of diet can be
helpful, but are wholly inadequate for understanding human nutrition (that is why the paleo model is so
appealing). Diet is inadequate unless it is integrated with physical and cognitive activity.
Arthur De Vany
NeXTMAIL, SUN Mail & MIME welcome http://www.socsci.uci.edu/mbs/personnel/devany/devany.html
Department of Economics Institute for Mathematical Behavioral Sciences 3151 Social Science Plaza Irvine,
CA 92697-5100
PALEODIET Archives
Subject: Marathon food
From: Ray Audette
Date: Tue, 25 Mar 1997 00:22:59 -0800
> Is it true that sprouted breads are just as problematic as those made from regularly processed and
> milled grains? Assuming the answer to that question is yes, or at least a qualified yes--well,
> then, what to do for someone like me who has been dependent on them for energy? Perhaps I just
> need to experiment more, or commit to a longer-term program of getting myself off grains, and
> maybe my energy for running wold eventually return to normal levels. But just wondered if anybody
> here who is an endurance athlete had any practical suggestions or examples from your own life
> specifically about how you made the transition.
My ancestors, French Canadian fur traders performed a 9 month marathon every year when they paddled
their canoes 16 hours a day in order to reach B.C. and return to Quebec before the rivers froze. During this
time they ate nothing but pemmican. From my own experience, I can tell you that this is the paleolithic
energy food you are looking for. Pemmican is made from raw red dehydrated meat saturated with tallow (by
calories 80% fat). It is very energy dense, easily absorbed and will keep without refrigeration for 200-300
years. It contains all the nutrients and vitamins a human requires and can be eaten exclusively for long
periods of time. It is also ideal baby food being very close to human milk in its' nutritional components. My
son Gray-Hawk has eaten it every day since age three weeks.
PALEODIET Archives
Subject: Longevity
From: Ray Audette
Date: Tue, 25 Mar 1997 00:33:04 -0800
> Anyway, let's assume caloric restriction in a modern protected lab environment might theoretically
> result in increased longevity.
Actually, it's reduced body fat that produces this result. The correlation between thinness and lifespan is well
known in humans and led to these studies in rodents. Reducing calories is the only way most researchers
know to lower body fat.
15/298 (1997)
My co-author Troy Gilchrist (NeanderThin 6 years) and I (NeanderThin 12 years) recently had our body fat
tested at a health fair we exhibited at. His was 4.8% and mine was 5.2%. This puts us at the high end of the
longevity scale!
PALEODIET Archives
Subject: Kagnoff Speech
From: Don Wiss
Date: Tue, 25 Mar 1997 00:43:57 -0500
While again this was written for a celiac aware audience, it does get into the various proteins in the grains
that celiacs find toxic. Fits in with the recent discussion of grains versus the "gluten" grains. Don.
"Genetics and What's New in Research"
------------------------------------a talk by Martin F. Kagnoff, MD summarized by Jim Lyles
Dr. Martin F. Kagnoff is the director of the Laboratory of Mucosal Immunology at the University of
California at San Diego, and well-known for his research in celiac disease, particularly with respect to
genetic factors. He gave a talk at the 1995 CSA/USA conference on October 5, 1995, in San Francisco,
California. What follows are some highlights of Dr. Kagnoff's talk.
Celiac Disease (CD) is associated with small bowel damage, which occurs when a celiac eats gluten
containing foods. "Gluten" is something of a misnomer. Gluten really refers to the disease- activating
proteins in wheat, and we know there are similar, related, but somewhat different proteins in other grains that
activate CD as well. However, gluten-free (GF) has come to mean free of the grains which are toxic to
celiacs.
Nutrients are not absorbed properly in an untreated celiac, due to the damage in the small bowel. This results
in a wide spectrum of different symptoms.
When a celiac consumes gluten, the damage to the small intestine may be slight or it may be extensive. It
depends on how sensitive that individual is to gluten, and on how much gluten is consumed. However, it is
not just the small intestine that is sensitive to gluten; the entire digestive tract including the large bowel is
sensitive. In a study done several years ago, wheat was placed at the very bottom of the small intestine,
where celiac damage does not usually occur. This caused the type of damage that is characteristic of CD.
More recently, Mike Marsh has inserted gluten into the rectum to help in diagnosing CD. He has found that
inflammation and changes in the rectal lining occur in celiacs exposed to gluten in this fashion.
Dr. Kagnoff showed slides with the two extremes: normal, healthy villi with small crypts and completely
flattened villi with elongated crypts. He said that there are many in-between situations, where the villi are
only partly gone or partly damaged. A healthy small intestine has many folds, with villi on the folds, and
microvilli on the villi. Altogether, this provides a surface area equivalent to two regulation-size tennis courts;
this is about 600 times as large as the surface area inside piece of tubing the same size and length as the
small intestine. As the villi are damaged and the microvilli disappear in active CD, the absorptive surface is
greatly reduced. The severity of the symptoms varies depending on the amount of absorptive surface that has
been lost.
Another point to consider is: What do you absorb in your small intestine, and where? One of the common
symptoms of untreated CD is iron deficiency. Some celiacs had iron deficiency for years, but were not
diagnosed until other symptoms began to show up as well. Dr. Kagnoff has a set of twins as patients that
were diagnosed with iron deficiency at age seven, are short in stature, and wasn't until they were over 40 that
they developed symptoms such as bloating and diarrhea which finally led to a diagnosis of CD. The reason
this can happen is that iron is absorbed in the very top portion of the small bowel. If the villi damage is not
severe and limited to that area, then other nutrients are absorbed further down in the intestine and only iron is
malabsorbed. Another common problem with untreated celiacs is iron malabsorption coupled with calcium
malabsorption. After malabsorbing calcium for years these people are susceptible to bone fractures, but
really don't have that full-blown "picture" of CD which is the underlying cause of these fractures.
16/298 (1997)
As the small bowel lining becomes more damaged and abnormal, one starts to malabsorb fat-soluble
vitamins such as D, E, A, and K. As the disease progresses, water soluble vitamins start malabsorbing as
well. However, if the damage is limited to the first foot or so of the small intestine, full-blown malabsorption
may never occur as the remaining 20 feet or so if small intestine will continue to absorb nutrients normally.
However, in these cases iron absorption will be a continual problem as iron is only absorbed in the earliest
portion of the small intestine.
In CD genes, environmental factors, and the immune system all play a role. Dr. Kagnoff touched on all three
of these factors.
Environmental Factors
--------------------We all know that ingesting certain grains activates CD: wheat, rye, barley, and if taken in large enough
quantities, oats. There is some debate in some groups as to whether or not oats are toxic to celiacs. We know
that rice, corn, and sorghum are fine, as long as they are not contaminated by one of the toxic grains. When
you look at the plant ancestry, you find that wheat, rye, and barley all come from a common ancestor. If you
go up one more level, you find a point where oats also shares a common ancestor. These grains all have a
high content of some alcohol-soluble proteins that are called prolamins. (The content is somewhat lower in
oats.) These prolamins have a very high content of glutamine and proline, which are two amino acids.
When we talk about a gluten-free (GF) diet, what we are really talking about are these alcohol-soluble
proteins, which are named as follows:
Grain Proteins -----------wheat gliadins barley hordeins rye secalins oats avenins
Note that we are not talking about a single protein. A variety of wheat may have 40 different gliadins
encoded on multiple genes within the wheat. Some of the chromosome specialists years ago tried to engineer
wheat that would lack the gliadins that active CD; but there were so many different genes encoding gliadins,
on different chromosomes, that they soon realized it was an almost impossible feat.
Within the wheat gliadins, there have been studies to determine which part(s) of the gliadin activate CD.
Gliadins (and the corresponding proteins of the other three toxic grains) are proteins made up of many
different building blocks that are called amino acids. We've found that only a small part of these proteins is
needed to activate CD, about 12-15 of these amino acids; these are called gliadin peptides. Studies are being
conducted all around the world, and some sort of consensus is being reached as to which peptide sequence
activates a celiac response.
One particular wheat gliadin (alpha-gliadin) has been studied in more detail. Don Kasarda, of the USDA
research facility, and his group purified this protein, and others at the facility isolated the nucleotide and
peptide sequences for alpha-gliadin. Other groups around the world have also worked with this single
protein. What they've found is this protein has 266 amino acids, with over 60 glutamines and over 30
prolines. This is very unusual; most proteins have a fairly random scattering of amino acids.
Tests with celiacs using alpha-gliadin have been conducted to isolate the actual amino acid sequence that
triggers a celiac-type response. Groups in Norway and England have isolated the same sequence, which
MAY be the part of alpha-gliadin that activates the disease.
Genetic Factors
--------------Is CD a genetic disease? The answer is probably "yes"; susceptibility to CD is certainly genetic. Certain
genetic factors are required; without them you don't get CD. However, even with them you might not get the
disease, so CD is not entirely genetic.
Within families of celiacs, depending on which studies you read, the incidence among other family members
is between 2% and 15%. This is a relatively small number, but still far greater than the incidence in the
population at large. What really points to a very strong genetic association is the incidence in monozygotic
(identical) twins: Where one twin has CD, at least 70% of the time the other also has CD. The fact that this
incidence is not 100% is another indication that there are other factors besides genetics involved in CD.
Susceptibility to CD is associated with HLA genes encoded on the sixth chromosome. The HLA genes are
among the most diverse set of genes encoded in humans or other mammals. They determine and govern why
we are different from one another in terms of our immune system and how it reacts and responds.
17/298 (1997)
Celiacs nearly always have one of two HLA genes: DQ2 or DQ8. These genes are relatively common among
Caucasians of European descent, occurring in about 25% of the population. These genes are not found in
Japan or Africa among the blacks; consequently CD is virtually unheard of in these areas of the world. Most
people with these HLA genes don't get CD, so there is still more to this puzzle than we currently know.
About 95% of the celiac population carry the DQ2 gene, another 5% carry the DQ8 gene, and far less than
1% would carry anything else.
If a celiac and a sibling share the same HLA genes, there is a 20-40% chance that the sibling will develop
CD also.
There are some studies going on which are trying to induce something similar to CD in animals. Dr.
Kagnoff's group has just submitted one for publication in which they cloned DQ2 and other HLA genes and
put them into mice. They are beginning to look at how the mice respond to gliadin.
The Immune System
----------------In CD, two types of T-cells come into play. The first type is intraepithelial T-lymphocytes, which exist
between the epithelial cells. In active CD, one of the striking features is an increase in the number and
density of these intraepithelial T-lymphocytes. These T-cells were thought to be responsible for the villi
damage, but recent studies suggest that these cells actually help in the growth and development of epithelial
cells. The increase in these T-cells during active CD may be an attempt to maintain the normalcy of the
epithelial lining. In fact, when the gene responsible for these cells is deleted from mice, the epithelial lining
is totally abnormal.
The T-cells in the lamina propria are the ones responsible for the villi damage, by reacting to the presence of
gliadin. During this reaction the T-cells release cytokines, and it is the cytokines which appear to cause the
damage to the villi.
Diagnostic Tests
---------------CD can present with a broad array of symptoms. Often the symptoms are very subtle and appear to be far
removed from the small intestine. This makes diagnosing CD difficult in many cases.
The blood tests can be useful for screening. Three of the four antibody tests can be highly sensitive, but only
when there is fairly marked damage to the villi. These tests generally do not come back positive when the
damage is mild. Also, we have to take into account how often these tests give a false positive. For a while the
endomysial antibody was felt to be nearly 100% specific, i.e., no false positives. In recent years that number
has fallen off some, as there have been some false positives detected. The bottom line is: These tests are
good as a screening device and to monitor compliance with the GF diet, but they cannot be used in place of
the small bowel biopsy for diagnosing CD. Dr. Kagnoff does not believe these tests would be useful in
screening the population at large; they are most useful in screening those in whom there is some suspicion of
CD due to the symptoms.
Next we need to look at HLA Class II DQ gene typing tests. These can be useful in eliminating the
possibility of CD, as CD is virtually unheard of unless you have one of the two DQ markers we discussed
earlier. Of course, the converse is not true: The vast majority of those which DO have one of these markers
also don't have CD, so all you can say in that case is that CD remains a possibility.
The HLA typing tests are also useful in determining for the siblings of a celiac if CD can be eliminated as a
potential future concern.
At this point Dr. Kagnoff answered some questions from the floor:
Q: What is the risk of small bowel lymphoma?
A: There is good (but not definitive) evidence that the increase in lymphoma is related to not being on a strict
GF diet. For celiacs on a strict GF diet, the risk of small bowel lymphoma is not significantly greater than it
is for non-celiacs. The question is, how much gluten is okay? Dr. Kagnoff has detected inflammation in
biopsies of individuals who only eat a small amount of gluten. We know from other malignancies that
ongoing inflammation is associated with increased risk.
On the other hand, the overall risk is still very small, even in studies where people with active CD have eaten
gluten for 30, 40, or 50 years. The risk is real, but the risk of an earthquake in California is probably higher.
However, I still recommend that celiacs maintain as GF a diet as they can.
Q: What is the risk of colon cancer in celiacs?
A: There is no evidence that there is an increase risk of colon cancer in celiacs. The increase in risk, which is
small, refers to cancers in the mouth, esophagus, oral pharynx, lymphoma of the small bowel, and cancer of
the small intestine (which is very rare, even in celiacs). There is no increased risk elsewhere.
Q: What is the possibility of developing a GF grain of wheat?
18/298 (1997)
A: Very unlikely. By the time you eliminated all of the gliadin-related genes from wheat, I'm not sure there
would be much left.
Q: Are you born with CD, or can it "develop" at any age?
A: First it must be triggered by some event in the environment, such as a certain kind of flu, stress, etc. Then,
once it is triggered, you continue to have the disease for the rest of your life.
PALEODIET Archives
Subject: Re: Glutenous Grains
From: Bob Avery
Date: Tue, 25 Mar 1997 03:21:05 EST
Dean or Ron or anyone,
It is common practice in the natural foods community to consume the juice of sprouted wheat and barley
grass. The grains are planted and allowed to sprout until they produce a short grass a few inches tall. The
grass is harvested and put through a juicer. The resulting juice is drunk as is (raw) or mixed with other raw
vegetable juices.
Do any of you know whether the proteins in these grasses are objectionable from the celiac patient's
perspective, or is their nutrient profile sufficiently different from that of the grains themselves so as not to be
a concern as regards "gluten" toxicity?
Bob Avery
PALEODIET Archives
Subject: Dairy products in the diet and evolution
From: John Allen
Date: Tue, 25 Mar 1997 14:11:05 UTC+1200
Dean Esmay (I believe) raised this point in a previous message:
> One might also wonder about dairy. I know of no evidence that the ancestral human diet would ever
> include dairy. In fact, although I eat dairy products myself, you could argue that the consumption
> of dairy is just about the most bizarre thing that modern humans do. Dairy products contain
> lactose, and compellingly, about 75% of the world population is lactose-intolerant. But lactose
> isn't the only foreign substance; casein is also in all dairy products, and is another substance
> which would be foreign to the human digestive tract, and which appears to cause at least some
> individuals problems. I know of no rigorous evidence that casien is a major danger, but it does
> seem logical to posit that substances unique to foods that would never have been eaten by humans
> in nature should be looked at with suspicion.
With Susan Cheer, I have recently published a paper in Current Anthropology called "The non-thrifty
genotype" (37:831-842, 1996), in which I provide a somewhat heterodox view of the Thrifty Genotype
concept and attempt to link lactose tolerance and use of dairy products to the issue of why European-derived
populations appear to be virtually unique in not possessing the Thrifty Genotype. Lactose is a simple sugar,
and those were (are) unusual in hunter-gather diets. In addition, the proteins in milk are evidently insulin
secretogogues, thus the insulin response to lactose in milk is much greater than to lactose alone (ie, mixed in
a solution of water). Anyway, I have tried to make a consistent evolutionary story about these facts and a few
others. The most fundamental observation raised in the paper is that populations with high lactose tolerance
rates have low rates of Type II diabetes; the relationship is quite a strong one despite all the other factors that
one would think would be involved.
If anyone would like a copy of the article, just send me an e-mail.
Cheers, John Allen
**********************************************************
Dr John S Allen Department of Anthropology University of Auckland Private Bag 92019 Auckland, NEW
ZEALAND 64-9-373-7599, Ext 8574 (office) 64-9-373-7441 (fax)
PALEODIET Archives
Subject: Re: Kitava
19/298 (1997)
From: Staffan Lindeberg

Date: Tue, 25 Mar 1997 19:00:45 +0100
Dean wrote:
> However, it seems quite possible that dietary carbohydrate might be a red herring, or a smaller
> ingredient than it is sometimes regarded as. The first thing to make me realize this was Staffan
> Lindeberg's studies on the Kitava (and Lindeberg is also a member of this listserv, BTW). If you
> wish I am Staffan to any of you. The Kitava are not hunter/gatherers, but are not exactly
> agriculturalists either; they would best be defined as primitive horticulturalists, as they mostly
> cultivate wild plants ...
Their staple crops are tubers: yam, sweet potato, taro, and tapioca.
> ... and do not grow or consume cereal grains (and if I'm not mistaken, do not eat dairy either).
Correct. 70% of the daily energy intake in a Western society like Sweden is provided by foods which are not
eaten in Kitava and which were unavailable during human evolution, namely dairy products, oils, margarine,
refined sugar and cereals.
Table 1. Estimated dietary intakes (daily medians) in Kitava.
------------------------------------------------------By weight Protein Fat Carbohydrate Energy (g) (g) (g) (g) (kJ)
------------------------------------------------------Tubers 1200 25 2 300 5600 (Yam, sweet potato, taro)
Fruit 400 3 <1 50 920 Coconut 110 4 43 7 1865 Fish 85 17 4 0 445 Other veg. 200 5 <1 14 360 Western
food <1 0 <1 <1 20
Total 2 000 54 50 370 9200
------------------------------------------------------> Their diet is relatively high in carbohydrate and somewhat low in fat, although saturated fat
> intake is fairly high.
It is high in saturated fat from coconut (not coconut oil which is devoid of fiber and minerals).
Table 2. Estimated dietary macronutrient composition expressed as per cent of total energy in Kitava, among
the general Swedish population, and as recommended to general western populations (Recommended dietary
allowances, RDA].
------------------------------------------------------Kitava Sweden RDA
------------------------------------------------------Total fat 21 37 30 -Saturated 17 16 <10 -Monounsaturated 2 16
> 10 -Polyunsaturated 2 5 5-10 Protein 10 12 10-15 Carbohydrate 69 48 55-60 Alcohol 0 2?
------------------------------------------------------> About 80% of them smoke cigarettes on a daily basis, and while they are physically active, they
> are only somewhat moreso than most Westerners. Yet their rates of obesity, diabetes, stroke, and
> heart attacks are vanishingly small. (I don't know if Lindeberg and his team ever looked for
> rheumatoid arthritis or cancer, two common autoimmune diseases typical to civilization. Perhaps he
> can tell us that himself.)
1. In our survey, protracted illness during several months or more was practically unknown, as were
successively growing visible tumours. One of the few exceptions was an elderly man who was reported to
have had an ulcer at the front of the lower part of one leg, and to have become ill and died after several years.
This case was known to the majority (and was presented almost identically by the different groups across the
island). One man had heard of an old lady who had had a growth at one of her breasts and who had died
within a rather short time. Another man aged 67, a betel-chewer but non-smoker, suffered since several
months, possibly years, from a dry, non-tender ulcer at the hard palate, which was examined by me. No other
case corresponding to superficially growing malignancies was known in Kitava.
20/298 (1997)
Comments: The ulcer of the hard palate was obviously an oral carcinoma, which has been the most common
malignancy among males in PNG [Wallington, 1986 #3676; Atkinson, 1964 #3294; Henderson, 1979
#3296], and which, since Kitavans are all betel chewers, is probably caused by the highly alkaline lime
component of the betel quid [MacLennan, 1985 #3295; Thomas, 1992 #3570; Boyle, 1990 #1581; Nair, 1990
#1580; Prokopczyk, 1991 #1576; Stich, 1991 #1578; Nishikawa, 1992 #1573; Sharan, 1992 #1570;
Sundqvist, 1992 #1662]. The man with a reported leg ulcer probably had a tropical phagedenic ulcer, which
are common in the area (J=FCptner H, personal communication) and in which squamous cell carcinomas
(cancer) occasionally develop [Meyer, 1991 #3293]. In sub-Saharan Africa, malignant change in poorly
treated tropical ulcers account for up to 10% of all malignant tumours in some groups [Ziegler, 1991 #3362].
Until the last 10-20 years, women have most of the time been stripped above their hips, and even today the
majority freely uncover their breasts. Nevertheless, Kitavans were unaware of superficial tumors, with the
possible exception of one reported woman who may have had breast cancer. J=FCptner, however, observed
one case during his five years in the 1960s as the only general practitioner (serving 12, 000 people) in
Kiriwina, the main Trobriand island. This was in a pregnant woman, whose mother and mother-in-law
refused to have her operated, and who developed enlargement of supraclavicular lymph nodes and died
within few months. It thus seems justified to consider breast cancer to be less common in the Trobriand
Islands than in the USA [Seidman, 1985 #3345]. In contrast, J=FCptner, who was a trained gynecologist,
diagnosed more than 10 cases of ovarian cancer among 12, 000 inhabitants in 5 years, which is a higher
incidence than in the USA (p<0.008) [Heintz, 1985 #3297] or as compared to the rest of Papua New Guinea
(p<0.02) [Mola, 1982 #3298]. It is tempting to speculate that the high intake of saturated fat from coconut
may be an explanation, since milk, an important source of saturated fat in westerners, has been suggested to
cause ovarian cancer [Rose, 1986 #3581; Mettlin, 1990 #3576], although much of the debate has concerned
lactose rather than saturated fat [Mettlin, 1991 #3579; Cramer, 1991 #3580; Harlow, 1991 #3583].
J=FCptner found no case of cervical carcinoma (the most common gynecological cancer in PNG [Mola,
1982 #3298]) and no other malignancies, but he made very few autopsies. The absence of growths
corresponding to lymphoma is thus confirmed by J=FCptner. Burkitt's lymphomas are fairly common in
those coastal areas of PNG where malaria transmission is intense [Henderson, 1979 #3296].
2. As to other non-communicable diseases, accidents were reported to be a fairly common cause of death,
and most cases had drowned or fallen from coconut trees (One 70-year-old non-attending man died after
falling from one tree during our expedition). Five of those who were older than 85, and who declined to
participate, referred to their aching legs, and four of them suffered from stiffness and pain of hips and/or
knees. Two of them had enlarged circumferences and flexion contractures of the knees, suggestive of chronic
arthritis. One case of severe emphysema in an elderly male smoker was encountered, but milder cases may
well have been present. Two cases of dementia were noted, most certainly due to mental retardation. Both
subjects were younger than 30 years. All the elderly seemed mentally well preserved. No case of severe
personality disorder was noted, although during an earlier visit on the island a man aged about 30 was seen
who was highly suspected of suffering from schizophrenia. (In Kiriwina I also met a man with obvious latent
psychosis. Incidentally, he had been separated from his parents as an infant.)
The majority of Kitavans were, on gross inspection, and by the brief discussions during the initial selection
procedures, in excellent condition. Starvation had not been experienced except for one month around 1927.
Food was abundant and considerable amounts were wasted. Many children aged 2-7 years had large
abdomens, but all appeared healthy. No evidence of malnutrition was found. Estimated protein intake in
adults averaged 55 g per day.
Comments: Accidents are expected to be common [Barss, 1984 #1613], and the same is true for infectious
arthritides [Theis, 1991 #3328]. There is more uncertainty regarding primary osteoarthritis, which is reported
to be extremely rare in Japan [Nakamura, 1987 #3329]. According to Theis, "primary osteoarthritis of the hip
is rarely seen among Chinese and [Asians] Indians, whereas the same condition is very common in the knee"
[Theis, 1991 #3328]. Osteoarthritis, which apparently is not primarily an inflammatory disorder, obviously
affects humans irrespectively of their lifestyle although unphysiological tearing may worsen it [References
below]. J=FCptner diagnosed a few cases of symmetric polyarthritis, primarily affecting the knees and
occasionally the joints of the hand. This MAY indicate the presence of rheumatoid arthritis, but other causes
are perhaps more likely.
21/298 (1997)
Among the most probable causes of the large abdomens are firstly intestines distended by voluminous foods
or by worms (Ascaris in particular) [Schwartzman, 1991 #3349; Barnish, 1992 #3348] and secondly
hepatosplenomegaly (enlarged liver and spleen) from chronic malaria [Strickland, 1991 #3351; Cattani, 1992
#3350]. Protein-energy malnutrition or vitamin deficiency has neither been diagnosed nor suspected by my
colleagues J=FCptner, Schiefenh=F6vel and Kame among Trobriand Islanders (personal communications).
In contrast, Stanhope reported, on the basis of government medical protocols and interviews of former
medical officers, two deaths from malnutrition among 17 deceased children between 1962 and 1967, and
suggested that "in bad yam seasons, malnutrition appears in [Kiriwina] inland villages and vitamin A
deficiency has been reported" [Stanhope, 1969 #1053]. On Kitava, however, there are no inland villages.
There is some evidence indicating that infection of Ascaris lumbricoides may cause stunting and possibly
even impaired vitamin A status in developing countries [Solomons, 1993 #3682], where carotene intake,
however, would be lower than in the Trobriands. The estimated protein intake in adults is expected to be
sufficient [Garlick, 1993 #3460].
According to J=FCptner, retained placenta was the most common cause of maternal death in the 1960s.
Chronic bronchitis and asthma are prevalent in PNG even in non-smokers [Anderson, 1992 #3352]. Further
comments on non-communicable diseases are best avoided at this stage.
In conclusion, accidents are thus common causes of death in Kitava. Malnutrition is virtually non-existent.
Whether non-communicable diseases other than cardiovascular disease (CVD), cancer and malnutrition are
uncommon cannot be assessed from the present findings.
> Genetics
> does not seem to be the explanation, either.
Substantial evidence from other surveys indicates that you are right, Dean, although the significance of
genetic factors for the virtual absence of CVD was not possible for us to study properly, since the
environment was essentially similar to all Kitavans and since both environment and ethnic descent differed
between Kitava and Sweden. The only migrant available to us, a man aged 44 who had grown up on Kitava
and who was now a businessman in Alotau, the provincial capital, came for a visit during our expedition. He
differed in several aspects from all other adults regardless of sex: he had the highest diastolic blood pressure
(120/92), the highest body mass index (28.0), the highest waist to hip ratio (1.06) and the highest PAI-1
activity (possibly indicating decreased clot-resolving capacity). The most obvious difference in his lifestyle,
as compared with non-migrant Kitavans, was the adoption of western dietary habits.
Although this finding is suggestive, one subject is not much to comment upon, but some general remarks
may be relevant. The risk of developing hypertension (high blood pressure), obesity, diabetes or CVD in
response to a certain environment undoubtedly differs between humans. Within western populations, familial
heritage apparently is a strong determinant of some cardiovascular risk factors. For instance, fibrinogen
seems largely to be determined by genetic heritability, which in one study explained an estimated 50% of the
variation of fibrinogen, while the combined effect of obesity and smoking accounted for only 3% [Hamsten,
1987 #3078]. =46urthermore, genetics may influence the risk of CVD on the population level, as in some
Pacific Islanders who seem to develop diabetes more easily than other ethnic groups after westernization
[King, 1992 #3749; Zimmet, 1979 #1020], and the same may be true for Maoris in New Zealand [Prior, 1974
#1032]. Even the higher CVD rates among blacks in the US [Gillum, 1982 #3374] or Asian Indians in the
UK [McKeigue, 1989 #3448] may hypothetically be due to lower resistance to the Western life style. The
prevalence of inherited disorders such as familial hypercholesterolemia may exert some influence on overall
death rates, for instance in South African whites [Rossouw, 1984 #430].
However, the environment is obviously more important to explain the vast differences in extent of coronary
atherosclerosis or occurrence of CVD and diabetes that have been found in cross-cultural surveys, migrant
studies and observations of secular trends [Tejada, 1968 #1835; Solberg, 1972 #3740; Trowell, 1981 #2064;
Keys, 1980 #3159; Prior, 1974 #1032; INTERHEALTH Steering Committee, 1991 #919; O'Dea, 1992
#1538; Dyerberg, 1989 #1637; Kevau, 1990 #1454; Hughes, 1986 #3449; World Health Organization, 1992
#3759]. It is reasonable to assume that environmental factors may actually be necessary requirements for the
development of CVD, and that cross-cultural differences only to a minor degree are explained in terms of
population genetics. Papua New Guinea is no exception, as is evident from the increasing number of
myocardial infarctions and diabetics in urbanized populations [Kevau, 1990 #1454; King, 1985 #3646]. As
yet there are no scientific reports on CVD rates in migrants from the Trobriand Islands. Sporadic interviews
that I made in Kiriwina indicate that at least one overweight Trobriander in Port Moresby may have been
struck by spontaneous sudden death.
22/298 (1997)
Genetics and environment as causes of CVD are not mutually exclusive [Smith, 1992 #3665]. Or, as it has
been put, "the answer to 'Why does this particular individual in this population get this disease?' is not
necessarily the same as the answer to 'Why does this population have so much disease?'" [Rose, 1985
#3645]. The two approaches are not in academic competition (they only compete for funding).
Conclusion: The findings in the only studied migrant suggest that Kitavans are not protected from
hypertension or androgenic obesity when exposed to western dietary habits. This would be consistent with
the emergence of obesity, diabetes, hypertension and IHD in Melanesia and other parts the Pacific.
I am sorry for the long answer.
Staffan Lindeberg
REFERENCES ON OSTEOARTHRITIS
Alexander, C. J. (1994). "Utilisation of joint movement range in arboreal primates compared with human
subjects: an evolutionary frame for primary osteoarthritis." Ann Rheum Dis 53(11): 720-5.
Beighton, P. and L. Solomon (1981). Arthritides in the negroid peoples of southern Africa. Western
Diseases: their Emergence and Prevention. Cambridge, Mass, Harvard University Press. 83-92.
Bridges, P. S. (1991). "Degenerative joint disease in hunter-gatherers and agriculturalists from the
Southeastern United States." Am J Phys Anthropol 85(4): 379-91.
Cohen, M. N. and G. J. Armelagos, Ed. (1984). Paleopathology at the origins of agriculture. London,
Academic Press.
Crawford Adams, J. and D. L. Hamblen (1995). Outline of orthopaedics. Edinburgh, Churchill Livingstone.
Nelson, D. T. (1993). "The course of osteoarthritis and factors that affect it." Rheum Dis Clin North Am
19(3): 607-15.
Nelson, D. T., M. T. Hannan, et al. (1991). "Occupational physical demands, knee bending, and knee
osteoarthritis: results from the Framingham Study." J Rheumatol 18(10): 1587-92.
Hoaglund, F. T., C. S. Oishi, et al. (1995). "Extreme variations in racial rates of total hip arthroplasty for
primary coxarthrosis: a population-based study in San Francisco." Ann Rheum Dis 54(2): 107-10.
Holm, S. (1993). "Pathophysiology of disc degeneration." Acta Orthop Scand 64 (Suppl 251): 13-5.
Joosab, M., M. Torode, et al. (1994). "Preliminary findings on the effect of load-carrying to the structural
integrity of the cervical spine." Surg Radiol Anat 16(4): 393-8.
Jumah, K. B. and P. K. Nyame (1994). "Relationship between load carrying on the head and cervical
spondylosis in Ghanaians." West Afr J Med 13(3): 181-2.
Jurmain, R. D. and L. Kilgore (1995). "Skeletal evidence of osteoarthritis: a palaeopathological perspective."
Ann Rheum Dis 54(6): 443-50.
Kraemer, J. (1995). "Natural course and prognosis of intervertebral disc diseases. International Society for
the Study of the Lumbar Spine Seattle, Washington, June 1994." Spine 20(6): 635-9.
Lane, N. E. (1995). "Exercise: a cause of osteoarthritis." J Rheumatol Suppl 43(3): 3-6. Lane, N. E. and L. B.
Kremer (1995). "Radiographic indices for osteoarthritis." Rheum Dis Clin North Am 21(2): 379-94.
Langeland, M. and F. Lingaas (1995). "Spondylosis deformans in the boxer: estimates of heritability." J
Small Anim Pract 36(4): 166-9.
Nakamura, S., S. Ninomiya, et al. (1989). "Primary osteoarthritis of the hip joint in Japan." Clin Orthop 111:
190-6.
Osti, O. L. and D. E. Cullum (1994). "Occupational low back pain and intervertebral disc degeneration:
epidemiology, imaging, and pathology." Clin J Pain 10(4): 331-4.
Panush, R. S. (1990). "Does exercise cause arthritis? Long-term consequences of exercise on the
musculoskeletal system." Rheum Dis Clin North Am 16: 827-36.
Rauschning, W. (1993). "Pathoanatomy of lumbar disc degeneration and stenosis." Acta Orthop Scand 64
(Suppl 251): 3-12.
Rogers, J. and P. Dieppe (1994). "Is tibiofemoral osteoarthritis in the knee joint a new disease?" Ann Rheum
Dis 53(9): 612-3.
Roos, H., M. Ornell, et al. (1995). "Soccer after anterior cruciate ligament injury--an incompatible
combination? A national survey of incidence and risk factors and a 7-year follow-up of 310 players [see
comments]." Acta Orthop Scand 66(2): 107-12.
Swanepoel, M. W., L. M. Adams, et al. (1995). "Human lumbar apophyseal joint damage and intervertebral
disc degeneration." Ann Rheum Dis 54(3): 182-8.
van Saase, J. L. C. M., L. K. J. van Romunde, et al. (1989). "Epidemiology od osteoarthritis: Zoetermeer
survey. Comparison of radiological osteoarthritis in a Dutch population with that in 10 other populations."
Ann Rheum Dis 48: 271-80.
23/298 (1997)
Videman, T., S. Sarna, et al. (1995). "The long-term effects of physical loading and exercise lifestyles on
back-related symptoms, disability, and spinal pathology among men." Spine 20(6): 699-709.
PALEODIET Archives
Subject: Re: Glutenous Grains
From: Don Wiss
Date: Tue, 25 Mar 1997 19:51:09 -0500
Bob Avery asked:
> It is common practice in the natural foods community to consume the juice of sprouted wheat and
> barley grass. Do any of you know whether the proteins in these grasses are objectionable from the
> celiac patient's perspective, or is their nutrient profile sufficiently different from that of the
> grains themselves so as not to be a concern as regards "gluten" toxicity?
This is what a leading US wheat protein expert has to say:
Date: Tue, 12 Dec 1995 16:15:38 PST Sender: Celiac/Coeliac Wheat/Gluten-Free List From: "Donald D.
Kasarda" Subject: Re: Query: sprouted wheat
Jules Levin asked:
> I just purchased an antioxidant from a health-food store, called "BIOGUARD". The label reads:
> "Bioguard is composed entirely of hydroponically grown wheat sprouts. Hypoallergenically free of
> wheat gluten and yeast."
Reply from Don Kasarda, Albany, California
Most sprouted wheat still has gluten or gluten peptides remaining. Although the sprouting begins enzymatic
action that starts to break down the gluten (a storage protein for the plant) into peptides and even amino
acids. Generally this is not a complete process for sprouts used in foods so some active peptides (active in
celiac disease) remain. I don't know anything about Bioguard specifically, but I would be cautious about it
until the company can say on what basis they are claiming "gluten-free." For example, how have they tested
this?
PALEODIET Archives
Subject: Re: Plant foods in paleodiets
Date: Wed, 26 Mar 1997 03:16:14 +0100
Ward Nicholson wrote:
> Recently I was talking privately with a Paleodiet researcher (who may or may not be on this list
> yet, I don't know), who said the often-cited estimate of a ratio of 65% plant/35% animal foods for
> humans during Paleolithic times has turned out to have been based on mistabulated ethnographic data.
This is a very important debate for all of us in order to know whether there is evidence of an optimal balance
of macronutrients (carbohydrate, fat and protein) for humans.
Let us start with asking what edible items were found in the African savanna, items which all contemporary
humans are expected to be adapted to. How much vegetable foods were available? I fear that we may only be
able to get learned guesses even from quarternary biologists and paleoclimatologists (do we have any on this
list?) but I am not sure. Incidentally I asked one today and I will forward the question to a couple of more of
them (Raymonde Bonnefille, Rachid Cheddadi, Daniel Livingstone and Jim Ritchie; Any other
suggestions?).
It has been put forward e.g. by Brand Miller (Brand Miller JC, Colagiuri S. The carnivore connection:
dietary carbohydrate in the evolution of NIDDM. Diabetologia 1994; 37: 1280-6) that human diet was low in
carbohydrate from the time of H. habilis up to sapiens leaving Africa, allegedly because dry climates during
the Ice Ages would result in grasslands being the main edible plants instead of roots and fruits.
I know at least two subscribers to our list who have well founded opinions on this matter: Loren Cordain and
John Allen. I hope both will give us their view.
Staffan Lindeberg
24/298 (1997)
PALEODIET Archives
Subject: Re: Our own diet
Date: Wed, 26 Mar 1997 03:20:38 +0100
Ward Nicholson wrote:
> So my question is: what do those of you in the Paleodiet research community do about your own
> diets, assuming you are trying to put into practice what you have learned in your research?
A typical day my lunch and dinner is meat or fish with plenty of tubers and vegetables including pulses.
Recently I eat less potatoes. For breakfast and in between meals I take fruits and nuts. I eat hardly any dairy
products, margarine, refined sugar or cereals. We add some rape-seed oil by cooking. My salt intake is below
30 mmol/24 hours compared to 100-250 for most Westerners and 1 (one) for the Yanomamo indians of the
Amazon. When in 1987 I started following this programme at the age of 37 I lost 9 kg of weight and
regained the weight of my youth (65 kg, BMI 20.5). My serum cholesterol dropped from 5.2 to 3.7 mmol/L
(201-143 mg/dL) and my blood pressure went from 130/82 to 120/65 in 6 months (9 measurements,
p=3D0.004).
> Is it really necessary to eat as high as 50-65% animal products for optimal health, or is there
> perhaps a *range* of say 10 or 20% to 60% that for all practical purposes might get close to the
> same results?
Good question. I would say the latter.
> And/or if not, are there other foods or supplements that might wisely be used to bridge the gap?
Probably not needed for you and me. Not without risks either.
Staffan
PALEODIET Archives
Subject: Re: Grains and primates
From: Don Wiss
Date: Wed, 26 Mar 1997 13:03:02 -0500
Ray Audette wrote:
> As humans have only been eating grains for about 350 generations,
Ray,
How long is a generation? If we exclude the longer rice eating Asians and stick with grain growing, we have
10, 000 years for people in the Near East, down to 5, 000 years for much of Europe, and less than 2, 000 for
some very far from the grain start. So it could be a lot less than 350. Maybe better presented with a range of
generations depending on where your ancestors are from.
I'm taking my numbers from this article:
Lutz, W.J., "The Colonisation of Europe and Our Western Diseases", Medical Hypotheses, Vol. 45, pages
115-120, 1995
I have a text version of the article that I can e-mail, but can't make available on the web or a list for copyright
reasons. It lacks exhibits so the real article is better. If you want this copy, please don't reply to this message
but e-mail me at
Don.
PALEODIET Archives
Subject: Re: Hunting on the Grasslands
From: Ray Audette
Date: Wed, 26 Mar 1997 21:57:58 -0800
As a hunter-gatherer who hunts every day on the grasslands in and around Dallas, Texas, I can tell you that
there is not much vegetable food to be had. Besides a few berries, nuts and edible roots found around the
creek beds which can be eaten only seasonally there is not much but grass. As grass is not edible to any
species of primate I must eat large amounts of game.
25/298 (1997)
The fat content of my diet depends on the game caught and thus the method used to hunt. My own method
uses no weapons as this is illegal within the city limits. Using only my Harris Hawk, I take rabbits, hares,
squirrels, ducks, geese, pheasant and quail. I never stay out longer than 1.5 hours and have about an 80%
success rate. I often feel (especially on the bad days) that I could do nearly as well only throwing rocks. As
all of these with the exception of the waterfowl (the most difficult to catch) are very low in fat eating only
what I could hunt and gather in this way would prove difficult. I would probably suffer from what the Inuit
call rabbit starvation.
Large game that has good fat reserves will require that I employ a weapon. At close range, a sharp stick will
kill any animal (many states in the U.S. allow hunting bear with spears). Getting close enough to use this
sharp stick is the problem even if it is propelled by a bow or spear-thrower. Using this method, I could still
surprise the occasional cow (or buffalo in the old days) at the watering hole and obtain enough fatty meat to
survive. As rustling is still considered very serious in Texas I don't regularly do this!
To take large game, I need dogs! Alone with a pack of dogs, I can out-hunt a dozen men armed only with
spears or bows or a pack of wolves. The dogs will bring the game to me. As the dogs will hold the animal at
bay, I run a lot less chance of injury (those horns hurt-ask any Texas cowboy) and can even employ a bow or
spear-thrower and further reduce my risk. When mankind teamed up with dogs through their mutual
neotenazation during the Mesolithic era, fatty large game became the food of choice. As wolves are
temperate creatures and lack our efficient cooling system, this symbiosis was most efficient in cooler
climates. Some have postulated that this resulted in the extinction of many species of large fat bearing
mammals (mammoths, ground sloths, wooly rhinos, etc.)and the predators who depended on them. In the old
world this neoteny took many thousands of years to fully develop. This extinction in the new world had to
wait for these hunting teams to arrive over the land bridge, but once they arrived it happened much faster.
Once the fattest large game was hunted to extinction, mankind began to associate with domesticated (ie
neotenized) animals who also carried fat reserves such as cows, pigs and sheep. When the limits of this
pastoral lifestyle were met the result was the Neolithic Revolution and current eating habits.
PALEODIET Archives
Subject: Message from Loren Cordain re: misc issues
From: Dean Esmay
Date: Wed, 26 Mar 1997 22:41:20 -0500
Loren is having a little trouble with his mail software. I'm working with him to solve this issue but in the
meantime here is a response he has written to various things that have been discussed this week. With luck
any further comments can come from him directly.
Dean
--[begin Dr. Cordain's letter]--Greetings! I have enjoyed reading the paleodiet digest to date but have been somewhat reticent to make any
comments simply because of my unfamiliarity with the format. Thanks to some helpful hints from Dean, I
hope that this message makes it through.
Both Staffan and Ward have commented upon the macronutrient content of preagricultural diets and Staffan
has suggested that I provide my input. What follows is a portion of a message that I have previously sent to
Staffan.
26/298 (1997)
Although Richard Lee (1) and others have suggested that the average macronutrient content of all world
wide hunter gatherers was derived from a subsistence pattern of 35% animal food and 65% vegetable food, it
has been shown that these figures are likely erroneous (2). Lee derived his macronutrient percent estimate
from compiled data from the Ethnographic Atlas (3), however it has been shown that he distorted the original
data by reducing the number of North American cases and by reclassifying shellfishing into a gathering
activity (2). A re-analysis of the data in the Ethnographic Atlas shows results much different from those
which Lee originally presented. Indeed for most (77%) of the societies listed in the Ethnographic Atlas,
gathered plant food contributes less than half the calories (2). Leonard et al. (4) in an analysis of 5 recently
and carefully studied hunter gatherer groups (!Kung, Ache, Hiwi, Inuit and Pygmies) has shown the mean
value for energy intake from animal food sources to be 59%. Leonard et al.'s (4) data include Lee's analysis
of the !Kung diet which contains 33% of its calories from animal food. However, careful analysis of the
!Kung diet shows that of their daily intake of 2, 140 calories, only 190 calories were derived from plant
foods other than mongongo nuts. Because of the close proximity of an enormous mongongo nut forest, it is
likely that the !Kung data is not representative of a typical hunter-gatherer. Since vegetable food is virtually
unavailable to the Inuit, who obtain 96% of their caloric intake from animal food, this data is also
unrepresentative of the typical hunter gatherer. An average value for the Leonard et al. (4) data without these
two extreme values would show that 56% of the calories were derived from animal foods. In her classic
study of Australian Aborigines temporarily reverting to a hunter-gatherer lifestyle, O'Dea (5) showed that
animal foods contributed 64 % of the total energy (6). The macronutrient breakdown was 54 % protein, 33%
carbohydrate and 13% fat (6). These values are significantly different than those now almost universally
accepted by my friend and co-author, Boyd Eaton et al. (7) of 34.2% protein, 44.3% carbohydrate and 21.5
% fat.
Clearly, the carbohydrate content of the average paleolithic diet varied according to geographic location,
latitude and season; however in aggregate, it almost certainly was significantly lower than the 55%
carbohydrate recommended by the American Heart Association Diet. Except for seasonal occurrences of
honey and dried fruit, its carbohydrates were rich in fiber and of a low glycemic index. The paleolithic diet
was devoid of starches from cereal grains, and starches from legumes and tubers generally contributed fewer
calories than those from animal derived foods. Prior to the regular use of fire, many tubers almost all
legumes would have been unavailable for consumption because of their high antinutrient load (8). Since
animal sources almost always contributed the majority of total daily calories (an average value would
probably be between 55-65%), it is unlikely that the carbohydrate content could have regularly exceeded
40% and under most circumstances was probably between 30-35%. As humans moved into more extreme
latitudes (40-45degrees N or S), carbohydrates would have contributed even fewer than 30-35% of the total
calories, particularly during winter or early spring. So, with this enormous caloric intake derived from animal
foods, how can the seeming paradox of low serum cholesterol (and presumably reduced risk from coronary
heart disease), observed in virtually all hunter gatherers, be explained? Recent studies by Wolfe and coworkers (9, 10, 11) have shown that isocaloric replacement of carbohydrate with animal derived protein
improves all lipid profile indices including total CHOL, HDL, LDL and VLDL. A high protein diet similarly
improves virtually all indices of type II diabetic control and symptoms of Syndrome X (5) whereas low fat,
high carbohydrate diets have been repeatedly shown (in tightly controlled dietary kitchen studies) to worsen
HDL, VLDL, triglyceride and total CHOL/HDL ratios (12, 13, 14).
On another unrelated matter, I have received notification that many scientific journals including NEJM will
now refuse to publish any material which has appeared previously on the Internet. Consequently, I think that
as scientists and authors, it is important that we use this forum to share ideas and thoughts on the paleolithic
diet, but to be somewhat guarded in putting out portions of our unpublished work for common disposal.
Clearly, individual e-mail messages between two scientists do not constitute a risk. Perhaps Dean could
comment upon this.
Cordially,
Loren Cordain, Ph.D.
References
1. Lee RB. What hunters do for a living, or how to make out on scarce resources. In Lee RB, DeVore I (Eds).
Man the Hunter. Chicago: Aldine, 1968:30-48.
2. Ember CR. Myths about hunter gatherers. Ethnology 1978;17:439-48.
3. Murdock GP. Ethnographic atlas: a summary. Ethnology 1967;6:109-236.
4. Leonard WR, Robertson ML. Evolutionary perspectives on human nutrition: the influence of brain and
body size on diet and metabolism. Am J Hum Biol 1994;6:77-88.
27/298 (1997)
5. O'Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian Aborigines
after temporary reversion to traditional lifestyle. Diabetes 1984;33:596-604.
6. Naughton JM, O'Dea K, Sinclair AJ. Animal foods in traditional Australian diets: polyunsaturated and low
in fat. Lipids 1986;21:684-90.
7. Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J
Med 1985;312:283-89.
8. Stahl AB. Hominid dietary selection before fire. Current Anthropology 1984;25:151-68.
9. Wolfe BM, Giovannetti PM. Short term effects of substituting protein for carbohydrate in the diets of
moderately hypercholesterolemic human subjects. Metabolism 1991;40:338-43.
10. Wolfe BM, Giovannetti PM. High protein diet complements resin therapy of familial
hypercholesterolemia. Clin Invest Med 1992;15:349-59.
11. Wolfe BM. Potential role of raising dietary protein intake for reducing risk of atherosclerosis. Can J
Cardiol 1995;11(supp G):127G-131G.
12. Gonen B, Patsch W, Kuisk I, Schonfeld G. The effect of short term feeding of a high carbohydrate diet
on HDL subclasses in normal subjects. Metabolism 1981;30:1125-29.
13. Coulston AM, Liu GC, Reaven GM. Plasma glucose, insulin and lipid responses to high carbohydrate
low-fat diets in normal humans. Metabolism 1983;32:52-56.
14. Chen YDI, Coulston AM, Zhou MY, Hollenbeck CB, Reaven GM. Why do low fat high carbohydrate
diets accentuate lipemia in patients with NIDDM? Diabetes Care 1995;18:10-16.
--[end Dr. Cordain's letter]-========================================================================= Date:
Wed, 26 Mar 1997 23:43:46 -0500 From: Dean Esmay Subject: On the issue of publication
Regarding Loren's concern about prior publication issues, I do not have a definitive answer. But I can
provide some information and suggestions that might be helpful:
As of today there are about 40 persons signed up for this list. I cannot imagine membership ever exceeding
about ten times that amount. The list is also not a "publication" per se, as what is written here is not generally
distributed to anyone other than list members. Considering a small group of maybe a few hundred people
exchanging informal comments a "publication" would be a stretch indeed. Which is not to say that some
hard-nosed editor couldn't possibly see it that way, but I would be surprised if one did.
However, all messages posted to this list are archived. We hope at some point to make these archives
available through the World Wide Web so they may be read by others who wish to learn about this field or
catch up on previous conversations. The existence of these archives, even though they can only be seen if
someone specifically goes looking for them, might arguably be considered a form of "publication" by the
editors of some journals. This is some cause for concern.
But I think there are a few things that can prevent any problems:
1) Any message you write to this list is, by current copyright law, automatically copyrighted by you. Which
means that, beyond the distribution to list members which you implicitely agreed to when you wrote to the
list, no one has any right to further redistribute anything you write without your express permission. This
does not mean that someone cannot do so, but they have no RIGHT to do so and have legally violated your
rights if they do.
2) Because anything written to the list by any list member is copyrighted by that member, I will, upon
request, remove any individual message from the archives. The messages are, after all, not my property.
3) You may also at any time further protect yourself by simply writing, at the top or bottom of any message,
a protective statement. An example would be: "This message is copyright 1997 by Dean Esmay. This
message may only be distributed privately to members of the Paleolithic Diet & Exercise Symposium
discussion group, and may not be reprinted or otherwise distributed by anyone to anyone. These constitute
informal comments to colleagues and are not for publication."
Technically, by copyright law, you do not have to attach such a statement to be protected. However, adding
such a statement will be additional protection, emphasizing the nature of the communication and serving as
an easy verification to anyone who asks that what you wrote was PRIVATE CORRESPONDENCE TO A
SMALL GROUP and not for publication. (And I will fully back anyone up on that if necessary.)
4) Most of the time common sense should be sufficient. If you don't say anything here that you wouldn't say
to a journalist from DISCOVER magazine who called you for an interview, it's unlikely you'll ever have any
real trouble.
I'm glad Loren brought this up though, as discussing it now may avoid grief later.
28/298 (1997)
PALEODIET Archives
Subject: Plant foods in paleodiets
From: Jeanne Sept
Date: Thu, 27 Mar 1997 15:23:14 -0500
Staffan Lindeberg wrote:
> Let us start with asking what edible items were found in the African savanna, items which all
> contemporary humans are expected to be adapted to. How much vegetable foods were available?
Let me refer you to my WWW page, which has links to an old syllabus/bibliography (not current, sorry) for a
class I teach called "Prehistoric Diet and Nutrition" and to my home page, which lists a number of recent
articles I have written on this topic.
http://www.indiana.edu/~origins/
Several points: - a long-term primate perspective on human diet is important for reconstructing early hominid
diets - the types of foods accessible depend upon the type of technology you have (e.g. digging tools? fire?)
and your guts, which we can only speculate about for extinct critters, in addition to teeth, etc, which
determine the costs/benefits of foraging decisions... e.g. can you cook your legumes, or do you eat them at an
immature stage before they are hard and tempered with secondary compounds? - the range of mixed
woodland & grassland environments of our African early hominid ancestors would have offered plenty of
opportunities for plant food foraging, including many patches of various types of large and small fleshy fruits
(mostly quite fibrous by modern standards) and legumes, and patches of tender "terrestrial herbaceous
vegetation" in riparian forests ; shallow corms, rhizomes, bulbs and deeply buried tubers in well-drained
and/or rocky soils (most wild tubers I am familiar with are high in dietary fiber, and simple carbos, but low
in starch). Honey is an often-overlooked woodland/forest food source. - archaeological evidence suggests
that at least some lean meat and marrow were a common component of the diets of early Homo, although no
one has been able to estimate relatively how important animal foods were for the early sites... for a variety of
reasons. Animal foods would have been increasingly important to early hominids invading the temperate
zones of Eurasia during the Pleistocene, and it is clear that folks were actively hunting by the Middle
Pleistocene. - if you want to trace nutritional inheritance to the origins of our species, you can also use a
tropical African model... though of course the % of animal foods will be habitat dependent... which is why
the !Kung-derived 70% veg model is not the best model for interpreting archaeological evidence for Upper
Paleolithic hunter-gatherers in western Europe (which is what Eaton and Konner did in their book).
Jeanne Sept
Anthropology Department Indiana University Bloomington IN 47405
PALEODIET Archives
Subject: Acidosis problems?
From: David Ross
Date: Thu, 27 Mar 1997 21:59:04 -0500
In light of some of the upwardly revised estimates of the percentage of protein in the paleo-diet (50-60%),
could someone comment on the possibility that early man (or contemporary hunter-gatherers for that matter)
was a victim of acidosis problems. I believe that there is a fair amount of evidence that the acid-ash of excess
protein (roughly, any more than 50 gms/day) can not, in the long run, be neutralized by the buffering systems
that maintain fluid PH levels at beneficial levels.
David Ross
PALEODIET Archives
From: Dean Esmay
Date: Thu, 27 Mar 1997 22:52:02 -0500
29/298 (1997)
It would seem, at least in my superficial reading, that perhaps Dr. Livingstone has misinterpreted the
question (through no fault of his own) to be about whether humans are omnivores or carnivores. Yet I do not
think that anyone now seriously believes that humans evolved as anything other than omnivores with a taste
for a wide variety of foods.
This may point out to a language difficulty. I have frequently seen Barry Sears' THE ZONE diet, which uses
40% carbohydrate, referred to as "low-carbohydrate." This absurdly lumps it in with other diets of less than
10% carbohydrate. On the other hand, the current dietary fashion in America is to that the ideal diet is 65%
carbohydrate. This would be quite high by some standards but is normal, and perhaps even a little bit low by
others (e.g. the rural Chinese).
I think we need to either standardize on phrasing (e.g. "moderately low carbohydrate" vs. "extremely low
carbohydrate") that is intuitively understandable, or try to stick more to numbers.
I wish we could get Boyd Eaton to join us, as he seems to have done an awful lot of work in this department.
PALEODIET Archives
Subject: Plant foods in paleodiets
Date: Fri, 28 Mar 1997 03:15:56 +0100
In order to learn more about carbohydrates in human evolution I sent a mail to Dr. Daniel Livingstone, a
highly respected paleoecologist and limnologist who holds the James B. Duke Professorship of Zoology and
Geology at Duke University, where he has been since 1956. He has worked in Nova Scotia, arctic Alaska,
and especially tropical Africa on lakes and their history. He is best known as the designer of the Livingstone
sampler for lake sediments, and for having been tasted and rejected by a large Nile crocodile. This is my
question ....
> It has been put forward e.g. by Brand Miller (Brand Miller JC, Colagiuri S. The carnivore
> connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia 1994; 37: 1280-6) that
> human diet was low in carbohydrate from the time of H. habilis up to sapiens leaving Africa,
> allegedly because dry climates during the Ice Ages would result in grasslands being the main
> edible plants instead of roots and fruits. Please give me your opinion on this issue which is
> important to evolutionary medicine in order to know wether there is evidence of an optimal balance
> of macronutrients for humans.
... and his answer:
The question may be of significance, but I doubt that my opinion on it is worth much.
However, for what it is worth, I wouldn't bet much on this idea. It rests on such a train of untested ideas that
the final conclusion doesn't have much weight.
First, very little is known about the environment of early paleolithic people. We know something from pollen
analysis about the nature of tropical African vegetation during the last part of the last ice age and the time
since then. We get a few glimpses of what things were like during earlier periods from studies of the isotopic
composition of old soils, marine cores, plant fossils, mainly leaves, buried under volcanic ash, and an
occasional pollen analysis of the sediment from paleoanthropological sites.
The picture that emerges is one of a complex mosaic of vegetation types. During the last ice age, and
presumably earlier ones as well, although this is not a well-tested presumption, the vegetation was richer in
grasses and poorer in trees than it has been during post-glacial time. It is not easy to place most
archaeological sites accurately in that shifting vegetational context, but Desmond Clark, the dean of African
prehistorians, believes that until Sangoan time, which may be 100, 000-200, 000 years ago or so, when a
culture developed that was intermediate between the late Acheulian and Middle Stone Age, people were not
adapted to life in a forest. This is an interesting idea, and well worth serious stratigraphic testing. I have tried
but failed to give it a usefully rigorous test.
It is likely that people from early paleolithic time onward lived in a more or less open vegetation. Paleolithic
sites seem to cluster around water, and it is likely that our ancestors, like ourselves, were obliged to drink
water, and not having containers larger than ostrich shells, could not carry it very far. There is always a
possibility that they had skin or gourd containers, but sewing up skins would probably require stone tools
such as burins, which don't show up until much later in the record. It is always possible that they could get
by without drinking water, as gorillas and some antelopes do, but the distribution of sites argues against this.
30/298 (1997)
In the African vegetation matrix, the local vegetation close to permanent water tends to be richer in trees than
the vegetation farther away. I don't mean to argue for gallery forest around every cluster of Olduwan tools,
but only to suggest that it is not likely that early Paleolithic people spent their lives far away from trees.
From watching baboons, and from keeping a Canadian countryman's eye on the resources that might be used
for food in an emergency, I don't think that even in a grassland early Paleolithic people would find it difficult
to consume carbohydrates. I would expect them to depend heavily on grass seeds, and from the time they had
digging sticks, on underground storage organs of vascular plants. I don't eat them in Africa, because some
are very poisonous and I don't know which are safe, but I have no reason to believe that our early Paleolithic
ancestors were so ignorant.
As for what those people actually ate, that is still an open question, so far as I know. There has been some
isotopic analysis of their bones, but I have not followed that closely enough even to tell if it suggests
membership in a food chain based on C-3 or C-4 plants. In this state of affairs, there is a place for speculative
papers suggesting that they did not consume appreciable quantities of carbohydrates, but that speculation
doesn't seem to me very solid, and I wouldn't modify my diet, nor advise you to modify your dietary advice,
in accord with it.
You really need to get in touch with paleoanthropologists about this. The people who work with Lower
Paleolithic cultures are excellent natural historians, they read the papers we publish on the paleoecology of
Africa, and they are in a better position to have currently valid opinions than I am. Try Dr. Robert J.
Blumenschine in the Anthropology Department of Rutgers University, Rutgers, New Jersey, USA .
Our African heritage affects our health in other ways. Our peculiar fluoride requirement looks like a legacy
of a prehistory spent where waters are fluoride rich. Possibly something similar is behind our lithium
requirement.
People tend to develop semi-religious feelings about questions of this sort. When I was a boy, much
influenced by the writings of Viljhalmur Steffansson, I believed that we were all natural carnivores, because
Innuit were heavy meat-eaters and free of dental caries. I was dragged kicking and screaming to acceptance
of the idea, based on studies of Kalihari Bushmen and the great apes, that our early ancestors were probably
omnivores, with a heavy component of plant material in their diets. Maybe I burn with the zeal of the newly
converted, and you should be wary of my opinion for that reason.
I think, though, that it is no such faith, but rather a cold assessment of what little we know about the history
of African vegetation that makes me skeptical of the idea that early Paleolithic people lived in an
environment so poor in potential carbohydrate foods that they had to eat other things. That is probably the
only part of my opinion that you care about, since you will know more than I do about the other stuff.
I hope that this helps.
Dan Livingstone
[end of included e-mail]
I have posted the same question to Dr Blumenschine.
Staffan
PALEODIET Archives
Subject: Important paper: The non-thrifty genotype
Date: Fri, 28 Mar 1997 03:16:51 +0100
> John Allen wrote:
> With Susan Cheer, I have recently published a paper in Current Anthropology called "The
> non-thrifty genotype" (37:831-842, 1996)...
This is in my opinion one of the more important papers on diet in human evolution and I expect it to become
a classic. It may not be coincidental that the paper is written by two scholars outside of the medical
profession. These two anthropologists can see the wood despite all the trees.
In his posting John offered a copy to be obtained from him by sending an e-mail to .
Staffan
PALEODIET Archives
Subject: Re: Publication and NIDDM
From: Art De Vany
31/298 (1997)
Date: Fri, 28 Mar 1997 11:36:14 -0800

This refusal to publish web-distributed papers is a rear guard action by traditional venues threatened by new
technology. It will pass. In the meantime, I do not submit papers to journals that make that stipulation. The
value of the journal outlet is the peer review process and the open criticism to which claims are subject. The
journal name becomes a quality signal that saves search costs. In the information age, these quality signals
will take many forms. Authority and knowledge will be decentralized and knowledge communities, such as
this one, will evolve the criteria that are appropriate to the problems they seek to address.
While much has been made of the racial and cultural distribution of the ravages of drugs and of the
destruction of inner city culture by the war on drugs, I see too little concern over the ravages of high
glycemic carbohydrate diet on Amerindians, Mexican Americans, and African Americans. NIDDM is near
epidemic proportions among these groups and African-American females, who already disproportionately
bear the burden of the war on drugs because of what it has done to the competition for mates, are at high risk
(a risk that may reach that of the Pima).
An african-american child, raised in a northern city, with too little sunlight and eating a high glycemic, high
carbohydrate diet, drinking whole milk and eating grains may be the prototype for a non-insulin dependent
diabetic adult. School lunch programs almost by design fit that pattern---they are nearly identical to the
federal food distributions that ravaged the american indians (Diabetes as a Disease of Civilization).
The AHA diet and the food industry (primarily carb producers) sponsored food pyramid are one-diet-fits-allpeople models. They are wrong and they are potentially highly destructive. They are (in my opinion, at least)
contrary to the health interests of people from nearly all cultures that adapted late to agriculture. I have no
evidence, but it does seem that "soul food" with its greens and fat and high protein beans is far better adapted
to an african american genetic profile which exhibits high proportions of lactose intolerance and insulin
resistance. (Any thoughts on that?)
Scotty Pippen endorsing milk and Oprah pushing carbs in her book are unwittingly harming those who share
their genetic and cultural heritage. Even as a NEPHS (northern european paleolithic homo sapien) I don't
touch this stuff.
Arthur De Vany NeXTMAIL, SUN Mail & MIME welcome
http://www.socsci.uci.edu/mbs/personnel/devany/devany.html Department of Economics Institute for
Mathematical Behavioral Sciences 3151 Social Science Plaza Irvine, CA 92697-5100
PALEODIET Archives
Subject: Grasslands
From: Loren Cordain
Date: Fri, 28 Mar 1997 14:27:42 -0500
Ray makes a good point that food calories from most of the plants located on grasslands are generally
unavailable to hominids. Further information on this concept can be found in: Foley R. A reconsideration of
the role of predation on large mammals in tropical hunter-gatherer adaptation. Man 1982;17:393-402.
Cordially,
Loren Cordain
PALEODIET Archives
Subject: Charter clarification & philosophical digression
From: Dean Esmay
Date: Fri, 28 Mar 1997 14:57:03 -0500
I have gotten a few private questions about this list's charter, so I thought I'd best make a brief statement.
This very new Symposium is open to discussion of any and all issues that relate to the pre-agricultural
lifestyle pattern for humans. The assumption is that you know enough about the subject to pose intelligent
questions or give reasonably authoritative answers, but otherwise discussion -can- be in any area desired.
Indeed, I hope that discussion turns at some point to issues like exercise, ethics, and biosustainability. Not
that there is any hurry; I just want to avoid anyone getting the impression that diet is the only -allowedsubject because it -happens- to be all that anyone is discussing at the moment.
32/298 (1997)
There is a greek word, "nomos, " which refers to the concept of spontaneous order--that is, when anarchy
somehow generates order. It's a concept implicit in Adam Smith's free market economic theories, for
example, and also to the theory of evolution. A mailing list like this one operates under similar principles,
and might even be considered as a living organism. It has certain set limitations and patterns, but what
happens within those parameters is rarely more than moderately predictable.
If discussion stays focused on any one topic, that will be solely because no member has chosen to bring
anything else up. There is nothing wrong with that, because whatever the group finds stimulating or
enlightening is perfectly acceptable. But if anyone should ever wish to turn the beast in a different direction,
he need only do one thing: post a message about a different subject. If the beast doesn't turn the first time, a
little patience and further prodding should produce the desired result. (Just don't prod too hard or you might
get an undesirable reaction.)
The only person "in charge" here is me, and my only function is to maintain the minimal order necessary to
prevent the organism from disintegrating. You as list members may bring up any subject you wish, so long
as it relates in a substantive way to the pre-agricultral lifestyle pattern for humans. Indeed, you are
encouraged to do so at any time, so long as it relates in a substantive and informed manner.
I hope this clears up any private misapprehensions. Please continue. :-)
PALEODIET Archives
Subject: Grains
From: Dean Esmay
Date: Fri, 28 Mar 1997 15:30:01 -0500
I had my preconceptions rocked this week. Which is always a healthy thing, but I'm still reeling from it.
My assumption has long been that most cereal grains and beans are foreign to the human digestive tract
because they can only be rendered edible by technology--i.e. extended cooking. Earliest evidence for use of
fire for cooking among humans seems to be 25, 000 years (I have no reference for that handy, let me know if
that's in dispute), which would indicate the potential for some adaptation to cooked foods. Yet it would seem
that the fact that grains and beans are inedible without things like cooking pots and mortar and pestle ought
to make us look with suspicion to those foods, since that all by itself would tend to indicate that humans
would never have eaten them in any appreciable quantity until around the time of agriculture.
Enter the members of the raw food community who I recently encountered online. These people eat
absolutely everything raw, on the belief that the molecular changes wrought by cooking foods are unnatural,
addicting, and carcinogenic. I am mildly skeptical of this belief system, although there is some rational
argument for it; humans ARE the only animals who cook food and most of the evidence I've seen suggests
that we haven't been doing it for very long.
But what really rocked me is that these people (and I've seen messages from more than one of them) eat
whole cereal grains and beans raw. They most commonly will use overnight soaking methods, either in pots
or jars or even just wrapping the stuff in moist rags. However they will also apparently eat them even
without this, eating them completely raw without even any soaking. Their claim is that if you haven't been
eating this way all your life it might take a week or two for your digestive tract to adjust, but that they
otherwise have no trouble at all living this way.
At first I was tempted to dismiss this as a bizarre cultish sort of thing. But if these people appear to be happy
eating this way. The very fact that it's POSSIBLE for them to do this should, at minimum, throw back open
to question whether or not humans have been eating cereal grains since before the advent of agriculture after
all. Although it's hard to imagine them making up the majority of the diet, if people can comfortably eat wild
grains without technology then there's not much reason to think they wouldn't, is there?
Once in a while you get shown the light/ In the strangest of places if you look at it right ---Robert Hunter
PALEODIET Archives
Subject: Re: Hunting on the Grasslands
Date: Fri, 28 Mar 1997 16:07:05 +0100
33/298 (1997)
Ray may be right that survival on the grasslands of our African ancestors depended on game rather than
vegetables, unless these grasslands differed from Ray's own hunting habitat. What we need to know is
whether our ancestors were mainly confined to such open grasslands during human evolution. Perhaps they
stayed near the waters and perhaps their habitats differed. As far as I can figure out we don't even know for
sure that there was savanna at the places in question and if so what kind of savanna. I would expect Ray's
diet to be very healthy, but the question is if saturating vegetables rich in carbohydrates with a low glycemic
index could have been part of lower Paleolithic diets and hence healthy too. Until further notice I consider
humans omnivores.
Staffan Lindeberg
PALEODIET Archives
Date: Sat, 29 Mar 1997 01:13:50 +0100
Loren Cordain wrote:
Although Richard Lee (1) and others have suggested that the average
> macronutrient content of all world wide hunter gatherers ... ... i.e. contemporary
> hunter-gatherers who may not be representative of paleolithic ones. The former have largely been
> forced aside by other populations while the latter could choose the best habitats for themselves.
> ... was derived from a subsistence pattern of 35% animal food and 65% vegetable food, it has been
> shown that these figures are likely erroneous (2). ... ... Clearly, the carbohydrate content of
> the average paleolithic diet varied according to geographic location, latitude and season; however
> in aggregate, it almost certainly was significantly lower than the 55% carbohydrate recemmended by
> the American Heart Association Diet.
I agree. But if, in some of their habitats during evolution, they depended on vegetables we would expect
them to have preserved their capacity to handle considerable amounts of carbohydrate. As Loren notes, the
available carbohydrates were, compared to typical Western ones, of low glycemic index and the foods in
question were rich in soluble fiber (which is quite different than cereal fiber in regard to metabolic effects).
Such carbohydrate-rich foods would also have been high in minerals and vitamins, some of which may be of
considerable importance to prevent common Western disorders. The probable depletion of these minerals
and vitamins in many of our contemporary high-tech plant foods could further exaggerate any differences in
the intake of these nutrients. Finally, dietary allowances may differ substantially due to other differences in
lifestyle.
In conclusion, it takes a lot more to convince me to stop eating plenty of fruit, nuts and saturating vegetables.
PALEODIET Archives
Subject: Raw foods diets (was Grains)
From: Secola/Nieft
Date: Sat, 29 Mar 1997 11:11:36 -0800
Hi all,
A large thank you to Dean Esmay for making this list happen. I very much appreciate the opportunity to
participate.
With this post I mark my failure to lurk this list without posting. I am a 8+ year happily-omnivorous raw
fooder (99.9% raw) who started out as a strict "instincto". Instinctos are the raw food fringe which most
closely matches a pre-fire paleolithic ideal. Briefly, an instincto eats one raw food at a time according to
sensory pleasure. S/he chooses the best smelling (with perhaps a little taste-test as well) food from a variety
of raw items and consumes that food alone until a "taste-change" or "stop" presents itself. The stop can be a
change in mouth-feel, rising acidity, blandness, burning, etc. It can also be a sense of repletion.
34/298 (1997)
In any case, the beginning instincto is instructed to "eat their fill" of the most attractive raw food available.
These foods include animal foods (fish, roe, shellfish, crustaceans, meat, organ meat, marrow, eggs, insects,
etc.) and plantfoods (fruits, veggies, nuts, honey, pollens, etc.). Grains and legumes "can" be eaten if
attractive in their raw state, though they rarely are unless sprouted and even then are not very tasty in
su=ignificant amounts. Great care is taken to obtain the most "instincto-quality" foods which means organic
or wild vs. chemically-farmed. Dairy is avoided and even sprouted wheat is avoided.
There are problems with nearly every instincto idea and practice but the biggest ones include overeating
modern too-sweet fruits, obtaining high-quality animal foods, fanaticism, and, of course, the social
limitations.
Dean Esmay writes:
> I had my preconceptions rocked this week. Which is always a healthy thing, but I'm still reeling
> from it.
Oh, Dean, if you could only see the majority of raw fooders (most who have vegan aspirations) try to deal
with the arguments for paleo-diets while maintaining their ethical superiority stances regarding animal foods.
_Their_ pre-conceptions are rocked as well. Many even continue to argue the nutritional and
anthropological(!) superiority of an all-plant diet. You have indeed stumbled into strange, but interesting
waters...but so have many vegetarians when they come across the paleo-diet ideations ;)
> Yet it would seem that the fact that grains and beans are inedible without things like cooking
> pots and mortar and pestle ought to make us look with suspicion to those foods, since that all by
> itself would tend to indicate that humans would never have eaten them in any appreciable quantity
> until around the time of agriculture. Enter the members of the raw food community who I recently
> encountered online. These people eat absolutely everything raw, on the belief that the molecular
> changes wrought by cooking foods are unnatural, addicting, and carcinogenic.
Very few of them eat absolutely everything raw. After you hang around them for a time you realize that most
are quite taken with the simplicity of rawism, but are constantly dealing with "cooked food addictions",
backsliding, and finding the "right" supplements. The track record of most raw regimes (including instincto)
is quite dismal.
> I am mildly skeptical of this belief system, although there is some rational argument for it;
> humans ARE the only animals who cook food and most of the evidence I've seen suggests that we
> haven't been doing it for very long.
I, too, am mildly skeptical. Yet it does seem to be something of a scientific black-hole as regards the utility
of cooking. I have spent many years trying to research what anthropology as to say about when humans
began widespread cooking and there are very few references to be found that are more edifying than
intriguing. Further, the difference between raw and cooked foods in digestion and metabolism appear to be
little studied. How science can overlook something so fundamental and obvious may be an example of
cultural blinders resulting from the "obvious a priori" that cooked food is natural for humans.
> But what really rocked me is that these people (and I've seen messages from more than one of them)
> eat whole cereal grains and beans raw. They most commonly will use overnight soaking methods,
> either in pots or jars or even just wrapping the stuff in moist rags. However they will also
> apparently eat them even without this, eating them completely raw without even any soaking. Their
> claim is that if you haven't been eating this way all your life it might take a week or two for
> your digestive tract to adjust, but that they otherwise have no trouble at all living this way.
You may grow weary of raw foodist's "claims" overtime as I have. But note that instinctos _rarely_ find
sprouted grains or legumes attractive for more than a mouthful or two. It may be that vegan-rawists are
simply extremely mis-nourished on only raw plant foods. Their tendency to rely on sprouts (and greenpowder-type supplements) to try to maintain some homeostasis may be a frustrating stop-gap effort to
maintain their vegan ideations with a second-class protein such as sprouts. Further, sprouts are usually spiced
or mixed in some way to mask the taste-change which would prevent their consumption in large amounts
otherwise.
> At first I was tempted to dismiss this as a bizarre cultish sort of thing.
From what I have seen you would be more right than wrong. Ward Nicholson's 3-part interview in Chet
Day's HEALTH & BEYOND is probably the best ever written on the subject (http://chetday.com/). The third
part (not on the webpage, but available as hardcopy) deals with these cultish and fanatical aspects in a very
straightforward manner.
35/298 (1997)
I am ambivalent about bringing up the topic on this list since there are plenty of rawists on it: I don't want to
debate raw food ideology! But neither do I want to witness a misrepresentation of all rawists as happy
healthy sprout-eaters. IMO, the fields of Darwinian medicine, evolutionary psychology, paleo-diet, and
instincto are on a collision course and may meet as a minor revolution down the road. Much of the rest of
rawist ideology (fruitarianism, "Natural Hygiene", sproutarian, etc.) seems unwilling or unable to modify its
tenets according to new information, anthropological or otherwise. In sum, I don't want some zealotrous rawvegans to alienate the paleo-diet community as they have many folks in the raw foods (and caloricrestriction) arenas.
> But if these people apparear to be happy eating this way. The very fact that it's POSSIBLE for
> them to do this should, at minimum, throw back open to question whether or not humans have been
> eating cereal grains since before the advent of agriculture after all.
How happy (or healthy) these people are is a matter for serious exploration. There is probably a reasonable
argument for the paleolithic consumption of grains/legumes as a "drought-food" or "survival-food" but I
seriously question why a human would bother unless animal foods were in _very_ short supply. The
extinctions of many (but clearly not all) large game animals which coincides with the last glacial retreat may
have played a part in such a scenario, but that begs the question of whether such grains are optimal for
human health. Cooked grains are clearly more denatured than raw grains, but...there is an interesting
instincto "claim" regarding bread: apparently when long-time instinctos have experimented with bread-eating
they find that, relative to the much-maligned "Wonder bread", whole-grain breads are much _harder_ to
digest and more likely to cause nervous tension after consumption. Wonder bread is problematic but _less_
so. The implication is that if bread is problematic, whole-grain bread is even more problematic than Wonder
bread, since whole grains have even greater molecular complexity than polished grains. Both may be best
left unconsumed.
> Although it's hard to imagine them making up the majority of the diet, if people can comfortably
> eat wild grains without technology then there's not much reason to think they wouldn't, is there?
Not unless there were no animal foods to be had. Modern rawists _decide_ to avoid animal foods for a
variety of "reasons". It is hard to imagine paleolithic folks prostelystising the evils of animal food
consumption, but perhaps an abundance of wild stands of grain, combined with a dearth of animal foods, and
perhaps some population pressure(?) played a part in the rise of agriculture.
Below is some text from "Instinctive Nutrition" by Severen Schaeffer (Celestial Arts, 1986) regarding the
onset/origin of cooking. I think it applies analogously to the idea of grain consumption as well. (Instinctos,
fruitarians, and every other rawist in between, seem to agree that cooked grains, esp bread, are perhaps the
most addictive class of denatured foods. This passage also serves as an example of the tenuous type of
ideation that keeps a raw fooder "motivated" when they need to see cooking as evil...
--------"Once humans discovered how fire could be used for cooking, they were on a one-way trip to metabolic
chaos and organic disharmony. They had tied a knot they couldn't undo, that we, their descendants, have
rendered practically inextricable.
"In order to understand this, let is imagine a tribe of Homo Erectus somewhere in the forest, say around 400,
000 B.C. They are gathered near a fire, eating yams and other foods collected earlier in the day. The ones
who are eating yams are those whose bodies need the nutrients yams contain: this is what makes them smell
and taste good. Those who do not need yams are not attracted to them.
"Whatever they're eating, they're eating it raw, the way it came off the tree or out of the ground. It has never
occurred to them to mix, grind, pound, heat, or do anything else to an attractive piece of food other than to
eat it.
"One member of the group, call him Onemug [a German pun for Einstein], has eaten less than a fourth of a
yam when the taste becomes unattractive. Carelessly he throws it down, and it rolls to the edge of the fire,
unnoticed. And there it begins to bake. And it begins to smell. And the smell is stronger than ever a yam
smelled before. The smell reaches Onemug's nose, and it is good. So Onemug follows his nose, and takes up
the baked yam and begins to eat it. He can do so now because the taste has become good again. So Onemug
eats the rest of the yam. The yams molecular structure, modified by heat, no longer causes its taste to change
from good to bad.
36/298 (1997)
"A day or so later, Onemug is hungry, but all the tribe has found to eat that day is yams. Thanks to cooking,
Onemug had been able to eat more yam than he actually needed, so his organism was still overloaded with it.
As a result, naturally, he finds the raw yam unattractive. But Onemug is a genius: he remembers that the hot
yam from the fire was good: he associates: fire + good = good. On an impulse, he pushes a yam into the fire.
And sure enough, after a while an attractive smell comes to his nose. And he is able to eat the yam with a
degree of pleasure until he is full.
"Of course, the other members of the tribe smelled the cooked yam too, and begin to follow suit. So all of
them begin to eat yams, not until the body has had its fill of the nutrients yams contain, but until the belly has
no room for more. And naturally, the next day, because they don't need them, none of them is attracted to
raw yams any longer.
"This brings upon the tribe an unexpected change in the way it lives. Up to now, yams in their natural state
were delicious. Now, however, they have to be cooked or they can't be eaten. Instinct has to be tricked or it
will stop the organism from overloading itself with substances it doesn't need.
"Thus is birth given to the artifice of cooking. It is not an 'art' in the sense of haute cuisine but it must
inevitably become one. For by disrupting the dynamic structure of food, cooking kills its taste: each
mouthful tastes just like the last. Since it will no longer trigger an alliesthetic response, it will not become
unpalatable. But it _will_ be boring, because the taste of cooked food does not vary.
"Over the centuries, ways will be found to 'enliven' it, to make it interesting and pleasurable to eat. Food in
its original state will of itself be more pleasurable than any artifice can make it, but only if the body needs it.
However, once the organism has become saturated with remnants of denatured foods (which it can neither
use nor eliminate because biochemically it 'doesn't know how'), then the senses of smell and taste themselves
become denatured and dulled. Thus must leaves, herbs, spices, ferments, oils, extracts, mixing, baking,
roasting, basting and boiling, etc. be called upon to provide flavor where none remains. The relationship
between the dynamic molecular effects of these procedures on the food, and the effects of the food on the
human organism, have only recently become a subject for scientific enquiry--which has generally assumed
along with everyone else, that cooking is perfectly 'natural' for humans."
----------------Whatcha think, paleo-listers?
Cheers, Kirt
Kirt Nieft / Melisa Secola
PALEODIET Archives
Subject: Fire and raw foods (was GRAINS)
Date: Sat, 29 Mar 1997 13:34:54 -0600
Dean Esmay writes:
> I had my preconceptions rocked this week. Which is always a healthy thing, but I'm still reeling
> from it. My assumption has long been that most cereal grains and beans are foreign to the human
> digestive tract because they can only be rendered edible by technology--i.e. extended cooking.
> Earliest evidence for use of fire for cooking among humans seems to be 25, 000 years (I have no
> reference for that handy, let me know if that's in dispute), which would indicate the potential
> for some adaptation to cooked foods.
From what I know from having combed through the research I have been able to find myself, the evidence
for earliest use of fire itself goes back much further than 25, 000 years, although it is very difficult to say
with any certainty just when cooking practices began as a result of previous familiarity with fire. About
controlled use of fire itself, however, even someone as skeptical as Steven James, in a review article of the
evidence for early fire use, concedes that by at least 230, 000 years ago, at the Terra Amata site in Spain, one
finds clear evidence. [James S, 1989, "Hominid use of fire in the lower and middle Pleistocene. A review of
the evidence." Current Anthropology, v.30:1-26] (Newer dating techniques may have pushed the date for this
site back to 300, 000 years, but I am not sure.)
37/298 (1997)
However, since this review-of-the-evidence article, there is now other recent evidence at, I believe, another 2
or perhaps 3 sites in Spain and/or France, including one in France (Menez-Dragan) that would push the
controlled-fire-use date back to around 380, 000 to 465, 000 years if the claims stand up to testing. Also of
significance is that burnt rhinocerous bones were found close to a hearth inside a cave at this site, leading the
researchers to tentatively conclude cooking had occurred, as it seemed unlikely to them the rhinocerous
bones could have gotten inside the cave otherwise. [reported by journalist Patel T 1995, "Burnt stones and
rhino bones hint at earliest fire." New Scientist, June 17, 1995, p.5]
I also believe (and would like to hear informed comment from those here better acquainted with the evidence
than I) that while some of the very earliest claims for control of fire by humans (approx. 1.5 million years
ago) at Zhoukoudian Cave in China have now been disputed or discredited, more recent analysis of the ash
layers in the cave dated to 230, 000 to 460, 000 years ago, in which animal skulls have been found, show
burn patterns around the teeth and skulls that would indicate cooking of the brains [Rowley-Conwy, Peter
1993, "What do the Zhoukoudian finds tell us?" In: Burenhult, Goran (ed.) The First Humans: Human
Origins and History to 10, 000 B.C. New York: Harper-Collins, p.65. This is a compendium put out by the
American Museum of Natural History, and not peer-reviewed, but Rowley-Conwy is a well-known authority
in the field, I believe.]
One thing I have heard only one writer discussing fire address is what can be inferred about cooking just
from the evidence for control of fire itself. Somehow the question of fire use seems to catch the researchers'
attention, but the advent of cooking--which seems to be just as much or more interesting a question to me-does not. But if one were going to suppose, doesn't it seem logical to infer--when you consider why hominids
would have been interested in controlling fire in the first place (why were they doing it at all?)--that it would
have been for either warmth or cooking food, or both? I wonder what others think about that supposition,
given that fire does not leave many useful traces behind, at least, according to what I have heard stated in the
literature. As is often said, "Absence of evidence is not evidence of absence."
Dutch writer Johan Goudsblom, in his 1992 book "Fire and Civilization" [Penguin Books: London; New
York] notes that animals in the wild, like birds of prey such as kites, quickly gather around burned-out
wildfires to eat the burnt victims, and other animals can be seen gathered round the wildfire-sites later at
night, apparently attracted by the warmth. The implication of this leads to the supposition, which I believe
was Goudsblom's point in bringing it up, that if other animals take advantage of fire in this way, then it
would seem unlikely that observant hominids would not also have followed suit with regard to its use for
warmth and possible processing of food fairly early on after first controlled use. (Ann Brower Stahl,
however--commenting in the follow-up section to James' Current Anthropology article--believes that fire's
use for warmth would have predated its use for cooking.)
The most relevant question, though, it seems to me, where Paleodiet is concerned, is when the use of fire for
cooking became *widespread* enough that it would have begun to constitute a serious evolutionary selective
pressure. On this point, Steven James notes that consistent evidence for fire use itself in a number of
different archeological locations is not seen until at least the late Paleolithic, which he defines as roughly (if I
am remembering correctly) 125, 000 years ago and more recently.
However, if it is true that ancient fires would not leave many traces behind archaeologically in most cases, it
may be we are faced with a paucity of evidence by the very nature of the question, which leaves us in a
dilemma. I don't know, though, what do others think?
Where hard evidence is concerned, though (as opposed to inference), there does not seem to be much
indication that *widespread* use of fire for cooking goes back more than about 40, 000-60, 000 years or so,
but I would like to hear more input from others more well-versed than I, since I have had trouble even
finding much interest, let alone data, in the fire-and-adaptation-to-cooking question in what Paleodiet
literature I have been able to unearth myself.
> Yet it would seem that the fact that grains and beans are inedible without things like cooking
> pots and mortar and pestle ought to make us look with suspicion to those foods, since that all by
> itself would tend to indicate that humans would never have eaten them in any appreciable quantity
> until around the time of agriculture. Enter the members of the raw food community who I recently
> encountered online. These people eat absolutely everything raw, on the belief that the molecular
> changes wrought by cooking foods are unnatural, addicting, and carcinogenic. I am mildly skeptical
> of this belief system, although there is some rational argument for it; humans ARE the only
> animals who cook food and most of the evidence I've seen suggests that we haven't been doing it
> for very long.
38/298 (1997)
I am still reserving judgment myself on the question of whether or to what degree cooking foods may render
them "unnatural, " addicting, or carcinogenic. (Cooking creates some carcinogens, but neutralizes others; and
most plant foods contain a certain level of "nature's pesticides" in the first place as a self-defense tactic to
discourage animals from eating them; so the question is not a cut-and-dried one. [See Ames, B 1983,
"Dietary carcinogens and anticarcinogens." Science, v.221 (Sept. 23, 1983), pp. 1256-1264])
However, one thing about the raw-foods community that I think should be strongly emphasized, which I
point out here based on my own first-hand experience as a former member of the raw-foods community
myself, is that the walk does not match up completely to the talk. You will hear lots of claims that someone
is eating 100% all-raw foods, but when you get them in private, or cross-examine them in public, most will
admit they can't or don't sustain the full regimen. This is not to say that there are not some very notable
examples of people who do, because there definitely are (and I know one or two of them on this listgroup).
But most avowed "raw-foodists" are actually eating more like 70% to 80%, perhaps 90%, raw foods. Still a
lot of raw food, of course, but it seems to me very significant that for the vast majority who try (and most
who become convinced it is the ultimate way to eat get pretty motivated about it and try hard) there seems to
be some sort of barrier preventing them from taking it all the way. (Also, it is important to note in saying this
that most raw-foodists are vegetarians as well, and the lack of animal-food intake could be affecting their
ability to otherwise successfully sustain a raw-food regime.)
I recently resigned the editorship of a small many-to-many newsletter on health and vegetarian raw foods
that I ran for 4 years, due to growing disillusionment with what I saw regarding preaching vs. practice, as
well as becoming increasingly familiar with the evolutionary Paleodiet literature. (Many-to-manys work just
like on-line listgroups as far as comment-and-response discussions, except they are distributed through
snailmail.) Many of the participants were, or claimed to be, or had tried to make a go of, eating all-raw foods.
But when their actual practices were flushed out through cross-examination, as near as I could tell, not more
than about 10-15% of them were actually successful at walking their talk over the long-term in good health.
And of those who had tried to eat all-raw foods but could not sustain it, most gave it up either because of
strong cravings they could not satisfy on the all-raw regimen, or because of health problems, or both. There
are no scientific studies or surveys of raw-foodists that I know of myself, but I wrote an article last year from
the "former insider" perspective about raw-foodists who follow the Natural Hygiene philosophy of natural
diet, which strongly emphasizes raw foods, and the problems many of them experience. (If anyone is
interested, I can snailmail a xerox of it for $2 (to cover my time and copying/mailing expense) to anyone
interested. (The article runs 12, 000 words.) Or I might see if I can't get it translated to ASCII here soon
instead to email to those who have an interest.
> But what really rocked me is that these people (and I've seen messages from more than one of them)
> eat whole cereal grains and beans raw. They most commonly will use overnight soaking methods,
> either in pots or jars or even just wrapping the stuff in moist rags. However they will also
> apparently eat them even without this, eating them completely raw without even any soaking. Their
> claim is that if you haven't been eating this way all your life it might take a week or two for
> your digestive tract to adjust, but that they otherwise have no trouble at all living this way.
As a former insider, this is true--at least for those 10-15% who succeed on the type of raw-foodist dietary
program that may include such practices (though not necessarily for the other 85-90% who don't succeed too
well). It should also be specifically noted in connection with this practice that most people who attempt a
raw-food vegetarian diet and fail are usually only able to later succeed on their dietary program by modifying
it to include some sort of concentrated starch or protein food. (Most end up including something like steamed
or cooked squash, potatoes, legumes, or grains.)
However, as Dean says, those who are really serious about continuing to eat only raw foods--but who resort
to eating grains or legumes to round out the diet to succeed--will soak or sprout them (for a day or two or
less) to be able to ingest them raw. And then there are a very few who, as Dean mentions, will also eat the
grains raw without even soaking them. (They may grind them first, of course.) Whether and how much of the
grain they are actually digesting when eaten this way is an open question. (Cooking helps neutralize the
trypsin inhibitors commonly found in legumes and grains that otherwise interfere with digestion, so it is
questionable how much raw grain eaters actually digest and assimilate of it, even if they can tolerate it fine.
[I don't know what a trypsin inhibitor is, but Ann Brower Stahl briefly discusses the situation in her 1984
paper, "Hominid dietary selection before fire, " Current Anthropology, April 1984, v.25, no.2, pp.151-168.])
But I agree with Dean's inference that Paleodiet researchers really ought to look into this and see what is
going on here physiologically with these folks.
39/298 (1997)
Regarding the many failures of those attempting a raw-food diet, I have also had conversations with a person
well-acquainted with the "instincto" segment of the raw foods community from the inside who I believe is on
this list. (Instinctos are raw-foodists who do not limit themselves to vegetarianism and freely include raw
meat in their diet.) This individual can comment here themselves if they like, but they have told me that in
their estimation the success rate for raw-food instinctos is no better than for the raw-food vegetarian crowd
(i.e., 10-15% or less, they thought, from widespread acquaintance).
In bringing all this up with a Paleodiet researcher (and again, if they are on this list, I'm sure they will speak
up for themselves) who believes humans are not yet genetically much-adapted to cooked foods, it seemed
their opinion was the raw-food failures were due to two things. First, since hominid diets have evolved over
the eons to include not only much more animal foods than our primate cousins--and these animal foods are in
general more concentrated, less fibrous, and more efficiently assimilated foods than plant foods--vegetarian
raw-foodists will have a hard time getting a concentrated enough stream of nutrients without including
concentrated vegetarian starch foods like grains or cooked tubers, etc. I.e., since every organ system comes at
a metabolic cost, and it takes a large gut to digest a diet high in fiber; and since humans have smaller guts
than their primate cousins, for which we have compensated by eating more concentrated, more nutrient-rich,
less-fibrous animal foods that allowed us to evolve a large metabolically costly brain, many people who
attempt a vegetarian diet are going to find they have to eat more food than they can realistically handlevolume wise unless they include more concentrated foods like grains, legumes, and tubers by way of cooking
them to make them edible. (And this supposition seems to agree very well with the actual results and
practices I have seen in the raw-foods community myself.)
Second, the reason the instincto raw-foodists (who include meat) may be having a hard time succeeding, is
that it seems from observations of modern hunter/gatherers eating meat that they go for the organ meats first
which they value most highly, also even the bone marrow. Muscle meats are eaten last and least valued, yet
those of us in the modern age have access to mostly only these muscle meats. So it appears that even most
raw-foodists who include animal foods have trouble because they do not eat the best portion of the animal,
and may be shorting themselves nutritionally.
My question in all this is: If hominids evolved eating nothing but raw foods, and we are not yet adapted to
the cooking practices begun relatively late in our evolution (though considerably more ancient than
agriculture), why then do so many people fail on raw-food diets, even the ones who eat plenty of meat? Do
the above reasons just given make sense to those of you who are researchers? I don't get the feeling from my
perusal of the literature that very many Paleodiet researchers have even thought to address the cooking vs.
raw-foods survival question, and whether homo is now adapted to a certain amount of cooked foods (or to
certain ones customarily cooked during evolution) or not, but I would be interested to hear comments. To
me, this consideration also bear on the question of how we might compensate these days for the fact that we
cannot obtain organ meats and bone marrow, and whether cooking of certain foods may be a necessary evil
to help make up the difference somehow.
> At first I was tempted to dismiss this as a bizarre cultish sort of thing. But if these people
> apparear to be happy eating this way. Actually, as I've said, most people who try to 100%
> raw-foods do not succeed at it over the long-term--though they will rave about it during the
> short-term and be most vocal before they start having problems--and a lot them are not very happy
> about that fact, or disguise it. However, as you also say...
> The very fact that it's POSSIBLE for them to do this should, at minimum, throw back open to
> question whether or not humans have been eating cereal grains since before the advent of
> agriculture after all. Although it's hard to imagine them making up the majority of the diet, if
> people can comfortably eat wild grains without technology then there's not much reason to think
> they wouldn't, is there?
Great question. It *is* possible to eat grains without technology, and some individuals that try it--mostly
vegetarians--are able to succeed healthwise at it. However, there is also the well-known fact that apparent
success or not, phytates in grains greatly impair mineral absorption which seems to indicate we are not yet
very well adapted to them, even if it is possible to eat them.
--Ward Nicholson Wichita, KS
PALEODIET Archives
Subject: Raw foods
From: Dean Esmay
Date: Sat, 29 Mar 1997 15:57:48 -0500
40/298 (1997)
My, what a lot to absorb.

I found Ward and Kirt's messages interesting and astonishingly in-depth, for which I am grateful. But I grow
a bit anxious. I wish to assiduously avoid this becoming any kind of debate center on obscure, semi-religious
side-roads in modern nutrition.
No criticism of anyone at all is implied (after all, I brought it up, and recent messages on the subject are
thoroughly informative), but let's all please be very careful just how far along this road we travel.
Speculation about use of fire for cooking and the possibility that grains and legumes were commonly
consumed prior to agriculture is perfectly valid of course, and that was really where I meant to steer
discussion.
PALEODIET Archives
Subject: Re: Odds and Ends
From: Loren Cordain
Date: Sat, 29 Mar 1997 16:04:00 -0700
A few comments from the last paleodigest:
1. Dean writes: I wish we could get Boyd Eaton to join us, as he seems to have done an awful lot of work in
this department.
I am in regular communication with Boyd, and I hope you all will read our most recent piece on ancestral
exercise patterns (Cordain L, Gotshall RW, Eaton SB. Evolutionary aspects of exercise. World Review of
Nutrition and Dietetics 1997 81:in press.). As far as I know, Boyd is not yet on line, but I am hopeful that
this will occur shortly, as I know he now has a computer.
2. David Ross writes: In light of some of the upwardly revised estimates of the percentage of protein in the
paleo-diet (50-60%), could someone comment on the possibility that early man (or contemporary huntergatherers for that matter) was a victim of acidosis problems. I believe that there is a fair amount of evidence
that the acid-ash of excess protein (roughly, any more than 50 gms/day) can not, in the long run, be
neutralized by the buffering systems that maintain fluid PH levels at beneficial levels.
Speth has written extensively on this topic. A good starting point is (Speth JD. Early hominid hunting and
scavenging: the role of meat as an energy source. J Hum Evol 1989 18:329-43) Dr. Speth suggests that 300
g/day or roughly 50% of one+s normal total daily caloric intake would be the upper limit of protein that
could be safely consumed on a regular daily basis without impairing health. Speth points out that the liver
apparently has difficulty metabolising excessive dietary amino acids and the kidneys may be unable to
adequately excrete the urea and purine by-products of excessive dietary protein intake. However, there is
scant experimental evidence in humans to critically confirm or deny this. The classic study of Stefansson+s
all meat diet indicated that when carbohydrates were excluded from the diet, the ad-libitum macro nutrient
intake was ~80% fat and 20% protein. Protein levels above 20% produced feelings of nausea and un-ease
(Stefansson V. The Fat of the Land. MacMillan, New York, 1960, p60-89). Note that this experiment was
conducted in Bellevue Hospital under metabolic ward conditions, and the results of this prolonged (1yr)
dietary trial were published in most of the major scientific journals of that era including JAMA, J Am
Dietetic Assn, and the J Biol Chem.
3. Staffan writes: As far as I can figure out we don't even know for sure that there was savanna at the places
in question and if so what kind of savanna.
Obviously, we can never know with absolute certainty the climatic conditions and the vegetation associated
with certain geographic locations 2-4 million years ago (MYA). However, recent studies of marine eolian
dust records corroborate marine oxygen isotopic records and clearly show that more arid conditions occurred
in East Africa near 2.8 MYA, and 1.7 MYA (deMenocal PB. Plio-pleistocene African climate. Science
1995;270:53-59.). These time frames coincide with the first appearance of H. habilis (2.4 -2.2 MYA) and H.
erectus/ergaster (1.9-1.7 MYA). The marine climatic data correlate well with core pollen data from east
Africa from this time as well as with fossils of herbivores known to inhabit savanna grassland. All of these
pieces of the puzzle point to a reduction of tropical forest and woodland and increases in open savanna areas
dominated by graminae species.
4. Dean writes: Earliest evidence for use of fire for cooking among humans seems to be 25, 000 years (I have
no reference for that handy, let me know if that's in dispute).
41/298 (1997)
I refer Dean to the classic paper (James SR. Hominid use of fire in the lower and middle pleistocene. Current
Anthropology 1989 30:1-26.). There is no single date at which fire was mastered by all hominids at all
locations on the earth. Obviously, dated evidence for early fire use varies upon geographic locale. Certainly,
the ability to make fire (flint stones or drills) came much later in man+s evolution in some locales and never
in others. The Efe still rely upon collecting naturally occurring lightening fires and transporting it from
hearth to hearth, and the Tasmanian aborigines at first contact did not even use fire. This method (collecting
lightening fires) of fire control was likely the procedure first used by our ancestors. Fire probably was not
used initially to cook meat - let alone plant foods, but was initially a strategy for overwintering in more
northern latitudes (keeping warm, thawing frozen scavenged meat) or perhaps utilized in hunting. James
(1989) suggests that fire was being used by hominids between 230, 000-400, 000 years ago in Europe and
that the date of 400, 000-500, 000 years would have been too early for the evidence at Zhoukoudian in
China. The first appearance of hearths (burned stones arranged in a circle or semi-circle) represents
unequivocal use of fire, and no actual hearths have been found until the appearance of the neanderthals at the
end of the middle pleistocene (~200, 000 years ago). The Lehringen wooden spear (dated to 125, 000 years
ago in Germany) recovered from between the ribs of an extinct straight tusked elephant has been reported to
be fire hardened (Movius HL. A wooden spear of third interglacial age from lower saxony . Southwestern J
Anthropol 1950 6:139-42). Actually, it is thought that burning of wooden spear tips was done to ease its
carving with stone shavers as well as to make it more hard (Oakley KP et al. A reappraisal of the clacton
spearpoint. Proc Prehistoric Soc 1977 43:13-30). Fire then was certainly part of most of our species
technological repertoire by the appearance of behaviorally modern men 35, 000-40, 000 years ago. The
manner in which it was controlled varied by geographic locale over time.
Dean further comments: Although it's hard to imagine them making up the majority of the diet, if people can
comfortably eat wild grains without technology then there's not much reason to think they wouldn't, is there?
People can put many plant items as well as non-edible items (stones, bones, feathers, cartilage etc) into their
gastrointestinal tracts by way of putting them into their mouths. The key here is the ability of the GI tract to
extract the nutrients (calories, protein, carbohydrate, fat vitamins and minerals). Bi-gastric herbivores have
evolved an efficient second gut with bacteria that can ferment the fiber found in leaves, shrubs, forbs and
grasses and thereby extract nutrients in an energetically efficient manner (that is, there is more energy in the
food than in the energy required to digest it). Humans can clearly put grasses and grass seeds into our
mouths, however we do not have a GI tract which can efficiently extract the energy and nutrients. The starch
and hence carbohydrate and protein calories in cereal grains occur inside the cell walls of the grain. Because
the cell walls of cereal grains are almost completely resistant to the mechanical and chemical action of the
human GI tract, cereal grains have been shown to pass through the entire GI tract and appear intact in the
feces (Stephen A. Whole grains - impact of consuming whole grains on physiological effects of dietary fiber
and starch. Crit Rev Food Sci Nutr 1994 34:499-511). In order to make the nutrients in cereal grains
available for digestion, the cell walls must first be broken (by milling) to liberate their contents and then the
resultant flour must be cooked. Cooking causes the starch granules in the flour to swell and be disrupted by a
process called gelatinization which renders the starch much more accessible to digestion by pancreatic
amylase (Stephen A, 1994). It has been shown that the protein digestibility of raw rice was only 25%
whereas cooking increases it to 65% (Bradbury JH et al. Digestibility of proteins of the histological
components of cooked and raw rice. Brit J Nutr 1984 52:507-513). The main cereal grains that humans now
eat (wheat, rice, corn, barley, rye, oats, millet, sorghum) are quite different from their wild, ancestral
counterparts from which all were derived in the past 10, 000 years.
We have deliberately selected for large grains, with minimal chaff and which are easily harvestable. The
wild counterpart of these grains were smaller and difficult to harvest. Further, separation of the chaff from
the grain was time consuming and required fine baskets for the winnowing process. Once the chaff is
separated from the grain, the grains have to be milled and the resultant flour cooked. This process is time
consuming and obviously could have only come about in very recent geologic times. Further, the 8 cereal
grains now commonly eaten are endemic to very narrow geographic locations and consequently by their
geographic isolation would have been unavailable to all but a selected few populations of hominids.
42/298 (1997)
Now Dean, I haven't even touched upon the issue of antinutrients in raw cereal grains, and believe me this is
an issue. There are components in raw cereal grains which wreak absolute havoc with human health and well
being. The primary storage form of phosphorous in cereal grains is phytate and phytates bind virtually all
divalent ions. Excessive (50-60% of total calories) consumption of whole grain, unleavened breads
commonly results in rickets and hypogonadal dwarfism, and iron deficiency anemia (will provide the
references upon request). The main lectin in wheat (wheat germ agglutinin) has catastrophic effects upon the
gastrointestinal tract (Pusztai A et al. Antinutritive effects of wheat germ agglutinin and other Nacetylglucosamine-specific lectins. Brit J Nutr 1993 70:313-21). Additionally the alkylrescorcinols of cereals
influence prostanoid tone and induce a more inflammatory profile (Hengtrakul P et al. Effects of cereal
alkylresorcinols on human platelet thromboxane production. J Nutr Biochem 1991 2:20-24) as well as
depressing growth (Sedlet K et al. Growth depressing effects of 5-n-pentadecylresorcinol: a model for cereal
alkylresorcinols. Cereal Chem 1984 61:239-41. So, Dean if you choose to eat raw cereal grains, please
perform this experiment. Go out and buy some whole grain wheat seeds and swallow a handful of them.
Monitor your fecal contents over the next couple of days and report to this forum what you have observed. If
you choose to eat raw legumes (beans) you can probably smell the results of this experiment before you see
it.
Sometimes you get shown the smell before you see the light and it oftentimes occurs in the strangest of
places. What a long strange trip its been.
PALEODIET Archives
Subject: Fire for cooking
From: Dean Esmay
Date: Sat, 29 Mar 1997 20:54:14 -0500
Let me be clear that I was aware that evidence for use of fire goes back a half-million years or so. The
careful reader will note that I was specifically referring to evidence of use of fire -for cooking-. However, as
I cannot remember where precisely I got that little factoid about 25, 000 years, I'll withdraw the comment in
face of greater knowledge and will humbly seek the Stahl paper for further enlightenment.
If the protein absorbability of raw rice is normally 25%, then that means you could live for a while on the
stuff, if not very well. It would probably be a safe bet that if forced to go on such a regimen the metabolism
might be able to adjust somewhat given time. But if we can also posit that wild grains are even less rich in
calories and more full of indigestible bulk than modern artificially grown and bred stuff, then most likely our
ancestors didn't eat much grain, not as a staple anyway. Nevertheless someone had to figure out that it was
worth cultivating, so likely someone was chewing on it now and then. So referring to cereal grains as "not
digestible" by humans without cooking is probably not the most precise way of phrasing things.
As for my experimenting with eating raw grains and beans and reporting the results: Doctor Cordain, I am
inspired by your suggestion, and in the interests of science am starting immediately. I will be saving all my
post-prandially produced materials for the next two weeks in tightly sealed thermos containers. However, I
suspect I would lack sufficient objectivity in the area of gas spectrum analysis; after all, like most people, I
am quite convinced that my natural output has no particularly redolent effluvium. Knowing your own keen
interest in this subject area, I will dispatch my un-fossilized coprolite on a daily basis to the Colorado State
University for your (I am sure) assiduous and fully objective evaluation. Perhaps we can then co-publish a
paper on the results.
Yours in science,
Dean Esmay, Esq. Q.E.D. P.D.Q.
PALEODIET Archives
Subject: Raw foods, esp cereals
Date: Mon, 31 Mar 1997 03:15:21 +0100
Since all contemporary human populations appear equally intelligent, I find it a bit hard to believe that the
ability to control fire is not at least as old as man himself, that is more than 150, 000 years. Whether the need
to use it was there is perhaps a more difficult question.
43/298 (1997)
Whatever the use of fire during human evolution, the concept of making grains or beans edible by way of
soaking, souring and fermenting needs further consideration. Whole meal cereals and other seeds as well as
beans have in their shells phytic acid which strongly binds to minerals like calcium, iron, zinc and
magnesium to form insoluble salts, phytates. There is overwhelming evidence that whole meal cereals
through this mechanism decrease the absorption of such minerals. In this way cereals are an important
contributing cause of iron deficiency in third world countries and possibly in the western world.
As to calcium deficiency the picture is less clear. Mellanby found back in the 30s that dogs got rickets when
they were fed oats from early age. The possible absence of rickets in preagricultural skeletons, its apparent
increase during medieval urbanization and its epidemic explosion during Western European industrialisation
can hardly be explained only in terms of decreasing exposure to sunlight and decreased length of breastfeeding, nor to sub-optimal intake of foods rich in vitamin D or calcium. An possible contributing cause is a
secular trend of increasing inhibition of calcium absorption by phytate from cereals since these apparently
increased in amount during the Middle Ages, and since old methods of reducing the phytate content such as
dampening and heat treatment may have been lost during the emergence of large-scale cereal processing
from the agricultural revolution. Old fashion sourdough baking decreases the amount of phytic acid by use of
phytases, enzymes which are also found in the cereals but which often are destroyed during industrial
processing.
Non-westernized Melanesians from Kitava, Trobriand islands, that we have surveyed had four times higher
magnesium levels in hair compared to Swedes, Asian Indians and westernized Polynesians of Tokelau (the
latter three groups had similar levels) while those of zinc were two-fold higher in Kitavans. Whether the very
low phytate intake in Kitava (they do not eat cereals) is involved remains speculative.
The claimed notion of members of the raw food community that it might take a week or two for your
digestive tract to adjust to raw cereals finds to my knowledge no support in the scientific literature, and then
I'm exclusively referring to phytates.
As to other potential dangers of cereals, I have not much to say in this context, but Loren certainly has,
though he may want to wait until after publication of his extremely interesting paper on cereals to come.
Let me know if you want references.
Staffan
PALEODIET Archives
Subject: Coprolites
From: Loren Cordain
Date: Mon, 31 Mar 1997 11:28:31 -0500
Dean writes:
> As for my experimenting with eating raw grains and beans and reporting the results: Doctor
> Cordain, I am inspired by your suggestion, and in the interests of science am starting
> immediately. I will be saving all my post-prandially produced materials for the next two weeks in
> tightly sealed thermos containers. However, I suspect I would lack sufficient objectivity in the
> area of gas spectrum analysis; after all, like most people, I am quite convinced that my natural
> output has no particularly redolent effluvium. Knowing your own keen interest in this subject
> area, I will dispatch my un-fossilized coprolite on a daily basis to the Colorado State University
> for your (I am sure) assiduous and fully objective evaluation. Perhaps we can then co-publish a
> paper on the results.
Although I have had a singular experience with this kind of work (Cordain L. et al. The effects of an aerobic
running program on bowel transit time. J Sports Med Phys Fitness 1986;26:101-04), I will forego Dean's
generous offer for analysis of his un-fossilized specimens and suggest that he submit the evidence to Dr.
Kristin Sobolik at Texas A&M, who is generally considered to be the -Dean- of coprolite analysis. Although
we are having a good laugh with this topic, it is indeed a valuable source of evidence for prehistoric diets and
should be considered a serious topic. I refer our subscribers to: Sobolik KD. Direct evidence for the
importance of small animals to prehistoric diets: A review of coprolite studies. North Am Archaeologist
1993 14: 227-44. Dr Sobolik has a Web page and perhaps Dean could convince her to join this august group!
PALEODIET Archives
Subject: The definition of cooking
44/298 (1997)
From: Dean Esmay

Date: Mon, 31 Mar 1997 13:22:01 -0500
A member of the list who prefers to remain a "lurker" (i.e. one who remains relatively anonymous by not
posting messages) posted some questions, and made an interesting comment, which I thought I would
forward here:
-begin forwarded commentsOne thing I would like to ask is the definition of cooking? There seem to be many ways of breaking down
cell walls to make the nutrients available to humans. not all involving heat
Also I would like to add, talking of the digestibility of plant foods, I have seen reports of reindeer hunters
relishing the half digested contents of the reindeers stomachs as a source of vitamin C. The reindeer
presumably having grazed on lichen which people would not eat in unaltered form.
-end forwarded comments-
PALEODIET Archives
Subject: Promotion of this group
From: Dean Esmay
Date: Mon, 31 Mar 1997 13:55:35 -0500
Staffan Lindeberg wrote me in email recently:
> I cannot tell you how happy I am about PALEODIET, which seems to turn out into something very
> important for my own research. ... If it is not too much trouble for you I would appreciate a few
> words about how its existence is spread to the global research community as well as to invited
> individuals. If you find this of general interest you can of course post the answer to the list
> group.
As this is very much a non-paying, volunteer enterprise for me, I have limited time and resources for
spreading the word about the Symposium. My hope is that list members (such as Staffan) will either send me
email addresses of people who I might send an announcement to, or will just send invitations themselves to
people or groups who will be interested (it is not necessary that I be the person to contact everybody).
Here is the current announcement which I use for selected groups, which any list member may send to any
person or group that you believe will be interested. My only stipulation would be that this NOT receive wide
distribution on groups on the internet full of intellectually questionable elements (such as rec.food.vegetarian
or alt.support.diet), and that you keep in mind that we are generally only interested in promoting the list to
serious-minded scholars and researchers:
The Paleolithic Diet Symposium listserv is a semi-private, semi-moderated symposium for researchers with
interest in and knowledge of primitive diets and their relevance to modern life. Our primary audience is
biologists, paleontologists, anthropologists, physiologists, and health care professionals. Students or
members the lay public are not necessarily excluded, but any messages submitted to the list membership will
be reviewed before distribution to assure that the information presented, or the questions posed, reflect an
appropriate level of understanding of the science underlying the subject under discussion.
If you would like to subscribe, please fill out the following questionnaire and send it to
This is a standard questionnaire for all prospective subscribers to PALEODIET. You are not required to give
us more than your name and email address, although we would appreciate having the other information. Any
information you give on this questionnaire is solely for the list owners' information, and will NOT be sold or
used for any form of business solicitation.
Name: Preferred E-mail Address: Title: Institution: Phone Number: Research Areas: Other Areas of Interest:
Your list membership will be confirmed by the Listowner. You should receive a message confirming your
membership within a few days of sending in your subscription request. Thanks for your interest!
Owner: Dean Esmay
PALEODIET Archives
Subject: Re: Dean of paleodiet
From: Ray Audette
Reply-To:
45/298 (1997)
Date: Tue, 1 Apr 1997 00:23:15 -0800

Automatic digest processor wrote: Dr. Kristin Sobolik at Texas A&M,
> who is generally considered to be the -Dean- of coprolite analysis.
Actually, Dr. Sobolik is now at the University of Maine. Her teacher at A&M was Dr. Vaugh Bryant, who is
the head of the Anthropology department and also a full professor of bio-chemistry. His papers on coprolite
analysis in the 70's caused quite a stir and changed the way he ate as well (see People Magazine Feb. 19,
1979). Also among his students were Art Devaney PhD. (author of "Evolutionary Fitness").
Dr. Bryant was kind enough to review my book "NeanderThin" before publication and his input resulted in
several important corrections. He has been published in the popular press as well as the scholarly journals
and would make a good contributor to this list.
PALEODIET Archives
Subject: Re: fresh coprolites
From: Ray Audette
Reply-To:
Date: Tue, 1 Apr 1997 00:40:25 -0800
Even more striking differences can be observed between the fecal remains of dogs fed commercial dog food
and that of wolves or (in Texas) coyotes. See "A field Guide to Animal Tracks" for illustrations of wild
canine feces and compare these to the mess on your lawn. My own dog's (fed a wolf diet) feces are very
different than the other dog's in our neighborhood and this makes cleaning the lawn much easier.
> Automatic digest processor Knowing your own keen interest in this subject area, I will dispatch my
> un-fossilized coprolite on a daily basis to the Colorado State University for your (I am sure)
> assiduous and fully objective evaluation. Perhaps we can then co-publish a paper on the results.
PALEODIET Archives
Subject: Coprolites and Weak Chins
From: Art De Vany
Reply-To:
Date: Tue, 1 Apr 1997 12:23:18 -0800
Actually, my training is in economics and mathematics and I do research in social and economic systems as
complex, adaptive systems (a glimpse of what I do is in last week's The New Yorker (Mar 31, 1997)). I was
a professor at Texas A & M. I have read much of Vaughan Bryant's research, but I disavow any knowledge
or experience with coprolites (did I even spell it right?).
Turning from the scatological to evolutionary psychology, I have this question to pose.
I think it is evident that the female attitude toward men with "weak chins" lies somewhere between
indifference and contemp. Unlike the many studies of male preference for female waist to hip ratio studies
(where it is shown that there is a strong preference for small ratios, but not too small), I know of no studies
on this aspect of male physiology). Am I right on this aspect of female sexual selectiveness?
If this is the case, and I have little doubt that it is, does a weak chin indicate poor nutritional status of the
male as a child and, therefore, represent information about skeletal and other deficiencies that spell low
capability?
Or is it a throwback to a period when the prominent chin of homo sapiens was beginning to be a clue to
"good" genes? If this is so, then sexual selection could readily have accelerated the transition from homo
habilis to homo sapiens.
Arthur De Vany Professor NeXTMAIL, SUN Mail & MIME welcome
46/298 (1997)
PALEODIET Archives
Subject: Acidosis
From: "Jeffrey P. Krabbe"
Date: Wed, 2 Apr 1997 01:20:02 EDT
Frieda Wallace writes:
PA
> What evidence actually exists that high-protein diets cause acidosis? In PA what groups has this
> ever actually been observed? The Inuit eat remarkable PA amounts of meat and don't seem to have
> trouble with acidosis. Do they have PA some kind of special buffering that other humans do not?
By high-protein diets we need to delineate them as either ketogenic or anti-ketogenic. On a ketogenic diet,
irrespective of the levels of the two main macronutrients (fat and protein) ketoacidosis by definition CAN
NOT occur in normal healthy human beings on this type of diet for the following reasons: 1. Ketoacidosis
envelops due to a total lack of insulin on a ketogenic diet, insulin's levels are indeed low, but the sensitivity
of tissues to insulin's anti-ketogenic nature is vastly increased, i.e. less insulin but greater sensitivity to it.
Contrast this to a type I diabetic (IDDM) in which they are insulin deficient and are also ketoacidosis-prone.
Type II diabetics are NOT ketoacidosis prone due to higher systemic insulin, but less tissue sensitivity, thus
insulin's antiketogenic effect is in place. 2. Ketoacidosis occurs due to a competition between fuels.
Ketoacidosis only occurs in IDDM and alcoholics. In IDDM ketosis occurs with hyperglycemia (high blood
glucose levels). Since the body is accustomed to using carbohydrates are a fuel (especially the brain) the
ketones are not used and accumulate in the bloodstream, bring down pH, and a coma will shortly ensue. 3.
Ketones are self-regulating. The most amazing thing about ketosis as on a low-carb diet is the ability of
ketone bodies to limit their production so as to never cross the maximal threshold. They accomplish this
mighty task by feedback regulation which includes the secretion of insulin to limit overproduction. In IDDM
with the lack of insulin this negative feedback inhibition is no longer present, and insulin is unable to reprise
it's role in limiting over production. In fact hyperketonemia, and the uncontrolled production of ketone
bodies is accepted among the other above statements as one the central reasons this will occur in IDDM.
There are other factors, but they require a working knowledge of interconversion rates between AcAc
(acetoacetate) and BHB (beta-hydroxybutyrate), and the normal ratios of these two substrates in the body in
normal vs. IDDM subjects.
Don't be fooled by anyone though. A ketogenic diet will lower pH some, but that only reflects the dietary
intake of a ketogenic diet, the products of metabolism, and the compensatory mechanisms at work like bicarb reabsorption, ammonia to glutamine, and the like. If you are referring to non-ketogenic diet, that I
highly doubt there would be any acidosis, and even then the protein intake would have to be substantial and
far above any reasonable and prudent intake, i.e. excessive.
JPK
PALEODIET Archives
Subject: Acidosis
Reply-To:
Date: Wed, 2 Apr 1997 01:20:02 EDT
Frieda Wallace writes:
PA
> What evidence actually exists that high-protein diets cause acidosis? In PA what groups has this
> ever actually been observed? The Inuit eat remarkable PA amounts of meat and don't seem to have
> trouble with acidosis. Do they have PA some kind of special buffering that other humans do not?
47/298 (1997)
By high-protein diets we need to delineate them as either ketogenic or anti-ketogenic. On a ketogenic diet,
irrespective of the levels of the two main macronutrients (fat and protein) ketoacidosis by definition CAN
NOT occcur in normal healthy human beings on this type of diet for the following reasons: 1. Ketoacidosis
envelops due to a total lack of insulin on a ketogenic diet, insulin's levels are indeed low, but the sensitivity
of tissues to insulin's anti-ketogenic nature is vastly increased, i.e. less insulin but greater sensitivity to it.
Contrast this to a type I diabetic (IDDM) in which they are insulin deficient and are also ketoacidosis-prone.
Type II diabetics are NOT ketoacidosis prone due to higher systemic insulin, but less tissue sensitivity, thus
insulin's antiketogenic effect is in place. 2. Ketoacidosis occurs due to a competition between fuels.
Ketoacidosis only occurs in IDDM and alcoholics. In IDDM ketosis occurs with hyperglycemia (high blood
glucose levels). Since the body is accostomed to using carbohydrates are a fuel (especially the brain) the
ketones are not used and accumulate in the bloodstream, bring down pH, and a coma will shortly ensue. 3.
Ketones are self-regulating. The most amazing thing about ketosis as on a low-carb diet is the ability of
ketone bodies to limit their production so as to never cross the maximal threshold. They accomplish this
mighty task by feedback regulation which includes the secretion of insulin to limit overproduction. In IDDM
with the lack of insulin this negative feedback inhibition is no longer present, and insulin is unable to reprise
it's role in limiting over production. In fact hyperketonemia, and the uncontrolled production of ketone
bodies is accepted amoung the other above statements as one the central reasons this will occur in IDDM.
There are other factors, but they require a working knowledge of interconversion rates between AcAc
(acetoacetate) and BHB (beta-hydroxybutyrate), and the normal ratios of these two substrates in the body in
normal vs. IDDM subjects.
Don't be fooled by anyone though. A ketogenic diet will lower pH some, but that only reflects the dietary
intake of a ketogenic diet, the products of metabolism, and the compensatory mechansims at work like bicarb reabsorption, ammonia to gluatmine, and the like. If you are refering to non-ketogenic diet, that I highly
doubt there would be any acidosis, and even then the protein intake would have to be substantial and far
above any reasonable and prudent intake, i.e. excessive.
JPK
PALEODIET Archives
Subject: Re: Late Pleistocene Extinctions and Man's Carnivorous Ways
From: Loren Cordain
Date: Wed, 2 Apr 1997 20:07:00 -0700
Ray Audette made an interesting comment in a previous digest, noting that a man with 6 dogs and an atlatl
would have been a formidable predator capable of mass extinction of large pleistocene mammals. Much has
been written on man's role in the wide scale extinctions of large mammals that occurred at the end of the
pleistocene:
1. Stuart AJ. Mammalian extinctions in the late pleistocene of northern eurasia and north america. Biol Rev
1991 66:453-62.
2. Martin PS. The discovery of America. The first Americans may have swept the western hemisphere and
decimated its fauna within 1000 years. Science 1973 179:969-74.
3. Diamond J. The American blitzkrieg: a mammoth undertaking. Discover 1987 June:82-88.
4. Diamond J. The golden age that never was. Discover 1988 Dec:71-79.
5. Martin PS. 40, 000 years of extinctions on the planet of doom. Palaeogeography, Palaeoclimatology,
Palaeoecology 1990 82:187-201.
6. Haynes CV. Elephant hunting in North America. Sci Am 1966 214:104-112.
7. Grayson DK. The chronology of North American late Pleistocene extinctions. J Archaeol Sci 1989
16:153-65.
8. Mosimann JE, Martin PS. Simulating overkill by paleoindians. Am Sci 1975 63:304-313.
48/298 (1997)
During this period, which presumably coincided with increasing technological development and increasing
human populations, South America lost 46 out of 58 genera (80%) of mammals exceeding 44 kg; Australia
15 out of 16 (94%); North America 33 out of 45 (73%). For Europe and Africa the figures are considerably
lower (7 out of 24 - 29%) and (2 out of 44 - 5%) respectively. These mass extinctions affected large
terrestrial mammals exclusively, whereas invertebrates, small to medium terrestrial vertebrates, plants and
marine vertebrates continued almost unscathed. Martin and others believe that human overkill was largely
responsible for the extinction of these large mammals and that many of these huge behemoths were
wastefully killed and only certain portions of the carcass were selectively consumed. Present day hunter
gatherers prefer fatty portions of the carcass (organs, brains, marrow, tongue, fat depots, fatty cuts of meat),
and it is likely that our ancestors did as well. Butcher marks on mammoths in a number of european sites
indicate cut marks which suggest that tongues were highly prized. Ray Audette suggested that many of the
mammals that became extinct during this period were those which stored the most adipose tissue, and hence
were selectively preyed upon. Although, we have no way of determining the body composition of extinct
animals, it is likely that high northern and southern latitude mammals probably had to store fat similar to
modern mammals living in seasonal climates to survive through the winter. Given modern man's preference
for fat, it is no less likely that our ancestors did not seek out fat and fatty animals as well. Further, because of
selective utilization of animal tissues (both pre-historically and in present day hunter-gatherers), the fat
content of the human diet could have easily exceeded estimates of 15-20% of the total caloric intake which
have been widely used as a model for the paleolithic diet. The other point worth noting here is that for most
"paleolithic meals" protein and fat would have almost always occurred together (since these two elements
always were present with the kill - except for small stores of liver and muscle glycogen, animals are virtually
devoid of carbohydrate), whereas carbohydrates from collected plant foods would have more often been
eaten separate from the protein/fat combination. The health implications of these ancestral macronutrient
combinations are critical for modern man. Recent studies show that high fat, high CHO meals tend to
increase post-prandial lipemia compared to lower CHO meals, and that elevated blood lipid levels in the
post-prandial period are a significant risk factor for CHD (Chen Y.D. et al. Effect of variations in dietary fat
and carbohydrate intake on postprandial lipemia in patients with noninsulin dependent diabetes mellitus. J
Clin Endocrin Metabol 1993 76:347-51.). Taken together with Wolfe's data (Wolfe BM. Potential role of
raising dietary protein intake for reducing risk of atherosclerosis. Can J Cardiol 1995 11:127G-131G)
showing isocaloric replacement of CHO with animal based protein results in lowered total CHOL, LDL,
VLDL, TG and increased HDL, these experiments tend to confirm that our ancestral eating habits of
combining fat with high amounts of protein produces a less atherogenic profile than combining high levels of
carbohydrate with high levels of fat. Preliminary data from our laboratory utilizing game meat consumption
confirms this general concept (Tillmans C, Cordain L, Harris et al. Game meat is an effective dietary
component in lowering serum cholesterol. Proc Rocky Mtn Chapt ACSM; abstract, 1995).
Cordially,
PALEODIET Archives
Subject: Re: Late Pleistocene Extinctions and Man's Carnivorous Ways
From: Loren Cordain
Reply-To:
Date: Wed, 2 Apr 1997 20:07:00 -0700
Ray Audette made an interesting comment in a previous digest, noting that a man with 6 dogs and an atlatl
would have been a formidable predator capable of mass extinction of large pleistocene mammals. Much has
been written on man's role in the wide scale extinctions of large mammals that occurred at the end of the
pleistocene:
1991 66:453-62.
2. Martin PS. The discovery of America. The first Americans may have swept the western hemisphere and
decimated its fauna within 1000 years. Science 1973 179:969-74.
3. Diamond J. The American blitzkrieg: a mammoth undertaking. Discover 1987 June:82-88.
4. Diamond J. The golden age that never was. Discover 1988 Dec:71-79.
49/298 (1997)
5. Martin PS. 40, 000 years of extinctions on the planet of doom. Palaeogeography, Palaeoclimatology,
Palaeoecology 1990 82:187-201.
6. Haynes CV. Elephant hunting in north America. Sci Am 1966 214:104-112.
7. Grayson DK. The chronology of Northa American late Pleistocene extinctions. J Archaeol Sci 1989
16:153-65.
8. Mosimann JE, Martin PS. Simulating overkill by paleoindians. Am Sci 1975 63:304-313.
During this period, which presumably coincided with increasing technological development and increasing
human populations, South America lost 46 out of 58 genera (80%) of mammals exceeding 44 kg; Australia
15 out of 16 (94%); North America 33 out of 45 (73%). For Europe and Africa the figures are considerably
lower (7 out of 24 - 29%) and (2 out of 44 - 5%) respectively. These mass extinctions affected large
terrestrial mammals exclusively, whereas invertebrates, small to medium terrestrial vertebrates, plants and
marine vertebrates continued almost unscathed. Martin and others believe that human overkill was largely
responsible for the extinction of these large mammals and that many of these huge behemoths were
wastefully killed and only certain portions of the carcass were selectively consumed. Present day hunter
gatherers prefer fatty portions of the carcass (organs, brains, marrow, tongue, fat depots, fatty cuts of meat),
and it is likely that our ancestors did as well. Butcher marks on mammoths in a number of european sites
indicate cut marks which suggest that tongues were highly prized. Ray Audette suggested that many of the
mammals that became extinct during this period were those which stored the most adipose tissue, and hence
were selectively preyed upon. Although, we have no way of determining the body composition of extinct
animals, it is likely that high northern and southern latitude mammals probably had to store fat similar to
modern mammals living in seasonal climates to survive through the winter. Given modern man's preference
for fat, it is no less likely that our ancestors did not seek out fat and fatty animals as well. Further, because of
selective utilization of animal tissues (both pre-historically and in present day hunter-gatherers), the fat
content of the human diet could have easily exceeded estimates of 15-20% of the total caloric intake which
have been widely used as a model for the paleolithic diet. The other point worth noting here is that for most
"paleolithic meals" protein and fat would have almost always occurred together (since these two elements
always were present with the kill - except for small stores of liver and muscle glycogen, animals are virtually
devoid of carbohydrate), whereas carbohydrates from collected plant foods would have more often been
eaten separate from the protein/fat combination. The health implications of these ancestral macronutrient
combinations are critical for modern man. Recent studies show that high fat, high CHO meals tend to
increase post-prandial lipemia compared to lower CHO meals, and that elevated blood lipid levels in the
post-prandial period are a significant risk factor for CHD (Chen Y.D. et al. Effect of variations in dietary fat
and carbohydrate intake on postprandial lipemia in patients with noninsulin dependent diabetes mellitus. J
Clin Endocrin Metabol 1993 76:347-51.). Taken together with Wolfe's data (Wolfe BM. Potential role of
raising dietary protein intake for reducing risk of atherosclerosis. Can J Cardiol 1995 11:127G-131G)
showing isocaloric replacement of CHO with animal based protein results in lowered total CHOL, LDL,
VLDL, TG and increased HDL, these experiments tend to confirm that our ancestral eating habits of
combining fat with high amounts of protein produces a less atherogenic profile than combining high levels of
carbohydrate with high levels of fat. Preliminary data from our laboratory utilizing game meat consumption
confirms this general concept (Tillmans C, Cordain L, Harris et al. Game meat is an effective dietary
component in lowering serum cholesterol. Proc Rocky Mtn Chapt ACSM; abstract, 1995).
Cordially,
PALEODIET Archives
Subject: Boxgrove site
From: Dean Esmay
Reply-To:
Date: Fri, 4 Apr 1997 07:16:46 -0500
One of our lurking researchers was kind enough to send me reference to the following article on the
Boxgrove Site excavation, written by the excavation's director Mark Roberts and published in BRITISH
ARCHAOLOGY late last year. A tantalizing tidbit:
> Hunting at this period of our hominid ancestry is a controversial subject. From the late 1960s to
> the present day, the concept of `Man the Hunter' has become less popular with academics studying
50/298 (1997)
> the Lower Palaeolithic, with the alternative of carcass-scavenging being proposed as the major way
> in which hominids procured their meat. The evidence from Boxgrove, however, suggests strongly
> that the hominids of the period did hunt their meat.
There's more detail in the article, which is worth a look. Fire up your web browser and point it to:
http://britac3.britac.ac.uk:80/cba/ba/ba18/ba18feat.html#roberts
The article is apparently part of a series. The next part, entitled "And then came clothing and speech, "
appears here:
http://britac3.britac.ac.uk:80/cba/ba/ba19/ba19toc.html
-=-=Once in a while you get shown the light/ In the strangest of places if you look at it right ---Robert Hunter
http://www.syndicomm.com/esmay
PALEODIET Archives
Subject: Dietary medicine and herbs
From: Michael Schubert
Reply-To:
Date: Fri, 4 Apr 1997 19:45:54 +1000
Dear Paleodiet,
I have been lurking for the last few weeks, and I'm finding this one of the most interesting and stimulating
lists I've seen. On to business. One of the things I do is teach aspects of botany and herbal medicine in the
only university-based programme in natural and complementary medicine (naturopathy) in Australia.
1. I have often speculated with my students that early humans were provided with many of the compounds
that would protect them from illness via their diet. These very same compounds (e.g. alkaloids, tannins,
glycosides) are the main/active constituents of the products that herbalists prescribe today. I cite empirical
evidence that the cultivation of foodstuffs has "watered down" the bitter and pungent chemical load,
favouring sweet and salty tastes. This has resulted in a diet in contemporary humans, which is lacking in
these compounds, and therefore lacking in the protection that these bitter and pungent compounds provide.
What do list members have to comment?
2. I also point out, that the paleodiet consisted of a food source of up to 1500 species, with 500 major
"vegetables" and that the contemporary diet is drawn from 200 species, with only 80 major "vegetables".
Whilst I am always dubious of such numbers, I cannot recall which reference I used to derive these figures. I
think the point is useful to make to my students, but wonder whether I'm using erroneous figures, or if I'm
right off the track.
Any assistance, criticism or comments would be helpful.
3. Thanks for the stimulating diversions into dietary habits. I've been trying to interest the nutrition lecturer
in this area, but I think she thinks I'm a bit strange, bringing up the paleodiet in 1997. I thought I'd heard of
every diet imaginable, having been involved in alternative medicine for almost 20 years, but I've learned a lot
from these discussions.
4. In passing, my background is in traditional and alternative medicine, with formal university degrees in
biology & ecology and sociology. My final questions relate to a teaching and research interest regarding the
application of herbs in healing. When is the first evidence for the use of plant material in healing? What sort
of practices or technologies were used in the application of plants (or animal bits, or minerals for that matter)
in healing?
Any comments would be welcomed.
Regards
Michael Schubert
_____________________________________________
Michael Schubert School of Natural & Complementary Medicine Southern Cross University P.O. Box 157,
Lismore N.S.W. 2480 AUSTRALIA Tel: (066) 20 3649 International: 61-66-203649 Fax: (066) 20 3904
International: 61-66-203904 Visit us at http://www.scu.edu.au
_____________________________________________
PALEODIET Archives
51/298 (1997)
Subject: The paleolithic diet

From: Dean Esmay
Reply-To:
Date: Sat, 5 Apr 1997 01:20:33 -0500
Here is an attempt at constructing a modern equivalent to the diet humans likely evolved to eat:
Eggs: Any variety Meat: Any variety. Nuts: Any variety, excepting peanuts and other "nuts" that are not nuts
at all. Fruits: Any variety. Berries: Any variety. Vegetables: Any that do not require cooking to be
comfortably edible.
There would be almost very, very little of any of the following:
Cereal grains Beans Dairy products of any sort (outside of infancy) *Tubers (Perhaps an occasional treat?)
Eggs, meat, and nuts would be eaten ad libitum and would probably make up a majority of the intake. Meat
would be raw, dried, or cooked over an open fire and most likely rare. Fruits would be eaten sparingly. A
majority of the rest of the food would be eaten fresh and raw most of the time.
Such a diet is very easy to live on even in this modern world; moderately expensive perhaps, but not
prohibitively so for most, especially if it brings health benefits.
The question would be: is this a realistic modern reconstruction? Or are there flaws to the model? What
possible negative health consequences might be associated with such a diet?
Comment is invited.
PALEODIET Archives
Subject: Down's Syndrome Plants
From: Ray Audette
Reply-To:
Date: Sat, 5 Apr 1997 01:30:54 -0800
I cite empirical evidence that the cultivation of foodstuffs has
> "watered down" the bitter and pungent chemical load, favouring sweet and salty tastes. This has
> resulted in a diet in contemporary humans, which is lacking in these compounds, and therefore
> lacking in the protection that these bitter and pungent compounds provide.
Domestication of plants and animals involves selecting for one of the most common forms of mutation neoteny. Neoteny is the retention of juvenile traits into adulthood and results in the the plant or animal being
arrested in its' development. Thus the thorobred horse looks like a spindly colt instead of the squat
undomesticated horse as pictured in cave dwellings. Corn is an even better example as it took hundreds of
years to discover its undomesticated form growing wild in Mexico because it so little resembles our corn.
In plants, the fruit growing stage may be prolonged resulting in more carbohydrates and preventing it from
forming chemicals that protect the mature fruit and cause it to drop from the stalk. Without neoteny, wheat
would have much more tough bran and be nearly impossible to harvest as it would fall from the stalks onto
the ground (domestic wheat requires threshing to reproduce).
Some of the chemicals lacking in this immature fruit would be used by the plant to ward off pathogens and
parasites that would hinder reproduction. These chemicals include antibiotics, anti-fungals and anti-virals.
Mostly, these result in the fruit lasting longer without spoiling thus enhancing reproductive sucess.
Other chemicals are used by plants to ward off larger animals. These are also greatly reduced in neotenized
fruit. Without this effect some common types of modern foods could be hazardous (new strains of lima beans
for instance must be tested for cyanides for this reason).
Compared to the total number of plants in the global biomass, Primates eat relatively few species. Vegetable
foods edible to humans in nature (i.e. without technology) are edible to all primates. Most primates are on the
move constantly looking for these plants traveling many miles surrounded by plants in the rain forest looking
for the just right ones. Tens of millions of years of evolution have made primates resistant to the toxins these
edible plants contain. They may even be used by primates to ward off pathogens. Our primate DNA
recognizes them and responds appropriately.
52/298 (1997)
As well as these toxins, nonedible plants contain non toxic proteins that are not recognized in the database
known as our DNA. Our bodies don't know weather these are toxins, pathogens or short term anomolies.
After reaching a threshold of exposure however, the immune system may mount an attack. When this attack
harms the body itself, you are said to have an autoimmune disease.
Among paleolithic people who only eat foods edible to primates, autoimmune diseases are as rare as they are
in wild animals (practilly nil). This is true even for those who eat no vegetables at all (Inuit). Among people
who get a large part of their nutrition from plants not edible to othe primates (i.e. grains, beans, potatoes),
autoimmune diseases are rampant. It has been estimated that 95% of all Americans die of such disorders.
Ref:
Ames, B.N. "Paleolithic Diet, Evolution and Carcinogens" Science 238, 1633-34
Budiansky, S. "The Covenant of the Wild:Why Animals Chose Domestication" New York, William Morrow
& Co., 1992
Stahl, A.B. "Hominid Dietary Selection Before Fire" Current Anthropology Vol. 25, No. 2, 4/84
Stefansson, V. "Cancer Disease of Civilization" New York, Hill and Wang, 1960
BTW the earliest example of a cultivated plant (several neatly planted rows - carbon dated to 25, 000 years)
was of a species of medicinal plant recently aproved for use (by referendum) in California.
PALEODIET Archives
Subject: Re: Uncultivated Plant Foods & Early hunting vs scavenging
From: Loren Cordain
Reply-To:
Date: Sat, 5 Apr 1997 10:38:00 -0700
In response to Michael Schubert+s comments about the role of non-cultivated plant foods in human
evolution, I suggest the following reference:
1. Eating on the Wild Side: the pharmacologic, ecologic and social implications of using non-cultigens. Etkin
NL (Ed.) The University of Arizona Press, Tucson & London, 1994.
This book represents the definitive statement on the medicinal values of wild plant foods used by huntergatherers.
In the last digest, Dean writes:
> Hunting at this period of our hominid ancestry is a controversial subject. From the late 1960s to
> the present day, the concept of `Man the Hunter' has become less popular with academics studying
> the Lower Palaeolithic, with the alternative of carcass-scavenging being proposed as the major way
> in which hominids procured their meat. The evidence from Boxgrove, however, suggests strongly
> that the hominids of the period did hunt their meat.
53/298 (1997)
There has been a recent trend in the anthropology community towards acceptance of wide scale hunting by
early hominids (H. erectus/ H. heidelbergensis/ archaic H. sapiens) inhabiting both europe and Asia circa
(~500, 000 - 300, 000 years before present (BP)). There are two recent finds which clearly support this
notion. Thieme and co-workers recently reported in Nature (Thieme H. Lower palaeolithic hunting spears
from Germany. Nature 1997 385:807-810) the discovery of four wooden throwing spears which were dated
to 400, 000 years BP. Thieme mentions that -all spears, although of different lengths, were manufactured to
the same pattern, with the maximum thickness and weight at the front; the tails are long, and taper towards
the proximal end. In all of these respects they resemble modern javelins, and were made as projectile
weapons rather than thrusting spears or lances-. He concludes by saying, -The discovery of spears designed
for throwing means that theories of the development of hunting capacities and subsistence strategies of
Middle Pleistocene hominids must be revised, as well balanced, sophisticated hunting weapons were
common from an early period of the Middle Pleistocene onwards. Accordingly, meat from hunting may have
provided a larger dietary contribution than has previously been acknowledged-. The second piece of
information which is highly suggestive of wide scale hunting during this period is the recent discovery of
stone artifacts in central Siberia which have been dated to more than 260, 000 year BP (Waters MR. et al.
Diring Yuriakh: A lower paleolithic site in central Siberia. Science 1997 275:1281-84). Because this site is
located at approximately 55 degrees N. latitude, even during warmer, interglacial periods, the climate of this
region would have been severe. Consequently for at least half or more months of the year, plant food which
could provide sustenance for hominids would have been unavailable. Additionally, to live in this climate, I
quote Waters, - would require sophisticated use of fire, clothing and shelter for survival-. Scavenging of
game would, at best, be an irregular affair and would not provide a regular caloric source - consequently it
seems likely that hunting provided these early humans with both clothing and food. Any scavenged game
that may have been acquired during the deep winter months would likely have been frozen and quite difficult
to eat; hence fire may have been used to thaw scavenged meat. Cordially,
PALEODIET Archives
Subject: Fat percentages in PaleoDiet
From: Kevin Tisdel
Reply-To:
Date: Sat, 5 Apr 1997 20:04:47 -0600
The idea seems to be that paleolithic diet was extremely high in fat and proteins, compared to our modern
diet of fat and carbohydrates. Since it is illogical to conclude that the people of this time could function at a
weight of 300 pounds or more, the conclusion seems to be that a high fat/ protein diet is quite a bit healthier
IN MODERN MAN than our current high fat/ carb. diet and that we could get along quite well with this diet.
My concern is that we aren't dealing with a level playing field. I understand that fat is an extremely efficient
energy souce, but the caloric requirements of paleolithic man must have been fantastic. I wonder what the
affects of a high fat/ CARBOHYDRATE diet would be on a modern human who walked perhaps 10-15
miles a day in search of food and shelter. Might the caloric expenditures be the real variable we should be
dealing with? With that amount of exercise, it would seem to me that it would take an exceptional amount of
carbohydrates to result in an unhealthy body. And what of long term side effects of a high fat/ protein diet?
Given paleolithic man was lucky to live into their twenties, is it logical to extend that diet to modern man
who lives almost four times as long? I do not question that the Paleolithic diet was appropriate for Paleolithic
man, but I am hesitant to extend that diet to modern man without further understanding of these other
variables. I am new to the list and appologize if this has been covered in other discussions.
Cordially, Kevin Tisdel
PALEODIET Archives
Subject: Paleolithic diet and longevity
Reply-To:
Date: Sun, 6 Apr 1997 09:23:30 -0600
54/298 (1997)
Kevin Tisdel writes:

> Given paleolithic man was lucky to live into their twenties, is it logical to extend that diet to
> modern man who lives almost four times as long? I do not question that the Paleolithic diet was
> appropriate for Paleolithic man, but I am hesitant to extend that diet to modern man without
> further understanding...
Maybe Loren can cite more recent references than I, but an interesting chart on Paleolithic longevity I have
seen had data indicating that late Paleolithic peoples actually lived into their early to mid-30s on average.
And even more interestingly, they were also perhaps slightly longer-lived (though not by much) than the
agricultural people who followed them and who ate less meat/fat and higher quantities of carbohydrates.
These longevity figures are for skeletons where the age at death was determined using standard
"paleopathological" techniques, for prehistoric humans who lived in the Eastern Mediterranean where a lot
of research has been done and the data is available. Main thing to note here about the short average lifespans
compared to modern times is that the major causes are thought to have been "occupational hazards, " i.e.,
accidents, trauma, etc., stresses of nomadism, and so forth. [Source: Angel, Lawrence J. (1984) "Health as a
crucial factor in the changes from hunting to developed farming in the eastern mediterranean." In:
Paleopathology at the Origins of Agriculture. (proceedings of a conference held in 1982) Orlando: Academic
Press. pp.51-73]
Median Lifespan (yrs) MALE FEMALE
- 30, 000 to 9, 000 B.C. 35.4 30.0 (late "Paleolithic" times)
- 9, 000 to 7, 000 B.C. 33.5 31.3 ("Mesolithic" transition period from Paleolithic to some agricultural
products)
- 7, 000 to 5, 000 B.C. 33.6 29.8 ("Early Neolithic, " i.e., agriculture first spreads widely)
- 5, 000 to 3, 000 B.C. 33.1 29.2 ("Late Neolithic, " i.e., the transition is mostly complete
- 3, 000 to 2, 000 B.C. ("Early Bronze" period) 33.6 29.4 - 2, 000 to 1, 450 B.C. ("Middle People/Bronze
Kings") 36.5 31.4 - 1, 450 to 1, 150 B.C. ("Late Bronze") 39.6 32.6 - 1, 150 to 650 B.C. ("Early Iron") 39.0
30.9 - 650 to 300 B.C. ("Classic") 44.1 36.8 - 300 B.C. to 120 A.D. ("Hellenistic") 41.9 38.0 - 120 to 600
A.D. 38.8 34.2 - Medieval Greece 37.7 31.1 - Byzantine Constantinople 46.2 37.3 - 1400 to 1800 A.D.
("Baroque") 33.9 28.5 - 1800 to 1920 A.D. ("Romantic") 40.0 38.4 - "Modern U.S. White" (1982-ish
presumably) 71.0 78.5
I am not entirely sure what to make of these figures, but all other things being equal (which they may not
have been, I don't know) longevity seems to have decreased slightly during the first several millennia after
the introduction of agricultural foods, then gradually rebounded. If true, wouldn't this indicate that
meat/protein consumption itself could not have been the factor responsible for decreased longevity? (Looks
like it would to me.) From some of the later time periods involved where civilizations were known to be on
the rise or fall, it appears that social factors have the biggest impact on longevity, particularly since longevity
never rose above about age 45 for long, often falling below that figure for centuries at a time, until the 1900s,
since which time it has almost doubled.
PALEODIET Archives
Subject: Meat or fruit or both
Reply-To:
Date: Mon, 7 Apr 1997 00:38:06 +0100
Remains of hominid hunters from cool and semi-arid sites outside Africa are important evidence that human
metabolism can handle large amounts of meat. They do however not seem to provide any clues as to whether
we also can handle carbohydrate-rich staple foods.
Contemporary humans may differ widely in their capacity to metabolize dietary carbohydrate. I can vaguely
see four groups represented by 1) non-western ethnic groups, 2) glucose tolerant westerners, 3) glucose
intolerant westerners and 3) diabetic westerners. There are no sharp boundaries between the three latter
groups. Considerable evidence shows that few if any middle-aged or elderly westerners have not at least one
disturbed variable related to this metabolic syndrome of insulin resistence (abdominal overweight, increased
blood pressure, low HDL-cholesterol etc). That is, virtually every adult westerner can improve one or more
of these by improving their lifestyle.
55/298 (1997)
Accordingly it may not be enough to study whether Pleistocene carbohydrate-rich foods appear detrimental
when eaten by westerners. We may have to compare some of the groups as to their carbohydrate sensitivity,
and to see what happens when they obtain a truly ideal weight. Contemporary hunter-gatherers can obviously
handle dietary carbohydrates much better than we can until they also become westernized. One important
cause seems to be their leanness. Nutrient-dense foods apparently help maintain a low body weight
irrespective of whether the are rich in carbohydrate, protein or fat. Satiety needs to be further studied.
Staffan
------------------------------------------------------------------Staffan Lindeberg M.D. Ph.D. Dept of Community Health Sciences, Lund University, Mailing address: Dr
Staffan Lindeberg, Primary Health Care Centre, Sjobo, S-22738 Sweden, +46 416 28140, Fax +46 416
18395 http://www.panix.com/~donwiss/paleodiet/sl1.shtml
-------------------------------------------------------------------
PALEODIET Archives
Subject: Herbs
Reply-To:
Date: Mon, 7 Apr 1997 00:38:16 +0100
Michael Scubert wrote:
> ... compounds that would protect [humans] from illness via their diet ... are the main/active
> constituents of the products that herbalists prescribe today.
Prescribing herbs is in most cases pharmacy rather than nutritional advice. Nobody knows if they shorten or
lengthen your life. Herbal drugs are a common cause of pathologically increased liver enzymes in Sweden.
There are at least 30 nutrients which are suspected by at least 10 authorities to protect from at least one
common western disorder and which were eaten in larger than present amounts by our remote ancestors.
There are at least another 50 substances that can find some kind of scientific support as being protective.
Epidemiology shows relationships but many variables are interrelated which may explain why giving
carotene to Finish smokers increased their mortality despite beneficial relations in earlier surveys.
Biochemical studies in laboratories can never take account of all the thousands of variables involved, many
of which are not yet discovered. Intervention trials on *total* mortality, not just incidence rates of the disease
under investigation, would solve the case. But they are very expensive and not often promoted by those who
have the money, and when they cannot be performed as double-blind placebo-controlled trials you would in
the end not be sure that you had not changed some other factor than the one you were studying.
These are just a few reasons why "ancient" foods are safer than drugs and why Michaels nutrition lecturer
friend should listen to him when he tells her about paleodiet. If he would ask her about the best diet for a
chimpanzee she would probably not suggest the foods they get in the zoo but the ones that were available
during chimpanzee evolution. But I suppose the main reason she considers paleodiet strange is that nobody
gave lectures on it during her training.
Anyway I think we have reason to be optimistic. Nutrition authorities I encounter in Europe are obviously
highly influenced by the concept of a "paleolithic diet standard" (for many of them it started with the paper
Paleolithic Nutrition by Eaton and Konner in N Engl J Med in 1985), although they seldom state it in public.
So keep swinging.
Regards, Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: Re: Age span of current hunter gatherers
From: Loren Cordain
Reply-To:
56/298 (1997)

Date: Mon, 7 Apr 1997 11:29:00 -0600
Ward has done a great job in presenting Angel's estimates of human age spans from paleolithic times to
present. I also disagree with Kevin Tisdel's statement saying "paleolithic man was lucky to live into their
twenties". The fossil record for the paleolithic period is obviously VERY incomplete and therefore there is
no means to provide an unbiased statistical analysis of life tables for populations living 20, 000-30, 000 years
ago or more. The entire number of fossil hominids ever found for this period could fit nicely into a small
room. We have very little evidence on how these people died, nor can the age at death be accurately
determined. We certainly can distinguish between child and adulthood, but relative age at death during
adulthood can only be broadly estimated. The best surrogate for studying the age distribution of pleistocene
humans is the age distribution of living hunter gatherers. This information is also inexact as most hunter
gatherers, because of illiteracy, do not keep precise records of age. The only data I know of in which life
tables have been established for living hunter gatherers is that of Neel's work with the South American
Yanomama (JV Neel. Health and disease in unacculturated Amerindian populations. Ciba Foundation
Symposium #49; 1977, 155-177.). During the early 1960's to the mid 1970's, Neel and colleagues made a
census of 29 Yanomama villages (there was minimal western contact at this time) and developed a life table
showing percentage of the population by age groups. He compared the life table curves of the Yanomama to
that in Japan (the world leader) during the mid 1960's and to that of India in 1900. Obviously, the Japanese
were far superior to the Yanomama at every point on the curve, however the Yanomama life table curves
were superior to those of Asians living in India until age 40 and were at least equal to those of the Asians
until age 80. This data is remarkable given that the Yanomama have no modern medicine, engage in constant
inter-tribal warfare and live in an environment where tropical diseases are rampant. So, this data suggests
that modern day hunter gatherers have higher mortality rates throughout their lifespan when compared to
modern, industrialized societies, but lower rates than in poor, agrarian societies. For estimates of the activity
levels of paleolithic man, I refer Kevin to our most recent paper on this concept (Cordain L, Gotshall RW,
Eaton SB. Evolutionary aspects of exercise. World Rev of Nutrition 1997 81:in press).
PALEODIET Archives
Subject: Modern foods for a paleodiet
From: Loren Cordain
Reply-To:
Date: Mon, 7 Apr 1997 18:36:45 -0400
Dean writes:
> Here is an attempt at constructing a modern equivalent to the diet humans likely evolved to eat:
> Eggs: Any variety Meat: Any variety. Nuts: Any variety, excepting peanuts and other "nuts" that
> are not nuts at all. Fruits: Any variety. Berries: Any variety. Vegetables: Any that do not
> require cooking to be comfortably edible. There would be almost none of any of the following:
> Cereal grains Beans Dairy products of any sort (outside of infancy) *Tubers
(* Perhaps an occasional treat?)
57/298 (1997)
Dean is to be commended at his attempt to reconstruct a paleolithic diet from commonly available
supermarket foods. I think Ray Audette has done quite a bit of work on this in his book, -Neanderthin-. Also,
we should not forget Boyd Eaton+s book, -The Paleolithic Prescription- which is perhaps the first effort at
re-creating ancestral diets with modern day foods. Although in his book, Boyd originally advocated cereal
grains and low fat dairy products, I have had numerous conversations with him indicating that this advice
came about because of his co-authors (Shostak & Konner) concerns, and he now would probably temper or
delete this advice. Our stoneage ancestors certainly consumed wild bird eggs, however this was only a
seasonal matter and likely provided a small percentage of their total yearly caloric consumption. Because
eggs are the genetic matter for procreation, natural selection has operated in a manner similar to the eggs (eg
seeds) of graminae (grains, grasses) by endowing eggs (the whites primarily) with antinutrients that can have
severe and adverse effects in humans and other predators when eaten raw. Raw egg white contains avidin, an
antinutrient which impairs the metabolism of the vitamin biotin, which is critical in carboxylase dependent
reactions such as chain elongation and desaturation of fatty acids. Avidin also impairs the metabolism of
other B vitamins. Additionally, eggs do no spoil in their shell (even though it is permeable to bacteria)
because egg white contains an iron binding lectin (conalbumin) which can impair iron absorption in humans
(Alderton G. et al. Identification of the bacteria-inhibiting, iron binding protein of egg white as conalbumin.
Arch Biochem 1946 11:9-13). Based upon studies of present day hunter-gatherers, our ancestors almost
certainly ate the tubers (storage roots) of many plants. These roots include raw, edible rhizomes, corms etc of
a wide variety of plants. The main tubers of agricultural man (potatoes, sweet potatoes, yams, cassava etc)
are inedible without cooking because of their high anti-nutrient load and their storage form of carbohydrate.
These tubers contain huge amounts of poorly digested starch which becomes more digestible during cooking
. Additionally many, but not all antinutrients are denatured or reduced with cooking and/or processing
(soaking in water or leaching in alkaline solutions). The difference between wild edible roots and
commercially available starchy tubers is that, the starch content is generally much lower in wild roots and
there tends to be more stored sachharides and less toxic antinutrients. Examples of domesticated roots which
certainly should be a part of a -modern paleolithic diet- would include carrots, beets, parsnips, radishes,
daikon, turnips or any other non-starchy root which is edible and non-toxic in its raw state. Potatoes are
clearly inedible in their raw state and there have been more than 30 deaths reported in humans in this century
from eating raw potatoes (Slanina P. Solanine (Glycoalkaloids) in potatoes: toxicological evaluation. Fd
Chem Toxic 1990 28:759-61.). Although Dean mentions that any fruit would be accepable on his version of
the -modern, paleolithic diet-, there may be some important exceptions here. The glycemic response of
virtually all wild fruits is generally quite low because of low sugar, and starch contents, bitterness and a high
fiber content. Modern fruits have been selected over the last 2-3 thousand years or more for a larger size, an
increased sugar content and a reduced fiber content (Spiegel R. Domestication of fruit trees. In: The Origin
and Domestication of Cultivated Plants. C. Barigozzi (Ed), Therefore, many of the super market fruits we eat
can induce a hyperinsulinemic response in susceptible individuals when eaten in excess, particularly dried
fruits (raisins, dates, figs etc) and starchy fruits (bananas). Berries and melons generally have low effective
glycemic responses. Although Dean advocates meats, he fails to mention organ meats. Clearly, our ancestors
ate brains, marrow, kidneys, gonads, (sometimes liver), thymus etc. Our research group is currently
examining the complete fatty acid spectrum of a wide variety of organ meats in North American wild
animals. As for a treat, I recommend good dry white or red wine. We have preliminary evidence to show that
moderate (2 glasses) consumption of wine does not promote weight gain and may in fact increase insulin
sensitivity so as to help prevent symptoms of syndrome X (Cordain L. et al. Influence of moderate daily
wine consumption upon body weight regulation and metabolism in healthy free living males. J Am Coll Nutr
1997 16: in press.). Additionally, moderate wine consumption has been shown to reduce the mortality from
CHD and the phytochemicals in wine have antineoplastic effects and a wide variety of other health
promoting effects.
Cordially,
PALEODIET Archives
Subject: Lifespan Numbers
From: Ray Audette
Reply-To:
Date: Mon, 7 Apr 1997 22:23:38 -0700
58/298 (1997)
The only data I know

> of in which life tables have been established for living hunter gatherers is that of Neel's work
> with the South American Yanomama (JV Neel. Health and disease in unacculturated Amerindian
> populations. Ciba Foundation Symposium #49; 1977, 155-177.).
As pointed out by Marvin Harris in "Cannibals and Kings:The Origins of Culture"(New York, Random
House 1977), the Yanomama raise crops and hunting sucess is tempered by the resulting population denisity.
Still if Neolithic people can obtain results like these, can true Paleolithic people do less.
A more interesting number might be arrived at by modeling the effects of the lack of auto-immune disease
noted by Tanchou and Stefansson (As documented in V.S.'s "Cancer Disease of Civilization, New York, Hill
and Wang, 1960) in true hunter-gatherers on American mortality rates. As 95% of all Americans currently
die of auto-immune diseases, the resulting number may be a lot closer to the ideal human life span (1
milliom hours) than is currently enjoyed in this country.
I'm no mathematician (Art Devanney, are you reading this?) so I don't know the practicality of this, but such
a number would interest the popular press and sell millons of books for several authors on this list! I have
received many letters from readers claiming remissions from several types of auto-immune disorders and
have personal experence with remissions from diabetes and rheumatoid arthritis (which is why I wrote my
book).
PALEODIET Archives
Subject: Physical activity
Reply-To:
Date: Tue, 8 Apr 1997 01:40:28 +0100
Kevin Tisdel seems to believe that paleolithic man would normally walk 10-15 miles a day in search of food
and shelter. I do not share his belief. Energy expenditure must have been higher than in sedentary westerners,
but construction workers and some other manual labourers of the first half of this century had probably a still
higher level of physical activity on an average. Nevertheless this has apparently not been dramatically
protective in terms of cardiovascular disease and diabetes among such groups [1].
As for contemporary hunter-gatherers, it is true that Australian Aborigines had a very high level of daily
physical activity [2], but those living in most other parts of the world apparently had not. On an average they
have spent 2-3 hours per day for subsistence activities [3-7]. But the variablity is large. On the one extreme,
a female Machiguenga of the Amazon dug up enough tubers in one hour to feed 25 adults for one day [7].
On the other extreme we find populations living in deserts, the Arctic or similar marginal habitats and who
have spent more than seven hours a day hunting or gathering [3]. The very high level of physical exercise
exerted by the Tarahumara Mayans of Mexico [8] can hardly be considered representative for traditional
human populations.
1. Dorn J, Trevisan M. Physical activity and cardiovascular disease: a review of the literature. Nutr Metab
Cardiovasc Dis 1992; 2: 40-6.
2. O'Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines
after temporary reversion to traditional lifestyle. Diabetes 1984; 33:596-603.
3. Hayden B. Subsistence and ecological adaptations of modern hunter-gatherers. In: Harding RDS, Teleki
G, ed. Omnivorous primates: gathering and hunting in human evolution. New York: Columbia University
Press, 1981: 344-421.
4. Sahlins M. Stone Age Economics. Chicago: Aldine, 1972
5. Taylor CB, Ho KJ. Studies on the Masai. Am J Clin Nutr 1971; 24:1291-3.
6. Lee RB. What hunters do for a living, or, how to make out on scarce resources. In: Lee RB, DeVore I, ed.
Man the hunter. Chicago: Aldine, 1968: 30-48.
7. Johnson A, Behrens CA. Nutritional criterioa in Machiguenga food production decisions: a linearprogramming analysis. Human Ecology 1982; 10:167-89.
8. Groom D. Cardiovascular observations on Tarahumara Indian runners--the modern Spartans. Am Heart J
1971; 81:304-14.
------------------------------------------------------------------Paleolithic Diet Symposium List
59/298 (1997)
Staffan Lindeberg M.D. Ph.D. Dept of Community Health Sciences, Lund University, Mailing address: Dr
-------------------------------------------------------------------
PALEODIET Archives
Subject: Paleolithic diet and longevity
Reply-To:
Date: Tue, 8 Apr 1997 02:42:56 +0100
I suppose life expectancy at birth for Pleistocene hominids may have been around 30 years but not
necessarily that low. The main cause of a low figure would be high mortality rates among infants, children
and adolescents. Life expectancy at 30 may very well have been an additional 25 years or more. How much
more can not be estimated by use of available osteological methods [Isan, M. Y., Kennedy, K. A. R. (1989).
Reconstruction of life from the skeleton. New York, Wiley-Liss].
Age estimations are very difficult after middle age and fossil remains are often classified as belonging to a
human aged "40 years or more". An age process is not equally rapid in different humans, samples are often
small and many of the age processes are influenced by lifestyle (e.g. bone loss). Other problems are lack of
contemporary autopsy material for comparison, bone changes occuring after death, selection bias, different
disease patterns during different times and insufficient standardization of age estimation methods.
By the way, don't we have any paleoanthropologists or paleopathologists in the group? If not we ought to go
and get some.
Staffan Lindeberg
PALEODIET Archives
Subject: Estrogenic compounds in the diet
From: Pat Stephens
Reply-To:
Date: Tue, 8 Apr 1997 18:29:43 -0400
I have been reading "Our Stolen Future" by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
with dismay. May I inquire of this list if all plant and manmade estrogenic compounds are heat stable? Are
any commonly found and eaten phytoestrogenic or chemical estrogen look-alike compounds heat labile?
Those prefering a raw food diet would find this information very valuable, indeed.
thank you,
Pat Stephens
Sat, 5 Apr 1997 19:00:03 -0400
> There are 3 messages totalling 204 lines in this issue. Topics of the day: 1. The paleolithic diet
> 2. Down's Syndrome Plants 3. Uncultivated Plant Foods & Early hunting vs scavenging
PALEODIET Archives
Subject: Honey & Beans & Omega 3 fats
From: Loren Cordain
Reply-To:
Date: Wed, 9 Apr 1997 19:37:09 -0400
Dean writes:
> Eaton, Shostak, and Konner also seem to feel (in this particular book) that honey is an important
> source of dietary carbohydrate, and use this in part to justify a recommendation that a majority
> (60%) of daily calories for modern humans should come from carbohydrate. But this seems absurd;
60/298 (1997)
> while I am quite certain that honey would be prized as a delicious treat by most any primitive
> peoples, it seems awfully unlikely that braving wild bee nests just to obtain a few ounces of
> honey would ever be a daily ritual. It also doesn't seem that there would be enough beehives with
> enough honey to make the stuff more than an occasional treat even if braving bees nests were trivial.
I understand that Dr. Janette Brand Miller is now a part of our group. She has recently written an article on
the role of honey in pre-industrial diets (Allsop KA, Brand Miller J. Honey revisited: a reappraisal of honey
in pre-industrial diets. Perhaps she can comment upon Dean's remarks.
Dean makes the comment:
> Yet this all seems odd; what form of wild beans exist and grow in such quantities that they could
> ever be a staple for anybody, and how are we to imagine most primitive peoples preparing them? Can
> they realistically be eaten without cooking? What cooking methods would be common if so? If beans
> are natural, why do they cause gas (which indicates fermentation of indigestible products in the
> gut)? If they aren't, what are we to make of accounts of the !Kung and other primitive peoples who
> -do- eat them?
Clearly, hunter gatherers have been documented eating legumes, however under most cases, the legumes are
cooked or the tender, early sprouts eaten raw rather than the mature pod. Some legumes in their raw state are
less toxic than others, however most legumes in their mature state are non-digestible and/or toxic to most
mammals when eaten in even moderate quantities. I refer interested readers to : (Liener IE. Implications of
antinutritional components in soybean foods. Crit Rev Food Sci Nutr. 1994 34:31-67; Gupta YP.
Antinutritional and toxic factors in food legumes: a review. Plant Foods for Human Nutrition 1987 37:20128; Noah ND et al. Food poisoning from raw red kidney beans. Brit Med J 1980 2:236-7; Pusztai A. et al.
The toxicity of Phaseolus vulgaris lectins. Nitrogen balance and immunochemical studies. J Sci Food Agric
1981 32:1037-46). These references summarize the basics about legume indigestibility/toxicity, however
there are hundreds if not thousands of citations documenting the antinutritional properties of legumes.
Legumes contain a wide variety of antinutrient compounds which influence multiple tissues and systems and
normal cooking procedures do not always eliminate these (Grant et al. The effect of heating on the
haemagglutinating activity and nutritional properties of bean (Phaseolus vulgaris) seeds. J Sci Food Agric
1982 33:1324-26). There are a variety of compounds in beans which cause gas. Mainly, these are the nondigested carbohydrates, raffinose, stachyose and sometimes verbascose which provide substrate for intestinal
microflora to produce flatus (Calloway DH et al. Reduction of intestinal gas forming properties of legumes
by traditional and experimental processing methods. J Food Sci 1971 36:251-55).
Dean states:
> There is also the issue of what are now popularly referred to as the "essential fatty acids, " the
> Omega-3 and Omega-6 groups of fats which are now acknowledged to be protective against a host of
> diseases. And yet the best sources of the Omega-3 family seem to come almost entirely from fish or
> refined vegetable oils, both of which seem like they would be largely unavailable in any great
> quantity to most primitive humans. This also brings up the issue of fish, by which I generically
> refer to all freshwater and saltwater fish, including shellfish, eels, etc., as well as seaweeds.
> How natural are these to the human animal? Some humans obviously have great access to them, but
> did we evolve with such ready access?
The answer to this one is fairly straight forward. Until about 40, 000 years ago, humans rarely exploited the
aquatic environment (Eaton SB. Humans lipids and evolution. Lipids 1992 27:814-20). This inference can be
made by the lack of fossil evidence for fish hooks, weirs, fishing spears etc; also by the absence of fossilized
fish bones in our ancestors camps. How then did our ancestors acquire N-3 fats unless they ate foods of
aquatic origin? There are different forms of omega 3 fats; the 18 carbon fat (linolenic acid) occurs widely in
the plant kingdom, particularly in green leafy vegetables. The 20 and 22 carbon omega 3 fats occur almost
exclusively in foods of animal origin. Data from our laboratory shows that the omega 6/omega 3 (N6/N3)
ratio for wild herbivore muscle tissue is between 3-4:1 whereas the lowest N6/N3ratio occurs in the brain of
wild herbivores and is about 1:1. Because plants contain small amounts of total fats and because their N3 fats
(linolenic acid) must be chain elongated and desaturated by the liver to form the 20 and 22 carbon fats which
are essential for cell structure and function, animal tissues provide a more readily available source of N3
fatty acids. Muscle and organ tissues of wild animals, because they provided the majority of the calories for
our ancestors were the environmental template which shaped our present day N3 and N6 requirements.
Estimates from our laboratories suggest that the evolutionary N6/N3 ratio would have been between 2.5 -4.0
which is much lower than current estimates of 10-15:1 for most western diets.
Cordially,
61/298 (1997)
PALEODIET Archives
Subject: Modern reconstruction
From: Dean Esmay
Reply-To:
Date: Mon, 7 Apr 1997 20:23:46 -0400
My purpose in my attempted construction was in the hopes that others would find faults with it, in the hopes
that we might reach something resembling consensus on what is closest to a natural diet for modern humans.
I had assumed that "meat" included organ meats, but as Loren points out it's probably best to mention them
explicitely, since at least in America so many people rarely or never eat them. (In such a large country you
can find someone somewhere eating just about anything of course; I am speaking of what is typical daily fare
for most.)
I have questions and critiques of the diets posted in both _Neander Thin_ by Ray Audette and _The
Paleolithic Prescription_ by Eaton, Shostak, and Konner. I have more criticism of _The Paleolithic
Prescription_ because Eaton et. al. seemed almost afraid to follow their own logic to its natural conclusions.
For example, they noted that hunter/gatherer diets average anywhere from 20% to about 60% protein, and
used this to recommended a diet of no more than 20% protein. They noted that dairy and cereal grains were
alien to humans in nature, but stated that these foodstuffs were "too valuable" to eliminate, without bothering
to say what was so valuable about them or even to open the question of whether that was a valid assumption.
Eaton, Shostak, and Konner also seem to feel (in this particular book) that honey is an important source of
dietary carbohydrate, and use this in part to justify a recommendation that a majority (60%) of daily calories
for modern humans should come from carbohydrate. But this seems absurd; while I am quite certain that
honey would be prized as a delicious treat by most any primitive peoples, it seems awfully unlikely that
braving wild bee nests just to obtain a few ounces of honey would ever be a daily ritual. It also doesn't seem
that there would be enough beehives with enough honey to make the stuff more than an occasional treat even
if braving bees nests were trivial.
I have always assumed that Eaton et. al. made these recommendations both out of prudent conservatism and
out of a desire not to face a strong backlash. The American nutritional establishment tends to worship at the
ground of whole grains and dairy products and to view both protein and fat with antipathy. Nevertheless this
also means that while the book is marvelously informative (and I highly recommend it to anyone interested
in this subject), on the subject of their explicit dietary recommendations (which make up only one chapter of
a lengthy and truly -excellent- book) their logic seems flawed.
As for Ray Audette's book _Neander Thin_: his diet recommendations (which I think are overall very
sensible) forbids even small amounts of alchohol or vinegar, which may or not be reasonable, depending on
whether humans in the wild ever eat over-ripe fruits. He also states rather unequivocally that potatoes and
beans are foreign to the human digestive tract, and yet we know that the African !Kung eat some forms of
beans (see _The Paleolithic Prescription_ again) and that some primitive peoples eat some forms of wild
tubers.
Loren's recent comments about wild tubers being radically different from the popular potatoes eaten by most
Westerners, however, make a great deal of sense. But this still leaves open the question of beans. It seems to
be commonly believed that primitive peoples eat beans. Eaton et. al. mention beans eaten by the !Kung San
in _The Paleolithic Prescription_, Ann Louise Gittleman states flatly that "Cavemen didn't eat grains.
Cavemen relied on meats, vegetables, BEANS, fruits, berries, and nuts." (Emphasis mine) (see Beyond
Pritikin_, Revised 1996 edition, p. 25, by Ann Louise Gittleman, M.S.) and I believe Barry Sears
recommends beans as part of a natural diet in his popular book _THE ZONE_. Yet this all seems odd; what
form of wild beans exist and grow in such quantities that they could ever be a staple for anybody, and how
are we to imagine most primitive peoples preparing them? Can they realistically be eaten without cooking?
What cooking methods would be common if so? If beans are so natural, why do they cause gas (which
indicates fermentation of indigestible products in the gut)? If they aren't, what are we to make of accounts of
the !Kung and other primitive peoples who -do- eat them?
There is also the issue of what are now popularly referred to as the "essential fatty acids, " the Omega-3 and
Omega-6 groups of fats which are now acknowledged to be protective against a host of diseases. And yet the
best sources of the Omega-3 family seem to come almost entirely from fish or refined vegetable oils, both of
which seem like they would be largely unavailable in any great quantity to most primitive humans.
62/298 (1997)
This also brings up the issue of fish, by which I generically refer to all freshwater and saltwater fish,
including shellfish, eels, etc., as well as seaweeds. How natural are these to the human animal? Some
humans obviously have great access to them, but did we evolve with such ready access?
I pose more questions than answers, in the hope of stimulating discussion of the issue among those who
know more than I. I will now be quiet and hope to hear from others.
PALEODIET Archives
Subject: Teeth and Longevity
From: Mavis Wood
Reply-To:
Date: Thu, 10 Apr 1997 15:41:11 +1200
May I, as a lurker, ask if the subject of teeth has been considered?
May one of the reasons for early death have been lack of the necessary teeth to process food and in the later
European Palaeolithic at least, skins and sinews. Worn down and uncared for teeth would also be liable to
form abscesses which, I presume could be fatal.
The teeth of people living on grain processed with rough stone querns would also be very worn it would
seem, are there any statistics on this available?
Would better tooth care since the 1920's be a factor in the present day longer life in the present day North
American population.
ME Emberson MA Hons Prehistoric Archaeology (Edin)
PALEODIET Archives
Subject: Interesting web links
From: Dean Esmay
Reply-To:
Date: Sat, 12 Apr 1997 22:54:15 -0400
Those with an interest in exploring a bit about fish in the ancient human diet may wish to see the following
URL, which has a bit of information and lots of contact information for researchers working in that field:
http://atlas.otago.ac.nz:800/~foss/ICAZ/icaz.htm
Also there is a short article by Mike Richards on the use of meat in ancient British Isles diets. The suggestion
is that the Brits were depending primarily on meat for their nutritition up to around 2000 b.c. There's not a lot
of detail but it's interesting anyway:
http://britac3.britac.ac.uk:80/cba/ba/ba12/ba12feat.html#richards
PALEODIET Archives
Subject: Re: Modern Lifespans
From: Art De Vany
Reply-To:
Date: Mon, 14 Apr 1997 15:48:30 -0700
The Vikings used to note the decline of a warrior with the phrase "long in the tooth" an indicator of gingivitis
and the eventual onset of the inability to consume adequate amounts of protein.
Audette's hypothesis is a compelling one that, to my knowledge, has not been tested. We do know that
displaced American Indians forced to rely on Federal food supplies to their remote areas suffered greatly:
1. The supply was unreliable and starvation was more or less common.
2. The foodstuffs were simple starchy substances, like highly refined flour, and canned fruit in high sugar
content syrup.
There was a complete lack of animal protein and fresh fruits and vegetables. The mortality associated with
this diet, and the imposed restrictions on mobility and hunting, was brutal.
63/298 (1997)
Even today, the rural diet is far inferior to the urban diet in most places around the globe. If you get off the
interstates and back into remote areas, it is appalling what they eat there.
Eskimo and Pima children consume far more simple carbs than even children in the city --- who are candy
junkies.
PALEODIET Archives
Subject: Life span
From: robert rosenstein
Reply-To:
Date: Mon, 14 Apr 1997 21:12:56 EDT
The following thoughts were prompted by Ray Audette's posting of 12 April concerning diet and life span.
LIFE EXPECTANCY The life expectancy of a group or a nation is a statistical figure based on past
mortality records. The life expectancy figure has nothing to do with nutrition, sanitation, medicine, or
environment. Whether any of these factors have anything to do with life expectancy is arguable. There is no
doubt that certain conditions would LOWER a person's life expectancy, but on the other hand there is no
evidence - at least that I am aware of - that a particular diet (all other things being equal) will determine a
person's life span.
A study of history, especially recent history, seems to indicate that other forces are at work. The increase in
life expectancy among the peoples of ghettos and of the Third World can not be explained on the basis of
sanitation or of diet. The same can be said of the population growth experienced in early Medieval times and
at the time of the Industrial Revolution - certainly the most unsanitary of times. (I dread to think that there
are evolutionary fores working over which we have no control :-()
WHY LIFE SPAN IS IMPORTANT Life span is important for several reasons:
1. A short life span affects population growth. If life expectancy is very short, as it probably was among the
Paleoindians, for example, it could mean
a. That there could be an equilibrium between births and deaths, in a word, a stable population. b. That there
could also be an equilibrium between the group and the available food resources. c. That "family" would
probably not exist because the necessity to reproduce could not be dependent on individual initiative. I would
wonder, too, especially at that stage of our development, and in particular in cold climates, whether the
sexual function was still periodic in nature.
2. A long(er) life expectancy would naturally lead to an increase in population and thus population pressures:
a. There eventually could be an imbalance between population and food supply. This usually has led to part
of the group splitting off. b. Social and political behavior in a larger population would develop along entirely
different lines.
It can be argued that over-population of groups is what led to the eventual populating of the hemisphere.
DIET In Linguistics, the statement used to be made that all languages were sufficient unto themselves. I
wonder if the same thing couldn't be said of all "natural" diets. The diets of all the people we know, or know
about, seems to have been adequate to the daily tasks they had to perform. This, unless I'm mistaken, would
hold for peoples in all climates and in all situations - except when faced with famine conditions. It is almost
as if having something to eat is more important than what is eaten (which may be a heretical statement :-))
TWO CENTS WORTH OF OPINION The subject of life expectancy has received very little attention from
the various disciplines studying our evolution. It has received a good deal of attention in recent years because
of the population explosion. It is a sad commentary on the mentality of our times that what should be looked
upon as a wonderful development and a blessing has been twisted into a condemnation of the same peoples
who have been so thoroughly victimized for the past six or seven hundred years. After all, an increase in life
expectancy should be looked upon with joy, as it should enable people to devote more of their life-time to
the development and exploration of those skills, talents and meditations which could give a life a meaning
beyond the humdrum round of sleep and labor. It is clearly insinuated that the peoples of the Third World
should stop procreating at the present rate: a classic example of blaming the victim.
robert
64/298 (1997)
PALEODIET Archives
Subject: Teeth & Lifespan
From: "Robert E. Wynman, DDS"
Reply-To:
Date: Wed, 23 Apr 1997 19:01:57 -0400
May one of the reasons for early death have been lack of the necessary teeth to process food and in the later
European Palaeolithic at least, skins and sinews. Worn down and uncared for teeth would also be liable to
form abscesses which, I presume could be fatal.
The teeth of people living on grain processed with rough stone querns would also be very worn it would
seem, are there any statistics on this available?
Would better tooth care since the 1920's be a factor in the present day longer life in the present day North
American population.
My OPINION only, based on study, research & practice in this area since 1965:
Teeth of our ancestors lasted as long as they were needed 'til the introduction of cooked food & the toxins
produced by that pyrolyzinf process. Rampant dental diseas apparently did not appear 'til the time sucrose
sugar was processed out of former foods & made cheaply available to the population. These conclusions
probably come mostly from the studies of Weston Price, DDS in the 20-30's & the writings of Guy Claude
Burger in the last 15 years out of France.
Hope that's helpful,
Robert E. Wynman, DDS, FAGD
PALEODIET Archives
Subject: Modern Lifespans
From: Ray Audette
Reply-To:
Date: Sat, 12 Apr 1997 23:53:16 -0700
The relationship between life span and medical (and dental) progress is not a very strong one. Although great
strides have been made in combating some forms of infection, auto-immune diseases still kill the majority of
people in the world.
Other areas of technological innovation may have added more years to our life indirectly.
A natural human diet consists of meats, fruits, vegetables edible raw, nuts and berries. All of these are much
more common in the average persons diet because of the invention of the railroads and refrigeration. The
increases seen in life span seem to follow these innovations more closely than any other factors. Before these
were invented people ate more non-primate foods such as grains, beans, potatoes, milk products(such as
cheese)and sugars which are less perishable.
Thus only technology allows us to afford a "stone age diet"!
PALEODIET Archives
Subject: What happened to the list?
From: Dean Esmay
Reply-To:
Date: Wed, 23 Apr 1997 19:33:59 -0400
A number of list members have likely been wondering why there has been no activity to speak of here on the
paleodiet list for the last week. A long and detailed answer would involve far more detail than anyone really
needs to know, but here's the short of it:
65/298 (1997)
This is a "moderated" list. This means that except for certain individuals, no messages submitted to the list
will be distributed until the list owner (yours truly) clears it. This is an automated process; when a message is
submitted to the list, it appears in my mailbox and if I approve it I send a special message to the listserv robot
telling it to go ahead and distribute the message. This is not a particularly time-consuming task under normal
circumstances; either I approve of the message or I write the person who wrote it and explain my problem
with it.
Last Monday I had a serious family emergency that was both unforeseen and unavoidable and which
required me to drive over 5, 000 miles in only one week. Upon leaving for the trip I brought my laptop
computer in the hopes of keeping up with essential functions like clearing list messages. However, technical
problems and practical matters regarding the trip left me with no free time whatsoever and no practical
ability to get online even if I did have an hour or two to spare. The upshot has been that until my return at
2:00 a.m. this morning. I was unable to clear any messages submitted to me, nor even to add new members
(and we have had several academics apply for membership in the last week, who were only finally added this
evening).
Under normal circumstances I would have simply had someone else take over moderation duties until my
return but the sudden and extraordinary circumstances didn't make that practical. There will, however, be no
repeat of this problem.
List members have my apology for unusual delays over the past week and my promise not to see this
problem repeated. It is not conceivable that I will be called away for such a lengthy time period while
completely unable to get online again.
Thanks all for your patience. Our list membership has now grown to over 100 people, the majority of whom
have doctorates, and most of the remainder with master's degrees or in graduate programs in related fields.
We have not seen a great deal of traffic but I expect that to pick up in the coming weeks, as we have had
many thought-provoking discussions so far and there is much more to discuss.
For those of you who are interested, archives of all previous discussios on this list are now available on the
World Wide Web. I especially encourage all new members to review this resource, as there is much
information to absorb from the conversations we have had in the last two months. All members should see
http://maelstrom.stjohns.edu/archives/paleodiet.html and probably bookmark it for future reference.
Thanks again, and welcome to our new members.
Dean Esmay, Paleodiet list owner
PALEODIET Archives
Subject: Late pleistocene extintions...
From: Dean Esmay
Reply-To:
Date: Wed, 23 Apr 1997 20:10:12 -0400
The following letter was sent to me by Jorge Martinez-Moreno, an assistant professor at Universitat
Autonoma de Barcelona:
Dear Dean Esmay,
Thanks for the information of Paleodiet List.
I will explain differents ideas about the letter of Loren Cordain (04/02/1997) about Megafauna extintions...
The comment of Ray Audette (wich I don't reed) about a man with 6 dogs and an atlatl is a formidable
predator is interesting and provocative, but I think is a old idea (for example see papers of P. Martin or Clive
Vance Haynes at 60's).
The extintions of megafauna at Late Pleistocene is a very controversial hypothesis, but the recent discovery,
at specially, the new datations or arrival of human groups to new continents are a critical factor in the debate.
For example, the arrival at Sahul, than the last number of archaeological journal Antiquity, T.D. Price has
new sites with termoluminiscence datations about 100.000 BP aprox. Egally, Monte Verde (Chile), suggets a
expansion of temporal span between megafauna and hunter-gathrerers.
This exemples critized the "blitzkrieg" notion. Evidently human are a factor important in the extintion of
megafauna, and in recent context humans are the causal factor, but during the Last Glacial, perhaps are a
secondary agent or an important factor into a mammals group very dammaged in a stress ambient.
66/298 (1997)
Reflexions about megafauna extintions and hunting subsistence Is very interesting the book of GAMBLE, C
(1993). Timewalkers. Penguin. Paper of Daniel FISHER at the book : The Evolution of Human Hunting
(Nitecki-Nitecki eds.) (1988) Plenum Press is a very interesting taphonomyc approach to resolution of
mastodont mortality at North America.
I will very interested in the reference concret cited for Loren Cordain: "bucher marks on mammoths in a
number of european sites indicate cut-marks....", because I don't know that bone modifications are really
"cut-marks" and the european sites.... For example in the superb Gary HAYNES book: Mammoths,
Elephants and Mastodonts not cite cut-marks at european sites.
I hope my message is not very difficult to read for you
Sincerely
Jorge Martinez
PALEODIET Archives
Subject: Honey
From: Jennie Brand Miller
Reply-To:
Date: Wed, 23 Apr 1997 21:54:35 -0400
Dear Everyone,
Thank you for the invitation to join this discussion group. I haven't read the archives yet but I learnt
something from reading today's correspondence. I'd like to add something to the debate about honey. Here is
the abstract of our paper on honey in the British Journal of Nutrition. Is there a word limit in our
correspondence?
Synopsis: In pre-industrial times, honey was the main source of concentrated sweetness in the diets of many
peoples. There are no precise figures for per capita consumption during most periods in history because
honey was part of either a hunter/gatherer or subsistence economy. Until now, historians and food writers
have proposed that it was a scarce commodity available only to a wealthy few. We do know, however, that in
a cash economy honey was sold in large units (gallons and even barrels) and it was present in such
abundance that mead was a common alcoholic drink made from honey. A reappraisal of the evidence in the
Stone-Age, Antiquity, the Middle Ages and early Modern times suggests that ordinary people ate much
larger quantities of honey than has previously been acknowledged. Intakes at various times during history
may well have rivalled our current consumption of refined sugar. There are implications therefore for the
role of sugar in modern diets. Refined sugar may not have displaced more nutrient rich items from our
present day diets but only the nutritionally comparable food, honey.
Below is the text about modern hunter-gatherer diets.
Modern hunter-gatherers Unfortunately, quantitative studies of hunter-gatherer diets are scarce. We know
that for the Hazda of Tanzania 'meat plus honey' constitute 20% of food eaten by weight (Woodburn 1963).
The remainder of the diet is of vegetable origin and so in energy terms 'meat plus honey' will contribute
much more than 20%. The Mbuti pygmies of the Congo obtain as much as 80% of their dietary energy from
honey during the honey season (Crane 1983), but this lasts for only two months of the year (Turnbull 1963).
The Veddas or Wild Men of Sri Lanka esteem honey so highly that they regularly risk their lives to obtain it
(Crane 1983). The local bees often nest in crevices on rock faces and these men will lower themselves into
the ravine suspended by only a bamboo ladder. The Veddas sometimes fill a hollow tree trunk with honey
and then place flesh in it as a means of preserving the meat for times of scarcity. This is certainly suggestive
of plentiful supplies of honey.
In the New World, the Guayaki Indians of Paraguay have honey as the very basis of their diet and culture
(Crane 1975). Vellard reports that, 'one group of fifteen people had seven large vessels holding at least forty
litres altogether.' Unfortunately we do not know how long this was to last them nor how many people were to
partake of it.
Many Australian Aboriginal tribes regard the honey of the native bee as 'the supreme delicacy' (Low 1989).
In the rest of the world it is usually the males of a tribe who hunt for honey, but amongst some Australian
Aborigines this task falls to the women. One method they employ involves capturing a bee and attaching a
small feather to its body, so that on release it can be more easily seen and followed all the way back to the
nest. On removing the contents, Australian Aborigines eat everything - honey, wax, dead bees and brood
(which provides protein) - with relish.
67/298 (1997)
In 1972-3 Meehan lived for a year with the native Anbarra people of Northern Australia (Meehan 1982).
Over four one-month periods, chosen to be representative of the different tropical seasons, she recorded the
weights of foods consumed. The results indicate an average intake of 2 kg honey per person per year.
However, Meehan points out that the wet season that year was unusually long and this may have diminished
honey foraging activity. In addition, this group of Anbarra had supplies of store food (providing 35-58% of
dietary energy) including refined sugar, which may have reduced the incentive to go about the tricky and
time-consuming activity of tracking down bees' nests.
The bees of the New World are stingless but may bite or burn with caustic liquids anyone who threatens the
nest. Yet neither this, nor the stings of Old World bees deter a hunter-gatherer in pursuit of honey. The
amount of honey available from one region to the next will vary greatly depending on the extent to which the
environment suits bee activity. The evidence suggests that the amount eaten by 'Stone-Age' people was
limited only by how much was available in their surroundings.
The Bushmen of South Africa lay claim to no personal possessions of any type, except that is, for bees' nests
(Free 1982). Perhaps it was to reduce the likelihood of such a nest being robbed that a man first carried it, in
its hollow log, back from the forest to a place near his dwelling. Perhaps that year was favourable for his
bees, which in their excess numbers swarmed, coming finally to rest in a clay pot their owner had discarded
in the grass, thus unknowingly inventing the first man-made hive.
Best wishes Jennie
Assoc. Professor Jennie Brand Miller Human Nutrition Unit, Dept. of Biochemistry G08 University of
Sydney, 2006, Australia FAX: 61.2.9351.6022 Ph: 61.2.9351.3759
PALEODIET Archives
Subject: More on teeth and health
From: Dean Esmay
Reply-To:
Date: Wed, 23 Apr 1997 19:17:10 -0400
Submitted by one of our list members who prefers to remain anonymous:
See the Times London for an article Science Briefing by Nigel Hawkes
Dental defects * Roost boost * Tracing tots
Roots of disease http://www.the-times.co.uk/news/pages/Times/frontpage.html?1529511 for April 21 1997.
It is a report of tha work of Professor Robert Genco in Buffalo NY on gum disease and it's connection to
other potentially fatal conditions.
-also submittedANTIQUITY http://intarch.ac.uk/antiquity/index.html
VOLUME 68 NUMBER 258 MARCH 1994 Sarah L.R. Mason, Jon G. Hather & Gordon C. Hillman
Preliminary investigation of the plant macro-remains from Doln Ve^stonice II, and its implications for the
role of plant foods in Palaeolithic and Mesolithic Europe You have to get the journal or photocopy (by
library interloan I expect)
Dental Microwear (evidences of past diet) Hominoids and hominids
http://comp.uark.edu/~pungar/referenc.html
I expect you have these already! Never mind the fun is in the chase! :-)
PALEODIET Archives
Subject: Re: Clocks and set points
From: Art De Vany
Reply-To:
Date: Thu, 24 Apr 1997 13:23:35 -0700
Aging and obesity research share an outlook that is misguided.
68/298 (1997)
Aging researchers are looking for the clock that times the onset of the aging process. This reminds me of the
time that brain researchers were looking for the command neuron in the brain that ran everything. It is an
error that comes from what I call the centralized mind set; the coordination of processes that appear to be
complex is attributed to a central commander. Nothing real and adaptive, like a human being, works that way
(think of it as the Soviet model of the organism).
There are many clocks in the human organism: the glucose clock, the unwinding of peptides, the
deterioration of the telemeres, the pulses of the calcium gradients over the cell membranes, the tidal rhythms
in the lungs, the heart beat. All these clocks are self-organized and lack any central control. They work the
way they do because that is the way things are--the chemistry and the dynamics make it happen, no
mysterical force or guidance does it.
All these clocks that have been tracked exhibit chaotic dynamics; their basins of atraction are not fixed
points, or even limit cycles but strange attractors. The clock beat (or return time on the attractor) pulses with
the rhythm of natural systems which is described by power laws. Such laws, where intensity is distributed
over frequency as 1/f, are the intrinsic dynamics of all natural systems that have been studied in enough
detail to make the determination. Our mail list shows the same kind of behavior, bursts of activity and
periods of stasis without characteristic scale; we share the statistical distribution of earthquakes and stock
market price changes.
The signature of chaos and adaptive dynamic systems is a mixing of many time and event scales. This is
precisely the situation in the human organism. There is no single clock. What makes us tick is the mixing of
millions of clocks, each running on their own attractors and pulsing at power law variations. The search for
an aging clock is doomed and misconceived.
The real issue is how all these clocks are coordinated. I suspect that cyclic amp, the ubiquitous second
messenger hormone is at work, among many other coordinating mechanisms. That is how slime mold
organisms become coordinated---a glucose crisis triggers a camp release which coordinates aggregation.
From then on, the aging of the organism follows a definite sequence.
A similar argument can be made for the fat set point (the idea confuses a basin of attraction with a point,
ignores how you move out of a basin, fails to specify how the set point is set, and neglects that a set point is
not evolutionarily elegant in design), but I have used up my space.
PALEODIET Archives
Subject: Megafaunal extinctions, Caries in Hunter-Gatherers, Honey
From: Loren Cordain
Reply-To:
Date: Fri, 25 Apr 1997 09:49:00 -0600
69/298 (1997)
I would like to welcome Professor Jorge Martinez to our group and appreciate his comments upon the "over
kill hypothesis" and megafaunal extinctions at the end of the pleistocene. I hope that my comments in a
previous edition did not imply that man was solely responsible for the disappearance of most large mammals
in all continents except Africa at the close of the Pleistocene. Clearly, climatic changes which altered habitat
have been implicated, however the criticism of this argument is that profound changes in climate were a
recurring feature throughout the Pleistocene. Previous transitions from cold to warm (interglacial) periods,
which are thought to have been very similar to the transition from the Last Cold Stage to the Holocene
(Postglacial), were not accompanied by mass extinctions. Because the fossil record (admittedly incomplete)
contains numerous examples of stone tools, imbedded in the remains of extinct megafauna, cut marks on the
bones of megafauna, and the remains of megafauna in many human habitation sites, the evidence clearly
indicates these beasts were hunted extensively and were an integral part of the human diet. Although the idea
that humans were the sole cause of the "coup de grace" of megafauna is clearly controversial, few are in
disagreement that expanding human populations at the end of the Pleistocene and its consequent increase in
hunting pressure, combined with dryer conditions which concentrated the remaining beasts in smaller
geographic locales together spellt disaster for these large beasts. A final observation concerning the overkill
hypotheses involves "Optimal Foraging Theory" which states that organisms tend to optimize energy
expended in acquiring food vs. the energy available in the food. For hunter gatherers, collecting plant food is
less energetically rewarding than hunting or scavenging animal food. It has been shown that the picking,
winnowing, grinding and cooking of grass seeds (grains) yields about 100-1, 300 kcal/hr whereas the returns
on encounters with game animals are in the range of 2, 500-15, 000 kcal/hr (Hawkes K et al. Optimal
foraging models and the case for the !Kung. Am Anthropologist 1985;87:401-05). It is obvious that the
killing of large beasts would be more energetically efficient than the killing of small beasts, hence our
ancestors would have preferentially chosen megafauna (once they were technologically advanced enough to
kill these beasts effectively) over smaller game (Webster D. et al. Optimal hunting and pleistocene
extinction. Human Ecology 1984;12:275-89). I am unable to easily find the citation showing cut mark on the
hyoid bone of mammoths in central europe. I remember having a conversation with Boyd Eaton about this,
and he indicated that the location of the bone cut marks suggested that the tongues of these behemoths may
have been a highly preferred part. Next time, I speak with him, I'll see if I can track down the citation. I can
provide a reference which shows a 2.40 meter wooden spear made of yew which was found between the ribs
of a skeleton of the extinct Straight-Tusked Elephant (Hesperoloxodon antiquus) and estimated to be ~125,
000 years old in Germany (Movius HL. A wooden spear of third interglacial age from lower saxony.
Southwest Journal of Anthropology 1950;6:139-42.). Clearly, if our ancestors were hunting these elephants,
they were butchering them and eating them as well.
IN REGARDS TO HONEY:
I would like to warmly welcome Dr. Brand-Miller aboard and look forward to any comments she may have
on the macronutrient content of ancestral diets and how this may have influenced our present day insulin
metabolism. Also, I am curious about the Crane, 1975 citation in which she says "the Guayaki Indians of
Paraguay have honey as the very basis of their diet and culture (Crane 1975).". The term Guayaki is the
earlier name used for the Ache Indians of Eastern Paraguay who have been extensively studied by Hawkes
and colleagues (Hill K, Hawkes K et al. Seasonal variances in the diet of Ache Hunter Gatherers in Eastern
Paraguay. Human Ecology 1984;12:101-35). Hawkes reports that "meat. . . .provided the most number of
calories daily (mean=56%), and varied little across seasons. The vegetable component of the diet is
characterized by low variance in absolute numbers of calories, but high variance iin species composition".
This data would appear to show that meat formed the basis of their diet, not honey as Crane's reference may
have suggested. Jenny, perhaps you could clarify your position?
A COMMENT ABOUT DENTAL CARIES
I enjoyed Dr. Wynman's comments and his references (especially the classic work of Weston Price). Perhaps
the most comprehensively documented review of dental caries in hunter gatherers has been reported by
Turner (Turner CG. Dental anthropological indications of agriculture among the Jomon people of central
Japan. Am J Phys Anthrop 1979;51:619-35). She reports on the incidence of caries in 19 hunter gatherers
ranging from Neanderthals to present day Eskimos and of 47, 672 teeth examined, the percent which
contained caries was 1.3%. This is in contrast to the caries rates (65% or greater) which can occur in
countries wherein sucrose and starch form the bulk of the diet.
Cordially,
Loren Cordain, Ph.D. Professor, Colorado State Univ.
70/298 (1997)
PALEODIET Archives
Subject: Re: PALEODIET Digest - 15 Apr 1997 to 24 Apr 1997
From: Dick
Reply-To:
Date: Fri, 25 Apr 1997 09:06:33 +0000
Re:
> I will very interested in the reference concret cited for Loren Cordain: "bucher marks on mammoths
> in a number of european sites indicate cut-marks....", because I don't know that bone
> modifications are really "cut-marks" and the european sites.... For example in the superb Gary
> HAYNES book: Mammoths, Elephants and Mastodonts not cite cut-marks at european sites. I hope
> my message is not very difficult to read for you Sincerely Jorge Martinez
There is a school of thought which maintains that cut marks on human bones are evidence of cannibalism,
especiaally when found in archaeo settings. However the cut marks are frequently on the _inner_ concave
surfaces of these bones and are incompatible with the idea of a sawing process such as you might use when
slicing meat or trying to separate it from bone. The pattern rather suggests ritual markings for religious
purposes. The tendency to want to believe in cannibalism is interesting one and was pointed up by Arens in
"The Man-eating Myth - Anthropophagy and Anthropology" OUP 1979.
Arens perhaps overstated the case against cannibalism but the controversy is not irrelevant in the light of
current debate about transfer of "prions" from animals to humans. This is supposed to be the mechanism in
the BSE-Creutzfeld Jacob disease transfer. The original idea of transmission of type of this disease by eating
was due to Gajdusek who studies alleged cannibalistic transmission of Kuru in New Guinea. However one
would not explain an epidemic of say measles in Manhatten by assuming that the natives were eating one
another, although many diseases could be transmitted in this way.
Food for thought?
Dick Bird School of Behavioural and Environmental Studies University of Northumbria NE1 8ST UK
PALEODIET Archives
Subject: More from Barcelona
From: Dean Esmay
Reply-To:
Date: Thu, 24 Apr 1997 16:55:40 -0400
The following message was sent to me by Professor Jorge Martinez of Barcelona :
Dear all (I am sorry for the cross-postings!),
I will inform you that the II MEETING ON HALLUCINOGENOUS SUBSTANCES:
ANTHROPOLOGICAL PERSPECTIVE AND TERAPEUTIC APPLICATIONS will take place in
Barcelona (Spain), 27-28 june 1997. If you are interested in to receive more information you can contact
with:
Josep M. Fericgla
Meeting place: Institut Municipal d'Investigacio Medica Dr.Aiguader 80, baixos (Vila Olimpica) 08003 BARCELONA
Some of the speakers: Jonathan Ott (ethnomicologist), Dr.Albert Hoffmann (chemist), Dr.Joan Laporte
(clinic pharmacologist, Universitat Autonoma de Barcelona), Dr. Jordi Cami (Clinic pharmacologist, Institut
Municipal d'Investigacio Medica), Dr. Jordi Riba (pharmacologist, Institut de Prospectiva Antropologica),
Dr.Manuel J. Barbanoj (pharmacologist, Institut de Recerca de St. Pau), Dr. Josep M. Fericgla
(Anthropologist, Universidad de Salamanca), Giorgio Samorini (ethnomicologist), Dr. Antonio Escohotado
(sociologist, UNED), Dr. Jose M. Poveda (Universidad Autonoma de Madrid), Joan Obiols (Universidad de
Barcelona)
PALEODIET Archives
Subject: Starch
71/298 (1997)
Reply-To:
Jennie Brand Miller
Date: Fri, 25 Apr 1997 10:25:06 +1000
Dear Everyone,
I have been having a little trouble replying to the list, so I'm hoping this one goes through OK.
Dean Esmay indicated a week or so ago, that there are good reasons to suggest that starch is a relatively
recent addition to human diets.
It intrigues me then, why humans have such extraordinary ability to secrete aplha-amylase, the starch
digesting enzyme, present in both saliva and pancreatic secretions. We have so much, that some biochemists
call it alph-amylase overkill. Any suggestions?
Jennie
PALEODIET Archives
Subject: Re: Starch digestion
From: Loren Cordain
Reply-To:
Date: Sat, 26 Apr 1997 15:28:00 -0600
In yesterday's digest, Jenny writes,
"Dean Esmay indicated a week or so ago, that there are good reasons to suggest that starch is a relatively
recent addition to human diets.
It intrigues me then, why humans have such extraordinary ability to secrete aplha-amylase, the starch
digesting enzyme, present in both saliva and pancreatic secretions. We have so much, that some biochemists
call it alph-amylase overkill. Any suggestions?
Jennie"
The highest levels of alpha amylase occur in human pancreas followed by the parotid glands. The amylase
isozyme levels in parotid glands are of an order of magnitude less than those in pancreas (Sobiech KA et al.
Determination of amylase by measurement of enzmatic acitivity anb y enzyme immunoassay and
radioimmunoassay. Arch Immunol Therap Exp 1983; 31:845-8). Because starch boluses do not remain in the
mouth for more than a few seconds, parotid derived alpha amylase has little influence upon immediate starch
digestion. Additionally, if the starch is wheat based, there are endogenous alpha amylase inhibitors in wheat
(also in legumes) which effectively inhibit salivary amylase (O'Donnell MD et al. Purification and properties
of an alpha amylase inhibitor from wheat. Biochimica et Biophysica Acta 1976;422:159-69.). Further, wheat
alpha amylase inhibitors also influence pancreatic amylase secretion (Buonocore V. et al. Wheat protein
inhibitors of alpha amylase. Phytochemistry 1977 16:811-820) and have been shown to result in pancreatic
hypertrophy in animal models (Macri A. et al. Adaptation of the domestic chicken, Gallus Domesticus, to
continuous feeding of albumin amylase inhibitors form wheat flour as gastro-resistant microgranules. Poultry
Science 1977; 56:434-441). Legume starch contains trypsin inhibitors which inactivate native pancreatic
trypsin so as to abnormally increase pancreatic cholecystokinin levels and also cause pancreatic enlargement
in animal models. (Liener IE. Implications of antinutritional components in soybean foods. Crit Rev Food
Sci Nutr 1994;34:31-67.). The point here is that humans obviously have adequate salivary and pancreatic
amylase levels to digest moderate amounts of certain kinds of starch, however, antinutrients in our main
starch sources (grains and beans), when consumed in excessive quantities may negatively impact endocrine
function.
Loren
PALEODIET Archives
Subject: Re: Starch
From: Jordi Juan-Tresserras
Reply-To:
72/298 (1997)
Date: Sun, 27 Apr 1997 23:34:22 +0200

Dear all,
I also enjoyed Prof.Jennie's comments. The question about alpha-amylase and starch consumption is a very
interesting subject. I hope that someone can contribute to inform us about this relationship.
One of my basic research is focused in the study of starch granules preserved in the human dental calculus of
prehistoric populations from the Iberian Peninsula. These starch granules are a type of resistant starch (we
have also documented these remains in grinding stones, potsherds, ...). At this moment, the starchy foods
documented in the prehistoric sites from the Iberian Peninsula are prepared with acorns, pulses and cereals.
I am very interested in knowing, if it is possible, if anyone have observed some differences and
characteristics of dental caries caused by carbohydrates from acorns (with high and/or low levels of tannins)
and/or cereal grains and pulses. Last day, we were discussing about this subject with Concha de la Rua
(University of the Basque Country, Bilbao) and she inform me about the possible relationship between acorn
consumption and cervical caries. Anyone know some information about it?
Cordially,
*************************************************************************
Jordi Juan i Tresserras Unitat d'Arqueobotanica SERP/Dept.Prehistoria, H. Antiga i Arqueologia
UNIVERSITAT DE BARCELONA Baldiri i Reixac, s/n Torre B pis 11 E-08028-Barcelona (Espanya,
Union Europea) e-mail:
Tel.909.32 85 82 International: tel. +34.09.32 85 82 Fax.(93) 449 85 10 fax. +34.3.449 85 10
"Cada epoca de la historia modifica el fogon, y cada pueblo come segun su alma, antes tal vez que segun su
estomago" - Emilia Pardo Bazan
**************************************************************************
PALEODIET Archives
Reply-To:
Jennie Brand Miller
Date: Mon, 28 Apr 1997 10:22:41 +1000
Dear Loren,,
Thanks for your well-documented facts about amylase inhibitors. My understanding is that these are all very
heat labile and denatured by cooking. If we eat raw starch we get a bad pain in the belly because raw starch
per se is resistant to digestion.
Best wishes Jennie
In message Paleolithic Diet Symposium List writes:
> There is one message totalling 54 lines in this issue.
> Topics of the day:
> 1. Starch digestion
> End of Topics (which are also called e-mail "Subject Lines")
>
------------=-=-=-=-=-=-=- IMPORTANT NOTICE -=-=-=-=-=-=-------------> ** Make sure you have a subject line that reflects your topic **
> ** Do not have a subject that says Re: PALEODIET Digest - ... **
> ** Selectively quote the previous message, do not repost it **
>
---------------------------------------------------------------------> Date: Sat, 26 Apr 1997 15:28:00 -0600
> From: Loren Cordain Subject: Re: Starch digestion
> In yesterday's digest, Jenny writes, "Dean Esmay indicated a week or so ago, that there are good
> reasons to suggest that starch is a relatively recent addition to human diets. It intrigues me
> then, why humans have such extraordinary ability to secrete aplha-amylase, the starch digesting
> enzyme, present in both saliva and pancreatic secretions. We have so much, that some biochemists
> call it alph-amylase overkill. Any suggestions?
> Jennie"
73/298 (1997)
>
> The highest levels of alpha amylase occur in human pancreas followed by the parotid glands. The
> amylase isozyme levels in parotid glands are of an order of magnitude less than those in pancreas
> (Sobiech KA et al. Determination of amylase by measurement of enzmatic acitivity anb y enzyme
> immunoassay and radioimmunoassay. Arch Imm. Therap Exp 1983; 31:845-8). Because starch boluses
> do not remain in the mouth for more than a few seconds, parotid derived alpha amylase has little
> influence upon immediate starch digestion. Additionally, if the starch is wheat based, there are
> endogenous alpha amylase inhibitors in wheat (also in legumes) which effectively inhibit salivary
> amylase (O'Donnell MD et al. Purification and properties of an alpha amylase inhibitor from wheat.
> Biochimica et Biophysica Acta 1976;422:159-69.). Further, wheat alpha amylase inhibitors also
> influence pancreatic amylase secretion (Buonocore V. et al. Wheat protein inhibitors of alpha
> amylase. Phytochemistry 1977 16:811-820) and have been shown to result in pancreatic hypertrophy
> in animal models (Macri A. et al. Adaptation of the domestic chicken, Gallus Domesticus, to
> continuous feeding of albumin amylase inhibitors form wheat flour as gastro-resistant
> microgranules. Poultry Science 1977; 56:434-441). Legume starch contains trypsin inhibitors which
> inactivate native pancreatic trypsin so as to abnormally increase pancreatic cholecystokinin
> levels and also cause pancreatic enlargement in animal models. (Liener IE. Implications of
> antinutritional components in soybean foods. Crit Rev Food Sci Nutr 1994;34:31-67.). The point
> here is that humans obviously have adequate salivary and pancreatic amylase levels to digest
> moderate amounts of certain kinds of starch, however, antinutrients in our main starch sources
> (grains and beans), when consumed in excessive quantities may negatively impact endocrine
> function.
> Loren
-----------------------------> End of PALEODIET Digest - 25 Apr 1997 to 26 Apr 1997
PALEODIET Archives
Reply-To:
Jennie Brand Miller
Date: Mon, 28 Apr 1997 09:50:50 +1000
Dear Everyone,
Loren asked me to confirm Crane's statement that 'honey was the very basis of their diet' (Ache or Guayaki
Indians of Eastern Paraguay). Eva Crane is arguably the world's expert on all aspects of honey. I don't have
her 1975 book on hand to check her sources right now but I'll try to do this shortly. I don't think she intended
to mean that all they ate was honey but perhaps it made up a significant fraction of their daily energy intake.
In the past meat was often eaten with honey for flavour and even preserved in it.
My hypothesis is that carbohydrate was in short supply during glacial periods and that humans adapted to the
the scarcity by becoming insulin resistant. Insulin resistance spares glucose for the brain and foetus which
use glucose exclusively as a source of fuel. Genetically determined insulin resistance was therefore a
selective advantage. In this way, populations with a high prevalence of insulin resistance emerged. Today
this characteristic is no longer an advantage and is, in fact, a disadvantage because it is increases one's risk of
developing non-insulin-dependent diabetes. This hypothesis was published in Diabetologia 1994;37:1280-86.
I think honey and all things sweet would have been highly sought after for this reason. What do you think?
Best wishes Jennie
PS In passing, Eva Crane is Elsie Widdowson's sister. McCance and Widdowson's The Composition of
Foods is the author of one of the best compilations on the composition of foods.
Best wishes Jennie
74/298 (1997)
PALEODIET Archives
Subject: Extinctions
From: by way of Dean Esmay
Reply-To:
Date: Mon, 28 Apr 1997 12:35:44 -0400
Dear Dean Esmay
I don't like polemice, but I'll explain my position about the Pleistocene Extintion. I haven't the solution of the
problem. In archeology, I think, "smoke guns" are very rarce. We work with a record very problematic
(admittedly incomplete in Loren Cordain terms) and megafauna extintion are only an example of the degree
of complexity that the archaeological discussion. Others examples of the discussion are the
scavenging/hunting at Plio-Pleistocene sites in East-Africa. This kind of discusion, for me, is demostrative
the an important teorethical change: we need an approach multicausal. The explanation of phenomens are
complex and posibily the combination of differents agents are more apropiate than monocausal explication.
I agree with Loren Cordain when says that previous changes from cold to warm were not accompanied by
mass extintions. That's rigth, with exceptions...for example, last ocurrence of hipopotamus in Europe are
situated in the Eem (Riss-Wurm). That's signifies the disparition of hipopotamus is consecuence of human
activity? I don't know...Along the Pleistocene, the reduction and finally the disparition at Europe of hyena,
leopard, cave bear and others carnivore are consecuence of human pressure?...Perhaps. Extintion are
historical complex phenomenon and posibily each phenomenon are their historical process. For example,
human impact at Madagascar island is sure, and the disparition of megafauna for consecuence of human
activity is very important. But Madagascar are "terra incognita" just the first milenium...
Now, in Europe are a controversial debate about the extintion of faunal island, for example the pigmy
hypopotamus of Cyprus. The people has worked at the island are differents opinions,
Don t worry for the citation about cut-marks in hyoides is only curiosity, but cut-marks and bone
modification in general are scarce at elephant bone (a good example is Bonnichsen and Sorg (eds.): Bone
Modifications).
Leringen spear are an example of sofisticated tecnological degree of the human arcaics very interesting.
Recently a Schoningen (Germany) H. Thieme describes 3 spears with 400.000 years old (Nature 385).
Posibily, pre-Sapiens are efficients hunters, but not only for they are tecnollogy efficients. Is necesary linked
with others atributes (social organization for example).
I disagree with the mecanical aplication of the Optimal Foraging Theory. Perhaps, energically are more
interesting mastodont hunting, but I don't sure this activity are easy and sure. Hunting are an habitual activity
for people arrived to America with an advanced technology. But that's no imply this people lives only with
mamut "entrecot"!. The overkill is an posibiliy but not are the only posibility.
In the last numbers of Journal of Human Evolution 1995 Tillier described Neandertals dental caries.
Jorge
Jorge Martinez Dpt. Antropologia Social i Prehistoria Universitat Autonoma de Barcelona
PALEODIET Archives
Subject: Cannibalism
From: by way of Dean Esmay
Reply-To:
Date: Mon, 28 Apr 1997 12:36:18 -0400
Excume, but I don't read Bird text.
Canniabalism are "aberrant" human behavior for us, and we prefer think others posibilities. Archeologically
we can know when an human bone is modified. The last years the bibliography are very important, for
example Bodo (African Middle Pleistocene) T. White described operational marks at the cranium. At TD-4
Atapuerca (Lower Pleistocene) the human remains have cut-marks and impact scarcs.
At 1985, Villa worked an interesting case at Fontbregoua (Neolithic french cave). The humans remains have
impact notch and cut-marks, and they are diposed with deer, roe deer, boar, etc.... I accept this pattern is
religious if you accept the same ritual for the deer, boar, ect...
75/298 (1997)
Arens books is very interesting, but recently are more information about cannibalism, and posibles
"functional context" associated. Not is the same Maya cannibalism (posibily they are a political and
cohercitive power in statal context) and the history of Fontbregoua people.
Yes, I'm a school of thougth wich maintains that bone modifications on human bones are evidence of human
manipulation.....Explanation are other history.....
Thought for food?
Jorge
PALEODIET Archives
Subject: Starch and a Short gut
From: Ray Audette
Reply-To:
Date: Sun, 27 Apr 1997 22:49:58 -0700
As the human large intestine is so short relative to other Primates, adaptations must occure to allow the
starches found in edible raw fruits and vegetables to be converted into simple sugars to be absorbed by the
small intestine. This deficiency of large intestine may also be expressed by our un-primate like cravings (as
noted by Goodall et al) of things both sweet and starchy.
That the sources of starches in agricultural diets inhibits the action of our naturally occuring starch digesting
enzymes only exasperates these cravings by cuting off the feed-back loop at the small intestine and only
allowing starches to be absorbed more slowly and less efficiently after bacterial action in the large intestine.
Most people who eat a paleolithic diet report that these cravings are greatly reduced in just a few days.
see:"The Expensive Tissue Hypothesis: The Brain and Digestive System in Human and Primate Evolution"
Current Anthropology vol. 36, #2 (April 1995) 199-221
PALEODIET Archives
Subject: Paleolithic diet list
From: Dean Esmay
Reply-To:
Date: Mon, 28 Apr 1997 14:40:14 -0400
I've been thinking it's really about time someone started a listserv devoted to everyday people who want to
adapt paleolithic nutrition principles into their own lives. Several people told me they'd be interested in
helping to run such a list, and I know now how to set one up. Unfortunately I can't remember who all was
interested in that, so I'd like to invite anyone who is interested in setting up and running such a list (a list for
non-academics, more for everyday people) to send me private mail and we'll discuss how to get that done.
Just shoot me some private email if interested.
PALEODIET Archives
Subject: Re: Alpha amylase inhibitors & cooking
From: Loren Cordain
Reply-To:
Date: Tue, 29 Apr 1997 08:47:00 -0600
In the last paleodigest, Jenny writes:
"Dear Loren,,
76/298 (1997)
Thanks for your well-documented facts about amylase inhibitors. My understanding is that these are all very
heat labile and denatured by cooking. If we eat raw starch we get a bad pain in the belly because raw starch
per se is resistant to digestion.
Best wishes Jennie".
Both alpha amylase inhibitors (in cereals and legumes) and trypsin inhibitors (primarily in legumes) are not
fully denatured by normal cooking processes. It is reported, "Protein alpha amylase inhibitors may represent
as much as 1% of wheat flour and, because of their thermostability, they persist through bread baking being
found in large amounts in the center of loaves." (Buonocore V. et al. Wheat protein inhibitors of alpha
amylase. Phytochemistry 1977;16:811-20). Further in his treatise on antinutrients, Liener states, "However
because of the necessity of achieving a balance between the amount of heat necessary to destroy the trypsin
inhibitors and that which may result in damage to the nutritional or functional properties of the protein, most
commercially available edible grade soybean products retain 5 to 20% of the trypsin inhibitor activity
originally present in the raw soybeans from which they were prepared." (Liener IE. Implications of
antinutritional components in soybean foods. Crit Rev Food Sci Nutr 1994;34:31-67.).
Cordially,
Loren
PALEODIET Archives
Subject: Re: Dental caries and acorns
From: Loren Cordain
Reply-To:
Date: Tue, 29 Apr 1997 09:31:00 -0600
Jordi Juan-Tresserras writes:
"I am very interested in knowing, if it is possible, if anyone have observed some differences and
characteristics of dental caries caused by carbohydrates from acorns (with high and/or low levels of tannins)
and/or cereal grains and pulses. Last day, we were discussing about this subject with Concha de la Rua
(University of the Basque Country, Bilbao) and she inform me about the possible relationship between acorn
consumption and cervical caries. Anyone know some information about it?
Cordially, "
In central California, before it was colonized by European settlers, the native Indian population utilized
acorns as a staple part of their diet for many thousands of years. Turner (Turner CG. Dental anthropological
indications of agriculture among the Jomon people of central Japan. Am J Phys Anthrop 1979;51:619-36)
reports in a sample of 289 teeth a caries rate of 2.4 % in acorn eating central California Indians which is
slightly higher than the 1.6 % for the aggregate of hunter-gatherers. It is possible that the higher levels of
tannins in this food source may increase the rate of enamel erosion, however these data indicate not much
difference.
Best Wishes,
Loren
PALEODIET Archives
Subject: The Non-Thrifty Genotype
From: Dean Esmay
Reply-To:
Date: Tue, 29 Apr 1997 09:45:12 -0400
I just finished reading THE NON-THRIFTY GENOTYPE, by John S. Allen and Susan M. Cheer, published
in CURRENT ANTHROPOLOGY, Volume 37, Number 5, December 1996, and would like to repeat
Staffan Lindeberg's kudos for this excellent paper and the recommendation that other list members look for it
if possible. It's quite worthwhile reading.
Thanks to John Allen for taking the time to send me a copy.
77/298 (1997)
PALEODIET Archives
Subject: Starch and dental caries
Reply-To:
Jennie Brand Miller
Date: Tue, 29 Apr 1997 10:35:34 +1000
To those interested,
Raw cereal starch is very slowly digested by human intestinal enzymes and also by the bacteria that cause
dental caries. We human beings over the years in our quest for more and more palatable food, have
coincidentally increased the rate of starch digestion in cereals by grinding (into flour) and cooking and more
recently by processes such as extrusion cooking (all the funny little shapes you find in snack foods and
breakfast cereals mean extrusion cooking has been used).
Recent research indicates that these quickly digested starches are more likely to cause dental caries than
slowly digested starches. In fact they are just as effective as the sugars in reducing the dental plaque pH.
One reference is:
Lingstrom P, Holm J, Birkhed D, Bjorck I. Effects of variously processed starch on pH of human dental
plaque. Scan J Dent Res, 1989, 97 : 392-400.
Best wishes Jennie
PALEODIET Archives
Subject: Detoxifying Plant Anti-Nutritional Factors
From: Luc De Bry
Reply-To:
Date: Tue, 29 Apr 1997 11:41:58 -0700
Good morning paleodiet digest participants,
Working on Plant-Food-Consumer interactions, I am very happy to have come across this listserver, and
thoroughly enjoyed reading the first paleodiet digests on my screen. A big thank to the organizers for this
well done job.
Commenting (very briefly, and with a few short-cuts) on information relevant to starch and carbohydrates
from Jennie Brand Miller and from Loren Cordain that were in the last two or three digests :
If leaves and some fruits, most notably banana, do contain some starch, the main starch source in humans'
diet comes from tubers and seeds, all of them belonging to the Group of the Angiosperms. Tubers and seeds
are progenies of mother plants. They cannot run away when comes a predator, a plant-eater. Hence, the
mother plant protects them, on the one hand with odour-silence to pass unoticed, and on the other hand, with
powerful anti-nutritional factors. Following T. Swain (1977, Annual review of Plant Physiology, 28 : 479501; according to ISI, one of the ten most cited papers of the plant science literature), plant anti-nutritional
factors may have evolved in response to overfeeding by dinosaurs, hence contributing to their demise over
some 35 long million years.
A few moulds, insects and grain-eating birds (successful dinosaurs) have adapted to the challenge of plant
anti-nutritional factors, and mutated some stomach genes to overcome plant chemical defences. For instance,
their trypsin is insentive to plant-anti-trypsin. Other animals, humans included cannot eat raw grains and
beans and tubers : anti-trypsins, anti-amylases, lectins, cyanogens, alkaloids, etc, would kill them.
So, when Jennie wrote
> Thanks for your well-documented facts about amylase inhibitors. My understanding is that these are
> all very heat labile and denatured by cooking.
It's correct : they are heat labile, but not always "very" heat labile. (If we go back to pre-historical baking
technology, we would need up to half a day to bake a bread.) There are now some papers going into the
depth of the physical-chemistry of this denaturation, even measuring the kinetics of the detoxification
phenomenon, which is of tremendous importance both to the food and feed industries as well as to the food
safety for the Consumers.
> If we eat raw starch we get a bad pain in the belly because raw starch per se is resistant to
78/298 (1997)
> digestion.
Here, I believe that Jennie meant "raw flour". Indeed, raw wheat flours can kill. Not because of starch, but
because of wheat toxic proteins, e.g. anti-amylases, dispersed in the endosperm between starch granules. And
indigestible-insufficiently-baked gluten balls in our stomachs do cause pains. Concerning uncooked or more
precisely ungelatinized starch itself, a good source of kilocalories, if it cannot be attacked by amylases and
hydrolysed down to dextrins, it can be hydrolysed (slowly) by glucoamylases (releasing glucose units).
Now, moving from the comments to a question :
All animals that I know, whether domestic or wild, whether fishes, rabbits or gorillas, once they tasted a
piece of bread or of chocolate, they just love to eat more when given an opportunity. The major difference
between them and humans, is that only humans can apply Fire Technology and the Maillard Reaction
"invented" by our Mother(s) Eve, for detoxifying plant anti-nutritional factors.
Could the abscence of fears from the fire be related to some human-specific genetic defect(s)???
Who knows?
Any comment?
Have a good day, and regards,
Luc
__ A paleo-thought : / \ / O______ __/\/\/\/\_ / ^^^^ / \ / **** / \_ / / <-_____----_____ _\
>
>
>/\
>/\/\
A Stegosaurus evolved from about 144 million years ago to 135 million years ago. A Tyrannosaurus rex
from 83 million years ago to about 65 million years ago. Thus, although often displayed together, a T. rex
never ate a steak of Stegosaurus. And as Angiosperms started to evolve some 120 million years ago, no
Stegosaurus could taste one of them and smell flower perfumes.
-- Luc De Bry, Ph.D.; Head of Research Department; DANONE BISCUITS NORTH De BeukelaerPareinlaan 1; B-2200 Herentals - Belgium Tel. 32 (0)14 241432; Fax 32 (0)14 241025; Email : URL Site
http://www.danonegroup.com
PALEODIET Archives
Subject: Hunger and Cannibalism
From: Luc De Bry
Reply-To:
Date: Tue, 29 Apr 1997 12:29:40 -0700
Good morning again,
On April 26-28, the Automatic digest processor reported about cannibalism and hunger
Jorge by way of Dean Esmay wrote a line among others:
> Canniabalism are "aberrant" human behavior for us, and we prefer think others posibilities.
and completed with
> Thought for food?
May I briefly comment, from a different background, and illustrate this with a rather modern case :
Well, "aberrant" may be as understood in today's over-fed Western Societies. I was born and raised in
Central Africa, and escaped (thank to my Parents) to horrors and savageries of both war and starvation, i.e.
hunger plus famine. Sadly enough, other friends, many from childhood time, did not have that "luck",
including in the present wars and starvations prevailing once again in Central Africa.
Here is a relevant and "1997" news about cannibalism and hunger, as "experienced" in another far remote
corner of our world, by some other "humans", that may be instructive in terms of "thought for food?"
The source of that article is WORLDWIDE REUTERS, dd 04/28/97, and is available today at URL site
http://www.agriculture.com/worldwide/AgricultureFarming/04_28_1997.reute-story-bckoreahunger.html
Title : North Koreans fear cannibalism amid hunger
BEIJING, April 28 (Reuter) - Hunger in North Korea is forcing peasants to sell clothes for food, to sneak
into China to steal animal feed and even to delay burials to prevent cannibalism, visitors to the border said on
Monday.
79/298 (1997)
However, many North Koreans are so terrified of official retribution they dare not cross into China over the
border that is marked in part of northern Jilin province by a shallow river that can be waded easily.
``The situation in North Korea is very bad, '' one recent visitor to the Jilin border town of Yanji quoted an
ethnic Korean salesgirl as saying.
``There is only corn to eat and very little of that, '' said the woman, who recently visited her sister who lives
across the border in the Stalinist hermit state. ``People have to sell their clothes to get the money to buy
food.''
The north of the country has been hardest hit by floods that wiped out crops for two consecutive years.
Pyongyang has appealed for food aid but has not allowed aid officials to the region and last week prevented
workers of World Vision International, a Christian charity that has worked in North Korea since 1995, from
touring the region.
Chinese in Yanji who have frequent contacts with the North said the situation appeared to be deteriorating.
One recent sign was the decision by some North Korea peasants to delay the burial of their dead for fear the
bodies would be dug up and eaten by other hungry farmers, a recent visitor quoted Yanji residents as saying.
Farmers now kept their dead in their homes until the corpse began to putrefy before burying it to prevent
cannibalism, several Chinese residents said.
For those desperate enough to sneak across the border and through North Korea's security net, punishment
can be brutal and swift, Chinese and ethnic Koreans told recent visitors.
Few make the journey because of the security and restrictions on obtaining visas, Yanji residents said.
Those who do are quickly spotted by a network of North Korean spies based in China who round up the
escapees as illegal immigrants and force them back across the border, they said.
Punishment is swift.
``The North Korean police put a metal wire through the nose of some people who escape, '' the visitor quoted
one Yanji resident as saying. ``It's like a brand that marks them out.''
Even children are not exempt.
``We can hear the screams of children when they put the metal wire through their nose because they do it as
soon as they cross into North Korea and the border is very close, '' the Yanji resident was quoted as saying.
``They don't dare to carry out this punishment in China but as soon as they are back in North Korea they can
do what they want, '' he was quoted as saying.
Many of those who flee into China do little more than slip into local cattlesheds to steal animal feed to eat
and then sneak back into the North, Yanji residents said. Residents said they turned a blind eye out of
sympathy.
Dean Hirsch, president of World Vision International, said last week that recent tours of two rural counties
near the capital, Pyongyang, convinced him that North Korea may be only 90 days away from starvation.
Repeated international appeals for food aid -- the latest being a U.N. World Food Programme appeal for
$95.5 million -- have drawn only a lukewarm response amid fears the food aid will go to Pyongyang's
military.
Copyright 1997 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content is
expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or
delays in the content, or for any actions taken in reliance thereon.
@g Worldwide | @griculture Online | Canada @griculture Online | Farmers Weekly Interactive | Interfax
News Agency
End of article.
Hunger and sadness look universal.
When we were kids, we had a joke: - "Do you know why there are no more cannibals?" - "Well, yesterday, I
ate the last one..."
Regards,
Luc -- Luc De Bry, Ph.D.; Head of Research Department; DANONE BISCUITS NORTH De BeukelaerPareinlaan 1; B-2200 Herentals - Belgium Tel. 32 (0)14 241432; Fax 32 (0)14 241025; Email : URL Site
http://www.danonegroup.com
PALEODIET Archives
Subject: 4. Starch
From: Bob Avery
Reply-To:
80/298 (1997)
Date: Tue, 29 Apr 1997 20:03:05 EDT

Jennie,
> Thanks for your well-documented facts about amylase inhibitors. My understanding is that these are
> all very heat labile and denatured by cooking. If we eat raw starch we get a bad pain in the belly
> because raw starch per se is resistant to digestion.
I eat lots of raw starch (rice, other grains, yams) with NO pains in the belly.
Bob Avery
PALEODIET Archives
Subject: Re: Cereal starches & dental caries & A question
From: Loren Cordain
Reply-To:
Date: Wed, 30 Apr 1997 10:50:00 -0600
A good paper showing the epidemiological relationship between cereal grain consumption and caries
incidence is: (Sreebny LM. Cereal availability and dental caries. Community Dent Oral Epidemiol
1983;11:148-55). The author, Leo Sreebny, did most of the original epidemiological work relating sucrose
consumption to dental caries.
QUESTION:
In our group over the last month or so, we have bandied about the idea of the ancestral macronutrient
compositions (i.e. %fat, %protein, % CHO) and how they influence health. Clearly, in the normal western
diet (~45-50% CHO, 35-40% fat and 10-15% protein) if dietary saturated fats are reduced, then total and
LDL cholesterol are also reduced. Keys (Keys A et al. Serum cholesterol response to changes in the diet. IV.
Particular saturated fatty acids in the diet. Metabolism 1965;14:776-87) has published an equation which has
been used extensively to predict changes in serum cholesterol from dietary lipids and cholesterol. Others
(Mensink et al) more recently, have confirmed Keys' Equation. In perhaps the most well controlled, modern,
dietary study of Greenland Eskimos, Bang and Dyerberg (Bang HO, Dyerberg J. Lipid metabolism and
ischemic heart disease in greenland eskimos. In: Advances in Nutrition Research, HH Draper (Ed), Vol 3,
N.Y., Plenum Press, 1980, 1-22.), it has been shown that ischemic heart disease is very uncommon in these
people (3.5 % vs 45-50% mortality rate in western countries). The dietary macronutrient content of these
partially westernized eskimos was (38% CHO, 39%fat and 23% protein) whereas the values for the control
group of Danish people was (47% CHO, 42% fat, and 11%protein). Mean total cholesterol levels in the
eskimos (5.03 mmol/liter) was significantly lower than in the Danes (6.18 mmol/liter) whereas the TG (0.57
vs 1.23 mmol/liter) and VLDL (0.43 vs 1.29 mmol/liter) were much lower in the eskimos and HDL levels
were significantly higher (4.00 vs 3.34 mmol/liter). Based upon the Keys et al. equation, the actual difference
between the Eskimos' total cholesterol levels should have been 0.67 mmol/liter, whereas in acutality it was
1.15 mmol/liter. This data suggests that the Keys equation may be invalid under circumstances wherein high
quantities of animal products replace traditionally cereal dominated diets. Possible reasons for this
discrepancy include: (1) higher protein levels in the face of lowered CHO may induce different lipoprotein
transport mechanisms (Wolfe BM. Potential role of raising dietary protein intake for reducing risk of
atherosclerosis. Can J Cardiol 1995;11:127G-31G) or different polyunsaturated fat (high N3 fats and high
levels of preformed long chain fats of both N3 and N6 families) between the two diets (Nelson GJ et al. Low
fat diets do not lower plasma cholesterol levels in healthy men compared to high fat dits with similar fatty
acid composition at constant caloric intake. Lipids 1995 30:969-76). The bottom line here is that present day
hunter gatherers maintain quite low serum lipid levels despite high consumptions of animal based foods.
Comments?
Cordially,
PALEODIET Archives
Subject: Book Review
From: Ray Audette
Reply-To:
81/298 (1997)

Date: Thu, 1 May 1997 11:10:23 -0700
"NeanderThin" is going to be reviewed in the May '97 issue of Healthy and Natural Journal. I've not seen it
yet so I don't even know if it's favorable.
Good or bad, I hope my readers will respond with a letter to the editor. If one of your letters get published,
it's better than an ad (which I can't afford anyway).
Thanks for all your support.
PALEODIET Archives
Subject: Fishing
From: Dean Esmay
Reply-To:
Date: Thu, 1 May 1997 11:29:01 -0400
African Exodus Chris Stringer & Robin McKie. 1996 London Jonathan Cape p4-5 (Zaire) In the neglected
western branch of the African Rift Valley ....sediments are being exposed which were laid down 90 000
years ago, just as Homo Sapiens was making its mark across Africa.
At the town of Katanda this erosion has produce an archaeological treasure trove;thousands of artefacts,
mostly stone tools, plus a few bone implements........Among the wonders they have uncovered are
sophisticated bone Harpoons and knives. Previously it was thought that the Cro-Magnons were the first
humans to develop such delicate carving skills-50 000 years later.......There were other surprises for
researchers, however. Apart from the finely carved implements, they found fish bones, including some from
two metre long catfish. It seems that the Katanda people were efficiently and repeatedly catching catfish
during their spawning season, indicating that systematic fishing is quite an ancient human skill and not some
relatively recently acquired expertise, as many archaeologists had previously thought. (The archaeologists
were John Yellen of the National Science foundation, Washington and Allison Brooks of George
Washington University)
PALEODIET Archives
Subject: Diet composition
Reply-To:
Jennie Brand Miller
Date: Fri, 2 May 1997 07:05:54 +1000
Dear Bob, Comments for Bob Avery
> I eat lots of raw starch (rice, other grains, yams) with NO pains in the belly.
Perhaps your gut has adapted to the presence of large amounts of raw starch by either increasing amylase
secretion in the small intestine or increasing the numbers and types of bugs in the large intestine. This
happens in lactose intolerant individuals who continue to drink milk.
(I'm sorry I don't have time to look up the reference that says this but if you want it I'll dig around for it.)
The type of resistant starch in raw cereals is easier to digest than that in raw potatoes. Most people complain
of symptoms when they eat raw potatoes or alot of raw green bananas. John Cummings et al at the Dunn
Nutrition Unit have divided up resistant starch into three types based on their crystallinity.
We need to remember that the food plants we eat today are a long, long way from the original wild types. We
have consistently bred them for improved characteristics like size and palatability and perhaps their ease of
digestion.
It's interesting that Australian Aboriginals used lots of processing techniques to rid plants of toxins but they
ate a very high protein diet just the same based on marine and land animals.
Comments for Loren
'The bottom line here is that present day hunter gatherers maintain quite low serum lipid levels despite high
consumptions of animal based foods'.
82/298 (1997)
The Keys equation does not consider the effect of amount and type of CHOs on insulin secretion.
Hyperinsulinaemia is turning out to be one of the biggest independent risk factors for CHD. High protein
diets and low glycaemic index diets both lower insulinaemia.
Best wishes Jennie
>
-----------------------------> Date: Wed, 30 Apr 1997 08:44:00 PDT
> From: "Ginsberg, Doug" Subject: Re: Alpha amylase inhibitors & Detoxifying plant foods
> Does anyone know if traditional food preparation techniques such as soaking, sprouting, and
> fermenting are effective responses to some of these plant toxicity issues; and were any of them
> used by paleolithic hunter-gatherers?
> Doug Ginsberg
>
>
-----------------------------> Date: Wed, 30 Apr 1997 10:50:00 -0600
> From: Loren Cordain Subject: Re: Cereal starches & dental caries & A question
> A good paper showing the epidemiological relationship between cereal grain consumption and caries
> incidence is: (Sreebny LM. Cereal availability and dental caries. Community Dent Oral Epidemiol
> 1983;11:148-55). The author, Leo Sreebny, did most of the original epidemiological work relating
> sucrose consumption to dental caries.
> QUESTION:
> In our group over the last month or so, we have bandied about the idea of the ancestral
> macronutrient compositions (i.e. %fat, %protein, % CHO) and how they influence health. Clearly, in
> the normal western diet (~45-50% CHO, 35-40% fat and 10-15% protein) if dietary saturated fats are
> reduced, then total and LDL cholesterol are also reduced. Keys (Keys A et al. Serum cholesterol
> response to changes in the diet. IV. Particular saturated fatty acids in the diet. Metabolism
> 1965;14:776-87) has published an equation which has been used extensively to predict changes in
> serum cholesterol from dietary lipids and cholesterol. Others (Mensink et al) more recently, have
> confirmed Keys' Equation. In perhaps the most well controlled, modern, dietary study of Greenland
> Eskimos, Bang and Dyerberg (Bang HO, Dyerberg J. Lipid metabolism and ischemic heart disease in
> greenland eskimos. In: Advances in Nutrition Research, HH Draper (Ed), Vol 3, N.Y., Plenum Press,
> 1980, 1-22.), it has been shown that ischemic heart disease is very uncommon in these people (3.5
> % vs 45-50% mortality rate in western countries). The dietary macronutrient content of these
> partially westernized eskimos was (38% CHO, 39%fat and 23% protein) whereas the values for the
> control group of Danish people was (47% CHO, 42% fat, and 11%protein). Mean total cholesterol
> levels in the eskimos (5.03 mmol/liter) was significantly lower than in the Danes (6.18
> mmol/liter) whereas the TG (0.57 vs 1.23 mmol/liter) and VLDL (0.43 vs 1.29 mmol/liter) were
> much lower in the eskimos and HDL levels were significantly higher (4.00 vs 3.34 mmol/liter).
> Based upon the Keys et al. equation, the actual difference between the Eskimos' total cholesterol
> levels should have been 0.67 mmol/liter, whereas in acutality it was 1.15 mmol/liter. This data
> suggests that the Keys equation may be invalid under circumstances wherein high quantities of
> animal products replace traditionally cereal dominated diets. Possible reasons for this
> discrepancy include: (1) higher protein levels in the face of lowered CHO may induce different
> lipoprotein transport mechanisms (Wolfe BM. Potential role of raising dietary protein intake for
> reducing risk of atherosclerosis. Can J Cardiol 1995;11:127G-31G) or different polyunsaturated fat
> (high N3 fats and high levels of preformed long chain fats of both N3 and N6 families) between the
> two diets (Nelson GJ et al. Low fat diets do not lower plasma cholesterol levels in healthy men
> compared to high fat dits with similar fatty acid composition at constant caloric intake. Lipids
> 1995 30:969-76). The bottom line here is that present day hunter gatherers maintain quite low
> serum lipid levels despite high consumptions of animal based foods. Comments?
> Cordially,
>
> Loren Cordain, Ph.D.
>
-----------------------------> End of PALEODIET Digest - 29 Apr 1997 to 30 Apr 1997
83/298 (1997)
PALEODIET Archives
Subject: Starch and dental caries
Reply-To:
Date: Mon, 5 May 1997 01:00:03 +0100
In due time I hope that we will have some scholars of dental paleopathology in the group. In the meantime I,
who know very little on the subject, refer to Lukacs JR. Dental paleopathology: Methods for reconstructing
dietary patterns. In: Isan MY, Kennedy KAR. Reconstruction of life from the skeleton. New York, WileyLiss 1989 who states that caries rates were low in prehistoric hunter-gatherers, intermediate in early farmers
and highest in full-blown agriculturalists. A later paper that I came across also supports a role of cereal starch
in caries: Littleton, J. Frohlich, B. Fish-eaters and farmers: dental pathology in the Arabian Gulf. Am J Phys
Anthropol 1993; 92: 427-47. Abstract: Twelve skeletal samples, previously published, from the Arabian Gulf
have been used to trace differences in diet and subsistence patterns through an analysis of dental pathology.
The skeletons date from 3, 000 BC to AD 1, 500 and cover a variety of geographical locations: off-shore
islands, Eastern Arabia, and Oman. The dental conditions analyzed are attrition, caries, calculus, abscessing,
and antemortem tooth loss (AMTL). Results indicate four basic patterns of dental disease which, while not
mutually exclusive, correspond to four basic subsistence patterns. Marine dependency, represented by the
Ras el-Hamra population, is indicated by severe attrition, low caries rates, wear-caused abscessing, and a
lack of AMTL. The second group of dental diseases--moderate attrition and calculus, low rates of caries,
wear-caused abscessing, and low-moderate rates of AMTL--affects populations subsisting on a mixture of
pastoralism or fishing and agriculture (Failaka, Umm an-Nar, Bronze Age Maysar, Bronze Age Shimal, and
Iron Age Galilah). Mixed farming populations (Iron Age Maysar and Islamic Bahrain) experienced lowmoderate attrition, high rates of caries and calculus, abscessing due to caries, and severe AMTL. The final
group of dental diseases affects populations practicing intensive gardening (Bronze and Iron Age Bahrain,
and Sites 3 and 5, Ras al-Khaimah). These groups experienced slight attrition, high rates of caries, low rates
of calculus deposition, and severe AMTL.
Sorry if I overemphasized what may already have been clear to you.
Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: Re: Dietary Macronutrient Content and Hyperinsulinemia
From: Loren Cordain
Reply-To:
Date: Mon, 5 May 1997 09:47:00 -0600
In a previous digest, Jenny wrote: "The Keys equation does not consider the effect of amount and type of
CHOs on insulin secretion. Hyperinsulinaemia is turning out to be one of the biggest independent risk factors
for CHD. High protein diets and low glycaemic index diets both lower insulinaemia.
Best wishes Jennie"
84/298 (1997)
This was exactly my point. Ancestral, pre-agricultural diets were quite high in animal protein and the
carbohydrate that was consumed was generally of a low glycemic index. These populations also selcetively
consumed the fatty portions of the killed animal (brain, marrow, depot fat, perinephral fat, mesenteric fat,
tongue, organs etc). However, available evidence from living hunter gatherers show that these surrogates of
our stone age ancestors maintain low risk factors for CHD (blood lipid profiles, blood pressure, insulin
sensitivity, body composition etc). All of this on a diet which contains 50-65% or more of its total calories
derived from animal foods. Clearly, the Key's equation breaks down when either the macronutrient content
(extremely high protein and low CHO) or the fatty acid composition of the diet (or both) varies beyond the
range of conditions in which Keys originally derived his regression. Although there is much circumstantial
evidence to indicate that the Key's equation is erroneous under these conditions, there is no empirical data
that I am aware of which has confirmed this concept.
Best wishes,
Loren
PALEODIET Archives
Subject: Re: Detoxifying plant foods
Reply-To:
Date: Tue, 6 May 1997 01:25:52 +0100
Apologies for repeating myself, but Doug Ginsberg wrote:
> Does anyone know if traditional food preparation techniques such as soaking, sprouting, and
> fermenting are effective responses to some of these plant toxicity issues...
Whole meal cereals and other seeds have in their shells phytic acid which is not toxic but strongly binds to
minerals like calcium, iron, zinc and magnesium to form insoluble salts, phytates. There is overwhelming
evidence that whole meal cereals through this mechanism decrease the absorption of such minerals to a point
where cereals are no longer an optimal human food. Phytates are most certainly an important contributing
cause of iron deficiency in third world countries and possibly in the western world. As to calcium deficiency
the picture is less clear.
Mellanby found back in the 30s that puppies got rickets when they were fed oats. The possible absence of
rickets in preagricultural skeletons, its apparent increase during medieval urbanization and its epidemic
explosion during industrialism can hardly be explained only in terms of decreasing exposure to sunlight and
descreased length of breast-feeding. An additional possible cause is a secular trend of increasing inhibition of
calcium absorption by phytate from cereals since these apparently increased in amount during the Middle
Ages, and since old methods of reducing the phytate content such as dampening and heat treatment may have
been lost during the emergence of large-scale cereal processing. Old fashion sourdough baking as well as
soaking and fermenting decrease the amount of phytatic acid by use of phytases, enzymes which are also
found in the cereals but which often are destroyed during industrial processing.
> ...and were any of them used by paleolithic hunter-gatherers?
I don't think there is any evidence of that. I suppose they would need pottery which they apparently did not
use.
Staffan
PALEODIET Archives
Subject: Re: Beyond saturated fat
Reply-To:
Date: Tue, 6 May 1997 03:20:49 +0100
Keys mainly considered low intake of saturates in lowering LDL cholesterol. This is obviously not enough
which Loren's Eskimo example shows.
85/298 (1997)
To add further to the evidence: Among subsistence horticulturalists of Kitava, Papua New Guinea
[http://www.panix.com/~donwiss/paleodiet/sl1.shtml], saturated fat intake was similar as in Sweden (1617% of daily energy intake, en%) but serum total cholesterol was lower, especially in the males (4.8 vs 5.8
mmol/L) [1]. Likewise, total cholesterol in healthy subjects in rural Sri Lanka was only 4.7 mmol/L despite
that saturated fat from coconut provided 19 en% [2]. And total cholesterol in middle-aged traditional
Polynesians from Tokelau was only 5.0 mmol/L in males and 5.5 in females, despite an estimated 45 en%
saturated fat, also mainly from coconut [3, 4]. In urbanised males and females who had migrated from
Tokelau to New Zealand and decreased their intake of saturated fat to 21 en%, TC was 5.6 and 5.8 mmol/L,
respectively, further indicating that other factors than saturated fat and dietary cholesterol are of importance,
such as the above. The same argument may be applied to the much higher TC in urbanized than rural Masai,
despite a higher intake of saturated fat from milk among the rural group [5, 6].
In this group Loren and Jennie suggest that LDL may decrease by high protein and/or low glycaemic index
diets through improved insulin sensitivity. I believe this is important and underestimated. But isn't it possible
that any satiating (e.g. nutrient dense, voluminous, water rich etc.) diet by way of reduced caloric intake and
reduced (abdominal) obesity could lower your LDL independently of these factors? If so it could in a sense
be more important to avoid empty calories than to find the best proportions of CHO, fat and protein.
Regards
Staffan
1. Lindeberg S, Nilsson-Ehle P, Ternt A, Vessby B, Scherstn B. Cardiovascular risk factors in a
Melanesian population apparently free from stroke and ischaemic heart disease - the Kitava study. J Intern
Med 1994; 236: 331-40.
2. Atukorala TM, Jayawardene MI. Lipid patterns and dietary habits of healthy subjects living in urban,
suburban and rural areas. Ceylon Med J 1991; 36:9-16.
3. Stanhope JM, Sampson VM, Prior IA. The Tokelau Island Migrant Study: serum lipid concentration in
two environments. J Chronic Dis 1981; 34:45-55.
4. Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a
natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr 1981; 34:1552-61.
5. Day J, Carruthers M, Bailey A, Robinson D. Anthropometric, physiological and biochemical differences
between urban and rural Maasai. Atherosclerosis 1976; 23:357-61.
6. Ho KJ, Biss K, Mikkelson B, Lewis LA, Taylor CB. The Masai of East Africa: some unique biological
characteristics. Arch Pathol 1971; 91:387-410.
-------------------------------------------------------------------
PALEODIET Archives
Subject: Re: High protein diets
Reply-To:
Jennie Brand Miller
Date: Tue, 6 May 1997 10:24:25 +1000
I was glad to see Staffan's comments about dental caries in agriculturists. A large majority of dietitians think
sugar is still the only cause of dental caries and recommend high starch diet on these grounds.
A question about high protien diets:
Have any of you any experience of putting people on high protein diets with little CHO?
I have read that most subjects (who were probably insulin sensitive Caucasians) find this sort of diet
nauseating and that experiments are usually terminated early.
One experiment succeeded because the investigators added very large amounts of salt to the high protein
diet. They did this becuase they noticed very high sodium excretion of unsalted high protein diets.
(Ref: Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL (1983) The human metabolic response to chronic
ketosis without caloric restriction: physical and biochemical adaptation. Metabolism 32: 757-768.)
I find this fascinating because it might explain the historical and current preoccupation with adding salt to
food.
86/298 (1997)
I wonder whether the ability to 'tolerate' high protein diets is determined by the degree of genetically
determined insulin resistance.
Best wishes Jennie
havIn message Paleolithic Diet Symposium List writes:
> There are 2 messages totalling 94 lines in this issue. Topics of the day: 1. Starch and dental
> caries 2. Dietary Macronutrient Content and Hyperinsulinemia End of Topics (which are also called
> e-mail "Subject Lines")
>
---------------------------------------------------------------------> Date: Mon, 5 May 1997 01:00:03 +0100
> From: Staffan Lindeberg Subject: Starch and dental caries
> In due time I hope that we will have some scholars of dental paleopathology in the group. In the
> meantime I, who know very little on the subject, refer to Lukacs JR. Dental paleopathology:
> Methods for reconstructing dietary patterns. In: Is=E7an MY, Kennedy KAR. Reconstruction of life
> from the skeleton. New York, Wiley-Liss 1989 who states that caries rates were low in prehistoric
> hunter-gatherers, intermediate in early farmers and highest in full-blown agriculturalists. A
> later paper that I came across also supports a role of cereal starch in caries: Littleton, J.
> Frohlich, B. Fish-eaters and farmers: dental pathology in the Arabian Gulf. Am J Phys Anthropol
> 1993; 92: 427-47.
> Abstract: Twelve skeletal samples, previously published, from the Arabian Gulf have been used to
> trace differences in diet and subsistence patterns through an analysis of dental pathology. The
> skeletons date from 3, 000 BC to AD 1, 500 and cover a variety of geographical locations: off-shore
> islands, Eastern Arabia, and Oman. The dental conditions analyzed are attrition, caries, calculus,
> abscessing, and antemortem tooth loss (AMTL). Results indicate four basic patterns of dental
> disease which, while not mutually exclusive, correspond to four basic subsistence patterns. Marine
> dependency, represented by the Ras el-Hamra population, is indicated by severe attrition, low
> caries rates, wear-caused abscessing, and a lack of AMTL. The second group of dental
> diseases--moderate attrition and calculus, low rates of caries, wear-caused abscessing, and
> low-moderate rates of AMTL--affects populations subsisting on a mixture of pastoralism or fishing
> and agriculture (Failaka, Umm an-Nar, Bronze Age Maysar, Bronze Age Shimal, and Iron Age Galilah).
> Mixed farming populations (Iron Age Maysar and Islamic Bahrain) experienced low-moderate
> attrition, high rates of caries and calculus, abscessing due to caries, and severe AMTL. The final
> group of dental diseases affects populations practicing intensive gardening (Bronze and Iron Age
> Bahrain, and Sites 3 and 5, Ras al-Khaimah). These groups experienced slight attrition, high rates
> of caries, low rates of calculus deposition, and severe AMTL. Sorry if I overemphasized what may
> already have been clear to you.
> Staffan
>
------------------------------------------------------------------> Staffan Lindeberg M.D. Ph.D. Dept of Community Health Sciences, Lund
> University, Mailing address: Dr Staffan Lindeberg, Primary Health Care
> Centre, Sjobo, S-22738 Sweden, +46 416 28140, Fax +46 416 18395
> http://www.panix.com/~donwiss/paleodiet/sl1.shtml
>
------------------------------------------------------------------>
-----------------------------> Date: Mon, 5 May 1997 09:47:00 -0600
> From: Loren Cordain Subject: Re: Dietary Macronutrient Content and Hyperinsulinemia
> In a previous digest, Jenny wrote: "The Keys equation does not consider the effect of amount and
> type of CHOs on insulin secretion. Hyperinsulinaemia is turning out to be one of the biggest
> independent risk factors for CHD. High protein diets and low glycaemic index diets both lower
> insulinaemia.
87/298 (1997)
> Best wishes Jennie"

> This was exactly my point. Ancestral, pre-agricultural diets were quite high in animal protein and
> the carbohydrate that was consumed was generally of a low glycemic index. These populations also
> selcetively consumed the fatty portions of the killed animal (brain, marrow, depot fat,
> perinephral fat, mesenteric fat, tongue, organs etc). However, available evidence from living
> hunter gatherers show that these surrogates of our stone age ancestors maintain low risk factors
> for CHD (blood lipid profiles, blood pressure, insulin sensitivity, body composition etc). All of
> this on a diet which contains 50-65% or more of its total calories derived from animal foods.
> Clearly, the Key's equation breaks down when either the macronutrient content (extremely high
> protein and low CHO) or the fatty acid composition of the diet (or both) varies beyond the range
> of conditions in which Keys originally derived his regression. Although there is much
> circumstantial evidence to indicate that the Key's equation is erroneous under these conditions,
> there is no empirical data that I am aware of which has confirmed this concept.
> Best wishes,
> Loren
>
-----------------------------> End of PALEODIET Digest - 1 May 1997 to 5 May 1997
PALEODIET Archives
Subject: Re: Fishing
Reply-To:
Date: Tue, 6 May 1997 19:09:40 +0100
Dean's report from 90 000 year old fishers makes sense. Why on earth would they not be fishing since they
were just as intelligent as we are and less preoccupied with millions of other obligations (like exploring
healthy diets). Perhaps their fishing tools were made from materials which are less prone to become
fossilized than other artifacts? Any comment from Foss Leach?
> African Exodus Chris Stringer & Robin McKie. 1996 London Jonathan Cape p4-5 (Zaire) In the
> neglected western branch of the African Rift Valley ....sediments are being exposed which were
> laid down 90 000 years ago, ...they found fish bones, including some from two metre long catfish.
> It seems that the Katanda people were efficiently and repeatedly catching catfish during their
> spawning season, indicating that systematic fishing is quite an ancient human skill...
-------------------------------------------------------------------
PALEODIET Archives
Subject: High-protein diets
From: Dean Esmay
Reply-To:
Date: Tue, 6 May 1997 20:41:40 -0400
> Have any of you any experience of putting people on high protein diets with little CHO? I have
> read that most subjects (who were probably insulin sensitive Caucasians) find this sort of diet
> nauseating and that experiments are usually terminated early.
88/298 (1997)
I hope we can find a way to draw out Michael Eades, who has been a member of our list for quite some time
but has been quiet so far. He's a physician with considerable experience treating his patients with highprotein, strictly carbohydrate-limited diets, with quite positive results.
Unfortunately, finding supporting research on this matter is very difficult. This sort of diet has a very bad
reputation, at least in the United States, but there is very little supporting research to back up this extremely
negative view. There is also very little peer-reviewed medical research which compellingly supports a
positive view either. This is because there is a lack of much research at all, and much of what has been done
is many decades old now.
For example, it is frequently claimed that high-protein, strictly carbohydrate-limited diets cause ketoacidosis
and muscle deterioration. There is no research which can be taken seriously that backs up these common
claims; about the only examples that are ever mentioned are studies of very low carbohydrate ketogenic
diets, but all such studies also involved severe calorie limitation--I have yet to see one which involved more
than 800 k/calories of total daily intake, and some involve as little as 400 k/cals per day. Similarly, while
very low carbohydrate diets sometimes cause nausea, no one has ever bothered to document how common
this really is, or how severe it usually is. It certainly does not affect all subjects this way but no one's
bothered to document more than that it does do this to some subjects, without even bothering to analyze
whether those who do get hit with nausea find it debilitating or only mildly annoying.
On the other hand, while a small handful of popular writers, including some physicians (e.g. Michael &
Mary Dan Eades, Robert Atkins, Richard Bernstein) have claimed significant health benefits from this sort of
diet, again there is very little in the way of clinical, peer-reviewed research to back up their claims. In fact,
while physicians like Eades and Atkins claim to have treated literally thousands of patients with this kind of
diet, improving all sorts of serious health problems, none have bothered to date to compile serious statistical
information and submit for peer review.
I can point out research which suggests that diets high in carbohydrate and/or low in fat raise risks for
diseases like cancer or heart disease (upon request). I can point to research which shows improvements in
athletic performance from very low carbohydrate diets. I can point to individuals I know (including myself)
whose health improved remarkably after using strictly carb-limited, high-protein diets, including the results
of my own survey of nearly 100 such people (most of whom are of European extraction but have weight
problems, by the way). But compelling data is limited--which is most frustrating for many of us.
PALEODIET Archives
Subject: Re: Plant breeding
Reply-To:
Date: Tue, 6 May 1997 19:09:50 +0100
Jennie wrote:
> We need to remember that the food plants we eat today are a long, long way from the original wild
> types. We have consistently bred them for improved characteristics like size and palatability and
> perhaps their ease of digestion.
What are the specific differences in nutrient density (amount of e.g. mineral per energy unit) between a wild
edible tuber and a cultivated (and hence bred) one? I posted exactly that question at the news group
sci.bio.food-science (which seems dominated by professionals) but I only got more questions. If nobody in
this group knows, could someone be so kind to take the time and effort to find an expert who has a good
answer?
Staffan Lindeberg
PALEODIET Archives
Subject: More on fishing
From: Dean Esmay
Reply-To:
Date: Tue, 6 May 1997 20:53:34 -0400
89/298 (1997)
> Perhaps their fishing tools were made from materials which are less prone to become fossilized
> than other artifacts?
The cat fish can apparently be caught by spear. At Wadi Kubbaniya c 16.000-15 000 BC (18000 BP) The
Nile flowed at higher levels than today. at this site catfish and other fish bones are found along with
waterfowl It is thought that the catfish swam into shallows in the flooding and were caught in the receding
waters, so I expect they could be caught by hand or net, too
18 000 BP was the high of the glaciation in Western Europe.
The reference which goes with this is <Loaves and Fishes: The prehistory of Wadi Kubanniya. > Wendorf
F, Schild R and A Close. Dallas: Southern Methodist Univ.1980 The same techniques would be useful for
atlantic salmon which were caught in the ice free salmon rivers of SW Europe in the same period.
None of this stuff is any of my own research, by the way. Certain list members seem to prefer a little
anonymity and so I'm happy to oblige by reposting for them.
PALEODIET Archives
From: Andrew Millard
Reply-To:
Date: Wed, 7 May 1997 08:42:39 +0100
> Doug Ginsberg wrote: [regarding cooking/detoxifying methods]
> ...and were any of them used by paleolithic hunter-gatherers? I don't think there is any evidence
> of that. I suppose they would need pottery which they apparently did not use.
We do have hunter-gathers using pottery in the Jomon culture of Japan for several thousand years, but not in
Palaeolithic cultures (any culture which had pottery would probably not be labelled Palaeolithic!). The
Jomon is usually considered to be similar to the Mesolithic of Europe.
On the other hand we do have farming cultures, notably the Pre-pottery Neolithic of the Near East, where
there is clearly massive reliance on cereal crops but no pottery in which to cook them. They clearly needed to
cook their crops, but we have little idea of how they did it.
Andrew Millard
========================================================================= Dr.
Andrew Millard Department of Archaeology, University of Durham, Tel: +44 191 374 4757 South Road,
Durham. DH1 3LE. United Kingdom. Fax: +44 191 374 3619 http://www.dur.ac.uk/~drk0arm/
=========================================================================
PALEODIET Archives
Subject: Re: High protein diets, fish and tubers
From: Loren Cordain
Reply-To:
Date: Wed, 7 May 1997 11:39:00 -0600
In the last digest, Jenny wrote:
"A question about high protien diets:
Have any of you any experience of putting people on high protein diets with little CHO?
I have read that most subjects (who were probably insulin sensitive Caucasians) find this sort of diet
nauseating and that experiments are usually terminated early.
One experiment succeeded because the investigators added very large amounts of salt to the high protein
diet. They did this becuase they noticed very high sodium excretion of unsalted high protein diets.
(Ref: Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL (1983) The human metabolic response to chronic
ketosis without caloric restriction: physical and biochemical adaptation. Metabolism 32: 757-768.)
I find this fascinating because it might explain the historical and current preoccupation with adding salt to
food.
90/298 (1997)
I wonder whether the ability to 'tolerate' high protein diets is determined bythe degree of genetically
determined insulin resistance.
Best wishes Jennie"
When Stefansson undertook his classic dietary experiment (metabolic ward controlled) in Bellvue hospital in
1922 in which he consumed an all meat diet for an entire year (Lieb CW. The effects of an exclusive, longcontinued meat diet. JAMA 1926;87:25-26), he reported nausea and illness after the 2nd day of eating large
quantities of "chopped fatless muscle" (Stefansson V. The Fat of the Land. Macmillan Company, New York,
1960, p60-89). Inclusion of fatty meats, brains and bacon remedied his nausea and he was able to continue
the experiment under metabolic ward conditions in which all food that was consumed was measured and its
nutrient and caloric content measured. Additionally his metabolic rate was continually monitored in a
metabolic chamber. The results of this case study were widely reported in the scientific and medical
literature of the late 1920's and early 30's (I can provide all of the references if you are interested). It turned
out that his ad libitum average caloric intake was 2, 650 calories/day of which 2, 100 calories consisted of fat
and 550 calories consisted of protein or about 79% fat & 21% protein. It is difficult to speculate upon
Stefansson's degree of insulin resistance, however because he was of Northern European extraction and
somewhat overweight while on a normal mixed diet, it is probable that he was not as insulin resistant as
recently acculturated peoples such as the Inuit, polynesians, Australian aborigines or Pima Indians. Speth has
written extensively about excess dietary protein and it seems likely that unless sufficient carbohydrate or fat
are available, the calories present in wild, lean game animals can only be eaten in limited quantities.(Speth
JD. Early hominid hunting and scavenging: the role of meat as an energy source. J Hum Evol 1989;18:32943; Speth et al. Energy source, protein metabolism, and Hunter-Gatherer subsistence strategies. J Anthropol
Archaeology 1983;2:1-31).
Staffan writes:
Dean's report from 90 000 year old fishers makes sense. Why on earth would they not be fishing since they
were just as intelligent as we are and less preoccupied with millions of other obligations (like exploring
healthy diets). Perhaps their fishing tools were made from materials which are less prone to become
fossilized than other artifacts? Any comment from Foss Leach?
The fossil record which is obviously incomplete generally doesnt show any evidence of exploitation of the
aquatic environment until about 35, 000 years ago. Clearly, part of the problem is that the technologies
which may have been used to capture fish: nets, lines, weirs and bone hooks likely disintegrated. However,
there should have been a record of fossilized portions (heads, tails, fins etc) of uneaten fish parts along with
other animal foods consumed in the caves and camps of our ancestors. Except for the recent report from
Africa 90, 000 years ago, there are virtually no reports showing evidence for large scale fish consumption.
The date of the African data has been challenged because of the difficulty in dating fossils in this general
time period (C14 dating only can go back about 40, 000yrs). Since humans reached Australia by 50, 000-60,
000 yrs ago, it can be inferred that they had mastered at least somewhat sophisticated boating/rafting
procedures - it is difficult to believe that they did not exploit the creatures in the medium in which they
sailed. Also, the sites of most of the coastal dwelling people (most likely to have consumed fish) are now
under water and generally unavailable for archaeological exploration. One final comment - optimal foraging
theory would suggest that the aquatic environment would generally not be exploited until more easily
obtained resources (i.e. large easily killed pleistocene beasts) were depleted.
Staffan wrote:
What are the specific differences in nutrient density (amount of e.g. mineral per energy unit) between a wild
edible tuber and a cultivated (and hence bred) one? I posted exactly that question at the news group
sci.bio.food-science (which seems dominated by professionals) but I only got more questions. If nobody in
this group knows, could someone be so kind to take the time and effort to find an expert who has a good
answer?
I know of no specific studies examining nutrient densities between wild and cultivated tubers, however in
Boyd Eaton's most recent article (Eaton SB et al. An evolutionary perspective enhances understanding of
human nutritional requirements. J Nutr 1996;126:1732-40) he provides a table of average nutrient densities
of 224 vegetable foods that hunter gatherers may have eaten. There are perhaps 30 or more references which
have been provided including some of Jenny Brand-Miller's data on Aboriginal foods. Perhaps somewhere in
one of these you may find a specific comparison of wild and cultivated tubers.
Cordially,
Loren
91/298 (1997)
PALEODIET Archives
Subject: Re: High-protein diets
From: Art De Vany
Reply-To:
Date: Wed, 7 May 1997 15:44:46 -0700
I think the stories about kidney or liver damage from high protein diets either are apocryphal or are based on
out-dated and challenged research. If so, this would coincide with what Dean said about nausea and
ketoacidosis and high protein diets.
I would like to see some of the references Dean mentioned regarding cancer and heart disease and athletic
performance.
As to peer-reviewed research, a lot of the research done in this area is of short duration and uses poor sample
design and questionable statistics. Research is always in a state of flux. That is one reason I find evolutionary
and anthropological evidence to be a good second test to apply to the laboratory research. When there is
agreement over these test modalities, you may have something. If, in addition, one can describe the
mechanisms and characterize how they operate in different subgroups of the population (insulin resistance,
and so on), then you do have something.
I can add one more data point to the sample of high protein/low carbohydrate eaters. It works for me. I eat
enormous amounts of food, probably 4000 plus calories, but the calories come only from meat, vegetables,
and fruit. I am physically active, as I imagine our ancestors were in the hunt, not in the frenetic daily routine
often prescribed to manage weight. The intermittent intensity maintains muscle mass so that I stay lean on
this diet and carry the lean body mass that might have been typical of a paleolithic ancestor.
I would be very interested in adding a discussion of activity patterns to this valuable discussion group's
topics and interests. Diet cannot be understood in the absence of and understanding of the activity patterns of
the organism.
Art De Vany
PALEODIET Archives
Subject: High Protein Diets
From: robert rosenstein
Reply-To:
Date: Wed, 7 May 1997 18:16:53 -0500
In the paragraph about Stephasson, it was noted:
"It turned out that his ad libitum average caloric intake was 2, 650 calories/day of which 2, 100 calories
consisted of fat and 550 calories consisted of protein or about 79% fat & 21% protein. "
New York is not the Arctic and the amount of energy expended daily in the city - even with exercise - could
not account for the dissapation of all those calories. Do you know whether he gained a lot of weight during
this time?
robert
PALEODIET Archives
Subject: PALEODIET BOOK REVIEW
From: Ray Audette
Reply-To:
Date: Thu, 8 May 1997 11:07:13 -0700
This is the review of NeanderThin in the May '97 issue of Healthy & Natural Journal. I hope my readers will
respond with a letter to the editor at the e-mail address below Ray Audette Author "NeanderThin: A
Caveman's Guide to Nutrition"
92/298 (1997)
"Diagnosed with rheumatoid arthritis and diabetes by the age of 34, Ray Audette relates in NeanderThin he
began reading about the probable causes and concluded they, along with allergies, colitis, multiple sclerosis,
Alzheimer's, lupus, many cancers and cardiovascular diseases, as well as obesity were associated with
civilization. Cut out our overpopulated, over-poluted, over-weight civilization, he reasoned, and you'll do
away with these devastating diseases. He began eating only the foods that would be edible if he were armed
with only a sharp stick and a rock. Well, almost. Audette is really more of a supermarket hunter-gatherer. His
diet eliminates technology-dependent foods such as grains, beans, potatoes, dairy products and sugars. But
he includes store-bought meats (lots of it), fruits, vegetables, nuts and berries, all preferably eaten raw,
though again he cooks quite a bit. He's especially keen on pemmican - equal parts of dried raw meat and suet
(beef fat). He assures us that the extra animal fat will be offset by not using vegetable oils, trans-fatty acids
and dairy fats. Caveman diets are nothing new -- pun intended. Every generation has had a few exponents,
some more persuasive than others. Audette, who hail from Texas -- where else?-- sounds sincere and his
little book has some insights -- for example, he argues that we should try living closer to nature and eating
less processed foods. I might be convinced by someone who heads for the wilderness and lives only on wild
animals and plants. But to consume animals and plants which have undergone tremendous genetic changes
over the generations that they have been domesticated, and which are pumped full of chemicals, pesticides,
hormones, synthetic feeds and increasingly bio-engineered, then to call that a caveman diet is a delusion. The
basic premise is also false: the "diseases of civilization" are associated primarily with Western civilization:
Asians, for example, who eat less meat are less prone to these diseases. Animal fat is not the nutrition
equivalent of fats derived from plants. Audette's arguments that humans are innately meat eaters is
contradicted by human dentition and the human digestive system, which are not those of carnivores. His
argument that the principle cause of animal extinction is the plow not the slaughterhouse (because farmland
denies wildlife habitat is ludicrous: what do domestic animals eat (it takes 7 pounds of grain to produce one
pound of beef) and where do they roam? His choice of Neanderthals as a model is unfortunate. Neanderthals
were probably not direct ancestors of ours, but a specialized adaptation to Ice Age Europe who died out - an
evolutionary dead cul de sac. Their average lifespan was 30, meaning they would not be prone to diseases
such as Alzheimer's and many cancers; yet they still suffered from arthritis, rickets and scurvy. They were
survived in Europe by Cro-Magnon who ate a more balanced diet of plants and meats."
Review by Alain Dessaint Posted with permission of Healthy & Natural Journal
PALEODIET Archives
Subject: Healthy & Natural Journal
From: Ray Audette
Reply-To:
Date: Thu, 8 May 1997 15:08:57 -0700
The e-mail address for H&N Journal is
I hope you will inform them of the factual errors in their review of my book.
Ray Audette
PALEODIET Archives
Subject: Re: Ancestral exercise patterns;meso/neolithic cereal consumption; Stefansson's weight
From: Loren Cordain
Reply-To:
Date: Thu, 8 May 1997 17:10:00 -0600
In the last digest, Art wrote:
I would be very interested in adding a discussion of activity patterns to this valuable discussion group's
topics and interests. Diet cannot be understood in the absence of and understanding of the activity patterns of
the organism.
Art De Vany
93/298 (1997)
Our group has writtten a paper which should appear in print shortly involving estimation of ancestral activity
patterns. I refer you to (Cordain L, Gothshall RW, Eaton SB. Evolutionary aspects of exercise. World
Review of Nutrition and Dietetics 1997;81:xx-xx). I can provide you with preprints if you directly e-mail
me. Also, I made a presentation on this topic at a National convention last month in which my co-presenter,
Dr. Jakicic presented data from his group. Enclosed is the abstract of his findings which supports Dr. De
Vany's concept of short term high intensity exercise bouts:
Jakicic JM. Wing RR. Butler BA. Robertson RJ. Prescribing exercise in multiple short bouts versus one
continuous bout: effects on adherence, cardiorespiratory fitness, and weight loss. International Journal of
Obesity & Related Metabolic Disorders 1995;19:893-901.
Abstract OBJECTIVE: To investigate whether prescribing exercise in several short-bouts versus one longbout per day would enhance exercise adherence, cardiorespiratory fitness, and weight loss in overweight
adult females in a behavioral weight control program. CONCLUSION: These results suggest that short-bouts
of exercise may enhance exercise adherence. Short-bouts of exercise may also enhance weight loss and
produce similar changes in cardiorespiratory fitness when compared to long-bouts of exercise. Thus, shortbouts of exercise may be preferred when prescribing exercise to obese adults.
Dr's Lindeberg and Millard wrote:
Andrew Millard wrote:
> We do have hunter-gathers using pottery in the Jomon culture of Japan for several thousand years,
> but not in Palaeolithic cultures (any culture which had pottery would probably not be labelled
> Palaeolithic!). The Jomon is usually considered to be similar to the Mesolithic of Europe. On the
> other hand we do have farming cultures, notably the Pre-pottery Neolithic of the Near East, where
> there is clearly massive reliance on cereal crops but no pottery in which to cook them. They
> clearly needed to cook their crops, but we have little idea of how they did it.
Could it be that they wrapped them in leaves and covered and baked them in the ground with heated stones
like for instance the Trobriand Islanders and many others traditionally did? Would this leave any traces?
Staffan Lindeberg
There are two references in the literature which suggest that early cereal consumption may have been done
by consumption of gruels & maybe even beers which perhaps were made in vessels of animal hides,
stomachs or intestines.
1. Katz SH et al. Bread and beer. The early use of cereals in the human diet. Expedition 1986;28(2):23-34.
2. Braidwood RJ. Did man once live by beer alone? Am Anthropologist 1953;55:515-526.
- Perhaps Dean could comment on the title of the last citation?
STEFANSSON'S WEIGHT:
In the paragraph about Stefansson, it was noted:
"It turned out that his ad libitum average caloric intake was 2, 650 calories/day of which 2, 100 calories
consisted of fat and 550 calories consisted of protein or about 79% fat & 21% protein. "
New York is not the Arctic and the amount of energy expended daily in the city - even with exercise - could
not account for the dissapation of all those calories. Do you know whether he gained a lot of weight during
this time?
robert
The answer to this one is a direct quote from Stefansson: "A phase of our experiment has a relation to
slimming, slenderizing, reducing: the various treatments of obesity. I was about 10 pounds overweight at the
beginning of the meat diet, by life insurance standards, and lost all of it." (Stefansson V. The Fat of the Land.
Macmillian, New York, 1960, p.84.). I believe his official body weight pre-post the one year of the all meat
diet was reported in (Lieb CW. The effect on human beings of a twelve month's exclusive meat diet. J Am
Med Assoc 1929;92:20-.).
PALEODIET Archives
Subject: Re: High protein diets, saltiness
Reply-To:
Date: Thu, 8 May 1997 23:29:37 +0100
94/298 (1997)
Case history: 59 year old man who was referred to me one month after he had been diagnosed with type 2
(non-insulin dependent) diabetes (NIDDM). Before we met he had got the advice to minimise fat intake
which he truly did to around 10 per cent of daily energy (E%) (Swedish average is 37) largely by eating
polymeric or elementary diets to which he had easy access. By use of a nutrition software that he and a
mutual friend of ours had developed he systematically explored the effects of varying proportions of CHO
and protein on weight, blood glucose (he has like most of our diabetics his own glucometer) and urinary
glucose while keeping fat intake at 10-12 E%. Before I even mentioned the ongoing discussions of high
protein intake in prudent diets he reported that the combination that helped him the best to lose weight was
45/45/10 of Prot/CHO/Fat (note that he never changed his fat intake). When CHO was increased to 70% his
blood sugar immediately went up. During the following 2 months his HbA1C (glycated hemoglobin which
reflects average blood glucose in the last 6-8 weeks) was almost normalised from 8.1% to 6.0 in 2 months.
Weight went from 115 to 102 kg, serum triglycerides from 2.1 to 0.7 mmol/L, serum cholesterol from 6.5 to
5.6 mmol/L and fasting serum insulin from 16 to 3 mU/L. We rarely succeed that well with our NIDDM
patients even if we give them antidiabetic medication (which by the way has not been shown to prevent early
death or coronary heart disease).
As for the saltiness of meat I refer to my personal experience which is that a low salt diet is easier to comply
with if it includes much meat. In April 1987 I started my life-long experiment on a no-salt everyday food
mainly based on meat, fish, tubers, fruit and nuts. During the first 8 months I made no exception and my 24
hour urinary sodium excretion was 14 mmol (most Westerners excrete 100-250). When after a couple of
months I was accustomed I experienced that meat is quite salty compared to vegetable foods, i.e. the
naturally occuring salt in meat is high as is also evident from food composition tables. There is no difference
in sodium content between wild and domesticated animals. Today heavily salted meat is virtually inedible to
me and my family.
Staffan
PALEODIET Archives
Reply-To:
Date: Fri, 9 May 1997 08:53:54 +0100
> Staffan Lindeberg wrote
> Andrew Millard wrote:
> On the other hand we do have farming cultures, notably the Pre-pottery Neolithic of the Near East,
> where there is clearly massive reliance on cereal crops but no pottery in which to cook them. They
> clearly needed to cook their crops, but we have little idea of how they did it. Could it be that
> they wrapped them in leaves and covered and baked them in the ground with heated stones like for
> instance the Trobriand Islanders and many others traditionally did? Would this leave any traces?
It is possible but we are talking about the earliest towns with large numbers of people living together, and
intensively farming the surrounding area, and given that leaves are likely to be a one-use cooking vessel their
environmental impact would have been very great. This might tie in with what is known from 'Ain Ghazal
(Jordan) where from the middle Pre-pottery Neolithic B (PPNB c. 7200-6500 C14 years BP) through the late
PPNB (6500-6000 C14 BP) to PPNC (6000-5500 C14 BP) we see a decrease in the size of posts used in
construction. The houses also had c.50 sq. m of lime plaster floor each. The excavator's interpretation was
that it would have consumed 10 mature trees per floor to make the plaster, and given the keeping of
domesticated goats, trees would not have regenerated, hence there would have been deforestation. The
occupation reached its greatest density in the late PPNB, in the PPNC we see types of house implying
changes in the structure of society, and in the following Yarmoukian period occupation density was much
less. (Information from a seminar given here by Gary Rollefson last December.) But perhaps leaf use also
contributed to the deforestation?
Andrew Millard
========================================================================= Dr.
=========================================================================
95/298 (1997)
PALEODIET Archives
Subject: Ecosystem map reconstructions
From: Dean Esmay
Reply-To:
Date: Fri, 9 May 1997 10:36:48 -0400
List members may find the following a useful reference:
http://www.esd.ornl.gov/ern/qen/adams1.html
Abstract:
A set of preliminary, broad-scale ecosystem map reconstructions is presented for the world at the Last
Glacial Maximum (18, 000 14C years ago) and the early Holocene (8, 000 14C years ago), the mid Holocene
(5, 000 14C years ago) and for comparison 'present-potential' maps that may be regarded as approximating
the late Holocene vegetation distribution as it would - or might - have been without agricultural modification.
The maps were produced through consultation with an extensive network of experts and a range of literature
and map sources, with the final decision in each case made by the editors. Accompanying each regional map
is a general background text detailing the principal sources of evidence and the major uncertainties within
this.
These maps are not intended as the 'last word' on the distribution of ecosystem types at these times - they are
merely a rough attempt at appraisal of current knowledge and opinion. Nevertheless, the maps and the
accompanying literature review should provide a valuable and readily accessible source of information on
current opinion in the Quaternary community. It is also hoped that they will act as a forum for discussion on
the distribution of palaeovegetation amongst those who are working in each region.
PALEODIET Archives
Subject: High Protein Diets
From: Dean Esmay
Reply-To:
Date: Fri, 9 May 1997 15:54:30 -0400
As someone who talks frequently with people who use high-protein, very low carbohydrate diets for health
reasons, I can say that people reporting energy and/or nausea problems quite often seem to be avoiding or
trying to cut back on fat intake, with the notion that avoiding fat will somehow help them lose weight better
or that fat will harm them somehow. This usually results in significant discomfort. The Inuit have a name for
this condition; they call it "rabbit sickness, " which is brought about from eating too much lean meat without
enough fat (in a nearly carbohydrate-free diet), which can be a problem especially during times of famine
when the game meat has become starved and has very little fat left on its body. The condition supposedly can
be fatal though I don't know if there have been any firsthand reports of this. It's always fixed by introducing
larger quantities of fat into the diet.
As for weight: Stefansson reported (see "Adventures in Diet Part 1, December 1929 Harper's Monthly) that
he had been ten pounds overweight at the start of the experiment and that these were eliminated by the end of
the experiment. During the experiment he was no more physically active than the average businessman in
New York.
There is a widespread belief that high-fat diets result in rapid weight gain but I've seen very little evidence
that the difference is all that compelling. Excess fat in the diet will convert more efficiently to body fat than
excess carbohydrate, but not very much. For example, see this abstract from the American Journal of Clinical
Nutrition 1995;62:19-29:
-=-
96/298 (1997)
Abstract: The purpose of this study was to determine whether and by what mechanism excess dietary fat
leads to greater fat accumulation than does excess dietary carbohydrate. We overfed isoenergetic amounts
(50% above energy requirements of fat and carbohydrate for 14 days each) to nine lean and seven obese
men. A whole-room calorimeter was used to measure energy expenditure and nutrient oxidation of days 0, 1,
7, and 14 of each over feeding period. From energy and nutrient balances we extimated the amount and
composition of energy stored. Carbohydrate overfeeding produced progressive increases in carbohydrate
oxidation and total energy expenditure resulting in 75-85% of excess energy being stored. Alternative, fat
overfeeding had minimal effects on fat oxidation and total energy expenditure, leading to storage of 90-95%
of excess energy. Excess dietary fat leads to greater fat accumulation than does excess dietary carcohydrate,
and the difference was greatest early in the overfeeding period. Significant tidbits:
> Fat Mass and Fat Free Mass increased significantly with carbohydrate overfeeding and fat overfeeding.
There were no significant differences between diets and/or groups in body weight or body-composition
changes.
> Fat accumulation was initially lower and carbohydrate accumulation higher with carbohydrate than with
fat overfeeding. However, with the progressive decline in fat oxidation, fat storage increased so that on day
14 there was no difference between diets in fat or carbohydrate storage.
> Greater than 75% of the excess energy consumed by our subjects was stored in the body, not expended,
regardless of the composition of the excess. However, our results demonstrate that excess carbohydrate
affects energy and nutrient balances differently than does excess fat. We found that for equivalent amounts
of excess energy, fat leads to more body fat accumulation than does carbohydrate.
> Regardless of the composition of the overfeeding diet, obese subjects oxidized proportionally more
carbohydrate and less fat than did lean subjects
-=While the experiment showed that excessive fat in overfeeding situations leads to faster accumulation of
body fat, it also demonstrated that the difference is statistically significant but not particularly compelling. It
also showed that the difference between the two sources' storage potential narrowed as time went on; it
would have been nice to know if that trend would have continued had the experiment gone on longer. And as
the experiment was so short-term, we can't know what the long-term effects of carbohydrate-overfeeding
would have been on insulin levels over a period of months or years, which might eventually lead to greater
appetite and/or general fat accumulation than a higher fat diet would.
It can be observed empirically that some obese individuals lose weight at a steady and comfortable pace over
a period of months on very high fat, high protein, very low carbohydrate diets. So far scientific interest in
exploring this phenomenon has been sadly low.
As for Art's question:
> I would like to see some of the references Dean mentioned regarding cancer and heart disease and
> athletic performance.
I'll get back to you on that early next week, I'm a little swamped this weekend!
PALEODIET Archives
Subject: More on Fishing
From: Ron Hoggan
Reply-To:
Date: Sat, 10 May 1997 12:26:36 -0600
I'm sorry to be so long in responding to this post, but my server was down for several days.
Tue, 6 May 1997 20:53:34 -0400 Dean Esmay said:
> Perhaps their fishing tools were made from materials which are less prone to become fossilized
> than other artifacts? The cat fish can apparently be caught by spear. At Wadi Kubbaniya c
> 16.000-15 000 BC (18000 BP) The Nile flowed at higher levels than today. at this site catfish and
> other fish bones are found along with waterfowl It is thought that the catfish swam into shallows
> in the flooding and were caught in the receding waters, so I expect they could be caught by hand
> or net, too
97/298 (1997)
As a kid, my brother was much better at fishing than I was, so I figured out a way to compete. The water
level rose and fell in the bow river. So I chose a spot where the water would form pools, and be isolated
when water levels were low, but would allow fish to enter when the levels were high. I also chose a place
that was shaded by trees, as the fish seemed to prefer that.
I dug a pool deeper, and lined the perimeter with rocks that were large enough that the gaps between them
would allow the minnows and smaller fish out, but hold in fish of a size I was interested in. During the
summer, I regularly caught several fish each day, until my brother followed me so he could have access to
my secret fishing hole.
While my brother considered himself cheated, I felt that I had proven myself to be the superior fisherman. :-)
I believe that my "net" was indistinguishable to most passers-by. No trace would have been left of it after a
few months.
As an adult, I was talking with a good friend. He told me that as a child (he was from a poor immigrant
family) he had developed a similar system for catching fish, in the same river, but a few miles upstream.
I don't think that paleolithic humans would have had much difficulty catching fish in a similar manner. And
my friend's similar "inspiration" suggests to me that it was not a unique insight on my part.
Best Wishes, Ron http://www.panix.com/~donwiss/hoggan/
PALEODIET Archives
Subject: Re: More on Fishing
Reply-To:
Date: Sun, 11 May 1997 01:29:22 +0100
So, if only one person in each group of Paleolithic humans were as intelligent as Ron Hoggan was as a boy,
:-), he/she would show his/her mates how to catch fish without leaving any traces for archaeologists.
Another possible source of bias is close to one of those Loren Cordain mentioned (see below): Could it be
that those ancestors that have been found exploited a habitat which for some reason were more likely to
become fossilized, or just happened to do so? The odds are heavily against any person or artifact becoming
fossilized AND coming up to the ground in this century AND being found before being destroyed in the
open air. However, I would expect fishing ancestors living near waters to be more likely to fall in the river
and thus be preserved, and if this is true we could actually overestimate the proportion of fishers.
As for optimal foraging theory, which according to Loren would suggest that the aquatic environment would
generally not be exploited until more easily obtained resources (i.e. large easily killed pleistocene beasts)
were depleted, I have a question: Does such theory consider our obvious urge for thrill and excitement (or
whatever made Ron go fishing although he probably didn't need it) in a habitat where only 2-3 hours per day
are needed for subsistence activities (as for contemporary hunter-gatherers)? And what would optimal
foraging theory have to say about my cat who mostly would want her mouse victims to give her much more
of a match before she eats them?
> Date: Sat, 10 May 1997 12:26:36 -0600
> From: Ron Hoggan Subject: More on Fishing
> Perhaps their fishing tools were made from materials which are less
>
> prone to become fossilized than other artifacts? The cat fish can apparently be caught by spear.
> At Wadi Kubbaniya c 16.000-15 000 BC (18000 BP) The Nile flowed at higher levels than today. at
> this site catfish and other fish bones are found along with waterfowl It is thought that the
> catfish swam into shallows in the flooding and were caught in the receding waters, so I expect
> they could be caught by hand or net, too
> As a kid, my brother was much better at fishing than I was, so I figured out a way to compete. The
> water level rose and fell in the bow river. So I chose a spot where the water would form pools,
> and be isolated when water levels were low, but would allow fish to enter when the levels were
> high. I also chose a place that was shaded by trees, as the fish seemed to prefer that. I dug a
> pool deeper, and lined the perimeter with rocks that were large enough that the gaps between them
> would allow the minnows and smaller fish out, but hold in fish of a size I was interested in.
> During the summer, I regularly caught several fish each day, until my brother followed me so he
> could have access to my secret fishing hole.
98/298 (1997)
> While my brother considered himself cheated, I felt that I had proven myself to be the superior
> fisherman. :-) I believe that my "net" was indistinguishable to most passers-by. No trace would
> have been left of it after a few months.
> As an adult, I was talking with a good friend. He told me that as a child (he was from a poor
> immigrant family) he had developed a similar system for catching fish, in the same river, but a
> few miles upstream. I don't think that paleolithic humans would have had much difficulty catching
> fish in a similar manner. And my friend's similar "inspiration" suggests to me that it was not a
> unique insight on my part.
Loren's posting: "The fossil record which is obviously incomplete generally doesnt show any evidence of
exploitation of the aquatic environment until about 35, 000 years ago. Clearly, part of the problem is that the
technologies which may have been used to capture fish: nets, lines, weirs and bone hooks likely
disintegrated. However, there should have been a record of fossilized portions (heads, tails, fins etc) of
uneaten fish parts along with other animal foods consumed in the caves and camps of our ancestors. Except
for the recent report from Africa 90, 000 years ago, there are virtually no reports showing evidence for large
scale fish consumption. The date of the African data has been challenged because of the difficulty in dating
fossils in this general time period (C14 dating only can go back about 40, 000yrs). Since humans reached
Australia by 50, 000-60, 000 yrs ago, it can be inferred that they had mastered at least somewhat
sophisticated boating/rafting procedures - it is difficult to believe that they did not exploit the creatures in the
medium in which they sailed. Also, the sites of most of the coastal dwelling people (most likely to have
consumed fish) are now under water and generally unavailable for archaeological exploration. One final
comment - optimal foraging theory would suggest that the aquatic environment would generally not be
exploited until more easily obtained resources (i.e. large easily killed pleistocene beasts) were depleted."
PALEODIET Archives
Subject: New List Announcement
From: Dean Esmay
Reply-To:
Date: Sun, 11 May 1997 12:33:16 -0400
This non-academic list for the general public may be of interest to some of our subscribers:
PALEOFOOD
This is a SUPPORT list for those interested in a Paleolithic Style Diet such as described in
"NEANDERTHIN" by Ray Audette or as prescribed as an experimental treatment for various diseases.
The principle aim of this list is to provide a discussion forum for people who feel their well being is better
served by a diet that excludes certain foods in the spirit of the Hunter-Gatherer.
Primary purpose of the list is to be a practical forum of support and information for those following a Preagriculture Hunter-Gatherer Lifestyle in today's Modern World.
The List is open to everyone but list content will be mostly concerned with the lifestyle as described by Ray
Audette in NeanderThin or similar works.
It is not possible to be a Vegetarian. If you are not comfortable with red meat consumption, then this list is
not for you.
Knowledge of "low carb" diets will be beneficial (carbohydrate restricted and/or ketogenic diets) especially
if weight loss is a goal and/or for the control and management of a specific disease.
The "mood" and "tone" will be that of informational to the curious and supportively helpful to those seeking
solutions for their personal challenges.
Our goal is to make a pre-agriculture Paleolithic diet do-able in today's world by sharing ideas, knowledge
and experience.
----> The Paleolithic Diet Page What the Hunter/Gatherers Ate Information at:
http://www.panix.com/~donwiss/paleodiet/ Come Join us
PALEODIET Archives
Subject: High fat vs high CHO diets
99/298 (1997)
Reply-To:
Jennie Brand Miller
Date: Mon, 12 May 1997 10:49:42 +1000
Last week Dean Esmay wrote: 'There is a widespread belief that high-fat diets result in rapid weight gain but
I've seen very little evidence that the difference is all that compelling. Excess fat in the diet will convert more
efficiently to body fat than excess carbohydrate, but not very much. For example, see this abstract from the
American Journal of Clinical Nutrition 1995;62:19-29'
Yes, under controlled feeding conditions like this, there is virtually no difference between a high fat and a
high CHO diet. But the key word here is 'controlled'. Under free-living conditions it's difficult to consume a
high CHO diet in excess. For example in the above study, the extra 1000 calories as CHO versus fat would
mean consuming an extra loaf of bread a day versus a packet of peanuts. You tell me which is easier!
One of the best studies looking at BMI and the composition of the diet involved 10, 000 people in Scotland
(International J. Obesity 1994, 18: 820-828). They found the best predictor of BMI was the ratio of fat to
CHO (especially sugar) ie the BMI increased as the ratio increased. The more fat and the less sugar, the fatter
people were. It explained almost 50% of the variation in the BMI.
I think it's very interesting neither starch, or fibre, or intrinsic sugars explained as much of the variation in
BMI. (By the way they excluded the dieters from the study). Whatever way you look at it, a high CHO diet
will weigh twice as much as a high fat diet, so it's more difficult to overeat it.
Best wishes Jennie
PALEODIET Archives
Subject: Cooking of cereals
Reply-To:
Jennie Brand Miller
Date: Mon, 12 May 1997 10:59:18 +1000
Last week Staffan lindeberg wondered how they might cook cereals without pottery.
The Australian Aboriginal people might be a good example here. They had no pottery.
First they roasted the cereals (or other seeds such as acacias) in the ashes of a fire. The women would then
separate the seeds from the dirt and ashes using a highly skilled shaking action in a coolamon (a curved
wooden dish). They would then grind the seeds on a grinding stone mixing in a little water. They woould eat
the paste with their fingers or alternatively cook the paste on a hot stone to form a kind of damper.
Best wishes Jennie
PS Thanks for all your comments about high protein diets. All very interesting. But more research needed!
PALEODIET Archives
Subject: Re: Fishing and optimal foraging theory
From: Loren Cordain
Reply-To:
Date: Mon, 12 May 1997 11:44:00 -0600
100/298 (1997)
Staffan suggested last time that optimal foraging theory may not adequately explain modern man's desire to
go fishing. I am in complete agreement with this - last Saturday, I took my two boys out for 4 hours of lazy
fishing and didnt even get a bite. In support of my experience, Hawkes in her classic study of Ache optimal
foraging behavior (Hawkes K et al. Why hunters gather: optimal foraging and the Ache of eastern Paraguay.
Am Ethnologist 1982;9:379-398) showed that the caloric return (calories derived from the food per handling
hour) from fishing ranked 9th out the top 12 foods regularly acquired by the Ache. Hawkes notes, "why dont
Ache fish more often?. . . . .five women spent 2.25 hr each fishing a small lagoon and stream. Their returns
were neglible: less than 2 kg of fish. This seemed to be viewed more as play than foraging. . . . . 38 adults
spent 5 hr each fishing the lagoon and took about 25 kg fish. The addition of these two incidents to the
figures results in a total of 288 forager-hours for 216 kg of fish, which is 1.3 hr/kg or about 733 Cal per
forager hour. These figures suggest that the Ache fish infrequently because they do better hunting." So, it
seems that in living hunter gatherers in inland tropical situations, they have the same problems as my sons
and I had - fishing generally has a low caloric return rate. Clearly, there are exceptions to this - witness the
salmon runs utilized by Inuit and other indigenous populations living at northern latitudes and the shellfish
mounds in coastal areas - however these resources only tended to be exploited towards the end of the
pleistocene, and as previously stated, there is little evidence of regular exploitation of the aquatic
environment for most of the time hominids have existed.
Best wishes,
Loren
PALEODIET Archives
Subject: On the subject of fat
From: Dean Esmay
Reply-To:
Date: Mon, 12 May 1997 13:30:42 -0400
Regarding fat: I keep hoping we can talk Mary Enig into sharing some of her wisdom on this subject with us.
But in the meantime, here are some preliminary references to check out regarding the negative and/or
questionable impact of low-fat diets:
-=Jeppeson, J., et. al. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in
postmenopausal women. Shows that low-fat, high-carbohydrate diets (15% protein, 60% carbohydrate, 25%
fat) increase risk of heart disease in post-menopausal women over a higher fat, lower carbohydrate diet (15%
protein, 40% carbohydrate, 45% fat). (American Journal of Clinical Nutrition, 1997;65:1027-33.)
Franceschi S et. al. Intake of macronutrients and risk of breast cancer. Lancet; 347(9012):1351-6 1996. In the
largest and most comprehensive study on diet and breast cancer to date, studying over 5, 000 women
between 1991 and 1994 showed that women with the lowest intake of dietary fat had a significantly higher
incidence of breast cancer than the women with the highest intake of dietary fat. It also found that women
with the highest intake of starch had a significantly higher incidence of breast cancer than the women with
the lowest intake of startch. The study found no evidence that saturated fat had any effect one way or the
other on breast cancer, but that unsaturated fat had a significantly protective effect against breast cancer.
"Our results do not support the recommendation of an isoenergetic high carbohydrate, low fat diet for
improving peripheral insulin action in adults with glucose intolerance ... the increase in insulin action that we
observed previously with vigorous exercise training was negated when combined with a diet high in
carbohydrates and fiber. ... The subjects in this study are at increased risk for developing NIDDM"
(American Journcal of Clinical Nutrition 1995;62:426-33)
Jorge Salmern et. al. Dietary Fiber, Glycemic Load, and Risk of Non-insulin-dependent Diabetes Mellitus
in Women. Journal of the American Medical Association. 1997;277:472-477. Abstract has an emphasis on
cereal fibre as a preventative against diabetes, but if you order the complete study and read carefully the
study also fully demonstrates that diets high in carbohydrate are likely to cause diabetes in women, even
independent of fibre intake, although cereal fibre intake seems to have a protective effect.
101/298 (1997)
Leibel RL. Energy intake required to maintain body weight is not affected by wide variation in diet
composition. Energy intake required to maintain body weight is not affected by wide variation in diet
composition. Even with extreme changes in the percentage of energy from fat (0% - 70%) there was no
detectable evidence of significant variation in energy need as a function of percentage fat intake. (American
Journal of Clinical Nutrition 1992;55;350-5)
In a study of 171 women on a two year low fat diet, maximum weight loss of 3.2 kg was reported at 6
months. By year 2 some of the weight was regained. The standard deviation was more than twice the average
weight loss. This shows that quite a few actually gained weight on the low fat diet, not counting the 13 that
dropped out of the program. (American Journal of Clinical Nutrition 1991;54:821-8.)
In the presence of dietary carbohydrate, the preferred fuel is glucose and the capacity to mobilize fat is
limited. Factors that increase blood glucose during dieting may stimulate insulin release and all the metabolic
sequelae of circulating insulin. Fatty acid synthesis is activated and lipolysis is profoundly inhibited by
insulin even at very low concentrations of the hormone. (American Journal of Clinical Nutrition
1992;56:217S-23S)
Conventional wisdom holds that low fat diets improve insulin sensitivity. Unfortunately, this is true only
after an ultra-low carbohydrate diet. No changes in glucose tolerance and substrate oxidation were measured
after a high-carbohydrate low fat diet. In addition, these studies confirm a growing body of evidence that
increasing dietary carbohydrate increases plasma triglycerides and decreases plasma high-density-lipoprotein
(HDL), increasing the risk of cardiovascular disease. (METABOLISM 1993:42:365-70)
The average U.S. daily fat consumption is 2.52 ounces, with 10% of males obese; the average Australian
daily fat consumption is much less, but 14% are obese. (LONGEVITY, May 1992)
Ascherio A et. al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United
States. British Medical Journal, 1996 Jul 13, 313:7049, 84-90. Study strongly suggests no link between fat
intake and heart disease in men and supports the contention that linolenic acid (a form of fat) is actually
preventative against heart disease.
Liu GC; Coulston AM; Reaven GM. Effect of high-carbohydrate-low-fat diets on plasma glucose, insulin
and lipid responses in hypertriglyceridemic humans. Metabolism, 1983 Aug, 32:8, 750-3. In which it was
shown that in humans with existing trouble with high triglycerides, low-fat high-carbohydrate diets
significantly increased metabolic risk factors for coronary artery disease.
Coulston AM; Liu GC; Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate lowfat diets in normal humans. Metabolism, 1983 Jan, 32:1, 52-6. In which it is shown that low-fat, high
carbohydrate diets in normal human males caused changes in insulin, TG, and HDL-cholesterol
concentrations which have been associated with an increase in incidence of coronary artery disease.
Heller, RF & Heller, RF. Hyperinsulinemic obesity and carbohydrate addiction: the missing link is the
carbohydrate frequency factor. Medical Hypotheses, 42: 5, 1994 May, 307-12. In which it is suggested that
high carbohydrate diets, especially diets in which carbohydrate intake is frequent throughout the day, has a
strong correlation with obesity, heart disease, diabetes, and a host of medical problems.
Olefsky JM; Crapo P; Reaven GM. Postprandial plasma triglyceride and cholesterol responses to a low-fat
meal. American Journal of Clinical Nutrition, 1976 May, 29:5, 535-9. Suggests that low-fat, highcarbohydrate meals lead to increases in plasma triglyceride levels.
Ginsberg H et. al. Induction of hypertriglyceridemia by a low-fat diet. J Clin Endocrinol Metab, 1976 Apr,
42:4, 729-35. Shows low-fat high-carbohydrate diets can induce hypertriglyceridemia.
Franceschini G. et. al. Omega-3 fatty acids selectively raise high-density lipoprotein 2 levels in healthy
volunteers. Metabolism, 1991 Dec, 40:12, 1283-6. Demonstrates that high intake of fats from the Omega-3
group increase HDL cholesterol levels, which is considered protective against heart disease. Obviously it
would be difficult to eat an Omega-3 rich diet while following a traditional fat-reduced diet (especially if one
were following one of the popular American diets that has one eating 20-30 grams of fat per day.) See also
Journal of the American College of Nutrition 1991:10(6);593-601.
Laugharne JD; Mellor JE; Peet M. Fatty acids and schizophrenia. Lipids, 1996 Mar, 31 Suppl:, S163-5.
Correlation between schizophrenia and deficiencies in fats from both the n-6 and n-3 series. Supplementation
with extra fats in these groups significantly improved symptoms of schizophrenia in most patients. Analysis
of patients' diet did not suggest unusual deficiency of fats although diets higher natural intake of n-3 fatty
acids showed less severe symptomatology. The possibility that diets generally low in fat might worsen
schizophrenia or even bring on the condition among those already predisposed toward the condition is hard
to ignore.
-=-=-
102/298 (1997)
Compellingly, despite more than a decade of American diet gurus recommending low-fat diets for weight
loss, there remains no reliable study which clearly shows that low-fat diets result in long-term weight loss
among the chronically obese. Indeed, according to the USDA, Americans' fat consumption has consistently
gone down over the last 20 or so years while the American national rates of obesity have gone up at precisely
the same time. Correlation is not causation and yet it hard to jive this fact with claims that high-fat diet is the
primary cause of obesity. Some explanations have been offered to continue to support the low-fat paradigm
as a workable weight-loss diet, but none are very compelling. For example, it has been noted that Americans
also increased their daily caloric intake ate during this same period of decreased fat intake, which supposedly
explains the differences. And yet the claim of most low-fat diet advocates been that lowering fat intake
causes people to naturally eat less food. One hypothesis is that Americans have just somehow, for no
apparent reason, become more piggish and less restrained in their eating habits, although there is no rational
explanation for why this would be, especially in a period wherein Americans have become more and more
conscious of health issues and striven harder and harder to eat "healthier" (lower fat, lower cholesterol) diets
and to exercise more often. The alternate hypothesis, that lowering fat intake and raising carbohydrate intake
results in higher insulin levels which results in higher hunger and more difficulty reaching satiaty has not
been well-studied.
How all of this relates to the concept of paleolithic nutrition is hard to say, but it's quite clear from where I
stand that the health benefits of low-fat diets is becoming increasingly questionable, especially when such
diets are combined with high intake of carbohydrate and low intake of protein. It seems clear that humans did
-not- evolve to eat high-carbohydrate diets, most especially diets rich in bioavailable carbohydrate. The best
figures I've seen on the mean average intake of macronutrients (Eaton BS, Konner M, Shostak M. Stone
Agers in the Fast Lane. American Journal of Medicine 1988;84:739-749) show the average worldwide for
hunter/gatherers to be 33% protein, 46% carbohydrate, and 21% fat, with most of the carbohydrate from
high-fibre sources relatively low on the glycemic index (and thus low in bioavailability). The only
meaningful exception seems to be honey, and just how common honey intake has historically been around
the world seems unclear to me. (Jennie Brand Miller has had some neat thoughts on that so far but I'm still
unclear from her comments what we can realistically think honey contributed to the diet of most preagricultural peoples.)
There is also the issue that what current hunter/gatherers eat may be different from what our paleolithic
ancestors ate. If megafauna such as the mammoths was much higher in fat, or if historical humans ate highfat organs such as brains, tongues, etc. preferentially to the lean muscle meat of wild game, fat intake may
have been higher than what is available to most modern hunter/gatherers.
As an individual data point I can say that I know a great number of chronically obese individuals whose
weight and health was massively improved by drastic lowering of carbohydrate intake and strong increase of
intake of both fat and protein. I happen to be one of those individuals; a low-fat, high-fibre, highcarbohydrate diet gave me very low HDL cholesterol, somewhat elevated trigylcerides, and a resting heart
rate of about 92 bpm, despite 60-90 minutes of daily exercise (resistance training + aerobics), calorie control,
and strictly holding fat intake to very low levels (20-30 grams per day). Moving to a high-protein, high-fat
diet, even with less exercise and an ad libitum eating pattern (no more calorie restriction), massively
improved my HDL/LDL ratios, dropped my triglycerides, dropped my resting heart rate by about 15 bpm,
and generally improved my health, not to mention helping me to lose 25 pounds of unwanted body fat
painlessly.
This experience, along with knowing others with similar experiences, has naturally led me to be very
skeptical of the general wisdom that dietary fat is a danger to health or a primary cause of obesity. But this
also makes me more likely to be biased on the matter, so of course anything I have to say on this subject
should be taken with a grain of salt.
PALEODIET Archives
Subject: Early Technology for Detoxifying Plant-Foods
From: Luc De Bry
Reply-To:
Date: Mon, 12 May 1997 15:34:58 -0700
103/298 (1997)
Good morning paleo-digest Readers,

Reading the Paleo-Digest of May 8-9th., my attention was attracted to what Dr. and Staffan Lindeberg wrote
about pottery, baking and cooking for detoxifying plant-foods.
AM:
> On the other hand we do have farming cultures, notably the Pre-pottery Neolithic of the Near East,
> where there is clearly massive reliance on cereal crops but no pottery in which to cook them. They
> clearly needed to cook their crops, but we have little idea of how they did it.
SL:
> Could it be that they wrapped them in leaves and covered and baked them in the ground with heated
> stones like for instance the Trobriand Islanders and many others traditionally did? Would this
> leave any traces?
AM:
> It is possible but we are talking about the earliest towns with large numbers of people living
> together, and intensively farming the surrounding area, and given that leaves are likely to be a
> one-use cooking vessel their environmental impact would have been very great. This might tie in
> with what is known from 'Ain Ghazal (Jordan) where from the middle Pre-pottery Neolithic B
> (PPNB c. 7200-6500 C14 years BP) through the late PPNB (6500-6000 C14 BP) to PPNC (6000> 5500 C14 BP) we see a decrease in the size of posts used in construction.
Not being a specialist in the History of Cooking Technologies, I am missing something here. I do not
understand this "pre-pottery" expression. How could a population rely on cereals crops without basic
cooking/detoxifying technology?
As far as I am aware, most if not all (always a few exceptions to confirm the rule) tubers and seeds (i.e.
grains and beans) must be detoxified before we can eat them safely. This implies the use of some "fire
technology" to inactivate a wide variety of anti-nutritional factors. For instance, today, that means cooking
for soybeans, baking for wheat grains, malting for barley grains, roasting for cocoa beans, etc. Yesterday, in
the abscence of this variety of technologies, it seems that grains and beans were all detoxified by grinding
them, by throwing them into water, and by cooking the mixture, the water-suspension. For instance, that is
how American Indians detoxified cocoa beans to get their original and safe "chocoatl" beverage, at the time
of C. Colombus. It's onbly in the 19th. Century that the roasting technology and chocolates were invented.
About dates : Man learnt to control and to use the fire some 700, 000 years ago. Millstones were used in
High-Egypt some 17, 000 years BC. The first cultures of cereals happened in the fertile crescent some 10,
000 years B.C. The technology to detoxify grains and beans must have existed BEFORE agriculture. Indeed,
without an ability to detoxify these poisonous foods, i.e. to cook them, there would have been no point at
developing agriculture. Thus, it seems, at least to me, but I may be wrong, that the synergy of fire technology
and cooking technology (in some kind of pot or jar, or something similar) must have been an essential prerequisite to the development of agriculture. Malting and brewing barley would have been just impossible
without adequate containers for liquid fermentation, and beer-drinking. And why would someone cultivate
barley if he cannot detoxify it?
So, shouldn't some kind of "pre-pottery" have been developed, or used-as-found, earlier than some 7, 500 BC
as mentionned in the exchange between Stefan and Andrew? Have some of you information, or references,
about the early technologies that must have been available for detoxifying plant-foods (tubers, grains and
beans), before the development of agriculture, i.e. before some 12, 000 years ago?
With anticipated thanks for you help, and kind regards to all,
Luc
-- Luc De Bry, Ph.D.; Head of Research Department; DANONE BISCUITS NORTH De BeukelaerPareinlaan 1; B-2200 Herentals - Belgium Tel. 32 (0)14 241432; Fax 32 (0)14 241025; Email : URL Site
http:/:www;danonegroup.com
PALEODIET Archives
Subject: Ancient bread
Reply-To:
Date: Tue, 13 May 1997 09:03:12 +0100
104/298 (1997)
This question appeared recently on BritArch mailing list, but there was no response. Does anyone here know
anything?
Andrew Millard
On Fri, 2 May 1997 10:46:00 +0100, Althea Davies {PG} wrote:
> I recently bought some sprouted wheat bread which claims on the packaging that this is how bread
> was made thousands of years ago. The ingredients consist only of sprouted wheat grains, germinated
> in spring water. Does anyone know if this claim is true and, even better, how it is made? I hope
> this query isn't too tangential.
PALEODIET Archives
Reply-To:
Andrew Millard
Date: Tue, 13 May 1997 09:25:40 +0100
Luc De Bry wrote:
> Not being a specialist in the History of Cooking Technologies, I am missing something here. I do
> not understand this "pre-pottery" expression. How could a population rely on cereals crops without
> basic cooking/detoxifying technology?
This is precisely the problem I wqas referring to: we have all the features of the Neolithic, i.e. domesticated
crops and animals, permanent settlements and even towns with 2 storey buildings, but we have no pottery.
So it is called the pre-pottery Neolithic meaning the Neolithic before pottery was invented. This period lasts
for 1500 years in some parts of Syria and Palestine. However we also know of a number of other aceramic
societies - The Neolithic and Iron Age of Ireland and the Iron Age and Early Medieval periods in Wales
appear to have been without pottery.
> About dates : Man learnt to control and to use the fire some 700, 000 years ago. Millstones were
> used in High-Egypt some 17, 000 years BC. The first cultures of cereals happened in the fertile
> crescent some 10, 000 years B.C.
Actually cultivation begins about 8000 BC / 10000 *BP*.
> The technology to detoxify grains and beans must have existed BEFORE agriculture.
Certainly. For example, we have the Natufian culture in Syria/Palestine immediately preceding the Neolithic,
with a dependence on collection of wild cereals, including grindstones
> Malting and brewing barley would have been just impossible without adequate containers for liquid
> fermentation, and beer-drinking. And why would someone cultivate barley if he cannot detoxify it?
It would be possible to ferment it in skins/stomachs as someone pointed out yesterday - and the narcotic
effect of alcohol might be sufficent reason to grow barley in small quantities. But cooking in such containers
would be more difficult.
But of course as Jennie Brand Miller wrote:
> The Australian Aboriginal people might be a good example here. They had no pottery. First they
> roasted the cereals (or other seeds such as acacias) in the ashes of a fire. The women would then
> separate the seeds from the dirt and ashes using a highly skilled shaking action in a coolamon (a
> curved wooden dish). They would then grind the seeds on a grinding stone mixing in a little water.
> They woould eat the paste with their fingers or alternatively cook the paste on a hot stone to
> form a kind of damper.
This is a possibility, but it sounds very labour intensive for an agricultural society where the main food
source may be cereals. Does anyone know of any ethnographic accounts of aceramic agricultural societies?
Andrew Millard
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: High fat/high protein diets and ancestral feeding patterns
105/298 (1997)
From: Loren Cordain

Reply-To:
Date: Tue, 13 May 1997 10:19:00 -0600
The subject of high fat/high protein diets to elicit weight loss and improve blood lipid profiles is clearly
controversial in the nutritional community. Dean has done a wonderful job in the last listing to highlight the
salient literature which supports the concept. Clearly, Reaven and the group at Stanford have strong data to
show that low fat, high carb diets tend to worsen many aspects of blood lipid profiles in both normals and in
NIDDM patients. However, to date neither they nor any other researchers that I am aware of have evaluated
extremely low carb diets or extremely high protein diets; nor have there been any experiments in which the
macronutrients (protein, fat, CHO) have been separated at each meal. The separation of macronutrients
would have been a frequent feeding pattern for pre-agricultural modern H. sapiens and perhaps the most
frequent feeding pattern for pre-modern hominids in which there is little evidence for storage of goods or
food (1). Consequently, when an animal was killed, it was entirely consumed within a 24 hr period, similar
to modern day hunter gatherers (2). Except for some stored hepatic and muscle glycogen, there is virtually no
carbohydrate in food derived from animal sources; therefore, protein and fat meals tended to be consumed
together. Carbohydrate sources came primarily from uncultivated fruits, vegetables, tubers, nuts and seeds
and tended to be consumed while they were gathered (2); consequently carbohydrates generally were
consumed separate from protein and fat. The concept of a regular sit down meal with a wide variety of foods,
both animal and plant based would have been a rare occurrance for most pre-modern hominids and many
contemporary hunter gatherers. Recent data has shown that the ubiquitious high fat, high carb meal of
western societies worsens elements of the postprandial lipid profile more so than simple high fat meals (3,
4). Consequently, it may be that separation of macronutrients similar to our evolutionary experience may be
an effective dietary procedure to prevent some of the health shortcomings of the traditional high fat, high
carb meal of the western world. There was a series of popular diet books in the 1930's in the USA which
advocated exactly this eating pattern (5, 6). Clearly, the separation of fat from carbohydrate has many
evolutionary clues pointing in its direction for improving health, but to date there have been no clinical trials
evaluating this concept.
REFERENCES
1. Ingold T. The significance of storage in hunting societies. Man 1983;18:553-71.
2. Hawkes K et al. Why hunters gather: optimal foraging and the Ache of eastern Paraguay. Am Ethnologist
1982;9:379-98.
3. Chen IYD et al. Effect of variations in dietary fat and carbohydrate intake on postprandial lipemia in
patients with noninsulin dependent diabetes mellitus. J Clin Endocrinol Metabol 1993;76:347-51.
4. Chen IYD et al. Effect of acute variations in dietary fat and carbohydrate intake on retinyl ester content of
intestinally derived lipoproteins. J Clin Endocrinol Metabol 1992;74:28-32.
5. Hay WH. Weight control. London Harrap, 1936.
6. Hay WH. A New Health Era. Mount Pocono, PA, Pocono Haven, 1936.
PALEODIET Archives
Subject: Hunter gatherers -which?
From: Mavis Wood
Reply-To:
Date: Tue, 13 May 1997 10:30:42 +1200
Dear Symposium Members
There is a difficulty for me when reading the Paleodiet symposium . I wonder often whether the contributors
are referring to the diet of early hominids, in the African savannah, or, the diet of the people of the glacial
refugia in Europe circa 18 0000 when there must have been a low population and consequently a bottleneck
in the genetic inheritance of those people who have any European ancestry at all. Which may involve
American with mainly African ancestors. Thirdly I often get the impression that we are talking about
Paleoindians of the Americas. These are of course mostly derived from Asia and must have their genetic
inheritance from ice free areas of Eurasia during the maximum glacial period. the same would hold for the
inhabitants of the Pacific, Australia and New Guinea excepted.
106/298 (1997)
I have interested in the diet of the Upper Palaeolithic in South West France and Iberia since I think I have
heard that the geneticists say that most Western Europeans are descended from them. I wonder how it has
affected our inheritance in digestive functions and perhaps in resistance to parasites? I think the
Scandinavians were excluded from this population Has any one on this list any up to date information about
this(ie 1997 information)? How about the Basques, are they like the Etruscans, later?
I would like it, if I might suggest it, just to keep things tidy in my archaeological mind, if list members would
specify which hunter gatherers they are citing when talking about ancient diets and the actual material
evidence for those diets.
Incidentally I am reading a book called <Time Walkers : The prehistory of global colonization
> by Clive Gamble which brings up to date information on the debate on hominid ancestries. and is
available in paperback from Penguin (though I don't know about the USA) it is also in hardback from Alan
Sutton Stroud. UK ISBN 0-7509-0321-X
gratefully
ME Wood MA Hons Edinburgh (Prehistoric Archaeology).
PALEODIET Archives
Subject: Re: Early grains
Reply-To:
Date: Tue, 13 May 1997 10:54:19 -0500
Luc De Bry wrote:
> crescent some 10, 000 years B.C.
And Andy Millard replied:
> Actually cultivation begins about 8000 BC / 10000 *BP*. The technology to detoxify grains and
> beans must have existed BEFORE agriculture. Certainly. For example, we have the Natufian culture
> in Syria/Palestine immediately preceding the Neolithic, with a dependence on collection of wild
> cereals, including grindstones
Just to clarify the dates further here. The question of control over fire is actually quite controversial, with
various estimates for earliest control ranging from 230, 000 years to 1.5 million years ago. Which figure you
take as definitive depends on which circumstantial evidence one is willing to accept as reliable, and how
critically you qualify what kind of behavior the circumstantial evidence actually signifies. Many recent
authorities do not seem to give reliable credit to any dates for control over fire much longer than about 400,
000 years ago, although that might well turn out in hindsight to be overly conserative. But nobody really
knows for sure right now. [See: James, SR (1989) "Hominid use of fire in the lower and middle Pleistocene.
A review of the evidence." Current Anthropology, 30:1-26, for the most extensive in-depth critique of known
fire-sites to that time. James will only credit 230, 000 years ago; however, there have been discoveries since
his paper that would push the date back some to around 400, 000 years, probably to the satisfaction of most
critics.]
Regarding grains: "Cultivation" is the key word regarding dating. *Wild* grains were in fact beginning to be
gathered by 17, 000 B.C. by people in the Levant (Middle East) and being ground into flour with mortar-andpestle at this time, though cultivation did not begin until considerably later as Andy states. The Natufians
were the successors to the very earliest grain-gatherers, and were themselves also gathering wild grains
intensively (also using grindstones) around 13, 000 B.C. prior to the introduction of agricultural cultivation.
[See the Smithsonian's "Timelines of the Ancient World, " 1993, ed. by Chris Scarre, New York: DorlingKinderley, pp. 56, 61, for a brief account.]
For those who have a special interest in this time period, The American Museum of Natural History has out a
beautifully produced full-color book with equal emphasis on photographs of archeological artifacts and sites,
as well as very absorbing articles understandable to the layperson, written by authorities in the field who
have authored peer-reviewed papers elsewhere. It covers the entire transition period from late Paleolithic to
Neolithic and the introduction of grains/farming. This book used to be $40 US, but has been on close-out in
recent months for $20 in our local Barnes & Noble bookstore chain. [See: "People of the Stone Age: HunterGatherers and Early Farmers" (1993) ed. by Goran Burenhult, New York: Harper-Collins.]
107/298 (1997)
PALEODIET Archives
Subject: Re: ancestral feeding patterns / food separation
Reply-To:
Date: Tue, 13 May 1997 13:21:14 -0500
Loren Cordain writes:
> The separation of macronutrients would have been a frequent feeding pattern for pre-agricultural
> modern H. sapiens and perhaps the most frequent feeding pattern for pre-modern hominids in which
> there is little evidence for storage of goods or food (1). Consequently, when an animal was
> killed, it was entirely consumed within a 24 hr period, similar to modern day hunter gatherers (2
> ). Except for some stored hepatic and muscle glycogen, there is virtually no carbohydrate in food
> derived from animal sources; therefore, protein and fat meals tended to be consumed together.
Just a socio-historical note here of possible interest on the idea of food-separation:
As a one-time follower (since reformed :-)) of the so-called "Natural Hygiene" school of raw-food
vegetarianism (I attempt to follow a Paleodiet approach now based on the evolutionary evidence), I can say
that many of its practitioners to this day follow a very similar practice which they somewhat mis-name "food
combining" (since it actually focuses more on food separation than combining). Theirs is the only current
group I personally know of with actual experience intentionally doing this type of thing.
However, in their philosophy, so-called "food combining" (actually "separation of macronutrients, " as Loren
calls it) is practiced due to a belief that foods will digest and assimilate better if eaten separately, rather than
a concern for effect on lipid profiles. Many adherents report better gastrointestinal function and reduction in
gas and/or digestive distress. Anecdotal of course, but interesting nonetheless.
The theory was that different macronutrients required different types of digestive enzymes for processing,
which would conflict with or partially neutralize the effectiveness of each other when digesting different
macronutrient food types mixed together at a meal. However, the Natural Hygienists never could point to
any documented evidence to support the practice other than ideas from musty physiology textbooks on
digestion that were decades old, and some, though not all, modern practitioners are beginning to abandon the
practice. It would be interesting, though, if the practice were to be found beneficial for the differing reasons
Loren cites.
Also, in direct opposition to what would have occurred during evolution, their belief has been that fats and
proteins should *not* be eaten together (for some kind of poorly-digested-that-way reason I don't recall). Of
course, this view doesn't square well with the evolutionary situation, where fats and proteins would have
been eaten together often since they occur naturally in foods like nuts and flesh. Another idea, among others,
in their food-combining philosophy were that fruits should be eaten alone and generally not combined with
protein foods. (This does happen to gibe with Loren's observation that carbs would not tend to have been
eaten together with proteins in Paleolithic times.)
Anyway, these observations are just to offer some additional food for thought and add to Loren's initial
observation out that the idea of food separation has been around for quite awhile (actually, it still is) in other
forms.
> There was a series of popular diet books in the 1930's in the USA which advocated exactly this
> eating pattern (5, 6). 5. Hay WH. Weight control. London Harrap, 1936. 6. Hay WH. A New Health
> Era. Mount Pocono, PA, Pocono Haven, 1936.
I checked the standard N.H. text on food-combining (the rather musty-by-now "Food Combining Made Easy,
" by Herbert Shelton from 1951, Natural Hygiene Press: Tampa, FL), but they do not mention Hay, so this
makes the historical notes even more interesting. (Instead they mention Howell's "Textbook of Physiology"
and McLeod's "Physiology in Modern Medicine" as sources, both probably out-of-print, and neither one of
which are footnoted so that they could be traced easily.)
--Ward Nicholson
PALEODIET Archives
Subject: Ancient bread
108/298 (1997)
From: Al Davis
Reply-To:
Date: Tue, 13 May 1997 19:58:02 -0400
> Date: Tue, 13 May 1997 09:03:12 +0100
> From: Andrew Millard Subject: Ancient bread
> This question appeared recently on BritArch mailing list, but there was no response. Does anyone
> here know anything? I recently bought some sprouted wheat bread which claims on the packaging
> that this is how bread was made thousands of years ago. The ingredients consist only of sprouted
> wheat grains, germinated in spring water. Does anyone know if this claim is true and, even better,
> how it is made? I hope this query isn't too tangential.
This sounds like what is usually sold as Essene Bread in the U.S. I have read descriptions of how is was
supposed to have been made by the ancient Essenes who lived in the deserts of the Middle East during and
before the time of Christ.
As I recall, the wheat berries were soaked in water until they swelled and then were kept moist until they
sprouted. When the sprouts were about the length of the berry, they would be crushed and ground for bread.
Sprouting releases enzymes which convert the starch in the berry to sugar and so the mash would be quite
sweet and would readily support the growth of naturally ocurring yeast which abounds everywhere. This
would cause the loaves to rise, somewhat. When they were ready, the loaves were placed on rocks in the
desert sun to bake. I don't recall if they mixed oil with the dough or not. I suspect they would have done so,
as sprouted wheat mash is very gummy and hard to handle, otherwise, and would have stuck to the rock and
become dry and hard as a brick without oil.(This is an educated guess, as I've not tried it, although I have
used sprouted wheat in baking and experimented with making malt (sprouted barley).
Maybe not too tangential. It could be accomplished with only rocks, and animal fat under very primitive
conditions, assuming suitable grass seeds were available. Hope this is helpful.
Al Davis
PALEODIET Archives
Subject: Re: Hunter gatherers -which?
Reply-To:
Date: Wed, 14 May 1997 01:13:51 +0100
Dear Mavis,
You wonder what diet we mainly refer to as the Paleolithic one. As for myself, 1) I want to know about the
diet(s) to which all humans as a group are genetically adapted. That would be the one(s) that (hominids and)
Homo, especially anatomically modern humans, had access to during evolution. Which would mean foods
available on the African savannah (and other habitats?) up to around 100, 000 years BP. When I do not
specify, this is the diet(s) I refer to. 2) I also want to consider the (obviously rather small) differences
between specific ethnic groups like for instance Caucasians and others as to the resistance to western dietary
habits and/or the possibility of one diet being optimal for some pre-agricultural populations but not for others
(which I principally doubt). A beautiful paper on resistance to western diet is (Allen JS, Cheer SM. The NonThrifty Genotype. Current Anthropology 1996; 37: 831-42). John Allen, one of the authors, subscribes to this
list.
Best wishes
Staffan
> Date: Tue, 13 May 1997 10:30:42 +1200
> From: Mavis Wood Subject: Hunter gatherers -which?
> Dear Symposium Members
> There is a difficulty for me when reading the Paleodiet symposium . I wonder often whether the
> contributors are referring to the diet of early hominids, in the African savannah, or, the diet
> of the people of the glacial refugia in Europe circa 18 0000 when there must have been a low
> population and consequently a bottleneck in the genetic inheritance of those people who have any
> European ancestry at all. Which may involve American with mainly African ancestors. Thirdly I
109/298 (1997)
> often get the impression that we are talking about Paleoindians of the Americas. These are of
> course mostly derived from Asia and must have their genetic inheritance from ice free areas of
> Eurasia during the maximum glacial period.
> The same would hold for the inhabitants of the Pacific, Australia and New Guinea excepted. I have
> interested in the diet of the Upper Palaeolithic in South West France and Iberia since I think I
> have heard that the geneticists say that most Western Europeans are descended from them. I wonder
> how it has affected our inheritance in digestive functions and perhaps in resistance to parasites?
> I think the Scandinavians were excluded from this population Has any one on this list any up to
> date information about this(ie 1997 information)? How about the Basques, are they like the
> Etruscans, later?
> I would like it, if I might suggest it, just to keep things tidy in my archaeological mind, if
> list members would specify which hunter gatherers they are citing when talking about ancient diets
> and the actual material evidence for those diets.
> Incidentally I am reading a book called <Time Walkers : The prehistory of global colonization by
> Clive Gamble which brings up to date information on the debate on hominid ancestries. and is
> available in paperback from Penguin (though I don't know about the USA) it is also in hardback
> from Alan Sutton Stroud. UK ISBN 0-7509-0321-X gratefully ME Wood MA Hons Edinburgh
(Prehistoric Archaeology).
> -----------------------------> Date: Tue, 13 May 1997 09:03:12 +0100
> From: Andrew Millard Subject: Ancient bread
> This question appeared recently on BritArch mailing list, but there was no
> response. Does anyone here know anything?
> Andrew Millard
> On Fri, 2 May 1997 10:46:00 +0100, Althea Davies {PG}
> wrote:
> I recently bought some sprouted wheat bread which claims on the packaging that this is how bread
> was made thousands of years ago. The ingredients consist only of sprouted wheat grains, germinated
> in spring water. Does anyone know if this claim is true and, even better, how it is made? I hope
> this query isn't too tangential.
> -----------------------------> Date: Tue, 13 May 1997 09:25:40 +0100
> From: Andrew Millard Subject: Early Technology for Detoxifying Plant-Foods
> Luc De Bry wrote:
> Not being a specialist in the History of Cooking Technologies, I am missing something here. I do
> not understand this "pre-pottery" expression. How could a population rely on cereals crops without
> basic cooking/detoxifying technology?
> This is precisely the problem I wqas referring to: we have all the features of the Neolithic, i.e.
> domesticated crops and animals, permanent settlements and even towns with 2 storey buildings, but
> we have no pottery. So it is called the pre-pottery Neolithic meaning the Neolithic before pottery
> was invented. This period lasts for 1500 years in some parts of Syria and Palestine. However we
> also know of a number of other aceramic societies - The Neolithic and Iron Age of Ireland and the
> Iron Age and Early Medieval periods in Wales appear to have been without pottery.
> crescent some 10, 000 years B.C. Actually cultivation begins about 8000 BC / 10000 *BP*. The
> technology to detoxify grains and beans must have existed BEFORE agriculture. Certainly. For
> example, we have the Natufian culture in Syria/Palestine immediately preceding the Neolithic, with
> a dependence on collection of wild cereals, including grindstones
> Malting and brewing barley would have been just impossible without adequate containers for liquid
> fermentation, and beer-drinking. And why would someone cultivate barley if he cannot detoxify it?
> It would be possible to ferment it in skins/stomachs as someone pointed out yesterday - and the
> narcotic effect of alcohol might be sufficent reason to grow barley in small quantities. But
> cooking in such containers would be more difficult.
> But of course as Jennie Brand Miller wrote:
> The Australian Aboriginal people might be a good example here. They had no pottery. First they
> roasted the cereals (or other seeds such as acacias) in the ashes of a fire. The women would then
110/298 (1997)
> separate the seeds from the dirt and ashes using a highly skilled shaking action in a coolamon (a
> curved wooden dish). They would then grind the seeds on a grinding stone mixing in a little water.
> They woould eat the paste with their fingers or alternatively cook the paste on a hot stone to
> form a kind of damper. This is a possibility, but it sounds very labour intensive for an
> agricultural society where the main food source may be cereals. Does anyone know of any
> ethnographic accounts of aceramic agricultural societies?
> Andrew Millard
> ==========================================================================
> Dr. Andrew Millard
> Department of Archaeology, University of Durham, Tel: +44 191 374 4757
> South Road, Durham. DH1 3LE. United Kingdom. Fax: +44 191 374 3619
> http://www.dur.ac.uk/~drk0arm/
> ==========================================================================
> -----------------------------> Date: Tue, 13 May 1997 10:19:00 -0600
> From: Loren Cordain Subject: High fat/high protein diets and ancestral feeding patterns
> The subject of high fat/high protein diets to elicit weight loss and improve blood lipid profiles
> is clearly controversial in the nutritional community. Dean has done a wonderful job in the last
> listing to highlight the salient literature which supports the concept. Clearly, Reaven and the
> group at Stanford have strong data to show that low fat, high carb diets tend to worsen many
> aspects of blood lipid profiles in both normals and in NIDDM patients. However, to date neither
> they nor any other researchers that I am aware of have evaluated extremely low carb diets or
> extremely high protein diets; nor have there been any experiments in which the macronutrients
> (protein, fat, CHO) have been separated at each meal.
> The separation of macronutrients would have been a frequent feeding pattern for pre-agricultural
> modern H. sapiens and perhaps the most frequent feeding pattern for pre-modern hominids in which
> there is little evidence for storage of goods or food (1). Consequently, when an animal was
> killed, it was entirely consumed within a 24 hr period, similar to modern day hunter gatherers (2
> ). Except for some stored hepatic and muscle glycogen, there is virtually no carbohydrate in food
> derived from animal sources; therefore, protein and fat meals tended to be consumed together.
> Carbohydrate sources came primarily from uncultivated fruits, vegetables, tubers, nuts and seeds
> and tended to be consumed while they were gathered (2); consequently carbohydrates generally were
> consumed separate from protein and fat. The concept of a regular sit down meal with a wide variety
> of foods, both animal and plant based would have been a rare occurrance for most pre-modern
> hominids and many contemporary hunter gatherers.
> Recent data has shown that the ubiquitious high fat, high carb meal of western societies worsens
> elements of the postprandial lipid profile more so than simple high fat meals (3, 4).
> Consequently, it may be that separation of macronutrients similar to our evolutionary experience
> may be an effective dietary procedure to prevent some of the health shortcomings of the
> traditional high fat, high carb meal of the western world. There was a series of popular diet
> books in the 1930's in the USA which advocated exactly this eating pattern (5, 6). Clearly, the
> separation of fat from carbohydrate has many evolutionary clues pointing in its direction for
> improving health, but to date there have been no clinical trials evaluating this concept.
> REFERENCES
> 1. Ingold T. The significance of storage in hunting societies. Man
> 1983;18:553-71.
> 2. Hawkes K et al. Why hunters gather: optimal foraging and the Ache
> of eastern Paraguay. Am Ethnologist 1982;9:379-98.
> 3. Chen IYD et al. Effect of variations in dietary fat and
> carbohydrate intake on postprandial lipemia in patients with noninsulin
> dependent diabetes mellitus. J Clin Endocrinol Metabol 1993;76:347-51.
> 4. Chen IYD et al. Effect of acute variations in dietary fat and
> carbohydrate intake on retinyl ester content of intestinally derived
> lipoproteins. J Clin Endocrinol Metabol 1992;74:28-32.
> 5. Hay WH. Weight control. London Harrap, 1936.
> 6. Hay WH. A New Health Era. Mount Pocono, PA, Pocono Haven, 1936.
> -----------------------------Paleolithic Diet Symposium List
111/298 (1997)
> End of PALEODIET Digest - 12 May 1997 to 13 May 1997

> ****************************************************
-------------------------------------------------------------------
PALEODIET Archives
Subject: Noodling
From: Becky Johnson
Reply-To:
Date: Wed, 14 May 1997 08:26:45 -0500
Large catfish can be caught by hand by a technique called "noodling". The noodler wades in the river along
the bank, feeling for holes in the bank. When one is found, the noodler may block the entrance with his/her
knee to prevent escape of the fish. Then the noodler reaches into the hole and grabs the catfish by the gills
and hauls it out. Of course part of the challenge is not to get jabbed by the fish's spines. Like rattlesnake
hunts, results of noodling competitions are occasionally published in newspapers in the southern U.S.
PALEODIET Archives
Subject: Re: Early Technology for Detoxifying Plant-Foods
From: Sarah Mason
Reply-To:
Date: Wed, 14 May 1997 09:49:19 +0000
Andrew Millard suggests skins/stomachs mnay have been used for fermenting grains, but suggests that:
> cooking in such containers would be more difficult. He also questions Jennie Brand Miller's
> suggestion of cooking 'dampers' as being a possibility, but it sounds very labour intensive for an
> agricultural society where the main food source may be cereals. Does anyone know of any
> ethnographic accounts of aceramic agricultural societies?
Not 'agricultural' societies, but some of the cooking technologies utilised by Native Californians may be
instructive - many seeds of both wild grasses and other plants were gathered and processed and cooked to
make 'pinole'. Chesnut [Chesnut, V.K. 1974. Plants Used by the Indians of Mendocino County, California.
First published (1902) in Contributions from the U.S. National Herbarium Vol. VII. Ukiah, California:
Mendocino County Historical Society.] for example describes (p. 312) this for the European introduction
Avena fatua (a form of wild oat) - the seeds gathered then parched in a shallow basket with live coals, before
grinding in a mortar. The flour was then eaten, usually dry. However, pinole could be mixed with water and
cooked by the process of stone-boiling, in tightly-woven baskets - stones heated in a fire added to the basket
and stirred to prevent burning. This method was used especially to cook acorn flour - containers such as
skins/stomachs or wooden bowls/hollowed-out logs, even clay-lined holes in the ground, etc could readily
substitute here. Acorn flour mixed with water was also cooked as a 'bread' by wrapping in leaves and
cooking in an earth oven (fire pit lined with rocks which heat up, fire removed and food added, pit covered
and left to cook for several hours/overnight, etc). So, there are plenty of potential non-pottery cooking
technologies - and the acorn soup or mush cooked by stone-boiling was a major staple, so presumably the
benefits outweighed any problems of labour-intensiveness. It is also possible to use some materials, such as
birch-bark containers, for cooking directly on a fire - the container will not burn as long as it contains water.
Sarah Mason Human Environment Section email: Institute of Archaeology, UCL Tel: +44 (0)171 387 7050 x
4757 31-34 Gordon Square Fax: +44 (0)171 383 2572 London, WC1H 0PY, UK
PALEODIET Archives
112/298 (1997)
From: ann
Reply-To:
Date: Wed, 14 May 1997 09:51:15 +0000
That pottery is not a prerequisite for plant food preparation is demonstrated currently in Ethiopia, for
instance. As I have observed, pottery in a home in the Highlands may be confined to a single water jar
(indeed often even this has been replaced by a plastic jerry can). Ground grains (teff preferably, but also
sorghum, wheat, pulses etc) are mixed with water and fermented in a container (basketry, stone, gourd,
wood, skin.... will do), the resultant batter is baked on a hot plate (flat surface of stone or clay) over a fire, to
make the bread "injera". The toxic seeds of grasspea are detoxified by being soaked in hot water (again any
container will do), dried, roasted (hot plate as before) and hulled, ground, spiced, mixed to a paste with water
and used as a sauce - no pots. Water, of course, may be heated in many containers other than pots, on or off
the heat source.
In many societies worldwide, pulses (esp. chickpea) and other grains are prepared by short roasting over a
fire, not only as snack food or as rations for travelling, but also as a staple.
Cheers, Ann
PALEODIET Archives
Subject: Magazine Article
From: Ray Audette
Reply-To:
Date: Wed, 14 May 1997 11:05:09 -0700
Psychology Today May/June '97 has a piece tittled "Caveman Diet"(pg. 18) outlining the work of Loren
Cordain and S.Boyd Eaton MD.
No mention of me but a nice piece never the less! Congrats guys!
Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition" http://ww.sofdesign.com/neander
PALEODIET Archives
Subject: Lancet Article
From: Ray Audette
Reply-To:
Date: Wed, 14 May 1997 12:02:35 -0700
From a Wall Street Journal article abstracting a recent Lancet Study:
"Diseases of affluence" such as heart disease and strokes are killing more people in the developing world
than in richer richer countries........
By 1990, therefore there were already 50% more cancer deaths in less developed countries than in developed
countries........
Dr. Christopher Murry. Harvard Center for Population and Development Studies Alan Lopez, World Health
Orginization
I feel this study dispells the myth that these disorders are found mostly in our decadent western societies (see
NeanderThin review).
It also, I feel, shows the benifits of a more paleolithic modern diet made possible by advanced transportation
methods and refridgeration. In examining historic life spans these seem to have a larger statistical effect than
even medical advances.
I also feel, high rates of these "diseases of civilization" should be seen in any primate species fed a
technolgy-dependent diet. As most lab primates are fed Purina Monkey Chow, I wonder if anyone has
looked at their disease rates (do they last that long?).
113/298 (1997)
PALEODIET Archives
Subject: Re: International Symposium
From: Loren Cordain
Reply-To:
Date: Wed, 14 May 1997 14:32:00 -0600
I just received a message indicating that at the upcoming XIV International Congress of Anthropological and
Ethnological Sciences there will be a symposium entitled "The Origins and Evolution of Human Diet".
Sounds interesting - I dont know where this Conference is to be held or even when, however the contact
person is: Dr. Peter S. Ungar, Department of Anthropology, University of ARkansas, Fayetteville AR 72701,
Tel 501-575-6361 (email:). Perhaps we could invite the organizer of the symposium to join our group.
Cordially,
Loren
PALEODIET Archives
Subject: detoxifying plant foods
From: "Kristen J. Gremillion"
Reply-To:
Date: Thu, 15 May 1997 13:00:11 -0400
Hello, everyone. I am new to the list and new to posting on the Internet so please excuse any breaches of
etiquette.
> On 12 May 1997, Luc De Bry wrote:
> As far as I am aware, most if not all (always a few exceptions to confirm the rule) tubers and
> seeds (i.e. grains and beans) must be detoxified before we can eat them safely. This implies the
> use of some "fire technology" to inactivate a wide variety of anti-nutritional factors.
Many, perhaps most, wild plant seeds, fruits, and tubers contain secondary compounds that are either
unpalatable or toxic to humans. Processing methods and/or selection under domestication are effective ways
to eliminate or reduce these toxins. However, many wild seeds and fruits are quite edible when eaten raw
(although perhaps not especially palatable or nutritious). For example, coprolites from Salts Cave and
Mammoth Cave in Kentucky, USA dating to ca. 300-600 B.C. contain remains of seed coats and pericarps of
Iva annua, Helianthus annuus, and Chenopodium berlandieri that show not obvious evidence of processing. I
certainly agree that effective processing techniques were (and remain) a crucial aspect of human dietary
adaptation (beginning well before the advent of food production), but I'm not sure that safety is always the
key factor. Nutrient extraction may be more important in many cases, e.g. with grass seeds.
So, shouldn't some kind of "pre-pottery" have been developed, or used-as-found, earlier than some 7, 500 BC
as mentionned in the exchange between Stefan and Andrew? Have some of you information, or references,
about the early technologies that must have been available for detoxifying plant-foods
(tubers, grains and beans), before the development of agriculture, i.e. before some 12, 000 years ago?
114/298 (1997)
I suspect that pottery greatly increases the efficiency of detoxifying & general cooking technology,
particularly if it is able to withstand direct heating (see for example Braun, D, 1987, "Coevolution of
sedentism, pottery technology, and horticulture in the central Midwest, 200 BC-AD 600" in W Keegan ed.
*Emergent horticultural economies of the Eastern Woodlands*, pp. 153-182, So. Illinois University at
Carbondale, Center for Arch. Investigations, Occasional Paper No. 7). However, there are a variety of
methods potentially available to traditional chemists who lack pottery. For example, California Indians
detoxified acorns by burying them in leaching pits. Manioc can be freed of cyanogenic glycosides by grating
and then exposure to air. Ingestion of clay may act to neutralize glycoalkaloids in tubers such as potatoes, as
suggested by Timothy Johns. His article, "A chemical-ecological model of root and tuber domestication in
the Andes" (in DR Harris and GC Hillman, eds., *Foraging and farming: the evolution of plant exploitation*,
Unwin Hyman, London, 1989, pp. 504-519), deals with this subject in detail. He remarks that although
cereals and legumes are made edible by heating, "generally speaking, non-seed foods such as roots and
tubers are characterized by non-protein secondary compounds, many of which are not destroyed by cooking"
(p. 505). He also proposes that sophisticated detoxifying methods may actually postdate the beginnings of
agriculture because they rely on a long period of association with particular species. Geophagy may
represent an earlier method.
Johns also has pointed out that retention of some secondary compounds in the diet is quite common and may
well be beneficial ("Ambivalence to the palatability factors in wild food plants", in *Eating on the wild
side*, ed. by N Etkin, pp. 46-61, U. of Arizona Press, Tucson, 1994)
Another very useful source is Stahl, A, "Plant food processing: implications for dietary quality", in Harris
and Hillman ed. (see above), pp. 171-194.
I look forward to learning more about the effects of plant processing on nutritional quality and
toxicity/palatability. I don't know of much archaeological evidence for pre-pottery detoxification, though
evidence of cooking (e.g., roasting pits) is quite common, at least here in North America.
cheers,
Kris Gremillion
*********************************
Kristen J. Gremillion Department of Anthropology Ohio State University 244 Lord Hall, 124 W. 17th Ave.
Columbus, Ohio, 43210 USA
*********************************
PALEODIET Archives
Subject: Re: Adaptation to one diet?
From: Dean Esmay
Reply-To:
Date: Fri, 16 May 1997 01:15:31 -0400
It seems to me that among the companion animals I have known (dogs, cats, ferrets, etc.), an awful lot of
them grow rather fat, and some I've encountered are really quite ridiculously fat. That, too, should be looked
at in addition to diabetes. I would certainly be interested in hearing about any data on either subject.
I'm not sure it would make sense to assume that all humans today should eat a certain diet just because our
paleolithic ancestors ate it. After all, it's been some 10, 000 years or more since the advent of agriculture, and
some adaptation has probably occurred since then. Yet we know that some groups have been eating highcarbohydrate, low-protein diets for considerable longer than others; my own Midwestern American Indian
(Miami tribe) and English, Irish, and French ancestors have been farmers a considerably shorter period of
time than the Chinese or the Indians, for example. I'm lactose-tolerant but my wife is definitely not. It seems
very clear to me that trying to find any one dietary method or protocol that universally applies to all humans
is to search for the golden fleece. And yet it seems equally clear that much can be learned from the dietary
habits of our ancestors.
Perhaps others will have more to say on this subject than I can, including offering some references that I
can't.
PALEODIET Archives
Subject: Lancet Article
115/298 (1997)

Reply-To:
Date: Fri, 16 May 1997 09:04:54 +0100
Ray Audette wrote:
> From a Wall Street Journal article abstracting a recent Lancet Study: "Diseases of affluence" such
> as heart disease and strokes are killing more people in the developing world than in richer richer
> countries........ By 1990, therefore there were already 50% more cancer deaths in less developed
> countries than in developed countries........ I feel this study dispells the myth that these
> disorders are found mostly in our decadent western societies (see NeanderThin review).
These facts do not surprise me. The population of the developing world is so much greater than the richer
countries (especially if the latter is narrowly defined) that to have more deaths of any disease in the former is
not unlikely. I would guess there are more deaths of AIDS, cholera, TB, and other causes unrelated to diet,
even road accidents, in the developing world. What is of more interest is the proportion of deaths in the
different parts of the world, and if we are to make inferences about diet we must allow for the better medical
facilities in the richer world - I expect the prevalence of, say, breast cancer is similar but the mortality is
higher in the developing world, simply from lack of treatment.
Andrew Millard
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Adaptation to one diet?
Reply-To:
Jennie Brand Miller
Date: Fri, 16 May 1997 10:56:24 +1000
It seems that many of us believe that animals and human beigns have evolved on one sort of diet and it's best
that we stick to the composition of that diet.
I wonder then, if there been much work on cats and dogs. They evolved as carnivores and carbs would have
been a very small component of their diet. But these days all the dry cat/dog food contains lots of
carbohydrate, up to 60%. I know there are a few fat cats around and some develop diabetes but has this been
connected to the high CHO diets. I think we can learn alot from the knowledge/experience of the animal
nutritionists. Can anyone comment?
Best wishes Jennie
PALEODIET Archives
Subject: Plant Food
From: Dean Esmay
Reply-To:
Date: Fri, 16 May 1997 12:00:37 -0400
Another report from one of our lurking members:
For those interested in ancient plant food remains, and the digestion, a very good survey of work from
Palaeolithic to Date: Gordon Hillman: Plant foods in Ancient Diet: the Archaeological Role of Palaeofaeces
in General and Lindow Mans's Gut Contents in Particular pp 99-116. In <Lindow Man, the Body in Bog
> British Museum Publications 1986 ISBN 0-7141-1386-7 (Gordon Hillman of the Institute of
Archaeology .UCL London)
also related papers in the same book:
116/298 (1997)
Timothy G Holden: Preliminary Report on the Detailed Analyses of the Macroscopic Remains from the Gut
of Lindow Man: pp 116-126
Robert G Scaife: Pollen in Human Palaeofaeces; and the Preliminary Investigation of the Stomach and Gut
Contents of Lindow Man.: pp 126-136
Don Robins Keith Sales Duro Oduwole Tim Holden Gordon Hillman Postscript: Last Minute Results from
ESR Spectroscopy Concerning the Cooking of Lindow Man's Last Meal.: pp 140-143
< thanks to Staffan Lindberg for his note in the Paleodiet digest. I really think he should read the <Time
Walkers > book. Things are moving relatively fast in paleoanthropology especially re Homo Sapiens (I
mean they are not moving at glacial speeds the way they did for years :-)) Clive Gamble has worked on the
paleolithic development of hominids with Chris Stringer of the Natural History Museum London. He is
located at Southampton University. It seems that many sites where it was presumed that man had hunted
animals and butchered them are now seen as places where the poor things were instead eaten by carnivorous
animals along with the other prey. This means that a lot of work on paleolithic diet will have to be rethought
if this is true.
>
PALEODIET Archives
Subject: Rethinking Paleodiet
From: Ray Audette
Reply-To:
Date: Sat, 17 May 1997 00:22:11 -0700
To fully grasp what humans were designed to eat is easy. Simply limit your technology to that which comes
naturally without any technology(naked with a sharp stick or rock) and eat accordingly. You will find that
you will eat only those things edible to any Primate in a similar state. All primates eat meat (insects and other
animals), raw fruits, raw vegetables, nuts and berries. Without technology, no primate can utilize grains,
beans, potatoes, other species milk or refined sugars or vegetable oils. Because of your hominid lateraly
asymetric brain, you have an inherent ability to aim and thus kill more animals than your monkey cousins
who lack this skill. This skill added to your bipedal gait and super efficient cooling system (lack of fur and
unique perspiration system)make you the most efficent hunter on earth (lions never attack elephants, but
pigmies do!). Because of your hominid short lower intestine, you can rely less on plant materials than any
other primate and will crave fatty meat as it is the highest energy food available to you.
This method is more reliable than fosil evidence. Get it wrong and you don't feel well! This method does not
depend on what your culture taught you or where on earth you find yourself.
Hunter-gather cultures lived closer to this ideal than any modern people. Their epidemeological data alone
are enough to support my decision to live this way (over 12 years).
Ray Audette Author"NeanderThin:A Caveman's Guide to Nutrition" http://www.sofdesign.com/neander
> It seems that many sites where it was presumed that man had hunted animals and butchered them are
> now seen as places where the poor things were instead eaten by carnivorous animals along with the
> other prey. This means that a lot of work on paleolithic diet will have to be rethought if this is true.
PALEODIET Archives
Subject: Re: Lancet Article
Reply-To:
Date: Sat, 17 May 1997 08:49:05 +0100
At 09.04 97-05-16, Andrew Millard wrote:
> "Diseases of affluence" such as heart disease and strokes are killing more people in the
> developing world than in richer countries........ By 1990, therefore there were already 50% more
> cancer deaths in less developed countries than in developed countries........ I feel this study
> dispells the myth that these disorders are found mostly in our decadent western societies (see
> NeanderThin review). These facts do not surprise me. The population of the developing world is so
117/298 (1997)
> much greater than the richer countries (especially if the latter is narrowly defined) that to have
> more deaths of any disease in the former is not unlikely. ... What is of more interest is the
> proportion of deaths in the different parts of the world, ...
In developing countries there is an emerging epidemic of cardiovascular disease which in many parts now
outnumber infectious and parasitic disease [5]. In 1993 some two-thirds of the estimated 14 million annual
cardiovascular disease deaths occured in the developing world [6]. The progressive aging of populations,
better medical facilities and the decline in infectious disease are only partial explanations for this trend, and
several studies strongly indicate that urbanization plays an important role [7, 9-17]. It is also well known that
urbanization, irrespective of ethnic origin of a population, leads to an increased mean level of blood pressure
[13, 44, 57, 58, 75, 81, 91, 93, 100, 101, 138-150] and body mass index [12, 13, 47, 57, 58, 81, 105, 139,
142, 146-148, 150-154], and that both of these cardiovascular risk factors only then start to increase with
age.
Substantial evidence indicates that most cases of cancer are caused by environmental factors (Doll R, Peto T.
The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. J Natl
Cancer Inst 1981; 66: 1192-1308), and the Swedish Cancer Committee has suggested that the proportion is
more than 80 per cent. The incidence rates of many cancers differ tenfold, and sometimes hundredfold,
between different countries in the world (Muir C, Waterhouse J et al. Cancer incidence in five continents.
IARC Sci Publ 1987; no 88).
The question is not if but how much atherosclerotic heart disease and cancer can be prevented.
Best regards, Staffan
5. Beaglehole R. Cardiovascular disease in developing countries. An epidemic that can be prevented. BMJ
1992; 305: 1170-1. 6. Report WD. Investing in health.Oxford: Oxford University Press, 1993 7. Kevau IH.
Cardiology in Papua New Guinea in the twenty-first century [editorial]. P N G Med J 1990; 33: 271-4. 9.
King H. The epidemiology of diabetes mellitus in Papua New Guinea and the Pacific: adverse consequences
of natural selection in the face of sociocultural change. In: Attenborough RD, Alpers MP, ed. Human
Biology in Papua New Guinea. The Small Cosmos. Oxford: Clarendon Press, 1992: 363-72.
118/298 (1997)
10. Vaughan JP. A review of cardiovascular diseases in developing countries. Ann Trop Med Parasitol 1978;
72: 101-9. 11. Sinnett PF, Kevau IH, Tyson D. Social change and the emergence of degenerative
cardiovascular disease in Papua New Guinea. In: Attenborough RD, Alpers MP, ed. Human Biology in
Papua New Guinea. The Small Cosmos. Oxford: Clarendon Press, 1992: 373-86. 12. Zimmet P.
Epidemiology of diabetes and its macrovascular manifestations in Pacific populations: the medical effects of
social progress. Diabetes Care 1979; 2: 144-53. 44. Gee RW. The epidemiology of hypertension in the South
Pacific. P N G Med J 1983; 26: 55-8. 47. Prior IA. Cardiovascular epidemiology in New Zealand and the
Pacific. N Z Med J 1974; 80: 245-52. 57. Eason RJ, Pada J, Wallace R, Henry A, Thornton R. Changing
patterns of hypertension, diabetes, obesity and diet among Melanesians and Micronesians in the Solomon
Islands. Med J Aust 1987; 146: 465-9. 58. Taylor R, Bennett P, Uili R, et al. Hypertension and indicators of
coronary heart disease in Wallis Polynesians: an urban-rural comparison. Eur J Epidemiol 1987; 3: 247-56.
75. Shaper AG. Cardiovascular disease in the tropics. IV. Coronary heart disease. B M J 1972; 4: 32-5. 81.
Trowell HC, Burkitt DP, ed. Western diseases: their emergence and prevention. Cambridge, Mass: Harvard
University Press, 1981: 91. Kean BH, Hamill JF. Anthropology of arterial tension. Arch Intern Med 1949;
83: 355-62. 93. Lowenstein FH. Blood-pressure in relation to age and sex in the tropics and subtropics. A
review of the literature and an investigation in two tribes of Brazil Indians. Lancet 1961; i: 389-92. 100. Prior
IAM, Stanhope JM. Blood pressure patterns, salt use and migration in the Pacific. In: Kesteloot H, Joosens
JV, ed. Epidemiology of Arterial Blood Pressure. The Hague: Martinus Nijhoff, 1980: 243-62. 101. James
GD, Baker PT. Human Population Biology and Hypertension: Evolutionary and Ecological Aspects of Blood
Pressure. In: Laragh JH, Brenner BM, ed. Hypertension: Pathophysiology, Diagnosis, and Management.
New York: Raven Press, Ltd, 1990: 137-145. 105. Mann GV. The serum lipoprotein and cholesterol
concentrations of Central and North Americans with different dietary habits. Am J Med 1955; 19: 25. 138.
Maddocks I. Dietary factors in the genesis of hypertension. In: Mills CF, Passmore R, ed. Proceedings of the
Sixth International Congress of Nutrition. Edinburgh: Livingstone, 1964: 137-47. 139. Walker ARP.
Overweight and hypertension in emerging populations. Am Heart J 1964; 68: 581-5. 140. Cruz-Coke R,
Etcheverry R, Nagel R. Influence of migration on blood pressure of Easter Islanders. Lancet 1964; i: 697-9.
141. Miall WE, Del CE, Fodor J, et al. Longitudinal study of heart disease in a Jamaican rural population. I.
Prevalence, with special reference to ECG findings. Bull World Health Organ 1972; 46: 429-41. 142.
Edwards FM, Wise PH, Thomas DW, Murchland JB, Craig RJ. Blood pressures and electrocardiographic
findings in the South Australian Aborigines. Aust N Z J Med 1976; 6: 197-205. 143. Zimmet PZ, Taylor R,
Jackson L, Whitehouse SL, Faaivaso S, Ainuu J. Blood pressure studies in rural and urban Western Samoa.
Med J Aust 1980; 2: 202-5. 144. Zimmet P, Jackson L, Whitehouse S. Blood pressure studies in two Pacific
populations with varying degrees of modernisation. N Z Med J 1980; 91: 249-52. 145. Poulter N. Blood
pressure in urban and rural East Africa: the Kenyan Luo Migrant Study. In: Cruickshank JK, Beevers DG,
ed. Ethnic Factors in Health and Disease. Oxford: Wright, 1989: 61-8. 146. Ahmed ME. Blood pressure in a
multiracial urban Sudanese community. J Hum Hypertens 1990; 4: 621-4. 147. Thouez JP, Eko JM, Foggin
PM, et al. Obesity, hypertension, hyperuricemia and diabetes mellitus among the Cree and Inuit of Northern
Cubec. Arct Med Res 1990; 49: 180-8. 148. Alpert JS, Goldberg R, Ockene IS, Taylor P. Heart disease in
native Americans. Cardiology 1991; 78: 3-12. 149. He J, Klag MJ, Whelton PK, et al. Migration, blood
pressure pattern, and hypertension: the Yi Migrant Study. Am J Epidemiol 1991; 134: 1085-101. 150. Nan L,
Tuomilehto J, Dowse G, Virtala E, Zimmet P. Prevalence of coronary heart disease indicated by
electrocardiogram abnormalities and risk factors in developing countries. J Clin Epidemiol 1994; 47: 599611. 151. Salmond CE, Prior IA, Wessen AF. Blood pressure patterns and migration: a 14-year cohort study
of adult Tokelauans. Am J Epidemiol 1989; 130: 37-52. 152. Collins V, Dowse G, Zimmet P. Prevalence of
obesity in Pacific and Indian Ocean populations. Diabetes Res Clin Pract 1990; 153. Taylor R, Badcock J,
King H, et al. Dietary intake, exercise, obesity and noncommunicable disease in rural and urban populations
of three Pacific Island countries. J Am Coll Nutr 1992; 11: 283-93. 154. O'Dea K, Patel M, Kubisch D,
Hopper J, Traianedes K. Obesity, diabetes, and hyperlipidemia in a central Australian aboriginal community
with a long history of acculturation. Diabetes Care 1993; 16: 1004-10.
-------------------------------------------------------------------
PALEODIET Archives
119/298 (1997)

Reply-To:
Jennie Brand Miller
Date: Mon, 19 May 1997 10:29:35 +1000
Australian Aborigines had no pottery but they detoxified a large proportion of their plant foods. In fact, when
the first Europeans arrived many of the foods they tried made them very sick and they decided that the native
plants of Australia were not worht eating. Australian Aborigines ate the very toxic cycad nuts (Macrozamia
spp) and a number of yams (Dioscorea spp).
They would cut up/grind the yams/seeds, place them in a dilly bag (a tightly woven grass bag) and leave
them suspended in running water for up to 7 days and then cook on hot coals. Another method was to soak in
shallow water for several days. These were then placed in a hole dug in a dry sandy place and covered with
sand and grass tree leaves. In a fortnight (2 weeks) the pulp encasing the cycad nut was eaten raw or roasted.
There may not have been much in the way of water-soluble vitamins and minerals at the end of all this, but it
seems it was worth the effort. They got sick of eating just protein foods (marine, land animals) and liked to
have a balance between animal foods and plant foods. A good book to read about all this is Mutooroo - Plant
use by Austalian Aboriginal People. Compiled by Gleen Leiper. ISBN 0 7242 1185 3.
Best wishes Jennie
PALEODIET Archives
Subject: some basic questions
From: Sarah Mason
Reply-To:
Date: Mon, 19 May 1997 15:50:12 +0000
As a new member who has looked through much of the archive, and read messages of the last week or so
with much interest, a few questions have arisen in my mind which as far as I can tell have not been
directly/explicitly addressed so far by the list. As someone who is not an expert in dietary/nutritional studies
I hope these questions are also not ones which are felt to be too basic!
A few selections from posts which brought these questions to mind first:
Jennie Brand Miller wrote:
> It seems that many of us believe that animals and human beigns have evolved on one sort of diet
> and it's best that we stick to the composition of that diet. while Dean Esmay questions that this
> is necessarily so: After all, it's been some 10, 000 years or more since the advent of agriculture,
> and some adaptation has probably occurred since then....It seems very clear to me that trying to
> find any one dietary method or protocol that universally applies to all humans is to search for
> the golden fleece. And yet it seems equally clear that much can be learned from the dietary habits
> of our ancestors.
While Ray Audette writes:
> To fully grasp what humans were designed to eat is easy. Simply limit your technology to that
> which comes naturally without any technology(naked with a sharp stick or rock) and eat accordingly
> [continuing to suggest that certain adaptations make meat (the?) preferred food] This method is
> more reliable than fosil evidence. Get it wrong and you don't feel well! This method does not
> depend on what your culture taught you or where on earth you find yourself. Hunter-gather cultures
> lived closer to this ideal than any modern people.
120/298 (1997)
My first question has already been brought up by Mavis Wood asking WHICH Palaeolithic peoples are
being referred to by list members, but did not apparently receive much response. My reading of messages
suggest most people are referring to early hominids/the Lower Palaeolithic, for which the direct
archaeological evidence relating to diet (especially any role for plant foods) is necessarily very sparse. There
seems to be an implicit assumption by some members that this is the diet that 'we' evolved to eat. But to what
extent has evolution of the species since the Lower Palaeolithic included changes in dietary 'adaptations'
which are in (large?) part related to such 'cultural' aspects as developments in technology, including use of
cooking and other processing technologies - in other words, has the species' evolution been influenced by
these? Presumably adaptations to environments other than savannah, with different kinds of available foods,
might also be involved. What kind of evidence is there for the speed at which genetic changes related to the
way the gut behaves (for instance) can occur - I think I'm right in thinking that evidence from such things as
lactose/glucose in/tolerance suggest that there can be quite rapid changes. So what basis is there for believing
that our guts are really the same as those of Lower Palaeolithic hominids?
In view of the paucity of evidence for the real nature of Palaeolithic diets (of whatever type) should we be
making such definitive claims as those of Ray Audette? Several posts make it clear that the verdict on the
likely nature of early hominid diet is still very much out. Ethnographically-recorded hunter-gatherer diets are
remarkably varied, especially in relation to the proportions of plant vs. animal foods, suggesting that there
may be great variability in human adaptations - and to what extent can any of these be regarded as analogous
with the diet of a Lower Palaeolithic hominid?
And a furher (partly related) question: in many discussions, particularly relating to toxicity of plant foods,
there has been much use of the word 'staple' - what evidence is there that our Palaeolithic ancestors (of
whichever type) subsisted on diets in which there necessarily was A staple? (however that is defined - IS
there a broadly-acepted definition?). In a broad-spectrum / omnivorous diet, which presumably is one
possibility, is it necessary to have a staple, and can problems of toxicity be overcome by eating small
amounts of many different foodstuffs, so that toxic foods are not eaten in suficient quantities to cause
problems?
regards,
Sarah Mason Human Environment Section email: Institute of Archaeology, UCL Tel: +44 (0)171 387 7050 x
4757 31-34 Gordon Square Fax: +44 (0)171 383 2572 London, WC1H 0PY, UK
PALEODIET Archives
Subject: PaleoAnthro Fully Moderated
From: Matt Fraser
Reply-To:
Date: Wed, 21 May 1997 15:30:56 -0400
Hello,
I would like to announce that the PaleoAnthro Discussion List (a list that is devoted to topics dealing with
Paleoanthropology, Physical Anthropology, Prehistoricn Archaeology, and Human and Non-human Primate
Evolution), has become totally moderated. This measure was taken to ameliorate certain problems, such as
forgetting to trim response posts, potential flaming situations and off-topic posts. Consequently, the total
volume of posts has been decreased.
In addition, I have added a digest version of the Discussion list, as well as an "Announcements Only" list for
those not interested in the discussions. The Discussion Lists also receive the announcements, so subscribing
to more than one list is unnecessary.
To subscribe to one of the lists, send an email message to
With one of the following three messages in the body of the email:
subscribe paleoanthro
subscribe paleoanthro-digest
subscribe pa-announce
The topics of these lists include Paleoanthropology, Physical Anthropology, Prehistoric Archaeology, and
Human and Non-human Primate Evolution.
For more information, see the PaleoAnthro Lists Home Page at:
http://www.pitt.edu/~mattf/PalAntList.html
Thanks,
121/298 (1997)
Matt Fraser List Owner and Moderator

_________________________________________________________
Matt Fraser Matt's Paleo Pages <http://www.pitt.edu/~mattf/PaleoPage.html
>
Where you can find The Paleo Award, PaleoNews, PaleoChat, The Paleo Forum, The PaleoAnthro Mailing
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PALEODIET Archives
Subject: Evolutionary changes in human gut: response to Sarah Mason
From: Loren Cordain
Reply-To:
Date: Fri, 23 May 1997 13:27:00 -0600
In the last digest, Sarah Mason wrote:
"What kind of evidence is there for the speed at which genetic changes related to the way the gut behaves
(for instance) can occur - I think I'm right in thinking that evidence from such things as lactose/glucose
in/tolerance suggest that there can be quite rapid changes. So what basis is there for believing that our guts
are really the same as those of Lower Palaeolithic hominids?"
122/298 (1997)
There are calculations which estimate how long it took to increase the adult lactase gene (ALP) in northern
europeans from a pre-agricultural incidence rate of 5% to its present rate of approximately 70% (1). In order
for the gene frequency to increase from 0.05 to 0.70 within the 250 generations which have occurred since
the advent of dairying, a selective advantage in excess of 5 % may have been required (1). Therefore, some
genetic changes can occur quite rapidly, particularly in polymorphic genes with wide variability in their
phenotypic expression. Because humans normally maintain lactase activity in their guts until weaning (~4
yrs of age in modern day hunter-gatherers), the type of genetic change (neoteny) required for adult lactase
maintenance can occur quite rapidly if there is sufficient selective pressure. Maintenance of childlike genetic
characteristics (neoteny) is what occurred with the geologically rapid domestication of the dog during late
pleistocene and mesolithic (2). The complete re-arrangement of gut morphology or evolution of new enzyme
systems capable of handling novel food types is quite unlikely to have occurred in humans in the short time
period since the advent of agriculture. Some populations have had 500 generations to adapt to the new staple
foods of agriculture (cereals, legumes and dairy) whereas others have had only 1-3 (i.e Inuit, amerindians
etc). Because anatomical and physiological studies among and between various racial groups indicate few
differences in the basic structure and function of the gut, it is reasonable to assume that there has been
insufficient evolutionary experience (500 generations) since the advent of agriculture to create large genetic
differences among human populations in their ability to digest and assimilate various foods. Of the
population differences in gastrointestingal function which have been identified, they generally are associated
with an increased ability to digest disachharides (lactose & sucrose) via varying dissacharidase activity.
Although insulin metabolism is not a direct component of the gastrointestinal tract, there is substantial
evidence to indicate that recently acculturated populations are more prone to hyperinsulinemia and its
various clinical manifestations, including non-insulin dependent diabetes mellitus (NIDDM), obesity,
hypertension, coronary heart disease and hyperlipidemia (3). It is thought that these abnormalities,
collectively referred to as syndrome X (4) are the result of a so called " thrifty gene" (5) which some groups
have suggested is glycogen synthase (6). Consequently, the ability to consume increasing levels of
carbohydrate without developing symptomes of syndrome X is likely genetically based and a function of
relative time exposure of populations to the higher carbohydrate contents of agriculture (3). There are no
generally recognized differences in the enzymes required to digest fats or proteins among human
populations. Additionally, all human groups regardless of their genetic background have not been able to
overcome the deleterious effects of phytates and other antinutrients in cereal grains and legumes. Iranian
populations, Inuit populations, european population and asian populations all suffer from divalent ion (Ca,
Fe, Zn, etc) sequestration with excessive ( > 50% total calories) cereal or legume consumption. All racial
groups also have not evolved gut characteristics which allow them to digest the food energy which is
potentially available in the major type of fiber contained in cereal grains. Further most of the antinutrients in
cereal grains and legumes (alklyrescorcinols, amylase inhibitors, lectins, protease inhibitors etc) wreak their
havoc upon human physiologies irrespective of differing genetic backgrounds. Thus, most of the available
evidence supports the notion that except for the evolution of certain dissacharidases and perhaps changes in
some genes involving insulin sensitivity, the human gut remains relatively unchanged from paleolithic times.
Cordially,
REFERENCES
1. Aoki K. Time required for gene frequency change in a deterministic model of gene-culture coevolution,
with special reference to the lactose absorption problem. Theoretical Population Biology 1991;40:354-68.
2. Budiansky S. The Covenant of the Wild. Why Animals Chose Domestication. New York, William
Morrow & Co., 1992.
3. Brand-Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM.
Diabetologia 1994;37:1280-86.
4. Reaven GM. Syndrome X: 6 years later. J Int Med 1994;236(supp 736):13-22.
5. Neel JV. Diabete mellitus: A "thrifty" genotype rendered detrimental by "Progress". Am J Hum Genetics
1962;14:353-62.
6. Schalin-Jantti C. et al. Polymorphism of the glycogen synthase gene in hypertensive and normotensive
subjects. Hypetension 1996;27:67-71.
PALEODIET Archives
Subject: Message from Mary Enig PhD and Sally Fallon
From: Dean Esmay
123/298 (1997)
Reply-To:
Date: Fri, 23 May 1997 13:29:09 -0400
Dear Dean and Fellow Paleodiet Colleagues
We have been lurkers so far but now throw our hat into the ring with the following article on the cave man
diet. It will appear in the Summer 1997 edition of the Price Pottenger Nutrition Foundation Health Journal.
We particularly wish to counter the notion that the paleolithic diet was low in saturated fat.
We also recommend that paleodieters become familiar with the work of Weston Price who studied many
isolated cultures in the thirties. His pioneering work Nutrition and Physical Degeneration can be obtained
from the Price Pottenger Nutrition Foundation by calling (619) 574-7763. You may also wish to order back
journals that dealt with the African and Eskimo diets. Or, visit our web site at http://members.aol.com/ppnf.
Another book that will be of interest is Handbook of Indigenous Fermented Food by Keith Steinkraus,
published by Marcel Dekker.
Sincerely yours, Sally Fallon MA and Mary G Enig PhD, authors of Nourishing Traditions: The Cookbook
that Challenges Politically Correct Nutrition and the Diet Dictocrats ProMotion Publishers (800) 231-1776
The Cave Man Diet Sally Fallon and Mary G. Enig, PhD
Low-fat diets, claim the pundits of medical orthodoxy, have been associated with good health and longevity
throughout the globe and since the dawn of time. The research of Weston Price proves otherwise. From the
Eskimo of Alaska to the hardy Alpiner, from Gaelic villager to African tribesman, Price discovered that all
healthy indigenous people had a plentiful source of animal fat in the diet. Such Neolithic groups could still
be found when Price embarked on his eventful travels back in the 1930s. But no one, of course, not even the
indefatigable Dr. Price, could visit our Paleolithic forbearers, the so-called cave men. The lack of direct
evidence about our hunter-gather ancestors--who by definition neither cultivated crops nor domesticated
farm animals--allows limitless conjecture about the content of their diets. The low fat school claims that the
cave man ate lean meat, supplemented by copious amounts of plant foods in the form of sprouts, roots, fruits,
berries and leaves; dissenting investigators assert that the cave man imbibed animal fat first and foremost,
along with the meat to which it was attached, and very little in the way of foods from the vegetable kingdom.
Both schools of thought are in agreement that the cave man diet was otherwise Spartan, lacking foodstuffs
that were either salty or sweet.
Dr. Walter L Voegtlin argues for the high fat model in his book the Stone Age Diet, published in 1975.
Humans are carnivorous animals he asserts, and the Stone Age diet was that of a carnivore--chiefly fats and
protein, with only small amounts of carbohydrates. He notes that like the carnivorous dog, man has canine
teeth, ridged molars and incisors in both jaws. His jaw is designed for crushing and tearing, and moves in
vertical motions. Mastication of his food is unnecessary and he does not ruminate. His stomach holds two
quarts, empties in three hours, rests between meals, lacks bacteria and protozoa, secretes large quantities of
hydrochloric acid and does not digest cellulose. His digestive tract is short relative to body length, his cecum
is nonfunctional and his appendix vestigial. His rectum is small, contains putrefactive bacterial flora and
does not contribute to the digestive process. The volume of feces is small; digestive efficiency borders on
100%; his gall bladder is active and well developed. Both the dog and man feed intermittently and can
survive without a stomach or colon. The herbivorous sheep, by contrast, lacks canines, has flat molars and
incisors only in the lower jaw. His jaw is designed for grinding and rotary movments. Mastication and
rumination are vital functions. His stomach holds eight and one-half gallons, contains bacteria and protozoa,
never empties and has but weak production of hydrochloric acid. His colon and cecum are long and
capacious; the cecum performs a vital function; the bacterial flora of his rectum is fermentative rather than
putrefactive; feces are voluminous; gall bladder function is weak or absent; and total digestive efficiency is
50% or less. The sheep feeds continuously. He cannot live without his stomach or colon. His entire digestive
tract is about five times longer, as a ratio of body length, than that of man and his dog.
Voegtlin argues that gross differences in the anatomy of man and the herbiverous animals make him unable
to successfully adapt to a diet based on plant foods, particularly carbohydrate-rich grains, as well as to a diet
in which milk products, rich in lactose, predominate; and that the whole range of modern diseases stems
from his abandonment of the food choices of his primitive ancestors, based largely on meat and rich in fat.
He notes that, with the exception of vitamins C and K, all essential nutrients can be derived from animal
foods, and that the cave man diet was certainly much richer in vitamins and minerals than our own. Modern
devitalized plant foods--such as sugar and white flour--only hasten our decline.
124/298 (1997)
A decade later, in 1988, Dr. Boyd Eaton published the Paleolithic Prescription in which he argues that the
cave man diet was low in fat, particularly saturated fat, low in salt and rich in dietary fiber from plant foods.
His Paleolithic prescription for optimum health is, in fact, very much akin to the so-called prudent diet of the
American Heart Association. The typical Paleolithic macronutrient profile, he asserts, contained 33% of total
energy from protein, principally but not entirely animal protein, 46% from carbohydrates and a mere 21%
from fat. Journalist Joe Friel translates these suppositions about Paleolithic eating habits into the following
dietary recommendations: Select the leanest cuts of meat (wild game, if possible), trim away all visible fat
from meat, include fish and fowl, eat low- or non-fat dairy products and include moderate amounts of
monounsaturated fat in the diet in the form of oils and spreads of almonds, avocado, hazelnut, macadamia
nut, olive and walnut. He lumps natural saturated fats in with newfangled hydrogenated oils as fats to be
avoided. The cave man, it seems, thriving on a diet of lean venison along with roots, shoots and fruits, was
altogether politically correct in his low-fat dietary habits,
Or was he? In a recently published collection of essays, Ice Age Hunters of the Rocky Mountains, we learn
that the hunter-gatherers of the North American continent ate the following animals: mammoth, camel, sloth,
bison, mountain sheep, small mammals including beaver, pronghorn antelope, elk, mule deer, horse, llama
and large members of the dog family. Mammoth, sloth, mountain sheep, bison and beaver are fatty animals
in the modern sense in that they have a thick layer of subcutaneous fat, as do the many species of bear and
wild pig whose remains have been found at Paleolithic sites throughout the world. The bison and camel have
humps composed largely of tallow.
Furthermore, if the dietary patterns of present day African hunter-gathers can serve as a guide, the Paleolithic
hunter preferred the fatty portions of the carcass including organs, brains, tongue, feet and marrow.
Archeological remains indicate that whereas meat from game carcasses was often left uneaten, the long
bones were carried back into camps and chopped onto pieces so that the marrow could be extracted. Organ
meats were eaten immediately--and often raw--but muscle meat was preserved by drying, or by mixing it
with tallow to make pemmican. Some investigators believe that the cave man's preference for the fatty
portions of his kill led to profligate practices--wastefully killing of mammoths simply to extract their fatty
tongues, for example--and that selective hunting of the fattier animals was a prime factor leading to the
extinction of large mammals such as mammoths, sloths and rhinoceros.
Bones of the bear predominate in many European sites. Archeologist Myra Shakley reports on an important
Neanderthal site in Hungary where 90 percent of the remains were those of bear. Whole carcasses were
brought to the site--not just portions as was the case for other animals--and the manner in which the
carcasses were cut up suggests that the skins were removed. Obviously the pelts were used to protect the
hunter-gather from the severe climate. The skins would also have provided a rich source of fat that could be
used for preserving other foods. Altars containing bear skulls found in caves in the Swiss Alps, and dated
back as far as 75, 000 years, indicated that the bear was worshiped as a sacred animal.
Present-day hunter-gathers, as well as those of the ancient past, possess greater dietary wisdom than the
majority of our modern Ph.D.s. They understood that a diet of lean meat, lacking in fat, was the surest route
to weakness, disease and death. Steffanson, who studied the Eskimos and Indians of the far north, reports
that when lean caribou was the only meat available, anxiety set in. These natives knew that a month or more
on such meat, without the addition of marine animals or fatty fish, would make them sick and prone to
disease. The ancient tribes of the Americans West would not eat female bison in the Spring because nursing
and pregnant bison cows burned off their fat reserves during the winter months. In fact, most bison hunts
occurred in the late Summer and Fall when the bison were naturally fattened on the ripe grain of prairie
grasses. Anthropologist Leon Abrams reports that the Aborigine will throw away a kangaroo he has killed if
he discovers that its carcass does not contain sufficient fat. Members of Randolph Marcys 1856 expedition
to Wyoming grew weak and sick consuming a politically correct low-fat regime of six pounds of lean horse
and mule meat per day; Dr. Wolfgang Lutz reports that a very efficient way of eliminating jailed political
prisoners in South and Central America is to feed them a diet composed exclusively of lean meat. They soon
develop severe diarrhoea and succumb. The explanation is that fats contain nutrients like vitamin A that the
body needs to utilize the amino acids and minerals in flesh foods; without fat in the diet, the body rapidly
uses up its own stores of fat soluble vitamins. When these vital nutrients are depleted, the human organism
can no longer fight off disease.
125/298 (1997)
Was the cave man diet simply rich in unsaturated fats, but low in saturated fats? Antelope and caribou fat is
over 50% saturated--about the same as beef--and mountain sheepfat would be the similar. Buffalo fat is 56%
saturated--more saturated than beef! All ruminant animals contain lots of saturated fat because the protozoa
in their capacious guts do an efficient job of saturating the oils found in plant foods--whether these oils come
from dried hay or green grass, from feedlot corn or the ripe grains of prairie grasses. (Of course naturally fed
meat is richer in vitamins and minerals.) The bison were hunted in the late Summer and Fall when their fat
stores would have been highest. Grazing animals spend several months eating the carbohydrate-rich seeds of
wild grasses, which begin to ripen as early as the month of May--grain fattening in feedlots merely mimics
this natural process.
Camel fat, from the kind of animal the Neanderthals apparently hunted to extinction, is a whooping 63%
saturated! Wild boar is about 41% saturated, exactly the same as lard from a domestic pig. Kidney fat--which
modern man avoids but which the cave man would have eaten--is highly saturated. Buffalo kidney is 58%
saturated, antelope kidney fat is 65% saturated, elk kidney is 62% saturated and mountain goat kidney fat is
66 % saturated. Caribou marrow has a preponderance of monounsaturated fat, and a small amount of
polyunsaturated, but still contains more than 27% saturated fat. Figures for elephant tongue are unavailable
but beef tongue is 45% saturated. Bears, which yield 48% of their kilocalories as fat, have a preponderance
of monounsaturated fat, the same kind found in olives, almonds and other nuts.
Seafood in coastal regions would also have provided fat for primitive man, particularly the valuable omega-3
fatty acids; insects, grubs and worms are a source of additional fat in all regions except the arctic.
So the high-fat proponents are the most likely winners of great Paleolithic fat debate; but they are probably
wrong in their assertions that plant foods, particularly grains, are new to the human diet. Remains of plant
foods at Paleolithic sites include seeds, berries, roots, leaves and bulbs. Sunflower seeds, prickly pear seeds,
amaranth seeds and limber pine seeds have been found at Rocky Mountain sites. Various types of nuts were
consumed by primitives in the Americas and on the European continent. The amount of plant food in the
cave man diet varied according to the climate and locality. Obviously plant foods were minimal in the diets
of those in arctic climates, but played a large role in tropical regions. Nuts, of course, provided additional fat.
The pecan, consumed in large quantities by the Indians of the Southeast, contains 85% of calories as fat. In
tropical regions, palm nuts and coconuts provide large quantities of saturated fats.
Present day hunter-gatherers employ special preparation methods for carbohydrate-rich foods. Acorns, for
example, are soaked in water and lye to remove tannins; tubers are buried in the ground, pounded or cooked
in hearth ashes; seeds are soaked, pounded and allowed to ferment in various ways. It is safe to assume that
the ancient hunter-gatherers employed similar techniques to neutralize the many enzyme inhibitors, irritants
and mineral blocking substances found in tubers and seeds. In fact, a large portion of the primitive womans
day was spent in just such preparations--pounding, soaking, sieving, souring and putting the finishing
touches on various types of root and seed foods. The men, on the other hand, divided their time between
dangerous hunting forays, in which physical stamina and strength was at a premium, and periods of idleness
when they would work on their weapons and gossip.
So the comparison of the human digestive tract with that of the dog, while interesting, does not tell the whole
story. Man can benefit from the many nutrients in plant foods as long as he takes care in their preparation.
Primitive plant preparation methods--pounding, soaking, and fermenting--imitate the time-consuming
processes that take place in the sheeps digestive tract, beginning with his flat grinding molars and ending
with the fermentative bacteria in his lower bowel. The Paleolithic hunter-gatherer had the good sense not
only to eat the fattier portions of meat, but to prepare his plant foods correctly. Modern man, particularly the
modern professor of nutrition, does not.
Dogs, apparently, were the first animal to be domesticated by man--or, as the current theory holds, the dogs
adopted man and went to work for him. A man with five or six dogs can track down and kill the largest of
wild animals. Dogs made hunting less dangerous, and allowed our intrepid cave man to stand back and kill
his prey with something he threw--an arrow or light spear--rather than with a lance that he physically had to
thrust in. Almost certainly, the advent of the dog at mans side hastened the extinction of the large fatty
animals that had given the cave man his physical prowess and resistance to disease. But the dog would also
have helped the hunter move into his Neolithic phase, by rounding up wild sheep, cattle and goats and
helping to keep them in flocks, so that their fatty meat and milk would be available throughout the year. Such
milk was much richer than milk from todays Holsteins which have been bred to produce low-fat milk The
neo-agriculturist would have been ruled by his tastebuds, rather than modern advertising, and consumed his
milk products whole.
126/298 (1997)
Assuming that mans tastebuds are not superfluous, but natures way of guiding him to the food he needs, let
us examine the notion that the cave man diet satisfied only the bitter, sour or pungent portion of his tasting
apparatus, and not the salty or sweet. A number of studies report that honey, far from being a rare delicacy,
contributed a substantial portion of the calories in many primitive diets. The Hazda of Tanzania, the Mbuti
pygmies of the Congo, the Veddas or Wild Men of Sri Lanka, the Guayaka Indians of Paraguay, the
Bushmen of South Africa and the Aborigines of Australia, all put a high value on honey and consumed it in
large amounts. East coast American Indians consumed plentiful portions of maple syrup, and used it in the
production of pemmican. Wild fruits and berries are incredibly sweet at the peak of ripeness, and can be
preserved in various ways for consumption throughout the year. Fermented foods of the Eskimo are
described as tasting as sweet as candy. Primitive man did not consume refined sweeteners, as we do, but
neither did he neglect his sweet tooth.
It is hard to imagine that he would have neglected his taste for salt. It occurs naturally in meat and blood and,
as animals seek out natural salt licks, so our sensible cave man would have done the same. The manufacture
of salt can be accomplished simply by filling a hollowed out log with sea water and letting the brine
evaporate. The evidence of place names in England indicates that salt was the earliest commodity to be
traded from the seacoast, or from salt pits, to other areas. In extremely remote locations, such as the
Himalayas or the interior of Africa, the ashes of sodium-rich marsh grasses are added to food. It is reported
that the members of the Yanomami tribe in the Amazon basin do not take in any added salt. In an apparant
adoptive measure, they also excrete almost no salt in the urine.
Milk is salty because mammals need salt for the production of hydrochloric acid and for the development of
the brain and nervous system. Without dietary salt, the human mind does not fully develop and man must
live, not by his wits like the ingenious cave man from the dawn of time, but as a brute, even if he happens to
be born in this modern age.
PALEODIET Archives
Subject: Re: Comments on Dr. Enig's and Sally Fallon's Cave Man Diet
From: Loren Cordain
Reply-To:
Date: Mon, 26 May 1997 15:43:00 -0600
First, I would like to welcome Mary Enig and Sally Fallon to our group. I have been a long time admirer of
Dr. Enig's work in the area of lipid metabolism and coronary artery disease. Her seminal work in pointing
out the lack of an association between per capita disposal rates of saturated fats and cancer (1) and
cardiovascular disease (2) clearly demonstrate the complexity of dietary practices and human health and well
being. Also, her realization of the health dangers of dietary trans fatty acids preceded more mainstream
recognition (3) of this data by 12-15 years. I have a number of questions/comments that perhaps Mary and
Sally could address:
127/298 (1997)
1. I was unaware of Dr. Walter L. Voegtlin's book, "The Stone Age Diet", published in 1975. Could you
provide a more complete citation. Also, a correction must be made regarding Voegtlin's assertion that "with
the exception of vitamins C and K, all essential nutrients can be derived from animal foods". Uncooked or
minimally cooked flesh and organs of animals apparently provide sufficient vitamin C levels to prevent
scurvy (4). 2. Although never explicitly stated in their recent posting, it seems the point, Dr. Enig and Sally
Fallon were making was that paleolithic humans ate considerable levels of saturated fats and likely did not
develop the degenerative diseases afflicting modern man such as atherosclerosis and coronary heart disease
(CHD). Therefore, if we follow this line of logic, present day consumption of high levels of saturated fats in
the western diet would not necessarily be associated with an increased risk for CHD. Therefore, modern man
should not limit consumption of saturated fats. There are a number of points which need to be clarified
regarding this line of logic. First, there is little doubt that paleolithic man consumed (probably preferentially)
the fatty portions of wild game animals and that during certain times of the year (late summer and early fall),
the total lipid content of large herbivorous animals was considerable; consequently consumption of saturated
fats could have been quite high. Despite a consumption of a largely animal based diet that frequently could
include high levels of saturated fats, most modern day hunter gatherers exhibit low serum cholesterol levels,
low blood pressure and low to non-existent mortality rates from (CHD) (5, 6). At first, this data seems
paradoxical in light of the almost universal recommendations of a low saturated fat, high carbohydrate diet in
the treatment of CHD. However, there are important and subtle differences between the high saturated
fat/animal based diets of pre-agricultural man and the high saturated fat diets of modern man which can
account for this paradoxical situation. 1. There is increasing recognition that for the atherosclerotic process to
occur, there must not only be elevated levels of LDL cholesterol, but that the lipids and cholesterol carried
by LDL must be oxidized (7). The macrophages which take up oxidized LDL molecules and eventually
become the foam cells of the atherosclerotic plaque have a scavenger receptor which is different from native
LDL receptors and which does not down regulate. Consequently, continually elevated levels of oxidized
LDL in the plasma tends to promote the atherosclerotic process. High levels of dietary linoleate increase
LDL oxidizabilty (8). Because refined vegetable oils were not present in pre-agricultural diets the linoleate
levels would have been lower than in western diets wherein the vegetable fat consumption has increased 300
% since 1910 and the animal fat consumption has decreased slightly (9). Thus, the relatively high levels of
vegetable oils consumed along with relatively high levels of saturated fats in the western diet promote a lipid
profile in which LDL cholesterol is elevated and more prone to oxidation and hence to the development of
CHD. 2. The protein content of the paleolithic diet was significantly higher than the average 12-15% of the
western diet. Recent studies (10, 11) show that isocaloric replacement of carbohydrate with protein lower
total cholesterol, LDL, VLDL and triglycerides (TG) while elevating HDL cholesterol. Consequently, a high
dietary protein content even in the face of increasing saturated fat serves to lower serum cholesterol levels
and reduce the risk for CHD. 3. The carbohydrate content of pre-agricultural diets was generally lower than
the 45-55% of the western diet. Consequently the post-prandial lipemic excursions, during which LDL
molecules are most prone to oxidation would have been reduced, since the addition of carbohydrate to a fat
rich meal exacerbates this swing (12). Pre-agricultural eating patterns show that fat and protein were
generally eaten together whereas, carbohydrate meals were eaten separately. This eating pattern would have
reduced post-prandial lipemic excursions. Additionally, the reduced carbohydrate content of pre-agricultural
diets would have improved the portions of the blood lipid profile (TG, VLDL, HDL, Lp(a)) which are
worsened by high carbohydrate diets (13). 4. Work from our laboratory, as well as that of others has shown
that the fatty acid profiles of storage as well as structural fat is quite different when contrasting wild to
domesticated animals. Of the dietary saturated fats, 12:0, 14:0 and 16:0 are known to elevate plasma
cholesterol levels whereas 18:0 is neutral or perhaps hypocholesterolemic. The saturated fat of marrow and
depot fat in wild animals contains greater levels of 18:0 and lower levels of 14:0 and 16:0 when compare to
domestic animals. Additionally, the structural lipid content in game meat is quite different than that in
domestic meat. There generally are higher levels of all n-3 fats and higher levels of all 20 and 22 carbon fats
of both the n-3 and n-6 variety in game meat. The N6/N3 ratio of beef averages about 15 whereas in wild
animals it is about 4-5. Again, higher levels of N6 lipids in domestic animals, particularly linoleate tend to
increase LDL oxidizability whereas the higher levels of N3 fats in game animals are cardioprotective.
Consequently, the consumption of saturated fats in pre-agricultural diets occured against a background of
dietary lipids which was much different than the background fats in the modern diet. Recent evidence clearly
shows that the fatty acid composition of a meal can improve serum lipid values despite widely varying fat
levels (14). 5. Pre-agricultural diets by definition would not have included dairy fats. In western diets, about
a third of the saturated fats is contibuted by dairy foods (milk, butter, cheese, ice cream). In metabolic ward
studies, butter fat raised LDL cholesterol levels significantly higher than beef tallow (15). Further, milk
128/298 (1997)
consumption is the best world wide predictor of CHD mortality of all dietary elements (16). Bovine milk fat
is quite low in the long chain cardioprotective N3 fats and has an high n6/ratio. Additionally the Ca/Mg ratio
in milk and dairy products is quite high compared to the average 1:1 ratio in foods available to preagricultural man. Elevated Ca/Mg ratios have been shown to be positively related to CHD (17). This data
suggests dairy products would be quite atherogenic, particularly when consumed in a background of other
dietary elements in the western diet. 6. Modern man eating a high saturated fat diet is generally quite inactive
compare to pre-agricultural man (18). High levels of activity serve to improve insulin sensitivity and lower
TG and VLDL while increasing HDL cholesterol.
So yes, in all liklihood, the dietary saturated fat levels of pre-agricultural man could have been quite high
(even by modern standards); however because of differing types and amounts of carbohydrate, protein and
fatty acids as well as differing levels of fiber and antioxidant vitamins and phytochemicals, these types of
diets generally did not elevate cholesterol levels, nor increase LDL oxidizablility.
One final comment - not only does the high sodium content of the western diet predispose us to
hypertension, osteoporosis, urinary tract stones, menierre's syndrome, stomach cancer, insomnia, asthma and
initiation and promotion of all types of cancer, it also seems to do the same in our closest relative, the chimp
(19).
REFERENCES
1. Enig MG, Munn RJ, Keeney M. Dietary fat and cancer trends-a critique. Fed Proc 1978;37:2215-2220.
2. Enig MG. Diet, serum cholesterol and coronary heart disease. In: (dont have exact title of book - perhaps
Dr. Enig can supply the rest of the citation)
3. Willett WC, Ascherio A. Trans fatty acids: Are the effects only marginal? Am J Pub Health 1994;84:72224.
4. Stefansson V. Observations on three cases of scurvy. JAMA 1918;71:1715-18.
5. Bang HO, Dyerberg J. Lipid metabolism and ischemic heart disease in Greenland Eskimos. In: Draper HH
(ed). Advances in Nutrition Research, vol 3, N.Y., Plenum Press, 1980, 1-22.
6. Leonard WR, et al. Correlates of low serum lipid levels among Evenki herders of siberia. Am J Hum Biol
1994;6:329-338.
7. Steinberg D et al. Beyond cholesterol: modifications of low-density lipoprotein that increase its
atherogenicity. N Engl J Med 1989;320:915-24.
8. Louheranta AM et al. Linoleic acid intake and susceptibility of very low ensity and low density
lipoproteins to oxidation in men. Am J Clin Nutr 1996;63:698-703.
9. ASCN/AIN Task Force on Trans Fatty Acids. Position paper on trans fatty acids. Am J Clin Nutr
1996;63:663-70.
Cardiol 1995;11(supp G):127G-131G.
11. Wolfe BM et al. Short term effects of substituting protein for carbohydrate in the diets of moderately
hypercholesterolemic human subjects. Metabolism 1991;40:338-43.
12. Chen YDI et al. Effect of acute variations in dietary fat and carbohydrate intake on retinly ester content
of intestinally derived lipoproteins. J Clin Endocrin Metabolism 1992;74:28-32.
13. Reaven GM. Pathophysiology of insulin resistance in human disease. Physiol Rev 1995 75:473-86.
14. Nelson GJ et al. Low fat diets do not lower plasma cholesterol levels in healthy men compared to high fat
diets with similar fatty acid composition at constant caloric intake. Lipids 1995;30:969-76.
15. Denke MA, Grundy SM. Effects of fats high in stearic acid on lipid and lipoprotein concentrations in
men. Am J Clin Nutr 1991;54:1036-40.
16. Artaud-Wild SM et al. Differences in coronary mortality can be explained by differences in cholesterol
and saturated fat intakes in 40 countries but not in France and Finland. A paradox. Circulation 1993;88:277179.
17. Varo P. Mineral element balance and coronary heart disease. Internat J Vit Nutr Res 1974;44:267-73.
18. Cordain L, Gotshall RW, Eaton SB. Evolutionary aspects of exercise. World Review of Nutrition and
Dietetics 1997;81: in press.
19. Denton D et al. The effect of increased salt intake on blood pressure of chimpanzees. Nature Medicine
1995;1:1009-16.
PALEODIET Archives
Subject: Bears
From: Dean Esmay
129/298 (1997)
Reply-To:
Date: Tue, 27 May 1997 14:03:51 -0400
Passed along from an anonymous member:
Timewalkers. Clive Gamble 1993 p194
< The excavator of the Drachenloch cast his alpine Palaeolithic finds as specialist cave bear hunters and
threw in some fanciful evidence for bear cults among the Ancients to support the case. These have proved
difficult to dislodge both from the archaeological and general literature but, however reluctantly, the much
illustrated stone "cupboards " with bear skulls stacked inside have to be dismantled. Bears frequently die
during hibernation and other sleepers in the cave will push bodies and skeletons out of the way and in doing
so create all sorts of interesting patterns with skulls and bones....... It is, however difficult to find clear
evidence for the specialist hunting of species. Well dated Middle Paleolithic sites as the Hortus cave in
Southern France and the early Upper Paleolithic site at Bacho Kiro in Bulgaria both have animal faunas
dominated by bones of mountain goat. However it is unclear how many of these bones are really the end
products of hunting since at both sites carnivores, which would be major predators on ibex, such as leopard,
wolf, and lynx are also common. This raises the distinct possibility that the human record is once again being
swamped by the archaeology of other species > see also Gamble 1986 The Palaeolithic Settlement of
Europe Cambridge University Press
The title of the book on the Neanderthals
Stringer C and C Gamble 1993 In Search of the Neanderthals : solving the puzzle of human origins. London
Thames and Hudson
PALEODIET Archives
Subject: "The Stone Age Diet"
Reply-To:
Date: Tue, 27 May 1997 16:22:52 EDT
The Stone Age Diet: based on in-depth studies of human ecology and the diet of man. Voegtlin, Walter L.,
1904- 1st ed. New York, Vantage Press, c1975 xvii, 277 p. bibliography: p.265-277.
I read this book cover-to-cover at least twice back in college. I would highly recommend that anyone
interested in either ketogenic diets or the diet of our ancestors to check with your local library and read it.
Jeffrey P. Krabbe
PALEODIET Archives
Subject: Question for Dr. Enig
From: Tammy Glaser
Reply-To:
Date: Tue, 27 May 1997 22:47:59 -0400
Having read the book "The Zone" by Dr. Barry Sears, I have become very interested in EFA metabolism,
specifically for my daughter who is autistic. She has done very well on a diet free of gluten and casein (based
upon the research of Reichelt (1), (2), (3), (4) and Shattock (5), (6), (7)). A search on medline revealed no
hits on autism and EFA metabolism, but it may be due to the fact it's been overlooked. Since the research on
gluten/casein originated from links to schizophrenia (8), (9), (10), I ran a search on schizophrenia and EFA
metabolism. I found many studies linking schizophrenia and altered cell membrane dynamics(11, (12),
impaired EFA/PGE1 metabolism (13), (14), (15), (16) and elevated PGE2 plasma levels (17), just to mention
a few anomalies mentioned in recent studies.
130/298 (1997)
In your research on today's hunter/gatherer societies, have you found people who fit the conditions of
schizophrenia or autism? (Obviously, there may be many other factors arising in our society that contribute
to these conditions.)
Tammy L. Glaser M.S., Operations Research
References: (1) "Dietary Intervention in Autistic Syndromes" by A M Knivsberg, K L Reichelt, et al., Brain
Dysfunction 3: 315-327 (1990) (2) "Gluten, Milk Proteins and Autism: Dietary Intervention Effects on
Behavior and Peptide Secretion" by K L Reichelt, J Ekrem, H Scot, Journal of Applied Nutrition, 42(1): 1-11
(1990) (3) "Nature and Consequences of Hyperpeptiduria and Bovine Casomorphins Found in Autistic
Syndromes" by K L Reichelt, A M Knivsberg, et al., Developmental Brain Dysfunction, 7: 71-85 (1994) (4)
"Probable Etiology and Possible Treatment of Childhood Autism" by K L Reichelt, A M Knivsberg, et al.
Brain Dysfunction, 4: 308-319 (1991) (5) "Proteins, Peptides and Autism: Part 1: Urinary Protein Patterns in
Autism as Revealed by Sodium Dodecyl Sulphate-Polyacrylamide Gel Electrophoresis and Silver Staining"
by K Williams, P Shattock, et al., Brain Dysfunction, 4: 320-322 (1991) (6) "Proteins, Peptides and Autism:
Part 2: Implications for the Education and Care of People with Autism" by P Shattock and G Lowdon, Brain
Dysfunction, 4: 323-334 (1991) (7) "Role of Neuropeptides in Autism and Their Relationships with Classical
Neurotransmitters, P Shattock, A Kennedy, et al., Brain Dysfunction, 3: 328-345 (1990) (8) "Cereals and
Schizophrenia - Data and Hypothesis" by F C Dohan, Acta Psychiatr. Scandinavia, 42: 125 (1966) (9)
"Schizophrenia: Possible Relationship to Cereal Grains and Celiac Disease" by F C Dohan in
"Schizophrenia: Current Concepts and Research" by S Sankar, P. J. D. Publications, Ltd., Hicksville NY
(1969) (10) "Relapsed Schizophrenics: More Rapid Improvement on a Milk and Cereal-Free Diet" by F C
Dohan, J Grasberger, et al., British Journal of Psychiatry, 115: 595 (1969) (11) Decreased tyrosine transport
in fibroblasts from schizophrenics: implications for membrane pathology. Ramchand CN; Peet M; Clark AE;
Gliddon AE; Hemmings GP. Prostaglandins Leukot Essent Fatty Acids, 1996 Aug, 55:1-2, 59-64 (12)
Abnormal incorporation of arachidonic acid into platelets of drug-free patients with schizophrenia. Yao JK;
van Kammen DP; Gurklis JA. Psychiatry Res, 1996 Feb 28, 60:1, 11-21 (13) The relationship between
schizophrenia and essential fatty acid and eicosanoid metabolism. Horrobin DF. Prostaglandins Leukot
Essent Fatty Acids, 1992 May, 46:1, 71-7 (14) Essential and other fatty acids in plasma in schizophrenics
and normal individuals from Japan. Kaiya H; Horrobin DF; Manku MS; Fisher NM. Biol Psychiatry, 1991
Aug 15, 30:4, 357-62 (15) Prostaglandin E1 suppression of platelet aggregation response in schizophrenia.
Kaiya H. Schizophr Res, 1991 Jul-Aug, 5:1, 67-80 (16) Polyunsaturated fatty acids, prostaglandins, and
schizophrenia. van Kammen DP; Yao JK; Goetz K. Ann N Y Acad Sci, 1989, 559:, 411-23 (17) Elevated
plasma prostaglandin E2 levels in schizophrenia. Kaiya H; Uematsu M; Ofuji M; Nishida A; Takeuchi K;
Nozaki M; Idaka E. J Neural Transm, 1989, 77:1, 39-46
PALEODIET Archives
Subject: State of the Paleodiet Symposium
From: Dean Esmay
Date: Sun, 1 Jun 1997 23:36:14 -0400
I would like to welcome all the new members who have joined our list in the last few weeks.
I'm pleased to say that after less than three months of operation, this listserv now boasts very nearly 200
members, the vast majority of whom have doctorates in fields such as biology, archaeology, paleontology,
medicine, and other (mostly related) fields. Even a majority of the non-degreed appear to be graduate
students. Our list is now also available generally on the World Wide Web at
http://maelstrom.stjohns.edu/archives/paleodiet.html and is undoubtedly read by others who are not currently
list members, since the web site is now linked in several other places and all messages posted to the list are
readable from that page.
Traffic on our list has been relatively low of late, but thoroughly informative. I would like to invite some of
you who may have been silent to date to feel free to take part in discussions; there is a tremendous pool of
knowledge and insight available from our list here, and I would like to encourage everyone to make use of it.
Thank you all for helping to make this list a success beyond my expectations.
PALEODIET Archives
Subject: Re: Animals (Was: Adaptation to one diet?)
131/298 (1997)
Date: Mon, 2 Jun 1997 00:26:55 +0100

At 01.56 97-05-16, Jennie Brand Miller wrote:
> It seems that many of us believe that animals and human beigns have evolved on one sort of diet
> and it's best that we stick to the composition of that diet. I wonder then, if there been much
> work on cats and dogs. They evolved as carnivores and carbs would have been a very small
> component of their diet. But these days all the dry cat/dog food contains lots of carbohydrate, up to
> 60%. I know there are a few fat cats around and some develop diabetes but has this been connected to
> the high CHO diets. I think we can learn alot from the knowledge/experience of the animal
> nutritionists. Can anyone comment?
As Jennie Brand Miller points out, we can learn a lot from animal nutrition. One area of research where
much (but far too little) has been done is atherosclerosis.
Fully developed lipid-rich atherosclerosis of the extramural coronary arteries (the largest branches
supporting the heart) is part of normal ageing in westernized populations and is seen in more than 90 per cent
of men aged 60 years or more [1-4], but it has to my knowledge not been demonstrated in other free-living
mammals [5-9]. However, early stages of atherosclerosis, with no or little deposition of fat in the arterial
wall, can appear 'spontaneously' in mammals like horses, swine, ruminants and some carnivores including
dogs [5-9]. In dogs, hyaline degeneration of smaller intramural coronary arteries, an entirely different
disorder, is rather common and often leads to severe heart failure [6, 10].
With the exception of strains with genetic hypercholesterolemia (rabbits etc), every studied case of lipid-rich
atheromas in non-human mammals (laboratory animals, domestic pigs etc) has thus apparently been
preceeded by a diet which is not eaten by the animal in its natural context. Neither smoking nor stress suffice
when feeding is not manipulated. Psychological stress can induce early atherosclerosis like fatty streaks and
fibrous plaques but not true atheromas [11]. Regression of atherosclerosis in an animal can be obtained if,
and apparently only if, the animal is fed a natural diet [12-14].
Animal species differ in their susceptibility to atherosclerosis when fed atherogenic diets. There are few
attempts in the literature to put the pieces together, but in 1965 Richard Fiennes, Pathologist at the
Zoological Society of London, suggested that "the dividing line between susceptible and insusceptible
groups is related more to dietary habits than to phylogenetic relationships" [15]. His following passage is
worth quoting in full: "Among birds, insusceptible species are those whose natural diet is grain, while the
most susceptible are those who feed normally on fruit or fresh animal food. Among mammals, the most
susceptible group is the primates, including man. Man in his original state fed on a mixed diet with a high
proportion of fruit and fresh animal protein. It may be suggested, therefore, that susceptible groups of
animals are those whose natural diet would be fruit or fresh uncooked food of animal origin and who, under
conditions of captivity, domestication, or civilization, are maintained on graminivorous diets. The analogy
holds good also in the case of susceptible rodent family members, such as guinea pigs, chinchillas, and
rabbits, who rely on fresh-growing vegetable foods for their diet. Rats and mice, on the other hand, naturally
graminivorous and adapted to life in sewers and ships and other places where fresh foods often are not
available, are atheroma-insusceptible. The domestic pig, fed largely on an unnatural diet of grain, suffers
from atheroma, while the wild pig, rooting for shoots and other germinating tuberous foods and killing rats
and snakes as a fresh animal supplement, is rarely affected. We have supposed, therefore, that the
development of atheroma in susceptible species may be primarily associated with enforced dietary habits of
an unnatural nature. The main association appears to be with secondary graminivorous habits, of which man
himself, the greatest atheroma sufferer, is supremely guilty."
I am not aware of any serious comment to Fiennes' 32 year old suggestion that cereals may be a cause of
atherosclerosis in animals.
Advanced 'spontaneous' atherosclerosis is thus common only in birds with wide variation between species,
strains and breeds (see 15 for some taxonomic details). For obvious reasons most studies were performed in
captive birds. Whether atherosclerosis was common in paleolithic birds is of course impossible to know but
may be worth considering, or rather what diets were available to these birds, and also whether 10, 000
generations of birds living near seed-producing humans could have led to speciation of some more resistant
strains.
132/298 (1997)
Another illustration of the difficulties of studying wild animals is the case of the elephant. Early stages of
coronary atherosclerosis are not uncommon in the wild African elephant but unlike humans their aorta is
much more affected [16]. Sikes compared the distribution of atherosclerosis in the aorta among two groups
of elephants living in two separate habitats, a 'natural' montane habitat where, among other things, diet was
varied, and a 'disturbed' habitat consisting of scrubland or grassland, a habitat which elephants would not
choose were they not confined there by encroaching human settlements. Atheromas were found only in
elephants from the 'disturbed' habitat [17].
As for humans, westernization obviously has a great impact on whether at all and to what extent they are
affected by atherosclerosis. In the 1960s Tejada et al compared the distribution of atherosclerosis in a defined
segment of one partical coronary artery in deceased men aged 45-55 in four different cities: New Orleans
(whites), Sao Paolo, Brazil (whites), Santiago, Chile, and Durban, South Africa (blacks) [4]. In only 14 of
156 men (9%) from New Orleans, less than 2% of the vessel was affected, compared to 108 of 142 (76%)
among the Durban black men. Today coronary heart disease in urban blacks of South Africa is still low but
increasing [18], while in the US it is about as high in blacks as in whites [19].
Essential hypertension, the common form of high blood pressure in westerners (which is absent in
contemporary hunter-gatherers and subsistence horticulturalists), has not been reported in animals [6]. I don't
know about diabetes or abdominal obesity in animals but I doubt that there is much data.
Best wishes, Staffan Lindeberg
1. Velican D, Velican C. Study of fibrous plaques occurring in the coronary arteries of children.
Atherosclerosis 1979; 33: 201-5. 2. Velican D, Velican C. Atherosclerotic involvement of the coronary
arteries of adolescents and young adults. Atherosclerosis 1980; 36: 449-60. 3. Velican C, Velican D.
Incidence, topography and light-microscopic feature of coronary atherosclerotic plaques in adults 26--35
years old. Atherosclerosis 1980; 35: 111-22. 4. Tejada C, Strong JP, Montenegro MR, Restrepo C, Solberg
LA. Distribution of coronary and aortic atherosclerosis by geographic location, race, and sex. Lab Invest
1968; 18: 509-26. 5. Robinson WF, Maxie MG. The cardiovascular system. In: Jubb KVF, Kennedy PC,
Palmer N, ed. Pathology of domesticated animals. New York: Academic Press, 1985. 6. Whitney JC. The
spontaneous cardiovascular diseases of animals. In: Pomerance A, Davies MJ, ed. The pathology of the
heart. Oxford: Blackwell, 1975: 579-610. 7. Stout LC, Bohorquez F. Significance of intimal arterial changes
in non-human vertebrates. Med Clin North Am 1974; 58: 245-55. 8. McCullagh KG. Arteriosclerosis in the
African elephant. Atherosclerosis 1972; 307-35. 9. Armstrong ML, Heistad DD. Animal models of
atherosclerosis. Atherosclerosis 1990; 85: 15-23. 10. Jonsson L. Coronary arterial lesions and myocardial
infarcts in the dog. A pathologic and microangiographic study. Acta Vet Scand Suppl 1972; 38: 1-80. 11.
Kaplan JR et al. Plaque changes and arterial enlargement in atherosclerotic monkeys after manipulation of
diet and social environment. Arterioscl Thromb 1993; 13: 254-63. 12. Moncada S, Martin JF, Higgs A.
Symposium on regression of atherosclerosis. Eur J Clin Invest 1993; 23: 385-98. 13. Kaplan JR, Manuck SB,
Adams MR, Williams JK, Register TC, Clarkson TB. Plaque changes and arterial enlargement in
atherosclerotic monkeys after manipulation of diet and social environment. Arterioscler Thromb 1993; 13:
254-63. 14. Malinow MR. Experimental models of atherosclerosis regression. Atherosclerosis 1983; 48: 10518. 15. Fiennes RNTW. Atherosclerosis in Wild Animals. In: Roberts JC, Straus R (eds). Comparative
Atherosclerosis. The morphology of spontaneous and induced atherosclerotic lesions in animals and its
relation to human disease. Harper & Row, New York, 1965: 113-26. 16. McCullagh KG. Arteriosclerosis in
the African elephant. Atherosclerosis 1972; 16: 307-35. 17. Sikes SK. The disturbed habitat and its effect on
the health of animal populations, with special reference to cardiovascular disease in elephants. Proc R Soc
Med 1968; 61: 2-3. 18. Walker A.R.P, Labadarios D, Glatthaar II. Diet-related disease patterns in South
African interethnic populations. In: Temple NJ, Burkitt DP. Western Diseases. Their Dietary Prevention and
Reversibility. 1994 Totowa, New Jersey, Humana Press, 29-66. 19. Manson JE, Ridker PM. Racial
differences in coronary heart disease incidence and mortality. Methodologic mythology? Ann Epidemiol
1990; 1: 97-100.
PALEODIET Archives
Subject: Cereal grains
From: Dean Esmay
Date: Mon, 2 Jun 1997 22:30:52 -0400
I have been intending to write an essay on cereal grains but alas the "real world" has left me far too busy
these last few weeks and an end is not in sight. So I thought I would offer a few brief comment:
133/298 (1997)
Enig and Fallon, in their piece submitted a few weeks ago, stated that Paleolithic Nutrition writers are
probably wrong about cereal grains being unnatural foods for humans. They then gave examples of the use
of acorns and seeds from non-grain plants. This sincerely seems to dodge the issue to me.
Many on this list have questioned of late whether it is really possible to construct a picture of the paleolithic
diet in humans. There also seems to have been some argument against man as a true, 100% meat-eating,
carbohydrate-free animal, although notably no one I'm aware of seems to have seriously taken that position
for quite some time. I think much of this may be time wasted; can it safely be said that it is generally
acknowledged that humans have always eaten a wide variety of foods, and that the "natural" diet for humans
will of necessity vary wildly in content depending upon region and climate and season?
A review of modern hunter/gatherer diets(1) shows tremendous variation in diet based on these factors and I
don't see how it's possible to argue that it has not always been so. In fact I think it can easily be argued that
one of man's primary evolutionary advantages has been the ability to adapt to an extremely wide array of
foods.
I think instead it seems easier to use deductive reasoning in trying to define a "paleodiet": it can probably
best be defined by what it lacks, rather than by what it contains. We can never know precisely what a prehuman living in plains 25, 000 years ago ate, but we can probably take very educated guesses about what he
did -not- eat, and from that as a starting point we can start adding in what we think he -did- eat within
reasonable guessing parameters.
From this perspective I do not think it can be successfully argued that cereal grains such as rice, wheat,
barley, and etc. were ever a part of the natural human diet prior to but a few millenia ago (2, 4). I have yet to
find any respectable scientific reference which seriously suggests this might be so. The best argument that
can be made is that possibly early man may have occasionally munched on wild grass seeds, but the idea that
this would ever have been a daily staple seems quite far-fetched. I would be extremely interested in hearing
about any research which suggests that it might be otherwise. Given the lack of evidence to the contrary and
the simple fact that the idea of eating large quantities of cereal grains on a daily basis seems extremely
difficult to imagine without a system of agriculture, it surely seems to that there's not much reason to think
that cereal grains as a staple are in any way natural to the human animal.
There is also significant evidence linking the advent of agriculture with bone and joint disease (2, 3). A study
of a people eating a high saturated fat diet that are nearly 100% free of heart disease seems to show that the
most significant difference between their diet and that of Westerners is a lack of dairy and cereal grain
products (5). There is evidence that the proteins in cereal grains provoke auto-immune reactions (6). There is
also the troubling existence of Celiac disease, which is a serious condition caused entirely by sensitivity to
the proteins in cereal grains, and which appears to be quite a bit more common among peoples who have
culturally only been agriculturalist a relatively short time, such as the Irish, compared to that of, say, the
Indians or the Chinese; I do not happen to have references on the incidence of Celiac right now but perhaps
Ron Hoggan can help us out there (Ron, are you still reading?). Also Staffan has given us numerous
references in the past which strongly suggest that the phytic acid in cereal grains causes calcium depletion; I
have seen these references posted in the past but apparently not to this list; Staffan, could I talk you into
posting specific references for this matter to this list?
I see that this message has rambled more than I intended, and there are more references that can be offered. It
does seem to me that while it is probably not possible to construct "a paleodiet" for all humans that gives
specific content, it can be said that there are probably things in common to most if not all pre-agricultural
diets, especially if you start your definition by what such diets -lack-.
Perhaps others can comment further; my time for this evening (and this month I suspect!) is done. :-)
Dean
1. Ember CR. Myths about hunter gatherers. Ethnology 1978;17:439-48.
2. Eaton S, Nelson D, "Calcium in evolutionary perspective" _Am. J. Clin. Nutr._1991; 54: 281S - 287S
3 Armelagos G, Van Gerven D, Martin D, Huss-Ashmore R, "Effects of Nutritional Change on the Skeletal
Biology of Northeast African (Sudanese Nubian) Populations" _From Hunters to Farmers The Causes and
Consequences of Food Production in Africa_ Clark & Brandt (eds.) 1984; II: 37-146
4. Lutz W J, "The Colonisation of Europe and Our Western Diseases" _Medical Hypotheses_ 1995; 45: 115120
5. Lindeberg S, et al. "Cardiovascular risk factors in a Melanesian population apparently free from stroke and
ischaemic heart disease: the Kitava study" _J Intern Med_ 1994 Sep.
6. 11. Ostenstad B, Dybwad A, Lea T, Forre O, Vinje O, Sioud M, "Evidence for monoclonal expansion of
synovial T cells bearing V Alpha 2.1/V beta 5.5 gene segments and recognizing a syntehtic peptide that
shares homology with a number of putative autoantigens"
134/298 (1997)
PALEODIET Archives
Subject: Cooking habits
From: Dean Esmay
Date: Tue, 3 Jun 1997 20:44:53 -0400
A wonderful document, ARCTIC DAWN -- The Journeys of Samuel Hearne, is to be found in its entirety at
http://web.idirect.com/~hland/sh/title.html
This is, essentially, the journals of an 18th Century Englishman as he explored the Canadian wilderness.
Here is some fascinating stuff about diet and cooking from this journal. Note especially the use of an
animal's stomach as a cooking implement. The phrasing is a little hard to follow in places because Hearne's
18th-Century King's English is a bit different from modern English (I believe "parts of generation" refers to
genitalia, for example) but hopefully others will find these observations as interesting as did I. (Thanks to
David Chapman for supplying this originally to me):
From: A Journey from Prince of Wales's Fort in Hudson's Bay to the Northern Ocean in the years 1769,
1770, 1771, 1772; Hearne, Samuel, 1745-1792, Strahan and Cadell, London, England, 1795.
13 July, 1771: ... Seeing some woods to the Westward, and judging that the current of the rivulet ran that
way, we concluded that the main river lay in that direction, and was not very remote from our present
situation. We therefore directed our course by the side of it, when the Indians met with several very fine buck
deer, which they destroyed; and as that part we now traversed afforded plenty of good firewood, we put up,
and cooked the most comfortable meal to which we had sat down for some months. As such favourable
opportunities of indulging the appetite happen but seldom, it is a general rule with the Indians, which we did
not neglect, to exert every art in dressing our food which the most refined skill in Indian cookery has been
able to invent, and which consists chiefly in boiling, broiling, and roasting: but of all the dishes cooked by
those people, a BEEATEE, as it is called in their language, is certainly the most delicious, at least for a
change, that can be prepared from a deer only, without any other ingredient. It is a kind of haggis, made with
the blood, a good quantity of fat shred small, some of the tenderest of the flesh, together with the heart and
lungs cut, or more commonly torn into small shivers; all which is put into the stomach, and roasted, by being
suspended before the fire by a string. Care must be taken that it does not get too much heat at first, as the bag
would thereby be liable to be burnt, and the contents to be let out. When it is sufficiently done, it will emit
steam, in the same manner as a fowl or a joint of meat; which is as much as to say, Come, eat me now: and if
it be taken in time, before the blood and other contents are too much done, it is certainly a most delicious
morsel, even without pepper, salt, or any other seasoning.
After regaling ourselves in the most plentiful manner, and taking a few hours rest, (for it was almost
impossible to sleep for the muskettoes,) we once more set forward, directing our course to the North West by
West; and after walking about nine or ten miles, arrived at that long wished-for spot, the Copper-mine River.
...
January, 1772 ....
The flesh of the buffalo is exceedingly good eating; and so entirely free from any disagreeable smell or taste,
that it resembles beef as nearly as possible: the flesh of the cows, when some time gone with calf, is
esteemed the finest; and the young calves, cut out of their bellies, are reckoned a great delicacy indeed.
... The tongue is also very delicate; and what is most extraordinary, when the beasts are in the poorest state,
which happens regularly at certain seasons, their tongues are then very fat and fine; some say fatter than
when they are in the best order; the truth of which, I will not confirm. ...
Though the flesh of the moose is esteemed by most Indians for both its flavour and substance, yet the
Northern Indians of my crew did not reckon either it or the flesh of the buffalo substantial food. This I should
think entirely proceeded from prejudice, especially with respect to the moose; but the flesh of the buffalo,
though so fine to the eye, and pleasing to the taste, is so light and easy of digestion, as not to be deemed
substantial food by any Indian in this country, either Northern or Southern. ...
Chapter IX: A Short Description of the Northern Indians, also a farther Account of their Country,
Manufactures, Customs, &c. ...
135/298 (1997)
The extreme poverty of those Indians in general will not permit one half of them to purchase brass kettles
from the Company; so that they are still under the necessity of continuing their original mode of boiling their
victuals in large upright vessels made of birch-rind. As those vessels will not admit being exposed to the fire,
the Indians, to supply the defect, heat stones red-hot and put them into the water, which soon occasions it to
boil; and by having a constant succession of hot stones, they may continue the process as long as it is
necessary. This method of cooking, though very expeditious, is attended with one great evil; the victuals
which are thus prepared are full of sand: for the stones thus heated, and then immerged in the water, are not
only liable to shiver to pieces, but many of them being of a coarse gritty nature, fall into a mass of gravel in
the kettle, which cannot be prevented from mixing with the victuals which are boiled in it. Besides this, they
have several methods of preparing their food, such as roasting it by a string, broiling it, &c; but these need no
farther description.
The most remarkable dish among them, as well as all the other tribes of Indians of those parts, both Northern
and Southern, is blood mixed with the half-digested food which is found in the deer's stomach or paunch, and
boiled up with a sufficient quantity of water, to make it of the consistence of pease-pottage. Some fat and
scraps of tender flesh are also shred small and boiled with it. To render this dish more palatable, they have a
method of mixing the blood with the contents of the stomach in the paunch itself, and hanging it up in the
heat and smoke of the fire for several days; which puts the whole mass into a state of fermentation, and gives
it such an agreeable acid taste, that were it not for prejudice, it might be eaten my those who have the nicest
palates. It is true, some people with delicate stomachs would not be easily persuaded to partake of this dish,
especially if they saw it dressed; for most of the fat which is boiled in it is first chewed by the men and boys,
in order to break the globules that contain the fat; by which means it all boils out, and mixes with the broth;
whereas, if it were permitted to remain as it came from the knife, it would still be in lumps, like suet. To do
justice, however, it their cleanliness in this particular, I must observe, that they are very careful that neither
old people with bad teeth, nor young children, have any hand in preparing this dish. At first, I must
acknowledge that I was rather shy in partaking of this mess, but when I was sufficiently convinced of the
truth of the above remark, I no longer made any scruple, but always thought it exceedingly good.
The stomach of no other large animal beside the deer is eaten by any of the Indians that border on Hudson's
Bay. In Winter, when the deer feed on fine white moss, the contents of the stomach is so much esteemed by
them, that I have often seen them sit round a deer where it was killed, and eat it warm out of the paunch. In
Summer the deer feed more coarsely, and therefore this dish, if it deserve that appellation, is then not so
much in favour. The young calves, fawns, beaver, &c. taken out of the bellies of their mothers are reckoned
most delicate food; and I am not the only European who heartily joins in pronouncing them the greatest
dainties that can be eaten. Many gentlemen who have served with me at Churchill, as well as at York Fort,
and the inland settlement, will readily agree with me in asserting, that no one who ever got the better of
prejudice so far as to taste of these young animals, but has immediately become excessively fond of them;
and the same may be said of young geese, ducks &c. in the shell. In fact, is almost become a proverb in the
Northern settlements, that whosoever wishes to know what is good, must live with the Indians.
The parts of generation belonging to any beast they kill, both male and female, are always eaten by the men
and boys; and though these parts, particularly in the males, are generally very tough, they are not, on any
account, to be cut with an edge-tool, but torn to pieces with the teeth; and when any part of them proves too
tough to be masticated, it is thrown into the fire and burnt. For the Indians believe firmly, that if a dog should
eat any part of them, it would have the same effect on their success in hunting, that a woman crossing their
hunting track at an improper period would have. The same ill-success is supposed also to attend them if a
woman eat any of those parts.
They are also remarkably fond of the womb of the buffalo, elk, deer, &c. which they eagerly devour without
washing, or any other process but barely stroking out the contents. This, in some of the larger animals, and
especially when they are some time gone with young, needs no description to make it sufficiently disgusting;
and yet I have known some in the Company's service remarkably fond of the dish, though I am not one of the
number. The womb of the beaver and deer is well enough, but that of the moose and buffalo is very rank, and
truly disgusting.*
* The Indian method of preparing this unaccountable dish is by throwing the filthy bag across a pole directly
over the fire, the smoke of which, they say, much improves it, by taking off the original flavour; and when
any of it is to be cooked, a large flake, like as much tripe, is cut off and boiled for a few minutes; but the
many large nodes with which the inside of the womb is studded, make it abominable. Those nodes are as
incapable of being divested of moisture as the skin of a live eel; but when boiled, much resemble, both in
shape and colour, the yolk of an egg, and are so called by the natives, and as eagerly devoured by them.
136/298 (1997)
The tripe of the buffalo is exceedingly good, and the Indian method of cooking it infinitely superior to that
practised in Europe. When opportunity will permit, they wash it tolerably clean in cold water, strip off all the
honey-comb, and only boil it about half, or three-quarters of an hour: in that time it is sufficiently done for
eating; and though rather tough than what is prepared in England, yet is exceedingly pleasant to the taste, and
must be much more nourishing that tripe that has been soked and scrubbed in many hot waters, and then
boiled for ten or twelve hours. The lesser stomach, or, as some call it, the many-folds, either of buffalo,
moose, or deer, are usually eaten raw, and are very good; but that of the moose, unless great care be taken in
washing it, is rather bitter, owing to the nature of their food.
The kidneys of both the moose and buffalo are usually eaten raw by the Southern Indians; for no sooner is
one of these beasts killed, than the hunter rips up its belly, thrusts in his arm, snatches out the kidneys, and
eats them warm, before the animal is quite dead. They also at times put their mouths to the wound the ball
has made, and suck the blood; which they say quenches thirst, and is very nourishing.
PALEODIET Archives
Subject: Re: Cereal grains (cont) & Marrow
From: Loren Cordain
Date: Tue, 3 Jun 1997 16:49:00 -0600
137/298 (1997)
I enjoyed Dean's recent piece on cereal grains. I would agree with his statement saying that Dr. Enig and
Sally Fallon are off base in suggesting that cereal grains have been a long term component of the human
dietary evolutionary experience. First off, as pointed out by Dean, Dr. Enig and Sally Fallon are incorrect in
suggesting that the consumption of plant seeds ("sunflower seeds, prickly pear seeds, limber pine seeds") at
pre-agricultural sites is a general indication of cereal grain consumption by pre-agricultural man. Cereal
grains are the seeds of grass and are botanically classified in the gramineae family. Consequently even
though the fossil record may indicate that pre-historic man may have consumed plant seeds, it cannot
necessarily be concluded that a specific type of seeds (gramineae) were consumed by paleolithic man as
well. There are a number of lines of logic which point to this conclusion. 1. There are 8 major cereal grains
which are consumed by modern man (wheat, rye, barley, oats, corn, rice, sorghum and millet) (1). Each of
these grains were derived from wild precursors whose original ranges were quite localized (1). Wheat and
barley were domesticated ~10, 000 years ago in the Near East; rice was domesticated approximately 7, 000
years ago in China, India and South East Asia; corn was domesticated 7, 000 years ago in central and south
america; millets were domesticated in Africa 5-6, 000 years ago; sorghum was domesticated in East Africa
5-6, 000; rye was domesticated ~5, 000 years ago in south west asia and oats were domesticated ~3, 000
years ago in europe. Consequently, the present day edible grass seeds simply would have been unavailable to
most of mankind until after their domestication because of their limited geographical distribution. Also, the
wild version of these grains were much smaller than the domesticated versions and extremely difficult to
harvest (2). 2. Clearly, grass seeds have a world wide distribution and would have been found in most
environments in which early man would have inhabited. However because almost all of these seeds are quite
small, difficult to harvest and require substantial processing before consumption (threshing, winnowing,
grinding and cooking), it would have been virtually impossible for pre behaviorally modern humans (circa
35, 000-40, 000) to exploit this food source. To harvest and process grains on a large scale, sickles,
winnowing trays (baskets), threshing sticks, grinding stones and cooking apparatus are required. There is no
reliable evidence to indicate that this combination of technology was ever utilized by hominids until the late
pleistocene. The advent of grinding stones in the mideast approximately 15, 000 years ago heralds the first
large scale evidence of regular cereal grain consumption by our species (3). There is substantial evidence that
certain modern day hunter gatherers such as the Australian Aborigine and the American Great Basin Indians
utilized grass seeds (1), however these grass seeds were not utilized as a staple and represented only a small
percentage of the total caloric intake and were eaten for only a few weeks out of the year. 3. Except for some
species of baboons, no primate consumes gramineae seeds as a part of their regular natural diet. Primates in
general evolved in the tropical rain forest in which dicotyledons predominate - consequently monocotyledons
(gramineae) would not have been available to our primate ancestors. 4. The primate gut is not equipped with
the enzyme systems required to derive energy from the specific types of fiber which predominate in
graminae. Consequently, unless cereal grains are milled to break down the cell walls and cooked to
crystallize the starch granules (&hence make them more digestible), the proteins and carbohydrates are
largely unavailable for absorption and assimilation. Thus, until the advent of regular fire use and control (as
evidenced by hearths ~125, 000) years ago, it would have been almost virtually energetically impossible for
our species to consume cereal grains to supply the bulk of our daily caloric requirements. 5. Eating raw
cereal grains (as well as cooked cereal grains) wreaks enormous havoc on the primate gut because of their
high antinutrient content. Additionally in virtually every animal model studied (dog, rat, guinea pig, baboon
etc - citations available if you want them), high cereal grain promotes and induces rickets. I havent even
touched upon the other antinutrients which inflict damage on a wide variety of human physiological systems
- these antinutrients include protease inhibitors, alkylrescorcinols, alpha amylase inhitors, molecular
mimicking proteins ect). Clearly, unprocessed cereal grains cannot contribute substantial calories to the diet
of primates unless they are cooked and processed. 6. Optimal foraging theory suggests that because of the
substantial amount of energy required to harvest, process and eat cereal grains, they generally would not be
eaten except under conditions of dietary duress (4).
A final note to Dr. Enig & Sally Fallon regarding the saturated fat argument. Recent unpublished data (we
will abstract this data for the Federation meeting this Fall) from our laboratory shows that although the lipid
content of wild animal marrow (a food commonly used by preagricultural man) is generally quite high in
total fat percent (~90%), it contains the lowest saturated fat content (20%) of four tissues we have studied
(brain, marrow, white adipose tissue and brain). Additionally it contains the highest level of
monounsaturated fats (~75%) of all tissues. Consequently, marrow would be generally non-atherogenic
because it contains such high levels of MS fats and quite low levels of saturated fat.
REFERENCES
1. Harlan JR. Crops and Man. American Society of Agronomy, Inc., Madison, WI, 1992.
138/298 (1997)
2. Zohary D. The progenitors of wheat and barley in relation to domestication and agricultural dispersal in
the old world. In: The Domestication and Exploitation of Plants and Animals. PJ Ucko, GW Dimbleby (Eds).
Aldine Publishing Co, Chicago, 1969;46-66.
3. Eaton SB. Humans, lipids and evolution. Lipids 1992;27:814-20.
4. Hawkes K, O'Connell JF. Optimal foraging models and the case of the !Kung. Am Anthropologist
1985;87:401-05.
PALEODIET Archives
Subject: Re: Cereal grains
From: Mark Leney
Date: Wed, 4 Jun 1997 09:40:36 +0100
Dean Esmay wrote:
> A review of modern hunter/gatherer diets(1) shows tremendous variation in diet based on these
> factors and I don't see how it's possible to argue that it has not always been so. In fact I think
> it can easily be argued that one of man's primary evolutionary advantages has been the ability to
> adapt to an extremely wide array of foods.
I'm not sure if we have been over this ground already, but it is perfectly possible to argue (and biologically it
must be the null assumption) that the vast majority of our nutritional requirements have (in the evolutionary
past) been satisfied by a relatively small number of food items.
Optimal foraging theory suggests that when all food types are ranked in terms of the time costs of processing
them and nutritional benefits resulting that a foraging indicidual can then be thought of as making a choice
when it encounters a potential food item, along these lines. Should I stop and eat this item or would my time
be better spent continuing my search for a more rewarding item. Stop and eat now will be common if the
processing time is very small or the density of better options is (or is likely) to be low. Leaving potential
food items will be common where processing times (including time taken to catch, dig-up, clean and eat
etc..) are high or the probablity of something better coming along soon is also high.
Following this simpel algorithim thorugh suggests that species will tend to minimize the number of food
species to that most efficient set. This is most likely to leave food resources for growth and reproduction
after maintainence. The assumption here is that the foragers is limited by a macronutrient. Micro-nutrient
limitation might complicate things.
Modern hunter-gatherers tend to live in environments where the costs of moving on to the next potential
resource are relatively high (!Kung women appear to have reached the point where foraging distance has
compromised their reproductive physiology), they take many sub-optimal items in their diet because the
density of optimal items is low and search costs are high, leading to dietary diversity. When there is a rich
and cheap source of food they concentrate on that (Mongogo nuts).
Our pre-agricultural ancestors in general did not live in the areas currently occupied by hunter-gatherers.
Because they occupied areas with richer resources now overun by agro/pastoralists the dynamic between
food choice and foraging time would be different. Less food species would be included in the diet as the
density of higher quality items increased. Therefore I would argue that dietary diversity amongst modern
HG's is derived and is not good evidence for the basic evolutionary dietary strategy adopted by humans in
the late Pleistocene.
If dietary diversity is a basic human adaptation then we have to conceive of humans as living largely in an
impoverished and marginal environment with few or no 'keystone' resource species (such as figs) providing
resource refugia during seasonal resource restrictions. Why would humans live in these places and where are
they?
All this mainly applies to the female diet, males will on the whole do more risky things, but then their
reproductive sucesss is not so closely linked to nutritional status as females. I am not arguing for an all meat
diet for these women, but I suggest that the basal dietary strategy may have been based on the efficient
exploitation of a few species at any one time and place. These key species would clearly vary accross space
and through time but then that kind of diversity is not what we are talking about when we look at modern
hunter-gatherers.
Well there you go, I'm an unreconstructed evolutionary ecologist so what would I know?
PALEODIET Archives
139/298 (1997)
Subject: Cereals in hunter-gatherer diets

Date: Wed, 4 Jun 1997 11:05:02 +1000
In his last posting, Dean writes:
I do not think it can be successfully argued that cereal grains such as rice, wheat, barley, and etc. were ever a
part of the natural human diet prior to but a few millenia ago (2, 4). I have yet to find any respectable
scientific reference which seriously suggests this might be so.
I'd like to add something here. Although rice, wheat and barley were not part of Australian Aboriginal diets,
it sees that other cereal grains played an important role.
I cite from Kirk's book (Aboriginal Man Adapting, RL Kirk, Oxford University Press, Melbourne, 1983).
"Although the collection of seed was widespread across the continent, it was the predominant actitivy in
more arid areas and became high specialised in the wide belt of grasslands which sweep across the north and
down through the east of the Continent (this means about 30% of Australia!). Seed gathering activity was a
major activity for the Bagundji in the Darling River Basin, although in the Murray River area, tubers were
the main dietary staple. Early in the last century Mitchell (one of the first European explorers of Australia)
observed as he travelled down the Darling River that grass had been gathered and piled in heaps. Sometimes
the heaped grass (native millet or Panicum sp.) was burnt and the seed collected form the ground. But storing
the green grass in heaps also allowed the seed to be kept fresh for several months so that a supply was
aailable during the leaner period of the year. Reports from other places suggest that storage of seed was not
uncommon. Howitt, for exapmple reported in 1862 a store of Portulaca seed wrapped in grass and coated
with mud, and more recently in central Australia nearly 1000 kg of grain was found stored in wooden dishes.
Certainly in the more favoured grassland areas there were extensive tracts of grass for harvesting and one
report from south-west Queensland speaks of Aborigines reaping areas of 1000 acres of Panicum,, using
stone knives to cut the stalks. Tindale argues that the wet-milled grass-seed economy was greater than that of
one based on the hard seed derived form the shrublands. This greater edfficiency is one of the dterminants of
the far larger population among the tribes of the grassland areas.'
JBM's interpretation of all this: various AA groups seemed to have relished the cereal grains and eaten them
in significant amounts but I'm sure that much of the carbohydrate in them must have been resistant to
digestion and that which wasn't would have been slowly absorbed.
Cheers Jennie
PALEODIET Archives
Subject: Insulin resistance and glucose scarcity in the paleolithic
From: Art De Vany
Date: Thu, 5 Jun 1997 17:06:12 -0700
Whether it is called Profactor H, Syndrome X, or the Western Disease, the complex of factors surrounding
insulin resistance and hyperinsulemia are at the heart of many of the degenerative and lethal diseases that
afflict modern human beings. I think of insulin resistance as glucose sparing for it impedes transfer across
membranes and, thus, preserves a higher level of circulating glocose. Such a mechanism would serve to
protect the glucose-demanding brain in the internal competition between muscle, organ, and adipose tissue
for scarce glucose. (Adipose tissue indirectly competes for glucose; when the free fatty acids are taken up by
adipose tissue, removing substrate for gluconeogenesis.)
By limiting the uptake by other tissues, insulin resistance spares glucose for the brain. Indeed, the evolution
of a measure of glucose-sparing insulin resistance in other tissues relative to the brain may have been an
essential step in the development of large-brained homo sapiens. The positive, non-linear feedback in which
hyperinsulemia promotes higher insulin resistance which promotes higher hyperinsulemia, is also evidence
of a glucose scarce ancestral habitat. Evolutionarily elegant design would require a negative loop.
This hypothesis could be tested by comparing the relative passage rates of glucose into the relevant tissues
among insulin resistant and non-insulin resistant subjects. Insulin resistance must be a property of adipose
tissue as well as muscle tissue according to this model.
The existence of Factor H is evidence of the scarcity of glucose in the ancestral habitat and of the relative
abundance in the modern habitat. Whatever our ancestors ate, glucose was relatively scarce.
140/298 (1997)
Diet is only one part of dealing with Factor H. Intense exercise that passes the anerobic threshold promotes
growth hormone release, which breaks the positive feedback loop. Growth hormone is antagonistic to insulin
and at the same time sensitizes insulin receptors. Moderate exercise is incapable of triggering the large,
pulsate GH releases that are essential to breaking the hypercycle. Control theory tells us that you regulate a
non-linear, positive feedback system by taking some of the non-linearity out of it (sensitizing the insulin
binding sites through GH release does this) and by hitting it with control pulses (the pulsate GH spikes do
this). Evolution seems to have settled on the same control principles.
Effective exercise should be aimed at promoting hormone drive, not at burning calories.
PALEODIET Archives
Subject: Cereal Grains
From: Ron Hoggan
Date: Thu, 5 Jun 1997 23:20:28 -0700
Dean Esmay wrote:
> There is also significant evidence linking the advent of agriculture with bone and joint disease
> (2, 3). A study of a people eating a high saturated fat diet that are nearly 100% free of heart
> disease seems to show that the most significant difference between their diet and that of
> Westerners is a lack of dairy and cereal grain products (5). There is evidence that the proteins
> in cereal grains provoke auto-immune reactions (6). There is also the troubling existence of
> Celiac disease, which is a serious condition caused entirely by sensitivity to the proteins in
> cereal grains, and which appears to be quite a bit more common among peoples who have culturally
> only been agriculturalist a relatively short time, such as the Irish, compared to that of, say,
> the Indians or the Chinese; I do not happen to have references on the incidence of Celiac right
> now but perhaps Ron Hoggan can help us out there (Ron, are you still reading?).
I'm still reading, but am very limited in time right now. That will change in a couple of weeks, but in the
interim, my comments will have to be very brief.
Depending on the means of determining gluten intolerance, as associated with serum antibodies against some
protein fractions of wheat, rather than mental illness or villous atrophy, the incidence ranges from 15% of a
random population sample in Iceland (1) to 4.75% of a sample taken from healthy blood donors in Maryland,
USA (2) I think it reasonable to deduce that something more than 5% of Westerners experience an immune
response to the commonest food in our diet.
The types of gluten intolerance that result in mental illness are given little creedence in mainstream
medicine, and I am unaware of any epidemiological data on that facet of gluten intolerance.
As for celiac disease itself, there is increasing serological evidence, both from Europe and the USA, that the
incidence among healthy blood donors is ~ 1:250 (3, 4, 5, 6, 7).
There is further evidence that in patient populations with neuropathies of unknown etiology, the incidence of
celiac disease runs as high as 35% (8).
To my knowledge, no epidemiological studies have been done among cancer patients, but there is some basis
for speculating that, while not a carcinogen per se, some fractions of the cereal grain proteins which are toxic
to celiacs, may also be involved in the downregulation of natural killer cell activation, thus contributing to
the incidence and progression of a variety of malignancies. (9)
1. Arnason J, Gudjonsson H, Freysdottir J, Jonsdottir I, valdimarsson H. Do adults with high gliadin
antibody concentrations have subclinical gluten intolerance? Gut 1992; 33 (2): 194-197.
2. Not T, Horvath K, Hill I, Fasano A, Hammed A, Magazzu G, "ENDOMYSIUM ANTIBODIES IN
BLOOD DONORS PREDICTS A HIGH PRVALENCE OF CELIAC DISEASE IN USA"
_Gastroenterology_ Supplement April, 1996; 110(4): A 351
3. Challacombe, David "When is coeliac" _Lancet_ 1994; 343: p188
4. Tighe & Ciclitira "The implications of recent advances in coeliac disease" _Acta Paediatr_ 1993; 82: 805810
5. Corrao G, Corazza G, Andreani M, Torchio P, Valentini R, Galatola G, Quaglino D, Gasbarrini G, di Orio
F, "Serological screening of coeliac disease: choosing the optimal procedure according to various prevalence
values" _Gut_ 1994; 35: 771-775
6. Ladinser B, Rossipal E, Pittschieler K, "Endomysium antibodies in coeliac disease: an improved method"
_Gut_ 1994; 35: 776-778
7. Malnick S, Lurie Y, Bass D, Geltner D, "Screening of coeliac disease" _Lancet_ 1994; 343: 675
141/298 (1997)
8. Hadjivassiliou M, Gibson A, Davies-Jones G, Lobo A, Stephenson T, Milford-Ward A, "Does cryptic

gluten sensitivity play a part in neurological illness?" _Lancet_ 1996; 347: 369-371
9. Hoggan R, "Considering Wheat, Rye, Barley, and Oats Proteins as Aids to Carcinogens" _Medical
Hypotheses_ In Press
From Loren Cordain's post of June 4:
5. Eating raw cereal grains (as well as cooked cereal grains) wreaks enormous havoc on the primate gut
because of their high antinutrient content. Additionally in virtually every animal model studied (dog, rat,
guinea pig, baboon etc - citations available if you want them), high cereal grain promotes and induces
rickets. I havent even touched upon the other antinutrients which inflict damage on a wide variety of human
physiological systems - these antinutrients include protease inhibitors, alkylrescorcinols, alpha amylase
inhitors, molecular mimicking proteins ect). Clearly, unprocessed cereal grains cannot contribute substantial
calories to the diet of primates unless they are cooked and processed.
Hi Loren,
I would appreciate such citations as you offer. I'm sure I have some. One on dogs done here in Canada, and
one on cats. But I've never heard of the others and would welcome them, as I'm sure many list members
would.
Thanks, Ron Hoggan
PALEODIET Archives
From: Sarah Mason
Date: Fri, 6 Jun 1997 16:04:50 +0000
Dean Esmay and Loren Cordain have made some interesting arguments against the role of cereal grains
(defined as the seeds of Gramineae - the grass family) in pre-agrarian diet. I would like to present some
discussion regarding some of the points raised:
1. Dean says:
> I think instead it seems easier to use deductive reasoning in trying to define a "paleodiet": it
> can probably best be defined by what it lacks, rather than by what it contains. We can never know
> precisely what a pre-human living in plains 25, 000 years ago ate, but we can probably take very
> educated guesses about what he did -not- eat, and from that as a starting point we can start
> adding in what we think he -did- eat within reasonable guessing parameters.
Such an argument fails to acknowledge the crucial role of archaeological data - we can construct -models- of
Palaeolithic diet based on deductive reasoning from many and varied sources, but we can only -test- these
models against finds from the archaeological record. These, unfortunately, can be more or less equivocal;
nevertheless, we can make weaker or stronger inferences about some of the foods that people are likely to
have been eating, based on the archaeological evidence. We can guess that it is -unlikely- that people ate
particular items, but, given the vagaries of the archaeological record, especially from early periods, absence
of evidence can never provide conclusive proof regarding this. So I would disagree with Dean on this point we can be -more- (though not wholly) definite about what people ate than about what they did not eat.
2. Dean continues:
> From this perspective I do not think it can be successfully argued that cereal grains such as
> rice, wheat, barley, and etc. were ever a part of the natural human diet prior to but a few
> millenia ago .... I have yet to find any respectable scientific reference which seriously suggests
> this might be so. The best argument that can be made is that possibly early man may have
> occasionally munched on wild grass seeds, but the idea that this would ever have been a daily
> staple seems quite far-fetched. I would be extremely interested in hearing about any research
> which suggests that it might be otherwise. Given the lack of evidence to the contrary and the
> simple fact that the idea of eating large quantities of cereal grains on a daily basis seems
> extremely difficult to imagine without a system of agriculture, it surely seems to that there's
> not much reason to think that cereal grains as a staple are in any way natural to the human animal.
Loren backs up Dean's arguments by citing the restricted distributions of wild ancestors of the major modern
domesticated cereals, and suggesting that
> Also, the wild version of these grains were much smaller than the domesticated versions and
> extremely difficult to harvest ...... Clearly, grass seeds have a world wide distribution and
> would have been found in most environments in which early man would have inhabited. However
142/298 (1997)
> because almost all of these seeds are quite small, difficult to harvest and require substantial
> processing before consumption (threshing, winnowing, grinding and cooking), it would have been
> virtually impossible for pre behaviorally modern humans (circa 35, 000-40, 000) to exploit this food
> source. To harvest and process grains on a large scale, sickles, winnowing trays (baskets),
> threshing sticks, grinding stones and cooking apparatus are required.
There is very good ethnobotanical, ecological, experimental and archaeobotanical evidence which can be
used to support a hypothesis of pre-agrarian grass seed use ('cereal' usually being confined to the seeds of
domesticated forms). As both Loren Cordain and Jennie Brand Miller have already suggested,
ethnoecological data, especially from Australia, western North America, and Africa suggest that wild grass
seeds can potentially contribute significantly to diet (see Harris, D. 1984. Ethnohistorical evidence for the
exploitation of wild grasses and forbs: its scope and archaeological implications. In Plants and Ancient Man.
W. van Zeist & W.A. Casparie (ed.), 63-69. Rotterdam: Balkema; Harlan, J.R. 1989. Wild grass-seed
harvesting in the Sahara and Sub-Sahara of Africa. In Foraging and Farming: The Evolution of Plant
Exploitation. D.R. Harris & G.C. Hillman (ed.), 79-98. One World Archaeology. London: Unwin Hyman).
Harlan's classic experiments demonstrated that wild grass seed harvesting can be extremely productive
(Harlan, J.R. 1967. A wild wheat harvest in Turkey. Archaeology 20: 197-201). Archaeobotanical evidence
for pre-agrarian Gramineae seed use (I'm excluding later pre-agrarian evidence here, since the arguments
seem to centre around Palaeolithic use, for which I'm assuming approximately a pre-Holocene cut-off point)
comes mainly from the Near East, with the best examples being the sites of Tell Abu Hureyra and Ohalo II
(though less categoric and/or relatively later finds have also been made in Epipalaeolithic levels from Wadi
Hammeh and Jericho) (see Hillman, G.C., S.M. Colledge & D.R. Harris. 1989. Plant-food economy during
the Epipalaeolithic period at Tell Abu Hureyra, Syria: dietary diversity, seasonality, and modes of
exploitation. In Foraging and Farming: The Evolution of Plant Exploitation. D.R. Harris & G.C. Hillman
(ed.), 240-268. One World Archaeology. London: Unwin Hyman; Kislev, M.E., D. Nadel & I. Carmi. 1992.
Epipalaeolithic (19, 000 BP) cereal and fruit diet at Ohalo II, Sea of Galilee, Israel. Review of Palaeobotany
and Palynology 73: 161-166).
3. The above cannot demonstrate, and nor am I suggesting that grass seeds necessarily ever constituted a major- portion of pre-agrarian diet, partly for reasons provided by Loren Cordain in his post (though in a
previous post I have also questioned the need to assume that foodstuffs were ever necessarily consumed as
'staples' equivalent to agricultural staples during the Palaeolithic). However, I am concerned particularly with
the way in which arguments surrounding this issue are apparently being used in the literature; and this brings
me to a crucial question surrounding the whole issue of 'palaeodiets'. Many of the references in opposition to
the use of cereal grains pre-agriculture are traceable to the work of Boyd Eaton (see Dean and Loren's
previous posts), whose reconstructions of 'Palaeolithic diet' derive from a combination of dietary studies of
recent peoples (both 'hunter-gatherers' and 'traditional agriculturalists'), and nutritional analyses of a range of
wild plant and animal foods. As an archaeologist I acknowledge the great usefulness of such data in erecting
hypotheses about pre-agrarian diet. However, I have two concerns about the use of such arguments by those
arguing for a 'Palaeolithic (dietary) prescription' for modern ailments. First, since much of the data used in
constructing arguments about a 'healthy' diet derives from studies of recent h-gs and traditional
agriculturalists, why is it felt necessary to go through the extra step of extrapolating such diets back to the
Palaeolithic to demonstrate that they might be good for us too? Notwithstanding arguments about our
common ancient genetic heritage, this seems to me an unnecessary step, replete as it is with the many
uncertainties that much of the debate on this list makes clear exist - if elements of dietary practice exhibited
by recent h-gs and agriculturalists can be demonstrated to be 'healthy', then any need to back this up by
referring to them as 'Palaeolithic' is not only superfluous, but may well be inaccurate. Which leads onto my
second point, which is that the desire to produce a model of Palaeolithic diet which supports
recommendations for a modern healthy diet is in many ways putting the cart before the horse, in that
arguments about the 'paleodiet' may be being influenced by opinions about what constitutes a 'healthy' diet;
and, most importantly (from my point of view anyway), may be preventing an objective approach to the true
nature of Palaeolithic diets.
PALEODIET Archives
Subject: More on cooking
From: Dean Esmay
Date: Fri, 6 Jun 1997 20:29:55 -0400
143/298 (1997)
Two interesting observations about the below:

1) Here is at least one hunter/gatherer people who seem to eat a fairly wide variety of foods (meats of many
varieties, corn, squash, melons, beans, edible tree bark, wild rice, although the meat seems most strongly
emphasized).
2) Here we have another example of a non-agriculturalist people eating grains, albeit that it is unclear what
percentage of the diet this would have been.
(Again, the below is supplied by Dave Chapman.)
From: Carver's Travels through North America in the Years 1766, 1767, and 1768 with Illustrations and
Maps, Carver, Jonathan, 1710-1780, J.Walter and S. Crowder, London, 1778.
CHAP. VI. Of Their Feasts.
Many of the Indian nations neither make use of bread, salt, or spices; and some of them have never seen or
tasted of either. The Naudowessies in particular have no bread, nor any substitute for it. They eat the wild
rice which grows in great quantities in different parts of their territories; but they boil it and eat it alone. They
also eat the flesh of the beasts they kill, without having recourse to any farinaceous substance to absorb the
grosser particles of it. And even when they consume the sugar which they have extracted fro the maple tree,
they use it not to render some other food palatable, but generally eat it by itself. Neither have they any idea
of the use of milk, although they might collect great quantities from the buffalo of the elk; they only consider
it as proper for the nutriment of the young of these beasts, during their tender state. I could not perceive that
any inconveniency attended the total disuse of articles esteemed so necessary and nutritious by other nations,
on the contrary, they are in general healthy and vigorous.
One dish however, which answers nearly the same purpose as bread, is in use among the Ottagaumies, the
Saukies, and the more eastern nations, where Indian corn grows, which is not only much esteemed by them,
but it is reckoned extremely palatable by all the Europeans who enter their dominions. This is composed of
their unripe corn as before described, and beans in the same state, boiled together with bears flesh, the fat of
which moistens the pulse, and renders it beyond comparison delicious. They call this food Succatosh.
The Indians are far from being canibals as they are said to be. All their victuals are either roasted or boiled;
and this in the extreme. Their drink is generally the broth in which it has been boiled.
Their food consists of the flesh of the bear, the buffalo, the elk, the deer, the beaver, and the racoon; which
they prepare in the manner just mentioned. The usually eat the flesh of the deer which is naturally dry, with
that of the bear which is fat and juicy; and though the latter is extremely rich and luscious, it is never known
to cloy.
In the spring of the year, the Naudowessies eat the inside bark of a shrub that they gather in same part of
their country; but I could neither learn the name of it, or discover from whence they got it. It was of a brittle
nature and easily masticated. The taste of it was very agreeable, and they said it was extremely nourishing. In
flavour it was not unlike the turnip, and when received into the mouth resembled that root both in its puplous
and frangible nature.
The lower ranks of the Indians are exceedingly nasty in dressing their victuals, but some of the chiefs are
very neat and cleanly in their apparel, tents, and food.
They commonly eat in large parties, so that their meals may properly be termed feasts; and this they do
without being restricted to any fixed or regular hours, but just as their appetites require, and convenience
suits. They usually dance either before or after every meal; and by this cheerfulness, probably, render the
Great Spirit, to whom they consider themselves as indebted for every good, a more acceptable sacrifice than
a formal and unanimated thanksgiving. The men and women feast apart: and each sex invite by turns their
companions to partake with them of the food they happen to have; but in their domestic way of living then
men and women eat together.
No people are more hospitable, kind, and free than the Indians. They will readily share with any of their own
tribe the last part of their provisions, and even with those of a different nation, if they chance to come in
when they are eating. Though they do not keep one common flock, yet that community of goods which is so
prevalent among them, and their generous disposition, render it nearly of the same effect.
When the chiefs are convened on any public business, they always conclude with a feast, at which their
festivity and cheerfulness knows no limits.
CHAP. XIX. Of the Trees, Shrubs, Roots, Herbs, Flowers, &c. ....
Farinaceous and Leguminous Roots, &c. Maize or Indian Corn, Wild Rice, Beans, the Squash, &c.
144/298 (1997)
MAIZE or INDIAN CORN, grows to the height of about five or six feet, on a stalk full of joints, which is
stiff and solid, and when green, abounding with a sweet juice. The leaves are like those of the reed, about
two feet in length, and three of four inches broad. The flowers which are produced at some distance from the
fruit on the same plant, grow like the ears of oats, and are sometimes white, yellow, or of a purple colour.
The seeds are as large as peas, and like them quite naked and smooth, but of a roundish surface, rather
compressed. One spike generally consists of about six hundred grains, which are placed closely together in
rows to the number of eight or ten, and sometimes twelve. This corn is very wholesome, easy of digestion,
and yields as good nourishment as any other sort. After the Indians have reduced it to meal by pounding it,
the make cakes of it and bake them before the fire. I have already mentioned that some nations eat it in cakes
before it is ripe, in which state it is very agreeable to the palate and extremely nutritive.
WILD RICE. This grain, which grows in the greatest plenty throughout the interior part of North America, is
the most valuable of the spontaneous productions of that country. Exclusive of its utility, as a supply of food
for those of the human species who inhabit this part of the continent, and obtained without any other trouble
than that of gathering it, in the sweetness and nutritious quality of it attracts an infinite number of wild fowl
of every kind, which flock from distant climes to enjoy this rare repast; and by it become inexpressibly fat
and delicious. In future periods it will be of great service to the infant colonies, as will afford them a present
support, until in the course of cultivation other supplies may be produced; whereas in those realms which are
not furnished with this bounteous gift of nature, even if the climate is temperate and the soil good, the first
settlers are often exposed to great hardships from the want of an immediate resource for necessary food. This
useful grain grows in the water where it is about two feet deep, and where it finds a rich muddy soil. The
stalks of it, and the branches or ears that bear the seed, resemble oats both in their appearance and manner of
growing. The stalks are full of joints, and rise more than eight feet above the water. The natives gather the
grain in the following manner: nearly about the time that it begins to turn from its milky state and to ripen,
they run their canoes into the midst of it, and tying bunches of it together just below the ears with bark, leave
it in this situation three or four weeks longer, till it is perfectly ripe. About the latter end of September they
return to the river, when each family having its separate allotment, and being able to distinguish their own
property by the manner of fastening the sheaves, gather in the portion that belongs to them. This they do by
placing their canoes close to the bunches of rice, in such position to receive the grain when it falls, and then
beat it out, with pieces of wood formed for that purpose. Having done this, they dry it with smoke, and
afterwards tread or rub it off the outside husk; when it is fit for use they put it into the skins of fawns or
young buffalos taken off nearly whole for this purpose and sewed into a sort of sack, wherein they preserve it
till the return of their harvest. It has been the subject of much speculation why this spontaneous grain is not
found in any other regions of America, or in those countries situated in the same parallels of latitude, where
the waters are as apparently adapted for its growth as in the climates I treat of. As for instance, none of the
countries that lie to the south and east of the great lakes, even from the provinces north of the Carolinas to
the extremities of Labradore, produce any of this grain. It is true I found great quantities of it in the watered
lands near Detroit, between Lake Huron and Lake Erie, but on enquiry I learned that it never arrived nearer
to maturity then just to blossom; after which it appeared blighted, and died away. This convinces me that the
northwest wind, as I have before hinted, is much more powerful in these than in the interior parts; and that it
is more inimical to the fruits of the earth, after it has passed over the lakes and become united with the wind
which joins it from the frozen regions of the north, that it is farther to the westward.
BEANS. These are nearly of the same shape as the European beans, but are not much larger than the smallest
size of them. They are boiled by the Indians and eaten chiefly with bear's flesh.
The SQUASH. They have also several species of the MELON or PUMPKIN, which my some are called
Squashes, and which serve many nations partly as a substitute for bread. Of these there is the round, the
crane-neck, the small flat, the large oblong Squash. The smaller sorts being boiled, are eaten during the
summer as vegetables; and are all of a pleasing flavour. The crane-neck, which greatly excels all the others,
are usually hung up for a winter's store and in this manner might be preserved for several months.
I am sensible the I have not treated the foregoing Account of the natural productions of the interior parts of
North America with the precision of a naturalist. I have neither enumerated the whole of the trees, shrubs,
plants, herbs, &c. that it produces, nor have I divided them into classes according to their different genera
after the Linnaean method: the limits of my Work, in its present state, would not permit me to pursue the
Subject more copiously. However, if the favour of the Public should render a future edition necessary, as I
trust, from the number of Subscribers who have already favoured me with their Names, will be the case, I
then propose the enlarge it considerably, and to insert many interesting particulars and descriptions, which
the size of the present Edition obliges me to curtail or entirely to omit.
145/298 (1997)
PALEODIET Archives
Subject: Re: More on cereal grains & response to Sarah Mason
From: Loren Cordain
Date: Sun, 8 Jun 1997 12:28:00 -0600
The following citations show that excessive whole cereal grain consumption ( > 50% of total calories) can
cause or exacerbate rickets and/or osteomalacia in both animals and man: (I inclued the articles on zinc
deficiency because it (zinc deficiency) has now been shown to retard skeletal growth (12).
1. Robertson I et al. The role of cereals in the aetiology of nutritional rickets: the lesson of the Irish National
Nutrition Survey 1943-8. Brit J Nutr 1981;45:17-22. 2. Ewer TK. Rachitogenicity of green oats. Nature
1950;166:732-33. 3. Sly MR. et al. Exacerbation of rickets and osteomalacia by maize: a study of bone
histomorphometry and composition in young baboons. Calcif Tissue Int 1984;36:370-79. 4. Ford JA et al. A
possible relationship between high extraction cereal and rickets and osteomalacia. Advances in Exp Med &
Biol 1977;81:353-62. 5. Ford JA et al. Biochemical response of late rickets and osteomalacia to a chupatty
free diet. Brit Med J 1972;ii:446-447. 6. MacAuliffe T. et al. Variable rachitogenic effects of grain and
alleviation by extraction or supplementation with vitamin D, fat and antibiotics. Poultry Science
1976;55:2142-47. 7. Hidiroglou M et al. Effect of a single intramuscular dose of vitamin D on concentrations
of liposoluble vitamins in the plasma of heifers winter-fed oat silage, grass silage or hay. Can J Anim Sci
1980; 60:311-18. 8. Reinhold JG. High phytate content of rural Iranian bread: a possible cause of human zinc
deficiency. Am J Clin Nutr 1971;24:1204-06. 9. Halsted JA et al. Zinc deficiency in man, The Shiraz
Experiment. Am J Med 1972;53:277-84. 10. Sandstrom B et al. Zinc absorption in humans from meals based
on rye, barley, oatmeat, triticale and whole wheat. J Nutr 1987;117:1898-1902. 11. Dagnelie PC et al. High
prevalence of rickets in infants on macrobiotic diets. Am J Clin Nutr 1990;51:202-08. 12. Golub MS et al.
Adolescent growth and maturation in zinc-deprived rhesus monkeys. Am J Clin Nutr 1996;64:274-82.
RESPONSE TO SARAH MASON'S LAST POSTING:
Clearly, present day and historical accounts of hunter-gatherers have shown that cereal grains have been
included in the human diet. Sarah's reference list on this topic is comprehensive and outlines most of the
better known citations. However, the point to be made here is that cereal grains rarely formed the bulk of the
daily caloric intake throughout the year of any of these peoples, and that for virtually all of the rest of the
studied hunter-gatherer populations, cereal grains were not consumed. Consequently, in view of optimal
foraging theory, it seems likely that during the late paleolithic and before, when large mammals abounded,
our ancestors would almost have never consumed the seeds of grass. As has been suggested by John Yudkin
almost 30 years ago, cereal grains are a relatively recent food for hominids and our physiologies are still
adjusting and adapting to their presence. Clearly, no human can live on a diet composed entirely of cereal
grains (for one thing they have no vitamin C). As I pointed out in my last posting, when cereal grain calories
reach 50% or more of the daily caloric intake, humans suffer severe health consequences. One has to look no
further than the severe pellagra epidemics of the late 19th century in America and the beri-beri scourges of
South East Asian to confirm this. The present day incidence of hypo-gonadal dwarfism in Iran (8, 9) lends
further support to this notion. Simoons classic work (Simoons FJ. Celiac disease as a geographic problem.
In: Food, Nutrition & Evolution, DN Walcher & N Kretchmer (Eds). NY, Masson Pub, 1981, 179-199) on
the incidence of celiac disease shows that the distribution of the HLA B8 haplotype of the human major
histocompatibility complex (MHC) nicely follows the spread of farming from the mideast to northern
europe. Because there is strong linkage disequalibrium between HLA B8 and the HLA genotypes which are
associated with celiac disease, it indicates that those populations with the least exposure to cereal grains
(wheat primarily) have the highest incidence of celiac disease. This genetic argument is perhaps the strongest
evidence to support Yudkin's observation that humans are incompletely adapted to the consumption of cereal
grains. Thus, the genetic evidence for human disease (in this case, I have used celiac disease, however other
models of autoimmune disease could have been used) is supported by the archeological evidence which in
turn supports the clinical evidence. Thus, the extrapolation of paleo diets has provided important clues to
human disease - clues which may have gone un-noticed without the conglomeration of data from many
diverse fields (archaeology, nutrition, immunology, genetics, anthropology and geography). So, in the case
of the celiac disease, we clearly are not putting the cart before the horse. For a celiac, a healthy diet is
definitely cereal free - why is this so - perhaps now the evolutionary data is finally helping to solve this
conundrum.
146/298 (1997)
PALEODIET Archives
Date: Sun, 8 Jun 1997 14:55:35 +0100
Dean asked for references to the notion that phytic acid in cereal grains causes calcium depletion. In 1992
Professor Harold H. Sandsted, who is Interim Editor-in-Chief of the American Journal of Clinical Nutrition,
the most important journal of nutrition, noted that "the evidence seems overwhelming that high intakes of
fiber sources that are also rich in phytate can have adverse effects on mineral nutrition of humans" and that,
"in view of the [reviewed] data, it appears that some health promoters who suggest that U.S. adults should
consume 30-35 g dietary fiber daily either have not done their homework or have simply ignored carefully
done research on this topic" [1]. My own opinion is that authorities who advocate cereals in a prudent
western diet largely do so for practical reasons [2].
So let's look do the homework. Whole meal cereals and other seeds have in their shells phytic acid which
strongly binds to minerals like calcium, iron, zinc and magnesium to form insoluble salts, phytates [1, 3-7]. It
is well known that whole meal cereals by this mechanism decrease the absorption of such minerals [1, 3-7].
There is apparently no adaptation to a habitual high intake of phytic acid [8] which is an important
contributing cause of iron deficiency in third world countries and possibly in the western world [9]. It is also
an important cause of mineral deficiency in vegetarians [10-12]. The most commonly studied minerals are
bound to phytic acid possibly in the following decreasing order: calcium, iron, zinc, magnesium (Fredlund K,
personal communication).
Mellanby found back in the 30s that young dogs got rickets when they were fed oatmeal [13]. He was made
aware of the calcium-binding effect of phytate [14] and showed that phytate was the dietary factor
responsible for inhibition of calcium absorption by oatmeal as well as the induction of rickets in dogs [15].
McCance and Widdowson found adverse effects of bread prepared from high-extraction wheat flour on
retention of essential metals by humans [16]. They also showed that destruction of phytate improved
retention of calcium [17]. Substantial evidence have later firmly established this negative impact of phytate
[1, 3-7]. Not even rats seem to be fully adapted to graminivorous diets since phytate adversely affects
mineral absorption in them as well [18].
In the archaeological record, rickets is rare or absent in preagricultural human skeletons, while the
prevalence increases during medieval urbanization and then explodes during industrialism [19]. In the year
1900, an estimated 80-90 per cent of Northern European children were affected [20, 21]. This can hardly be
explained only in terms of decreasing exposure to sunlight and descreased length of breast-feeding. An
additional possible cause is a secular trend of increasing intake of phytate since cereal intake increased
during the Middle Ages (Morell M, personal communication) and since old methods of reducing the phytate
content such as malting, soaking, scalding, fermentation, germination and sourdough baking may have been
lost during the agrarian revolution and industrialism by the emergence of large-scale cereal processing. The
mentioned methods reduce the amount of phytic acid by use of phytases, enzymes which are also present in
cereals [22-26]. These enzymes are easily destroyed during industrial cereal processing [27, 28].
It should be noted that dietary fiber alone has no impact on mineral absorption [5, 29] why a high intake of
fiber from fruits and tubers can safely be recommended, at least from this point of view.
Best regards to all of you,
Staffan
147/298 (1997)
1. Sandstead HH. Fiber, phytates, and mineral nutrition. Nutr Rev 1992; 50: 30-1. 2. Walker ARP, Walker
BF I. I. Fiber, phytic acid, and mineral metabolism. Nutr Rev 1992; 50: 246-7. 3. Spivey Fox MR, Tao S-H.
Antinutritive effects of phytate and other phosphorylated derivatives. In: Hathcock JN, ed. Nutritional
Toxicology. New York: Academic Press, 1989: 59-96. vol 3). 4. Harland BF. Dietary fibre and mineral
bioavailability. Nutr Res Rev 1989; 2: 133-47. 5. Rossander L, Sandberg A-S, Sandstr=F6m B. The
influence of dietary fibre on mineral absorption and utilisation. In: Schweizer TF, Edwards CA, ed. Dietary
fibre - a component of food. Nutritional function in health and disease. London: 1992: 6. Sandberg AS,
Hasselblad C, Hasselblad K, Hulten L. The effect of wheat bran on the absorption of minerals in the small
intestine. Br J Nutr 1982; 48: 185-91. 7. Morris ER. Phytate and dietary mineral bioavailability. In: Graf E,
ed. Phytic acid: Chemistry and applications. Minneapolis: Pilatus Press, 1986: 57-76. vol 4). 8. Brune M,
Rossander L, Hallberg L. Iron absorption: no intestinal adaptation to a high-phytate diet. Am J Clin Nutr
1989; 49: 542-5. 9. Hallberg L, Rossander L, Skanberg AB. Phytates and the inhibitory effect of bran on iron
absorption in man. Am J Clin Nutr 1987; 45: 988-96. 10. Harland BF, Smith SA, Howard MP, Ellis R, Smith
JJ. Nutritional status and phytate:zinc and phytate x calcium:zinc dietary molar ratios of lacto-ovo vegetarian
Trappist monks: 10 years later. J Am Diet Assoc 1988; 88: 1562-6. 11. Ellis R, Kelsay JL, Reynolds RD,
Morris ER, Moser PB, Frazier CW. Phytate:zinc and phytate X calcium:zinc millimolar ratios in selfselected diets of Americans, Asian Indians, and Nepalese. J Am Diet Assoc 1987; 87: 1043-7. 12. Gibson
RS. Content and bioavailability of trace elements in vegetarian diets. Am J Clin Nutr 1994; 59(5 Suppl):
1223S-1232S. 13. Mellanby E. A story of nutrition research.Baltimore: Williams & Wilkins Co, 1950 14.
Bruce H, Callow R. Cereals and rickets. The role of inositolhexaphosphoric acid. Biochem J 1934; 28: 51728. 15. Harrison D, Mellanby E. Phytic acid and the rickets-producing action of cereals. Biochem J 1934; 28:
517-28. 16. McCance R, Widdowsos E. Mineral metabolism of healthy adults on white and brown bread
dietaries. j Physiol 1942; 101: 44-85. 17. McCance R, Edgecombe C, Widdowson E. Mineral metabolism of
dephytinized bread. J Physiol 1942; 101: 18. Fairweather TS, Wright AJ. The effects of sugar-beet fibre and
wheat bran on iron and zinc absorption in rats. Br J Nutr 1990; 64: 547-52. 19. Stuart-Macadam PL.
Nutritional deficiency diseases: a survey of scurvy, rickets, and iron-deficiency anemia. In: Is=E7an MY,
Kennedy KAR, ed= . Reconstruction of life from the human skeleton. New York: Wiley-Liss, 1989: 201-22.
20. Gibbs D. Rickets and the crippled child: an historical perspective [see comments]. J R Soc Med 1994; 87:
729-32. 21. Hernigou P. Historical overview of rickets, osteomalacia, and vitamin D. Rev Rhum Engl Ed
1995; 62: 261-70. 22. Sandberg AS. The effect of food processing on phytate hydrolysis and availability of
iron and zinc. Adv Exp Med Biol 1991; 289: 499-508. 23. Svanberg U, Sandberg A-S. Improved iron
availability in weaning foods using germination and fermentation. In: Southgate DAT, Johnson IT,
=46enwick GR, ed. Nutrient Availability: Chemical and biological aspects. Cambridge: Cambridge
University press, 1989: 179-81. 24. Larsson M, Sandberg A-S. Phytate reduction in bread containing oat
flour, oat bran or rye bran. J Cereal Sci 1991; 14: 141-9. 25. Navert B, Sandstrom B, Cederblad A. Reduction
of the phytate content of bran by leavening in bread and its effect on zinc absorption in man. Br J Nutr 1985;
53: 47-53. 26. Caprez A, Fairweather TS. The effect of heat treatment and particle size of bran on mineral
absorption in rats. Br J Nutr 1982; 48: 467-75. 27. Sandberg A-S. Food processing influencing iron
bioavailability. In: Hallberg L, Asp N-G, ed. Iron Nutrition in Health and Disease. London: John Libbey,
1996: 349-58. 28. Sandstrom B. Food processing and trace element supply. In: Somogyi JC, Muller HR, ed.
Nutritional Impact of Food Processing. Bibl Nutr Dieta. Basel: Karger, 1989: 165-72. 29. Andersson H,
Navert B, Bingham SA, Englyst HN, Cummings JH. The effects of breads containing similar amounts of
phytate but different amounts of wheat bran on calcium, zinc and iron balance in man. Br J Nutr 1983; 50:
503-10.
PALEODIET Archives
Subject: Re: Add to the dangers of vegging out....
Date: Tue, 10 Jun 1997 01:08:57 +0100
> According to Professor Uri Seligson, insufficient levels of vitamin B-12 can lead to nervous
> system damage. He noted that these symptoms could develop in people strict vegetarians who eat no
> meat, dairy products or eggs.
> Awwww, that's not fair. As people age, they lose the "intrinsic factor" in their stomachs which is
> necessary for the absorption of B12. That's why they have sublinguals and shots of B12.
148/298 (1997)
Very fair indeed. It is well established knowledge, not just a notion by Seligson, that long term vegetarians,
most notably vegans, are at increased risk of vitamin B12 deficiency [Herbert V. Staging vitamin B-12
(cobalamin) status in vegetarians. Am J Clin Nutr 1992; 59: 1213S-22S].
"As people age..." should better be "As western people age...". Although this particular aspect of human
aging has not been studied in non-western populations, there are many other aging processes that are not
seen in such people. Accordingly, aging in the West is sometimes obviously quite different than true
biological aging.
Best regards
Staffan
PALEODIET Archives
From: Dean Esmay
Date: Wed, 11 Jun 1997 13:33:55 -0400
In response to Sarah mason's piece on Friday:
I believe Sarah makes a justifiable point. She is also not the first archaeologist to raise this objection. Just
days before her note to the list, another archaeologist made a similar point to me in private email. In
contemplating their messages I suspect that most archaeologists probably have very similar concerns and
may well be wondering if the rest of us are all daft.
From the point of view of an archaeologist, much if not most of our discussions are putting the cart before
the horse. They understand better than anybody the available evidence for what pre-agricultural humans ate
really is, how slim it is on certain points, how much debate there has been in this area, and where and how
those debates continue. It is in those debates that they center their attention. From the view of the
archaeologist, the object of "paleolithic nutrition" is to find out very specifically what exactly people ate
during a very specific and exact time period; to them the discussion is about that specific point. The idea of
applying this to modern life probably seems a bit odd. From their perspective a lot of the deductions made
about human diet prior to written history are only speculation and often not particularly scientific by the
standards of their field.
What I think some archaeologists may be missing is that they'll probably never have a complete picture and
will always have debate over many specific points. They may also miss that the results of their hunt in this
area has serious ramifications for those far beyond their field. The question of what humans evolved to eat is
an important one which may have tremendous impact on medicine and nutrition.
In fact, the concept of paleolithic nutrition as a model for a healthy diet for modern humans started among
anthropologists (Vilhjalmur Stefansson seems to have been the first), with people in medicine and nutrition
taking a strong interest some time later. That interest waxed and waned for a while but got serious I think
after Boyd Eaton revived serious interest in the subject in the 1980s.
The very name "paleolithic nutrition" probably suggests something far different and far more specific to an
archaeologist than it does to people outside that field. To the nutritionist, "Paleolithic nutrition" is about how
humans ate prior to agriculture; to the archaeologist, it implies examinatioon of precisely that particular
period in prehistory from about 750, 000 b.c. to roughly 15, 000 b.c. and furthermore would be about various
periods within the paleolithic, and various regions during those time periods.
I suspect that a lot of archaeologists are simply lost on a lot of these discussions because they're not entirely
sure what some of us are babbling about, and are probably wondering quite frequently why many of us are
generalizing strongly about certain things that, to them, ought not to be generalized about at all.
Sarah suggests that:
> First, since much of the data used in constructing arguments about a 'healthy' diet derives from
> studies of recent h-gs and traditional agriculturalists, why is it felt necessary to go through
> the extra step of extrapolating such diets back to the Palaeolithic to demonstrate that they might
> be good for us too? Notwithstanding arguments about our common ancient genetic heritage, this
> seems to me an unnecessary step, replete as it is with the many uncertainties that much of the
> debate on this list makes clear exist - if elements of dietary practice exhibited by recent h-gs
> and agriculturalists can be demonstrated to be 'healthy', then any need to back this up by
> referring to them as 'Palaeolithic' is not only superfluous, but may well be inaccurate. Which
> leads onto my second point, which is that the desire to produce a model of Palaeolithic diet which
> supports recommendations for a modern healthy diet is in many ways putting the cart before the
149/298 (1997)
> horse, in that arguments about the 'paleodiet' may be being influenced by opinions about what
> constitutes a 'healthy' diet; and, most importantly (from my point of view anyway), may be
> preventing an objective approach to the true nature of Palaeolithic diets.
The very concept of paleolithic diet (or exercise) as a healthy modern lifestyle is a theoretical model, not a
proven proposition. And it is much more a medical or biological model than an archaeological one. Although
it may be of some interest to the archaeologist, I don't think the archaeologist should take it very seriously in
his quest to learn -in his field-. The biological model may be an interesting thing for him to contemplate and
might provide him with a flash of insight, but might equally be a distraction or lead him in directions he
needn't necessarily go.
But without the evidence from the evolutionary record, the medical side of this discussion grinds to a halt.
Who would seriously suggest that the diet of the Pygmie, the Australian Aborigine, the Watusi, and the Inuit
have something in common, or anything meaningful to contribute to modern ideas of nutrition? What
compelling basis would there be for any such theory? The only basis, realistically, seems to lie in the fact
that most of the evidence suggests that modern hunter/gatherers have a lifestyle that probably more closely
resembles that of pre-historic humans than anything or anyone else in the modern world (although
Lindeberg's work with the Kitava provides an interesting, if closely related, alternative view). The only
reason we would think their lifestyle would have much to teach us in the field of nutrition is because they
appear to be the peoples closest to the evolutionary roots we sprang from.
Medical research is full of conflicting theories and ideas. Nutritional research as a field is chaotic and filled
with a shameful amount of politics; large corporate agricultural interests fund research testing the alleged
health benefits of vegetarianism or whole grain foods, ethical vegetarians fund studies to test the proposition
that meat is carcinogenic and atherogenic, margarine manufacturers fund studies attempting to show that
butter kills and vegetable oil is "heart-healthy, " egg manufacturers fund studies showing that eggs are good
for you, and so on and so forth. And because human biology is such a very complicated thing, it is terribly
easy to come up with facts that support a wide variety of theories. Furthermore, the pace of much medical
research is achingly slow and terribly specific to the point at times of being not very useful without much
more research. The simple question of whether or not saturated fat is atherogenic has been fought over for
decades, and just when the issue seemed settled has started again in recent years with people on both sides
growing quite vociferous. In general medical research in areas like this one moves in terribly tiny
increments.
Furthermore, a tremendous amount of research in nutrition, ever since the earlier parts of this century
(starting with Kellogg, I think) has been driven by people who advocate vegetarianism or near-vegetarianism
as the "natural" human diet. In fact it's surprising how often you'll hear well-educated people in the field of
nutrition or medicine claim that human beings evolved as herbivores! Such claims are -astonishinglycommon--not in the published literature per se, but in medical schools, schools of nutrition, and popular
books on nutrition written by people who really ought to know better. Nutritional research itself doesn't
suggest this openly, but a great deal of research in this area is driven, consciously or unconsciously, by these
kinds of assumptions. Paleontology and archaeology ought to be helping us answer these questions, and a
great many others.
Let me use another example: Start as a medical researcher with the proposition that humans did not evolve to
eat large amounts of cereal grains on daily basis. Examine the archaeological evidence for this. Find that
there is some support for this common-sense theory, and not much to refute it. Now from the perspective of
an archaeologist perhaps you haven't gotten anything, but to the medical researcher you've opened up a vast
new field of inquiry. You can test this idea further and see if you can't find a link between certain medical
problems and widespread grain consumption. If you can then find a correlation (and some have done so), you
can try direct lab research to see if you can figure out what about the grains might be troublesome, if
anything.
This chain of events can't happen without having that theoretical model in the first place. If indeed there IS
something in cereal grains that causes many modern diseases, you might spend years, even centuries, before
you stumble upon that link if you didn't have that theoretical model to base your explorations on. Who
otherwise would look to the harmless and wholesome bread everyone so enjoys as a possible cause of
rheumatoid arthritis, multiple sclerosis, or cancer? Yet there are researchers seriously looking at such
questions now--some of them are on this list. For example, there is at least one researcher on this list who is
looking at a "paleolithic diet" model of nutrition as a possible treatment for multiple sclerosis.
150/298 (1997)
The discomfort of the archaeologist in these discussions is both understandable and serious, but also may be
missing an important point. If archaeology can provide useful insights to people in other fields, then that is a
tremendous contribution. To be more melodramatic, if archaeological data can provide inspiration and
insight into theories in medicine which eventually lead to improving the quality of life for millions of people,
even saving lives, that's impressive indeed. It's probably not why you got into archaeology, in fact that was
probably the furthest thing from your mind at the time, but it represents (to me) one of the most exciting
ways in which one field can cross-pollinate with another to bring about wonderful results.
To me it seems that the goal for the archaeologist, when discussing the medical model of "paleolithic
nutrition, " would be to either ignore it completely as a distraction (which may well be the best course of
action), or to attempt to test that model, disproving its assumptions if possible or adding supporting data if
not.
This does leave me in a difficult position with this list. It seems that the archaeologists may have a
completely different agenda for what they want to talk about than the biologists and physicians. My hope has
been that the archaeologists among us (and we have at least a dozen among our membership, most of whom
have remained silent so far!) would be able to provide data which either supports or contradicts the medical
model--or to give simple insights to various points of contention such as, "Well yes there is some support for
that, and here's why, " or "No I don't think you can find support for that, and here's way." I had also hoped
that archaeologists would be able to glean some ideas and insights from other fields, and perhaps share data
with each other, but perhaps that's not possible?
PALEODIET Archives
Subject: Re: More on cereal grains & response to Sarah Mason
From: Sarah Mason
Date: Wed, 11 Jun 1997 16:40:01 +0000
Loren Cordain responded to my own previous post on cereal grains by emphasising that:
> .... the point to be made here is that cereal grains rarely formed the bulk of the daily caloric
> intake throughout the year of any of these [ethnographically-recorded] peoples, and that for
> virtually all of the rest of the studied hunter-gatherer populations, cereal grains were not
> consumed. Consequently, in view of optimal foraging theory, it seems likely that during the late
> paleolithic and before, when large mammals abounded, our ancestors would almost have never
> consumed the seeds of grass.
> As has been suggested by John Yudkin almost 30 years ago, cereal grains are a relatively recent
> food for hominids and our physiologies are still adjusting and adapting to their presence.
> Clearly, no human can live on a diet composed entirely of cereal grains (for one thing they have
> no vitamin C). As I pointed out in my last posting, when cereal grain calories reach 50% or more
> of the daily caloric intake, humans suffer severe health consequences.....[the] genetic argument
> [regarding celiac disease] is perhaps the strongest evidence to support Yudkin's observation that
> humans are incompletely adapted to the consumption of cereal grains.
151/298 (1997)
I would suggest that there is a very big difference between never consuming the seeds of grass and a point
where they comprise as much as 50% of caloric intake. Most research on hunter-gatherer diets indicates the
broad range of resources which are utilised, and their consequent dietary diversity; and current theories and
evidence surrounding the transitions to an agricultural economy, though they may approach the subject from
varying angles, almost all inevitably imply a decrease in the number and range of foodstuffs utilised (as a
cause, or consequence, of increasing focus on the small range of domesticated resources) [for summaries see
especially Hillman, and Hillman et al. in Foraging and Farming: The Evolution of Plant Exploitation. D.R.
Harris & G.C. Hillman (ed.), 240-268. One World Archaeology. London: Unwin Hyman; also Hillman in
Harris, D.R. (ed.). 1996. The Origins and Spread of Agriculture and Pastoralism in Eurasia. London: UCL
Press]. Thus I suspect that few hunter-gatherer peoples are likely to have fulfilled as much as 50% of their
caloric needs from -any- single resource - e.g., the highest estimate that I know of for the role of acorns in
the diet of native Californians, who are frequently cited as being at the extreme end of high reliance on one
wild resource (though even here, several different species of oak were invariably involved), was suggested
by Steven Powers in 1877 to have been as much as 56%, but subsequent research suggests this is likley to be
very much an overestimate, and has emphasised the high diversity of diet even within this group of peoples
[Heizer, R.F. & A.B. Elsasser. 1980. The Natural World of the California Indians. California Natural History
Guides 46. Berkeley: University of California Press; McCorriston, J. 1994. Acorn eating and agricultural
origins: California ethnographies as analogies for the ancient Near East. Antiquity 68: 97-107]. The only
possible exceptions to this that I can think of are perhaps some of the Arctic groups - but did even they
obtain more than 50% over the year from any one animal species? If the adverse dietary consequences of
cereal intake are not great until an intake of 50% or so is reached, could this not imply that genes providing
adaptations to cereals would have little selective advantage with a lower proportion in the diet? If that was
the case, then absence of adaptations would not necessarily imply an absence of some (less than 50%) role in
diet before agriculture (I'm not clear to what extent the proteins related to celiac diseases are, in any case,
present in all wild grasses). To say that cereals formed less than 50% of diet (which in any case is far greater
than any estimate I imagine would seriously be given by even the more strenuous advocates of a large role
for plant foods in pre-agrarian diet) is quite different from saying that 'our ancestors would almost have never
consumed the seeds of grass'. As Loren suggests, many estimates, (see, e.g., those cited by Hillman in some
of the above publications), often based on some from of optimal foraging argument do indeed suggest that
wild grasses would only be a -favoured- resource, and become more intensively-utilised in certain
specialised circumstances, such as inceased resource stress.
In other words I'm happy to agree with Loren that, in the case of celiac disease the coming together of data
from the fields of archaeology, nutrition, immunology, genetics, anthropology and geography...
has provided important clues to human disease but would argue that this is most informative in relation to
arguments regarding the role of cereals in the diet of people, and the spread of intensive cereal use -after- the
introduction of agriculture; I'm also happy to agree that -it's likely that- wild grasses are unlikely to been the
sole major provider of calories for pre-agrarian peoples. However, I would argue that while the
genetic/evolutionary argument can certainly allow us to suggest that cereals were not important enough in
pre-agrarian diet to have led to any significant adaptations to their use, it cannot be used to argue that they
cannot have had -any- significant role. Evidently, semantics may be one problem here (depending on how
one wishes to define significant); and as I've suggested in previous posts, I think that assumptions about the
fact that pre-agrarian/Palaeolithic peoples must have utilised 'staples' (in the sense of single, or a very small
number of, foods which comprised the bulk of their diet) may also be responsible for producing conflicting
hypotheses about the potential roles of different foods in palaeodiets.
PALEODIET Archives
Subject: Re: Just a little bit more on cereal grains
From: Loren Cordain
Date: Wed, 11 Jun 1997 17:39:00 -0600
152/298 (1997)
I agree in principal with Sarah's comments & suspect, as Sarah mentioned, that most of our differences
perhaps lie in the semantics of the argument. Clearly our ancestors were opportunistic and relied upon a wide
variety of species (both plant and animal) to sustain themselves. The point to be made here is that the
archaelogical data supports the clinical, biochemical and genetic data indicating that the human dietary
experience with cereal grain consumption is quite recent and that our present day physiologies have not
completely adapted to consumption of this ubiquitous food. As a discussion group, we have not even touched
upon the role cereal grains have in inducing autoimmune disease (except for a few discussions upon celiac
disease). There is substantial evidence (both epidemiological, and clinical) showing the role cereal grains
may play in the aetiology of such diverse autoimmune diseases as MS, Insulin dependent diabetes mellitus
(IDDM), rheumatoid arthritis, sjogrens syndrome, dermatitis herpetiformis, and IgA nephropathy. Although
this proposal may at first seem preposterous, there is strong data to suggest that cereal grains may be
involved in all of these diseases through a process of molecular mimicry whereby certain amino acid
sequences within specific poly peptides of the gramineae family are homologous to a variety of amino acid
sequences in mammalian tissue. These homologous amino acid sequences can ultimately confuse our
immune systems so that it becomes difficult to recognize "self" from "non-self". When this happens, T-cells
among other immune system components, launch an autoimmune attack upon a body tissue with AA
sequences similar to that of the the dietary antigen. It seems that grass seeds (gramineae) have evolved these
proteins with similarity to mammalian tissue to protect themselves from predation by mammals, vertebrates
and even insects. This evolutionary strategy of molecular mimicry to deter predation or to exploit another
organism has apparently been with us for hundred's of millions of years and is a quite common evolutionary
strategy for viruses and bacteria. It has only been realized since about the mid 80's (Oldstone MBA.
Molecular mimicry and autoimmune disease. Cell 1987;50:819-20) that viruses and bacteria are quite likely
to be involved in autoimmune diseases through the process of molecular mimicry, and with a little bit of
luck, our group will hopefully publish a review paper in the next 6 months or so compiling the evidence (and
it is extensive) implicating cereal grains in the autoimmune process. As Dean mentioned, without the
evolutionary template and without the evidence provided us by the anthropological community showing that
cereal grains were not part of the human dietary experience, the idea that cereal grains had anything to do
with autoimmune disease would probably had never occurred to us. This new electronic medium has allowed
instant cross fertilization of disciplines which probably would have rarely occurred as recently as 5 yrs ago.
Cordially,
Loren
PALEODIET Archives
From: Ron Hoggan
Date: Wed, 11 Jun 1997 18:27:08 -0700
Let me begin by saying that I am thirlled by today's posts from Sarah Mason and Dean Esmay. Such
discussions are the very reasons I wanted to participate in this list.
On Wed, 11 Jun 1997 13:33:55 -0400 Dean Esmay wrote:
> What I think some archaeologists may be missing is that they'll probably never have a complete
> picture and will always have debate over many specific points. They may also miss that the results
> of their hunt in this area has serious ramifications for those far beyond their field. The
> question of what humans evolved to eat is an important one which may have tremendous impact on
> medicine and nutrition.
This is, in my opinion, an extremely important point worth exploring just a little further. In: Armelagos G,
Van Gerven D, Martin D, and Huss-Ashmore R, "Effects of Nutritional Change on the Skeletal Biology of
Northeast African (Sudanese Nubian) Populations" _From Hunters to Farmers_ Clark J, & Brandt S. eds. U
of California Press, 1984
They indicate that concommitant with the advent of agriculture, associated skeletal remains revealed
significant skeletal changes including: cranial morphology; porotic hyperostosis; bone growth patterns;
microdefects in dentition; and premature osteoporosis in juvenile and young women.
153/298 (1997)
These conditions could be attributed, for the most part, to a dietary crisis which preceeded the cultivation of
cereals, rather than the result of such cultivation. There is, however, an exception to this generalization.
Porotic hyperostosis is well established as the result of iron deficiency anemia. It happens that the proximal
duodenum is both the site of earliest damage to the intestinal microvilli, in gluten reactions, and the site of
most iron absorption.
Without such archaeological evidence, medical assessment could not occur.
> First, since much of the data used in constructing arguments about a 'healthy' diet derives from
> studies of recent h-gs and traditional agriculturalists, why is it felt necessary to go through
> the extra step of extrapolating such diets back to the Palaeolithic to demonstrate that they might
> be good for us too?
That is not quite how I see this as working. The arguments used to deny the pathogenic nature of cereals
point to the long, healthy heritage of their cultivation and consumption. A fair response to such an argument
is to offer evidence to the contrary.
> Which leads onto my second point, which is that the desire to produce a model of Palaeolithic diet
> which supports recommendations for a modern healthy diet is in many ways putting the cart before
> the horse, in that arguments about the 'paleodiet' may be being influenced by opinions about what
> constitutes a 'healthy' diet; and, most importantly (from my point of view anyway), may be
> preventing an objective approach to the true nature of Palaeolithic diets.
But if we can have a sense of human dietary habits during the bulk of the evolution of our predecessors, we
may be able to counter some of the malignacy and autoimmunity which is torturing and killing much of the
Western world. Modern medicine does much to aid us in our battle against bacteria and injury, but they are
quite ineffective when it comes to civilizatory diseases.
> The discomfort of the archaeologist in these discussions is both understandable and serious, but
> also may be missing an important point. If archaeology can provide useful insights to people in
> other fields, then that is a tremendous contribution. To be more melodramatic, if archaeological
> data can provide inspiration and insight into theories in medicine which eventually lead to
> improving the quality of life for millions of people, even saving lives, that's impressive indeed.
> It's probably not why you got into archaeology, in fact that was probably the furthest thing from
> your mind at the time, but it represents (to me) one of the most exciting ways in which one field
> can cross-pollinate with another to bring about wonderful results.
And there is some possibility of aiding in archaeological discovery. For instance, declines of certain
populations might be explained in light of evidence that suggests that cereal grains may be a factor in
lukemia and lymphoma. Increased consumption of cereals might lead to increases in consequent deaths. I
would think that could be a powerful bit of information in the hands of an archaeologist trying to unravel a
mystery involving lost civilizations.
PALEODIET Archives
Subject: Re: Molecular mimicry and evolution
Date: Thu, 12 Jun 1997 21:57:19 -0500
Jennie Brand Miller writes:
> In her last posting, Loren wrote:
> 'This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism
> has apparently been with us for hundred's of millions of years and is a quite common evolutionary
> strategy for viruses and bacteria.' Wouldn't this mean that the foods that we have exploited most
> often for the longest period of time, should be the highest source of these molecules, not the
> foods (like cereals) that we've adopted most recently?
154/298 (1997)
It might if one assumed that plants were constantly evolving strategies of molecular mimicry while the
animals that preyed on the plants weren't countering the mimicry with ever-evolving immune-system
strategies of their own. One key evolutionary characteristic of the predator/prey relationship (in this case
foraging animals vs. the plants that are their "prey") is that it is an *arms race*--i.e., it is *ongoing*, not a
situation of evolutionary stasis that allows one side to continue developing its arsenal while the other side
simply stands still becoming a victim. (Or more accurately, if one side cannot cope over evolutionary time
and *does* become a victim, then it goes exteinct.) Each side tends to be continually responding to the need
to evolve new survival strategies in response to whatever "opponents" they face change what *they* do over
time.
Thus, just because plants that we have been associated with for long periods of evolutionary time could be
expected to evolve ever-more-sophisticated strategies of molecular mimicry against a long-familiar
adversary doesn't mean that we the adversary have a biology or physiology that is just sitting there doing
nothing about it. Because we are a moving target. Our bodies, too, are continually evolving new strategies to
counter the deterrent mechanisms of the plants that counter ours. But of course when changes are introduced
suddenly (as would be the case with grains in the human diet right now) there is something of a time lag
where "evolutionary discordance" prevails while the species is still working out an evolutionary coping
strategy.
However, so far, this way of looking at it only considers *adversarial* evolutionary relationships. It is easy
to overlook--when characterizing plants' and animals' evolutionary strategies in regard to each other as
adversarial--that just as importantly relationships may end up being *symbiotic* instead. For example, take
the classic example of fruits. Fruits in some sense symbiotically exploit the animals that eat them by using
them as seed dispersers (through their feces). So the relationship in this kind of situation is advantageous to
both sides.
On yet a third hand, sometimes the relationship between predator and prey is at the same time a complex
mixture of both symbiois *and* that of adversary. For instance, carnivores that prey on herbivores may help
keep the herds thinned out which keeps them from overgrazing the landscape and going through seasonal
die-offs from overshooting the landscape's capacity to support them. Things can get complicated.
However, one would still expect as a general rule that those foods (or environmental conditions, or any input
or stressor for that matter) that a species has had the least exposure to would be the ones with which
*mutual* evolutionary coping strategies would not yet have been worked out (mutual is the key word here)-whether that mutual relationship be symbiotic in nature or adversarial, or what-have-you (however complex).
Think of the cases where species alien to another environment (starlings, Dutch elms, etc.) have been
suddenly introduced. The result is normally a period of instability before things settle down into some sort of
long-term balance.
No matter what the selective pressures are--whether they be food, environment, or whatever--one of the
foundational assumptions of evolution as a paradigm (and of the things that gives it part of its explanatory
and predictive power) is that *anything* significantly new in evolutionary terms is almost inevitably going to
be *discordant* with the species adaptation; and there will necessarily be a time lag before evolutionary
selective processes have a chance to weed things out to establish more of a balance. Even if that "balance" is
a dynamically shifting one as in an arms race, or one of symbiosis, or both.
--Ward Nicholson
P.S.--By the way, Loren Cordain is not a she--he is a he! :-)
PALEODIET Archives
Subject: Practical Paleodiet
From: Ray Audette
Date: Thu, 12 Jun 1997 22:40:13 -0700
From the response I have received from my book, I know perhaps better than anyone how effective a
paleolithic diet can be for a wide variety of "diseases of civilization".
Although NeanderThin is primarily a high-fat, high-calorie weight loss book, I have never been overweight.
I wrote of my own experience in ridding myself of diabetes and rheumatoid arthritis (it took 1 week) by
following only one rule - Only eat that which is edible when you are naked with a sharp stick! From my
mail, it seems to reduce weight and blood sugar problems in all primates!
155/298 (1997)
Others have reported great results on a wide variety of health problems including colitis, MS, ALS, ADD,
Bipolar disorder (manic/depression), high cholesterol and blood preasure and many other auto-immune
problems. Readers have also reported improved muscle tone, stamina and recovery in athletic endevors.
Could these results be only a placebo effect of my charismatic writing style? In spite of my "mesiah
complex", I think not. If this rule was more widly applied would it save human suffering and billions of
health care dollars? I think so and have dedicated my life to this end.
That my self-published work is the only book currently in print on the topic of paleolithic nutrition is a very
sad state of affairs. Many of the members of this list (who have better credentials than my BS degree and
Mensa card)could correct this easily. The potential for fame and fortune is great (Dr. Adkins has sold over 30
million books)but more importantly, millions of people despritly need this information.
PALEODIET Archives
Subject: Molecular mimicry
Date: Fri, 13 Jun 1997 10:59:05 +1000
In her last posting, Loren wrote:
'This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism has
apparently been with us for hundred's of millions of years and is a quite common evolutionary strategy for
viruses and bacteria.'
Wouldn't this mean that the foods that we have exploited most often for the longest period of time, should be
the highest source of these molecules, not the foods (like cereals) that we've adopted most recently?
PALEODIET Archives
Subject: Re: Molecular mimicry
From: Kurt Starsinic
Date: Fri, 13 Jun 1997 16:32:49 -0400
Jennie Brand Miller writes:
> In her last posting, Loren wrote:
> 'This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism
> has apparently been with us for hundred's of millions of years and is a quite common evolutionary
> strategy for viruses and bacteria.' Wouldn't this mean that the foods that we have exploited most
> often for the longest period of time, should be the highest source of these molecules, not the
> foods (like cereals) that we've adopted most recently?
It is worth emphasizing that human consumption of grain is consumption of _ground_ seed. We don't
disperse viable grain seeds through our feces, as with fruit and vegetable seeds; and we cultivate and inbreed
grains, thus limiting diversification. Humans are, to the best of my understanding, the primary "predators" of
cereal grains. Evolutionarily speaking, if I were wheat, I would "have it in" for humans.
PALEODIET Archives
Subject: Re: Response to molecular mimicry comments
From: Loren Cordain
Date: Mon, 16 Jun 1997 14:07:00 -0600
156/298 (1997)
I appreciate Jenny's recent comment about my original posting on molecular mimicry. Having had a busy
weekend, I didnt get a chance to answer, but upon my return, I see that Ward Nicholson has done a superb
job in covering this topic. My only follow-up on this idea concerns the genetic evidence which supports the
concept. In the human immune system, there are a number of individual mechanisms which allow the body
the ability to determine self from non self so that foreign proteins (ie bacteria, viruses etc) can be recognized,
destroyed and eliminated. Perhaps the most complex system which nature and evolution have engineered to
accomplish this is the human leucocyte antigen (HLA) system. This system was discovered when early
physicians found out that tissue from one human could not be grafted to another without rejection. The
physiological function of this system was not to foil the efforts of transplant surgeons, but to initiate an
immune response to parasites (viruses, bacteria). All cells of the body manufacture HLA proteins, whose
function is to bind short peptides (protein fragments) and display them on the cell surface. Most of the
peptides are derived from the body's own proteins (self peptides), however when the body is infected by a
virus or bacteria, the HLA molecules pick up peptides derived from broken down proteins of the virus or
bacteria and present them to T lymphocytes. The purpose of T-lymphocytes is to continually scan the
surfaces of other cells to recognize foreign peptides while ignoring self peptides. Once a T cell receptor
"recognizes" a foreign peptide, a complex series of steps is set into play which ultimately destroys the cell
presenting the foreign peptide as well as living viruses or bacteria in the body which also have peptide
sequences similar to those which were presented. When the HLA system loses the ability to recognize self
(self peptides) from non-self (foreign peptides), T- lymphocytes attack self tissue resulting in what is known
as an autoimmune disease (i.e. celiac disease, IDDM, MS, Dermatitis Herpetiformis, ankylosing spondylitis
etc). The HLA proteins which present foreign peptides to circulating T lymphocytes are coded by DNA
sequences on chromosome 6. The entire HLA system includes more than 100 genes and occupies a region
more than four million base pairs in length which represent 1/3, 000 of the total human genome. On
chromosome 6, the HLA is sub-divided into Class I (HLA-A, HLA-B, HLA-C) and Class II segments (HLADR, HLA-DQ, HLA-DP). Individuals with autoimmune disease inherit characteristic HLA combinations
which identify their disease. People with celiac disease have genetic markers (HLA-DR3, HLA -B8 and
HLA-DQ2) which are associated with the disease; people with insulin dependent diabetes mellitus (IDDM)
almost always have DQ and DR genotypes. Thus, the manner in which foreign proteins are presented to
circulating T cells by HLA proteins tends to be different for individuals with auto-immune diseases
compared to those without these maladies. As I mentioned in a previous post, the incidence of a variety of
autoimmune diseases follows a southeasternly gradient from northern europe (highest incidence) to the
mideast (lowest incidence) - can provide citations if wanted. This gradient occurs because the incidence of
susceptible HLA haplotypes increases as one moves north westerly from the mideast. This gradient which
occurs for both the incidence of autoimmune diseases and HLA haplotypes is not a serendipitous relationship
but occurred as a result of the spread of agriculture from the mideast to northern europe (Simoons FJ. Celiac
disease as a geographic problem. In: Food, Nutrition & Evolution. DN Walcher & N Kretchmer (Eds), NY
Masson Pub, 1981, 179-199). Consequently, as agriculture spread into Europe there were environmental
elements associated with this demic expansion which progressively selected against HLA haplotypes
(combinations of HLA genes inherited from the two chromosomes in each cell) which were originally
present in the pre-agrarian peoples of Europe. Now, the question is, what were those environmental selective
elements? In the case of celiac disease, it doesnt take a rocket scientist to determine that it was wheat.
Increasing consumption of wheat caused increased mortality from celiac disease - thus, the incidence of
celiac disease and its susceptible HLA haplotypes (HLA-B8, HLA-DQ, HLA-DR) are lowest in those
populations with the most chronologic exposure to wheat (mideasterners and southern europeans) and
greatest in those populations with the least exposure (northern europeans). Similar arguments can be made
for IDDM and a host of other autoimmune diseases. There are a substantial number of animal studies
showing that consumption of wheat by rats increases the incidence of IDDM - citations available if wanted.
How is it that wheat can wreak such havoc with the autoimmune system? Our group believes that wheat
contains peptide sequences which remain undigested and which can enter into systemic circulation. These
peptide sequences are homolgous to a wide variety of the body's tissue peptide sequences and hence induce
autoimmune disease via the process of molecular mimicry (eg. macrophages ingest the circulating wheat
peptides and HLA molecules within the macrophage present amino acid sequences of the fragmented peptide
to circulating T-lymphocytes which through clonal expansion create other T cells to "attack" the offending
dietary antigen and any other self antigen which has a similar peptide sequence - i.e. the bodies own tissues).
The original non-agricultural HLA haplotypes conferred selective advantage because these genotypes
provided enhanced immunity from certain types of infectious diseases, however with the advent of cereals in
the diet they represented a liability. Thus, the genetic data clearly shows that a recently introduced food type
157/298 (1997)
has resulted in genetic discordance between our species and those from the gramineae family.
Cordially,
Loren Cordain, Ph.D. Professor, Colorado State University
-And yep! I'm not a her, but a him!
PALEODIET Archives
Subject: Announcement
From: STONE and SPEAR
Date: Thu, 19 Jun 1997 01:05:31 -0700
A variety of diets help a variety of folks in a variety of ways. Here are three private email Listserv groups
that cover three Lifestyles that I have found beneficial in controlling and dealing with my challenges leading
to more energy and a feeling of well being.
LC-DIABETES for Persons with Diabetes who control their carbohydrate intake to assist in the management
of their diabetes. Especially popular is the new book by a 50+ year Type I Richard K. Bernstein MD, the
Endocrinologist. But all diets and lifestyles are welcome. Archives at:
http://maelstrom.stjohns.edu/archives/lc-diabetes.html To subscribe email: put in the body of the message:
SUB LC-DIABETES YourFirstName YourLastName
PALEOFOOD is a Support Group for those who shy away the from grains, legumes and dairy products of
the post-agricultural era and instead consume fresh meat, fruit and veggies that would have been safely eaten
by Hunters & gatherers of the pre-agricultural period. Based on Ray Audette's NeanderThin "A Caveman's
Guide to Nutrition". Archives at: http://maelstrom.stjohns.edu/archives/paleofood.html To subscribe email:
put in the body of the message: SUB PALEOFOOD YourFirstName YourLastName
ATKINS-NEW is a Support Group who have discovered the benefits of low carbing by following the work
of Robert C. Atkins MD along with his approach to weight loss and dietary advice for disease control and
management as explained in his book Dr. Atkins' "New Diet Revolution". Archives at:
http://maelstrom.stjohns.edu/archives/atkins-new.html To subscribe email: put in the body of the message:
SUB ATKINS-NEW YourFirstName YourLastName
Looking forward to seeing you in one or more of the Groups
Grant
PALEOFOOD--> Hunter-Gatherer Lifestyle following "NeanderThin" LC-DIABETES-- All carbohydrate counting
> diets for Diabetes control ATKINS-NEW--- for followers of Dr. Atkins "New Diet Revolution"
> More information at: http://www.mountain-inter.net/~magnuson/
PALEODIET Archives
Subject: Counterfactuals
From: Art De Vany
Date: Thu, 19 Jun 1997 15:05:00 -0700
It is sometimes helpful to look at counterfactuals when seeking a deeper understanding. This strikes me as a
useful way to try to understand what features of the human adaptation evolved during the Paleolithic. How
much of our humanity, intelligence and failings emerged during this period? Who knows?
But, think of it this way. Ask the question: But for the Paleolithic, humans would be ... and fill in the blanks.
The essential features strike me as the abundant big game, the cold, the seasonality, and the big-game
hunting adaptation. So, here is the proposition (others on the list will have their own counterfactuals to
supply I hope)
Proposition: Paleolithic big-game hunting required courage, strength, and endurance. It also required wit and
a deep understanding of the animals, their migratory patterns, the seasons of the earth, and its topography.
These are the requirements of the Paleolithic human lifeway and they shaped every aspect of modern human
physiology and function.
158/298 (1997)
Had it not been for this critical period and its unique environment, human beings of our form would not have
evolved. But for the Paleolithic adaptation, humans would be smaller, have larger stomachs, and smaller
brains. They would be less intelligent. They would have less preference for meat as a food. They would not
have such a strong liking for fat. And they would be less capable of storing fat on their bodies. They would
be less cooperative and far less capable of thinking ahead. They probably would not bury their dead. And
they would be nearly devoid of spiritual beliefs.
PALEODIET Archives
Subject: Re: Counterfactuals
Date: Mon, 23 Jun 1997 10:01:26 +0100
On Fri, 20 Jun 1997, Art De Vany wrote:
> It is sometimes helpful to look at counterfactuals when seeking a deeper understanding. This
> strikes me as a useful way to try to understand what features of the human adaptation evolved
> during the Paleolithic. How much of our humanity, intelligence and failings emerged during this
> period? Who knows? But, think of it this way. Ask the question: But for the Paleolithic, humans
> would be ... and fill in the blanks.
We must be very careful when doing this as the Palaeolithic is a long period of time (at least 2.5 million
years).
> The essential features strike me as the abundant big game, the cold, the seasonality, and the
> big-game hunting adaptation. So, here is the proposition (others on the list will have their own
> counterfactuals to supply I hope)
This is an a high latitude Palaeolithic scenario, which applies to the last 5-700, 000 years of human
occupation in Europe, northern Asia and northern North America, it is not necessarily true of the rest of the
world. If we are interested here in anatomically modern humans then we must consider this to apply only to
the last 40, 000 years of human occupation in those high latitude regions.
> Proposition: Paleolithic big-game hunting required courage, strength, and endurance. It also
> required wit and a deep understanding of the animals, their migratory patterns, the seasons of the
> earth, and its topography. These are the requirements of the Paleolithic human lifeway and they
> shaped every aspect of modern human physiology and function. Had it not been for this critical
> period and its unique environment, human beings of our form would not have evolved.
Not entirely true. Most modern humans have a body shape which is not adapted for the cold of the last
glacial in Europe - our body shape is essentially that required for an African climate. (Although some
peoples have a body shape better adapted to cold than others [e.g. Eskimo].)
> But for the Paleolithic adaptation, humans would be smaller, have larger stomachs, and smaller
> brains. They would be less intelligent. They would have less preference for meat as a food. They
> would not have such a strong liking for fat. And they would be less capable of storing fat on
> their bodies. They would be less cooperative and far less capable of thinking ahead.
Much of the increase in brain size relative to other apes (measured by encephalisation quotient) had occurred
prior to the Palaeolithic when stone tool use began. Gut length was also decreasing to keep the body in
energy balance, according to the expensive tissue hypothesis. As the other deductions here follow on from
this we may deduce that they had also started to occur to a greater or lesser extent prior to the appearance of
the genus homo.
> They probably would not bury their dead. And they would be nearly devoid of spiritual beliefs.
These traits do not appear until the Upper Palaeolithic. We have hardly any evidence for burial of the dead
(which is construed as religious belief) until well into the Upper Palaeolithic of Europe. There are only 2 or 3
definite burials of Neanderthals and these have no sign of ritual practices. The earliest grave goods and art
are associated with Upper Palaeolithic humans, whose ancestors appear to have had the same anatomical
form for many tens of millenia before this time. The appearance of ritual is thus not linked to brain size or
anatomical form and is something of a mystery. It is however linked to changes in tool manufacture and the
introduction of bone tools alongside stone tools, which suggests some sort of mental change which cannot be
observed anatomically.
159/298 (1997)
The scenario described by Art as influencing human evolution is in fact one which modern humans adapted
to when they entered Europe c.45-35, 000 years ago, and after which point we can detect very little change to
their anatomy, although technology is changing. This "Palaeolithic human lifeway" is thus *not* what
moulded our evolution, but something which we adapted to in certain parts of the world.
PALEODIET Archives
Subject: Re: citations showing wheat's diabetogenicity
From: Loren Cordain
Date: Mon, 23 Jun 1997 11:52:00 -0600
In a previous posting, I mentioned that certain wheat peptides have been implicated in animal models of
insulin dependent diabetes mellitus (IDDM). The following references may be of interest to readers wanting
more information.
1. Scott FW et al. Evidence for a critical role of diet in the development of insulin dependent diabetes
mellitus. Diabetes Research 1988;7:153-57.
2. Elliott RB et al. Dietary protein: a trigger of insulin-dependent diabetes in the BB rat? Diabetologia
1984;26:297-99.
3. Hoofar J. et al. Prophylactic nutritional modeification of the incidence of diabetes in autoimmune nonobese diabetic (NOD) mice. Brit J Nutr 1993;69:597-607.
4. Scott FW et al. Diabetogenicity of various protein sources in the diet of the diabetes prone BB rat. In:
Advances in Experimental Medicine and Biology. RA Camerini-Davalos, HS Cole (Eds); vol 246; Plenum
Press, NY, 277-85.
5. Storlien LH et al. Laboratory chow-induced insulin resistance: a possible contributor to autoimmune type I
diabetes in rodents. Diabetologia 1996;39:618-20.
6. Effects of wheat germ agglutinin on insulin binding and insulin sensitivity of fat cells. Am J Physiol
1980;238:E267--E275.
7. Schechter Y. Bound lectins that mimic insulin produce persistent insulin like activities. Endocrinology
1983;113:1921-26.
8. Scott FW et al. Conference summary: Diet as an environmental factor in development of insulindependent diabetes mellitus. Can J Physiol Pharmacol 1991;69:311-319.
PALEODIET Archives
Subject: Re: New book
From: Art De Vany
Date: Tue, 24 Jun 1997 15:34:34 -0700
There is yet another new evolutionary diet book titled: Dr. Citron's Evolutionary Diet and Cookbook. I
haven't seen it and don't know the publisher, but Citron is doing some LA book signings this week. It was
featured in a Crown Books ad.
I, for one, do best on a modified evolutionary diet; it is more or less a mediterranean diet without the grains,
no milk or dairy products, and with rather more animal sources of protein, like eggs and lean meat. The focus
in this diet, for me, is on the antioxidant content of the olive oil, the fresh plant foods and fruits including the
vitamins C and E, the carotenoids, and the flavonoids. Plenty of variety is essential in order to (as Marge
Profet would say) diversify your toxins.
The sulpher containing amino acids that I get from eggs also contribute to endogenous antioxidant
production. The utility of 2 glasses of wine a day, and the resolution of the "French paradox", comes from
the flavonoids in the wine (I prefer beer which has the same flavonoid content). A red onion in your salad
with olive oil and balsamic vinegar is a far better way to get your flavonoids. B. Halliwell, "Antioxidants in
Human Health and Disease, " Amer. Rev. Nutr. 1996, 16:33-50.
A diet higher in fat, which I briefly tried, left me ravenous and I went from less than 8% body fat to around
11%. Since I had no visible fat, it was easy to see where I gained it --- it was in the adominal area over the
kidneys, the worst place. Sarah Mason has pointed to this connection in an earlier post. See also J. Blundell,
et. al. "Control of Human Appetite...." Amer. Rev. Nutr. 1996, 16:285-319.
160/298 (1997)
Given the seasonal variation in the fat content of big game in the upper paleolithic (I stand corrected for
using "paleolithic" rather too broadly, thanks to Andrew Millard's excellent posting), a selectively favorable
adaptation would have been a weak appetite suppression from the consumption of fat. Fattening up for the
winter by over-feeding on summer-fattened animals at the seasonal peak of caloric abundance would have
been adaptive.
Is the wide-spread, and seemingly culturally universal, antipathy to obesity also a selective strategy that
stems from the impending dietary stress at the onset of winter?
PALEODIET Archives
Subject: antipathy to obesity
From: "Kristen J. Gremillion"
Date: Wed, 25 Jun 1997 16:47:11 -0400
> On Tue, 24 Jun 1997, Art De Vany wrote:
> Given the seasonal variation in the fat content of big game in the upper paleolithic (I stand
> corrected for using "paleolithic" rather too broadly, thanks to Andrew Millard's excellent
> posting), a selectively favorable adaptation would have been a weak appetite suppression from the
> consumption of fat. Fattening up for the winter by over-feeding on summer-fattened animals at the
> seasonal peak of caloric abundance would have been adaptive. Is the wide-spread, and seemingly
> culturally universal, antipathy to obesity also a selective strategy that stems from the impending
> dietary stress at the onset of winter?
Antipathy to obesity is not a cultural universal. In fact, I believe it is primarily a recent phenomenon
confined largely to the world of Western European and descendant populations. Take a look at indigenous
representational art from around the world--including that of the European Upper Paleolithic. Assuming that
artistic representations are often (if not always) embodiments of the aesthetic sensibilities of a culture, body
fat is not/has not been cross-culturally reviled as either unhealthy or unattractive. In fact, many traditional
cultures consider obesity to be a sign of prosperity and therefore desirable in a potential spouse. I am not a
cultural anthropologist, and I don't have the references right at hand, but I can find them if necessary. There
is no doubt that many dietary practices that are adaptive in some way are supported by cultural values. I am
just questioning the generalization about attitudes toward obesity.
PALEODIET Archives
Subject: Calcium
Date: Thu, 26 Jun 1997 23:16:49 +0100
Paleolithic diets are expected to be beneficial for calcium balance for three reasons:
1 Calcium INTAKE from vegetables is high. This is because vegetables are rich in calcium when this is
measured in mg per unit of energy, actually close to dairy products, and because much of the western foods
are low in calcium (e.g. margarine, oil, sugar and cereals).
2 Calcium BIOAVAILABILITY is high when cereals, maize and beans are absent. These are rich in phytic
acid which strongly binds to calcium (and iron, zinc and magnesium) so that this is excreted without being
absorbed (Sandstead HH. Fiber, phytates, and mineral nutrition. Nutr Rev 1992; 50: 30-1).
3 Calcium LOSSES are apparently less when salt intake is low. A high sodium intake increases urinary
losses of calcium (Evans C, Eastell R. Adaptation to high dietary sodium intake. In: Burckhardt P, Heaney
RP, ed. Nutritional aspects of osteoporosis '94. Rome: Ares-Serono Symposia, 1995: 413-8. vol 7; Shortt C,
Flynn A. Sodium-calcium inter-relationships with specific reference to osteoporosis. Nutr Res Rev 1990; 3:
101-15; Schaafsma G, van BE, Raymakers JA, Duursma SA. Nutritional aspects of osteoporosis. World Rev
Nutr Diet 1987; 49: 121-59) and one study suggests that this may increase the risk of osteoporosis (Devine
A, Criddle RA, Dick IM, Kerr DA, Prince RL. A longitudinal study of the effect of sodium and calcium
intakes on regional bone density in postmenopausal women. Am J Clin Nutr 1995; 62: 740-5).
Several studies suggest that bioavailability and urinary losses of calcium are more important than intake
(Nordin BEC, Need AG, Morris HA, Horowitz M, Chatterton BE, Sedgwick AW. Bad habits and bad bones.
In: Burckhardt P, Heaney RP, ed. Nutritional aspects of osteoporosis '94. Rome: Ares-Serono Symposia,
1995: 1-25. vol 7).
161/298 (1997)
A no-salt no-cereal diet rich in saturating vegetables would thus seem to prevent osteoporosis.
PALEODIET Archives
Subject: Leon Chaitow
From: Dietmar Hartl
Date: Sat, 28 Jun 1997 04:27:23 -0700
I believe his surname is actually "Chaitow". He's a British/US/Jewish osteopath who's written TONS of
books (from "Acupuncture Treatment of Pain" & "Amino Acids in Therapy" to "Osteopathic SelfTreatment" & "Varicose Veins", among the 23 listed in my 1993 edition of "Ost. Self-Tx"). So he's definitely
"in the writing business", maybe more than in the "helping" business"? My own personal jury is out,
although I WAS happy with the 2 books of his that I've read.
PALEODIET Archives
Subject: Enig & Fallon Reply to Dr. Cordain
From: Date: Sun, 29 Jun 1997 09:26:30 -0400
To: Dr. Cordain and members of the Paleodiet Group Re: Answers to questions of May 26, 1997
First, many apologies for taking so long to respond to your excellent questions and comments of May 26.
Our replies follow:
1. You now have the reference for Voegtlin's book. As you point out, Voegtlin errs in asserting that plant
foods are needed to prevent scurvy. Uncooked or minimally cooked flesh of organs of animals contain either
vitamin C or a vitamin-C-like substance that prevents scurvy. Dr. Weston Price made this discovery when
studying the Indians of Northern Canada. (1) When they killed an animal, the Indians immediately divided
up the adrenal glands and gave a piece--raw--to every member of the tribe, and they understood that this
would prevent scurvy. Dr. Voegtlin is also wrong about vitamin K, which is found in butter and animal fats.
So it can be said that all the known vitamins, minerals and needed macronutrients can be obtained from
animal foods. However, we should not rule out the possibility that the various phyto-chemicals, alkaloids,
etc. found in plant foods, while not classified as vitamins, are necessary for optimal health, at least to some
individuals.
2. We have consistently argued that the current high levels of CHD have nothing to do with the consumption
of saturated fat from animal sources, (2, 3, 4) but rather are due to foods relatively new to the human diet-particularly excess polyunsaturates, hydrogenated oils and refined carbohydrates. The anti-cholesterol, antianimal-fat campaign is a phoney issue invented and promulgated by the vegetable oil and fabricated food
industries during the 50s and 60s in order to get the upper hand in marketing their products. It amounts to
propaganda designed to denigrate nutritious traditional foods so that the consumer will buy highly refined
and processed food items instead. The amount of saturated fat in the American diet remained the same
between 1935 and 1974--the period of greatest increase in heart disease.
3. The LDL/HDL issue is also phoney and does not stand up to rigorous scrutiny. LDL is necessary to carry
cholesterol from the liver to the cells, particularly to the brain cells, which unlike other cells in the human
body, do not manufacture cholesterol. However, it is true that oxidized LDL is a problem, and does initiate
foam cells in the arteries. Oxidized cholesterol is found in products that have been heated to very high
temperatures in the presence of oxygen, such as powdered eggs and milk. Powdered eggs are added to many
processed foods and powdered milk is added to 1% and 2% milk to give it body. People drinking reduced fat
milk in order to "avoid heart disease" are actually taking in large quantities of oxidized cholesterol which is a
causative factor. You are also right in pointing out that high levels of commercial polyunsaturated oils
(virtually all of which have a high N6 to N3 ratio) increase LDL oxidizability. It is the excess of
polyunsaturated oils that cause the problem--not the saturated fats, whether in the modern diet or in
traditional cuisines. In fact, SFAs have been shown to lower Lp(a) which, unlike total serum cholesterol,
HDL or LDL, is a very good marker for increased risk of CHD. (5)
162/298 (1997)
4. We believe that the amount of protein in the diet as related to CHD is another phony issue. One can point
to populations with relatively high protein consumption (30-40%) with little or no CHD, and to populations
with relatively low protein consumption (15-20%) with little or no CHD. In any event, we have no way of
knowing the exact ratios of macronutrients in the Paleolithic diet, and in fact, there probably was a lot of
variation depending on season, locality and tribal custom. The danger lies, as we pointed out in our article, in
diets high in animal protein but low in fat. This seems to have been generally recognized by the huntergatherer.
5. We would like to know what kind of fat combined with carbohydrates exacerbate the postprandial lipemic
excursions. We can well believe that excess polyunsaturated or trans fats would do this. We know that fats
taken with carbohydrates, especially traditional fats such as butter or any of the tropical oils, lower the
glycemic index, thereby preventing blood sugar swings. We are not aware of any studies showing
carbohydrates were eaten separately in pre-industrial societies. American Indians made pemmican from meat
or fish, fat, maple syrup and cranberries; succatash was made from meat, fat, beans and corn. Orthodox
dieticians/nutritionists contend that high carbohydrate diets improve blood lipid profiles. All this emphasis
on protein and carbohydrate content is, we believe, misplaced. The real issue is the kind and quality of the
macronutrients--how they are produced, processed and prepared.
6. We look forward to seeing your research and intriguing findings about the varying lengths of SFAs in wild
and domesticated animals. Stearic acid (18:0) has been shown to raise cholesterol in some studies--and in
any event, the whole cholesterol issue is bogus. There may be differences in the N6/N3 ratios in wild and
domesticated ruminant adipose tissue, but in both overall total PUFA is low. The real imbalances come with
modern farming methods (for eggs, fish, vegetables, etc.) and with the introduction of high N6 oils into the
diet. Excess N6/N3 ratios result in profound imbalances at the cellular level that can lead to MI, cancer and
many other diseases. (6, 7) We certainly do agree that high levels of N6 in the diet are a problem, but the
source of excess N6 is not domesticated beef and lamb.
7. We do not know when milk product consumption became general, but it is fair to assume that the adoption
of a nomadic/herder life-style--and therefore the domestication of animals--preceded agriculture. We cannot
understand how dairy products per se can be blamed for the CHD epidemic. Counter examples include
France (low CHD, high consumption of butter and cheese); Soviet Georgia (famed for longevity, high
consumption of whole milk products); the Masai (high consumption of whole milk products, no CHD);
Switzerland and Austria (life span almost as long as Japan, diet rich in butterfat and whole milk products)
and America at the turn of the century (diet loaded with butterfat and whole milk products, very little CHD.)
If CHD is associated with milk consumption within individual countries, the finger must be pointed at
modern production methods (inappropriate feed for the cows, cows bred to have a low butterfat content)
processing (pasteurization, homogenization) and additives (powdered skim milk containing oxidized
cholesterol and synthetic vitamin D2 or D3. Synthetic D2 has been very conclusively shown to cause
calcification of the soft tissues including the arteries, and large amounts of synthetic D3, which has largely
replaced D2 as an additive to milk, have been implicated as a causative factor in the initiation of pathogenic
lesion development in the arteries. (8) The N6-N3 ratio of the small amounts of PUFAs in bovine milk fat is
excellent--about 2/1--whereas total N6/N3 in the modern diet exceeds 20/1. So once again, while we agree
that high levels of N6 in the diet are a problem, the source of excess N6 is not butterfat. Dietary saturated fats
contribute to improved assimilation of EFAs. (9) In other words, we need less of the EFAs when there are
enough SFAs in the diet. Magnesium does seem to protect against CHD. The fault lies not with high levels of
calcium from milk products, but with the deficiency of magnesium in modern diets. Weston Price found that
the diets of healthy "primitives" contained at least four times the amount of calcium as the American diet of
his day (and ten times the fat-soluble vitamins A and D!) (1) Sources of magnesium include nuts, meat and
grains such as buckwheat.
8. As we stated earlier, modern man is not consuming high levels of SFAs compared to pre-agricultural man.
The blame for inactivity should be placed on the lower nutrient content of the total diet, composed as it is of
high levels of refined and devitalized foods. When the diet supplies all the needed factors, humans need no
incentives to exercise.
163/298 (1997)
9. Finally, on the question of salt, a distinction must be made between processed salt, which contains many
problematic chemicals including aluminium, and from which the magnesium salts and all the valuable trace
minerals have been removed. Modern salt comes attached to modern food products, which are invariably
refined, rancid and laced with additives; and it is difficult to separate salt from these other variables in
dietary research surveys. Some studies have shown that with low salt diets, hypertension becomes worse. In
the 1930s, researcher McCance demonstrated that when dietary salt is lowered, all manner of inappropriate
physiological responses ensue--including cramps, weakness, lassitude, loss of taste sensation and severe
cardiorespiratory distress on exertion. (10) The recent contribution to this debate, describing various
American Indian methods for using salty blood in the preparation of their meat, supports our contention that
Paleolithic diets contained sodium chloride. Salty animal blood and urine form an important part of the diet
in salt-poor Africa. The concentration of population, and the rise and fall of civilizations throughout the
world, can be positively correlated with the availability of salt. (11)
To summarize, the hypothesis that modern chronic diseases like CHD and cancer are due to consumption of
saturated fats, red meat, milk products and salt does not stand up to careful scrutiny. These have been in the
diets of healthy population groups for millennia. Media denigration of such traditional foods is a distraction
that diverts the attention of both the public and the scientific community from the real culprits--modern
farming techniques, inappropriate processing, refined carbohydrates, commercial vegetable oils, food
additives and rancid & altered fats.
P.S. The rest of citation #2 is Coronary Heart Disease: The Dietary Sense and Nonsense, George V Mann,
ed, Janus Publishing, 1993, available from the Price-Pottenger Nutrition Foundation (619) 574-7763. Mann's
involvement with the Framingham Study, and his studies of the Masai, whose diet is high in saturated fat but
who do not suffer from CHD, led him to the following conclusion: "The diet-heart hypothesis has been
repeatedly shown to be wrong, and yet, for complicated reasons or pride, profit and prejudice, the hypothesis
continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental
agencies. The public is being deceived by the greatest health scam of the century." Confirmation of Mann's
statement comes from none other than William Castelli, Director of the Framingham Study, who stated, "In
Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories
one ate, the lower peoples serum cholesterol. . . we found that the people who ate the most cholesterol, ate
the most saturated fat, ate the most calories weighed the lease and were the most physically active."
(Archives of Internal Medicine, 1992)
1. Price, Weston A DDS, Nutrition and Physical Degeneration, 1945 Keats Publishing, Price Pottenger
Nutrition Foundation (619) 574-7763
2. Fallon, Sally with Mary G Enig, PhD and Pat Connolly, Nourishing Traditions: The Cookbook that
Challenges Politically Correct Nutrition and the Diet Dictocrats, 1996 ProMotion Publishing (800) 231-1776
3. Fallon, Sally and Mary G Enig, PhD, "Diet and Heart Disease: Not What You Think", Consumers
Research Magazine, July 1996 (615) 337-3322
4. Fallon, Sally and Mary G Enig, PhD, "Our Friend Cholesterol", Health Freedom News, April-May 1996,
National Health Federation (818) 303-0642
5. Pramod Khosla, PhD and K C Hayes, DVM, PhD "Dietary Trans-Monounsaturated Fatty Acids
Negatively Impact Plasma Lipids in Humans: Critical Review of the Evidence" Journal of the American
College of Nutrition, Vol 15, No 4 3250-339 (1996)
6. Horrobin, David F, PhD, "The regulation of prostaglandin biosynthesis by manipulation of essential fatty
acid metabolism, " Reviews in Pure and Applied Pharmacological Sciences, Vol 4, 339-383, Freund
Publishing House, 1983
7. Fallon, Sally and Mary G Enig PhD, "Tripping Lightly Down the Prostaglandin Pathways", Price
Pottenger Nutrition Foundation Health Journal, Vol 20, No 3 Fall 1996 25-29.
8. Huang, William Y, Akinori Kamio, S-J C Yeh and Fred A Kummerow, "The Influence of Vitamin D on
Plasma and Tissue Lipids and Atherosclerosis in Swine", Artery 3(5):439-455 (1977)
9. Garg, M L et al, FASEB Journal 2:4:A852 (1988)
10. McCance, R A, "Experimental Sodium Chloride Deficiency in Man", Nutrition Reviews, Vol 48, 145147 (Mar 1990)
11. Bloch, M R, "The Social Influence of Salt", Scientific American 121-129 (July 1963)
PALEODIET Archives
Subject: Re: Stearic Acid and Blood Lipids
From: Robert Crayhon
164/298 (1997)
Date: Mon, 30 Jun 1997 00:03:37 -0400

Dear Dr. Enig and Sally Fallon,
You said in your very interesting response to Dr. Cordain that stearic acid (18:0) raises cholesterol in some
studies--did you mean lower it? From what literature I have read, it would seem to lower it, which seemed to
fit the drift of your argument more.
Also, can you comment on the difference between studying saturated fatty acids in the context of the diet and
foods they come in, versus the animal studies that often examine them in a purified form? Thank you.
By the way, as a practicing nutritionist, I have files filled with clients whose blood cholesterol came DOWN
on a diet with plenty of eggs, meat, and other animal products once sugar, margarine, and excessive
consumption of grains, fruits and fruit juices was decreased. HDL goes up, total cholesterol goes down,
triglycerides plummet. Most important, the clients FEEL better. I have seen this with over 200
hyperlipidemic clients over the past 12 years.
PALEODIET Archives
Subject: Followup questions for Fallon & Enig
From: Dean Esmay
Date: Mon, 30 Jun 1997 16:48:17 -0400
I would like to see specific documentation for the following assertions:
1) The claim that Americans' fat intake was constant betweeen 1935 and 1974.
2) The claim that saturated fats have been shown to reduce Lp(a) levels. (I've checked Medline and I cannot
find the Promod/Hayes reference.)
3) The claim that HDL/LDL cholesterol levels have no meaningful correlation with heart disease.
I understand that #3 may be a great deal of effort to document, and I don't expect to see mountains moved,
but a brief summary with a few specific references would be helpful.
In general I am sympathetic to Enig and Fallon's view that warnings about the dangers of fat are bogus and
quite possibly dangerous; my opinions on this are best summarized by an article I wrote which appears at
http://www.syndicomm.com/lowfat.html -- I invite any criticism or comment on this article from anyone on
this list, including Enig or Fallon (in fact Dr. Enig is briefly quoted in the article so she may want to have a
look for that reason alone. ;-).
PALEODIET Archives
Subject: Corrected reposting of Fallon & Enig article
From: Dean Esmay
Reply-To:
Date: Tue, 1 Jul 1997 19:54:49 -0400
Sally Fallon asked me to re-post this article, correcting some problems with punctuation codes caused by
transmission errors (and my carelessness) the first time, and also correcting an error regarding calcium. Here
it is again; I'll try to remember to re-do the archives to fix this.
To: Dr. Cordain and members of the Paleodiet Group Re: Answers to questions of May 26, 1997
First, many apologies for taking so long to respond to your excellent questions and comments of May 26.
Our replies follow:
1. You now have the reference for Voegtlin's book. As you point out, Voegtlin errs in asserting that plant
foods are needed to prevent scurvy. Uncooked or minimally cooked flesh of organs of animals contain either
vitamin C or a vitamin-C-like substance that prevents scurvy. Dr. Weston Price made this discovery when
studying the Indians of Northern Canada. (1) When they killed an animal, the Indians immediately divided
up the adrenal glands and gave a piece--raw--to every member of the tribe, and they understood that this
would prevent scurvy. Dr. Voegtlin is also wrong about vitamin K, which is found in butter and animal fats.
So it can be said that all the known vitamins, minerals and needed macronutrients can be obtained from
animal foods. However, we should not rule out the possibility that the various phyto-chemicals, alkaloids,
etc. found in plant foods, while not classified as vitamins, are necessary for optimal health, at least to some
individuals.
165/298 (1997)
2. We have consistently argued that the current high levels of CHD have nothing to do with the consumption
of saturated fat from animal sources, (2, 3, 4) but rather are due to foods relatively new to the human diet-particularly excess polyunsaturates, hydrogenated oils and refined carbohydrates. The anti-cholesterol, antianimal-fat campaign is a phoney issue invented and promulgated by the vegetable oil and fabricated food
industries during the 50s and 60s in order to get the upper hand in marketing their products. It amounts to
propaganda designed to denigrate nutritious traditional foods so that the consumer will buy highly refined
and processed food items instead. The amount of saturated fat in the American diet remained the same
between 1935 and 1974--the period of greatest increase in heart disease.
3. The LDL/HDL issue is also phoney and does not stand up to rigorous scrutiny. LDL is necessary to carry
cholesterol from the liver to the cells, particularly to the brain cells, which unlike other cells in the human
body, do not manufacture cholesterol. However, it is true that oxidized LDL is a problem, and does initiate
foam cells in the arteries. Oxidized cholesterol is found in products that have been heated to very high
temperatures in the presence of oxygen, such as powdered eggs and milk. Powdered eggs are added to many
processed foods and powdered milk is added to 1% and 2% milk to give it body. People drinking reduced fat
milk in order to "avoid heart disease" are actually taking in large quantities of oxidized cholesterol which is a
causative factor. You are also right in pointing out that high levels of commercial polyunsaturated oils
(virtually all of which have a high N6 to N3 ratio) increase LDL oxidizability. It is the excess of
polyunsaturated oils that cause the problem--not the saturated fats, whether in the modern diet or in
traditional cuisines. In fact, SFAs have been shown to lower Lp(a) which, unlike total serum cholesterol,
HDL or LDL, is a very good marker for increased risk of CHD. (5)
4. We believe that the amount of protein in the diet as related to CHD is another phony issue. One can point
to populations with relatively high protein consumption (30-40%) with little or no CHD, and to populations
with relatively low protein consumption (15-20%) with little or no CHD. In any event, we have no way of
knowing the exact ratios of macronutrients in the Paleolithic diet, and in fact, there probably was a lot of
variation depending on season, locality and tribal custom. The danger lies, as we pointed out in our article, in
diets high in animal protein but low in fat. This seems to have been generally recognized by the huntergatherer.
5. We would like to know what kind of fat combined with carbohydrates exacerbate the postprandial lipemic
excursions. We can well believe that excess polyunsaturated or trans fats would do this. We know that fats
taken with carbohydrates, especially traditional fats such as butter or any of the tropical oils, lower the
glycemic index, thereby preventing blood sugar swings. We are not aware of any studies showing
carbohydrates were eaten separately in pre-industrial societies. American Indians made pemmican from meat
or fish, fat, maple syrup and cranberries; succatash was made from meat, fat, beans and corn. Orthodox
dieticians/nutritionists contend that high carbohydrate diets improve blood lipid profiles. All this emphasis
on protein and carbohydrate content is, we believe, misplaced. The real issue is the kind and quality of the
macronutrients--how they are produced, processed and prepared.
6. We look forward to seeing your research and intriguing findings about the varying lengths of SFAs in wild
and domesticated animals. Stearic acid (18:0) has been shown to raise cholesterol in some studies--and in
any event, the whole cholesterol issue is bogus. There may be differences in the N6/N3 ratios in wild and
domesticated ruminant adipose tissue, but in both overall total PUFA is low. The real imbalances come with
modern farming methods (for eggs, fish, vegetables, etc.) and with the introduction of high N6 oils into the
diet. Excess N6/N3 ratios result in profound imbalances at the cellular level that can lead to MI, cancer and
many other diseases. (6, 7) We certainly do agree that high levels of N6 in the diet are a problem, but the
source of excess N6 is not domesticated beef and lamb.
166/298 (1997)
7. We do not know when milk product consumption became general, but it is fair to assume that the adoption
of a nomadic/herder life-style--and therefore the domestication of animals--preceded agriculture. We cannot
understand how dairy products per se can be blamed for the CHD epidemic. Counter examples include
France (low CHD, high consumption of butter and cheese); Soviet Georgia (famed for longevity, high
consumption of whole milk products); the Masai (high consumption of whole milk products, no CHD);
Switzerland and Austria (life span almost as long as Japan, diet rich in butterfat and whole milk products)
and America at the turn of the century (diet loaded with butterfat and whole milk products, very little CHD.)
If CHD is associated with milk consumption within individual countries, the finger must be pointed at
modern production methods (inappropriate feed for the cows, cows bred to have a low butterfat content)
processing (pasteurization, homogenization) and additives (powdered skim milk containing oxidized
cholesterol and synthetic vitamin D2 or D3. Synthetic D2 has been very conclusively shown to cause
calcification of the soft tissues including the arteries, and large amounts of synthetic D3, which has largely
replaced D2 as an additive to milk, have been implicated as a causative factor in the initiation of pathogenic
lesion development in the arteries. (8) The N6-N3 ratio of the small amounts of PUFAs in bovine milk fat is
excellent--about 2/1--whereas total N6/N3 in the modern diet exceeds 20/1. So once again, while we agree
that high levels of N6 in the diet are a problem, the source of excess N6 is not butterfat. Dietary saturated fats
contribute to improved assimilation of EFAs. (9) In other words, we need less of the EFAs when there are
enough SFAs in the diet. Magnesium does seem to protect against CHD. The fault lies not with high levels of
calcium from milk products, but with the deficiency of magnesium in modern diets. Weston Price found that
the diets of healthy "primitives" contained at least four times the amount of calcium as the American diet of
his day (and ten times the fat-soluble vitamins A and D!) (1) Sources of magnesium include nuts, meat and
grains such as buckwheat.
8. As we stated earlier, modern man is not consuming high levels of SFAs compared to pre-agricultural man.
The blame for inactivity should be placed on the lower nutrient content of the total diet, composed as it is of
high levels of refined and devitalized foods. When the diet supplies all the needed factors, humans need no
incentives to exercise.
9. Finally, on the question of salt, a distinction must be made between processed salt, which contains many
problematic chemicals including aluminium, and from which the magnesium salts and all the valuable trace
minerals have been removed. Modern salt comes attached to modern food products, which are invariably
refined, rancid and laced with additives; and it is difficult to separate salt from these other variables in
dietary research surveys. Some studies have shown that with low salt diets, hypertension becomes worse. In
the 1930s, researcher McCance demonstrated that when dietary salt is lowered, all manner of inappropriate
physiological responses ensue--including cramps, weakness, lassitude, loss of taste sensation and severe
cardiorespiratory distress on exertion. (10) The recent contribution to this debate, describing various
American Indian methods for using salty blood in the preparation of their meat, supports our contention that
Paleolithic diets contained sodium chloride. Salty animal blood and urine form an important part of the diet
in salt-poor Africa. The concentration of population, and the rise and fall of civilizations throughout the
world, can be positively correlated with the availability of salt. (11)
To summarize, the hypothesis that modern chronic diseases like CHD and cancer are due to consumption of
saturated fats, red meat, milk products and salt does not stand up to careful scrutiny. These have been in the
diets of healthy population groups for millennia. Media denigration of such traditional foods is a distraction
that diverts the attention of both the public and the scientific community from the real culprits--modern
farming techniques, inappropriate processing, refined carbohydrates, commercial vegetable oils, food
additives and rancid & altered fats.
P.S. The rest of citation #2 is Coronary Heart Disease: The Dietary Sense and Nonsense, George V Mann,
ed, Janus Publishing, 1993, available from the Price-Pottenger Nutrition Foundation (619) 574-7763. Mann's
involvement with the Framingham Study, and his studies of the Masai, whose diet is high in saturated fat but
who do not suffer from CHD, led him to the following conclusion: "The diet-heart hypothesis has been
repeatedly shown to be wrong, and yet, for complicated reasons or pride, profit and prejudice, the hypothesis
continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental
agencies. The public is being deceived by the greatest health scam of the century." Confirmation of Mann's
statement comes from none other than William Castelli, Director of the Framingham Study, who stated, "In
Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories
one ate, the lower peoples serum cholesterol. . . we found that the people who ate the most cholesterol, ate
the most saturated fat, ate the most calories weighed the lease and were the most physically active."
(Archives of Internal Medicine, 1992)
167/298 (1997)
1. Price, Weston A DDS, Nutrition and Physical Degeneration, 1945 Keats Publishing, Price Pottenger
Nutrition Foundation (619) 574-7763
2. Fallon, Sally with Mary G Enig, PhD and Pat Connolly, Nourishing Traditions: The Cookbook that
Challenges Politically Correct Nutrition and the Diet Dictocrats, 1996 ProMotion Publishing (800) 231-1776
3. Fallon, Sally and Mary G Enig, PhD, "Diet and Heart Disease: Not What You Think", Consumers
Research Magazine, July 1996 (615) 337-3322
4. Fallon, Sally and Mary G Enig, PhD, "Our Friend Cholesterol", Health Freedom News, April-May 1996,
National Health Federation (818) 303-0642
5. Pramod Khosla, PhD and K C Hayes, DVM, PhD "Dietary Trans-Monounsaturated Fatty Acids
Negatively Impact Plasma Lipids in Humans: Critical Review of the Evidence" Journal of the American
College of Nutrition, Vol 15, No 4 3250-339 (1996)
6. Horrobin, David F, PhD, "The regulation of prostaglandin biosynthesis by manipulation of essential fatty
acid metabolism, " Reviews in Pure and Applied Pharmacological Sciences, Vol 4, 339-383, Freund
Publishing House, 1983
7. Fallon, Sally and Mary G Enig PhD, "Tripping Lightly Down the Prostaglandin Pathways", Price
Pottenger Nutrition Foundation Health Journal, Vol 20, No 3 Fall 1996 25-29.
8. Huang, William Y, Akinori Kamio, S-J C Yeh and Fred A Kummerow, "The Influence of Vitamin D on
Plasma and Tissue Lipids and Atherosclerosis in Swine", Artery 3(5):439-455 (1977)
9. Garg, M L et al, FASEB Journal 2:4:A852 (1988)
10. McCance, R A, "Experimental Sodium Chloride Deficiency in Man", Nutrition Reviews, Vol 48, 145147 (Mar 1990)
11. Bloch, M R, "The Social Influence of Salt", Scientific American 121-129 (July 1963)
PALEODIET Archives
Subject: Fat, milk and salt
Reply-To:
Date: Tue, 1 Jul 1997 22:23:31 +0100
Mary Enig and Sally Fallon, in two postings rich in statements but poor in references, have written:
> From the Eskimo of Alaska to the hardy Alpiner, from Gaelic villager to African tribesman, Price
> discovered that all healthy indigenous people had a plentiful source of animal fat in the diet.
I do not know how Price defined healthy, but there have been many traditional populations with a low intake
of animal fat (including dairy products and fat from meat) who also have had low rates of cardiovascular
disease, hypertension, obesity and diabetes prior to westernization [1-102].
> We cannot understand how dairy products per se can be blamed for the CHD epidemic.
But I can. Per capita intake of milk is the single environmental factor which is most strongly related to
international ischaemic heart disease death rates [103], and for males of 19 OECD countries the negative
relation between mortality from ischaemic heart disease and wine or alcohol intake was reduced to nonsignificance by controlling for dairy products [104]. But epidemiology can never prove causality. The cause
could be some undiscovered lifestyle factor which is related to milk intake.
168/298 (1997)
Or it could be something else in the milk than saturated fat. Dr Jeffrey Segall has suggested that it is lactose
[105] and recently argued that 'International data show stronger correlations of mortality from ischaemic
heart disease with per capita supply of dairy products excluding fat than with dairy fat, and of estimated
lactose than with dairy fat or margarine and other processed fats (positively) and vegetable oils and fats, fat
of fish or wine (negatively). Butter and cheese, which have a low content of lactose, show moderate and zero
correlations, respectively. Populations with low or intermediate prevalence of adult lactose absorbers have a
lower supply of dairy products excluding butter (and therefore of lactose), and a lower mortality from
ischaemic heart disease, than populations with a high prevalence of absorbers. Specific national and ethnic
data suggest that a diet low or relatively low in lactose, in populations with low or relatively low prevalence
of lactose absorbers, is more consistently associated with protection against ischaemic heart disease than are
high intakes of unsaturated fatty acids, wine, alcohol or dietary fibre. In seven countries with a high
consumption of dairy products (six at least with a high prevalence of lactose absorbers), trends in ischaemic
heart disease mortality appear to have reflected changes in the supply of milk (and therefore of lactose), but
not consistently of butter or inversely of unsaturated fatty acids. The findings reviewed in this paper call for
further investigation of the subject, epidemiologically and biochemically' [106].
In order to be absorbed, lactose is split by the intestinal enzyme lactase into glucose and galactose.
Paleolithic human adults did not drink milk and were probably, like most adults of the world today,
incapable of absorbing lactose [107]. Accordingly, galactose is one of the few nutrients that did not enter the
metabolic system of adults during human evolution.
> ...the Masai (high consumption of whole milk products, no CHD)...
Segall states that, among the Masai, 'the milk is consumed largely lactose-fermented, and the prevalence of
lactose absorbers in adults can be assumed to be low because that in children aged 5-14 years is estimated to
be 38 per cent [108]' [106].
This is crucial. Does anyone else know whether the Masai really ferment(ed) their milk?
> Assuming that man's tastebuds are not superfluous, but nature's way of guiding him to the food he
> needs, let us examine the notion that the cave man diet satisfied only the bitter, sour or pungent
> portion of his tasting apparatus, and not the salty or sweet.
Obviously our tastebuds lead us to the sweet, but sweet foods during evolution differed dramatically from
most sweet foods today regarding nutrient density. Personally I would be at least 25 kg heavier if I had let
my tastebuds guide me through the supermarket.
> It is hard to imagine that he would have neglected his taste for salt. It occurs naturally in meat
> and blood and, as animals seek out natural salt licks, so our sensible cave man would have done
> the same.
Yes of course, we are all very similar. But meat and blood are low salt foods and substantial evidence
suggests that, since nature has not prepared the cave man and his woman for excess salt, increasing their salt
intake to western standards would increase their risk of hypertension, stroke, heart failure, esophageal and
gastric cancer, kidney stones and osteoporosis [109]. Hunter-gatherers by the sea may have added sea water
or even sea salt to their foods. But sea salt is only 65 per cent sodium chloride, the rest is potassium chloride
and magnesium sulphate, and in any case the sodium to potassium ratio would not have been as high as for
westerners.
> It is reported that the members of the Yanomami tribe in the Amazon basin do not take in any added
> salt. In an apparant adoptive measure, they also excrete almost no salt in the urine.
Yes, they excrete 1 mmol per 24 hours, which corresponds well with their intake [110]. But this is not
specific for them, all human are capable of adopting to a low-salt diet [111]. Last time I checked my urinary
excretion of sodium it was 14 mmol per 24 hours compared to 150-300 in the West.
> Milk is salty because mammals need salt for the production of hydrochloric acid and for the
> development of the brain and nervous system. Without dietary salt, the human mind does not fully
> develop and man must live, not by his wits like the ingenious cave man from the dawn of time, but
> as a brute, even if he happens to be born in this modern age.
I am not aware of any evidence that that we do not get more salt than we need from unsalted meat, fruit and
saturating vegetables [111]. If Enig and Fallon have references please share them with us. I have several
thousand colleagues here in Sweden who would be very happy to find arguments for giving pills in stead of
dietary advice to patients with high blood pressure (although the effect of pills on their health is lousy [112114]).
> Some studies have shown that with low salt diets, hypertension becomes worse.
169/298 (1997)
But the bulk of evidence suggests the contrary [115]. Any cause-effect relationship will by chance be
'reversed' in one or two studies out of many, and readers who pick out such single studies are possibly in love
with some hypothesis.
But who is not? :-)
170/298 (1997)
1. Breinl A. On the occurence and prevalence of diseases in British New Guinea. Ann Trop Med Parasitol
1915; 9: 285-. 2. Clements FW. A Medical Survey in Papua: Report of the First Expedition by the School of
Public Health and Tropical Medicine to Papua, 1935. Med J Aust 1936; 1: 451-. 3. Devine HD. Rheumatic
Heart Disease in New Guinea: Including a Cardiovascular Survey of 200 Native Papuans. Ann Intern Med
1946; 24: 826-. 4. Backhouse TC. Melanesian natives and vascular disease: A note based on autopsy records,
1923-1934. Med J Aust 1958; 36-. 5. Whyte H. Body fat and blood pressure of natives in New Guinea:
Reflections on essential hypertension. Aust Ann Med 1958; 7: 36-46. 6. Barnes R. Incidence of Heart
Disease in a Native Hospital of Papua. Med J Aust 1961; 2: 540-. 7. Campbell C, Arthur R. A study of 2000
admissions to the medical ward of Port Moresby General Hospital. Med J Aust 1964; 1: 989-992. 8.
Dewdney JCH. Maprik Hospital - a review of 3888 consecutive admissions, February 1963 to July 1964.
Papua New Guinea Med J 1965; 8: 89-96. 9. Kariks J, McGovern VJ. Heart disease in the territory of PapuaNew Guinea: a preliminary report based on a necropsy study. Med J Aust 1967; 1: 176-7. 10. Verlee DL.
Ophthalmic survey in the Solomon Islands. Am J Ophthalmol 1968; 66: 304-19. 11. Stanhope JM. Mortality
and population growth: Losuia area, Kiriwina, Trobriand Islands. Papua New Guinea Med J 1969; 12: 42-48.
12. Vines AP. An epidemiological sample survey of the highlands, mainland and island regions of the
Territory of Papua and New Guinea. In: Department of Public Health, Territory of Papua and New Guinea,
Port Moresby, 1970: 13. Conyers RA. Myocardial infarction in a New Guinean. Med J Aust 1971; 2: 412-7.
14. Aiken GH, Lytton DG, Everingham S. Atherosclerotic heart disease in urbanised Papua New Guineans.
P N G Med J 1974; 17: 248-50. 15. Hornabrook RW, Crane GG, Stanhope JM. Karkar and Lufa: an
epidemiological and health background to the human adaptability studies of the International Biological
Programme. Philos Trans R Soc Lond Biol 1974; 268: 293-308. 16. Mathews CL. Cardiovascular disease in
Lae- a five year review. P N G Med J 1974; 17: 251-62. 17. Page LB, Damon A, Moellering RJ. Antecedents
of cardiovascular disease in six Solomon Islands societies. Circulation 1974; 49: 1132-46. 18. Sinnett P,
Buck L. Coronary heart disease in Papua New Guinea: present and future. P N G Med J 1974; 17: 242-7. 19.
Somers K. Cardiology in Papua New Guinea. P N G Med J 1974; 17: 235-41. 20. Hornabrook RW. Editorial:
neurology in Papua New Guinea. P N G Med J 1975; 18: 193-6. 21. Nagurney JT. Neurological admissions
to Goroka Base Hospital - an eight month survey. P N G Med J 1975; 18: 220-6. 22. Sinnett P. The people of
Murapin.Oxford: EW Classey Ltd, 1977(Research PNGIoM, ed. Monograph Series No 4 23. McGarvey ST,
Baker PT. The effects of modernization and migration on Samoan blood pressures. Hum Biol 1979; 51: 46179. 24. Korner N. Cardiovascular disease in Papua New Guinea. Med J Aust 1980; 1: 1-7. 25. Martin FI,
Wyatt GB, Griew AR, Mathews JD, Campbell DG. Diabetic surveys in Papua New Guinea - results and
implications. P N G Med J 1981; 24: 188-94. 26. Palmer P. Autopsies at Goroka hospital from 1978-1982: a
review. P N G Med J 1982; 25: 166-7. 27. Ree GH. Elderly ailing Highlanders of Papua New Guinea. P N G
Med J 1982; 25: 93-6. 28. Gee RW. The epidemiology of hypertension in the South Pacific. P N G Med J
1983; 26: 55-8. 29. Savige J. Diabetes mellitus in the Tolais of the Gazelle Peninsula, New Britain. P N G
Med J 1982; 25: 89-92. 30. Patel MS. Diabetes, the emerging problem in Papua New Guinea [editorial]. P N
G Med J 1984; 27: 1-3. 31. King H. Glucose tolerance in Papua New Guinea: past and future studies. P N G
Med J 1985; 28: 283-9. 32. Jenkins C. Medical anthropology in the Western Scrader range, Papua New
Guinea. Nat Geogr Res 1987; 3: 412-30. 33. Kevau IH. Clinical documentation of twenty cases of acute
myocardial infarction in Papua New Guineans. P N G Med J 1990; 33: 275-80. 34. Sinnett PF, Kevau IH,
Tyson D. Social change and the emergence of degenerative cardiovascular disease in Papua New Guinea. In:
Attenborough RD, Alpers MP, ed. Human Biology in Papua New Guinea. The Small Cosmos. Oxford:
Clarendon Press, 1992: 373-86. 35. Hunter JD. Some epidemiological aspects of coronary artery disease in
New Zealand and the Cook Islands. Ann N Y Acad Sci 1963; 97: 908-19. 36. Stanhope JM. Blood pressures
of the Tinam-Aigram people, near Simbai, Madang District. P N G Med J 1968; 11: 60-1. 37. Labarthe D,
Reed D, Brody J, Stallones R. Health effects of modernization in Palau. Am J Epidemiol 1973; 98: 161-74.
38. Prior IA. Cardiovascular epidemiology in New Zealand and the Pacific. N Z Med J 1974; 80: 245-52. 39.
Pathik B, Ram P. Acute myocardial infarction in Fiji: a review of 300 cases. Med J Aust 1974; 2: 922-4. 40.
Beaglehole R, Salmond CE, Prior IA. Prevalence of coronary heart disease in samples of New Zealand
Maoris and Pakehas. N Z Med J 1975; 82: 119-22. 41. Reed DM. Current health problems in the South and
Central Pacific. N Z Med J 1977; 85: 326-9. 42. Zimmet P. Epidemiology of diabetes and its macrovascular
manifestations in Pacific populations: the medical effects of social progress. Diabetes Care 1979; 2: 144-53.
43. Jackson L, Whitehouse S, Zimmet P, Sloman G. Electrocardiographic findings in a partly urbanised
Polynesian population. The Funafuti survey. N Z Med J 1980; 91: 210-2. 44. Zimmet PZ, Taylor R, Jackson
L, Whitehouse SL, Faaivaso S, Ainuu J. Blood pressure studies in rural and urban Western Samoa. Med J
Aust 1980; 2: 202-5. 45. Zimmet P, Jackson L, Whitehouse S. Blood pressure studies in two Pacific
populations with varying degrees of modernisation. N Z Med J 1980; 91: 249-52. 46. Beaglehole R, Prior IA,
171/298 (1997)
Foulkes MA, Eyles EF. Death in the South Pacific. N Z Med J 1980; 91: 375-8. 47. Prior IAM, Stanhope JM.
Blood pressure patterns, salt use and migration in the Pacific. In: Kesteloot H, Joosens JV, ed. Epidemiology
of Arterial Blood Pressure. The Hague: Martinus Nijhoff, 1980: 243-62. 48. Zimmet P, Faaiuso S, Ainuu J,
Whitehouse S, Milne B, DeBoer W. The prevalence of diabetes in the rural and urban Polynesian population
of Western Samoa. Diabetes 1981; 30: 45-51. 49. Crews DE, MacKeen PC. Mortality related to
cardiovascular disease and diabetes mellitus in a modernizing population. Soc Sci Med 1982; 16: 175-81. 50.
Finau SA, Prior IA, Evans JG. Ageing in the South Pacific. Physical changes with urbanization. Soc Sci Med
1982; 16: 1539-49. 51. Reed DM, Feinleib M. Changing patterns of cardiovascular disease in the Pacific
Basin: report of an international workshop. J Community Health 1983; 8: 182-205. 52. Kasl SV, Berkman L.
Health consequences of the experience of migration. Annu Rev Public Health 1983; 4: 69-90. 53. Taylor R.
Prevention and control of non-communicable diseases in Pacific Island nations. Prospects and constraints.
Med J Aust 1983; 2: 389-94. 54. King H, Zimmet P, Bennett P, Taylor R, Raper LR. Glucose tolerance and
ancestral genetic admixture in six semitraditional Pacific populations. Genet Epidemiol 1984; 1: 315-28. 55.
Tuomilehto J, Ram P, Eseroma R, Taylor R, Zimmet P. Cardiovascular diseases and diabetes mellitus in Fiji:
analysis of mortality, morbidity and risk factors. Bull World Health Organ 1984; 62: 133-43. 56. Taylor R,
Thoma K. Mortality patterns in the modernized Pacific Island nation of Nauru. Am J Public Health 1985; 75:
149-55. 57. Baker PT, Hanna JM, Baker TS, ed. The Changing Samoans Behavior and Health in Transition.
Oxford: Oxford University Press, 1986: 58. Taylor R, Nemaia H, Connell J. Mortality in Niue, 1978-82. N Z
Med J 1987; 100: 477-81. 59. Eason RJ, Pada J, Wallace R, Henry A, Thornton R. Changing patterns of
hypertension, diabetes, obesity and diet among Melanesians and Micronesians in the Solomon Islands. Med J
Aust 1987; 146: 465-9. 60. Taylor R, Bennett P, Uili R, et al. Hypertension and indicators of coronary heart
disease in Wallis Polynesians: an urban-rural comparison. Eur J Epidemiol 1987; 3: 247-56. 61. Finlayson
PJ, Caterson LD, Rhodes KM, Plehwe WE, Hannelly T, Silink M. Diabetes, obesity and hypertension in
Vanuatu. P N G Med J 1988; 31: 9-18. 62. Tuomilehto J, Zimmet P, Kankaanpaa J, et al. Prevalence of
ischaemic ECG abnormalities according to the diabetes status in the population of Fiji and their associations
with other risk factors. Diabetes Res Clin Pract 1988; 5: 205-17. 63. Crews DE, Pearson JD. Cornell Medical
Index responses and mortality in a Polynesian population. Soc Sci Med 1988; 27: 1433-7. 64. Salmond CE,
Prior IA, Wessen AF. Blood pressure patterns and migration: a 14-year cohort study of adult Tokelauans.
Am J Epidemiol 1989; 130: 37-52. 65. Dowse G, Collins V, Zimmet P, Finch C. Cross-sectional and
longitudinal relationship between obesity, hypertension and coronary heart disease in Micronesian Nauruans.
Diabetes Res Clin Pract 1990; 10: S179-83. 66. Tukuitonga CF, Stewart A, Beaglehole R. Coronary heart
disease among Pacific Island people in New Zealand. N Z Med J 1990; 103: 448-9. 67. Tuomilehto J,
Zimmet P, Nan L, Dowse G. ECG abnormalities in relation to glugose tolerance and other risk factors in men
of the developing Pacific nation of Kiribati. Nutr Metab Cardiovasc Dis 1991; 1: 195-200. 68. Dowse GK,
Zimmet PZ, King H. Relationship between prevalence of impaired glucose tolerance and NIDDM in a
population. Diabetes Care 1991; 14: 968-74. 69. King H, Finch C, Koki G, King LF, Alpers M, Zimmet P.
Glucose tolerance in Papua New Guinea: comparison of Austronesian and non-Austronesian communities of
Karkar Island. Diabet Med 1991; 8: 481-8. 70. Yatsu FM. Strokes in Asians and Pacific-Islanders, Hispanics,
and Native Americans. Circulation 1991; 83: 1471-2. 71. King H. The epidemiology of diabetes mellitus in
Papua New Guinea and the Pacific: adverse consequences of natural selection in the face of sociocultural
change. In: Attenborough RD, Alpers MP, ed. Human Biology in Papua New Guinea. The Small Cosmos.
Oxford: Clarendon Press, 1992: 363-72.
172/298 (1997)
72. O'Dea K. Diabetes in Australian Aborigines: impact of the western diet and life style. J Intern Med 1992;
232: 103-117. 73. Groom D. Cardiovascular observations on Tarahumara Indian runners--the modern
Spartans. Am Heart J 1971; 81: 304-14. 74. Connor WE, Cerqueira MT, Connor RW, Wallace RB, Malinow
MR, Casdorph HR. The plasma lipids, lipoproteins, and diet of the Tarahumara indians of Mexico. Am J
Clin Nutr 1978; 31: 1131-42. 75. Burns-Cox CJ, Maclean JD. Splenomegaly and blood pressure in an Orang
Asli community in West Malaysia. Am Heart J 1970; 80: 718-9. 76. Oliver WJ, Cohen EL, Neel JV. Blood
pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a "no-salt" culture.
Circulation 1975; 52: 146-51. 77. Spielman RS, Fajans SS, Neel JV, Pek S, Floyd JC, Oliver WJ. Glucose
tolerance in two unacculturated Indian tribes of Brazil. Diabetologia 1982; 23: 90-3. 78. Baruzzi R, Franco
L. Amerindians of Brazil. In: Trowell H, Burkitt D, ed. Western diseases: their emergence and prevention.
Cambridge, Mass: Harvard University Press, 1981: 138-153. 79. Donnison CP. Blood pressure in the African
native. Its bearing upon the tiology of hyperpiesia and arterio-sclerosis. Lancet 1929; i: 6-7. 80. Vint FW.
Postmortem findings in the natives of Kenya. East Afr Med J 1937; 13: 332-40. 81. Muwazi E. Neurological
disease among african natives of Uganda: A review of 269 cases. East Afr Med J 1944; 2-19. 82. Davies J.
Pathology of central african natives. IX: Cardiovscular diseases. East Afr Med J 1948; 25: 454-467. 83.
Higginson J, Pepler WJ. Fat intake, serum cholesterol, and atherosclerosis in the South African Bantu. Part
II. Atherosclerosis and coronary artery disease. J Clin Invest 1954; 33: 1366-71. 84. Hutton PW.
Neurological disease in Uganda. East Afr Med J 1956; 33: 209-223. 85. Trowell HC. Non-infective diseases
in Africa.London: Edward Arnold Ltd, 1960:74-152. 86. Thomas W, Davies J, O'Nea lR, Dimakulangan A.
Incidence of myocardial infarction correlated with venous and pulmonary thrombosis and embolism. A
geographic study based on autopsies in Uganda, East Africa and St Louis, USA. Am J Cardiol 1960; 5: 4147. 87. Lowenstein FH. Blood-pressure in relation to age and sex in the tropics and subtropics. A review of
the literature and an investigation in two tribes of Brazil Indians. Lancet 1961; i: 389-92. 88. Reef H,
Isaacson C. Atherosclerosis in the Bantu. Circulation 1962; 25: 66-72. 89. Walker ARP. Mortality from
coronary heart disease and from cerebral vascular disease in the different racial populations in South Africa.
South Afr Med J 1963; 37: 1155-9. 90. Seftel HC, Keeley KJ, Walker ARP. Characteristics of South African
Bantu who have suffered from myocardial infarction. Am J Cardiol 1963; 12: 149-56. 91. Billinghurst JR.
The pattern of adult neurological admissions to Mulago hospital, Kampala. East Afr Med J 1970; 47: 653-63.
92. Truswell AS, Kennelly BM, Hansen JD, Lee RB. Blood pressures of Kung bushmen in Northern
Botswana. Am Heart J 1972; 84: 5-12. 93. Solberg LA, McGarry PA. Cerebral atherosclerosis in Negroes
and Caucasians. Atherosclerosis 1972; 16: 141-54. 94. Dodu S. Clinical aspects of ischaemic heart disease
(IHD) in Ghana. Ghana Med J 1972; 11: 203-214. 95. Merimee TJ, Rimoin DL, Cavalli SL. Metabolic
studies in the African pygmy. J Clin Invest 1972; 51: 395-401. 96. Joffe BI, Jackson WP, Thomas ME,
Toyer MG, Keller P, Pimstone BL. Metabolic responses to oral glucose in the Kalahari Bushmen. B M J
1971; 4: 206-8. 97. Edginton ME, Hodkinson J, Seftel HC. Disease patterns in a South African rural Bantu
population, including a commentary on comparisons with the pattern in urbanized Johannesburg Bantu. S
Afr Med J 1972; 46: 968-76. 98. Okuwobi B, Strasser T. Heart disease in Nigeria. World Health 1972; 2425. 99. Walker AR. The epidemiological emergence of ischemic arterial diseases. Am Heart J 1975; 89: 1336. 100. Truswell AS, Hansen JDL. Medical research among the !Kung. In: Lee RB, DeVore I, ed. Kalahari
Hunter-gatherers. Cambridge, Mass.: Harvard University Press, 1976: 166-95. 101. Isaacson C. The
changing pattern of heart disease in South African Blacks. S Afr Med J 1977; 52: 793-8. 102. Trowell HC,
Burkitt DP, ed. Western diseases: their emergence and prevention. Cambridge, Mass: Harvard University
Press, 1981: 103. Artaud WS, Connor SL, Sexton G, Connor WE. Differences in coronary mortality can be
explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and
Finland. A paradox. Circulation 1993; 88: 2771-9. 104. Popham RE. Variation in mortality from ischaemic
heart disease in relation to alcohol and milk consumption. Med Hypotheses 1983; 12: 321-9. 105. Segall JJ.
Is milk a coronary health hazard? Br J Prev Soc Med 1977; 31: 91-5. 106. Segall JJ. Dietary lactose as a
possible risk factor for ischaemic heart disease: review of epidemiology. Int J Cardiol 1994; 46: 197-207.
107. Allen JS, Cheer SM. The Non-Thrifty Genotype. Current Anthropology 1996; 37: 831-42. 108. Jackson
RT, Latham MC. Lactose malabsorption among Masai children of East Africa. Am J Clin Nutr 1979; 32:
779-82. 109. Antonios TF, MacGregor GA. Salt - more adverse effects. Lancet 1996; 348: 250-1. 110.
Mancilha-Carvalho JJ, de Oliveira R, Esposito RJ. Blood pressure and electrolyte excretion in the
Yanomamo Indians, an isolated population. J Hum Hypertens 1989; 3: 309-14. 111. Michell AR.
Physiological aspects of the requirement for sodium in mammals. Nutr Res Rev 1989; 2: 149-60. 112.
Lindholm L, Ejlertsson G, Scherstn B. High risk of cerebro-cardiovascular morbidity in well treated male
hypertensives. A retrospective study of 40-59-year-old hypertensives in a Swedish primary care district. Acta
Med Scand 1984; 216: 251-9. 113. Strandgaard S, Haunso S. Why does antihypertensive treatment prevent
173/298 (1997)
stroke but not myocardial infarction? Lancet 1987; ii: 658-61. 114. Berglund G. Does antihypertensive
treatment precipitate myocardial infarctions? [editorial]. Acta Med Scand 1987; 222: 193-4. 115. Beilin LJ.
Non-pharmacological management of hypertension. In: Swales JD, ed. Textbook of Hypertension. Oxford:
Blackwell, 1994: 1165-77.
18395 http://www.panix.com/~paleodiet/lindeberg/
-------------------------------------------------------------------
PALEODIET Archives
From: Pamela Davis
Reply-To:
Date: Thu, 3 Jul 1997 16:30:35 -0400
Staffan Lindeberg writes:
> Per capita intake of milk is the single environmental factor which is most strongly related to
> international ischaemic heart disease death rates [103], and for males of 19 OECD countries the
> negative relation between mortality from ischaemic heart disease and wine or alcohol intake was
> reduced to non-significance by controlling for dairy products [104].
This is a naive question but why would we exclusively consume one food for the first 2-4 years of our lives
and then abandon it altogether?
PALEODIET Archives
Subject: Milk and the Masai
Reply-To:
Date: Thu, 3 Jul 1997 17:59:53 -0500
I very much enjoyed Mary Enig and Sally Fallon's posting; however, I have a question regarding the
following two passages in which the Masai (who are large milk-drinkers) are mentioned:
> 7. We do not know when milk product consumption became general, but it is fair to assume that the
> adoption of a nomadic/herder life-style--and therefore the domestication of animals--preceded
> agriculture. We cannot understand how dairy products per se can be blamed for the CHD epidemic.
> Counter examples include France (low CHD, high consumption of butter and cheese); Soviet Georgia
> (famed for longevity, high consumption of whole milk products); the Masai (high consumption of
> whole milk products, no CHD); P.S. The rest of citation #2 is Coronary Heart Disease: The Dietary
> Sense and Nonsense, George V Mann, ed, Janus Publishing, 1993, available from the Price-Pottenger
> Nutrition Foundation (619) 574-7763. Mann's involvement with the Framingham Study, and his studies
> of the Masai, whose diet is high in saturated fat but who do not suffer from CHD.
The above comments about the Masai having no CHD, apparently based in part on George Mann's 1993
paper, seems to conflict with an earlier study of Mann's which reports on their significant levels of
atherosclerosis. Let me just here condense and rephrase something I posted to the Paleofood list a few weeks
ago on this Subject: While it is true that the Masai are (or were) athletic and could be considered to be in
good health compared to Westerners, the Masai have been shown to have significant levels of
atherosclerosis.
My limited knowledge of the situation is that there may be some confusion about studies of the Masai, which
probably got its start from field studies of them in the 1960s done by George Mann (mentioned above by
Enig and Fallon), published in his paper, "Physical fitness and immunity to heart disease in the Masai, "
Lancet, 12/25/65, p.308]. However, Lee Hitchcox points out in his book Long Life Now (1996, Celestial
Arts, p.161), that this early study by Mann depicting the Masai as free of heart disease was funded by a
vested interest in how the study turned out: the National Livestock and Meat Board.
174/298 (1997)
When Mann did later independent studies of the Masai, his published findings were curiously different:
Autopsies showed the Masai to have significant levels of atherosclerosis. These levels of atherosclerosis
were present even in the face of low blood lipids--exemplified in the Masai by cholesterol levels in the range
of 115 to 145 [Mann G. et al 1972, "Atherosclerosis in the Masai, " American Journal of Epidemiology,
95:1, Jan. 1972, pp. 26-37]. I mention this because if true, it would be interesting to know what the
mechanism for the atherosclerosis would be given their low blood cholesterol levels.
If I am remembering Mann's research correctly, one interesting point in the later study (which again may be
responsible for some of the differing interpretations of the Masai's health) was that the Masai were spared
many of the repercussions from atherosclerosis that might affect Westerners for the reason that the diameters
of their arteries were much larger than average, presumably due to the effect of their superior cardiovascular
fitness from high levels of physical activity. In other words, they still had enough arterial volume despite the
atherosclerosis to support good blood flow. I am not clear on the what the clinical definition of CHD is and
whether it includes atherosclerosis itself, or subsequent symptoms usually caused by it, which were
(apparently) absent in the Masai.
If the 1993 Mann reference that Mary and Sally cite has information that would supersede Mann's
conclusions from his earlier 1972 study which they could explain in further detail here on the list, I would
find them helpful in the interest of clearing up these issues about the Masai.
--Ward Nicholson
PALEODIET Archives
Subject: New genetic research dates dogs' origins to 100, 000 years ago
Reply-To:
Date: Thu, 3 Jul 1997 18:40:04 -0500
I just received the latest Science News (6/28/97 issue) which contains a very interesting article on a new
genetic clock study dating the early lineage of dogs. The information may prove of interest here in light of
Ray Audette's observation on the listgroup some weeks ago that small bands of hunters armed only with
atlatls and aided by dogs could be fearsome hunters capable of taking down the largest of mammals. I'll just
summarize the basic points here.
Titled, "Stalking the Ancient Dog: Man's Best Friend May Go Way Back, " the results of the new
mitochondrial DNA studies (widely used in genetic dating, though still controversial) indicate that the origin
of the dog goes back much further than previous estimates of 10, 000-20, 000 years ago--perhaps to well
beyond 100, 000 years ago. The studies weren't able to determine the original geographic origin of dogs but
they did eliminate from consideration any parent species other than the wolf (which has long been
suspected). They also suggest that dogs may have evolved from wolves, not once, but several different times,
as well as the possibility that dogs may have interbred with wolves from time to time.
The study, published in the 6/13/97 issue of Science (no refs given) by Robert K. Wayne et al of UCLA,
looked at DNA from 162 wolves taken from 27 populations in Europe, Asia, and North America, and
compared it with DNA from 140 modern dogs from 67 different breeds around the world. There was such a
wide range of variability between modern dogs and wolves that researchers close to the case say it is
impossible for the genetic variability observed to have evolved in the traditional assumed timeframe of just
10 to 20 thousand years. (This interpretation assumes of course that the molecular-clock dating technique,
which is still controversial, holds up.)
The more ancient timeframe for the origin of the dog can be explained, say the researchers, because even
though the fossil record for dogs is obscure beyond about 14, 000 years ago (after which dog bones are often
found in association with human bones), it has been overlooked until now that wolf bones can be found in
association with human bones going back beyond the 100, 000-year horizon. Thus what were formely
considered "wolves" may in fact have been "dogs-in-process." If wolves and humans were indeed associating
with each other this early in symbiotic fashion, it suggests that we may be looking at a different type of
mutually beneficial relationship than the traditional assumption of "domestication." In other words, 100, 000
years ago or before, wolves might have been "tamed" in some way that did not lead to changes that would
show up in the fossil record. Then with the impending advent of agriculture, late mesolithic or early neolithic
peoples might have begun actually breeding dogs selectively to become different kinds of hunters than
before, or into herders, guards, etc.
175/298 (1997)
Says Elaine Ostrander, a molecular biologist collaborating on a study of the dog genome who works at the
Fred Hutchsinson Cancer Research Center in Seattle, "When we became an agricultural society, what we
needed dogs for changed enormously, and a further and irrevocable division occurred at that point. That may
be the point--at which dogs and wolves were noticeably different physically--that stands out in the fossil
record."
--Ward Nicholson
PALEODIET Archives
From: Ron Hoggan
Reply-To:
Date: Thu, 3 Jul 1997 18:51:53 -0600
First, I would like to thank Staffan for his very interesting and instructive post.
> From: Staffan Lindeberg Subject: Fat, milk and salt
> We cannot understand how dairy products per se can be blamed for the CHD epidemic. But I can. Per
> capita intake of milk is the single environmental factor which is most strongly related to
> international ischaemic heart disease death rates [103], and for males of 19 OECD countries the
> negative relation between mortality from ischaemic heart disease and wine or alcohol intake was
> reduced to non-significance by controlling for dairy products [104]. But epidemiology can never
> prove causality. The cause could be some undiscovered lifestyle factor which is related to milk intake.
Or it could be associated with an autoimmune response to alpha casein. Attachment of milk-derived proteins
to vascular walls could incite a lymphocyte attack that would result in vascular leakage, increased fibrinogen,
and consequent plaquing of the vascular walls. It is a concept I have previously voiced suggesting a gliadininduced autoimmune attack on the vascular walls. But perhaps the facts support a milk-derived protein as the
primary major pathogen in much CHD.
> Or it could be something else in the milk than saturated fat. Dr Jeffrey Segall has suggested that
> it is lactose [105] and recently argued that 'International data show stronger correlations of
> mortality from ischaemic heart disease with per capita supply of dairy products excluding fat than
> with dairy fat, and of estimated lactose than with dairy fat or margarine and other processed fats
> (positively) and vegetable oils and fats, fat of fish or wine (negatively). Butter and cheese,
> which have a low content of lactose, show moderate and zero correlations, respectively.
These might equally be interpreted as suggestive of causation by milk-derived proteins. But, as you said, a
correlation does not constitute causation. Can anyone instruct me as to the content of intact milk protein in
cheese?
> Populations with low or intermediate prevalence of adult lactose absorbers have a lower supply of
> dairy products excluding butter (and therefore of lactose), and a lower mortality from ischaemic
> heart disease, than populations with a high prevalence of absorbers.
Again, the hypothesis of a protein-driven autoimmune attack on vascular walls might find considerable
support in this correlation.
> Specific national and ethnic data suggest that a diet low or relatively low in lactose, in
> populations with low or relatively low prevalence of lactose absorbers, is more consistently
> associated with protection against ischaemic heart disease than are high intakes of unsaturated
> fatty acids, wine, alcohol or dietary fibre.
> In seven countries with a high consumption of dairy products (six at least with a high prevalence
> of lactose absorbers), trends in ischaemic heart disease mortality appear to have reflected
> changes in the supply of milk (and therefore of lactose), but not consistently of butter or
> inversely of unsaturated fatty acids.
What is the protein content of butter?
> The findings reviewed in this paper call for further investigation of the subject,
> epidemiologically and biochemically' [106].
Thanks to previous posts from Staffan, I am aware that a great deal of antibody testing has been done in
association with atherosclerosis. Is anyone aware of any specific anti-casein testing? What about antiendomysium? Anti-reticulin? anti-gliadin?
I would be very grateful for information along these lines.
176/298 (1997)
> In order to be absorbed, lactose is split by the intestinal enzyme lactase into glucose and
> galactose. Paleolithic human adults did not drink milk and were probably, like most adults of the
> world today, incapable of absorbing lactose [107]. Accordingly, galactose is one of the few
> nutrients that did not enter the metabolic system of adults during human evolution.
Did lactase develop in some populations, in response to some other evolutionary pressure or accident? Does
it serve some other dietary function besides splitting lactose?
> ...the Masai (high consumption of whole milk products, no CHD)...
As the traditional Masai diet does NOT include gluten, perhaps they lack the intestinal permeability
necessary for the absorption of intact milk-derived proteins. Perhaps the multifactorial cultural mix of a
highly glutenous diet, to induce the intestinal permeability, in combination with milk consumption, and
perhaps other factors, are all necessary to the current epidemic of CHD.
> Segall states that, among the Masai, 'the milk is consumed largely lactose-fermented, and the
> prevalence of lactose absorbers in adults can be assumed to be low because that in children aged
> 5-14 years is estimated to be 38 per cent [108]' [106]. This is crucial. Does anyone else know
> whether the Masai really ferment(ed) their milk?
It is only crucial if you are looking at the sugars, not the combination of proteins.
> Assuming that man's tastebuds are not superfluous, but nature's way of guiding him to the food he
> needs, let us examine the notion that the cave man diet satisfied only the bitter, sour or pungent
> portion of his tasting apparatus, and not the salty or sweet. Obviously our tastebuds lead us to
> the sweet, but sweet foods during evolution differed dramatically from most sweet foods today
> regarding nutrient density. Personally I would be at least 25 kg heavier if I had let my tastebuds
> guide me through the supermarket.
Or, perhaps, we evolved eating a great deal of fats and meats, and in their current dietary paucity, we have
learned to substitute those foods which are sweet and energize us. As a celiac, I have experienced dramatic
changes in my taste for sweets.
> Yes of course, we are all very similar. But meat and blood are low salt foods and substantial
> evidence suggests that, since nature has not prepared the cave man and his woman for excess salt,
> increasing their salt intake to western standards would increase their risk of hypertension,
> stroke, heart failure, esophageal and gastric cancer, kidney stones and osteoporosis [109].
> Hunter-gatherers by the sea may have added sea water or even sea salt to their foods. But sea salt
> is only 65 per cent sodium chloride, the rest is potassium chloride and magnesium sulphate, and in
> any case the sodium to potassium ratio would not have been as high as for westerners.
Loren Cordain has also asserted a connection between gastric cancer and salt consumption, but I'm afraid I
lack the biochemical background to grasp the concept. Could someone suggest a resource that would bring
me up to speed on that point?
> I am not aware of any evidence that that we do not get more salt than we need from unsalted meat,
> fruit and saturating vegetables [111]. If Enig and =46allon have references please share them with
> us. I have several thousand colleagues here in Sweden who would be very happy to find arguments
> for giving pills in stead of dietary advice to patients with high blood pressure (although the
> effect of pills on their health is lousy [112-114]).
Salt cravings are very common among celiac patients. And, given recent postings on the celiac listserv,
reduced HCL is also a common problem among celiacs. Would any one be willing to speculate on this issue?
I would be very interested in citations supporting this claim. If these reports included other dietary
information, they might hold some very valuable clues to an enhanced understanding of the underlying
pathology.
For instance, if the dietary gluten or casein intake is high, in these rogue investigations that show increased
hypertension on low salt, then there is support for the notion of an underlying autoimmunity. If, conversely,
magnesium is low, the hypertension may reflect dietary deficiencies in minerals and vitamins.
Some very interesting work is currently demonstrating that some vitamins aid some cancer patients in their
battles against malignancy. But that is another story.
Again, I am always grateful to Staffan (along with many other list members) for his very informative posts.
Best Wishes, Ron Hoggan Calgary, Alberta, Canada http://www.panix.com/~donwiss/hoggan/
PALEODIET Archives
Subject: Re: Fat, milk and salt
177/298 (1997)

Reply-To:
Date: Fri, 4 Jul 1997 00:00:05 +0100
At 01.51 97-07-04, Ron Hoggan wrote:
> Or [coronary heart disease] could be associated with an autoimmune response to alpha casein.
Which, like galactose, is another of the few substances for which the adult human metabolic system was not
designed.
> What is the protein content of butter?
According to Swedish food composition tables it is 0.6 mg per 100 g or 0.2 g per MJ (megajoule).
> Loren Cordain has also asserted a connection between gastric cancer and salt consumption, but I'm
> afraid I lack the biochemical background to grasp the concept. Could someone suggest a resource
> that would bring me up to speed on that point?
Case-control studies: Tuyns A. Salt and gastrointestinal cancer. Nutr Cancer 1988; 11: 229-32. Haenszel W
et al. Stomach cancer among Japanese in Hawaii. J Natl Cancer Inst 1972; 49: 969-88. Coggon D et al.
Stomach cancer and food storage. J Natl Cancer Inst 1989; 81: 1178-82. Graham S et al. Diet in the
epidemiology of gastric cancer. Nutr Cancer 1990; 13: 19-34. Hu J et al. Diet and cancer of the stomach: a
case-control study in China. Int J Cancer 1988; 41: 331-5.
Epidemiology and reviews: Howson CP et al. The decline in gastric cancer: epidemiology of an unplanned
triumph. Epidemiol Rev 1986; 8: 1-27. Cordle F. The use of epidemiology, scientific data, and regulatory
authority to determine risk factors in cancers of some organs of the digestive system. 5. Stomach cancer.
Regul Toxicol Pharmacol 1986; 6: 171-80. Joosens JV, Geboers J. Dietary salt and risks to health. Am J Clin
Nutr 1987; 45: 1277-88.
Experimental studies in rats: Shirai T et al. Effects of butylated hydroxyanisole, butylated hydroxytoluene,
and NaCl on gastric carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine in F344 rats. J Natl
Cancer Inst 1984; 72: 1189-98. Takahashi M et al. Effects of sodium chloride, saccharin, phenobarbital and
aspirin on gastric carcinogenesis with N-methyl-N'-nitro-N-nitrosoguanidine. Gann 1984; 75: 494-501. Kim
JP et al. Co-carcinogenic effects of several Korean foods on gastric cancer induced by N-methyl-N'-nitro-Nnitrosoguanidine in rats. Jpn J Surg 1985; 15: 427-37. Tatematsu M et al. Effects in rats of sodium chloride
on experimental gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline-1oxide. J Natl Cancer Inst 1975; 55: 101-6.
> I would be very interested in citations supporting this claim. If these reports included other
> dietary information, they might hold some very valuable clues to an enhanced understanding of the
> underlying pathology.
I am only aware of one such study. It showed unaltered blood pressure but worsened serum total and HDL
cholesterol in patients with non insulin-dependent diabetes (del Rio A, Rodriguez-Villamil JL. Metabolic
effects of strict salt restriction in essential hypertensive patients. J Intern Med 1993; 233: 409-14):
OBJECTIVE. Some observations suggest that a strict low-salt diet may induce unfavourable metabolic sideeffects. The main aim of this study was to analyse the possible consequences of severe salt restriction in
mildly hypertensive patients. DESIGN. The study was carried out through a randomized double-blind
protocol. SUBJECTS. Forty-seven ambulatory patients proceeding from the hypertension unit were initially
admitted: 17 were lost, and 30 non-diabetic mildly hypertensives (DBP 90-104 mmHg) with normal renal
function completed the protocol. INTERVENTION. After a wash-out period, patients were maintained on a
low-salt intake (2.8 +/- 1.0 g day-1 of NaCl) and placebo for 2 weeks, and the same diet and salt supplements
(11.7 +/- 2.5 g day-1 of NaCl) for another 2 weeks, separated by a second wash-out period. MEASURES. At
the end of each dietary period, blood pressure (BP) and body weight were measured, and a blood sample was
taken for determination of routine serum chemistries, plasma lipid and apolipoprotein concentrations,
immunoreactive insulin (IRI), and plasma renin activity (PRA). Urinary 24 h excretion of sodium and
potassium were measured. RESULTS. During the salt restriction period BP did not change, weight lowered,
and PRA raised. There was a significant increase in serum level of creatinine, uric acid, IRI, total cholesterol
and apo B, and a decrease in HDL cholesterol and apo A-I. CONCLUSION. As previously suggested, these
observations seem to indicate that strict salt restriction may cause, at least in the short-term, adverse
metabolic changes in hypertensive patients".
178/298 (1997)
In a recent (1994) textbook of hypertension (1328 pages), edited by JD Swales who is a well known critic of
salt restriction in hypertension, there are are two chapters dealing with salt. I can not find one single study
there (out of many) which suggests that blood pressure would increase by a decreased intake of salt. What
they did show was either a decrease or no effect.
Cheers,
Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: Fat, milk, and salt
From: Dean Esmay
Reply-To:
Date: Sat, 5 Jul 1997 12:05:49 -0400
To the best of my knowledge, there is no animal which consumes milk outside of infancy--except man.
To the best of my knowledge, there is also no animal which consumes the milk of -other species- in any
significant quantity--except man.
Moreover, it would be wrong to say that man regularly consumes milk, because most humans do not. It is
only in the West (and some limited parts of Africa) that people eat dairy on a regular basis. In most of the
world, regular consumption of the milk of animals would be considered either disgusting or simply a bizarre
aberration of white Westerners.
Both the carbohydrates (especially lactose) and the proteins (such as casein and lactoglubulin) are quite
different in character than the proteins or carbohydrates humans normally encounter in their other foods.
It's not clear to me when humans started the practice of herding animals in order to drink their milk. Perhaps
some more knowledgeable member of the list can share with us some thoughts on that?
PALEODIET Archives
Subject: Answers to questions concerning our latest contribution
From: Reply-To:
Date: Sat, 5 Jul 1997 19:09:44 -0400
Thank you all for the lively debate. Following are answers to queries that have come in.
A. Replies to Dean Esmay:
1. Our figures come from the USDA. We stated that SATURATED fat intake remained the same between
1935 and 1974--total fat consumption rose between 1935 and 1974 (from about 150 grams/capita/day to
about 170 g/c/d.) Animal fat consumption actually declined (from 100 g/c/d to about 90 g/c/d) but there was
an increase in consumption of vegetable oils (from just over 50 g/c/d to over 80 g/c/d.) We cannot say,
however, that saturated fat intake declined during this period, because vegetable oils contain some SFAs.
2. The authors of the reference about SFAs reducing Lp(a) are Khosla and Hayes. Please let us know if you
cannot find this on Medline. You should also be able to find it on Agricola. As the abstract of this review
article does not mention the effect of SFAs on Lp(a), we will quote directly from the relevant passage on
page 330: A subsequent analysis of frozen plasma from this study revealed that the trans diet also resulted in
significantly higher concentrations of Lp(a) than those resulting from the oleic acid-rich diet. However, a
surprising, but unheralded, aspect of the Lp(a) analysis was that the saturated fatty acid-rich diet produced
significantly lower Lp(a) concentrations than the oleic acid-rich diet.
179/298 (1997)
3. The whole HDL/LDL hypothesis comes from the Framingham study, whose coordinators utilized
questionable methodologies and made many omissions in reporting the data. For an excellent discussion of
this issue see Smith, Russell, L "Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of
the Literature" (1991) Volume 2, pp 3-78 to 3-100. Smith concludes: "In 40 years of several hundred
Framingham reports, this writer has found neither an actual correlation coefficient published for either total
or LDL cholesterol nor a figure showing the CHD mortality and/or morbidity rate as a function of LDL level
. . . Examination of published Framingham data. . . indicate that the correlation between CHD and total or
LDL cholesterol is probably under 0.3. The objective and statistically sophisticated scientist would consider
these correlations as unrepresentative of cause and effect relationships and would analyze the associated data
base to find reasons why the observed correlations occurred at all." (pp1-2 to 1-3) An interesting sidelight to
this issue is an item reported in a recent newsletter from Dr. Atkins, who states that high HDL levels are
indicative of an underactive thyroid. If this is the case, then the logical conclusion is that high HDL
predisposes to CHD, and not the reverse.
4. Regarding your most recent contribution about milk consumption, one could also say that man is the only
animal that uses tools, lives in houses, wears clothes, speaks and writes books--and uses milk products. Is the
use of milk products thus one of those attributes that sets man apart from the beasts? We reiterate that the use
of milk produsts is associated with long and healthy life in many parts of the world--Soviet Georgia, Hunza,
Vilcabamba in Equador, and the supremely healthy Swiss villagers studied by Weston Price in the 1930s.
B. To Robert Crayhon:
4. Regarding stearic acid, we do mean that some studies have shown stearic to raise blood cholesterol--some
studies show it to be neutral and some studies show 18:0 to lower cholesterol. Thus nothing can be
concluded about the effect of stearic acid on cholesterol levels. However, Dr. Cordain was arguing that
modern beef feeding methods lowered components that lower cholesterol (stearic acid) and raised
components that raise cholesterol (16:0 and 14:0). We were merely demonstrating that no real conclusions
can be drawn about the differences between wild and domesticated meat in regards to its effect on serum
cholesterol levels.
5. Without giving specific references, we think it is a given that the different fatty acids given in pure form
would not have the same effect as those fatty acids given as components of whole foods--this certainly is the
case with amino acids. Remember also, that in many of the animal experiments, animal fats were given to
vegetarian animals (such as rabbits) which of course led to pathological responses.
6. We hope you will publish the results you have had with hyperlipidemic clients using eggs, meat and other
animal products while eliminating the fabricated foods and refined carbohydrates. We need to have more
citations in the literature about these kinds of real-world results. What you have here is a healthy lowering of
cholesterol levels because the body does not need to have as much cholesterol to serve as an antioxidant and
protective mechanism against rancid vegetable oils; rather than the kind of pathological reduction that often
temporarily occurs when individuals are put on a high-PUFA diet. This latter situation forces cholesterol into
the tissues to give them body and stability in the absence of sufficient SFAs.
C. To Don Weiss and Dean Esmay:
Regarding the study by Kaneko et al. The abstract is very clear. When 27-year-old females ate meat, they
absorbed more calcium. Since they were evidently in calcium balance, they excreted more calcium, i.e. the
excess that they did not need. They also excreted the extra sulfur from the sulfur-containing amino acids
which are found in abundance in meat, but are deficient in soy proteins (soy formula for infants must have
added methionine to overcome this deficiency.) The results of the added meat is as would be expected in
normal homeostasis. We would expect someone in appropriate calcium balance to do just that. When the soy
protein was fed, there was no increased absorption and excretion of calcium; this too is as expected since the
soy contains components that inhibit uptake of calcium. We do not have the actual paper so do not know if in
fact the soy might have caused a negative balance in some of the subjects.
Correctly interpreted, the abstract does not show that eating meat causes a loss of calcium. For further
research on this subject, see the careful studies of Herta Spencer, who did not find that eating meat caused
calcium loss. (Spencer, et al "Effect of a high protein (meat) intake on calcium metabolism in man" Am J
Clin Nutr 31 (12):2167-2180 (Dec 1978); and Spencer et al, "Further studies of the effect of a high protein
diet as meat on calcium metabolism" Am J Clin Nutr 37 (6):924-929 (Jun 1983.)
PALEODIET Archives
Subject: Answers to questions concerning our latest contribution
From: Dean Esmay
180/298 (1997)
Reply-To:
Date: Sat, 5 Jul 1997 20:41:00 -0400
Fallon & Enig write, in response to my recent generalizations about dairy:
> Regarding your most recent contribution about milk consumption, one could also say that man is the
> only animal that uses tools, lives in houses, wears clothes, speaks and writes books--and uses
> milk products. Is the use of milk products thus one of those attributes that sets man apart from
> the beasts?
I chuckled when I read this, but I must emphasize that when I pointed out that man appears to be the only
animal on the planet that regularly consumes milk, I was answering the point of a person who had inquired,
"why would we exclusively consume one food for the first 2-4 years of our lives and then abandon it
altogether?" My response to this question was rhetorical and meant to point out the obvious: cow and goat
milk are nature's way of feeding infant cows and goats, not adult humans, and there's no animal on the planet
that requires its own milk outside of adulthood, let alone that of a different species.
Now I'll ad a tongue-in-cheek response to Enig & Fallon: It is difficult to imagine what metabolic
pathologies might be caused by daily consumption of tools, houses, or books, but I hope you will grant the
possibility that if we all started chewing on hammers, huts, and Hawthorne, we might get sick. ;-)
More seriously, my point was that there I no reason to suggest that there is any NEED for dairy outside of
infancy. I know of no evidence that adults who drink milk are healthier than adults who do not. Most
humans, in fact, are lactose-intolerant, and even that minority which continues to secrete lactase into
adulthood frequently lose this ability later in life (references available upon request). Casien and
lactoglobulin, the primary proteins in cow's milk, are both rather different from the proteins found in meats,
eggs, and nuts, and a number of people are allergic to one or both. There are even studies suggesting a link
between casein and the development of autism in children, with some interesting and promising studies
going on right now with treating autistic people with dairy-free diets (references for this also available upon
request; in fact I hope to get more information from researchers working on this in the near future). I'm not
sure what to make of the assertions Enig & Fallon make versus the countering data provided by Lindeberg;
both clearly require some contemplation.
By the way, for an interesting analysis of the difference between human and cow milk (which I'm sure Fallon
& Enig are entirely aware of, but which others on the list may want to look at out of simple curiosity), have a
look at http://classes.aces.uiuc.edu/AnSci308/HumanLact.html#Macro -- the differences are quite
substantial.
PALEODIET Archives
Subject: Origins of milk-drinking / problems of milk
Reply-To:
Date: Sun, 6 Jul 1997 11:02:53 -0500
Dean Esmay asked about the timescale of the origins of milk-drinking. Here is some information from a
paper by Frederick J. Simoons (1988) "The Determinants of Dairying and Milk Use in The Old World:
Ecological, Physiological, and Cultural, " In JRK Robson (ed.), Food, Ecology and Culture: Readings in the
Anthropology of Dietary Practices. New York: Gordon and Breach. (pp. 83-91)
First a few statistics about modern milk tolerance:
- 70% of the world's population is lactose-intolerant. This figure includes: - 90-100% of Asians. - 75% of
African-Americans. - 80% of Native Americans. - 50% of Hispanics worldwide. - 20% of CaucasionAmericans.
[taken from: Mogelonsky, Marcia (1995) "Milk Doesn't Always Do a Body Good, " American
Demographics, Jan. 1995 issue.]
Babies are born with the capacity to digest the lactose in milk via production of the digestive enzyme lactase.
Starting around 3-4 years old, however (if I am remembering correctly), this capacity is normally lost. This
would have been the baseline *normal* state of affairs prior to the advent of agriculture.
181/298 (1997)
The 30% of the world's population that does not exhibit adult lactose intolerance can trace its heritage very
closely to the earliest populations of humans that began the practice of herding animals for their milk. The
earliest milking populations in Europe, Asia, and Africa began the practice probably around 4, 000 BC.
Simoons says:
"The distributional pattern and historical record of milking and nonmilking in the Old World suggests that
the milking habit developed somewhere within the Eurasian-African landmass and spread outward. The
earliest convincing evidence we now have of milking is for the Sahara Desert, during the middle of the socalled Pastoral Period (circa 5500-2000 BC) of the Neolithic. [Elsewhere Simoons puts the best-estimate
date at approx. 4000 BC.] At that time the desert was somewhat rainier and able to support pastoralists,
whose most prominent animals were common cattle. The pastoralists' abundant, naturalistic rock drawings,
reminiscent of Lascaux and Altamira in Europe, include clear milking scenes. We cannot, however, be
certain that the milking habit originated in the Sahara; whether, as many scholars suspect, it originated
somewhere in Southwest Asia, or whether it developed elsewhere."
Simoons goes on to delineate the world's lactose-intolerant populations today, saying:
"Of special significance are the world patterns of high and low incidence of primar adult lactose
malabsorption, for these bear a considerable similarity to the traditional patterns of milking and nonmilking
sketched previously. For example, many groups with a high prevalence of such malabsorption, have
traditionally been nonmilking. These include Greenland Eskimos, various American Indian tribes, Americanborn Negroes and Orientals, Yoruba and Ibo in Southern Nigeria, Bantu agriculturalists of the Congo,
Bushmen, Chinese, Japanese, Thais, Indonesians, Filipinos, native Fijians, Australian aborigines, and natives
of New Guinea. Indeed, all groups tested so far whose origins lie in the traditional zone of nonmilking have
high prevalences of primary adult lactose malabsorption. Of the groups found to have low prevalences of
such malabsorption, moreover, all seem to come from long backgrounds of consuming abundant dairy
products in lactose-rich forms. These include Danes and certain other northwest Europeans, their overseas
decendants in the Americas and Australia, the pastoral Fulani of Nigeria, the Hima and Tussi of East Africa,
Bedouin and other Saudi Arabs, and various groups in the northwest of the Indian subcontinent. Differences
in the prevalence of primary adult lactose malabsorption are particularly striking in the United States, whose
people are quite varied in the ethnic and racial origins."
After a lengthy analysis, Simoons concludes, "The strong suggestion is that we are dealing with a genetic
condition, that primary adult lactose malabsorption is the normal state in animals and man, and that selection
for high group prevalence of absorption has developed during a long history of using lactose-rich dairy
products." [i.e., only in those populations with a history of it]
One estimate of the time needed for lactose tolerance to become the norm rather than the exception in a
population where milk-drinking is regular is that it could occur in as little as 1, 150 years in populations with
sufficiently strong cultural pressures for it [Cavalli-Sforza et al 1994 "The History and Geography of Human
Genes. Princeton, NJ: Princeton Univ. Press. p.13]. For Northern Europeans, there is research showing the
prevalence of lactose tolerance developing from 5% to approx. 70% in about 250 generations (roughly 5000
years). [Aoki K. (1991) "Time required for gene frequency change in a deterministic model of gene culture
coevolution, with special reference to the lactose absorption problem. Theoretical Population Biology vol.
40, pp.354-68.] (Thanks to Loren Cordain for pointing out this latter reference to me.)
However, lactose tolerance is probably only one among a number of adaptations that would have to occur for
full adaptation to the consumption of other animals' milk products to take place without health repercussions.
(Dean mentions the casein and lactoglobulins in animals milk differ substantially from human milk, for
example.)
Perhaps Loren might expand on other troubles with milk, prominent among them, the calcium/magnesium
ratio, I believe, which he mentioned to me briefly in a separate conversation. Basically the situation as I
recall it is that in the Paleolithic diet the Ca:Mg ratio is approx. 1.0. In milk and dairy products the ratio is
12.0, and can skew the overall dietary ratio to 4.0 when added to the usual American diet. (How it would
affect the overall ratio in an otherwise Paleolithic diet I am not sure.) Loren, perhaps you could go into the
health repercussion of excessive calcium relative to magnesium?
I might add here that an interesting side-question I have not seen answered to my satisfaction is whether
despite such problems, dairy products in moderation might prove of some help in other ways to those who
eschew meat (i.e., vegetarians) and serve as something of a poor-second-cousin meat substitute. Having run a
newsletter in the past for vegetarians, it seemed to be the case that those who were having troubles on a
vegetarian diet diet often improved when they included animal by-products such as dairy and/or eggs, if they
completely ruled out any meat (as they almost inevitably did, of course). The potential negative long-term
consequences of doing so, however, and whether they would be worth any positives, would be the issue here.
182/298 (1997)
--Ward Nicholson
P.S. Mary and Sally: In your Saturday post addressing questions to your previous post, I did not see any
commentary regarding my question about George Mann's research on atherosclerosis in the Masai (large
milk-drinkers). (Perhaps my question was overlooked due to a subject line not tied to your original post?)
Would be most interested in any knowledge you have of later research by Mann or anyone else on the Masai.
Thanks.
PALEODIET Archives
From: Reply-To:
Date: Sun, 6 Jul 1997 21:30:25 -0400
Regarding Simoons assertion that milk drinking dates back only 4000 years, there was recently an exhibition
of ancient statues from Jordan at the Smithsonian Institution here in Washington DC. The site from which
the statues were excavated dates back to 7200 BC. We quote from the brochure: "The people of Ain Ghazal
lived year-round at the site, relying for their subsitence on hunting, herding and farming. They ate meat and
milk products from the goats they herded and grew wheat, barley, lentils, peas and chickpeas. . . " So milk
drinking dates back at least 9000 years. (By the way, we have the upmost respect for Simoons whose book
Food In China should be read by all.)
When we consider how milk products are processed in traditional societies, the debate over lactose
intolerance becomes moot. The fermenting of milk into yoghurt, cheese or any one of the myriad of
fermented milk products found throughout the world, partially or fully digests the lactose and makes milk
products tolerable to the vast majority, even the lactose intolerant. On the other hand, even those with a high
tolerance for milk products may have a hard time digesting modern supermarket milk which is pasteurized,
has a low milk fat content and comes from freak pituitary cows eating inappropriate feed.
To Ward Nicholson: We missed your question on the Masai--could you repost?
Sally and Mary
PALEODIET Archives
Subject: Re: PALEODIET Digest - 6 Jul 1997 to 7 Jul 1997
From: Niccolo Caldararo
Reply-To:
Date: Wed, 9 Jul 1997 01:31:19 -0400
Dear Sally and Mary:
Your post contains quite a number of assertions supported by no evidence. Beginning with the 7, 200 B.C.
milk use statement, one would expect a better citation than a Smithsonian brochure (I have the utmost
respect for the Smithsonian, but really....). It is interesting to hear that there is only one kind of lactoseintolerance and that all the world's people respond to yogurt the same as well as to "supermarket milk".
Niccolo Caldararo
PALEODIET Archives
Subject: More from Sally and Mary
From: Reply-To:
Date: Wed, 9 Jul 1997 12:04:53 -0400
Re: Ward Nicholsons queries about the Masai and Lactose intolerance
183/298 (1997)
In the introduction to his book "Coronary Heart Disease" (available from Price-Pottenger Nutrition
Foundation 619-574-7763) Mann states on page 7: "In the 1960s we examined about 1500 Masai subjects in
Kenya and Tanzania. The Masai are a pastoral, nomadic people who consume mainly milk and meat, and in
large quantities since they are active people. We found them to have cholesterol levels below 170 mg/dl and
our autopsies of 50 adult males showed little evidence of atheroma. . . The coronary vessels often showed
fibrotic scarring, but the subjects coronary arteries enlarge in lumenal dimensions with increasing age. Thus,
these animal fat eaters show neither hypercholesteremia, nor atheroma, nor heart attacks."
Fibrotic "scarring" is a phenomenon that occurs universally at certain locations in the blood vessels in
response to pressure gradients. This phenomenon is discussed in a chapter by the pathologist Meyer Texon in
the same volume. The gradual buildup of such lesions is a protective device, and not the same as
atherosclerosis which involves pathogenic plaques that may occlude the arteries. These contain large
amounts of calcium and fatty material that is oxidized and polymerized. By the way, the International
Atherosclerosis Project, in which 31, 000 autopsies from 15 different countries were examined, determined
that vegetarians have just as much atherosclerosis as meat eaters, and there was no correlation between
amount of fat in the diet nor the level of serum cholesterol with the amount or degree of atherosclerosis. (Lab
Invest 1986 18:465)
Continuing the debate on milk products, we are arguing that even those with adult lactase deficiency can
tolerate fermented milk products in which the lactose has been wholly or partially converted. See "Modern
Nutrition in Health and Disease" 8th Edition 1994, page 40, from which we quote: "Adult lactase deficiency
is the most common of all enzyme deficiencies; well over half the worlds adults are lactose intolerant. Small
quantities of lactose can be tolerated, however, and most individuals can tolerate up to 100 ml of milk (5 g
lactose) without any symptoms."
Geographic areas where the inhabitants traditionally consumed milk products include the most of Europe,
Middle Europe and Russia, the entire Mediterranean basin, Asia Minor, northern Africa, parts of central
Africa, Ethiopia and some areas on the east African coast, all areas inhabited by Arab groups, all of India and
the Himalayas, Southeast Asia and northern China.
To sum up: Milk products have been around a long time, and have been consumed by many population
groups. Most people can consume them to advantage provided they have been properly produced and
processed. In fact, consumption of milk products is associated with longevity and good health in several
traditional societies. Such products provide many important nutrients including saturated fats, fat soluble
vitamins, protein, calcium and many other minerals. The fact that modern milk products are so poorly
tolerated, and associated with a number of diseases, should serve as a warning against the kind of factory
farming, genetic manipulation, inappropriate feeding and industrial processing that dominates today's milk
industry.
PALEODIET Archives
Subject: Re: Chinle Dialysis Center
From: Art De Vany
Reply-To:
Date: Wed, 9 Jul 1997 12:20:18 -0700
Chinle is a small town in Northern Arizona that is the gateway to Canyon de Chelly, a smaller and lesser
know competitor to the Grand Canyon. Chelly's intense, pure, iron oxide reds, narrow span, and sheer, even
concave, rocky cliffs and stark towers of rock are a sharp contrast to the broader vistas, mixed colors, and
sloping walls of the Grand Canyon. Some think it is more beautiful even than the Grand Canyon.
The town is deep in Navajo country, but the signs are subtle. It looks like any rural town that is just getting
by; there are no pueblos, or adobe dwellings, just the same kind of run down houses and gas stations that you
could find anywhere in America's backcountry. The houses and garages are littered with the kind of rural
junk --- dead cars and tires and farm machinery, discarded refrigerators and household detritus --- that seems
to infect rural America where ever you go.
The first tell-tale sign that this is indian country are the blighted, government-issue, housing projects that
have replaced the beautiful, traditional indian pueblos and adobe dwellings in much of Navajo country. (Can
you write a government spec for adobe? Probably not, so you have to build these wretched little boxes about
two feet apart and put them behind chain link.)
184/298 (1997)
The second tell-tale sign is the absence of liquor stores. These carbohydrate intolerant, insulin-resistant
peoples have tried strictly to limit the presence of liquor stores, or prohibited them outright, on lands they
control. A correlated sign that the nearest liquor store is some distance down the highway are the twisted
remains of horrific traffic accidents --- most of them head-on collisions --- scattered along the backlots of the
town's gas stations and garages. Some distance out of town, I saw an industrial strength liquor store
surpassing even Tony's at Westwood and Santa Monica in West LA. A drive up window, huge steel doors
that could be pulled over the automatic glass entry to block late-night entry (the building also was steel),
pallets of beer stacked to the ceilings, whiskey bottles of every size (some larger than I have ever seen
before), and no floor or refrigerator space wasted on GatorAde or magazines.
The most chilling sign that we were in Indian country was the dialysis center. Chinle is a small town for a
dialysis center, we thought, but this pattern repeated itself in many of the small settlements we passed
through on our way to Santa Fe. My wife is (juvenile onset) diabetic and we know all too well what a
dialysis center signifies: near epidemic levels of adult-onset non-insulin dependent diabetes among the
Amerindians of all tribes, not just the Navajo, but the Zia, and Pueblo, and Pima and all the other tribes
throughout New Mexico and Arizona. Each settlement we passed through became a depressing search for the
dialysis center and the government issue housing, reliefed only by the beautiful country, the splendid
pueblos, and a surprising sign in Jemez, in the hills south of Los Alamos Labs, that read "Archery Range" (a
favorite recreation for indians, or a place to keep skills intact for an uprising?).
In Chinle, the dialysis center is on a dusty side road, right across the road from the swap meet. We wandered
through the swap meet, but quickly felt like intruders and left. We felt awkward standing there looking at the
frank poverty displayed on the blankets and tables and pick up truck beds where goods were offered for sale.
But, a deeper, starker irony was this: if you looked around the ring of displays, at regular intervals you saw
huge colorful bottles of sweet syrups on large tables. They were there to flavor the ice cones the children
were eating. Nearly a quarter of all the booths were selling icy, sugary syrup, setting the kids up for the
dialysis center just across the road.
Adults were drinking sugary cokes; there was not a diet drink to be found (they may not be all that great
either, with their foreign proteins and sugary-mimicking properties). The other substance being offered at
food booths was Navajo fry bread, a tortilla-like, flat bread made of refined white flour (government issue,
straight from the subsidized, carbohydrate producing giants like Archer-Midland) and some lard.
Judging from what is for sale at the swap meet (never the best food anyway) and the convenience store,
where at least 90 per cent of the calories on the shelves are simple carbohydrates, the Navajo diet has them
on the fast track to adult-onset diabetes. You and I would have diabetes if we ate like this.
Arthur De Vany Professor http://www.socsci.uci.edu/mbs/personnel/devany/devany.html Institute for
PALEODIET Archives
Subject: Paleo Art
From: Art De Vany
Reply-To:
Date: Thu, 17 Jul 1997 12:03:07 -0700
I have tried without success to find paleolithic art reproductions that I might hang on my office walls.
None of the graphics, or repro shops, or galleries carry cave art, here in the US or even in France. Nor can
one find listings in the catalogues the stores order from.
While there are many beautiful books containing wonderful cave art, there seem to be no life size
reproductions around.
Has anyone else out there had success in finding paleolithic art in a size and format suitable for display?
Art De Vany
PALEODIET Archives
Subject: The Cancer Connection
From: Ron Hoggan
Reply-To:
185/298 (1997)
Date: Fri, 18 Jul 1997 22:47:30 -0600

To those of you who are also on the celiac list, I apologize for posting it where you will see this twice. It was
actually someone on this list whose comments prompted me to write this, and as it pertains to some of the
discussion here, it seemed appropriate to post it.
Best Wishes, Ron
The Cancer Connection by Ron Hoggan
There is much evidence linking untreated celiac disease with malignancy. I have recently been notified of
publication of a report I have written on that connection, which is promised for the September, 1997 issue of
_Medical Hypotheses_ (1). In that report, I combine a review of the literature with an ouline of a possible
biochemical pathway whereby psychoactive peptides derived from the pepsin digests of wheat, rye and
barley may downregulate the activation of natural killer cells, the body's first line of defence against
malignancy. This is not a postulation that glutenous grains are carcinogenic. Humankind has been exposed to
carcinogens throughout its ~two million year evolution. But it is only in recent centuries that malgnancy has
increased exponentially, and has struck so many children and adolescents. This is clearly a counterevolutionary trend when youngsters are afflicted, because the incidence should be decreasing over time, as
these youngsters' genes are being pruned from the gene pool. There is some evidence which has come to
light since my aforementioned report, which will be of interest to celiacs and members of their families.
M.Stanislas Tanchou, a truly visionary physician, who campaigned with Napoleon Bonaparte, presented a
paper to the Paris Science Society in 1843, which was a complex statistical examination of malignancy,
offering evidence of increased malignancy with increased civilization(2). One of the prime indicators of a
civilizing trend was a diet which included cereal grains. The greater the consumption of these foods, the
greater the incidence of malignancy (3).
Dr. Chris Reading, an orthomolecular psychiatrist, in Australia, has documented the treatment of five cancer
patients for depression (4). His testing for food allergies, and subsequent treatment of depression with dietary
exclusion of cereal grains resulted in total remission of the cancers (which were also given conventional
treatments) in all five patients he reports treating. One of these patients did die, but that was from the cancer
treatment.
There are also two reports in the _Journal of Clinical Gastroenterol_(5) _Lancet_ (6) which I cite in my
_Medical Hypotheses_ article. These reveal a total remission of malignancy in each patient. One report then
recants the original diagnosis, and identifies the correct diagnosis as lymphadenopathy. In the other report,
which spurs a heated debate, the original diagnosis is supported by a resected section of malignant bowel,
and there can be no doubt as to the correct diagnosis.
Further, in a 1977 report, in _Nutrition and Cancer_ (8), from Stanford University, *all* the children
suffering from radiation and chemotherapy damage to the small bowel recovered fully from their chronic
enteritis, and suffered *no* relapse of either the bowel obstruction or the disease. The treatment they were
given was a gluten-free, dairy-free, low fat, low residue diet.
In an obscure Czech journal, a report has recently indicated that one or more of the gliadins, a sub-set of
proteins in gluten, may also interfere with natural killer cell activation in peripheral blood (9). They tested
the levels of natural killer cell activation in normals, and in treated celiacs, and found no significant
difference. BUT, after 30 minutes' exposure of the celiacs' blood to gliadin, there was a reduced activation of
natual killer cells.
For the last hundred years, billions of dollars have been spent identifying carcinogens. Most of what we
encounter in our environment appears to have some measure of carcinogenic potential. Unfortunately, we
have failed to recon that Humanity has been exposed to most of these carcinogens throughout its evolution.
Conventional wisdom has pointed to the the increasing levels of chemical pollution and environmental
damage. And I do not doubt that these factors are contributing to the current epidemic of malignacy. What I
do doubt is that segment of the population, variously reported at 20% to 30%, which has the HLA factors
which predispose to celiac disease and many other autoimmune diseases, can mount an adequate immune
response, with natural killer cells, against malignancy.
Sources:
1. Hoggan R, "Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens" in press _Medical
Hypotheses_ ;1997
2. Tanchou S, "Statistics of Cancer" _London Lancet_ 1843; Aug 5, 593
3. Audette R, personal communication
4. Reading C, Meillon R, _Your Family Tree Connection_ Keats; New Canaan, Conn.: 1988
186/298 (1997)
5. Wink A, et. al. "Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Deit in Celiac Sprue"
_J. Clin. Gastroenterol_1993; 16(4): 317-319
6. Wright DH, et. al. "Coeliac disease and Lymphoma" _Lancet_ 1991; 337:1373
7. Wright DH, et. al. letter _Lancet_ 1991; 338: 318-319
8. Donaldson SS, "Effect of Nutrition as Related to Radiation and Chemotherapy" _Nutrition and Cancer_
Winick ed. 1977; Wiley & Sons, New York, 137153
9. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H, "Natural killer cell activity in coeliac
disease: effect of in vitro treatment on effector lymphocytes and/or target lymphoblastoid, myeloid and
epithelial cell lines with gliadin" _Folia Microbiol_ 1995 (Praha) 40; 6: 615-620
* Posters are asked to summarize private replies back to the List *
PALEODIET Archives
Subject: Peter D'Adamo's Eat Right 4 Your Type
From: "John P. Hughes"
Reply-To:
Date: Wed, 23 Jul 1997 10:31:15 -0400
Peter D'Adamo, in his book Eat Right 4 Your Type, posits that no diet is right for everyone. His argument
centers around the body's response to lectins as determined by blood type. I'm interested in opinions
regarding his work.
*********************************************
John Hughes Jr.
PALEODIET Archives
Subject: Neanderthal DNA
From: Ray Audette
Reply-To:
Date: Sat, 19 Jul 1997 00:08:24 -0700
A recent analysis of DNA extracted from a single Neanderthal bone has led some to speculate that they were
not our direct ancestor because the split seems to occured much longer ago than the fossil record would
indicate.
NeanderThin comes from the gracile form of Neanderthal. In structure, a modern human is a slender form of
Neanderthal, one having less muscle mass and a smaller head (and brain). Many examples of gracile forms
of wild animals becoming our domestic animals through neoteny exist including the dog and the horse.
Just as the bones of Neanderthal indicate that this split occured only 60, 000 years ago and the DNA sugests
600, 000 years ago, so bones recognizable as dogs appear only 14, 000 years ago even though DNA suggest
the split from wolves occured 135, 000 years ago. The similarity in ratios may tell us something about
neoteny and the evolutionary time scale necesarry to achieve it through enviromental presures.
These presures may have included the earlier beginings of the ice age on the tropical homidid and the later
warming of the earth for the temperate/arctic wolf. It is only when both species underwent a significant
amount of this process and existed in the same enviroment that domestication appeared.
Regardless of the time scale involved, wolves are still considered to be the progenitors of dogs and I have no
doubt that Neanderthals are the progenitors of NeanderThins. The complexities of the processes involved are
not fully understood yet to say otherwise. Isolated popultions of wolves still exist despite dedicated efforts to
wipe them out and the vastly higher population of dogs, making the premise stated by these scientists based
on only one sample somewhat suspect. If we could mate with Neanderthals and produce fertile offsprings, as
wolves do with dogs (thus being the same species) is not answered by this experiment on only one sample.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 18 Jul 1997 to 19 Jul 1997
187/298 (1997)
Reply-To:
Date: Wed, 23 Jul 1997 14:30:01 +0100
Ray Audette wrote:
> A recent analysis of DNA extracted from a single Neanderthal bone has led some to speculate that
> they were not our direct ancestor because the split seems to occured much longer ago than the
> fossil record would indicate. NeanderThin comes from the gracile form of Neanderthal. In
> structure, a modern human is a slender form of Neanderthal, one having less muscle mass and a
> smaller head (and brain). Many examples of gracile forms of wild animals becoming our domestic
> animals through neoteny exist including the dog and the horse.
The modern human form is not simply a gracile or neotonous form of the Neanderthal form. We do have a
smaller head and brain but realitve to our bodysize they are larger. The few Neanderthal juveniles whixch
have been studied have many of the features (e.g. browridges) which distinguish hth two species (or subspecies depending on your point of view).
> Just as the bones of Neanderthal indicate that this split occured only 60, 000 years ago and the
> DNA sugests 600, 000 years ago, so bones recognizable as dogs appear only 14, 000 years ago even
> though DNA suggest the split from wolves occured 135, 000 years ago. The similarity in ratios may
> tell us something about neoteny and the evolutionary time scale necesarry to achieve it through
> enviromental presures.
We have 100ka modern humans at Qafzeh and Skhul in Israel and also in of similar age. Neanderthals
existed from 2-300ka through to 27ka. Therefore we cannot place a divergence at 60ka: the late
Neanderthals, including the Neander Valley 1 specimen analysed for mtDNA must have diverged from
modern humans at a minimum of 100ka if there was any descent from Neanderthals to modern humans and
possibly before 200ka if Neanderthals and modern humans share their most recent common ancestry in homo
erectus. Can you give a reference for the dog domestication genetics please?
> These presures may have included the earlier beginings of the ice age on the tropical homidid and
> the later warming of the earth for the temperate/arctic wolf. It is only when both species
> underwent a significant amount of this process and existed in the same enviroment that
> domestication appeared. Regardless of the time scale involved, wolves are still considered to be
> the progenitors of dogs and I have no doubt that Neanderthals are the progenitors of NeanderThins.
Who then are NeanderThins? The Neanderthals only occupied Europe and the western part of Asia, and it is
clear that if modern humans descend from them, then modern humans derive from a number of ancient
populations around the world of which Neanderthals as the ancestors of Europeans were but one race or subspecies. This is the multi-regional hypothesis of modern human origins in its extreme form. In any more
moderate statement Neanderthals are the population of ancient hominids least likely to have contributed to
the modern gene pool, due to the temporal overlap described above.
> The complexities of the processes involved are not fully understood yet to say otherwise. Isolated
> popultions of wolves still exist despite dedicated efforts to wipe them out and the vastly higher
> population of dogs, making the premise stated by these scientists based on only one sample
> somewhat suspect. If we could mate with Neanderthals and produce fertile offsprings, as wolves do
> with dogs (thus being the same species) is not answered by this experiment on only one sample.
The question of interbreeding will never be answered by DNA studies. Genetic studies alone might lead one
to believe that a Great Dane could mate with a Chihuahua, but it is actually a physical impossibility. We will
never know just what the Neanderthal softparts were like and so the question of interbreeding will never be
answered. In thye same way if wolves were extinct we would never know whether they could interbreed with
dogs, but we could still make the deduction that the two populations (whether the same species or not) had a
last common ancestor at 135ka, and that the groups of ancient canids which gave rise to wolves and dogs
have been diverging from that point, even if they have not yet reached the point of speciation. A wolf subspecies which has arisen in the last 135ka will not be ancestral to the domesticated dog although it is related.
For humans the situation is similar but different: we have a last common hominid ancestor for Neanderthals
and modern humans at 600ka, which is before the known appearance time of both of them and thus shows
that the Neanderthals were not the ancestors of modern humans.
Andrew Millard
Reference Stringer, C & Gamble, C "In Search of the Neanderthals" Thames & Hudson 1993
188/298 (1997)
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Glucose sparing
Reply-To:
Jennie Brand Miller
Date: Thu, 24 Jul 1997 11:56:53 +1000
Dear Everyone,
In Arthur de Vany's last posting, he talked about the rationale for insulin resistance being a mechanism that
spares glucose for the brain in an environment where dietary CHO is scarce. To my knowledge, we were the
first to put this hypothesis forward in our paper 'The carnivore connection: dietary carbohydrate in the
evolution of NIDDM' in Diabetogia, 1994; 37: 1280-86.
We postulated that the ice ages (over the last 2 million years of human evolution) resulted in a diet for many
human groups dominated by game and marine animals with very few plants and therefore high in protein and
fat and low in carbohydrate. We believe this diet would select for more insulin resistant genotypes.
We are in the process are obtaining more support for this hypothesis. We have shown that the plasma glucose
profile after protein feeding is more favourable (ie higher) in insulin-resistant people compared with insulin
sensitive ones (the latter show a decline in blood glucose). We've published this in abstract form only
(Proceedings of the Nutrition Society of Australia (1994, full details on request) and are about to submit the
full paper.
It is also interesting to note that acute exercise has exactly the same effect on glucose metabolism at the
cellular level as a pulse of insulin ie it promotes glucose uptake into the muscle cells. Thus relative insulin
resistance would not compromise exercise performance (fight or flight!). I can give you the ref details on
request.
Best wishes Jennie
PS I thought Sarah Mason's points were very good ones.
PALEODIET Archives
Subject: Low salt diet for all?
Reply-To:
Date: Sat, 26 Jul 1997 14:12:26 +0100
> Dr. Alderman said a low salt diet doesn't look like a good idea and before you go mucking about in
> the lives of 250 million Americans, you have to have evidencae that it improves lives. His
> researach showed that those who ate the least salt, had the most heart attacks. (Don Wiss read and
> forwarded this message.)
Yes, Michael Alderman and colleagues found that among 1, 900 men with hypertension who were all on
medication, urinary sodium excretion was gradually inversely related to the risk of myocardial infarction
(heart attack) during an average follow-up of 3.8 years [Alderman M et al. Urinary sodium excretion and
myocardial infarction in hypertensive: a prospective cohort study. Am J Clin Nutr 1997; 65(suppl): 682S6S]. In the four equally large groups excreting less than 89, 89-126, 127-174 and more than 174 mmol/day
there were, respectively, 22, 10, 10 and 4 cases of myocardial infarction. It is therefore concievable, but far
from certain, that salt restriction is dangerous in such patients, and if so I would start looking at whether the
danger is to combine antihypertensive medication and salt restriction. I would also suggest such patients to
discuss their lifestyle changes with their doctor, although he may unfortunately not know enough about these
things (but who does?). In the future it may furthermore be possible to find subgroups of patients who can
lower their salt intake safely (remember there are other potential health risks with too much salt).
189/298 (1997)
Obviously a very low salt intake was without risks during human evolution, and the Yanomamo indians of
the Amazone safely eat only 1 (one) mmol/day. However, this does not necessarily apply to all contemporary
humans, depending on medication and other lifestyle factors. We must keep in mind that none of our
medicines have been tested in humans eating a paleolithic diet. Accordingly, much more research is needed,
and this was the official conclusion drawn by Alderman in his article although he may act differently in other
circumstances.
The information I (presently) give to my own hypertensive patients is that if they cannot change their
lifestyle (less empty calories, more exercise, weight reduction and so on) radically enough to get rid of their
antihypertensive medication (which many of them theoretically can), it may not be without risk to restrict
their sodium intake below, say 100 mmol/day.
Anyone who is interested in the possible adverse effects of salt restriction should read parts of the February
issue of Am J Clin Nutr or, if the language is to technical, suggest it to be read by someone else.
-------------------------------------------------------------------
PALEODIET Archives
Subject: Re: A new perspective on the spread of agriculture in Europe
From: Art De Vany
Reply-To:
Date: Mon, 28 Jul 1997 15:52:07 -0700
Those may well be the attributes of a conquering people if the diseases they brought with them killed the
indigenous population. The agriculturalists may have adapted to the plague, cholera, and smallpox that
accompanied sedentary agriculture; diseases to which the indigenous hgs may have had no immunity.
If the evolutionary record shows a wave of extinctions, followed by a decline in stature and evidence of
anemia, that would be consistent with the extinction by imported disease hypothesis.
If the conquest of the Incan empire were to have occured in prehistory, I imagine the skeletal remains would
tell a story like this.
Art De Vany
PALEODIET Archives
Subject: Re: A new perspective on the spread of agriculture in Europe
From: Don Wiss
Reply-To:
Date: Mon, 28 Jul 1997 18:55:40 -0400
Ron Hoggan wrote:
> I just read an article in the July 5/97 issue of _New Scientist_ beginning on page 32, that offers
> a rather revolutionary view of the spread of agriculture in Europe.
The entire article can be found on the web at:
http://www.newscientist.com/ns/970705/features.html
Don.
PALEODIET Archives
Subject: A new perspective on the spread of agriculture in Europe
From: Ron Hoggan
Reply-To:
Date: Tue, 29 Jul 1997 16:40:10 -0600
190/298 (1997)
Hi All, This may be old news to many on this list, but I just read an article in the July 5/97 issue of _New
Scientist_ beginning on page 32, that offers a rather revolutionary view of the spread of agriculture in
Europe.
It runs directly contrary to the Cavalli-Svorza work with Rh factors. This latter, of course, is suggestive of
the spread of an agricultural People who displace the previous inhabitants as they move in with their new
technology.
Bryan Sykes, et. al., at Oxford's Institute of Molecular Medicine, are offering a new perspective, but it all
hinges on the constancy of the rate of mutation of mitochondral DNA.
Sykes hints that currently ongoing DNA testing of pre-Neolithic bones is supportive of his group's
hypothesis, but no definite statement is offered.
The Oxford results are highly supportive of both my common sense notion that the hunter-gatherers would
not just vacate their homes peacefully, and allow the cultivators to supplant them, and my understanding that
the transition to agriculture would be accompanied by reduced stature, bone quality, and the onset of anemia.
These latter are not the physical characteristics I would associate with a conquering people. On the other
hand, agriculture did spread throughout Europe, so alternative explanations appeal to me.
I would welcome instruction on these issues.
Best Wishes, Ron Hoggan
PALEODIET Archives
Subject: Osteoporosis in Eskimos
Reply-To:
Date: Tue, 29 Jul 1997 21:36:46 +0100
Dear friends,
(cross posted)
I. OSTEOPOROSIS IN 20TH CENTURY ESKIMOS Ward Nicholson started a thread in PALEOFOOD
(which I occasionally read):
One study of the Eskimos showed them to have high rates of osteoporosis. [1] ... I believe this study was of
Eskimos prior to acculturation, eating their traditional diet.
This has been found in several studies. From the late 1960s to the late 1970s, Eskimos of Northern Alaska
and Canada have been investigated regarding osteoporosis by use of forearm dual energy absorptiometry
and, in one study, with radiography [1-4]. The findings are consistent and hard to dispute, although whole
body dual energy x-ray absorptiometry (DXA) is a better method in the living (the best method has yet to be
determined). Bone density (i.e. the volume of bone in relation to soft tissue) is generally low compared to US
Whites, and bone loss starts at an earlier age and proceeds at a greater rate than in other populations. I am not
aware of any scientific paper which claims the opposite. Osteoporosis is expected to be a greater health
problem in the Eskimos than in other populations in the future.
---------------------------------------------------------------1. Mazess RB, Mather WE. Bone mineral content of North Alaskan Eskimos. Am J Clin Nutr 1974; 27: 916925. 2. Pawson IG. Radiographic determination of excessive bone loss in Alaskan Eskimos, Human Biology
1974; 46: 369-80. 3. Mazess RB, Mather WE. Bone mineral content in Canadian Eskimos. Human Biology
1975; 47: 45-63. 4. Harper AB, Laughlin WS, Mazess RB. Bone mineral content in St Lawrence Island
Eskimos. Human Biology 1984; 56: 63-78.
---------------------------------------------------------------> Ward believes that the first study was of Eskimos prior to acculturation, eating their traditional
> diet. which Ron Hoggan put in doubt: But this incidence is long after the Inuit had adopted the
> Western diet ...
191/298 (1997)
From what I have read, Ron seems to be close to the truth. To be more certain please check up further
references in the cited literature. The 1974 paper of Mazess [1] deals with Wainwright Eskimos in Northern
Alaska studied in 1968-69. According to the diet surveys carried out by the International Biological
Programme in 1971 and 1972 which is cited by Draper [5], Wainwright adults at that time obtained 32 per
cent of their calories from carbohydrate compared to an estimated 2 per cent in premodern Arctic Eskimos.
Native foods accounted for nearly half of the calories in Wainwright. Protein intake was 25 per cent of
calories, not much less than the estimated 32 per cent in the premodern Eskimos (12 per cent would be
typical for US or Northern European populations). The authors do not mention alcohol which provides much
of the calories today, at least in Greenland (and which adversely affects bone mass). Point Hope Eskimos a
bit south of Wainwright obtained 43 and 22 per cent of calories from carbohydrate and protein, respectively,
and had more hypertensives, 13 per cent compared to 5 in the Wainwright group. A still higher rate, 23 per
cent, was found in the southwestern sister villages of Kasigluk and Nunapitchuk, and this "was correlated
with the increased use of processed foods and the decay of the traditional life-style". In a letter in 1975 [6]
George Mann, who had studied Alaskan Eskimos in 1958 [7], commented on the Mazess study on
Wainwright Eskimos [1]. Mann stated that "the meat diet which we associate with [the Eskimos] has been
importantly diluted by these modern foods", that "Eskimo adults are [now] a sedentary people" and that "the
early loss of bone mineral is more likely attributable to physical inactivity than to high intake of phosphate,
sulphate, and other anions". Mazess replied that "meat remains a mainstay of the diet and intakes are quite
high". Berkes and Farkas provide some insight into the history of changing dietary patterns among the Inuit
of Labrador and they give some references but no figures on percentages of modern foods since their main
focus is on the James Bay Cree Indians [8]. Resource depletion started to become intense already in the
1800's due to fur trade (the Hudson Bay Company started trading fur in the late 1600's) and whaling (land
mammals like caribou and muskox, and sometimes walrus, were depleted from feeding the whalers). Berkes
and Farkas also cite Shephard and Godin who in 1976 calculated that the Igloolik Eskimos of North-west
Territories (at about the same latitude as Wainwright) obtained only about 31 per cent of the needs from wild
food energy [9]. Rode and Shephard recently presented anthropometric data on Igloolik Inuit [10] which
shows that lifestyle has been further deteriorated after 1970. Males aged 40-49 years increased their
percentage of body fat (estimated from triceps, subscapular and suprailiac skinfolds according to Durnin and
Womersley) from 11 per cent in 1970 to 17 and 23 per cent in 1980 and 1990, and corresponding figures for
females were 22, 29 and 38 per cent. I have not seen nutritional data from 1920-70 but the Eskimo lifestyle
may have changed a lot in that time period. This is a crucial question with regard to the Wainwright Eskimos
surveyed around 1970. Additionally, we must always be aware of secular trends when interpreting crosssectional surveys in a group of people who have been changing their lifestyle for some decades. If a secular
trend would explain the age-related decrease of bone mass in contemporary Eskimos (which I highly doubt)
it would mean that older persons would have lower bone mass than younger ones not because their bone
mass had decreased as they grew older but because younger persons at the time of the study had higher bone
mass than the old ones had had in their youth.
---------------------------------------------------------------5. Draper HH. The Aboriginal Eskimo diet in modern perspective. Am Anthropol 1977; 79: 309-16. 6. Mann
GV (and reply by Mazess RB). Bone mineral content of North Alaskan Eskimos. Am J Clin Nutr 1975; 28:
566-7. 7. Mann GV et al. The health and nutritional status of Alaskan Eskimos. A survey of the
Interdepartmental Committee on Nutrition for National Defense-1958. Am J Clin Nutr 1962; 11: 31-. 8.
Berkes F, Farkas CS. Eastern James Bay Cree Indians: changing patterns of wild food use and nutrition. Ecol
Food Nutr 1978; 7: 155-72. 9. Shephard RJ, Godin G. Energy balance of an Eskimo community. In:
Shephard RJ, Itoh S (eds). Circumpolar health. Univ Toronto Press, Toronto. 1976: 106-12. 10. Rode A,
Shephard RJ. Body fat distribution and other cardiac risk factors among circumpolar Inuit and nGanasan.
Arct Med Res 1995; 54: 125-33. See also Lippe-Stokes S. Eskimo story-knife tales: reflections of change in
food habits (which I have not read). In: Robson JRK (ed). Food, ecology and culture. Readings in the
anthropology of dietary practices. Gordon and Breach 1976(?): 75-82 (which I have not read).
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192/298 (1997)
II. SOME PROBLEMS OF MEASURING BONE MASS IN ANCIENT POPULATIONS Studies of

osteoporosis in archaeological skeletons are problematic, and one researcher recently stated that "in
archaeological bone, studies of prosoty, density, and mineralization are almost impossible" [11]. One of the
reasons is that when bones lie in the ground for long periods they undergo changes (diagenesis) which in our
case may result in falsely low or falsely high levels of bone mass. Another problem is that estimations of age
at death are very unreliable after the age of 50 and the methods have not been standardized [12-13] (i.e. all
investigators do not do it in the same way). Subjects with estimated ages above 50 years are commonly put
in one group which seriously hampers investigations of disorders which have limited influence before that
age. Our group is starting up studies on bone mass in a fairly large population of prehistoric hunter-gatherers
by the sea from Gotland, Sweden (not Eskimos). My colleague Dr Peter Johansson, who is in charge of these
studies, suspects that dual energy absorptiometry, which mainly measures trabecular (inner) bone, may not
necessarily be the method of choice in archaeological skeletons. Possibly quantitative computerized
tomography (QCT) is better. Then you can measure cortical (outer) bone as well as trabecular. Osteoporosis
is characterized, histologically, by a decrease in cortical thickness and in the number and size of the
trabeculae (the bar-like inner structures of bone). Trabecular bone has often been overemphasized in
osteoporosis research, partly depending on the used methods of measurement. A major reason why, in the
West, bone loss is higher in women than in men is that there is a gradual thinning of cortical bone in women
[14]. This is because resorption on the inside is greater and formation on the outside is less [15].
Furthermore, the strength of a bone depends not only on bone mass and even here the importance of cortical
thickness may have been underestimated [16-17].
---------------------------------------------------------------11. Jackes M. Paleodemography: problems and techniques. In: Saunders SR, Katzenberg MA. Skeletal
biology of past peoples: research methods. Wiley-Liss, 1992: 189-224. 12. Iscan MH, Loth SR. Osteological
manifestations of age in the adult. In: Iscan MH, Kennedy KAR (eds). Reconstruction of life from the
skeleton. Wiley-Liss 1989:23-40. 13. Stout SD. Methods of determining age at death using bone
microstructure. Skeletal biology of past peoples: research methods. Wiley-Liss, 1992: 21-35. 14. Kalender
WA et al. Reference values for trabecular and cortical vertebral bone density in single and dual-energy
quantitative computed tomography. Eur J Radiol 1989; 9: 75-80. 15. Ruff CB, Hayes WC. Sex differences in
age-related remodeling of the femur and tibia. J Orthop Res 1988; 6: 886-96. 16. Mazess RB. Fracture risk: a
role for compact bone [editorial]. Calcif Tissue Int, 1990; 47: 191-3. 17. Ruff C. Biomechanical analyses of
archaeological human skeletal samples. In: Saunders SR, Katzenberg MA (eds). Skeletal biology of past
peoples: research methods. Wiley-Liss 1992: 37-58.
----------------------------------------------------------------
193/298 (1997)
III. OSTEOPOROSIS IN PREHISTORIC ESKIMOS Archaeological data suggest that even prehistoric
Eskimos were at higher age adjusted risk of osteoporosis than contemporary Westerners [18-21]. Accelerated
loss of bone mass after 50 years has been noted rather than low peak bone mass at early adulthood. Harper
[4] states that "studies based upon skeletonized ancestral-antecedent populations of Aleuts, Yupik Eskimos,
and Inupiaq Eskimos have revealed a major cline [i.e. a gradual geographic difference, my comment] in bone
cortical thickness [which] is highest in the ancestral Umnak-Kodiak homeland of the Bering Sea Mongoloids
and decreases in populations north along the Alaskan coast to the Arctic Circle, the approximate demarcation
point between Yupik and Inupiaq Eskimo. Cortical thickness values diminish even more in the Inupiaq
Eskimos extending east across north Alaska, Canada and Greenland. The difference between the terminal
isolates, Aleuts and Greenland Inupiaq Eskimos, are as great as the differnce in cortical thickness between
male and female in the same isolate. Similarly, femoral BMC [bone mineral content of the thigh-bone]
measured by direct photon absorptiometry mirrors the highly significant differences between the Aleuts, on
one hand and northern Eskimos on the other". Merbs found the extinct Sadlermuit to have a high prevalence
of spinal compression fractures (from vertical forces on the vertebral column) [22-23]. Such fractures were
present in 36 of 80 adult Eskimos. The author considers "the high incidence ... attributable primarily to riding
on a komitak, a simple platform sled lacking any form of shock absorber. As the vehicle moves rapidly over
ice roughened by pressure ridges or rocks hidden by snow, vertical forces, sometimes quite violent, are
transmitted directly to the vertebral column of the rider. The Eskimo condition is thus similar to one known
in orthopedics as 'snowmobiler's back', also characterized by vertebral compression fractures...". Thus, as
Dean suggests, the commonly expressed notion that the findings of Merbs are further evidence of
osteoporosis in Eskimos may be open for debate. In a study on the non-sledding Aleut Eskimos, cited by
Merbs, the frequency of vertebral compression fractures was 22 per cent [24]. For comparison, women aged
50 years and over from Rochester, Minnesota, had a prevalence of vertebral deformity of 25.3 per cent (95%
confidence interval 22.3-28.2) [25]. The incidence of clinically diagnosed vertebral fractures among women
in the same population was 5.3 per 1, 000 person-years, suggesting that around 30% of such deformities in
women receive clinical attention. I am sure there must be much more data on the occurence of fractures in
arcaeological Eskimo skeletons. It should be noted that the complete absence of a disease in a non-western
population not always occurs to the author as being important. He or she would nevertheless probably be
delighted to be asked about it. Try e-mail by the Worldwide list of universities at
<http://www.mit.edu:8001/people/cdemello/univ.html
---------------------------------------------------------------18. Mazess RB. Bone density in Sadlermuit Eskimos. Hum Biol 1966; 38: 42-9. 19. Thompson DD,
Gunness-Hey M. Bone mineral-osteon analysis of Yupik-Inupiaq skeletons. Am J Phys Anthropol1981; 55:
1-7. 20. Laughlin WSB et al. New approaches to the pre- and post-contact history of Arctic peoples. Am J
Phys Anthropol 1979; 51: 579-87. 21. Richman EA et al. Differences in intracortical bone remodelling in
three American aboriginal populations: possible dietary factors. Calcif Tissue Int 1979; 28: 209-14. 22.
Merbs CF. Patterns of activity-induced pathology in a Canadian Inuit population. National Museum of Man
Mercury Series, Arcaelogical Survey of Canada Paper No. 119. 23. Merbs C. Trauma. In: Iscan MH,
Kennedy KAR (eds). Reconstruction of life from the skeleton. Wiley-Liss 1989:161-89. 24. Yesner DR.
Degenerative and traumatic pathologies of the Aleut vertebral column. Arch Calif Chirop Assoc 1981; 5: 4557. 25. CooperC, O'Neill T, Silman A. The epidemiology of vertebral fractures. Bone 1993; 14 Suppl 1: S8997.
---------------------------------------------------------------It is not easy to draw conclusions about the role of diet, physical activity, sunlight and genetics for the
allegedly high risk of osteoporosis in prehistoric Eskimos. If diet is a cause I would not suspect calcium
INTAKE in the first place since absorption and losses of calcium seem to overshadow intake, at least in
westernized populations [26], and furthermore I would expect the meat and fish diet of Eskimos to provide
sufficient amounts of calcium (In fish the amount of calcium per 10 MJ averages about 1, 000 mg). Calcium
absorption would probably be high due to the absence of phytic acid from cereals (see
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9706&L=paleodiet&O=T&P=850). The most common
nutritional explanation in the literature is the high protein intake (see below). I suppose vitamin C deficiency
would be another possibility [27].
---------------------------------------------------------------26. Nordin BEC. Bad habits and bad bones. In: Burckhardt P, Heaney RP (eds). Nutritional aspects of
osteoporosis '94. Rome, Ares-Serono Symposia 1995: 1-25. 27. New SA et al. Nutritional influences on bone
mineral density: a cross-sectional study in premenopausal women. Am J Clin Nutr 1997; 65: 1831-9.
---------------------------------------------------------------Paleolithic Diet Symposium List
194/298 (1997)
IV. BONE LOSS IN HUNTER-GATHERERS Perzigian studied bone density of the forearm by use of
photon absorptiometry in two prehistoric north American groups of hunter-gatherers, one of whom were said
to supplement its hunting and gathering with part-time agriculture [28]. He concluded that age related
trabecular bone loss in the latter group was higher than in the exclusive hunter-gatherers which had similar
bone loss as contemporary populations.
---------------------------------------------------------------28. Perzigian AJ. Osteoporotic bone loss in two prehistoric Indian populations. Am J Phys Anthropol 1973;
39: 87-96.
---------------------------------------------------------------V. PROTEIN INTAKE AND CALCIUM LOSSES Many metabolic trials and epidemiological surveys have
been performed regarding the role of dietary protein for calcium losses. Most of them show that an increased
protein intake leads to higher urinary losses of calcium, possibly because of an increased acidic load [29-33].
In epidemiological surveys, dietary protein, in particular animal protein (although some investigators do not
differ between protein from meat and milk products), has been associated with higher rates of osteoporotic
fractures across cultures [34] and among US nurses [35]. Epidemiological studies are often biased by
confounding, when a hidden cause (like smoking) is related to a variable (like yellow fingers) which in turn
is found to be related to the disease in question (like lung cancer). Therefore we need intervention studies for
proof (although in the case of smoking we got convinced without them). Such studies have to my knowledge
not been able to show that a change from low/moderate to high protein intake increases the rate of kidney
stones or bone loss in animals or humans. In one study, rats were fed a control diet (15% soy protein plus
0.2% methionine) or a high protein diet (control plus 20% lactalbumin) for 10 months [36]. Rats which were
fed the high protein diet exhibited increases in urinary calcium but no change in bone composition. In
another study, 99 persons who had calcium oxalate kidney stones for the first time were randomly assigned
to either a control diet or a low animal protein, high fiber diet and followed regularly for up to 4.5 years [37].
In the intervention group of 50 subjects, stones recurred in 12 (7.1 per 100 person-years) compared with two
(1.2 per 100 person-years) in the control group (p = 0.006), suggesting that a *low* animal protein diet
increased the risk of urinary stones. Furthermore, when Orwoll et al studied growing rats fed a diet low in
protein (5%) for 4, 6, and 8 wks (n = 10 animals/group) and compared them with animals pair-fed with a
protein-replete (18%) diet, skeletal dimensions were *reduced* in the protein-deprived rats but there were no
significant differences in bone mineral content between control and low-protein animals at 4, 6, and 8 wks
[38]. Hence, they found that dietary protein deprivation resulted in slower growth but bone mineral density
was maintained when there was a marked reduction in urinary calcium excretion.
---------------------------------------------------------------29. Kerstetter JE, Allen LH. Dietary protein increases urinary calcium. J Nutr 1989; 120: 134-6. 30. Do
protein and phosphorus cause calcium loss? J Nutr 1988; 118: 657-60. 31. Burtis WJ et al. Dietary
hypercalciuria in patients with calcium oxalate kidney stones. Am J Clin Nutr 1994; 60: 424-9. 32. Trinchieri
A et al. The influence of diet on urinary risk factors for stones in healthy subjects and idiopathic renal
calcium stone formers. Br J Urol 1991; 67: 230-6. 33. Breslau NA et al. Relationship of animal protein-rich
diet to kidney stone formation and calcium metabolism. J Clin Endocrinol Metab 1988; 66: 140-6. 34.
Abelow BJ, Holford TR, Insogna KL. Cross-cultural association between dietary animal protein and hip
fracture: a hypothesis. Calcif Tissue Int 1992; 15: 14-8. 35. Feskanich D, Willett WC, Stampfer MJ, Colditz
GA. Protein consumption and bone fractures in women. Am J Epidemiol 1996; 143: 472-9. 36. Whiting SJ,
Draper HH. Effect of chronic high protein feeding on bone composition in the adult rat. J Nutr 1981; 111:
178-83. 37. Hiatt RA, Ettinger B, Caan B, Quesenberry CP Jr, Duncan D, Citron JT. Randomized controlled
trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am
J Epidemiol 1996; 144: 25-33. 38. Orwoll E; Ware M; Stribrska L; Bikle D; Sanchez T; Andon M; Li H.
Effects of dietary protein deficiency on mineral metabolism and bone mineral density. Am J Clin Nutr 1992;
56: 314-9.
---------------------------------------------------------------I do not agree with the following statements of Dean:
> There is no evidence at all that meat proteins cause calcium loss. Every study which has shown
> loss of calcium and other minerals from high protein intake has involved soy and other
> non-animal-source proteins. Studies which use meat proteins show no such loss of calcium. (1, 2, 3)
> 1) Spencer H; Kramer L; DeBartolo M; Norris C; Osis D. Further studies of the effect of a high
> protein diet as meat on calcium metabolism. Am J Clin Nutr, 1983 Jun, 37:6, 924-9 2) Osteoporosis,
> calcium requirement, and factors causing calcium loss. Spencer H; Kramer L. Clin Geriatr Med, 1987
> May, 3:2, 389-402 3) Do protein and phosphorus cause calcium loss? Spencer H; Kramer L; Osis D.
195/298 (1997)
> J Nutr, 1988 Jun, 118:6, 657-60

Rather, the debate goes on [39]. When different sources of protein have been compared it is usually the
animal protein diet that has resulted in the greatest loss of urinary calcium [33, 40], and in epidemiologic
surveys the case is also rather against meat [35, 41]. From what I know today I would personally not advice a
lady to live only on an Eskimo diet. Nevertheless, my working hypothesis (which some day may be able to
test) is that prehistoric hunter-gatherers from the equator to the temperate zones had strong bones at old age.
---------------------------------------------------------------39. Spencer H, Kramer L. Does dietary protein increase urinary calcium? [Letter with reply by Kerstetter JE
and Allen LH] J Nutr 1991; 121: 152-3. 40. Schuette SA, Linkswiler HM. Effects on Ca and P metabolism in
humans by adding meat, meat plus milk, or purified proteins plus Ca and P to a low protein diet. 41. Hu J-F
et al. Dietary intakes and urinary excretion of calcium and acids: a cross-sectional study of women in China.
Am J Clin Nutr 1993; 58: 398-406.
---------------------------------------------------------------Best regards,
Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: On the subject of low-carbohydrate diets
From: Dean Esmay
Reply-To:
Date: Mon, 11 Aug 1997 23:53:22 -0400
A message forwarded from another online forum, reposted here with permission of the author:
> From: (Jon Bayh) Date: 29 Jul 1997 06:51:22 GMT
...I recently read a book titled "The Foraging Spectrum, " by Robert L. Kelly, associate professor of
anthropology. It's a very dense read, and I'm not sure I would recommend it unless one is very motivated.
However, some points from it were very interesting. First and foremost, Kelly concludes that there is so
incredibly much variance in "hunter-gatherer" lifestyles that it is impossible to draw accurate conclusions
about what the h-g lifestyle _is_. He further concludes that it is unlikely that we can infer from modern h-g
groups how ancient h-g groups lived. Oh, we may get glimpses, but these won't tell us a whole lot about how
our ancestors were living. Also, there is virtually no h-g group, even in records dating back to the 18th
century, that has not been influenced by contact with---what? ---modern?---western?---civilized?(HAH!)--culture, and therefore isn't tainted as to what the "primordial" hunter-gatherer culture is.
Another point is that the relative contribution of hunting (which contributes mostly protein and lipids) and
gathering (which contributes carbohydrates, lipids, and some protein, mostly in that order) depends a lot on
the solar radiation (latitude) but also on the local climate and vegetation. For instance, in another post you
mentioned knowing of only the Inuit as deriving calories almost exlusively from hunting. Kelly has a list of
hunter-gatherer societies and the approximate relative contribution of hunting, fishing, and gathering, in
relation to solar radiation and local plant life. The relative percentages are all over the map, with groups such
as the Comanche, Cheyenne, Kiowa-Apache, Seri (Mexico), Anbarra (Northern Australia), Mbuti (Africa)
all deriving less than 30% of volume of diet from gathering. These are just examples---of 123 groups, about
75 derive 30% or less by volume of food from gathering, but these are heavily weighted to northern,
extreme-climate groups. Only 19 groups derive 60% or more (by volume) from gathering. Only 4 groups
derive as much as 80-85%, and among these are the Ju/'hoansi (this book's designation for the !Kung). So,
citing the !Kung may be picking an extreme on a large range of behavior.
196/298 (1997)
Of those who hunt more than expected, "Many of these are tropical groups who trade meat for carbohydrates
(Mbuti, Aeta, possibly Aweikoma), northern groups who do not have direct access to substantial aquatic
resources [hence no fishing] and who cannot turn to plant food as a substitute (Nunamiut, Tanana), and
Plains hunters who, like tropical forest groups, trade meat for carbohydrates (in this sample, corn grown by
Pueblo or other horticultural peoples) and who live in interior grasslands where much of the primary
production [local plant life] cannot be eaten by humans and where aquatic resources are not abundant
(Kiowa, Comanche, Cheyenne, Crow, Kiowa-Apache, Sarsi, Blackfoot)." Obviously, this throws a wrench
into the works---a given people may show a given percentage of hunting/gathering/fishing behavior, but
these products may be traded with other people for goods that better balance the nutrition picture. "The
Foraging Spectrum" is frustratingly (oh, SO FRUSTRATINGLY!) silent on the topic of exact balance of
calories between protein/lipids/carbs. There are hints here and there, but no definitive conclusions.
In sum, modern (last 300 years) hunter-gatherers tell us precious little about the diet(s) that humans evolved
on, and there may have been very widespread changes in human diets as climates and geographies shifted.
The theory has been advanced lately that early hominids (perhaps Homo habilis, perhaps earlier) were
scavengers. They would find the carcass of an animal after the predators were done with it, and split open the
denser bones with tools (rocks) to eat the marrow. Such a diet would be very high fat, medium protein, and
(unless suplemented) essentially zero carbohydrate. While the evidence for this model is pretty limited, the
theory sounds fairly reasonable to me. It suggests incremental, stepwise advancement to hunting behavior
(which is very likely by the time of Homo erectus). Still, the bottom line is that we just don't know, and that
human diet behavior is extremely diverse.
Part of the problem, of course, is that we're talking about what diets contribute to long life, and the simple
fact is that most of the diseases we're talking about (heart disease, cancer) tend (except in extreme cases) to
hit late in life. Nature really cares very little about what happens to animals late in their breeding lifespan
(and breeding, in early hominids, probably started at 15-18).
...I wanted to follow up on this post with the book in front of me, because the chart is really quite startling.
There are four data points that interest me beyond others, for orangutans (Pongo pygmaeus), chimps (Pan
troglodytes), gorillas (Gorilla gorilla), and humans (Homo sapiens). Now, near as anybody can tell, none of
these four critters have had a common ancestor for at least 4 to 8 million years. Gorillas have never been
known to consume animal flesh or much insect protein in the wild---they live mostly on leaves and fruits.
Orangs emphasize fruit a little more than gorillas do; I don't know whether they eat meat or insects, but I
certainly haven't heard so. Of three great apes, chimps actively seek out and hunt meat, and often eat insects.
(It's frustrating that pygmy chimps aren't on the chart; I would find that data point very, very interesting).
Now picture the graph. It is a two-dimensional plot that varies (virtually, anyway), from -10 to +15 on the Xaxis and -10 to +10 on the Y-axis. Carnivores are in a rectangular-ish block off to the upper right, ranging
from (2, -3) to (15, 4) to (13, 10) to (1, 3). Frugivores are in a diamond centered at (-3, 1) and ranging +/- 3
on X and +/-4 on Y. "Midgut-fermenting folivores" (primates and horses, for example) are off to the far left
side, and "foregut-fermenting folivores" like rabbits and some monkeys in a separate block to the "south".
What is most amazing about all this is that, even in spite of the variance of chimps from orangs and gorillas,
and a separation of at least 4 million years from any common ancestor, they are all within a radius of 1 unit
of each other. Orangs are at (-4, 1), gorillas at (-4, 0), and chimps shifted just a tiny little bit toward
carnivores at (-3, 0). Gorillas and orangs are almost in the folivores with horses.
Humans are at (1, 4) ! They are very nearly in the carnivore block, but not quite there. We've got three
species that have barely shifted by a unit of 1 in, conservatively, 4 million years, and one species that has
shifted by a radius of about 5 in the same period.
Disclaimer: I am _not_ convinced of the wisdom of low-carbohydrate diets, especially for long-term use. My
comments here are not intended to show the widespread use of low-carb diets among hunter-gatherers, but
rather to show the diversity in diet and dietary behavior in hunter-gatherers, especially considering the trade
of nutrients between groups. Furthermore, due to the diverse behavior in modern h-g groups, very little
inference can be drawn to establish the behavior of our ancient hominid ancestors. The fossil evidence
concerning diet among hominids is much more equivocal than folks with an axe to grind (especially those
with self-help diet books to sell) are willing to admit.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 29 Jul 1997 to 12 Aug 1997
From: Jon Bayh
Reply-To:
197/298 (1997)

Date: Tue, 12 Aug 1997 14:39:48 -0700
Folks, I should point out that the re-post of my comments from another forum were edited from two or three
different posts, and a few details were left out. In particular, one could get the impression that the chart that I
was talking about was in the book _The Foraging Spectrum_. In fact, it was from _The Cambridge
Encyclopedia of Human Evolution_. One person asked for references for the chart, and I posted the
following; I figured someone here might be interested:
----------------------------------------------------------------------The label on the chart is a bit vague as to exactly what is being measured. It says:
Multidimensional plot of indices for surface areas of stomach, small intestine and caecum + colon for 80
primates and other mammals.
The Cambridge Encyclopedia of Human Evolution is an edited book, with individual contributors writing
various chapters. The author of this particular chapter is Dr. David J. Chivers, of the University of
Cambridge. The suggested further reading for this section lists:
Chivers, D.J. and Hladik, C.M. Morphology of the gastrointestinal tract in primates: comparisons with other
mammals in relation to diet. Journal of Morphology 166:337-86 (1980). Chivers, D.J. et al. (eds). Food
Acquisition and Processing in Primates. New York: Plenum Press, 1984. Clutton-Brock, T.H. (ed.) Primate
Ecology: Studies of Feeding and Ranging in Lemurs, Monkeys and Apes. London and New York: Academic
Press, 1977. Davies, A.G. et al. Natural foods as a guide to the nutrition of Old World primates. In Standards
in Laboratory Animal Management, pp. 225-44. Potters Bar, Herts: Universities Federation for Animal
Welfare, 1984. Hill, W.C.O. Pharynx, oesophagus, small and large intestine: form and position. Primatologia
3: 139-207 (1958). Hladik, C.M. Diet and the evolution of feeding strategies among forest primates. In
Omnivorous Primates: Gathering and Hunting in Primate Evolution (eds R.S.O. Harding and G. Teleki), pp.
215-54. New York: Columbia University Press, 1981. MacLarnon, A.M. et al. Gastro-intestinal allometry in
primates and other mammals including new species. In Primate Ecology and Conservation (eds J.G. Else and
P.C. Lee), pp 75-86. Cambridge: Cambridge University Press, 1986. Martin, R.D. et al. Gastrointestinal
allometry in primates and other mammals. In Size and Scaling in Primate Biology (ed.W.L. Jungers), pp. 6189. New York: Plenum Press, 1985.
Me, I'd check the first reference and the last two references, first. Matter of fact, I might do just that, if I can
find a source---they look interesting.
Jon
-----------------------------------------------------------------------
PALEODIET Archives
Subject: Re: Responses to June & July Messages
From: Loren Cordain
Reply-To:
Date: Thu, 14 Aug 1997 16:13:00 -0600
Due to a well needed 6 week vacation at Lake Tahoe, I have not been in correspondence with this wonderful
group of people that comprise our paleodiet digest. However, upon my return, I have been able to review
most of what has "gone done" in the past six weeks, and I see that there has been a number of lively debates
on a variety of issues. Let me humbly add my two cents to some of these conversations (I will reply to Dr.
Enig & Sally Fallon in a couple of days):
June 24: I only recently became aware of Leon Chaitlow's, "Stone Age Diet" book and have ordered it
through interlibrary loan. I will try to do a short review on it when I receive it. I'd be interested to know if Art
DeVaney has a more complete reference for "Dr. Citron's Evolutionary Diet and Cookbook". Another older
book on paleodiets which apparently was a "classic" but is rather obscure these days is: DeVries, Arnold.
Primitive Man and His Food. Chicago, 1962. - I dont know the publisher, and have not read the book yet, but
have ordered it through interlibrary loan. Are any of our readers familiar with this book?
198/298 (1997)
June 27: There is another reason why paleodiets are beneficial for calcium balance in addition to the three
reasons Staffan mentioned. In pre-agricultural diets consisting of meats, fruits, vegetables, nuts etc., the
Calcium to Magnesium ratio is approximately 1:1. Because the Ca:Mg ratio of milk and dairy products is
12:1 (1), the inclusion of milk and milk products into post-agricultural diets can raise the Ca:Mg ratio to 34:1 (1). In animal models, it has been shown that rats develop clinical signs of Mg deficiency after three
weeks on high calcium, normal magnesium diets (2, 3, 4). Ironically, high calcium diets may have a
deleterious effect upon bone mineralization because of their hypomagnesic effect. Mg deficiency is a known
cause of hypocalcemia (5). The resultant hypocalcemia stems from PTH unresponsiveness (6), since the
effects of PTH are magnesium dependent (7). Gross, clinical hypocalcemia and hypomagnesia tend not to
occur in otherwise healthy post-menopausal, osteoporotic women; however, serum measures of magnesium
concentrations are not good indicators of magnesium status, and subjects with magnesium deficiencies (as
measured intracellularly) frequently maintain normal serum magnesium levels (8). Consequently, over a
lifetime, a marginal or reduced intracellular Mg level may adversely influence PTH responsivity which in
turn likely compromises bone mineral content. A recent review article (9) showed that post-menopausal
women given magnesium supplements over a 2 yr period had a significant increase in their bone mineral
density, whereas meta-analyses of calcium supplementation and bone mineral density have been equivocal.
REFERENCES
1. Varo P. Mineral element balance and coronary heart disease. Int J Vit Nutr Res 1974;44:267-73. 2. Evans
GH et al. Association of magnesium deficiency with blood pressure lowering effects of calcium. Journal of
Hypertension 1990;8:327-337. 3. Luft FC et al. Effect of high calcium diet on magnesium, catecholamine,
and blood pressure of stroke-prone spontanneously hypertensive rats. Proc Soc Exp Biol Med 1988;187:47481. 4. Sellig MS et al. Magnesium interrelationnships in ischemic heart disease: a review. Am J Clin Nutr
1974;27:59-79. 5. Rude et al. Functional hypoparathyroidism and parathyroid hormone end organ resistance
in human magnesium deficiency. Clin Endocrinol 1976;5:209-224. 6. Rude et al. Parathyroid hormone
secretion in magnesium deficiency. J Clin Endocrinol Metab 1978;47:800-06. 7. Estep H, et al.
Hypocalcemia due to hypomagnesemia and reversible parathyroid hormone unresponsiveness. J Clin
Endocrinol 1969;29:842-48. 8. Ryzen E, et al. Low intracellular magnesium in patients with acute
pancreatitis and hypo calcemia. West J Med 1990;152:145-48. 9. Sojka JE et al. Magnesium
supplementation and osteoporosis. Nutr Rev 1995;53:71-4.
PALEODIET Archives
Subject: Cooked meat
From: Mavis Wood
Reply-To:
Date: Fri, 15 Aug 1997 11:51:40 +1200
To PALEODIET LIST SYMPOSIUM
The list readers may be interested in the report of a four hundred thousand year old hearth in The Electronic
Telegraph issue 809 entitled *Barbecues a Thing of the Past*, by Aisling Irwin
Archaeologists from Liverpool University in Suffolk have discovered what could be a hearth with animal
bones and knives.
http://www.telegraph.co.uk
Mavis Wood MA hons Prehistoric Archaeology Edinburgh.
*Domine*Dirige*Nos
> )M(<<<<<
PALEODIET Archives
Subject: Ron Hoggan on Radio this Sunday evening at 9:30 PM EST
From: Don Wiss
Reply-To:
Date: Fri, 15 Aug 1997 14:32:40 -0400
Hi all,
199/298 (1997)
Fellow list subscriber Ron Hoggan will be a guest on Robert Crayhon's nutrition show "The Voice of
Wellness" via telephone, this Sunday evening for about 20 minutes or so. 9:30-10:00 PM Eastern time. It
will be on WOR, which is 710 AM in the NYC area, and the program is also nationally syndicated. But
easier than trying to figure out which WOR affiliate carries it or not, the station can be heard live on the web.
One does need a sound card and a 28.8K baud modem. You can find WOR at http://www.wor710.com/
Ron will be asked about his hypothesis regarding gluten and the cancer connection, why he feels that a
strong focus on diagnosing celiac disease, and gluten sensitivity would constitute an effective cancer
prevention program, and a little bit about Ron's brother, although he seems less interested in that angle.
Crayhon also wants to talk about the Paleolithic diet, and what that means to wellness.
I hope we all can tune in.
Don.
PALEODIET Archives
Subject: Re: Wine and beer
From: Art De Vany
Reply-To:
Date: Mon, 18 Aug 1997 13:37:48 -0700
The radio just gave a summary of a new study that claims to show white wine and beer are as effective as red
wine in promoting health (or preventing some atherosclerosis).
As I said in an earlier post, they should be equally effective because they contain approximately the same
levels of flavonoids (I will try to dig out a reference, but I am not as good at that as Loren and Staffan---don't
expect a theoretician to become an empiricist over night).
Of course, there are far better sources of flavonoids such as onions, garlic, fresh fruits and salads.
I would suggest that the culprit in the low flavonoid content of the Western diet is the lack of fresh plants and
fruits and the generally low antioxidant status of Westerners in general. High carbohydrate diets contribute to
the antioxidant depletion (elevated blood glucose promotes formation of free radicals and glycosylation of
body tissue).
No, Loren, I have not found Citron's book. Our library doesn't have it and I don't plan to buy it. I am
perfectly happy with my own evolutionary diet.
One comment on Staffan's wonderful piece on osteoporosis among the Eskimo. The remodelling of bone
(loss of cortical mass and increased cross webbing) is just what would happen if the bone were being
redesigned from a load bearing column to a beam, whose stress comes from shearing forces. It's like taking a
Mack truck and making a race car out of it. This may be a consquence of a shift from hunting and gathering,
with its high load bearing stresses, to factory work, where I think light, shear forces dominate. I lift
something equal to one or more multiples of my body weight several times a week.
PALEODIET Archives
Subject: Breakfast, and other things
Reply-To:
Date: Wed, 20 Aug 1997 10:32:10 +1000
Having followed the list with great interest for some time now, I have a few questions - which are of a more
practical nature.
What does a paleodietitian eat for breakfast? How many times a day/week did our ancestors eat? Evidence or
theory? Is the frequency of eating factored into paleodietary strategies? What literature managing database
do some of you use, to be able to respond so effectively?
Regards
Michael
________________________________________________
200/298 (1997)
Michael Schubert School of Natural and Complementary Medicine Southern Cross University P.O. Box 157,
Lismore, N.S.W. 2480, Australia Telephone 61-2-6620 3649 Visit us at
<http://www.scu.edu.au/schools/ncm/index.html
> ________________________________________________
PALEODIET Archives
Subject: Re: Response to Michael Schubert
From: Loren Cordain
Reply-To:
Date: Mon, 25 Aug 1997 15:05:00 -0600
1. What does a paleodietitian eat for breakfast.
I suspect that Ray Audette or Art DeVaney could give a bit of practical advice here. Pre-agricultural people
would probably not have consumed cereal grains, dairy products, vegetable oils, refined carbohydrates,
legumes, yeast containing foods or salted foods on a regular basis for any meal. All meals would have been
derived from mimimally processed foods which could be obtained in the local environment according to
season and availability. Modern paleodietitians have a much wider plate from which to choose. We can
obtain virtually any fruit, vegetable, nut, seed, tuber or animal product in unlimited quantities all year round,
and if we are willing to pay the price from virtually any locale. However, our foods are almost always
limited to domesticated fruits, vegetables and meats which can be obtained at the supermarket. Clearly there
are nutritional differences between wild foods (both plant and animal) and domesticated foods. Through
artificial selection, farmers have succeeded in developing plant foods which are generally, sweeter, larger
and have less fiber and seed than the wild version. Domesticated meats are quite different in macronutrient
composition from wild meats, particularly in their lipid composition (1, 2) and our ancestors would not have
thrown out the organs (brain, marrow, liver, spleen, kidney, gonads, mesenteric fat etc) as we do today. I
have had a number of conversations with Boyd Eaton who has suggested that the morning meal of present
day hunter gatherers may have consisted of a "little bit" of what was consumed at the previous evening's
meal. So, if a kangaroo was bagged, it may have been remaining portions of the carcass. There are many
excellent descriptions of hunter gatherer meals in a wide variety of anthropological texts describing the food
habits of these peoples. Perhaps one of our anthropologists on the listserve could provide a reference or two.
Modern day "paleodietitians" could eat a bowl of mixed nuts(brazil nuts from South American, pecans from
American, almonds from the Mid East, walnuts and hazel nuts from Europe) with dried fruit (raisins from
California, dates from Iraq, pineapple from hawaii etc) and honey. Obviously, a meal like this could never
have been reconstructed by our ancestors, nor was it likely that this kind of food combination was consumed
at a single meal (nuts, dried fruit and honey) except under very unusual situations. However a modern day
"paleodietitician" could consume this meal every day of the week if he/she so desired. Because of its high
sugar content (dried fruit and honey) and fat content, this so-called "paleo meal" could produce the very
same hyperinsulinemic and dyslipidemic profile characteristic of western "civilized", high fat, high carb
meals. I sometimes wonder if the extreme obesity represented by the "Venus" figurines found throughout
europe at the close of the pleistocene (3) were representations of female "godesses" who were fed a diet of
the choicest foods of the time (honey, dried fruit, nuts, marrow and fatty meats). 2. How many times a
day/week did our ancestors eat?
Now that Boyd Eaton and his son are on our listserve, perhaps they could comment. I offer the information
that the modern meal pattern of breakfast, lunch and dinner is a fairly recent phenonmenon (4, 5). Also,
because the killing of game and the location of edible plant food was not a "sure thing", meal timing and
frequency would have been somewhat dependent upon the availability of resources. 3. What literature
managing database do some of you use, to be able to respond so effectively.
I can't speak for others, and I'm not so sure that I respond effectively - However, I have a personal library of
articles totaling ~15-20, 000 that are arranged into ~25 subcategories. Each subcategory contains anywhere
from 50-100 files which contain my articles. I would like to someday put all of my articles on a database for now I use my memory which seems to fail more frequently as I approach 50. I typically use MEDLINE
or CARL (UNCOVER) to locate information on a topic. I'd be interested in hearing from our colleagues in
the anthropological sciences which on line reference data bases they employ. By the way, MEDLINE is now
available for free on the web at: ww4.ncbi.nlm.nih.gov/PubMed/
Cordially,
201/298 (1997)
Loren
REFERENCES
1. Eaton SB. Humans, lipids and evolution. Lipids 1992;27:814-20. 2. Sinclair AJ, O'Dea K. Fats in human
diets through history: Is the western diet out of step? In: Reducing fat in Meat Animals. JD Wood & AV
Fisher (Eds). Elsevier Applied Science, New York, 1990, 1-47. 3. Pontius AA. Stone age art venuses as
heuristic clues for types of obesity: contributions to iconodiagnosis. Perceptual and Motor Skills
1986;63:544-46. 4. Fenton A, Kisban E. Food in Change: Eating Habits from the Middle Ages to the Present
Day. John Donald Publishers, Glasgow, 1986. 5. Tannahill R. Food in History. Crown Publishers, New
York, 1988.
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Tue, 26 Aug 1997 19:01:21 -0400
> ww4.ncbi.nlm.nih.gov/PubMed/
I believe Loren made a small typing error here; I believe the proper URL is:
http://www.ncbi.nlm.nih.gov/PubMed/
Note that Medline is also available for free at:
http://www.healthgate.com/ -- just click the link for "Free Medline" when you arrive at this site. If you look
carefully on the Medline search screens on this site, you will see an "advanced search" option that allows
more flexibility than what I see available at the NIH site Loren mentions. It's still not ideal as there are search
capabilities it could have but doesn't, but it's fairly advanced and quite useful (and quite free).
When I am being good on my dietary regimen, breakfast for me might consist of eggs and meat and/or
berries and nuts. Lunch will usually be steak or chicken or fish with some olive-oil based mayonaise (made
with eggs, lemon juice, and olive oil) and perhaps some fresh salsa. Supper might be fruit, fresh green
vegetables, and usually some other form of meat. Snacks are usually nuts, green leafy vegetables, olives,
perhaps some jerky. An infinite variety of dishes can be made from a base of meats, nuts, eggs, green
vegetables, fruits (including cucumbers, tomatoes, and other fruits commonly thought of as vegetables),
berries, and flavorful stuffs such as black pepper, oregano, marjoram, sage, mustard, jalapeno, cayenne,
garlic, onions, celery, and so on.
The basic rule would seem to be: whatever can be eaten raw, or with only minimal cooking, is acceptable.
Ray Audette has an interesting book with interesting recipes on it; you can find the book referenced at
http://www.sofdesign.com/neander/
An essential diagram of what modern paleolithic nutritionists would be something like this:
Meat--any variety, including fish. Eggs--any variety. Nuts--any variety, so long as it is a true nut (peanuts,
for example, are not nuts, they are legumes and are quite poisonous in their raw state; they must be roasted or
boiled to remove toxic molds and other antinutrients) Fruit--any variety so long as it can be eaten raw
Berries--any variety.
Staffan Lindeberg has a certain disagreement with some on this issue as he seems to feel that potatoes are
just fine in moderation, while some purists insist that the potato is inedible in the wild and therefore would
not be part of the ancestral human diet. Some also seem to feel that eggs should not be allowed except
occasionally.
Some seem uncomfortable with significant meat consumption, apparently since vegetarianism and attacks on
red meat have made such major inroads into modern nutrition. But the overwhelming bulk of the data I'm
aware of says that meat is and always has been an important part of human diet. (I invite serious
disagreement if anyone is familiar with peer-reviewed data contrary to this proposition.)
A few seem to feel that all foods should be eaten raw. This is an extremist position that's difficult to support
as there is considerable evidence of use of fire by hominids going back quite some time, including at least
one recent archaeological dig of what appears to be a 500, 000 year-old hearth (as Mavis recently referred us
all to).
Fruit is also something of an item of controversy because as Loren points out, modern fruits have been
adapted to be more sugary and less fibrous than their natural cousins. Some seem to feel this should not be a
major issue while others caution that such fruits should only be eaten in moderation.
202/298 (1997)
As Jennie Brand-Miller has so excellently documented in her work, honey appears to be a very common
source of food that is far more common among primitive peoples than would seem intuitively obvious. This
may be a too-often overlooked food source for early humans, if bees were as ubiquitous in the past as they
are today.
There seems to be fairly universal agreement that cereal grains, dairy products, and most legumes would
either be nonexistant or only an occasional part of the ancestral human diet. Enig & Fallon are the only ones
to date to make a very strong defense of dairy. Some others doubt whether the ancestral human diet really
has much relevance to modern people and view this as an entirely intellectual matter with no practical
application.
Eaton has suggested in his published work that the basic paleolithic diet would be relatively low in fat. A few
of us have taken issue with this and feel that fat, most particularly animal fats, have been attacked quite
inappropriately in the last couple of decades.
A crucial question that has also not been addressed strongly is whether or not a pre-agricultural diet (which is
what most of us really mean when we say "paleolithic diet" --although archaeologists are understandably a
bit disturbed by this since the paleolithic period is a huge one and constructing an exact human diet based
solely on archaeological data is impossible without invoking deductive reasoning they are rightfully skittish
of) is really the most appropriate diet for current humans living in advanced Western societies. There is
clearly much to discuss in this area alone.
And this is entirely leaving aside discussions of the actual archaeological evidence and what can be said
definitively there (and what cannot), which we hope the archaeologists among us can help us understand
better. For example, it seems fairly clear from the literature that humans have always eaten animal proteins
of some form, but can more than this be said with conviction from the archaeological record?
I'm hoping at some point to see Loren expand on why he feels that cereal grains are a serious health issue for
humans; although Staffan has elaborated at length about the issue of phytates, and Loren has spoken briefly
about some of the antinutrients to be found in cereals, and a few of us have glanced briefly at the possible
autoimmune reactions caused by the unusually large and complex proteins in most cereals, this seems to bear
much more discussion.
I offer more questions and equivocations than answers, but this may help explain to some what we're trying
to learn about here.
The important thing to remember is that this group does not exist to put forward any particular proposition
(except, perhaps, that there is such a thing as a pre-agricultural diet and that it is worth talking about). We are
here to discuss the data, hypothesize, and learn from each other. There are no limits here, no preconceived
ideas. While I have my own opinions, I'd be quite happy to see someone with a considerable array of facts,
figures, and references to suggest that everything I believe is wrong and that humans evolved eating nothing
but ruminant feces--if the data were legitimate and the reasoning well-articulated (although we would, I
hope, dispense with suggested recipes).
Sharing data, putting forward hypotheses, and testing them to the best of your ability is science at its very
best, no?
-=- "Rest not! Life is sweeping by; go and dare before you die. Something mighty and sublime, leave behind
to conquer time." Goethe (1749-1832)
PALEODIET Archives
Subject: Paleo breakfasts and sugars
Reply-To:
Date: Wed, 27 Aug 1997 10:03:33 +0700
Dear Everyone,
I very impressed with Loren's memory! My memory is not up to giving you a reference, but I know I have
read in a reputable source that some Australian Aboriginal groups (AA) would eat for breakfast whatever
was left over from the dinner the night before. This might include some vegetable foods as well as animal
foods. But often there was nothing left over!
This same source said that the dinner was the main meal of the day and represented the large 'prizes' from the
day's hunting and gathering.
203/298 (1997)
They tended to do the gathering and hunting during the early morning or late afternoon when the
temperatures were less hot. During these expeditions they would nibble on what ever they could see and
would always be on the lookout for sugarbag (honey) and would eat this on the spot.
So in terms of frequency, we can see a nibbling and gorging pattern in one day.
In the Loren's last posting, he wrote
'Because of its high sugar content (dried fruit and honey) and fat content, this so-called "paleo meal" could
produce the very same hyperinsulinemic and dyslipidemic profile characteristic of western "civilized", high
fat, high carb meals.'
It is incorrect to assume that sugary foods will produce high glucose and insulin responses. Fruits tend to
have low glycaemic index values (1). Wolever (2) showed that in current diets, the higher the sugar content,
the LOWER the overall glyaemic index (GI) of the diet. This is because most of the sugary foods we eat
have lower GIs than modern starchy foods.
Of course, the paleo starchy foods had a low GI but so too did their sugary foods. The GI of sugarbag (native
honey) is only 43 on a scale where glucose = 100 (1). When we measured the GI of Australian commercial
honey, we got a value of only 58 while Jenkins got a value of 87 for Canadian honey (1). I suspect the
Canadian honey may have been 'glucose enriched'.
My guess is that paleo diets generated a relatively low demand for insulin and that high insulin responses in
modern diets do indeed produce a greater predisposition to body fat accummulation. We have unpublished
evidence to support this and there is some published work that supports it in humans (3) and animals.
Best wishes Jennie
References
(1) Foster-Powell K, Brand Miller J. International tables of glycemic index. Am J Clin Nutr, 1995, 62 :
871S-93S.
(2) Wolever TMS, Nguyen P, Chiasson J, Hunt JA, Josse RG, Palmason C, Rodger NW, Ross SA, Ryan EA,
Tan MH. Determinants of diet glycemic index calculated retrospectively from diet records of 342 individuals
with non-insulin-dependent diabetes mellitus. Am J Clin Nutr, 1994, 59 : 1265-9.
(3) Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of a low-insulin-response, energyrestircted diet on weight loss and plasma insulin concentration in hyper insulinemic obese females. Am J
Clin Nutr, 1994, 60 : 48-53.
Jennie Brand Miller PhD Associate Professor in Human Nutrition Department of Biochemistry G08
University of Sydney NSW 2006 Australia Phone: (61 2) 9351 3759 Fax: (61 2) 9351 6022
PALEODIET Archives
Subject: Help request
From: Dean Esmay
Reply-To:
Date: Wed, 27 Aug 1997 11:41:11 -0400
I have an archaeobotanist from the University of Bradford in England attempting to join the list. However
she appears to have trouble with her email configuration so she can get mail out but I cannot get mail to her.
Would anyone know the proper domain name to send to a person at the University of Bradford? (i.e.)
bradford.ac.uk does not work.
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Wed, 27 Aug 1997 17:03:24 -0400
Er, a correction to myself. I mistyped the below:
> including at least one recent archaeological dig of what appears to be a 500, 000 year-old hearth (as
> Mavis recently referred us all to).
204/298 (1997)
That should have said what appears to be a 400, 000 year-old hearth. Curse my slippery fingers. Or was it a
slippery memory? :-).
PALEODIET Archives
Subject: Re: Eggs
From: Loren Cordain
Reply-To:
Date: Wed, 27 Aug 1997 17:25:00 -0600
In the last digest, Dean mentioned that eggs might be part of his modern day paleodiet for breakfast. It is
without question that our early ancestors would have scavenged and even actively pursued eggs from the
nest of birds. However, because in the wild, eggs only occur seasonally, pre-agricultural man could never
have consumed 2 eggs for breakfast every morning of the year, as may be the case for western man.
Although the in vitro nutritional content of eggs are quite good, there would have been substantial "in vivo"
nutritional problems with regular egg consumption for early man. Prior to the regular controlled use of fire
(~150, 000 y BP - 40, 000 y BP), hominids would have had to consume any eggs that were found in the raw
state. Raw egg white contains a protein called avidin, which is a potent inhibitor of biotin and other B
vitamins. Additionally egg white contains the lectin conalbumin which is a powerful binding protein for iron
and which would inhibit its absorption (1). Additionally, egg white protein is one of the more common
allergenic food proteins. Consequently, there are some nutritional/evolutionary arguments which would
contraindicate egg consumption on a daily basis for some people.
Reference 1. Alderton G. et al. Identification of the bacteria-inhibiting, iron binding protein of egg white as
conalbumin. Arch Biochem 1946;11:9-13.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 26 Aug 1997 to 27 Aug 1997
From: Linda Scott Cummings
Reply-To:
Date: Wed, 27 Aug 1997 23:13:09 -0400
Dean,
What is this archaeobotanist's name that you can't reach? I am also an archaeobotanist and belong to the
archaeobotany list. Perhaps I could reach this person for you. I've been "lurking" on your list for awhile
trying to form an opinion of the topic and conversations.
Now, to address one paragraphy from the most recent post:
> And this is entirely leaving aside discussions of the actual archaeological evidence and what can
> be said definitively there (and what cannot), which we hope the archaeologists among us can help
> us understand better. For example, it seems fairly clear from the literature that humans have
> always eaten animal proteins of some form, but can more than this be said with conviction from the
> archaeological record? The archaeological and especially the archaeobotanic literature has many
> examples of pre-agricultural diet. Most of this literature is "gray" or unpublished, which means
> that if you don't know an archaeobotanist, it's hard to find.
The best data on diet comes from the study of human coprolites (feces). There are coprolites representing the
diet of pre-agricultural people in Texas in the literature -- primarily as MA theses and Ph.D. dissertations. To
find these, one should search through University Microfilms, since they sell copies of theses and
dissertations. I don't have a good memory for exact titles of publications, so I'll need to look at some of this
information on my bookshelf to post for this group.
At the present, I'm examining the remains from two probable human coprolites about 6000 years old from
Wyoming -- definitely pre-agricultural. The contents are very interesting and would lead most people to the
conclusion that these coprolites are not from humans.
205/298 (1997)
I'm surprised to read so many opinions about the "paleolithic diet" as if it was similar around the world. Not
so. In some areas pre-agricultural diets include many insects. Often they have been cooked. In some areas
rodents are a common component of the diet, usually consumed complete with bones, hair, stomach contents,
and meat. We have good evidence of the consumption of rodent hair and bones and assume the stomach
contents and meat part. In fact, in some areas rodent consumption persisted into the agricultural period. In
the northwest coast area of North America pre-agricultural diet included large amounts of fish, berries, and
roots. Camas bulbs were a staple in portions of the American northwest. This can be documented through the
archaeologic record.
If there is interest out there for an archaeobotanic accound of the pre-agricultural diet, I'll put together an
abstract and begin on a book for publication.
Linda Scott Cummings Paleo Research Golden, CO
PALEODIET Archives
Subject: Implementing Paloediet
Reply-To:
Date: Thu, 28 Aug 1997 07:26:51 -0400
As a clinical nutritionist/author/Ph.D. candidate who has been a fish eating vegetarian for 11 years, I have
gone back to meat these past two months and have eliminated grains. I eat meat at each meal, and my
physique is much leaner. I have more muscle without any extra exercise, and I have much better muscle
definition. No supplement changes--just a more Paleo diet, with 4-6 ounces of animal protein 3 times per
day.
Regarding saturated fats, there is a lot of argument as to whether they are "good" or "bad." I think that there
is bit too much saturated fat phobia, even among people I have the highest respect for. People can point to
studies showing that more saturated fats are linked to more heart disease, but I think you cannot separate
saturated fats downside from omega 3 fatty acid deficiency. A low fat diet with no EFAs will cause heart
disease, and a high saturated fat diet with plenty of omega 3s will keep arteries clear (Eskimos). I wish we
could see fats as a symphonic event, and not say oboes are good, timpani drums are bad, etc. And the
advantage of saturates over too many omega 6s is that saturated do not compete with omega 3s for
elongation. Saturates alone increased may worsed insulin problems, but combined with omega 3s may help
insulin metabolism. See the excellent review article "Dietary Fats, Membrane Phospholipids and Obesity, "
Pan P et al, Journal of Nutrition 124: 1555-1565, 1994. As I tell my clients, we are more often killed by what
we fail to eat than by what we eat.
Love Paleodiet--thanks Dean. Great to be part of this forum with all these wonderful contributors.
"Progress, far from consisting in change, depends on retentiveness"
-- Santayana
Cheers-Robert Crayhon, MS
PALEODIET Archives
From: John Martinson
Reply-To:
Date: Thu, 28 Aug 1997 09:19:51 -0700
Many Thanks to Loren for the NLM/NIH website (even if he did make a little typo). What the heck, "W" and
"4" are close on the Sholes keyboard. And I don't think Loren is losing memory as he approaches 50 (even if
his typing skills are suffering). What happens as time goes by (and he continues to read, study, learn etc.) is
that his hard disk is filling up. Loren, you haven't lost anything--quite the opposite--but your retrieval time is
getting longer. And I speak as someone who has personally experienced this process about 20 years longer
than you have. So don't be discouraged, and keep up the good work. You just have to be patient in your
retrieval efforts.
206/298 (1997)
P.S. I recommend the following website to anyone interested in more efficient keyboard skills-http://www.ccsi.com/~mbrooks/dvorak/ It will take you into the whole world of the Dvorak keyboard for
typing. A vast improvement on the Sholes that we all use. And now software is available to convert your
Sholes keyboard to the Dvorak if you really want to improve your keyboard effectiveness.
PALEODIET Archives
Subject: Re: Help request
Reply-To:
Date: Thu, 28 Aug 1997 10:05:13 +0100
> Date: Wed, 27 Aug 1997 11:41:11 -0400
> From: Dean Esmay
> I have an archaeobotanist from the University of Bradford in England attempting to join the list.
> However she appears to have trouble with her email configuration so she can get mail out but I
> cannot get mail to her. Would anyone know the proper domain name to send to a person at the
> University of Bradford? (i.e.) bradford.ac.uk does not work.
The ones in my addressbook are of the form, or, except one which is of the form There is a directory of
mailnames on the Bradford webserver http://www.brad.ac.uk/contacts.htm
Andrew
========================================================================= Dr.
=========================================================================
>
>
-----------------------------> End of PALEODIET Digest - 26 Aug 1997 to 27 Aug 1997
>
****************************************************
>
PALEODIET Archives
Subject: Re: comments to Robert Crayhon & John Martinson
From: Loren Cordain
Reply-To:
Date: Thu, 28 Aug 1997 15:38:00 -0600
207/298 (1997)
Robert C makes the comment that "a low fat diet with no EFAs will cause heart disease, and a high saturated
fat diet with plenty of omega 3s will keep arteries clear (Eskimos)". I believe that Robert has got the first part
of this correct. Indeed low levels of EFAs (essential fatty acids - particularly the chain elongated 20 and 22
carbon forms of both n6 and n3 families are inversely related to coronary heart disease (CHD). Paradoxically
(at least in terms of the AHA dietary recommendations), Hindu vegetarians from India whose diet is
composed largely of low fat grains and pulses (legumes) maintain CHD rates equal to (1) or higher (2) than
those in the USA and countries of Europe despite their lower total fat content when compared to American
and European diets. Indian populations have consistently exhibited high plasma N6/N3 ratios; low levels of
20:5n3 and 22:6n3 and high levels of 18:2n6 when compared to western populations (2, 3, 4, 5). All of these
EFA profiles are conducive to CHD and occur because of the lack of an appropriate balance of N6/N3 and
because of the almost total lack of 20 and 22 carbon fatty acids in commonly consumed plant based foods.
Robert is partially correct in saying that omega 3 fats provide protection against CHD, but it has little to to
with keeping the arteries clear (i.e. atherosclerosis). Omega 3 (n3) fats provide protection from CHD in that
they lower triglycerides and perhaps VLDL; additionally they reduce platelet adhesitivity and decrease
thrombotic tendencies as well as reducing cardiac arrhythmias (6). However, recent large scale meta analyses
(7) show that N3 fats actually cause a 5-10% rise in LDL cholesterol and a small rise (1-3%) in HDL.
Eskimo populations indeed do consume higher levels of both saturated fat and N3 fats than do Western
populations; they also exhibit significantly lower serum LDL and total Cholesterol levels than europeans (8).
Thus, logic (derived from the meta analytical data) dictates that the N3 fats are not the element responsible
for the lower total and LDL serum Cholesterol in these populations. Careful analysis of Bang and Dyerberg's
data (8) reveals a much higher protein intake (26% of total calories) compared to the 11% value in Danes.
High protein intakes are known to cause drastic inhibition of hepatic VLDL synthesis (9) - (VLDL's are the
source of LDL's) and high protein diets in humans have been clinically shown to reduce total cholesterol,
LDL cholesterol, and triglycerides while simultaneously increasing HDL (10, 11). Further, acute
consumption of high levels of low fat (6.5%), lean beef protein is not associated with a post prandial rise in
insulin but rather an increase in glucagon levels (12). Consequently, the major reason why eskimo diets keep
serum cholesterol levels low and atherosclerosis at bay is because of their high protein content primarily.
There is no doubt that N3 fats also contribute to lowering CHD, but it is not directly mediated by a lowering
of LDL cholesterol but rather by other mechanisms previously outlined.
REFERENCES 1. Begom R. et al. Prevalence of coronary artery disease and its risk factors in the urban
population of south and north India. Acta Cardiologica 1995;50:227-240. 2. Miller GJ. et al. Dietary and
other characteristics relevant for coronary heart disease in men of Indian, West Indian and Eruopean descent
in London. Atherosclerosis 1988;70:63-72. 3. Reddy S. et al. The influence of maternal vegetarian diet on
essential fatty acid status of the newborn. Eur J Clin Nutr 1994;48:358-68. 4. Ghafoorunissa. Essential fatty
acid nutritional status of apparently normal Indian men. Human Nutrition: Clinical Nutrition 1984;38C:26978. 5. McKeigue PM et al. Diet and risk factors for coronary heart disease in asians in northwest London.
Lancet 1985;ii:1086-90. 6. Leaf A et al. Cardiovascular effects of n-3 fatty acids. N Engl J Med
1988;318:549-557. 7. Harris WS. n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr
1997;65(supp): 1645s-54s. 8. Bang OB et al. Lipid metabolism and ischemic heart disease in Greenland
Eskimos. In: Draper HH (ed). Advances in Nutrition Research, Vol 3, NY, Plenum Press, 1980; 1-22. 9.
Kalopissis AD et al. Inhibition of hepatic very low density lipoprotein secretion in obese Zucker rats adapted
to a high protein diet. Metabolism 1995;44:19-29. 10. Wolfe BM. Potential role of raising dietary protein
intake for reducing risk of atherosclerosis. Can J Cardiol 1995;11:127G-131G. 11. Wolfe BM et al. Short
term effects of sutstituting protein for carbohydrate in the diets of moderately hypercholesterolemic human
subjects. Metabolism 1991;40:338-43. 12. Westphal SA. et al. Metabolic response to glucose ingestion with
various amounts of protein. Am J Clin Nutr 1990;52:267-72.
Thanks to John Martinson for pointing out the Dvorak key board to us - can we really teach old dogs new
tricks? John has some interesting ideas concerning hominid brain encephalization and nutrition during
pregnancy which perhaps he could share with us. Also, let us not forget his realization that insects have
substantial amounts of n3 fats. I've got the references for this, if anyone is interested.
Cordially,
Loren
PALEODIET Archives
Subject: Re: Eggs
From: Art De Vany
208/298 (1997)
Reply-To:
Date: Thu, 28 Aug 1997 15:40:09 -0700
I can add only a few observations to what Loren and Dean put forth as the paleo diet.
I eat abundant amounts of eggs: boiled or scrambled in a teflon pan using nothing, or residual fat from a ham
steak or bacon. Typical breakfast is half a large ham steak or 5 pieces of bacon with 4 or 5 eggs (tossing out
a yolk or two) and half a cantalope (maybe a pear half an hour later). Lunch is a tuna on a bowl of lettuce
with plenty of raw vegs and fresh spices. Olive oil and balsamic vinegar. If I eat at campus, a beef sandwich
(tossing about half of the bread) with fresh fruit and selzer water. Dinner is steamed vegs with two or three
chicken breasts along with a large salad. When I eat out, I like a good steak house with a great salad bar. I
just order the steak and tell them to hold the potatoes and bread and gather fruit and vegs at the salad bar.
Snacks, if any, are fresh fruits, especially melons and pears. Watermelon is high in glutathione, the body's
primary antioxidant.
It is amusing to order breakfast and watch the server's response when you say don't give me any toast or
pancakes or potatoes or rolls or butter; substitute fruit if you can. Eggs and bacon and a bowl of truit is about
the best thing you can get in Denny's. Many mexican restaurants will substitute vegs for beans and rice.
I never eat potatoes or rice or cereals. No milk or cheese. By the way, milk produces an enormous blood
sugar response. This seems to be undocumented, but my wife and son are both diabetics, and we know this to
be true. The effectiveness of milk in countering insulin reactions is medical folk wisdom among diabetics
and many of their doctors. It may be proteins in the milk; it is known that certain proteins elevate blood
glucose.
What I can add that has not been stressed enough (in my opinion and experience) is that I believe it is
essential to vary the amount one eats. A bit of chaos is essential to all living things. I eat more on days when
I workout heavy. I do something active nearly every day, but 3 or 4 days include brief, high intensity
workouts or hikes with uphill sprints. My caloric intake is absurdly high on days that I work out; probably 4
or 5000 calories (I never count). On other days, it may be between 2000 and 3500. Once in a while, I fast
lightly, eating only a meal or two or eating fruit only. I used to flip a coin to decide if it was going to be a
day with a succesful hunt and feasting or a lean day. Now I just randomize in my mind and by feel. But, I do
randomize.
Since a large part of the battle is against hyperinsulemia, one should strive to produce abundant growth
hormone pulses as a countermeasure. This is where the intense exercise plays a crucial role.
Never drink these sports drinks before or after exercising; they are high glycemic and kill the GH response
you are after in your exercise. Post exercise food or drink should be low glycemic to maximize the GH
response. Also, high blood sugar after a workout caused the elevated blood lipids to precipitate onto the
vessels and the insulin helps the fats to migrate into the lining.
I add once more that it is inadequate to consider diet alone; paleo diets go with paleo life rhythms and paleo
activity patterns. I discuss this on my Evolutionary Fitness web page, which can be reached from my
personal web page, whose url is below.
Mathematical Behavioral Sciences
"The more corrupt the republic, the more laws multiply." Tacitus
PALEODIET Archives
Subject: Protein
From: Todd Moody
Reply-To:
Date: Fri, 29 Aug 1997 21:58:34 -0400
On Fri, 29 Aug 1997, Loren Cordain wrote:
> Careful analysis of Bang and Dyerberg's data (8) reveals a much higher protein intake (26% of
> total calories) compared to the 11% value in Danes. High protein intakes are known to cause
> drastic inhibition of hepatic VLDL synthesis (9) - (VLDL's are the source of LDL's) and high
> protein diets in humans have been clinically shown to reduce total cholesterol, LDL cholesterol,
> and triglycerides while simultaneously increasing HDL (10, 11). Further, acute consumption of high
209/298 (1997)
> levels of low fat (6.5%), lean beef protein is not associated with a post prandial rise in insulin
> but rather an increase in glucagon levels (12).
Very interesting. I had the idea that fat intake has little effect on the insulin/glucagon response to food, so
that the rise in glucagon levels would result from a given amount of protein, whether it be fatty or low-fat. Is
this incorrect? It's interesting that Sears' "zone" diet calls for 30% of calories *at each meal* to be protein,
with total daily recommended protein intake linked to lean body mass. That is, if Sears is right, the favorable
glucagon response depends not only on the right percentage of protein but on *absolute* protein sufficiency.
Is this consistent with the data referenced above?
Todd Moody
PALEODIET Archives
From: Luc De Bry
Reply-To:
Date: Sun, 31 Aug 1997 21:59:49 -0700
PROTEIN * FAT MIXTURE
Just one comment on the exchange of views concerning fat and proteins doses, between Loren Cordain and
Todd Moody in the sole message of Paleodiet Digest of August 29th :
There is one little detail of tremendous importance which is missing. It's not just the fat "per se" that is
important, or the protein "per se".
There is a kind of synergy between dose effects from proteins and fat, AND relative proportions between fat
and proteins. Indeed, fat and protein do form a "mixture"; a two-component mixture!
Very few people have realized and are measuring this fact. First insights came from Plant Physiology and
Nutrition in the 1950's at the French-speaking Free University of Brussels (Belgium). (Well yes, plants obey
to a number of basic nutrition principles too. The difference with us, is that their food is called "fertilizers"
and "sun energy"). Prof. Homes and Van Schoor have published their major results in French in the early
1960's. Their books are out of print.
Similarly to the genetic results of Mendel, these results have been buried and forgotten. Now, some 30 years
later, they are reapearing with more mathemathics to support them, in English this time. The ones not too
averse to statistics and maths may enjoy cross-fertilising their work with this master-piece :
EXPERIMENTS WITH MIXTURES Designs, Models and the Analysis of Mixture Data John A. Cornell
(Univ. of Florida) Wiley Interscience Publication - 1990 ISBN 0-471-52221-X
It's a bit more rough to digest than Homes and Van Schoor's books, but how valuable it is to pay attention to
the combination between dose effect and relative proportions between the doses. Furthermore, today's
relevant softwares can do most of the work for you.
Best wishes for many results,
Luc -- Luc De Bry, Ph.D., Head of Research Department GENERAL BISCUITS BELGIE De BeukelaerPareinlaan 1 B-2200 Herentals - Belgium
Email : An Operating Company of http://www.danonegroup.com
PALEODIET Archives
Subject: Response to Todd Moody
From: Loren Cordain
Reply-To:
Date: Tue, 2 Sep 1997 09:20:00 -0600
210/298 (1997)
As far as I know, there are no good, recent data evaluating the effects of varying protein/fat mixtures upon
insulin/glucagon responses in humans. Most of the data involves manipulating CHO, with varying amounts
of fat; protein is usually held constant. The Westphal et al paper (1) evaluates protein/CHO mixtures on
serum glucagon responses. Pure dietary CHO (50 gm glucose) shows no rise in plasma glucagon whereas
pure protein (actually 93.5% lean beef, 6.5% fat) causes the greatest rise in glucagon after 1hr; with roughly
equal areas under the curve after 3hrs when comparing pure protein to protein/CHO mixtures (50 gm
glucose/50 gm protein). Thus, there appears to be a dose response with protein/CHO mixtures and from the
data, it can probably be interpreted that there is a dose response effect with pure protein. Fat/CHO mixtures
cause a greater rise in insulin that CHO meals alone, presumably because of the stimulatory effect of fat
upon glucose dependent insulinotropic peptide (GIP) (2). Thus, as Todd has surmised, there is a dose
dependent effect of dietary protein upon glucagon secretion which is largely independent of either CHO or
Fat.
REFERENCES
1. Westphal SA et al. Metabolic response to glucose ingested with various amounts of protein. Am J Clin
Nutr 1990;52:267-72. 2. Collier GR et al. The acute effect of fat on insulin secretion. J Clin Endocrionology
and Metabolism 1988;66:323-26.
PALEODIET Archives
Subject: Strange problem
From: Dean Esmay
Reply-To:
Date: Wed, 3 Sep 1997 13:18:28 -0400
Recently, I discovered that the welcome message sent to new subscribers of this list was mixed up.
Somehow, the welcome message for the LOW-CARBOHYDRATE TECHNICAL DISCUSSION LIST was
being sent to new subscribers of the PALEOLITHIC DIET & EXERCISE SYMPOSIUM. I recently fixed
this error; I'm not sure how long it's been going on.
I've received a few messages from people who were confused by this in the last few days, but I'm not sure
how long the problem was going on before that.
For those of you who received the erroneous welcome message, here is the proper group charter & welcome
message for this symposium:
[Important! PLEASE save a copy of this message in a handy place in, on or near your computer. You may
need to refer to it again in the future if you have any questions or problems with the Paleolithic Nutrition
list.]
WELCOME!
You have been added to the Paleolithic Diet Symposium list. This is a semi-moderated, semi-formal
discussion group on the nature, benefits and drawbacks of pre-agricultural diet and lifestyles, and their
potential application to modern life.
We strongly suggest that all new subscribers point their web browsers at
http://maelstrom.stjohns.edu/archives/paleodiet.html and bookmark that page. This page contains the
complete archives of all messages ever posted to the Paleodiet Symposium. As a new subscriber you should
probably review recent messages on this web site to catch up on discussions.
The primary objective of the list is to provide a forum for communication and discussion among
investigators of pre-agricultural nutrition. It is hoped that this forum will facilitate discussion of both
published and unpublished findings and ideas, foster potential collaborations between investigators, and
develop into an information resource.
If you are knowledgeable in this field, we encourage you to share your thoughts and information with us.
Messages or questions sent to the list should be based on research. Because the concept of paleolithic
nutrition covers many fields, discussion may at times seem free-ranging; nutrition, biology, paleontology,
anthropology, and other areas of science all touch on this subject. But any message is potentially of value so
long as it serves to provide illumination in a substantive manner to the subject of evolution and the human
diet.
211/298 (1997)
The Paleolithic Diet Symposium is primarily intended for researchers, but accepts others who have a welldefined need or interest, including physicians or nutritionists. Even members of the lay public will be
allowed to read the messages from this list. However, the list is moderated, and only messages submitted by
those with appropriate credentials, or demonstrating significantly advanced understanding of the subject
under discussion, will be distributed to the list membership. Debate is welcome and even encouraged, but
only in a form which demonstrates a serious level of understanding of the subject area.
(In short, your message only goes to the list if the moderators agree that you know what you're talking about
and aren't wasting people's time. With all that said, please do not be timid if you believe you have
meaningful question to ask or appropriately supported data to share.)
If you know of other persons who might have a legitimate interest in this list, we encourage you to tell them
about it. The more accumulated knowledge and wisdom that we can pool here, here more useful this resource
will become.
-=-=RULES FOR SENDING MESSAGES TO THE LIST:
--------------------------------------1. Include only relevant lines from messages you are quoting. Including a complete message wastes
resources and readers' time.
2. Do not contact the Postmaster, or anyone else at St. Johns with questions or complaints about our list. The
computer staff at St.Johns maintains hundreds of internet discussion groups and cannot get involved in
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3. If you decide to remain subscribed to this mailing list, your doing so indicates agreement by you to the all
the policies outlined in this Welcome message, including the terms and conditions to be found in the
following two paragraphs. PLEASE unsubscribe from this list if you are unable to agree.
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5. By your use of this mailing list, you agree to hold harmless the PALEODIET List forum leaders/owners,
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If you do not agree to the provisions of the two paragraphs immediately above, or with any other policy
included in this Welcome message, please unsubscribe from the PALEODIET list immediately. (see below)
-=-=PALEODIET LIST ADDRESSES:
------------------------The following e-mail addresses are used in relation with this list:
1. The list address:
Messages sent to this address go to all list members. This is called "posting" to the list.
You can only post to the list from the account under which you are subscribed. If your post is rejected for no
apparent reason, contact Dean Esmay at
2. The listserv address:
This is the address to which you sent your subscription request, and it should be used for all requests that can
be handled automatically by the LISTSERV program. This includes changing your name or address,
unsubscribing, changing your subscription options, retrieving files from the file server, searching the list
archives, etc. You will find a list of the most commonly used LISTSERV commands in the next section.
3. The listowners' addresses:
Primary Owner: Dean Esmay
Co-Owners: Don Wiss Staffan Lindeberg
These are the people in charge of keeping the list running. If you have ANY problem that you cannot solve
with LISTSERV commands, contact one of the listowners.
COMMON LISTSERV COMMANDS:
------------------------Here are some of the common commands that you may find useful as a member of the Paleodiet mailing list.
Send any of these commands in the body of a letter addressed to (NOT to the paleodiet address) and it will
be taken care of.
This is not a complete list of commands, but should include every command you might need.
212/298 (1997)
Remember to send commands to ; don't send them to, which is the address where you post messages for
everyone else to read.
The common commands are as follows:
1. SIGNOFF PALEODIET
This command removes you from the PALEODIET list.
---------2. SET PALEODIET NOMAIL
Sets your subscription option so that you will receive no mail from the list. You are still able to post
messages to the list. This is useful if you have more than one mail account (so you can post messages from
any account but only read from one), or if you want to leave the list temporarily (e.g. when going on
vacation). Use "SET PALEODIET DIGEST" to go back to normal.
---------3. SET PALEODIET NODIGEST
Sets your subscription option to individual messages instead of receiving a daily digest. You will receive
each message as it is posted. To return to digest, use SET PALEODIET DIGEST.
---------4. INDEX PALEODIET
This returns a list of all the PALEODIET files available from the file server, including our archives of
previous messages.
--------5. GET
This retrieves a named file from the file server, eg. GET PALEODIET LOG703 will retrieve the March 1997
(97 = year, 03 = month) archive of all message traffic to the PALEODIET list.
---------6. INFO
Returns a complete list of LISTSERV help files. Send "INFO REFCARD" for a reference card on
LISTSERV commands, to see every command available (as opposed to this short of common commands).
----------Replying to messages
-------------------------When you reply to a message someone has posted on the PALEODIET list, you need to give some thought
as to where you send the reply. If it is a personal reply, or only of interest to a very few people, then you
should send the reply to the individual who posted the message. If you believe your reply would be of
interest to more than a very few list subscribers, then you should send it to the list. We have set the "reply-to"
field in the message header such that with most mail programs, this happens automatically.
If you have any questions or problems, please send them directly to me, and I will try to help you.
With all that out of the way, let me again say, welcome. We hope this list provides you with a useful
resource.
Dean Esmay
PALEODIET Archives
Subject: Questions on digestibility of cooked foods
Reply-To:
Date: Wed, 3 Sep 1997 17:58:02 -0500
At the request of a friend of mine on the Raw-Food listgroup, I'm posting a few questions here that he put to
me on the subject of cooked vs. raw-food digestibility, in the hopes that someone with a technical
background here will have answers. (References would also be nice, and score you bragging-rights bonus
points. :-)) Note that those in the all-raw-foodist camp are intensely skeptical of any reasoning or data that
might support the cooking of food in any way, so should you have something along those lines, references
would be most appreciated where you have them. (Same goes for opposing views of course, as well.)
213/298 (1997)
I would be interested in any comments/ answers/ musings those with biochemistry/ physiology backgrounds
have on these questions. These are the types of questions that get asked all the time on groups like the RawFood and Raw listgroups for which no one ever seems to have definitive answers, and over which much
foofaraw is made. It has always been a bit surprising to me that these questions are also not topics of
occasional conversation here on the Paleodiet group, given their relevance to evolutionary diet. In any event,
they are topics of practical concern among those of us actually trying to fashion our diets according to some
semblance of what the evolutionary picture of human diet is thought to have been. Again, any answers
welcomed and appreciated. Thanks,
--Ward Nicholson
P.S. In hopes of stimulating comment (possibly about how erroneous my own ideas are :-)), I will be posting
a rather conjectural follow-up reply of my own to Tom's questions here on the Paleodiet list shortly, should it
make it through Dean Esmay's "B.S." filter.
*****************************************************************************
Subject: QUESTIONS ON DIGESTIBILITY OF COOKED FOODS To: Ward Nicholson From: Tom
Billings Date: 9-3-97
On the question of adaptation to eating cooked food, one question came to me. I don't recall offhand if this
was addressed in the research on this (my apologies for forgetting if it was), so thought I would raise it:
Are cooked foods close enough in composition to their raw counterpart that we can digest them anyway (as
we are omnivores, able to digest a wide variety of foods and survive on radically different diets)? As an
example, can I digest cooked starch because my ancestors ate raw starch foods in pre-fire days, and the
chemical composition is altered some, but not that much, by cooking?
This also raises the questions:
Is grain close enough in chemical composition to say, tubers, that we can digest it OK?
Is dairy close enough in chemical composition to other foods (that is, it is similar to an average of meat +
fruit, hence within the "range" of digestible "original" foods), that many of us can digest it?
(Re: the above two questions: I acknowledge the serious problems some people have with gluten and lactose.
I'm not suggesting everyone can digest them.)
You are free to post this on the Paleo lists if you wish - if you do that, I would be interested in any significant
replies to these questions.
Regards, Tom Billings
****************************************************************************
PALEODIET Archives
Subject: Re: PALEODIET Digest - 1 Sep 1997 to 2 Sep 1997
From: Todd Moody
Reply-To:
Todd Moody
Date: Wed, 3 Sep 1997 18:54:57 -0400
On Tue, 2 Sep 1997, Loren Cordain wrote:
> Thus, there appears to be a dose response with protein/CHO mixtures and from the data, it can
> probably be interpreted that there is a dose response effect with pure protein. Fat/CHO mixtures
> cause a greater rise in insulin that CHO meals alone, presumably because of the stimulatory effect
> of fat upon glucose dependent insulinotropic peptide (GIP) (2). Thus, as Todd has surmised, there
> is a dose dependent effect of dietary protein upon glucagon secretion which is largely independent
> of either CHO or Fat.
Thank you for this clarification. The picture that seems to emerge from the data is that humans tolerate
dietary fat quite well (assuming that the fat is not deficient in certain fatty acids) when carbohydrate intake is
moderate. To think of it in another way, if either fat intake or carbohydrate intake is high, then the presence
of the other macronutrient in large amounts becomes problematic. Current low-fat dietary "wisdom" takes
for granted high levels of dietary carbohydrate, and the safest way to eat lots of carbs is to eat very little fat
along with them.
214/298 (1997)
Health seems to require a trade-off between fats and carbs, as well as sufficient consumption of protein. I am
not a scientist, but this picture certainly causes me to wonder what evolutionary pressures might bring about
this trade-off condition. The answer that suggests itself is this: The human body would "prefer" to run on
animal protein and fat, primarily, but because hunting is a dicey thing, backup systems are needed. So, when
animal protein and fat are not available, we can eke out a living on carbs. During certain seasons, we might
be able to do little better than lean meat and carbs, but what would normally never happen to a huntergatherer, I suppose, is to have a long-term a diet composed mainly of carbs and fats.
So, if we have a fair idea of what components of the civilized diet are conducive to CHD, it is interesting to
ask whether it is even possible to have a CHD-prone diet without resorting to agricultural foods...
Todd Moody
PALEODIET Archives
Subject: Questions on digestibility of cooked foods
Reply-To:
Date: Wed, 3 Sep 1997 18:18:13 -0500
I don't know the answers to very many, if any, of Tom Billings' questions, but I'll take a few speculative
stabs here that might hopefully stimulate comment from the rest of you about just how foolish my musings
here are, if nothing else. :-)
> Are cooked foods close enough in composition to their raw counterpart that we can digest them
> anyway (as we are omnivores, able to digest a wide variety of foods and survive on radically
> different diets)?
That sounds plausible enough. It would seem to me that while cooking changes things about foods, and the
changes may seem like significant changes--from the point of view total-raw-food enthusiasts--in the overall
the changes may not always amount to all that much in terms of digestibility. I.e., they may be enough to
introduce some additional toxins perhaps, or change the character of the starch in some foods to make them
more digestible, or whatever.
But it's not as if all of a sudden the foodstuff was changed into something so completely foreign to the
digestive tract--like polybicarbonate plastic or something :-) --that all of a sudden it becomes totally
indigestible, or even largely indigestible. Wouldn't the supposition hold that if the protein in the food is still
protein, the starch and sugars and other carbs still carbs, the fats still fats, the body is going to digest it?
To me the question is not so much digestibility, but more whether any potential side-effects due to the
cooking might create any problems of undue toxicity significantly above the level of toxins and antinutrients
that may be in raw foods to begin with. Although in some cases, of course, cooking makes the foods a lot
*more* digestible and less toxic than they would be raw (many root vegetables, grains, etc.)--which of
course might beg the question of whether we ought to be eating these foods to begin with, even though many
people do eat them raw. (And that's whether or not they are digesting very much of them even if they *can*
eat them raw, and have them go through their digestive tract without experiencing noticeable problems or
distress.)
Actually, I would think these same considerations apply to raw foods just as much as with cooked foods, as
far as the ratio or equation of usable nutriment vs. waste/ toxic matter goes (playing the part of equalopportunity muckraker here :-)). Obviously cooking affects digestibility and/or assimilation, or we wouldn't
do it in the case of grains and tubers, to mention two items; and obviously many people in today's world exist
most of their lives on mostly cooked food. So to me in most cases it seems like more a question of degrees
and gradations of digestibility, not either/or.
> As an example, can I digest cooked starch because my ancestors ate raw starch foods in pre-fire
> days, and the chemical composition is altered some, but not that much, by cooking?
Well, this question of course presupposes there wasn't any cooking in prehistoric times for a long enough
time to have affected the human genome, and there may have in fact been--these days I am not convinced by
what evidence is available one way or the other. However, supposing for the moment that were the case (no
adaptation to cooking yet), I would tend to think so (that the starch is digestible to what degree it is cooked
based on prior adaptations to raw starch). However, the kicker here is that from what I understand, the starch
in many root veggies and probably all grains is much MORE digestible when cooked.
215/298 (1997)
So the sword can cut both ways here, and when it cuts this latter way, it sort of begs the question of how
certain cooked foods could be more digestible than raw if we hadn't encountered those cooked foods in
evolution before. The two possible answers would seem to be that: (1) we HAVE encountered those foods
cooked before and made more successful use of them cooked than raw, or (2) we HAVEN'T encountered
those foods, and we aren't that well-adapted to them raw, but for whatever reason cooking renders them--by
fortuitous circumstance--more digestible given our previously evolved digestive mechanisms.
> Is grain close enough in chemical composition to say, tubers, that we can digest it OK?
Hmmm. To my mind, the question would be not how close grains are to tubers, but rather how compatible
each _on_its_own_ would be with the human digestive system. Comparing their digestbility based just on
the criterion of starch content may be rather arbitrary on our part. Since tubers and grains are in two different
biological classes of plants, the fact they both are high in starch is just a similarity we happen to notice
between them because, say, that might be one way we classify foods according to some recipe for eating. But
that seems like it might be something of an arbitrary scheme to me. They may be enough dissimilar in other
respects that you can't use the digestibility of one as a gauge for the other. I wouldn't know enough to say.
> Is dairy close enough in chemical composition to other foods (that is, it is similar to an average of
> meat + fruit, hence within the "range" of digestible "original" foods), that many of us can digest it?
Again, I wonder if it really makes sense to be comparing dairy against an "average" of meat/ fruit--rather
simply on its own merits. Or according to some sort of *independent* standard, to the degree that one is
possible, for what types of things are digestible in the human tract, and why. (Such as, perhaps, the above
hypothetical postulated thinking about carb/ fat/ protein content, or should that not be the applicable
standard, whatever else actually does apply, etc.) To me the question would be not so much how similar one
food is to another by some subjective classification scheme, but rather what specific molecular compounds
and elements they contain and in what array, and which are attackable by the enzymes and so forth that the
digestive system can bring to bear. That may or may not correspond to our own subjective classification
schemes.
From having subscribed to the Paleodiet list here, it seems that everything comes down to very specific
biochemical pathways, in terms of either enzymes or other controlling factors determined by specific genes,
or in terms of specific autoimmune response to food antigens, etc.
> (Re: the above two questions: I acknowledge the serious problems some people have with gluten and
> lactose. I'm not suggesting everyone can digest them.)
Agreed. Interesting in this connection, though, is that it takes a specific enzyme (lactase) to digest lactose
which is coded for by a specific gene. I forget the process by which some people can handle gluten without
generating an auto-immune response (Ron Hoggan, aren't you the expert on that?), but again, it is something
that comes down to certain specifics. In general, I think these two examples may be a good illustration of
how the general type of reasoning used in alternative diet circles as to digestibility partakes too much of
woolly thinking and vagueness; when, if you get right down to it, everything probably has to do with
*specific* enzymes and if the food contains the specific class of substrates attackable by those enzymes
without too much leftover waste matter or toxic material that the digestive system doesn't have ways of
buffering sufficiently, or is capable of eliminating it within the safety parameters of the body's design for
elimination.
> You are free to post this on the Paleo lists if you wish - if you do that, I would be interested in any
> significant replies to these questions.
Me too.
--Ward Nicholson
PALEODIET Archives
Subject: A new data point on paleo diet and exercise.
From: Art De Vany
Reply-To:
Date: Thu, 4 Sep 1997 11:22:08 -0700
216/298 (1997)
This is a report from a former student no longer in fear of grades and free to say what he wants to say. It is an
almost controlled experiment, longer in time scale than most fitness studies, and lacking only in sample size.
The young man is of Vietnamese and French genetic heritage. He had been drinking protein shakes,
consuming engineered fat loss food, and taking "fat burners" of every description. He is 5'10", 22 years old
and seemed to me to be insulin-resistant. Parents are border-line NIDDM. He had worked out for years
according to what body builder magazines prescribed---high volume, repetitive, daily or sometimes twice
daily training. He had a cold all the time and seemed to be chronically overtrained. He stopped eating and
exercising the way he had been for the past 3 years and followed the Evolutionary Fitness program (or nonprogram, given its variation).
* Well, it's been nine months of fitness under your advice through "Evolutionary Fitness" and the results
have been extrordinary. Back in January, I was weighing in at 230 lbs. with a fat count of around 23.9%.
Today, I'm weighing in at 188 lbs. with a fat count of only 8.9%. For my age, I'm still not at "lean body
mass" of 6 to 7% for a 22yr. old male, but the improvements are very satisfying. Through your workout and
advice, I have seen dramatic results in fat burnning and an increase in overall strength. I am still trying to
implement cardivascular exercises into my workout, but it is amazing how much fat can be lost through your
workout and diet. I have completely eliminated rice, most grains, and patatoes from my diet and have
increased my intake of protien enriched foods, especially red meats which is very appealing to my apitite. I
have finally decreased enough fat on my body to where I can seriously notice how your exercises have given
me better shape. I am especially pleased with the results of the upper chest, thanks to your emphasis on
inclines rather than flat benching. Thanks for all your great advice. I've been trying to reduce fat since the
summer of '96 and nothing has induced a dramatic result as your fitness program. You're not only a great
professor, but a great fitness guru also.
Mathematical Behavioral Sciences
"The more corrupt the republic, the more laws multiply." Tacitus
PALEODIET Archives
Subject: Status update and reminder
From: Dean Esmay
Reply-To:
Date: Fri, 5 Sep 1997 18:06:33 -0400
A quick reminder for members of the Symposium: If you opt to submit a message to the Symposium, please
remember to change the SUBJECT line of your email. Our archiving system (at
http://maelstrom.stjohns.edu/archives/paleodiet.html) is a searchable archive of all traffic to have appeared to
date. Subject lines are frequently one of the most useful ways of finding messages regarding specific
subjects, but this is not useful if messages always have a subject that merely says, "Paleodiet Archive - 4 Sep
1997 to 5 Sep 1997" (or whatever date).
Our membership is continuing to grow on a regular basis. Since starting in late March of this year, we have
reached well over members, with more joining on an almost daily basis. The large majority of our members
have doctorates in fields such as paleontology, biology, biochemistry, anthropology, medicine, dentistry,
nutrition, and archaeology (including more than one archaeobotanist, archaeological dentist, and others with
related specialties). The remaining minory are by and large graduate students or practicing degreed
professionals.
I hope those of you who have joined us in the last month or so have found the time to review our archives (as
mentioned above), as we have had many fascinating discussions to date, many on issues deserving of further
analysis.
I would also ask that if any of you know of other academics and researchers who would be interested in
joining our esteemed group, please send me email so that I may contact them and invite them to join.
I want to thank you all for being a part of this splendid community we've built.
PALEODIET Archives
217/298 (1997)
Subject: Answers on digestibility of cooked foods

From: Luc De Bry
Reply-To:
Date: Sat, 6 Sep 1997 00:51:21 -0700
Dear Members,
Answering to a few questions on digestibility of cooked foods of the Paleodiet digest of 3-4 Sept. 1997,
either asked or forwarded by Ward Nicholson :
Some of the answers can already be found in the archives of Paleodiet digests of May 5-17, 1997. For a start,
look for comments from Jennie Brand Miller and Andrew Millard about aborigenes and pottery in cooking.
> Obviously cooking affects digestibility and/or assimilation, or we wouldn't do it in the case of
> grains and tubers, to mention two items; and obviously many people in today's world exist most of
> their lives on mostly cooked food. So to me in most cases it seems like more a question of degrees
> and gradations of digestibility, not either/or.
You are right. There is a difference between pre-cooking toxicity from efficient plant anti-nutritional factors
which can kill very fast (e.g. lectins from 5-8 Ricinus beans, or cyanogens from manihot are enough to kill
an adult overnight; for wheat anti-nutritional factors, weaker poisonous activities selected for 100s of years
require a few more days to kill an adult), and post-cooking toxicity arising from over-cooked (or burnt)
foods, and containing man-made carcinogens. These latters are rather slow-killers, requiring more time to
kill someone than plant anti-nutritional factors.
> As an example, can I digest cooked starch because my ancestors ate raw starch foods in pre-fire
> days, and the chemical composition is altered some, but not that much, by cooking?
Cooking does two things for starch : on the one hand, it modifies its physical (not chemical) properties, i.e.
once at 68-72C, it gelatinzes the starch granules, hence rendering them hydrolysable by alpha-amylases; and
on the other hand, cooking inactivates anti-amylase activities of plant anti-nutritional factors (e.g. in wheat
two thirds of the albumins, i.e. water soluble proteins, have anti-amylase activities).
> Well, this question of course presupposes there wasn't any cooking in prehistoric times for a long
> enough time to have affected the human genome,
If ever affected, the human genome must have been affected BEFORE cooking. Indeed, all animals fear the
fire. Only humans have "domesticated" it. All animals that I know, whether birds, turtles, cats, dogs rabbits,
horses, etc, love to eat a piece of bread or of chocolate or of cooked potato, when given the opportunity. The
major difference between animals and humans is that only humans can cook potatos, bake a bread or roast
cocoa beans before manufacturing any piece of chocolate or of food. Without mastering of the Fire
Technology, there would have been no invention of the cooking process. This suggests that that fire and
cooking technologies may have arisen thank to a genetic defect, a defect which allowed humans "to
experiment and to play" with the fire; a defect which does not look fixed as yet...
> and there may have in fact been--these days I am not convinced by what evidence is available one
> way or the other.
What evidence do you refer to? - If you want, I can refer you to more convincing evidences published in
other scientific disciplines. (I just reviewed 188 of them, but the list itself is too long for an email).
> However, supposing for the moment that were the case (no adaptation to cooking yet),
There may have been no need "to adapt" to cooking. Rather, recent studies on Plant-Food-Consumer
Interactions suggest that there may have been a need to adapt to changing environmental conditions and
increased competitive pressures, forcing humans (and other mammals) either to starve from hunger, or to
find a way to enhance calorie intake, while at the same time overcoming plant anti-nutritional factors. As
stated above, our ancestors seem to have achieved this maybe thank to a genetic defect unique to humans.
> I would tend to think so (that the starch is digestible to what degree it is cooked based on prior
> adaptations to raw starch). However, the kicker here is that from what I understand, the starch in
> many root veggies and probably all grains is much MORE digestible when cooked.
As said above, at the end of proper cooking, no more active anti-amylase coupled to starch gelatinization,
that is an enhancement of both food safety and nutritional properties, for the benefit of plant/grain-eaters.
> So the sword can cut both ways here, and when it cuts this latter way, it sort of begs the
> question of how certain cooked foods could be more digestible than raw if we hadn't encountered
> those cooked foods in evolution before. The two possible answers would seem to be that: (1) we
> HAVE encountered those foods cooked before and made more successful use of them cooked than
> raw,
218/298 (1997)
Around the World, we still keep improving their cooking today.

> or (2) we HAVEN'T encountered those foods, and we aren't that well-adapted to them raw, but for
> whatever reason cooking renders them--by fortuitous circumstance--more digestible given our
> previously evolved digestive mechanisms.
Plants seem to have evolved an ability to biosynthesize anti-nutritional factors in response to over-feeding by
phytophagous predators. In their turn, grain eating-birds and insects evolved digestive biochemical
mechanism to overcome these new plant anti-nutritional factors. Not humans! The latter may have benefited
from a genetic defect allowing them not to have any fear from the fire, hence opening the way to human
specific cooking/detoxifying technology. The formers (birds and insects) may have benefited from a genetic
advantage, i.e. in their stomach, they have a pH of 4, versus 1.5 for the humans. At pH 4, toxic plant proteins
with anti-nutritional activities precipitate (isoelectric pH), hence anihilating poisonous action without any
need for the fire technology...
> Is grain close enough in chemical composition to say, tubers, that we can digest it OK?
Starch granules may look somewhat different in size, and in side-chains between grains and tubers, but
ultimately, all starch granules, whatever their source (tubers, grains or beans) are all composed solely of
glucose units. Some proteins, as the wheat friabilins, may be attached to granules, but they are not part of
starch granules.
> Is dairy close enough in chemical composition to other foods (that is, it is similar to an average
> of meat + fruit, hence within the "range" of digestible "original" foods), that many of us can
> digest it?
As a matter of fact, and from the energy (calories) angle of approach, human mother milk is fairly close to
milk chocolate, the latter being (a lot) more concentrated than the former, or the former being (a lot) more
diluted (high water content) than the latter.
> And answering to a question of Ward's second message by another question: At the request of a
> friend of mine on the Raw-Food listgroup, I'm posting a few questions here that he put to me on
> the subject of cooked vs. raw-food digestibility, in the hopes that someone with a technical
> background here will have answers. (References would also be nice, and score you bragging-rights
> bonus points. :-))
Are you sure that you desire references? - There are so many around.
> Note that those in the all-raw-foodist camp are intensely skeptical of any reasoning or data that
> might support the cooking of food in any way, so should you have something along those lines,
> references would be most appreciated where you have them. (Same goes for opposing views of
> course, as well.)
Sounds like a group knowing what fun means, doesn't it?
> Are cooked foods close enough in composition to their raw counterpart that we can digest them
> anyway (as we are omnivores, able to digest a wide variety of foods and survive on radically
> different diets)? As an example, can I digest cooked starch because my ancestors ate raw starch
> foods in pre-fire days, and the chemical composition is altered some, but not that much, by cooking?
As stated above, sorry to repeat : NO! - Upon cooking, you can digest grain and bean starch because seed
anti-amylases have been inactivated. And you can digest banana starch without cooking. Bananas do not
contain any anti-amylase activity : they are fruits, not seeds. (Indeed, in terms of plant life, fruits and seeds
do not have the same biological function).
That was long enough for this answer. Have a good day and "raw" food regards from the Kingdom of
Belgium,
Tel 32 (0)14 24 14 32 Fax 32 (0)14 24 10 25
Email :
An Operating Company of http://www.danonegroup.com -- Views expressed above are from the author,
according to his today's limited knowledge, and not necessarily from the Organization. Neither the author,
nor the Organization can be made liable for the use, misuse or abuse of data and views presented herein.
PALEODIET Archives
Subject: 2. Answers on digestibility of cooked foods
From: Bob Avery
Reply-To:
219/298 (1997)

Date: Sat, 6 Sep 1997 20:12:29 -0400
Question for Luc: I enjoyed your Paleodiet post, but little mention has been made thus far on this list about
the practices of raw fooders such as myself of soaking overnight and/or sprouting seeds, nuts, or even grains
to neutralize the anti-nutritive factors (chiefly digestive enzyme inhibitors, I understand) contained in these
foods. Given that humans have not always had fire under control, it would seem to me that the discovery of
this method of neutralizing plant toxins could easily have pre-dated the use of fire. This method offers a
"best of both worlds" scenario to my mind since the anti-nutritive factors are neutralized without the
production of the carcinogens created by firing the starches (in the case of grains, for example). I admit I
have not tried this method with tubers, however, and wonder whether there might be something to gain from
doing it with them too. Any comment?
Bob Avery
PALEODIET Archives
Subject: Raw food diets
Reply-To:
Date: Tue, 9 Sep 1997 10:06:00 +0700
Dear Everyone,
It might interest the raw foodies that Professor David Jenkins at the University of Toronto has been
following a Simian (monkey) diet for the past few years and he has a trial going to look at the effects on
blood lipids in a group of people etc. The Simian diet involves eating only fruit and vegetables, but not
grains or starchy roots and tubers. He has told me personally that although they intended the diet to be based
on raw foods, they found that they were not able to eat sufficient calories for their requirements because of
the sheer bulk of of raw fruit and veges. So the trial continues but with cooked veges.
Best wishes Jennie
PALEODIET Archives
Subject: Soaking tubers
Reply-To:
Date: Tue, 9 Sep 1997 19:38:28 +1000
Bob
You are speculating as to whether it might be a good idea to soak tubers overnight to presumably rid them of
some of the anti-nutritive factors. Herbalists call this a cold infusion (like a cup of tea made with cold water,
usually soaked overnight). The aim is to extract water soluble chemicals that may be heat-labile. I would
therefore suggest that it might not be such a good idea, given that along with various vitamins and
carbohydrates, you are likely to extract a whole host of substances which may not be so user friendly - e.g.
tannins, mucilages, gums, some glycosides, minimal but detectable alkaloids and essential oils. It would
naturally depend on the chemical profile of the tuber.
In response to : Bob Avery " little mention has been made thus far on this list about the practices of raw
fooders such as myself of soaking overnight and/or sprouting seeds, nuts, or even grains to neutralize the
anti-nutritive factors (chiefly digestive enzyme inhibitors, I understand) contained in these foods. . . . . I
admit I have not tried this method with tubers, however, and wonder whether there might be something to
gain from doing it with them too. Any comment?
Michael
________________________________________________
220/298 (1997)
Michael Schubert School of Natural and Complementary Medicine Southern Cross University P.O. Box 157,
Lismore, N.S.W. 2480, Australia Telephone (02) 6620 3649 or International + 61-2-6620 3649 Facsimile
(02) 6620 3647 or International + 61-2-6620 3647 Visit us at
<http://www.scu.edu.au/schools/ncm/index.html
> ________________________________________________
PALEODIET Archives
Subject: Comparing Diets
From: Luc De Bry
Reply-To:
Date: Thu, 11 Sep 1997 19:16:16 -0700
Good morning everyone,
Two comments about comparing diets, inspired by two messages of the last two Paleodigests A comment to
the news of this information-message which was communicated on and by : Tue, 9 Sep 1997 10:06:00
+0700; From: Jennie Brand Miller; ; Subject: Raw food diets
> ... (snipped) ... The Simian diet involves eating only fruit and vegetables, but not grains or
> starchy roots and tubers. has told me personally that although they intended the diet to be based
> on raw foods, they found that they were not able to eat sufficient calories for their requirements
> because of the sheer bulk of of raw fruit and veges. So the trial continues but with cooked veges.
How amusing! When living in Central Africa, simians used to come to grab eventual remains of our meals
on our terrace, even sometime daring to venture into our kitchen and, at the great dismay of my mother,
transforming it into something like hell.
This summer, while completing a research project, my wife and me, we asked our 8 years old daughter to
exercise at some calculations, with the following problem : Average in our latitudes, a human being requires
some 2, 500 kcal/day/person to live. The following figures are medians, as found in our village : Lettuces (8
kcal/100g), or apples (50 kcal/100g) and bananas (91 kcal/100g) are collected through gathering activities
(including in today's supermarkets); fish (120 kcal/100g), beef (230 kcal/100g), and pork (350 kcal/100g) are
from hunting activities (including in the next door farms when hungry); and bread (250 kcal/100g), biscuit
(440 kcal/100g) and hazelnut chocolate (650 kcal/100g) are from cooking (i.e. detoxifying) activities. In
order to fulfill your daily energy requirements (for the moment being, let's keep essential nutrients out of the
energy question), how many grammes of each of these food products will you need to eat?
When our second daugther, 6.5 years old heard the figures, talking about the vast amount of lettuces that one
should eat for surviving, she simply said : "I hate lettuces; I do not want to eat all day like a cow and to listen
to Mummy saying "keep grazing, it's good for you!""
Our son, 5 years old, stated : "I love the chocolate, let's get it".
Our second son, 3 years old did not say anything : he expressed his agreement with his sister's calculations
by eating the chocolate, and brought the lettuces to our rabbits.
And our dog, not very good at calculations, ate the wrapping paper, begging for more, while our cat was
stealing the fish from the kitchen table...
It is a true story. If ever you have hard to believe it, just do the same calculations. We are very proud of our
children.
Second comment, in answer to Bob's question in message of Sat, 6 Sep 1997 20:12:29 -0400; Bob Avery ;
Question for Luc:
> I enjoyed your Paleodiet post, but little mention has been made thus far on this list about the
> practices of raw fooders such as myself of soaking overnight and/or sprouting seeds, nuts, or even
> grains to neutralize the anti-nutritive factors (chiefly digestive enzyme inhibitors, I
> understand) contained in these foods.
You are right : soaking seeds (grains and beans) and tubers induces the germination and/or sprouting process.
This induction triggers the start of the hydrolysis of the seed storage proteins, 85% or more of them having
anti-nutritional properties, hence contributing to the detoxification. The drawback is that it also induces the
hydrolysis of the energy reserves of the seeds, most notably starch and oil. Once starch, oil and proteins have
been converted into new roots and the first leaves, then the photosynthesis process takes over for responding
to the next energy requirements of the seedling.
221/298 (1997)
It may be worth observing that soaking is the first part of barley malting, fermenting and brewing into beer,
and of cocoa fermentation and roasting towards chocolate. In both cases, soaking alone is not enough to
detoxify barley and cocoa, and certainly not to enable you to enjoy the tsate and flavour of beers and
chocolate. (If ever you stop these two processes at the soaking step, my friends and my kids will hate you.)
In the cooking process, provided that you refrain from overcooking, i.e. burning, you do not loose the starch
and oil. But you do need to pay the energy required to detoxify your food.
In any case, whether you soak or cook, one cannot win both ways : you will loose some energy.
> .... Given that humans have not always had fire under control, it would seem to me that the
> discovery of this method of neutralizing plant toxins could easily have pre-dated the use of fire.
For soaking, you need some kind of recipient, pottery or equivalent. Back in May, there were discussions in
this listserver on pottery dating. Personnally, I have never done any dating experiment. But I use references.
My favourite ones come from good old neighbours of Central Africa, who were my heroes while I was a kid,
i.e. members of the Leakey family. (From time to time, even as a scientist, I do not mind to be emotional.
And I am longing for Africa.) In his latests books, Richard Leakey wrote that the fire must have been
invented some 700, 000 years ago. Pottery must have come later. (If proven wrong, do not worry, I shall
adapt.)
> This method offers a "best of both worlds" scenario to my mind since the anti-nutritive factors
> are neutralized without the production of the carcinogens created by firing the starches (in the
> case of grains, for example).
When you cook right, you eliminate the anti-nutritional activities, and you prevent the formation of
carcinogens before it burns. The delicate balance between pre-cooking toxicity and post-cooking toxicity can
be recognized thank to the Maillard aroma. A good Maillard aroma, e.g. the aroma that one can smell from
well baked bread of well roasted coffee beans or cocoa beans is an organoleptic indicator of food safety.
Thus, anosmic excepted (i.e. the few without any sense of smell, i.e. who are smell-blind), everyone of us
has a chance to be a good cook.
Now, for soaking, when the astringency has been reduced to a minimum, then, what you are used to soak
may be safe. But well, what's the point at missing that then fantastic Maillard aroma that goes with food
safety and quality, and all the good anti-oxidants that have been developed throughout the Maillard reaction
during a well run cooking process!
Ask our kids : the best of both world is called "food diversity", isn't it?
Have nice diets, and kind regards,
Tel 32 (0)14 24 14 32 Fax 32 (0)14 24 10 25
Email :
An Operating Company of http://www.danonegroup.com -- Views expressed above are from the author,
according to his today's limited knowledge, and not necessarily from the Organization. Neither the author,
nor the Organization can be made liable for the use, misuse or abuse of data and views presented therein.
PALEODIET Archives
Subject: Gentle reminder
From: Dean Esmay
Reply-To:
Date: Thu, 11 Sep 1997 22:42:51 -0400
I would like you all to consider the calibre of the membership of this list, and where we want it to go.
While it is not our purpose to advocate any one position, or to demand absolutely rigid standards of behavior,
I have noticed lately that some messages have made sweeping generalizations without references, made
claims about unreproducible anecdotal data (or data no one's as yet had the discipline to describe to make it
reproducible), tried to find justifications for obscure dietary regimens with little underlying them but vague
theories, and generalized about that which shouldn't be.
A small amount of this is fine. But a good thing in small doses isn't always a good thing in large doses.
222/298 (1997)
I would encourage everyone, before submitting to this list, to realize that a large number of our membership
are distinguished scientists with multiple peer-reviewed papers to their credit. Do we want to use this forum
as an overblown bull session? Or do we want a genuine forum which seeks to expand real knowledge and
cross-fertilize between important disciplines?
No individual should feel this message is addressed to him. It is just something I would like us all to keep in
mind.
PALEODIET Archives
Subject: Amer Diabetes Assoc. abstract on CHO-induced fatty acid synthesis and insulin resistatnce
From: Art De Vany
Reply-To:
Date: Mon, 22 Sep 1997 10:46:57 -0700
Here is an interesting abstract exploring fatty acid synthesis on low fat diets. It is located at
http://www.diabetes.org/ada/res1.html.
My reading is that it seems to confirms results previously posted to this list: a higher proportion of CHO is
synthesized to fatty acids the higher is the ratio of CHO to fat in the diet. The subjects in this case were
insulin-resistant; there were no normals in the study.
If the fatty acid synthesis of these insulin resistant subjects exceeds that of normals, then this is suggestive of
a mechanism for a "thrifty gene". The abstract fails to separate an increase in the RATE of fatty acid
synthesis from the LEVEL accumulated in blood trigyceride. It is clear the rate increased and it seems the
level as well.
Abstract follows:
Clinical Research Grant
Sensitivity to Carbohydrate-Induced Fatty Acid Synthesis in the Insulin Resistance Syndrome
Lisa Cooper Hudgins, MD New York, NY
Summary of Results: In the first year, using solid food diets composed of commonly consumed foods, my
project explored the effects of a reduction in the amount of dietary fat and an increase in the amount of
carbohydrate on the body's own production of fat in normal and obese, insulin-resistant volunteers. In seven
normal volunteers studied for one month in the controlled environment of the Rockefeller Clinical Research
Center, we found that when the dietary carbohydrate was high in simple sugars and low in complex
carbohydrate, the body converted the carbohydrate to fat when 30% of calories were fat, and even more
when 10% of calories were fat. When fat production increased, the newly formed saturated (animal) fat
accumulated in the blood triglyceride with potential adverse effects on heart disease and diabetes. An
important finding was that there was no change in body weight or metabolic rate between the high fat and
low fat diets. Surprisingly, two obese subjects with high fasting insulins and other characteristics of the
insulin resistance syndrome showed less, rather than the predicted greater, fat production on the two diets.
More subjects need to be studied to confirm this finding that may be a consequence of decreased
responsiveness to insulin.
PALEODIET Archives
Subject: Re: CHO-induced fatty acid synthesis
Reply-To:
Date: Mon, 22 Sep 1997 22:55:02 +0100
The composition of fatty acids (FA) in serum cholesterol esters (CE) to some extent reflects FA intake. We
measured CE-FA in subsistence horticulturalists of Kitava, Trobriand Islands (1, 2). Despite a very low
intake of total fat and palmitic acid (16:0, the dominating saturated fatty acid in the West), the level of
CE16:0 was higher in Kitava than in Sweden.
223/298 (1997)
When total fat intake is low, CE16:0 may preferentially reflect endogenous fat synthesis from carbohydrates
rather than dietary intake of 16:0 (3). This may also explain the fact that, in multivariate analysis, we found
CE16:0 in both sexes to be positively related to TG and negatively to HDL-C, since TG is elevated and
HDL-C is reduced by an increased intake of carbohydrates (4), at least when dietary fat provides less than 25
en% and carbohydrates more than 60 en%, as is the case in Kitava. Similar negative relations between
CE16:0 and HDL-C in healthy males from Finland (5) and France (6) suggest, on the other hand, that there
may be additional explanations.
1 Lindeberg S, Vessby B. Fatty acid composition of cholesterol esters and serum tocopherols in Melanesians
apparently free from cardiovascular disease - the Kitava study. Nutr Metab Cardiovasc Dis 1995; 5: 45-53. 2
Lindeberg S, Nilsson-Ehle P, Vessby B. Lipoprotein composition and serum cholesterol ester fatty acids in
non-westernized Melanesians. Lipids 1996; 31: 153-8. 3 Gurr, M. (1993) "Fats", in Human Nutrition and
Dietetics (Garrow, J.S. and James, W.P.T., eds.) 77-102, Edinburgh, Edinburgh. 4 Liu, G., Coulston, A.,
Hollenbeck, C. and Reaven, G. (1984) "The effect of sucrose content in high and low carbohydrate diets on
plasma glucose, insulin, and lipid responses in hypertriglyceridemic humans", J Clin Endocrinol Metab 59,
636-42. 5 Marniemi, J., Lehtonen, A., Inberg, M., Niittymaki, K., Maatela, J., Alanen, E. and Seppanen, A.
(1989) "Fatty acid composition of serum lipids in patients with a coronary bypass operation", J Intern Med
225, 343-7. 6 Cambien, F., Warnet, J.M., Vernier, V., Ducimetiere, P., Jacqueson, A., Flament, C., Orssaud,
G., Richard, J.L. and Claude, J.R. (1988) "An epidemiologic appraisal of the associations between the fatty
acids esterifying serum cholesterol and some cardiovascular risk factors in middle-aged men", Am J
Epidemiol 127, 75-86.
At 18.46 97-09-22, Art De Vany wrote:
> Here is an interesting abstract exploring fatty acid synthesis on low fat diets. It is located at
> http://www.diabetes.org/ada/res1.html. My reading is that it seems to confirms results previously
> posted to this list: a higher proportion of CHO is synthesized to fatty acids the higher is the
> ratio of CHO to fat in the diet. The subjects in this case were insulin-resistant; there were no
> normals in the study. If the fatty acid synthesis of these insulin resistant subjects exceeds that
> of normals, then this is suggestive of a mechanism for a "thrifty gene". The abstract fails to
> separate an increase in the RATE of fatty acid synthesis from the LEVEL accumulated in blood
> trigyceride. It is clear the rate increased and it seems the level as well.
> Abstract follows: Clinical Research Grant Sensitivity to Carbohydrate-Induced Fatty Acid Synthesis
> in the Insulin Resistance Syndrome Lisa Cooper Hudgins, MD New York, NY
> Summary of Results:
> In the first year, using solid food diets composed of commonly consumed foods, my project explored
> the effects of a reduction in the amount of dietary fat and an increase in the amount of
> carbohydrate on the body's own production of fat in normal and obese, insulin-resistant
> volunteers. In seven normal volunteers studied for one month in the controlled environment of the
> Rockefeller Clinical Research Center, we found that when the dietary carbohydrate was high in
> simple sugars and low in complex carbohydrate, the body converted the carbohydrate to fat when
> 30% of calories were fat, and even more when 10% of calories were fat. When fat production
> increased, the newly formed saturated (animal) fat accumulated in the blood triglyceride with
> potential adverse effects on heart disease and diabetes. An important finding was that there was no
> change in body weight or metabolic rate between the high fat and low fat diets. Surprisingly, two
> obese subjects with high fasting insulins and other characteristics of the insulin resistance syndrome
> showed less, rather than the predicted greater, fat production on the two diets. More subjects need to
> be studied to confirm this finding that may be a consequence of decreased responsiveness to insulin.
-------------------------------------------------------------------
PALEODIET Archives
Subject: Alzheimer's disease and fat
Reply-To:
224/298 (1997)
Date: Tue, 23 Sep 1997 16:12:01 +0100

Here is something interesting. W Grant has found a cross-cultural relationship between fat intake and
Alzheimer's Disease. Read the full paper in a peer-reviewed journal on-line at
http://www.coa.uky.edu/ADReview/contents.htm
> Dietary Links to Alzheimer's Disease
> William B. Grant, PhD
> 803 Marlbank Drive, Yorktown, VA 23692-4353
> Extended Abstract
> Based on recent findings that elderly African- and Japanese-Americans have much higher prevalence
> of AD (6.24% and 4.1%, respectively) than those still living in their ethnic homelands (<2%), a
> meta-analysis of epidemiological (population) data of Alzheimer's disease (AD) was conducted.
> Regression analyses were performed on the prevalence of AD in the 65+ age population for 11
> countries obtained from 18 community- wide studies versus components of the national diets. The
> primary findings are that fat and total caloric supply have the highest correlations with AD
> prevalence rates (r2 = 0.932 and 0.880, respectively (p<0.001)). Regression analysis performed on
> a subset of 7 European and North American countries also indicates that fish consumption reduces
> the risk of developing AD, which is consistent with a recent study in The Netherlands. The results
> of the statistical analysis are also consistent with previous studies showing that excess fat
> (linoleic acid) consumption leads to inflammation and that both fat and excess caloric consumption
> contribute to oxidative stress from free radicals. Cross-correlations between the prevalence of
> dementia and other chronic degenerative diseases (CDDs) in 8 geopolitical regions of the world
> show very high correlations between dementia and many brain disorders, cancers, and cardiovascular
> diseases, most of which have been linked to diet, especially to fat. Statistical analyses applied
> to both AD incidence and prevalence rates indicate that the diet just prior to the development of
> AD is the most critical in determining the risk for developing AD. A review of the literature on
> diet/nutrition and CDD suggests that diets high in total calories including acidic drinks,
> alcohol, fat, salt and sugars promote trace mineral imbalances and elevated free radical
> production in the body. Several dietary components and supplements have been found effective in
> delaying the onset of AD, including antioxidants, estrogen (for post-menopausal women), fish or
> fish oil, and anti-inflammatory substances. The prevalence of AD in the U.S. is estimated to be
> 5.1+0.6% of those over the age of 65 years. This translates to 1.7+0.2 million over the age of 65
> and 0.4+0.1 under the age of 65. This gives a 0.87+0.10% probability of having AD at the age of
> 65, with the probability increasing by a factor of 1.146 for each additional year of age. The
> total cost to the U.S. is estimated to be $100 billion per year. While the results of this study
> suggest that diet is an important risk factor for the development of Alzheimer's disease, and that
> AD is, thus, preventable in many cases, additional research is, of course, warranted.
-------------------------------------------------------------------
PALEODIET Archives
Reply-To:
Andrew Millard
Date: Wed, 24 Sep 1997 08:58:58 +0100
> The composition of fatty acids (FA) in serum cholesterol esters (CE) to some extent reflects FA
> intake. We measured CE-FA in subsistence horticulturalists of Kitava, Trobriand Islands (1, 2).
> Despite a very low intake of total fat and palmitic acid (16:0, the dominating saturated fatty
> acid in the West), the level of CE16:0 was higher in Kitava than in Sweden.
225/298 (1997)
This can be paralleled by the results of controlled feeding experiments in pigs. Stott et al [1] measured the
stable isotope composition of individual lipids as part of a study to investigate the routing of dietary carbon
into different body tissues. They examined bone lipids to enhance our understanding of studies on bone
lipids from archaeological populations. They found that the C13 content of fatty acids (16:0, 18:0 and 18:1)
and cholesterol reflected accurately the isotopic compostion of the whole diet, but that of linoleic acid (18:2),
an essential fatty acid, reflected direct incorporation from the diet. Further studies are underway by the same
workers to examine the isotopic compostion of lipids in rats fed on diets with controlled isotopic
compositions of various components [2].
[1] Stott, AW, Davies, E, Tuross, N & Evershed RP (1997) Monitoring the routing of dietary and
biosynthesised lipids through compound-specific stable isotope (delta C-13) measurements at natural
abundance Naturwissenschaften 84 (2) 82-86
[2] Jim, S, Stott, AW, Ambrose, SH, Rogers, JM, Tuross, N & Evershed, RP "Compound specific stable
isotope analysis of bone lipids: tracing the dietary carbon flux into animals raised on isotopically controlled
diets." Paper presented at Archaeological Sciences '97 Durham 2-4 September 1997, Durham, UK
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Fat in the Paleolithic diet
From: "Steve Meyers, Lawrence Berkeley Laboratory"
Reply-To:
Date: Wed, 24 Sep 1997 16:59:52 PDT
[ I wrote the following as part of a "conversation" with a friend, but thought that folks on the list would have
some perspectives on the topic.]
Fat in the Paleolithic Diet
There seems to be some controversy regarding the role of fat in the diet of Paleolithic humans. One reason
for disagreement is that people tend to speak of a typical Paleo diet, when in fact it stands to reason that the
diet differed considerably according to geography and climate. Diets of 20thC HGers certainly exhibit much
diversity, with a large range in the relationship of plant and animal food in the diet, and in the types of
animal food.
In The Paleolithic Prescription (PP), Eaton et al. construct an average diet for Late Paleolithic humans that
has 21% of total calories coming from fat (slightlyly less than half from animal sources). The amount of
animal fat is based on the average fat content of 43 species of present-day wild game from three continents.
The average is 4.3%, with a range from around 1-8%. This is far below choice beef sirloin at 27%.
One question is: to what extent does the composition of present-day wild game approximate that of the game
hunted by Paleo humans? Many of the animals hunted by Paleo humans -- at least in Europe and North
America -- no longer exist.
It seems that here too geography and climate would play a major role. Much of the period in which homo
sapiens sapiens has lived (roughly the last 100, 000 years) was characterized by very cold climate, at least in
the temperate regions. Since fat is an insulator, it seems likely that at least some of the hunted animals in
these regions had a higher fat content than that of present-day wild game, but probably still much less than
domesticated cattle. It is also worth bearing in mind that modern humans arrived relatively late in colder
regions such as Northern Europe and Siberia (beginning around 35, 000 years ago), and much of the preagric human population adapted to wild game that was available in the tropics (presumably less fatty?).
In their article The Cave Man Diet (PPNF Health Journal, Vol. 21, No. 2), Fallon and Enig argue that the
Paleo diet was both higher in fat and higher in saturated fat than the typical diet proposed by Eaton et al.
Drawing on the collection Ice Age Hunters of the Rocky Mountains, they list a number of animals that were
hunted, and say that many of them are fatty animals. However, two animals that they cite as fatty (bison and
beaver) are listed by Eaton et al. as having fat content of only 3.8% and 5.1% respectively. However,
Fallon/Enig also refer to the cave mans preference for the fatty portions of his kill. The fat contents cited by
Eaton et al. refer to portion of fat in muscle meat. But other portions (organs, brains, tongue, marrow) are
prized by many 20thC HGers, and these are usually higher in fat content.
226/298 (1997)
Eaton et al. also argue that the animal fat in the Paleo diet was low in saturated fat compared to that of
domesticated red meat. This too is based on the fat content of present-day wild game. Saturated fat as % of
all fatty acids is generally in the 60-70% range, well below domestic beef/pork/veal. Fallon/Enig report
similar data.
So, have Eaton et al. understated the role of fat in the Paleo diet? It seems that may be so with respect to
people living in Europe and No. America, and perhaps the colder regions of Asia. Plant foods were less
abundant in these regions, so animal foods played a larger role than indicated by the typical diet in the PP.
And it makes sense that people in cold climates would want to get as much calorie-dense fat as possible. For
Paleo people in other regions who lived in a less cold climate, perhaps the role of fat suggested in the PP is
closer to the truth?
Stephen Meyers Berkeley, CA
PALEODIET Archives
Reply-To:
Date: Thu, 25 Sep 1997 00:09:04 +0100
At 08.58 97-09-24, Andrew Millard wrote:
> They examined bone lipids to enhance our understanding of studies on bone lipids from
> archaeological populations.
How old may bones be for such methods to be applicable?
PALEODIET Archives
Subject: Fat in the Paleolithic diet
From: Dick Dawson
Reply-To:
Date: Thu, 25 Sep 1997 02:29:29 -0400
Steve Meyers posted:
> Fat in the Paleolithic Diet
[..]
Might this help?
Kenneth L Feder in _The_Past_in_Perspective_ Mayfield 1996 isbn 1-55934-384-2 refers to megafauna
hunting ~18-10kya. He cites finds of kills of woolly rhino & mammoth, various bison and deer and horse.
Would 10kya old members of species that exist today have fat content much different from that of modern
examples? Do we know anything about body fat of the now extinct woolly rhino and mammoth?
If I recall correctly _PP_ acknowledges a wide variation of reliance on animal food sources; cites the
extreme of the Eskimo/Inuit's heavy reliance on seal and other high fat animals, ~95% of diet; also extremes
in other regions where HG folk lean toward vegetable food.
Someone recently noted that reliance on modern HGs as models for paleolithic HGs is somewhat uncertain.
Dick http://smith.syr.edu/~ddawson
PALEODIET Archives
Reply-To:
Date: Thu, 25 Sep 1997 11:38:54 +0100
On Thu, 25 Sep 1997, Staffan Lindeberg wrote:
> At 08.58 97-09-24, Andrew Millard wrote:
227/298 (1997)
> They examined bone lipids to enhance our understanding of studies on bone lipids from
> archaeological populations. How old may bones be for such methods to be applicable?
The oldest report is of 75000+-15000 years for whale bones, where the integrity of the signal was verfied by
comparison of cholesterol with collagen.[1] Collagen survival is often taken as an indicator of general
organic survival in bones, and we have collagen from bones of 2-3 times that age, so we may be reasonably
confident of going back 200, 000 years and in principle further. However, survival of organic matter in bones
varies from site to site and become rarer the further back one goes. Actually making useful statements about
real diets will require a lot more work, and that the diet under consideration had isotopically distinguishable
parts. That last caveat is particularly appropriate in Europe, where there are plants of only one photosynthetic
pathway, so that apart from the terrestrial/marine divide there are only subtle differences in isotopic content
of foods.
[1] Stott, AW, Evershed, RP, Tuross, N (1997) Compound-specific approach to the delta C-13 analysis of
cholesterol in fossil bones Organic Geochemistry 26 (1-2) 99-103
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Isotopic bone dating & Fat in the Paleolithic Diet
From: Loren Cordain
Reply-To:
Date: Thu, 25 Sep 1997 20:38:00 -0600
I would like to point out that relative components of ancient diets can be estimated utilizing stable carbon
isotopic analysis (i.e. the 13C/12C ratio). 13C/12C analysis has been used to determine presumed dietary
intake of Australopithecus robustus from 1.8 -1.0 million years ago (1). The stable carbon isotope ratio
(13C/12C) distinguishes the relative proportions of plants utilizing either the C3 or C4 photosynthetic
pathways. During photosynthesis, C3 plants fix CO2 into a 3 carbon molecule, while C4 plants fix CO2 into
a 4 carbon molecule. C3 plants tend to have lower 13C/12C ratios than do C4 plants because 13C (the
heavier isotope) is not as readily incorporated into the tissues of these plants as C4 plants. Grasses are almost
exclusively C4 plants whereas trees, shrubs and forbs are more generally C3 plants. The carbon isotopes
(13C and 12C) from plants are incorporated into the bones and teeth of the animals who consume these
plants. Grass eating herbivores and the carnivores feeding on them can then be identified by the higher
C13/C12 ratio they maintain in their bones and teeth. Lee-Thorp et al.'s data (1) suggest Australopithecus
robustus consumed a mixed diet containing both C3 and C4 foods. Although, the interpretation is more
difficult, strontium calcium ratios (Sr/Ca) have also been used to estimate dietary components of ancient
diets (2).
228/298 (1997)
I would like to respond to Steve Meyers comments regarding the fat level in the paleolithic diet. As I have
mentioned in a previous post, there is considerable controversy regarding the macronutrient (PRO/FAT/CHO
%) content of pre-agricultural diets. Clearly, there was no single "paleolithic diet" and its macronutrient
content varied according to latitude, season and local environmental conditions. Boyd Eaton's widely quoted
estimate (3) suggests a breakdown of 37% protein, 41% carbohydrate and 22% fat. This is based upon an
estimation of 65% of derived calories emanating from plant foods and 35% of total calories emanating from
animal foods. Boyd used Richard's Lee analysis of the Ethnographic Atlas (4) to arrive at the 65/35 ratio;
however Carole Ember (5) has pointed out that Lee incorrectly tabulated the data and that in 77% of the
societies examined in the Atlas, plant derived foods represented less than 50% of the calories. Carefully
studied recent hunter-gatherer societies (Hiwi, Inuit, Ache, Pygmy, !Kung) show a mean value for the
calories derived from animal foods to be 59% (6). If one throws out the high value for the Inuit (96% animal
food) and the low value for the !Kung (33%), the value would show that 56% of the average hunter-gatherer
diet was derived from animal foods. Thus, the average macronutrient breakdown would probably show a
slightly lower CHO % and slighly higher protein intake when compared to Boyd's estimate. If fatty portions
of the animal being consumed were preferentially eaten and lean not consumed, then the fat % could have
been significantly higher. This clearly would have had to be true for populations living in northern latitudes
wherein the plant food intake would have been seasonally restricted or eliminated. In northern latitudes
wherein no plant foods were consumed, expecially during winter months, the dietary intake was solely
reliant upon animal protein and fat. Speth (7) has pointed out that the maximal protein intake cannot
constitute more than 50% of total calories (when there is no CHO available) and probably cannot exceed
35% for long periods of time unless CHO is available. High dietary protein induces diarhea, lethargy and
eventual death and was called "rabbit starvation" by early trappers, explorers and others forced to eat only
lean meat. The famous Stefansson experiment at Bellevue Hospital (utilizing an all meat diet) showed that
when only meat and fat were available, self selected diets contained an 80% fat/ 20% protein mix. Although
many of the animals that were hunted by paleolithic humans have become extinct and we will never know
the total carcass lipid content, many prey animals survived to modern times. Cave drawings as well as
taphonomical analyses of human occupation sites indicate animals such as ibex, horse, european elk, deer
and other cervids were widely hunted. Data from our laboratory as well as data presented by Speth and
colleagues (7) shows that cervid total body fat content can range from 6 to as high as 15% . It is quite likely
that large northern pleistocene mammals may have had similar if not greater values. Remember that there is
significant seasonal variation in these numbers and certain African ruminants have been reported to have
total body fat percentages of less than 1%, which clearly must approach physiological limits. Average body
fat % of wild ruminants tend to be higher and 4-6% seems to be a pretty good overall estimate, based upon
the few whole body analyses reported in the literature (7).
REFERENCES
1. Lee-Thorp JA et al. Diet of Australopithecus robustus at Swartkrans from stable carbon isotopic analysis. J
Hum Evol 1994;27:361-72. 2. Sillen A et al. Strontium calcium ratios and strontium isotopic ratios of
Australopithecus robustus and Homo sp. from Swartkrans. J Hum Evol 1995;28:277-85. 3. Eaton SB et al.
Paleolithic nutrition revisited: A twelve year retrospective on its nature and implications. Eur J Clin Nutr
1997;51:207-16. 4. Lee RB. What hunters do for a living, or how to make out on scarce resources. In Lee
RB, DeVore I, (eds). Man the Hunter. Chicago: Aldine, 1968:30-48. 5. Ember CR. Myths about hunter
gatherers. Ethnology 1978;17:439-48. 6. Leonard WR et al. Evolutionary perspectives on human nutrition:
the influence of brain and boyd size on diet and metabolism. Am J Hum Biol 1994;6:77-88. 7. Speth JD et al.
Energy source, protein metabolism, and hunter-gatherer subsistence strategies. J Anthropological
Archaeology 1983;2:1-31.
PALEODIET Archives
Subject: Re: Fat in the Paleolithic diet
Reply-To:
Date: Fri, 26 Sep 1997 09:18:27 +0100
On Wed, 24 Sep 1997, Steve Meyers wrote:
> In The Paleolithic Prescription (PP), Eaton et al. construct an average diet for Late Paleolithic
> humans that has 21% of total
229/298 (1997)
What is meant by Late Paleolithic? The usual term is Upper Palaeolithic from c.40ka-10ka, but the Late
Upper Palaeolithic is only the final part of this.
> calories coming from fat (slightlyly less than half from animal sources). The amount of animal fat
> is based on the average fat content of 43 species of present-day wild game from three continents.
> The average is 4.3%, with a range from around 1-8%. This is far below choice beef sirloin at 27%.
But as you note later this does not account for marrow, etc., which feature heavily in reconstructions of the
food utility of animal parts, notably in Binford's various utility indices. This is not really my field: are there
any zooarchaeologists on the list who could comment in more detail?
> One question is: to what extent does the composition of present-day wild game approximate that of
> the game hunted by Paleo humans? Many of the animals hunted by Paleo humans -- at least in
> Europe and North America -- no longer exist.
Some no longer exist, many do, we may not have mammoth, woolly rhino, or aurochs but we do have horse,
reindeer, deer, and many of the smaller species.
> It seems that here too geography and climate would play a major role. Much of the period in which
> homo sapiens sapiens has lived (roughly the last 100, 000 years) was characterized by very cold
> climate, at least in the temperate regions. Since fat is an insulator, it seems likely that at
> least some of the hunted animals in these regions had a higher fat content than that of
> present-day wild game, but probably still much less than domesticated cattle.
May be, may be not. In a cold climate animals will put on a layer of fat for the winter, which many modern
western breeds of domestic animals do not need to do, becasue they are cossetted by us. If it is sufficently
cold, then it is possible to kill animals at the beginning of winter and cache the meat for several months, thus
allowing access to high fat meat when the animals roaming the area are getting lean. This was the strategy of
eneolithic h-gs on the steppes of Kazakhstan with respect to the wild horses which were their main source of
food.
> In their article The Cave Man Diet (PPNF Health Journal, Vol. 21, No. 2), Fallon and Enig argue
> that the Paleo diet was both higher in fat and higher in saturated fat than the typical diet
> proposed by Eaton et al. Drawing on the collection Ice Age Hunters of the Rocky Mountains, they
> list a number of animals that were hunted, and say that many of them are fatty animals.
It seems to me that taking N American Ice Age Hunters as a basis for a generalised Palaeolithic diet is risky.
Humans probably didn't arrive in the Americas more than 14, 000 years ago (though arrival before 30, 000
cannot entirely be ruled out), and these were people adapting to a new environment, in which there were
animals which had never been hunted before. They thus represent a relatively recent adaptation and it is quite
possible that their diet was different to that of their ancestors and cousins in the Old World.
> However, two animals that they cite as fatty (bison and beaver) are listed by Eaton et al. as
> having fat content of only 3.8% and 5.1% respectively. However, Fallon/Enig also refer to the cave
> mans preference for the fatty portions of his kill. The fat contents cited by Eaton et al. refer
> to portion of fat in muscle meat. But other portions (organs, brains, tongue, marrow) are prized
> by many 20thC HGers, and these are usually higher in fat content.
Marrow was consumed by ancient h-gs, as evidence by the many bones split for acccess to the marrow, some
parts of the kill would also be neglected as they were of little value, and they would be left at the kill site
rahter than transported to the "home base" (this is known as the schlepp effect).
> So, have Eaton et al. understated the role of fat in the Paleo diet? It seems that may be so with
> respect to people living in Europe and No. America, and perhaps the colder regions of Asia. Plant
> foods were less abundant in these regions, so animal foods played a larger role than indicated by
> the typical diet in the PP. And it makes sense that people in cold climates would want to get as
> much calorie-dense fat as possible. For Paleo people in other regions who lived in a less cold
> climate, perhaps the role of fat suggested in the PP is closer to the truth?
It is very difficult to know the vegetable/meat ratio fron preserved remains as we usually ony have the
animal bones, but it should be possible to deduce whether the marrow and other fatty portions were being
utilised from bone fracture patterns. I know little of the non-European data, so I can't comment on that.
Andrew
========================================================================= Dr.
=========================================================================
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PALEODIET Archives
Subject: isotopic analysis of bone
Reply-To:
Date: Mon, 29 Sep 1997 09:00:47 +0100
On Thu, 25 Sep 1997, Loren Cordain wrote:
> I would like to point out that relative components of ancient diets can be estimated utilizing
> stable carbon isotopic analysis (i.e. the 13C/12C ratio). 13C/12C analysis has been used to
> determine presumed dietary intake of Australopithecus robustus from 1.8 -1.0 million years ago
> (1). The stable carbon isotope ratio (13C/12C) distinguishes the relative proportions of plants
> utilizing either the C3 or C4 photosynthetic pathways. <snip Grasses are almost exclusively C4
> plants whereas trees, shrubs and forbs are more generally C3 plants.
It is important to note that it is only **tropical** grasses, the grasses of Europe and most of N. America are
not C4 flora. This limits the usefulness of this technique. There is also a very small shift in isotope content
from herbivore to carnivore, but this is much more difficult to use, except in situations where there are one to
one predator-prey relationships.
> The carbon isotopes (13C and 12C) from plants are incorporated into the bones and teeth of the
> animals who consume these plants. Grass eating herbivores and the carnivores feeding on them can
> then be identified by the higher C13/C12 ratio they maintain in their bones and teeth. Lee-Thorp
> et al.'s data (1) suggest Australopithecus robustus consumed a mixed diet containing both C3 and
> C4 foods. Although, the interpretation is more difficult, strontium calcium ratios (Sr/Ca) have
> also been used to estimate dietary components of ancient diets (2).
Interpretation is in fact very much more difficult, as the Sr/Ca work is rarely accompanied by assessment of
postmortem changes to bone mineral. I have a PhD student starting in a weeks time who will be taking a long
hard look at just what it is that Sr/Ca analysis is extracting from bones.
Andrew Millard
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Alzheimer's disease and fat
From: Art De Vany
Reply-To:
Date: Mon, 29 Sep 1997 18:12:29 -0700
Following Staffan Lindeberg's posting of Dietary Links to Alzheimer's Disease by William B. Grant, PhD, I
scanned the article, focusing on its statistical methods and results. My apologies if this is too technical, I do
think the conclusions are worth examining.
I hardly agree with the conclusions of this article, though I accept the many linkages it develops between
oxidative stress and Alzheimer's disease (among those 65+).
Its results suggest that among the factors related to Alzheimer's are total caloric intake and fat intake.
There are 11 data points, 7 in the European/North American cluster. The data are highly aggregate measures
of diet and Alzheimer's incidence showing national rates. They are crudely adjusted for age distribution.
There are few degrees of freedom because of the small sample size. Consequently, outliers are influential.
The equation for fat is: AD prevalence rate = -0.203+(0.0312*fat (grams/day)). A large negative intercept
term and a positive slope, leading to the author's conclusion. A large negative intercept often indicates a nonlinear relationship (which these data surely exhibit). Because fat intake varies so much among countries,
compared to total caloric intake, the differences among countries are expanded in the regressions using fat as
the dependent variable. This exaggerates the influence of outliers.
231/298 (1997)
Take a look at this graph from the ariticle http://www.coa.uky.edu/ADReview/Grant_Images/grantf1.gif and

you will see that there are two groups: developed Northern American and European countries and Asian and
African countries. There are no points in the middle and a vast gulf between the data clusters.
Within the developed cluster there is no relation between fat consumption and Alzheimer's.
Measurement error is all over these data: different reporting rates, more thorough surveys, and genetic
composition of the populations are just a few.
This is compounded by multicolinearity: fat and total calories are highly correlated and so is the % of
cereals. You can't put them in the same equation and get any precision in your estimates. The relationship
between total calories and Alzheimer's is less problematic (statistically speaking). But, Europeans and
Americans are bigger and must eat more than Asians and Nigerian pastoralists.
Grant's article is excellent on other grounds, but the statistics show nothing, or they hint at a genetic
disposition to Alzheimer's more than an environmental one.
Arthur De Vany Professor http://www.socsci.uci.edu/mbs/personnel/devany/devany.html University of
California Institute for Mathematical Behavioral Sciences 3151 Social Science Plaza Irvine, CA 92697-5100
PALEODIET Archives
Subject: Sr/Ca ratios in 'fossils'
From: Mark Leney
Reply-To:
Date: Mon, 29 Sep 1997 23:56:04 +0100
I was interested in the comments about Sr/Ca ratios in fossils and stable isotope work in general. Andrew
Millard suggested that there are difficulties in interpreting the signals. I may not be up to date on this but I
remember that sequential washes were used to remove the diagenic signal and the remaining signal was
taken to be an indication of the biogenic ratios. This seemed to make sense because there were differences
between definte herbivores and definite carnivores from the same deposits (presumably subjected to the
same diagenic regime). This leaves the possibility that bones are entering the deposit with different signals
based less on their trophic level but more on differences between the background levels of trace elements/
rare isotopes between the localities where they 'grew' their bone/ laid down the mineral signal; i.e. a suprious
signal ante-mortem, or there are some other post-mortem processes such as different bone chemistry
unrelated to diet leading to a 'false' signal in the fossils even after all the washes. Both these 'spolier'
hypotheses seems unlikely and in any case, the first one would show up with more sampling... are their
grounds for the second? I would love to know more as it is an intriguing line of evidence. Can Dr Millard,
(or anyone else) fill us in or cite some of the up to date references so we (I) can read some of the criticism of
this provoking work.
Mark
-- Mark Leney New College University of Oxford
PALEODIET Archives
From: Art De Vany
Reply-To:
Date: Tue, 30 Sep 1997 11:39:38 -0700
I agree with Steffan Lindeberg's statement completely when he says
Grant's study is interesting since there is so little cross-cultural data on Alzheimer's disease (AD) in relation
to diet. If the noted statistical relation to fat intake (or total energy intake) can be confirmed, I would be
interested to see more research on intake of micronutrients (e.g. antioxidants) which is negatively related to
fat intake (or total energy intake) in most cross-cultural settings.
And I thank him for putting the discussion group on to Grant's paper which is thorough and a gold mine of
references. I have long had a hunch that oxidation was a source of brain degradation and the death of many
runners from brain cancer (anecdotal evidence only at this stage) may also be related to antioxidant depletion
from long training and free radical stress to brain tissue from oxygen-laden blood. To protect my brain, I
have taken antioxidants for many years (though Staffan may argue that it hasn't worked!).
232/298 (1997)
My quarrel is with the lack of diagnostics in the statistics, the lack of testing of alternative specifications, and
with the false sense of precision which the regression equations and correlation coefficients convey about the
information contained in these crude, aggregate data (and the way they are used to calculate risks). I do not
love hypotheses and believe we should attempt to falsify them and test them against alternatives.
Didn't these sorts of cross-country, epidemiological studies provide much of the early emphasis for low fat,
high carbohydrate diets? I don't know the history.
PALEODIET Archives
Reply-To:
Date: Tue, 30 Sep 1997 19:34:23 +0100
Grant's study is interesting since there is so little cross-cultural data on Alzheimer's disease (AD) in relation
to diet. If the noted statistical relation to fat intake (or total energy intake) can be confirmed, I would be
interested to see more research on intake of micronutrients (e.g. antioxidants) which is negatively related to
fat intake (or total energy intake) in most cross-cultural settings.
At 02.12 97-09-30, Art De Vany wrote:
> There are few degrees of freedom because of the small sample size. Consequently, outliers are
> influential. As you can see on the graph at
> http://www.coa.uky.edu/ADReview/Grant_Images/grantf1.gif there are no obvious outliers. The
> equation for fat is: AD prevalence rate = -0.203+(0.0312*fat (grams/day)). A large negative
> intercept term and a positive slope, leading to the author's conclusion. A large negative
> intercept often indicates a non-linear relationship (which these data surely exhibit).
The intercept is actually close to zero and could be negative by chance. If we change only the Chinese AD
prevalence rate from 1.2 to 1.4 per cent the intercept becomes positive.
> Because fat intake varies so much among countries, compared to total caloric intake, the
> differences among countries are expanded in the regressions using fat as the dependent variable.
> This exaggerates the influence of outliers.
This argument is applicable in any similar epidemiological study.
> Take a look at this graph from the ariticle
> http://www.coa.uky.edu/ADReview/Grant_Images/grantf1.gif and you will see that there are two
> groups: developed Northern American and European countries and Asian and African countries.
> There are no points in the middle and a vast gulf between the data clusters.
I would say the data fit the regression line better than in many important surveys.
> Within the developed cluster there is no relation between fat consumption and Alzheimer's.
Yes there is. Within this cluster R2=0.77 (p=0.0062) for fat intake versus AD, meaning that fat intake
explains 77 per cent of the variation of AD between these countries. Actually, in the Asian/African cluster
the correlation is not far from significant either (R2=0.81, p=0.065).
> Measurement error is all over these data: different reporting rates, more thorough surveys, and
> genetic composition of the populations are just a few.
Quite true. If the paper was on some disease which had been studied more in relation to nutrition it would not
bring much new input. But in this case it is definitely interesting.
> Grant's article is excellent on other grounds, but the statistics show nothing, or they hint at a
> genetic disposition to Alzheimer's more than an environmental one.
A rather tendentious statement it seems. What hypothesis are you in love with?
-------------------------------------------------------------------
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PALEODIET Archives
Reply-To:
Date: Tue, 30 Sep 1997 22:32:36 +0100
> Didn't these sorts of cross-country, epidemiological studies provide much of the early emphasis
> for low fat, high carbohydrate diets? I don't know the history.
Yes they did. A famous example is The Seven Countries Study back in the 1950s showing a positive
relationship with saturated fat intake and coronary heart disease death rates in westernized populations
including Cretans. That relation was not more convincing than Grant's between fat and AD. And the outliers
loooked more like outliers.
Keys A. Seven Countries. A Multivariate Analysis of Death and Coronary Heart Disease.Cambridge, Mass.:
Harvard University Press, 1980.
PALEODIET Archives
Subject: Re: Sr/Ca ratios in 'fossils'
Reply-To:
Andrew Millard
Date: Wed, 1 Oct 1997 09:56:51 +0100
On Mon, 29 Sep 1997, Mark Leney wrote:
> I was interested in the comments about Sr/Ca ratios in fossils and stable isotope work in general.
> Andrew Millard suggested that there are difficulties in interpreting the signals. ....... Can Dr
> Millard, (or anyone else) fill us in or cite some of the up to date references so we (I) can read
> some of the criticism of this provoking work.
OK my major criticism is contained in the project proposal for my new PhD student, whose work will
include:
a critical analysis of Sillen's solubility profile technique for obtaining palaeodietary information from Sr/Ca
and 87Sr/86Sr ratios of bone through selectively leaching of mineral phases of differing solubility. The
actual phases dissolved have never been identified, which casts some doubt over the validity of the
technique, even though it has produced some convincing results.
My own studies of bone crystallinity suggest that in many cases the solubility behaviour ought not be as
simple as it appears to be in Sillen's system. I have also heard a paper presented by one of his co-workers, but
as far as I know not published yet, where they examined a worst case scenario of a terrestrial animal buried
in marine sediments, and showed that its Sr isotope ratio was altered to that of the sediments in bone, dentine
and tusk, but not in enamel, but the enamel showed variation in isotope ratio through the solubility profile.
There is very strong evidence from stable isotope and radiocarbon studies that the carbonate in bone mineral
is fairly readily exchanged with the environment and the increases in U and F content of bone with time have
been well known for a century or more. Whilst U uptake does not necessarily involve the interior of bone
mineral crystals, F uptake does and so does the increase in crystallinity of bones which is widely observed.
Processes invlolving the interior of crystals can only be happening on archaeological timescales if they
involve dissolution and reprecipitation of the crystals, and this process will open them up to exhange of all
trace elements with percolating groundwaters.
I think that there is no reason why one of the solubility compartments in Sillen's work should contain only
biogenic material as the dissolved material in a single wash will contain some newly dissolving crystals,
surface etching of other crystals and the interior parts of crystals previously etched.
In short I cannot see why the Sillen Solubility Profile method should work, but as you say it appears to give
good results separating carnivores and herbivores.
I hope this has not been too technical for the list. I was asked to provide a criticism, which I don't believe is
in print anywhere, though parts of the above are. 9 years in bone diagenesis studies has made me sceptical of
any technique which claims to overcome diagenesis in general, as it is such a multifaceted thing.
Andrew
234/298 (1997)
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Biotin deficiency in Lindow Man
From: Loren Cordain
Reply-To:
Date: Wed, 1 Oct 1997 17:03:00 -0600
Lindow Man, whose preserved body was found in a peat bog in Cheshire, England in 1984 is one of the
more extensively studied of the so called "bog mummies" (1). The principal last meal of Lindow Man likely
consisted of a non-leavened wholemeal bread probably made of emmer wheat, spelt wheat and barley.
Unleavened, whole grain breads such as this represented a dietary staple for most of the less affluent classes
during this time. Excessive consumption of unleavened cereal grains negatively impacts a wide variety of
physiological functions which ultimately present themselves phenotypically. The well documented phytates
of cereal grains sequester many divalent ions including Ca, Zn, Fe and Mg which can impair bone growth
and metabolism. Further, there are antinutrients in cereal grains which directly impair vitamin D metabolism
(2, 3), and rickets are routinely induced in animal models via consumption of high levels of cereal grains (4).
Less well appreciated are the ability of whole grains to impair biotin metabolism. My colleague, Bruce
Watkins (5), as well as others (6, 7) have shown that biotin deficiencies can be be induced in animal models
by feeding them high levels of wheat, sorghum and other cereal grains. Biotin dependent carboxylases are
important metabolic pathways of fatty acid synthesis, and deficiencies severely inhibit the chain elongation
and desaturation of 18:2n6 (linoleate) to 20:4n6 (arachidonic acid). Human dietary supplementation trials
with biotin have shown this vitamin to reduce fingernail brittleness and ridging that are associated with
dificiencies of this vitamin (8). Careful examination of the photograph of Lindow's man fingernail (still
attached to a phalange of the right hand, reference (1, p66) show the characteristic "ridging" of biotin
deficiency. It is likely that regular daily consumption of high levels ( > 50% daily calories) of unleavened
cereal grain breads, which Lindow man may have consumed, caused a biotin deficiency, which in turn
caused nail ridging.
REFERENCES
1. Stead IM, Bourke JB & Brothwell. Lindow Man. The Body in the Bog. Ithaca, N.Y., Cornell University
Press, 1986. 2. Batchelor AJ et al. Reduced plasma half life of radio labelled 25- hydroxy vitamin D3 in
subjects receiving a high fiber diet. Brit J Nutr 1983;49:213-16. 3. Clement MR et al. A new mechanism for
induced vitamin D deficiency in calcium deprivation. Nature 1987;325:62-65. 4. Sly MR et al. Exacerbation
of rickets and osteomalacia by maize: a study of bone histomorphology and composition in young baboons.
Calcif Tissue Int 1984;36:370-79. 5. Watkins BA. Dietary biotin effects on desaturation and elongation of
14C linoleic acid in the chicken. Nutr Res 1990;10;325-34. 6. Blair R et al. Biotin bioavailability from
protein supplements and cereal grains for growing broiler chickens. Int J Vit Nutr Res 1989;59:55-58. 7.
Kopinksi JS et al. Biotin studies in pigs. Biotin availability in feedstuffs for pigs and chickens. Brit J Nutr
1989;62:773-780. 8. Hochman LG et al. Brittle nails: response to daily biotin supplementation. Cutis
1993;51:303-05.
Cordially,
Loren Cordain, Ph.D. ESS Dept Colo State Univ
PALEODIET Archives
Subject: Pemmican
From: Art De Vany
Reply-To:
Date: Thu, 2 Oct 1997 13:47:06 -0700
235/298 (1997)
Members of the PaleoDiet group will know pemmican as a mixture of fat and dried meat, with fruit
sometimes added, long used by North American indians and frontier people. So important a source of food
was pemmican that Pemmican wars were fought to control its distribution.
I broke a long standing tradition of staying out of "health food" stores and buying any packaged or processed
food yesterday to buy some pemmican to use as an afternoon snack. I bought it without reading the label and
now find that what is sold as "pemmican" is not pemmican.
Here are the ingredients: malted corn and barley, nonfat milk, honey, wheat germ, raisins, soy flour, walnuts,
soy oil, wheat bran, pecans, grape juice.
Aside from walnuts and pecans, there is nothing in this list that a PaleoEater like myself (and, I gather, most
of you) ever eats. Its macronutrient profile is fat 20%, protein 34% and carbohydrate 20%. But, more than
half the CHO is sugars.
The taste was repulsive to someone who has eaten Paleo for so long (15 years or so).
I also glanced over most of the "balance" or 30-30-40 or "power" bars and found them to be about like this
"pemmican". I wasn't surprised to see that hundreds of new "miracle" diet and fat-burning, muscle growing
"explosive energy" products had been invented in years since I had last been in a health food store. The
people in there don't look any better or seem any more energetic though, in spite of these new innovations.
What did strike me, in my more informed perspective about macronutrients gained from this group, is that
the products on the shelves of health food stores are as far out on the CHO abuse scale as what you find in
any store. This health food store seemed to be a candy store in disguise where you can feel good about
carbohydrate abuse.
Its back to the Stone Age for me at the produce and meat counter.
PALEODIET Archives
Reply-To:
Date: Sun, 5 Oct 1997 23:44:47 +0100
FROM: William Grant,
Congratulations to Art De Vany for spotting some of the reasons the Alzheimer's Association issued a press
release shooting down my paper - the data in Figure 1. Other reasons included "flawed methodology" and
"confusing strokes with Alzheimer's disease. However, one should remember that the Alzheimer's
Association has the Reagan Foundation for Alzheimer's Disease Research, and if the donors knew that an
atmospheric scientist found the major risk factor for AD in 300 hours, the funds they receive might dry up.
In response to their concern that the Alzheimer's disease rate vs. fat supply did show two distinct groupings,
and the concerns of others that the European countries showed lots of rate variation for small variations in
fat, I did another analysis using only European and North American countries. The results are given in Table
4, but the figures are not included because the editor thought that a multiple regression with fat and fish was
too complicated. What the fat/fish multiple regression shows (using data from Table 2) is that 1 calorie of
fish counters 4.3 cal. of fat . The mechanism is likely that fish oil reduces inflammation through
prostaglandin 3s, while fat promotes inflammation through prostaglandin 2s. In the unpublished figure, the
European countries now lie in a straight line, and r2 = 0.937.
Regarding genetic vs. environmental causes of Alzheimer's disease. I got interested in this topic because Lon
White showed that Japanese-Americans have 2.5 times the AD rate of native Japanese. I later learned that
African-Americans have 4 times the rate of AD as Nigerians, in both cases age-adjusted to the U.S.
population distribution over 65 years of age. This does not look like a genetic factor to me.
236/298 (1997)
As far as experimental uncertainty goes, I included 4 values from Japan, which range from 1.5 to 2.4%, and
4 from Taiwan (not used in the analysis), which range from 0.6 to 2.6%. The U.S. data range from 3.5 to
6.24%. The Alzheimer's Association also questioned the use of national dietary supply data as a measure of
local dietary consumption. It is well known that Japanese-Americans still eat much fish and rice, while
African-Americans eat more fat and salt than the average American. I averaged the two ethnic groups in
determining an average U.S. AD rate. So, yes, there is experimental uncertainty in the data. However, the
statistical analysis was able to spot the fact that data from the period prior to 1980 were not comparable with
data after 1980, with the reason being, I learned later, that the clinical determination of AD changed in 1980.
The way my results should be viewed as a hypothesis which should then be tested using case control studies.
Such studies are already underway. I refer to the one by Kalmijn et al., which actually got me to look at the
multiple regression for fat and fish. Also, Mark Smith, referenced for other works, has participated in some
case control work which shows that those with AD maintained the same caloric intake in their 60s as they
did in their earlier years, while the controls reduced their caloric intake by 400 calories. Another study
showed that those with AD have reduced intakes of vitamins and minerals compared to controls. Dharma
Singh Khalsa in Tucson is treating people in the early stages of AD with a progam consistent with my
findings and is able to slow the progression or reverse cogintive impairment or AD.
I think that if people look at the supporting documentation, such as the use of NSAIDs to reduce the risk of
AD, and the use of vitamin E to slow the progress of AD (both referenced in my paper), the changes in the
Japanese-American and African-American populations compared with native populations, the recent case
control results, the changes in metal ion concentrations in the brains of those with AD, the high crosscorrelations with diseases associated with dietary fat, the results of the Nuns Study showing that AD is a
vascular disease, etc., they would be hard- pressed to find a better hypothesis. If anyone does, please let me
know.
The epidemilogic approach linking diet and disease was very useful in the 1970s and 1980s in reestablishing
the link between dietary fat and cancer. John Weisburger sent me some papers in 1991 which later provided
the model for my work. Ancel Keys and John Yudkin had also used the approach to show that animal fat and
sugar were associated with heart disease. I have submitted manuscripts linking meat and sugar to rheumatoid
arthritis and animal fat and sugar as links to heart disease (animal fat for men, sugar for women). I also have
a letter to the editor on fat and cancer which should be in the NY Times for Oct. 3.
PALEODIET Archives
From: Art De Vany
Reply-To:
Date: Mon, 6 Oct 1997 11:16:55 -0700
This subject is of great interest substantively and methodologically.
On genetic vs. environmental causes of Alzheimer's disease: Africans living in France apparently do not
show the pattern found among African-Americans relative to Nigerians or native Africans. Nor do Japanese
living in Peru show the elevated Alzheimer's rates found among those living in the US. This may further pin
point the US environment as a contributory factor; or simply reflect the higher reporting rates in the US.
Cavilli-Sforza reports that the genotypic variation among a small population of Africans contains all the
variation that exists among humans. A more diverse population will show some incidence of almost any
disease (or adaptive characteristic and talent as well). Thus, the African-American experience tells us
something about the vulnerabilities of us all.
A methodological note. I, for one, have a hard time with these macronutrient measures. They omit so much:
vitamins, antioxidants, glycemic index (not all carbs are equal), and so on. Most high fat eaters are also
sweet carb browsers. At a barbeque restaurant the other day I ate ribs, a salad, and steamed vegetables, while
most everyone around me ate ribs, bread, and potatoes and sweetened beans and drank cokes. They ingested
no fruit or vegetables and loaded the glyco-oxidative pathway with sugar and fat. It is a high insulin response
that triggers the eicosanoid pathway that produces an inflammatory response (Protein Power by the Eades is
a too-simple source, but one I have at hand).
237/298 (1997)
My colleague, the distinguished econometrician Jack Johnston (Econometric Methods) is fond of saying that
r square values can be too high. In a cross-country regression, anything above 0.7 should be suspect. Nature
isn't that orderly and linear (untestable, I know, but sound advice). Values exceeding this level are often the
result of what he calls "partial identities" which are transformations of the data that put the same variable on
both sides of the regression. Something is fishy about these regressions (speaking for myself and attributing
no motives to anyone) and it isn't prostaglandin 3.
But, what do they show anyway? In the all-country sample, no country is near the mean---it lies in that
empty middle between two far-flung clusters. The regression and risk assessment express the change in the
expected value of the dependent variable (incidence of Alzheimer's) conditional on a change in the mean of
the independent variable (fat or whatever). The correct interpretation of the coefficient is that if the fat intake
among all 11 countries falls by enough to lower the mean fat intake among all 11 countries by X, then the
mean incidence of Alzheimer's will fall by the coefficient value times X.
Where this sort of calculation leads to bad policy is when it is applied to a population or an individual. There
is no representative population or individual to which this world sample applies and it does not follow that
your risks or my risks are related in any way to our fat intake. They may be, and the mechanisms elucidated,
along with the extensive cited literature, may be a cause for reassessing one's own diet.
For all that, I think the Grant article is one of the most stimulating I have read in some time.
PALEODIET Archives
Subject: Re: Alzheimer's Disease, Trans Fatty Acids and Aluminum
From: Loren Cordain
Reply-To:
Date: Mon, 6 Oct 1997 15:59:00 -0600
238/298 (1997)
The search for environmental risk factors for Alzheimer's Disease has shown an increased level of aluminum
in the brains of Alzheimers's patients (1, 2). More recent studies utilizing laser microprobe mass analyzers
(which have concentration resolutions of 1-2 parts per million and a spatial resolution of 1 micrometer) have
demonstrated a specific and selective accumulation of aluminum within neurofibrillary tangle (NFT) bearing
neurons when compared with adjacent NFT free neurons (3). Animal experiments (4) have shown that
administration of chelated aluminum compounds seriously worsened the learning ability of rats and resulted
in diminished cholinergic activity, a characteristic of Alzheimer's Disease. Insoluable aluminum compounds
did not influence learning ability. Studies of miners exposed to "McIntyre Powder" (finely ground aluminum
and aluminum oxide) showed impaired cognitive performance consistent with the putative neurotoxicity of
chronic aluminum exposure (5). These experiments clearly implicate aluminum as one of perhaps many
environmental etiologic risk factors for Alzheimer's disease. Because the form in which aluminum is
ingested seems to influence its ultimate concentration in the brain (4), then environmental sources of
aluminum which are highly soluable and which would be readily incorporated into brain tissue should be
scrutinized. One potential source of brain aluminum stems from the consumption of trans fatty acids (the
primarily fat of hardened vegetable oils, ie. margarines, shortenings etc). In order to synthesize trans fatty
acids, hydrogen is bubbled through vegetable oil in the presence of a catalyst called "Raney Nickel". Merck's
Index reveals that Raney Nickel is prepared by fusing 50 parts nickel with 50 parts aluminum. The alloy is
pulverized and most of the aluminum is dissolved out with sodium hydroxide, however residual aluminum,
amounting to several percent, remains and appears to be necessary for proper catalytic activity. During the
hydrogenation process which forms trans fatty acids, Raney Nickel (in the form of its oxide) is used in
amounts of 0.5 to 1 per cent of the weight of the oils. Although the metal is filtered from the oil, an
appreciable amount remains dissolved in the oil, presumably in the form of a soap consisting of nickel,
aluminum and the mixture of lipids formed after the hydrogenation process. It is possible that these aluminonickel soaps formed during the synthesis of trans fatty acids provide a stable and highly soluable vehicle for
the biological uptake and transport of aluminum into the membrane and storage lipids of body tissues,
including brain. To date, I believe no radio tracer studies have either confirmed or denied this hypothesis.
How does this relate to paleonutrition. Obviously, aluminum exposure in the environment of pre-industrial
man would have been minimal. The trans fatty acids produced via the hydrogenation of vegetable oils have
only been with us since shortly after the turn of the century. Meat from ruminants which humans have been
consuming for at least 2 million yrs or more, contain small amounts of trans fatty acids, but these fatty acids
(trans vacenic acid primarily) are apparently benign (compared to the trans fat, elaidic acid produced during
hydrogenation) and do not contain either aluminum or nickel because they are produced by biohydrogenation occuring in the rumen.
Cordially,
Loren Cordain, Ph.D. Professor, Colo State Univ
REFERENCES
1. Crapper DR et al. Brain aluminum distribution in Alzheimer's disease and experimental neurofibrillary
degeneration. Science 1973;180:511-513. 2. Crapper DR et al. Aluminum, neurofibrillary degeneration and
Alzheimer's disease. Brain 1976;99:67-80. 3. Good PF et al. Selective accumulation of aluminum and iron in
the neurofibrillary tangles of Alzheimers Disease: A laser microprobe (LAMMA) study. Ann Neurol
1992;31:286-92. 4. Bilkei-Gorzo A. Neurotoxic effect of enteral aluminium. Fd Chem Toxic 1993;31:35761. 5. Rifat SL et al. Effect of exposure of mineres to aluminum powder. Lancet 1990;336:1162-65.
PALEODIET Archives
Subject: Accounting for "finer points" of diet in human nutrition studies
Reply-To:
Date: Wed, 8 Oct 1997 11:06:50 PDT
Art De Vany's point about researchers not accounting for the "finer" points of subjects' diets in their studies
is one that seems to apply in so many cases, no? Of course, it's understandable given the difficulties of
obtaining data, yet it does undercut the robustness of the findings.
What Art pointed out about "not all carbs are equal" (esp. in this case given the insulin/eicosanoid
connection) is perhaps even more the case with respect to fats and the studies linking fat consumption with
cancer and satfat consumption with CHD, no?
239/298 (1997)
I imagine similar issues apply for claimed links between animal protein consumption and various diseases.
Not only does one need to consider the type of macronutrient and the diet and health of the source (for
animals and plants too!), but also the cooking method. A steady diet of crispy BBQ ribs from "industrial
cattle" may be trouble, while the same amount of rare (or raw for those so inclined) wild game may be quite
healthful! (at least it seems to have been for our forebears)
Steve Meyers Staff Scientist Lawrence Berkeley Natl. Lab. Berkeley, CA
PALEODIET Archives
Subject: Re: PALEODIET Digest - 7 Oct 1997 to 9 Oct 1997
From: Aaron Hirschhorn
Reply-To:
Date: Thu, 9 Oct 1997 17:31:47 -0400
Topic: eicosanoids and insulin
Yesterday someone mentioned the "eicosanoid/insulin connection." After reading Barry Sear's book I began
to try to unearth some more data documenting this connection. Unfortunately, the only article that Sears
himself cites is one by Brenner (1982) which worked with rats. I have been unable to find any other
documentation, which to me smells of some academic fraud. If any one else has any ideas or knows of more
information, please let me know.
-Aaron
Brenner, R.R. Nutrtional and hormonal factors influencing desaturation of essential fatty acids. 1982. Prog
Lipid Res. 20; 41-47.
PALEODIET Archives
Subject: Loren Cordain responds to Enig & Fallon (Part 1)
From: Dean Esmay
Reply-To:
Date: Thu, 9 Oct 1997 20:46:33 -0400
The following was written by Loren Cordain. I'm posting it for Loren as he is having technical problems at
the moment.
Those wishing to refer back to the messages Dr. Cordain is responding to here may wish to see
http://maelstrom.stjohns.edu/archives/paleodiet.html and to do a search an "Enig" or "Fallon" to read the
relevent messages.
Cordain's message follows:
-=-=-=This commentary represents my rebuttal to Dr. Enig's and Sally Fallon's response of June 29. I realize that
this rebuttal comes in rather late, however I was unable to respond during the summer because I was out of
town. I have tried to preface the original questions so that our members can determine what issues were
being discussed.
1. Thank you for your followup comments on Dr. Voegtlin's book. We are in agreement that an all animal
based diet can provide all the known nutrients needed for adequate nutrition. I am in complete agreement
that for optimal nutrition, diets based upon both plant and animal foods probably provide superior nutrition
than do diets based solely upon animal derived foods. Not only do plant foods provide necessary vitamins,
minerals and soluable fiber, but they provide a source of phytochemicals which are increasingly being found
to benefit human health in a wide variety of ways.
240/298 (1997)
2. Dr. Enig and Sally Fallon say "We have consistently argued that the current high levels of CHD have
nothing to do with the consumption of saturated fat from animal sources, but rather are due to foods
relatively new to the human diet--particularly excess polyunsaturates, hydrogentated oils and refined
carbohydrates". I agree that there is now substantial evidence that hydrogenated oils are atherogenic via their
hypercholesterolemic effects (1); however in terms of their cholesterol raising properties they may be worse
than saturated fats because they cause a decrease in HDL cholesterol (2). Refined carbohydrates (sucrose in
particular) has been known for more than 30 years (3) to be implicated in its CHD promoting effects,
probably through increases in VLDL, triglycerides, total cholesterol and perhaps decreases in HDL (4).
Recently it has been recognized that although dietary polyunsaturates may lower serum cholesterol levels,
they may actually increase the risk for CHD by increasing the susceptibility of LDL to oxidation (5). So we
are in agreement that hydrogenated fats, refined carbohydrates and excessive polyunsaturated fats (primarily
linoleic acid, 18:2n6) contribute to the development of CHD via hypercholesterolemic and LDL oxidizing
mechanisms. However, I cannot agree with the statement that saturated fats from animals having nothing to
do with CHD. It may be possible that the hypercholesterolemic effects of saturated fats (12:0, 14:0. 16:0) can
be negated or somewhat ameliorated by extremely low levels of dietary carbohydrates (particularly in insulin
resistant subjects) or by high levels of dietary protein ( > 20% of total calories) via protein's VLDL
suppressing effects (6); however it is clear beyond a shadow of a doubt that dietary saturated fats (12:0, 14:0
and 16:0) elevate serum cholesterol levels within the context of the "average American diet". A recent meta
analysis of 224 published studies encompassing 8, 143 subjects (many under metabolic ward conditions) has
unequivocally demonstrated the hypercholesterolemic effect of dietary saturated fats (7). The cellular basis
for the this observation stems from the regulation of low density lipoproteins. When the amount of
cholesterol or saturated fat into the body is increased, there is an expansion of the sterol pools within liver,
and to a lesser extent, peripheral cells, which causes a down regulation of LDL receptors. As a consequence
LDL in plasma increases (8). Some have argued that increases in total plasma cholesterol and LDL may not
necessarily have a direct relationship to mortality from CHD (9). Clearly, there are a wide variety of
independent risk factors for CHD including hypertension, homocysteine (vitamins B6, B12 and folic acid),
catecholamines, n6/n3 fatty acid ratio, antioxidant status (vitamins e, c beta carotene, phytochemicals
etc.)dietary fiber, cigarette smoking and ethanol consumption which influence a variety of physiological
systems involved with CHD. However, there is powerful evidence (n = 356, 222) to indicate that the
relationship between serum cholesterol levels and the risk of premature death from CHD is continuous and
graded (9). Therefore, the recommendation to consume high levels of dietary saturated fats within the
context of the "average American diet" appears to not only be erroneous, but probably deadly. Our hunter
gatherer ancestors consumed high levels of animal food (probably > 55% of their total daily calories),
however the context under which this was done was much different than present day conditions. As I have
previously mentioned, the carbohydrate content of the diet was low (~< 35 % of total calories) and composed
of plant foods with high soluble fiber and low starch content. The protein content of the diet would have
exceeded 20% and may have been as high as 30-40 %. The fats consumed would have had a low n6/n3 ratio
and there would have been both ample levels of 20 and 22 carbon fats of both the n6 and n3 variety. Since
marrow contains, 70-75% monounsaturated fats (MS) and was a favored food, it is likely that although the
fat content of the diet may have been as high as 40%, it was composed of higher levels of MS and non
atherogenic saturated fats such as stearic acid (18:0).
3. Wholesale dismissal of the LDL/HDL ratio as a risk factor for CHD without either rationale or references
is difficult to respond to. Perhaps Dr. Enig and Sally can provide further detail. Low HDL cholesterol levels
are strongly associated with coronary heart disease, and many factors that produce lower HDL cholesterol
levels increase the risk of coronary heart disease; examples are smoking, obesity, lack of physical activity,
abstinence from alcohol and low levels of dietary ascorbate. The induction of high HDL cholesterol levels in
animals retards atherogenesis, and the infusion of HDL protein retards the development of fatty streaks (10).
I agree that the oxidized cholesterol in powdered milk, eggs and aged cheeses is a powerful promoter of
atherogenesis. In our laboratories, we routinely induce atherosclerosis in miniature swine using a diet with
high levels of oxidized cholesterol. Except for trans fatty acids which elevate Lp (a), Lp(a) is remarkably
unresponsive to dietary manipulations (11). I would enjoy seeing the references showing that saturated fat
consumption actually decreases it.
241/298 (1997)
4. Dr. Enig and Sally Fallon dismiss the idea that dietary protein has any influence upon cardiovascular
disease with the argument that there is no difference in CHD incidence in populations consuming either
"high protein consumption (30-40%)" or "relatively low protein consumption (15-20%)". Once again no
references are cited to substantiate this argument. I would first like to point out that global surveys of the
world's populations indicate a remarkably limited range of protein consumption that varies from about 10 to
15% of total calories (12). Further, except for reports of Inuit and Eskimo diets, I know of no references
showing any contemporary populations consuming 15-20% of their calories as protein, much less 30-40%.
Please provide your sources. Speth (12) has extensively studied protein intakes in contemporary world wide
populations and notes that most human populations today obtain between 10-15% of their total energy
requirements from protein. For Americans the value is 14%, for Swedes it is 12%; for Italian shipyard
workers it is 12.5-12.8%; for Japanese, it is 14.4% and for West Germans it is 11.1%. Even among athletes
values rarely exceed 15%. Speth (12) shows that Italian athletes consumed between 17-18% of their caloric
intake as protein; Russian athletes consumed 11-13%; Australian athletes competing at the 1968 Olympic
games consumed 14.4% of their daily calories as protein. This data clearly demonstrates the relative
homgeneity amongst contemporary global populations in their protein consumption levels. That protein
consumption may have anything to do with the atherosclerotic process and hence CHD is an obscure topic
which has been rarely examined by the medical and nutritional communities. I am not surprised that Dr. Enig
and Sally Fallon are unaware of the literature which supports this concept. There are at least three human
clinical trials (13, 14, 15) demonstrating that isocaloric substitution of protein (daily caloric protein intakes
ranging from 17-27% of total calories) for carbohydrate reduces triglycerides, VLDL, LDL and total
cholesterol while increasing HDL cholesterol. Further, acute consumption of high levels of beef protein
without carbohydrate evokes an extremely small rise in serum insulin levels and a concomitant substantial
rise in glucagon (16). Both of these acute responses would tend to be associated with a reduced risk for
CHD. Lastly, in animal models, high levels of protein are known to dramatically inhibit hepatic VLDL
synthesis (6). VLDL are the precursor molecules for LDL cholesterol. In their classic study of Inuit, Bang
and Dyerberg (17) have shown that the serum cholesterol levels of the Inuit were 0.48 mmol/liter lower than
what would have been predicted by the Keys equation which estimates plasma lipid levels from dietary
saturated fats, polyunsaturated fats and cholesterol . At the time (1980), it was suggested that the
paradoxically low serum cholesterol levels may have resulted from the higher omega 3 (n3) fats found in the
Eskimo's seafood based diet. However after almost 30 years of research, meta analytical studies have shown
that n3 fatty acids, slightly elevate (5-10%) LDL cholesterol concentrations, but do not materially affect total
cholesterol (18). Consequently, it may have been the higher dietary protein intake (23-26% of total calories)
in the Inuit compared to the Danish Controls (11% of total calories as protein) which may have accounted for
these differences. However, since the Key's equation considers dietary monounsaturated fats as neutral
(which more recent research (19) indicates is not the case), it is possible that the higher monounsaturared fat
content (57.3% of total fat) in the Inuit diet (Vs 34.6% in the Danes) may have also contributed to the plasma
cholesterol differences. Many people on this list would argue that the cholesterol lowering effect of the
Eskimo diet stemmed from its low carbohydrate content. However, in one of the few (and best controlled)
metabolic ward trials of a carbohydrate free (<20 gm/day) diet, Phinney and colleagues (20) demonstrated a
rather large rise in serum cholesterol (159 to 208 mg/dl) in nine lean, healthy males who participated in this
35 day in patient trial. The protein content of the diet was estimated to be 15%, whereas the fat content of the
diet represented between 83-85% of total daily calories. Consequently, during the dietary trial, the protein
content remained similar to the average daily intake in the US and was not increased. This experiment shows
that a carbohydrate diet free diet composed of "ground beef, breast of chicken, water packed tuna fish,
powdered egg solids, and cheddar cheese with mayonnaise, heavy cream, sour cream, and cream cheese as
primary lipid sources" was definitely hypercholesterolemic. In a less well publicized, but highly controlled
clinical research center (CRC) study, Gray (21) showed similar results in a 3 week study of 10 healthy males
who consumed a diet composed of 73-75% fat, 7-9% CHO and 16-20% protein. Compared to their standard
(normal carbohydrate diet), the high fat diet increased total cholesterol from 156.5 mg/dl to 167.6 mg/dl and
LDL cholesterol increased from 46.6 mg/dl to 55 mg/dl. The total CHOL/HDL ratio actually improved on
the high fat diet going from 3.36 to 3.20. High fat, low carbohydrate diets such as the Phinney (20) and Gray
(21) studies characteristically induce other beneficial lipid profiles such as increased HDL levels and
(Continued in Part 2)
PALEODIET Archives
242/298 (1997)
From: Dean Esmay

Reply-To:
Date: Thu, 9 Oct 1997 20:46:38 -0400
...and Gray (21) studies characteristically induce other beneficial lipid profiles such as increased HDL levels
and decreased triglyceride levels. These blood lipid changes (increased HDL and reduced TG) have also
been frequently demonstrated in reduced carbohydrate diets (22, 23) in which CHO has been reduced but not
as drastically as in the Phinney (20) and Gray (21) studies .
So, in summary the animal foods of our stone age ancestors were probably non atherogenic because they
contained high levels of protein ( > 20% of total calories), lower levels of saturated fats, higher levels of
monounsaturated fats, higher levels of N3 fats, little or no trans-fats, and higher levels of HUFA ( > 18
carbon) fats of both the N6 and N3 varieties than modern, western meat based diets. The higher consumption
of animal based foods would have necessarily reduced the carbohydrate content of the diet and this would
have also benefited certain aspects of the lipid profile which I have previously enumerated.
5. In a previous comment, I suggested that pre-agricultural meals tended to produce less of a glycemic
response than western meals. This was based on the observation that hunter gatherer meals generally were
not the elaborate mixtures of fat/carbohydrate/protein that are typical of western meat/potato meals. Hunter
gatherers quite often would eat only the animal killed for a meal without added plant courses. Thus,
protein/fat macronutrient mixtures were the norm. Carbohydrates generally were consumed as they were
collected or separate from animal based meals. It has been well established that by mixing fat with
carbohydrate, the glycemic response worsens (24).
6. I presented our data on the fatty acid distribution in tissues of wild animals at a recent conference on the
return of n3 fats to the food supply, held at NIH in Bethesda. The abstract should be published this Spring in
the World Review of Nutrition and Dietetics.
I disagree with Dr. Enig's contention that the overall PUFA in wild animal tissues is low. To the contrary, it
is relatively high in both brain (26%) and muscle (36%) as our data shows and which corroborates earlier
work of Crawford (25). The difference in PUFA between the western diet and the so called "paleolithic diet"
is that the PUFA in the western diet is predominantly based upon 18 carbon lipids (vegetable oils) with huge
amounts of 18:2n6 (linoleic acid) predominating. The PUFA content of the paleolithic diet is higher than that
of the western diet (19.2% vs. 12.7% - see reference 17) with much higher levels of HUFA ( > 20 carbon
lipids) of both the N6 and N3 families.
7. Dr. Enig contends that "dairy products cannot be blamed for the CHD epidemic". However, as has been
pointed out previously by Staffan Lindeberg, some of the highest dietary correlates to CHD in world wide
epidemiological studies come from consumption of milk and dairy products (26, 27). Milk and dairy
products are thought to produce their atherogenic effects through a variety of mechanisms. The most obvious
is their high saturated fat content. Recent NHANES data indicates that saturated fat from dairy products
(whole milk, cheese, butter and ice cream) represents one of the highest sources for the atherogenic fats
(12:0, 14:0, and 16:0) in the US diet.
In addition to high levels of saturated fats, the Ca:Mg ratio of milk is about 12:1. The inclusion of milk
products in western diets can easily raise the Ca: Mg ratio to about 5:1(28). Because high levels of Ca tend to
impair Mg assimilation, consumption of dairy products without concomitant consumption of high levels of
Mg will ultimately reduce intracellular Mg stores (29). Supplementation studies of Mg show that it reduces
CHD risk via its serum lipid lowering effects (30), by its ability to prevent cardiac arrhythmias (31), by its
ability to decrease VLDL and LDL peroxidizability (32) and by its ability to increase insulin sensitivity and
reduce thromboxane synthesis (33). In "pre-agricultural" diets, estimates from our laboratory suggest that the
Ca:Mg ratio would have been about 1:1. Therefore, with the development of agriculture and the concomitant
increase in dairy product consumption, the Ca:Mg ratio would have become significantly elevated. This
chronic disproportionate increase in dietary Ca relative to Mg can over a lifetime lead to reduced
intracellular levels of Mg which can significantly increase the risk for CHD via the enumerated mechanisms.
In addition to its high saturated fat content and disproportionate Ca:Mg ratio, milk has been implicated in
CHD via a number of other mechanisms. Numerous epidemiological studies have shown dietary lactose (the
disaccharide in milk) to be a prominent risk factor for CHD (34). High consumption of lactose is used to
routinely induce copper deficiencies in laboratory animals which in turns causes increased exacerbation of
heart pathology and mortality (35). High levels of lactose in the diet from milk and milk products are thought
to induce their cardiovascular damaging effects via reduction of tissue levels of the bodies endogenous
antioxidants, copper-zinc superoxide dismutase and cytochrome c oxidase (36).
243/298 (1997)
Milk also contains significant quantities of xanthine oxidase(37) which has been shown to enter the
circulation (37, 38). Because xanthine oxidase is routinely used to induce LDL oxidation in vitro (39), it may
be that part of milk's pro atherogenic effect stems from its ability to increase LDL oxidation. Alternatively,
there is increasing recognition of the involvement of the immune system in atherosclerosis, and there is now
substantial evidence to indicate the presence of activated macrophages and T-lymphocyte in human arterial
fatty streaks indicating a cell mediated immune response (40). In milk drinking populations, human sera has
been shown to exhibit extraordinarily high concentrations (20 to 100 times higher than for other
autoantibodies) of IgG antibodies to xanthine oxidase which are specifically directed against the xanthine
oxidase antigen present in endothelial cells of capillaries and arterioles (41). Specificity for xanthine oxidase
has been demonstrated by immunoblotting in capillary endothelium, and there is cross reactivity with the
human and bovine xanthine oxidase polypeptide (41). Further, IgA antibodies to bovine xanthine oxidase are
significantly elevated in patients with severe atherosclerosis when compared to controls (42). It is quite
possible that the high titers of xanthine oxidase specific auto-antibodies in human serum (41) are induced by
bovine milk xanthine oxidase that has been taken up with dairy products and which has escaped digestion.
Because the basement membranes of arterial endothelial cells may share epitopes with xanthine oxidase, the
initial lesion to the endothelial lining which is characteristic of the first stage of atherosclerosis, likely occurs
because of an immune response directed against the bodies own tissues. The loss of self tolerance occurs
because there is molecular mimicry (similar amino acid sequences) between bovine xanthine oxidase and
proteins within the endothelium. Activated T-lymphocytes therefore cannot distinguish self from non self
and cause continual damage to endothelial linings of arterioles. The hypothesis that a cow milk protein may
be involved in an autoimmune response related to CHD is not new and Davies has written extensively on the
topic (43).
Clearly no, humans consumed milk of any kind after weaning prior to the domestication of animals,
therefore milk or dairy products of any kind have little or no precedent in the human evolutionary
experience. It is not surprising that they wreak havoc in human health.
By the way, autopsies done on 50 Masai men (milk drinking populations) have revealed extensive
atherosclerotic lesions in coronary artery cross sections "which equaled that of old U.S. men" (44). Thus, the
earlier reports of freedom from atherosclerosis in the Masai were shown to be incorrect.
8. I disagree with Dr. Enig's comment that " modern man is not consuming high levels of SFAs compared to
pre-agricultural man". Bang and Dyerbergerg's data (17) on Eskimo populations shows precisely the
contrary. Of the total dietary fats, saturated fats comprised 22.8% in Inuit people whereas saturated fats
comprised 52.7% of the total dietary fats in a control population of Danes.
9. Dr. Enig and Sally Fallon made three points regarding sodium and human health. (1) Modern processed
sodium contains other substances which negatively influence human health. (2) Modern processed sodium is
depleted of other minerals which are of benefit to human health and (3) It is difficult to distinguish sodium's
putative deleterious health effects from those of the processed foods from which it is added.
I agree that modern processed salts have been purified to an extent that most other trace minerals are
depleted and that anti-caking agents and pouring enhancing agents have been added as well as iodine.
However, these manipulations only make a generally bad product even worse, and the major constituents of
salt; sodium and chloride remain as its major deleterious product whether one chooses to consume sea salt or
Morton's Table salt. High levels of dietary sodium (high levels are simply normal levels in western societies)
disrupt intracellular ionic balance whether one is sodium sensitive or not (45) and therefore alter fundamental
cellular homeostasis such that intracellular Na and Ca increase while Mg and pH are lowered. These
observations have been made repeatedly over the past 30 years including experiments utilizing recently
developed sophisticated nuclear magnetic resonance techniques (45). It is not completely clear how dietary
sodium elicits these intracellular ionic changes however it is thought to occur primarily through endogenous
digoxin like molecules (46) or perhaps other hormonal like peptides which impair the Na/K ATPase pump
and which in turn, indirectly influences other ion channels. Increases in intracellular Ca in smooth muscle are
thought to be in part responsible for sodium's hypertensive effect (45) as well as for its asthma inducing
effects (47). Calcium channel blocker drugs, such as nifedipine, work by reversing the ionic effects of dietary
salt loading by reducing intracellular levels of Ca and by increasing intracellular Mg and pH.
244/298 (1997)
Because the kidney must obligatorily excrete calcium with sodium (48), high levels of dietary sodium are
now generally recognized to be the greatest dietary risk factor for osteoporois (49, 50, 51). Additionally,
because of the associated hypercalciuria induced by high dietary sodium intake, there is an increased risk for
kidney stones with high salt intake (52). There is also powerful epidemiological (53) as well as experimental
evidence to show that high dietary sodium is a strong inducer/promoter of gastric cancer. Further, Menierre's
syndrome (ear ringing) (54) and insomnia (55) are known to be ameliorated or eliminated by reductions in
dietary sodium. Recently, motion sickness has also been linked to high dietary sodium intake (56). Most
ominous of all is the epidemiological (57) as well as theoretical (58) work that suggests that mitogenesis and
hence oncogenesis (cancer) are facilitated by the changes in resting membrane potential that are elicited by
the characteristic intracellular ionic changes which occur when people consume high levels of dietary
sodium.
10. Dr. Enig and Sally Fallon sum up their last response by saying, "the hypothesis that modern chronic...
(Continued in Part 3)
PALEODIET Archives
Subject: Re: insulin/eicosanoid connection
From: Art De Vany
Reply-To:
Date: Fri, 10 Oct 1997 15:04:11 -0700
Responding to Aaron's investigations of the insulin/eicosanoid connection as presented by Sears, the Eades
in their book, Protein Power, do not give references for their assertions (there are no references at all in their
book, though they are available on the Internet).
The Eades make these points:
1. The 1982 Nobel prize was awarded for research on eicosanoids (who? what findings?)
2. That a high carbohydrate diet (as well as trans fatty acids and alpha linolenic acid) inhibits Delta 6
desaturase, the enzyme controlling the conversion of Linoleic acid to eicosanoids.
3. That the pathway synthesizing linoleic acid to series one (prostacyclins or good eicosanoids) or series two
eicosanoids (thromboxanes and leukotrienes or bad ones) is activated by insulin, which favors the series two
profile, and down regulated by glucagon.
I can't evaluate these claims.
Gurr in "Fats", Garrow and James eds. Human Nutrition and Dietetics at page 91 concludes agnostically:
"The mechanisms by which the relative proportions of the different eicosanoids are regulated, particularly
how diet influences this regulation, and the quantitative relationship between the requirements for essential
fatty acids, which are measured in grams, and the daily production of eicosanoids, which is measured in
micrograms, are subjects for further research."
One of his charts does indicate that antioxidants prevent the conversion of arachidonic acid to hydroperoxy
acids from which leukotrine B4 is synthesized. Leukotrine B4 is inflammatory. N3 acids may inhibit the
formation of leukotrine B4. Gurr states further: "In general, the potency of eicosanoids derived from n-3
polyunsaturated fatty acids is less than that of those derived from n-6 polyunsaturated fatty acids.
I hope we can track through this topic which is a central theme in two huge selling diet books and of interest
to us all. One of the references in Loren's brilliant post suggests an insulin/eicosanoid connection mediated
through magnesium deficiency: 33. Nadler JL et al. Magnesium deficiency produces insulin resistance and
increased thromboxane synthesis. Hypertension 1993;21:1024-29.
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Thu, 9 Oct 1997 20:48:32 -0400
245/298 (1997)
Parts/Attachments:
text/enriched (342 lines)
10. Dr. Enig and Sally Fallon sum up their last response by saying, "the hypothesis that modern chronic
diseases like CHD and cancer are due to consumption of saturated fats, red meat, milk products and salt does
not stand up to careful scrutiny. These have been in the diets of healthy populations groups for millennia.
Media denigration of such traditional foods is a distraction that diverts the attention of both the public and
the scientific community from the real culprits-- modern farming techniques, inappropriate processing,
refined carbohydrates, commercial vegetable oils, food additives and rancid & altered fats."
This summary response indicates a naivet and lack of understanding of the chronological magnitude of the
human evolutionary experience as it relates to diet. The first member of the human genus, Homo, was Homo
habilus who has now been dated to ~ 2.33 million years ago (MYA) (59). Homo erectus who had postcranial body proportions similar to modern men appeared in Africa by about 1.7 MYA and is thought to have
left Africa and migrated to Asian by 1 MYA or perhaps even earlier (60). Archaic Homo Sapiens (called by
some, Homo heidelbergensis) have been dated to 600, 000 yrs in Africa and to about 400, 000 yrs in Europe
or perhaps earlier (61). Anatomically modern Homo Sapiens appear in the fossil record in Africa and the
Mideast by about 90, 000-110, 000 years ago and behaviorally modern H. Sapiens are known in the fossil
record by ~50, 000 years ago in Australia and by about ~40, 000 yrs ago in Europe. The so called
"Agricultural Revolution" (primarily the domestication of animals, cereal grains and legumes) occurred first
in the Near East about 10, 000 years ago and spread to Northern Europe by about 5, 000 years ago (62). The
industrial revolution occurred roughly 200 years ago, and the technological revolution which brought us
packaged, processed foods is primarily a development that has occurred in past 100 years and has seen
enormous growth in the last 50 years.
To gauge how little geologic or evolutionary time humans have been exposed to foods wrought by the
agricultural revolution, let's do a little paper experiment. Take a stack of computer paper (the kind in which
each page is connected to one another) and count out 212, eleven inch pages. Then unravel the stack of paper
and lay it out end to end - it will form a continuous 194 ft strip. Now, let's assume that 1 inch equals 1, 000
years in our 194 foot strip of computer paper; thus, the first part of the first page represents the emergence of
our genus 2.33 MYA and the last part of the last page represents the present day. Now, take a slow walk
down all 194 ft of the computer paper, and carefully look at each of the individual eleven inch sections.
When you get to the very last eleven inch section (the 212th section), this represents the beginning of
agriculture in the Mideast, 10, 000 years ago; therefore, during the preceding 211 sheets humanity's foods
were derived from wild plants and animals. This little experiment will allow you to fully grasp how recent in
the human evolutionary experience are cereal grains, dairy products, salt and the fatty meats of domesticated
animals.
246/298 (1997)
Humans may have indeed eaten these foods for "millennia", but millennia (even 10 millennia) in the overall
time frame of human existence represents 0.4%. Because the estimated amount of genetic change (0.005%)
which has occurred in the human genome over this time period is negligible, the genetic makeup of modern
man has remained essentially unchanged from that of pre-agricultural man (63). Consequently, the human
genome is ideally adapted to those foods which were available to pre-agricultural man, namely lean muscle
meats, limited fatty organ meats, and wild fruits and vegetables. High levels of saturated fat consumption on
a year round basis only became possible when domesticated animals were bred and fed in a manner which
allowed accumulation of depot fat on a year round basis. Wild animals almost always show a seasonal
variation in storage fat, and even the very fattest wild land mammals contain 60-75% less total fat than the
average domesticated animal. Thus, until the advent of the "Agricultural Revolution", it would have been
extremely difficult, or perhaps impossible, to eat high levels of saturated fat on a daily basis throughout the
year. Milk and dairy products are without question a recent addition to the human diet, and as evidenced by
lactose intolerance in virtually all of the world's peoples except Northern Europeans, represent a food which
are not part of the natural human dietary repertoire. Sodium is found in low concentrations throughout the
terrestrial environment, whereas potassium is quite common. Consequently, the vertebrate kidney (including
primates) has been shaped by evolution to conserve sodium and excrete potassium (64). Unless, sodium salts
are actively mined, or collected and added to foods, it is virtually impossible to consume more than about 2,
000mg of sodium per day from wild game meats, and undomesticated fruits and vegetables. The highest
concentration of sodium from naturally occurring foods is from the tissues (meat) of animals. Assuming one
ate 7.8lbs of buffalo meat in a day (this represents 4, 662 kcal), the total amount of ingested sodium would be
2, 016 mg, whereas the potassium intake would be 11, 172 mg. Thus the highest Na:K ratio one could ever
obtain on naturally occurring wild foods would be about 1: 5. In the western diet, this ratio has been almost
entirely reversed and now is 5:1 and easily can approach 10:1 when salt laden "traditional foods" that
humans have eaten for "millennia" such as feta cheese, olives, sausages, salted meat and salted fish are
included in the diet. Consequently, even traditional foods which have been available for millennia, may in
fact, represent relatively new foods to the human dietary experience, and as such they are discordant with our
optimal dietary needs as determined over eons of evolutionary experience.
Cordially,
Professor, Dept. of ESS
Colorado State University
Fort Collins CO, 80523
(970) 491-7436
FAX (970) 491-0445
REFERENCES
1. Willett WC et al. Trans fatty acids: are the effects only marginal. Am J Public Health 1994;84: 722-24.
2. Ascherio A et al. Health effects of trans fatty acids. Am J Clin Nutr 1997;66:1006s-10s.
3. Yudkin J. Sucrose and cardiovascular disease. Proc Nutr Soc 1972;31:331-37.
4. Hollenbeck CB et al. Effects of sucrose on carbohydrate and lipid metabolism in NIDDM patients.
Diabetes Care 1989;12:62-66.
5. Louheranta AM et al. Linoleic acid intake and susceptibility of very low density and low density
lipoproteins to oxidation in men. Am J Clin Nutr 1996;63:698-703.
6. Kalopissis, AD et al. Inhibition of hepatic very low density lipoprotein secretion on obese Zucker rats
adapted to a high protein diet. Metabolism 1995;44:19-29.
7. Howell WH et al. Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta analysis.
Am J Clin Nutr 1997;65:1747-64.
8. Dietschy JM. Theoretical considerations of what regulates low density lipoprotein and high density
lipoprotein cholesterol. Am J Clin Nutr 1997;65:1581S-9S.
9. Stamler J et al. Is relationship between serum cholesterol and risk of premature death from coronary heart
disease continuous and graded? JAMA 1986;256:2823-28.
10. Vega GL et al. Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary
heart disease. Curr Opin Lipidology 1996;7:209-16.
11. Mensink RP et al. Effect of dietary cis and trans fatty acids on serum lipoprotein (a) levels in humans. J
Lipid Res 1992;33:1493-1501. patients with noninsulin dependent diabetes mellitus. J Clin Endocrinol
Metab 1993;76:347-51.
12. Speth JD. Early hominid hunting and scavenging: the role of meat as an energy source. J Hum Evolution
1989;18:329-43.
247/298 (1997)
13. Wolfe BM et al. Short term effects of substituting protein for carbohydrate in the diets of moderately
hypercholesterolemic human subjects. Metabolism 1991;40:338-43.
14. Wolfe BM et al. High protein diet complements resin therapy of familial hypercholesterolemia. Clin
Invest Med 1992;15:349-59.
Cardiol 1995;11 (supp G):127G-31G.
16. Westphal SA et al. Metabolic response to glucose ingested with various amounts of protein. Am J Clin
Nutr 1990;52:267-72.
17. Bang HO, Dyerberg J. Lipid metabolism and ischemic heart disease in Greenland Eskimos. Adv Nutr
Res 1980;3:1-22.
18. Harris WS. n-3 Fatty acids and serum lipoproteins: human studies. Am J Clin Nutr 1997;65:1645s-54s.
19. Gardner CD et al. Monounsaturated versus polyunsaturated dietary fat and serum lipids. A meta analysis.
Arterioscler Thromb Vasc Biol 1995;15:1917-27.
20. Phinney SD et al. The human metabolic response to chronic ketosis without caloric restriction: physical
and biochemical adaptation. Metabolism 1983;32:757-68.
21. Gray CG et al. The effect of a three week adaptation to a low carbohydrate/ high fat diet on metabolism
and cognitive performance. Naval Research Center Report No. 90-20. Naval Health Research Center, San
Diego CA.
22. Jeppesen J et al. Effects of low fat, high carbohydrate diets on risk factors for ischemic heart disease in
postmenopausal women. Am J Clin Nutr 1997;65:1027-33.
23. Coulston AM et al. Plasma glucose, insulin and lipid responses to high carbohydrate, low fat diets in
normal humans. Metabolism 1983;32:52-56.
24. Collier GR et al. The acute effect of fat on insulin secretion. J Clin Endocrinol Metab 1988;66:323-26.
25. Crawford MA et al. Linoleic acid and linolenic acid elongation products in muscle tissue of syncerus
caffer and other ruminant species. Biochem J 1969;115:25-27.
26. Artaud-Wild S et al. Differences in coronary mortality can be explained by differences in cholesterol and
saturated fat intake in 40 countries but not in France and Finland. Circulation 1993;88:2771-79.
27. Renaud S et al. Dietary lipids and their relation to ischaemic heart disease: from epidemiology to
prevention. J Int Med 1989;225 (supp 1):39-46.
28. Varo P. Mineral element balance and coronary heart disease. Int J Vit Nutr Res 1974;44:267-73.
29. Evans GH et al. Association of magnesium deficiency with the blood pressure lowering effects of
calcium. J Hypertension 1990;8:327-337.
30. Rasmussen HS et al. Influence of magnesium substitution therapy on blood lipid composition in patients
with ischemic heart disease. Arch Int Med 1989;149:1050-53.
31. Horner SM et al. Efficacy of intravenous magnesium in acute myocardial infarction in reducing
arrhythmias and mortality. Meta analysis of magnesium in acute myocardial infarction. Circulation
1992;86:774-79.
32. Guex E. et al. Oxidative modification of triglyceride rich lipoprotein in hypertriglyceridemic rats
following magnesium deficiency. Lipids 1993;28:573-75.
33. Nadler JL et al. Magnesium deficiency produces insulin resistance and increased thromboxane synthesis.
Hypertension 1993;21:1024-29.
34. Segall JJ. Dietary lactose as a possible risk factor for ischeemic heart disease: review of epidemiology.
Int J Cardiol 1994;46:197-207.
35. Fields M et al. Copper deficiency in rats: the effect of type of dietary protein. J Am Coll Nutr
1993;12:303-06.
36. Lynch SM, Strain JJ. Effects of copper deficiency on hepatic and cardiac antioxidant enzyme activities in
lactose and sucrose fed rats. Brit J Nutr 1989;61:345-54.
37. Deeth HC. Homogenized milk and atherosclerotic disease: A review. J. Dairy Sci 1983;66:1419-35.
38. Muscari A et al. Association of serum IgA antibodies to milk antigens with severe atherosclerosis.
Atherosclerosis 1989;77:251-56.
39. Napoli C et al. Human low density lipoproteins are peroxidized by free radicals via chain reactions
triggered by the superoxide radical. Cardiologica 1991;36:527-32.
40. Munro JM et al. An immunolohistochemical analysis of human aortic fatty streaks. Hum Pathol
1987;18:375-80.
41. Bruder G. et al. High concentrations of antibodies to xanthine oxidase in human and animal sera. J Clin
Invest. 1984;74:783-94.
248/298 (1997)
42. Muscari A et al. Association of serum IgA antibodies to milk antigens with severe atherosclerosis.
Atherosclerosis 1989;77:251-56.
43. Davies DF et al. Antibodies to reconstituted dried cow's milk protein in coronary heart disease. J
Atherocler Res 1969;9:103-07.
44. Mann GV et al. Atherosclerosis in the Masai. Am J Epidemiology 1972;95:26-37.
45. Resnick LM et al. Intracellular ionic consequences of dietary salt loading in essential hypertension. J Clin
Invest 1994;94:1269-76.
46. DeWardener HE et al. Dahl's hypothesis that a saluretic substance may be responsible for a sustained rise
in arterial pressure: its possible role in essential hypertension. Kidney Int 1980;18:1-9.
47. Carey OJ. Effect of alterations of dietary sodium on the severity of asthma in men. Thorax 1993;48:71418.
48. Nordin BEC et al. The nature and significance of the relationship between urinary sodium and urinary
calcium in women. J Nutr 1993;123:1615-22.
49. Matkovic V et al. Urinary calcium, sodium and bone mass of young females. Am J Clin Nutr
1995;62:417-25.
50. Devine A et al. A longitudinal study of the effect of sodium and calcium intakes on regional bone density
in postmenopausal women. Am J Clin Nutr 1995;62:740-5.
51. Cappuccio FP. Dietary prevention of osteoporosis: are we ignoring the evidence? Am J Clin Nutr
1996;63:787-8.
52. Massel LK, Whiting SJ. Dietary salt, urinary calcium and kidney stone risk. Nutrition Reviews
1995;53:131-9.
53. Joossens JV et al. Nutrition and gastric cancer. Proc Nutr Soc 1981;40:37-46.
54. Proctor CA et al. Etiology and treatment of fluid retention (Hydrops) in Meniere's syndrome. Ear, Nose
and Throat Journal 1992;71:631-35.
55. Miller MM. Low sodium chloride intake in the treatment of insomnia and tension states. J Am Med
Assoc 1945;129:262-66.
56. Lindseth G et al. The relationship of diet to airsickness. Aviation, Space and Environ Med 1995;66:53741.
57. Jansson B. Geographic cancer risk and intracellular potassium/sodium ratios. Cancer Detection and
Prevention 1986;9:171-94.
58. Cone CD. Unified theory on the basic mechanism of normal mitotic control and oncogenesis. J Theor.
Biol 1971;30:151-81.
59. Kimbel WH et al. Late pliocene Homo and oldowan tools from the Hadar formation (Kada Hadar
Member), Ethiopia. J Hum Evol 1996;31:549-61.
60. Larick R, Ciochon RL. The African emergence and early dispersals of the genus Homo. Am Scientist
1996;84:538-51.
61. De Castro JMB et al. A hominid from the lower pleistocene of Atapuerca, Spain: possible ancestor to
neandertals and modern humans. Science 1997;276:1392-95.
62. Cavalli-Sforza LL et al. Demic expansions and human evolution. Science 1993;259:639-46.
63. Eaton SB et al. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med
1985;312:283-89.
64. Meneely GR et al. High sodium-low potassium environment and hypertension. Am J Cardiol
1976;38:768-85.
PALEODIET Archives
Subject: eicosanoids and insulin
From: Ron Hoggan
Reply-To:
Date: Fri, 10 Oct 1997 17:47:05 -0600
Hi Aaron, I located the one below, on my hard drive, within 2 minutes of reading your post (I get the digest).
If I felt the need, I'm pretty sure I could find a few more.
While I don't yet know enough about this topic to comment in depth, I think there is rather a lot of data
supporting Sears' assertions.
Sincerely, Ron Hoggan
249/298 (1997)
Green IC, 1988 "Opiate-prostaglandin interactions in the regulation of insulin secretion from rat islets of
Langerhans in vitro." Life Sci 42(21), 2123-2130
PALEODIET Archives
Subject: Abstinence from Alcohol
From: Robert Rosenstein
Reply-To:
Date: Sat, 11 Oct 1997 18:43:46 -0500
In Loren Cordain's posting of Oct. 7/9, he notes:
"Low HDL cholesterol levels are strongly associated with coronary heart disease, and many factors that
produce lower HDL cholesterol levels increase the risk of coronary heart disease; examples are smoking,
obesity, lack of physical activity, abstinence from alcohol and low levels of dietary ascorbate."
I don't understand the "abstinence from alcohol". Have I and our Paleo ancestors been missing out on
something - or have I misread this?
If Dr. Cordain will site suitable references, I will most certainly change the liquid part of my diet :-) .
robert
PALEODIET Archives
Subject: Re: Alcohol and Coronary Heart Disease.
From: Loren Cordain
Reply-To:
Date: Mon, 13 Oct 1997 10:41:00 -0600
In my last post, I mentioned that abstinence from alcohol consumption is known to characteristically reduce
HDL in population surveys (1, 2). Further, experimental studies have shown that moderate alcohol
consumption elevates HDL cholesterol (3, 4, 5). Because of this effect and others, moderate alcohol
consumers have a lower mortality rate from CHD than do tee totalers (6, 7). Work from our research group
(8) suggests that moderate alcohol consumption may improve a wide variety of CHD risk factors via its
known ability to improve insulin sensitivity (9, 10). Clearly, it would have been difficult or impossible for
pre-agricultural man to produce ethanol, and the first evidence for regular production of fermented drinks
comes much after the agricultural revolution of 10, 000 yrs ago. Therefore, it is apparent that ethanol was not
a part of the human dietary experience from an evolutionary perspective, and in the backdrop of a preagrarian diet is without a doubt harmful when consumed in other than moderate quantities. The question may
then be posed, "Why do moderate consumers of ethanol in the western world have a reduced mortality from
all causes combined from a substance which is foreign to the human evolutionary experience?". It is likely
that the backdrop of the average western diet (high in refined CHO, saturated fat, salt, trans fats, N6 fatty
acids, low in fiber, low in phytochemicals, low in antioxidant vitamins, low in protein etc) alters our
physiologies in such a way (primarily via Syndrome X: hyperinsulinemia, hypertension, dyslipidemia etc)
that moderate alcohol consumption may reverse some of these symptoms of Syndrome X as well as other
deleterious physiological changes wrought via western diets (11). I am not advocating moderate ethanol
consumption as part of an optimal modern re-creation of a stone age diet. There are more healthful ways to
ameliorate symptoms of Syndrome X (see my previous post) that have none of the nutritional and
physiological problems associated with elevated levels of alcohol consumption.
Cordially,
Loren Cordain, Ph.D. Professor, ESS Dept Colo State Univ Fort Collins CO 80523 (970) 491-7436
REFERENCES
250/298 (1997)
1. Suh I et al. Alcohol use and mortality form coronary heart disease: the role of high density lipoprotein
cholesterol. Ann Int Med 1992;116:881-887. 2. Razay G et al. Alcohol consumption and its relation to
cardiovascular risk factors in British women. Brit Med J 1992;304:80-83. 3. Haskell WL et al. The effect of
cessation and resumption of moderate alcohol intake on serum high density lipoprotein subfractions N Engl J
Med 1984;310:805-10. 4. Handa K et al. Alcohol consumption, serum lipids and severity of angiographically
determined coronary artery disease. Am J Cardiol 1990;65:287-89. 5. Amarasuriya RN et al. Ethanol
stimulates apoprotein A-I secretion by human hepatocytes: implications for a mechanism for atherosclerosis
protection. Metabolism 1992;41:827-32. 6. Fuchs CS et al. Alcohol consumption and mmortality among
women. N Engl J Med 1995;332:1245-50. 7. Klatsky Al et al. Alcohol and mortality. Ann Int Med
1992;117:646-564. 8. Cordain L et al. Influence of moderate daily wine consumption on body weight
regulation and metabolism in healthy free living males. J Am Coll Nutr 1997;16:134-39. 9. Kiechl S et al.
Insulin sensitivity and regular alcohol consumption: large, prospective, cross sectional population study
(Bruneck study). Brit Med J 1996;313:1040-4. 10. Facchini F et al. Light to moderate alcohol intake is
associated with enhanced insulin sensitivity. Diabetes Care 1994;17:115-119. 11. Bisson LF et al. The role of
moderate ethanol consumption in health and human nutrition. Am J Enol Vitic 1995;46:449-62.
PALEODIET Archives
Subject: Sucrose and CHD
Reply-To:
Date: Mon, 13 Oct 1997 11:27:10 +0700
Dear Everyone,
I thought Loren's reply to Enig and Fallon was very balanced.
I would like to comment on one issue, however, that of sucrose and CHD. Loren cites John Yudkin but I
should tell you that most nutrition experts dismiss any causative relationship between sucrose and CHD.
Yudkin omitted data so that the correlation looked fine. Most of the data that makes sucrose look bad has
been done in animals fed impossibly high levels of sucrose (something like > 80% energy) which doesn't
relate the levels that human eat ad libitum (total sugars 10-20%).
Sucrose would have been one of one of the major sources of energy in primate diets coming from the fruits
and berries in roughly equal proportions with glucose and fructose. Thus high levels of sugars have been in a
diet since the beginning of evolution of humans. Even though sucrose is the starting product in many sweet
foods, by the time we eat it it has been hydrolysed to glucose and fructose (bt heat, acid, time).
While high insulin responses may indeed be detrimental, sucrose and most sugary foods, elicit lower glucose
and insulin responses than modern starchy foods, like bread (1, 2).
I think humans have evolved an instinctual desire for sweet things because glucose is the obligatory fuel for
the brain and foetus. We can't make enough via gluconeogenesis alone. Honey was highly prized in
paleolithic diets, way out of proportion to the amounts of energy it might supply. Furthermore, the amounts
eaten might have rivalled that eaten as sucrose today (3).
My main message here is that sugar is not the villain people might imagine, but quickly digested starch could
be (4-8).
Best wishes Jennie
(1) BRAND MILLER J, Pang E, Broomhead L. The glycemic index of foods containing sugars: comparison
of foods with naturally occurring versus added sugars. Brit J Nutr 1995; 73: 613-623.
(2) Wolever TMS, BRAND MILLLER J. Sugar and blood glucose control. Am J Clin Nutr,
1995;62(suppl):212S-27S.
(3) Allsop K, BRAND MILLER JC. Honey revisited: a reappraisal of honey in pre-industrial diets. Br J
Nutr; 75: 513-20.
(4) BRAND MILLER J, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of noninsulin dependent diabetes. Diabetologia 1994; 37: 1280-86.
(5) Byrnes S Denyer G, BRAND MILLER J, Storlein L. The effect of amylose vs amylopectin feeding on
development of insulin resistance in rats. J. Nutr 1995; 125: 1430-7.6
(6) Wiseman, CE, Higgins JA, Denyer GS, BRAND MILLER JC. Amylopectin starch induces nonreversible
insulin resistance in rats. J Nutr 1996, 126;410-5.
251/298 (1997)
(7) Higgins JA, BRAND MILLER JC, Denyer GS. Development of insulin resistance in the rat is dependent
on the rate of glucose absorption from the diet. J Nutr 1996;126: 596-602.
(8) BRAND MILLER JC, Foster-Powell K, Colagiuri S. The G.I. Factor. Sydney: Hodder Headline, 1996.
PALEODIET Archives
From: Melissa Darby
Reply-To:
Date: Mon, 13 Oct 1997 22:30:10 -0700
> Date: Monday Oct 12 10:21 pm
> From: Melissa Darby
> Subject: Abstract of thesis on Wapato
Greetings; I have had several requests for more information about my thesis re WAPATO, Sagittaria
latifolia. Below is the abstract.
ABSTRACT
An abstract of the thesis of Melissa Cole Darby for Master of Arts in Anthropology presented May 28, 1996.
Portland State University, Portland Oregon, USA Title: WAPATO FOR THE PEOPLE: An ecological
approach to understanding the Native American use of Sagittaria latifolia on the Lower Columbia River.
Sagittaria latifolia Willd. was an important root food and trade commodity for the Indians who lived along
the Lower Columbia River in early historic times. This plant was prolific in the extensive wetlands of the
Lower Columbia from about the great Cascades to the Kalama River. The tubers of this plant were called
'wapato' in Chinook Jargon, the local trade language. The wetlands, and this plant that grew there, occupied a
vast extent of the Lower Columbia territory; so much so that this valley was named 'WapatoValley' by Lewis
and Clark in 1805. This thesis will provide pertinent information on botanical characteristics, habitat,
productivity, and traditional harvesting and preparation techniques of this species. Nutritional analyses show
that wapato could have provided meaningful quantities of energy (carbohydrates), fiber, and trace elements.
Ecological data pertaining to this species, and ethnographic and archaeological data from North America and
especially the Lower Columbia, are used to address the following research question: Was wapato intensively
exploited by the Indians of the Greater Lower Columbia River (Hajda 1984) in early historic times? A test of
root food intensification using ecological and ethnohistoric data demonstrated: 1) that wapato was a cost
effective food to harvest; 2) that the annual productivity of this root food in Wapato Valley could have fed a
larger population than was estimated to exist in the valley at contact; 3) that root food intensification may not
always be indicated by the presence of large earth ovens and ground stone tools. In this study I conclude that
wapato was sufficiently productive and predictable to be intensively exploited and to function as a staple
food resource. This assessment illustrates the need to reconsider some commonly accepted ideas about the
intensification of root foods and the archaeological characteristics of root processing sites.
Thesis is available for $25, payable to Melissa Darby 3327 NE Simpson Portland Oregon 97211. Or free as a
zip file (does not include some photographs and charts).
I am writing an article about the post-glacial distribution of Sagittaria latifolia in North America and the
implications of this with regards to the diet of late Pleistocene, early Holocene hunter-gatherers.
If anyone has pollen data or has found macro remains I would be interested in hearing from you.
PALEODIET Archives
Subject: Re: Loren Cordain's response to Enig and Fallon
From: David Ross
Reply-To:
Date: Wed, 15 Oct 1997 10:40:33 -0400
> I agree that the oxidized cholesterol in powdered milk, eggs and aged cheeses is a powerful
> promoter of atherogenesis. I assume that oxidized cholesterol is present in cooked eggs, not raw
252/298 (1997)
> eggs.Could you please clarify that for me. More generally, could you comment on the use of raw
> eggs in the paleo-diet and perhaps the effects of eggs from free-roaming, organically fed chickens
> in the modern diet. However, as has been pointed out previously by Staffan Lindeberg, some of the
> highest dietary correlates to CHD in world wide epidemiological studies come from consumption of
> milk and dairy products (26, 27). Milk and dairy products are thought to produce their atherogenic
> effects through a variety of mechanisms. The most obvious is their high saturated fat content. In
> addition to high levels of saturated fats, the Ca:Mg ratio of milk is about 12:1. Numerous
> epidemiological studies have shown dietary lactose (the disaccharide in milk) to be a prominent
> risk factor for CHD (34). Milk also contains significant quantities of xanthine oxidase(37) which
> has been shown to enter the circulation.
Do these remarks about dairy apply to goat milk and its derivatives? Do you know of any epidemiological
data from populations who make significant use of goat/sheep/mare milk rather than cow milk?
Loren, thank you very much for your contributions to this list.
David
PALEODIET Archives
Subject: Re: Answers to David Ross
From: Loren Cordain
Reply-To:
Date: Wed, 15 Oct 1997 15:03:00 -0600
Oxidized fats, oils and cholesterol have been known to induce greater levels of atherogenesis in animal
models than their non-oxidized counterparts for at least 30 years (1, 2, 3). Heating of fats, oils and
cholesterol increases the number and amounts of lipid peroxide products, and these peroxides are thought to
be the main reason why oxidized lipids induce an elevated atherogenic response (3). When cholesterol
containing diets were fed to rabbits, fried or hard boiled eggs produced the highest serum cholesterol levels
(10-14 times greater than pre-experimental values), scrambled or baked eggs caused elevation of serum
cholesterol to 6 to 7 time the pre-experimental level. Raw or soft boiled eggs only increased serum
cholesterol levels 3 to 4 times the pre-experimental level (4). There is little doubt that pre-agricultural man
would have consumed wild bird eggs when they were seasonally available, and for most of man's history
they would have been consumed raw, because fire was not in use. However, as I have pointed out in a
previous post, regular consumption of raw eggs can induce a number of nutritional problems. One of the
functions of the egg white is to protect the entire egg from decomposition by bacterial contamination. Raw
egg white prevents bacterial contamination largely because of an iron binding lectin (glycoprotein), called
conalbumin (5). Additionally, raw egg white contains avidin, a substance which tightly binds certain B
vitamins including biotin. Biotin deficiencies are routinely induced in animal models via avidin feedings.
Therefore, regular consumption of high levels of raw eggs can potentially impair human nutrition. Because,
pre-agricultural man only consumed eggs on a seasonal basis, there would be no chronic health problems
associated with their sporadic consumption. I know of no epidemiological studies contrasting the effects of
goat vs. cow milk consumption upon human health. The percentage composition of major components in
goat's milk resembles that of cow's milk, although there tends to be more variability in the total amount of fat
and in the fatty acid profiles (6). Therefore, from a purely lipid/atherogenesis perspective, one would not
expect to find differences. I have never seen data on the Ca/Mg ratio for goats milk, and am therefore unable
to comment upon its potential for atherogenicity in this regard. The same can be said for its xanthine oxidase
levels, although because of its ubiquitous nature in mammals, I suspect that goat's milk also contains
significant amounts of this enzyme. Whether or not there is cross reactivity between goat and human
xanthine oxidase is not known. The only milk which humans have evolutionary experience in drinking is
mother's milk and this only for the 2-4yr period prior to weaning.
253/298 (1997)
REFERENCES 1. Taylor CB et al. Spontaneously occurring angiotoxic derivatives of cholesterol. Am J Clin

Nutr 1979;32:40-57. 2. Kummerow FA. Nutrition imbalance and angiotoxins as dietary risk factors in
coronary heart disease. Am J Clin Nutr 1979;32:58-83. 3. Kubow S. Lipid oxidation products in food and
atherogenesis. Nutr Rev 1993;51:33-40. 4. Pollak OJ. Serum cholesterol levels resulting from various egg
diets -- experimental studies with clinical implications. J Am Ger Soc 1958;6:614-18. 5. Alderton G et al.
Identification of the bacteria inhibiting, iron binding protein of egg white as conalbumin. Arch Biochem
1946;11:9-13. 6. Lawton R. Goat's milk. In: Health Hazards of Milk, DLJ Freed (Ed), Bailliere Tindal,
London, 1984, 150-56.
PALEODIET Archives
Subject: Cooking eggs
Reply-To:
Date: Fri, 17 Oct 1997 09:19:59 +0100
On Thu, 16 Oct 1997, Loren Cordain wrote:
> There is little doubt that pre-agricultural man would have consumed wild bird eggs when they were
> seasonally available, and for most of man's history they would have been consumed raw, because
> fire was not in use.
What is meant by "most of man's history"? If you mean the period of existence of anatomically modern
humans then there is good evidence for the use of fire for most of that 100, 000 year period. For example at
Kebara and Hayonim Caves, where in teh middle Palaeolithic levels "there are certain areas ... in which at
least 3m of ... [ash derived] sediments exist" and "it would take roughly tens of thousands of years for 1m or
so ... to accumulate" (Schiegl et al. 1996). If you wish to take the 2 million years or so of the genus Homo,
then there are fairly good claims for the use of fire for more than the lst quarter of that period, for example,
Schiegl et al. cite a number of studies in Africa, and there has been recent press publicity about a 400-500,
000 year old hearth at Beeches Pit in Suffolk, England (Daily Telegraph 12 August 1997, available online
via http://www.telegraph.co.uk/).
It seems to me that you cannot deny that fire has been available for a significant amount of evolutionary
time. Whether these early humans could cook eggs is another matter. Once they could boil eggs though I
have no doubt that this would be preferable: a boiled egg is a much easier thing to carry for sustenance on a
trip than a raw one!
Andrew
Reference
Schiegl, S, Goldberg, P, Bar-Yosef, O & Weiner, S (1996) Ash deposits in Hayonim and Kebara Caves,
Israel: Macroscopic, microscopic and mineralogical observations, and their archaeological implications.
Journal of Archaeological Science 23 763-781
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Fire & lactose
From: Loren Cordain
Reply-To:
Date: Fri, 17 Oct 1997 16:17:00 -0600
FIRE:
254/298 (1997)
It seems we have had numerous discussions in this group about the origins of fire with a multiplicity of
references. Since our genus Homo, now dates to ~2.33 MYA (1) and since everybody is pretty much in
agreement that the appearance of hearths signals the first regular, controlled use of fire, then regular cooking
probably did not occur until this event transpired. James, in his comprehensive review (2) indicates that no
structured hearths are found until the appearance of Neanderthals at the end of the middle pleistocene.
Therefore, for most (~90%) of the evolutionary history of our genus, cooking of food was rarely if ever done.
It seems likely that the earlier use of fire may have occurred by capturing and controlling natural fire,
however, it is doubtful that the ability to make fire occurred until much later. The antinutrients in raw egg
white still impair modern human nutrition, just like they did to our ancestors, and allergy to eggs remains one
of the most frequently occurring allergies (3). Clearly, we have had insufficient evolutionary experience as a
species to adapt resistance to the proteins in this food.
References
1. Kimbel WH et al. Late pliocene Homo and oldowan tools from the Hadar formation (Kada Hadar
Member), Ethiopia. J Hum Evol 1996;31:549-61. 2. James SR. Hominid use of fire in the lower and middle
pleistocene. Curr Anthropol 1989:30:1-26. 3. Noma T et al. Cytokine production in children outgrowing hen
egg allergy. Clin Exp Allergy 1996;26:1298-1307.
LACTOSE:
In response to Jennie's inquiry regarding lactose as an epidemiological risk factor for CHD, independent of
its saturated fat, I cite the following references (4, 5, 6, 7, 8, 9, 10). There are numerous animal experiments
to show that added lactose increases the severity of atherosclerosis in animal models (10, 11, 12, 13). As I
mentioned in my original post, the most likely explanation for lactose's atherogenicity is that high milk diets
induce copper deficiencies (15, 16) presumably via high levels of lactose (10, 14). Copper deficiencies in
turn reduce the levels of the bodies natural antioxidants such as the Cu-Zn form of superoxide dismutase (13,
14, 17). Lowered levels of endogenous antioxidants presumably increase the susceptibility of LDL to
oxidation and therefore increase the risk for CHD.
References
4. Segall JJ. Dietary lactose as a possible risk factor for ischaemic heart disease: review of epidemiology. Int
J Cardiol 1994;46:197-207. 5. Segall JJ. Lactose. In: Health Hazards of Milk. DLJ Freed (Ed.). Bailliere
Tindall, London, 1984, 229-39. 6. Segall JJ. Hypothesis: is lactose a dietary risk factor for ischaemic heart
disease. Int J Epidemiol 1980;9:271-76. 7. Lember M et al. Lactose absorption and milk drinking habits in
Estonians with myocardial infarction. Brit Med J 1988;296:95-96. 8. Popham RE et al. Variation in mortality
from ischemic heart disease in relation to alcohol and milk consumption. Med Hypotheses 1983;12:321-29.
9. Pearce RJ. Correlation of coronary heart disease with milk consumption: is protein or some other factor
involved? Med Hypothesis 1984;14:259-63. 10. Strain JJ. Milk consumption, lactose and copper in the
aetiology of ischaemic heart disease. Med Hypotheses 1988;25:99-101. 11. Wells WW, Anderson SC. The
increased severity of atherosclerosis in rabbits on a lactose containing diet. J Nutr 1959;68:541-49. 12.
Wostmann B et al. Effect of dietary lactose at levels comparable to human consumption on cholesterol and
bile acid metabolism of conventional and germfree rats. J Nutr 1976;106:1782-90. 13. Carville DGM et al.
The effect of copper deficiency on blood antioxidant enzymes in rats fed sucrose or sucrose and lactose diets.
Nutr Rep Int 1989;39:25-33. 14. Lynch SM et al. Effects of copper deficiency on hepatic and cardiac
antioxidant enxyme activities in lactose and sucrose fed rats. Brit J Nutr 1989;61:345-54. 15. Stemmer KL et
al. Copper deficiency effects on the cardiovascular system and lipid metabolism in the rat; the role of dietary
proteins and excessive zinc. Ann Nutr Metab 1985;29:332-47. 16. Fields M et al. Copper deficiency in rats:
the effect of type of dietary protein. J Am Coll Nutr 1993;12:303-06. 17. Lynch SM et al. Effects of
skimmed milk powder, whey or casein on tissue trace element status and antioxidant enzyme activities in rats
fed control and copper deficient diets. Nut Res 1990;10:449-60.
Cordially,
Loren Cordain, Ph.D. Professor, Dept of ESS Colo State Univ, Ft Collins, CO 80523
PALEODIET Archives
Subject: Lactose and CHD
Reply-To:
Date: Fri, 17 Oct 1997 16:33:04 +0700
255/298 (1997)
Loren wrote:
Numerous epidemiological studies have shown dietary lactose (the disaccharide in milk) to be a prominent
risk factor for CHD (34).
This is new to me. What would be the mechanism? Could it not be that the saturated fat in dairy products is a
confounder in this association. It seems strange that the major source of carbohdyrate in human milk would
actually encourage a disease process.
Best wishes Jennie
PALEODIET Archives
Subject: Re: Lactose and CHD
From: Edward Campbell
Reply-To:
Date: Sat, 18 Oct 1997 01:06:42 -0400
Jennie Brand Miller,
According to research cited in the May '96 issue of Dr. Atkins' newsletter, the allergy that many people have
to milk comes not from lactose but from the antibody reaction to its proteins.
With regards to CHD, Atkins cites a theory in the literature concerning whether the the enzyme Xanthine
oxidase (XO), a potential source of free-radical activity that's found in high quantity in homogenized cow's
milk, causes heart attacks and heart related chest pain.
Homogenization makes XO invulnerable to digestive enzymes that otherwise would destroy it. Once
ingested, XO is carried by the lymph system to the arteries, where, according to the oxidation theory of
disease, it damages fatty acids, resulting in atherosclerotic lesions that eventually lead to heart attacks. In one
comparative measurement, people who had a heart attack possessed higher levels of the XO antibody than
did people who had not had a heart attack (Atherosclerosis, vol 77, pp 251-6, 1989).
For someone who has been a milk drinker, Atkins suggests prescription doses of folic acid (10-40 mg) and
the bioflavonoids like quercetin. The nutrients have been shown in several studies to inhibit XO (Jour of
Nutr Sci and Vitaminology, vol 32, pp 635-42, 1986; Jour of Biological Chemistry, vol 261, pp 11, 242-6,
1986).
Atkins concludes that milk consumption, particularly pasteurized and homogenized, should not be a part of
any human's diet after infancy.
Ed Campbell, DC, CSCS
PALEODIET Archives
Subject: Use of fire by modern man
From: Dick
Reply-To:
Date: Sat, 18 Oct 1997 12:21:20 +0000
Andrew Millard said:
> Subject: Cooking eggs
> On Thu, 16 Oct 1997, Loren Cordain wrote:
> There is little doubt that pre-agricultural man would have consumed wild
> bird eggs when they were seasonally available, and for most of man's
> history they would have been consumed raw, because fire was not in use.
> What is meant by "most of man's history"? If you mean the period of
> existence of anatomically modern humans then there is good evidence for
> the use of fire for most of that 100, 000 year period.
> It seems to me that you cannot deny that fire has been available for a
> significant amount of evolutionary time.
256/298 (1997)
But if this was the period of the existence of modern man, anatomically like us, what is the evidence for
much evolution during this period? This is surely rather a period of _non-evolutionary_ time, during which
the ability to digect has not altered very much? If people could or could not eat certain foods to advantage
then, what is the evidence this has changed since 100 000 BP?
Dick Bird School of Behavioural and Environmental Sciences University of Norhtumbria UK NE1 8ST
PALEODIET Archives
Subject: Alcohol
From: Dean Esmay
Reply-To:
Date: Tue, 21 Oct 1997 13:32:30 -0400
Loren wrote me this note last week but due to the birth of my son I am only now getting caught up with old
mail. Loren suggested that if I found this sufficiently interesting I could repost it to the list. I do, so I have.
---begin letter from Loren--Dean,
In order for pre-agricultural man to make ethanol, he had to have had a water tight container, yeast and a
very large source of concentrated carbohydrate whose food calories could be "wasted" to produce an ethanol
containing drink. Although these requirements could have easily been put together by post-agricultural man,
I maintain that it would have been difficult or impossible (particularly in higher latitudes) for pre-agricultural
man to produce ethanol, primarily because of the lack of a readily available carbohydrate source which could
be afforded to be "wasted". The first documented production of beer is known from a beer recipe written in
Sumerian on clay tablets from the 3rd millennium BC in Mesopotamia (1). Making ethanol from grain is
more difficult than making ethanol from fruits with high sugar content because the starch in the grain must
first be converted into sugars. Therefore, it could be assumed as Mavis Wood has suggested, that preagricultural man made ethanol containing drinks by fermenting fruits with high sugar contents. However,
there is scant information from either the fossil or written anthropological record to suggest that this was
done. In North America, no alcoholic beverages were made in pre-Columbian times North of Mexico (2). I
am unaware of any reports of hunter-gatherers consuming alcohol, and this consensus is similar to Boyd
Eaton's (3).
Cordially,
Loren Cordain, Ph.D. Professor, ESS Dept Colo State Univ
REFERENCES
1. Katz SH, Voigt MM. Bread and beer: the early use of cereals in the human diet. Expedition 1987;28:2334. 2. Braidwood, RJ et al. Did man once live by beer alone? American Anthropologist 1953;55:515-26. 3.
Eaton SB et al. The Paleolithic Prescription. Harper & Row, NY, 1989, p.45.
PALEODIET Archives
Subject: Early Human Adaptation in the Northern...
From: Dean Esmay
Reply-To:
Date: Tue, 21 Oct 1997 13:58:26 -0400
A note from another list member:
New books listed in `The Bookseller' this week include:
Stopp, Marianne P `Early human adaptation in the northern hemisphere and the implications of taphonomy',
136pp, BAR International Series, no 669, pbk, 32UKP, July 1997, ISBN 1 84058 001 1
PALEODIET Archives
Subject: Folic acid
257/298 (1997)
From: Jon Bayh

Reply-To:
Date: Tue, 21 Oct 1997 23:45:26 -0700
> From: Edward Campbell For someone who has been a milk drinker, Atkins suggests prescription
> doses of folic acid (10-40 mg)
I don't know if Atkins' recommendation is for short term use or long term use. If long term, this seems like
overkill, by quite a bit, and dangerous advice for some individuals. The RDA for folic acid is 200
micrograms for adults, 400 micrograms for pregnant women. The RDA, tenth edition, under folate, says:
Excessive Intakes and Toxicity
Folic acid and the anticonvulsant drug phenytoin inhibit the uptake of each other at the gut cell membrane
and possibly at the brain cell membrane (Charnarin, 1979; Colman and Herbert, 1979). Very large doses of
folic acid (100 or more times the RDA) may precipitate convulsions in persons whose epilepsy is in
continuous control by phenytoin (Colman and Herbert, 1979). In laboratory animals, very large doses of folic
acid given parenterally may precipitate in the kidneys, producing kidney damage and hypertrophy (Colman
and Herbert, 1979). No untoward effects have been reported in women given 10 mg/day of folic acid
continuously for 4 months (Butterworth et al., 1988). However, without evidence of benefit and with some
potential for toxicity, excessive intakes of supplemental folate are not recommended.
I'd be skeptical of a 4-month trial being very indicative of possible long term consequences, and kidney
damage isn't something to play with lightly.
Jon Bayh
PALEODIET Archives
Subject: Re: Alcohol
Reply-To:
Andrew Millard
Date: Wed, 22 Oct 1997 14:42:08 +0100
On Tue, 21 Oct 1997 Dean Esmay quoted Loren Cordain:
> The first documented production of beer is known from a beer recipe written in Sumerian on clay
> tablets from the 3rd millennium BC in Mesopotamia (1). 1. Katz SH, Voigt MM. Bread and beer: the
> early use of cereals in the human diet. Expedition 1987;28:23-34.
Whilst this is the earliest documentary record there is evidence to suggest brewing had been around for some
time. Alan Millard argues [1] that leavened bread was being produced in bevelled rimmed bowls from early
in the 4th millenium BC in the Uruk culture. Further he argues that given the mastery of yeast and the fact
that early beer was made with a mash similar to part risen bread, it is likely that they made beer as well. This
is supported by comparison of certain drinking vessels with the symbol for beer in Sumerian.
Loren's arguments for the need for containers and a warm climate still apply.
[1] Millard, AR (1988) "The bevelled rimmed bowls: their purpose and significance" Iraq 50 49-57
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Soluble fiber
Reply-To:
Date: Wed, 22 Oct 1997 17:26:16 PDT
258/298 (1997)
In his original (26 May) post with comments to Enig and Fallon regarding human consumption of saturated
fat and the relationship with CHD, Loren Cordain identified a number of factors in the presumed paleolithic
diet that would have been cardio-protective -- factors that are absent in the typical modern diet.
In his latest post (9 Oct), he elaborated on many of these factors, and mentioned one other, but only in
passing. So for the sake of completeness, I thought I would mention it: namely, the high level of SOLUBLE
FIBER in the paleo diet. Soluble fiber has been shown to modify cholesterol metabolism in ways that can
lower serum closterol levels (is its effect on LDL/HDL known?)
While oat bran was not available to our Paleo ancestors, they may well have consumed large amounts of
soluble fiber from fruits and veggies. The "typical" late Paleo diet constructed by Eaton et al. (1) based on
diets of modern HGers shows a daily fiber intake of ~150 g (compared to 20 g for US average), with much of
this coming from soluble fiber.
Among peoples with a higher share of animal food in their diet than in this typical diet, of course, the level of
soluble (and insoluble) fiber could be much lower. Which brings me to a question:
Given that levels of insoluble fiber (which promotes bowel transit time) would be rather low in the diets of
HGers relying heavily on animal foods (and here we could include Cro Magnon man), one wonders if they
had any troubles with constipation. Perhaps the lack of fiber was balanced by their high level of physical
activity? But what about in winter, when they are less active and plant foods are even less available?
Any thoughts/data on this?
(1) Eaton et al., The Paleolithic Prescription, 1988.
Steve Meyers Staff Scientist Lawrence Berkeley Lab. Berkeley, CA
PALEODIET Archives
Subject: Interesting study
From: Dean Esmay
Reply-To:
Date: Fri, 24 Oct 1997 03:51:29 -0400
Ed Campbell pointed this out to some of us in email recently and I pulled it out of Medline, thinking it may
be of some interest. I haven't read more than this abstract but it certainly is interesting.
Title
Food groups and risk of colorectal cancer in Italy.
Author
Franceschi S; Favero A; La Vecchia C; Negri E; Conti E; Montella M; Giacosa A; Nanni O; Decarli A
Address
Servizio di Epidemiologia, Centro di Riferimento Oncologico, Aviano (PN), Italy.
Source
Int J Cancer, 1997 Jul 3, 72:1, 56-61
Abstract
The proportion of colorectal cancer attributed to dietary habits is high, but several inconsistencies remain,
especially with respect to the influence of some food groups. To further elucidate the role of dietary habits, 1,
225 subjects with cancer of the colon, 728 with cancer of the rectum and 4, 154 controls, hospitalized with
acute non-neoplastic diseases, were interviewed between 1992 and 1996 in 6 different Italian areas. The
validated food-frequency questionnaire included 79 questions on food items and recipes, categorised into 16
food groups. After allowance for non-dietary confounding factors and total energy intake, significant trends
of increasing risk of colorectal cancer with increasing intake emerged for bread and cereal dishes (odds ratio
[OR] in highest vs. lowest quintile = 1.7), potatoes (OR = 1.2), cakes and desserts (OR = 1.1), and refined
sugar (OR = 1.4). Intakes of fish (OR = 0.7), raw and cooked vegetables (OR = 0.6 for both) and fruit other
than citrus fruit (OR = 0.7) showed a negative association with risk. Consumption of eggs and meat (white,
red or processed meats) seemed uninfluential. Most findings were similar for colon and rectum, but some
negative associations (i.e., coffee and tea, and fish) appeared stronger for colon cancer. Our findings lead us
to reconsider the role of starchy foods and refined sugar in light of recent knowledge on the digestive
physiology of carbohydrates and the insulin/colon cancer hypothesis. The beneficial role of most vegetables
is confirmed, with more than 20% reduction in risk of colorectal cancer from the addition of one daily
serving.
---Paleolithic Diet Symposium List
259/298 (1997)
Franceschi's group is the one that published a study last year finding a correlation between high starch intake
and breast cancer (see Franceschi S et. al. Intake of macronutrients and risk of breast cancer. Lancet;
347(9012):1351-6 1996)
PALEODIET Archives
Subject: Re: Response to alcohol, folic acid and soluble fiber
From: Loren Cordain
Reply-To:
Date: Fri, 24 Oct 1997 10:16:00 -0600
Andrew Millard points out that beer making may have been invented as early as the 4th millenium BC
because of the presence of beveled rimmed bowls. This is likely, and it wouldnt surprise me if evidence is
eventually found for beer brewing even earlier. There is evidence (McGovern PE, Fleming S, Katz S. The
origins and ancient history of wine. The Biblical Archaeology Review 1997;23:62-68) that wine making may
have occurred even earlier than beer brewing.
Jon Bayh argues that Atkins' recommendation of 10-40 mg folic acid is excessive. I would tend to agree
given that the RDA is 200-400 mcg. However, folic acid insufficiency/ deficiency is quite common in
industrialized countries (1) primarily because the best sources of folic acid are leafy green vegetables, organ
meats, fruits and other vegetables, and in most western countries fruits and leafy green vegetables are eaten
infrequently and in small quantity (2). Hunter-gatherers would have little trouble achieving dietary folate
levels of 400 mcg given their regular consumption of organ meats and fruits and vegetables. Low folate
levels are known to be involved in the etiology of neural tube defects (3), coronary artery disease via their
hyper-homocysteinemic effects (4) colon cancer (5) and cervical cancer (6). Primarily because of the neural
tube defect data, the U.S. government has now decided to fortify cereal grain with folate (7). Alcohol
consumption and oral contraceptives impair folate metabolism, and given the generally low level of folate
consumption in this country, supplementation would go a long way in preventing many health problems.
REFERENCES
1. Rosenberg IH. Folic acid and neural tube defects- time for action? N Engl J Med 1992;327:1875-77. 2.
Patterson BH et al. Fruit and vegetables in the american diet: data from the NHANES II survey. Am J Pub
Health 1990;80:1443-49. 3. Czeizel AE et al. Prevention of the first occurrence of neural tube defects by
periconceptual vitamin supplementation. N Engl J Med 1992;327:1832-5. 4. Graham IM et al. Plasma
homocysteine as a risk factor for vascular disease. JAMA 1997;277:1775-81. 5. Stampfer MJ et al.
Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer.
Cancer Research 1997;57:1098-102. 6. Butterworth CE et al. Folate deficiency and cervical dysplasia.
JAMA 1992;267:528-33. 6. Romano RS et al. Folic acid fortification of grain: an economic analysis. Am J
Pub Health 1995;85:667-676.
In regards to soluble fiber, there are numerous literature citations to show that it improves lipid profiles
primarily by lowering LDL cholesterol. Most trials show little or no improvement in HDL cholesterol,
however there is at least one recent study (1) showing a lowering of the LDL/HDL with psyllium fiber. Meat
contains significant amounts of non-digestible connective tissues and is therefore not devoid of fiber. High
meat diets have been shown to not decrease stool weight or fecal transit time and are therefore considered to
not cause constipation (2). I believe Ray Audette has previously commented upon this from his personal
experience with stone age diets.
REFERENCES
1. Jenkins DJA et al. Effect of pysllium in hypercholesterolemia at two monounsaturated fatty acid intakes.
Am J Clin Nutr 1997;65:1524-33. 2. Cummings JH et al. The effect of meat protein and dietary fiber on
colonic function and metabolism. Am J Clin Nutr 1979;32:2086-93.
Cordially,
PALEODIET Archives
Subject: Soluble Fiber
From: Rob't Beck
Reply-To:
260/298 (1997)
Date: Fri, 24 Oct 1997 13:19:41 -0400

Steve Meyers, of Lawrence Berkeley Laboratory questioned the degree of constipation experienced by HG's
that do not ingest copious quantities of soluble fiber.
Please excuse a certain lack of daintiness in what follows. There are probably more clinical terms to describe
the phenomena below, but they escape me....
In my experience, a diet consisting largely of animal-derived protein and fat causes the body to give up
water, so that the stool is quite loose and, judging by the amount of "floaters", highly hydrated. Bowel transit
time is very short - about 8 hours. This is consistent with the descriptions of the digestive process in "Protein
Power" by Eades, and "Neanderthin", by Audette. Neither of those books purports to be very scientific, but
there is a wealth of practical knowledge in them.
It is my understanding that soluble fiber functions largely by absorbing water from the gut -- That being the
case, and if my experience is typical, there is essentially no difference (vis-a-vis bowel function) between the
HG that eats soluble fiber and the one that eats only animal meat.
I would like to add a data point to the general paleo-diet discussion: Since eliminating milk and grain
products from my diet in January 1997, the following has happened --Weight down from 210 to 165 lb. (still losing, but slowly). -BP down from 165/110 to 125/75 (no more
debilitating medication!) -Total cholesterol down from 200+ to 180 -Ratio of HDL to Total Cholesterol
down from 7.9 to 3.9 -Triglycerides down significantly
The experiment continues.
Robert Beck
****************************************************
"...it is almost certain that someday they will collect our skulls and call us Early Man."
****************************************************
PALEODIET Archives
Subject: Fibre
Reply-To:
Date: Fri, 24 Oct 1997 16:31:38 +0700
Steve Meyers wrote:
> Given that levels of insoluble fiber (which promotes bowel transit time) would be rather low in
> the diets of HGers relying heavily on animal foods (and here we could include Cro Magnon man), one
> wonders if they had any troubles with constipation.
We have just completed a review of the nutritional composition of Australian Aboriginal plants foods in
which we generated an average figure for fibre per 100 g plant foods (Brand Miller and Holt. Nutritional
Research Reviews, in press). This figure turned out to be 11 11(SD) g fibre per 100g.
The data enable us to calculate the absolute contribution of plant foods to total food and nutrient intake of
traditional living AA. If plants provided 20-40% of the energy in the diet (the most likely range), then plants
would have contributed 22-44 g protein, 18-36 g fat, 101-202 g carbohydrate, 40-80 g fibre and 90-180 mg
vitamin C in a 12, 500 kJ (3000 Cal) diet.
Thus fibre intake would have been very high by our standards even when plant food intake was relatively
low.
Best wishes Jennie
PALEODIET Archives
Subject: Re: 'protein power'
From: Susanne Holt
Reply-To:
Date: Mon, 27 Oct 1997 11:46:54 +1100
261/298 (1997)
Robert Beck wrote:

> Since eliminating milk and grain products from my diet in January 1997, the following has happened
> -- -Weight down from 210 to 165 lb. (still losing, but slowly). -BP down from 165/110 to 125/75
> (no more debilitating medication!) -Total cholesterol down from 200+ to 180 -Triglycerides down
> significantly The experiment continues.
I am a nutrition research scientist and I would like to suggest that it is important to consider all the factors
responsible for these 'benefits' before ascribing them solely to the decreased carb and increased protein
contents of the new diet.
By adjusting one's diet to completely eliminate grain and dairy products, the following things may occur
which could also contribute to the beneficial effects: 1. a decrease in total fat and calorie intake; 2. a decrease
in saturated fat intake; 3. an increase in total fibre intake; 4. a decrease in the amount of rapidly-digested
carbohydrate consumed; and 5. a possible reduction in sodium intake.
In addition, other healthy lifestyle changes which often accompany committed dietary changes, -such as a
reduction in the amount of alcohol and caffeine consumed and an increase in daily exercise - could also
partly explain the beneficial effects.
Robert is to be congratulated for his commitment to improving his health by changing his dietary habits.
However, I just want to stress that change is often due to a number of factors and that not all grain products
are necessarily unhealthy. The apparent lack of degenerative diseases in paleoman and contemporary huntergatherers or third-world farmers consuming mostly traditional indigenous foods, is obviously due to their
high level of physical activity and the composition of their diet. Modern man does not generally expend as
much energy in daily life and may not require such high levels of protein. Controlled metabolic research has
shown that any excess protein consumed is oxidised by the body as a fuel (which pushes both carb and fat
into storage) since the body is unable to store excess protein.
Changing the types of carbohydrate-rich foods which form the basis of one's diet can also produce
substantial health benefits, it may not be necessary to eliminate all grain products from the diet. The health
benefits experienced by Robert are also similar to the benefits arising from low-fat diets based on low-GI
carb-rich foods (Triglycerides may show a transient increase in some people, secondary to an increased
consumption of carbs). The carb-containing foods consumed by hunter-gatherers and early agricultural
societies were most likely to be tubers and roots, legumes and coarsely ground cereal products - which have
a lower glycaemic impact than their modern counterparts. These traditional foods are also likely to be more
satiating and therefore they may not have been eaten in such large amounts. Dr Susanne Holt CSIRO Division of Human Nutrition PO Box 52 NORTH RYDE NSW 2113 AUSTRALIA
Ph (+61) 02 9490 8425 Fax (+61) 02 9887 8511 Email
PALEODIET Archives
Subject: Questions for Dr. Holt and Dr. Brand-Miller
From: Dean Esmay
Reply-To:
Date: Mon, 27 Oct 1997 17:51:19 -0500
For Dr. Holt:
Regarding the claim that "not all cereal grains are necessarily unhealthy" -- can Dr. Holt elaborate on which
ones she feels are not unhealthy, and what criteria she uses to reach this conclusion?
Also: Regarding the claim that health benefits of substantial weight loss (over 20% total body mass),
decreased triglycerides, and increased HDL cholesterol could be ascribed to a low-fat diet--what is this based
on? Every study I have seen on low-fat diets among westerners has shown a trend toward decreased HDL
cholesterol. Increases in triglycerides are also a common result. Furthermore, after more than a year of
reviewing research on low-fat diets, I have found not one study which boasts more than very small weight
loss benefits, usually on the order of a kilogram or two, awong obese subjects--and some studies show
substantial weight gain in some subjects using such diets. Lowered fat and lowered caloric intake over the
last decade in the United States have correlated with record increases in obesity and diabetes.
(These are issues we have discussed before, so I will offer peer-reviewed references upon request, assuming
everyone has seen them already. Just ask if you want them reposted, however.)
262/298 (1997)
Are there any studies which show substantial weight loss among the obese, increased HDL cholesterol, and
substantially lowered triglyceride from reducing fat intake? If so, where have they been published? I would
very much like to see them.
Similarly, to the claim that hunter/gatherers exercise significantly more than modern westerners: this seems
self-evident. But I'd like to know if research exists to closely compare the amount and type of exercise
experienced on a daily basis by hunter/gatherers as compared to, say, the average construction worker, police
officer, or office worker who exercises for one hour three times per week at a health club. How substantial is
the difference? And what evidence is there that exercise results in more than moderate weight loss among
most subjects?
Finally, to the claim that excess protein is oxidized by the body as fuel, "which pushes both carb and fat into
starage", can Dr. Holt elaborate? Is she suggesting that in two diets of, say, 2000 kCals daily, one of 15%
protein and the other of 30% protein, the latter will cause faster storage of fat than the former? Does protein
not have a lower glycemic index value than most forms of carbohydrate?
For Dr. Brand-Miller:
Regarding your message of last week, you stated that Yudkin omitted data to make a correlation between
sucrose and CHD appear to be there. Has this been documented anywhere?
Also, you stated that sucrose would have been one of the major sources of energy in primate diets, coming
from fruits and berries in roughly equal proportions with glucose and fructose (which would obviously
amount to about the same thing as sucrose). I don't dispute this, but would it also not be the case that sugars
consumed in nature would also be eaten with massive amounts of fibre, thus slowing down the absorption of
those sugars? Wild fruits and berries have a higher amount of fibre than most domesticated fruits, and are not
generally so sweet as their domesticated cousins. It should also be the case that, due to natural dry seasons,
droughts, and winters most pre-agricultural humans would probably go through semi-regular periods of
weeks or even months with only small amounts of such foods available, no?
And while I appreciate that sucrose itself has been shown to have a glycemic index no worse than that of
white bread, does this suggest that sucrose is harmless--or might it not just suggest that bread is not so
benign as it is often thought to be? Are there any wild fruits which have such a strong glycemic reaction?
Your own study on wild honey showed even that to have a lower glycemic response than pure sucrose, did it
not?
You also stated your that glucose is the obligatory fuel for the brain and fetus, and that we can't make enough
glucose via gluconeogenesis alone. But Cahill (Cahill, G. and Aoki, T.T., Medical Times 98, 1970) found
that the brain will utilize ketones preferentially to glucose, once a brief period of adjustment of 1-3 weeks is
made.
It is also well known that the Inuit eat almost no carbohydrate, and must therefore use gluconeogenesis and
ketones for most of their fuel needs. But certainly they manage to have children. There is also at least one
diabetologist who is a member of this symposium who has treated more than one pregnant diabetic with a
very-low-carbohydrate diet, and normal infants have (so far) been the norm for his patients. (Perhaps we can
get Dr. Bernstein to tell us more about his results with his patients, if he is reading still.)
It is frequently asserted that glucose is a necessary fuel but there is research suggesting that neither brain nor
muscle tissue requires it so much as is commonly believed. Not only did Cahill find that the brain will use
ketones preferentially to glucose, but recent research has also shown that athletes, particularly endurance
athletes, tend to show performance increases on very low carbohydrate, high protein, high fat diets, after a 13 week adaptation period (See European Journal of Applied Physiology and Occupational Physiology, vol.
69, no. 4, 287-93 1994. See also Journal of Applied Physiology, vol. 71, no. 1, p.197, 1991. See also Science
News, vol. 149, p. 287, 5/4/96. See also Townsand Letter for Doctors and Patients, June 1996. See also
Anabolic Research Review, vol. 1, no.2).
None of this is to suggest that a carbohydrate-free diet would be the ideal diet for any primate, including
homo sapiens sapiens. But it does suggest to me that the common assertion that high carbohydrate intake is
necessary to meet the human animal's fuel needs should be looked at with a more jaundiced eye.
PALEODIET Archives
Subject: Re: Protein Power
From: Loren Cordain
Reply-To:
Date: Tue, 28 Oct 1997 12:52:00 -0700
263/298 (1997)
I'd like to welcome Susanne Holt to our listserve group and appreciate the expertise she brings to us with her
studies and publications regarding satiety. I agree with her conclusions that modern "paleo diets" can elicit
body weight changes by many potential mechanisms. In regards to satiety, there is at least one report in the
literature to show that fish meals have a greater satiety value than either chicken or beef meals (1). I wonder
if game meat based meals would have an effect similar to fish. On an acute basis, high protein meals cause
an increase in circulating glucagon levels (2). Because elevated glucagon will stimulate hormone sensitive
lipase, high protein meals will cause an increased mobilization of fats, not an increased storage. It is possible
that this effect will influence satiety. Chronic administration of high protein diets (~60% energy) has been
shown to improve insulin sensitivity and result in weight loss in at least two studies (3, 4). In one of these
studies involving a 62% (of total energy) protein diet (3), the authors concluded, "three subjects could not eat
enough to maintain constant body weight". Presumably this weight loss occurred because of a reduction in
satiety elicited by the high protein diet. It is tempting to suggest that the loss in body weight in these two
dietary trials came about as a reduction in appetite by higher circulating glucagon levels, however this is not
known. There have been a number of clinical trials showing the efficacy of high protein, low calorie diets
upon body weight regulation (5, 6), but few involving ad libitum consumption of protein and fixed
consumption of fat and CHO. Consequently, the potential weight reduction benefits of high protein (low
carbohydrate, moderate to low fat) diets, similar to what humans evolved with are almost completely
unknown. It cannot be assumed that excessive protein will cause increased de novo lipogenesis, in fact the
contrary has been shown in animal models (7). Because of the metabolic changes which are known to occur
in animal models utilizing high protein diets (increased ureagenesis, and gluconeogenesis, decreased
lipogenesis and increased glucagon levels (8)), it is possible that similar effects could occur in humans and
which may have important modulating effects upon body weight regulation, independent of the simple in
vitro caloric considerations.
Cordially,
REFERENCES
1. Uhe AM, Collier GR, O'Dea K. A comparison of the effects of beef, chicken and fish protein on satiety
and amino acid profiles in lean male subjects. J Nutr 1992;122:467-72. 2. Westphal SA et al. Metabolic
response to glucose ingested with various amounts of protein. Am J Clin Nutr 1990;52:267-72. 3. O'Dea K et
al. The effects of diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II
diabetes. J Am Diet Assoc 1989;89:1076-86. 4. O'Dea, K. Marked improvement in carbohydrate and lipid
metabolism in diabetic Australian Aborigines after temporary reversion to a traditional lifestyle. Diabetes
1984;33:596-603. 5. Apfelbaum M. The effects of very restrictive high protein diets. Clin Endocrinol Metab
1976;5:417-30 6. Scheen AJ et al. Hormonal and metabolic adaptation to protein supplemented fasting in
obese subjects. Int J Obes 1982;6:165-174. 7. Katsurada A et al. Effects of dietary nutrients on substrate and
effector levels of lipogenic enzymes, and lipogenesis from tritiated water in rat liver. Biochim Biophys Acta
1986;878:200-208. 8. Kalopissis AD et al. Inhibition of hepatic very low density lipoprotein secretion in
obese Zucker rats adapted to a high protein diet. Metabolism 1995;44:19-29.
PALEODIET Archives
Subject: Question to Loren Cordain
From: David Ross
Reply-To:
Date: Wed, 29 Oct 1997 06:54:02 -0500
In a recent post to this list, Loren Cordain offered the following:
" I agree that the oxidized cholesterol in powdered milk, eggs and aged cheeses is a powerful promoter of
atherogenesis."
Loren, are you suggesting that the aging process itself leads to the oxidation of cholesterol in cheese (and, if I
might extend the point, in meat as well)? I have assumed that at least in raw cheese, oxidation would be an
insignificant factor.
david
264/298 (1997)
PALEODIET Archives
Subject: Re: Hunter-Gatherer Exercise Patterns
From: Loren Cordain
Reply-To:
Date: Wed, 29 Oct 1997 09:37:00 -0700
In the last paleodigest, Dean E, requested information about Hunter-Gatherer exercise patterns. I believe our
recent article (Cordain L, Gotshall RW, Eaton SB. Evolutionary aspects of exercise. World Rev Nutr Diet
1997;81:49-60) is one of the few treatises on the topic. Boyd Eaton, my co-author has written on the topic as
well (Eaton SB et al. The first fitness formula. In: The Paleolithic Prescription. New York, Harper & Row,
168-199). Enclosed is an abstract of our recent article. If any readers are interested, I can send you an e-mail
attachment of the full document if you specifically request it.
Cordially,
Abstract A wealth of scientific reports points to the inescapable conclusion that human fitness and health
improve when previously sedentary individuals begin to exercise. Despite the enormous literature describing
the frequency, intensity, duration and mode of exercise required to elicit both fitness and health effects, the
vast majority of this information deals with proximate mechanisms relating exercise to health and fitness. In
order to understand, ultimately, why a causal relationship exists between exercise and health and fitness, an
evolutionary perspective must be examined. Similar to all other organisms, humans have evolved species
specific exercise capacities, limitations and requirements in order to successfully compete in their
environmental niche. The environmental niche which humans have occupied since the first appearance of our
genus (Homo habilis) over 2 million years ago, until the agricultural revolution of 10, 000 years ago was that
of a hunter gatherer. Mitochondrial DNA evidence suggests that the modern human genome is almost
identical to that of paleolithic humans who lived 40, 000 years ago. Hence the exercise capacities and
requirements of modern humans remain similar to those which had been originally selected by evolution for
stone age humans living in a hunting and gathering environment. Hunter-gatherers have activity patterns
which have been described as regular, intermittent with days of intense physical activity alternating with
days of relative rest. Daily activities stress both aerobic and strength pathways and can include such activities
as walking, running, butchering, tool making, dancing, carrying objects, and shelter construction. Huntergatherer males typically expend between 19.6 to 24.7 kcal/kg/day in physical activity whereas the sedentary
office worker, even including a 3 mile walk, would still only expend 8.7 kcal/kg/day in physical activity. It is
this discordance between our genetically determined exercise requirements and those of modern, sedentary
societies which directly contributes to many of the chronic degenerative diseases which plague western,
civilized populations. For the hunter-gatherer, energy expenditure was directly linked to food procurement.
Because technological achievement and social organization have disrupted the evolutionary relationship
between food procurement and energy expenditure, contemporary man's biology has become so disordered
that physiological and biochemical risk factors affecting the cardiovascular system, the skeleton, and our
carbohydrate metabolism are now unprecedentedly common. In each case, departure from exercise patterns
which prevailed during evolution plays a fundamental role.
PALEODIET Archives
Subject: Re: Question for Loren Cordain
From: Loren Cordain
Reply-To:
Date: Wed, 29 Oct 1997 16:04:00 -0700
265/298 (1997)
David Ross wanted to know if the aging process used for many cheeses increased the quantity of oxidized
cholesterol within the cheese, and if "raw" cheese contained less oxidized cholesterol. As far as I know, there
never has been a quantitative study examining oxidized cholesterol in various cheeses. According to Taylor
et al. (1), "Some cheeses, particularly those exposed to air at room temperature for long periods during
processing and later stored at room temperature may also contain significant quantities of toxic cholesterol
derivatives". Based upon this data and other studies, I suspect that aged, dry cheeses, such as parmesan
would contain greater amounts of oxidized cholesterol, whereas cheeses which havent been aged would
probably have lesser amounts of oxidized cholesterol. Interestingly, Hindu immigrants from India have one
of the highest coronary disease mortality rates in the world, and it has been theorized that this may be due in
part to the high consumption of ghee, a clarified butter product which is high in cholesterol oxides (2). Dairy
products were obviously not part of the human evolutionary dietary experience and whether they are taken as
milk, cheese, low fat yogurt, butter, ghee, ice cream, powdered skim milk or what have you, they can
potentially disrupt health from many different mechanisms. I have written extensively on the health problems
associated with dairy foods in a past paledigest posting to Mary Enig and Sally Fallon. You may also want to
try to obtain a book written by a deceased acquaintance, Frank Oski (Past president of the American
Academy of Pediatrics and Endowed Chair at Johns Hopkins Univ), who brilliantly outlines many of the
health/nutritional problems associated with dairy product consumption (3).
Cordially,
REFERENCES
1. Taylor CB et al. Spontaneously occurring angiotoxic derivatives of cholesterol. Am J Clin Nutr
1979;32:40-57. 2. Jacobson MS. Cholesterol oxides in Indian ghee: possible cause of unexplained high risk
of atherosclerosis in Indian immigrant populations. Lancet 1987;ii:656-58. 3. Oski FA. Dont drink your milk.
Syracuse, N.Y., Mollica Press, Ltd., 1983.
REFERENCES
1.
PALEODIET Archives
Subject: Protein Power
From: Rob't Beck
Reply-To:
Date: Thu, 30 Oct 1997 06:51:13 -0500
Dr. Susanne Holt wrote that my health improvements may be due to other than the elimination of grains &
dairy products from my diet:
> By adjusting one's diet to completely eliminate grain and dairy products, the following things may
> occur which could also contribute to the beneficial effects: 1. a decrease in total fat and
> calorie intake; 2. a decrease in saturated fat intake; 3. an increase in total fibre intake; 4. a
> decrease in the amount of rapidly-digested carbohydrate consumed; and 5. a possible reduction in
> sodium intake.
To my best estimate, total fat and saturated fat probably remained fairly constant. Total caloric intake was
lower. Total fiber intake decreased markedly, (along with digestive & bowel problems (heartburn, gas,
bleeding, general discomfort)). Rapidly-digested CHO was eliminated, while sodium may have increased
due to large amounts of meat ingested (I use KCl instead of NaCl at table). CHO in my diet came largely
from green & leafy vegetables and, sparingly, from fruits
Exercise was not so much increased as shifted from entirely aerobic to a mix of strength and aerobic training.
Exercise levels are low to moderate.
Just for the record, I am 57 years old, 69" tall, and presently weigh 160 lbs. My Total Cholesterol to HDL
ratio is 3.9 (not the inverse ratio, as I had it in my original post). My resting heart rate is now 50-55 BPM,
whereas it was 70-75 BPM for the past 25 years. My wife (55 yrs, 67", 120 lbs) is doing very well on a diet
consisting mainly of complex CHO (which I used to eat) and aerobic exercise only. Genetic diversity?
Marital diversity, for sure!
266/298 (1997)
I agree completely that there are many factors at work here. The subject is so complex that it is difficult to
begin to discuss it in a short post. The evidence is "anecdotal", and slim at best, but my best guess is that my
own personal metabolic processes do not perform at their optimum level with high CHO intake -- animal
fat/protein is the preferred fuel, supplemented by low glycemic index vegetables. I also believe that this
condition has become more pronounced with time, i.e., when I was a lad I could process CHO much better
than I do now.
It would be enormously beneficial if nutritionists would study and report on the short- and long-term results
of high-protein, moderate fat, eucaloric diets vs. high-CHO, low fat diets as promulgated by conventional
wisdom. The study would preferably take into account, and look for, differences in digestive system
phenotypes. There must be more going on than is currently reported, or the number of people on animal
protein-based diets would be decreasing due to increased mortality. I have searched high & low for
comparative information of that sort, to no avail. Since the CSIRO has a Human Nutrition Division, perhaps
the good Dr. Holt can help....
If people of the caliber of Drs Cordain, Brand-Miller and Holt could be persuaded to develop the protocols,
there are probably enough interested, motivated people among the participants (and lurkers, one of which I
have been until now) of this paleo-diet list to provide a cross-section of diets, geno/phenotypes, and controls,
as well as serve as record-keepers and other functionaries in a controlled, well-planned test of the concepts of
paleo-diets.
Rob't Beck
****************************************************
****************************************************
PALEODIET Archives
Reply-To:
Date: Fri, 31 Oct 1997 14:11:32 +0700
In the last post, Loren writes:
> Dairy products were obviously not part of the human evolutionary dietary experience ...
But human milk is a dairy product! Humans would have been drinking human milk for the first 4-5 years of
life in hunter-gatherer societies. Although cow's milk is obviously of somewhat different composition, it is
still a mammalian milk. Lactase sufficiency in adulthood was genetically selected in some population groups
because milk drinking offered a survival advantage. To exploit an animal's milk is really no different to
exploiting it's flesh or bones or blood. If early man selectively killed pregnant and lactating animals (and
there is evidence that this is so), milk would have been always part of our evolutionary experience.
Re sucrose: I am still preparing my answer to Dean Esmay's questions. Stay tuned.
Best wishes Jennie
> -----------------------------> Date: Thu, 30 Oct 1997 06:51:13 -0500
> From: Rob't Beck Subject: Protein Power
> Dr. Susanne Holt wrote that my health improvements may be due to other than the elimination of
> grains & dairy products from my diet: By adjusting one's diet to completely eliminate grain and
> dairy products, the following things may occur which could also contribute to the beneficial
> effects: 1. a decrease in total fat and calorie intake; 2. a decrease in saturated fat intake; 3.
> an increase in total fibre intake; 4. a decrease in the amount of rapidly-digested carbohydrate
> consumed; and 5. a possible reduction in sodium intake.
>
> To my best estimate, total fat and saturated fat probably remained fairly constant. Total caloric
> intake was lower. Total fiber intake decreased markedly, (along with digestive & bowel problems
> (heartburn, gas, bleeding, general discomfort)). Rapidly-digested CHO was eliminated, while sodium
> may have increased due to large amounts of meat ingested (I use KCl instead of NaCl at table). CHO
> in my diet came largely from green & leafy vegetables and, sparingly, from fruits Exercise was not
> so much increased as shifted from entirely aerobic to a mix of strength and aerobic training.
267/298 (1997)
> Exercise levels are low to moderate. Just for the record, I am 57 years old, 69" tall, and
> presently weigh 160 lbs. My Total Cholesterol to HDL ratio is 3.9 (not the inverse ratio, as I had
> it in my original post). My resting heart rate is now 50-55 BPM, whereas it was 70-75 BPM for the
> past 25 years. My wife (55 yrs, 67", 120 lbs) is doing very well on a diet consisting mainly of
> complex CHO (which I used to eat) and aerobic exercise only. Genetic diversity? Marital diversity, for
sure!
> I agree completely that there are many factors at work here. The subject is so complex that it is
> difficult to begin to discuss it in a short post. The evidence is "anecdotal", and slim at best,
> but my best guess is that my own personal metabolic processes do not perform at their optimum
> level with high CHO intake -- animal fat/protein is the preferred fuel, supplemented by low
> glycemic index vegetables. I also believe that this condition has become more pronounced with
> time, i.e., when I was a lad I could process CHO much better than I do now.
> It would be enormously beneficial if nutritionists would study and report on the short- and
> long-term results of high-protein, moderate fat, eucaloric diets vs. high-CHO, low fat diets as
> promulgated by conventional wisdom. The study would preferably take into account, and look for,
> differences in digestive system phenotypes. There must be more going on than is currently
> reported, or the number of people on animal protein-based diets would be decreasing due to
> increased mortality. I have searched high & low for comparative information of that sort, to no
> avail. Since the CSIRO has a Human Nutrition Division, perhaps the good Dr. Holt can help.... If
> people of the caliber of Drs Cordain, Brand-Miller and Holt could be persuaded to develop the
> protocols, there are probably enough interested, motivated people among the participants (and
> lurkers, one of which I have been until now) of this paleo-diet list to provide a cross-section of
> diets, geno/phenotypes, and controls, as well as serve as record-keepers and other functionaries
> in a controlled, well-planned test of the concepts of paleo-diets.
> Rob't Beck
>
> ****************************************************
> "...it is almost certain that someday they will
> collect our skulls and call us Early Man."
> ****************************************************
> -----------------------------> End of PALEODIET Digest - 29 Oct 1997 to 30 Oct 1997
> ****************************************************
PALEODIET Archives
Subject: Re: protein power
From: Susanne Holt
Reply-To:
Date: Mon, 3 Nov 1997 11:50:08 +1100
Robert Beck wrote:
> Dr. Susanne Holt wrote that my health improvements may be due to other than the elimination of
> grains & dairy products from my diet:...... To my best estimate, total fat and saturated fat
> probably remained fairly constant. Total caloric intake was lower. Total fiber intake decreased
> markedly, (along with digestive & bowel problems (heartburn, gas, bleeding, general discomfort)).
> Rapidly-digested CHO was eliminated, while sodium may have increased due to large amounts of
> meat ingested (I use KCl instead of NaCl at table). CHO in my diet came largely from green & leafy
> vegetables and, sparingly, from fruits Exercise was not so much increased as shifted from entirely
> aerobic to a mix of strength and aerobic training.
268/298 (1997)
I would like to stress again - that the health improvements Robert Beck has experienced are due to the
combination of changes he has made to his diet and lifestyle, and Robert seems to be agreeing with this
conclusion at the end of his last email. It would be beneficial to conduct a controlled cross-over study using a
group of healthy lean subjects, a group of healthy overweight subjects, and a group of subjects with
symptoms of insulin resistance consume each of the 3 following diets for a period of several months, in
random order: 1. a diet that includes refined cereal products; 2. a diet that contains less refined/wholegrain
cereal products; and 3. a diet that completely eliminates cereal products.
This kind of study would provide some more objective evidence to either confirm the hypothesis that all
grain products result in undesirable physiological responses in all people. Obviously, it would be good to
keep the macronutrient and total energy contents of these 3 diets the same, but this could be a bit of a
challenge. Furthermore, it would be beneficial to ensure that the people within each subject group
commenced the study at a similar physiological state and nutritional status. Ideally, this kind of study would
be done in a metabolic ward setting.
Robert also wrote: <<If people of the caliber of Drs Cordain, Brand-Miller and Holt could be persuaded to
develop the protocols, there are probably enough interested, motivated people among the participants....to
serve as record-keepers and other functionaries in a controlled, well-planned test of the concepts of paleodiets
> We are certainly motivated enough to carry out these kind of studies, and indeed continue to submit such
protocols to various scientific bodies in control of awarding research grants. Unfortunately, nutrition-related
research often does not have a high priority rating, so it is incredibly difficult to get enough money to
perform these large controlled dietary trials.
Dean Esmay wrote: Regarding the claim that "not all cereal grains are necessarily unhealthy" -- can Dr. Holt
elaborate on which ones she feels are not unhealthy, and what criteria she uses to reach this conclusion?
> The long-term consumption of diets which induce relatively high blood glucose and insulin responses
after eating, (ie based on highly-refined cereal products) appear to be associated with the development of
insulin resistance and other related health problems (refs 1-3). Less refined cereal products produce lower
but more sustained elevations in blood glucose levels and are also more difficult to eat and more satisfying
(eg ref 4). Again, health problems are likely to be due to a combination of dietary, lifestyle and genetic
factors. Not all grain eaters suffer from heart disease, overweight etc.
However, a very very high-Carb diet that does not have much fat or protein could be unhealthy, particularly
if people are avoiding whole food groups like meats and dairy products.
Dean Esmay also wrote: <<Regarding the claim that health benefits of substantial weight loss, decreased
triglycerides, and increased HDLcholesterol could be ascribed to a low-fat diet--what is this based on? Every
study I have seen on low-fat diets among westerners has shown a trend toward decreased HDL cholesterol.
Increases in triglycerides are also a common result. Furthermore, after more than a year of reviewing
research on low-fat diets, I have found not one study which boasts more than very small weight loss benefits,
usually on the order of a kilogram or two, awong obese subjects--and some studies show substantial weight
gain in some subjects using such diets. Lowered fat and lowered caloric intake over the last decade in the
United States have correlated with record increases in obesity and diabetes.
I did not ever make a claim that low-fat, high-carb diets are effective in producing weight loss in obese
people. This was not an issue I introduced. Re: the effects of diet on weight loss, it is essential to consider the
group of subjects being studied and how the dietary information was collected. For example, many of the
obese subjects in dietary trials are the hard-core difficult cases in hospital clinics with a very long history of
failed diets. Do you really expect to see substantial weight loss maintained over time? There is also quite a
bit of evidence now to confirm that obese people tend to underreport their actual food intake in diet
diaries/food frequency questionnaires etc. Low-fat, high-carb diets have been shown to be useful in
preventing weight gain in some studies (if the total amount of energy is decreased) and have resulted in the
loss of a few kilos in normal weight subjects (who didn't need to lose weight anyway). It is important to
consider the types of foods used in the studies, since a high-carb diet based on relatively energy-dense highcarb foods (white bread, honey, fruit juice, mashed potato, lentil dhal) will facilitate a greater energy intake
than less energy-dense carb foods which contain less energy per gram and usually more intact fibre
(wholegrain bread, whole fruit, boiled unpeeled potato, boiled whole lentils) (see review ref 5). Perhaps the
energy density of the average USA diet has increased (ie calories per gram food eaten) while energy
expenditure has decreased? Quite a few of the low- to zero-fat processed foods available in the USA have
had the fat replaced with dense carbohydrates - so they don't really contain any less calories.
269/298 (1997)
Sucessful weight loss requires the individual to make dietary and lifestyle changes that they can maintain in
order to consume fewer calories than they are expending. It is a very individual thing. Some people lose
weight by skipping breakfast, most people don't, etc etc. An excellent book which describes the individual
changes made by people who have successfully lost weight and maintained this loss is called "Thin for life 10 keys to success from people who have lost weight and kept it off" by Anne M Fletcher, published by
Chapters publishers and booksellers, 2085 Shelburne RD, Shelburne VT 05482, USA.
Dean Esmay also wrote re:<<the claim that excess protein is oxidized by the body as fuel, "which pushes
both carb and fat into starage", can Dr. Holt elaborate? Is she suggesting that in two diets of, say, 2000 kCals
daily, one of 15% protein and the other of 30% protein, the latter will cause faster storage of fat than the
former?
There is a growing body of metabolic research which confirms that there appears to be a hierarchy (protein,
CHO, fat) in the extent to which the stores of the macronutrients are autoregulated by oxidation. An excess
carb intake tends to promote fat storage (but not de novo fat synthesis) (See ref 6). Fat storage will also be
influenced by: total fat intake; total energy intake vs total energy expenditure; and possibly by the type of
proteins and carbs ingested.
References
1. Slabber et al (1994)Effects of low-insulin response, energy-restricted diet on weight loss and plasma
insulin concentrations in hypoerinsulinemic obese females. Am J Clin Nutr 60:48-53.
2. Salmeron et al (1997) Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care 20: 545-50.
3. Salmeron et al (1997) Dietayr fiber, glycemic load and risk of NIDDM in women. J Am Med Assoc
(JAMA) 12: 472-77.
4. Holt & Brand Miller (1994) Particle size, satiety and the glycaemic response. Eur J Clin Nutr 48: 496-502.
5. Poppitt and Prentice (1996) Review on energy density and energy intake. Appetite. Dr Susanne Holt
CSIRO - Division of Human Nutrition PO Box 52 NORTH RYDE NSW 2113 AUSTRALIA
Ph (+61) 02 9490 8425 Fax (+61) 02 9887 8511 Email
PALEODIET Archives
Subject: High-protein diets
From: Rob't Beck
Reply-To:
Date: Tue, 4 Nov 1997 09:37:24 -0500
1. Dr. Holt & I seem to be in agreement, however, I would not go so far as to suggest that _all_ people
respond in the same way to any given dietary regime. A major part of an ideal study would determine
conclusively if genetic differences exist, and define those differences.
2. Given the amount of human suffering caused by various dietary problems (obesity here, starvation there,
malnutrition everywhere), it is amazing that it is so difficult to pry loose a few millions of dollars for
nutritional studies so that man might begin to understand his _most_ basic need. It seems to me that those
studies would quickly pay for themselves in reduced costs for remedial treatments for nutritional
deficiencies/ excesses.
3. Several people in this list have referred, more or less obliquely, to a connection between fat storage and
ingestion of combinations of food, e.g., eating CHO with fat may be more conducive to fat storage than
eating iso-caloric amounts of CHO alone, or fat alone. This has been referred to (disparagingly) as foodmixing theory by conventional nutritionists. The concept is appealing in its apparent simplicity.... There
seem to be no first-principle reasons why it might not be correct. Unfortunately, Dr. Holt's reference 6 was
apparently inadvertently omitted. Could she supply it? Does anyone else have evidence for or against this
theory? Does the success of some people on high-protein diets constitute evidence for the theory?
****************************************************
****************************************************
PALEODIET Archives
Subject: Fitness and diet
From: Dick
Reply-To:
270/298 (1997)

Date: Tue, 4 Nov 1997 14:00:27 +0000
On: Wed, 29 Oct 1997 09:37:00 -0700 Loren Cordain said:
> Subject: Re: Hunter-Gatherer Exercise Patterns . .
> Mitochondrial DNA evidence suggests that the modern human genome is almost identical to that of
> paleolithic humans who lived 40, 000 years ago. Hence the exercise capacities and requirements of
> modern humans remain similar to those which had been originally selected by evolution for stone
> age humans living in a hunting and gathering environment.
How strong is the evidence suggesting that the paleolithic human genome is nearly identical to that of
modern man, and how large are the differences? Small differences in the genome can make a big difference
to the phenotype (e.g sickle-cell anaemia) so if there are differences, even small ones, surely they may
contribute to quite radical differences in diet?
Conversely, if there has been _no_ selection since 40 000 years ago, what is the evidence that diet has played
any part in anything except individual health - i.e. that it has contributed anything to the fitness of the
species?
Dick Bird School of Behavioural and Environmental Studies University of Northumbria Newcastle upon
Tyne NE1 8ST
PALEODIET Archives
Subject: Re: Fitness and Diet
From: Loren Cordain
Reply-To:
Date: Tue, 4 Nov 1997 16:21:00 -0700
Dick Bird's questioned the evidence regarding differences between modern man's genome and that of
paleolithic man. Clearly, the suggestion that there are minimal differences can only be inferred. The amount
of mitochondrial DNA diversity in various human racial groups from around the world has been determined
(1), additionally the rate of mitochondrial DNA change can also be estimated (1, 2). Based upon this rate of
mDNA change, as well as similar nuclear DNA studies (3), the genetic differences between humans living
40, 000 yrs ago and those living today ago can be estimated. A similar approach has been used to determine
if Neanderthals were precursors to modern humans or were separate species (4). I agree that small genotypic
differences can result in large phenotypic differences. Also, there are a number of genotypic differences
among various human populations that are known to have been elicited by diet (i.e. adult lactase persistence
and a variety of hemoglobinopathies, and perhaps the degree of insulin resistance/sensitivity) since the
agricultural revolution. Consequently, modern human genomes (particularly in those populations with the
greatest exposure to agriculture) are not identical to our paleolithic ancestors, and some of these slight
genetic differences may have important health ramifications for modern man. However, basic human
nutritional needs seem not to have varied significantly since paleolithic times. All humans require similar
ranges of both macro and micronutrients and all human groups have similar anatomical, physiological and
endocrine functions in regard to diet and nutrition. The reason for these similarities is because of our
common evolutionary experience - we were all hunter gatherers dependent upon wild plants and animals and these dietary selective pressures shaped our present day nutritional requirements.
Cordially,
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Wed, 5 Nov 1997 12:14:00 -0500
Loren forgot to include the references with his post. Here they are. :)
271/298 (1997)
1. Penny D et al. Improved analyses of human mtDNA sequences support a recent African origin for Homo
sapiens. Mol Biol Evol 1995;12:863-82. 2. Hedges B et al. Human origins and analysis of mitochondrial
DNA sequences. Science 1992;255:737-39. 3. Hammer MF. A recent common ancestry for human Y
chromosomes. Nature 1995;378:376-78. 4. Krings M et al. Neandertal DNA sequences and the origin of
modern humans. Cell 1997;90:19-30.
PALEODIET Archives
Subject: Very worthwhile reading
From: Dean Esmay
Reply-To:
Date: Wed, 5 Nov 1997 18:23:42 -0500
One of the best things to ever appear on the 'net on the subject of diet and human evolution can be found
here:
http://www.syndicomm.com/nicholson
It's an interview of Paleodiet Symposiom Ward Nicholson by health newsletter editor Chet Day (who by
complete coincidence was my boss a number of years ago when I worked on the Genie network).
Of highest interest are probably parts 1 & 2 of the interview. Part 1 starts with a discussion of Ward's
personal history, and may seem rather pointless until he starts discussing actual scientific research--and once
that happens the interview takes off on what is probably the most meticulously documented, closely detailed,
well-researched discussion of diet and evolution I have ever read.
Note that the interviewer and interviewee are both coming from a perspective of discussing "Natural
Hygiene, " an all- or mostly-raw, usually vegetarion dietary philosophy--Day is writing from the perspective
of a practitioner of this philosophy, whereas Nicholson in writing from the perspective of one who has
largely abandoned such dietary concepts. Don't let any of this deter you from reading the interview, however.
It is a must-read item.
PALEODIET Archives
Subject: Sucrose - not a villain after all
Reply-To:
Date: Sat, 8 Nov 1997 14:33:43 +1100
Dear Everyone,
I apologise for the delay in answering Dean's questions about the role of sucrose in the diet. I managed to
lose the first draft of the reply and had to start again.
1. Yudkin omitted data to make a correlation between sucrose and CHD appear to be there. Has this been
documented anywhere?
Sucrose was first implicated as a risk factor for CHD by Yudkin and although the hypothesis gained popular
credibility, it was quickly refuted. In univariate analysis, Liu et al (1) showed that both saturated fat and
refined sugars were highly correlated with CHD in 20 industrialised nations. However, in subsequent
multivariate analysis sucrose was no longer significantly related to CHD mortality. Thus one of the causes of
the confusion is that saturated fat and sucrose correlate with each other in population studies (but not in
individual diets).
Truswell (2) reviewed 10 case-control studies of sucrose and CHD and found that none supported the
hypothesis. The international community thinks so little of the Yudkin's hypothesis that 'no prevention trial
of CHD with sugar has been completed, started, planned or even contemplated.'
2. but would it also not be the case that sugars consumed in nature would also be eaten with massive amounts
of fibre, thus slowing down the absorption of those sugars?
272/298 (1997)
While it may be true that sugars in nature are often eaten with massive amounts of fibre, this is not to say that
they give metabolic responses any lower that refined products. We found that there was a wide range of
glycaemic and insulin responses (an indirect measure of rate of absorption) among 40 naturally-occurring
sugars and refined sugar-containing foods (3). In Australia, commercial honey, bush honey and refined
sucrose have similar GIs.
There are plenty of sugary foods in western diets with a low GI. This includes most of the sweetened dairy
products and chocolate confectionery. We have just completed GI studies of 10 Mars
confectionary/chocolate items. Many have a GI in 30-50 range (the same as legumes). One reason for this
low GI is that the high fat content slows down gastric emptying. The high saturated fat content is a concern
but not the sugar. On the other hand there are tropical fruits with GIs in the 70s. I'm using the GI scale where
glucose = 100.
In a study of the diets of 342 people with diabetes, Wolever et al (4) found that the GI of the diet was
*inversely* related to the proportion of carbohydrate that was sugars (both natural and refined). Thus, the
higher the sugars content, the lower the overall diet GI. He also found that the lower the GI, the lower their
glycosylated hemoglobin (a measure of average blood glucose levels).
Some studies also suggest that insulin sensitivity is better on high sugar (vs high starch) diets (5).
3. sucrose itself has been shown to have a glycemic index no worse than that of white bread, does this
suggest that sucrose is harmless--or might it not just suggest that bread is not so benign as it is often thought
to be?
Yes, I agree with you on this one. I am always stunned by the very high sustained glycaemic and insulin
response we see to white or wholemeal bread. But note that on average sugar-containing foods have a lower
GI than most western starchy staples (3).
4. You also stated your that glucose is the obligatory fuel for the brain and fetus, and that we can't make
enough glucose via gluconeogenesis alone. But Cahill (Cahill, G. and Aoki, T.T., Medical Times 98, 1970)
found that the brain will utilize ketones preferentially to glucose, once a brief period of adjustment of 1-3
weeks is made.
Yes, it's true that brain can utilise ketones when itmust but the state of ketonemia is generally regarded as
undesirable. It has been shown to be associated with impaired cognitive function and teratogenic effects on
the fetus (6, 7). See below for further details.
5. It is also well known that the Inuit eat almost no carbohydrate, and must therefore use gluconeogenesis
and ketones for most of their fuel needs. But certainly they manage to have children.
Yes, I am very much aware of this and it forms one of the links in our 'carnivore connection' hypothesis (8).
We hypothesised that a human females exposed to diets in which there was little carbohydrate would be
advantaged by a state of genetically determined insulin resistance. This would spare glucose for the fetus and
increase the capacity of the liver to produce glucose from non-glucose precursors.
Female dogs fed a carbohydrate-free diet with 26% protein became hypoglycaemic and ketotic towards the
end of gestation and over a third of the puppies were stillborn (9-11). Adequate synthesis of glucose from
gluconeogenic amino acids may be accomplished if dietary protein is sufficiently high. For example, dogs
are able to reproduce on a carbohydrate-free diet when the protein intake is sufficiently high (10, 11). This
fits well with the evolutionary development of the dog as a hunter, since the body of prey would have
supplied only a little available carbohydrate but large amounts of protein. The dog therefore falls halfway
between a carnivore and an omnivore (and perhaps we humans do too).
In true carnivorous animals like the cat, gluconeogenesis is also more or less permanently 'switched on' (40)
with maximal gluconeogenesis occurring in the absorptive phase immediately following a meal. Carnivorous
animals like the cat who have evolved and reproduce well on a low carbohydrate intake, appear to be
genetically insulin resistant (12). Moreover, they appear to develop NIDDM when exposed to a high
carbohydrate diet (13).
6. ..recent research has also shown that athletes, particularly endurance athletes, tend to show performance
increases on very low carbohydrate, high protein, high fat diets, after a 1-3 week adaptation period.
My understanding of the literature is that high carbohydrate diets (and carbohydrate loading) enhance
prolonged strenuous exercise because the level of glycogen stores is the limiting factor here (for review see
14).
273/298 (1997)
High carbohydrate diets (vs high fat diets) have been shown to produce higher glycogen stores. When
exercise is sufficiently strenuous (above 70% VO2max), only glucose can be utilised as fuel by the muscle
because free fatty acids cannot enter the cell fast enough. As exercise progresses (and the same high
VO2max is maintained), glycogen stores gradually fall. The sensation of 'hitting the wall' corresponds with
glycogen stores becoming fully depleted. It is likely that other forms of exercise (sprint events) are not
affected by diet.
Perhaps Loren Cordain (if he's still reading!) might like to comment here.
Summing up For a major recent review of all health aspects of sugars, I refer readers to a supplement number
1 of the Am J Clin Nutr 1995 (Volume 62). Apart from lingering concerns about TG levels and very high
carbohdyrate diets, sucrose is given a clean bill of health.
I am in the process of writing a paper titled 'Sugar - not a villain after all'. In it I provide the accumulated
scientific evidence (most of it from the last 5-10 years) that restricting sugar may do more harm than good.
This is because low sugar diets in HUMANS (not rats!) are associated with:
1. an increase in fat, especially saturated fat, intake (the sugar-fat seesaw) 2. an increase in obesity and
overweight 3. an increase in the glycaemic index of the diet 4. a decrease in insulin sensitivity 5. diversion of
millions of research and consumer dollars to non-sucrose sweeteners.
I would be happy to post the summary to the review when it's finished.
Best wishes Jennie
References
1. Liu et al. Dietary lipids, sugar, fiber and mortaolity from coronary heart disease. Arteriosclerosi 1982; 2:
221-7.
2. Truswell AS. Sugar and health: a review. Food Technol Aust 1987; 39: 134-40.
3. Brand Miller J, Pang E, Broomhead L. The glycemic index of foods containing sugars: comparison of
foods with naturally occurring versus added sugars. Brit J Nutr 1995; 73: 613-623.
4. Wolever TMS, Nguyen P, Chiasson J, Hunt JA, Josse RG, Palmason C, Rodger NW, Ross SA, Ryan EA,
Tan MH. Determinants of diet glycemic index calculated retrospectively from diet records of 342 individuals
with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1994;59: 1265-9 214. Wolever
5. Piatti PM et al. Insulin sensitivity and lipid levels in obese subjects after slimming diets with different
complex and simple carbohdyrate content. In J Obesity 1993; 17:375-81.
6. Veneman T et al. Effect of hyperketonemia and hperlactatacidemia on symptoms, cognitive function...
during hypoglycaemica in normal humans. Diabetes 1994; 43: 1311-7.
7. Reece et al. Multifactorial basis of the syndrome of diabetes embyropathy. Teratology 1996; 54: 171-82.
8. Brand Miller J, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of noninsulin dependent diabetes. Diabetologia 1994; 37: 1280-86.
9. Rosmos DR, Palmer HJ, Muiruri KL, Bensink MR (1981) Influence of a low carbohydrate diet on
performance of pregnant and lactating dogs. J Nutr 111: 678-689.
10. Kienzle E, Meyer H, Lohrie H (1985) Influence of carbohydrate-free rations with various protein/energy
relationships on foetal develpoment, viability of newborn puppies and milk composition. Advances in
Animal Physiology and Animal Nutrition 16: 78-99.
11. Blaza SE, Booles D, Burger IH (1989) Is carbohydrate essential for pregnancy and lactation in dogs? In:
Berger IH, Rivers JPW (eds) Nutrition of the dog and cat. Cambridge University Press, Cambridge, pp 229243.
12. MacDonald ML, Rogers QR, Morris JG (1984) Nutrition of the domestic cat, a mammalian carnivore.
Ann Rev Nutr 4: 521-62.
13. O'Brian TD, Hayden DW, Johnson KH, Stevens JB. High dose glucose tolerance test and serum insulin
glucagon levels in diabetic and non-diabetic cats: relationships to insular amyloidosis. Vet Path 22:255-261.
14. Sherman WM. Metabolism of sugars and physical performance. Am J Clin Nutr 1995; 62: 212S-227S.
PALEODIET Archives
Subject: Fat/carbohydrate mix and glycemic response
Reply-To:
Date: Sat, 8 Nov 1997 20:44:12 PST
274/298 (1997)
In their reply to Loren Cordain of June 29, Sally Fallon and Mary Enig state that "fats taken with
carbohydrates, esp. traditional fats such as butter..., lower the glycemic index" (no reference cited). I also
thought this was the case, due to the role of fat in increasing the time that the carbs are kept in the stomach.
But in his reply of Oct. 9, Prof. Cordain says "it has been well established that by mixing fat with
carbohydrate, the glycemic response worsens" (he cites a 1988 paper by Collier et al).
If indeed the latter is correct, could someone kindly explain why fat would cause this effect.
Stephen Meyers Lawrence Berkeley National Laboratory Berkeley, CA 94720 USA E-mail:
PALEODIET Archives
Subject: Macronutrient mixtures in hunter-gatherer meals
Reply-To:
Date: Sat, 8 Nov 1997 21:07:42 PST
In his post of 26 May, Loren Cordain stated that "pre-agric. eating patterns show that fat and protein were
generally eaten together whereas carbohydrate meals were eaten separately" (no citation).
In their reply to Loren Cordain of June 29, Sally Fallon and Mary Enig question this claim.
In his reply of Oct. 9, Prof Cordain again states that "Hunter gatherers quite often would eat only the animal
killed for a meal without added plant courses. Thus, protein/fat macronutrient mixtures were the norm.
Carbohydrates generally were consumed as they were collected or separate from animal based meals."
Presumably there is considerable data on this issue with respect to 20th C. hunter-gatherers. I thought that it
has been not uncommon for a main meal to consist of both meat/fish from the hunt and plant foods that had
been gathered that day or before. Could anyone who is up on the literature comment?
For Paleolithic peoples living in climates with minimal plant food (or in winter), of course, one would
imagine that the pattern suggested by Prof. Cordain would have been common. But this situation corresponds
to a relatively short part of the ~2 million year evolutionary period of Homo sapiens, does it not?
PALEODIET Archives
Subject: Low-carb diet and blood lipid profiles
Reply-To:
Date: Sat, 8 Nov 1997 21:21:56 PST
In his post of 26 May, Loren Cordain stated that "the reduced carbohydrate content of per-agric. diets would
have improved the portions of the blood lipid profile (TG, VLDL, HDL, Lp(a)) which are worsened by high
carb diets". He cites a 1995 paper by Reaven.
In their reply to Loren Cordain of June 29, Sally Fallon and Mary Enig say that "orthodox nutritionists
content that high carb. diets improve blood lipid profiles."
In his reply of Oct. 9, Prof Cordain provides further references for positive blood lipid changes resulting
from reduced carbohydrate diets.
So, are the orthodox nutritionists wrong?
PALEODIET Archives
Reply-To:
Date: Tue, 11 Nov 1997 16:38:51 +0000
275/298 (1997)
Due to some transatlanic holdup the 5 Nov digest only reached me after 6 days! Thus this response may be
rather belated, I hope it is still relevant.
On Tue, 4 Nov 1997 Loren Cordain wrote:
> Dick Bird's questioned the evidence regarding differences between modern man's genome and that of
> paleolithic man. Clearly, the suggestion that there are minimal differences can only be inferred.
> The amount of mitochondrial DNA diversity in various human racial groups from around the world
> has been determined (1), additionally the rate of mitochondrial DNA change can also be estimated
> (1, 2). Based upon this rate of mDNA change, as well as similar nuclear DNA studies (3), the
> genetic differences between humans living 40, 000 yrs ago and those living today ago can be
> estimated. A similar approach has been used to determine if Neanderthals were precursors to modern
> humans or were separate species (4).
But all these studies have been conducted on what are believed to be non-coding unselected parts of the
genome, and cannot be extrapolated to rates of change in parts of the genome which are under selection. A
stronger argument can be built from the following facts:
a) mtDNA and nuclear DNA evidence shows that there has been a recent (100-200ka ago) population
bottleneck follwed by rapid expansion, which explains the lack of genetic diversity amongst modern humans,
and:
b) a conservative reading of the archaeological evidence shows that modern human populations were present
throughout the Old World by 40ka
Thus given our species recent origin, and geographical dispersion, we can argue that there will be no
nutritional selective pressures common to all Homo sapiens. The nutritional niche for which we are selected
will either be that of the founding population, or more or less modified versions of it, varying between
regions. So there may be entire populations or large proportions of populations with genetic adaptations to
local food resources.
As Loren says, we observe some of these:
> there are a number of genotypic differences among various human populations that are known to
> have been elicited by diet (i.e. adult lactase persistence and a variety of hemoglobinopathies, and
> perhaps the degree of insulin resistance/sensitivity) since the agricultural revolution.
> Consequently, modern human genomes (particularly in those populations with the greatest exposure
> to agriculture) are not identical to our paleolithic ancestors, and some of these slight genetic
> differences may have important health ramifications for modern man.
BUT these are minor variations:
> All humans require similar ranges of both macro and micronutrients and all human groups have
> similar anatomical, physiological and endocrine functions in regard to diet and nutrition. we
> therefore may conclude that: The reason for these similarities is because of our common
> evolutionary experience - we were all hunter gatherers dependent upon wild plants and animals > and these dietary selective pressures shaped our present day nutritional requirements.
When in the past should we look for this palaeolithic diet which is the common inheritance of all humans? It
must be before the population dispersal which allowed regionally varying diets to arise. We cannot then look
at Upper Palaeolithic diets, as they are certainly after the dispersal. Accepting the genetic evidence for a
bottleneck mentioned above leads us acceptance an Out Of Africa II scenario rather than a Multiregional
Evolution scenario for the origin of modern humans, and thus to place the dispersal event of interest at c.120100ka. Therefore it is amongst archaic Homo sapiens and possibly late Homo erectus *in Africa* that we
should seek this diet, and probably in some smaller (but as yet undefined) part of Africa.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Out of Africa
Reply-To:
Date: Wed, 12 Nov 1997 16:23:36 PST
276/298 (1997)
Andrew Millard's interesting post of 11 Nov concluded:

> Accepting the genetic evidence for a bottleneck mentioned above leads to acceptance of an Out Of
> Africa II scenario rather than a Multiregional Evolution scenario for the origin of modern humans,
> and thus to place the dispersal event of interest at c.120-100ka. Therefore it is amongst archaic
> Homo sapiens and possibly late Homo erectus *in Africa* that we should seek this diet, and
> probably in some smaller (but as yet undefined) part of Africa.
His post reinforced some thoughts I have had, namely that the focus that some seem to have on the diet of
Upper Paleolithic temperate zone peoples as a guide for our "evolutionary diet" may be misplaced. Andrew's
idea also would cast some doubt on the approach taken by Eaton et al to approximate our "evolutionary diet"
(i.e., averaging across modern-day HGers). If we accept the Out of Africa scenario, then we might do better
by looking at the diets of modern HGers living in environments that approximate the conditions under which
our African forebears evolved. But maybe the problem with such an approach is the fact that modern HGers
have been pushed to more marginal environments (forest, arid zones, etc.) than the ones in which their
ancestors lived in.
I have a question for Andrew: Why do you only go as far back as late Homo erectus?
Steve Meyers Lawrence Berkeley National Laboratory Berkeley, CA 94720 USA E-mail:
PALEODIET Archives
Subject: Re: Response to Steve Meyers
From: Loren Cordain
Reply-To:
Date: Thu, 13 Nov 1997 11:24:00 -0700
1. Steve said:
In his post of 26 May, Loren Cordain stated that "the reduced carbohydrate content of per-agric. diets would
have improved the portions of the blood lipid profile (TG, VLDL, HDL, Lp(a)) which are worsened by high
carb diets". He cites a 1995 paper by Reaven. In their reply to Loren Cordain of June 29, Sally Fallon and
Mary Enig say that "orthodox nutritionists content that high carb. diets improve blood lipid profiles." In his
reply of Oct. 9, Prof Cordain provides further references for positive blood lipid changes resulting from
reduced carbohydrate diets.
So, are the orthodox nutritionists wrong?
What was once outlandish is now orthodox and what was once orthodox is now outlandish. Science moves
forward, new data is generated, new hypotheses are generated and tested and new theories are ultimately
developed. A perfect example of this is vitamin E. In the mid to late 60's vitamin E was thought by orthodox
nutritionists to have little or no function - today it's role as an antioxidant is firmly known and accepted by
"orthodox" nutritionists. The dogma of orthodox nutritionists regarding macronutrient intake for the past 2025 years has been that a high carb, low fat diet was the optimal diet for humans and benefitted virtually all
pathological conditions ranging from heart disease to cancer. In the past 10 years, this concept has been
seriously questioned in terms of deleterious changes (elevated TG, and VLDL and lowered HDL) which
occur in blood lipid profiles from such advice. Increasingly, influencial scientists (Scott Grundy, Walter
Willett, Gerald Reaven) and institutions (Harvard School of Public Health) have recognized this shortcoming
of high carb, low fat diets and are now recommending monounsaturated fat in lieu of carbohydrate (1, 2).
This message is now being taught to our nutrition students in the University - when they get out into the real
world, this message may become their dogma and as surely as one generation will replace the next, new
ideas will replace "orthodox" ideas.
REFERENCES
1. Grundy SM. Comparison of monosaturated fatty acids and carbohydrates for lowering plasma cholesterol.
N Engl J Med 1986;314:745-48. 2. Mensink RP et al. Effects of monounsaturated fatty acids versus complex
carbohydrates on high density lipoproteins in healthy men and women. Lancet 1987;1:122-25.
A second question from Steve is:
277/298 (1997)
"In their reply to Loren Cordain of June 29, Sally Fallon and Mary Enig state that "fats taken with
carbohydrates, esp. traditional fats such as butter..., lower the glycemic index" (no reference cited). I also
thought this was the case, due to the role of fat in increasing the time that the carbs are kept in the stomach.
But in his reply of Oct. 9, Prof. Cordain says "it has been well established that by mixing fat with
carbohydrate, the glycemic response worsens" (he cites a 1988 paper by Collier et al). If indeed the latter is
correct, could someone kindly explain why fat would cause this effect."
We need to clarify our terms on this one. The ingestion of fat with carbohydrate results in lower blood
glucose but higher insulin levels compared to carbohydrate ingestion alone (1, 2). Fat ingestion stimulates
the secretion of glucose dependent insulino-tropic polypeptide (GIP) and it is thought that the additional rise
in insulin is mediated by the effects of GIP (3).
REFERENCES
1. Collier G, O'Dea K. The effect of co-ingestion of fat on the glucose, insulin and gastric inhibitory
polypeptide responses to carbohydrate and protein. Am J Clin Nutr 1983;37:941-45. 2. Collier G. et al.
Effect of co-ingestion of fat on the metabolic responses to slowly and rapidly absorbed carbohydrate.
Diabetologia 1984;26:50-56. 3. Collier G et al. The acute effect of fat on insulin secretion. J Clin Endocrinol
1988;66:323-26.
A third point Steve brings up:
In his post of 26 May, Loren Cordain stated that "pre-agric. eating patterns show that fat and protein were
generally eaten together whereas carbohydrate meals were eaten separately" (no citation). In their reply to
Loren Cordain of June 29, Sally Fallon and Mary Enig question this claim. In his reply of Oct. 9, Prof
Cordain again states that "Hunter gatherers quite often would eat only the animal killed for a meal without
added plant courses. Thus, protein/fat macronutrient mixtures were the norm. Carbohydrates generally were
consumed as they were collected or separate from animal based meals." Presumably there is considerable
data on this issue with respect to 20th C. hunter-gatherers. I thought that it has been not uncommon for a
main meal to consist of both meat/fish from the hunt and plant foods that had been gathered that day or
before. Could anyone who is up on the literature comment? For Paleolithic peoples living in climates with
minimal plant food (or in winter), of course, one would imagine that the pattern suggested by Prof. Cordain
would have been common. But this situation corresponds to a relatively short part of the ~2 million year
evolutionary period of Homo sapiens, does it not?
Most foraging mammals including primates (1) consume food as they encounter it in their day to day travels
throughout their range. Because food sharing occurs infrequently in chimpanzees, man's closest relative, all
individuals in the foraging group, except for nursing infants, are responsible to obtain their own food (1).This
pattern of foraging almost certainly would have been true for Australopithecines (2). Consequently,
organized meals in which multiple foods, collected from the environment and brought back to a home base
to be shared by all members of the foraging group is quite unlikely until the development of 1), a home base
and 2) containers. The transport and sharing of meat does not require a container (only a stone tool to
dismember the carcass), whereas the transport of plants back to a home base requires a container. It is likely
that the scavenging/hunting of animals preceded the invention of containers (primitive baskets or animal
membrane bags) (2). So, the concept of a home base likely developed in conjuction with the transport and
sharing of meat only and plant foods would still have been foraged by each individual in the manner of most
non-human primates (2). Food sharing by the inclusion of dispersed vegetable foods would have come later
in man's evolution, consequently early Homo species would have eaten meats separate from vegetable foods.
This pattern of food consumption would have prevailed throughout much of early man's evolution and the
concept of bringing multiple plant and animal foods together to be shared by all members of a troop for an
organized meal surely only arose much later in man's evolution as behavioral complexity increased. The
anthropological literature is full of descriptions of hunter-gatherers consuming plant foods "on the run", that
is as they move through their environment. These foods are eaten as they are encountered by both men and
women (without mixing them with animal foods that may have been killed earlier. Groups of men who make
a kill while out on a hunt, generally eat portions of the animal immediately without stopping to gather plant
foods to make a "balanced" meal. I refer interested readers to (3).
Steve further comments:
For Paleolithic peoples living in climates with minimal plant food (or in winter), of course, one would
imagine that the pattern suggested by Prof. Cordain would have been common. But this situation corresponds
to a relatively short part of the ~2 million year evolutionary period of Homo sapiens, does it not?
278/298 (1997)
Steve's assumption here is incorrect. Humans left Africa for more northerly latitudes by at least 1 million
years ago and probably quite earlier (4). We now have strong evidence that hominids lived in Spain ( > 40
degrees North latitude) by at least 750, 000 years ago, in England ( > 50 degrees North latitude) by at least
500, 000 years ago and in Germany ( > 50 degrees North latitude) by at least 400, 000. There is astonishing
evidence that early man may have lived as far north as (60 degrees North latitude) by 260, 00 years ago (5).
As, Steve has surmised, the consumption of plant based foods (edible by primates) is severly seasonally
restricted at higher latitudes, so it seems likely for these populations that plants would have been rarely
consumed simultaneously with animal foods, and this pattern of eating (plants separate from animals) has
been with humans from the very beginings of the evolution of our species..
REFERENCES
1. Suzuki A. An ecological study of chimpanzees in a savanna woodland. Primates 1969;10:103-48. 2. Isaac
G. The diet of early man: aspects of archaeological evidence from lower and middle pleistocene sites. 3.
Bicchieri MG. Hunters and Gatherers Today. New York, Holt, Rinehart & Winston Inc, 1972. 4. Larick R,
Ciochon RL. The african emergence and early dispersals of the genus Homo. Am Scientist 1996;84:538-51.
5. Waters MR et al. Diring Yuriakh: a lower paleolithic site in central siberia. Science 1997;275:1281-84.
Cordially,
PALEODIET Archives
Subject: BBC programme
From: Dean Esmay
Reply-To:
Date: Thu, 13 Nov 1997 16:42:36 -0500
Comments sent to me by a subscriber:
I have been watching a programme made by the BBC Horizon documentary group. I videoed it because it
shows at 4.00am in NZ. It was about the BOXGROVE excavations. I believe that the videos of these
programmmes are available from the BBC. See the Web site. http://www.bbc.co.uk/ Some of the list
members may like to look at it. It is entitled *The Butchers of Boxgrove*
Further:
The Horizon Library sells videos of many (though not all) Horizon programmes. They can be contacted by
telephone at 0181 576 2541 (or 44 181 576 2541 if you are calling from outside UK)
I am told that videos may only be purchased for educational use, and are not available for rent.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 6 Nov 1997 to 8 Nov 1997
Reply-To:
Date: Thu, 13 Nov 1997 21:00:58 -0500
"Beware of sweet dainties; they are a deceitful food" -- Proverbs 23:3
The problems with sugar are well documented in major medical journals worldwide. Yet we continue to
ignore the warnings. Sugar has been shown to:
Increase the risk for breast cancer Double the risk for biliary tract cancer Interfere with the absorption of
calcium and magnesium Increase cholesterol and insulin levels Raise blood pressure Raise triglycerides
Weaken the immune system Cause a deficiency of copper Cause to varicose veins Damage the kidneys
Cause or worsen arthritis Cause migraine headaches Cause gallstones Contribute to obesity (All of the above
statements are referenced below.)
Sugar is not a pick-me-up. It is a drag-you-down. As sugar burns out our blood sugar balancing mechanisms,
it makes us want more. We can no longer keep our own sugar levels balanced, and want sugar as often as
possible to relieve depression or low energy levels. We are caught in a vicious circle. The way out is to avoid
it completely.
279/298 (1997)
Sugar also depresses immune function by encouraging the overgrowth of a yeast organism known as candida
albicans. Candida is a yeast naturally present in small amounts in everyone's intestinal tract. But when sugar
is consumed, candida may overgrow, leading to bloating, gas, depression, low energy levels, and a host of
other problems. Sugar in and of itself does not always lead to candida overgrowth. Consuming sugar
regularly, however, significantly increases the chances that the yeast organism known as candida albicans
will change into its fungal form, overgrow in the GI tract and elsewhere in the body, and cause health
problems.
In China, sugar is applied externally to help wounds heal. That's the first genuinely beneficial use for sugar
I've ever heard
Robert Crayhon
References
"Dietary Factors in Hormone-Dependent Cancers", Carroll, K.K., in Current Concepts in Nutrition, Vol. 6.,
Nutrition and Cancer, New York, John Wiley and Sons, 1977, 25-40.
"Diet and Breast Cancer: The Possible Connection with Sugar Consumption", Seely, S., Horrobin, D.F.,
Medical Hypotheses, 11 (3): 319-27, 1983.
"Dietary Sugar Intake in the Etiology of Biliary Tract Cancer", Moerman, Clara J., et al, International
Journal of Epidemiology, 1993; 22: 207-214.
"Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium",
Lemann, J., Journal of Laboratory and Clinical Medicine, 70: 236-245.
"Diets High in Glucose or Sucrose and Young Women", Kelsay, J., et al, American Journal of Clinical
Nutrition, 1974, 27: 926-936.
"Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease", Reiser, S., Nutritional
Health, 1985, 3:203-216.
"Carbohydrates and Blood Pressure", Hodges, R. and Rebello, T., Annals of Internal Medicine, 1983, 98:
838-841.
"The Effect of Dietary Sucrose on Blood Lipids, Serum Insulin, Platelet Adhesiveness and Body Weight in
Human Volunteers", Scanto, S., and Yudkin, John, Postgraduate Medical Journal, 1969, 45: 602-607.
"Role of Sugars in Human Neutrophilic Phagocytosis", Sanchez, A., et al, American Journal of Clinical
Nutrition, November, 1973, pp. 1180-84.
"Sucrose, Neutrophilic Phagocytosis and Resistance to Disease", Ringsdorf, W., Cheraskin, E., and Ramsay,
R., Dental Survey, 52, 12: 46-48.
"Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets", Fields, M.
et. al., Journal of Nutrition, 1983, 113: 1335-1345.
Diabetes, Coronary Thrombosis and the Saccharine Disease, Cleave, T. and Campbell, G., Bristol, England,
John Wright and Sons, 1960.
"Effects of High Dietary Sugar", Yudkin, J., et al, British Journal of Medicine, November 22, 1980, 281: 139
"Placebo Controlled Blind Study of Dietary Manipulation Therapy in Rheumatoid Arthritis", Darlington, L.,
Ramsay and Mansfield, Lancet, February 6, 1986, pp. 236-238.
"Food Allergies and Migraine", Grand, E., Lancet, 1979, 1:955-959
"The Sweet Road to Gallstones", Heaton, K., British Medical Journal, April 14, 1984, 228: 1103-4.
"Nutrient Intake, Adiposity and Diabetes", Keen H., et al, British Medical Journal, 1974, 655-658.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 6: Sucrose / Sugar
From: Robert Rosenstein
Reply-To:
Date: Thu, 13 Nov 1997 21:02:59 -0500
I am confused by Jennie Brand Miller's conclusion to her posting of 8 November. In it she states:
"I am in the process of writing a paper titled 'Sugar - not a villain after all'. In it I provide the accumulated
scientific evidence (most of it from the last 5-10 years) that restricting sugar may do more harm than good.
This is because low sugar diets in HUMANS (not rats!) are associated with:
1. an increase in fat, especially saturated fat, intake (the sugar-fat seesaw) 2. an increase in obesity and
overweight 3. an increase in the glycaemic index of the diet 4. a decrease in insulin sensitivity 5. diversion of
millions of research and consumer dollars to non-sucrose sweeteners."
280/298 (1997)
The use of sugar, as "sugar" in diets was not prevalent until well into the 17th century and for perhaps more
than a century after that it was not a general part of anyone's diet.
The use of foods from which sugars are naturally derived such as fruits, have not, at least to my knowledge,
been a common part of any diet, anywhere in the past - or the present.
If "sugsr" is as important to the diet as Jennie indicates, it brings up the question of what was included in the
diet of the world's peoples from Paleolithic times to almost the present that counteracted the four harmful
effects Jennie has presented?
I must add that I am disturbed by Jennie's fifth statement regarding the waste of consumer dollars on
irrelevant research. Although it was not intentional, this sounds like an out and out blurb for the sugar
industry. It is also implies that certain other researches and product developments never should have taken
place.
robert
robert rosenstein :
PALEODIET Archives
Subject: Out of Africa II
Reply-To:
Date: Fri, 14 Nov 1997 11:50:52 PST
In his post of 13 Nov, Loren Cordain stated;
"Humans left Africa for more northerly latitudes by at least 1 million years ago and probably quite earlier
(4). We now have strong evidence that hominids lived in Spain ( > 40 degrees North latitude) by at least
750, 000 years ago, in England ( > 50 degrees North latitude) by at least 500, 000 years ago and in
Germany ( > 50 degrees North latitude) by at least 400, 000. There is astonishing evidence that early man
may have lived as far north as (60 degrees North latitude) by 260, 00 years ago (5). As Steve has surmised,
the consumption of plant based foods (edible by primates) is severly seasonally restricted at higher latitudes,
so it seems likely for these populations that plants would have been rarely consumed simultaneously with
animal foods, and this pattern of eating (plants separate from animals) has been with humans from the very
beginings of the evolution of our species."
Prof. Cordain has not yet commented on Andrew Millard's post regarding the Out of Africa II hypothesis and
its implications for our "evolutionary" diet, but if we accept this hypothesis, is it not the case that the dietary
patterns (and other adaptations) of hominids post Out of Africa I would not be relevant to modern humans?
My (somewhat limited) understanding is that the Out of Africa II hypothesis is becoming increasingly
accepted among paleontologists, based on both genetic and archaeological evidence.
Of course, if we rely mainly on an Africa-centered model for the evolutionary experience that is relevant for
modern humans, there would be no conflict with Prof. Cordain's points regarding eating patterns with respect
to animal/plant food combinations. However, there would probably be implications in other areas, such as
the proportion of plant/animal foods and the amount of fat in wild game.
I look forward to views of others on this topic.
Steve Meyers
PALEODIET Archives
Subject: Re: Out of Africa
Reply-To:
Date: Fri, 14 Nov 1997 17:20:16 +0000
On Wed, 12 Nov 1997 Steve Meyers wrote:
> Andrew Millard's interesting post of 11 Nov concluded:
> Accepting the genetic evidence for a bottleneck mentioned above leads to acceptance of an Out Of
> Africa II scenario rather than a Multiregional Evolution scenario for the origin of modern humans,
> and thus to place the dispersal event of interest at c.120-100ka. Therefore it is amongst archaic
281/298 (1997)
> Homo sapiens and possibly late Homo erectus *in Africa* that we should seek this diet, and
> probably in some smaller (but as yet undefined) part of Africa.
> I have a question for Andrew:
> Why do you only go as far back as late Homo erectus?
Essentially I was arguing when our *most recent* common ancestral diet was, which is clearly that of
archaic Homo sapiens in Africa. Homo erectus is another species, although ancestral, and therefore more
removed from us. The late African Homo erectus (sensu lato) were presumably moving towards being like
modern humans, but the further back you go, the more likely it is that the diet was different, particularly
given the glacial-interglacial cycles occurring at the time of H.s. arising from H.e. It is quite possible that the
speciation involved a dietary shift. Hence I would prefer to look at our own species if possible, and if not
then the most closely related part of another species.
Of course if you take the regional continuity hypothesis, then the common ancestral diet is that of early H.e.,
but, given the apparently rapid spread of that species around the world, the best we can do might be to look
at late H. habilis.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Sucrose
Reply-To:
Date: Fri, 14 Nov 1997 13:08:33 +0700
To answer Robert Rosenstein's questions:
> The use of sugar, as "sugar" in diets was not prevalent until well into the 17th century and for
> perhaps more than a century after that it was not a general part of anyone's diet.
True, but honey was a general part of most people's diets (1) and in nutritional terms, honey and refined
sugar are rougly equivalent.
> The use of foods from which sugars are naturally derived such as fruits, have not, at least to my
> knowledge, been a common part of any diet, anywhere in the past - or the present.
Are you suggesting that fruits were not a common part of past diets? That's new to me. Our pre-human
ancestors evolved on diets based on fruits and berries (2). Australian Aboriginal people ate fruit, much of it
in the form of dried fruit with concentrated sugars (3). Humans have also availed themselves of the
concentrated sweetness in honey ants, dried dates and figs, maple syrup, manna etc
> If "sugsr" is as important to the diet as Jennie indicates, it brings up the question of what was
> included in the diet of the world's peoples from Paleolithic times to almost the present that
> counteracted the four harmful effects Jennie has presented?
As above. Honey, dried fruit etc. High levels of physical activity in the past meant people needed
concentrated sources of energy. Fat would have been most helpful in this respect. So in the past a high fat
diet did not lead to obesity. On the contrary, it would have spared us from excessive weight loss associated
with high energy expenditure or large intakes of bulky high carbohydrate foods. The amount of dietary fat
and the rising prevalence of obesity are only important because we are so sedentary.
> I must add that I am disturbed by Jennie's fifth statement regarding the waste of consumer dollars
> on irrelevant research. Although it was not intentional, this sounds like an out and out blurb for
> the sugar industry. It is also implies that certain other researches and product developments
> never should have taken place.
It might sound like a blurb for the sugar industry but that doesn't mean it shouldn't be said. I do not have any
financial association with the sugar industry and I say it simply because I believe it to be true and worth
saying - low joule substitutes for refined sugar cost a lot of money to develop, test and market. Aspartame
was the most expensive food additive ever to be launched. Yet there is little evidence that low joule
sweeteners are effective for weight loss or weight maintenance. (In fact, there is some evidence that they
stimulate appetite and lead to higher energy intake).
282/298 (1997)
The sugar issue is not the first time nutritionists have misled the food industry. The 'great protein fiasco' of
the 1970's and all the research that went into novel proteins was based on nutritionists' assessment that the
world was short on protein specifically. Secondly, the idea that milk was a perfect food and good for
everyone led to the introduction of dairy technology in countries where the whole population lacked the
enzyme lactase.
References
1. Allsop K, Brand Miller JC. Honey revisited: a reappraisal of honey in pre-industrial diets. Br J Nutr; 75:
513-20.
2. Lee RB, DeVore I (1968). Man the Hunter. Aldine, Chicago.
3. Brand Miller J, James K, Maggiore P. Tables of composition of Australian Aboriginal foods. Aboriginal
Studies Press, Canberra, Australia, 1993.
PALEODIET Archives
Subject: Re: Sugars, Fruits, & Archaeology
Reply-To:
Date: Sun, 16 Nov 1997 00:52:55 -0500
A quick recap:
> The use of foods from which sugars are naturally derived such as fruits, have not, at least to my
> knowledge, been a common part of any diet, anywhere in the past - or the present. Are you
> suggesting that fruits were not a common part of past diets? That's new to me. Our pre-human
> ancestors evolved on diets based on fruits and berries (2). Australian Aboriginal people ate
> fruit, much of it in the form of dried fruit with concentrated sugars (3). Humans have also
> availed themselves of the concentrated sweetness in honey ants, dried dates and figs, maple syrup,
> manna etc
The archaeological record from most continents supports the interpretation that fruits and berries have long
been a part of the human diet. In fact, for much of the American west there is good evidence that prickly pear
cactus fruits also were eaten. These are very high in sugar. In one coprolite report for Texas it was suggested
that consumption of large amounts of prickly pear cactus fruits was responsible for the high number of caries
(cavities) for that population. Mesquite bean pod flour also has a high sugar content. So does roasted agave.
I've had several requests to comment on evidence for diet in the archaeological record. Most of my research
has been on the North American continent with sites within the last 10, 000 years. Just a blink of an eye for
the time periods that many of you are talking about. However, as a preview (I don't have time to enter
references at the moment -- and I'm at home and my references are at the office), we have lots of evidence
for numerous plants such as grass seeds, cattail roots, Chenopodium sp. (goosefoot) seeds, Amaranthus sp.
(pigweed) seeds, seeds of several members of the mustard family such as Descurainia, various Polygonum
(knotweed, smartweed) seeds, Eriogonum (wild buckwheat) seeds, Cleome (beeweed) greens and seeds,
Opuntia (prickly pear cactus) seeds, Opuntia fruits and pads. Cholla buds are steamed and eaten (and taste
something like asparagus). This is just the tip of the iceberg concerning plants that were eaten. Some foods,
such as acorns, needed to be processed before they were eaten. Leaching acorns usually involves grinding
the acorns and rinsing them in water or burying them. Leaching (rinsing) Cleome seeds also is a good idea.
Roots and tubers were important parts of the diet for people living in portions of North America. Camas
bulbs, bitterroot, lomatium, mariposa lily, and others were roasted and eaten.
Evidence for eating meat includes most of the game animals that we can think of and many animals that we
wouldn't consider. Mammoths (now extinct), bison, pronghorn (known to most of you as antelope), mountain
sheep, rabbits, deer, elk, moose, and many more game animals. Rodents were consumed -- and more than the
obvious squirrels. Mice, packrats, and other small rodents were eaten in many areas. Certainly some of the
historic populations ate these animals whole (fur, bones, stomaches, and all), which suggests that prehistoric
people may have done the same. Insects were popular with some groups, particularly those in California and
the Great Basin -- Grasshoppers, crickets, grubs, worms, and many, many more. I've had opportunities to
taste many native foods. Most are surprisingly tasty or at least acceptable. Some are not. Cooked insects are
surprisingly tasty.
283/298 (1997)
I'll post a list of references of ethnobotanic studies of historic Native American groups from the office next
week. At present it's mixed with references to the edibility of plants in North America -- which I will leave in
for the benefit of those who are interested.
It's been my observation that diet varies with geography. It's very hard to generalize about "prehistoric diet"
as if it applied to people over a vast area. At least during the Holocene (last 10, 000 years or so) people in
many areas tended to eat both animal and plant foods during the same day, if not during the same meal. The
remains are mixed in the coprolites. While this is not proof of consumption of a mixure of plant and animal
foods at a single meal, it would be very hard to prove that many prehistoric people had a regular practice of
eating these foods either separately or together. Consumption of small rodents (the entire animal) means
eating both the meat of the rodent and the plant foods that the rodent ate (stomach contents) at the same time.
After having worked with the archaeological record for over 25 years, I'd have to throw my opinion with
those of you who believe that paleodiet included both animal and plant foods that may or may not have been
consumed together -- but that the deciding factor was probably availability of individual foods. Sometimes
plants and animal foods were available together and sometimes not. Sometimes a fresh kill dominated a meal
(or day or more of meals), when people gorged themselves. Sometimes plant foods were mixed with meat
(pemmican). Remember we're still in North America and still in the Holocene when people had grinding
tools.
At any rate, that's a very quick review (sans references) for a part of the North American diet.
Just one quick comment. Since I've been lurking on this list nearly all the foods mentioned are ones that
modern Americans consider palatable. Certainly the true paleodiet contained many more insects that we care
to think about. Shouldn't we be considering the insect population "fair game"?
Linda Scott Cummings
PALEODIET Archives
Subject: Re: Sucrose - not a villain after all
Reply-To:
Date: Mon, 17 Nov 1997 00:54:58 +0100
Jennie Brand Miller suggests that
> restricting sugar may do more harm than good. This is because low sugar diets in HUMANS (not
> rats!) are associated with: 1. an increase in fat, especially saturated fat, intake (the sugar-fat
> seesaw) 2. an increase in obesity and overweight 3. an increase in the glycaemic index of the diet
> 4. a decrease in insulin sensitivity 5. diversion of millions of research and consumer dollars to
> non-sucrose sweeteners.
May I add 6. an increase in salt intake?
Nothing of this happens in my family where sugar-rich foods are mainly replaced by fruits and nuts.
Nevertheless, Jennie's point is noteworthy. Perhaps even some cookies are healthier than many sandwhiches?
Cheers,
Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: Fruits and insects
Reply-To:
Date: Mon, 17 Nov 1997 11:28:42 +0700
284/298 (1997)
Thank you to Linda Scott Cummings for the expert account of native Northwest American food habits. I'm
glad someone else agrees that the diet for at least some groups was high in fruits and sugars. We don't have
such a strong instinctual desire/taste for sweetness for nothing. Fat on the other hand is comparatively
tasteless.
But I wonder what an instinctual desire for sweetness offered? Concentrated energy? Only half as much as
fat and no better than starch or protein. Alternatively, perhaps sweetness was an obvious sign of the
carbohydrate that was essential for survival? Any other suggestions?
I agree that we tend to ignore the contribution of insects. Australian Aborigines relished the 'wittchetty grub'
(a huge moth larva) which has a composition of 20% protein and 30% fat.
In table of Composition of Australian Aboriginal foods (1), there are 14 pages devoted to insect foods and
their products, including bobong moths (a staple food for months of the year for some groups), honey ants,
sugar bag, galls, lerps, green ants.
Kind regards Jennie
(1) Brand Miller J, James K, Maggiore P. Tables of composition of Australian Aboriginal bushfoods.
Aboriginal Studies Press: Canberra, 1993
PALEODIET Archives
Subject: alcohol
From: Dick Dawson
Reply-To:
Date: Tue, 18 Nov 1997 15:14:55 -0500
Becky Johnson wrote:
Interesting suggestion:
> Gourds would have provided readily available containers for fermentation. My bet is if wild fruit
> was gathered in gourds, fermentation was discovered very early on.
Some have said that the first guys to milk a goat stored the milk in a goat rumen (first stomach) and the
stomach lining enzymes (rennet) made cheese of it.
Archaeological evidence for sufficient domestication of animals to allow milking first appears ~10kya; long
after H sapiens arose. K Feder _The_Past_in_Perspective_ Mayfield 1996.
I don't recall the first instances of fruit storage or discovery contexts.
Dick http://smith.syr.edu/~ddawson
PALEODIET Archives
Subject: macronutrient mixtures
From: "Mazer, C. & Blank, J."
Reply-To:
Date: Thu, 20 Nov 1997 00:21:57 -0500
Steve Meyers writes (8 Nov):
> Presumably there is considerable data on this issue with respect to 20th C. hunter-gatherers. I thought
> that it has been not uncommon for a main meal to consist of both meat/fish from the hunt and plant
> foods that had been gathered that day or before. Could anyone who is up on the literature comment?
I'm not "up on the literature, " but Marvin Harris, in his _Our Kind_, pp. 306-7, writes:
285/298 (1997)
"The first priority of a hungry person's body is to convert whatever food it consumes into energy. Supplied
with nothing but lean meat, the body uses the protein in it for energy rather than for body-building and bodyrugulating functions. One way to 'spare' the protein in meat is to eat it along with calorie-rich starchy
foods.... Among the Yanomami the protein-sparing combination is meat and plantains. Kenneth Good has
told me that the Yanomami absolutely refuse to eat meat if it is not accompanied by plantains, although they
will eat plantains without meat. The best protein-saving combination of all, however, is fatty meat, since fat
contains twice as many calories per gram as starch.... ... the conversion of calories into body fat during good
times is essential for survival during bad times. In order to build up fat reserves, the body has to expend
calories. If the food to be converted to fat is a strach, almost a quarter of of its caloric value is wasted as a
cost of the conversion and storage process. But if the source of the stored fat is fat itself, only 3 percent of
the ingested calories are lost...."
So there you have it: the Yanomami anyway eat their meat with starch, even if generally speaking meat with
fat would be more efficient.. I would imagine this would be true of cultures in the Pacific Islands where yams
and seafoods are staples -- but I'm not that up on the literature.
Hope this helps.
John Blank
PALEODIET Archives
Subject: Saturated fat and coronary heart disease
Reply-To:
Date: Tue, 25 Nov 1997 13:02:42 PST
Loren Cordain's response (9 Oct 97) to Fallon and Enig regarding the positive association between dietary
saturated fat and heart disease risk was to my mind rather convincing, but the role of saturated fat in
contributing to CHD relative to other factors still seems somewhat uncertain.
It seems we would agree that "moderate" intake of saturated fat probably does not pose a problem, esp. if it is
a higher proportion of 18:0 relative to 12:0, 14:0 and 18:0, and if the various factors that may also contribute
to CHD are minimized, and if the factors that are cardio-protective are incorporated in diet and lifestyle. I
suspect that the "concensus view" in this symposium would support a saturated fat intake higher than that
currently advocated by the medical establishment, if the various other factors are in a reasonable balance.
Perhaps this view is supported by the point made by Enig and Fallon that the amount of SF in the American
diet remained the same between 1935 and 1974, a period of great increase in heart disease. I don't have the
data at my disposal, but my sense is that the level of CHD was fairly low in the pre-1935 period, despite a
high (relative to the current recommendations) intake of SF. Certainly many of the other risk factors for
CHD were present to a lesser extent during that time, and factors such as n6/n3 ratio were "better." And I
suspect that the % of wild game (with it's lower SF than domesticated meats and higher % of 18:0 SF) as %
of total animal food was higher (esp. before 1900).
I'd be interested in thoughts of others on this.
Steve Meyers
PALEODIET Archives
Subject: Saturated fat and coronary heart disease
Reply-To:
Date: Thu, 27 Nov 1997 09:12:37 +0000
On Tue, 25 Nov 1997 Steve Meyers wrote:
> Perhaps this view is supported by the point made by Enig and Fallon that the amount of SF in the
> American diet remained the same between 1935 and 1974, a period of great increase in heart
> disease. I don't have the data at my disposal, but my sense is that the level of CHD was fairly
> low in the pre-1935 period, despite a high (relative to the current recommendations) intake of SF.
286/298 (1997)
But this is not necessarily a significant observation against a link between SF and CHD. CHD is to a large
extent a disease of the 50+ age group, and I would be surpised if the proportion of them in the population did
not increase significantly in this period. There is also a danger in using average dietary SF in a population:
there may be a level above which SF is a risk factor, so if the average remains the same but the range of SF
values increases, then there may be more people at risk. Wasn't this a period of increasingly sedentary
lifestyles? Just look at the increase in car use.
The data quoted show that SF may not be the only risk factor, but they do not show that it is not a risk factor.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: New book
From: Dean Esmay
Reply-To:
Date: Fri, 28 Nov 1997 19:01:08 -0500
I just got word about this book. Haven't read it, haven't got a copy, this is all the information I have:
Larsen, Clark Spencer `Bioarchaeology: interpreting behavior from the human skeleton', 468pp, 34 ill,
Cambridge Studies in Biological Anthropology, no 21, UKP55, 00, Cambridge University Press, November
1997, ISBN 0 521 49611
PALEODIET Archives
Subject: New book
From: Dean Esmay
Reply-To:
Date: Mon, 1 Dec 1997 14:35:44 -0500
From some private correspondence I recently got from Steve Meyers, reposted here with permission:
--[snip]-Along those lines, I recently read an interesting article that summarizes a number of studies in the 1980s that
used skeletal analysis to look at relative pathology of various groups of (late) hunter-gatherers and early
cultivators. The data are not entirely conclusive, but generally point in the direction of better health for the
HGers.
Mark Cohen, The significance of long-term changes in human diet and food economy, in Harris and Ross
(eds), Food and Evolution (1987).
Steve
BTW -- I'll be off on vacation for much of December, so the absence of postings from me doesn't mean I've
lost interest.
--[snip]-...I thought the reference might be a bit dated, and no doubt more such studies have been done since this
guy's review, but perhaps it's still relevant. His motivation is trying to sort out whether the increasingly broad
spectrum of food resources utilized from Late Paleolithic to Mesolithic to Neolithic was more a function of
need ("stress") rather than progress; he tends to be of the "stress" school, and this review tends to support this
view.
BTW, there is another good article in the same book: Katherine Milton, Primate diets and gut morpholgy:
implications for hominid evolution.
Steve
PALEODIET Archives
287/298 (1997)
Subject: Re: Out of Africa II, Sugars Fruits & Archaeology, Macronutient M ixtures, Saturated Fat & CHD
From: Loren Cordain
Reply-To:
Date: Mon, 1 Dec 1997 17:00:00 -0700
My contributions to the listserve have been minimal in the past couple of weeks because of the arrival of our
third son two weeks ago and because of a concerted effort to complete my cereal grain manuscript, which is
now complete & hopefully should appear in a forth coming issue of the World Review of Nutrition and
Dietetics.
In regards to the out of Africa hypothesis and its relationship to diet, I think the data supports the concept
that early humans left Africa by at least 1 MYA or possibly earlier and were replaced by anatomically and
behaviorally modern humans in the past 40-60, 000 years. Anatomically modern humans likely evolved in
Africa and first appear in the fossil record ~100-120 kYA. Therefore, this population in theory would
represent the last common ancestor for which all modern humans could trace a common gene pool and
ideally could serve as the model for the genetic nutritional requirements of all present day humans before the
confounding influence of various environments wrought by migration etc. upon our genome. However, it is
inappropriate to dismiss the nutritional evolutionary experience of all hominids prior to the split between
anatomically modern humans and their predecessors because, we share more genes with these hominids than
those for which we differ. In order for encephalization (increase in brain size relative to body mass) to
proceed, early hominids had to increase the nutrient density of their predominantly plant based diets (1). This
increase in the size and metabolic activity of the brain occurred as a result of a decrease in the size and the
metabolic activity of the gut (2). The most obvious nutrient dense foods that early hominids began to include
in their diet were animal based foods, including scavenged bones containing marrow and skulls containing
brain. Early stone tools presumably (inferred from cut marks on associated butchered fossil bones) were
manufactured to facilitate the dismembering of either hunted or scavenged carcasses. This consumption of
animal based foods which led to a relatively smaller and less metabolically active gut is still with us today.
So presumably all hominids (including modern humans) share the basic gastrointestinal physiology that
evolved in response to a high meat based diet. Further, all modern humans have poor ability to desaturate
and chain elongate 18 carbon lipids to 20 and 22 carbon lipids (3). Similar to cats (complete carnivores) the
inability to efficiently desaturate and chain elongate plant based 18 carbon lipids to the 20 and 22 carbon
lipids needed for membrane and eicosanoid function has occurred because the selective pressure for
desaturation and chain elongation has been relaxed. Humans like cats eat higher up on the food chain (ie.
other animals), in which 20 and 22 carbon lipids are present - thus there is little need to retain genes for lipid
desaturation and chain elongation of plant based 18 carbon lipids. Similar arguments can be made for the
synthesis of taurine (a conditionally essential amino acid) and the conversion of beta carotene to vitamin A.
Thus, the basic physiological adaptation to a meat based diet occurred early on and was likely complete by
the time early hominids migrated to northern latitudes. Fruit eating hominids could not have left the environs
of the tropics until they began to utilize a food source that was present not only in the tropics but elsewhere.
The remains of archaic humans in Germany ~ 400, 000 yrs ago as well as their wooden hurling spears (3)
clearly indicates that these people were meat eating hunters, genetically well adapted to their prey. There is
no evidence whatsoever that this pattern of diet in which meat predominates had changed in Africa at the
time of or after the evolutionary split between anatomically modern humans. In fact, to the contrary, it
appears that anatomically modern humans became even more efficient hunters as they appeared in the fossil
record in europe, asia and north america. Thus, deviation from these basic dietary patterns have only
occurred relatively recently in the meso and neolithic. Consequently, it seems likely that there may have
been many basic nutritional similarities between anatomically modern humans and their predecessors.
REFERENCES
1. Leonard WR et al. Evolutionary perspectives on human nutrition: the influence of brain and body size on
diet and metabolism. Am J Human Biol 1994;6:77-88. 2. Aiello LC et al. The expensive tissue hypothesis.
Curr Anthropology 1995;36:199-221. 3. Thieme H. Lower palaeolithic hunting spears from Germany.
Nature 1997;385:807-10.
288/298 (1997)
I enjoyed Linda Scott Cummings wonderful post on pre-agricultural diets in North America during the
holocene based upon her work done with coprolites. I would agree with her that during this period, there was
a world wide increase in the exploitation of small animals, the aquatic environment and many plant based
foods that was coincident with the extinction of numerous large pleistocene mammals (1, 2). Also, I'm sure
that she would agree that the consumption of the meat or organs of large mammals is still technically
difficult or impossible to determine in coprolites. Also, coprolite evidence generally could not distinguish the
relative timing of plant vs: animal meal consumption. Clearly a plant based meal followed hours later by an
animal based meal would produce mixed fecal material.
1. Stuart A.J. Mammalian extinctions in the late pleistocene of northern eurasia and north america. Biol Rev
1991;66:453-62. 2. Webster D, Webster G. Optimal hunting and pleistocene extinction. Human Ecology
198412:275-89.
I agree with John Blank's mention of the value of carbohydrate in the consumption of high protein meals.
There is an absolute limit to the amount of non-fat protein which can be consumed, and it has been estimated
to be roughly 300 g and/or 50% of total calories (1). Thus, there would have been a protein constraint for all
humans following the killing of a large game animal, and they would have had to either selectively eat fatty
portions of the carcass along with the lean meat or they would have had to include plant based carbohydrate
with the lean meat (but not necessarily at the exact same moment). As John pointed out, carbohydrate
generally will allow a greater protein intake than will fat. At higher latitudes and during winter months
(wherein plant foods are restricted), the only way out of this protein conundrum is to selectively eat fatter
animals or the fatty portions of the carcass to the exclusion of the lean meat. Despite this protein ceiling, a
survey of 181 world wide hunter gatherer societies (2) show that in 61.3% of the societies, plant foods
comprised 35% of less of the total food energy and that the most frequently occurring plant: animal
subsistence ratio would have been 16-25% plant : 66-75% animal.
REFERENCES
1. Speth JD. Early hominid hunting and scavenging: the role of meat as an energy source. J Hum Evolution
1989;18:329-43. 2. Murdock GP. Ethnographic Atlas: a summary. Ethnology 1967;6:109-236.
In response to Steve Meyers, I stand by my guns that saturated fat is atherogenic, particularly in western
based diets wherein the protein intake is low (12-15% energy) relative to that which potentially was available
from pre-agricultural diets (35-50%). I have firmly stated my position on this in my lengthy Oct 9, 1997 post.
I agree with Dr. Millard's conclusion that there are confounding variables which make the data Enig and
Fallon offer difficult to interpret. Stone age diets, although high in animal based food were low in saturated
fat, even when fattier portions of the carcass were consumed. Our analysis of the lipid composition of
portions of wild animal carcass which we recently presented in Bethesda (1) confirm this concept. The
combined total amount of polyunsaturated and monounsaturated fat in wild animals would have almost
always equaled or exceed the saturated fat content.
REFERENCES
1. Cordain L et al. The fatty acid composition of muscle, brain, marrow and adipose tissue in elk:
evolutionary implications for human dietary lipid requirements. World Rev Nutr Diet 1998, in press.
PALEODIET Archives
Subject: Re: Out of Africa II, Sugars Fruits & Archaeology,
From: "Loren Cordain (by way of Dean Esmay)"
Reply-To:
Date: Tue, 2 Dec 1997 09:15:21 -0500
On the last post I sent in today, I messed up my references for the first section. The first reference (3) should
be: Salem N et al. Arachidonic and docosahexaenoid acids are biosynthesized from their 18-carbon
precursors in human infants. Proc Natl Acad Sci 1996;93:49-54. The second (3) in the text should actually be
(4) and the reference (3) in the list of references should be labeled (4).
PALEODIET Archives
Subject: Out of Africa
From: Dick Dawson
Reply-To:
289/298 (1997)

Date: Tue, 2 Dec 1997 15:21:59 -0500
[..]
> I have a question for Andrew: Why do you only go as far back as late Homo erectus? Steve Meyers
> Lawrence Berkeley National Laboratory Berkeley, CA 94720 USA
Archaeological evidence of teeth of Australopithecines suggests heavy vegetable diets; probably largely
seeds and grain. Huge molars, small incisors, much abraded wear on molars. This is most exaggerated in A.
robustus, A. boisei etc. But perhaps these more specialized Australopithecines weren't our ancestors; rather
they might have been on other branches of the Hominid tree and have no living descendants. Depends on
one's choice of cladistics.
Our pre-primate ancestors were primarily insectivorous. Some suggest their diet has influenced our needs:
for protein, fat, vitamins etc. Insects are a fine source of nutrition although generally abhorred in European
diets.
Perhaps our dietary needs developed over ongoing evolutionary time and changes.
Perhaps the evidence of some modest number of healthy 'old' (80yr) skeletons suggests our paleo period
ancestors ate right and that careful study of modern h-g diets confirm this per Boyd et. al:
_Paleolithic_Prescription_.
I'm not sure we have the final answer to this study.
Dick http://smith.syr.edu/~ddawson SU Rifle Club: http://smith.syr.edu/~ddawson/surifleclub.html
PALEODIET Archives
Subject: List announcements
From: Dean Esmay
Reply-To:
Date: Tue, 2 Dec 1997 16:10:31 -0500
I have sent written an announcement about the Paleolithic Diet & Exercise Symposium to the following
journals:
European Journal of Clinical Nutrition Hertfordshire UK
American Journal of Human Biology East Lansing Michigan USA
American Journal of Clinical Nutrition Berkeley California USA
Journal of the American College of Nutrition Miami Florida USA
Journal of Nutrition Urbana Illinois USA
The Journal of Applied Nutrition Austin Texas USA
Medical Anthropology Atlanta Georgia USA
Journal of Human Evolution London UK
American Journal of Physical Anthropology Dartmouth USA
Current Anthropology St. Louis Missouri USA
The announcement includes a description of our group, the URL for the archives, and instructions on how to
join the Symposium. With any luck this should see our little group expand significantly.
If anyone has suggestions for other journals that would be worth sending this information to, please send me
email. I will need not just the journal name, but a mailing address as well. Electronic mail is preferred since
postage has to come out of my personal pocket, but a regular mailing address is fine. Also if anyone,
especially those outside of North America, would like to volunteer to send announcements to significant
journals in their part of the world, please email me and I'll send you a copy of the announcement.
Overall our little group is doing well. New membership has slacked off considerably but membership
remains comfortably stable--and I expect it to pick up considerably once we let the journals know we're here.
Thanks all for your continued participation.
PALEODIET Archives
Subject: Paleo Christmas
290/298 (1997)
From: Art De Vany

Reply-To:
Date: Tue, 2 Dec 1997 22:47:27 -0800
List members may find the Skull Duggery web site of interest.
They offer an Hominid Series of full-size replicas of our ancestors and their near relatives.
Included are: Australopithecus afarensis Cranium
Australopithecus africanus Cranium
Homo habilis Cranium
Homo erectus Cranium
Neandertal Cranium
I am getting Homo erectus for my desk and plan to put a huge Smilodon next to it. Just to give me an
evolutionary perspective on the challenges of modern life.
Many other fossil and miniatures of dinosaurs, dire wolf, etc. are available.
Their web site URL is http://www.skullduggery.com/store.htm
Art De Vany
PALEODIET Archives
Subject: Question on Vanadium
From: Dean Esmay
Reply-To:
Date: Tue, 2 Dec 1997 22:56:40 -0500
I've been asked to post this question on behalf of Stan Angilley, the author of: "A MULTIDISCIPLINARY
APPROACH TO DIABETIC NEUROPATHY TREATMENT" located at:
http://www.nsd.uib.no/yngve/helse/neuropat.shtml
We are seeking to get some idea of the daily intake of vanadium from "natural" sources pre- and postagricultural "revolution".
1) is it true that the major dietary source of vanadium for humans was unprocessed oils and animal fats? if so
how much and in what form?
2) the purported success of the ancient Roman treatment of diabetes: "gorge yourself on meat and fat every
day" would provide exactly how much vanadium and what form would this vanadium take?
PALEODIET Archives
Subject: Oxygen, Eve, and Bottlenecks
From: Art De Vany
Reply-To:
Date: Thu, 4 Dec 1997 04:04:27 -0800
Some theoretical speculations spurred by the recent discussion of Out of Africa.
The oxygen content of the air reached a minimum over the past 250K years between 145 and 118, 000 years
ago (see the jpg chart attached). This time just precedes or coincides with the earliest findings of homo
sapiens. It was a very warm period as well, representing a 30, 000 year peak temperature that is much
warmer than the preceding 20, 000 years and the ensuing 100, 000 years. Starting about 118, 000 ybp (years
before present), the climate cooled dramatically. And the oxygen content of the atmosphere increased from
about 32 per cent to closer to 40 per cent. The present warm, interglacial period shows few temperature and
oxygen deviations and the oxygen content is about 36 per cent.
The high oxygen content of the atmosphere during the period of the emergence of homo sapiens may have
been a factor contributing to homo's adaptation. An atmosphere with high oxygen content produces a free
radical load. Free radicals are a well-known source of mutations to the RNA and DNA and may have
increased the rate of mutation and hence the diversity of early homos and their rate of adaptation to the
changing climate and atmosphere.
291/298 (1997)
The Eve bottleneck occurs near this period as does the appearance of anatomically modern humans. The
ability to adapt rapidly to the changing environment of falling, rising and then falling temperatures and a
highly variable oxygen level are likely to have been the selective pressures that led to homo sapiens
If African Eve lived about 140ky ago it would coincide with the abrupt change in temperature and oxygen
density that took place then. In just a few hundred years, the temperature jumped about 22 degrees and
oxygen density plummeted from about 40 percent to 32 percent. This could have produced the population
bottleneck that the Eve hypothesis proposes.
A notable change in the shape of the human rib cage occured during this time which coincides with the
appearance of anatomically modern humans. The upper thorasic area of the chest expanded relative to homo
sapiens' predecessors, probably in response to the rapidly diminishing oxygen content from 150, 000 to 130,
000 years ago. The ability to remain mobile and active in a world of diminishing oxygen would have been an
enormous selective advantage. Coupled with the evolution of sweat glands, the widening thorasic crest and
expanding lung capacity would have given our first modern ancestors enormous competitive advantages over
their predecessors. With the ability to utilize more oxygen would come a concommitant need to shed heat. A
human adapted to a lower oxygen density would have been able to move more rapidly and for much longer
periods than prey that had not so quickly adapted to low oxygen levels. Along with the increasing grassy
areas and large game, the mobility advantage is leveraged into hunting prowess.
Art De Vany
PALEODIET Archives
Subject: F W Scott's Research- Smoking Gun Evidence
From: Dean Esmay
Reply-To:
Date: Thu, 4 Dec 1997 13:18:59 -0500
I became interested in the concept of a Paleolithic Diet in a circuitous way which began with the diagnosis of
my oldest son with multiple sclerosis two and a half years ago. I hit the med library soon after I was told that
there was no known cause and no effective treatment for MS. My goal was to determine the most likely
cause and to then devise a therapy which countered this cause. After reading hundreds of papers and
countless more abstracts I reached the conclusion that the main cause of MS is dietary and that dairy, gluten
and saturated fat were the three main offending foods. I have summarized this analysis in an essay which is
at http://aspin.asu.edu/msnews/emb11297.htm
The file is about 120k and I'll be glad to email it to anyone who wants it. It contains about 75 references to
the published literature and is about a year out of date.
The evidence I used to reach my interpretation was a combination of epidemiology, theory (molecular
mimicry) and anecdotal data. After the essay was on the web I was contacted by Loren Cordain who pointed
out that the foods implicated in MS were "recently introduced" to the human diet from a genetic point of
view and he gave me the references to Boyd Eaton's classic papers on Paleolithic Nutrition. From my
geological background this concept seemed eminently reasonable so now I had an excellent unifying concept
to go along with all the other data. One shortcoming of the evidence was that it was all circumstantial. There
was no "smoking gun" evidence, that is, empirical evidence which demonstrates beyond a reasonable doubt
that food proteins really do cause cell-mediated, organ-specific autoimmunity.
As a dutiful civil servant, I made one of my required pilgrimages to Ottawa last week to participate in
various mind-numbing meetings. I had a free afternoon so I went out to the Nutrition Research Division of
Health Canada where I had the good fortune to meet with Dr Fraser Scott. Dr. Scott has been studying the
effect of diet on the development of Type 1 Diabetes in BBdp rats for 20 years. He and co-workers have
demonstrated conclusively that Type 1 diabetes can be generated by proteins derived from wheat, soy and
milk. So now I had found the smoking gun. Food proteins can indeed induce cell-mediated autoimmunity
and not surprisingly the foods which supply the pathogenic proteins are those added to the human diet during
the Neolithic. I believe Dr. Scott's work is of great significane for understanding the cause of autoimmune
disease and strongly supports Eaton's suggestion the the diet of our ancestors is the best defence against the
diseases of civilization.
The best reference for Scott's work is: Scott, FW, 1996, Food-induced Type 1 Diabetes in the BB Rat.
Diabetes/Metabolism Reviews, v.12, p. 341-359. This paper summarizes all his results up to 1996 and
contains references to all his earlier work.
292/298 (1997)
As a postscript my son has been on a modified Paleolithic Diet for over 2 years now and has never been
healthier.
PALEODIET Archives
Subject: F W Scott's Research- Smoking Gun Evidence
From: Dean Esmay
Reply-To:
Date: Thu, 4 Dec 1997 13:25:57 -0500
Er, I made a significant error in my last posting. The geologist Ashton Embry emailed me his message and
asked if I would post it for him. I did but I foolishly neglected to mention that it was HIS message, not mine.
So in reading the above, please keep in mind that it's Ashton Embry's message, not mine, and address any
inquiries about it to him (or to the list, if it seems appropriate).
-=- Bugs: You be quiet. He doesn't have to shoot you now. Daffy: He does so have to shoot me now. I
demand that you shoot me now!
PALEODIET Archives
Subject: Soy Protein and a Question to the group
From: BOBDFH
Reply-To:
Date: Mon, 15 Dec 1997 16:52:35 EST
One hears a constant mantra of the benefits of soy protein in lowering cholesterol, yet not enough
questioning of what kind of cholesterol is being lowered. In a recent study (Sugiyama K et al. Methionine
content of dietary proteins affects the molecular species composition of plasma phosphatidylcholine in rats
fed a cholesterol-free diet. J. Nutr. 1997; 127: 600-607.) HDL cholesterol was lowered over 40%! This is
hardly desirable or cardioprotective. LDL was also lowered, and the upshot from this animal study is that the
HDL:total cholesterol ratio remains about the same. The absolute HDL apart from the ratio is gaining
increasing importance, and therefore questions whether lowering is always beneficial if HDL is brought
down with LDL. It may be doing more harm than good.
Question: Does anyone in the group know the n6/n3 ratio of grasses that animals in the wild forage upon? I
am trying to figure out the effect of animals eating grasses on the fatty acid profile of their meat. Thanks.
Happy holiday to this esteemed and fun group!
Robert Crayhon, M.S.
PALEODIET Archives
Subject: Status of list
From: Dean Esmay
Reply-To:
Date: Tue, 16 Dec 1997 13:07:12 -0500
I have recently recieved letters from people wondering where the Paleodiet Digest has gone since no one has
received one in quite some time.
A few things to keep in mind:
1) Digests only get sent out when someone sends a message to the list.
2) At this time we only have a couple of hundred subscribers. Though this may change in the next few
months, and we know there are a number of people reading the Symposium's contents strictly through the
web without being "subscribers" per se, this does naturally limit the amount of messages we are likely to see.
3) Our standards for accepting messages are much higher than most other lists, with a pretty high rejection
rate.
293/298 (1997)
4) While we don't forbid informality, speculation, or humor, we strongly urge use of references whenever
making important statements of fact that may not be common knowledge. This tends to make it a bit more
work to post something than might
5) Most of our subscribers are professors or practicing researchers, who only have so much time after all.
It's not that we have the rigorous requirements of a peer-reviewed journal--we are a semi-formal discussion
forum, not a repository for doctoral theses--but combine all these factors and it should be understandable that
sometimes days may go by without any messages being issued. If this goes on too long (more than a week or
two) then the list moderator will likely post a message or two trying to "goose" the list back into activity. But
under normal circumstances it's not unusual for the list to go through periods of inactivity.
I am hoping our membership base will increase after the peer-reviewed journals I mentioned a while ago
receive the announcement I sent out about what we're doing here. I continue to be interested in any
suggestions anyone has for journals or other publications we might write to to attract the interest of more
researchers in various fields. Please email me if you have any ideas in that regard.
Thanks all.
-="If in the last few years you haven't discarded a major opinion or acquired a new one, check your pulse, you
may be dead."--Gelett Burgess
PALEODIET Archives
Subject: Soy Protein and a Question to the group
From: Ron Hoggan
Reply-To:
Date: Tue, 16 Dec 1997 17:27:48 -0700
Hi Robert, As you know, your question falls outside the realm of my usual participation. Still, Fraser Scott's
papers (courtesy of Ashton Embry) suggest that soy protein can induce type 1 diabetes in genetically
susceptible rats.
At 04:00 PM 12/16/97 -0400, Robert Crayhon wrote:
> Question: Does anyone in the group know the n6/n3 ratio of grasses that animals in the wild forage
> upon?
I attended a conference in Vancouver, B.C., last month, where a Dr. Pizzorno, ND, spoke. If memory serves,
he indicated that in wild, ranging animals, the balance between omega 6 and omega 3 was about equal. In
grain fed animals, however, there was a huge increase of omega 6, leading to an imbalance.
As I said, this not an area I've focussed on, so I wouldn't know if I have missed some critical feature of what
he said, or if I have gotten it wrong. I'm just repeating what I think I heard. Still, it seems a question well
worth pursuing.
best wishes, Ron Hoggan
PALEODIET Archives
Subject: Grasses and meat fatty acid composition
Reply-To:
Date: Wed, 17 Dec 1997 08:44:00 +0000
On Mon, 15 Dec 1997 BOBDFH wrote:
> upon? I am trying to figure out the effect of animals eating grasses on the fatty acid profile of
> their meat. Thanks.
I can't speak for meat directly, but in cooking residues left in pottery it is the type of animal that determines
the fatty acid composition, and the major distinction that can be made is between ruminant and non-ruminant
(milk can also be distinguished) [1].
What are n3 and n6 abbreviations for?
294/298 (1997)
[1] Evershed, RP "Organic residues in archaeological ceramics: current status and future prospects" Paper
presented at British Association for Near Eastern Archaeology Conference 11 Dec 1997
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: n6/n3 ratio
From: Loren Cordain
Reply-To:
Date: Wed, 17 Dec 1997 17:17:00 -0700
I would like to respond to Robert's question regarding the ratio of omega 6 fatty acids to omega 3 fatty acids
in grasses. Grasses are members of the gramineae plant family of which cereal grains are a prominent
member. Grasses are composed of both leaves and seeds, and the seeds (grains) of commonly consumed
grasses (wheat, rye, barley, oats, maize, millet, sorghum) form the staple food of virtually all of the people
on earth. Polyunsaturated fats are classified by the length of the fatty acid carbon chain, by the number of
double bonds and by the location of the last double bond from the omega end of the fatty acid carbon chain.
Linoleic acid (a common fatty acid found in salad oils) is labeled 18:2n6 (that is, there are 18 carbon atoms
forming the fatty acid chain; there are 2 double bonds; and the terminal double bond is located 6 carbon
atoms from the omega end of the fatty acid chain). Alpha linolenic acid is a common omega 3 (n3) fattty acid
and is labeled 18:3n3 (there are 18 carbon atoms forming the fatty acid chain; there are 3 double bonds and
the last double bond is located 3 carbon atoms from the omega end of the fatty acid chain). There are other
polyunsaturated fats of both the n6 and n3 families with carbon lengths greater than 18 (20, 22 primarily)
which are mainly found in animal food sources. The 18 carbon fatty acids of both n6 and n3 families are
primarily, but not exclusively found in foods of plant origin. The ratio of dietary n6/n3 fatty acids has
important human health implications including the development of coronary heart disease, cancer and
autoimmune diseases. The estimated n6/n3 ratio in modern western diets is about 10-15:1, whereas in preagricultural diets, it has been estimated to be from 2:1 to about 4:1. The high n6/n3 ratio in western diets
stems from the excessive consumption of vegetable oil based fats (margarines, salad oils, etc) which have
been incorporated into the food supply since about 1913 and particularly after WWII. In my soon to be
published manuscript on the deleterious effects of cereal grains upon human health, we report the average
n6/n3 ratio of the 8 most commonly consumed cereal grains to be 21.6. Thus, the seeds of grasses are quite
high in n6 fats, and extremely low in n3 fats. The exact opposite situation is to be found in the leaves. Salem
(1) has shown the n6/n3 ratio to range from 0.09 to 0.12 in the leaves of two grass species. Because the
leaves of grasses form a much greater bulk of the entire plant, it would be expected that for a foraging
herbivore consuming the entire grass plant (grains and leaves), the dietary n6/n3 ratio would quite likely be
less than 1. Since the type of lipid an animal consumes is directly reflected in the type of lipids in both
storage and structural fat, then free ranging animals consuming grasses will have lower n6/n3 ratios in their
tissues compared to feedlot animals consuming only the grains of grasses. Humans consuming the tissues of
free ranging animals will also have lower n6/n3 ratios in their own tissues than compared to individuals
consuming feedlot animals which have been "finished" upon cereal grains. The consumption of free ranging
animals is a very old human practice - the consumption of feedlot fed animals is a relatively new practice,
and with obvious health ramifications.
REFERENCES
1. Salem N. Omega-3 fatty acids: molecular and biochemical aspects. In: New Protective Roles for Selected
Nutrients. GA Spiller, J Scala (Eds). Alan R. Liss, New York, 1989, p. 127.
PALEODIET Archives
Subject: Re: a Question to the group
From: "DOUGLAS A. JEEVES"
Reply-To:
295/298 (1997)

Date: Wed, 17 Dec 1997 20:14:21 -0500
> upon? I am trying to figure out the effect of animals eating grasses on the fatty acid profile of
> their meat. Thanks. well, there is an effect on milk. check this article:
Linkname: Science News Online - Food for Thought - 10/11/97 URL:
http://www.sciencenews.org/sn_arc97/10_11_97/food.htm
the article is called 'why grass makes better milk'. it discusses research on the production of conjugated
linoleic acid (CLA) in cow's milk, a fatty acid which research suggests offers protection against certain
malignancies. cows eating nothing but grass produced five times as much CLA as those on typical feed.
check it out, it has citations.
if you go in at the main page you can check out the other 'Food for Thought' articles, too.
Douglas in Pittsburgh to us will be years and long days with false kings and withering fruit-crops - Merlin:
Hoianau -
PALEODIET Archives
Subject: n6/n3 ratio in grasses
Reply-To:
Date: Fri, 19 Dec 1997 09:22:47 +1100
I would like to add something to the discussion about fatty acid patterns of grasses and the resulting pattern
in animals that feed on these grasses. My understanding of this issue is that the ratio of n3/n6 or the level of
polyunsaturated fatty acid content in grasses is not reflected in the meat/milk of ruminant grazing animals.
This is because the rumen bacteria do a good job of hydrogenating all the PUFAs and the animal absorbs
only saturated fatty acids. Thus the meat and milk of cattle and sheep are fairly saturated irrespective of what
you feed them. On the other hand, pigs and chickens (which are not ruminants) show a fatty acid pattern
which reflects the diet they are getting. I am not sure where caribou etc stand.
Best wishes Jennie
PALEODIET Archives
Subject: Re: n6/n3 ratio
From: Dean Esmay
Reply-To:
Date: Mon, 22 Dec 1997 01:50:40 -0500
For a concise and readable summary of how fats are constructed, what this N6/Omega 6, N3/Omega 3,
double-bond, cis and trans fat stuff is all about, see the following message from Dr. Ed Blonz from another
mailing list I run:
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9712&L=lowcarb&O=A&P=6624
PALEODIET Archives
Subject: Fatty acids and ruminants
Reply-To:
Date: Sat, 27 Dec 1997 15:13:59 +1100
296/298 (1997)
Thank you Loren for correcting my out-of-date information. But I'm still confused! If the majority of the
fatty acids eaten with meat come from the muscle triglcerides and subcutaneous adipose tissue, then surely
the difference in muscle phosholipid fatty acid pattern is of only limited significance.
Alot of work was done in Australia in the 1970's (where cattle are mainly pasture-fed) to increase the PUFA
content by feeding the animals 'protein-protected' PUFAs. The ruminant bacteria were not able to
hydrogenate the PUFAs because of a coating of treated protein. The process worked but there was limited
consumer acceptance of this 'new' meat and its unusual flavour.
Best wishes Jennie
PALEODIET Archives
Subject: pre-primates was: Out of Africa II, Sugars Fruits & Archaeology, Macronutient M ixtures,
Saturated Fat & CHD
From: Dick Dawson
Reply-To:
Date: Sun, 28 Dec 1997 02:20:00 -0500
[..]
> In regards to the out of Africa hypothesis and its relationship to diet I think the data supports
> the concept that early humans left Africa by at least 1 MYA or possibly earlier and were replaced
> by anatomically and behaviorally modern humans in the past 40-60, 000 years. Anatomically modern
> humans likely evolved in Africa and first appear in the fossil record ~100-120 kYA. Therefore this
> population in theory would represent the last common ancestor for which all modern humans could
> trace a common gene pool and ideally could serve as the model for the genetic nutritional
> requirements of all present day humans before the confounding influence of various environments
> wrought by migration etc. on our genome. It is inappropriate to dismiss the nutritional
> evolutionary experience of all hominids prior to the split between anatomically modern humans and
> their predecessors because we share more genes with these hominids than those for which we differ.
[..]
> either hunted or scavenged carcasses. This consumption of animal based foods which led to a
> relatively smaller and less metabolically active gut is still with us today. So presumably all
> hominids including modern humans share the basic gastrointestinal physiology that evolved in
> response to a high meat based diet. Further, all modern humans have poor ability to desaturate and
> chain elongate 18 carbon lipids to 20 and 22 carbon lipids (3). Similar to cats (complete
> carnivores) the inability to efficiently desaturate and chain elongate plant based 18 carbon
> lipids to the 20 and 22 carbon lipids needed for membrane and eicosanoid function has occurred
> because the selective pressure for desaturation and chain elongation has been relaxed. Humans like
> cats eat higher up on the food chain (ie. other animals) in which 20 and 22 carbon lipids are
> present thus there is little need to retain genes for lipid desaturation and chain elongation of
> plant based 18 carbon lipids. Similar arguments can be made for the synthesis of taurine (a
> conditionally essential amino acid) and the conversion of beta carotene to vitamin A. Thus the
> basic physiological adaptation to a meat based diet occurred early on and was likely complete by
> the time early hominids migrated to northern latitudes. Fruit eating hominids could not have left
> the environs of the tropics until they began to utilize a food source that was present not only in
> the tropics but elsewhere. The remains
[..]
Looking back before the paleolithic era at our evolutionary roots:
One physical anthropologist claims that the predecessors of the first primates were insectivores and that the
whole of the primate evolution has been influenced by that gastric formation. I assume that these insectivores
were rather similar to cats in many ways and may have had a common ancestor with cats a few million years
before ie: maybe 20-50mya. But we see that some primates are essentially herbivorous eg: Gorilla gorilla,
various Australopithecines (by dentition) eg: A. boisei. Perhaps some species have adapted at least partially
to a more herbivorous diet. There's great dentitional difference between gorilla and Australopithecine thus
more to study on their herbivoral adaptations.
297/298 (1997)
Depending on one's cladistics perhaps the robust Australopithecines were not ancestors of various Homo ie:
perhaps there's another line of descent from the pre-primate insectivores to H. sapiens than through
Australopithecus or perhaps a branch early in the development of Australopithecines.
source: Syracuse University lectures in physical anthropology by Prof. Mark Fleischman spring 1997.
I'd be interested in analyses of the success of the herbivouous Australopithecines and their apparent
replacement by early Homo. Is this simply a result of encephalization or are there other factors eg: social
adaptations, climatic and other environmental changes etc?
Both Dr. Cordain's scheme and the descent from insectivorous ancestors lead me to suspect the high protein
and fat intake we associate with paleo diet might be most appropriate for most modern humans; something
our physical nature requires or is best adapted for.
Dick http://smith.syr.edu/~ddawson SU Rifle Club: http://smith.syr.edu/~ddawson/surifleclub.html
PALEODIET Archives
Subject: Re: N6/N3 fats
From: Loren Cordain
Reply-To:
Date: Sun, 28 Dec 1997 13:19:00 -0700
In the last digest, Jennie wrote:
"Thank you Loren for correcting my out-of-date information. But I'm still confused! If the majority of the
fatty acids eaten with meat come from the muscle triglcerides and subcutaneous adipose tissue, then surely
the difference in muscle phosholipid fatty acid pattern is of only limited significance.
Alot of work was done in Australia in the 1970's (where cattle are mainly pasture-fed) to increase the PUFA
content by feeding the animals 'protein-protected' PUFAs. The ruminant bacteria were not able to
hydrogenate the PUFAs because of a coating of treated protein. The process worked but there was limited
consumer acceptance of this 'new' meat and its unusual flavour.
Best wishes Jennie"
I would agree that the majority of fat in domestic, grain fed cattle is derived from inter-muscular and
subcutaneous triglycerides, and that these tissues are minimally influenced by dietary lipid manipulations.
However, in wild animals, because there is no inter-muscular fat storage (marbling), and because
subcutaneous fat stores almost never represent more than 4% (seasonally) of total body wt (compared to 3545% for grain fed cattle), the differences in muscle phospholipid fatty acid patterns caused by free ranging
foraging (as opposed to grain feeding) represents a significant difference when compared to domestic
animals. Obviously, the tissue phospholipid fatty acid patterns of individuals consuming free foraging
animals will reflect this difference. The level of enrichment of DHA (22:6n3) by fish oil feedings in cattle is
remarkable and approaches 500%. Mandell (1) has recently shown an increase of DHA (mg/100 fresh wt)
from 1.8 to 11.0, however, as Jennie has pointed out, it is unclear whether this may have a real influence
upon the consumer, since the level of both DHA and EPA (20:5n3) combined, when expressed as a
percentage of total fatty acids rose from 0.2 to 1.0, and fish oil supplementation at this level (10%) definitely
imparts a fish flavor to the meat. The western diet is overburdened by a high dietary n6/n3 ratio (estimated to
be about 10:1), and any attempts to influence the food supply of the average consumer in order to improve
this ratio (closer to the estimated 2-4 to 1 in paleolithic diets) should not be discouraged. Grass fed cattle,
allowed to free forage will not only have a more favorable fatty acid pattern in muscle and organ
phospholipids, but they will have less storage trigylcerides because of the energy expenditure required for
free foraging. Clearly, the massive consumption of foods high in omega 6 fats (certain vegetable oils,
margarines, shortenings) and low in omega 3 fats is vastly at odds with the fats derived from foods available
to our stone age ancestors and is associated with many of the chronic illnesses (cardiovascular disease,
cancer and inflammatory and autoimmune diseases) which plague modern man.
Cordially,
Loren Cordain, Ph.D. Professor, ESS Dept Colorado State University Fort Collins, CO 80523
REFERENCES
1. Mandell IB et al. Omega-3 fatty acid enrichment of Beef. J Anim Sci, in press.
298/298 (1997)
PALEODIET Archives
Subject: Teeth
From: Dean Esmay
Reply-To:
Date: Sat, 10 Jan 1998 12:07:46 -0500
One of the most common arguments advanced by advocates of vegetarianism, and by some other
commentators on health, is that humans evolved as vegetarian or mostly-vegetarians. The most frequently
forwarded argument to advance this position is that human tooth and jaw structrure are clearly those of
herbivores, with flat molars, excellent sideways chewing motion, and with a clear lack of sharp teeth for
killing prey.
I most recently heard a snippet of this line of thinking on a popular news show here in America called
"Nightline" in which a medical doctor and health writer advanced this view.
I wonder if anyone among our membership would like to comment on this line of reasoning?
PALEODIET Archives
Subject: Re: Teeth
Reply-To:
Date: Mon, 12 Jan 1998 08:47:10 +0000
On Sat, 10 Jan 1998 Dean Esmay wrote:
> One of the most common arguments advanced by advocates of vegetarianism, and by some other
> commentators on health, is that humans evolved as vegetarian or mostly-vegetarians. The most
> frequently forwarded argument to advance this position is that human tooth and jaw structrure are
> clearly those of herbivores, with flat molars, excellent sideways chewing motion, and with a clear
> lack of sharp teeth for killing prey. I most recently heard a snippet of this line of thinking on
> a popular news show here in America called "Nightline" in which a medical doctor and health writer
> advanced this view. I wonder if anyone among our membership would like to comment on this line of
> reasoning?
One must remember that teeth are only a part of the dentition. According to Hillson (1986, p13-14) The
dentition functions in eating (not necessarily its only function) for crushing, slicing or grinding food. "Most
of these functions are accomplished by the jaw muscles, but it is also to do with the hinges points, the
temporomandibular joints (TMJ for short) ..... The complexity of these joints varies."
Carnivores cut up their food by shearing one sharp-ridged tooth against another, only requiring an up and
down movement. Hence the TMJ is limited. The same is true of insectivores which merely crush food
between sharp sets of cusps.
Herbivores tend to specialise in side to side (e.g. ungulates) or back and forth (e.g. rodents) lower jaw
movements to grind their food.
Humans use a complex process of up and down, side to side and back and forth motions.
This suggests to me that we are omnivores, with some herbivore and some carnivore features. "Flat" molars
(technically bunodont, with low rounded cusps rather than sharp ridges) are found in primates, bears and
suiform artiodactyls, as well as some generalised carnivores within Musteildae, Viverridae and Canidae
(Hillson p17) so one cannot argue from molar shape alone, or one would have to argue that badgers,
mongooses and racoon-dogs are all vegetarian!
Reference
Hillson, S (1986) Teeth. Cambridge Manuals in Archaeology. Cambridge University Press: Cambridge, UK
Andrew Millard
========================================================================= Dr.
=========================================================================
1/147 (1998)
PALEODIET Archives
Subject: Re: PALEODIET Digest - 28 Dec 1997 to 10 Jan 1998
From: Clark Larsen
Reply-To:
Date: Mon, 12 Jan 1998 09:05:32 -0500
On Sat, 10 Jan 1998, Automatic digest processor wrote:
> Topics of the day: 1. Teeth One of the most common arguments advanced by advocates of
> vegetarianism, and by some other commentators on health, is that humans evolved as vegetarian or
> mostly-vegetarians. The most frequently forwarded argument to advance this position is that human
> tooth and jaw structrure are clearly those of herbivores, with flat molars, excellent sideways
> chewing motion, and with a clear lack of sharp teeth for killing prey.
As a biological anthropologist with an interest in teeth and function, let me take a stab at this argument. First,
there is plenty (and growing) evidence that humans evolved with a very generalized rather than "vegetarian
or mostly-vegetarian" diet. This evidence is based on stable isotope analysis, trace element analysis,
microwear, archaeological remains, etc. Regarding teeth, my take on the evidence is that the human dentition
is adapted especially for generalized diet ranging in some populations that consume a great deal of plant
foods to some populations consuming a heck of a lot of meat (e.g., traditional Eskimos). Although I've been
studying humans, their past remains, and diet for a couple of decades, I am always struck by the amazing
variability in diets, past and present, and the remarkable versatility of the dentition. Although the argument
can be made that humans lack a canine that can be used for cutting--or for killing prey--the additional
versatility of culture and technology provides more than sufficient means for acquisition of food via hunting.
The point here is not that the human dentition and jaw structure is not adapted to consumption of plant foods,
but rather than the dentition and jaws a adapted to a wide range of foodstuffs.
Some key resources that readers may want to look at are:
(1) Conroy, Glenn C. (1990) Primate Evolution. New York: Norton.
(2) Conroy, Glenn C. (1997) Reconstructing Human Origins. New York: Norton.
(3) Hillson, Simon (1986) Teeth. Cambridge: Cambridge Univ. Press.
(4) Hillson, Simon (1996) Dental Anthropology. Cambridge: Cambridge Unv. Press.
For information on dietary reconstruction in ancient bones and teeth, I present an overview in:
(5) Larsen, Clark Spencer (1997) Bioarchaeology: Interpreting Behavior from the Human Skeleton.
Cambridge: Cambridge University Press.
There is a great deal of information in the biological anthropology and paleoanthropology literature on past
diet and adaptation. I think most will come to the conclusion that advocates of vegetarianism have a too
simplistic perspective on adaptation, at least with respect to the masticatory apparatus. From my perspective,
it is the complexity of the issue, however, that makes the problem interesting and exciting, especially when it
comes to human origins and evolution.
PALEODIET Archives
Subject: Re: More on teeth and hominid diet
From: Loren Cordain
Reply-To:
Date: Thu, 15 Jan 1998 16:31:00 -0700
2/147 (1998)
I am in agreement with both Clark and Andrew's previous posts that human dentition is adapted for a
generalized diet composed of both plant and animal foods and that human populations show amazing
variability in their plant to animal subsistence ratios. However, it is important to recognize that hominids
have evolved important metabolic and biochemical adaptations which are indicative of an increasing
physiological dependence upon animal based foods. Further, comprehensive compilations of hunter gatherer
subsistence strategies indicate that whenever it is ecologically possible, humans will almost always consume
more animal food than plant food. We have recently compiled the plant:animal subsistence ratios data in the
Ethnographic Atlas (1) for all world wide181 hunter gatherer populations which have been studied either
historically or by contemporary anthropologists. The analysis shows that in the majority (61.3%) of world
wide hunter-gatherers, gathered plant food represents 35 % or less than the total foods utilized. Only 2.2% of
the world's hunter gatherers derive 66% or more of their total foods from plants; further not a single hunter
gather population derives 86 % or more of its total calories from plant foods. The most frequently occurring
(mode) plant:animal subsistence ratio for world wide hunter gatherers is (16-25% plant): (66-75% animal),
and the median value is (26-35% plant): (56-65% animal). These values corroborate 5 careful modern studies
of hunter gatherers showing a mean energy intake from animal food sources to be 59% (2). Pongids, because
thier diet is largely plant based, must maintain large and metabolically active guts to process the fibrous plant
foods which compose over 93% or greater of their dietary intake. In contrast, the human gut is much smaller
and less metabolically active than the ape gut. Presumably this adaptation (reduction in gut size and
metabolic activity) evolved in humans because the inclusion of nutrient dense, animal based foods by our
early hominid ancestors allowed the selective pressure for a large metabolically active gut to be relaxed (2,
3). In addition to the smaller gut that humans maintain relative to apes, there are other metabolic and
biochemical clues which point to increased utilization of animal food by humans over our evolutionary
history. By evaluating the metabolic and biochemical dietary adaptations of cats (obligate carnivores) and
those in humans (omnivores), it becomes apparent that evolution has shaped both hominid and feline
metabolic machinery towards a diet in which animal food was predominant. Obligate carnivores, such as
cats, must obtain all of their nutrients from the flesh of other animals and have therefore evolved certain
biochemical adaptations which are indicative of their total dietary dependence upon animal based foods.
Most of these biochemical adaptations involve either the loss (or reduced activity) of certain enzymes
required for the synthesis of essential nutrients. These adaptations generally occurred because the selection
pressure to maintain these metabolic pathways was relaxed as cats gradually increased the amount of animal
food in their diet as they evolutionarily progressed from omnivory into obligate carnivory. Vitamin B12 is an
essential nutrient for both herbivorous and carnivorous mammals. Because B12 is not found in higher plants,
herbivorous mammals must soley rely upon absorption of B12 from bacteria which synthesize it in their gut.
Cats can neither synthesize B12, nor absorb it from their gut, consequently they have become wholly
dependent upon animal flesh as their source for this essential nutrient. Humans, like cats are unable to
synthesize or absorb vitamin B12 and are also reliant upon animal based sources of this essential vitamin,
since it does not occur in a biologically active form in any of the plant foods which humans normally eat.
The absence of the ability of humans to either synthesize or absorb bacterially produced B12 is indicative of
the long evolutionary history of animal based foods in our diet. Taurine is an amino acid which is not found
in any plant based food (4) and which is an essential nutrient in all mammalian cells. Herbivores are able to
synthesize taurine from precursor amino acids derived from plants, whereas cats have completely lost the
ability to synthesize taurine (5). Since all animal based foods (except cow milk) are rich sources of taurine
(4), cats have been able to relax the selective pressure required for taurine synthesis because they obtain all
of this nutrient that they need from their exclusive meat based diet. Humans, unlike cats, still maintain the
ability to synthesize taurine in the liver from precursor substances, however this ability is quite limited and
inefficient when compared to herbivores. Vegan vegetarians following diets devoid of animal products
display unusally low levels of both plasma and urinary taurine (6) - levels which are indicative of the poor
ability of humans to synthesize taurine. Similar to cats, this inability to efficiently synthesize taurine has
come about because the selective pressure to produce this amino acid has been gradually reduced due to
human kind's long reliance upon animal food, a food which is quite high in taurine. Plant based foods contain
18 carbon fatty acids of both the omega 3 and omega 6 families, but are virtually devoid of the 20 and 22
carbon fatty acids which are required for the normal functioning of all mammalian cells, whether the
mammal is a herbivore or carnivore. Herbivores have evolved hepatic enzymes (desaturases and elongases)
which allow these precursor plant based 18 carbon fatty acids to be chain elongated and desaturated to their
20 and 22 carbon products. Cats have extremely low levels of the enzymes required to make 20 and 22
carbon fatty acids (7). Again, the selection pressure to synthesize 20 and 22 carbon lipids has been almost
entirely removed because cats obtain sufficient quantities of these long chain fatty acids by eating animal
3/147 (1998)
tissues which are rich sources of these lipids. Similarly, humans also have inefficient elongase and desaturase
enzymes (7). Again, this metabolic change has occurred largely because the need to desaturate and chain
elongate 18 carbon plant fatty acids to their 20 and 22 carbon products has been reduced because humans,
like cats, have obtained their 20 and 22 carbon lipids directly by eating other animal tissues. All animals,
whether herbivore or carnivore require vitamin A. Vitamin A is not found in any plant based food;
consequently, herbivores must synthesize it in the liver from beta carotene consumed from plant based foods.
Cats have lost the ability to synthesize vitamin A from beta carotene (8), and must obtain all of their vitamin
A from the organs (liver, kidney) of their prey. Again, cats have lost the ability to synthesize vitamin A
because the selective pressure (need) to provide adaptive energy for the synthesis of proteins needed to
catalyze the production of vitamin A were reduced as cats progressively increased the amount of animal
foods in their diets. Recently, it has been shown that humans also have limited capactity to synthesize
vitamin A from beta carotene (9), presumably because humans, like cats, have consumed vitamin A rich
animal food sources for eons and are in a transitional state from omnivory to obligate carnivory. These
metabolic and biochemical adaptations in humans in response to increasingly meat based diets as well as the
anthropological evidence provided by both contemporary and historical studies of hunter gather diets provide
strong evidence for the central role of meat and animal tissues in the human diet. Although it is true that
human populations can survive under broad plant:animal subsitence ratio's, the consensus evidence supports
the notion that whenever it was ecologically possible, animal calories would have always represented the
majority of the total daily energy intake.
Cordially,
Loren Cordain, Ph.D. Dept of ESS Colorado State University Fort Collins, CO 80523 (970) 491-7436
REFERENCES
1. Murdock GP. Ethnographic atlas: a summary. Ethnology 1967;6:109-236. 2. Leonard WR et al.
Evolutionary perspectives on human nutrition: the influence of brain and body size on diet and metabolism.
Am J Hum Biol 1994;6:77-88. 3. Aiello LC, Wheeler P. The expensive tissue hypothesis. Current
Anthropology 1995;36:199-221. 4. Laidlow SA et al. The taurine conte of common foodstuffs. J Parenteral
Enteral Nutr 1990;14:183-88. 5. Knopf K et al. Taurine: an essential nutrient for the cat. J Nutr
1978;108:773-778. 6. Laidlow SA. Plasma and urine levels in vegans. Am J Clin Nutr 1988;47:660-3. 7.
Salem N et al. Arachidonate and docosahexaenoate biosynthesis in various species and compartments in
vivo. World Rev Nutr Diet 1994;75:114-19. 8. MacDonald ML et al. Nutrition of the domestic cat, a
mammalian carnivore. Ann Rev Nutr 1984;4:521-62. 9. de Pee S, West CE et al. Lack of improvement in
vitamin A status with increased consumption of dark leafy green vegetables. Lancet 1995;346:75-81.
PALEODIET Archives
Subject: Emergence of stroke in Papua New Guinea
Reply-To:
Date: Thu, 15 Jan 1998 21:33:25 +0100
We have recently returned to Sweden from a reconnaissance trip to Port Moresby, the capital of Papua New
Guinea. Our aims are twofold: 1) To study the effects of urbanization among traditional subsistence
horticulturalists on the incidence and prevalence of cardiovascular disease (spontaneous sudden death,
retrosternal effort angina, aphasia and hemiparesis) and on cardiovascular risk factor levels. 2) To facilitate
necessary efforts of preventing the emergence of cardiovascular disease in developing countries.
We are sorry to tell you that stroke is rapidly becoming a major health problem among urbanized Papuan
New Guineans, even more so than myocardial infarction which is however also coming up [1]. We saw one
obvious case of stropke; hemiplegia and aphasia in a 47 year old smoking male. There are almost two stroke
cases every week at the Port Moresby General Hospital where the first was reported in the mid 70s (Kevau I,
personal communication). We roughly estimate that the hospital serves some 300 thousand inhabitants.
Thus, history repeats itself; the same pattern was seen in Uganda from the 1940s and onwards when stroke
emerged from virtual absence in the 1930s to similar prevalences as in the West around 1970 [2-4]. This was
parallelled by a dramatic change in diet and lifestyle.
The effect of a paleolithic lifestyle in the prevention of stroke may be heavily underestimated by the medical
community.
4/147 (1998)
1. Kevau IH. Clinical documentation of twenty cases of acute myocardial infarction in Papua New Guineans.
P N G Med J 1990; 33: 275-80. 2. Muwazi E. Neurological disease among african natives of Uganda: A
review of 269 cases. East Afr Med J 1944; 2-19. 3. Hutton PW. Neurological disease in Uganda. East Afr
Med J 1956; 33: 209-223. 4. Billinghurst JR. The pattern of adult neurological admissions to Mulago
hospital, Kampala. East Afr Med J 1970; 47: 653-63.
Staffan Lindeberg and Dan Petersson Dept of Community Health Sciences, Lund University, Sweden
PALEODIET Archives
Subject: Rickets in Dorset 1600 A.D.
Reply-To:
Date: Thu, 15 Jan 1998 23:20:13 +0100
Rickets, or "the English disease", may have emerged around Dorset and Somerset in the early 17th century.
Some remarks made on this topic by myself, Martha Sherwood at the Dept of Ecology and Evolution,
University of Oregon, and by the historian Thomas Jackson may be of interest to some of our readers.
Perhaps any of you has something to add or time enough to check up some of the suggested lines.
------------------------------------I wrote to a listserv on the history of England and Wales:
IN BRIEF Rickets is a disease of infancy and childhood which causes marked skeletal changes that can
easily be identified by osteologists. The disease is rare or absent in preagricultural human skeletons, while
the prevalence seems to have increased during medieval urbanization, at least in some cities, and then to
have exploded shortly before industrialization starting in southwestern England in the early 17th century. In
the year 1900 more than 80 per cent of Northern European children may have been affected. This dramatic
increase can hardly be explained only in terms of decreasing exposure to sunlight (which is important for the
activation of vitamin D), not even after considering descreased length of breast-feeding (milk is a good
source of vitamin D). Another possible contributing factor is an increasing inhibition of calcium absorption
by phytate from cereals since their intake increased during the Middle Ages, and since old methods of
reducing phytate from cereals (dampening, heat treatment, sourdough baking etc) appear to have been lost
during the emergence of yeast baking and large-scale cereal processing.
5/147 (1998)
IN DETAIL The first adequate description of rickets is attributed to Soranus of Ephesus (A.D. 98-138), who
observed more cases in the neighborhood of Rome than in other places including Egypt. He specifically
stated that it did not affect Greek children. Apparently, the term rickets was first mentioned in the mortuary
tables of London in 1634, when 14 of 10, 900 persons were reported to have died from rickets. Shortly
before 1645, Dr. Francis Glisson (1597-1677), who was born in the village of Rampisham in Dorset,
reported to the College of Physicians about the disease. In 1650, after more than five years of discussions
within the college he wrote a book on the subject, entitled De Rachitide sive Morbo Puerili qui Vulgo The
Rickets Dicitur (On rachitis or a disease which ordinary people call the rickets). One year later Glisson and
two others stated that "This disease became first known as near as we could gather from the relation of
others, after sedulous inquiry, about thirty years since, in the counties of Dorset and Somerset since which
time the observation of it hath been derived unto all the southern and western parts of the Kingdom". At
about the same time, and possibly without knowledge of the mentioned discussions, Thomas Fuller (16081661) a divine living in Exeter, noted that "There is a disease of infants .... having scarcely as yet gotten a
proper name in Latin, called the rickets; wherein the head waxeth too great, whilst the legs and lower parts
wane too little". Shortly thereafter the disease had spread to other parts of England and later throughout
Europe. It cannot be excluded that the spread was slightly earlier, considering that Floyer in 1706 wrote that,
"In the time of King Charles" (who was born in 1600 and was king from 1625 until his execution in 1649)
rickets "was almost epidemical, few families escaping it". From what I have gathered, in the 1600s it was
mainly the children in the high and middle ranks of society who appear to were affected, while two centuries
later it was rather those of the lowest ranks. Scrutinizing cereals is not as far fetched as it may seem. Cereals
and other seeds have in their shells phytic acid which strongly binds to minerals like calcium, iron, zinc and
magnesium to form insoluble salts, phytates. It is well known that whole meal cereals by this mechanism
decrease the absorption of such minerals. There is apparently no adaptation to a habitual high intake of
phytic acid, why this is an important contributing cause of iron deficiency in third world countries. It is also
an important cause of mineral deficiency in vegetarians. Mellanby found back in the 30s that young dogs got
rickets when they were fed oatmeal. He was made aware of the calcium-binding effect of phytate and
showed that phytate was the dietary factor responsible for inhibition of calcium absorption by oatmeal as
well as the induction of rickets in dogs. McCance and Widdowson found adverse effects of bread prepared
from high-extraction wheat flour on retention of essential metals by humans. They also showed that
destruction of phytate improved retention of calcium. Substantial evidence have later firmly established this
negative impact of phytate. Contemporary Asian Indians are at high risk of rickets which can be healed or
prevented by removal of chapatti bread from the diet. Not even rats seem to be fully adapted to
graminivorous diets since phytate adversely affects mineral absorption in them as well. Accordingly, in
addition to lower intake of meat, fish and dairy products (which are important sources of vitamin D) during
and after the Middle Ages, as well as decreased exposure to sunlight and earlier weaning during
industrialization, a possible contributing cause of rickets is thus a secular trend of increasing intake of
phytate. This could be the case if cereal intake increased during the Middle Ages and if old methods of
reducing the phytate content such as malting, soaking, scalding, fermentation, germination and sourdough
baking were lost by the emergence of large-scale cereal processing and the introduction of yeast baking. The
mentioned methods reduce the amount of phytic acid by use of phytases, enzymes which are also present in
cereals and which are easily destroyed during industrial cereal processing. So, what happened in Dorset and
Somerset in the early 17th century and later in the rest of England? Since my knowledge of history may be
less than that of your worst students of history, it may be rather daring when I propose that the practice of
using beer-yeast in bread baking was first introduced from France to Dorset, where Dorchester was
apparently once famous for its breweries. Nor do I know when and where enclosure first became widespread
and what impact such a spread would have on the availibility of small game and fish to common people.
Finally, what conclusions can be drawn from the fact that between 1500 and 1650 the purchasing power of
wage rates decreased by more than 50 per cent while the price of agricultural products increased by 700 per
cent after both had been stable for at least 50 years? Would this imply that poverty was increasing and that
access to milk, cheese and meat declined markedly while common people had to rely ever more on cereals? I
should mention another possible contributing dietary factor: salt. Urinary excretion of calcium is directly
related to sodium intake which accordingly theoretically may deprive the body of calcium from the skeleton.
However, I would expect salt intake to have increased much earlier than 1600. Any relevant information is
most welcome.
6/147 (1998)
REFERENCES Caprez A, Fairweather TS. The effect of heat treatment and particle size of bran on mineral
absorption in rats. Br J Nutr 1982; 48: 467-75. Thirsk J (Ed). Chapters from the Agrarian History of England
and Wales. Vol 1-5. Cambridge Univ Press 1990. Gibbs D. Rickets and the crippled child: an historical
perspective. J R Soc Med 1994; 87: 729-32 [Comment by Black J in J R Soc Med 1995; 88: 363-4]. Gibson
RS. Content and bioavailability of trace elements in vegetarian diets. Am J Clin Nutr 1994; 59(5 Suppl):
1223S-1232S. Harrison D, Mellanby E. Phytic acid and the rickets-producing action of cereals. Biochem J
1934; 28: 517-28. Hernigou P. Historical overview of rickets, osteomalacia, and vitamin D. Rev Rhum Engl
Ed 1995; 62: 261-70. McCance R, Edgecombe C, Widdowson E. Mineral metabolism of dephytinized bread.
J Physiol 1942; 101: Mellanby E. A story of nutrition research. Baltimore: Williams & Wilkins Co, 1950
Pettifor JM. Privational rickets: a modern perspective. J R Soc Med 1994; 87: 723-5. Sandberg AS. The
effect of food processing on phytate hydrolysis and availability of iron and zinc. Adv Exp Med Biol 1991;
289: 499-508. Sandstead HH. Fiber, phytates, and mineral nutrition. Nutr Rev 1992; 50: 30-1. StuartMacadam PL. Nutritional deficiency diseases: a survey of scurvy, rickets, and iron-deficiency anemia. In:
Iscan MY, Kennedy KAR, eds. Reconstruction of life from the human skeleton. New York: Wiley-Liss,
1989: 201-22.
------------------------------------Martha Sherwood wrote: I found your posting on the English History list most interesting. Two things that
might be relevant, both anecdotal: An observation one runs across frequently in travel literature from the late
18th-early 19th century is the surprisingly good health of the Irish peasantry, despite their extreme poverty.
One would expect a population that relied on potatoes as a starch base to have a lower incidence of rickets
than one which relied on grains. The incidence of dental caries also seems to follow the sort of pattern you
are describing. I ran across something in a literary source that suggested that rickets was epidemic in the
children of people exiled to northern regions of the Soviet Union in the 30's and 40's, though not particularly
common in the regions these people had come from or among native peoples of Siberia. This would have
been a population forced by extreme poverty to rely on a diet consisting almost entirely of grain. Middleaged people in Russia in general have very poor teeth, again probably ascribable to childhood calcium
deficiency. From: (Martha Sherwood)
------------------------------------Thomas Jackson wrote: This is not my topic, I am a local historian living in the North of England but I found
the question interesting as I used to work in the food industry. Have you looked at a book called Food in
England by Dorothy Hartley, I do not have a copy but it may have something which is relevant. Have you
looked at the timing of mortality crisis in the SW of England in Wrigley and Schofield The population
history of England 1541-1871 in case harvest failures could have caused diet changes? Could there have
been a reduction in the milk intake of Dorset children due to increased demand for cheese outside the county,
Dorset blue vinney is a famous English cheese. Could a reduction of the use of salted meat as cattle began to
be fed on winter forage during the 17th century make the addition of salt directly to food at higher
concentrations more likely. Dorothy George in her book London life in the 18th Century, says that in London
the number of deaths from ricketts in the Bills of Mortality declined steadily which was attributed to the
more maternal attention to the suckling and rearing of children. Do you know there is a local history list on
mailbase in the UK, it is not very active but it might get an answer from someone in Dorset. From: Thomas
Jackson
-------------------------------------
7/147 (1998)
Martha Sherwood also wrote: I had some more thoughts, very general and not fully formed, on the subject of
phytate sequestration of essential minerals in heavily graniverous populations. (1). Did Greeks and Romans
have different techniques for baking bread? I read somewhere that the teeth of Greek skeletons were in
significantly better shape than contemporary Romans. Were the Greeks and Egyptians more likely to be
processing grain at home? (2). Does alkalai neutralize phytate? Soaking in alkalai is practiced by many
traditional American cultures as a means of processing corn. Also, in the type of oven used throughout the
mideast until comparatively recently and in Europe in the Middle Ages, bread is baked in flat loaves in ashes
in the fire chamber, which results in an alkaline ash-impregnated crust. Would switching to an oven with a
separate fire chamber increase exposure to phytates? This would I think be consistent historically with the
pattern that is observed in England for rickets. Maybe also consistent with what is observed in India, where
chapati and nan used to be baked in tandoori ovens, which work on the same principle, but are now more
likely to be baked on kerosene-fired grills. (3). A sketchy survey of the anthropological literature reveals
what looks like a short-lived phase in the growh of agricultural communities where there is a high incidence
of bone abnormalities and dental caries, does this correspond to a period where burgeoning population
decreased people's access to game and livestock, but a usable technique for reducing phytate intake had not
yet been discovered by trial and error. (4). Childhood rickets is a contributing cause to high infant and
childbirth mortality. Is it possible that our picture of the prevalence of these in the past is skewed by much of
the hard data coming from the early modern period in England? Another thing comes to mind, re previous
communication. Those healthy Irish potato eaters underwent a population explosion in the latter eighteenth
century. It would be interesting to get hold of records from representative parishes of the period and calculate
things like infant mortality and life expectancy, comparing them with England. (5). I think this may have a
bearing on a question that has been puzzling me for years. Grain eaters from high latitudes have a notorious
prediliction for preferring to consume their starch base in fermented form. The increase in rickets in England
does correlate with the rise of puritanism, in attitudes such as frowning on children drinking beer for
breakfast. The people responsible for the "disease theory of alcoholism" account for the latitudinal variation
in rates of alcoholism (which depends more on where your ancestors came from than where you were born
and raised) by postulating that since people in mediterranean cultures have had many more generations over
which their ancestors had access to alcohol, so the trait has been selected against in their populations. I
reasoned that one cannot acount for a high-frequency deleterious hereditary trait solely on the basis that it
has not in the past been selected against; there has to have been some compensatory advantage. If the beer
drinkers suffered fewer skeletal defects and thus had better reproductive success than the teetotalers, one
would have a situation where a taste for beer was selected for. Before widespread access to distilled liquor, it
would have been uncommon in any case for people to drink enough to suffer really adverse health effects
before they reached the end of their reproductive years. Hogarth's prints, "Beer alley" and "gin lane" come to
mind, the beer drinkers are depicted as being in robust good health and the gin drinkers as wallowing in
misery. Beer drinking was considered in 18th century England to be particularly beneficial for nursing
mothers; contracts for wet nurses often specified a generous beer allowance. (6). Natives of northern Russia
and Siberia are fond of kvas, made of fermented rye bread. In an area of northwestern China the preferred
way of preparing maize, the dietary staple, is to steam cornmeal mush and then allow it to ferment (the
fungal fermentation used produced carcinogens, which only became a problem when the average life
expectancy in the area increased under Communism). (7). Heavy taxation of the rural peasantry to finance
development in Meiji Japan led to increased reliance on rice bran and seeds of wild grasses as a food source;
one sees an increase in mineral deficiency diseases associated with it. I'll let you know what else I come up
with.
------------------------------------My comment: Optimal pH for degradation of phytic acid by phytases is 5.15. Accordingly alkali would not
be of any help. A more probable reason why traditional populations have treated cereals or maize with alkali
is to prevent pellagra. Read more about this and other cereal issues in a very, very interesting review by - the
one and only - Loren Cordain: Cereal Grains: Humanity's Double Edged Sword. World Rev Nutr Diet 1998,
in press.
-------------------------------------
8/147 (1998)
Thomas Jackson also wrote: Have you looked at Norman Moore' The history of the first treatise on rickets'?
He also wrote Cause and Treatment of rickets, and probably wrote the account in the DNB of Francis
Glisson. That is where I got those references, he implies that while Glisson may have described the disease
on observations in his native Dorset, that the disease had always occurred where infants were fed solid food
during suckling. This is written in 1885 before the work on vitamin D. This may mean there is no factor
unique to Dorset which can be related back to Glisson's initial work . I used to be an information officer in
industry so find it difficult to get out of the habit of searching.
------------------------------------Any further comments?
Best regards
Staffan
-------------------------------------------------------------------
PALEODIET Archives
Subject: Teeth
Reply-To:
Date: Fri, 16 Jan 1998 14:46:25 +1100
I'm finding the current discussion about teeth fascinating. I would like to ask Clark Larsen if there is any
evidence of genetically determined differences in tooth and jaw structure from one human population to
another. Specifically, is there evidence that one population was evolving on more meat and less plant matter
versus another? Do the Eskimos have different teeth/jaws to the !Kung bushmen?
Best wishes Jennie
PALEODIET Archives
Subject: Teeth and adaptation
From: Mark Leney
Reply-To:
Date: Sat, 17 Jan 1998 09:14:39 -0500
A brief comment on the tooth form and diet issue. This is really a very old chestnut indeed. While it is
perfectly possible to attribute subtle changes in dentition to changes in diet in most species, the fact that
Homo has been processing its food for at least 2.5 million years means that the pattern of adaptation has
become somewhat uncoupled. Broadly early hominids have broader and flatter molars than their primate
ancestors suggesting a somewhat tougher diet, perhaps more dry and fibrous plant material as opposed to the
fruit and soft leaf diet of chimps. However given that chimps and baboon eat significant quantities of meat
and yet have relatively high-crowned teeth this all starts to look a little wobbly. Orang-utans have
superficially more human looking teeth but little is known of their evolutionary ecology. From the early
hominid pattern we see the megadonty of the robust 'australopithecines' with their large mill-stone like
molars popularly but not exclusively attributed to a diet of tough vegetable matter. The progressive reduction
of the human dentition in the Homo lineage is generally held to represent a shift to food processing before it
was put in the mouth rather than a change in diet per se. Thus the flat molars of humans are probably
explained by a shift to tougher/gritier food than the other great apes around 5 million years ago, the side to
side motion facilitated by the reduction in the size of the canine and the loss of the canine/premolar complex.
But by 2 million years ago Homo was a committed meat eater; that this is not reflected in the teeth merely
emphasizes the role of stone tools.
9/147 (1998)
Mark Leney Institute of Biological Anthropology Oxford
PALEODIET Archives
Subject: Teeth
From: Ron Hoggan
Reply-To:
Date: Sat, 17 Jan 1998 12:09:21 -0700
Parts/Attachments:
Fri, 16 Jan 1998 14:46:25, Jennie Brand Miller said:
>
>
I'm finding the current discussion about teeth fascinating.
I agree.
I would like to ask Clark Larsen if there is any evidence of genetically determined differences in tooth and
jaw structure from one human population to another. Specifically, is there evidence that one population was
evolving on more meat and less plant matter versus another? Do the Eskimos have different teeth/jaws to the
!Kung bushmen?
Yes, I would be very interested in that too. Although I have never seen a Kung bushman, I have seen Inuit
people (Eskimos) and they do appear to have a distinct jaw line. I have also noticed (although I've never
really looked inside an Inuit's mouth) that some have front teeth which appear shorter and broader than those
of other racial origins. This may be due to softening hide but if memory serves, the Inuit men also had
similar tooth shapes, and my memory is that they do not, typically, chew hides.
I am looking back ~35 years, and I did not pay much attention to teeth at the time, so I am very open to
correction on this issue.
On the same topic, I appreciate Loren Cordain's discussion of Humanity's metabolic preference for a diet
dominated by meat.
best wishes,
Ron Hoggan
PALEODIET Archives
Subject: Teeth
From: Dean Esmay
Reply-To:
Date: Sat, 17 Jan 1998 17:23:09 -0500
I'm told that the Inuit usually have the shovel shaped incisors and that Christie Turner has done some work
on that. Apparently this type of tooth turns up in people whose ancestors were from NE Asia, and they are
considered diagnostic of these human type by some.
Anyone know more about this?
PALEODIET Archives
Subject: Re: Teeth
Reply-To:
Date: Mon, 19 Jan 1998 00:01:25 +0100
Dean Esmay has been told
10/147 (1998)
> that the Inuit usually have the shovel shaped incisors and that Christie Turner has done some work on >
that. Apparently this type of tooth turns up in people whose ancestors were from NE Asia, and they are
> considered diagnostic of these human type by some.
According to Mayhall [1], "The frequency of the occurence of shovel-shaped incisors is generally held to be
greatest in Mongoloid populations and lower in other groups. ... In general, populations native to Asia and
North America have the deepest lingual fossae (larger than 0.9 mm), South Americans having intermediate
depths (0.5-1.0 mm) and Europeans the shallowest (0.3-0.7 mm). If only the larger expressions (shovel and
semishovel) are included, one can generalize and show that North and South American natives demonstrate
an occurence of 70%-95%, Asians about the same as the Amerindians, Melanesians approximately 6%-20%,
Australian Aborigines about 60%-90%, Europeans 5%-50% and Teso and Bantu from Africa between 10%
and 20% [2]. In North America, Indians and Inuit have about the same occurence of the trait, but the Indians
have the larger expressions [3].
In his review, Mayhall states that "the use of dental morphological traits such as Carabelli's trait, shovelshaped incisors, molar cusps and groove patterns, and protostyloid continues to be valuable in general
population identification and comparison", although he is oviously concerned about the lack of
standardization of techniques [1].
1 Mayhall JT. Techniques for the Study of Dental Morphology. In: Saunders SR, Katzenberg MA. Skeletal
Biology of Past peoples: Research Methods. Wiley-Liss 1992, 59-78: 2 Mizoguchi Y. Shovelling: A
statistical analysis of its morphology. Univ Tokyo Bull 1985; 26: 1-176. 3 Mayhall JT. Dental morphology
of Indians and Eskimos: Its relationship to the prevention and treatment of caries. J Can Dent Assoc 1972;
38: 152-4.
------------------------------------------------------------------Staffan Lindeberg M.D. Ph.D. Dept of Community Health Sciences, Lund University, Mailing address:
Primary Health Care Centre, Sjobo, S-22738 Sweden, +46 416 28140, Fax +46 416 18395
http://www.panix.com/~paleodiet/lindeberg/
-------------------------------------------------------------------
PALEODIET Archives
Subject: Re: PALEODIET Digest - 14 Jan 1998 to 16 Jan 1998
From: Clark Larsen
Reply-To:
Date: Mon, 19 Jan 1998 07:41:39 -0500
Thanks to Loren Cordain for his very interesting discussion of plant and meat intakes, and the evidence for
increased use of animal food by humans in evolutionary history. The survey he did in the Ethnographic Atlas
is revealing. Loren, I hope you are planning a publication.
> I'm finding the current discussion about teeth fascinating. I would like to ask Clark Larsen if
> there is any evidence of genetically determined differences in tooth and jaw structure from one
> human population to another. Specifically, is there evidence that one population was evolving on
> more meat and less plant matter versus another? Do the Eskimos have different teeth/jaws to the
> !Kung bushmen?
Clearly, there is some genetic basis for tooth and jaw size and structure, but this is very poorly known. Tooth
size probably has a greater genetic basis than bone size, but regardless, both have a signficant environmental
influence. There are differences in some aspects of morphology in teeth between Eskimos and !Kung San,
but the overall pattern of morphology similar. Eskimos have larger teeth than !Kung San, and this likely
reflects differences in diet. The presence of shovel-shaped incisors in Asian and Asian-descent populations
(e.g., Native Americans) perhaps reflects different dietary histories, and at least in part is associated with
large anterior teeth (incisors). An excellent overview of morphological differences seen in modern humans
is:
Scott, G. Richard, and Christy G. Turner II (1997) The Anthropology of Modern Human Teeth: Dental
Morphology and Its Variation in Recent Human Populations. Cambridge: Cambridge University Press.
An important source dealing with tooth size:
Kieser, J.A. (1991) Human Adult Odontometrics. Cambridge: Cambridge University Press.
A number of papers presented on tooth size, morphology, and tooth use and adaptation are presented in an
edited volume:
11/147 (1998)
Kelley, Marc A., and Clark Spencer Larsen (eds.) (1991) Advances in Dental Anthropology. New York:
Wiley-Liss.
PALEODIET Archives
From: Clark Larsen
Reply-To:
Date: Mon, 19 Jan 1998 07:58:50 -0500
> Yes, I would be very interested in that too. Although I have never seen a Kung bushman, I have
> seen Inuit people (Eskimos) and they do appear to have a distinct jaw line. I have also noticed
> (although I've never really looked inside an Inuit's mouth) that some have front teeth which
> appear shorter and broader than those of other racial origins. This may be due to softening hide
> but if memory serves, the Inuit men also had similar tooth shapes, and my memory is that they do
> not, typically, chew hides.
Eskimos do indeed have a "distinct jaw line, " at least in traditional Eskimo societies. This jaw line results
from extremely high mechanical demands placed on the jaws and teeth, in relation to chewing of tough foods
and preparation of animal hides. This morphology is clearly related to environmental influences. You're right
that females do most of the hide chewing, but regardless, both sexes engage in behaviors--masticatory and
extramasticatory--placing heavy demands on the jaws and teeth.
PALEODIET Archives
Subject: Re: 'Carnivorous' adaptations
Reply-To:
Date: Mon, 19 Jan 1998 11:44:36 +1100
Thank you to Loren Cordain for the excellent summary of the evidence that humans have adapted
metabolically and biochemically to a largely meat-based diet. I'd like to add to more items that I think are
additional evidence:
1. Iron nutrition in infants. Human infants become iron depleted after 4-6 months of breast-feeding because
human milk provides little iron and iron stores become low by this time. All the infant weaning foods based
on cereals need to be iron-fortified to cater for this need. In the past, a meat-based weaning diet would have
given infants all the iron they needed. Iron deficiency in childhood is extremely serious, recent studies
suggesting that it interferes with both physical and intellectual development (1).
2. Insulin resistance. We have hypothesised that insulin resistance is common today because in the past it
offered an advantage to people dependent on a diet of meat containing lots of protein but little carbohydrate
(2). Insulin resistance would have spared glucose for the brain and foetus which have an obligatory
requirement for glucose. Cats are inherently insulin resistant and increasingly diagnosed with diabetes,
possibly because new commercial dry feeds contain an abundance of carbohydrate (3).
References
1.Lozoff B. Iron deficiency and infant development. J Pediatrics 1994;125:577-8.
2. Brand Miller J, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM.
Diabetologia, 37:1280-86.
3. Struble AL, RW. Non-insulin-dependent diabetes in cats and humans. The Compendium, 1997; 19: 93545.
Jennie Brand Miller PhD
Associate Professor in Human Nutrition
Department of Biochemistry G08
University of Sydney
NSW 2006 Australia
Phone: (61 2) 9351 3759
Fax: (61 2) 9351 6022
12/147 (1998)
PALEODIET Archives
Subject: Adaptation
From: Todd Moody
Reply-To:
Todd Moody
Date: Mon, 19 Jan 1998 22:12:08 -0500
> Date: Tue, 4 Nov 1997 16:21:00 -0700
> From: Loren Cordain Subject: Re: Fitness and Diet
> [much deleted]
> differences may have important health ramifications for modern man. However, basic human
> nutritional needs seem not to have varied significantly since paleolithic times. All humans
> require similar ranges of both macro and micronutrients and all human groups have similar
> anatomical, physiological and endocrine functions in regard to diet and nutrition. The reason for
> these similarities is because of our common evolutionary experience - we were all hunter gatherers
> dependent upon wild plants and animals - and these dietary selective pressures shaped our present
> day nutritional requirements.
A somewhat belated response and query...
As a result of the fact that attempting to follow a paleolithic diet has resulted in seriously elevated LDL
cholesterol in my own case, I have been trying to understand the extent to which the reasoning above may or
may not shed light on the problem.
In his recent book "Eat Right 4 Your Type", naturopathic physician Peter D'Adamo argues that the
appearance of the ABO blood groups mark the emergence of populations with significantly different dietary
adaptations. Type A appeared about 15, 000 years ago; the B and AB types more recently, during historic
times. Although D'Adamo's theories have much to do with the body's immune response to dietary lectins, I
shall not pursue that aspect here (other than to note that some interesting messages on this list concerning
"molecular mimicry" lend at least some plausibility to his idea). But D'Adamo also claims that it is well
known that type As have generally lower levels of gastric acid, making them less able to digest animal
protein. He asserts that they also have the lowest levels of the enzyme alkaline phosphatase, which creates a
problem for breaking down dietary cholesterol. I have been unable to verify these claims, but there does
seem to be ample evidence that blood types are correlated with different health problems.
I am puzzled by the fact that some people can go to a meat-dominated paleolithic style diet and experience
actual improvement in their blood lipids while others, such as myself, find that they worsen. Perhaps the
classic demonstration of this puzzle is the Bellevue experiment of 1928 in which Vilhjalmur Stefansson and
Karsten Andersen ate only meat for a year. A study of two people can hardly be the basis for generalizations,
but it is nevertheless interesting that Stefansson's total cholesterol dropped slightly during the year while
Andersen's climbed all the way to 800, but returned quickly to normal levels after the conclusion of the
experiment. We don't know HDL/LDL ratios, unfortunately. We also know that Stefansson favored lamb,
while Andersen favored beef.
Anyway, the question that I am leading up to is this: Even though the basic nutritional needs of all humans
are the same, is there much evidence to support the contention that some populations are more adapted to
agricultural diets, and perhaps somewhat disadapted to hunter/gatherer diets, than others? Blood type could
be a marker for such adaptation/disadaptation, or perhaps there are other markers.
Ref: Clarence Lieb, MD, The effects on human beings of a twelve months' exclusive meat diet. JAMA, July
6, 1929, 20-22.
Todd Moody
PALEODIET Archives
Subject: Teeth again
Reply-To:
13/147 (1998)
Date: Tue, 20 Jan 1998 09:22:39 +1100

In Steffan Lindberg's last post he wrote:
According to Mayhall [1], "The frequency of the occurence of shovel-shaped incisors is generally held to be
greatest in Mongoloid populations and lower in other groups. ... In general, populations native to Asia and
North America have the deepest lingual fossae (larger than 0.9 mm), South Americans having intermediate
depths (0.5-1.0 mm) and Europeans the shallowest (0.3-0.7 mm). If only the larger expressions (shovel and
semishovel) are included, one can generalize and show that North and South American natives demonstrate
an occurence of 70%-95%, Asians about the same as the Amerindians, Melanesians approximately 6%-20%,
Australian Aborigines about 60%-90%, Europeans 5%-50% and Teso and Bantu from Africa between 10%
and 20% [2]. In North America, Indians and Inuit have about the same occurence of the trait, but the Indians
have the larger expressions [3].
As I read this, I was struck by the fact these same prevalence figures could be applied to the genetic trait of
insulin resistance which results in non-insulin-dependent diabetes (NIDDM) under adverse environmental
conditions. If 'shovel-shaped incisors' tell us anything about diet, then this same diet may have selected for
insulin resistance. Or alternatively, the very shallow lingual fossae of Europeans might tell us why
Europeans have such a low prevalence of NIDDM.
So what exactly do 'shovel-shaped' (or the opposite) incisors tell us about diet? Are we guessing or are their
some facts?
Best wishes Jennie
PALEODIET Archives
Subject: Diet and Body Type
From: LSCummings
Reply-To:
Date: Wed, 21 Jan 1998 18:06:55 EST
Todd,
In your last post, I think your questions/concluding remarks are another way to sum up the literature about
equating diet with blood types, body types, etc. Seems to be a lot of anecdotal evidence to support this.
Personally, I do very poorly on a high carbohydrate diet. This also leads me to question your statement "even
though the basic nutritional needs of all humans are the same.." ..... are they?? I'm not so certain that we
should be starting out from this premise. I think that the existence of RDA provides a facade to fool us into
thinking that human nutritional requirements are not unique for different groups and that we all require the
same stuff. If we look at diets around the world, nutrient quantities probably vary significantly between
populations.
Linda Scott Cummings
> Anyway, the question that I am leading up to is this: Even though the basic nutritional needs of
> all humans are the same, is there much evidence to support the contention that some populations
> are more adapted to agricultural diets, and perhaps somewhat disadapted to hunter/gatherer diets,
> than others? Blood type could be a marker for such adaptation/disadaptation, or perhaps there are
> other markers. Ref: Clarence Lieb, MD, The effects on human beings of a twelve months' exclusive
> meat diet. JAMA, July 6, 1929, 20-22.
> Todd Moody
PALEODIET Archives
Subject: 1. Adaptation 1. Adaptation
From: Bob Avery
Reply-To:
Date: Thu, 22 Jan 1998 00:16:25 -0500
14/147 (1998)
Todd Moody wrote:

> puzzle is the Bellevue experiment of 1928 in which Vilhjalmur Stefansson and Karsten Andersen ate
> only meat for a year. A study of two people can hardly be the basis for generalizations, but it is
> nevertheless interesting that Stefansson's total cholesterol dropped slightly during the year
> while Andersen's climbed all the way to 800, but returned quickly to normal levels after the
> conclusion of the experiment. We don't know HDL/LDL On another newslist, I saw the actual
> cholesterol levels of these men posted. Both were over 300 at the conclusion of the experiment. I
> would hardly call that "normal." Mine is 152.
Bob Avery
PALEODIET Archives
Subject: Fire
From: Matt Fraser
Reply-To:
Date: Thu, 22 Jan 1998 12:27:32 -0500
Hello All,
Apologies if this has already been discussed. I'm having a hard time keeping up with things these days.
Aside from the some of the more obvious uses of fire, such as fire-hardening wood, metallurgy,
"landscaping" for agriculture, protection from predators, etc., has it ever been hypothesized that one of the
biggest benefits of fire was in food preparation and inadvertant STERILIZATION (bacterial, viral and
parasite) of food products, specificallymeats, along with potential detoxification of both meats and
vegetables (assuming that some raw foods have endogenous toxins that might be heat labile). Can an
argument be made that surival was enhanced by this factor, AND (the following is HIGHLY speculative, and
may be hard to chew for some) can the argument be made that mostly all foods became easier to masticate,
thereby driving selection away from hominid robusticity (which appears to be associated with more robust
and vegetarian dentition)?
Thanks,
Matt
_________________________________________________________
Matt Fraser Matt's Paleo Pages <http://www.pitt.edu/~mattf/PaleoPage.html
>
Where you can find The Paleo Award, PaleoNews, PaleoChat, The Paleo Forum, The PaleoAnthro and The
Evolution of Language Discussion Lists, and The Paleo Ring Webring!
_________________________________________________________
PALEODIET Archives
Subject: Re: Adaptation
From: Loren Cordain
Reply-To:
Date: Thu, 22 Jan 1998 14:06:00 -0700
In the last paleodiet Todd Moody asked, " is there much evidence that some populations are more adapted to
agricultural diets, and perhaps somewhat disadapted (sic) to hunter gatherer diets . . . "
15/147 (1998)
It took roughly 5, 000 years for agriculture to spread from the mideast to the far reaches of northern europe.
In this part of the world, agrarian diets were characterized by a cereal staple (wheat or barley early on; later
rye and oats), legumes, dairy products, salt and the flesh of domesticated animals (sheep, goats, cows and
swine). There is strong evidence to suggest that the retention of lactase (the enzyme required to digest lactose
in milk) into adulthood is related to the spread of dairying (1). Most of the world's populations which were
not exposed to dairying did not evolve the gene coding for adult lactase retention. Favism is an acute
hemolytic anemia triggered by ingestion of fava beans in genetically susceptible subjects with severe
deficiency of glucose-6-phosphate dehydrogenase (G6PD). G6PD deficiency is thought to confer protection
against malaria only in those geographic areas where favism exists (2). A substance in fava beans called
isouramil (IU) triggers the hemolytic anemia in G6PD deficient individuals, and it is this interaction of IU
with G6PD erythrocytes which renders these red blood cells incapable of supporting the growth of the
malarial pathogen (Plasmodium falciparum). Thus, the spread of agriculture (fava beans in this case) to
geographic locations surrounding the Meditteranean was responsible for the selection of G6PD in early
farmers. Celiac disease is an autoimmune disease in which the body's white blood cells (T lymphocytes)
destroy intestinal cells causing malabsorption of many nutrients. The disease is caused by consumption of
gliadin (a peptide found in wheat, rye, barley and possibly oats). Withdrawal of gliadin containing cereals
causes complete remission of the disease symptoms. Only genetically susceptible individuals (certain HLA
haplotypes) develop the disease upon consumption of gliadin containing cereals. There is a geographic
gradient of susceptible HLA haplotypes in europe with the lowest incidence of susceptible HLA haplotypes
in the mideast and the highest frequency in northern europe that parallels the spread of agriculture from the
mideast 10, 000 years ago. This information is interpreted as showing that agriculture (via i.e wheat, rye and
barley) genetically altered portions of the human immune system (3). Diseases of insulin resistance,
particularly non-insulin dependent, diabetes mellitus (NIDDM) occur in greater frequency in populations that
are recently acculturated compared to those with long histories of agriculturally based (high carbohydrate)
diets. It has been hypothesized that insulin resistance in hunter-gatherer populations perhaps is an asset, as it
may facilitate consumption of high animal based diets (4), whereas when high carbohydrate, agrarian based
diets replace traditional hunter gatherer diets, it (insulin resistance) becomes a liability (4) and promotes
NIDDM. In regard to D'Adamo's ideas concerning ABO blood groups, diet and disease susceptibility, I
suspect that the relationship is significantly more complex than what he has proposed. There are numerous
examples in the literature showing an association with blood types and diet related disease (5, 6) however it
is unclear whether a causal relationship is present. It is generally conceded that human blood types have
evolved in response to infectious disease (7). Because there are 30 common blood cell surface antigens
(groups) in addition to the ABO group, it seems improbable that if blood typing is associated with certain
dietary induced maladies, that they would be exclusively a function of only ABO groups. The two references
I have cited demonstrate a relationship with Lewis blood types not ABO. Consequently, It is more probable
that a complex relationship exists between blood cell surface antigens, diet and disease that likely involves
multiple blood group types. Further, because of the confounding effect of genetic disequilibrium (the
associated inheritance of genotypes that do not follow Hardy Weinberg equilibrium patterns), the
relationship may only be seredipitous in nature and not causal as proposed by D'Adamo. Finally, I would like
to comment upon Todd's remark "As a result of the fact that attemmpting to follow a paleolithic diet has
resulted in seriously elevated LDL cholesterol in my own case". This listserve represents a forum wherein
scholars, academicians and persons interested in paleodiet can correspond and discuss issues salient to
paleodiet. Speaking strictly for myself (but I hope for most of the others in this group), my intent has never
been to offer specific dietary or health recommendations or advice to single individuals (perhaps we need
some legal clarification by Dean Esmay on this one). There are multiple, personal health issues that vary
from person to person and which must be evaluated in their entirety before dietary change is made.
Obviously, any major change in diet should be made in conjunction with the advice and supervision of
qualified medical and health practioners. As I have pointed out previously, there are subtleties in the macro nutrient composition of paleodiets which would be difficult to replicate using modern diets based upon
commercially available domestic meats. I have little doubt that the inclusion of large amounts of high fat
domestic meat will raise LDL and total cholesterol in the diets of most people. Paleo diets were characterized
by extremely high protein intakes (35-50% energy), intakes with extraordinarily low fat intakes. Let's use an
example of a male requiring 3, 000 kcal/day energy intake. In order to get 50% of total energy (1, 500 kcal)
from protein, he would have to consume 2.57 lbs of elk meat (assuming a nutrient density of 145.9 kcal per
100 gm meat). It would take 3.3 lbs of hamburger (assuming a nutrient density of 275.3 kcal per 100 gm
meat) to reach 1, 500 kcal of protein yet the total fat would increase from 22.2 gms with the elk meat to
288.4 gms of fat with the hamburger (a 13 fold increase). Worse still is the saturated fat content which would
16/147 (1998)
increase from 8.2 gms with the elk to 113.3 with the hamburger (a 14 fold increase). Finally, in order to get
1, 500 kcal from protein with the hamburger, it would be impossible to stay within the daily 3, 000 kcal/day
limit, as the total daily caloric limit would rise to 4, 165 kcal, whereas with the elk, it would be at 1, 704
kcal. The huge increase in saturated fat intake with domestic meat would predictably (using either the Keys
or Mensink equations) cause an enormous rise in both LDL and total cholesterol. Thus, it is unwise and
unwarranted to try to replicate paleodiets using commercially available, high fat modern meats. Only when
one has unlimited access to low fat game meat, low fat seafood, or certain types of poultry prepared and
cooked in a manner to remove and minimize fat should paleodiets be attempted in a modern setting.
Somewhere down the road, I think that a popular book could be written explaining what it would take to try
to replicate a paleodiet utilizing foods which are available to modern people. Clearly, such a diet would be
quite expensive and not universally applicable to all.
Cordially
Loren Cordain, Ph.D. Professor, ESS Dept Colorado State University Ft. Collins, CO 80523
REFERENCES
1. Simoons FJ. The geographic hypothesis and lactose malabsorption. A weighing of the evidence. Dig Dis
1978;11:963-80. 2. Golenser J et al. Inhibitory effect of a fava bean component on the in votro development
of plasmodium falciparum in normal and glucose-6-phosphate dehycrogenase deficient erythrocytes. Blood
1983;61:507-10. 3. Simoons FJ: Celiac disease as a geographic problem; in Walcher DN, Kretchmer N (eds):
Food, Nutrition and Evolution. New York, Masson Publishing, 1981, pp 179-199. 4. Brand Miller JC,
Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia
1994;37:1280-86. 5. Hein HO et al. The lewis blood group--a new genetic marker of ischaemic heart disease.
J Intern Med 1992;232:481-87. 6. Dickey W et al. Lewis phenotype, secretor status, and coeliac disease. Gut
1994;35:769-70. 7. Berger SA et al. Relationship between infectious diseases and human blood type. Eur J
Clin Microbiol Infect Dis 1989;8:681-89.
PALEODIET Archives
Subject: Andersen and Adaptation
From: Todd Moody
Reply-To:
Date: Thu, 22 Jan 1998 17:41:10 -0500
> Date: Thu, 22 Jan 1998 00:16:25 -0500
> From: Bob Avery Subject: 1. Adaptation 1. Adaptation
> Todd Moody wrote:
> only meat for a year. A study of two people can hardly be the basis for generalizations, but it is
> nevertheless interesting that Stefansson's total cholesterol dropped slightly during the year
> while Andersen's climbed all the way to 800, but returned quickly to normal levels after the
> conclusion of the experiment. We don't know HDL/LDL On another newslist, I saw the actual
> cholesterol levels of these men posted. Both were over 300 at the conclusion of the experiment. I
> would hardly call that "normal." Mine is 152.
Andersen's total cholesterol, a few weeks after the conclusion of the experiment, was 200; Stefansson's was
218. Both values would be considered normal, I think. But Stefansson's cholesterol never went way up the
way Andersen's did.
I have to emphazise that without knowing the HDL/LDL values we are not in a very good position to guess
at the health implications of these cholesterol readings, although I confess that I find it difficult to believe
that Andersen's peak readings of 600 and 800 could be a good thing.
I'd like to try stay connected to the subject matter of this list, however. On the (reasonable) assumption that
Andersen's total cholesterol values were problematic from a health standpoint, the question to ask is why he
might have had this response to the diet while Stefansson did not. I mentioned that Stefansson preferred
lamb, while Andersen preferred beef. The fatty acid composition of these meats are somewhat different.
Furthermore, I believe that even in 1928 cows for slaughter were more likely to be grain-fattened than were
lambs. Recent discussions on this list suggest the hypothesis that this could have been relevent; I would
gladly hear other opinions on this.
17/147 (1998)
Or it is possible that Andersen was descended from people who, for whatever reason, had become disadapted
to a meat-dominated diet. Of course, we can't test that hypothesis directly but it becomes plausible only if
there is good reason to believe that there is such a thing as genetic disadaptation of this sort.
And of course it is also possible that Andersen suffered from sort of metabolic disorder that interfered with
his ability to tolerate dietary fats, if there is such a disorder.
Todd Moody
PALEODIET Archives
Subject: General comments
From: Dean Esmay
Reply-To:
Date: Thu, 22 Jan 1998 22:33:19 -0500
Some points on recent discussions:
1) I remain confused at the assertion that glucose is the obligatory fuel for the human brain. Research has
shown that the human brain uses ketones preferentially over glucose when it has the opportunity. I've posted
references on this point before. I don't understand why the claim that glucose is required for the brain to
function is so often repeated (and I read it quite frequently in much popular literature, and hear it fairly often
from dietitians) when research has shown that the human brain uses fat as fuel just fine. Other major organs,
such as the heart and kidneys, also prefer fat to sugar.
2) On the matter of high-meat diets: I run another mailing list for medical doctors, researchers, and others
interested in low-carbohydrate diets as a treatment for diabetes, obesity, epilepsy, and other serious medical
conditions. One of the things a number of physicians and individuals in our group there has noticed is that in
some people, high saturated fat intake does not seem to raise LDL cholesterol. Indeed, in a high-protein, lowcarbohydrate intake dietary pattern, many have repeatedly documented reductions in LDL cholesterol (in
some cases very dramatic reductions, in others more minor reductions), increases in HDL cholesterol, and
lowered serum triglyceride levels with diets loaded with large quantities of butter, cream cheese, eggs,
steaks, and other supposedly dangerous and unhealthy foods--some documenting intakes of well over 3000
calories a day of food intake, with the majority of the caloric intake in animal fats. This is often accompanied
by substantial body fat loss (in some cases well over 50 kilograms), substantial -increases- in lean muscle
mass, decreases in systolic and diastolic blood pressure, and other positive health affects.
Some members of that list are professional researchers already working on research for formal publication
but who are not yet finished, so I can't say much more--but what I -can- say is that what we have seen, over
and over again, is that there are numerous individuals like Todd who seem to fit the pattern currently
predicted by most nutritionists (that high saturated fat intake will increase LDL cholesterol and possibly
other problems), but other individuals who respond quite favorably to the same kind of diet that causes
people like Todd problems.
It does seem that those individuals who respond favorably to high-fat diets tend to be people who have have
not responded well to the current high-carb, low-fat, low-cholesterol diet most often recommended as
healthy. I wish we had more concrete data on that but at this time we don't.
One thing that has long bothered me is that much research on nutrition seems to posit that if a group of
subjects has an "average" response to a certain dietary pattern, that any individuals within the test group
respond differently, those who respond differently are merely calculated in as part of the standard deviation.
There are, in fact, individuals who eat lots of saturated fat and never see increases in LDL cholesterol--just
stating this fact seems to really upset some people, but it's a plain truth that many physicians can tell you
from what they see in their own patients.
Researchers who test drugs always assume that whatever drug they are testing will have negative affects on
some individuals and will just plain not work on others, because after all humans are all individuals. Some
people become suicidal when given certain (usually very useful) antidepressants like fluoxetine; some people
become nauseated when given antibiotics like erythromycin that most people have no trouble with. Yet if
you suggest that, for example, saturated fat may not be poisonous to every human on the planet, some people
seem to become quite agitated and sometimes even angry.
18/147 (1998)
I once asked a friend of mine who knows a great deal more about nutrition than I do a pointed question that
he never gave me a straight answer to: if a specific individual eats a lot of saturated fat--eats more saturated
fat, in fact, than most Americans ever do--and that individual has perfectly good lipid profiles (great LDL,
high HDL, low triglycerides, etc.), what possible justification could there be for telling that person he was at
high risk for developing heart disease if he keeps eating lots of saturates?
It seems to me that nutritional researchers ought to start treating food like drug researchers treat drugs, by not
assuming that a general positive or negative reaction to any specific dietary measures will work universally
the same on every single individual.
But that's just my opinion--I could be wrong. :)
-=- Anger will never disappear so long as thoughts of resentment are cherished in the mind. Anger will
disappear just as soon as thoughts of resentment are forgotten.
Buddha (B.C. 568-488)
PALEODIET Archives
Subject: Re: Adaptation
From: Lorraine Heidecker
Reply-To:
Date: Fri, 23 Jan 1998 00:16:17 -0700
I would appreciate a reference or two for Todd Moody's statement about the relatively recent appearance of
the A and B allele in human blood types. It was my understanding that the ABO blood groups occur in all
African hominoids. I have checked my (admittedly limited) resources and have no information on this topic.
Lorraine Heidecker Department of Anthropology California State University Sacramento
PALEODIET Archives
From: Gary Ditta
Reply-To:
Date: Fri, 23 Jan 1998 09:51:57 -0800
> On another newslist, I saw the actual cholesterol levels of these men posted. Both were over 300
> at the conclusion of the experiment. I would hardly call that "normal." Mine is 152.
> Bob Avery
The original data for the total cholesterol values of Stefansson and Anderson during the Bellevue experiment
are to be found in the following reference: Tolstoi, E. (1929) J Biol Chem 83: 753-758. The starting value
(before meat diet) for Stefansson was 263, that for Andersen was not determined. The last value taken while
still on the meat diet, one year later, was 211 for Stefansson and 415 for Andersen. Two weeks later, after
eating a general diet, Stefansson's value was 218. After 4 weeks of general diet Andersen's was 200.
It was noted that the plasma of the men showed a cloudiness at the beginnning of the experiment due to the
increased fat intake (lipemia) of the all meat diet. This was also noted during the experiment for Andersen.
The fat intake for the two men was listed at 200-300 g/day. One thing to keep in mind is that this range of
values would allow for a sizable difference in the amount of fat consumed by the two men, if Stefansson
were eating at the low end Andersen at the high.
I hope this digression does not detract from Todd's very interesting question about the possibility of different
populations being differentially adapted to agricultural diets.
Gary Ditta
PALEODIET Archives
Subject: Dean's comments: another data point
From: Art De Vany
Reply-To:
19/147 (1998)
Date: Fri, 23 Jan 1998 11:44:12 -0800

My diet contains about 65% of its calories from animal sources, right in the range Loren Cordain has
documented.
It consists of cooked egg whites, fish, chicken, beef, veal, etc. The rest is made up of fresh vegetables, whole
fruit, some nuts, lots of fresh spices, and olive oil. I eat WAY beyond 3000 Kcals per day, but no refined
products, manufactured foods, fruit juices, soft drinks, or grains, potatoes. I also do not mix fat with carbs,
only fat with protein or carbs with protein in my meals, again following Loren's discussion and my own
reading ancestral opportunistic feeding patterns.
I eat less fat than most paleo eaters, no rinds, bacon is drained, trimmed meat grilled over fire to rend out fat,
boiled egg whites with fresh fruit for breakfast (with a yolk or two, but tossing most yolks), ham steaks, pork
chops or whatever I feel like and haven't eaten recently. I go for free range animal sources as much as is
practical (and affordable)
I often skip a meal (maybe twice a week) as though hunting is lean. I may eat nothing but fruit some
mornings. Other times nothing but meat. Snacks of fresh fruits and lean meat such as smoked turkey. The
quantities of food I eat are prodigious (and expensive).
But, I carry so much lean body mass (203 lbs, less than 8% body fat) that my basal metabolism consumes
something like 2800 Kcals per day . And, using the Ache' to approximate my activity level (a model I follow
in my evolutionary fitness system), I expend about 4800 Kcals per day.
Total cholesterol in the mid 150s to mid 160s. Triglcerides/HDL about 0.68. Scans of my carotid show a
completely clear vessel of very large cross section. All this at age 60.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Arthur De Vany Professor Institute for Mathematical Behavioral Sciences 3151 Social Science Plaza Irvine,
CA 92697-5100 714-5269 http://www.socsci.uci.edu/mbs/personnel/devany/devany.html
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
PALEODIET Archives
Subject: Message from Mary and Sally
From: Reply-To:
Date: Sun, 25 Jan 1998 01:38:28 -0500
To: All Paleodieters From: Reply to Loren Cordain, Part I, from Mary and Sally
We apologize for taking so long to reply to Loren Cordains submission on October 9. We will take his
points in order.
1. We stated that the necessary macronutrients and known vitamins and minerals can all be obtained from
animal foods. We speculated that the various phyto-chemicals MAY be necessary for optimum health, at
least to some individuals. Certainly plant foods add variety to the diet and make eating more fun. But plant
foods can have their drawbacks, particularly if improperly prepared. Grains, legumes and other seed foods
contain antinutrients such as phytic acid, enzyme inhibitors and goitrogenic substances (including
isoflavones, genistein and diadzen in soy foods.)(1)
2. We did not say that hydrogenated oils are atherogenic BECAUSE they raise cholesterol. We have stated
that cholesterol is a non issue--neither serum nor dietary cholesterol is good predictor of CHD. Trans fats
interfere with many processes on the cellular level that can lead to CHD. Several recent studies have linked
consumption of trans fats with increased CHD.(2) Nor did we say that polyunsaturated fats contribute to
heart disease BECAUSE they raise cholesterol It is generally accepted that polyunsaturated oils LOWER
cholesterol in the short term. We stated that excess n6 oils is a problem because, among other things, it
disrupts prostaglandin balance. In this regard, we highly recommend a recent paper by Okuyama, "Dietary
Fatty Acids--the n6/n3 balance and chronic elderly diseases. Excess linoleic acid and relative n3 deficiency
syndrome seen in Japan." (3)
The fact that saturated fats raise cholesterol in short term feeding studies, many in metabolic ward
conditions, has no relevance to our argument. Often studies done in metabolic wards involve the use of
purified fats, cholesterol, proteins, etc., which are not the same as eating real food. A Finnish study found
that over the long-term, the reduction of saturated fats in the diet does not affect plasma cholesterol.(4)
20/147 (1998)
The effect of fatty acids on serum cholesterol levels is dependent on the original serum cholesterol levels:
high serum cholesterol decreases with most fatty acids including all saturates; low serum cholesterol
increases with many of the fatty acids including saturates, monounsaturates and sometimes the
polyunsaturates. Over time, cholesterol levels tend to return to baseline levels (that is, levels appropriate for
the individual) regardless of changes in amount or type of dietary fat.
We are among those arguing that a wide variety of risk factors contribute to CHD, all of which may be
summarized as the inappropriate application of industrial techniques to farming, animal husbandry and food
processing.
You cite a 1986 JAMA article by Grundy in which he states that the relationship between serum cholesterol
and risk of premature death from CHD is continuous and graded. Researchers in the MRFIT study did indeed
find that the relationship was continuous and graded, with deaths from CHD rising in a straight line from the
cholesterol levels between 140 and 299. What Grundy failed to mention was that the relationship was also
trivial, with total CHD death at less than 1 per 1000 at 140, and slightly less than 2 per 1, 000 at 299. This
was similar to findings of the Framingham study which found virtually no difference in coronary -events- for
cholesterol levels between 180 and 300--the vast majority of the US population. What the MRFIT
investigators did find was that the total deaths were 6 per 1000 for those with cholesterol levels less than
140, twice as high as total deaths for those in the 140 to 260 range.
If the consumption of saturated fat within the context of the "average American diet" is "deadly, " why was
heart disease so rare among Americans at the turn of the century, who consumed large amounts of saturated
fat from dairy products, lard, tallows and coconut oil? The answer is that, like our hunter gatherer ancestors,
-the context under which this was done was much different than present day conditions, - namely the
introduction of altered foodstuffs into the food supply, including trans fats and the other factors you mention
such as large amounts of refined carbohydrates and a high n6/n3 ratio. The fault is not with the saturated fats,
but with the -context.You are arguing that the Paleolithic diet contained higher levels of monounsaturated fats, stearic acid and n3
fatty acids than the modern diet, but lower levels of overall saturates. The crux of your argument seems to be
that the Paleolithic diet had far lower amounts of all saturates than the modern diet, saturates that we obtain
from meat and butterfat. The following table combines data from USDA and from your laboratories on elk
killed in the Fall 1996 hunting season:(5)
ELK Brain Muscle Adipose Marrow Kidney
Saturates 41.3% 34.2% 53.4% 20.0% 66.0%
Mono 33.0% 28.8% 34.0% 75.5% 32.3%
Poly 26.0% 35.5% 8.6% 4.9% 1.7%
N6/N3 ratio 1.14 3.72 3.39 5.23 NA
P/S ratio 0.63 1.04 0.16 0.24 ~0.03
BEEF (USDA)
Saturates 44.3% 44.9% 53.3% NA 44.9%
Mono 35.9% 50.8% 43.2% NA 28.2%
Poly 19.8% 4.3% 3.2% NA 26.9%
N6/N3 ratio 0.52 2.84% 3.6% NA 66.0
P/S ratio 0.45 0.09 .06 NA 0.60
Your laboratories found that fat from elk muscle tissue was 2-4%, compared to domesticated beef at 25-30%.
Beef muscle fat is more saturated than elk muscle fat (and presumably contains a significant portion of "nonatherogenic" stearic acid). It contains far more "beneficial" monounsaturated and a better N6/N3 ratio (2.84
vs 3.72). Doesn't that imply that the large amount of muscle fat is a plus for beef?
These tables indicate that elk adipose is just as saturated as beef adipose fat. Your laboratories did not
provide a figure for adipose fat as a percentage of total meat. For domesticated beef, this ranges from about 9
to 27 percent. We need this data before we can determine whether the elk or the domesticated cow is a better
overall source of saturated fat, including the so-called atherogenic 14:0 and 16:0 fatty acids. You found that
14:0 was 5.1% and 16:0 was 33.1% in elk tallow for a total of 38.2%, compared to 5.2% of 14:0 and 23.6 of
16:0 in beef tallow for a total of 28.8%. In other words, beef has less of the so-called atherogenic fatty acids
than elk as a percentage of the total. The question is, how do the totals compare?
Unfortunately, we have no figures for beef marrow, but beef brain and elk brain have similar fatty acid
profiles, with beef brain slightly more saturated, slightly higher in monounsaturated and slightly lower in
polyunsaturates. Beef brain has a better N6/N3 ratio (0.52 vs 1.14).
21/147 (1998)
We have evidence that Paleolithic man consumed the marrow and organ meats by preference, (possibly
leaving much of the muscle meat at the site of the kill.) Traditional cultures also ate these portions. Modern
man does not eat these fatty organs and marrow portions of red meat (although he should) so it can be argued
that his intake of monounsaturates and polyunsaturates is less, assuming other factors in the diet are similar.
But modern man does not eat the kidney fat either--which probably totals 20 pounds on a large ruminant-which the Paleolithic man almost certainly did, particularly as this highly saturated fat has very good keeping
qualities. So it can be just as easily argued that modern man consumes less saturated fat from beef than
Paleolithic man consumed from wild game.
As for the lean meat in wild game, American Indian practices would indicate that earlier man mixed this with
tallow or bear fat to make more palatable products, similar to pemmican, succatash or haggis. After all, why
would anyone eat dry, tough lean meat when it tastes so much better mixed with fat, unless the entire
medical establishment and food industry were urging him to do so?
Finally, regarding the purported atherogenicity of lauric, myristic and palmitic acid, you may wish to note
the recently published work of Tratwein which found that olive oil produced the higher total cholesterol
relative to palm and coconut oil in the lipid sensitive hamster. (6) In humans, there have been numerous
studies with added coconut oil to the diet that resulted in lowering of cholesterol or no difference. (7)
Current recommendations to increase monounsaturated fats and reduce saturated fats should, we believe, be
viewed with caution. While more research is needed, we can cite a study by Kramer, et al which found that
feeding canola oil to rats caused increased incidence of myocardial lesions. When highly saturated cocoa
butter was added to the diet, there was a significant decline in the incidence of myocardial lesions. (8)
Researchers ascribed the adverse effects of the canola oil to its unique fatty acid composition--high in oleic
and n3 but low in saturated fatty acids. There is also some evidence that excess oleic acid in the diet
interferes with prostaglandin production in a similar fashion to excess n6.(9) We find it interesting that the
monounsaturates became "politically correct" just about the time that canola oil came on the market.
3. The Framingham study found that higher levels of HDL were associated with lower incidence of CHD. In
order to protect the lipid hypothesis, they were obliged to pinpoint LDL as the villain. We urge you to read
the discussion of this issue by Russell Smith, which we mentioned before and which we will now repeat. "In
40 years of several hundred Framingham reports, this writer has found neither an actual correlation
coefficient published for either total or LDL cholesterol nor a figure showing the CHD mortality and/or
morbidity rate as a function of LDL level. . . Examination of published Framingham data. . . indicate that the
correlation between CHD and total or LDL cholesterol is probably under 0.3. The objective and statistically
sophisticated scientist would consider these correlations as unrepresentative of cause and effect relationships
and would analyze the associated data base to find reasons why the observed correlations occurred at all."
(10)
We did not say that oxidized cholesterol in aged cheeses is a powerful promoter of atherogenesis. If this is
true, why do the French, Italians, and Greeks, who eat large quantities of aged cheeses, have generally lower
rates of CHD? The type of damaging oxidation we are talking about occurs when milk and eggs are
"powdered" by blowing them out of a small hole at high temperatures and pressures, thereby exposing a
large surface area to oxygen. Perhaps oxidized cholesterol was found in commercial "grated" (actually
powdered) Parmesan cheese, which remained for many months on the grocers shelf. If so, it is a gross
deception to tar traditional aged cheeses, which are a wholesome, nutrient-dense food, with the black brush
of commercial powdered--and probably rancid--Parmesan.
4. You object to our statement that "one can point to populations with relatively high protein consumption
(30-40%) with little or no CHD, and to populations with relatively low protein consumption (15-20%) with
little or no CHD." Our analyses of diet descriptions and menus at the turn of the century indicates that the
American diet contained about 20% protein, 40% fat and 40% carbohydrate. (11) Higher amounts would be
found in primitive diets that contain no plant foods, such as the Eskimo, Canadian Indians and groups that
subsist exclusively on milk, meat and blood like the Masai, although if one assumes a fat:protein ratio of 2:1,
then the upper limit for protein would be about 30%. As the prevailing viewpoint in this discussion is that
paleodiet was high in protein, but nonatherogenic, we are at a loss to understand your objections. You state
that the high-protein Paleolithic diet was nonatherogenic because the diet contained a different fatty acid
profile than the modern diet. This is a different issue than the protein issue, and is in fact the crux of our
debate--whether or not modern diets contain more saturated fats, particularly those you contend are
atherogenic (12:0, 14:0 and 16:0)--and if so, whether these fats are contributing to the modern plague of
heart disease. Can you show us statistics indicating that modern consumption of 12:0, 14:0 and 16:0 is much
higher today than in 1900?
22/147 (1998)
Regarding the ability of SFAs to lower serum Lp(a), we have already cited one reference. (12) We now have
another, from the USDA laboratories. (13)
5. There has been considerable discussion regarding your statement that the hunter gatherer did not consume
carbohydrates mixed with protein and fat. We cited succatash and pemmican as counter examples, and
another interesting example was given of the Yamani Indians in the Amazon basin who never consume meat
without plantains. The consensus seems to be that the paleodiet was mixed, and that our ancestors placed no
strictures on consuming carbohydrates with protein and fat. Are you suggesting that by consuming
protein/fat and carbohydrates at separate meals, we can eliminate CHD?
You state that it is "well established" that mixing fat with carbohydrate, the glycemic response worsens. In
fact, studies of glycemic response show that carbohydrates mixed with fat elicit a lower glycemic response.
For example, Jenkins and colleagues found that a Mars bar had a glycemic index of 68, compared to honey
with an index of 87 and lucozade at 95; and potato chips had an index of 51 compared to potatoes at 70. (14)
The fact that fats taken with meals regulate the too-rapid entry of glucose into the blood stream is so well
established as to be found in all the textbooks. In fact, recent study by Rasmussen and colleagues (15) found
that carbohydrate (in the form of potato) mixed with largely saturated butter provoked a lower glucose
response than carbohydrate mixed with largely monounsaturated olive oil.
6. We did not state that overall PUFA in wild animal tissues is low. We stated that the PUFA in modern
ruminant adipose tissue does not differ significantly from the PUFA in wild ruminant adipose tissue. We did
not include monogastric animals, and we were clearly referring only to the adipose of ruminant animals. We
pointed out that modern diets generally have much larger amounts of PUFA, particularly n6 PUFA, than
traditional diets because of the introduction of commercial vegetable oils, and not because we are eating
more animal fats.. The hunter/gatherer got significant amounts of fat from bone marrow and organ meats-nutritious foods that should be returned to American tables. These provide moderate amounts of both n6 and
n3 PUFA, along with monunsaturated and saturated fatty acids. The Eskimo diet is unusual in the fact that it
contains relatively high amounts of PUFA, particularly n3 PUFA, which we have agreed is very deficient in
western diets. Some have argued that higher levels of elongated n3's are necessary in cold climates, (16) but
there is no reason to assume that the levels of PUFA found in the Eskimo diet were characteristic of
hunter/gatherer diets from temperate climates based on game, or on those from the tropics which would have
included coconut and palm oils.
You cite NHANES data for the fatty acid profiles of dairy products without giving a reference. In all
likelihood, you are referring to the work of Gladys Block. Block reported on the NHANES II data in several
papers, but the fatty acid composition for all of NHANES II was and still is in great error (17). Much ice
cream today, for example, is made with skim milk and vegetable oil.
--continued next message--
PALEODIET Archives
From: Reply-To:
Date: Sun, 25 Jan 1998 01:59:57 -0500
To: All Paleodieters From: Mary and Sally Reply to Loren Cordain, Part II
7. You cite a study by Artaud to support the assertion that the "highest dietary correlates to CHD in world
wide epidemiological studies come from consumption of milk and dairy products." This study was
conducted by dieticians (who are trained to dispense fabricated foods) and William E Connor who is an avid
supporter of the lipid hypothesis. We note that the study contains no tables of actual food consumption, so
we are unable to assess some of their surprising claims, such as the assertion that the French consume much
larger amounts of vegetable oil than the Finns. In fact, consumption of vegetable oil is remarkably low in
France at 5 pounds per person per year (compared to 18 in the US) with 8 pounds of trans fats (compared to
24 in the US.) As there are many societies that consume dairy products and suffer little or no heart disease
(not only France, but also the Masai studied by George Mann and the primitive Swiss studied by Weston
Price), we would caution against basing any conclusions about milk on this paper. It should be noted that
Switzerland and Austria have the longest lifespan of the western countries, almost the same as Japan,
consuming a diet rich in dairy products. The Greeks are slightly behind, on a diet containing lots of rich (and
salty) feta cheese. (Goat milk has 25% more fat than cow's milk.)
23/147 (1998)
You continue to argue that dairy fats as sources of 12:0, 14:0 and 16:0 are "atherogenic." Our question is
this: Why were these fats not atherogenic at the turn of the century when the American diet was just loaded
with butter, whole milk and cream? Why are they not atherogenic to the French? Why are they not
atherogenic to the Masai? Why are they not atherogenic to peoples in the tropics who consume large
amounts of coconut? Why are they not atherogenic to the peoples of Soviet Georgia? Why are they not
atherogenic to babies drinking mother's milk, which contains more medium chain fatty acids (12:0 at 2.56
g/32 fl oz, 14:0 at 3.15 g/32 fl oz and 16:0 at 9.05 g/32 fl oz) than stearic acid (2.85 g/32 fl oz)? As we stated
earlier, just because these fats raise cholesterol levels in short term metabolic ward studies does not mean
that they cause heart disease.
You also argue that milk consumption results in an unfavorable Ca:Mg ratio. The Ca:Mg ratio of cow's milk
is about 9:1, which is "better" than the ratio of 11:1 found in mother's milk, and very close to serum Ca:Mg
ratios of 8:1. Weston Price found that calcium levels in primitive diets were about 4 times higher than the
calcium levels in the American diet of his day. Those people who did not consume dairy products got their
calcium from preparations made from bone, particularly bone broths, which are a distinguishing feature of
traditional diets. Small fish consumed with their bones contain considerably more calcium than milk, and it
is safe to assume that insects, consumed with their hard shells, were also an excellent source of calcium. Of
course, it is likely that magnesium levels were also higher in the Paleolithic diet. Magnesium is very
important for the health of the cardiovascular system--but so is calcium. You give no reference for your
assertion that the Ca:Mg ratio in "pre-agricultural" diet was 1:1.
The body's mechanism for regulating calcium intake is complex, involving signals from the parathyroid
gland when calcium is needed, and the action of special calcium binding proteins in the gut to transport
calcium across the intestinal wall. These mechanisms guard against overabsorption of calcium should it be
superabundant in the diet. The emphasis in modern diets should be on increasing magnesium from
organically grown green vegetables and nuts and grains that have been properly prepared to neutralize phytic
acid content (which can block magnesium absorption)--not on decreasing calcium.
The theory that the lactose component of milk is a cause of CHD is an interesting one and deserves more
study. It is one explanation for the fact that France has a low incidence of CHD with a high consumption of
dairy products. In France, dairy products are rarely consumed as milk, but as fermented products such as
cheese, yoghurt, butter and sour cream. Alternative explanations are the relatively low fat content in modern
milk, leading to a vitamin A deficiency (18), and the addition of additives such as powdered milk containing
oxidized cholesterol to reduced fat milks. Any one of these explanations supports our argument that the
problem lies not with consumption of milk products per se, but in the abandonment of traditional processing
methods (cheese-making, natural yoghurt, natural fermentation to make clabber, etc.) all of which do in fact
reduce lactose content. Genetic selection in favor of low-fat-producing cows, use of inappropriate feed,
pasteurization (which destroys lactase) and homogenization are other possible explanations.
The study you cite regarding copper deficiencies involved rats on copper deficient diets that contained 62%
fructose. Feeding powdered lactoalbumin exacerbated the effects of copper deficiency more than casein or
egg white--but lactoalbumin was not the cause of copper deficiency. These experiments have little relevance
for populations that do not have a high level of fructose consumption and that eat well-mineralized food and
properly processed dairy products. Hunter/gatherers and traditional societies got sufficient copper from
frequent consumption of liver and other organ meats.
7. Regarding xanthine oxidase, an enzyme found all over the human body and widely spread in animal
products including milk, you might want to check a web site on the subject
(http://www.bath.ac.uk/Departments/Biosciweb/roger2.htm) describing research examining the possibility
that IgM anti-XO antibodies have a protective role in controlling free radicals and other reactive oxygen
species. A study by White, et al, which found that high cholesterol induced release of xanthine oxidase in
non-milk drinking rabbits, is a further indication that XO plays a protective role. (19)
As we have given many examples of healthy populations that consume dairy products (usually fermented
dairy products), we do not agree that foods derived from milk "wreak havoc in human health." But we do
feel that modern commercial milk--pasteurized, fat-depleted and adulterated with additives--is best avoided.
24/147 (1998)
Referring to Mann's 1972 study of the Masai, you state that "...autopsies done on 50 Masai men (milk
drinking populations) have revealed extensive atherosclerotic lesions in coronary artery cross
sections...[noting that]...earlier reports of freedom from atherosclerosis in the Masai were shown to be
incorrect." We find this statement rather curious. In 1993, George Mann quoted this same reference, which
was Mann's own work, in the first chapter of his book Coronary Heart Disease: The Dietary Sense and
Nonsense (GV Mann, ed, Janus Publishing Co, London, 1993). Mann said "...and our autopsies of 50 adult
males showed little evidence of atheroma...[and also stated that]...these animal fat eaters show neither
hypercholesteremia, nor atheroma, nor heart attacks." Two other references you cite for their protein research
(i.e., 13 and 14, Wolfe and Giovanetti, 1991 and 1992) happened to have referred to Mann's findings with the
Masai (as Mann had reported in 1964) as showing "...undetectable coronary heart disease...and...undetectable
arteriosclerotic heart diseases..." Thus, we are doubly perplexed by your statement, and we are inclined to
accept Mann's 1993 description of his own earlier work.
8. We discussed SFA content of pre-agricultural man earlier. As we stated, the slightly higher PUFA content
of the Eskimo diet is not typical of other pre-industrial societies. Most of the fat in the Eskimo diet comes
from marine mammals, not fish, which is rich in monounsaturated fatty acids and also provides moderate
amounts of saturates.
9. Regarding the supposed calciuric effects of salt, Whiting et al found that calcium excretion with sodium
chloride or phosphate could not be detected. (20) If salt causes osteoporosis, why do the Orientals, who
consume very high levels of salt, have low levels of osteoporosis? Human skeletons of Huguenot women
ages fifteen to eighty-nine recently exhumed in London showed no bone loss among the elderly. The English
diet at the time was rich in salt, principally from salted meat and fish. (21)
10. Your thesis is that we have not done any adapting to any of the post agricultural diets, and that all of our
modern ills are due to the fact that we are not eating like the hunter=gatherers. But we were not eating like
the hunter-gatherers a hundred years ago and we were not suffering from all of the modern day chronic
ailments, so obviously there are some other variables to account for the increase in degenerative disease.
What we are all trying to determine is what these variables are.
We think it is important to keep in mind that it is virtually impossible to determine the overall health status
(including infant mortality, length of life, etc.) of Paleolithic man, particularly as he was subject to the
vagaries of the hunt, periodic famine, drought, etc., although the fossil record indicates that the
hunter/gatherer was in general well formed, well muscled and had good bone mineralization.
We have better data about some Neolithic groups, principally from the pioneering work of Weston Price who
found 14 societies in which virtually all members of the tribe or village were well formed, robust and
enjoyed freedom from degenerative disease including tooth decay. The particulars of these diets varied
considerably. Some contained milk products, some did not. Some contained grains and other plant foods;
others were almost devoid of plant foods. Some were based on fish; others on animals of the hunt. Some
contained much raw food and others consisted mostly of food that was cooked. The underlying
characteristics of these healthy diets are summarized as follows:
1. The diets of healthy primitive and nonindustrialized peoples contain no refined or denatured foods such as
refined sugar or corn syrup; white flour; canned foods; pasteurized, homogenized, skim or low-fat milk;
refined or hydrogenated vegetable oils; protein powders; artificial vitamins or toxic additives and colorings.
2. All traditional cultures consume some sort of animal protein and fat from fish and other seafood; water
and land fowl; land animals; eggs; milk and milk products; reptiles; and insects.
3. Primitive diets contain at least four times the calcium and other minerals and TEN times the fat soluble
vitamins from animal fats (vitamin A, vitamin D and the Price Factor) as the average American diet.
4. In all traditional cultures, some animal products are eaten raw.
5. Primitive and traditional diets have a high food enzyme content from raw dairy products, raw meat and
fish; raw honey; tropical fruits; cold-pressed oils; wine and unpasteurized beer; and naturally preserved,
lacto-fermented vegetables, fruits, beverages, meats and condiments.
6. Seeds, grains and nuts are soaked, sprouted, fermented or naturally leavened before being consumed.
7. Only about 4% of calories come from polyunsaturated oils naturally occurring in grains, pulses, nuts, fish,
animal fats and vegetables (compared to modern diets with values as high as 30% from polyunsaturates.) The
balance of fat calories comes from monounsaturated and saturated fats. (An exception is the Eskimos with
higher total fat from polyunsaturates.)
8. Traditional diets contain nearly equal amounts of omega-6 and omega-3 essential fatty acids.
9. All primitive diets contain some salt.
10. Primitive and traditional cultures use make use of animal bones, principally by preparation and
consumption of mineral- and gelatin-rich bone broths.
25/147 (1998)
11. Traditional cultures make provisions for the health of future generations by providing special nutrientrich foods for parents-to-be, pregnant women and growing children; by proper spacing of children; and by
teaching the principles of right diet to the young.
In summary, we feel that the debate over dairy products, saturated fat and salt is misplaced. The conquest of
degenerative diseases need not entail deleting nutritious and delicious foods like cheese, butter, sauces,
gravies, salt and whole grains from our diet. Rather it requires more wisdom in our application of technology
to the entire chain of food production, including the cultivation of plant foods so that they will be rich in
vitamins and minerals; humane and natural animal husbandry; the delivery of fresh foods to the marketplace
through a well-maintained infrastructure and appropriate packaging (rather than sterilization, pasteurization,
additives and irradiation); a return to traditional preservation and preparation techniques including lactofermentation and the making of broth; and the elimination of refined, devitalized and denatured foods
including modern vegetable oils, trans fats, sugar and white flour, soft drinks, most canned foods and protein
powders. Rather than "lean meat, occasional organ meats and wild fruits and vegetables, " (and we wonder
how we would obtain those wild fruits and vegetables and still have time to participate in the paleodebate)
may we suggest a varied and interesting diet that includes juicy well-marbled steaks served with Bernaise or
a nice reduction sauce, sauteed liver with onions, traditional (but not genetically engineered) cultivars of
organic vegetables (lightly steamed and dressed with butter or in salads with dressings composed of raw
vinegar, extra virgin olive oil and cold pressed flax oil), and a variety of delicious fruits served with oldfashioned cream.
References
1. Divi and George, Proceedings of the ISSX, 1996
2. W. C. Willett et al, Intake of trans fatty acids and risk of coronary heart diseases among women. Lancet
1993; 341:581-585; F.B Hu et al, Dietary fat intake and the risk of coronary heart disease in women. N Engl
J Med 1997; 337:1491-1499
3. Harumi Okuyama, et al, Prog Lipid Res, Vol 35, No 4, pp 409-457 1997
4. Tatu A Meittinen, et al, JAMA Oct 18, 1985 vol 254, No 15, pp 2097 - 2102; and Timo Strandberg, et al,
JAMA September 4, 1991 vol 266, No 9 pp 1225 - 1229
5. Loren Cordain et al, Abstract presented at the International Conference on the Return of N-3 Fatty Acids
Into the food Supply: I. Land-Based Animal Food Products. Natcher Conference Center, NIH, Bethesda, MD
1997.
6. Trautwein et all, British Journal of Nutrition 77:605-620, 1997
7. M. G Enig, "Health and Nutritional Benefits From Coconut Oil and Its Advantages Over Competing Oils,
" 1995 Indian Coconut Journal 26:2-10
8. J.K.G. Kramer et al, Lipids, Vol 17, No 5, 1982, pp 372-382
9. David F. Horrobin, "The regulation of prostaglandin biosynthesis by manipulation of essential fatty acid
metabolism, " Reviews in Pure and Applied Pharmacological Sciences, Vol 4, pp 339 - 383, Freund
Publishing House, 1983.
10. Russell L Smith, "Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of the
Literature, " 1991, Vol 2, pp 3-18 to 3-100.
11. Americans: Then and Now, Price-Pottenger Nutrition Foundation Health Journal, Vol 20, No 4, 1996
12. P Khosla and K. C. Hayes, Dietary trans-monounsaturated fatty acids negatively impact plasma lipids in
humans: critical review of the evidence. J Am Coll Nutr 1996; 15:325-339
13. B. A. Clevidence et al, Plasma lipoprotein (a) levels in men and women consuming diets enriched in
saturated, cis-, or trans-monounsaturated fatty acids. Arterioscler Thromb Vasc Biol 1997; 17:1657-1661
14. David J. A. Jenkins et al, Glycemic index of foods: a physiological basis for carbohydrate exchange. Am
J Clin Nutr 1981; 34:362-366
15. O. Rasmussen et al, Differential effects of saturated and monounsaturated fat on blood glucose and
insulin responses in subjects with non-insulin- dependent diabetes mellitus. Am J Clin Nutr 1996; 63:249253
16. Okuyama, op cit.
17. M. G. Enig et al, "Comparisons of Fatty Acid Profiles Used in NHANES II Data Base and Data
Available in the Literature." Abstract #2509, FASEB 73rd Annual Meeting; and M. G. Enig "Trans Fatty
Acids in Diets and Data Bases." 1996, Cereal Foods World 41:58-63
18. Sally Fallon, "Vitamin A Vagary" Price-Pottenger Nutrition Foundation Health Journal, Vol 19, No 2,
1995
19. White et al, Proceed Nat Acad Sci 1996:93:8745-8749
20. Whiting et al, Am J Clin Nutr 1997:65:1465-72
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21. B Lees et al, "Differences in proximal femur bone density over two centuries, " Lancet, March 1993,
341:673-675.
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Sun, 25 Jan 1998 14:19:03 -0500
A few comments:
1) I would like to welcome the return of Sally Fallon and Mary Enig to our discussions. Their comments are
always a thought-provoking welcome here.
2) I would like to take a couple of minor exceptions to their recent comments to our membership. However, I
want to be clear that they should be taken without prejudice--that is, that my comments are not "leading"
toward any point of view or to be taken as an attack on any other statement made by Enig & Fallon or
anyone else. They address the specific points they address and nothing more--period.
3) Enig and Fallon state that "...the prevailing viewpoint in this discussion is that paleodiet was high in
protein, but nonatherogenic..." This is probably correct, but it is worth noting that this viewpoint can only
safely be said to "prevail" with the two or three people who have actually put it forward. No one has strongly
attacked this viewpoint to date, but this should not necessarily be taken to mean that the 99% of the
membership who have remained silent on the point are in complete agreement with the 1% who have
espoused it.
4) I feel than Enig and Fallon are somewhat guilty of sidestepping the issue of cereal grains, inasmuch as it
seems almost impossible that cereals could have been more than a minor or occasional component to the
human diet prior to the neolithic revolution.
PALEODIET Archives
From: Todd Moody
Reply-To:
Todd Moody
Date: Sun, 25 Jan 1998 15:37:33 -0500
> Date: Thu, 22 Jan 1998 14:06:00 -0700
> From: Loren Cordain Subject: Re: Adaptation Finally, I would like to comment upon Todd's remark
> "As a result of the fact that attemmpting to follow a paleolithic diet has resulted in seriously
> elevated LDL cholesterol in my own case". This listserve represents a forum wherein scholars,
> academicians and persons interested in paleodiet can correspond and discuss issues salient to
> paleodiet. Speaking strictly for myself (but I hope for most of the others in this group), my
> intent has never been to offer specific dietary or health recommendations or advice to single
> individuals (perhaps we need some legal clarification by Dean Esmay on this one).
Quite right. My attempt to follow a paleolithic diet is a personal initiative, and that's all. While this listserv is
a source of information, I do not look to it as a source of advice. Period. I seek relevant information wherever
I can find it and make my own decisions.
> I have little doubt that the inclusion of large amounts of high fat domestic meat will raise LDL
> and total cholesterol in the diets of most people.
And yet, as Dean points out in a separate message, it appears that a good number of people do not experience
this consequence, if they are following ketogenic diets. Of course, based on what I have read here, it seems
unlikely that the typical paleolithic diet was ketogenic. If this is correct, it would seem that there has been
little selection pressue toward adaptation to long-term ketosis, with the exceptions of populations such as
Eskimos and Plains Indians, whose particular metabolic adaptations probably cannot be generalized to the
rest of us. In any case, their ketogenic diets would not have resembled what one could easily get at a
supermarket meat counter.
> Date: Fri, 23 Jan 1998 00:16:17 -0700
27/147 (1998)
> From: Lorraine Heidecker Subject: Re: Adaptation

> I would appreciate a reference or two for Todd Moody's statement about the relatively recent
> appearance of the A and B allele in human blood types. It was my understanding that the ABO blood
> groups occur in all African hominoids. I have checked my (admittedly limited) resources and have
> no information on this topic.
I got the information originally from Peter D'Adamo's popular diet book, but later did some checking of
sources. I believe I found the sources A.E. Mourant, _Blood Relations: Blood Groups and Anthropology_
(Oxford: 1983) and R.R. Race & R. Sanger, _Blood Groups in Man_ (Blackwell Scientific: 1975) to support
his contention that the A blood group appears in the fossil record between 25K and 15K years ago, and
proliterated in concert with the spread of agriculture. The B and AB groups came even later, in historical
times.
D'Adamo, for the record, concedes the point made by Loren Cordain, to the effect that there are many blood
groups besides the ABO serotypes, and that these may be relevant to diet. His reason for emphasizing the
ABO blood groups is that, unlike other blood groups, these types also apply to tissues other than blood. As
he puts it, they are more like "tissue types" and so have more global implications for immune response to
dietary lectins.
I gather that it is not controversial that lectins that cause hemagglutination in cells of one blood type do not
do so in cells of another type. What remains controversial about D'Adamo's ideas is his contention that (a) a
significant amount of lectin gets into the bloodstream; and (b) one there the lectin causes harm, instead of
just being swept up by macrophages. His idea is simple enough: By avoiding those lectins that demonstrably
cause hemagglutination in one's blood type one also avoids whatever health problems might be caused by
those lectins (or the body's immune response to them). I am not qualified to evaluate this line of thinking, but
I am trying to understand it better. I'm not sure if it falls properly into the subject matter of this list, though.
Todd Moody
PALEODIET Archives
Subject: Re: Response to Mary & Sally
From: Loren Cordain
Reply-To:
Date: Mon, 26 Jan 1998 15:25:00 -0700
I've enjoyed the spirited debate that we have carried on over the past 6 months. The extensive post by Mary
and Sally on January 25, 1998 was a rebuttal to my lengthy post of October 9, 1997 which in turn was a
response to Mary and Sally's post of June 29, 1997. Interested readers may access this on-going debate by
viewing the Archives of this list serve(http://maelstrom.stjohns.edu/archives/paleodiet.html). Except for a
few points which I will address, I feel that my viewpoint and perspective in regard to Dr. Enig's and Sally
Fallon's interpretation of paleodiets has been adequately expressed in my post of October 9th. We clearly
differ on a number of issues but also seem to be in agreement on others. A few brief responses to Mary and
Sally's post are in order.
1. I agree to disagree with Mary and Sally on the role of dietary saturated fat and coronary heart disease.
28/147 (1998)
2. The total fat content of elk muscle ranges from 1.5-2.0 % by weight or between 12-16% by calories. Thus
a 100 gm (~1/4 lb) sample would contain 1.5 gms total fat and about 0.5 gm saturated fat. Most wild
herbivore muscle contains a similarly low fat content. In contrast, a 100 gm lean sirloin beef steak (USDA
data) would contain 7.2% total fat by weight and 35% fat by calories with 2.8 gms of saturated fat. Thus, a
lean beefsteak contain 560% more saturated fat than does a comparable 100gm elk steak. This increase in fat
content of domesticated animals is a result of selective breeding and feedlot provisioning which induces
intramuscular lipid storage that is not found in wild animals. My contention is that it would have been
extremely difficult or impossible for pre-agricultural man to have had a regular source of dietary saturated
fat. Since dairy fats (cream, butter, cheese) were not part of man's diet until about 5-6, 000 yrs ago and since
wild animals regularly consumed by pre-agricultural man have extremely low levels of saturated fat, there
would not have been an unlimited source for the atherogenic fats (12:0, 14:0, 16:0) as there is today with
dairy products and fatty meats. One of the few ways in which pre-agricultural man could have obtained
regular high levels of dietary saturated fat would have been by selective butchering in which fatty portions of
the carcass were consumed to the exclusion of the rest of the carcass. This is assuming that the animal even
had fatty storage depots - most wild animals have seasonal variations in body fat, and only in late summer
and early winter are moderate (~3-5% total body weight) fat stores present. Peri-nephral, marrow and
subcutaneous fat stores, are not present in most northern latitude large herbivores for many months of the
year. From an energetic perspective (i.e. optimal foraging theory (1)), it is functionally inefficient to kill
large animals and consume only the the fatty portions of the animal. Clearly, the maximal amount of lean
flesh that could have been consumed, would have been consumed. Despite this, much of the lean carcass
would have been unavailable for consumption, particularly when carbohydrate food (plants) was limited
because of the ceiling or limit to the amount of protein which humans can consume. As I have pointed out in
many previous postings, there is an upper limit to human dietary protein intake which is roughly 50% of total
calories or about 300 gm (2). Thus, without either a source of added carbohydrate or fat, much of the
potential energy from the lean muscle of wild animals is unavailable for consumption. Optimal foraging
theory would predict that pre-agricultural man would have always eaten close to this upper limit for protein,
especially when large herbivorous animals formed the bulk of the dietary intake. This macronutrient intake
pattern (40-50% protein, 15-25% fat; 25-35% carbohydrate) represents the dietary pattern for which preagricultural humans are adapted and which provides optimal health in this group. High intake of animal
based diets (65% total calories or more) are not atherogenic in this context because of the
hypocholesterolemic effect of the enormous protein intake (3, 4), the relatively low saturated fat intake and
the relatively high intake of monounsaturated fats, and long chain polyunsaturates (20 carbon or > ) of both
the n6 and n3 varieties. The low levels of carbohydrate (pre-agricultural humans did not consume grains) in
paleodiets served to further prevent coronary heart disease by reducing triglycerides and VLDL cholesterol
while elevating HDL cholesterol.
3. I agree that that carbohydrate mixed with fat generally results in a lower glycemic (blood glucose)
response. My point here was that the insulin response to fat + carbohydrate is greater than to carbohydrate
alone because of the stimulatory effect of fat ingestion upon glucose-dependent insulino-tropic polypeptide
(GIP) (5).
4. I suggest that Mary and Sally carefully read some of the previous references I have provided in my Oct 9
posting. Mann et al. (6) have clearly shown in coronary artery biopsies performed post mortem on Masai
warriors the evidence for extensive atherosclerosis on a high saturated fat diet of mik and blood. This article
even shows an example photograph of atherosclerotic lesions in coronary artery cross sections.
5. It is sheer folly to deny the calciuretic effects of sodium. This effect has been known for more than 40
years and the evidence in humans is unequivocal (7). In the paper (8) that Mary and Sally cite to support
their contention that sodium is not calciuretic, the reason that sodium did not cause a calciuretic effect is
because an acute load was given rather than a chronic load. The authors of the article even acknowledge this
by saying, "Results from study 1 suggest that the use of acute load tests for studying the effect of sodium
chloride on urinary calcium excretion is inappropriate. Because urinary sodium excretion did not change
significantly from fasting concentrations, it appeared that dietary sodium was retained for the 3h that urinary
excretions was monitored and it is possible that the expected changes in urinary calcium were prolonged past
the collection period of the acute load test".
29/147 (1998)
The type of foods (milk, cheese, butter, cream, salt, fatty meats, whole grains etc) which Mary and Sally
recommend as healthful are all foods which are recent additions to the human dietary experience and which
were only incorporated as staple foods in the past 10, 000 years as humans made the transition from huntergather to farmer. High dietary intakes of sodium, saturated fat, dairy foods and cereal grains are inconsistent
with human evolutionary experience. It is this discordance between our genetically determined nutritional
needs and the recent foods ushered in by the "agricultural revolution" which invariably cause nutritionally
related health problems.
Cordially,
Loren Cordain, Ph.D. Professor, ESS Dept Colorado State University Fort Collins, CO 80523
REFERENCES
1. Hawkes K, Hill K, O'Connell JF. Why hunters gather: optimal foraging and the Ache of eastern Paraguay.
Am Ethnologist 1982;9:379-98. 2. Speth JD. Early hominid hunting and scavenging: the role of meat as an
energy source. J Hum Evolution 1989;18:329-43. 3. Wolfe BM. Potential role of raising dietary protein for
reducing risk of atherosclerosis. Can J Cardiol 1995; 11 (suppl G):127G-131G. 4. Wolfe BM et al. Short
term effects of substituting protein for carbohydrate in the diets of moderately hypercholesterolemic human
subjects. Metabolism 1991;40:338-43. 5. Collier GR et al. The acute effect of fat on insulin secretion. J Clin
Endocrionol 1988;66:323-26. 6. Mann GV et al. Atherosclerosis in the Masai. Am J Epidemiology
1972;95:26-37. 7. Nordin BEC et al. The nature and significance of the relationship between urinary sodium
and urinary calcium in women. J Nutr 1993;123:1615-22. 8. Whiting et al. Calciuretic effects of protein and
potassium bicarbonate but not of sodium chloride or phosphate can be detected acutely in adult women and
men. Am J Clin Nutr 1997;65:1465-72.
PALEODIET Archives
Subject: Re: Adaptations
From: Loren Cordain
Reply-To:
Date: Mon, 26 Jan 1998 17:26:00 -0700
30/147 (1998)
There has been considerable discussion in the past week regarding human blood lipid responses to high and
low carbohydrate diets and whether or not there is a genetic basis for differential responders. To follow up on
this discussion, I would like to point out that there is substantial evidence to show that blood lipid response
to variation in dietary fat and cholesterol intake varies widely among individuals (1, 2, 3) and that this
variability is likely attributable to genetic factors with polymorphisms at several genetic loci including genes
for apolipoproteins and for low density lipoprotein (LDL) particle size and density (4). There is a LDL
subclass called pattern "B" which is characterized by a preponderance of small, dense LDL particles,
elevated triglycerides, low high density (HDL) cholesterol and increased coronary heart disease (CHD) risk.
LDL pattern B occurs in ~30% of the male population (5). LDL subclass pattern "A" is characterized by
larger more buoyant LDL particles. Low fat, high carbohydrate diets induce a reduction in the atherogenic
small dense LDL in individuals displaying pattern "B" and also cause reductions in LDL cholesterol that are
greater than in subjects displaying pattern "A" (6). These data clearly suggest that low fat, high carbohydrate
diets may be more effective in lowering LDL cholesterol and small dense LDL in about 30% of the
population, and less effective in 70% of the population. LDL subclass pattern B is influenced by a major
gene or genes with a prevalence in the American population estimated to be 0.25 (5). The specific gene or
genes responsible for this trait have not been identified, but there is evidence to show linkage to polymorphic
markers near the LDL receptor gene on chromosome 19p (7). To date, there are no experimental data
evaluating the effects of quite low carbohydrate diets (<30% of total energy) upon blood lipid responses in
LDL subclasses A or B, however Krauss et al. (8) have clearly shown that all subjects (n=105) whether
subclass A or B responded to a high fat diet (46% energy) by substantial increases in LDL cholesterol and
responded to a low fat diet (23.9% energy) by decreases in LDL cholesterol. This information does not
support Dean's contention in a previous post that differential responders to high and low fat diets bias
interpretation of dietary intervention trials, nor does it lend support to his proposal that high fat diets can
improve blood lipid profiles. I contend that any improvement in total cholesterol or LDL cholesterol by
uncontrolled, self administered low carbohydrate diets (such as followed by Dean and others) are an artifact
of (a) reductions in total caloric intake, (b) increases in total protein, (c) unknowing changes in the dietary
P:M:S ratio, (d) and combination of the three. Further, improvements in TG, VLDL and HDL can be mainly
attributable to reductions in carbohydrate. Under isocalorically controlled conditions in which dietary
saturated fat is increased at the expense of any other lipid or macronutrient, there will be a characteristic
increase in LDL cholesterol as shown time and again with meta analyses (9) under metabolic ward
conditions (10) and corroborated by in vitro and in vivo data showing that LDL receptors are down regulated
by dietary saturated fat (11).
Cordially,
Loren
REFERENCES
1. Mistry F et al. Individual variation in the effects of dietary cholesterol on plasma lipoproteins and cellular
homeostasis in man. J Clin Invest 1981;67:493-502. 2. Jacobs DR et al. Variability in individual serum
cholesterol response to change in diet. Arteriosclerosis 1983;3 3. Katan MB et al. Congruence of individual
responsiveness to dietary cholesterol and to saturated fat in humans. J Lipid Res 1988;29:883-92. 4. Dreon
DM et al. Gene-diet interactions in lipoprotein metabolism. Monographs in Human Genetics 1992;14:32549. 5. Austin MA et al. Inheritance of low-density lipoprotein subclass patterns:results of complex
segregation analysis. Am J Hum Genet 1988;43:838-46. 6. Dreon DM, Krauss RM. Diet-gene interactions in
human lipoprotein metabolism. J Am Coll Nutr 1997;16:313-24. 7. Nishina PM et al. Linkage of atherogenic
lipoprotein phenotype to the low density lipoprotein receptro locus on the short arm of chromosome 19. Proc
Natl Acad Sci 1992;89:708-12. 8. Krauss RM, Dreon DM. Low density-lipoprotein subclasses and response
to a low-fat diet in healthy men. Am J Clin Nutr 1995;62:478s-87s. 9. Howell WH et al. Plasma lipid and
lipoprotein responses to dietary fat and cholesterol: a meta analysis. Am J Clin Nutr 1997;65:1747-64. 10.
Phinney SD et al. The human metabolic response to chronic ketosis without caloric restriction: physical and
biochemical adaptation. Metabolism 1983;32:757-68. 11. Brown MS, Goldstein JL. Receptor mediated
control of cholesterol metabolism. Science 1976;191:150-4.
PALEODIET Archives
Subject: Raising cholesterol
From: Ray Audette
Reply-To:
31/147 (1998)
Date: Mon, 26 Jan 1998 23:41:41 -0800

> Date: Thu, 22 Jan 1998 14:06:00 -0700
> From: Loren Cordain
> Subject: Re: Adaptation
> I have little doubt that the inclusion of large amounts of high fat domestic meat will raise LDL
> and total cholesterol in the diets of most people.
Low fat diets have been shown to raise LDL (by 24%) and triglycerides (by 23%) very rapidly (under 6
weeks)in insulin resistant individuals (1). As many overweight individuals have this condition (2), limiting
fat intake may not be a good idea for these the majority of Americans.
People who traditionally eat a low fat diet such as Sumo wrestlers also have very highest rates of arterial
disease (3). A recent report in the Lancet (May, 97?) also pointed out the high rates of these disorders in
areas of low fat consumption world wide.
1. Garg "Effects of varying Carbohydrate Consumption in Non-Insulin Dependent Diabetes Mellitus" JAMA
vol. 271, #18 (May 11, 1994)pg 1421-1428
2. Eades, "Protein Power" NY Bantam 1995
3.Roach, "Advice from the World's Biggest Weight Experts" Health (March/April 1993) pg 62-72
PALEODIET Archives
Subject: Re: Response to Mary & Sally
From: Jean-Louis Tu
Reply-To:
Date: Tue, 27 Jan 1998 09:41:34 -0500
> I agree that that carbohydrate mixed with fat generally results
> in a lower glycemic (blood glucose) response. My point here was that
> the insulin response to fat + carbohydrate is greater than to
> carbohydrate alone because of the stimulatory effect of fat ingestion
> upon glucose-dependent insulino-tropic polypeptide (GIP) (5).
> 5. Collier GR et al. The acute effect of fat on insulin secretion.
> J Clin Endocrionol 1988;66:323-26.
I would like to point out what I think is an inaccuracy in the last statement. I looked up in the articles
published by Collier et al. (1, 2, 3), and the results were:
From (1): The effects of co-ingestion of 50 g fat (butter) with 50 g carbohydrate (potato) compared with
potato alone: markedly decreased glucose, very slightly decreased insulin, markedly increased GIP.
From (2): Similar experiments and results with 75 g carbohydrate (438 g potato or 121 g lentils) with or
without 37.5 g fat (46.5 g butter). Of course, all the effects are more important with the rapidly absorbed
carbohydrate (potato) than with the slowly absorbed carbohydrate (lentils).
From (3): The aim of that article was to test the conjecture that the rate of rise of GIP, rather than the steady
state level achieved, stimulates insulin secretion when fat and carbohydrate are ingested together. To do that,
the authors administered a 5 g iv bolus dose of glucose 15 minutes after the meal, when the RATE of rise of
GIP was highest but the level still LOW, and observed the insulin response. It appears that the peak insulin
after the mixed meal was 60% higher than after the carbohydrate meal. That seems to confirm their
hypothesis.
It should be noted that, in a practical situation, nobody will inject you some glucose after lunch, so, that the
insulin peak is higher after such a practice following a mixed meal shouldn't be of concern.
So, in summary, 50 grams of carbohydrates+50 grams of fat is much "better" on the blood glucose point of
view, and only slightly "better" on the insulin point of view than 50 grams of carbohydrates alone.
Now, in a practical situation, a man would have the choice between:
A) 50 grams carb. at breakfast, 50 grams fat at lunch B) 50 grams carb and 50 grams fat at breakfast, no
lunch C) 25 grams carb and 25 grams fat at each meal
Obviously, from the preceding, B is "better" than A, and I think most people will agree that C is better than
B.
32/147 (1998)
So, that's in favor of mixed meals. Now, the problem is, fat is often co-ingested with protein. The effect of
carbohydrate+protein has been studied by Westphal et al. (4), but Westphal's findings contradict earlier
findings (5, 6).
So, I realize it's not clear, but the effect of mixed meals on blood glucose nevertheless shouldn't be
underestimated, since it is thought that high blood glucose can cause insulin resistance or exacerbate an
underlying insulin resistance state (7-14).
Best wishes,
Jean-Louis Tu
REFERENCES
1. Collier et al., The effect of co-ingestion of fat on the glucose, insulin and gastric inhibitory polypeptide
responses to carbohydrate and protein, Am J Clin Nutr 37:941
2. Collier et al., Effect of co-ingestion of fat on the metabolic responses to slowly and rapidly absorbed
carbohydrates, Diabetologia 26:50-54
3. Collier et al., The acute effect of fat on insulin secretion, J Clin Endocrin. Metabolism 66:323 (1988)
4. Westphal et al., Metabolic response to glucose ingested with various amounts of protein, Am J Clin Nutr
1990 (62):267-272
5. Spiller et al., Effect of protein dose on serum glucose and insulin response to sugars, Am J Clin Nutr 1987
(46):474-80
6. Rabinowitz D, et al., Patterns of hormonal release after glucose, protein, and glucose plus protein, Lancet.
1966 Aug 27; 2(7461): 454-456
7. Yki-Jarvinen H. Acute and chronic effects of hyperglycemia on glucose metabolism, Diabetologia
1990(33):579-585
8. Yki-Jarvinen H. Glucose toxicity, Endocrine Rev. 1992(13):415-431
9. Anderson CM et al., Relative expression of insulin receptor isoforms does not differ in lean, obese and
NIDDM subjects, J Clin Endocrinol Metab 1993(80):1037-1044
10. Rossetti L et al., Effect of chronic hyperglycemia on in vivo insulin secretion in partially pancreatomized
rats, J Clin Invest 1987(80):1037-1044
11. Rossetti L et al., Correlation of hyperglycemia with phlorizin normalizes tissue sensitivity to insulin in
diabetic rats, J Clin Invest 1987(79):1510-1515
12. Garvey WT et al., The effects of insulin treatment on insulin secretion and action is type II diabetes
mellitus, Diabetes 1985(34):222-234
13. Henry RR et al., Diabetes 1986(35):990
14. Kolterman OG et al., The acute and chronic effects of sulfonylurea therapy in type II diabetics, Diabetes
1984(33):346
PALEODIET Archives
Subject: n6/n3 ratio in grasses
From: Dick Dawson
Reply-To:
Date: Wed, 28 Jan 1998 11:17:18 -0500
it's old but Jennie wrote:
> About fatty acid patterns of grasses and the resulting pattern in animals that feed on these
> grasses: My understanding of this issue is that the ratio of n3/n6 or the level of polyunsaturated
> fatty acid content in grasses is not reflected in the meat/milk of ruminant grazing animals. This
> is because the rumen bacteria do a good job of hydrogenating all the PUFAs and the animal absorbs
> only saturated fatty acids. Thus the meat and milk of cattle and sheep are fairly saturated
> irrespective of what you feed them. Pigs and chickens, not ruminants, show a fatty acid pattern
> that reflects the diet they are getting. I am not sure where caribou etc. stand.
Caribou are deer family. Also moose, elk, elg (same as NA moose in norden), deer. All ruminants but not
bovine family. Perhaps different acid conversion. I don't know about antelope & pronghorn.
PALEODIET Archives
Subject: Re: Response to Mary and Sally
33/147 (1998)
From: Edward Campbell

Reply-To:
Date: Sat, 31 Jan 1998 01:32:54 EST
Loren wrote:
> I agree to disagree with Mary and Sally on the role of dietary
> saturated fat and coronary heart disease.
> The type of foods (milk, cheese, butter, cream, salt, fatty meats, whole
> grains etc) which Mary and Sally recommend as healthful are all foods
> which are recent additions to the human dietary experience and which
> were only incorporated as staple foods in the past 10, 000 years as
> humans made the transition from hunter-gather to farmer.
Mary and Sally wrote:
> If the consumption of saturated fat within the context of the "average American
> diet" is "deadly", why was heart desease so rare among Americans at the turn of
> the century, who consumed large amonts of saturated fat from dairy products,
> lard, tallows and coconut oil?
I feel this is a good question. During a recent lecture, Robert Atkins, MD also cited this evidence. He
mentioned that all the great anatomists of the 19th Century rarely reported on seeing any atheroscerlosis in
the many autopsies performed. Atkins says that it was not until around 1912 that atheroscerlotic plaques
began to be observed upon autopsy. This was approx. 20-30 years after "altered foodstuffs" (flour, cereals,
refined sugars, trans fats, etc.) began to be common components of the American diet (this coorelates to
Cleave's "Law of 20's").
Also, the 10/21/97 issue of Circulation contained an article called: "Fasting Triglycerides (TG) and HDL and
Risk for Myocardial Infarction". This Harvard study concluded that the ratio of TG:HDL was the most
significant risk factor in developing CHD. The TG:HDL ratio was a better predictor than total cholesterol
(TC), better than TC:HDL ratio, and better than LDL:HDL ratio.
Reducing carbohydrates, particularly refined ones and other "altered foodstuffs", is the best way to reduce
TG levels. Maybe this is one explaination for why 19th Century Americans and primitive cultures that
consumed some dairy products and whole grains were remarkably clear of atherscelosis and CHD.
Comments?
Ed Campbell, DC, CSCS
PALEODIET Archives
Subject: Glucose and insulin responses
Reply-To:
Date: Mon, 2 Feb 1998 10:43:50 +1100
Parts/Attachments:
We have tested the glucose and insulin responses to hundreds of foods over the last 10 years. Generally
among high carbohdyrate, low fat foods you find that glucose and insulin responses correlate well (r around
0.7), but there are many examples where they become 'unhooked'. This is particularly true when we are
dealing with high fat foods. Recently we published the first insulin index of foods based on 1000 kJ portions
of common foods. The abstract of this paper is reproduced below. Several foods which were high fat/high
CHO combinations gave the highest insulin responses.
Just lately we tested the glucose and insulin responses to 12 confectionery candy type products. I was
surprised to find no correlation at all (if anything the trend was inverse) between glucose and insulin despite
a wide range of responses among both. In fact the food with the lowest GI gave the highest insulin response.
My conclusion is that we haven't tested enough high fat/high CHO combinations (such as we find in many
common foods) to understand the real situation.
34/147 (1998)
In the end I think it will be the insulin response which is the signficant factor from a disease risk point of
view, not the glucose response.
Best wishes Jennie
> 1. Foster-Powell K, Brand Miller J. International tables of glycemic index. Am J Clin Nutr 1995; 62:
871S-93S
2. Holt SHA, Brand Miller JC, Petocz P. An insulin index of foods: insulin demand generated by 1000 kJ
portions of common foods. Am J Clin Nutr, 1997; 66;1264-76.
The aim of this study was to quantify postprandial insulin responses to isoenergetic 1000 kJ (240 kcal)
portions of a large number of common foods. Thirty-eight foods separated into six food categories (fruits,
bakery products, snacks, carbohydrate-rich foods, protein-rich foods, breakfast cereals) were fed to groups of
11-13 healthy subjects. Finger-prick blood samples were obtained every 15 min over 120 min. Insulin index
(II) scores were calculated from the area under the insulin response curve for each food using white bread as
a reference food (=100%). Significant differences in insulin responses were found both within and among the
food categories and also among foods containing a similar amount of carbohydrate. Overall, plasma glucose
and insulin responses were highly correlated (r = 0.70, P<<0.001, n = 38). However, the protein-rich foods
and the bakery products (rich in fat and refined carbohydrate) tended to elicit insulin responses which were
disproportionately higher than their glycemic responses. Total carbohydrate (r = 0.42, P<<0.01, n = 38) and
sugar (r = 0.44, P<<0.44) contents were positively related to the mean II scores, whereas fat (r = - 0.32,
P<<0.05) and protein (r = - 0.24, NS) contents were negatively related. Consideration of II values may
improve the dietary management of diabetes and aid in the estimation of preprandial insulin requirements.
NSW 2006 Australia
Phone: (61 2) 9351 3759
Fax: (61 2) 9351 6022
PALEODIET Archives
Subject: Re: PALEODIET Digest - 31 Jan 1998 to 2 Feb 1998
From: "Maurice Sonnenwirth M.D."
Reply-To:
Date: Mon, 2 Feb 1998 18:44:27 EST
In a message dated 98-02-02 16:01:25 EST, you write:
<< Date: Mon, 2 Feb 1998 10:43:50 +1100 From: Jennie Brand Miller Subject: Glucose and insulin
responses
We have tested the glucose and insulin responses to hundreds of foods over the last 10 years. Generally
among high carbohdyrate, low fat foods you find that glucose and insulin responses correlate well (r around
0.7), but there are many examples where they become 'unhooked'.=20
Is there any way to get a list of the foods, and the responses? I would, of course, like to find out which foods
were on the "unhooked" list, and those where the response was opposite of that it was thought it would be. I
have read that fat and alternatively protein would slow down the carb absorption and the insulin response,
but apparently, at least with certain foods this is not so. Would love to have the "rest of the story".
Maurice Sonnenwirth
PALEODIET Archives
Subject: Saturated fat and risk of CHD
Reply-To:
Date: Fri, 6 Feb 1998 16:49:20 PST
35/147 (1998)
Here is an attempt to perhaps hone in a bit further on some of the points that have been made in this quite
interesting discussion:
Mary Enig and Sally Fallon recently posted:
> If the consumption of saturated fat within the context of the "average American diet" is "deadly",
> why was heart desease so rare among Americans at the turn of the century, who consumed large
> amonts of saturated fat from dairy products, lard, tallows and coconut oil?
On Sat, 31 Jan 1998 Edward Campbell posted:
> I feel this is a good question. During a recent lecture, Robert Atkins, MD also cited this
> evidence. He mentioned that all the great anatomists of the 19th Century rarely reported on seeing
> any atheroscerlosis in the many autopsies performed. Atkins says that it was not until around 1912
> that atheroscerlotic plaques began to be observed upon autopsy. This was approx. 20-30 years after
> "altered foodstuffs" (flour, cereals, refined sugars, trans fats, etc.) began to be common
> components of the American diet (this coorelates to Cleave's "Law of 20's").
It does seem that the jury is still out wrt to the relationship between dietary sat. fat and CHD. However, it is
important to recognize that when we are dealing with a condition that is influenced by many factors (such as
CHD), single-variable correlations within a given population (whether US in late 19th C or France today) are
weak evidence (at best) of a causative relationship (or lack thereof). There are numerous factors that could
explain the relative low rate of CHD in a population despite its having a relatively high per capita
consumption of sat. fat. I think it would be difficult to do a good multi-variate cross-country analysis to
determine the role of various factors due to lack of data for some of the variables.
One cautionary note wrt relying on the low rate of CHD in the US up to early 20th C (actually, I haven't seen
anyone provide statistics on this) was made a few months ago: that CHD is mainly a condition of the elderly,
and since the life expectancy was lower back in the good old days, the rate of CHD across the whole adult
population would have been lower than today even if the rate among the elderly was the same as today. Of
course, anecdotal evidence regarding low rate of etheroscerlosis back then has been presented, and in fact I
am very willing to believe that the CHD rate AMONG THE ELDERLY was lower than today due to higher
prevalence of cardio-protective factors such as exercise and lower prevalence of factors contributing to CHD
such as smoking and others that have been mentioned on this list.
But logically that does not allow one to give sat. fat a "clean bill of health" wrt CHD.
For example, Loren Cordain recently posted:
<Under isocalorically controlled conditions in which dietary saturated fat is <increased at the expense of any
other lipid or macronutrient, there will <be a characteristic increase in LDL cholesterol as shown time and
again <with meta analyses (9) under metabolic ward conditions (10) and <corroborated by in vitro and in
vivo data showing that LDL receptors are <down regulated by dietary saturated fat (11).
On the other hand, Mary and Sally raised concerns regarding the relevance of short-term feeding studies
under metabolic ward conditions -- do others share their concern?
Mary and Sally also question the linkage between LDL cholesterol level and incidence of CHD from the
Framingham study -- can anyone comment on this point?
Mary and Sally also raised strong doubts regarding the relationship between serum cholesterol and risk of
death from CHD (perhaps it would be better if the Grundy study had looked at incidence of CHD rather than
CHD death?) -- does Loren or anyone else have a rebuttal to their points here?
Ed continued:
> Also, the 10/21/97 issue of Circulation contained an article called: "Fasting Triglycerides (TG)
> and HDL and Risk for Myocardial Infarction". This Harvard study concluded that the ratio of TG:HDL
> was the most significant risk factor in developing CHD. The TG:HDL ratio was a better predictor
> than total cholesterol (TC), better than TC:HDL ratio, and better than LDL:HDL ratio. Reducing
> carbohydrates, particularly refined ones and other "altered foodstuffs", is the best way to reduce
> TG levels. Maybe this is one explaination for why 19th Century Americans and primitive cultures
> that consumed some dairy products and whole grains were remarkably clear of atherscelosis and CHD.
Could be, but note that this study only considered the standard blood lipid risk factors for CHD, not the
whole range of risk factors.
Can anyone provide a reference for the higher effect on reduced TG of reducing REFINED carbs?
Steve Meyers
PALEODIET Archives
Subject: Insulin index
36/147 (1998)

Reply-To:
Date: Wed, 4 Feb 1998 08:41:26 +1100
Dear Maurice
> Is there any way to get a list of the foods, and the responses?
The full reference tells you all. If you do not have access to this journal, let me know your address and I will
put a reprint in the mail.
Best wishes jennie
PALEODIET Archives
Subject: New book
From: Dean Esmay
Reply-To:
Date: Sun, 15 Feb 1998 10:41:05 -0500
Just received the following info on a new book:
Brothwell, D R & P Brothwell `Food in antiquity: a survey of the diet of early peoples', 248pp, 254 ill, new
ed, pbk, UKP13.00, Johns Hopkins Univ Press, January 1998, ISBN 0 8018 5740 6
I have no other information on this book at all.
PALEODIET Archives
From: Buji Kern
Reply-To:
Date: Thu, 19 Feb 1998 04:44:25 -0800
From Mary and Sally> We have stated that cholesterol is a non issue--neither
> serum nor dietary cholesterol is good predictor of CHD
The clinical model, which is always under revision, seems to be that the progress of atherosclerosis is
affected by hemodynamic factors secondary to blood pressure and vascular anatomy, to lipid and cholesterol
metabolism, to carbohydrate metabolism, and its interactions with lipids and cholesterol, and probably to
factors having to do with clotting, and inflammatory reactions. Some of these may have more effect on the
formation of the thrombus, some on the degradation of the vascular wall prior to the thrombotic event. Also,
various authorities (including Mary and Sally), question one or more parts of this story.
Many people and doctors concerned with prevention or avoidance of CHD, follow lipid profiles, blood
glucose, and blood pressure, not because these are necessarily the whole story, but because they are thought
to be relevant, they are relatively cheap and non invasive to monitor.But there is a big unstated assumption:
that the only cost to tailoring diets to optimize these readings is the loss of pleasure. In a Puritan culture like
the US, that is almost a plus.
If cholesterol doesn't count, or at least LDL and total cholesterol taken alone don't count, things are quite a
bit different. For example there are many diabetics, and obese people, for whom a relatively low
carbohydrate diet improves blood pressure, contributes to weight loss, and lowers blood sugar readings. But
it may well raise LDL and total cholesterol. If these people, or more likely their doctors, feel that the
degradation in cholesterol readings dominates the other improvements, they are back to square one. So what
is being treated is a number. It is extremely important to establish that that number is clinically important, or
alternatively, that it is not.
37/147 (1998)
What would be needed, is an alternate marker, that clinicians and patients can follow. At the present time, it
may possibly expose an MD to malpractice litigation to ignore cholesterol, the institutional acceptance of the
cholesterol - CHD hypothesis is so great.
Could Mary and Sally suggest blood chemistries, or other markers, that they feel may be more relevant to the
progress of atherosclerosis?
Thanks,
Michael Kern, MD
PALEODIET Archives
Subject: gender differences
From: Herr Hflechner
Reply-To:
Date: Sat, 21 Feb 1998 19:31:50 +0100
In January there has been a discussion about differences in dietary adaptations between human populations. I
have a similar question: Is it imaginable, that there are gender differences in dietary adaptations?
Anatomically the digestive tracts of humans and great apes are very similar (1). Allometric scaling however
shows, that the human gut is markedly small in relation to body size and in comparison with our closest
relatives (2). This suggests, that we are adopted for a relatively high-energy diet, for instance meat.
If dimensions of the digestive tract are indicators of dietary adaptations, how can we explain the following?
In the experience of many endoscopists colonoscopy in women is more difficult than in men. To investigate
a possible anatomic basis for this finding Saunders et al. analysed barium enemas of more than 300 patients
(3). Results: Total colonic length was greater in women (median, 155 cm) compared to men (median, 145
cm), despite womens smaller stature (p<0.0001). This difference is most prominent in the transverse colon
and these findings are in keeping with those of Sadahiro et al. (4).
Some other observations: Dispite food-sharing behavior the per capita consumption of meat by male
chimpanzees is greater than the amount of meat eaten by females (5). Similar differences may be observed in
humans: Data from the 1987 National Health Interview Survey (and from my own family) show that women
eat more fruits and vegetables and less meat.
Are the observed differences in colonic length accidental findings without any significance, acquired
modifications, or could it be, that they are the result of (at least) 2 million years "man the hunter" and
"woman the gatherer"?
1. Stevens CE & Hume ID (1995). Comparative physiology of the vertebrate digestive system. Cambridge,
Cambridge University Press. 2. Martin RD et al. (1985). Gastrointestinal allometry in primates and other
mammals. In: Size and scaling in primate biology (Jungers WL, ed.). New York, Plenum Press. 3. Saunders
BP et al. (1996). Why is colonoscopy more difficult in women? Gastrointestinal Endoscopy 43/2:124-126. 4.
Sadahiro S et al. (1992). Analysis of length and surface area of each segment of the large intestine according
to age, sex and physique. Surgical and Radiologic Anatomy 14:251-257. 5. Stanford CB (1996). The hunting
ecology of wild chimpanzees: Implications for the evolutionary ecology of Pliocene hominids. American
Anthropologist 98:96-113. 6. Patterson BH (1995). Food choices of whites, blacks, and Hispanics: data from
the 1987 National Health Interview Survey. Nutrition and Cancer 23:105-119.
PALEODIET Archives
Subject: Posting from Mary and Sally
From: SAFallon
Reply-To:
Date: Sun, 1 Mar 1998 20:57:18 EST
To: All Paleodieters From: Mary and Sally
Following are some miscellaneous comments for the ongoing debate.
38/147 (1998)
1. George Mann did not find pathogenic build up of plaque in the Masai, but rather the normal intimal
thickening of the arterial wall that occurs in all individuals, regardless of diet. The pathologist William
Stehbens has reported on this and we quote from his work. (The Pathology of Atherosclerosis, in Coronary
Heart Disease, George Mann ed., available from the Price-Pottenger Nutrition Foundation (619) 574-7763):
For many years it has been acknowledged that at birth the intima of the aorta is thickened, more so distally
than proximally, with similar intimal thickenings occurring at forks of distributing arteries. . . . It is also
recognized that the intima thickens throughout life progessively but not uniformly. The process does not
cease at physical maturity, like other maturation phenomena, even though some vessels remain unaffected or
virtually unaffected for most of the subjects life. This sclerotic change has been referred to as
arteriosclerosis and is often considered to be an aging phenomenon, while the accumulation of the lipid-rich
rich debris in the thickened intima was thought by some to be a separate disorder, i.e. atherosclerosis.
However the two disorders have not been satisfactorily differentiated, and so confusion has abounded for
many years over the use of the two terms. . . Logically, in seeking the cause of atherosclerosis, we should
investigate the earliest demonstrable lesions which appears to be the intimal pads of cushions about arterial
forks and junctions. Ultrastructurally, these intimal proliferations exhibit evidence of granulo- vesicular
degeneration and loss of elastica even in the neonate, and their localization is consistent with their being of
hemodynamic origin. These thickenings progressively enlarge and exhibit evidence of considerable muscle
cell degeneration with the accumulation of myriads of vesicles in the cell matrix and also plasma membrane
fragments, abnormal collagen, loss of elastic, and dystrophic basement membranes with separation of muscle
and endothelial cells from the multilaminated basement membranes. The accumulation of lipid and
calcification is a later phenomenon. . .(end quote)
In other words, atherosclerosis is initiated in the breakdown of normal thickened arterial tissue that occurs in
locations of pressure gradients due to the fluid dynamics of blood flow. Such breakdown may be due to
nutritional deficiencies or to irritations from viruses or free radicals from oxidized cholesterol and rancid
dietary fats.
2. A 1962 study of coronary artery disease in Thailand is germane to our discussion of saturated fats. (A
comparison of atherosclerosis of the aorta and coronary arteries in Bangkok and Los Angeles, Am J Clin
Path Vol 38, No 2, pp162-170.) Researchers found that in Thailand, a diet which is low in total fat
[compared to Thais living in Los Angeles] but relatively high in the proportion of saturated fat was found to
be compatible with a low severity of coronary atherosclerosis. Sources of saturated fat in the Thai diet are
lard used in cooking; and coconut oil, which contains over 50% of total fat as the supposedly atherogenic C12, C-14 and C-16 fatty acids. These fats strengthen immune system function, which may by why Thailand
has the lowest overall cancer rate (for both men and women) of all the 50 countries included in the National
Cancer Institute surveys.
3. Newly released USDA data show a decrease in the consumption of SFAs since the turn of the century (57
grams per person per day in 1909 versus 52 in 1994.) (CNI, February 13, 1998 pp 4-6.) Levels for
monounsaturated fatty acids increased from 49 and 65 grams per capita per day and levels of polyunsaturated
fatty acids increased from 13 to 31 grams per capita per day. Total fat contributions from red meat have
generally declined throughout this period. In the early years, red meat contributed about one-third of the fat,
but by 1994 its contribution decreased by almost one-half. However, contributions from salad oils were 10
times higher in 1994 than in 1909. Total fats and oils have increased from 41 pounds in 1909 to 70 pounds
per capita in 1994. It is hard to conclude from this data that consumption of saturated fats (from butter,
tropical oils and animal sources) is the cause of the steep rise in CHD that has characterized the 20th century.
In fact, these statistics indicate that the so-called heart healthy monounsaturated fats should be more closely
examined as a possible contributing factor, at least in the context of the American diet.
4. We still lack one key piece of data, and that is the amount of adipose tissue as a percentage of the total in a
large wild ruminant such as an elk or moose, during the late Summer and early Fall. Without this we cannot
make a true comparison between the saturated fat available to Paleolithic man, compared to his modern beefeating counterpart. Are there any hunters in the group who can enlighten us? Even a visual estimate would be
helpful. How thick is the subcutaneous fat on such an animal at the height of its fat stores?
39/147 (1998)
5. There was a question about traditional preparation of maize (corn) which involves an alkaline treatment to
release niacin. This seems to contradict assertions that grains should receive an acid treatment (lactic acid
fermentation) to neutralize phytic acid and other nutrients. Actually, corn in South American cultures was
first treated with lye before cooking; but the cooked gruel then underwent a long period of acid fermentation.
Examples are Cherokee bread, made from a cooked gruel of corn and beans, wrapped in corn husks and
allowed to ferment for at least two weeks. A similar preparation is Pozol, from southern Mexico, made by
wrapping cooked corn gruel in banana leaves and allowing at least two weeks for fermentation. The bread
becomes covered with green mold. Pozol seems to be a complete food, supporting good health without the
addition of other foodstuffs (insect parts and the mold itself would supply animal factors). A high enzyme
content and antibiotic factors in the mold would provide protection against gastrointestinal distress in the hot
moist jungle environment.
6. The politically correct interpretation of the Paleolithic diet is one of lean meat, occasional organ meats,
nuts, monounsaturated oils, fruits and vegetables. Some have found that their blood parameters worsen on
such a diet, and we submit that a likely cause is low levels of saturated fats, and inadequate levels of fat
soluble vitamins A and D, such as are found in dairy fats, shell fish, egg yolks and organ meats. We are
especially concerned about the use of this diet for growing children, who tend to dislike organ meats and
who have traditionally obtained vitamins A and D from dairy fats and egg yolks. Calcium deficiency is also a
potential problem. Traditional societies obtained sufficient calcium either from dairy products or from
preparations made from bones--generally bone broths. Vegetables will not supply adequate calcium for
growing children, due to a number of blocking factors such as oxalic acid, and nuts will not be a good source
either, unless properly prepared to neutralize phytic acid content. Adequate vitamin A and D are needed for
calcium absorption.
PALEODIET Archives
Subject: Re: Total body fat content of wild ungulates
From: Loren Cordain
Reply-To:
Date: Mon, 2 Mar 1998 17:12:00 -0700
40/147 (1998)
In a recent post, Mary Enig & Sally Fallon solicited information on the fat content of wild game animals. My
colleague, Boyd Eaton, has previously summarized the fat content of lean game muscle meat (1), but did not
present data on total carcass fat content. Speth (2) has compiled data from 33 analyses of whole body fat %
of 11 different species of wild ungulates. The mean value of 3.6% fat is similar to other estimates (2-5%)
based upon compiled data (3). In contrast the total body fat content of a domesticated, grain fed steer ranges
between 33-40% (2). In wild animals, the total fat content changes seasonally (at higher latitudes it is lowest
during late winter and early spring, whereas in lower latitudes it is lowest during the dry season). During late
summer & early fall, certain North American species have been reported to have total fat levels as high as
17% (2), whereas some African species have been shown to have values as high as 6% (2). Stefansson (4)
noted that "the largest slab of back fat which I have seen taken from a caribou on the Arctic coast was from a
bull killed near Langton Bay early in September, the fat weighing 39 lbs". Large caribou bull can weigh
between 350-400lbs, so the subcutaneous back fat of high northern ungulate species could conceivably
represent 10% of the total weight under the best of conditions during early fall. However, remember that
after the rut and into winter total fat % drops back down to an average of 1.3% (2) for caribou. This
reduction of total fat percentage occurs for all tissues except brain, and results mainly from reductions in
subcutaneous storage fat. Wild ungulates unlike domesticated cattle do not store depot fat (saturated
primarily) intra-muscularly (i.e. marbling) Thus, it is apparent that high levels of total fat intake could have
only occurred seasonally (perhaps 2-4 months) in early man dependent upon wild ungulates for the bulk of
daily energy. Higher levels of fat intake could conceivably occur with selective butchering in which fatty
tissues were eaten to the exclusion of lean. This proposition however, is quite wasteful and over the long
haul, contradicts optimal foraging theory (5). In all likelihood, fatty tissues would have always been
preferred over lean (3), but the fatty tissues mainly consumed over the course of the entire year would have
been organs (marrow, brain, perinephral fat, mesenteric fat, spleen, tongue, gonads, retro-orbital fat, liver,
kidney, thymus, heart) rather than subcutaneous depot fat; simply because subcutaneous fat depots are
negligible for most of the year. The fatty acid composition of organs is quite different from that of
subcutaneous fat depots in which saturated fat prevails. Most organs are quite high in long chain PUFA of
both n3 and n6 varieties; often times they are also quite high in MUFA; rarely if ever do they contain higher
levels of saturated fat relative to the combined PUFA and MUFA (6). Further, the total amount of organ
meats, relative to muscle meat in a single animal is quite small. Consequently, even with the selective
consumption of organ meats, the total fat energy in the diet would still not approach western levels because
of the diluting influence of high consumption of lean meat (as predicted by optimal foraging theory) which
averages ~2% by weight or 17% by energy. The muscle meat of wild animals is much less saturated than is
that of domesticated animals (3). The saturated fat content of 3 domesticated muscle meats (lamb, beef, pork
- averaging 4.2% total fat) has a mean saturated fat content of 42% (3). In contrast, the saturated fat content
of 5 wild animals (rabbit, buffalo, sambar deer, kangaroo, wild pig - averaging 1.4% total fat) has a mean
saturated fat content of 32% (3). It is apparent that both the relative and absolute amounts of saturated fats in
game muscle meat is considerably lower (particularly when total energy estimates are used rather than per
weight measures). Pre-agricultural diets were characterized by extremely high (by modern standards) protein
intakes (35-45% total energy), low carbohydrate intakes (25-35% total energy) and low to moderate fat
intakes (25%-35%). Saturated fats would have almost always comprised less than 40% of the total fat intake.
Thus, it would have been difficult or impossible for pre-agricultural man to consume a high fat ( >
40%energy) diet in which saturated fats were predominant.
REFERENCES
1. Eaton SB. Humans, lipids and evolution. Lipids 1992;27:814-20. 2. Speth JD. Energy source, protein
metabolism, and hunter-gatherer subsistence strategies. J Anthropological Archaeology 1983;2:1-31. 3.
Sinclair AJ, O'Dea K. Fats in human diets through history: is the western diet out of step. In: Wood JD,
Fisher AV (Eds). Reducing Fat in Meat Animals. Elsevier Applied Science, New York, 1990, 1-47. 4.
Stefansson V. The Fat of the Land. MacMillan Company, New York, 1960, pp 28-29. 5. Hawkes K et al.
Why hunters gather: optimal foraging and the Ache of eastern Paraguay. Am Ethnologist 1982;9:379-98. 6.
Cordain L et al. The fatty acid composition of muscle, brain, marrow and adipose tissue in elk: evolutionary
implications for human dietary lipid requirements. World Rev Nutr Diet (abstract), 1998, in press.
PALEODIET Archives
Subject: Re: organ meat weight vs. muscle meat
From: Buji Kern
Reply-To:
41/147 (1998)

Date: Tue, 3 Mar 1998 08:04:53 -0800
Loren Cordain presented very interesting data on the composition of wild ungulates. The one thing I wonder
about, not from any formal data collection, but from the practical experience of hunting and butchering
game, is with his statement immediately below.
Further, the total amount of organ meats, relative to muscle meat in a single animal is quite small
I would guess that if one took the cleaned liver, spleen, pluck, stomach, bowel, pancreas, kidneys, testicles,
and marrow fat, and brains, and piled it on one side of a scale, and put the boned musle on the other side, in
an average size deer, it is going to challenge the statement that the organs are relatively "quite small". Of
course the amount of depot fat remaining on the muscle would affect this, but as Loren has pointed out,
usually it amounts to very little.
This probably would not change the overall hypothesis that saturated fat could not have been a major early
dietary factor, due to the fatty acid composition of the organ meats. But it may suggest that one way that our
modern diets differ from those of early men, is that we don't eat near enough guts.
Michael Kern
PALEODIET Archives
Subject: Fat in wild mammals
Reply-To:
Date: Tue, 3 Mar 1998 09:05:10 +0000
On Sun, 1 Mar 1998 SAFallon wrote:
> Subject: Posting from Mary and Sally
> 4. We still lack one key piece of data, and that is the amount of adipose tissue as a percentage
> of the total in a large wild ruminant such as an elk or moose, during the late Summer and early
> Fall. Without this we cannot make a true comparison between the saturated fat available to
> Paleolithic man, compared to his modern beef-eating counterpart. Are there any hunters in the
> group who can enlighten us? Even a visual estimate would be helpful. How thick is the subcutaneous
> fat on such an animal at the height of its fat stores?
Archaeozoologists have been generating this type of data for certain animals. In order to interprete animal
bone assemblages, a series of studies have established Utility Indices for different skeletal parts, particularly
with reference to the amount of fat, meat and marrow they carry. There are probably archaeozoologists on
the list who could supply better information than I can. A random selection of work that I have come across
recently is:
Binford, LR (1978) Nunamuit Ethnoarchaeology. New York: Academic Press (for sheep and caribou)
Outram AK & Rowley-Conwy, PA (in press) Meat and marrow indices for horse (Equus). Journal of
Archaeological Science
Diab, MC (1998) Economic utility of the ringed seal (Phoca hispida): implications for arctic archaeology.
Journal of Archaeological Science 25 1-16
Diab also cites the following:
Blumenschine RJ & Caro, TM (1986) Unit flesh weights of some East African bovids. African Journal of
Ecology 24 273-286
Lyman RL, Savelle, JM & Whitridge, P (1992) Derivation and application of a meat utiltiy index for phocid
seals. Journal of Archaeological Science 19 531-556
Brink, JW (1997) Fat content in leg bones of Bison bison, and applications to archaeology. Journal of
Archaeological Science 24 259-274
Savelle, JM, Friesen, TM & Lyman RL (1996) Derivation and application fo an otariid utility index. Journal
of Archaeological Science 23 705-712
Whilst they do not necessarily use the fat content in their calculations, they may well do as Diab does and
record the amounts of fat removed.
Andrew
42/147 (1998)
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: CHD Theories and Markers
From: SAFallon
Reply-To:
Date: Wed, 4 Mar 1998 12:12:34 EST
To: All Paleodieters From: Mary and Sally
In response to Michael Kern, MD, we would like to address blood chemistries or other markers that are
alternatives to serum cholesterol, as predictors for heart disease. First, however, let us list various theories
other than the lipid hypothesis that have been proposed as causes of CHD, and for which the evidence is
superior or at least equally compelling. In fact, we would suggest that all of these theories merit funding for
additional research, but have not been pursued because they cannot be used to justify the imitation food
industry.
Price (Weston A, DDS) Deficiency of fat soluble vitamins A, D and the Price Factor Yudkin, Ahrens
Refined carbohydrates Kummerow, Mann Trans fatty acids from hydrogenated fats Hodgson Excess omega6 from refined vegetable oils Addis Oxidized cholesterol and oxidized fats Shute Vitamin E deficiency
Pauling Vitamin C deficiency McCully Deficiency of folic acid, B6 and B12 Annand Heated milk protein
(i.e. pasteurization) Anderson Magnesium deficiency Huttunen Selenium deficiency Ellis Microbial agents
Benditt Monoclonal tumor theory (viruses, bacteria) de Bruin Thyroid deficiency LaCroix Coffee
consumption Morris Lack of exercise Stern Exposure to carbon monoxide
Assuming most or all of the above factors to be true, the underlying cause of CHD might be summed up as
changes in our environment and food supply due to the unwise application of technology to farming and food
production, the abandonment of traditional foodways, and above all the insidious penetration of imitation
foods into the food supply of western nations.
We would make the following suggestions to the physician who is trying to determine the susceptibility of
his patients to CHD:
1. A thorough 2-week dietary survey to determine the level of trans fats, high omega-6 vegetable oils and
refined carbohydrates in the patients diet.
2. Assessment of the condition of teeth and gums. (High levels of caries and/or gum disease is a marker for
susceptibility to CHD.)
3. Blood test for homocysteine markers (indicating deficiencies in folic acid, B6 and B12)
4. Blood test for Lp(a). (High levels indicated proneness to CHD.)
5. Blood test for the true level of net HDL, now available from Romark Diagnostics of New Jersey. (High
levels of HDL may indicate protection against CHD.)
The following dietary guidelines summarize the suggestions that may be given to improve the various
chemical markers, and to eliminate atherogenic substances from the diet:
43/147 (1998)
Guidelines: 1. Eat whole, natural foods. 2. Eat only foods that will spoil, but eat them before they do. 3. Eat
naturally-raised meat including fish, seafood, poultry, beef, lamb, game, organ meats and eggs. 4. Eat whole,
naturally-produced milk products, preferably raw and/or fermented, such as whole yogurt, whole cheeses and
fresh and sour cream. 5. Use only traditional fats and oils including butter and other animal fats, extra virgin
olive oil, expeller expressed sesame and flax oil and the tropical oilscoconut and palm. 6. Eat a variety of
fresh fruits and vegetables, preferably organic, in salads and soups, or lightly steamed with butter. 7. Use
whole grains and nuts that have been prepared by soaking, sprouting or sour leavening to neutralize phytic
acid and other anti-nutrients. 8. Include enzyme-enhanced lacto-fermented vegetables, fruits, beverages and
condiments in your diet on a regular basis. 9. Prepare homemade meat stocks from the bones of chicken,
beef, lamb or fish and use liberally in soups and sauces. 10. Individuals sensitive to caffeine should use
acceptable substitutes. 11. Use spring water for cooking and drinking. 12. Use unrefined Celtic seasalt and a
variety of herbs and spices for food interest and appetite stimulation. 13. Make your own salad dressing
using raw vinegar, extra virgin olive oil and expeller expressed flax oil. 14. Use natural sweeteners in
moderation, such as raw honey, maple syrup, dehydrated cane sugar juice and stevia powder. 15. Use only
unpasteurized wine or beer in strict moderation with meals. 16. Cook only in stainless steel, cast iron, glass
or good quality enamel. 17. Use only natural supplements. 18. Get plenty of sleep, exercise and natural light.
19. Think positive thoughts and minimize stress. 20. Practice forgiveness.
Dietary Dangers:
1. Dont eat commercially processed foods such as cookies, cakes, crackers, TV dinners, soft drinks,
packaged sauce mixes, etc. 2. Avoid all refined sweeteners such as sugar, dextrose, glucose, concentrated
fruit juices and high fructose corn syrup. 3. Avoid excessive white flour, white flour products and white rice.
4. Avoid all hydrogenated or partially hydrogenated fats and oils. 5. Avoid all vegetable oils made from soy,
corn, safflower, canola or cottonseed. 6. Do not use polyunsaturated oils for cooking, sauteing or baking. 7.
Avoid fried foods. 8. Do not practice strict vegetarianism (veganism); animal products provide vital nutrients
not found in plant foods. 9. Avoid products containing protein powders. 10. Avoid pasteurized milk; do not
consume low fat milk, skim milk, powdered milk or imitation milk products. 11. Avoid battery produced
eggs and factory farmed meats. 12. Avoid highly processed luncheon meats and sausage. 13. Avoid rancid
and improperly prepared seeds, nuts and grains found in granolas, quick rise breads and extruded breakfast
cereals, as they block mineral absorption and cause intestinal distress. 14. Avoid canned, sprayed, waxed or
irradiated fruits and vegetables. 15. Avoid artificial food additives, especially MSG, hydrolyzed vegetable
protein and aspartame, which are neurotoxins. Most soups, sauce and broth mixes and commercial
condiments contain MSG, even if not so labeled. 16. Avoid caffeine-containing beverages such as coffee, tea
and soft drinks. Avoid chocolate. 17. Avoid aluminum-containing foods such as commercial salt, baking
powder and antacids. Do not use aluminum cookware or aluminum-containing deodorants. 18. Do not drink
fluoridated water. 19. Avoid synthetic vitamins and foods containing them. 20. Do not drink distilled liquors.
21. Do not use a microwave oven.
For additional information and practical recipes, see our book Nourishing Traditions, available from the
Price-Pottenger Nutrition Foundation (619) 574-7763
PALEODIET Archives
Subject: Teeth
From: Dick Dawson
Reply-To:
Date: Tue, 10 Mar 1998 02:29:00 -0500
Waaay back Dean wrote:
> One of the most common arguments advanced by advocates of vegetarianism and by some other
> commentators on health is that humans evolved as vegetarian or mostly-vegetarians. The most
> frequently forwarded argument to advance this position is that human tooth and jaw structrure are
> clearly those of herbivores with flat molars, excellent sideways chewing motion and with a clear
> lack of sharp teeth for killing prey.
Homo has lousy sideways grinding compared to real hervivores: bovines, horses etc. Our jaw doesn't work
very well that way by comparison.
We lack the long gut of horses and/or multiple stomachs of ruminants that are essential to their ability to
process raw grain and more appropriately grass and/or browse.
44/147 (1998)
We don't process green leaves of most plant species. Cabbage, kale, lettuce etc. sure. Grape leaves somewhat
if very young/early. Not much else other than fruit. Try eating whole grain w/o milling and extensive
cooking: you'll break your teeth. Try eating a minimally significant amount of grass: it won't stay down.
We don't process grain (seeds of grasses) well unless cooked.
We handle nuts and some seeds fine.
We've evolved using other tools for handling meat: hands and cultural adaptations: stone tools. We got into
stone tools long before the rise of Homo; stone tools appropriate for processing animals for meat, hides and
other tool material, not for processing grain until very recently (5000-8000ya, then as microblades for
scythes and concurrent with rise of agriculture demonstrated by other artifacts).
I think _Paleolithic_Prescription_ details our evolution very well.
You want a real herbivorous hominoid: look at the robust Australopithecines: A. boisei; A. robustus. Their
molars were easily twice the dimensions of ours; their incisors and canines easily less than half the size of
ours. They had large sagittal crests: attachment for huge chewing muscles. Their teeth are found to be
heavily worn as by dirt etc. in their food implying grain and seed eating. Depending on one's cladistics they
are high probability a divergent branch of our ancestral A. afarensis (Lucy), not as likely our direct ancestors.
They're extinct.
Other herbivores: Gorilla gorilla. Much more evident canines than ours. Similar molars.
Omnivores: Pan paniscus & Pan troglodytes: the chimps. Dentition much like the gorillas.
I think we must conclude that dentition isn't much of a guarantee of dietary interpretations.
I saw a moose mandible yesterday. The molars looked more like a dog's than man's. !
> I most recently heard a snippet of this line of thinking on a popular news show here in America
> called "Nightline" in which a medical doctor and health writer advanced this view. I wonder if
> anyone among our membership would like to comment on this line of reasoning?
Perhaps such 'reasoning' is more likely rationalizing.
Ah... noting that chimps are regular hunters and meat eaters and their primary meat source is other primates
perhaps one can imagine as Joseph Campbell (_The_Way_of_the_Animal_Powers_) did that the extinction
of the robust vegetarian Australopithecines is at least partly due to the dietary practices of various carnivores
including early Homo.
Physical anthropology shows that the last of the ancestors of the primates were insectivores this probably
being responsible for our dependence on concentrated vitamin, protein and fat sources.
PALEODIET Archives
Subject: Chlorine
From: Dean Esmay
Reply-To:
Date: Tue, 10 Mar 1998 20:26:18 -0500
I received a question from someone that I thought interesting enough to post:
> Subject: Tap water.
> In Stockholm, where I live, 130 million cubic meters of tap water is annually pruduced. To this
> is, among some other things, 37 tons of chlorine added. This equals to 0.3 mg/liter, and varies so
> that there is more added in the summer and less in the winter. Stockholm water is probably lower
> on chlorine than that of most cities in the world. A person who drinks mainly tap water can well
> get half a milligram of chlorine a day. Is there anyone on this list who has got the slightest
> idea of what that does to our bodies?
PALEODIET Archives
Subject: Foreign proteins
From: Art De Vany
Reply-To:
Art De Vany
Date: Wed, 11 Mar 1998 17:20:00 -0800
45/147 (1998)
Members of this list may find this of interest. I composed it for the members of the evolutionary fitness list,
but it is entirely applicable to the issues discussed in the Paleodiet list.
John wrote:
"Art, you mentioned some research that really sounds interesting. I would be very interested to hear of your
work in the area of . . . . (was it?) the microbiological content of the paleolithic diet. Neanderthin refers to
agriculture based proteins as "foreign." This suggests that even though it is fairly easy to achieve "complete"
proteins through combining, in doing so we may be getting some other biochemical substances in quantities
that we are simply not evolutionarily equipped to handle."
John's question is one I am trying to answer using both data and mathematical modelling of carcasses, plants,
stomach capacity, etc. I am far from finished and have many other things to do (including a week of lectures
in Mexico later this month).
One hint at the issues revolving around foreign proteins is to realize that the space of possible proteins is so
large that all the computational resources that ever existed in the universe are not enough even to enumerate
the members on the list (only about 10^120 or so are feasible using every particle and nanosecond in the
universe for as long as it existed as your computer). The protein space contains approximately 20^200
members, that is 20 to the 200 power.
The dimension of this space is so vast that there are an infinite number of novel proteins to which the
immune system may have no defenses or which it may confuse with pathogens, etc.
The amino acid chains that comprise the proteins fold into geometric objects and are recognized as "self" or
"foreign" on the basis of their shape, as well as the complex of antigens on their surface. Each protein has a
unique shape because of the way the amino acids are sequenced and bind.
The thymus is the "editor" that deletes non-self proteins and, like any editor, it only has so much critical
ability. Both the novelty as well as the total flux of foreign proteins may present a critical threshold where
autoimmune diseases are triggered. That is why one of my eating strategies is to diversify your toxins and
proteins by having a varied and changing diet, within the scope of evolutionary eating. The underlying key
strategy is to attempt to choose foods edible in the evolutionary period (of your choice, though mine is about
40, 000 years ago) for they would be least likely to present novel proteins.
It took about half of the time life existed on earth to evolve multicelled creatures. This has puzzled many, but
the answer may lie in the vast dimension of the possible proteins. Evolution may have needed that long to
work through space of possibilities to discover proteins capable of sustaining multicellular life. From that
point on, the possibilities for life form became very great. The last 2 billion years are a period of
experimentation on the possibilities.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
CA 92697-5100 714-824-5269 http://www.socsci.uci.edu/mbs/personnel/devany/devany.html
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
PALEODIET Archives
Subject: Cancer in hunter-gatherers
From: Jean-Louis Tu
Reply-To:
Date: Wed, 11 Mar 1998 20:06:27 -0500
I was wondering if there was some data available on the prevalence of cancer in some H-G populations.
Does anyone here have some references?
Many thanks in advance,
Jean-Louis Tu
PALEODIET Archives
Subject: Teeth and tools
Reply-To:
Date: Thu, 12 Mar 1998 08:51:10 +0000
46/147 (1998)
On Tue, 10 Mar 1998 Dick Dawson wrote:

> We've evolved using other tools for handling meat: hands and cultural adaptations: stone tools. We got
> into stone tools long before the rise of Homo; stone tools appropriate for processing animals for meat,
> hides and other tool material, not for processing grain until very recently (5000-8000ya, then as
> microblades for scythes and concurrent with rise of agriculture demonstrated by other artifacts).
I wuld deny that there is any strong evidence that stone tools were around before the rise of Homo, although
they cannot be unequivocally linked with Homo. The earliest stone tools are at Gona, Ethiopia at 2.52+/-0.08
Ma (Semaw et al 1997) the next are at Riwat, Pakistan (Dennel et al. 1988) at 1.90-2.01 Ma, the next are
Oldowan tools at c. 1.8 Ma in various African sites. The earlist Homo specimens are H. habilis at Olduvai
1.80+/-0.08 Ma (Johanson et al 1887), and H. erectus in Java 1.6-1.8 Ma (Swisher et al 1994) and possibly at
Dmanisi, Georgia 1.77-1.95 Ma (White et al 1994). These dates and their wide geographical spread suggest
that we have not yet found the earliest Homo, and given the sparseness of the stone tool finds, it is quite
possible that Homo and tools appear about the same time.
References
Dennel, RW, Rendell, H & Hailwood, E (1988) Early tool-making in Asia: two-million-year-old artefacts in
Pakistan. Antiquity 62 (234) 98-106
Johanson, DC et al. (1987) New partial skeleton of Homo habilis from Olduvai Gorge, Tanzania Nature, 327
205-209
Semaw, S, Renne, P, Harris, JWK, Feibel, CS, Bernor, RL, Fesseha, N & Mowbray, K (1997) 2.5-millionyear-old stone tools from Gona, Ethiopia. Nature 385 333-336
Swisher, CC, Curtis, GH, Jacob, T, Getty, AG, Suprijo, A & Widiasmoro (1994) Age of the earliest known
hominids in Java Indonesia. Science 263 1118-1121
White, TD, Suwa, G & Asfaw, B (1994) Nature 371 306-312
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Blood group references
From: Todd Moody
Reply-To:
Date: Thu, 12 Mar 1998 11:40:39 -0500
A while back I mentioned Peter D'Adamo's theory that the ABO blood groups represent not only adaption to
infectious disease but also adaptation to dietary changes. Although the core of his theory is that dietary
lectins affect tissues differently in the different blood ABO types, he asserts that there are also other
differences that have dietary implications. If he is correct, this would have considerable significance, since
the ABO types would correlate with the transition to post-paleo eating patterns.
One of the claims that he makes is that gastric acid levels are highest in type Os and lowest in type As.
Another claim is that concentrations of the intestinal enzyme alkaline phosphatase are also highest in Os and
lowest in As. I asked for references, and he kindly provided a few. For those who might be interested in this
sort of thing, here they are:
J. Steen, et al. Basal serum gastrin concentration related to complications, blood groups, and season in
duodenal ulcer. Scand J Gastroentero. 1982 Jun; 17(4): 529-532.
GP Jori, et al. Influence of blood group and secretor status on gastric acidity. Am J Dig Dis. 1969 Jun; 14(6):
380-384.
MA Demborough. ABO glood group, secretor status and gastric secretion. Australas Ann Med. 1966 Nov;
15(4): 314-317.
U Domar, K Hirano and T Stigbrand. Serum levels of human alkaline phosphatase isozymes in relation to
blood groups. Clin Chim Acta; 203(2-3) 1991 Dec 16.
AP Day, et al. Triglyceride fatty acid chain length influences the post prandial rise in serum intestinal
alkaline phosphatase activity. Ann Clin Biochem; 29(pt 3): 287-92 1992 May.
47/147 (1998)
The basic idea is that lower levels of gastric acid diminish one's ability to digest animal protein, and lower
levels of ALP diminish one's ability to digest fats and cholesterol.
The A group appeared about 20K years ago, but didn't really proliferate until agricultural times. B and AB
came later. If the theory is right, the A blood type would have been a liability to hunter-gatherers, but
perhaps the disadvantage was outweighed by the advantage of greater resistance to infection, as compared to
the O type. When agriculture arrived, the A type turned out to have a secondary advantage, the ability to
make better use of non-meat protein sources, such as legumes, as compared with type O. The later B and AB
types would represent more complete adaptation to agricultural and pastoral diets. For example, B blood is
common in semitic peoples who have had domesticated herds for a long time. Supposedly they also tolerate
dairy foods well.
I am ignoring the whole lectin dimension and looking solely at the ABO-linked phenotype considerations.
Does any of this make sense?
Todd Moody
PALEODIET Archives
Subject: tools and Homo
From: Jeanne Sept
Reply-To:
Date: Thu, 12 Mar 1998 18:54:37 -0500
> I would deny that there is any strong evidence that stone tools were around before the rise of
> Homo, although they cannot be unequivocally linked with Homo. The earliest stone tools are at
> Gona, Ethiopia at 2.52+/-0.08 Ma (Semaw et al 1997) ... The earlist Homo specimens are H. habilis
> at Olduvai 1.80+/-0.08 Ma (Johanson et al 1887), and H. erectus in Java 1.6-1.8 Ma (Swisher et al
> 1994) and possibly at Dmanisi, Georgia 1.77-1.95 Ma (White et al 1994). These dates and their wide
> geographical spread suggest that we have not yet found the earliest Homo, and given the sparseness
> of the stone tool finds, it is quite possible that Homo and tools appear about the same time.
> ==========================================================================
> ==========================================================================
Regarding the comment above, here's an update for those of you interested in early stone tools and the
appearance of Homo... Gona is the earliest site with well-dated stone tools currently known. There are also
several sites in the Turkana basin dated between 2.3 and 2.0 mya (e.g. at different stratigraphic levels at the
Omo and at West Turkana)... see Rogers et al 1994 "Changing patterns of land use by Plio Pleistocene
hominid in the Lake Turkana basin" Journal of Human Evolution 27: 139-158, for an overview, in addition
to references in the Semaw et al article cited by Millard.
Similarly, in addition to fragmentary Homo specimens found at the Omo a number of years ago, (recently
summarized in Suwa, White and Howell 1996 (American J. Physical Anthro 101 (2): 247-282), recent
discoveries have placed potential "Homo" specimens older close to 2.4 my in Malawi (e.g. Schrenk et al
1993 in Nature 365: 833-836); and northern Kenya (Hill et al 1992, in Nature 355: 719-722). Of course,
there is a debate about whether these early Homo specimens fall into one or two species, and there are
several contemporary australopithecine species in both eastern and southern Africa, all potential tool makers.
Jeanne Sept Anthropology Dept Indiana University, Bloomington IN
Jeanne Sept Anthropology Department Indiana University Bloomington IN 47405
PALEODIET Archives
Subject: Pasteurised Milk
From: "M E Wood (by way of Dean Esmay)"
Reply-To:
48/147 (1998)
Date: Thu, 12 Mar 1998 19:02:41 -0500

May I ask as a lowly lurker about the recommendation to drink unpasteurised milk? Is it not dangerous
especially in New Zealand where there is a reservoir of tuberculosis in the possum(Australian) population in
the bush which has been shown to infect cattle? I do not believe it is possible to purchase unpasteurised milk
in this country. I think I have read that TB is on the increase in the Pacific so I wonder if it might be better
just to avoid milk. -*Domine*Dirige*Nos
>
>
> )M(<<<<<
PALEODIET Archives
Subject: Cancer in hunter-gatherers
From: Ron Hoggan1
Reply-To:
Date: Fri, 13 Mar 1998 18:46:45 +0000
Hi Jean-Louis,
Stefansson, Vilhjalmur _Cancer: Disease of Civilization?_ Hill and Wang, New York, 1960
The author lived among the Inuit for 10 years, on the Northern Coast of Canada. He provides a fascinating
discussion of the absence of cancer among those who were not consuming a Western diet. (In 1906, when he
began his observations, few of the Canadian Inuit had yet been significantly exposed to our diet.)
It is a very enjoyable read. But perhaps you are already familiar with it, and you know that I have not done it
justice.
> I was wondering if there was some data available on the prevalence of cancer in some H-G
> populations. Does anyone here have some references? Many thanks in advance,
> Jean-Louis Tu
> Ron Hoggan Calgary, Alberta, Canada
PALEODIET Archives
Subject: Saturated fat and heart disease
From: Dean Esmay
Reply-To:
Date: Sat, 14 Mar 1998 20:55:21 -0500
I begin to feel that the subject of fat on this list has become worn to death. While I am a critic of low-fat,
high-carbohydrate diets, there are a number of views on the subject and I think we should all realize that.
There are a number of topics which this group could also be putting its time to discussing: the nature of the
need for exercise and the activity patterns that typified human evolution, the role of fishing, the positive and
negative effects of high protein intake as typified in most hunter/gatherer diets, whether the "thrifty
genotype" hypothesis is correct in explaining the prevalence of hyperinsulinism and its related health
problems, the consumption of insects, how much evidence there is that humans started eating animal milk in
any significant quantity prior to genuine herding activity, the role of minerals, and many other subjects.
I have perhaps let these discussions of fat go on too long because it's a pet obsession of mine. But I feel it's
begun to be a distraction from other equally interesting issues.
I would appreciate it if Symposium members would take a breather on this subject for a while, or take it into
private email, at least until we've had some time to examine other issues.
This comment should not in any way be interpreted as a rebuke to anyone, I simply think it's time we moved
on to something else for a while.
Thanks as always to everyone for contributing to our discussions.
-=-
49/147 (1998)
"If in the last few years you haven't discarded a major opinion or acquired a new one, check your pulse, you
PALEODIET Archives
Subject: Saturated fat and heart disease
Reply-To:
Date: Sat, 14 Mar 1998 10:19:30 PST
In the light of the recent post by Mary and Sally regarding saturated and monounsaturated fat and heart
disease, I wonder if Mary and Sally or someone else would care to comment on the Harvard study that was
published in the New England Journal of Medicine last November (11/20/97) (sorry, I don't have the citation;
I only have a short description of the study from Andrew Wiel's Feb 1998 newsletter).
According to the summary, the study involved 80, 000 women over a 14-year period. It found a 17% greater
risk of heart disease from saturated fat in comparison to the same caloric intake from carbohydrates (not
clear to me why results reported in this way), and a 19% lower risk associated with monounsaturated fat.
(There was a 93% higher risk associated with TFAs! -- and a 38% lower risk associated with TFA-free
polyunsaturated fat). As usual, it's not clear to what extent other factors that might account for development
of "heart disease" were accounted for in the study.
Steve Meyers
PALEODIET Archives
Subject: Re: Cancer in hunter-gatherers
Reply-To:
Date: Sun, 15 Mar 1998 15:01:23 +0100
The World Cancer Research Fund in association with the American Institute for Cancer Research has
published an excellent review on food and cancer (670 pages) [1] from which I quote:
"It has often been said that cancer was rare among gatherer-hunter and pastoral peoples living in remote parts
of the world, such as the Himalayas, the Arctic and equatorial Africa, when these were first visited by
explorers and missionaries [2-4]. A summary of these early accounts can be found in Cancer Wars [5]. Such
accounts have been taken to mean that cancer was generally rare in early history. The African explorer, Dr.
David Livingstone, suggested that cancer is a 'disease of civilisation' [6]. Practically nothing is known about
rates of cancer until careful records were first kept in Europe in the eighteenth century. These suggest that,
historically, cancer might have been a relatively uncommon disease."
Theoretical considerations by Eaton et al, based on calculated age at menarche (16), age at birth of first child
(19.5), duration of lactation per child (2.9 years), number of children (6), and age at menopause (47), in
combination with beneficial dietary habits and much exercise, suggest that cancers of breast, uterus and
ovary were very uncommon among hunter-gatherers [7].
1. Food, nutrition and the prevention of cancer: a global perspective. World Cancer Research Fund. 1997: 35.
2. Williams WR. The natural history of cancer, with special reference to its causation and prevention. New
York, William Wood, 1908. 3. Bulkley JL. Cancer among primitive tribes. Cancer 1927; 4: 289-95. 4.
Scweitzer A. Preface to: Berglas A. Cancer. Paris, 1957. 5. Proctor RN. Cancer War: How politics shapes
what we know and don't know about cancer. New York, Basic Books, 1995. 6. Maugh TH. Cancer and
environment: Higginson speaks out. Science 1979; 205: 1363-6. 7. Eaton SB, Pike MC, Short RV et al.
Women's reproductive cancers in evolutionary context. Quart Rev Biol 1994; 69: 353-67.
At 20.06 -0500 98-03-11, Jean-Louis Tu wrote:
> I was wondering if there was some data available on the prevalence of cancer in some H-G
> populations. Does anyone here have some references? Many thanks in advance,
> Jean-Louis Tu
50/147 (1998)
Staffan Lindeberg, M.D. Ph.D. Dept of Community Health Sciences, Lund University, Mailing address:
PALEODIET Archives
Subject: Web site on fishing
From: Dean Esmay
Reply-To:
Date: Sun, 15 Mar 1998 17:08:56 -0500
Here's an excellent resource for those interested in exploring fishing in paleolithic cultures:
http://atlas.otago.ac.nz:800/~foss/ICAZ/icaz.htm
PALEODIET Archives
Subject: Teeth
From: Dick Dawson
Reply-To:
Date: Tue, 17 Mar 1998 04:40:10 -0500
ancient email:
> I'm told that the Inuit usually have the shovel shaped incisors and that Christie Turner has done some
> work on that. Apparently this type of tooth turns up in people whose ancestors were from NE Asia, and
> they are considered diagnostic of these human type by some. Anyone know more about this?
Syracuse Univ. physical anthro and human variation courses assert that shovel shaped incisors are nearly
universal in Asiatic humans. This includes nearly all 'native' Americans. Excepting probably poor bedivviled
Mr Kenniwick.
Anecdotally: a friend whose father is Japanese and mother Anglo-American has them; a friend whose father
is Polish-American and mother is Korean has them.
It's a longitudinal groove in the back face of the incisors roughly half the width of the tooth but somewhat
variable.
PALEODIET Archives
Subject: Re: Seminar where Loren will talk
From: BOBDFH
Reply-To:
Date: Tue, 17 Mar 1998 17:45:18 EST
Dear Dean,
I don't know if this is something you would post on your site, but I am putting on a conference this August
13-15 in Boulder, CO where Loren Cordain, Ph.D. will be the keynote speaker. He will talk for 2 1/2 hours
on the Paleolithic Diet, grains and their problems, macronutrient ratios, and related topics. Those interested
my email me their snail mail address at and I will send them a flyer on the conference.
Thanks!
Robert Crayhon, MS
PALEODIET Archives
Subject: WAC4
51/147 (1998)
From: Dean Esmay

Reply-To:
Date: Wed, 18 Mar 1998 07:17:33 -0500
World Archaeology Congress 4 Cape Town: 10 - 14 January 1999 Theme: Global Archaeology at the Turn
of the Millennium
WAC, the World Archaeology Congress, was inaugurated at its first congress in Southampton in 1986, and
last met in New Delhi in 1994. Its conferences and inter-congresses have continued to develop the global
dimension of archaeology and the social role that archaeologists play as interpreters of the past. We expect
more than a thousand delegates in Cape Town, and we are planning an exciting and stimulating programme
that will do justice to the turn of the millennium.
It is appropriate that WAC4 should be held in South Africa. The World Archaeology Congress was formed
in opposition to apartheid, highlighting the relationship between the study of the past and the politics of the
present. South Africa's first democratic elections in 1994 ended a long, bitter era and archaeologists here are
now free to be part of a world community of scholarship.
The academic programme of the Congress will be organised around symposia. These will be half-day, fullday or running themes, each organised by a Symposium Convenor. Papers will be available electronically to
registered delegates prior to the Congress, and full details of the programme will be posted on our website as
they become available.
The Congress will be structured around three broad themes: time; archaeology in a global context, and the
future. This will provide a rich vein of intellectual stimulation, offering a truly global perspective on a
discipline that has stimulated and satisfied many for well over a century.
If you would like to attend the Congress, please visit our website (URL below) and register electronically, or
complete the registration form in the Second Announcement which will be mailed shortly.
Should you wish to deliver a paper, organise a symposium or workshop, present a poster or screen a film on
an archaeological topic, demonstrate an archaeology-related computer program or multimedia product, or
rent exhibition space at the Congress, please contact the Congress Secretariat :
Contact: Carolyn Ackermann WAC4 Congress Secretariat Address: PO Box 44503 Claremont 7735 South
Africa Telephone: +27 (21) 762 8600 Fax: +27 (21) 762 8606 e-mail: Website:
http://www.uct.ac.za/depts/age/wac
Important dates:
30 April 1998: Closing date for submission of abstracts and symposium convenor's packages with deposits
where appropriate.
31 July 1998: Preliminary programme to be mailed. Applicants to be notified of acceptance of
abstracts/symposia.
15 November 1998: Papers to be made available on the congress website.
PALEODIET Archives
Subject: Re: - Shovel Incisors
From: M E Wood
Reply-To:
Date: Thu, 19 Mar 1998 13:35:56 +1300
> Date: Tue, 17 Mar 1998 04:40:10 -0500
> From: Dick Dawson Subject: Teeth
> ancient email:
> Syracuse Univ. physical anthro and human variation courses assert that shovel shaped incisors are
> nearly universal in Asiatic humans. This includes nearly all 'native' Americans. Excepting
> probably poor bedivviled Mr Kenniwick. It's a longitudinal groove in the back face of the incisors
> roughly half the width of the tooth but somewhat variable.
52/147 (1998)
I had read some time ago that the shovel incisor was considered to be diagnostic of Northern Eurasian people
and that SE Asian people did not have the same incidence. I think that the shovel incisor was coupled with a
small peg molar as an indicator of geographical origin. Does anyone know if this view is still current? Do
Polynesian peoples ever show this dentition pattern? Has the shovel incisor any advantages over the plainer
incisor? Is it stronger? Is it more useful as a tool for processing such items as food and sinews, skins. In other
words, does it give an advantage? Or is a family trait?
ME Wood
PALEODIET Archives
Subject: Re: PALEODIET Digest - 18 Mar 1998 to 19 Mar 1998 (#1998-9)
Reply-To:
Date: Fri, 20 Mar 1998 11:20:44 -0700
Dredging up the information I was given regarding the incidence of shovel shaped incisors (I do not have
references - this is information I received during my own training) shovel shaped incisors appear in all
human populations in low frequency but the incidence is much higher among northern Asian and Native
american populations.
Lorraine Heidecker California State University Sacrament Department of Anthropology
PALEODIET Archives
Subject: Andersen and Adaptation
From: Dick Dawson
Reply-To:
Date: Sat, 21 Mar 1998 19:01:46 -0500
anciently Todd Moody wrote:
> only meat for a year. A study [..] I mentioned that Stefansson preferred lamb while Andersen
> preferred beef. The fatty acid composition of these meats are somewhat different. I believe that
> even in 1928 cows for slaughter were more likely to be grain-fattened than were lambs. Recent
> discussions on this list suggest the hypothesis that this could have been relevent; I would gladly
> hear other opinions on this.
Perhaps already considered by now but: 'lamb' suggests very young animals. Most modern Americans don't
like mutton. A young animal might not have developed heavy muscle tissue saturation with various fatty
results of grain feeding. The 'beef' that Andersen preferred was perhaps from 2 - 4 year old animals that
might have had time to accumulate substantially different fatty acids.
2 guys is a rather small study. ! Perhaps a larger sample and involving reliable and consistent allocations of
meat types including buffalo (Bison bison), venison, other deer species, antelope, range fed beef, feedlot
beef, veal, mutton, lamb, turkey, chicken, ostrich etc. could yield further info.
Perhaps preparation technique will be a factor: roasts, fried steaks, char broiled steaks, jerked meat etc.
I'll volunteer for the buff or venison if someone's got a grant. :)
PALEODIET Archives
Subject: Eskimos, Longevity, and Diet
From: Gary Ditta
Reply-To:
Date: Thu, 26 Mar 1998 07:31:31 -0800
Did the flame burn brighter but shorter for the Eskimo?
53/147 (1998)
The following passage from Viljhalmur Stefansson's monograph "Adventures in Diet" (1) illustrates his
belief that the Eskimos of Coronation Gulf aged more rapidly than normal. He attributed this to their all meat
diet which he also felt provided them with above average health and vitality:
"While meat eaters seem to average well in health, we must in our conclusion draw a caution from the most
complete modern example of them, the Eskimos of Coronation Gulf. Mr. Diamond Jenness...concluded from
his experience in the Gulf, when he was anthropologist on my third expedition, that the two chief causes of
death were accidents and old age. This puts in a different form my saying that these survivors of the stone
age were the healthiest people I have ever lived among. I would say the community, from infancy to old age,
may have had on the average the health of an equal number of men about twenty, say college students. The
danger is that you may reason, with too much confidence in a single factor, from this good health to a
necessarily great average longevity. So far as we can tell, the Eskimos, before the white men upset their
physiological as well as their economic balance, lived on the average at least ten years less than we. Now
their lives average still shorter; but that is partly from communicated diseases. If it be true that the good
average health of meat eaters is not necessarily accompanied by a great average length of life, the
explanation may be along the line of what has been said, ante, that I found the exclusive meat diet in New
York to be stimulating - I felt energetic and optimistic both winter and summer. Perhaps it may be
considered that meat is, over all, a stimulating diet, in the sense that metabolic processes are speeded up. You
are then living at a faster rate, which means you would grow up rapidly and get old soon. This is perhaps
confirmed by that early maturing of Eskimo women ...It may be that meat as a speeder-up of metabolism
explains in part both that Eskimo women are sometimes grandmothers before the age of twenty-three, and
that they usually seem as old at sixty as our women do at eighty."
Note here that Stefansson's belief that meat in some way "speeds up" metabolism cannot be taken exactly
literally. During the studies at Bellevue while on an all meat diet, neither he nor Andersen showed any
increase in basal metabolic rate (2).
In later years Stefansson made a point that Eskimos of advanced years could be identified (3). Nevertheless,
his initial observation came to be generally accepted and, as discussed below, seems to be in accord with
modern gerontological research.
While aging is clearly a multifactorial process and numerous mechanisms have been proposed, oxidative
stress (free radical damage) is one that is likely to be of fundamental importance (4, 5). The case for
involvement of oxidative stress in aging has direct experimental support in that genetically engineered fruit
flies with elevated levels of the free radical scavenging enzymes superoxide dismutase and catalase have
significantly extended lifespans (6).
Considerations of oxidative stress are particularly relevant for the ketogenic Eskimo diet. On a ketogenic
diet, energy is derived primarily from lipid oxidation, resulting in greater utilization of aerobic metabolism
due to the lower respiratory quotient (RQ) for fats (0.7) as opposed to protein (0.8) or carbohydrate (1.0).
The lower the RQ the greater the amount of oxygen necessary to produce a given amount of energy.
Stefansson noted in FAT OF THE LAND (7) that high fat diets would be expected to work less well at high
altitudes due to the increased oxygen requirement: "A physiologist who has been in charge of instruction for
high-altitude work in World War II puts it that if a high fat-protein dietis fed to aviators 'immediately before
as well as during flight, the capacity to tolerate oxygen lack and to work at high altitudes is reduced. On a
high carbohydrate diet similarly taken a definite increase in altitude tolerance is observed. The results are
probably due to the fact that, in comparison with carbohydrates, proteins and fats require for use relatively
larger amounts of oxygen, which is less available at high altitudes.'"
A diet high enough in fats should cause significantly increased oxidative stress and accelerated aging. This
would seem to be the case with the Eskimos Stefansson observed. If Stefansson is also correct about
increased health and vigor associated with a high fat diet (I know of no theoretical basis for this), the long
term cost of a high fat diet might be offset by increased early survival and reproduction for primitive peoples.
I would be very grateful if anyone in the group could offer data, argument, or comment relevant to these
ideas. In particular, I'd appreciate hearing from anyone familiar enough with Eskimo studies to more
properly evaluate Stefansson's comments than myself.
(1) Stefansson, V. (December, 1935 and January, 1936) Harper's Magazine. "Adventures in Diet" pp. 34-35.
(2) McClellan, W.S. et al (1931). J Biol Chem 93(2): 419. (3) Stefansson, V. (1958) Science 127: 16-19. (4)
Harman, D. (1956) J. Gerontol 11:298. (5) Sohal, R.S. and R. Weindruch (1996) Science 273: 59. (6) Orr,
W.C. and R.S. Sohal (1994) Science 263: 1128. (7) Stefansson, V. (1957) THE FAT OF THE LAND,
pp.266-267.
Gary Ditta
54/147 (1998)
PS My apologies to Dean for another fat question, but the point here is a bit different than usual I think and
I've been wondering about this for some time.
PALEODIET Archives
Subject: Evidence for human watercraft 800, 000 years ago
From: Dean Esmay
Reply-To:
Date: Thu, 26 Mar 1998 09:02:52 -0500
The March 27 issue of Science Week (which should be available by tomorrow at http://scienceweek.com/)
reports new evidence that Homo Erectus was capable of repeated water crossings. The evidence hinges on
the fact that the species reached the islands of Wallacea, which were not land-connected to any continent at
the time Homo Erectus existed. This may call for a reappraisal of H. Erectus' cognitive abilities. It might also
give one pause for thought on the issue of fishing and fish in the ancestral human diet.
Apparently the full paper by M.J. Morwood and colleagues was published in the 12 Mar 98 NATURE.
-=- "Doubt is the vestibule through which all must pass before they can enter into the temple of wisdom."
Colton (1780-1832)
PALEODIET Archives
Subject: W.M. Haenzel
From: Dean Esmay
Reply-To:
Date: Thu, 26 Mar 1998 09:11:54 -0500
The 27 March 98 SCIENCE WEEK also reports on the death of epidemiologist W.M. Haenzel at age 87.
Haenzel, among other things, designed and set up the first national system in the U.S. (SEER) to track cases
of cancer and their possible causes. This system produced some of the strongest early evidence of a link
between lung cancer and smoking. It also demonstrated that high stomach rates in Japan were no longer
found in Japanese who emigrated to Hawaii, identifying a correlation between diet and cancer.
PALEODIET Archives
Subject: Inuit and Longevity
From: Ray Audette
Reply-To:
Date: Sat, 28 Mar 1998 03:01:23 -0800
As Stefansson points out in "Hunters of the Great North" (Harcourt, Brace & Co., 1922), the Inuit he met
were in a period of great stress. Their way of life had been disturbed by the white man's trade goods and
hunger for furs for over 100 years when he met them. The whalers who were the first to make actual contact
with them only hastened the process by trading groceries in return for virtually all of the caribo to be found
on the costal plains, leading to periods of near famine for some.
More recently "The Georgia Centenarian Study:Nutritional Patterns of Centenarians" (The International
Journal of Aging & Human Development Vol. 34(1) (1992) 57-76) noted in its findings that 100 year olds do
not shun saturated animal fats - much to the surprise of the researchers.
PALEODIET Archives
55/147 (1998)
From: Mary
Reply-To:
Date: Sun, 29 Mar 1998 06:14:08 -0800
Dear List,
I have a 5, almost 6 year old son diagnosed with autism. Most, but not all, of the so called autistic symptoms
have disappeared with a paleo type of diet.
I would like to connect with a researcher or grad student who may be interested in this topic. There are
literally thousands of these kids coming up thru the system, with damaged intestines/colons from
antibiotics/vaccines.[See Wakefield's study in the Feb lancet regarding the MMR and so called autism] with
resulting brain damage.
Can a paleo diet heal these children?
If this topic interests you, please email me privately, I would love to connect with one of Loren's grad
students for example so we could put our heads together.
Thanks,
Moira
PALEODIET Archives
Subject: Re: Eskimos
From: M E Wood
Reply-To:
Date: Sun, 29 Mar 1998 08:23:26 +1200
While I know nothing about fat in the diet I wonder if the short life of the Eskimos in question might have
been caused in some part by the use of fat burning lamps, which heated the winter houses, where the
smoking of the fat would have left a deposit of carbon on the interior surface of the lungs and affected the
eyes? I have read somewhere that there have been studies of the "mummies" of women and babies found in
Greenland or somewhere like that. The women seemed to have died as the result of breathing the smoke for
long hours. Their eyes were also affected, I think. This may have been a factor in all primitive dwelling
where the fire or heating source was inside the dwelling especially the small winter houses of northern
people. The invention of the chimney must have contributed to health as well as comfort.
Sorry there is still fat in the post !
M E Wood
PALEODIET Archives
Subject: Re: Autism and paleodiets
From: Loren Cordain
Reply-To:
Date: Mon, 30 Mar 1998 10:19:00 -0700
56/147 (1998)
I would like to respond to Moira's post which indicated improvement in symptoms in an Autistic child
following adoption of a paleodiet. Autism in children is a neuro-developmental disorder characterized by few
or no language and imaginative skills, repetitive-rocking and self-injurious behavior, and abnormal responses
to sensations, people, events and objects. The cause of the syndrome is unknown, but there is increasing
evidence that it may be auto-immune in nature. Reed Warren's group (1) found that 58% of autistic children
maintained antibodies to myelin basic protein (a protein found in the myelin sheaths of nerves and suspected
of being the target protein [self antigen] for T-lymphocytes in the autoimmune disease, Multiple Sclerosis).
Additional support for the concept that Autism may be autoimmune in nature comes from work showing that
46% of autistic children maintain major histocompatibility complex (MHC) alleles associated with the
disease (2). The function of the MHC is to present self and foreign peptides to circulating T-lymphocytes at
the surface of all cells throughout the body. Thus, if foreign peptides are presented by the MHC,
circulatingT-lymphocytes can mount an immune response on the cell or cells which present, via the MHC,
that foreign peptide and destroy them. The MHC not only presents foreign peptides, but it also presents
peptides derived from the proteins of genes comprising the MHC itself. The susceptiblity genes for autism
are: DRB1*0404, DRB1*401 and DRB1*0101 (2). In a particular portion of these genes (the third
hypervariable region [HVR-3]), there is a common amino acid sequence shared by all three genes. This
amino acid sequence is either QKRAA (glutamine-lysine-arginine-arginine-alanine-alanine) or QRRAA.
Thus, either the QKRAA amino acid motif or the QRRAA amino acid motif can be presented to circulating
T-lymphocytes. This particular shared epitope increases the susceptibility to a number of autoimmune
diseases, including rheumatoid arthritis (3). The QKRAA or QRRAA amino acid motif also occurs quite
frequently in pathogens which reside in the human gastro-intestinal tract including Escherichia coli, Proteus
mirabilis, lactobacillus lactis, Brucella ovis and many other anaerobic gut bacteria (3). The QKRAA or
QRRAA sequences are found specifically in a particular type of protein contained in gut bacteria, called
DnaJ proteins. DnaJ proteins normally have a bacterial partner/ligand protein called heat shock proteins
(HSP70). It is the QKRAA or QRRAA amino acid sequence of DnaJ which allows it to bind HSP70. When
the MHC presents endogenously derived DRB1 alleles which contain the QKRAA or QRRAA amino acid
motif, then circulating HSP70 proteins (which normally bind DnaJ proteins) can bind the body's own MHC
presented QKRAA or QRRAA sequences. Circulating CD4+ T-lymphocytes recognize this HSP70/QRRAA
sequence as foreign and mount an immune response on all cells presenting this (HSP70) amino acid motif.
We believe that myelin basic protein contains an amino acid sequence that is homologous to an A.A.
sequence found in HSP70, and it is this three way mimicry between DRB1 peptides, bacterial peptides and
self peptides which causes self tolerance to be broken. So, how does a paleodiet have anything to do with this
process? Paleodiets are characterized by their lack of cereal grains, legumes, dairy products, and yeast
containing foods. Both cereal grains and legumes contain glycoproteins called lectins which bind intestinal
epithelial cells and change the permeability characteristics of these intestinal cells (4, 5). Not only do these
lectins cause an increase of the translocation of gut bacteria to the peripheracy, they cause an increased
overgrowth of gut bacteria as well as a change in the gut flora (4, 5). Further, cereal and legume derived
lectins (WGA, PHA respectively) cause increased expression of intracellular adhesion molecules (ICAM) in
lymphocytes (6) which allow bacterial/immune complexes to move from gut to the affected tissue.
Additionally, cereal and legume lectins increase lymphocytic expression of common inflammatory cytokines
such as tumor necrosis factor alpha (TNFa), interleukin 1 (IL-1) and IL-6 which are known promoters of
autoimmune disease. The cell walls of cereals and legumes contain a storage protein, GRP 180, which also
can act as a ligand to self presented MHC peptides (7). Further, peptides contained in dairy proteins (bovine
serum albumins - BSA, among many) also may contain peptide sequences which can interact with
endogenously presented peptides (8). Cereal, legume, dairy and yeast free diets potentially have therapeutic
benefit in many autoimmune related disorders via their ability to reduce gut permeability and decrease the
exogenous antigenic load both from pathogenic bacteria and from potentially self mimicking dietary
peptides.
REFERENCES
57/147 (1998)
1. Singh VK et al. Antibodies to myelin basic protein in children with autistic behavior. Brain, Behavior and
Immunity 1993;7:97-103. 2. Warren RP et al. Strong association of the third hypervariable region of HLADR beta 1 with autism. J Neuroimmunol 1996;67:97-102. 3. Auger I et al. A function for the QKRAA amino
acid motif: mediating binding of DnaJ to DnaK. J Clin Invest 1997;99:1818-22. 4. Liener IE. Nutritional
significance of lectins in the diet. In: The Lectins: Properties, Functions, and Applications in Biology and
Medicine. IE Liener (Ed), Academic Press, Orlando, pp 527-52. 5. Pusztai A. Dietary lectins are metabolic
signals for the gut and modulate immune and hormone functions. Eur J Clin Nutr 1993;47:691-99. 6. Koch
AE et al. Soluble intercellular adhesion molecule-1 in arthritis. Clin Immuunol Immunopathol 1994;71:20815. 7. Dybwad A et al. Increases serum and synovial fluid antibodies to immunoselected peptides in patients
with rheumatoid arthritis. Ann Rhem Dis 1996;55:437-41. 8. Perez-Maceda B et a. Antibodies to dietary
antigens in rheumatoid arthritis--possibel molecular mimicry mechanism. Clin Chim Acta 1991;203:153-65.
PALEODIET Archives
Subject: From Britarch mailing list
From: Dean Esmay
Reply-To:
Date: Thu, 2 Apr 1998 07:29:56 -0500
Tue, 31 Mar 1998 10:56:20 GMT From: "Keri Brown" Organization: Dept. Chem Eng - UMIST (FS1) To:
M.Sc in Biomolecular Archaeology 1998-99 A one-year M.Sc degree by teaching and research covering the
methods and applications of ancient DNA, protein and lipid analysis in archaeology. Taught at the
Department of Biomolecular Sciences, UMIST, Manchester (5A in RAE) and the Department of
Archaeology and Prehistory, University of Sheffield (5* in RAE). The course includes extensive training in
basic techniques in molecular biology (at UMIST) and in palaeobotany and osteoarchaeology (at Sheffield).
Applications of ancient biomolecules: human sex identification and kinship analysis, human population
studies, human origins and migrations, human evolution, palaeodisease, plant and animal domestication,
origins and development of agriculture.
The course is suitable for graduates in biological or archaeological subjects.
Entrance requirements: Honours degree in a biological science, archaeology or a related subject.
For further information and application forms contact Dr. Terry Brown, Department of Biomolecular
Sciences, UMIST, P.O. Box 88, Manchester M60 1QD. Phone 0161 200 4173 Fax 0161 236 0409 email
Subject: PhD Studentships at Oxford Date: Wed, 1 Apr 1998 15:18:25 +0100 (GMT Daylight Time) From:
Christopher Salter To:
Notice of two PhD studentships
UNIVERSITY OF OXFORD RESEARCH LABORATORY FOR ARCHAEOLOGY PhD Studentships in
Archaeological Science Applications are invited for two NERC funded PhD Studentships from October 1998
at the Research Laboratory for Archaeology and the History of Art, University of Oxford. The general topics
available are: Study of ancient diet (humans and animals) using isotopic and molecular information; Lead
isotope provenance studies of Islamic glazes; Luminescence dating. Candidates should have, or expect to
obtain, a first or upper second class degree, normally in either a physical or biological science, depending on
the area of interest. Letters of application indicating the preferred project area and accompanied by a CV and
names and addresses of two referees should be sent to Professor Robert Hedges, Research Laboratory for
Archaeology & the History of Art, 6 Keble Road, Oxford OX1 3QJ who will welcome enquiries on 01865
273930 or by e-mail Applications should be received by Monday 18 May 1998. The University is an Equal Opportunity
Employer
PALEODIET Archives
Subject: Bone conference
From: Dean Esmay
Reply-To:
Date: Sat, 4 Apr 1998 14:37:19 -0500
58/147 (1998)
Human bones conference Date: Fri, 3 Apr 1998 11:43:13 -0500 From: margaret cox To: britarch
As the forerunner to an important new publication on the subject, the School of Conservation Sciences,
Bournemouth University in conjunction with English Heritage are holding a major conference:' Human
osteology a British perspective: current practice and future potential' from Monday 29th June to Thursday
2nd July 1998.
The conference will be held at bournemouth University and a cast of stars, each an expert in their particular
field, will be presenting papers on biological and dental anthropology setting out what can be done and what
we hope to achieve in the near future. Speakers include, Charlotte Roberts, Margaret Cox, Simon Mays,
Juliet Rogers, Angela Childe, Tony Waldron, Richard Neave, Terry & Keri Brown, Jacky McKinley and
many others. Registration costs 35 (20 for students). For further details and a booking form please contact: or
Fax (attention of Anne Gifford) 01202 595255
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Sun, 12 Apr 1998 10:16:41 -0400
I have been a bit surprised that Herr Hflechner's thought-provoking and well-referenced message of 21
February (see
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9802&L=paleodiet&P=R334&D=0&H=0&O= T&T=1)
received no apparent notice by our membership.
My reading of the literature would support Hflechner's suggestion, given that the pattern of men doing most
of the hunting and women most of the gathering in foraging societies seems to be as close to a universal
constant as one can find in human social arrangements. At least that's my reading of the literature. Does
anyone have counterexamples or further thoughts on the matter?
-=-=Judge not, that ye be not judged. For with what judgment ye judge, ye shall be judged; and with what
measure ye mete, it shall be measured to you again. Jesus (B.C. 6?-30? A.D.)
Dean Esmay -- http://www.syndicomm.com/esmay
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Sun, 12 Apr 1998 10:04:18 -0400
Commentary on the apparent lack of cancer (and heart disease) among hunter-gatherers (and primitive
horticulturalists, as Staffan's work has shown) in this forum has been interesting, but a few people have sent
me messages asking about the average lifespan of such peoples. What data is available on this question?
PALEODIET Archives
Subject: Gender Differences
Reply-To:
Date: Mon, 13 Apr 1998 10:32:20 -0700
In rsponse to Esmay's note regarding Hoflechner's posting -- It is important to remember when searching the
ethnographic literature thatthose who wrote them had their own cultural prejudices. Thus the term "hunting"
often describes an activity that results in the killing of large game (Bear, Elk, Antelope, etc). I agree the
literature does reflect thatsuch activity tends to be limited almost exclusively to men.
59/147 (1998)
However, a search for diet often reveals the inclusion of many kinds of "small meat" which can make up the
bulk of the dietary protein intake. Large game hunting is an activity that is fraught with danger and
uncertainly - no matter the skill of the hunter. It is not to be depended on for a dietary staple, supplying
instead an occasional tasty and much-appreciated bonus.
The lesser protein sources: birds and small mammals that can be caught with traps and snares, insects,
shellfish, fish taken bythe use of paralyzants such as turkey mullen or through the use of weirs and a myrid
other creatures that are not so much "hunted" as "taken:, usually are taken by women, children, old people, or
by community effort. These are the dependable animal protein resources. They can be preserved and
stockpiled against a lean time and, except in Northern latitudes, are generally available in one form or
another, year-around.
PALEODIET Archives
Subject: Re: gender differences
Reply-To:
Date: Mon, 13 Apr 1998 11:06:27 +0100
> Is it imaginable, that there are gender differences in dietary adaptations? ...women eat more
> fruits and vegetables and less meat.
What a fascinating thought: That women are more resistant to western foods because these have something
in common with what was gathered during evolution!
PALEODIET Archives
Subject: Re: Autism and paleodiets (reposted to fix format errors)
From: "Loren Cordain (by way of Dean Esmay)"
Reply-To:
Date: Mon, 13 Apr 1998 19:29:01 -0400
60/147 (1998)
I would like to respond to Moira's post which indicated improvement in symptoms in an Autistic child
following adoption of a paleodiet. Autism in children is a neuro-developmental disorder characterized by few
or no language and imaginative skills, repetitive-rocking and self-injurious behavior, and abnormal responses
to sensations, people, events and objects. The cause of the syndrome is unknown, but there is increasing
evidence that it may be auto-immune in nature. Reed Warren's group (1) found that 58% of autistic children
maintained antibodies to myelin basic protein (a protein found in the myelin sheaths of nerves and suspected
of being the target protein [self antigen] for T-lymphocytes in the autoimmune disease, Multiple Sclerosis).
Additional support for the concept that Autism may be autoimmune in nature comes from work showing that
46% of autistic children maintain major histocompatibility complex (MHC) alleles associated with the
disease (2). The function of the MHC is to present self and foreign peptides to circulating T-lymphocytes at
the surface of all cells throughout the body. Thus, if foreign peptides are presented by the MHC,
circulatingT-lymphocytes can mount an immune response on the cell or cells which present, via the MHC,
that foreign peptide and destroy them. The MHC not only presents foreign peptides, but it also presents
peptides derived from the proteins of genes comprising the MHC itself. The susceptiblity genes for autism
are: DRB1*0404, DRB1*401 and DRB1*0101 (2). In a particular portion of these genes (the third
hypervariable region [HVR-3]), there is a common amino acid sequence shared by all three genes. This
amino acid sequence is either QKRAA (glutamine-lysine-arginine-arginine-alanine-alanine) or QRRAA.
Thus, either the QKRAA amino acid motif or the QRRAA amino acid motif can be presented to circulating
T-lymphocytes. This particular shared epitope increases the susceptibility to a number of autoimmune
diseases, including rheumatoid arthritis (3). The QKRAA or QRRAA amino acid motif also occurs quite
frequently in pathogens which reside in the human gastro-intestinal tract including Escherichia coli, Proteus
mirabilis, lactobacillus lactis, Brucella ovis and many other anaerobic gut bacteria (3). The QKRAA or
QRRAA sequences are found specifically in a particular type of protein contained in gut bacteria, called
DnaJ proteins. DnaJ proteins normally have a bacterial partner/ligand protein called heat shock proteins
(HSP70). It is the QKRAA or QRRAA amino acid sequence of DnaJ which allows it to bind HSP70. When
the MHC presents endogenously derived DRB1 alleles which contain the QKRAA or QRRAA amino acid
motif, then circulating HSP70 proteins (which normally bind DnaJ proteins) can bind the body's own MHC
presented QKRAA or QRRAA sequences. Circulating CD4+ T-lymphocytes recognize this HSP70/QRRAA
sequence as foreign and mount an immune response on all cells presenting this (HSP70) amino acid motif.
We believe that myelin basic protein contains an amino acid sequence that is homologous to an A.A.
sequence found in HSP70, and it is this three way mimicry between DRB1 peptides, bacterial peptides and
self peptides which causes self tolerance to be broken.
So, how does a paleodiet have anything to do with this process? Paleodiets are characterized by their lack of
cereal grains, legumes, dairy products, and yeast containing foods. Both cereal grains and legumes contain
glycoproteins called lectins which bind intestinal epithelial cells and change the permeability characteristics
of these intestinal cells (4, 5). Not only do these lectins cause an increase of the translocation of gut bacteria
to the peripheracy, they cause an increased overgrowth of gut bacteria as well as a change in the gut flora (4,
5). Further, cereal and legume derived lectins (WGA, PHA respectively) cause increased expression of
intracellular adhesion molecules (ICAM) in lymphocytes (6) which allow bacterial/immune complexes to
move from gut to the affected tissue. Additionally, cereal and legume lectins increase lymphocytic
expression of common inflammatory cytokines such as tumor necrosis factor alpha (TNFa), interleukin 1
(IL-1) and IL-6 which are known promoters of autoimmune disease. The cell walls of cereals and legumes
contain a storage protein, GRP 180, which also can act as a ligand to self presented MHC peptides (7).
Further, peptides contained in dairy proteins (bovine serum albumins - BSA, among many) also may contain
peptide sequences which can interact with endogenously presented peptides (8). Cereal, legume, dairy and
yeast free diets potentially have therapeutic benefit in many autoimmune related disorders via their ability to
reduce gut permeability and decrease the exogenous antigenic load both from pathogenic bacteria and from
potentially self mimicking dietary peptides.
REFERENCES
61/147 (1998)
1. Singh VK et al. Antibodies to myelin basic protein in children with autistic behavior. Brain, Behavior and
Immunity 1993;7:97-103. 2. Warren RP et al. Strong association of the third hypervariable region of HLADR beta 1 with autism. J Neuroimmunol 1996;67:97-102. 3. Auger I et al. A function for the QKRAA amino
acid motif: mediating binding of DnaJ to DnaK. J Clin Invest 1997;99:1818-22. 4. Liener IE. Nutritional
significance of lectins in the diet. In: The Lectins: Properties, Functions, and Applications in Biology and
Medicine. IE Liener (Ed), Academic Press, Orlando, pp 527-52. 5. Pusztai A. Dietary lectins are metabolic
signals for the gut and modulate immune and hormone functions. Eur J Clin Nutr 1993;47:691-99. 6. Koch
AE et al. Soluble intercellular adhesion molecule-1 in arthritis. Clin Immuunol Immunopathol 1994;71:20815. 7. Dybwad A et al. Increases serum and synovial fluid antibodies to immunoselected peptides in patients
with rheumatoid arthritis. Ann Rhem Dis 1996;55:437-41. 8. Perez-Maceda B et al. Antibodies to dietary
antigens in rheumatoid arthritis--possible molecular mimicry mechanism. Clin Chim Acta 1991;203:153-65.
PALEODIET Archives
From: Ruediger Hoeflechner
Reply-To:
Date: Tue, 14 Apr 1998 08:05:58 -0400
I am no advocate of a simple antiquated "man the hunter - woman the gatherer" model. On the other hand I
believe there is no doubt, that in all human populations there is more or less division of labor and at least in
many pulations there are certain dietary gender differences.
In his book "The foraging spectrum: diversity in hunter-gatherer lifeways" R.L.Kelly writes: "Food is not
shared equally, and men and women in a hunter-gatherer camp may eat very different diets, with women
often eating less meat than men." (p. 23)
The question is not if there are any dietary gender differences in humans, but
1) how frequent and considerable are such differences in human populations? 2) are there universal patterns
of dietary differences between men and women? 3) do these dietary differences have effects on the nutrient
composition of the diet? (Do women eating less big game meat get the same amount of protein from small
animal or vegetable resources?) 3) Are observed dietary differences recent cultural adaptations or long-time
(how long?) trends, which exert a selective pressure?
In my last message I mentioned two studies about differences in colonic length between men and women.
Again a question to all paleodieters: Have you ever heard about such differences in the digestive tract of
humans? Supposing it were so: wouldn't this have implications? Any other explanation for these differences?
Best wishes Ruediger Hoeflechner
PALEODIET Archives
Reply-To:
Date: Tue, 14 Apr 1998 14:30:10 +0100
On Sun, 12 Apr 1998 Dean Esmay wrote:
> Commentary on the apparent lack of cancer (and heart disease) among hunter-gatherers (and
> primitive horticulturalists, as Staffan's work has shown) in this forum has been interesting, but
> a few people have sent me messages asking about the average lifespan of such peoples. What data is
> available on this question?
62/147 (1998)
The average lifespan will not be particularly informative. What is needed is information on the age structure
of the populations. To take an exaggerated, (and hypothetical) example: a population with average lifespan
30 years could have: (a) 50% dying age 1 and 50% dying age 59, or (b) 50% dying age 29, 50% dying age
31. The former population will have a higher incidence of age-related diseases like cancer, heart disease, and
arthritis. Diseases of extreme old age (e.g. Paget's disease which is unknown under 50 years of age, and
reaches prevalences of 10-15% in Caucasians over 90 [1]) are seen in archaeological populations with
average age of death of 30 years or so, because there were many individuals who died young, but also some
who reached old age.
The average age of the living, rather than the dead, might be more informative, but still not as good as the
age structure of the living population.
[1] Roberts, C & Manchester, K (1995) The archaeology of disease. 2nd ed. Ithaca, NY: Cornell University
Press pp.184-185
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Women and hunting
Reply-To:
Date: Tue, 14 Apr 1998 15:45:10 +1100
I don't think it's necessarily true that men did the hunting and women the gathering, at least in the case of
Australian Aborigines. There is some evidence (which I'm afraid is not in my files) plus a recent study that
was reported in the newspaper this month, that Aboriginal women brought home most of the food - full stop.
They hunted small animals like goannas, snakes and wallabies as well as gathered shellfish, yams, honey,
bush fruit, nuts and seeds, and prepared the seed cakes. According to the paper, the men hunted the big
animals but were unsuccessful most of the time. I can dig around for the references if people want them.
Best wishes Jennie
PALEODIET Archives
Subject: Re: Life Tables of Hunter Gatherers
From: Loren Cordain
Reply-To:
Date: Tue, 14 Apr 1998 17:16:00 -0600
In a previous post, Dr. Millard made the excellent point that :
"The average lifespan will not be particularly informative. What is needed is information on the age structure
of the populations. To take an exaggerated, (and hypothetical) example: a population with average lifespan
30 years could have: (a) 50% dying age 1 and 50% dying age 59, or (b) 50% dying age 29, 50% dying age
31. The former population will have a higher incidence of age-related diseases like cancer, heart disease, and
arthritis. Diseases of extreme old age (e.g. Paget's disease which is unknown under 50 years of age, and
reaches prevalences of 10-15% in Caucasians over 90 [1]) are seen in archaeological populations with
average age of death of 30 years or so, because there were many individuals who died young, but also some
who reached old age. The average age of the living, rather than the dead, might be more informative, but still
not as good as the age structure of the living population."
63/147 (1998)
In this regard, there has only been a single study published showing the life table of hunter gathers (1). The
following Table (I hope it comes throught in a proper order) was constructed using data from a large sample
of Yanomama males. Column A is the mortality schedule (the chance that those who reach the age class will
die before reaching the next age class. Column B is the chance of surviving the age class or 1-A. Column C
is the number of survivors left at the beginning of the age class out of every 100 born. Here we go:
Age A B C 0 .26 .73 100 1 .16 .84 73 5 .11 .89 62 10 .08 .91 55 15 .14 .86 50 20 .15 .85 43 25 .16 .84 36 30
.16 .84 30 35 .16 .84 26 40 .16 .84 21 45 .17 .83 18 50 .17 .82 15 55 .21 .79 12 60 .28 .72 10 65 .36 .64 7 70
.47 .53 4 75 .61 .39 2 80+ 1.0 0.00 1
Thus, as Dr. Millard has pointed out, the age structure of the entire population tells us more about mortality
than a simple average life span. In the Yanomama, the constant warfare that goes on takes a high toll of
young adults and adults - also notice the high infant mortality rates (27%). Still a considerable percentage of
the population lives beyond age 50. Data for women is found in reference (1) for interested readers.
REFERENCE
1. Neel JV. Health and disease in unacculturated Amerindian populations. Ciba Foundation Symposium
1977;49:155-77.
PALEODIET Archives
Subject: Re: Life Tables
From: Loren Cordain
Reply-To:
Date: Thu, 16 Apr 1998 14:55:00 -0600
Thank you Andrew - I stand corrected. By the way how does the Hazda data look compared to the
Yanomamo?
Loren
On Tue, 14 Apr 1998 Loren Cordain wrote:
> In this regard, there has only been a single study published showing the life table of hunter
> gathers (1). 1. Neel JV. Health and disease in unacculturated Amerindian populations. Ciba
> Foundation Symposium 1977;49:155-77.
I was surprised at this and checked the references cited by Eaton et al [1]. Looking only at one which was
readily accessible to me [2] I found an estimated life table for the Hazda for three census dates, and cites for
other similar work including one study on the !Kung. Life table data is obviously out there in the literature,
but not necessarily tied directly to disease incidence rates.
[1] Eaton, SB, et al. (1994) Women's reproductive cancers in evolutionary context. Quarterly Review of
Biology 69 (3) 353-367 [2] Blurton-Jones et al (1992) Demography of the Hazda, an increasing and high
density population of savanna foragers. American Journal of Physical Anthropology 89 159-181
PALEODIET Archives
Subject: Re: Life Tables of Hunter Gatherers
Reply-To:
Andrew Millard
Date: Thu, 16 Apr 1998 17:18:19 +0100
On Tue, 14 Apr 1998 Loren Cordain wrote:
> In this regard, there has only been a single study published showing the life table of hunter
> gathers (1). 1. Neel JV. Health and disease in unacculturated Amerindian populations. Ciba
> Foundation Symposium 1977;49:155-77.
I was surprised at this and checked the references cited by Eaton et al [1]. Looking only at one which was
readily accessible to me [2] I found an estimated life table for the Hazda for three census dates, and cites for
other similar work including one study on the !Kung. Life table data is obviously out there in the literature,
but not necessarily tied directly to disease incidence rates.
64/147 (1998)
[1] Eaton, SB, et al. (1994) Women's reproductive cancers in evolutionary context. Quarterly Review of
Biology 69 (3) 353-367 [2] Blurton-Jones et al (1992) Demography of the Hazda, an increasing and high
density population of savanna foragers. American Journal of Physical Anthropology 89 159-181
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Thu, 16 Apr 1998 19:37:30 -0400
In reading Dr. Heidecker's note, I find myself confused. The implication appears to be that hunting done by
men is largely unnecessary and that they could bring in more food by gathering and chasing small game
close at hand. If this is so, why would men bother hunting? Would it not conflict with Optimal Foraging
Theory to have men regularly devoting large amounts of time and energy, and taking significant risks, to
chase after unreliable, not-particularly-valuable food sources?
I would be interested in any references on this.
PALEODIET Archives
Subject: Blood group references
From: Todd Moody
Reply-To:
Date: Fri, 17 Apr 1998 13:36:59 -0400
For anyone interested in pondering the question of whether the A, B and AB blood types represent
adaptations away from the paleolithic (O-type) diet, Peter D'Adamo has recently posted a rather large
collection of abstracts at his web site. The URL is
http://www.dadamo.com/aanp-r.htm
Todd Moody
PALEODIET Archives
Reply-To:
Date: Fri, 17 Apr 1998 16:50:00 -0700
In response to your question regarding why men participate in large game hunting if it is a dangerous, lowyield activity the answer is two fold.
First, in many cases, men are free to particpate in an activity that does not predictably yield a food resource
because the gathering activities of the other members of thier group produces a sufficient amount of food for
them. (It should also be noted that hunters will gather food while engaged in hunting activity, either to feed
themselves if the hunt is long or to bring back to camp.) For hunter/gatherer peoples that have not been
recently forced into marginal environments, gatherable food resources are usually plentiful throughout the
year.
65/147 (1998)
Second, hunting is a prestige activity that yields a much-valued food. A successful hunter has much to gain
in terms of social standing, improved reproductive opportunities and having the werewithal to build social
and politcal alliances. The scarcity of this food resource, and its high price in terms of the time and
technology necessary to obtain accounts for its high value, and the benefits that accrue to an individual who
can supply it.
I agree that meat from large-game is a valuable, high-quality protein addition to the diet. However, if it is not
available there are other resources that can supply the same foodstuff. The group can obtain their protein
needs through the consumption of nestling birds, songbirds, eggs, lizards, mice, insects, rabbits, etc. etc. etc..
As long as the total calorie intake is sufficient, a relatively small amount of dietary protein will suffice to
keep the females fertile and lactating, the children and adolescents growing at optimal speed and the adults
healing and manufactuirng any polypeptides necessary for maintenance and upkeep.
References on the diets and food-getting activities of hunter-gatherer groups are scattered throughout the
ethnographic literature, and much information on this topic can be obtained through a search in the Human
Relation Area Files. I can also refer you to such workds as Richard Lee and Irven DeVore"s Man the Hunter
(Aldine, Chicago, 1968), M. G. Bicchieri's Hunters and Gatherers Today, (Holt, Reinhart and Winston,
1972) and Frances Dahlberg's Woman the Gatherer (Yale University Press, 1981)
PALEODIET Archives
Subject: Our hunting fathers
From: Dick
Reply-To:
Date: Sat, 18 Apr 1998 11:36:52 +0100
In reply to:
> Date: Thu, 16 Apr 1998 19:37:30 -0400
> From: Dean Esmay Subject: Re: gender differences
> In reading Dr. Heidecker's note, I find myself confused. The implication appears to be that
> hunting done by men is largely unnecessary and that they could bring in more food by gathering and
> chasing small game close at hand. If this is so, why would men bother hunting? Would it not
> conflict with Optimal Foraging Theory to have men regularly devoting large amounts of time and
> energy, and taking significant risks, to chase after unreliable, not-particularly-valuable food
> sources?
I would submit an hypothesis, which is that not everything is done for Optimal Foraging reasons, either now
or in the past. Hunting large beasts may have been done for primarily ritual and religious reasons, rather than
for food.
I note three things of interest:
1. Some of the oldest symbols to which we have access are the runic symbols, and one, the Aurochs (Ur-Ox)
denotes the young man who has taken part in the successful hunt of a ferocious beast - the Aurochs. This
marks his passage from boyhood to manhood and was a gender specific rite. [N.B. A secondary note - we
presently lack such an established rite in our society, save when war visits our country. This lack may have
important psychological and social consequences.]
2. The religion of Mithras and, before it Zoroaster, which was first associated with the middle east in the area
of modern Iran, are connected with bull-slaying. Whatever the cosmological significance of the myth may
be, the social significance seems to have been again to lay stress on male heroism.
3. No issue is guaranteed to arouse more social upheaval in the United Kindom than that of hunting,
especially fox-hunting. Deaths occur at hunts, once only among the hunters, now also among the antihunting activists.Repeated attempts to ban hunting have failed despite governments of many political
colourations. It is difficult not to accept that hunting still has a powerful significance for this country at least.
I propose that hunting is of gender-specific, ritual importance, and that is the reason for its pursuit through
the ages.
Dick Bird Department of Psychology University of Northumbria Newcastle upon Tyne NE1 8ST
(0) 191 227 4521
66/147 (1998)
PALEODIET Archives
Subject: hunting and gathering
Reply-To:
Date: Sat, 18 Apr 1998 15:19:07 -0400
How important is hunting for human subsistence? It depends on the environment.
Hunter-gatherer diet is systematically related to environmental characteristics, especially the effectice
temperature and primary plant production. There is no question that many tropical and subtropical huntergatherers rely primarly on plant food (with women bringinging home most of the food).
But the colder the environment, the more food is derived from hunting and fishing (and the more food is
directly procured by men). I do not believe that Homo sapiens would have been so successfull in northern
latitudes without hunting large animals. What else than big game provides enough food for a hunter and
gatherer in a long and cold winter? In these regions hunting is not primarily a ritual or religious exercise but
a matter of death and life.
PALEODIET Archives
Subject: Food scarcity
Reply-To:
Date: Mon, 20 Apr 1998 10:20:22 +1100
I would like to see a debate on the issue of cycles of food abundance and food scarcity in hunter gatherer
diets. In a recent post, Lorraine Heidecker wrote 'For hunter/gatherer peoples that have not been recently
forced into marginal environments, gatherable food resources are usually plentiful throughout the year'.
Why is it that many scientifically trained people think hunter-gatherers regularly starved to death, allowing
natural selection of the 'thrifty genotype' (one susceptible to overweight and obesity today)? Is it true that we
often starved - what is the evidence? Overweight now affects nearly half of all adults in industrialised
countries and the experts are trying to explain it in these terms.
The current issue of Diabetologia has a debate on a new theory proposed by Gerald Reaven called the 'notso-thrifty genotype' followed by an article by the author of the 'thrifty phenotype' hypotheses (Hales). Both
authors are trying to explain the 'insulin resistance' syndrome. All of the theories are based on the notion that
starvation or food scarcity was common among our ancestors. None of them give any evidence to document
it - it's as if it's inarguable.
It puzzles me that humans could become taller and taller throughout the paleolithic while simultaneously
being exposed to fluctuating but significant periods of starvation. I'd like to hear your comments?
Best wishes Jennie
PALEODIET Archives
Subject: Re: food scarcity
Reply-To:
Date: Mon, 20 Apr 1998 08:12:43 -0400
An addition to Jenny Brand Miller's very interesting question:
Is a thrifty geno/phenotype really a hominid acquisition that gives us information about food scarcity in the
last four million years? Isn't it a much older vertebrate strategy to survive long periods of low food
availability? In captivity most vertebral species - including chimpanzees and gorillas - suffer from obesity
and other "western diseases" if fed ad libitum. Is starvation (to death?) common amoung great apes?
Best wishes Ruediger Hoeflechner
67/147 (1998)
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Tue, 21 Apr 1998 09:14:34 -0400
Kristen Hawkes, Kim Hill, and others have conducted careful and detailed analyses of the caloric intake
patterns of the Ache, a tribe of lowland foragers in Paraguay. Richard Lee and others have claimed that meat
intake will only be high in groups dwelling at high lattitudes, but their very careful study of the Ache
confounds that prediction. Despite abundant edible plant resources, the Ache derive about four times as
much of their caloric intake from animal sources as plant sources.
A very careful analysis of the total calories invested in garnering foods clearly shows why: medium and
larger-sized game animals produce more calories per hour invested in foraging than almost any other
resource. Only honey and oranges were able to compete with meats in terms of the amount of calories they
delivered vs. the amount of hours needed to put in to utilize those foods--and even then, many forms of game
animals (e.g. peccary, armadillo, coati, paca) still far out-produced both these resources.
Insects such as palm larvae did not produce as much caloric intake per hour of investment in obtaining them
as did almost any medium- or larger-sized game animal.
Furthermore, very small game, such as birds and snakes, produced far -less- food value than anything else
the Ache ate. Very small game such as these were highly undependable and required almost more effort to
garner than they were worth.
See:
Hawkes K et. al. Why Hunters Gather: Optimal Foraging and the Ache of eastern Paraguay. American
Ethnologist, pp 379-398, Vol 9, 1982
Hill K et. al. Seasonal Variance in the Diet of Ache Hunter-Gathererrs in Eastern Paraguay. Human Ecology,
Vol. 12, No. 2, 1984
PALEODIET Archives
Subject: Re: Food scarcity
Reply-To:
Date: Tue, 21 Apr 1998 09:38:23 +0100
On Mon, 20 Apr 1998 Jennie Brand Miller wrote:
> Why is it that many scientifically trained people think hunter-gatherers regularly starved to
> death, allowing natural selection of the 'thrifty genotype' (one susceptible to overweight and
> obesity today)? Is it true that we often starved - what is the evidence?
And on Mon, 20 Apr 1998 Ruediger Hoeflechner wrote:
> Is a thrifty geno/phenotype really a hominid acquisition that gives us information about food
> scarcity in the last four million years? Isn't it a much older vertebrate strategy to survive long
> periods of low food availability? In captivity most vertebral species - including chimpanzees and
> gorillas - suffer from obesity and other "western diseases" if fed ad libitum. Is starvation (to
> death?) common amoung great apes?
It seems to me that for there to be a selective effect it does not have to be starvation to death, but a level of
starvation which prevents successful reproduction - any capacity to reproduce in the face of food shortages
would be advantagous.
My immediate question is: do these overweight captive animals also suffer from diabetes?
Jennie also wrote:
> It puzzles me that humans could become taller and taller throughout the paleolithic while
> simultaneously being exposed to fluctuating but significant periods of starvation. I'd like to
> hear your comments?
68/147 (1998)
Adult height is determined both genetically and by childhood nutrition, so that with increasing nutrition in
the western world today each generation is taller than the last. However the differences over the palaeolithic
(the last 2.5Ma) also involve species differences where there may be a variety of selective effects acting. One
major factor is likely to have been the introduction of cooking which reduces the energy required for
digestion and therefore allows a greater proportion of dietary energy to be directed into growth. Increasing
brain size presumably lead to greater hunter efficiency, through strategy changes and improved hunting
equipment. In the Upper Palaeolithic (last 40ka) we begin to to see regional (and wider) exchange networks
which may have provided some cultural back-up to finding food resources in times of localised food scarcity.
Age at death may also affect the final apparent height of populations, as a poorly nourished individual will
continuing growing for a longer period. In C19th England the lowest social classes did not attain maximum
height until 29 years of age [1]. So if adult life expectancy* were low in palaeolithic hunter-gatherers, and
nutrition was poor, then we might expect to underestimate the final adult height, as our sample will include a
number of adults who are still growing.
* that is the life expectancy of those reaching an age of 18.
[1] Mays, S (1998) The archaeology of human bones. London & New York: Routledge. p70
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Hereditary Hemochromatosis
From: Gary Ditta
Reply-To:
Date: Thu, 30 Apr 1998 08:26:36 -0700
Like all animals, humans are under constant selective pressure from their food supply. The evolutionarily
recent switch from a predominantly meat-based hunter-gatherer diet to a predominantly plant-based
agricultural diet represents a profound change that is most assuredly reshaping our genetics. How much
adaptation has taken place? Not much, the argument goes, given the limited time available. Still, there are
assumptions involved in making this judgment and the general tendency is to err on the side of
underestimation rather than overestimation when considering the rapidity of possible genetic change. Nature
almost always works more efficiently than we think.
One candidate for such genetic adaptation that has not been fully appreciated is the mutation responsible for
hereditary hemochromatosis (HH) (1). This is a particularly interesting situation insofar as its prevalence
within the population can be viewed as the result of strong (positive) selective pressure for dietary change,
while the altered gene itself, once established, can also be viewed as the agent of weaker (negative) selective
pressure for the same dietary change.
HH is the predominant member of a class of disorders referred to collectively as iron overload disease. In
these diseases, massive amounts of iron (up to 5-10x normal) gradually accumulate in the body leading to
any of a panoply of health problems such as cirrhosis, arthritis, diabetes, impotence, heart failure and even
death. The iron is deposited in the form of a storage compound (hemosiderin) in major organs such as liver,
pancreas, heart, joints, and endocrine glands. Tissue damage, once evident, is at best only partially reversible
if at all. Iron overload in HH is progressive over an individual's lifetime. Most people (usually males, as
females are protected to a large extent due to menstruation) present clinically between the ages of 40 and 60.
The primary treatment is early detection and frequent phlebotomy (blood-drawing), usually accompanied by
a diet low in meat and other iron-rich foods. Phlebotomy works to prevent and/or partially reverse HH
because a certain amount of iron can be mobilized to form new red blood cells. Significant early mortality is
associated with lack of treatment.
69/147 (1998)
It is not generally appreciated that HH is the most common inherited metabolic disorder among whites
worldwide (2). It is also the most underdiagnosed. Recently the HH gene has been identified and cloned (3).
It is now known that more than 80% of HH cases are due to the identical mutation which probably arose
somewhere in Northern Erurope (3-5). Large scale studies have shown that HH is present in European
populations (or derivatives) at frequencies of 10-16% (6). This number represents heterozygotes having one
good copy of the HH gene and one mutated. It is obviously an extremely high value. Heterozygotes do not
show disease symptoms. The corresponding frequency for homozygous individuals having two copies of the
mutated gene is 0.3-0.8% (6). On a normal diet and in the absence of intervention, homozygotes will
progress to disease.
How did the frequency of this mutation get to be so high? Conceivably it could be a chance event resulting
from a population bottleneck (genetic drift). A more powerful argument, however, is that there has been
strong selective pressure for enrichment. This can easily be envisioned considering the mechanism by which
iron overload occurs: through increased absorption of dietary iron. Iron absorption is normally regulated in
humans such that rates rise only in response to anemia. In HH, however, absorption remains high regardless
of iron status. Given that iron deficiency problems most likely increased for humans following the transition
from hunter-gatherer modes to agricultural life (it is currently one of the most prevalent nutritional
deficiencies in the world), the presence of this mutation would prove extremely useful to individuals faced
with reduced meat intake (meat is a particularly good source of bioavailable iron) and/or increased reliance
on cereals or other plants containing inhibitors of iron absorption such as phytates or polyphenols (7) and/or
increased milk intake, which is an inhibitor of iron absorption due to casein, calcium, whey protein and
phosphates (see 8). Iron overload is in fact rare in populations existing primarily on cereal diets, even for
individuals homozygous for HH.
The fact that heterozygous asymptomatic individuals also absorb increased, though lesser, quantities of iron
(9) is particularly significant and could be the primary basis for penetrance of HH into the population. The
situation here would be somewhat analogous to that for sickle cell anemia, where strong selection is
maintained for heterozygosity as protection against malaria.
Lastly, one can imagine that, once present, HH itself implements weak negative selective pressure in the
direction of a reduced iron diet. Selection is weak owing to the generally post-reproductive nature of the
pathology. Factors that can be considered in this regard include: early-presenting situations of severity
(which do occur), speculative neonatal effects (10), increased bacterial infections (e.g Yersinia
enterocolitica, which is normally iron-dependent for infection), or group selection mechanisms.
1) Bothwell and MacPhail (1998) Seminars in Hepatology 35(1) 55-71. 2) Bonkovsky et al (1996)
Hepatology 24(3): 718-29. 3) Feder et al (1996) Nature Genet 12: 399-408. 4) Risch (1997) Nature Genetics
17: 375-376. 5) Merryweather-Clarke et al (1997) J Med Genet 34: 275-278. 6) Niederau et al (1994) Adv
Exp Biol Med 356: 303-308. 7) Hurrell (1997) Euro J Clinical Nutr (1997) 51: Suppl, S4-S8. 8) Olivares et
al (1997) J of Nutr 127(7):1407-11. 9) Bulaj et al N Eng J Med (1996) 335: 1799-1805. 10) Parkilla et al
(1997) Proc Nat Acad Sci 94(24): 13198-202.
Gary Ditta
PALEODIET Archives
Subject: Re: Fat is back!
From: Gregg M Burton
Reply-To:
Date: Fri, 1 May 1998 03:05:18 -0700
Hi Andrew!!!
> I found the following on Elsevier's Science Channel www.sciencechannel.nl, and was surprised not
> to have seen it discussed here. Anyone know any more
> Andrew Millard
-----------------------> Fat is back!
> April 23, 1998
70/147 (1998)
Yes I heard about this I think on Monday, or at least in the beginning of the week, on the Early Morning
News since I don't usually get to bed till about 6:00 or 7:00 in the Morning since I'm a Night Owl. In the
Segment one Doctor from Harvard University said they've know about this for Decades. The Story was about
Good Fats vs. Bad Fats and they said Fats like Olive Oil and Canola Oil were Good and I don't remember
what they said were Bad. I just thought it was interesting how they knew this for Decades and yet just about
every so-called Expert was telling People to go on this Stupid and Dangerous - in my Opinion - Low Fat
Diet, yet all the Data I've ever seen shows that it exactly the Opposite and that in fact it's a High Fat Diet that
is Good for you - Of course, it depends on the Fat and I'm talking mostly Animal Fats and NonHydrogenated Vegetable Fats. After the guy from Harvard spoke one Stupid Lady was saying that we still
had to be careful because of all the Calories that Olive Oil has and it had 120 Calories per Tablespoon and so
High Calorie and too many Calories is not good for us. Well she didn't look very Healthy to me and I'm
suppose to listen to her Propaganda? - I Don't Think So!!! You ever notice how Unhealthy most of these
Nutritionists, Doctors, and Researchers look and yet they're telling us what to Eat and how to Live - Nooooo
Thank You!!! - Not For Me!!!
Anyway, if anyone here has some really good Data and Studies on the Benefits of a High Fat Diet and some
good Resources for that Data I'd really appreciate - Thanks!!! - :)!!!
- Take Care!!!
- Gregg!!!
PALEODIET Archives
Subject: Fat is back!
Reply-To:
Date: Fri, 1 May 1998 09:26:20 +0100
I found the following on Elsevier's Science Channel www.sciencechannel.nl, and was surprised not to have
seen it discussed here. Anyone know any more
Andrew Millard
-----------------------Fat is back! April 23, 1998
A recent study which will contribute to new US Department of Agriculture (USDA) dietary guidelines for
the year 2000, concludes that a low fat diet at the expense of food variety isnAt always healthy. The study
conducted by researchers from the University of Michigan found that diversity and quality contributed as
much to health as a low fat diet.
The researchers compared French diets with American eating habits. What was intriguing about the French
diet was that men and women ate more foods with higher levels of fat, saturated fat and cholesterol than
Americans, but suffered less from heart disease and were generally less obese than their American
counterparts.
When compared to the USDA recommendations for healthy eating French diet fell short on all levels, but
still provided better health prospects. The researchers concluded that a monotonous diet quality of life.
Greater dietary variety, diversity and food quality goes hand in hand with over all health.
Story by: T. Garcia Compilation (c), 1998 Elsevier Science. All rights reserved.
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Problems
From: Dean Esmay
Reply-To:
Date: Fri, 1 May 1998 20:14:08 -0400
71/147 (1998)
There seems to be a bit of a problem with our list software. Normally most messages to this list go through a
human moderator, and messages lacking a certain level of intellectual rigor, or accidentally sent to the list
instead of as private correspondence, are not passed on to the membership. But lately some messages are
getting through without any review at all. I'm not sure how that's happening, but I'm looking into the
problem.
Thanks all for your patience. We seem to be having a number of small quirks with our software right now
(others have appeared behind the scenes, so hopefully won't have been noticed by most).
Nothing to worry about, just wanted everyone to know that strange things are afoot and if something weird
appears don't take it too seriously (for now).
PALEODIET Archives
Subject: Water Consumption
From: Don Wiss
Reply-To:
Date: Sat, 2 May 1998 19:08:42 -0400
I often see on the Net the recommendation to drink 8 glasses of water a day. On another mailing list they are
now talking about 8-10 glasses a day. I would think one should only drink when they are thirsty. As one that
looks to our ancestors for answers, I find it hard to believe Paleolithic people consumed this much, especially
as the only containers they might have had is animal bladders.
Has anybody done research into this? Is it possible that eating Neolithic foods increases the need for water?
But there is the argument that someone on a high protein diet needs more water. A paleo diet would have
been higher protein.
When do modern hunter/gatherer populations drink water? On this other list the argument is to drink plenty
of water between meals, but little with the meal. They say too much water will dilute the hydrochloric acid
and food will not digest properly. If HGs didn't have bladders filled with water, I can see them not drinking
water with meals, as they would have to go to the stream or pond to drink.
There are even books that claim drinking water cures all sorts of pains and degenerative diseases, e.g. stressinduced peptic ulcer disease, hypertension, and arthritis. But these are civilizatory diseases.
Don.
PALEODIET Archives
Subject: Re: Water Consumption
Reply-To:
Date: Sun, 3 May 1998 12:36:52 +0100
> I would think one should only drink when they are thirsty.
We cannot trust our senses in the modern community where food is salty and low in water and our bodies are
more or less damaged from early age which creates new needs for us. For those who stick to a western
lifestyle there are numerous interventions which may limit such damage. Hormone replacement therapy,
vitamin-D and lipid lowering statins are some of them. A high intake of water may hypothetically be another
example. In elderly westerners its benefits seem rather convincing to me [Vellas B, Albarede JL, Garry PJ
(eds). Hydration and Aging. Springer, NY, 1998].
When I started eating unsalted "paleolithic" foods 11 years age I became less thirsty and drank less than
previously while urine volumes increased. The latter is because the new diet is rich in water. Juice is not
richer in water than fresh fruit. Below is the average (standard deviation) water content of some food groups
in Sweden (g/kg).
Meat 709 (59) Fish 743 (121) Fruit 842 (50) Tubers 851 (67) Vegetabl. 886 (74) Nuts 105 (152) - excluding
chestnut and coconut 48 (13)
72/147 (1998)
Fats/oils 306 (250) Cereals 200 (174) Dairy pr. 643 (229) Juice 846 (122)
PALEODIET Archives
Subject: Re: Water consumption
Reply-To:
Date: Sun, 3 May 1998 22:34:29 -0700
In response to Don Wiss' query about water consumption it is important to remember that the majority of
hominid sites uncovered are found near a site of fresh water. Thus it would be relatively simple for hominids
from very early times to drink water throughout the day as long as they stayed near home. It would only be
those who were foraging some distance or who were perhaps journeying to another place that would need to
carry water and even these would doubtless have knowledge of water sources on the way unless they were
exploring new territory.
If we go back further, to a savannah primate model, then we find primates such as a baboon troup for
example, visiting a water source twice a day.
Lorraine Heidecker California State University Sacramento
PALEODIET Archives
Subject: Re: Plant:Animal Subsistence Ratios & Latitude
From: Loren Cordain
Reply-To:
Date: Mon, 4 May 1998 13:51:00 -0600
In a previous post, Ruediger Hoeflechner, wrote:
"How important is hunting for human subsistence? It depends on the environment.
Hunter-gatherer diet is systematically related to environmental characteristics, especially the effectice
temperature and primary plant production. There is no question that many tropical and subtropical huntergatherers rely primarly on plant food (with women bringinging home most of the food).
But the colder the environment, the more food is derived from hunting and fishing (and the more food is
directly procured by men). I do not believe that Homo sapiens would have been so successfull in northern
latitudes without hunting large animals. What else than big game provides enough food for a hunter and
gatherer in a long and cold winter? In these regions hunting is not primarily a ritual or religious exercise but
a matter of death and life."
73/147 (1998)
This issue (the relationship of food subsistence types to latitude in hunter gatherer societies) has been poorly
examined from an objective basis in the anthropological literature. It is commonly assumed, but rarely
quantified, that the relative amount of food derived from hunting increases with increasing latitude (i.e. a
positive correlation). In one of the few citations, I am aware of (I qualify this statement because eagle eyed
Andrew may slip in an additional citation), Foley (1) proffered data showing a moderate to weak correlation
of hunted food resources to latitude (r = 0.45; r squared x 100 = 20%). Foley used Richard's Lee's
compilation (2) of the Ethnographic Atlas (3) to make his calculations. As I have pointed out in a number of
previous posts, and has been pointed out elsewhere (4), Lee's compilation of the Ethnographic Atlas is
incomplete and therefore erroneous because he has only included 116 of the 181 hunter gatherer societies.
Further, he did not consider animal foods derived from fishing (including shellfishing and the pursuit of large
aquatic mammals). We have re-analyzed the original data from the Ethnographic Atlas utilizing all 181
Hunter Gatherer Societies and have included all three subsistence categories available to hunter gatherers
(gathering, hunting, fishing). The relationship of foods derived from hunting yields a non-significant (p >
0.05) "r" of 0.08 and a shared variance of 0.6%, meaning that latitude has almost zero influence upon food
calories derived from hunting. However, this does not mean that hunted animals were not important
components of hunter-gatherer diets, it simply means that latitude had relatively little influence upon the
mean estimated (26-35%) hunted animal food intake for all 181 Hunter Gatherer Societies. Therefore,
calories derived from hunted animal foods remains relatively constant in all hunter gatherer societies
regardless of latitude. Obviously, variables other than latitude need to be considered when evaluating
variations in hunter gatherer caloric intake derived from hunted animal food. Despite a relatively constant
animal food intake in hunter gatherer societies, there is a moderate to strong inverse relationship (r = -0.67;
p<0.001) between gathered plant foods and latitude (meaning as latitude increases, the total amount of plant
derived food decreases). So, if plant food decreases with increasing latitude and hunted animal food doesn't
increase, what makes up the difference. Ah, I can see Andrew beaming as he guesses this one correctly Fishing derived food? Yep! The relationship of fished animal foods to latitude is a moderate correlation (r=
0.48, p<0.001). So, presumably more and more aquatic based animal foods are included in the diet to replace
plant foods which decrease in frequency with increasing latitude. I hope to publish our complete analysis of
the Ethnographic Atlas as it relates to the diet of hunter gatherers in the near future.
References
1. Foley R. A reconsideration of the role of predation on large mammals in tropical hunter-gatherer
adaptation. Man 1982;17:393-402.
2. Lee RB. What hunters do for a living, or how to make out on scarce resources. In Lee RB, DeVore I,
(Eds). Man the Hunter. Chicago: Aldine, 1968:30-48.
3. Murdock GP. Ethnographic atlas: a summary. Ethnology 1967;6:109-236.
4. Ember CR. Myths about hunter-gatherers. Ethnology 1978;17:439-48.
Cordially,
Loren Cordain, Ph.D. Professor, ESS Dept Colo State Univ, Ft. Collins, CO 80523 (970) 491-7436 (970)
491-0445
PALEODIET Archives
Subject: Re: Food Scarcity; hemochromatosis; clarification of latitude & s ubsistence ratios
From: Loren Cordain
Reply-To:
Date: Tue, 5 May 1998 12:23:00 -0600
First, I'd like to thank Gary Ditta for his informative and interesting post on Hemochromatosis - Kudos Gary
- you should expand upon this and publish it.
I would like to respond to Jenny's comment:
74/147 (1998)
Implicit in JV Neel's original "thrifty gene" hypothesis (1) is the assumption that pre-agricultural man must
have gone through regular, periodic episodes of starvation that negatively impacted reproductive potential
and hence resulted in the selection of a gene or genes which would have survival value during the
fluctuations between "feast and famine". This concept is frequently invoked to explain the high incidence of
diseases of insulin resistance (non-insulin dependent diabetes mellitus (NIDDM), hypertension, obesity,
coronary artery disease) among recently acculturated populations (2, 3). John Allen (one of our members - if
he is still listening in the ether) has proposed the existence of a "non-thrifty genotype" (4) which is more
prevalent in westernized populations in which these putative adaptations to feast and famine do not occur.
Although Neel's hypothesis has become "one of the orienting concepts of nutritional and biomedical
anthropology" (4), it is founded upon an assumption which cannot be corroborated by the available
ethnographic data derived from living hunter gatherer populations nor by the fossil record. Indeed, periodic
starvation became more frequent and nutritional status declined when hunter gatherer populations made the
transition to agriculture (5, 6). Diamond has pointed out that starvation among early agriculturalist was quite
common because of the dependence upon a few staple cereal crops (7). If one staple food crop failed,
farmers ran a greater risk of starvation than did hunter gatherers who could utilize a much broader range of
wide plant and animal foods. Modern studies of hunter gatherers show that there is a seasonal fluctuation in
body weight, but these studies do not indicate any evidence of starvation or chronic malnutrition (8, 9). I
havent carefully examined the northern latitude studies, but Stefanson has reported that starvation did not
occur among the Copper Eskimos (10). In a review of 51 references examining human populations from
around the earth and from differing chronologies, as they made the transition from hunter gatherers to
farmers, Cohen (11) concluded that there was an overall decline in both the quality and quantity of life.
Generally, in most parts of the world, whenever cereal based diets were first adopted as a staple food
replacing the rich variety of wild animal and plant based foods of hunter gatherers, there was a characteristic
reduction in stature (4, 17, 18, 19) an increase in infant mortality (19, 20), a reduction in life span (19, 20),
an increased incidence of infectious diseases (19, 20, 21, 22), an increase in iron deficiency anemia (19, 20,
22), an increased incidence of osteomalacia, porotic hyperostosis and other bone mineral disorders (4, 19, 20,
22) and an increase in the number of dental caries and enamel defects (19, 20, 23). Clearly, early farming
brought on not a reduced mortality from starvation and nutritionally related diseases, but to the contrary, an
increase. If this is the case, then the advent of agriculture would not have reduced the selection for a thrifty
genotype, but would have actually increased it. Obviously, population and epidemiological data indicate this
is not the case. Therefore, the assumption that starvation was the single and only factor selecting for a
putative "thrifty genotype" could not be correct. Alternatively, my colleague Jenny Brand Miller (17) has
suggested that the high protein intake of pre-agricultural diets would have represented a more likely
environmental pressure responsible for selecting for multiple genes originally hypothesized by Neel to be
"thrifty genes". It is likely that Neel's concept of "thrifty" is a misinterpretation of the true function of these
multiple genes. I refer interested readers to Jenny's mechanistic explanation for this phenomenon (17) &
perhaps she could comment upon this. By the way, as a matter of interpretation - there seems to be a bit of
confusion concerning my previous post correlating latitude to animal based hunted foods. I indicated that the
mean dietary subsistence percentage for hunted animal foods for world wide hunter-gatherers is 26-35%.
This value is indeed correct - it differs from previous values I have presented in this forum because those
previous values (56-65%) represented the combined animal foods derived both from hunting and fishing.
These data support Jenny's contention that a high protein diet would have been the norm for our stone age
ancestors, and that this nutritional pressure may have favored the selection of genes which promoted survival
in the face of ultra high protein intakes. The sudden (in geological terms) switch to the high carbohydrate
diet with the advent of agriculture would have produced disssonace (or as my friend Boyd Eaton says,
"discordance") between genes that previously enhanced survival and a novel environmental pressure (low
protein, high carbohydrate diets).
Cordially,
Loren Cordain, Ph.D. Colorado State University Fort Collins, CO 80523
REFERENCES
75/147 (1998)
1. Neel JV. Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress". Am J Hum Genet
1962;14:353-62. 2. Wendorf M et al. Excavation of the "Thrifty" genotype. Diabetes 1991;40:161-65. 3.
West KM et al. Diabetes in american Indians and other native populations of the new world. Diabetes
1974;23:841-55. 4. Allen JS et al. The non-thrifty genotype. Current Anthropology 1996;37:831-42. 5.
Buikstra JE. The Caribou Eskimo:general and specific disease. Am J Physical Anthropol 1976;45:351-68. 6.
Cassidy CM. Nutrition and health in agriculturalists and hunter-gatherers: A case study of two prehistoric
populations. In: Nutritional Anthropology: Contemporary approaches to diet and culture. Jerome NW,
Kendal RF, Pelto GH (Eds). pp117-146. Bedford Hills, NY: Redgrave. 7. Diamond J. Agriculture's mixed
blessings. In: The Third Chimpanzee. Harper Perennial, NY, 1993, 180-191. 8. Wilmsen EN. Seasonal
effects of dietary intake on Kalahari San. Federation Proceedings 1978;37:65-72. 9. Bronte-Stewart B et al. S
Afr J Lab Clin Med 1960;6:187-. 10. Stefansson V. The Fat of the Land. MacMillan, NY, 1960. 11. Cohen,
M.N. (1987). The significance of long-term changes in human diet and food economy. In: Food and
Evolution. Toward a Theory of Human Food Habits. Temple University Press, Philadelphia, 261-283. 12.
Eaton, S. B. and Nelson, D.A. (1991). Calcium in evolutionary perspective. American Journal of Clinical
Nutrition, 54, 281s-287s. 13. Angel, J.L. (1975). Paleoecology, paleodemography and health. In: Polgar, S.
(Ed.), Population, Ecology and Social Evolution. Mouton, The Hague, 167-190. 14. Nickens, P.R. (1976).
Stature reduction as an adaptive response to food production in Mesoamerica. Journal of Archaeological
Science, 3, 31-41. 15. Lallo, J.W., Armelagos, G.J. and Mensforth, R.P. (1977). The role of diet, disease, and
physiology in the origin of porotic hyperostosis. Human Biology, 49, 471-483. 16. Turner, C.G. (1979).
Dental anthropological indications of agriculture among the Jomon people of central Japan. American
Journal of Physical Anthropology, 51, 619-636. 17.
PALEODIET Archives
Subject: Re: Water Consumption
From: M E Wood
Reply-To:
Date: Mon, 4 May 1998 16:45:52 +1200
If we are talking of lower Paleolithic hominids did they not eat their marrow bones etc by the side of
waterholes or streams? In which case they could drink by lapping or cupping their hands. Cupping their
hands would allow them to keep an eye on approaching predators so would be the better bet.
If we are talking about Upper Paleolithic people they could make containers of leather, since they had awls
and needles, or of birch bark. Leather bottles were in use until the eighteenth or nineteeth century in Europe
and birch bark was a very useful material for containers which could be made waterproof with resin or "tar"
in Northern Eurasia and North America into this century. It would be interesting to find out if rock shelters
caves and open air sites were situated close to sources of water. Though in the case of springs and streams
these would have dried up since.
M E Wood Christchurch New Zealand
PALEODIET Archives
Subject: Role of hunted food in hunter-gatherer diets
Reply-To:
Date: Tue, 5 May 1998 12:44:36 PDT
Loren Cordain's recent post was quite interesting. However, there was one statement that puzzled me:
"Therefore, calories derived from hunted animal foods remains relatively constant in all hunter gatherer
societies regardless of latitude."
It was my understanding from previous postings that the studies show a reasonably large range in this
variable. Is that not the case?
With regard to the relationship with latitude, I wonder if the relationship with respect to role of fishing is
somewhat skewed because the sample may be heavily represented by very high latitude HG groups that rely
greatly on fishing.
76/147 (1998)
I would suspect (and perhaps Loren can answer this) that the sample from the Ethnographic Atlas largely
contains HG groups in the tropics and the very high latitudes, since historic HG groups have been largely
eliminated from the temperate zone.
Steve Meyers
PALEODIET Archives
Subject: Re: Role of hunted food in hunter-gatherer diets
From: Loren Cordain
Reply-To:
Date: Tue, 5 May 1998 15:17:00 -0600
In the last digest, Steve Meyers, asked if there was "a reasonably large range" in the relative percentage of
hunted animal foods in hunter gatherer diets. The answer to this one is a statistical answer (YES), which may
be somewhat misleading. The range of dietary subsistence for HUNTED animal foods is (6-15%) to (86100%), but remember that the statistical range tells us nothing about the distribution of values. For instance
there are only 5 hunter gatherer populations (The Selung, the Yurok, the Karok, the Hupa, and the Wiyot)
out of 181 listed in the Ethnographic Atlas who obtain animal food from HUNTING at subsistence levels of
(6-15%) and remember, this number represents subsistence for animal foods derived from HUNTING only;
it doesnt include animal foods derived from FISHING. As I have mentioned many times in previous posts,
the mean subsistence percentage for animal based foods (both from HUNTING and FISHING combined) for
all 181 world wide hunter gatherer societies is (56-65%); the mode (most frequently occurring value) is (6675%) and the median (middle value for all 181 societies) is (56-65%). Steve also suggested that the sample
may be skewed regarding the increasing role of fishing with increasing latitude. This is not exactly the case
here. I dont want to let all of the cats out of the proverbial bag, before I publish our findings in a scientific
journal, but indeed the sample is skewed, but not necessarily in the way in which Steve suggested. Of the
181 samples, 93 societies are found in a latitude that ranges from the equator to 43 N or S latitude and 88 are
found from a latitude of 45-78 N or S. I am working (as we speak) on frequency histograms by every 10
degrees N or S latitude to fully answer this question. Also, Steve's suggestion that the distribution contains
HG groups largely from the tropics and very high latitudes is also incorrect. Of the 181 societies, 74 are to be
found from 30 N to 45 S (also 30 S to 45 S). Virtually the entire USA can be found between these two
latitudes, so the distribution is not necessarily skewed in this regard either. The ethnographic atlas contains
population information about HG societies which was collected over a long historical period from early
anthropological surveys as well as from more contemporary studies. Obviously, this record is but a small
fraction of all HG societies that have walked the earth, and certainly must be flawed in many respects, but it
clearly represents the largest, most comprehensive listing which is currently available in the literature (of
course unless Andrew can produce another source). Hope this helps to qualify some previously unanswered
questions. I hope to get this manuscript out in with all of the details in the next couple of months.
Cordially,
Loren
PALEODIET Archives
Subject: Re: PALEODIET Digest - 4 May 1998 to 5 May 1998 (#1998-33)
From: Gary Ditta
Reply-To:
Date: Wed, 6 May 1998 08:20:58 -0800
Staffan Lindeberg wrote on 5/5 in response to a question on hemochromatosis by Jennie Brand Miller:
> ...If agriculture arose in the Middle East and spread gradually to Europe, why don't Arabs have an
> even higher prevalence of HH? Supposedly because that particular mutation never took place in that
> population.
77/147 (1998)
This would be the simplest explanation for the HH mutation that is predominant among whites. A more
general question is whether one might not expect other kinds of hemochromatosis mutations in other
racial/ethinic groups that have been exposed to agricultural selection. Not necessarily, but it does seem that
the harder iron overload disease is looked for, the more evident it becomes. It has now been reported as
common (though not so much as the Caucasian form) in both African (1) and Hispanic (2) populations based
on assays involving transferrin saturation (a biochemical measure). It would be interesting to see a similar
analysis carried out on those of middle eastern descent.
I also want to point out to the group that although I did synthesize the evolutionary aspect of HH from
scratch, I was pretty sure similar ideas had to be around among HH researchers. They do seem pretty obvious
once you're familiar with hemochromatosis. Sure enough, yesterday I came across a reference where it is
specifically suggested that HH confers a selective advantage to heterozygotes by protecting against iron
deficiency (3), so not too much credit to me after all. Tracking down this story has got me to wondering,
though, about the extent to which one might be able to paint a broader theoretical picture about the genetic
impact of agriculture by looking at some of the more common inherited metabolic diseases and trying to
visualize scenarios similar to that for HH.
1) Gordeuk et al (1992) N Engl J Med 326: 95-100. 2) Felitti et al (1996) Morbidity Mortality Weekly
Report 45: 991-3. 3) Crawford et al (1995) Am J Human Genet 57(2): 362-7.
Gary
PALEODIET Archives
Subject: Re: Food Scarcity
From: Loren Cordain
Reply-To:
Date: Wed, 6 May 1998 08:59:00 -0600
In my previous post regarding food scarcity and the "thrifty" gene, I completely messed up my reference
numbering in paragraph #3 from cutting and pasting errors. The correct version of that post is as follows:
I would like to respond to Jenny's comment:
78/147 (1998)
Implicit in JV Neel's original "thrifty gene" hypothesis (1) is the assumption that pre-agricultural man must
have gone through regular, periodic episodes of starvation that negatively impacted reproductive potential
and hence resulted in the selection of a gene or genes which would have survival value during the
fluctuations between "feast and famine". This concept is frequently invoked to explain the high incidence of
diseases of insulin resistance (non-insulin dependent diabetes mellitus (NIDDM), hypertension, obesity,
coronary artery disease) among recently acculturated populations (2, 3). John Allen (one of our members - if
he is still listening in the ether) has proposed the existence of a "non-thrifty genotype" (4) which is more
prevalent in westernized populations in which these putative adaptations to feast and famine do not occur.
Although Neel's hypothesis has become "one of the orienting concepts of nutritional and biomedical
anthropology" (4), it is founded upon an assumption which cannot be corroborated by the available
ethnographic data derived from living hunter gatherer populations nor by the fossil record. Indeed, periodic
starvation became more frequent and nutritional status declined when hunter gatherer populations made the
transition to agriculture (5, 6). Diamond has pointed out that starvation among early agriculturalist was quite
common because of the dependence upon a few staple cereal crops (7). If one staple food crop failed,
farmers ran a greater risk of starvation than did hunter gatherers who could utilize a much broader range of
wide plant and animal foods. Modern studies of hunter gatherers show that there is a seasonal fluctuation in
body weight, but these studies do not indicate any evidence of starvation or chronic malnutrition (8, 9). I
havent carefully examined the northern latitude studies, but Stefanson has reported that starvation did not
occur among the Copper Eskimos (10). In a review of 51 references examining human populations from
around the earth and from differing chronologies, as they made the transition from hunter gatherers to
farmers, Cohen (11) concluded that there was an overall decline in both the quality and quantity of life.
Generally, in most parts of the world, whenever cereal based diets were first adopted as a staple food
replacing the rich variety of wild animal and plant based foods of hunter gatherers, there was a characteristic
reduction in stature (11, 12, 13, 14) an increase in infant mortality (6, 11), a reduction in life span (6, 11), an
increased incidence of infectious diseases (6, 7, 11, 15), an increase in iron deficiency anemia (6, 11, 15), an
increased incidence of osteomalacia, porotic hyperostosis and other bone mineral disorders (6, 11, 12, 15)
and an increase in the number of dental caries and enamel defects (6, 11, 16). Clearly, early farming brought
on not a reduced mortality from starvation and nutritionally related diseases, but to the contrary, an increase.
If this is the case, then the advent of agriculture would not have reduced the selection for a thrifty genotype
would have actually increased it. Obviously, population and epidemiological data indicates this is not the
case. Therefore, the assumption that starvation was the single and only factor selecting for a putative "thrifty
genotype" could not be correct. Alternatively, my colleague Jenny Brand Miller (17) has suggested that the
high protein intake of pre-agricultural diets would have represented a more likely environmental pressure
responsible for selecting for multiple genes originally hypothesized by Neel to be "thrifty genes". It is likely
that Neel's concept of "thrifty" is a misinterpretation of the true function of these multiple genes. I refer
interested readers to Jenny's mechanistic explanation for this phenomenon (17) & perhaps she could
comment upon this. By the way, as a matter of interpretation - there seems to be a bit of confusion
concerning my previous post correlating latitude to animal based hunted foods. I indicated that the mean
dietary subsistence percentage for hunted animal foods for world wide hunter-gatherers is 26-35%. This
value is indeed correct - it differs from previous values I have presented in this forum because those values
(56-65%) represented the combined animal foods derived both from hunting and fishing. These data support
Jenny's contention that a high protein diet would have been the norm for our stone age ancestors, and that
this nutritional pressure may have favored the selection of genes which promoted survival in the face of ultra
high protein intakes. The sudden (in geological terms) switch to the high carbohydrate diet with the advent of
agriculture would have produced disssonace (or as my friend Boyd Eaton says, "discordance") between
genes that previously enhanced survival and a novel environmental pressure (low protein, high carbohydrate
diets).
Cordially,
Loren Cordain, Ph.D. Colorado State University Fort Collins, CO 80523
REFERENCES
79/147 (1998)
1962;14:353-62. 2. Wendorf M et al. Excavation of the "Thrifty" genotype. Diabetes 1991;40:161-65. 3.
West KM et al. Diabetes in american Indians and other native populations of the new world. Diabetes
1974;23:841-55. 4. Allen JS et al. The non-thrifty genotype. Current Anthropology 1996;37:831-42. 5.
Buikstra JE. The Caribou Eskimo:general and specific disease. Am J Physical Anthropol 1976;45:351-68. 6.
Cassidy CM. Nutrition and health in agriculturalists and hunter-gatherers: A case study of two prehistoric
populations. In: Nutritional Anthropology: Contemporary approaches to diet and culture. Jerome NW,
Kendal RF, Pelto GH (Eds). pp117-146. Bedford Hills, NY: Redgrave. 7. Diamond J. Agriculture's mixed
blessings. In: The Third Chimpanzee. Harper Perennial, NY, 1993, 180-191. 8. Wilmsen EN. Seasonal
effects of dietary intake on Kalahari San. Federation Proceedings 1978;37:65-72. 9. Bronte-Stewart B et al. S
Afr J Lab Clin Med 1960;6:187-. 10. Stefansson V. The Fat of the Land. MacMillan, NY, 1960. 11. Cohen,
M.N. (1987). The significance of long-term changes in human diet and food economy. In: Food and
Evolution. Toward a Theory of Human Food Habits. Temple University Press, Philadelphia, 261-283. 12.
Eaton, S. B. and Nelson, D.A. (1991). Calcium in evolutionary perspective. American Journal of Clinical
Nutrition, 54, 281s-287s. 13. Angel, J.L. (1975). Paleoecology, paleodemography and health. In: Polgar, S.
(Ed.), Population, Ecology and Social Evolution. Mouton, The Hague, 167-190. 14. Nickens, P.R. (1976).
Stature reduction as an adaptive response to food production in Mesoamerica. Journal of Archaeological
Science, 3, 31-41. 15. Lallo, J.W., Armelagos, G.J. and Mensforth, R.P. (1977). The role of diet, disease, and
physiology in the origin of porotic hyperostosis. Human Biology, 49, 471-483. 16. Turner, C.G. (1979).
Dental anthropological indications of agriculture among the Jomon people of central Japan. American
Journal of Physical Anthropology, 51, 619-636. 17. Brand Miller JC, Colagiuri S. The carnivore connection:
dietary carbohydrate in the evolution of NIDDM. Diabetologia 1994;37:1280-86.
PALEODIET Archives
Subject: Food Scarcity
Reply-To:
Date: Wed, 6 May 1998 10:28:24 +1100
Parts/Attachments:
In his last post Loren Cordain wrote:
'....Neel's hypothesis has become "one of the orienting
concepts of nutritional and biomedical anthropology" .....
So very true, and not just anthropology but nutritional biochemistry and molecular biology too. Just about
every paper on the origins of obesity and diabetes mentions it. It's as if Neel's hypothesis is considered
proven beyond reasonable doubt.
Loren suggested I might elaborate on the mechanisms behind our hypothesis (1) that 'ultra' high protein diets
selected for the insulin resistant genotype rather than cycles of feast and famine (ie the thrifty genotype
hypothesis).
The mechanism relates to both the high protein intake as well as the simultaneously low carbohdyrate intake.
We hypothese that the need to spare carbohdyrate for the brain and fetus which use glucose as their preferred
fuel would have required metabolic mechanisms that re-directed glucose away from the muscles. That's
exactly what insulin resistance does best! What's more insulin resistance in the liver promotes
gluconeogenesis even in the face of the moderate insulinaemia which accompanies high protein meals.
We have had the opportunity to revise the hypothesis for World Review of Nutrition and Dietetics (in press).
Here is the abstract from that paper (I'd appreciate any new feedback):
Insulin resistance may provide valuable insights into past human existence and diet. A critical role is
proposed for the quantity and quality of dietary carbohydrate in the pathogenesis of the insulin resistance and
hyperinsulinemia which characterise the metabolic syndrome, non-insulin-dependent diabetes mellitus
(NIDDM) and heart disease. Our hypothesis, the carnivore connection, proposes that an insulin-resistant
genotype evolved to provide survival and reproductive advantages to populations adapted to a high meat,
low plant food (low carbohydrate) nutritional environment.
80/147 (1998)
Unlike true carnivores, humans have a limited capacity for gluconeogenesis even on a high protein diet.
Insulin resistance would have maximised gluconeogenesis and redirected glucose away from muscles
facilitating the preferential utilisation of glucose by the brain, fetus and mammary gland. But about 10, 000
years ago, following the end of the last Ice Age, carbohydrate intake increased with the development of
agriculture in the Middle East and Europe and the selection pressure for insulin resistance was relaxed.
Hence the prevalence of the insulin-resistant genotype decreased in Europeans and other groups exposed to a
high carbohydrate diet for sufficiently long.
The Mongoloid ancestors of both Pima Indians and Nauruans occupied the Siberian mammoth steppe during
the final 20, 000 years before the end of the last Ice Age. These groups depended on a high meat diet and did
not develop agriculture until 2, 000 years ago. Australian Aborigines never developed agriculture and until
this century ate an animal-based diet. Thus Pima Indians, Nauruans and Australian Aboriginals have had
only recent exposure to a high carbohydrate diet and currently have among the highest rates of NIDDM in
the world. While their traditional carbohydrate foods have a low glycaemic index and stimulate only modest
increases in plasma insulin, westernisation is associated with the intake of refined, high glycaemic index
carbohydrate which results in pronounced postprandial hyperinsulinemia. In this context the insulin resistant
genotype is disadvantageous and predisposes to the development of the metabolic syndrome, NIDDM and
heart disease.
(1) Brand Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of
NIDDM. Diabetologia 37: 1280-1286, 1994.
Best wishes Jennie
NSW 2006 Australia
Phone: (61 2) 9351 3759
Fax: (61 2) 9351 6022
PALEODIET Archives
Subject: Thrifty Genotype
Reply-To:
Date: Wed, 6 May 1998 11:48:12 -0700
Many thanks to Loren Cordain for his interesting post on Neel's idea of the thrifty genotype. I wounder if he
could clear up a point of confusion forme? It was my understanding the the "thrifty genotype" was set up not
to deal with periods of starvation but with a lifestyle in which carbohydrates were in short supply. Thus,
when the rare, high-carbohydrate meal was ingested, the body responded with high insulin production so as
to give the body more time to process and/or store this windfall before it was flushed out by the kidneys.
Also, women with this genotype gave birth to higher birth weight babies.
The two characteristics formed the basis for the selective advantage of the genotype.
So, have I confused this matter and is there a link to general periods of starvation that I have missed?
PALEODIET Archives
Subject: Optimum percentage for animal based foods
Reply-To:
Date: Thu, 7 May 1998 11:39:33 -0400
81/147 (1998)
A question to Loren Cordain: The mean subsistence percentage for animal based foods for all 181 world
wide hunter gatherer societies is 56-65% - does that imply that this is the percentage of animal based foods
we are adapted to? Is this the percentage of meat and fish (+organ meat, bone marrow, blood....) we should
recommend our patients?
Modern man, his digestive tract and metabolism evolved in Africa. There have been some adaptations (to
higher latitudes, to agriculture, ..) in some populations in the last 100.000 - 200.000 years, but the human
genetic constitution has changed relatively little since humans have diverged and migrated from Africa. The
differences between us and our last African ancestor cannot exceed the differences between modern
Europeans and Africans. Isn't there still an African gut under our fair skin?
In modern hunter gatherer societies plant food increases with decreasing latitude. Can mean percentages for
all hunter-gatherer societies (including Eskimos and other populations with nearly 100 % calories derived
from animal food) provide a model for the diet of today=B4s Africans and Mediterraneans? If the mean
percentage for animal foods in African hunter-gatherers is less than 56-65% and if they are representatives of
our ancestors, what's a reasonable percentage for modern humans? An approach to Boyd Eatons values?
Ruediger Hoeflechner
PALEODIET Archives
Subject: Thrifty Genotype vis-a-vis Fasting
Reply-To:
Date: Thu, 7 May 1998 11:54:35 -0500
With the recent discussion on the list in regard to the thrifty genotype hypothesis and periods of starvation,
can anyone offer an evolutionary rationale for why the practice of fasting (intentional, controlled, monitored
"starvation" within safe limits, if you will) should be not merely adaptive in an undependable environment,
but actually beneficial to health? That is what is claimed, at any rate, by numerous alternative health
advocates who claim great things for it and that it "renews" the body. (Analogies are sometimes made with
animals that seasonally fast like hibernating bears, and who (supposedly) live longer than non-hibernating
animals of the same size; caterpillars turning into butterflies while ingesting no food and existing on stored
nutritional reserves; fur bull seals expending enormous amounts of energy at the height of the mating season
while fasting during a time their fertility must be at a high, etc.)
There has been some work by a Scandinavian research group with fasting and arthritis that someone here on
the list provided me a reference about some time back, but I have not gotten around to checking it out.
[Kjeldsen-Kragh et al. "Antibodies against dietary antigens in rheumatoid arthritis patients treated with
fasting and a one year vegetarian diet." Clin Exp Rhematol 1995;13:167-72.]
One hypothesis I have heard suggested is that in itself fasting may be of note not so much for anything it
does on its own, but rather that it simply temporarily eliminates potentially offending foods in the diet that
may be adversely impacting one's metabolism. Thus if one were to subsist on a diet not containing any such
potentially offending foods, the thinking goes that one would see no material difference between the positive
benefits of that vis-a-vis fasting. The standard theory among alternative health advocates, however, is that
fasting has unique things to offer because it "detoxifies" the body. But on the other hand, I have heard it
asserted (unfortunately no one has been able to produce references for this point) that there are clinical
studies showing that the production of certain enyzmes specific to certain detoxification pathways in the
body is negatively impacted by fasting.
Several years ago I did some personal experimentation with lengthy fasting, and seemed to get relief from
symptoms I had been experiencing as well as improvement in sensitive blood sugar. However, I also
experienced fasting to be one of the most extreme physical stresses I have ever experienced. (Some
individuals apparently find it fairly easy, however.) Because of this, I have in retrospect become much more
skeptical and wondered if it is really such a positive thing, and find it difficult to conceive how there could
be any evolutionary justification for it other than as a survival mechanism.
I find this a confusing area and wondered if anyone here has insights to offer regarding evolutionary
adaptation and starvation/fasting that may illuminate the issue. Thanks.
--Ward Nicholson
82/147 (1998)
PALEODIET Archives
Subject: Re: Plant:Animal Subsistence Ratios & Latitude
Reply-To:
Date: Thu, 7 May 1998 11:56:19 -0400
On Monday, 4 May 1998, Loren Cordain wrote: "...latitude had relatively little influence upon the mean
estimated (26-35%) hunted animal food intake for all 181 Hunter Gatherer Societies......Despite a relatively
constant animal food intake in hunter gatherer societies, there is a moderate to strong inverse relationship
between gathered plant foods and latitude...... The relationship of fished animal foods to latitude is a
moderate correlation. So, presumably more and more aquatic based animal are included in the diet to replace
plant foods which decrease in frequency with increasing latitude."
Robert L. Kelly analyzed data from 123 hunter-gatherer societies (not a random sample, biased toward
nontropical environments, and also geographically biased with 77 percent of the cases coming from North
America) with similar results
(1): "For the 123 groups effective temperature and primary production predict the dependence on gathering
quite well (r =3D0.75, p<0.01), however ET and PP do not predict dependence on hunted food very well (r
=3D0.14, p > 0.05)........The use of aquatic resources tends to be higher in colder than in warmer climates.
In general, northern waters are relatively more productive than the adjoining terrestrial environment, perhaps
making the former more attractive than the latter."
His table of hunter-gatherer societies shows, that in Africa there are some hunter-gatherers relying primarily
on plant food (gathering - including small animals? - contributes up to 80 percent to subsistence), but with
increasing latitude hunting and fishing becomes more and more important.
This data refer to modern hunter-gatherers. What about ancient humans? I once again cite Loren Cordain (7
May 1997):
"The fossil record which is obviously incomplete generally doesnt show any evidence of exploitation of the
aquatic environment until about 35, 000 years ago. Clearly, part of the problem is that the technologies
which may have been used to capture fish: nets, lines, weirs and bone hooks likely disintegrated. However,
there should have been a record of fossilized portions (heads, tails, fins etc) of uneaten fish parts along with
other animal foods consumed in the caves and camps of our ancestors......Since humans reached Australia by
50.000-60.000 yrs ago, it can be inferred that they had mastered al least somewhat sophisticated
boating/rafting procedures - it is difficult to believe that they did not exploit the creatures in the medium in
which they sailed. Also, the sites of most of the coastal dwelling people (most likely to have consumed fish)
are now under water and generally unavailable for archaeological exploration. One final comment - optimal
foraging theory would suggest that the aquatic environment would generally not be exploited until more
easily obtained resources (i.e. large easily killed pleistocene beasts) were depleted."
Another very strong argument against an early exploitation of the aquatic environment is the frequency of
fish and shellfish allergies in humans.
260.000 years ago there were already humans (which were not our ancestors) in central Siberia (2) and
Europe. If fishing technologies are recent acquisitions of Homo sapiens, the basis of there subsistence could
only have been hunting.
Are aquatic resources really important for our paleolithic diet? Or: Fish as a brain-specific nutrition with a
significant potential to affect hominid brain evolution?(3) Has Homo erectus been the first sailor (and fishconsumer?) 800.000 years ago?(4).
1) Kelly RL (1995). The foraging spectrum. Diversity in hunter-gatherers lifeways. Washington and London,
Smithsonian Institution Press.
2) Waters MR et al. (1997). Diring Yuriakh. A lower paleolithic site in central Siberia. Science 275:12811284.
3) Broadhurst CL et al. (1998). Rift Valley lake fish and shellfish provided brain-specific nutrition for early
Homo. British Journal of Nutrition 79:3-21.
4) Morwood MJ et al. (1998). Fission-track ages of stone tools and fossils on the east Indonesian island of
Flores. Nature 392:173-176.
PALEODIET Archives
83/147 (1998)
Subject: Subject: Food Scarcity

From: Gary Ditta
Reply-To:
Date: Thu, 7 May 1998 13:36:08 -0800
On 5/6 Jennie Brand Miller wrote:
> Our hypothesis, the "carnivore connection", proposes that an insulin-resistant genotype evolved to
> provide survival and reproductive advantages to populations adapted to a high meat, low plant food
> (low carbohydrate) nutritional environment. ... Unlike true carnivores, humans have a limited
> capacity for gluconeogenesis even on a high protein diet. Insulin resistance would have maximised
> gluconeogenesis and redirected glucose away from muscles facilitating the preferential utilisation
> of glucose by the brain, fetus and mammary gland.
I hope it's not pressing Jennie too much to enquire a bit more about the nature of the selective pressure(s) for
insulin-resistance. Given the biochemical and physiological parameters outlined above, exactly how do you
envision a high protein/low carb/low GI h-g diet being disadvantageous in terms of survival and reproduction
for those lacking insulin resistance? This could have some measure of practical significance for modern-day
individuals thinking of adopting a heavily meat-based h-g diet if they have no tendency toward insulin
resistance.
Gary Ditta
PALEODIET Archives
Subject: Re: Thrifty genotype; Plant animal subsistence ratios & latitude
From: Loren Cordain
Reply-To:
Date: Fri, 8 May 1998 10:05:00 -0600
Let me first respond to Lorraine Heidecker's questions of May 6.
In 1962, JV Neel first proposed that diabetes mellitus might be due to the presence of a "thrifty genotype"
that previously had selective advantage to hunter gatherer populations, but was later rendered detrimental
with the advent of "civilized" or "westernized" environments (1). Neel further hypothesized that this
"genotype" arose as a response to periodic "feast" and "famine" conditions that were presumably endemic in
hunter gatherer societies. Individuals with the "thrifty genotype" were selected, presumably because they
were able to make more efficient utilization of food resources than individuals lacking this genotype. Neel
(2) suggested that members of societies who had the thrifty gene were characterized by increased response of
insulin to ingested food, leading to increased deposition of adipose tissue. This increase in stored energy
would enable such individuals to function better and survive longer during periods of low energy. The thrifty
gene would increase over time and survive as long as there were marked fluctuations in food availability.
Neel did not specifically state that the "thrifty genotype" arose exclusively as a response to carbohydrate
availability in the diet, however he did not necessarily preclude this possibility in part (3). A few likely genes
which may comprise portions of the "thrifty genotype" have been identified, including the gene coding for
the protein, glycogen synthase (4), which facilitates the storage of glucose in skeletal muscle; however, by
and large, the genetic basis for hyperinsulinemia in susceptible populations remains elusive.
REFERENCES
1962;14:353-62. 2. Neel JV. The thrifty genotype revisited. In: The Genetics of Diabetes Mellitus, J
Kobberling and J Tatttersall (Eds). New York, Academic Press, pp 283-93. 3. Spielman RS, Fajans SS, Neel
JV et al. Glucose tolerance in two unacculturated indian tribes of Brazil. Diabetologia 1982;23:90-93. 4.
Schalin-Jantti C et al. Polymorphism of the glycogen synthase gene in hypertension and normotensive
subjects. Hypertension 1996;27:67-71.
Let me respond to Ruediger Hoeflechner's questions:
84/147 (1998)
In a previous post, I mentioned that the mean subsistence percentage for animal based foods for all
181hunter gatherer societies is 56-65%; the mode (most frequently occurring value) is 66-75%, and the
median (middle value) is 56-65%. Ruediger asked, "does that imply that this is the percentage of animal
based foods we are adapted to?". This is a difficult question for which I suspect there is no single answer.
Perhaps insulin resistant individuals will do better on high protein, low carbohydrate diets than individuals
who are more insulin sensitive. O'Dea has conducted at least two preliminary studies which is suggestive that
this may be the case (1, 2). Despite the thousands, perhaps tens of thousands of clinical trials which have
been conducted manipulating the macronutrient (protein, carbohydrate, fat) content of diet, there are perhaps
no more than a half dozen which have examined the influence of a low fat, high protein, low carbohydrate
diet upon human health and metabolism. This is somewhat ironic, in that this macronutrient pattern appears
to be the one which nourished mankind for all of our time on this planet, except fort the last 10, 000 years.
Ruediger asked, "The difference between us and our last African ancestor cannot exceed the differences
between modern Europeans and Africans. Isnt there still an African gut under our fair skin". The answer to
this one is mixed, Yes and No. Yes, our basic physiological gastrointestinal machinery is virtually identical
from one so called "race" to the next. However, there are some important adaptations in gut enzyme activity
and susceptibility to G.I. tract maladies which have evolved in certain racial groups but not others. The
example of adult lactase (actually beta-galactosidases) persistence in caucasians is perhaps the most obvious.
Ruediger also brought up a good point regarding whether or not data from modern hunter gatherers can be
extrapolated to ancient hunter gathers. In the case of plant: animal subsistence ratios; a qualified maybe.
Remember that the average animal based subsistence ratio for modern hunter gatherers, based on data from
the Ethnographic Atlas is 56-65%, however of this amount, about 35% of the total calories are derived from
HUNTED animals and the balance from FISHED animals. Thus, fish make up a substantial percentage of the
animal based subsistence of modern hunter gatherers. As previously mentioned, fish intake increases with
latitude at the expense of plant based foods. Would ancient hunter gatherers have included this much
aquatically based foods in their diet? Probably not, as I have pointed out in past posts, the fossil record
indicates that aquatic environment was generally not exploited until about 35, 000 years ago. So, it seems
that if an animal subsistence ratio of 56-65% would have been maintained during the early and middle
paleolithic, it probably would have had to be maintained by an increased reliance upon hunted animal foods.
Given the low human population density and the high ungulate density during these times, this scenario
certainly appears likely.
1. O'Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic australian aborigines
after temporary reversion ot traditional lifestyle. Diabetes 1984;33:596-603. 2. O'Dea K et al. The effects of
diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II diabetes. J Am
Dietetic Assoc 1989;89:1076-86.
PALEODIET Archives
Subject: Re: Thrifty genotype; Plant animal subsistence ratios & latitude
From: Art De Vany
Reply-To:
Arthur De Vany
Date: Fri, 8 May 1998 11:40:53 -0700
I have long thought that the Neel "Thrifty Gene" hypothesis is lacking a compelling physiological basis, just
in terms of the metabolic processes posited. And I find theJenny Brand Miller "Glucose Sparing" hypothesis
more compelling and more surely based on underlying metabolic processes. Given the lack of evidence of
starvation in the ancient record, the Brand Miller hypothesis gains more credence.
To a non-linear thinker, there is a defect in the dynamics proposed by Neel. It is well known (1) that insulin
resistance increases with the accumulation of body fat. Thus, under the Neel hypothesis, our insulin resistant
ancestors who readily gain fat (and selective advantage) become more insulin resistant and, thus, deposit fat
even more readily. This is an explosive dynamic which we see culminating in NIDDM among insulinresistant people (virtually everyone if the measure is taken against the CHO load imposed by the modern
Western diet).
Were insulin resistance adapted to transitory starvation, it would have a contracting, not an exploding
dynamic. That is to say, insulin resistance (and the associated rate of fat deposition) would decrease rather
than increase with the accumulation of fat.
85/147 (1998)
The other issue that troubles one about the Neel hypothesis is that the evidence Loren Cordain and Jenny
Brand Miller point to indicates there was little carbohydrate in the ancestral diet to trigger the large insulin
response assumed by the Neel hypothesis. A starving ancestor gorging on mammoth would have little insulin
response and would succeed in laying down little fat. The glucose would have to come from
gluconeogenesis, for which humans have small capacity as Jenny Brand Miller points out. Were the glucose
to trigger a sharp insulin response, the brain would get llittle of it and an ancestor with low blood sugar
would be a "sitting duck" for predators.
In contrast, if insulin resistance spares glucose for the brain, then an ancestor lacking CHO in the diet would
conserve the limited glucose derived through gluconeogenesis from the animal-based food for the brain. As
to the consistency of an expansive dynamic in the mapping from insulin resistance to body fat, I do not see
that it conflicts with the glucose-sparing hypothesis, but I haven't thought it through.
This reasoning suggests to me, though I haven't filled in the steps, that few ancients were fat. Obesity is a
modern disease resulting from the CHO load which the modern diet imposes on a metabolism adapted to low
CHO.
Refs. 1. David Bernstein, Dr. Bernstein's Diabetes Solution, 1998. 2. @ARTICLE{ miller:94, AUTHOR =
{Jenny Brand Miller and S. Colagiuri}, TITLE = {The Carnivore Connection - Dietary Carbohdrate in the
Evolution of NIDDM}, JOURNAL = {Diabetologia}, YEAR = 1994, VOLUME = 37, NUMBER = 12,
PAGES = {1288-186}, MONTH = {Dec}
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
PALEODIET Archives
Subject: Stomach cancer
From: Dean Esmay
Reply-To:
Date: Sun, 10 May 1998 12:45:21 -0400
International Journal of Epidemiology 24(1): 33-41 1995
"Dietary Factors and Stomach Cancer: A Case-Control Study in Korea"
Background. Stomach cancer is the most common cancer among Koreans. There is wide agreement that
dietary factors are important in gastric carcinogenesis, but the role of many Korean food items remains
unknown.
Methods. A case-control investigation involving 213 incident cases of histologically confirmed stomach
cancer and an equal number of controls, matched by age (within 2 years) and sex, was conducted from June
1990 to October 1991.
Results. An increased risk of stomach cancer was noted among those with high consumption of stewed foods
such as soybean paste stew and hot pepper-soybean stew, broiled fish, and those who liked salty food.
However, mung bean pancake, tofu (soybean curd), cabbage, spinach, and sesame oil decreased the risk of
stomach cancer. Stratified analysis by salt in combined foods, such as stewed foods and pickled vegetables,
disclosed salt as being an important risk factor. Analysis of cooking methods showed that broiling and
salting increased the risk of stomach cancer, but that frying tended to decrease the risk. These suggest that
the cooking method might modify the gastric carcinogenicity of foods. As non-dietary factors, smoking and a
family history of stomach cancer increased the risk, but use of a refrigerator decreased the risk of cancer.
Conclusions. Heavy salt consumption and cooking methods like broiling and salting seem to play to play a
major role in gastric carcinogenesis among Koreans.
PALEODIET Archives
Subject: Ancestral human diet
Reply-To:
Date: Sun, 10 May 1998 13:32:32 PDT
86/147 (1998)
Ruediger asked, "The difference between us and our last African ancestor cannot exceed the differences
between modern Europeans and Africans. Isnt there still an African gut under our fair skin"?
Back in November 1997 there was an interesting post on this issue by Andrew Millard. For those new to this
list, I attach it below (the comments that Andrew responds to are by Loren Cordain).
At the time, there was no response to Andrew's point. One implication that I get from it is that the diet
subsistence pattern of 20th C HGers living in environments similar to those of the Lower Paleolithic African
populations that Andrew refers to might be a better guide to the pattern that modern humans are adapted for
than an average over 20th C HG groups scattered across a variety of environments (these 20th C groups
might better reflect diet patterns of Upper Paleolithic humans -- post Out of Africa II).
Steve Meyers
---------------------------------------------------Date: Tue, 11 Nov 1997 16:38:51 +0000 From: Andrew Millard
COMMON ANCESTRAL DIET
> Dick Bird questioned the evidence regarding differences between modern man's genome and that of
> paleolithic man. Clearly, the suggestion that there are minimal differences can only be inferred.
> The amount of mitochondrial DNA diversity in various human racial groups from around the world
> has been determined (1), additionally the rate of mitochondrial DNA change can also be estimated
> (1, 2). Based upon this rate of mDNA change, as well as similar nuclear DNA studies (3), the
> genetic differences between humans living 40, 000 yrs ago and those living today ago can be
> estimated. A similar approach has been used to determine if Neanderthals were precursors to modern
> humans or were separate species (4).
But all these studies have been conducted on what are believed to be non-coding unselected parts of the
genome, and cannot be extrapolated to rates of change in parts of the genome which are under selection. A
stronger argument can be built from the following facts:
a) mtDNA and nuclear DNA evidence shows that there has been a recent (100-200ka ago) population
bottleneck follwed by rapid expansion, which explains the lack of genetic diversity amongst modern humans,
and:
b) a conservative reading of the archaeological evidence shows that modern human populations were present
throughout the Old World by 40ka
Thus given our species recent origin, and geographical dispersion, we can argue that there will be no
nutritional selective pressures common to all Homo sapiens. The nutritional niche for which we are selected
will either be that of the founding population, or more or less modified versions of it, varying between
regions. So there may be entire populations or large proportions of populations with genetic adaptations to
local food resources.
As Loren says, we observe some of these:
> there are a number of genotypic differences among various human populations that are known to have
> been elicited by diet (i.e. adult lactase persistence and a variety of hemoglobinopathies, and
> perhaps the degree of insulin resistance/sensitivity) since the agricultural revolution.
> differences may have important health ramifications for modern man.
BUT these are minor variations:
> All humans require similar ranges of both macro and micronutrients and all human groups have
> similar anatomical, physiological and endocrine functions in regard to diet and nutrition. we
> therefore may conclude that: The reason for these similarities is because of our common
> evolutionary experience - we were all hunter gatherers dependent upon wild plants and animals > and these dietary selective pressures shaped our present day nutritional requirements.
When in the past should we look for this palaeolithic diet which is the common inheritance of all humans? It
must be before the population dispersal which allowed regionally varying diets to arise. We cannot then look
at Upper Paleolithic diets, as they are certainly after the dispersal. Accepting the genetic evidence for a
bottleneck mentioned above leads us acceptance an Out Of Africa II scenario rather than a Multiregional
Evolution scenario for the origin of modern humans, and thus to place the dispersal event of interest at c.120100ka. Therefore it is amongst archaic Homo sapiens and possibly late Homo erectus *in Africa* that we
should seek this diet, and probably in some smaller (but as yet undefined) part of Africa.
> I asked: Why do you only go as far back as late Homo erectus?
87/147 (1998)
Essentially I was arguing when our *most recent* common ancestral diet was, which is clearly that of
archaic Homo sapiens in Africa. Homo erectus is another species, although ancestral, and therefore more
removed from us. The late African Homo erectus (sensu lato) were presumably moving towards being like
modern humans, but the further back you go, the more likely it is that the diet was different, particularly
given the glacial-interglacial cycles occurring at the time of H.s. arising from H.e. IT IS QUITE POSSIBLE
THAT THE SPECIATION INVOLVED A DIETARY SHIFT. HENCE i WOULD PREFER TO LOOK AT
OUR OWN SPECIES IF POSSIBLE, and if not then the most closely related part of another species.
Of course if you take the regional continuity hypothesis, then the common ancestral diet is that of early H.e.,
but, given the apparently rapid spread of that species around the world, the best we can do might be to look
at late H. habilis.
Dr. Andrew Millard Department of Archaeology, University of Durham, Tel: +44 191 374 4757 South Road,
Durham. DH1 3LE. United Kingdom. Fax: +44 191 374 3619
PALEODIET Archives
Subject: CHO quality vs quantity
Reply-To:
Date: Sun, 10 May 1998 13:34:41 +0100
At 11.40 -0700 98-05-08, Art De Vany wrote:
> Obesity is a modern disease resulting from the CHO load which the modern diet imposes on a
> metabolism adapted to low CHO.
However, contemporary Trobriand Islanders in Kitava are very lean and obesity is absent despite a
carbohydrate intake which is higher than in Western populations (approximately 70 per cent of calories).
There is food in abundance and no starvation. Low serum insulin levels (extremely well predicted from their
body mass index) which decrease with age suggest rarity or absence of insulin resistance (Lindeberg et al,
submitted).
Possibly, the quality rather than the quantity of carbohydrates is important; carbohydrate-rich foods with a
low glycemic index and a high nutrient density (per energy unit), such as Kitavan tubers and fruit, may be
preferable to cereals and sugar (and potatoes?).
Similar diets were sometimes available during human evolution. Whether they are well tolerated by
westerners with overweight and insulin resistance remains to be tested.
1. Lindeberg S. Apparent absence of cerebrocardiovascular disease in Melanesians. Risk factors and
nutritional considerations - the Kitava Study [M.D. Ph.D.]. University of Lund, 1994. 2. Lindeberg S, Lundh
B. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study
in Kitava. J Intern Med 1993; 233: 269-75. 3. Lindeberg S, Nilsson-Ehle P, Ternt A, Vessby B, Scherstn
B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart
disease - the Kitava study. J Intern Med 1994; 236: 331-40. 4. Lindeberg S, Vessby B. Fatty acid
composition of cholesterol esters and serum tocopherols in Melanesians apparently free from cardiovascular
disease - the Kitava study. Nutr Metab Cardiovasc Dis 1995; 5: 45-53. 5. Lindeberg S, Nilsson-Ehle P,
Vessby B. Lipoprotein composition and serum cholesterol ester fatty acids in non-westernized Melanesians.
Lipids 1996; 31: 153-8. 6. Lindeberg, Berntorp E, Carlsson R, Eliasson M, Marckmann P. Haemostatic
variables in Pacific Islanders apparently free from stroke and ischaemic heart disease - The Kitava Study.
Thromb Haemost 1997; 77: 94-8. 7. Lindeberg S, Berntorp E, Nilsson-Ehle P, Ternt A and Vessby B. Age
relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. AJCN
1997;66:845-52. 8. Srikumar TS, Kllgrd A, Lindeberg S, ckerman PA, kesson B.Trace element
concentration in hair of subjects from two South Pacific islands, Atafu (Tokelau) and Kitava (Papua New
Guinea). J Trace Elem Electrolytes Health Dis 1994; 8: 21-6.
PALEODIET Archives
Subject: Re: Stomach cancer
88/147 (1998)

Reply-To:
Date: Sun, 10 May 1998 19:10:10 +0100
The Korean survey is in line with several studies suggesting that sodium chloride causes stomach cancer.
*Epidemiology and reviews: 1 Cordle F. The use of epidemiology, scientific data, and regulatory authority to
determine risk factors in cancers of some organs of the digestive system. 5. Stomach cancer. Regul Toxicol
Pharmacol 1986; 6: 171-80. 2 Joosens JV, Geboers J. Dietary salt and risks to health. Am J Clin Nutr 1987;
45: 1277-88. 3 Howson CP et al. The decline in gastric cancer: epidemiology of an unplanned triumph.
Epidemiol Rev 1986; 8: 1-27.
*Case-control studies: 4 Coggon D et al. Stomach cancer and food storage. J Natl Cancer Inst 1989; 81:
1178-82. 5 Graham S et al. Diet in the epidemiology of gastric cancer. Nutr Cancer 1990; 13: 19-34. 6 Tuyns
A. Salt and gastrointestinal cancer. Nutr Cancer 1988; 11: 229-32. 7 Haenszel W et al. Stomach cancer
among Japanese in Hawaii. J Natl Cancer Inst 1972; 49: 969-88. 8 Hu J et al. Diet and cancer of the stomach:
a case-control study in China. Int J Cancer 1988; 41: 331-5.
*Experimental studies in rats: 9 Shirai T et al. Effects of butylated hydroxyanisole, butylated
hydroxytoluene, and NaCl on gastric carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine in
F344 rats. J Natl Cancer Inst 1984; 72: 1189-98. 10 Takahashi M et al. Effects of sodium chloride, saccharin,
phenobarbital and aspirin on gastric carcinogenesis with N-methyl-N'-nitro-N-nitrosoguanidine. Gann 1984;
75: 494-501. 11 Kim JP et al. Co-carcinogenic effects of several Korean foods on gastric cancer induced by
N-methyl-N'-nitro-N-nitrosoguanidine in rats. Jpn J Surg 1985; 15: 427-37. 12 Tatematsu M et al. Effects in
rats of sodium chloride on experimental gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine or
4-nitroquinoline-1-oxide. J Natl Cancer Inst 1975; 55: 101-6.
PALEODIET Archives
Subject: Insulin resistance
Reply-To:
Date: Mon, 11 May 1998 10:29:17 +1100
Parts/Attachments:
In a previous post Gary Ditta wrote:
'I hope it's not pressing Jennie too much to enquire a bit more about the
nature of the selective pressure(s) for insulin-resistance. Given the
biochemical and physiological parameters outlined above, exactly how do you
envision a high protein/low carb/low GI h-g diet being disadvantageous in
terms of survival and reproduction for those lacking insulin resistance?'
We postulate that being insulin sensitive when the diet is high protein/low carbohydrate would result in a
degree of hypoglycaemia, nauseousness, vomiting and diarrhea that would compromise brain function and
survival of the foetus.
It is well recognised that humans become phenotypically insulin resistant on exposure to a very high
protein/low CHO diet in order to cope with the surfeit of protein and scarcity of CHO. In fact, many studies
of this nature don't get off the ground because the subjects (Caucasians) cannot tolerate the diet.
Furthermore, all women become insulin resistant during pregnancy to help re-direct glucose way from the
muscles and to boost gluconeogenesis (even on ordinary western diets) so that the foetus has a good supply
of glucose. The foetus uses only glucose from the mother as its energy source, not free fatty acids. If the
mother fails to ingest enough food or carbohydrate, then she becomes ketotic and foetal survival is
compromised (apologies to Dean, he won't agree with me on this one).
89/147 (1998)
Studies in dogs fed low CHO diets show that the mother (bitch) becomes increasingly hypoglycaemic
towards the end of pregnancy and many of the pups are stillborn. The references to all these statements can
be found in our hypothesis paper (1).
I think that being genetically insulin resistant would result in a more profound or more useful type of insulin
resistance that allows the person to reproduce more successfully on a combined high protein/low CHO
intake.
An analogy is to this situation is the effect of the sun on skin colour. In a Caucasian, the sun results in a
phenotypic change in skin colour that is semi-effective in providing protection from the harmful effects of
the sun's rays. But an African person with genetically determined dark skin colour obviously has much better
survival possibilities in circumstances where sun exposure is unavoidable. Any feedback is very welcome
Best wishes Jennie
NSW 2006 Australia
Phone: (61 2) 9351 3759
Fax: (61 2) 9351 6022
PALEODIET Archives
Subject: Re: Sodium and cancer
From: Loren Cordain
Reply-To:
Date: Mon, 11 May 1998 10:31:00 -0600
90/147 (1998)
In a previous post, Staffan and Dean noted that there is strong experimental as well as epidemiological
evidence to incriminate dietary salt (actually sodium) in the etiology of stomach cancer. Less well
appreciated is the evidence to suggest that dietary sodium may act as a universal promoter of multiple
cancers separate from the gastrointestinal tract. Although the notion that dietary sodium may influence the
development of a wide variety of cancers may at first seem to be unfounded, there is sufficient data from a
number of lines of evidence to point to this connection. There is a well established link between dietary
sodium and hypertension. Therefore, if sodium is somehow related to the promotion of cancer, there should
be an epidemiological relationship between hypertension and cancer mortality. And indeed there is, although
the information is relatively obscure and unrecognized. I have included 4 references (1, 2, 3, 4) which show
this link. Certainly, epidemiological studies cannot establish cause and effect, and the relationship could
simply be a spurious one existing because of confounding variables. In the four studies which show the
correlation between oncogenesis and hypertension, no attempt was made to mechanistically explain the
relationship. In human hypertension, there is a well documented increase in the intracellular Na+
concentration. In basically what amounted to a meta analysis, Hilton (5) reviewed 20 studies (involving 965
hypertensives and 1, 857 controls) and found the pooled data revealed an increased (p<0.001) intracellular
erythrocyte sodium concentration in the hypertensives. A more recent study (6) utilizing sophisticated NMR
analyses has shown that dietary salt loading caused intracellular sodium to increase in all subjects, whereas
in salt sensitive subjects there were additional elevations cytosolic free calcium and suppression of
intracellular pH and free magnesium levels. More than 20 years ago, Cone (7, 8) pointed out that sustained
lowering of the transmembrane potential initiates the mitogenic process and that processes which reduce
activity of the sodium pump in the cell surface membrane will initiate and sustain mitosis. A prediction of
Cone's model is that the intracellular concentration of sodium will be elevated in rapidly dividing normal and
tumor cells. Burns and Rozengurt (9) have shown that sodium influx is a necessary event in the mechanism
whereby peptide growth factors stimulate initiation of DNA synthesis and that changes in Na fluxes
influence the movement of other ions, namely K+ and H+. Thus, sodium fluxes universally represent an
early mitotic event whereby quiescent cells are stimulated to proliferate. There is a wealth of information in
the hypertension literature to show that the expanded extracellular fluid volume brought about by ingestion
of sodium chloride likely causes an increase in endogenous natriuretic substances which inhibit the sodium
pump (10) which ultimately leads to the increased intracellular sodium concentrations demonstrated in
hypertensive subjects. It is likely that this same mechanism alters the ionic flux in cancer patients. Should
dietary sodium inhibit the sodium pump, then it would be reasonable to expect to find elevated sodium
concentrations in a wide variety of tumor cells. Indeed, this is the case (11, 12, 13, 14, 15). An additional, but
not so convincing line of evidence is the observation made by many early 20th century frontier doctors
treating unacculturated peoples (who generally had limited access to dietary sodium) was the general
absence of all types of cancer (16). In summary, a lifetime of high (relative to our evolutionary levels)
dietary sodium tends to inhibit the Na/K ATPase pump via endogenous natriuretic factors; the inhibition of
the pump changes ionic flux across the membrane such that intracellular Na and Ca levels are increased; and
K+, Mg+, H+ levels are reduced. Changes in intracellular ionic concentrations are necessary early events in
both mitosis and oncogenesis causing quiescent cells to proliferate. Interested readers can find more on this
topic by my friend Birger Jansson who is the originator of this fascinating concept (17).
Cordially,
Loren Cordain, Ph.D. ESS Dept Colorado State University Ft. Collins, CO 80523 (970) 491-7436 FAX (970)
491-0445
References
91/147 (1998)
1. Goldbourt, U., Holtzman E., Yaari, S., Cohen, L. Katz, L. & Neufeld, H.N. (1986). Elevated blood
pressure as a predictor of long-term cancer mortality: analysis by site and histologic subtype in 10, 000
middle-aged and elderly men. Journal of the National Cancer Institute, 77: 63-70. 2. Khaw, K., BarrettConnor, E.B. (1984). Systolic blood pressure and cancer mortality in an elderly population. American
Journal of Epidemiology, 120: 550-558. 3. Dyer, A.R., Stamler, J., Berkkson, D.M. et al. (1975). High blood
pressure: a risk factor for cancer mortality? Lancet, 1: 1051-1064. 4. Svardsudd, K., Tibblin G. (1979).
Mortality and morbidity during 13.5 years' follow-up in relation to blood pressure. Acta Medica
Scandinavica, 205: 483-92. 5. Hilton, P.J. (1986). Cellular sodium transport in essential hypertension. New
England Journal of Medicine, 314: 222-29. 6. Resnick LM, Gupta RK, Difabio B, Barbagallo M, Mann S,
Marion R, Laragh JH. (1994). Intracellular ionic consequences of dietary salt loading in essential
hypertension. Journal of Clinical Investigation, 94: 1269-1276. 7. Cone, C.D. (1971). Unified theory on the
basic mechanism of normal mitotic control and oncogenesis. Journal of Theoretical Biology, 30: 151-81. 8.
Cone, C.D. (1974). The role of the surface transmembrane potential in normal and malignant mitogenesis.
Annals of the New York Academy of Sciences, 238: 420-35. 9. Burns CP, Rozengurt E. (1984).
Extracellular Na and initiation of DNA synthesis: role of intracellular ph and K. The Journal of Cell Biology
98: 1082-89. 10. Kramer, H.J., Meyer-Lehnert, H., Michel, H., Predel H. G. (1991). Endogenous natriuretic
and ouabain-like factors. Their roles in body fluid volume and blood pressure regulation. American Journal
of Hypertension, 4: 81-89. 11. Pieri, C., Giuli, C., and Bertoni-Freddari, C. (1983). X-ray microanalysis of
monovalent electrolyte contents of quiescent, proliferating as well as tumor rat hepatocytes. Carcinogenesis,
4: 1577-81. 12. Zs. Nagy et al. (1983). Correlation of malignancy with the intracellular Na+:K+ ratio in
human thyroid tumors. Cancer Research 43: 5395-5402. 13. Davies, R.J. et al. (1987). Sodium transport in a
mouse model of colonic carcinogenesis. Cancer Research, 47: 4646-50. 14. Davies, R.J. et al. (1990).
Uncoupling of sodium chloride transport in premalignant mouse colon. Gastroenterology, 98: 1502-08. 15.
Zs. Nagy et al. (1981). Intracellular Na:K ratios in human cancer cells as revealed by energy dispersive x-ray
microanalysis. The Journal of Cell Biology 90: 769-777. 16. Stefansson V. (1960). Cancer: Disease of
Civilization? New York: Hill & Wang. 17. Jansson B. Geographic cancer risk and intracellular
potassium/sodium ratios. Cancer Detection and Prevention 1986;9:171-94.
PALEODIET Archives
Reply-To:
Date: Mon, 11 May 1998 10:54:48 +1100
Thanks Art for your comments. I'm so pleased to hear someone agrees with me in this era of the thrifty
genotype.
On the suject of fat, deposition, I have a hunch that it is the COMBINATION of high fat and high GI
carbohdyrate that triggers weight gain. When we eat this type of meal (which is most of the time), the insulin
stimulated by the high GI carbohdyrate (mainly wheat flour and potatoes by the way, not sugar), the body's
response is to switch off lipolysis in the adipose tissue stores (this is one of the most important functions of
insulin) so that free fatty acids are no longer secreted into the bloodstream. Glucose becomes the main source
of fuel when insulin is high. This means that the fat in the meal needs to be 'tucked away' somewhere to
await oxidation when insulin levels decline. We all know where it gets tucked away. What's more, the
adipose tissue is staying put while ever insulin levels remain high.
Because insulin resistant individuals have an extremely pronounced insulin response to CHO feeding
(especially high GI CHO), insulin levels remain high for longer and free fatty acids remain unoxidised for
longer. Over the course of years this imbalance in CHO/fat oxidation lends itself to a steady accumulation of
body fat.
I think very high CHO, low fat diets 'work' (in limiting weight gain) partly because they are generally bulky,
satiating and hard to ingest in excess, but partly because they mean that there is less fat to be 'tucked away',
for burning later on.
We have rat experiments in progress at the moment to test this hypothesis.
Best wishes Jennie
92/147 (1998)
PALEODIET Archives
Subject: From: Art De Vany
Reply-To:
Arthur De Vany
Date: Mon, 11 May 1998 12:23:32 -0700
Further support for the linkages posited by Jenny Brand Miller between insulin resistance and fecundity
comes from this study by my colleagues here at Univ of Cal, Irvine. In this case the evidence is of the effects
of a surfeit of CHO, rather than a deficit. In two groups of women with gestational diabetes, large gestational
age infants tend to be borne by women who are on higher CHO diets. Large gestational age infants are
difficult children to birth, risky both to the mother and the child. Consistent with the "carnivore-connection"
hypothesis, insulin resistant females would be poor procreators in a CHO abundant environment and would
have a selective advantage were CHO scarce. (Abstract from PubMed follows.)
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Obstet Gynecol 1998 Apr;91(4):600-604
The effects of carbohydrate restriction in patients with diet-controlled gestational diabetes.
Major CA, Henry MJ, De Veciana M, Morgan MA
University of California, Irvine Medical Center, Department of Obstetrics and Gynecology, Orange 92686,
USA.
OBJECTIVE: To determine the effect of carbohydrate restriction on perinatal outcome in patients with dietcontrolled gestational diabetes mellitus (GDM). METHODS: Women with diet-controlled GDM were
divided non-randomly into two groups based on their dietary carbohydrate content: those with low dietary
carbohydrate content (below 42%) and those with high dietary carbohydrate content (exceeding 45%).
Subjects kept dietary accounts and were followed with daily fasting and postprandial glucose assessments.
Subjects also were tested daily for urinary ketones. Glycosylated hemoglobin, mean fasting and postprandial
glucose values, incidence of macrosomia and large for gestational age (LGA) infants, cesarean deliveries for
cephalopelvic disproportion and macrosomia, and need for insulin therapy were compared between the
groups. RESULTS: The two groups were identical in terms of demographic characteristics. Significant
reductions in the postprandial glucose values were seen among subjects in the low-carbohydrate group (P <
.04). Fewer subjects in the low-carbohydrate group required the addition of insulin for glucose control (P <
.047; relative risk [RR] 0.14; 95% confidence interval [CI] 0.02, 1.00). The incidence of LGA infants was
significantly lower in the low-carbohydrate group (P < .035; RR 0.22; 95% CI 0.05, 0.91). Subjects in the
low carbohydrate group also had a lower rate of cesarean deliveries for cephalopelvic disproportion and
macrosomia (P < .037; RR 0.15; 95% CI 0.04, 0.94). CONCLUSION: Carbohydrate restriction in patients
with diet-controlled GDM results in improved glycemic control, less need for insulin therapy, a decrease in
the incidence LGA infants, and a decrease in cesarean deliveries for cephalopelvic disproportion and
macrosomia.
PALEODIET Archives
Subject: The Trobriand Islanders Paradox
From: Art De Vany
Reply-To:
Arthur De Vany
Date: Mon, 11 May 1998 12:36:58 -0700
Staffan Lindeberg made this very interesting point:
"However, contemporary Trobriand Islanders in Kitava are very lean and obesity is absent despite a
carbohydrate intake which is higher than in Western populations (approximately 70 per cent of calories).
There is food in abundance and no starvation. Low serum insulin levels (extremely well predicted from their
body mass index) which decrease with age suggest rarity or absence of insulin resistance (Lindeberg et al,
submitted).
93/147 (1998)
Possibly, the quality rather than the quantity of carbohydrates is important; carbohydrate-rich foods with a
low glycemic index and a high nutrient density (per energy unit), such as Kitavan tubers and fruit, may be
preferable to cereals and sugar (and potatoes?)."
I wonder if Staffan could indicate something of the nature of the physical activties, and their patterns over
the season and by age, of these islanders. Surely, their fitness would be a factor so that, even with a very high
CHO intake, they might retain their insulin sensitivity. Is it not also true that insulin resistance increases as
body fat accumulates, particularly in the abdominal area? Might not the leanness of these peoples be a
factor? If they are active, have adequate lean body mass, and (therefore) retain insulin sensitivity, then
perhaps the Trobriand Islanders Paradox can be explained. The quality of the food may also be a contributing
factor, as this assures a good lean body mass among all ages.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
PALEODIET Archives
Subject: Body fat and cold climate
Reply-To:
Date: Wed, 13 May 1998 12:09:41 +1100
I would like to know what people think of the idea that a tendency to gain extra body fat may be a survival
stategy to cope with cold temperatures, rather than periodic starvation.
If animals that occupy the coldest parts of our planet such as whales and seals have large deposits of fat for
this reason, it may have been helpful to humans too. It may even explain the disposition to put the fat around
the abdomen, thereby insulating the heart and other organs.
Is there any scientific evidence in humans of differences in ability to survive cold temperatures as a function
of body fat? I wonder if two groups of people of similar BMI but different waist-to-hip ratios have different
capacities to cope in cold tempertures.
PALEODIET Archives
From: John Martinson
Reply-To:
Date: Thu, 14 May 1998 11:19:48 -0700
Two comments in response to Jennie Brand's recent post on cold climates and body fat: 1. I think the idea
that seals and whales live in one of the coldest climates might be challenged by oceanographers and
climatologists. The whales are obligate ocean dwellers, the seals facultative, but in either case the ocean is
nowhere close to the terrestrial temperatures in the polar regions. The penguins of Antarctica would be a
better species choice. And they go IN and OUT of the water in addition to surviving brutal temperatures. But
I think the focus should be on conditions affecting HEAT loss rather than TEMPERATURE. Whatever the
temperature, the conductivity of water is the crucial factor compared to air. I believe people have succumbed
to hypothermia in the summer in the Sierra Nevada after falling into a cold mountain stream and coming out
with soaking wet clothing just as a serious (though not necessarily cold) wind comes up.
94/147 (1998)
2. While penguins probably have fat layers I doubt they compare with whale blubber. But most animals
adapted to cold do have less exposure of their extremities. In hot climates the reverse is functional, e.g., the
large ears of elephants which serve as cooling surfaces, esp. important for large animals like elephants since
body surface expands as the square of body dimensions while mass (and therefore metabolic heat capacity)
expands as the cube of linear dimensions. Whatever their body fat content, I suspect that modern penguins
are descended from species with much greater wing surfaces (relative to body mass) than the extant
penguins.
An analogous argument has been presented in regard to human evolution, i.e., the tall thin Masai have a
greater surface to mass ratio than short stocky Aleuts, Eskimos, or Yakuts--but how good is the data unless it
reflects a comprehensive view of many ethnic groups over a wide geographic range?
John Martinson Facilities Planning Univ of Nevada-Reno
PALEODIET Archives
Subject: Re: Body fat and cold climate
From: Art De Vany
Reply-To:
Arthur De Vany
Date: Thu, 14 May 1998 16:14:28 -0700
Jenny asked:
"If animals that occupy the coldest parts of our planet such as whales and seals have large deposits of fat for
this reason, it may have been helpful to humans too. It may even explain the disposition to put the fat around
the abdomen, thereby insulating the heart and other organs.
Is there any scientific evidence in humans of differences in ability to survive cold temperatures as a function
of body fat? I wonder if two groups of people of similar BMI but different waist-to-hip ratios have different
capacities to cope in cold tempertures."
It is on the basis of this sort of argument that the Aquatic Ape hypothesis was constructed (there was a
popular book with this title by a journalist, whose name I forget). Humans have abdominal fat, it is
subcutaneous, and widely distributed. I doubt anyone on the list would subscribe to the Aquatic Ape theory,
but it does fit the stylized facts about human fat distribution.
On the other hand, I have seen citations that give the body fat percentage of male Eskimos at 11.5%. Not
different from, and perhaps even a bit lower, than other HGs in warmer climates.
Also, many individuals who carry large amounts of fat have reduced capacity for thermogenesis and have
virtually inactive brown adipose tissue, hardly the relationship one would expect were fat depots an Ice Age
survival strategy.
In line with Jenny's question, I doubt that our ancestors beyond 15 thousand years back were fat. The few
Venus figures that might be evidence of obesity are only of females and could have been stylized or rare
instances. There are no cave drawings between 15, 000 and 30, 000 years ago of obese males or females. It is
difficult to put on fat in a world of scarce carbohydrate and only moderate amounts of seasonally available
animal fat. The Paleolithic activity patterns, which mix intermittent intense activities (which release growth
hormone, an antagonist to insulin) with a high basal activity rate would have made the attainment of obesity
rare. This is precisely the kind of food and activity pattern that would have made insulin resistence a useful
adaptation.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
PALEODIET Archives
Subject: Body fat and heat
From: Dick
Reply-To:
Date: Fri, 15 May 1998 10:26:34 +0100
95/147 (1998)
> Jennie Brand Miller wrote

> I would like to know what people think of the idea that a tendency to gain extra body fat may be a
> survival stategy to cope with cold temperatures, rather than periodic starvation.
It seems to me there is a possibility that the extra body mass, far from protecting the body against cold, will
in fact cool it down, for two reasons.
First the extra fat will act as a heat sink, absorbing heat produced by the body. This is familiar to fat people
because their layers of fat are not warm but cold, once equilibrium with a cold environment has been
established.
The supply of heat to the extra fatty tissue will reduce heat available for the rest of the body, and therefore
produce a lower temperature in the body as a whole.
Second, the envelope of the body grows in area with more mass (albeit proportional to the sqare root of the
mass) and so more heat is lost to the environment.
These points both of course assume constant heat output by metabolism and constant distribution by heart
action. It is possible that fat people can metabolise faster, though I would have thought the reverse was true,
otherwise they would not be fat in the first place.
It is also possible that exercise given to the heart by carrying the extra body mass around (like running with a
back pack on, except it is a stomach one) will develop its muscular power and thus increase its output.
Whales and other mammals carrying fat as a sepcies may be adapted to some benefits; however this would
not seem to argue for specific advantages for the fatter individual members of a species.
Dick Bird School of Behavioural and Environmental Sciences University of Northumbria Newcastle upon
Tyne NE1 8ST
PALEODIET Archives
Subject: Re: Body fat and heat
From: Dean Esmay
Reply-To:
Date: Sat, 16 May 1998 17:00:15 -0400
Dick Bird wrote:
> Second, the envelope of the body grows in area with more mass (albeit proportional to the sqare
> root of the mass) and so more heat is lost to the environment.
Dick may want to rethink his physics. Fat people should have less surface area for every kilogram of body
mass than thin people. The amount of fat will grow much faster than the skin needed to contain it. In this
sense extra fat would provide a warming effect.
That said I have never seen any meaningful correlation between body fat and warm or cold climates. -=The mind is not a vessel to be filled. It's fire to be lit. - Plutarch
PALEODIET Archives
Subject: Surface area and heat loss
From: Dick
Reply-To:
Date: Mon, 18 May 1998 11:50:41 +0100
Dean Esmay riposted
> Subject: Re: Body fat and heat
> Dick Bird wrote:
> Second, the envelope of the body grows in area with more mass (albeit proportional to the sqare
> root of the mass) and so more heat is lost to the environment. Dick may want to rethink his
> physics. Ouch! Fat people should have less surface area for every kilogram of body mass than thin
> people. The amount of fat will grow much faster than the skin needed to contain it. In this sense
> extra fat would provide a warming effect. Ah! but I went on to say: These points both of course
> assume constant heat output by metabolism and constant distribution by heart action.
96/147 (1998)
I wasn't arguing that there would be MORE heat loss per pound mass, there will obviously be less. But if we
assume heat production is constant then heat loss from the organism increases with mass.
What reason is there for assuming greater production of heat in fat people? In the light of known facts about
IBAT, not much I would contend.
************************************************
"Ye canna change the laws of physics" - Scotty.
************************************************
Dick Bird School of Behavioural and Environmental Sciences University of Northumbria Newcastle upon
Tyne NE1 8ST
PALEODIET Archives
Subject: Re: The Trobriand Islanders Paradox
Reply-To:
Date: Tue, 19 May 1998 22:52:52 +0100
The level of physical activity of Kitavans was roughly estimated at 1.7 multiples of the basal metabolic rate
(BMR) [1]. BMR multiples for westerners with low occupational activity level who are non-active at leisure
time is 1.4 for both sexes, while moderately active persons at work as well as during leisure time is 1.7 for
males and 1.6 for females [2]. For 18-30 year old Kitavan males the estimated energy expenditure was 9.4
MJ, while their estimated total daily calorie intake from diet history was 9.2 MJ. Energy expenditure
decreased with aged in both populations. In the Swedish population self reported physical activity during
work and leisure time were each coded to a three-point scale (low, medium and high level of physical
activity) using a questionnaire [3].
Men spend their time gardening, relaxing, fishing, building houses, carving and playing football (soccer),
while women most of the time are weaving, cooking, gardening, relaxing or washing clothes. The two single
most common activies are gardening and sitting still. The annual variation of physical activity is
considerable, particularly for men. It seems to decrease slightly with age in both sexes. Individual levels of
physical activity were not assessed.
Although the precision in the calculated energy expenditure is low, it is obvious that Malinowski's statement
that "half of the natives' working life is spent in the garden" [5] will falsely suggest that Kitavan life is filled
with hardship. On the other hand, if "working life" means time for production of food, clothing and houses,
Malinowski's figure seems accurate.
The given figure of estimated energy expenditure is too uncertain to admit any strict comparison with other
traditional populations or with westerners [6]. Nevertheless, by modern western standards, the annual mean
level of physical activity appears high, although a considerable proportion of western labourers evidently
work more strenuously and have less time for leisure activities. Furthermore, the leisure activities of many
westerners are quite heavy and time-consuming.
In conclusion, the mean level of physical activity was higher in Kitava than in Sweden, although overlapping
between the two populations appears considerable (which it was not for leanness). Although the higher level
of physical activity may explain some of the beneficial health status of Kitavans, diet appears even more
important. Unfortunately this is not much more than a guess because our survey methods preclude any
detailed judgement.
A fairly low level of physical activity has been the rule among many traditional populations, particularly
hunter-gatherers and tribal horticulturalists, who have spent an average of three hours or less each day on
food production [7-10]. On the one extreme, a female Machiguenga of the Amazon dug up enough tubers in
one hour to feed 25 adults for one day [11]. On the other extreme we find populations living in deserts, the
Arctic or similar marginal habitats and who have spent more than seven hours a day hunting or gathering [7].
The very high level of physical exercise exerted by the Tarahumara Mayans of Mexico [12] can hardly be
considered representative for traditional human populations. Loren may however not agree on this last one
[13].
97/147 (1998)
Physical activity undoubtedly exerts a number of potentially beneficial effects on cardiovascular risk factors,
including reduction of blood pressure, body weight and waist to hip ratio, and elevation of HDL-C [14].
Higher levels of physical activity are furthermore prospectively associated with lower mortality [15, 16].
Besides its possible genuine effects, exercise may facilitate an adequate intake of essential nutrients by way
of increased energy expenditure [17]. Nevertheless, available evidence do not suggest that exercise is as
efficient as dietary changes to lower body weight [14] or blood pressure [18] and exercise alone is apparently
insufficient to fully prevent insulin resistance [4]. My personal impression from cross-cultural surveys is not
that a high level of physical activity is a necessary condition for very low rates of IHD.
As for fitness, this is very difficult to evaluate. Does fitness give health or does health give fitness?
Best wishes, Staffan
1. McNeill G. Energy. In: Garrow JS, James WPT, ed. Human Nutrition and Dietetics. Edinburgh:
Edinburgh, 1993: 24-37. 2. Department of Health. Dietary Reference Values for Food, Energy and Nutrients
for the United Kingdom.London: HMSO, 1991 3. Eliasson M, Asplund K, Evrin P-E. Regular leisure time
physical activity predicts high activity of tissue plasminogen activator: the Northern Sweden MONICA
Study. Int J Epidemiol 1996; 25: 1182-8. 4. Eriksson J, Taimela S, Koivisto VA. Exercise and the metabolic
syndrome. Diabetologia 1997; 40: 125-35. 5. Malinowski B. Argonauts of the Western Pacific.London:
Routledge & Kegan Paul Ltd, 1922 6. Leslie PW, Bindon JR, Baker BT. Caloric requirements of human
populations: a model. Human Ecology 1984; 12: 137-60. 7. Hayden B. Subsistence and ecological
adaptations of modern hunter-gatherers. In: Harding RDS, Teleki G, ed. Omnivorous primates: gathering and
hunting in human evolution. New York: Columbia University Press, 1981: 344-421. 8. Sahlins M. Stone Age
Economics.Chicago: Aldine, 1972 9. Taylor CB, Ho KJ. Studies on the Masai. Am J Clin Nutr 1971; 24:
1291-3. 10. Lee RB. What hunters do for a living, or, how to make out on scarce resources. In: Lee RB,
DeVore I, ed. Man the hunter. Chicago: Aldine, 1968: 30-48. 11. Johnson A, Behrens CA. Nutritional
criterioa in Machiguenga food production decisions: a linear-programming analysis. Human Ecology 1982;
10: 167-89. 12. Groom D. Cardiovascular observations on Tarahumara Indian runners--the modern Spartans.
Am Heart J 1971; 81: 304-14. 13. Cordain L, Gotshall RW, Eaton SB. Evolutionary aspects of exercise.
World Rev Nutr Diet 1997; 81: 49-60. 14. Chandrashekhar Y, Anand IS. Exercise as a coronary protective
factor. Am Heart J 1991; 122: 1723-39. 15. Shaper AG, Wannamethee G, Weatherall R. Physical activity
and ischaemic heart disease in middle-aged British men [published erratum appears in Br Heart J 1992
Feb;67(2):209]. Br Heart J 1991; 66: 384-94. 16. Sandvik L, Erikssen J, Thaulow E, Erikssen G, Mundal R,
Rodahl K. Physical fitness as a predictor of mortality among healthy, middle-aged Norwegian men [see
comments]. N Engl J Med 1993; 328: 533-7. 17. strand PO. Physical activity and fitness. Am J Clin Nutr
1992; 55(6 Suppl): 1231S-1236S. 18. Arroll B, Beaglehole R. Does physical activity lower blood pressure: a
critical review of the clinical trials. J Clin Epidemiol 1992; 45: 439-47.
At 12:36 -0700 98-05-11, Art De Vany wrote:
> Staffan Lindeberg made this very interesting point:
> "However, contemporary Trobriand Islanders in Kitava are very lean and obesity is absent despite a
> carbohydrate intake which is higher than in Western populations (approximately 70 per cent of
> calories). There is food in abundance and no starvation. Low serum insulin levels (extremely well
> predicted from their body mass index) which decrease with age suggest rarity or absence of insulin
> resistance (Lindeberg et al, submitted). Possibly, the quality rather than the quantity of
> carbohydrates is important; carbohydrate-rich foods with a low glycemic index and a high nutrient
> density (per energy unit), such as Kitavan tubers and fruit, may be preferable to cereals and
> sugar (and potatoes?)." I wonder if Staffan could indicate something of the nature of the physical
> activties, and their patterns over the season and by age, of these islanders. Surely, their
> fitness would be a factor so that, even with a very high CHO intake, they might retain their
> insulin sensitivity. Is it not also true that insulin resistance increases as body fat
> accumulates, particularly in the abdominal area? Might not the leanness of these peoples be a
> factor? If they are active, have adequate lean body mass, and (therefore) retain insulin
> sensitivity, then perhaps the Trobriand Islanders Paradox can be explained. The quality of the
> food may also be a contributing factor, as this assures a good lean body mass among all ages.
PALEODIET Archives
Subject: Food scarcity
From: Dick Dawson
Reply-To:
98/147 (1998)

Date: Sun, 31 May 1998 06:16:34 -0400
Andrew wrote:
[..]
> It seems to me that for there to be a selective effect it does not have to be starvation to death
> but a level of starvation which prevents successful reproduction. Any capacity to reproduce in the
> face of food shortages would be advantagous.
From studies of physical anthro and human variation, Syracuse Univ. courses:
This is about 'evolution' which might better be understood as 'adaptation'.
Anthropologists identify 4 forces of evolution: 1. mutation 2. natural selection 3. gene flow 4. gene drift
1. Mutation is the rise of genetic changes in a population of a species. These are changes in DNA occuring
during meiosis: the formation of reproductive cells.
most relevant to this discussion:
2. Natural selection has been known as 'survival of the fittest' but might better be considered as differential
reproductive success. The key here is 'differential'. If a genetically transmitted characteristic allows even a
slightly greater number of offspring who in turn produce a slightly greater number of offspring that
characteristic will survive and dominate. Some characteristic might be present in small quantity in a
population for many generations but rather abruptly increase in frequency due to some shift in environment.
An example might be some ability to thrive on grain based diet that might respond favorably to a shift from
h-g subsistence to grain farming.
3. Gene flow is the phenomenon of sharing of genes throughout a large area population. It's the reason that
man is exactly 1 species on this planet.
4. Gene drift is a sampling error that results from sufficiently long total isolation of a part of a species'
population from the rest of the species. Random mutation can cause an isolated population to change to a
different species. Gene drift would prevent sharing of genotype with the rest of the original population.
> immediate question: do these overweight captive animals also suffer from diabetes?
Can studies of these animals be made?
> Jennie also wrote:
> It puzzles me that humans could become taller and taller throughout the paleolithic while
> simultaneously being exposed to fluctuating but significant periods of starvation. I'd like to
> hear your comments? Adult height is determined both genetically and by childhood nutrition so that
> with increasing nutrition in the western world today each generation is taller than the last.
I've seen informal publication drawn apparently from research papers claiming that increases in height in
Japan are due to massive increases in meat and milk in infant and child diet.
PALEODIET Archives
Subject: Evolutionary Fitness
From: Art De Vany
Reply-To:
Arthur De Vany
Date: Tue, 9 Jun 1998 17:12:47 -0700
I have posted on the web the diet and fitness theories that I developed in my research for my (nearly
finished) book: Evolutionary Fitness.
The diet and activity models are a blend of ideas from complex adaptive systems theory and evolution. A lot
of guidance to the research literature on the diet side came from this group (though nothing I have seen in the
research has changed the diet I have followed for some 15 years).
The key strategies and a precise of my book along with a short preview of chapter 1 may be accessed from
URL:
http://www.socsci.uci.edu/mbs/personnel/devany/EvolutionaryFitness.html
I would be interested in comments and even vigorous criticism.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
99/147 (1998)
PALEODIET Archives
Subject: Does Animal Protein Increase Calcium Excretion?
Reply-To:
Date: Thu, 11 Jun 1998 09:03:27 EDT
In the March American Journal of Clinical Nutrition, 67: 438-444, 1998, there is a study entitled "Dietary
Protein Intake and Urinary Excretion of Calcium: A Cross-Sectional Study in a Healthy Japanese
Population."
They found that animal protein increases calcium excretion--but are the numbers significant? Quote from
page 441 of the study:
"From the multiple regression equations contained, it was estimated that an increase in urinary calcium
excretion was 1-2 mg with a 1 gram increase in protein catabolized to energy."
And did the Paleodiet, probably high in animal protein, cause osteoporosis?
Question: how much of protein is catabolized to energy? The calcium loss was only significant after
adjustments for other variables in the elderly Japanese (50-79 yo subjects.) Their muscle mass is probably
lower than younger people, who would use more protein to maintain lean mass.
More importantly, even if you are eating 50 grams more protein than your body needs, is the loss of 50 to
100 mg of calcium significant? The same can be lost from habitual coffee consumption.
Populations that have eaten five pounds of meat or more per day when settling the West did not show any
evidence of osteoporosis. It is this kind of data that makes me question whether this study of elderly Japanese
should really have us that concerned.
Robert Crayhon
PALEODIET Archives
Subject: Re: More on: "1. Does Animal Protein Increase Calcium Excretion?"
From: Loren Cordain
Reply-To:
Date: Thu, 11 Jun 1998 15:48:00 -0600
In the last paleodiet post, Robert Crayhon discusses the issue of high protein and bone loss in the diets of our
hunter gatherer ancestors. Three recent papers which also concern the topic of high dietary protein intake and
bone loss are:
1. Heaney RP. Excess dietary protein may not adversely affect bone. J. Nutr 1998; 128:1054-57. 2. Massey
LK. Does excess dietary protein adversely affect bone? Symposium overview. J Nutr 1998;128:1048-50. 3.
Barzel US, Massey LK. Excess dietary protein can adversely affect bone. J Nutr 1998;128:1051-53.
100/147 (1998)
Heaney et al (1) concluded that if the calcium to protein ratio (mg:g) is greater than or equal to 20, then there
is probably adequate protection for the skeleton. Using an assumed plant:animal subsistence ratio of 35:65,
the Ca:protein ratio for modern diets based upon stone age food categories (fruits, vegetables, and lean meats
including fish, poultry, shellfish, game meat and organ meats), would be about 2.47. If one assumes a
subsistence ratio exactly opposite (65% plant and 35% animal), as my colleague Boyd Eaton has (4), and use
his wild plant and animal food data base, then the Ca:protein ratio would be 6.29 for stone age humans. The
median Ca:protein ratio for 50-59 year old women as shown using NHANES III data is 9.30 (1). From these
data, it appears tha it would be virtually impossible for stone age man, living in his native environment,
eating wild plant and animal foods to have come remotely close to a dietary Ca:protein ratio equaling or
exceeding 20. Paradoxically, the fossil record shows stone age man to have thick bones with large cortical
cross sectional areas (5). Consequently, it is likely that the skeleton of stone age man and woman would have
been more robust and fracture resistant than that of western, industrialized men and women (5, 6). How
could this apparent paradox be possible? Stone age men and women did not consume supplemental dietary
sodium chloride, which like protein can also cause an increased calciuresis (7) and loss of bone mass (8).
Further, the Ca:Mg ratio was about 1:1 in pre-agricultural diets, whereas in western diets it can be as high as
4:1 (9). High dietary calcium can can cause magnesium deficiencies, even when normal levels of magnesium
are ingested (10). Because supplemental magnesium appears to prevent bone fractures and can result in
increased bone density (11), it is possible that the high consumption of dairy products, at the expense of
magnesium rich fruits and vegetables may unexpectantly result in a reduced bone mineral density.
Additionally, bone mass is also dependent upon the relative acid/alkaline dietary load (2, 3). Acid generated
by the diet is excreted in the urine and can cause calciuresis. Meat and fish have a high potential renal acid
load (PRAL) whereas fruits and vegetables have a negative PRAL, meaning they reduce acid excretion. The
human kidney cannot excrete urine with a pH lower than 5; consequently the acids (mainly phosphate and
sulfate) of acid producing foods such as meats, fish and some cereals must be buffered partially by calcium
which is ultimately derived from the skeleton (2, 3). Because fruits and vegetables can act as alkaline buffers
for the acids derived from meats and fish, they have been recently shown to decrease urinary calcium
excretion even when dietary protein and calcium were constant (12). Thus, the high levels of fruits and
vegetables that stone age people consumed, may have partially counteracted the calciuretic efffects of high
protein diets. Finally, our stoneage ancestors would have likely had higher plasma levels of vitamin D than
modern man because of their greater exposure to sunlight. Vitamin D, synthesized in the dermis via
ultraviolet radiation enhances calcium absorption and can prevent bone loss. Lastly, because our ancestors
were more active than modern man (6), their increased activity levels may have also improved their bone
mass despite a high protein intake.
Cordially,
Loren Cordain, Ph.D. ESS Dept Colorado State University Fort Collins, CO 80523
REFERENCES
4. Eaton SB et al. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med
1985;312:283-89 5. Ruff CB et al. Post cranial robusticity in Homo 1. Temporal trends and mechanical
interpretation. Am J Phys Anthrop 1993;91:21-53. 6. Cordain L et al. Evolutionary aspects of exercise.
World Rev Nutr Diet 1997;81:49-60. 7. Nordin BEC et al. The nature and significance of the relationship
between urinary sodium and urinary calcium in women. J Nutr 1993;123:1615-22. 8. Devine A et al. A
longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal
women. Am J Clin Nutr. 1995;62:740-5. 9. Varo P. Mineral element balance and coronary heart disease. Int
J Vit Nutr Res 1974;44:267-73. 10. Evans GH, Weaver CM et al. Association of magnesium deficiency with
the blood-lowering effects of calcium. J Hypertension 1990;8:327-337. 11. Sojka JE, Weaver CM.
Magnesium supplementation and osteoporosis. Nutr Rev 1995;53:71-74. 12. Appel LJ et al. A clinical trial
of the effects of dietary patterns on blood pressure. N Engl J Med 1997; 336:1117-24.
PALEODIET Archives
Subject: Animal protein and Ca excretion
Reply-To:
Date: Fri, 12 Jun 1998 09:32:04 +1100
101/147 (1998)
In the last post, Robert Crayhon suggests that the apparent increase in Ca excretion with diets that are high
protein may not be biologically important. I agree with him.
Early hunter-gatherers would have obtained huge quantities of calcium from the bones of small animals. We
analysed the foods consumed by the Wopkaimen people in Papua New Guinea in the 1980's (1). Their foods
included very tiny birds, frogs, fish etc that they cooked over the ashes and the WHOLE animal was
consumed including the bones which softened by the high heat (but even raw they were not hard to eat). We
found that the Ca content was 1000-4000 mg/100g wet weight of food. This is higher than milk and dairy
products and it would have been a highly absorbably form of Ca.
Best wishes Jennie
(1) Brand JC, Thomas De, Hyndman D. Composition fo the subsisteance fodd of the Wopkamin people of
Papua New Guinea. PNG Medical J 1991; 34:35-48.
PALEODIET Archives
Subject: Exceptional new web site
From: Dean Esmay
Reply-To:
Date: Tue, 23 Jun 1998 13:18:00 -0400
The following is a link to a new academic web site devoted to discussion of evolution and the human diet:
http://www.cast.uark.edu/local/icaes/index.html
The group also hosts their own discussion group. This appears to be a high-quality site. -=The mind is not a vessel to be filled. It's fire to be lit. - Plutarch
PALEODIET Archives
Subject: Honey, alcohol, famine, cooking, insects, toxic plants
From: Sean McBride
Reply-To:
Date: Tue, 14 Jul 1998 02:07:57 -0400
I am a new member of the list and have just finished reading the archives (both fascinating and at times
confusing). I would like to comment on some of the points raised:
Honey- Since here in Australia native bees produce about 1.5 kg of honey compared to around 50 kg from an
introduced native bee (1) perhaps the usage wasnt as great as we might think. (Although Jenny Brand Miller
would be much more knowledgeable on this). I am aware that honey was something of a staple of
Aboriginal people in the Kimberleys (2), yet Meehan (3) gives figures for the Anbarra diet of Arnhem Land
of 6 kg of honey consumed out of a total diet of 2280 kg of food consumed for April, 1973: and 2 kg out of
2101 for May, with none consumed in January. Of course store bought sugar and other factors may have
affected traditional consumption patterns. Meehan also cites Bose (4) with a figure of 15 kg of honey out of
1144 kg total food consumed in one month for the Onge people of Little Andaman Island.
Perhaps an overlooked form of sweetness is the nectar of flowers, widely used by Australian Aboriginal
people. In my experience large amounts of nectar may be obtained from Grevillia spp, banksia spp and
Xanthorrhoea spp and others. The flower is generally tapped on to the palm of the hand and the nectar licked
off. This use of flowers leads to my next subject
Alcohol -complicated technology is not needed to produce alcohol. Roth (5) mentions an alcoholic brew,
prepared by soaking blossoms (of Banksia from memory) in bark containers. Isaacs (4) mentions a drink
called mangaitju which was made by soaking the flower heads of grass trees (Xanthorrhoea spp.) in water
and allowing it to ferment for several days. Basedow (6) also mentions a cider like drink from Pandanus
spiralis. The cider gum of Tasmania (Eucalyptus gunni) is known to have supplied a potent alcoholic drink
for Tasmanian Aborigines (7).
102/147 (1998)
Nutritional Stress and Famine Loren Cordain and others mentioned a lack of evidence for famine. I am not
sure how common famine was, but nutritional stress does seem to have been fairly common as evidenced by
harris lines in bone, dental hypoplasia and Cribra orbitalis (8) indicating inadequate food supplies at certain
times of the year, anaemia and other nutritional stresses. Perhaps this would have some bearing on the thrifty
genotype debate in that those able to withstand the greater nutritional deficiencies survived compared to
those who died from nutritional stresses. Simplistic I know but others more knowledgeable than myself
might comment.
Cooking The simplest cooking method I have used involves simply heating rocks in a fire, digging a hole,
lining it with paper bark. In 2 hours (or sooner depending on heat of fire) the rocks are placed in the whole
with tubers and meat. The tubers are sliced in 2 cm thicknesses to cook them through and the meat (animals
such as chickens, ducks, or rabbits are gutted) has hot rock/s put in the abdominal cavity as well as around it.
The pit is covered with bark and sealed with dirt. The food is ready in 2 hours allowing other work to be
done in the meantime without having to watch the food. I dont know how much archaeological trace this
would leave, since no ashes or coals are in the pit, and the rocks can be reused till they break up. I have also
used this method in the initial stages of detoxifying Moreton Bay Chestnut (Castanospermum australe) a
rainforest Aboriginal food.
Poisonous plants Cycads (Cycas spp.) were a staple but very poisonous unless processed. Beck (9) mentions
that naturally aged seeds of cycad were sometimes eaten after careful selection (without processing) since
ageing diminished the poison content. If this is the case then our ancestors may have been eating what appear
to us to be poisonous plants but in reality are not if the seeds are aged. The selection of less toxic seeds
involves smelling them. Since no processing would be involved nothing would turn up in the archaeological
record.
Insects As to insects in the diet...many people around the world consume insects but not so much in the west.
In a classic study by Bernton and Brown (1967) extracts of seven common food infesting insects were
utilised in skin sensitivity tests of subjects with and without known allergies. The insects were the rice
weevil, Indian meal moth, lesser grain borer, confused flour beetle, red flour beetle larvae and adults,
sawtoothed grain beetle and the fruit fly (I can supply scientific names for those interested). The results were
as follows:
Of the 230 allergic patients, 68 (29.6%) reacted positively to one or more of the dialized insect extracts.
Surprisingly of the 194 non-allergic subjects 50 (25.8) showed sensitivity to at least one extract. A total of
333 positive reactions were observed. The degree of overall sensitivity was practically the same for both
groups, with the Indian meal moth extract eliciting the most positive reaction...these allergies (of the nonallergic group) are (likely) the result of ingesting small quantities of insect material in food over a lifetime.
So does this mean that insect eating is in the same boat as lactose intolerance (although to a lesser/greater
degree) in that we have not been eating them long enough to have adapted to the proteins etc contained in
them?. Also are other people around the world with a longer history of insect consumption better able to
handle them.?
Thanks for a great list. Sean McBride Australia
References 1) Heard, Tim (1996). Stingless Bees. Nature Australia, Spring 1996:51-55. 2) Isaacs, J (1987)
Bush Food. Weldons. Sydney 3)Meehan, Betty (1982). Shell Bed to Shell Midden. Australian Institute of
Aboriginal Studies. Canberra. 4)Bose, S.(1964) Economy of the Onge of Little Andaman. Man in India
44:289-310 5)Roth W.E. (1903) Notes of savage life in the early days of West Australian
settlement..Proceedings of the Royal Society of Queensland 17: 45-69 6)Basedow, H.(1918) Narrative of an
expedition of exploration in North West Australia. Proceedings of the Royal Geographical Society. XV111
7)Low, T.(1988) Wild Food Plants of Australia. Angus and Robertson. Sydney. 8)Webb, S.(1995)
Palaeopathology of Aboriginal Australians. Health and disease across a hunter gatherer continent.
Cambridge University Press. Cambridge. 9)Beck, W. (1985) Technology, Toxicity and Subsistence.
Unpublished PhD thesis, Division of Prehistory, LaTrobe University, Victoria 10) Bernton H.S. and H.
Brown (1967). Insects as potential sources of ingestant allergens. Annals of Allergy 25:381-387.
PALEODIET Archives
Subject: Re: Honey, alcohol, famine, cooking, insects, toxic plants
Reply-To:
Date: Wed, 15 Jul 1998 09:55:25 +1000
103/147 (1998)
A big welcome to Sean McBride who obviously has a lot more practical experience than some of us 'ivory
tower' types (maybe I'm the only one!).
Re the honey issue, I don't think that Betty Meehan's study can give us a true sense of how much honey was
eaten, given that refined sugar was in plentiful supply to this group and they satisfied their hunger for
sweetness in this way. I agree that the only cap on honey consumption would have been the extent of
availability. While the native bees may have produced much less than domestic bees, there seems to have
been plentiful hives and thousands of bees in each hive. The honey ant was also a source of concentrated
sweetness and as, Sean says, flowers were a source of sugars as well. I have also read references to the fact
that fermented flower water was consumed as a beverage. I don't have the expertise to comment on the
allergy paper but I'm not sure if allergy tests to whole insects are appropriate when the proteins are digested
to amino acids before absorption. Loren Cordain could comment here but he is out of email contact as
present.
Best wishes Jennie
PALEODIET Archives
Subject: Re: Honey, alcohol, famine, cooking, insects, toxic plants
Reply-To:
Date: Thu, 16 Jul 1998 08:55:41 +0100
On Wed, 15 Jul 1998 Jennie Brand Miller wrote:
> I don't have the expertise to comment on the allergy paper but I'm not sure if allergy tests to
> whole insects are appropriate when the proteins are digested to amino acids before absorption.
> Loren Cordain could comment here but he is out of email contact as present.
But allergies to foods develop mostly as antigens to the proteins in foods. Allergy tests for people with, for
example, eczema, are conducted on whole foods and seem to successfully identify the foods which are
causing the allergic reaction. Antigenic reactions need not only be to proteins, but could arise from peptide
fragments, and other complex molecules including secondary metabolites, which can be absorbed.. However
the whole food approach to identifying allergens is likely to give some false positive results because, as
Jenny says, many components of food will be digested and unavailable to become antigens, and these may
include substances which mimic antigens from other sources.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Human evolution in China
From: Dean Esmay
Reply-To:
Date: Sun, 19 Jul 1998 09:44:28 -0400
Here's a fascinating web site:
http://www.cruzio.com/~cscp/index.htm -=Diplomacy is saying "nice doggy" until you find a rock.
PALEODIET Archives
Subject: crops
104/147 (1998)
From: Bronwen Humphreys

Reply-To:
Date: Tue, 25 Aug 1998 12:03:54 +0100
An interesting question was recently forwarded to me via email. Has any source ever seriously examined the
question of why humans would have gravitated toward cereal grains as a primary crop for agriculture? Do
these plants yield a superior caloric density or protein content to other vegetation, such as tubers?
Grains have a higher protein content than many tubers, (wheat about 10g per 100g compared to 2g for
potatoes) but I believe that potatoes will support the greater number of people per acre planted. (I just
remember this from a lecture, I'm afraid I don't have any references).
I would imagine that grains are easier and more compact to store and carry around as you are considering a
dried product. Tubers are very bulky.
Bronwen Humphreys
PALEODIET Archives
Subject: Grains vs. other foods
From: Dean Esmay
Reply-To:
Date: Sun, 23 Aug 1998 17:38:33 -0400
An interesting question was recently forwarded to me via email.
Has any source ever seriously examined the question of why humans would have gravitated toward cereal
grains as a primary crop for agriculture? Do these plants yield a superior caloric density or protein content to
other vegetation, such as tubers?
PALEODIET Archives
Subject: grains vs tubers
From: Bob Pastorio
Reply-To:
Date: Mon, 24 Aug 1998 16:51:43 -0400
Automatic digest processor wrote:
> Has any source ever seriously examined the question of why humans would
> have gravitated toward cereal grains as a primary crop for agriculture? Do
> these plants yield a superior caloric density or protein content to other
> vegetation, such as tubers?
I don't know of any research on the subject but would like to offer some speculations and consideration.
Grains are little self-contained units that require no special storage conditions beyond a reasonable dryness.
They remove themselves from their husks with the most minimal of processing once dehydrated. They are
tidily portable and virtually any mobile person, children included, can easily carry enough for several days
eating. Dehydrated, they provide a rather dense source of nutrients with merely the addition of water to make
them edible. Or, they can be ground and used for other kinds of foods. You can see the crop you will get and
can plan accordingly. Grains can be harvested several times during a temperate climate growing season and
the straw has other uses as well including thatching, bedding and fodder. Grasses can grow on thin soil.
105/147 (1998)
Tubers are wet and therefore heavy. To transport them, they either need to be carried with all their water still
in them or they need to be processed to remove the water and that adds labor and time to the pre-preparation.
Tuber developement and therefore crop size can't be tracked during the growing season because they're
buried. Storing tubers can be a tricky process in a very low technology society. Currently, I'm of the
impression that tubers produce less available tonnage per unit of ground than grains; it may be that in the
technological past that could have been different. Tubers require plowing, burial of cuttings and weeding.
Plowing is mandatory in most soils to get maximum yields. Tubers can be harvested only once in a single
growing season. Tops of tuberous plants don't offer many other uses and are, in some cases, toxic. Tubers
require friable soils for good growth and yields.
Bob Pastorio
PALEODIET Archives
Reply-To:
Andrew Millard
Date: Wed, 26 Aug 1998 08:50:06 +0100
On Mon, 24 Aug 1998 Bob Pastorio wrote:
> Automatic digest processor wrote:
> Has any source ever seriously examined the question of why humans would have gravitated toward
> cereal grains as a primary crop for agriculture? Do these plants yield a superior caloric density
> or protein content to other vegetation, such as tubers? I don't know of any research on the
> subject but would like to offer some speculations and consideration. Grains are little
> self-contained units that require no special storage conditions beyond a reasonable dryness. They
> remove themselves from their husks with the most minimal of processing once dehydrated.
This is not true of the primitive wheats (e.g. spelt and emmer). They were not free-threshing like modern
wheats (e.g. bread and durum wheats). However this is an advantage for storage, as grain with its glume still
attached can be stored successfully at higher moisture contents than free grain. The Romans introduced bread
wheat to Britain, but they also had to introduce the corn-drier to process the grain before storage.
Does anyone know the processing and storage properties of primitve or wild versions of the other major
cereal crops (after wheat come rice, maize, barley and sorghum)?
The rest of your argument seems sensible to me. I would add that the edible crop and the seed crop are one
and the same for grains, but not necessarily for tubers. It may also be worth considering the location of the
transition to agriculture. For the Near Eastern case, it is thought that some sort of increasing pressure on
resources, perhaps including climatic changes, led grass harvesting peoples to become grass planting ones in
an environment where the choice of resources was limited by climate and neighbouring populations. My
impression is that tubers have been domesticated in environments which are not so marginal, and where there
is a greater diversity of food resources available, so that they are not the initial crops to be domesticated.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Tubers vs Grains
Reply-To:
Date: Wed, 26 Aug 1998 09:07:46 +1100
Hi Everyone,
106/147 (1998)
It may also be relevant that one has to eat 400 g of potato or 1 kg carrots to get 250 calories but only 100 g
bread (round figures). People find it difficult to eat so much bulk (its too satiating). Most tubers are not as
starchy as potatoes and yield much less energy. If hunter-gatherers needed 3000 cal a day, they wouldn't get
a great deal of this from tubers.
Best wishes Jennie
PALEODIET Archives
From: Melissa Darby
Reply-To:
Date: Wed, 26 Aug 1998 09:21:58 -0700
Date: 25 August 1998 From: Melissa Darby Subject: grains vrs tubers
I have done research on the tuber of the Sagittaria latifolia. It is a wetland plant that grows in standing water
in ponds and lakes or along a wet shoreline. I would like to respond to Bob's discussion on this subject.
He stated that grains are little self-contained units that require no special storage conditions beyond a
reasonable dryness.
Sagittaria l. tubers contain about 50% water, and dry readily to a hard nugget similar to a bean. Ddried tubers
need to be soaked before they are cooked, or the tuber can be ground into a flour. It is very starchy, and
resembles a potato in taste and texture when fresh. Sagittaria l. tubers are light and easy to transport once
dehydrated.
Sagittaria l. tubers are harvestable from October through mid-May on the lower Columbia River, with a less
productive time during the February high water in some of the patches that are adjacent to or connected to
the river. The Chinook people harvested the tubers in the fall when they were first ready, and continued
harvest through the winter according to Lewis and Clark. My experiments suggest that efforts during the fall
and spring are the most cost effective; the winter harvest was cold and the water was high.
The tubers are harvested by wading into the pond and with ones feet, agitating the silty soft substrate that the
tubers are suspended in, at which time they are released from the substrate, and float to the surface of the
water. Ducks geese and swans use this method to obtain them. Many of the First Americans reported
harvesting the tubers in this manner. Cosmopolitan in distribution, Sagittaria l. is found from Nova Scotia to
British Columbia, and south to the Great Basin, Mississippi Delta, and Florida. A close relative is found in
China, Siberia, Poland and other sites in Europe.
According to Bob 'Tubers are wet and therefore heavy'. The Chinook made their winter villages in the
wetlands of the river, perhaps to take advantage of several resources including Sagittaria l. tubers, waterfowl
and muskrats. The third most common mammal bone found in archaeological sites of the area is muskrat
(after elk and deer). They did not need to be transported in this context very far. However, they could be
transported while they are drying out or dry, they are not 'fragile' and can dry slowly or quickly with little
spoilage. Fresh tubers cook in ten minutes in hot ashes or by boiling. They do not need to be trimmed or
peeled.
Bob also mentioned that 'Tuber development and therefore crop size can't be tracked during the growing
season because they are buried." I check the patch by pulling one up, and that tells me how far along they
are. When the plant's biomass dies back, the tubers are at their largest. The bigger the plants, the bigger the
tubers. The average weight of the tubers from my latest work is 13.3 grams based on a harvest of 231 tubers
in a very productive patch that had big plants, no cattle in the area and no carp (both are predators). This was
in a 3 meter by 3 meter area. The average below-ground primary productivity of Sagittaria l. tubers is
between 600-800 fresh grams per meter. However not all float at any one time.
It was also mentioned that storing grains can be tricky. Storing Sagittaria l. tubers was done in pit cellers by
the Chinook, in sheds by the Klamath (recent). Some people in the mid-west dried it on strings in the eaves
of their houses.
It was mentioned that the tops of tubers are often toxic. Not the case with Sagittaria l. which had medicinal
uses, and could be used for tea, forage for horses. Cattle eat it when they have access to it.
107/147 (1998)
On the lower Columbia River, Sagittaria l. tubers grow in a silty soil which overlays a grey 'gley' clay.
Wetland soils are of course wet. Nutrients, especially nitrogen are added to the water by waterfowl
excretions.
Sagittaria l. tubers are a wild food and need no plowing, weeding, planting. On the lower Columbia and
elsewhere it grows in solid monocultures, like a crop, very thick. It looks like a corn field except the leaves
are a different shape and the plants reach a height of about 1 meter. Sagittaria trifolia grows in Japan and
China. The tubers are grown as a crop and used as food, and the foliage is used to feed cattle. Wetlands are
highly productive, more productive than grasslands.
I want to put Sagittaria l. tubers on the radar screen of those who study paleolithic diet so that we may now
be able to look for evidence of its use. Sagittaria tubers have been found in boggy deposits a Calowanie, a 9,
000 y BP site in the Polish Plain (Kubiak-Martens 1996). This is the first evidence for the possible use of
plant foods other than hazel nuts or water-chestnuts in the diet of hunter-gatherers on the North European
Plain during the Palaeolithic and Mesolithic. There may have been a similar pattern in North America. Tuber
fragments of Sagittaria species have also been found in coprolites from Dryden Cave, Nevada and perhaps in
Lovelock Cave (Neumann et al 1989).
As the ice was melting at the end of the last glaciation, wetlands were prolific; one of the pioneer plants that
spread to the recently glaciated disturbed region was Sagittaria latifolia, which is spread by waterfowl (the
seeds are consumed by the birds, and also have a barb and a sticky surface which sticks to the skin on the
legs of waterfowl). As the wetlands dried up, the plant was not as prolific. Wetlands produce more calories
per square meter than grassland. If it was indeed present and prolific in the environment of North America
10, 000 y BP, Sagittaria l. tubers would have been good food for people, and the leaves good forage for
Mammoths. It is currently grown in China for forage, and cattle are known to be very fond of it. When the
ice sheet melted, and the wetlands shrunk, this food and forage would have become limited as well. The
implications are...
I would be interested in feedback on the possible use of this plant by the First Americans and/or Mammoths.
I have some pollen data to support the contention that this plant was prolific, but I would like more data that
either refutes this theory or supports it. Since stone tools or fire cracked rock are not indicators of its use, it is
generally invisible in the archaeological record.
Neumann, Alan, Richard Holloway and Colin Busby 1989 Determination of prehistoric use of arrowhead
(Sagittaria, Alismataceae) in the Great Basin of North America by scanning electron microscopy. Economic
Botany 43(3) 1989, pp 287-296.
Kubiak-Martens, L. et al. Evidence for possible use of plant foods in Paleolithic and Mesolithic diet from the
site of Calowanie in the central part of the Polish Plain. Kubiak-Martens, L.; Vegetation History and
Archaeobotany (1996) 5:33-38.
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Wed, 26 Aug 1998 16:36:58 -0400
The following reference was recently emailed to me:
http://www.vegan-straight-edge.org.uk/GW_paper.htm
I have not had time to do more than glance at it yet, won't for at least another week, so it may be silliness or
may be interesting. Rather than sit on it I thought I'd go ahead and post the reference. Highly speculative
stuff but an interesting bibliography. -=- Anger will never disappear so long as thoughts of resentment are
cherished in the mind. Anger will disappear just as soon as thoughts of resentment are forgotten.
Buddha (B.C. 568-488)
PALEODIET Archives
From: Dean Esmay
Reply-To:
108/147 (1998)
Date: Wed, 26 Aug 1998 17:03:37 -0400

Er, I retract the "may be silliness" comment, I hadn't noticed that it was a reprinted article from a peerreviewed source. (Mumbling excuses about fine print.) It's probably not silliness. I really need to find more
time in the day. -=- Anger will never disappear so long as thoughts of resentment are cherished in the mind.
Anger will disappear just as soon as thoughts of resentment are forgotten.
Buddha (B.C. 568-488)
PALEODIET Archives
Reply-To:
Date: Thu, 27 Aug 1998 06:14:22 -0400
Some data about the productivity of wild-grass seeds From: Harlan, Jack R. (1989). Wild-grass seed
harvesting in the Sahara and Sub-Sahara of Africa. In: Foraging and farming: the evolution of plant
exploitation (Harris, DR & Hillman GC, eds). London, Unwin Hyman:
Over 60 species of grasses have been harvested for their grains in Africa. Most of these are famine or
scarcity foods or are harvested casually and opportunistically. Several species, however, have provided food
on a massive scale and have been staples for a number of tribes.
Natural stands of wild grass can give very respectable yields of high-quality food. Yields of 500-800 kg/ha
are not uncommon and 1 ton/ha can occasionally be obtained. This is in the range of many subsistence
farmers growing domesticated cereals and as much or more than farmers in England obtained from
domesticated wheat in the Middle Ages. Harlan cites Chevalier, who described an African wild-grass harvest
and stated that one adult could easily gather 10 kg in a mornings effort. In an experiment with wild einkorn
wheat in Turkey Harlan himself yielded almost 1 kg of pure-grain equivalent per hour of work, and the
grains were far more nutritious than domesticated wheat. This wild wheat harvest returned 40-50 kcal of
energy for every kcal expended. Harlan stated, that this was far more efficient in terms of the ratio of
consumable output energy to energy expended in harvesting than any form of agriculture so far studied.
Another interesting question is the toxicity of many tubers. In the following article Jones hypothesizes that
the first farmers may have preferred toxic plants. Maybe less susceptibility to pests is one reason why in
many parts of the world cereals are a primary crop for agriculture?
Jones DA (1998). Why are so many food plants cyanogenic? Phytochemistry 47(2):155-162
Abstract: A disproportionately large number of the most important human food plants is cyanogenic. The
accumulated research of numerous people working in several different disciplines now allows a tenable
explanation for this observation. Cyanogenesis by plants is not only a surprisingly effective chemical defence
against casual herbivores, but it is also easily overcome by careful pre-ingestion food processing, this latter
skill being almost exclusive to humans. Moreover, humans have the physiological ability to detoxify cyanide
satisfactorily, given an adequate protein diet. It appears that early in the domestication of crop plants the
cyanogenic species would have been relatively free of pests and competitive herbivores, as well as having
good nutritional qualities, and thus ideal candidates for cultivation by the first farmers.
PALEODIET Archives
Subject: grains vs. tubers
From: Rick Strong
Reply-To:
Date: Thu, 27 Aug 1998 07:38:06 -0400
The following appears in Guns, Germs, and Steel, the Fates of Human Societies, by Jarred Diamond, (Norton
1998):
109/147 (1998)
" Instead of being enclosed in a poppable pod, wild wheat and barley seed grow at the top of a stalk that
spontaneously shatters, dropping the seeds to the ground where they can germinate. A single-gene mutation
prevents the stalks from shattering. In the wild that mutation would be lethal to the plant, since the seeds
would remain suspended in the air, unable to germinate and take root. But those mutant seeds would have
been the ones waiting conveniently on the stalk to be harvested and brought home by humans. When humans
then planted those harvested mutant seeds, any mutant seeds among the progeny again became available to
the farmers to harvest and sow, while normal seeds among the progeny fell to the ground and became
unavailable. Thus, human farmers reversed the direction of natural selection by 180 degrees: the formerly
successful gene suddenly became lethal, and the lethal mutant became successful. Over 10, 000 years ago,
that unconscious selection for nonshattering wheat and barley stalks was apparently the first major human
"improvement" in any plant. That change marked the beginning of agriculture in the Fertile Crescent."
Diamond, p. 120.
PALEODIET Archives
Subject: grains v tubers
From: Dick
Reply-To:
Date: Thu, 27 Aug 1998 11:40:08 +0100
On Wed, 26 Aug 1998 08:50:06 +0100 Andrew Millard said
> Subject: grains vs tubers
> The rest of [the] argument seems sensible to me. I would add that the edible crop and the seed
> crop are one and the same for grains, but not necessarily for tubers. It may also be worth
> considering the location of the transition to agriculture. For the Near Eastern case, it is
> thought that some sort of increasing pressure on resources, perhaps including climatic changes,
> led grass harvesting peoples to become grass planting ones in an environment where the choice of
> resources was limited by climate and neighbouring populations. My impression is that tubers have
> been domesticated in environments which are not so marginal, and where there is a greater
> diversity of food resources available, so that they are not the initial crops to be domesticated.
> Andrew
> ==========================================================================
> ==========================================================================
>
However, if grains can be eaten as well as planted, they are different in kind from tubers, since in extremis
one can eat the potential crop ("eating the seed-corn") at the risk of future starvation if one is wholly
dependent on these crops. Does this have implications for the stability of grain-dependent cultures, which
may collapse in such a situation due to a rash decision?
Dick Bird University of Northumbria Newcastle upon Tyne NE1 8ST UK
PALEODIET Archives
Subject: Grains vs Tubers
From: Bronwen Humphreys
Reply-To:
Date: Thu, 27 Aug 1998 15:22:16 +0100
Further to my earlier message - I just happened to be looking up a reference for one of our members in:
Agriculture and the Citizen by Colin R W Spedding/Chapman & Hall. ISBN 0-412-71520-1 and I found a
table listing how many people whose protein requirement could be met per hectare of land, planted to
various crops.
110/147 (1998)
Cabbage 34 Field Beans 26 Peas 24 Potatoes 22 Wheat 20 Sugar beet 17 Maize 16 Rice 16 Barley 15
If energy requirements rather than protein are considered, sugar beet comes out top with 33 people per
hectare, potatoes second with 22, the best cereal is rice at 19.
Bronwen Humphreys The Vegetarian Society (UK)
PALEODIET Archives
Subject: Publisher seeks Manuscripts
From: Ray Audette
Reply-To:
Date: Sat, 29 Aug 1998 08:43:07 -0700
In a recent rejection letter from Keats Publishing, Aquistions Editor Thomas Hirch writes of Paleolithic
Nutrition: "It is a topic we have an interest in and have been considering publishing on. While your treatment
strikes us as personal and anecdotal, we are seeking a different basis to cover this subject."
Send proposals to:
Thomas Hirsch Keats Publishing 27 Pine Street (P.O. Box 876) New Canaan, CT. 06840-0876 203-9668721
BTW, the self-published version of my book is currently in the top 1/10 of 1% of all books sold on
Amazon.com (the worlds largest on-line bookstore). Ratings on Amazon.com are calculated hourly.
PALEODIET Archives
Subject: Civilization as a Pathology
From: Ron Hoggan
Reply-To:
Date: Tue, 1 Sep 1998 23:14:56 -0600
Hi All, I just read a very interesting article which offers another perspective on what may have moved
hunter-gatherers to take up agriculture and domestication of animals. The evidence is presented to suggest
that the comfort-inducing, addictive peptides from the partial digests of cereal and dairy proteins may have
been the motivating factor. This article can be seen at:
http://www.vegan-straight-edge.org.uk/GW_paper.htm
best wishes, Ron Hoggan
PALEODIET Archives
Subject: U of Southampton web site
From: Dean Esmay
Reply-To:
Date: Mon, 14 Sep 1998 13:49:10 -0400
A sharp-eyed member recently forwarded this interesting URL to me on prehistoric Italy:
http://www.arch.soton.ac.uk/Research/Italy/
PALEODIET Archives
Subject: Fw: Questions about meat in chimp diets/cooked foods... (to Jane Goodall)l
From: Bob Avery
Reply-To:
Date: Sun, 6 Sep 1998 20:09:57 -0400
111/147 (1998)
The following came from another internet newslist. I thought it might be of interest to some here.
Bob Avery
--------Begin forwarded message
---------> From: Jen Williams Date: 11 June 1998 20:51
> Subject: re:your letter to Jane Goodall
>
> Hi John,
> Dr. Goodall recently forwarded your letter of 27/11/97 to us at the Center for Primate Studies, so
> here are some answers to your questions. I haven't read Diamond's "The Third Chimpanzee", but the
> idea that males share meat more frequently with sexually receptive females is more of a
> supposition, in that it has not been tested with data. Male chimps are certainly more likely to
> hunt than females, but females do hunt, especially smaller prey. Hunts at Gombe do not appear to
> be ritualized. If anything, the Gombe chimps are more successful in catching colobus monkeys
> (their most frequent prey) when the hunt is very chaotic. Christophe Boesch in the Tai Forest (in
> Cote d'Ivore) claims that his chimps do in fact hunt in a cooperative way. He's published several
> papers on this (one is in "Chimpanzee Cultures, " 1995 ed. by Wrangham et al). One of the students
> here at the Center for Primate Studies is looking at the importance of meat as a social tool. If
> his suppositions are correct, meat may serve as currency in a service economy (de Waal has a
> recent paper on evidence for a service economy functioning in his captive colony, I don't have the
> full reference).
> As for your query re: whether chimps may have developed liking for foods that override their
> nutritional ideal, chimp reproduction seems to be very limited by food (i.e. nutrition), so we
> assume that individuals exhibiting non-optimal food choice wouldn't pass on very many of their
> genes. Given this assumption, the chimp desire for meat, termites, etc. is probably an effective
> way for them to get enough protein and fat. Unnutritional cravings are only an issue in humans
> because we have released ourselves from being limited by food (to support this, chimps in
> captivity do become very overweight when they are allowed to eat based on their cravings). re:
> data collection of feeding data, yes most of the time people record time spent foraging, rather
> than recording how much they ingest. A few studies have looked at ingestion (though I don't think
> in chimps), this usually entails counting the number of items put in the mouth, and assuming each
> item is an average mass. This is extremely difficult & time consuming since the observer
> frequently can't see the animal putting items in its mouth, so no, we don't generally correct for
> this. Since we frequently have no idea of the nutritional content of the species eaten in Gombe,
> we'd be hard-pressed to relate feeding time to exact nutritional gain in any case. The data you
> quote on Kanyawara chimps is from Richard Wrangham (chapter in "Ecology and Social Evolution",
> 1986, ed. by Rubenstein & Wrangham, I believe).
> As for your interest in lactation etc., I know very little about any of this - I'm sure such work
> has been done in captivity. Chimps wean their offspring around age 4-5 years, but young chimps are
> probably getting most of their nutrition from food for about a year of that. Finally, re: the
> article you read in which the author claimed that humans have adapted to eating cooked food in
> 1100 years, I find that rather questionable. Certainly large changes can occur under extreme
> selection in a short period of time, but I can't see why such strong selection would have been
> taking place during that period. Seems more likely that we broadened our diet by cooking things
> that are not nutritional raw, due to disease risk or toxic plant compunds. Hope this answers most
> of your questions (and that you have a copy of them, still, to refer to). As far as I know, Jane
> has no direct access to email or other handy modes of communication while traveling, which as you
> probably know is about 90% of the time.
> Yours, Jen Williams
> --------------------------------------------------------------------> Research Coordinator
> The Jane Goodall Institute's Center for Primate Studies
> Department of Ecology, Evolution and Behavior, U. of Minnesota
> 1987 Upper Buford Circle, St. Paul, MN 55108
> phone:612-624-6714; fax:612-624-6777
> email:
112/147 (1998)
>
--------End forwarded message
----------
PALEODIET Archives
Subject: Eat right for your type
Reply-To:
Date: Wed, 23 Sep 1998 17:22:28 -0400
O One of the strangest diet books of the last years is Peter D'Adamos "Eat right for your type". D'Adamo
tries to explain his blood group specific dietary recommendations with human adaptations to different
environments (O: oldest human blood group/hunter-gatheres, A: adaptation to
agriculture/vegetarianism/caucasian, B:adaptation to colder climates/dairy/mongoloid).
I believe it's necessary to state clearly: D'Adamo's diet has nothing to do with the topic of paleolithic
nutrition. Without doubt - there are a lot of documented links between blood type and risk of various
diseases. I also don't question the possibility of immunological reactions between blood group antigens and
certain foods. But until now there is no scientific basis for the conclusion, that each blood type requires its
own diet. D'Adamo has blown up a mouse to an (bestselling) elephant without showing any new data. And
his basic assumptions are simply wrong.
The idea that O is the original blood group of hunter-gatherers and blood type A and B came up later in
history is entirely antiquated. It can be traced back to Hirschfeld & Hirschfeld (1), Ruggles Gates (2), and
Raymond Dart (3). Today we know that A and B antigens are present not only in humans but also in many
other primate species, including chimpanzees, gorillas, orangutans, gibbons and macaques (4, 5, 6, 7). Karl
Landsteiner compared ABO-antigens of apes and humans already in the twenties (8, 9). He wrote: "The
group reactions which we have observed by the various methods in anthropoid bloods correspond in every
respect with the group reactions in human blood".
Irrespective of a convergent or transspecific evolution of the ABO-polymorphism in monkeys, apes and
humans (10, 11): Phylogenetic analysis suggests that the human A and B allels are at least a few million
years old (4, 12). Sorry, Mr. D'Adamo: blood group A and B are as paleolithic as blood group O. They are
ancient, no adaptations to mesolithic or neolithic dietary changes, and can also be found in most recent
hunter-gatherer societies.
References:
(1) Hirscheld, L. & Hirschfeld, H. (1919). Serological differences between the blood of different races.
Lancet 2:675-679.
(2) Ruggles Gates, R. (1939). Rise and spread of the A and B blood groups from the mutationist point of
view. Z. Rassenkunde 9:58-63.
(3) Dart, R. (1951). African serological patterns and human migrations. Capetown, Publ. South Afr Archeol
Soc
(4) Walter, H. (1998). Populationsgenetik der Blutgruppensysteme des Menschen. Stuttgart, Schweizerbart.
(5) Socha, W.W. et al. (1976). Blood groups of bonnet macaques (Macaca radiata), with a brief introduction
to seroprimatology. Am J Phys Anthrop 45:485-491.
(6) Schmid, D.O. & Buschmann, H.G. (1985). Blutgruppen bei Tieren. Stuttgart, Ferdinand Enke.
(7) Schmitt, J. (1968). Immunbiologische Untersuchungen bei Primaten. Ein Beitrag zur Evolution der Blutund Serumgruppen. Basel-New York, Karger.
(8) Landsteiner, K. & Miller, C.P. (1925). Serological observations on the relationship of the bloods of man
and the anthropoid apes. Science 61:941-942.
(9) Landsteiner, K. (1928). Sur les propri=E9t=E9s s=E9rologiques du sang des Anthropoides. C Rend Soc
Biol 99:658-660.
(10) Doxiadis, G.G. et al. (1998). Characterization of the ABO blood group genes in macaques: evidence for
convergent evolution. Tissue Antigens 51:321-326.
(11) Martinko, J.M. et al.(1993). Primate ABO glycosyltransferases: evidence for trans-specific evolution.
Immunogenetics 37:274-278.
113/147 (1998)
(12) O'hUigin, C. et al. (1997). Evidence for convergent evolution of A and B blood group antigens in
primates. Hum Genet 101(2):141-148.
Ruediger Hoeflechner, blood type O
PALEODIET Archives
Subject: Blood type comments
From: Todd Moody
Reply-To:
Date: Sun, 27 Sep 1998 13:56:09 -0400
> Date: Wed, 23 Sep 1998 17:22:28 -0400
> From: Ruediger Hoeflechner Subject: Eat right for your type
> O One of the strangest diet books of the last years is Peter D'Adamos "Eat right for your type".
> D'Adamo tries to explain his blood group specific dietary recommendations with human adaptations
> to different environments (O: oldest human blood group/hunter-gatheres, A: adaptation to
> agriculture/vegetarianism/caucasian, B:adaptation to colder climates/dairy/mongoloid).
> I believe it's necessary to state clearly: D'Adamo's diet has nothing to do with the topic of
> paleolithic nutrition. Without doubt - there are a lot of documented links between blood type and
> risk of various diseases. I also don't question the possibility of immunological reactions between
> blood group antigens and certain foods. But until now there is no scientific basis for the
> conclusion, that each blood type requires its own diet. D'Adamo has blown up a mouse to an
> (bestselling) elephant without showing any new data. And his basic assumptions are simply wrong.
D'Adamo's diet program is actually based on several loosely connected theories. One is that, although the
blood type alleles may have been present forever, the different types didn't flourish until certain historical
epochs. He explains this as a consequence of the fact that different foods agglutinate blood cells of different
typies. Another theory has to do with metabolic types and diet. He claims that type As, for example, produce
the least amounts of gastric acid and intestinal alkaline phosphatase. This supposedly makes it harder for
them to digest meats and animal fats. Yet another theory is that lectin-caused hemagglutination is linked to
particular diseases and health issues. Unlike other blood types, ABO types are not a "true" blood type. That
is, the type is not limited to blood cells but includes other cells as well, such as cells of the intestinal lining.
Put it all together and you get a diet book. Speaking as a layman, I have the impression that the specific
interactions of lectins with various tissue types is something well worth exploring, and may well have
implications for the history of major dietary transitions. When lentils were introduced into the food supply,
for example, there may have been a sudden and strong selection pressure against type Os, whose cells are
supposedly agglutinated by lentil lectin. Type As would have done much better. But the hypothesis needs a
lot more confirmation, in my opinion.
I suspect the metabolic type theory goes nowhere.
I await more informed opinions with interest. (Rather, I await with interest more informed opinions.)
Todd Moody
PALEODIET Archives
Subject: my own diet
From: "Robert M. Threlkeld"
Reply-To:
Date: Fri, 25 Sep 1998 15:33:15 -0700
I have been lurking on this list for a couple of months would appreciate your thoughts on my own diet and
the rationale behind it. I am currently eating primarily flesh of various types, green and other low
carbohydrate vegetables, plus small amounts of nuts and dried berries. I feel wonderful, have lost 15 pounds,
and am happy with this new way of eating. My energy level is up and I'm jogging at a level I did six years
ago. I'm 55 years old.
My rationale is based on the following, gleaned largely from this list and other reqadings,
114/147 (1998)
1. If one can trace one's ancestors back to arrival in the new world (assuming one isn't a native American),
we pretty know that our relatives have been resident in that region (Britain, Germany, etc.) for a very long
period of time, assuming no substantial migrations.
2. Virtually all my relatives are from either the UK or Scandinavia.
3. Agriculture came late to northern Europe, like 3, 000 BC.
4. Therefore, my most healthy diet is clearly preagricultural and based on what folks in that area ate prior to
3, 000 BC. Which I think is largely meat of some sort, with some green vegetables, roots, nuts, and berries.
Does this all make sense?
---------------------Robert Threlkeld, Dean Learning and Technology Director, Academic Innovation Center California State
University, Fresno 2225 East San Ramon Ave. Fresno, CA 93740-0121 cell phone (best bet) 209.250.7647
phone: 209.278.2058 fax: 209.278.7026 e-mail:
PALEODIET Archives
Reply-To:
Date: Mon, 28 Sep 1998 15:18:45 -0400
Todd, you encourage me to write a new diet book:
Do you know Kleiber's law? It describes the relationship between mammalian body weight and energy
requirements and indicates that, although larger mammals obviously require more energy, smaller mammals
have higher basal metabolic rates per unit body weight. Therefore smaller-bodied animals need more energyrich food than larger animals.
My conclusion: Human diet should depend on weight. People up to 60 kg should mainly feed on meat and
nuts, 60 - 90 kg should rely on milk and grains, and people with more than 90 kg should prefer fruits and
vegetables.
Whats wrong with my new diet book? Unfortunately body weight is only related to energy requirements.
Adaptation to certain foods, however, needs hundreds of steps. And the activity of enzymes in the gut, the
thrifty genotype, all the genes involved in the cholesterol-, carbohydrate- and calcium-metabolism are
inherited independent of height and weight. If you compare two isolated populations or species, body weight
may be an indicator for different selective pressures. In this case maybe you find an association between
weight and the frequency of other alleles. But in an interbreeding population all these traits are exposed to
the same environment - giants and dwarfs have the same vitamin and trace element requirements. Within a
population dietary recommendations can never be based on a single gene (with the exception of specific
diseases). Even the (hypothetical) thrifty genotype does not imply, that people with and without this type
have different micro- or macronutrient needs.
To illustrate the scientific qualification of Peter D'Adamo, just one sentence from the first chapter of his
book, dealing with hominid evolution (I have only a german edition and try to re-translate it - excuse my
English): "Neanderthals, the first known human beings, developed perhaps 50.000 years ago." Is this the sort
of information, we can trust? And we have to trust, because we don't get data.
Long lists of recommended and forbidden foods..... Blood type O: very wholesome: lamb, beef, salmon...
neutral: duck, rabbit, tuna..... avoid: goose, pork, catfish.....
data?? references?? clinical or epidemiological studies??
Peter D'Adamo found a mouse (increased incidence of peptic ulcers in blood type O), concludes: more
gastric acid (and Helicobacter pylori??) - better denaturation of protein - better suited for meat digestion and has blown it up into an elephant (type O should eat more meat than A and B). Data for this elephant??
references?? clinical or epidemiological studies??
Could it be, that the spread of agriculture promoted blood type A? Why not? But we need data und should be
careful with interpretations. Some food for thought: Peter D'Adamo believes that indigenous Americans have
only blood type O. Indeed - O has an extremly high frequency in Central and South America, in some
populations up to 100%. On the other hand blood type A and B has been shown in precolumbian mummies
(1 - 4). Why didn't blood type A flourish in America?
(1) Boyd, W.C. & Boyd, L. (1937). Blood grouping tests on 300 mummies. J Immunol 32:307-319
(2) Candela, P.B. (1943). Blood group tests on tissues of Paracas mummies. Am J Phys Anthrop 30:65-67.
115/147 (1998)
(3) Allison, M. et al. (1978). ABO blood groups in Chilean and Peruvian mummies. Am J Phys Anthrop
49:139-142.
(4). Llop, E. & Rothhammer, F. (1988). A note on the presence of blood groups A and B in Pre-Columbian
South America. Am J Phys Anthrop 75:107-111.
Best wishes
Ruediger Hoeflechner (blood type 0; I love lentils, though they are not "Paleo". No clinical symptoms of
agglutinated cells)
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Mon, 28 Sep 1998 15:41:48 -0400
Ruediger Hoeflechner humorous example is apropriate--a lot of popular books and articles on diet are based
on similarly silly logic and total lack of any real research. While popular publications shouldn't be expected
to be as rigorous and exquisitely detailed as peer-reviewed publications, the majority of writers of such
books lack even the most haphazard standards of support or proof.
Witness the number of vegetarians who continue to insist that the evolutionary record supports the notion
that humans evolved to be vegetarians because we have flat molars and no sharp fangs, or who state that
"almost no primate ever eats meat." I have heard fully qualified medical doctors make statements like these,
and heard the same from a number of degreed dieticians and others promoting popular books on human diet.
The fact that D'Adamo's book has been a bestseller in the United States (and is apparently now being
translated and sold in different countries) indicates that there is much popular interest in this subject. But it
also demonstrates that almost no one out there telling the public what really is known (and not known) in this
area. -=- The greatest mistake you can make in life is to be continually fearing you will make one. ---Elbert
Hubbard (1859-1915)
PALEODIET Archives
Subject: Popular article
From: Dean Esmay
Reply-To:
Date: Tue, 6 Oct 1998 05:13:42 -0400
An article appeared recently in the San Diego Union newspaper on the application of paleolithic diet
concepts to modern Western diets. It can be found in the paper's archives at:
http://www.uniontrib.com/news/utarchives/cgi/libsearch.cgi
It will unfortunately require membership to the newspaper's web site, but fortunately the membership is free
and takes only a few clicks to obtain.
Thanks to Dr. Ed Blonz for forwarding the URL. The article is an interesting snapshot of where the popular
imagination is on a lot of the issues we discuss. -=The mind is not a vessel to be filled. It's a fire to be lit. - Plutarch
PALEODIET Archives
Subject: Buffalo meat and fat and Native population
From: Mary
Reply-To:
Date: Tue, 6 Oct 1998 13:14:12 -0700
Does anyone know of people who are researching the Native American use of buffalo meat and fat as part of
their paleo diet?
116/147 (1998)
I'm trying to find out how Native populations utilized the fat, in particular.
It is highly saturated and tastes chalky. When Native populations made pemmican out of it, how did they
make the fat palatable?
I talked to a researcher at North Dakota State who said the native peoples made their pemmican out of dried
meat and berries only (no fat)
I'm looking for other sources of information, as well.
Thanks,
Mary
PALEODIET Archives
Subject: Re: Buffalo meat and fat and Native population
From: Dave Chapman
Reply-To:
Date: Wed, 7 Oct 1998 14:08:00 -0700
> Does anyone know of people who are researching the Native American use of buffalo meat and fat as
> part of their paleo diet? I'm trying to find out how Native populations utilized the fat, in
> particular. It is highly saturated and tastes chalky. When Native populations made pemmican out of
> it, how did they make the fat palatable? I talked to a researcher at North Dakota State who said
> the native peoples made their pemmican out of dried meat and berries only (no fat) I'm looking for
> other sources of information, as well.
I have made a few posts in the past to the Paleofood list quoting explorers & travellers on the preparaton of
pemmican by Aboriginals. If I remember correctly they all used fat - sometimes in the ratio of 60% fat to
40%meat. Berries were not always used. Searching the Paleofood achives at:
http://maelstrom.stjohns.edu/archives/PALEOFOOD.html will find the posts.
Best of luck, Dave Chapman
PALEODIET Archives
Subject: popular article
From: Dean Esmay
Reply-To:
Date: Wed, 7 Oct 1998 19:36:38 -0400
Update/correction:
The popular article on evolutionary nutrition I mentioned earlier is to be found at the following URL:
http://www.uniontrib.com/news/utarchives/cgi/idoc.cgi?411317+unix+desmay+ads.uni
ontrib.com..80+Union-Tribune+Union-Tribune+Library+Library++%28evolutionary
This will still require membership at the Times-Union web site, which is free. -="It is impossible for a man to learn what he thinks he already knows." Epictetus (50-138 A.D.)
PALEODIET Archives
Subject: Pemmican
From: Dean Esmay
Reply-To:
Date: Wed, 7 Oct 1998 19:42:41 -0400
Chapman's posts on Pemmican and related historical accounts of eating habits among Native Americans can
most easily be found at:
http://maelstrom.stjohns.edu/CGI/wa.exe?S2=paleofood&q=&s=& ctoria.bc.ca&a=&b=
I'll probably see if I can't just reprint the best of them here to our list. -=It was said that when people heard Cicero speak, they said, "What a clever fellow is Cicero, " but when they
heard Demosthenes speak they said, "Let us march against Philip."
117/147 (1998)
PALEODIET Archives
Subject: Re: Pemmican
From: Loren Cordain
Reply-To:
Date: Thu, 8 Oct 1998 16:32:01 -0600
In response to Mary's question:
Does anyone know of people who are researching the Native American use of buffalo meat and fat as part of
their paleo diet?
I'm trying to find out how Native populations utilized the fat, in particular.
It is highly saturated and tastes chalky. When Native populations made pemmican out of it, how did they
make the fat palatable?
I talked to a researcher at North Dakota State who said the native peoples made their pemmican out of dried
meat and berries only (no fat)
I'm looking for other sources of information, as well.
Our research group here at Colorado State University has been studying the lipid composition of wild game
tissue (muscle, brain, marrow, tongue, depot fat and other organs) in terms of its potential health benefits (1,
2, 3). We believe that the types and amounts of fats that pre-agricultural people consumed (via their
consumption of wild plants and animals only) were much different than those which are now consumed by
people in western industrialized countries. In regards to your specific question about pemmican, I refer you
to perhaps the most extensive review of this subject which has been written (4). In his classic book, The Fat
of the Land, Stefansson devotes five chapters (9. The Nature and Early History of Pemmican, 10. The First
Pemmican War, 11. The Romance of Pemmican, 12. Pemmican in Transition, 13. The Second Pemmican
War) and more than 136 pages to discussing all aspects of pemmican that were known as of 1960.
Specifically, the Plains Indians made pemmican by cutting buffalo muscle meat into thin strips and drying it
in the sun. Once dried, the meat was then pounded into a fine powder and any remaining pieces of sinew,
tendon and/or bone were removed. The dried meat powder was mixed with melted fat and packed in sacks of
hide. The preferred fat was marrow or peri-nephral fat (4), however subcutaneous storage fat was used if
marrow was limited. The powdered muscle and fat were mixed by weight in a ratio of roughly 50:50 which
roughly yields a protein/fat ratio of 20:80 (4). Although such a mix at first appears to be highly atherogenic
because of its high relative fat content, our analysis of the fatty acid composition of wild game marrow
shows this not to be the case. Wild game marrow can contain up to 92% of its total energy as fat, and of this
fat, monounsaturated fats (16:1 and 18:1) are predominant and typically make up 75% of all the fatty acids in
marrow (1). Monounsaturated fats such as those found in olive oil, nuts and avocados do not elevate serum
cholesterol levels (5) and decrease the susceptibility of LDL to oxidation (6). Therefore, their consumption is
associated with a reduced risk of mortality from coronary artery disease (7). Because the types and levels of
fatty acids found in marrow are similar to those found in olive oil and most nuts, marrow likely would also
not promote elevated cholesterol or the predisposition towards atherosclerosis and coronary artery disease.
Stefansson reports that berries were rarely, if ever mixed in the pemmican made by the Plains Indians (4).
REFERENCES
1. Cordain L, Martin C, Florant G, Watkins BA. (1998). The fatty acid composition of muscle, brain, marrow
and adipose tissue in elk: evolutionary implications for human dietary lipid requirements. The World Review
of Nutrition and Dietetics, 83: 225.
2. Cordain L, Tillmans CL. (1998). Muscle fatty acid composition in elk (Cervus Elaphus). Nutritional
considerations. The FASEB Journal, 12(4): A622a.
3. Eaton SB, Eaton SB Jr, Cordain L, Mann N, Sinclair A. (1998). Dietary intake of long chain
polyunsaturated fatty acids during the paleolithic. World Review of Nutrition and Dietetics, 83: 12-23.
4. Stefansson V. The Fat of the Land. The Macmillan Company, NY, 1960.
5. Gardner CD et al. Monounsaturated versus polyunsaturated dietary fat and serum lipids. A meta analysis.
Arterioscler Thromb Vasc Biol 1995;15:1917-27.
6. Bonanome A et al. Effect of dietary monounsaturated and polyunsaturated fatty acids on the susceptibility
of plasma low density lipoproteins to oxidative modification. Arteriosclerosis and Thrombosis 1992;12:52933.
118/147 (1998)
7. Keys A et al. The diet and 15 year death rate in the seven countries study. Am J Epidemiol 1986;124:90315.
Cordially,
Loren Cordain, Ph.D. Professor, Department of Exercise & Sport Science Colorado State University Fort
Collins, CO 80523 TEL: (970) 491-7436 FAX: (970) 491-0445 email:
PALEODIET Archives
Subject: Re: Stefansson's all meat diet
From: Loren Cordain
Reply-To:
Date: Tue, 13 Oct 1998 15:38:50 -0600
The following list of citations represents all of the scientific publications which occurred as a result of
Vilhjalmur Stefansson's famous "Year Long, All Meat Diet" Experiment which was conducted at Bellvue
Hospital in New York starting in January of 1928. Stefansson's diet consisted entirely of animal based food
with no plant foods and contained a fat:protein energy ratio of 20% protein and 80% fat. During the year
long experiment, Stefansson's serum cholesterol levels ranged from 212 mg/dl to 315mg/dl (14) with a mean
value of 269 mg/dl (14). Additionally, the all meat diet caused a persistent hypercalciuria and Stefansson was
in negative calcium balance for the entire year of the experiment (10). Although Stefansson followed a
similar all meat diet when he lived with Eskimo people on his expeditions to the far North, I suspect that
there were key differences in the manner in which the aboriginal Eskimo all meat diet differed from
Stefansson's "civilized" all meat diet. The storage fat in marine mammals (whales, seals, walrus etc) contains
much higher levels of monounsaturated fat and less saturated fat (16) than does the storage fat of commercial
meats. Additionally, the muscle tissue of caribou, moose and other ungulates of the far north contain much
lower levels of saturated fat than does domestic meat. Marrow and organ meats were consumed regularly in
the aboriginal eskimo diet, whereas Stefansson's dietary staples were mainly fatty meats. Marrow contains
approximately 75% of its total lipids as monounsaturated fats, and organ meats from wild animals contain
lipid profiles which tend to be non-atherogenic because of their high levels of both N6 and N3
polyunsaturates (17). Further, the dietary protein intake of eskimos has been reported to range from 27-45%
of their total energy (16, 18), and because protein is more effective in lowering serum cholesterol levels than
is carbohydrate (19), Stefansson's lower protein intake (20%energy) relative to aboriginal intakes may have
contributed to the hypercholesterolemia produced by his "civilized all meat diet". Finally, fish played an
important role in the Eskimo diet, and fish consumption is known to have a beneficial influence upon
cardiovascular health (20). It is not known how much fish Stefansson included in his "all meat" civilized
diet. These points underscore the difficulty in trying to emulate so called "paleodiets" with modern foods.
STEFANSSON REFERENCES:
1. Lieb CW. The effects of an exclusive long-continued meat diet. JAMA 1926;87:25-26. 2. Lieb CW. The
effects on human beings of a twelve months exclusive meat diet. JAMA 1929;93:20-22. 3. Lieb CW, Tolstoi
E. Effect of an exclusive meat diet on chemical constituents of the blood. Proc Soc Exp Biol Med
1929;26:324-25. 4. Lieb CW. A years's exclusive meat diet and seven years later. Am J Digestive Dis Nutr
1935;2:473-75. 5. Lieb CW. Statement. Am J Digestive Dis Nutr 1936;2:732. 6. McClellan WS, Toscani V.
Changes in the rate of excretion of acetone bodies during the twenty-four hours. J Biol Chem 1928;80:65358. 7. McClellan WS, Spencer HJ, Falk EA, DuBois EF. A comparison of the thresholds of ketosis in
diabetes, epilepsy, and obesity. J Biol Chem 1928;80:639- 8. McClellan WS. Der einfluss einer einhahrigen
ausschliesslichen fleischkost bei zwei menschen. Klin. Woch. 1930;9:931-32. 9. McClellan WS, DuBois EF.
Prolonged meat diets with a study of kidney function and ketosis. J Biol Chem 1930;87:651-80. 10.
McClellan WS, Rupp VR, Toscani V. Prolonged meat diets with a study of the metabolism of nitrogen,
calcium and phosphorous. J Biol Chem 1930;87:669-80 11. McClellan WS. The effect of the prolonged use
of exclusive meat diets on two men. J Am Diet Assoc 1930;6:216-28. 12. McClellan WS, Spencer HJ, Falk
EA. Prolonged meat diets with a study of the respiratory metabolism. J Biol Chem 1931;93:419-34. 13.
Tolstoi E. The effects of an exclusive meat diet lasting one year on the carbohydrate tolerance of two normal
men. J Biol Chem 1929;83:747-52. 14. Tolstoi E.The effect of an exclusive meat diet on the chemical
constituents of the blood. J Biol Chem 1929;83:753-58. 15. Torrey JC, Montu E. The influence of an
exclusive meat diet on the flora of the human colon. J Infect Dis 1931;49:141-76.
NON-STEFANSSON REFERENCES
119/147 (1998)
16. Bang HO, Dyerberg J. Lipid metabolism and ischemic heart disease in Greenland Eskimos. Adv Nutr
Res 1980;3:1-22. 17. Cordain L, Martin C, Florant G, Watkins BA. (1998). The fatty acid composition of
muscle, brain, marrow and adipose tissue in elk: evolutionary implications for human dietary lipid
requirements. The World Review of Nutrition and Dietetics, 83: 225. 18. Krogh A, Krogh M. A Study of the
Diet and Metabolism of Eskimos. Bianco Luno, Copenhagen, 1913. 19. Wolfe BM. Potential role of raising
dietary protein intake for reducing risk of atherosclerosis. Can J Cardiol 1995;11:127G-31G. 20. Wolmarans
P et al. Plasma lipoprotein response to substituting fish for red meat in the diet. Am J Clin Nutr
1991;53:1171-6.
Cordially,
Loren Cordain, Ph.D. Professor, Department of Exercise & Sport Science Colorado State University Fort
Collins, CO 80523 TEL: (970) 491-7436 FAX: (970) 491-0445 email:
PALEODIET Archives
Subject: Stefansson's Cholesterol
From: Ray Audette
Reply-To:
Date: Thu, 15 Oct 1998 09:08:43 -0700
Loren Cordain Wrote:
> Stefansson's lower protein
> intake (20%energy) relative to aboriginal intakes may have contributed to the hypercholesterolemia
> produced by his "civilized all meat diet".
Actually it was probally the only vegetable allowed on this diet that contributed the most to the high
cholesterol seen by Stefansson and to a much greater extent by Anderson. While in Belvue both drank coffee
prepared by Anderson in the traditional Scandinavian method - boiling!
Boiled coffee (as opposed to percolated or filtered) raises cholesterol higher and faster than any other method
known (including an extremly high fat diet). As Stefansson spent far less time drinking this potent brew and
more time time outside the hospital (he left the hospital after the first month and would have had access only
to percolated coffee) his hypercholesterolemia would have been far less than Anderson's (as was the case).
See: "Discovery: The Autobiography of Vilhjalmur Stefansson" and: CLINICAL NUTRITION Volume 65
Number 2 February 1997 Separate effects of the coffee diterpenes cafestol and kahweol on serum lipids and
liver aminotransferases
Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition"
PALEODIET Archives
Subject: Hunter/Gatherer meeting
From: Dean Esmay
Reply-To:
Date: Sun, 18 Oct 1998 18:29:24 -0400
HUNTER-GATHERERS: AN INTERDISCIPLINARY PERSPECTIVE a meeting of the Biosocial Society
organised by Catherine Panter-Brick, Robert Layton and Peter Rowley-Conwy UNIVERSITY OF
DURHAM, ENGLAND, 7 MAY 1999
The meeting will comprise the following eleven presentations:
ROBERT LAYTON, CATHERINE PANTER-BRICK and PETER ROWLEY-CONWY (University of
Durham, UK): Hunter-Gatherers: why a new synthesis?
STEVEN KUHN and MARY STINER (University of Arizona, USA): The antiquity of hunter-gatherers.
PETER ROWLEY-CONWY (University of Durham, UK): Time, change and the archaeology of huntergatherers: how original is the original affluent society?
BRUCE WINTERHALDER (University of North Caroline, USA): The behavioral ecology of huntergatherers: recent work.
MARK JENIKE (Pomona College, USA): Nutritional ecology: diet, growth, physical activity and health.
RENEE PENNINGTON (University of Utah, USA): Hunter-gatherer demography.
120/147 (1998)
ALAIN FROMENT (Laboratoire ERMES, France): Biological anthropology of hunter-gatherers: genetic

evolution and environmental constraints.
PATRICK MCCONVELL (Griffith University, Australia): Language shift and language spread among
hunter-gatherers.
ROBIN TORRENCE (Australian Museum): Hunter-gatherer technology as optimal solutions.
MEG CONKEY (University of California, USA): Hunting for images, gathering up meanings: the life of art
and art for life in hunting-gathering societies.
ROBERT LAYTON (University of Durham, UK): Indigenous rights.
The papers will provide up-to-date reviews of the literature on hunter-gatherers by leading researchers in
each field.
For further information contact Catherine Panter-Brick and the Department of Anthropology, University of
Durham, Old Elvet, Durham DH1 3HN, UK. Telephone +44-(0)191-374-2854; fax +44-(0)191-374-2870; e
mail
--- "What can be done with fewer assumptions is done in vain with more." William of Occam 1285-1347
PALEODIET Archives
Subject: Re: PALEODIET Digest - 14 Oct 1998 to 16 Oct 1998 (#1998-72)
From: Todd Moody
Reply-To:
Date: Fri, 16 Oct 1998 21:46:32 -0400
> Date: Thu, 15 Oct 1998 09:08:43 -0700
> From: Ray Audette Subject: Stefansson's Cholesterol
> Loren Cordain Wrote:
> Stefansson's lower protein intake (20%energy) relative to aboriginal intakes may have contributed
> to the hypercholesterolemia produced by his "civilized all meat diet". Actually it was probally
> the only vegetable allowed on this diet that contributed the most to the high cholesterol seen by
> Stefansson and to a much greater extent by Anderson. While in Belvue both drank coffee prepared by
> Anderson in the traditional Scandinavian method - boiling!
The trouble with this hypothesis is that Andersen's cholesterol returned to normal (200) two weeks after the
conclusion of the experiment [1]. Unless there is reason to suppose that he suddenly gave up drinking coffee
at this time (and unfiltered coffee was the norm in 1928), something else must explain the sudden drop in
cholesterol.
Todd Moody
[1] Tolstei, E. (1929) J. Biol Chem. 83: 753-758. "The effect of an exclusive meat diet on the chemical
consituents of the blood"
PALEODIET Archives
Subject: Stefansson's all meat diet
From: Art De Vany
Reply-To:
Date: Mon, 19 Oct 1998 11:42:34 -0800
Stefansson's experiment does show that an all meat diet can sustain life for a year. But that is all; I see no
other implications beyond that. Whether plaque may have formed in their blood vessels during that year or
what possible longer term effects the experiment may have had are open questions.
But, my main point is this: how does any one live for a year in a hospital? What are the consequences of this
virtual imprisonment? How does the induced stress of confinement and restricted activities, stimulation, and
variety impact on health?
It may be too much to read dietary implications from this highly artificial experiment, when we know so
little of the consequences of the impaired physical environment. Is it not true that blood chemistry is
influenced by imprisonment? Surely, their catecholamine levels were elevated.
121/147 (1998)
Arthur De Vany Professor Department of Economics Institute for Mathematical Behavioral Sciences
University of California Irvine, CA 92697-5100 949-824-5269
http://www.socsci.uci.edu/mbs/personnel/devany/devany.html
PALEODIET Archives
Subject: Re: Stefansson's all meat diet
From: Dean Esmay
Reply-To:
Date: Mon, 19 Oct 1998 20:43:53 -0400
Art, you may want to review the referenced papers on the all-meat diet again. The subjects were not kept
locked in prison conditions, they exercised on a regular basis, and after the first month or so Stefansson
himself travelled freely about the country, while always in the company of an observer and under strict oath
to eat nothing but meat.
The purpose of this experiment was (first and foremost) to demonstrate empirically that it was possible to
survive with no major ill effects on an all-meat diet, and in that they succeeded quite well. The common
predictions at the time were that anyone who tried this would be horribly crippled by gout or acidosis or
kidney failure or scurvy or other problems, including possible ill mental effects. Some had called Stefansson
and others liars for suggesting that the Inuit actually survived this way. However, after a year there were no
serious ill effects (mental or physical) except elevated cholesterol. Long-term negative effects were not
examined, although Stefansson is known to have lived into his 80s.
Beyond just demonstrating that it was possible for humans to survive and be healthy, all the experimenters
did was try their best to document various aspects of the subjects' health while on the diet. Making much
more out of this experiment would be hazardous.
--- "What can be done with fewer assumptions is done in vain with more." William of Occam 1285-1347
PALEODIET Archives
Subject: meat based formula for infatns with food allergies
From: Ron Hoggan
Reply-To:
Date: Thu, 22 Oct 1998 22:48:28 -0600
Hi all, I wonder if I could get your help? My grandson, now 3 months old, can't tolerate milk, so he is on soy
formula. Unfortunately, he is showing some evidence of reacting to that too. I have recently heard that there
is such a thing as a meat-based formula, but I can't find any information on it.
If you have any information on this, I would appreciate it.
Thanks in advance for your help. best wishes, Ron Hoggan Calgary, Alberta, Canada
PALEODIET Archives
Subject: [Fwd: Re: [Fwd: PALEODIET Digest - 20 Oct 1998 to 23 Oct 1998 (#1998-76)]]
From: luc de bry
Reply-To:
Date: Sat, 24 Oct 1998 01:14:29 -0700
Good evening Ron,
From the Paleodiet Digest of 20-23 Oct., I had forwarded your email to the Food Law listserver of the
Institute of Food Technologists, http://www.ift.org/
Here forwarded is a first answer from Dr. Beverly McCabe. Hope that it will be of some help to your
grandson.
Regards,
122/147 (1998)
Luc -- Luc De Bry, Ph.D., Head of Research Department GENERAL BISCUITS BELGIE De BeukelaerPareinlaan, 1 B-2200 Herentals - Belgium
Tel 32 (0)14 24 14 32 Fax 32 (0)14 24 10 25 Email internal : Email external :
An Operating Company of http://www.danonegroup.com
PALEODIET Archives
From: Kirsten Emmott
Reply-To:
Date: Sat, 24 Oct 1998 20:51:44 -0700
This meat formula might be Cho-Free, if they still make it: or perhaps Nutramigen, an amino-acid based
formular. Better than either, though, and very much cheaper, would be mother's milk, which just about all
babies can tolerate. Very severely allergic babies sometimes miraculously gain weight on donated milk. Call
the nearest big hospital and see if they have access to a human milk bank; or contact the local La Leche
League for local donors. I once set up a human milk bank in Victoria, BC. The Vancouver bank sent over a
couple of weeks' worth of donated milk for my little patient, who weighed only ten pounds at five months of
age. So many mothers in Victoria donated their extra milk, which the hospital lab agreed to store in their
freezer, that the baby doubled its weight in a month. Eventually she tolerated cow milk once again. She
started sleeping through the night on the third day of donor milk and sat up for the first time within a week.
Tactfully suggest to your grandson's mom that she breastfeed her next. Incidentally, if she really wants to,
she can relactate, even at 3 months. The La Leche League can help her. She'll need a Medela nursing
supplementer, which she uses to feed donor milk or formulaa while the baby is at her breast. It takes about
ten days. Babies usually cooperate pretty well.
Dr. K. Emmott
> I wonder if I could get your help? My grandson, now 3 months old, can't tolerate milk, so he is on
> soy formula. Unfortunately, he is showing some evidence of reacting to that too. I have recently
> heard that there is such a thing as a meat-based formula, but I can't find any information on it.
> Ron Hoggan
> Calgary, Alberta, Canada
PALEODIET Archives
From: Reply-To:
Date: Sun, 25 Oct 1998 15:56:36 EST
To Ron Hoggan from Mary and Sally,
We have a recipe for a meat based formula in our book Nourishing Traditions. The first edition is almost
sold out but the Price-Pottenger Nutrition Foundation has some copies left. Their number is (619) 574-7763.
You will also want to order The Ploy of Soy from them to find out just how inappropriate soy formula is for
infants. There is also an article on problems with soy-based formulas in the latest edition of the PPNF
journal.
When making the formula, be sure to include the coconut oil, called for in the recipe, as it is the only source
of saturated fatty acids in the formula and these are very necessary for a number of reasons.
Hope this helps, Sally Fallon
PALEODIET Archives
Subject: World Congress of Food Science and Technology
Reply-To:
Date: Mon, 26 Oct 1998 13:31:21 +1100
123/147 (1998)
Hi Everyone,
I've been assigned the task of arranging speakers for a symposium on Indigeous Foods at the World
Congress of Food Science and Technology which will be held in Sydney next October. I've decided to give it
a paleolithic nutrition emphasis. I'm trying to find speakers from outside of the USA, Europe, or Australia
(from which we already have numerous speakers). Would anyone on this list be aware of anyone in South
America, Africa, China or SE Asia with an interest in paleolithic nutrition? If so please email me at We are
primarily interested in speakers with established backgrounds as researchers or academics or medical
professionals.
Best wishes Jennie
PALEODIET Archives
From: Reply-To:
Date: Mon, 26 Oct 1998 17:11:34 EST
For Ron Hoggan,
For a commercial meat formula, Gerber meat formula was developed by the allergist Albert H. Rowe, Sr.,
M.D. and was still in use in the 1950s. Gerber may know if they still can make it on special order. MeadJohnson has had a meat formula in the past called Cemac (which included some vegetables). They do not list
it in any of their current literature, but there was still a meat formula available on special order 20 years ago.
Nutramagin is a casein hydrolysate plus added amino acids (and casein is from cow's milk).
CHO-free was a carbohydrate-free soy formula made by Syntex which has been off the market since it and
the other Syntex formula, NeoMullSoy, were both found to be chloride-deficient in the late 1970s.
The suggestion of relactation is a good one if you can convince the mother to get help and to really try.
The recipe in Sally's cookbook works very well, but needs to be made carefully following the directions
fully.
Mary G. Enig, Ph.D., F.A.C.N., L.N., C.N.S.
PALEODIET Archives
Subject: Sugestions requested
From: Ray Audette
Reply-To:
Date: Tue, 27 Oct 1998 11:47:47 -0800
I am now working on the expanded hardcover edition of NeanderThin which will be published in the spring
of 1999 by St. Martin's Press of NYC.
I have several additional chapters in mind but would like sugestions of topics from those members of this list
who are familar with my work and it's current deficiencies. Potential chapter titles in Biblical style are
optional!
Ray Audette Author "NeanderThin:A Caveman's Guide to Nutrition" 1-800-577-3977
PALEODIET Archives
From: Reply-To:
Date: Tue, 27 Oct 1998 16:36:47 EST
October 26, 1998
To: Paleodieters From: Sally and Mary Subject: Pemmican
124/147 (1998)
Pemmican was a concentrated food used by the Eskimos and Indians of North America as a convenience or
travel food. Stefansson reports that a pemmican ration of 1 1/2 to 2 pounds could support a large man doing
heavy physical labor throughout the day.
From published reports and Stefanssons analysis we know that the ratio of fat to protein in pemmican was
80:20. The question we are debating is the fatty acid profile of this fat. In his long discussion of pemmican,
Stefansson mentions the use of marrow fat as a component only once. Pemmican made with marrow fat was
called fine pemmican. (The Fat of the Land, p 192) Stefansson goes on to say that this was not the usual type
of fat used, because relatively unsaturated marrow fat would not have good keeping qualities--and pemmican
was known to keep for as long as 20 years.
According to Stefansson, The Eskimos of northwestern Canada believe, for the caribou, that the fats which
resist rancidity best are from the kidneys and from the back slab, the layer on the back that extends from the
horns to the tail and a little way down along the flanks. Kidney fat is the hardest. Less hard is the fat from the
ribs and brisket. Softest of all, and most easily spoiled is the marrow fat. For pemmican to have good
keeping qualities, Some form of tallow would be used, certainly. (p192) Marrow, on the other hand, was
usually eaten alone (p 26), usually raw. Interestingly, the Indians preferred the hip and shoulder marrow
which is described as hard and tallowy. (p 27)
The explorer Thompson says, the fat of the Bison is of two qualities, called hard and soft; the former is from
the inside of the animal, which when melted is called hard fat (properly grease) the latter is made from the
large flakes of fat that lie on each side of the back bone, covering the ribs, and which is readily separated,
and when carefully melted resembles Butter in softness and sweetness. (p 218)
John Lame Deer, a full-blooded Sioux born eighty years ago on the Rosebud Reservation in South Dakota
states that pemmican was meat pounded together with berries and kidney fat.
MacKenzie said that the fat used was the inside fat and that of the rump, and adds that the rump fat is much
thicker in these wild than our domestic animals. (p 217) Stefansson confirms that wild animals in their prime
carried a large slab of back fat, weighing as much as 40 to 50 pounds. (p 28) The Indians and Eskimo hunted
older male animals preferentially because they wanted the fat. They recognized that a diet of lean meat
without enough fat quickly brought on sickness. (p 31)
It seems that the vast majority of pemmican was made with a mixture of cavity fat and subcutaneous fat.
Assuming the cavity fat to be 75% saturated, and the back slab fat to be 50% saturated (55% in the buffalo),
then the fat of pemmican could contain at least 65% saturated fat--more if only kidney fat was used.
Of course, pemmican was eaten only under special circumstances. Normally, according to Stefansson, the
diet consisted of dried or cured meat eaten with fat. (p 198) There is no reason to believe that this fat was
other than cavity and back slab fat, given that this fat was easily separated from the animal and that the
marrow was consumed on its own. Hugh Brody (The Living Arctic) reports that raw liver was mixed with
small pieces of fat (p 55); and that strips of dried or smoked meat were spread with fat or lard. (p 57).
Assuming that the kidney fat from a large animal weighs 30 pounds, and the back slab weights 40 to 50
pounds, that means there is at least 70 pounds of easily accessible fat that is mostly saturated on a large game
animal--possibly more on a buffalo whose hump is composed mostly of tallow. According to Stefansson,
much of the lean meat from a large animal was given to the dogs (p 26) which means that the proportion of
highly saturated fat to lean meat in daily meals for humans could easily have been 80:20.
Of course, the hunter-gather consumed organ meats and obtained some lipids from cell membranes in muscle
meat. A textbook on lipids states the following: The lipids of muscle and of most of the organs are, for the
most part, typical membrane lipids with high proportions of phospholipids containing relatively large
amounts of polyunsaturated long-chain acids and the saturated acid, stearate. (J F Mead et al, Lipids:
Chemistry, Biochemistry and Nutrition, 1986, p 70) As the phospholipids carry two fatty acids, usually one
is a long-chain polyunsaturated and the other a stearate. So approximately 50% of the cell membrane
phospholipids in organs and muscle are saturated, and only small amounts are monounsaturated. As not all
the fatty acids in the cell membranes are in the phospholipids, total SFAs are somewhat lower. In game
animals, total SFAs in the membranes of muscle and organ meats is about 40-45%, as reported by the
USDA. Thus organ and muscle meat are another, albeit smaller, source of SFAs in the hunter-gatherer diet.
125/147 (1998)
We need to be careful not to manipulate what we know about the hunter-gatherer in order to support the
current politically correct agenda, which extols monounsaturated fatty acids from commercially available
oils like olive oil, canola oil and high oleic safflower oil. Just because these oils lower cholesterol in shortterm experiments does not mean that they protect us from heart disease. Most serum cholesterol lowering is
merely a shifting of cholesterol from the blood to the cell membranes in order to give them better melting
characteristics. When the cell membranes become too rich in unsaturated fatty acids, due to high amounts in
the diet, cholesterol is driven into the cells to give the cell wall more integrity or stiffness. The overall
amount of cholesterol in the body is not reduced in such circumstances; in fact, the body usually responds by
making more cholesterol, so that over time, total cholesterol is increased. In any event, serum cholesterol
levels are not a good marker for proneness to heart disease.
The popular food writer Jean Carper recently described an arty meal of arugula salad with canola oil and
balsamic dressing, followed by lean meat and more vegetables, as the modern equivalent of the cave man
diet! From all accounts, the hunter-gather dined on guts and plenty of grease, not lean soy-fed meat and
designer oils.
PALEODIET Archives
Subject: Interesting mummy project
From: Dean Esmay
Reply-To:
Date: Mon, 9 Nov 1998 06:22:18 -0500
http://www.mcc.ac.uk/museum/general/mummy.htm -=The mind is not a vessel to be filled. It's a fire to be lit. - Plutarch
PALEODIET Archives
Subject: Re: PALEODIET Digest - 17 Nov 1998 to 19 Nov 1998 (#1998-85)
From: Buji Kern
Reply-To:
Date: Sat, 14 Nov 1998 00:45:24 -0800
I would like to commend Loren Cordain, PhD, for his interesting answer to the question of data reliability,
relevance, etc. of paleodiet principles.
I am particularly interested in the question, does the genotype that was selected by paleo conditions,
including paleodiets, also mean that modern simulations of paleo-diets would have positive health
implications for modern people?(People who are supposedly more interested in longevity than in early
maturity and fecundity.)
Although it is very complicated, I think the answer is yes, and I think that two lines of reasoning support this.
First, recent evidence has shown that the grandmother generation of gatherers are very economically
productive, being more or less free from heavy duty child rearing. So the older people are an important
survival asset to the tribe. It follows from this that the paleodiet could not have selected solely for early
reproductive success, at the expense of the health of the older generation. What counts, then as today, is the
overall persistance of the group. The ability to have short generation times, while definitely positive, is only
one factor to be considered.
And second, many diseases which cause middle aged and geriatric mortality, also markedly decrease
fecundity, during childbearing years. One prominent example is diabetes mellitus. This illness is
skyrocketing in modern populations, particularly in populations which are not European or Mediterranean,
and who have a shorter history of agricultural life. In females who have genetic susceptibility to this disease,
it is common to show gestational diabetes with the second or later pregnancy. This state is extremely
prejudicial to fetal development, and constitutes a high risk pregnancy. High risk for the fetus and the
mother. The baby is often oversize, presenting the need for C-section. Emergencies such as pre-eclampsia,
eclampsia, premature placental separation, and post-partum hemorrhage are all much more common in the
diabetic mother, and seem to be a function of her hyperglycemia. Needless to say, in primitive conditions
this would have been selected out.
126/147 (1998)
Since this genotype is still very much with us, it seems that the paleo- environment and diet protected against
the emergence of this disease. Much the same argument could be made for many illnesses which today are
mainly considered to be problems of middle or old age- hypertension, auto-immune disease such as lupus,
etc.. These are also big obstetric problems, and cause increased fetal and maternal mortality even today, with
our very advanced obstetric practices.
Overall, it is probable that the same diet which creates healthy young adults, also favors the creation of
healthy middle aged and older adults.
Michael Kern, MD
PALEODIET Archives
Subject: Paleo Querries
From: "Brian J. Mac Lean"
Reply-To:
Date: Mon, 16 Nov 1998 18:56:16 -0400
I have recently investigated the Paleolithic diet literature and a number of basic issues interest and puzzle
me. First, it seems that to identify with a particular lifestyle or practice, one requires a reasonable body of
empirical knowledge of the aforementioned. It appears that this basic condition is not satisfied in the case of
aspiring modern day Paleolithic nutritional adepts. The available information on Paleolithic peoples is so
scanty that it seems specious to believe that one can follow their nutritional practices with more than a
modicum of accuracy. The picture we have of contemporary hunter-gatherers suggests that few conclusions
can be drawn due to the high variability of nutritional patterns across different populations, in addition to the
difficulty of the contaminating influences of contact with industrial and post-industrial cultures.
Two of the assumptions that appear to be held in common by most who write about the Paleolithic diet is
that there was generally an absence of grains and dairy products (1). Furthermore, it is often suggested that
there has not been a long enough evolutionary time period to physiologically adapt to the metabolic
requirements of these substances, which has often led to the breakdown of healthy functioning (2).
Experimental and anthropological investigations of pathology and longevity suggest a picture which appears
somewhat at variance with some of the current Paleolithic practitioners' beliefs. With regard to
anthropological evidence, it appears that modern day Hunza and Vilcambas peoples demonstrate
considerable disease-free extended life spans (3). Although problems arise ascertaining the exact ages of the
the older members of Hunzaland, evidence suggests an absence of cardiovascular disorders (4). Both of these
populations are agricultural and subsist on a very restricted calorie diet which includes grains, legumes, dairy
and very small quantities of meat. Regarding experimental research, the most robust finding seems to be that
a calorie restricted diet is positively correlated with longevity and reduced rates of pathology (5). No other
nutritional variables appear to be reliably associated with longevity. With regard to pathology, a high intake
of red meat has been associated quite consistently with the development of cancers (6).
Perhaps the Paleolithic diet (if there is such a thing?), in the form of a relatively high fat and protein intake
by today's standards, was evolutionarily selected because it was the most effective to develop the human
form for the first two decades of life with the goal of effective reproduction. It may be that the genetic
agenda has loaded the psychobiological developmental trajectory towards reproductive fitness rather than
longevity. A diet higher in protein and fat, and lower in carbohydrates than that promulgated by current
mainstream thinking, may have been necessary to ensure the viability of the human species, but may be out
of step with current conditions. It hardly seems that reproductive prowess is a trait useful in the face of the
current population explosion and the ever dwindling food supplies for the planet.
One wonders if instead of chasing the chimera of 'Paleolithic man', we should not be looking more carefully
at the evidence from the 20th century. Any comments on these points would be appreciated.
References
1. DeVany, A. "Evolutionary Fitness, " 14, 1997. 2. Eaton, S.B ., Shostak, M., et al. The Paleolithic
Prescription: A Program of Diet & Exercise and a Design for Living: 41. New York: Harper & Row, 1988. 3.
Leaf, A. National Geographic, 143:93, 1973. 4. White, P.D., & Toomey, E.G., American Heart Journal,
Dec., 1964. 5. Walford, R.L. & Weindruch, R. The Retardation of Aging and Disease by Dietary Restriction.
Springfield, Illinois Charles C. Thomas, 1988. 6. Campbell, T. Colin; Chen, J"Diet and chronic degenerative
diseases: perspectives from China." American Journal of Clinical Nutrition, vol. 59, 1153S-1161S., 1994.
127/147 (1998)
PALEODIET Archives
Subject: Re: Response to Brian MacLean's Paleo Querries
From: Loren Cordain
Reply-To:
Date: Wed, 18 Nov 1998 14:46:09 -0700
Brian brings out some excellent points which we have discussed in previous posts over the last year or two.
At the risk of repeating myself, let me briefly address some of his comments.
1. "The available information on Paleolithic peoples is so scanty that it seems specious to believe that one
can follow their nutritional practices with more than a modicum of accuracy". I dont think few scientists
studying paleodiets would argue this point. However there are some obvious deductions which allow basic
generalizations which have enormous impact upon present day health (i.e. dairy products could not have
been a component of stone age diets). Similar arguments can be made for salt (sodium chloride), trans-fatty
acids (except for trans vaccenic acid - trans 11, 18:1), cereal grains, refined carbohydrates, fatty meats and
other "modern" foods.
2. "The picture we have of contemporary hunter-gatherers suggests that few conclusions can be drawn due to
the high variability of nutritional patterns across different populations, in addition to the difficulty of the
contaminating influences of contact with industrial and post-industrial cultures." There is little doubt that
studies of contemporary hunter-gatherers, particularly those done in the past 30 years or so are influenced by
the relative degree of contact these peoples have had with industrialized societies. Many of these
contaminating influences of civilization upon dietary practices have been noted and qualified, particularly in
the more recent (in this century) studies of hunter-gatherers (eg. carbohydrate in the diet of the Inuit (1-4)).
The information that has been garnered by ethnologists and anthropologists has value and provides insight
into what the components of the completely aboriginal diet would have been prior to contact and
acculturation. We have comprehensive and detailed lists of wild plants and animals that were consumed by
hunter-gatherers all over the world. These lists have been compiled in the recent past in partially accultured
peoples, as well as in the 18th and 19th century in completely unacculturated hunter gatherers. The
qualitative substance of what these people ate is not so much in question as is the quantitative issue. Data
from our research group indicates that the range of diet in terms of plant:animal (P:A) subsistence ratios (and
hence macronutrient variation) was large (0-5%P:95-100%A to 76-85%P:15-24%A), however the variation
was surprisingly narrow relative to the central tendency. In all world wide hunter gatherers (n=229) listed in
Murdock's Ethnographic Atlas, the median and modal values for animal food subsistence is 56-65% whereas
the median and modal value for plant food subsistence is 26-35%. If the data is expressed as ratio level data,
then the mean value for animal food subsistence with its SD is 6.77 + 1.85. The mean value 6.77 would fall
within the 66-75% animal subsistence level. The meaning of this ethnographic data is clear. In virtually all
world wide hunter gatherer populations (whereever it was ecologically possible), animal food would have
always comprised more than half of the dietary intake. Therefore, the variability in diet among worldwide
hunter gatherers is not as quantitatively variable (in terms of macronutrients) as has previously been
assumed. Not a single world wide hunter gatherer society derives its entire subsistence solely from plant
foods, and only 10% of the total (n=229) studied, derive 56% to 85% of their food calories from plant food.
3. The third issue brought up by Brian is the issue of longevity. I think that most gerontologists are in
agreement (at least in terms of animal experiments) that caloric restriction extends lifespan. Whether or not
this general principal applies to humans is not known. However, in humans, it appears that there is a strong
genetic component which is independent of environmental factors (5). The reported longevity of Hunzas and
Vilcambas may have a genetic basis or it may be a function of diet or a combination of both. Although Brian
suggests that " No other nutritional variables appear to be reliably associated with longevity", this clearly is
not the case. Apparently Brian is unfamiliar with Harman's classic free radical theory reviewed in (6) and
generally accepted as a contributor to the ageing process by most nutritionists and gerontologists (7-9).
Because the hunter gatherer diet contained few or no cereal grains and high levels of fruits and vegetables
(compared to modern standards), the antioxidant intake from phytochemicals and vitamins would have been
quite high. In analyzing hunter-gatherer subsistence ratios using modern foods, computerized dietary
analyses by our research group has shown that a diet composed of lean meats (55% total energy) and fruits
and vegetables (45% energy) yields much higher antioxidant levels than for grain and dairy based diets.
128/147 (1998)
4. "With regard to pathology, a high intake of red meat has been associated quite consistently with the
development of cancers (6)." There is no doubt that multiple epidemiological studies have shown an
association between high consumption of red meat intake and many types of cancers. However, there is just
as strong epidemiological evidence to show a relationship between saturated fat intake and cancers (checkout
medline, there are thousands of references). Because, modern commercially available red meat contain
enormous amounts of saturated fat (a t-bone steak with 10% fat by weight contains 50% fat by energy), it is
quite difficult if not impossible for epidemiological studies to untangle the effects of the meat protein with
the meat fat. There is very little experimental evidence to show that protein is a mutagen whereas there
numerous animal studies and in vitro cell studies indicate that high fat diets can serve as promoters of many
diverse cancers. The fat content of muscle meat in wild game animals ranges from 1-2% by weight or about
10-20% by energy. Thus, the muscle of game meat (the staple food of hunter-gatherers) is almost entirely
protein.
5. "Perhaps the Paleolithic diet (if there is such a thing?), in the form of a relatively high fat and protein
intake by today's standards" Reconstructed "paleolithic diets" by my colleague Boyd Eaton (10), as well as
estimates that we will soon publish, do not indicate that such diets were high in fat. During certain times of
the year, these types of diets, particularly in northern latitude hunter gatherers, may have equaled or
exceeded the fat content of modern diets, however the aggregate data suggests that the total fat content was
either equal to or lower than that in modern diets. An important distinction here is the type of fats that were
consumed. As we have previously shown, the fatty acid composition of pre-agricultural diets would have
been much different than the modern diet (11).
6. "Perhaps the Paleolithic diet (if there is such a thing?), in the form of a relatively high fat and protein
intake by today's standards, was evolutionarily selected because it was the most effective to develop the
human form for the first two decades of life with the goal of effective reproduction." Evolutionary theory
certainly agrees with this concept, at least in context. The diet that humans evolved with is the diet which we
are genetically adapted to, and the diet that tends to optimize reproductive potential. Most nutritionists would
agree that diets high in fruits and vegetables such as the "paleodiet" would be healthful not only during the
reproductive years, but also during the post-reproductive years. Similarly, the low fat content and fat balance
(high N3, high monounsaturates, low trans fat, low saturated fat) of stone age diets would also promote
health in the post-reproductive years. If a high protein intake is countered by a high fruit and vegetable
intake, the potential deleterious influence high protein intake upon acid/base balance and hence calcium
metabolism can be overcome. Indeed the potential renal acid load (PRAL) of a diet in which 45% of the
caloric intake is composed of fruits and vegetables will result in a net alkaline load (12). I also suspect that a
salt restricted diet (such as the paleodiet) would also be just as beneficial for older people, if not more so,
than for those in their prime reproductive years.
7. "One wonders if instead of chasing the chimera of 'Paleolithic man', we should not be looking more
carefully at the evidence from the 20th century".
Indeed!, What was it that Santayana said? Something like: those who are unfamiliar with the past are
condemned to repeat it? (Dean - help me out on this quote - you are the quote master). By ignoring the
genetic and evolutionary basis for our present day dietary requirements, we are essentially throwing out eons
of evolutionary experience - experience that is still far wiser than the mind of 20th century man and his
fledgling science.
Cordially,
Loren Cordain, Ph.D., Professor Department of Exercise and Sport Science Colorado State University Fort
Collins, CO 80523 tel: (970) 491-7436 fax:(970) 491-0445 email:
http://www.colostate.edu/Colleges/CAHS/ess/cordain.htm
REFERENCES
129/147 (1998)
1. Bang HO, Dyerber J. Lipid metabolism and ischemic heart disease in Greenland eskimos. Adv Nutr Res
1980;3:1-22. 2. Sinclair HM. The diet of canadian indians and eskimos. Symposium Proc 1953;12:69-82. 3.
Heinbecker P. Studies of the metabolism of eskimos. J Biol Chem 1928;80:461-75. 4. Krogh A, Krogh M. A
study fo the diet and metabolism of eskimos undertaken in 1908 on an expedition to Greenland. Meddelelser
om Gronland 1913:51:1-52. 5. Mueller LD, Rose MR. Evolutionary theory predicts late-life mortality
plateaus.Proc Natl Acad Sci 1996;93:15249-53. 6. Harman D. The aging process. Proc Natl Acad Sci
1981;78:7124-28. 7. Cutler RG. Antioxidants and aging. Am J Clin Nutr 1991;53:373s-9s. 8. Ames BN et al.
Oxidantss are a major contributor to aging. Ann NY Acad Sci 1992 ;663:85-96 9. Sohal RS. Relationships
between antioxidants, prooxidants and the aging process. Ann NY Acad Sci 1992 ;663:74-84 10. Eaton, S.B
., Shostak, M., et al. The Paleolithic Prescription: A Program of Diet & Exercise and a Design for Living:
New York: Harper & Row, 1988. 11. Eaton SB, Eaton SB 3rd, Sinclair AJ, Cordain L, Mann NJ. Dietary
intake of long-chain polyunsaturated fatty acids during the paleolithic.World Rev Nutr Diet 1998;83:12-23.
12. Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. J Am Diet Assoc 1995
;95:791-7 .
PALEODIET Archives
Subject: Re: PALEODIET Digest - 15 Nov 1998 to 17 Nov 1998 (#1998-84)
From: M E Wood
Reply-To:
Date: Wed, 18 Nov 1998 16:49:51 +1300
> Topics of the day: > 1. Paleo Queries
I am at a loss to reconcile Paleolithic mans diet with contaminating influences from industrial societies.
Paleolithic man lived by definition before agriculture and therefore before cities and industrialisation.
Therefore he must have subsisted by hunting, gathering and fishing. Before agriculture any wild grains
would be harvested, if at all, when the seeds were ripe and are unlikely to have been a major part of the diet.
Milk is usually provided by managed herds of cattle camels or horses. How far paleolithic man, who lived
during the last glacial period and in its various warmer intervals, was following and milking herds is a matter
of controversy
Perhaps Mr MacLean is confusing paleolithic man with more modern " hunter gatherers" and has been
misled by the nomenclature used by anthropologists and archaeologists which may be some what specialised
but which we use unconciously now.:-)
M E Wood M A Hons Prehistoric Archaeology (Edinburgh)
"What can be done with fewer assumptions is done in vain with more." William of Occam 1285-1347.
PALEODIET Archives
Subject: Interesting web pages
From: Dean Esmay
Reply-To:
Date: Sat, 21 Nov 1998 19:51:07 -0500
From BBC News Online, a piece on milk in ancient diets:
http://news.bbc.co.uk/low/english/sci/tech/newsid_218000/218473.stm
From Science Magazine, a piece on a 9000 year-old settlement once thought to be agricultural:
http://www.sciencemag.org/cgi/content/full/282/5393/1441
-="What is wanted is not the will to believe, but the will to find out, which is the exact opposite." --Bertrand
Russell (1872-1970)
PALEODIET Archives
130/147 (1998)
Subject: Notes from the Moderator, and a Quote for Loren

From: Dean Esmay
Reply-To:
Date: Sat, 21 Nov 1998 20:09:20 -0500
Update: Our list continues to grow, but slowly. Our grouup consists of two hundred-odd members, a majority
with Ph.D.'s in various fields, a large number of the remainder being graduate students or people with
Master's degrees in fields such as paleontology, biology, archaeology, etc.
I would, however, like to see our list grow to include even more members in academia or professional
research. Thus I would like to encourage those of you who are professional scientists to mention the
Paleodiet Symposium to your colleagues. Being added to our (completely non-commercial, non-profit, and
free) mailing list is a simple matter of dropping a note to me at:
As for Loren's request to me (at
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9811&L=paleodiet&F=&S=&P=446): so far as I know
Santayana exactly said, "Those who cannot remember the past are condemned to repeat it." A good
sentiment, but Loren may have been searching for something more like this:
"A generation which ignores history has no past--and no future." (Robert Heinlein, TIME ENOUGH FOR
LOVE.)
Obligatory disclaimer: this message neither implies nor denies any endorsement or non-endorsement I may
or may not make of any position he may or may not take on any of the issues Brian so eloquently brought to
our attention.
Random thought: if there's a prize somewhere for squeezing eight or more equivocations into one sentence,
can I claim it now?
Dean Esmay, your ever-humble moderator, host, and Keeper of Odd Knowledge
-=Ad astra per aspera
PALEODIET Archives
Subject: Subject: 1. Response to Brian MacLean's Paleo Queries
From: Bob Avery
Reply-To:
Date: Sun, 22 Nov 1998 00:33:24 -0500
In response to Brian MacLean's questions, Loren Cordain wrote:
> hunter gatherers (n=229) listed in Murdock's Ethnographic Atlas, the median and modal values for
> animal food subsistence is 56-65% whereas the median and modal value for plant food subsistence is
> 26-35%.
Loren, just to clarify, when these percentages are bandied about, are we referring to (1) caloric values, (2)
volume, or (3) weight?
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PALEODIET Archives
Subject: gestational diabetes
From: kbemmott
Reply-To:
Date: Sun, 22 Nov 1998 11:39:50 -0800
Dr. M. Kern wrote:
131/147 (1998)
"....And second, many diseases which cause middle aged and geriatric mortality, also markedly decrease
fecundity, during childbearing years. One prominent example is diabetes mellitus. This illness is
skyrocketing in modern populations, particularly in populations which are not European or Mediterranean,
and who have a shorter history of agricultural life. In females who have genetic susceptibility to this disease,
it is common to show gestational diabetes with the second or later pregnancy. This state is extremely
prejudicial to fetal development, and constitutes a high risk pregnancy. High risk for the fetus and the
mother. The baby is often oversize, presenting the need for C-section. Emergencies such as pre-eclampsia,
eclampsia, premature placental separation, and post-partum hemorrhage are all much more common in the
diabetic mother, and seem to be a function of her hyperglycemia. Needless to say, in primitive conditions
this would have been selected out."
Oh, I don't know. If the pregnant woman is not an insulin dependent diabetic, there doesn't seem to be such a
high risk. Some authorities have stated flatly that there's no point in even screening for gestational diabetes
because treatment doesn't make any real improvement in fetal well being. I no longer screen women under
25, and I suspect a lot of Paleolithic births took place in under-25s. If a Paleolithic woman had juvenile,
insulin dependent diabetes, she would not live to grow up, and if she did, she would not give birth. Prior to
1922 the Joslin Clinic for diabetics had NEVER had a live birth to a diabetic woman. Most of the mothers
died, too.
PALEODIET Archives
Subject: Red meat and cancer
Reply-To:
Date: Sun, 22 Nov 1998 13:21:51 PST
Brian MacLean posted, and Loren Cordain responded:
4. "With regard to pathology, a high intake of red meat has been associated quite consistently with the
development of cancers (6)."
There is no doubt that multiple epidemiological studies have shown an association between high
consumption of red meat intake and many types of cancers. However, there is just as strong epidemiological
evidence to show a relationship between saturated fat intake and cancers (checkout medline, there are
thousands of references). Because, modern commercially available red meat contain enormous amounts of
saturated fat (a t-bone steak with 10% fat by weight contains 50% fat by energy), it is quite difficult if not
impossible for epidemiological studies to untangle the effects of the meat protein with the meat fat. There is
very little experimental evidence to show that protein is a mutagen whereas there numerous animal studies
and in vitro cell studies indicate that high fat diets can serve as promoters of many diverse cancers. The fat
content of muscle meat in wild game animals ranges from 1-2% by weight or about 10-20% by energy. Thus,
the muscle of game meat (the staple food of hunter-gatherers) is almost entirely protein.
-----------------------------------------------------In addition to the role that the saturated fat in modern meat may be playing in contributing to cancer, I would
like to mention 2 other possible factors (which were not present in the Paleo diet):
1) Pesticide residues from animal feed that concentrate in the fat (perhaps this could partly explain the
correlation between saturated fat intake and cancer?)
2) Modern meat consumption generally takes place place in the context of a low-fiber diet and relative
inactivity, whereas the Paleo diet was probably high in fiber (at least in plant-rich regions) and high in
activity. Both of these would contribute to quicker passage of any negative (possibly carcinogenic) residues
from animal protein digestion through the digestive system.
Steve Meyers Lawrence Berkeley Natl Lab
PALEODIET Archives
Subject: Recent postings
From: Dean Esmay
Reply-To:
Date: Sun, 22 Nov 1998 20:34:22 -0500
132/147 (1998)
1) What is the scientific evidence regarding the existence of pesticide residues in modern meats? What is the
extent of evidence that said residues are carcinogenic? And what is the evidence regarding whether or not
plant foods are somehow safer in this regard?
2) What medical authorities have advanced the suggestion that standard treatment protocols for gestational
diabetes are ineffective?
3) Is there a reference to support the claim that prior to 1922 the Joslin Clinic had never had a live birth to a
live woman?
While this is only a semi-formal forum, I urge members to provide specific evidence for any claims.
Speculation is not disallowed here. However we have members from many diverse fields. While we do want
to be able to relax and just talk here, I urge members to remember that not everyone may share the same
background, and that the bigger a claim is, the more it demands some form of objective source to verify it.
Much thanks for all efforts in this regard.
Russell (1872-1970)
PALEODIET Archives
Subject: Re: More on the Ethnographic Atlas & Longevity
From: Loren Cordain
Reply-To:
Date: Mon, 23 Nov 1998 11:54:30 -0700
In a previous post, Bob Avery had the following question,
"In response to Brian MacLean's questions, Loren Cordain wrote:
> hunter gatherers (n=229) listed in Murdock's Ethnographic Atlas, the median and modal values for
> animal food subsistence is 56-65% whereas the median and modal value for plant food subsistence is
> 26-35%.
Loren, just to clarify, when these percentages are bandied about, are we referring to (1) caloric values, (2)
volume, or (3) weight?"
Murdock did not stipulate this information in his compilation of the Ethnographic Atlas; he simply referred
to the data as "subsistence dependence". He compiled his admittedly rough numbers from ethnographic
observations made by anthropologists and ethnographers who in most cases neither weighed the food nor
attempted to estimate its caloric value. If one examines the original publications cited by Murdock (there are
about 400 references total), many of the references pre-date caloric theory, therefore, it is likely that most of
the observations were made by rough visual estimation of volume and/or weight. Consequently, there is an
inherent imprecision in the conversion of these estimates to caloric values. However, this is the nature and
shortcomings of ethnographic data & since, these hunter gatherer societies no longer exist (in their aboriginal
state), the ethnographic observations represent the only information available on the nutrient intake of these
societies. I suspect that Murdock realized these shortcomings, and his estimates have been divided into fairly
large ranges for each class interval (i.e. 16-25%, 26-35% etc).
133/147 (1998)
Dr. Kern makes some excellent points in his post of November 14th regarding selection for longevity in the
paleo- environment. Many of these same points have been eloquently written up by Jared Diamond
(Diamond J. Why women change. Discover Magazine 1996 (July):131-37). The persistence of female
menopause in our species is a powerful example in which post-reproductive selection pressures influence the
gene pool. Females of our species are quite unusual in the animal world; except for a single species of whale,
no other mammal experiences menopause. How is it that natural selection could have ever selected for early
shut down of reproductive capacity before the end of the full lifespan? Surely, women with a longer
reproductive span will produce more offspring and thereby increase the probability of increasing the number
of their genes in the gene pool. Thus, any theory attempting to explain menopause must show that by making
fewer babies, in actuality more babies are made (i.e more of the mothers genes survive with the surviving
offspring). Infants of older mothers are increasingly unlikely to survive or be healthy, because the risks of
abortion, still birth, low birth weight and genetic defects rise as the mother grows older. Thus, not only are
the children of older mothers more likely to die, but the chances of the older mother dying in or after
childbirth are also increased. Further, as a woman gets older she is also likely to have accumulated more
children, consequently her survival directly impacts the survival not just of her present child, but of her
previous children. Thus, each succeeding pregnancy not only puts her at risk, but also all of her previous
children. By shutting down reproduction before the end of the lifespan (menopause), apparently more of the
mothers children, and hence her own genes will survive. In hunter gatherer societies, a woman's survival is
not only important to her children, but also to her grandchildren. Studies of hunter-gatherer grandmothers
show that they share their excess gathered food harvest with grand children and grown children.
Consequently, in the case of humans, natural selection appears to be acting in an unusual a priori manner in
which the ultimate reproductive (total individual genes in the gene pool) potential is acting postreproductively. Humans are different from other animals in that we have a culture and language in which we
can transmit knowledge about our environment (present and past) to our offspring which may influence their
survival and hence our own genes' survival. Because old people represent the repository of knowledge in preliterate societies, they can influence the survival of hundreds of people who bear their genes by providing
information during times of stress (eg. where to find water or plants when the 40 yr drought arrives). In
hunter-gatherer societies, the old person is the tribe's library. The old person knows more about the local
environment than anyone else and is the sole person with accurate knowledge of events that happened long
ago. The accumulated experience that the elderly remember is important to the survival of the entire tribe.
Hence, because of our culture and ability to transmit knowledge, we in effect have an a priori influence upon
genes which we can no longer influence merely by direct transmission (i.e reproduction).
Cordially,
PALEODIET Archives
Subject: Re: Meat and cancer
From: Dana Carpender
Reply-To:
Date: Mon, 23 Nov 1998 20:20:30 -0500
Curious to know: have any of the studies of meat consumption and cancer development been done on people
who ate a very low carb diet, or at least ate no sugar or refined flour products of any kind? I've read some
interesting stuff in Medline about ketogenic diets slowing tumor growth, and in some cases even shrinking
tumors, while preventing cachexia. The ketogenic diet used was high in MCTs; have no idea what
importance that has to the positive results. From what I can gather, cancer is a glucose-hog, and limiting the
glucose load is the theoretical cause of the positive results. Thoughts? Studies?
Dana
PALEODIET Archives
Subject: Menopause in the hunter gatherer?
From: Sandy Rzetelny
134/147 (1998)
Reply-To:
Date: Tue, 24 Nov 1998 10:52:51 EST
In a message dated 11/24/98 3:28:32 AM Eastern Standard Time, writes:
<< Females of our species are quite unusual in the animal world; except for a single species of whale, no
other mammal experiences menopause. How is it that natural selection could have ever selected for early
shut down of reproductive capacity before the end of the full lifespan?
Is there evidence indicating that the paleo hunter gatherer woman did undergo menopause?
Thanks Sandy Rzetelny
PALEODIET Archives
Subject: Seeds Not Important in Paleolithic Diet???
Reply-To:
Date: Wed, 25 Nov 1998 03:36:10 EST
ME Wood writes: << Paleolithic man lived by definition before agriculture and therefore before cities and
industrialisation. Therefore he must have subsisted by hunting, gathering and fishing. Before agriculture any
wild grains would be harvested, if at all, when the seeds were ripe and are unlikely to have been a major part
of the diet.
I'm at a loss about the interpretation that Paleolithic man was unlikely to have included seeds as a major part
of the diet, if they were present at all. Where does this come from? Is there any evidence? Certainly
agricultural grains are not the only seeds available to or exploited by humans. Non- cultivated seeds have
been an important part of the diet in pre-agricultural populations, as well as for many populations with
agriculture. I think this statement reflects a bias (supposition?) not supported by data or might refer to a
specific econiche.
For instance, pre-agricultural man in North America exploited many native seeds including members of the
genera _Chenopodium_ and _Amaranthus_, the Asteraceae family, the Cruciferae family, the genus
_Portulaca_, to name a few. Pre-agricultural man in the Old World also exploited seeds including
_Chenodium_ and many others. These seeds are very nutritious, easy to gather and prepare. Where's the
evidence that they were absent from the diet or neglected as a food source?
Linda Scott Cummings, Ph.D. Paleo Research Golden, CO
PALEODIET Archives
Subject: diabetes and infertility reference
From: kbemmott
Reply-To:
Date: Thu, 26 Nov 1998 10:41:27 -0800
3) Is there a reference to support the claim that prior to 1922 the Joslin Clinic had never had a live birth to a
live woman?
There was a review article in the american Journal of Obstetrics and Gynecology about 1985, from the Joslin
Clinic. I'll try and track it down. Dr. K. Emmott
PALEODIET Archives
Subject: Ruediger Hoeflechner
Reply-To:
Date: Thu, 26 Nov 1998 13:37:18 -0500
135/147 (1998)
On Mon, 23 Nov 1998, Loren Cordain wrote: "Females of our species are quite unusual in the animal world;
except for a single species of whale, no other mammal experiences menopause."
Maybe we are less unique.... The following article quotes some other female mammals with a postreproductive phase:
Reproductive cessation in female mammals.
Packer C, Tatar M, Collins A
Department of Ecology, Evolution and Behavior, University of Minnesota, St Paul 55108, USA.
In female mammals, fertility declines abruptly at an advanced age. The human menopause is one example,
but reproductive cessation has also been documented in non-human primates, rodents, whales, dogs, rabbits,
elephants and domestic livestock. The human menopause has been considered an evolutionary adaptation,
assuming that elderly women avoid the increasing complications of continued childbirth to better nurture
their current children and grandchildren. But an abrupt reproductive decline might be only a non-adaptive
by-product of life-history patterns. Because so many individuals die from starvation, disease and predation,
detrimental genetic traits can persist (or even be favoured) as long as their deleterious effects are delayed
until an advanced age is reached, and, for a given pattern of mortality, there should be an age by which
selection would be too weak to prevent the onset of reproductive senescence. We provide a systematic test of
these alternatives using field data from two species in which grandmothers frequently engage in kin-directed
behaviour. Both species show abrupt age-specific changes in reproductive performance that are characteristic
of menopause. But elderly females do not suffer increased mortality costs of reproduction, nor do postreproductive females enhance the fitness of grandchildren or older children. Instead, reproductive cessation
appears to result from senescence.
Nature 1998 Apr 23;392(6678):807-11
PALEODIET Archives
Subject: Paleolithic centenarians?
Reply-To:
Date: Thu, 26 Nov 1998 13:45:01 -0500
An appendix to Brian Mac Lean=B4s question and Loren Cordain=B4s post about paleolithic longevity: The
existence of a female menopause in humans is a strong evidence for a maximal paleolithic lifespan that
widely exceeds average life expectancy. Can we suppose, that the paleolithic population pyramid of Homo
sapiens was slim (due to higher mortality rates in each decade), but had the same height as a modern one? In
Austria (8 million inhabitants) we have more than 300 centenarians. Were there sporadic centenarian humans
100.000 or 15.000 years ago? Or in modern paleolithic surrogates: There is no question, that some of them
live to the age of sixty - but are there Queen Mummies in the !Kung or Yanomamo?
In all industrialized countries average lifespan increases. Only average lifespan or maximal lifespan too? A
similar example are some animals in captivity, for instance more than 50 years old apes. Is this only the
broadened top of the demographic iceberg or has the top become higher?
PALEODIET Archives
Subject: Re: Meat and cancer
From: Ron Hoggan
Reply-To:
Date: Thu, 26 Nov 1998 17:35:18 -0700
Hi Dana, You have raised some *very* interesting points. The results of the ketogenic diets certainly weaken
the results of studies suggesting that meat consumption and associated saturated fat is a cause of cancer.
136/147 (1998)
You might be interested in looking at the articles cited below. The first two indicate that some proteins from
cereals and milk may inhibit our ability to battle malignancy. Celiac disease provides an example which
identifies those at one end of the spectrum. The second two indicate an association between cancer risk and
cereal consumption. The picture is, of course, much more complicated than that. I have summarized in the
interest of brevity.
1.Hoggan, R. (1997). Considering wheat, rye, and barley proteins as aids to carcinogens. Medical
Hypotheses. 49, 285-288.
2. Castany MA, et al. (1995) Natural killer cell activity in coeliac disease: effect of in vitro treatment on
effector lymphocytes and/or target lymphoblastoid, myeloid and epithelial cell lines with gliadin. Folia
Microbiol (Praha). 1995;40(6):615-20.
3. Favero A, et al. Diet and risk of breast cancer: major findings from an Italian case-control study. Biomed
Pharmacother. 1998;52(3):109-15.
4. Ji BT, et al. Dietary habits and stomach cancer in Shanghai, China. Int J Cancer. 1998 May 29;76(5):65964.
best wishes, Ron
PALEODIET Archives
Subject: Hyperinsulinemia and colon cancer
From: Paul Bergner
Reply-To:
Date: Thu, 26 Nov 1998 18:42:01 -0700
To Dana's question about refined carbohydrates being a possible confounding factor in studies relating meat
consumption with the development of cancer, here is slightly tangential but not too far afield response
Recent studies in animals have demonstrated a tumor promoting effect for hyperinsulinemia. See, for
instance,
Koohestani N, Tran TT, Lee W, Wolever TM, Bruce WR. Insulin resistance and promotion of aberrant crypt
foci in the colons of rats. on a high-fat diet. Nutr Cancer 1997;29(1):69-76
Tran TT, Medline A, Bruce WR. Insulin promotion of colon tumors in rats. Cancer Epidemiol Biomarkers
Prev 1996 Dec;5(12):1013-5
-- Paul Bergner, Editor, Medical Herbalism. Email: Web: http://medherb.com Bio and affiliations:
http://medherb.com/STAFF.HTM Books: http://medherb.com/PBBOOKS.HTM Mail: P.O. Box 20512,
Boulder, Colorado 80308, USA. Fax: 303-415-9196
PALEODIET Archives
Subject: Seeds Not Important in Paleolithic Diet???
From: Dean Esmay
Reply-To:
Date: Fri, 27 Nov 1998 16:53:17 -0500
Regarding Linda Scott Cummings' comments on seeds in the paleolithic diet: I offer no opinion on the
matter, but I point out that Mavis' point seems to have been that it's unlikely that wild grass seeds could have
been a -primary- food source in most of the world, since these are a seasonal item and are just one of a wide
variety of foods available to pre-agricultural peoples.
Analysis of human coprolites would probably tell us more about this issue than any amount of speculating.
I've been wishing for some time that we could find someone with a background in that area, but alas all the
people with such backgrounds I've tried to reach so far have not responded to my inquiries.
Russell (1872-1970)
PALEODIET Archives
137/147 (1998)
Subject: Scientific American article

From: Dean Esmay
Reply-To:
Date: Sat, 28 Nov 1998 10:58:38 -0500
Here is a nice article on medicine and evolution from Scientific American:
http://www.sciam.com/1998/1198issue/1198nesse.html
-="Gimme that ring, ya hairy-footed varmint! Gimme that ring or I'll blast ya!" --Yosemite Nazgul
PALEODIET Archives
Subject: Re: Seeds & Menopause
From: Loren Cordain
Reply-To:
Date: Sat, 28 Nov 1998 13:47:00 -0700
In her post of November 26, Linda Scott Cummings brings up an important point regarding seed
consumption in hunter-gatherers which often times seems to be frequently misunderstood or perhaps
misinterpreted in this listserve. As she points out, there is ample evidence from a variety of sources that
indicate seeds of a variety of species were consumed by pre-agrarian people (1-4). Also, there is substantial
evidence to indicate that grass seeds were sporadically consumed by certain hunter gatherer societies during
the post-pleistocene (Holocene) epoch (5). The issue here is the quantitative assessment of grass seed and
other seed consumption in the diets of hunter-gatherers. Generally, grass seeds only comprised significant
energy on a regular basis for hunter-gatherer societies living in marginal areas such as in the American Great
Basin (5), Certain parts of the arid Australian outback (4, 5, 6) and portions of Africa (5). Many of these
marginal areas only became inhabited by humans in the post-pleistocene epoch when human populations
numbers increased and large mammal numbers declined. Because the caloric return for energy expended in
the harvesting of grass seeds is low compared to animal foods (6), grass seed consumption generally occurs
under marginal environmental conditions when other food choices are unavailable. Seeds from species other
than graminacea often times yield a greater caloric return per energy expended (6) and would be expected to
be part of the diet of hunter-gatherers. However, it is quite unlikely that any seed ever represented the
majority of the daily energy intake in any human group until the advent of agriculture and the domestication
of cereal grains.
In regards to menopause, Ruediger Hoeflechner brings up data (7) of which I was unfamiliar and which
clearly does not support Jared Diamond's contention (8) that menopause is an almost unique function of
humans. I certainly do not claim expertise in this area. Perhaps we could get Dean to solicit the opionion of
either Dr. Diamond or Dr. Packer.?
REFERENCES 1. Renfrew JM. Paleoethnobotany. The Prehistoric Food Plants of the Near East and Europe.
Columbia University Press, N.Y., 1973. 2. Sobolik KD (Ed.). Paleonutrition and Health of Prehistoric
Americans. Center for Archaeological Investigations, Carbondale, Ill, 1994. 3. Gilbert RI, Mielke JH (Eds).
The Analysis of Prehistoric Diets. Academic Press, N.Y., 1985. 4. Brand-Miller JC, Holt SHA. Australian
aboriginal plant foods: a consideration of their nutritional composition and health implications. Nutr Res Rev
1998;11:5-23. 5. Harlan JR. Wild grass seed harvesting and implications for domestication. In: Prehistoire de
L'Agriculture:Nouvelles Approches Experimentales et Ethnographiques. Monographie du CRA no. 6, ed
CNRS, 1992. 6. O'Connell JF, Hawkes K. Food choice and foraging sites among the Alyawara. J. Anthropol
Res 1984;40:504-35. 7. Packer C, Tatar M, Collins A.Reproductive cessation in female mammals. Nature
1998 Apr 23;392(6678):807-11 8. Diamond J. Why women change. Discover Magazine, July 1996:131-37.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 29 Nov 1998 to 2 Dec 1998 (#1998-93)
138/147 (1998)
From: Reply-To:
Date: Fri, 4 Dec 1998 21:27:10 EST
To: All Paleodieters From: Sally Fallon and Mary G Enig, PhD Re: Queries by Brian J MacLean
We would agree that few conclusions can be made from the scanty evidence available on Paleolithic man. If
we are to use anthropological data to guide us in determining optimum diets for modern man, we would do
better to make careful and in depth studies of the dietary habits of living isolated primitive groups. We
emphasize the words careful and in depth, because cursory examinations often miss important details, such
as food preparation methods or unusual dietary choices like insects.
In the Human Diet Series we are writing for the Price-Pottenger Nutrition Foundation quarterly journal, 1 we
have noted certain underlying characteristics of traditional diets including a preference for animal protein
and fat (often to the point of gorging on these foods when they are available); use of animal bones (or
shellfish shells) to make pastes or broths; careful preparation of grains and legumes to neutralize antinutrients commonly found in these foods; and the widespread practice of lactofermentation to make
enzyme-enriched and nutrient-enhanced condiments, preserves and beverages.
Milk products and grains need not be avoided; they have nourished healthy population groups for thousands
of years. But care must be taken in production and preparation methods. Modern whole grain products
contain mineral blocking phytic acid and enzyme inhibitors; modern milk products have been denatured and
stripped of their valuable enzyme content through pasteurization; they come from cows that have been bred
to produce high- protein, low-fat milk, and that are fed inappropriate feed. A return to traditional farming and
preparation methods would solve the vast majority of problems association with milk and grain consumption.
(See www.realmilk.com)
The people of Hunza consume large amounts of whole goat milk products. Goat milk is higher in fat, and
contains more saturated fat, than cows milk. The people of Vilcabamba consume whole cows milk and the
principle meat is fatty pork. The long lived people of Soviet Georgia consume a diet high in animal protein
and fat from whole milk products and pork. In fact, the greatest longevity among inhabitants of Soviet
Georgia is found in those who consume the most meat and fat.2
No good studies have shown that calorie restriction contributes to a longer life in humans. The Framingham
study found that those who consumed the greatest number of calories weighed the least, had the lowest
serum cholesterol and were the most physically active.3 Animal studies showing reduced numbers of tumors
in animals on restricted-calorie diets also found that the restricted-calorie groups had larger and more
virulent tumors than those on nonrestricted diets.4
The Cornell Study did not find that consumption of red meat was associated with increased rates of cancer,
nor of any disease; nor did the study find that large amounts of dietary plant protein correlated with reduced
rates of disease (with the exception of a weak correlation of with less nasal cancer and less TB), in spite of
claims made by the studys authors.
In any event, the Cornell China study is seriously flawed, and cannot be used to determine the relationship
between diet and health. For example, egg consumption is given as ranging from averages of about 15 grams
per day in the northern most parts of China to amounts bordering on zero in the impoverished area around
Sian in central China. In the Shanghai region the average is given as 12 grams per day. (An egg weighs about
50 to 60 grams.) These figures are at odds with statistics that show per capita egg consumption in all of
China to be roughly one third that of the United States5, as well as with another study showing per capita egg
consumption of 50 to 80 grams per day in the northern part of China6, and yet another showing egg
consumption as high as 340 grams per day in lactating women.7 American egg consumption is roughly 40
grams per day, yet the Cornell study showed egg consumption at expected ratios in only two underpopulated
northern areas and in the Shanghai region. Such low values for egg consumption suggest that the participants
in the Cornell study were not truly representative of the Chinese populationyet consumption figures for this
nonrepresentative group are correlated with data for total overall mortality. No valid conclusions can be
drawn from this methodology.
The study indicated that egg eaters had more cancers of the brain, lung and bowel, perhaps because large
numbers of them live in the polluted Shanghai region. This example highlights yet another problem with the
Cornell study, namely that it encompasses huge numbers of variables, making it impossible to draw
conclusions about cause and effect. Much more meaningful would have been a comparison of egg
consumption and disease patterns within Shanghai itself, so that other variables would have been constant.
(Nevertheless, we cant help pointing out that the study found no significant correlation of egg consumption
with heart disease.)
139/147 (1998)
We wonder whether the Cornell researchers were dismayed or amused when they found that meat
consumption had no correlation, either positive or negative, with any disease, but a strong correlation with
the taking of snuff! (Because meat consumption is very high among herdsmen in the western most province,
where tobacco is taken in the form of snuff.)
Hunter-gatherer societies do indeed value animal fats as necessary for successful reproduction. As both
Weston Price and Francis Pottenger predicted, human fertility has declined with the advent of commercial
vegetable oils and the gradual disappearance of the fat soluble vitamins exclusive to animal fats. This may
send the population reductionists into paroxysms of glee, but it is a tragedy for those couples desiring
children and unable to conceive (currently an estimated 25% of all US couples.) With decreased fertility
comes an increase in birth defects, low birth weight babies and developmental problems, including learning
disabilities and attention deficit disorders. Better to encourage a diet that ensures the production of healthy,
well-formed children and allow population restriction to be a matter of free choice by well-informed and
conscientious parents.
1. Health and Healing Wisdom, Price-Pottenger Nutrition Foundation, San Diego, CA, (619) 574-7763
(Eskimos, Vol 20, No 3; America, Vol 20, No 4; Africa, Vol 21 No 1; Cave Man, Vol 21, No 2; China, Vol
21, No 3; England, Vol 21, No 4; Korea, Vol 22, No 1; Australian Aborigines, Vol 22, No 2; Thailand, Vol
22, No 3) 2. Pitskhelauri, G Z, The Long Living of Soviet Georgia, 1982, Human Sciences Press, New York,
NY 3. Castelli, William, Archives of Internal Medicine, Jul 1992, 152:7:1371-1372 4. Mary, need reference.
5. Sylvan Wittwer, et al, Feeding a Billion: Frontiers of Chinese Agriculture, Michigan State University
Press, East Lansing, 1987 6. William E Connor, et al, Human and Clinical Nutrition, 1995:2993-2994 7. Z Y
Chen, et al, Lipids, (1997) 32:(10):1061-1067
PALEODIET Archives
Subject: Neanderthal & Iodine
From: Dean Esmay
Reply-To:
Date: Sun, 6 Dec 1998 15:26:24 -0500
An interesting popular article:
http://oakridger.com/stories/112598/new_salt.html
Popular articles on scientific subjects can be very frustrating, however. Does anyone have more information
on the subject of this article?
PALEODIET Archives
Subject: Re: Menopause in the hunter gatherer?
Reply-To:
Date: Tue, 8 Dec 1998 12:55:11 +0000
On Wed, 2 Dec 1998 Staffan Lindeberg wrote:
> At 10.52 -0500 98-11-24, Sandy Rzetelny wrote:
> ... Is there evidence indicating that the paleo hunter gatherer woman did undergo menopause? Oh,
> yes. Available data suggest an average age at menopause of approximately 47 years.
How was this data obtained for *paleo* H-G women? Ref 1 gives a method for living H-G women to
determine whether they are pregnant/ not pregnant/ menopausal using luteinising hormone (LH) in urine.
This will be very difficult to detect in skeletal remains. Any method based on population statistics or
examination of menopausal skeletal changes (if there are any unequivocal ones) will fall down on our
inability to precisely age the skeletons of people aver 40 years of age.
> 1 Phillips JCM et al. New field techniques for detection of female reproductive status. Am J Phys
> Anthropol 1991; 85: 143. Actually AJPA 1991; Supplement 12: 143 2 Wood J. Fertility and
> reproductive biology. In Attenborough R and Alpers M (eds). The Small Cosmos. Oxford University
140/147 (1998)
> Press 1991.

Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Use of nuts in diet
From: Dean Esmay
Reply-To:
Date: Mon, 14 Dec 1998 12:51:56 -0500
Support for the contention that the human animal may have evolved a need for monosaturated fats in the
diet:
"Frequent Nut Consumption and Risk of Coronary Heart Disease in Women: Prospective Cohort Study"
British Medical Journal 317: 1341-1345 November 14, 1998
Abstract:
Objective: To examine the relation between nut consumption and risk of coronary heart disease in a cohort of
women from the Nurses' Health Study.
Design: Prospective cohort study.
Setting: Nurses' Health Study. Subjects: 86, 016 women from 34 to 59 years of age without previously
diagnosed coronary heart disease. stroke or cancer at baseline in 1980. Main outcome measures: Major
coronary heart disease including non-fatal myocardial infarction and coronary heart disease.
Results: 1255 major coronary disease events (861 cases of non-fatal myocardial infarction and 394 cases of
fatal coronary heart disease) occurred during 14 years of follow up. After adjusting for age, smoking, and
other known risk factors for coronary heart disease, women who ate more than five units of nuts (one unit
equivalent to 1 oz of nuts) a week (frequent consumption) had a significantly lower risk of total coronary
heart disease (relative risk 0.65, 95% confidence interval 0.47 to 0.89, P for trend = 0.0009) than women
who never ate nuts or who ate less than one unit a month (rare consumption). The magnitude of risk
reduction was similar for both fatal coronary heart disease (0.61, 0.35 to 1.05, P for trend = 0.007) and nonfatal myocardial infarction (0.68, 0.47 to 1.00, P for trend = 0.04). Further adjustment for intakes of dietary
fats, fibre, vegetables, and fruits did not alter these results. The inverse association persisted in subgroups
stratified by levels of smoking, use of alcohol, use of multivitamin and vitamin E supplements, body mass
index, exercise, and intake of vegetables or fruits.
Conclusions: Frequent nut consumption was associated with a reduced risk of both fatal coronary heart
disease and non-fatal mycardial infarction. These data, and those from other epidemiological and clinical
studies, support a role for nuts in reducing the risk of coronary heart disease.
Additional quotes from text of the report:
"When the analysis was restricted to non-smokers and women who were teetotaller or who drank
occasionally (<=1 drink per week), the inverse association was particularly strong (relative risk of coronary
heart disease for consumption of nuts > =5 times per week was 0.48 (0.27 to 0.84, P for trend 0.008)).
In analyses of peanuts and other nuts (assessed in 1986 separately, we combined the two highest categories
because of small number of cases. After adjusting for age, consumption of peanuts and other nuts were both
inversely associated with risk of coronary heart disease.
Consumption of peanut butter was only weakly associated with risk of coronary heart (multivariate relative
risk comparing women consuming peanut butter was 0.92 (0.74 to 1.15, P for trend 0.94). The relative risk
was slightly stronger for fatal coronary heart disease (0.76, 0.50 to 1.15, P for trend = 0.09). ......... Peanut
butter was only weakly associated with a risk of coronary heart disease, but this may be due to the addition
of hydrogenated fat to major American brands."
ALSO:
"Low Fat-monosaturated Rich Diets Containing High-oleic Peanuts Improve Serum Lipoprotein Profiles."
Lipids 32(7): 687-695 Jul 1997
Abstract:
141/147 (1998)
Postmenopausal hypercholesterolemic women are at risk for cardiovascular disease and are encouraged to
follow low-fat (LF) (< or = 30% energy) diets. However, these diets may have undesirable effects on high
density lipoprotein cholesterol (HDL-C), apolipoprotein A-I (apo A-I) and triglycerides, whereas diets high
in monosaturated fats do not. Twenty postmenopausal hypercholesterolemic women previously consuming
high-fat diets (34% energy) were placed on a low fat-monosaturated rich diet (LFMR: 26% 14% energy,
respectively) for 6 mon. Sixteen women already eating LF diets (24% energy) were also followed to monitor
variations in serum lipids due to seasonal variations. Twenty-five women successfully completely the study
(LFMR = 12, LF = 13). Serum cholesterol decreased 10% (264 to 238 mg/dl, P< or = 0.01) and low density
lipoprotein cholesterol (LDL-C) decreased 12% (182 to 161 mg/dl, P < or = 0.01) in the LFMR group, but
did not change in the LF group. The reduction in serum cholesterol in the LFMR group was greater than
estimated by predictive formulas. Serum triglycerides and apo A-I did not change in both groups, but only
the LFMR group showed a trend toward toward beneficial changes in LDL-C/HDL-C and apo A-Vapo B
ratios. Overall, the LFMR was well tolerated and resulted and resulted in an improved serum lipid and
apolipprotein profile.
PALEODIET Archives
Subject: Re: Nuts and Dean Esmay
From: Loren Cordain
Reply-To:
Date: Mon, 14 Dec 1998 15:07:24 -0700
As the moderator of this listserve, I know that Dean has an avid interest in nuts (heh, heh), so I think the
following post may be appropriate.
In regards to the recent reference claiming beneficial health effects from peanut and peanut oil consumption
("Low Fat-monosaturated Rich Diets Containing High-oleic Peanuts Improve Serum Lipoprotein Profiles."
Lipids 32(7): 687-695 Jul 1997), I have to disagree with the conclusions of the authors. My disagreement
was published in a subsequent issue of Lipids as a letter to the letter (Cordain L. Atherogenic potential of
peanut oil-based monounsaturated fatty acids diets. Lipids 1998 33;229-30.). The full contents of the letter is
reprinted below:
142/147 (1998)
Dear Editor, In the dietary management of coronary heart disease there is increasing recognition (1, 2) that
the traditionally recommended high carbohydrate, low fat diet for hypercholesterolemia (3) may elicit
undesirable blood lipid changes, including reductions in high density lipoproteins (HDL) and apolipoprotein
A-1, while concurrently elevating triglycerides (TG) and very low density lipoproteins (VLDL) (4-6).
Because of these untoward blood lipid changes induced by high carbohydrate, low fat diets, substitution of
monounsaturated fats (MUFA) for saturated fats may be a more effective strategy than substituting
carbohydrate for saturated fats in order to lower total and LDL serum cholesterol levels without adversely
influencing HDL, VLDL, TG and apo A-I (7-9). Most experimental diets have employed olive oil or canola
oil as the MUFA source, however other MUFA rich foods such as nuts (10) and avocados (11) have also
been demonstrated to improve blood lipid profiles. In a recent report to Lipids, O'Bryne et al. (12) have
shown that a low fat, high MUFA (14% energy) diet based upon high MUFA (76-80%) peanuts improved
total and LDL serum cholesterol levels in 12 post-menopausal women. Although diets based upon MUFA
rich peanuts (Arachis hypogea) should, in theory, be non-atherogenic because they reduce total and LDL
cholesterol, there is substantial evidence to indicate that peanut oil, despite its hypo-lipidemic effects, is
highly atherogenic. Although the total MUFA content of peanut oil is high and can range from 36 to 59%,
dependent upon the specific cultivar (13), it has been shown to be unexpectedly atherogenic when fed to
laboratory animals (monkeys, rabbits and rats) as part of a cholesterol rich or a cholesterol free diet (13, 14,
15, 16). Because peanut oil can so rapidly produce atherosclerotic lesions which have similar biochemical
and pathological characteristics to those in human atherosclerosis, it is routinely used in rabbit models to
induce atherosclerosis (17, 18). The reason for the high atherogenicity of peanut oil is unclear, however it
has been suggested that it may be due to residual lectins (glycoproteins with high affinity binding to cellular
carbohydrate residues) found in the oil, since peanut oil induces fibromuscular arterial lesions in contrast to
other vegetable oils which induce fatty lesions (19). Alternatively, the specific triglyceride structure may also
be responsible for it's atherogenicity (20). In native peanut oil, all of the long chain PUFA are found in the
sn-3 position of glycerol, however by utilizing a process to randomize the fatty acids within the triglyceride,
the atherogenicity of peanut oil has been shown to be reduced (21). It should be pointed out that the
randomization process may also reduce peanut oil's lectin content (20, 21). When contrasting olive to peanut
oil, laboratory animals which were fed peanut oil showed a higher frequency of arterial lesions, more intimal
proliferation and thicker intimas than did rabbits fed olive oil (15). Peanut oil containing atherogenic diets
induce a preferential increase in intimal collagen and result in a characteristic fibromuscular lesion in intimal
plaques that is attributable to the addition of peanut oil to the atherogenic diet (22, 23). It has been suggested
that residual peanut lectin (PNA) found in peanut oil, because of its specificity for D-galactose residues, may
bind arterial smooth muscle cells expressing these sugar residues and thereby induce its characteristic
fibromuscular lesions (19). In support of this concept, is data which has shown that PNA stimulates in vitro
vascular smooth muscle cell proliferation and that added lactose could inhibit the PNA induced stimulation
(24). A similar in vivo experiment would be able to distinguish if peanut oil's atherogenicity is more
attributable to its PNA content or to its specific triglyceride structure. Although there are no direct
epidemiological studies evaluating the atherogenic potential of peanut oil, there is suggestive information
from India which implicates peanut oil with higher mortality rates from coronary heart disease (CHD). In
India, wherein vegetable oils constitute 80% of the per capita fat consumption, there are regional preferences
in the choice of oils, and peanut oil is preferred in southern states, whereas northern states use mustard oil
(25). In southern India, the mortality rate from CHD 30 years ago was reported to be seven times higher than
that in northern India and similar to that in the U.S. and England (26, 27). A more recent report showed the
prevalence of CHD to be 61.6% higher in southern Indians compared to their more northerly counterparts
(28). It is possible that these regional differences may be due, in part, to different levels of peanut oil
consumption. In contrast to peanut oil, which is a fairly recent addition to the human diet, olive oil has been
part of the traditional Mediterranean diet for thousands of years (29) and has been shown both
epidemiologically (30) and clinically (31) to reduce the risk for CHD. These studies make a strong point for
the superiority of olive oil over peanut oil in terms of its cardiovascular health benefits. Until further trials
are conducted, it would be prudent not to recommend peanut oil as part of high MUFA diets for the
management of CHD.
Loren Cordain Department of Exercise and Sport Science Colorado State University Fort Collins, CO 80523
143/147 (1998)
References 1. Katan, M.B., Grundy, S.M., and Willett, W.C. (1997) Beyond Low-fat Diets. N. Engl. J. Med.
337, 563-566. 2. Grundy, S.M. (1989) Monounsaturated Fatty Acids and Cholesterol Metabolism:
Implications for Dietary Recommendations. J. Nutr. 119, 529-533. 3. Connor, W.E., and Connor, S.L. (1997)
Should a Low-Fat, High-Carbohydrate Diet Be Recommended for Everyone? N. Engl. J. Med. 337, 562-563.
4. Jeppesen, J., Schaaf, P., Jones, C., Zhou, M.Y., Ida Chen, Y.D., and Reaven, G.M. (1997) Effects of LowFat, High Carbohydrate Diets on Risk Factors for Ischemic Heart Disease in Postmenopausal Women. Am. J.
Clin. Nutr. 65, 1027-1033. 5. Denke, M.A., and Breslow, J.L. (1988) Effects of a Low-Fat Diet With and
Without Intermittent Saturated Fat and Cholesterol Ingestion on Plasma Lipid, Lipoprotein, and
Apolipoprotein Levels in Normal Volunteers, J. Lipid Res. 29, 963-969. 6. Mensink, R.P., and Katan, M.B.
(1992) Effect of Dietary Fatty Acids on Serum Lipids and Lipoproteins: a Meta-Analysis of 27 Trials.
Arterioscler. Thromb. 12, 911-919. 7. Grundy, S.M. (1986) Comparison of Monounsaturated Fatty Acids and
Carbohydrates for Lowering Plasma Cholesterol. N. Engl. J. Med. 314, 745-748. 8. Mensink, R.P., and
Katan, M.B. (1987) Effect of Monounsaturated Fatty Acids Versus Complex Carbohydrates on High-Density
Lipoproteins in Healthy Men and Women. Lancet 1, 122-125. 9. Wahrburg, U., Martin, H., Sandkamp M.,
Schulte, H., and Assmann G. (1992) Comparative Effects of a Recommended Lipid-Lowering Diet Vs a Diet
Rich in Monounsaturated Fatty Acids on Serum Lipid Profiles in Healthy Young Adults. Am. J. Clin. Nutr.
56, 678-683. 10. Dreher, M.L., Maher, C.V., and Kearney, P. (1996) The Traditional and Emerging Role of
Nuts in Healthful Diets. Nutr. Rev. 54, 241-245. 11. Colquhoun, D.M., Moores, D., Somerset, S.M., and
Humphries, J.A. (1992) Comparison of the Effects on Lipoproteins and Apolipoproteins of a Diet High in
Monounsaturated Fatty Acids, Enriched with Avocado, and a High-Carbohydrate Diet. Am. J. Clin. Nutr. 56,
671-677. 12. O'Byrne, D.J., Knauft, D.A., and Shireman R.B. (1997) Low Fat-Monounsaturated Rich Diets
Containing High-Oleic Peanuts Improve Serum Lipoprotein Profiles. Lipids 32, 687-695. 13. Kritchevsky,
D., Tepper, S.A., Scott, D.A., Klurfield, D.M., Vesselinovitch, D., and Wissler, R.W. (1981) Cholesterol
Vehicle in Experimental Atherosclerosis. Part 18. Comparison of North American, African and South
American Peanut Oils. Atherosclerosis 38, 291-99. 14. Kritchevsky, D., Davidson, L.M., Weight, M., Kriek,
N., and duPlessis J.P. (1982) Influence of Native and Randomized Peanut Oil on Lipid Metabolism and
Aortic Sudanophilia in the Vervet Monkey. Atherosclerosis 42, 53-58. 15. Kritchevsky, D., Tepper, S.A.,
Klurfeld, D.M., Vesselinovitch, D., and Wissler, R.W. (1984) Experimental Atherosclerosis in Rabbits Fed
Cholesterol Free Diets. Part 12. Comparison of Peanut and Olive Oils. Atherosclerosis 50, 253-59. 16. Bond,
M.G., Bullock, B.C., Bellinger, D.A., and Hamm T.E. (1980) Myocardial Infarction in a Large Colony of
Nonhuman Primates with Coronary Artery Atherosclerosis. Am. J. Pathol. 101, 675-692. 17. Saso, Y.,
Kitamura, K., Yasoshima, A., Iwasaki, H.O., Takashima, K., Doi, K., and Morita, T. (1992) Rapid Induction
of Atherosclerosis in Rabbits. Histol. Histopathol. 7, 315-320. 18. Kolodgie, F.D., Katocs, A.S., Largis, E.E.,
Wrenn, S.M., Cornhill, J.F., Herderick, E.E., Lee, S.J., and Virmani, R. (1996) Hypercholesterolemia in the
Rabbit Induced by Feeding of Low-Level Cholesterol. Methodological Considerations Regarding Individual
Variability in Response to Dietary Cholesterol and Development of Lesion Type. Arterioscler. Throm. Vasc.
Biol. 16, 1454-64. 19. Klurfeld, D.M., Kritchevsky, D. (1987) Isolation and Quantitation of Lectins from
Vegetable Oils. Lipids 22, 667-68. 20. Kritchevsky, D. (1991) Dietary Fat and Experimental Atherosclerosis.
Int. J. Tissue React. 13, 59-65. 21. Kritchevsky, D. (1988) Cholesterol vehicle in experimental
atherosclerosis. A brief review with special reference to peanut oil. Arch Pathol Lab Med 112, 1041-44. 22.
Ehrhard, L.A. and Holderbaum, D. (1980) Aortic Collagen, Elastin and Non-Fibrous Protein Synthesis in
Rabbits Fed Cholesterol and Peanut Oil. Atherosclerosis 37, 423-32. 23. Opsahl, W.P., DeLuca, D.J., and
Ehrhart, L.A. (1987) Accelerated Rates of Collagen Synthesis in Atherosclerotic Arteries Quantified in Vivo.
Arteriosclerosis 7, 470-476. 24. Sanford, G.L., and Harris-Hooker, S. (1990) Stimulation of vascular cell
proliferation by beta-galactoside specific lectins. FASEB J. 4, 2912-2918. 25. Ghafoorunissa. (1996) Fats in
Indian Diets and Their Nutritional and Health Implications. Lipids 31, S-287-S-291. 26. Malhotra, S.L.
(1967) Geographical Aspects of Acute Myocardial Infarction in India with Special Reference to Patterns of
Diet and Eating. Brit. Heart J. 29, 337-344. 27. Subramaniam, R., and Kulangara, A.C. (1967) Incidence of
Atherosclerotic Lesions at Madras, South India. Brit. Heart J. 29, 333-336. 28. Begom, R., and Singh, R.B.
(1995) Prevalence of Coronary Artery Disease and Its Risk Factors in the Urban Populations of South and
North India. Acta Cardiol. 50, 227-240. 29. Haber, B. (1997) The Mediterranean Diet: a View from History.
Am. J. Clin. Nutr. 66, 1053S-1057S. 30. Keys, A., Menotti, A., Karvonen, M.J., Aravanis, C., Blackburn, H.,
and Buzina, R. (1986) The Diet and 15-Year Death Rate in the Seven Countries Study. Am. J. Epidemiol.
124, 903-915. 31. Gardner, C.D., and Kraemer, H.C. (1995) Monounsaturated Versus Polyunsaturated
Dietary Fat and Serum Lipids. A Meta Analysis. Arterioscler. Thromb. Vasc. Biol. 15, 1917-1927.
144/147 (1998)
PALEODIET Archives
Subject: Use of nuts in diet, more support...
From: JJM van den Broek
Reply-To:
Date: Tue, 15 Dec 1998 00:38:36 -0800
More
> Support for the contention that the human animal may have evolved a need for monosaturated fats in
> the diet
Science News Online (11/21/98): High-Fat and Healthful,
http://www.sciencenews.org/sn_arc98/11_21_98/Bob1.htm for full text of article and "further reading"
excerpt:
> ...The good news is that not all of this high-fat fare is necessarily bad for ones health. In
> fact, some of the treats could serve as a springboard to a healthier diet, a variety of
> researchers believe. The trickand, of course, there is a trickis not only to sample these foods
> in moderation but also to steer toward those that derive a large proportion of their calories from
> monounsaturated fats.... Unlike liquid oils, nutswhich can derive up to 80 percent of their
> calories from fatappeal as snacks...Hazelnuts, macadamias, almonds, pecans, and pistachios all
> furnish 57 to 83 percent of their fats as monounsaturates...Brazil nuts, walnuts, and cashews
> deliver at least one-quarter of their fats as monounsaturates...a different rule now appears to
> apply to foods rich in monounsaturates. Indeed, a host of new dietary trials indicates that
> high-mono-fat diets lower the risk of cardiovascular diseasein some cases, even more effectively
> than do the standard low-fat diets that t! he American Heart Association (AHA) advocates... < -> From Science News, Vol. 154, No. 21, November 21, 1998, p. 328-330. Copyright 1998 by Science
> Service.
> References:
> Curb, J.D., et al. 1998. High monounsaturated fat macadamia nut diets; effects on serum lipids and
> lipoproteins. FASEB Journal Abstracts Part I 12(March 17):506. Davis, P.A., B.M. Burton-Freeman,
> and B.O. Schneeman. 1998. Postprandial lipemia: Effects of fat from whole almonds versus almond
> oil. FASEB Journal Abstracts Part I 12(March 17):A506. Mattes, R.D., and S.K. Voisard. 1998.
> Effects of peanuts on hunger and food intake in humans. FASEB Journal Abstracts Part I 12(March
> 17):A506. Morgan, R.L., . . . and P.M. Kris-Etherton. 1998. Effects of diets high in
> peanuts-peanut butter (P/PB) and peanut oil (PO) on the susceptibility of LDL to oxidative
> modification. FASEB Journal Abstracts Part II 12(March 20):A649. Pearson, T.A., T.D. Etherton . .
> . and P.M. Kris-Etherton. 1998. High-mufa diets with peanuts-peanut butter (P/PB) or peanut oil
> (PO) lower total cholesterol (TC) and LDL-C identically to a step 2 diet but eliminate the
> triglyceride (TG) increase. FASEB Journal Abstracts Part I 12(March 17):A506. Sacks, F.M., and K.
> McManus. 1998. Weight reduction: A comparison of a high unsaturated fat diet with nuts vs a low
> fat diet. FASEB Journal Abstracts Part II 12(March 20):A649. Spiller, G.A., et al. 1998. Nuts and
> plasma lipids: An almond-based diet lowers LDL-C while preserving HDL-C. Journal of the American
> College of Nutrition 17(June):285. -- Judith van den Broek ICQ4120171
PALEODIET Archives
Subject: Nuts
From: Dean Esmay
Reply-To:
Date: Wed, 16 Dec 1998 07:46:20 -0500
I suppose this is almost too obvious and trivial to mention, but peanuts are not nuts.
-=Paleolithic Diet Symposium List
145/147 (1998)
Ad astra per aspera
PALEODIET Archives
Subject: Nuts and peanuts
From: JJM van den Broek
Reply-To:
Date: Wed, 16 Dec 1998 14:38:23 -0800
> I suppose this is almost too obvious and trivial to mention, but peanuts are not nuts. Dean,
> that's right, it is ALMOST too obvious and trivial to mention 8-).
If you are referring to the Science Online article and its references, the full body of the article clearly states
the difference between legumes and true nuts...I'd rather assumed the full text of the article would be read by
those interested, and the references were provided to show the breadth of the studies; finally, if I remember
correctly, the clear "winner" in the nuts/nut oils/lipids was, overall, whole almonds; the argument holds.
-- Judith J. van den Broek ICQ4120171
PALEODIET Archives
Subject: Re: Nuts, Nuts & more nuts
From: Loren Cordain
Reply-To:
Date: Wed, 16 Dec 1998 14:34:19 -0700
For a review of nut eating by the massive jawed Australopithecus boisei and other hyper-robust
australopithecines, interested readers are directed to:
Peters CR. Nut-like oil seeds: food for monkeys, chimpanzees, humans, and probably ape-emen. Am J Phys
Anthropol 1987 73:333-363.
PALEODIET Archives
Subject: SCIENCE article
From: Dean Esmay
Reply-To:
Date: Sun, 20 Dec 1998 21:27:58 -0500
An interesting web page:
http://www.sciencemag.org/cgi/content/full/282/5393/1448
PALEODIET Archives
Subject: PALEODIET Membership Application
From: Dean Esmay
Reply-To:
Date: Mon, 21 Dec 1998 18:59:57 -0500
The Paleodiet Symposium recently reached 270 members, I'm pleased to announce.
A question has come up as to how researchers and academics should be invited to the listserv. For those who
wish to encourage their colleagues to join our discussion group, simply forward the following to them:
146/147 (1998)
----[snip here]---THE PALEOLITHIC DIET & EXERCISE SYMPOSIUM is a non-profit, semi-private, semi-formal online
discussion forum for professional scientists and educated laymen to discuss evolution as it involves the
human diet and physical activity patterns. Members are made up primarily of biologists, archaeologists,
paleontologists, medical doctors, dietetians, and graduate students in related fields.
There is absolutely no commercial interest tied to the Symposium, nor any charge of any kind for
membership. Message traffic is on the order of a few per week.
To join, simply fill out the following information and email it to Dean Esmay at :
Name: Preferred E-mail Address: Title: Institution: Phone Number: Research Areas: Other Areas of Interest:
ALL INFORMATION IS KEPT STRICTLY CONFIDENTIAL, and only name and email address are
mandatory. Under no circumstances is any information given out to any third party for any reason.
Please feel free to pass this announcement out to others via email, or to post to news grops, private servers,
or commercial systems.
Russell (1872-1970)
PALEODIET Archives
Subject: Book for the overweight teenager
From: Raymond Peterson
Reply-To:
Date: Mon, 28 Dec 1998 19:15:29 +0300
I am a pediatrician with an extensive research and clinical background. Together with my son, a cardiologist,
we are writing a book for the parents of overweight teenagers regarding the utility of the "paleodiet". Our
considerable clinical experience with patients prompts us to assemble the substantial data on this subject in a
form that will be credible and understandable to the lay public.
Although this subject is well known amongst professionals, such as the subscribers to the paleolist, we find it
is almost completely foreign to the layman. When known it is in the form of infomercials and books that, to
us at least, appear motivated primarily in selling something. While this doesn't alter the message, it does its
credibility.
We seek feedback from our fellow subscibers regarding: a) whether our preception regarding the detraction
of linking "selling something" to the message limits the credibility of the message, and, b) whether any of the
readers might be interested in joining us in this endeavor.
Raymond D.A. Peterson, M.D. Craig R.D. Peterson, M.D.
PALEODIET Archives
Subject: Neanderthal & Iodine
From: Dean Esmay
Reply-To:
Date: Thu, 31 Dec 1998 15:40:50 -0500
A better URL for the iodine/Neanderthal issue:
http://www.mindspring.com/~edobson/jdobson/neander.html
147/147 (1998)
PALEODIET Archives
Subject: Re Book for the overweight teenager
From: ALLEN EWART GALE
Reply-To:
Date: Sun, 3 Jan 1999 13:43:23 +1000
> Date: Mon, 28 Dec 1998 19:15:29 +0300
> From: Raymond Peterson Subject: Book for the overweight teenager
> I am a pediatrician with an extensive research and clinical background. Together with my son, a
> cardiologist, we are writing a book for the parents of overweight teenagers regarding the utility
> of the "paleodiet".,,,,,,,,,,,,,,, we find it is almost completely foreign to the layman.
Agreed. It is highly significant that the Hellers dedicated one of their books to Semmelweiss
I suggest you publish your book & advertise it ; if your book is good, the word will spread, as good books on
this topic are few.
> Raymond D.A. Peterson, M.D.
> Craig R.D. Peterson, M.D.
I will be pleased to list it on my web page Allen URL http://people.enternet.com.au/~agale/
--------------------------------From:- Dr Allen E Gale Consultant Physician (Allergy) & Adelaide Aerobiology Laboratory
PALEODIET Archives
Subject: Book for the overweight teenager
From: Dean Esmay
Reply-To:
Date: Sun, 3 Jan 1999 13:56:53 -0500
Doctors Peterson & Peterson ask in their message of 28 December 1998 about whether popularization of
dietary theories limits the credibility of the theories espoused. In that regard I have some thoughts:
A disturbing trend I've noticed in our discussion group has been the apparent assumption by some members
that there is a universally acknowledged definition of a "paleolithic diet" (or pre-agricultural diet). This
seems to revolve around the work of people like Boyd Eaton and analyses of the dietary patterns of preagricultural groups that exist now or did exist in the last few centuries which all seem to point to a highprotein, moderated carbohydrate and moderated fat diet quite low in cereal grains, high in fibre from fruits
and vegetables, moderate to low in sodium, high in potassium, calcium and magnesium, and with types of
fats balanced differently from what is typical today in Western diets. But has it been established that there is
a general consensus on this issue in every field?
The authors of a popular book advocating a "paleolithic diet" would be well advised, in my view, to seek
rigorous criticism before they publish. Asking for criticism from experts in fields other than biology and
medicine would be an important part of that. Our own group here seems to have insufficient input from
archaeologists, paleontologists, and anthropologists (something I'd very much like to see changed).
I'd also say that it would only be ethical in a popular book to be clear about what you can state as a fact, and
what you can state as reasoned theory. A depressing number of popular book authors constantly state theory
as fact, and make airy generalizations about what "the scientific evidence shows" without being clear what
evidence they're talking about or even mentioning the existence of contrary evidence and opinions from
respected scientists.
It's certainly the case that when scientists publish popular books and articles, they are sometimes looked
down on by their colleagues, sometimes unfairly so. But I would think that a good way to lessen that
problem would be to work hard at seeking criticism from sources in multiple fields, and to avoid the nasty
habit that popular authors have of presenting theories as facts.
PALEODIET Archives
1/46 (1999)
Subject: Re: methyl mercaptan

From: sean
Reply-To:
Date: Mon, 4 Jan 1999 11:33:06 +1000
I thought this might be of interest. While reading a book the other day on human senses and oddities I saw
mention of the fact that the smell that humans are supposedly most sensitive to is Methyl Mercaptan. It
seems that this a major component of the smell of rotting meat. This seems important to me. Why would we
evolve such a sensitivity? My thinking is that it is a survival sense thatt would have allowed us to avoid
eating the carcases of animals that had decomposed too far and hence were dangerous from the point of view
of food poisoning, although one of my lecturers here at uni had an alternative view. If we were scavenging
carcasses our sensitivity to methyl mercaptan may have led us to a carcass. I am open to the possibilities and
would be interested in other viewpoints.
A brief search of the net revealed much about methyl mercaptan but more from a chemical/industrial slant,
with nothing Paleodiet/human sense related, so if anyone can add to my info I'd appreciate it. Methyl
Mercaptan is added to gas so that we can smell it for safety reasons.
Cheers
Sean McBride
PALEODIET Archives
Subject: Re Book for the overweight teenager
From: ALLEN EWART GALE
Reply-To:
Date: Mon, 4 Jan 1999 23:32:29 +1000
From: ALLEN EWART GALE Subject: Re Book for the overweight teenager
> The authors of a popular book advocating a "paleolithic diet" would be well advised, in my view,
> to seek rigorous criticism before they publish. Asking for criticism from experts in fields other
> than biology and medicine would be an important part of that. Agreed. Have a look at the Vancouver
> Document at :- http://www.mja.com.au/public/information/uniform.html A relevant passage reads:> "Medical Journals and the Popular Media The public's interest in news of medical research has led
> the popular media to compete vigorously to get information about research as soon as possible.
> Researchers and institutions sometimes encourage the reporting of research in the popular media
> before full publication in a scientific journal by holding a press conference or giving
> interviews. The public is entitled to important medical information without unreasonable delay,
> and editors have a responsibility to play their part in this process. Doctors, however, need to
> have reports available in full detail before they can advise their patients about the reports'
> conclusions. In addition, media reports of scientific research before the work has been peer
> reviewed and fully published may lead to the dissemination of inaccurate or premature
> conclusions." Allen Jan5'99
PALEODIET Archives
Subject: The advantages of nuts
From: Todd Moody
Reply-To:
Date: Sat, 9 Jan 1999 22:35:46 -0500
In light of recent postings concerning the benefits of nut consumption, in conjunction with the fact that nuts
would have been part of the human diet during most or all of our evolutionary history, I want to share a
conjecture or two. Since I am not a scientist or any sort of expert in nutrition, I hope those who are more
qualified will comment.
2/46 (1999)
Anyway, in the course of browsing through Medline I noted that the protein casein can be used in laboratory
studies to induce elevated cholesterol in animals [1]. The explanation for this is, apparently, the fact that the
casein protein has a low arginine:lysine ratio. Another study [2] also suggests that the arg:lys ratio has a
significant effect on cholesterol.
Most of the literature on the health benefits of nuts deals with their monounsaturated fat content, which is
high. I had the idea of checking their arg:lys ratio in the USDA database and discovered that many nuts have
quite high ratios, among the highest of any foods that I looked at. Here are some samples:
Food arg:lys ratio
----------------------------walnuts 5.1 filberts 5.5 brazil nuts 4.8 almonds 4.2 lentils 1.1 milk .4 beef .7 sardines .7 whole wheat flour
1.5 chicken breast .8 turkey .8 peanuts 3.4 black beans .9 sunflower seeds 2.7
Well, that gives some idea. The arg:lys ratio of the nut proteins is significantly higher than that of most other
foods, with the interesting exception of peanuts. Loren Cordain recently posted some information on the
atherogenic properties of peanut oil. Yet another (partisan) study suggests that whole peanuts are associated
with reduced CHD risk [3]. The suggested explanation is that the peanut contains resveratrol, but perhaps the
arg:lys ratio is another factor.
Todd Moody
1. Kurowska EM, Carroll KK. Effect of high levels of selected dietary essential amino acids on
hypercholesterolemia and down-regulation of hepatic LDL receptors in rabbits. Biochim Biophys Acta 1992
Jun 22;1126(2):185-191
2. Rajamohan T, Kurup PA. Lysine: arginine ratio of a protein influences cholesterol metabolism. Part 1-Studies on sesame protein having low lysine: arginine ratio. Indian J Exp Biol 1997 Nov;35(11):1218-1223
3. http://www.peanut-institute.org/Resveratrol_Abstract.html
Todd Moody
PALEODIET Archives
Subject: Arg:lys ratio and legumes
From: Todd Moody
Reply-To:
Date: Mon, 11 Jan 1999 13:59:59 -0500
On Mon, 11 Jan 1999, John Apsley wrote:
Off the top of my memory, bovine (cow) dairy products actually have a relatively high amount of arginine
compared to lysine, hence many people with herpes I or II, which may be activated or aggravated by too
much Arginine, can take lysine to hasten recovery from herpes painful lesion outbreaks. In your references,
the second one clearly states the ratio as Lysine:Arginine, not Arginine: Lysine. This means, if I am correct,
that your table is headed incorrectly. The ratios may all be for Lysine::Arginine, or am I incorrect?
The Rajamohan article indicates that a *low* lys:arg ratio is hypocholesterolemic, but a low lys:arg ratio is
equivalent to a high arg:lys ratio. The Kurowska article indicated the hypercholesterolemic effects of amino
acids other than arginine. I chose to report arg:lys ratios so that arginine would be first, since it appears to be
the one to watch.
According to the USDA, whole milk has .119g arg per 100g and .261g lys per 100g. This gives an arg:lys
ratio of .45, which is I think what I reported.
I assume that the effect of the arg:lys ratio on herpes is independent of its effect on serum cholesterol, but I
certainly don't question that effect. This only illustrates the point that in the realm of human physiology
many things are not unequivocally "good" or "bad."
To tack back toward the subject matter of this list, however, I'd like to bring up the issue of legumes in preagricultural diets. The legume proteins that I have checked also tend to have high arg:lys ratios, though not
as high as nuts. They also tend to have low glycemic index, based on my browsing of on-line GI lists.
One argument is that legumes could not have been part of paleolithic diets because they are not edible raw,
or if they are edible it is only for a brief time. Another argument is that they contain anti-nutrients, such as
trypsin inhibitors and phytic acid, and so would have had unfavorable effects. Nevertheless, I conjecture that
it is impossible to generalize about legumes in this way. Some legumes, such as lentils, can be eaten after
soaking for several hours, and soaking seens to me to be a technology within reach of paleolithic humans. It
does not require durable pottery vessels but can be done with animal bladders.
3/46 (1999)
Is there evidence that pre-agricultural people gathered and ate lentils or other legumes?
Todd Moody
PALEODIET Archives
Subject: the advantages of nuts
From: Mark Moore
Reply-To:
Date: Mon, 11 Jan 1999 21:13:10 -0700
Hello,
On Sat. 9 Jan 1999, Todd Moody wrote:
> The arg:lys ratio of the nut proteins is significantly higher than that of most other foods...
This is a thought provoking concept for a layman like me that unhealthy foods might have a certain amino
acid profile.
Has anyone ever seen an amino acid breakdown for beef from organic, free-range cows? Would the ranking
of amino acids be different than that in beef from grain-fed cows? How difficult would it be for an individual
to have a lab run an amino acid analysis on both types of meat?
Thanks, mark
PALEODIET Archives
Subject: Re: PALEODIET Digest - 10 Jan 1999 to 12 Jan 1999 (#1999-5)
From: Bob Avery
Reply-To:
Date: Tue, 12 Jan 1999 19:43:49 -0500
Todd Moody wrote:
> One argument is that legumes could not have been part of paleolithic diets because they are not
> edible raw, or if they are edible it is only for a brief time. Another argument is that they
> contain anti-nutrients, such as trypsin inhibitors and phytic acid, and so would have had
> unfavorable effects. Nevertheless, I conjecture that it is impossible to generalize about legumes
> in this way. Some legumes, such as lentils, can be eaten after soaking for several hours, and
> soaking seens to me to be a technology within reach of paleolithic humans. It does not require
> durable pottery vessels but can be done with animal bladders.
In my experience, almost all legumes can be sprouted at any time of year and the sprouts eaten. It takes no
more than a week of daily or twice daily watering and rinsing to grow bean sprouts and no technology is
required. While I use glass jars with handy metal-sieve lids for rinsing, I'm sure an empty skull-bone dragged
through a stream would work just as well.
It is my understanding that sprouting neutralizes most of the enzyme inhibitors and other bad guys.
Bob Avery
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Internet access to use free Internet e-mail. Get completely free e-mail from Juno at
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PALEODIET Archives
Subject: Interesting links
From: Dean Esmay
Reply-To:
Date: Sat, 16 Jan 1999 11:31:01 -0500
Forwarded from a subscriber:
4/46 (1999)
http://news.bbc.co.uk/low/english/sci/tech/newsid_255000/255725.stm for links to several sites also see

http://www.sciencemag.org/ 15 Jan 1999
PALEODIET Archives
Subject: Conference notice
From: Dean Esmay
Reply-To:
Date: Sat, 16 Jan 1999 18:18:48 -0500
INTERNATIONAL SYMPOSIUM ETHNOBOTANY Medicinal Plants: Folk Traditions, History,
Pharmacology 14-18 September, 1999. San Jos (Costa Rica)
Organised by: Geodata Center, Costa Rica, Sciences et Lettres, Belgium, under the auspices of: Universidad
para la Paz, Costa Rica
From 14 to 18 September 1999, the 1st International Symposium on the History and Folk tradition of
Medicinal Plants will be organised in Costa Rica, the largest biodiversity center of the World. The amin
topics will be the history of medicicnal plants from antiquity to present times, folk traditions (past and
present), scientific knowledge, integration of folk tradition into medicine, ethnobotany and pharmacology,
with a special emphasis in temperate and neo-tropical floras. Comparative, transperiod and interdisciplinary
studies are welcome, as well as works and projects dealing with the use of multimedia means in the field.
The sicentific programme of the unique event of this kind, which will include plena-ry lectures, papers,
posters, round tables and free discussions, aims to encourage the sutdy of a patrimony of Humanity exposed
to disappearence, and to contribute to the preservation of flora worldwide, among others by the recuperation
of historical tradition and plant lore. Its proceedings are expected to constitute and indispensable tool and a
work of reference on this subject. The Symposium is a non profit event devoted to promote study, scientific
research and divulgation in the field. Held in the heart of the Tropical Forest, it is designed to be an
international forum open to physicians, pharmacists, chemists, botanists, historians, philologists,
ethnolingusits, ethnobotanists, anthropologists and everybody wishing to hear communications of major
world specialists in the field, to contribute personally with the presentation of original works, and to
participate in focused discussions on the current state of research in medicinal plants, their meaning for man,
culture and science through Worlds History.
For participation and further information please contact the organisers: SIMPOSIO P.O.BOX 6131, 1000
San Jos Prof. Ronald Chaves Prof. Alain Touwaide Fax : + (506) 283 02 63 Costa Rica Fax : + (506) 283
02 63 Spain e-mail
Visit us at: http://www.costarica.com/wg/simposio
INTERNATIONAL SYMPOSIUM ETHNOBOTANY FOLK TRADITIONS, HISTORY AND
PHARMACOLOGY San Jose, Costa Rica, Sept., 14-19, 1999
Scientific Programme: Preliminary Version Draft for Discussion
I. Mankind. Society and Medicinal Plants:Future challenges 1.1 Addresses from North America, Europe,
Mesoamerica, South America, Africa, China, Australia and India. Open to other geographical areas or
regions.
II. Medicinal Plants and Technology 2.1 Arts and Horticulture of Medicinal Plants 2.2 Satellite Imagery and
vegetation cartography 2.3 Global Positioning Systems and Vegetation Maps 2.4 Bioclimatic Mapping of
Medicinal Plants 2.5 Physiology of Medicinal Plants 2.6 Pharmacognosy of Medicinal Plants 2.7 Iterative
Data Banks 2.8 Germoplasm Data Banks 2.9 Cellular Biology 2.10 Genetic Biology 2.11 Medicinal Plants as
tracers of Environments
III. The Legay of Ancient Cultures 3.1. China, India, Australasia (Specialists are encouraged to say hello!)
3.2. Mesopotamia, Greece, Bizance, Rome 3.3. Arab World 3.4. Africa 3.5. The Preservation of Traditions in
the Middle Age: Registers, Papirs, Pergamon: The Pre-Systematic of Medicinal Plants 3.6. The Production
of Ancient Texts. The First essays of Pharmacopeas
IV. The Medicinal Plants of the World: Folk Traditons, History, Pharmacology, Biogeography 4.1 North
America 4.2 Mesoamerica 4.3 Amazonia 4.4 Andean Region 4.5 Pampean Region 4.6 Caribbean Region 4.7
Finno-Scandia 4.8 Mitteleuropa 4.9 Eurasia 4.10 Mediterranea 4.11 Africa (Papers and Communications
from other regions are welcome).
V. The Contribution of Ethnobotanics for Understanding Cultures. A Common Legacy: Ethology and
Medicinal Plants.
5/46 (1999)
VI. Working Groups 6.1 New Technologies 6.2 Biotechnology 6.3 Ethnomedicine 6.4 Herboristery 6.5
Pharmacology 6.6 Pharmacognosy 6.7 Ethnobotany 6.8 Ricovery of Ancient Texts
VII. SYMPOSIUM Preliminary Conclusions
PALEODIET Archives
Subject: Questions (forwarded)
From: Dean Esmay
Reply-To:
Date: Sun, 24 Jan 1999 15:04:38 -0500
Noemi Creagan asked me to re-post this message here for her.
Please send responses either to the Paleodiet list and/or directly to her in the email she gives below.
Dean
---------From: Noemi F. Creagan To: Subject: diabetes Date: Wednesday, January 20, 1999 4:53 PM
Hello,
I am looking for articles that deal with genetic and anthropological implications (or explanations) of diabetes
in North and/or South American Indians. I have found a few articles: Jason S. Shapiro (1997). Non-insulindependent Diabetes Mellitus among American Indians: a problem in human ecology American Indian culture
and research journal. 21:2 pp 197-227.
Introduction to type 2 diabetes / produced by the Nashville Area IHS Diabetes Program in cooperation with
IHS Diabetes Program, HQW ; Beth Drabant. HE 20.302:D 54/8(call number)
Prevention and control of diabetes among native Americans : hearing before the Select Committee on Indian
Affairs, United States Senate, Ninety-ninth Congress, second session, on S. 1988 ... April 15, 1986,
Washington, DC.PublisherWashington : U.S. G.P.O. : For sale by the Supt. of Docs., Congressional Sales
Office, U.S. G.P.O., 1986. "Y 4.In 2/11:S.hrg.99-764" (call number)
please let me know if I am in the right track
Thank you Noemi
PALEODIET Archives
Subject: Re: diabetes
Reply-To:
Date: Mon, 25 Jan 1999 23:51:04 +0100
My own focus has not been on the American continent but rather on the South Pacific. Nevertheless I can
point at some papers dealing with the relation between diabetes and acculturation in Amerindians: [1-9]. The
unaccultured Yanomamo Indians showed a "supernormal" glucose tolerance test, i.e. a very modest increase
of blood glucose and serum insulin after drinking a glucose solution [9].
Although familial heritage apparently is a strong determinant for cardiovascular risk within westernized
populations, genetic factors do not appear to explain the rarity of cardiovascular disease and diabetes among
traditional populations. On the contrary (and this may have been your point), after adopting a western
lifestyle subsistence horticulturalists like the Amerindians seem more prone to develop diabetes and
cardiovascular disease than populations of northern european ancestry [10-16], athough some of them
apparently more so than others [10, 17, 18].
From these and other studies it is reasonable to assume that environmental factors may actually be necessary
requirements for the development of non-insulin dependent diabetes mellitus but also that the susceptibility
to a western lifestyle differs slightly between populations.
Genetics and environment as causes of diabetes are thus not mutually exclusive. Or, as the late Geoffrey
Rose put it, "the answer to 'Why does this particular individual in this population get this disease?' is not
necessarily the same as the answer to 'Why does this population have so much disease?'" [19]. The two
approaches should not be in academic competition. But they do compete for funding.
I also suggest you search the Medline by use of some of these names for more references.
6/46 (1999)
Best wishes, Staffan Lindeberg

1. Newman WP, Middaugh JP, Propst MT, Rogers DR. Atherosclerosis in Alaska Natives and non-natives.
Lancet 1993; 341: 1056-7. 2. Thouez JP, Eko JM, Foggin PM, et al. Obesity, hypertension, hyperuricemia
and diabetes mellitus among the Cree and Inuit of Northern Cubec. Arct Med Res 1990; 49: 180-8. 3. West.
North American Indians. In: Trowell H, Burkitt D, ed. Western diseases: their emergence and prevention.
Cambridge, Mass: Harvard University Press, 1981: 129-37. 4. Alpert JS, Goldberg R, Ockene IS, Taylor P.
Heart disease in native Americans. Cardiology 1991; 78: 3-12. 5. Knowler WC, Bennett PH, Hamman RF,
Miller M. Diabetes incidence and prevalence in Pima Indians: a 19-fold greater incidence than in Rochester,
Minnesota. Am J Epidemiol 1978; 108: 497-505. 6. Groom D. Cardiovascular observations on Tarahumara
Indian runners--the modern Spartans. Am Heart J 1971; 81: 304-14. 7. Connor WE, Cerqueira MT, Connor
RW, Wallace RB, Malinow MR, Casdorph HR. The plasma lipids, lipoproteins, and diet of the Tarahumara
indians of Mexico. Am J Clin Nutr 1978; 31: 1131-42. 8. Baruzzi R, Franco L. Amerindians of Brazil. In:
Trowell H, Burkitt D, ed. Western diseases: their emergence and prevention. Cambridge, Mass: Harvard
University Press, 1981: 138-153. 9. Spielman RS, Fajans SS, Neel JV, Pek S, Floyd JC, Oliver WJ. Glucose
tolerance in two unacculturated Indian tribes of Brazil. Diabetologia 1982; 23: 90-3. 10. King H. The
epidemiology of diabetes mellitus in Papua New Guinea and the Pacific: adverse consequences of natural
selection in the face of sociocultural change. In: Attenborough RD, Alpers MP, ed. Human Biology in Papua
New Guinea. The Small Cosmos. Oxford: Clarendon Press, 1992: 363-72. 11. Zimmet P. Epidemiology of
diabetes and its macrovascular manifestations in Pacific populations: the medical effects of social progress.
Diabetes Care 1979; 2: 144-53. 12. Neel JV. Diabetes mellitus: a "thrifty" genotype rendered detrimental by
progress? Am J Hum Genet 1963; 14: 353-62. 13. Neel JV. The thrifty genotype revisited. In: Kobberlong J,
Tattersall R, ed. The genetics of diabetes mellitus. London: Academic Press, 1992: 283-93. 14. Brand Miller
JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia
1994; 37: 1280-6. 15. Hales CN, Barker DJP. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty
phenotype hypothesis. Diabetologia 1992; 35: 595-601. 16. Allen JS, Cheer SM. The Non-Thrifty Genotype.
Current Anthropology 1996; 37: 831-42. 17. Cruickshank JK, Beevers DG, ed. Ethnic Factors in Health and
Disease. Oxford: Wright, 1989: 18. Nelson RG, Sievers ML, Knowler WC, et al. Low incidence of fatal
coronary heart disease in Pima Indians despite high prevalence of non-insulin-dependent diabetes.
Circulation 1990; 81: 987-95. 19. Rose G. Sick individuals and sick populations. Int J Epidemiol 1985; 14:
32-8.
> From: Noemi F. Creagan To:
> Subject: diabetes
> Date: Wednesday, January 20, 1999 4:53 PM
> Hello,
> I am looking for articles that deal with genetic and anthropological implications (or
> explanations) of diabetes in North and/or South American Indians. I have found a few articles:
> Jason S. Shapiro (1997). Non-insulin-dependent Diabetes Mellitus among American Indians: a problem
> in human ecology American Indian culture and research journal. 21:2 pp 197-227. Introduction to
> type 2 diabetes / produced by the Nashville Area IHS Diabetes Program in cooperation with IHS
> Diabetes Program, HQW ; Beth Drabant. HE 20.302:D 54/8(call number) Prevention and control of
> diabetes among native Americans : hearing before the Select Committee on Indian Affairs, United
> States Senate, Ninety-ninth Congress, second session, on S. 1988 ... April 15, 1986, Washington,
> DC.PublisherWashington : U.S. G.P.O. : For sale by the Supt. of Docs., Congressional Sales Office,
> U.S. G.P.O., 1986. "Y 4.In 2/11:S.hrg.99-764" (call number) please let me know if I am in the right track
> Thank you
> Noemi
http://www.paleodiet.com/lindeberg/
PALEODIET Archives
Subject: Just a comment to researchers
From: Donna H
Reply-To:
Date: Tue, 26 Jan 1999 15:00:26 -0800
7/46 (1999)
I haven't researched the Western diet vs. the rest of the world to any sizable extent, but the more I hear about
it, the more I wonder how much data there is about those *not* in the West who adopt a Western diet.
Do we know that the same rate of disease prevails among Westerners living in Europe or Asia but with the
eating habits usually attributed to Americans?
What I'm getting at is... how do we rule out that there is something about physically being in America or
nearby that's contributing (our local corn supplies, water, approved pesticides, or who knows what).
This question may have been answered early on in major research, and I just haven't seen the studies. It *is*
something I've wondered about.
Donna
PALEODIET Archives
Subject: Saturated fat and heart disease, revisited
Reply-To:
Date: Thu, 28 Jan 1999 13:47:27 -0800
Many of you may recall the very interesting dialogue that took place last year between Loren Cordain and
Sally Fallon and Mary Enig. Two of the main points of contention were:
(1) The levels of saturated fat that were likely present in Paleolithic diets, and
(2) The association between dietary saturated fat and coronary heart disease (CHD).
I thought a number of good points were made on both sides, and I was left wanting to learn more. I
eventually asked Mary Enig if she had perhaps written a comprehensive "defense" of saturated fat in terms of
its association with CHD. She said that she had not, but said:
"The most comprehensive work on the entire cholesterol/saturated fat = issue with a scientific defense of
saturated fat in one collection is by = Uffe Ravnskov, M.D., Ph.D. from Sweden. He has put together a
website = addressing "The Cholesterol Myths". It is an absolute masterpiece. I = have never actually met
him, but have corresponded with him for several = years and have seen a number of his papers. This
collection of essays, = complete with the critical references is brilliant. There is a good = discussion of the
saturated fat issue in number 3; You will find it all = at http://home2.swipnet.se/~w-25775/"
I am far from being an expert on the literature on this topic, but I thought that his essays made a rather strong
case. I thought that others might be interested to check this out. If anyone does and has comments, I would
be interested.
Steve Meyers
PALEODIET Archives
Subject: Sugars in the Paleolithic diet
From: Mandi Smallhorne
Reply-To:
Date: Fri, 12 Feb 1999 14:33:44 +0200
Are any subscribers to the Paleolithic Diet Symposium aware of any published information or any research
into the kinds of sugars which would have formed part of the paleolithic diet? I am especially interested in
results concerning fructose, and the overall balance of sugars as opposed to other carbohydrates. Mandi
Smallhorne, editor, PhysioForum South Africa
PALEODIET Archives
Subject: New popular book
From: Dean Esmay
Reply-To:
Date: Sat, 13 Feb 1999 18:58:10 -0500
8/46 (1999)
I know nothing about this book or its contents but it may be of interest:
http://www.amazon.com/exec/obidos/ASIN/1577330277/
PALEODIET Archives
Subject: Sugars in Paleo diet
Reply-To:
Date: Sat, 13 Feb 1999 21:21:20 -0800
Here's a post from a while back that I happened to save; maybe Jennie has more to add...
Date: Mon, 13 Oct 1997 11:27:10 +0700 From: Jennie Brand Miller
Sucrose would have been one of the major sources of energy in primate diets coming from the fruits and
berries in roughly equal proportions with glucose and fructose. Thus high levels of sugars have been in a diet
since the beginning of evolution of humans. Even though sucrose is the starting product in many sweet
foods, by the time we eat it it has been hydrolysed to glucose and fructose (bt heat, acid, time).
While high insulin responses may indeed be detrimental, sucrose and most sugary foods elicit lower glucose
and insulin responses than modern starchy foods, like bread (1, 2).
I think humans have evolved an instinctual desire for sweet things because glucose is the obligatory fuel for
the brain and foetus. We can't make enough via gluconeogenesis alone. Honey was highly prized in
paleolithic diets, way out of proportion to the amounts of energy it might supply. Furthermore, the amounts
eaten might have rivalled that eaten as sucrose today (3).
My main message here is that sugar is not the villain people might imagine, but quickly digested starch could
be (4-8).
(1) BRAND MILLER J, Pang E, Broomhead L. The glycemic index of foods containing sugars: comparison
of foods with naturally occurring versus added sugars. Brit J Nutr 1995; 73: 613-623.
(2) Wolever TMS, BRAND MILLLER J. Sugar and blood glucose control. Am J Clin Nutr,
1995;62(suppl):212S-27S.
(3) Allsop K, BRAND MILLER JC. Honey revisited: a reappraisal of honey in pre-industrial diets. Br J
Nutr; 75: 513-20.
(4) BRAND MILLER J, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of noninsulin dependent diabetes. Diabetologia 1994; 37: 1280-86.
(5) Byrnes S Denyer G, BRAND MILLER J, Storlein L. The effect of amylose vs amylopectin feeding on
development of insulin resistance in rats. J. Nutr 1995; 125: 1430-7.6
(6) Wiseman, CE, Higgins JA, Denyer GS, BRAND MILLER JC. Amylopectin starch induces nonreversible
insulin resistance in rats. J Nutr 1996, 126;410-5.
(7) Higgins JA, BRAND MILLER JC, Denyer GS. Development of insulin resistance in the rat is dependent
on the rate of glucose absorption from the diet. J Nutr 1996;126: 596-602.
(8) BRAND MILLER JC, Foster-Powell K, Colagiuri S. The G.I. Factor. Sydney: Hodder Headline, 1996.
Steve Meyers
PALEODIET Archives
Subject: Sugars in paleolithic diets
Reply-To:
Date: Mon, 15 Feb 1999 18:15:16 +1000
Hi Mandy,
9/46 (1999)
I am interested in the sugars in paleolithic diets. As far as I'm aware there's almost nothing on the individual
sugar ratios. However, my guess it that there would have been more fructose than glucose or sucrose. Honey
is a rich source of fructose and many fruits have higher amounts of fructose than other sugars. Although
domesticated fruit have higher sugars content, I think the present individual sugar ratios would be a
reasonable estimation of paleolithic ratios.
Fructose is also the builing block of fructo-oligosaccharides and inulin which are found in many vegetables.
However, both of these are not digested and absorbed in the small intestine. The colder the climate, the more
likely a root or tuber will contain inulin rather than starch. I can give your references if need be. Jennie
PALEODIET Archives
Subject: Darwinian Diet and Exercise Program
Reply-To:
Date: Sat, 27 Feb 1999 13:20:51 -0400
Del Thiessen, Professor of Evolutionary Psychology at the University of Texas in Austin, and member of our
Symposium has written a book with the title "The Darwinian Diet and Exercise Program". On his homepage
you can find more information about it, a newsletter, and some links:
http://www.savagedawn.com/
Sounds interesting Rdiger Hflechner
PALEODIET Archives
Subject: Response to Loren Cordain and Sally Fallon & Mary Enig
Reply-To:
Date: Mon, 1 Mar 1999 11:02:43 -0800
To: All Paleodieters From: Brian J. MacLean Re: Response to Loren Cordain and Sally Fallon and Mary
Enig
This letter is in Reponses to comments made by Loren Cordain on November 18, 1998 and by Sally Fallon
and Mary Enig on December 4, 1998 to a letter I posted on November 16, 1998 (Paleo Querries). I apologize
for the delay in response, but I have been off the net and intensively 'studying' free radicals' effects on the
skin in the Florida and California sun (Loren's right-there's really something to that theory- I've got all kinds
of new wrinkles!). I t was a pleasure to return and find the interesting above responses to my 'Paleo
Querries.'
In reply to Loren Cordain's points:
10/46 (1999)
1. I stated that " The available information on Paleolithic peoples is so scanty that it seems specious to
believe that one can follow their nutritional practices with more than a modicum of accuracy." Loren
responded that by studying paleodiets, "there are some obvious deductions which allow basic generalizations
which have enormous impact upon present day health (i.e., dairy products could not have been a component
of stone age diets)." It seems that if the deductions are 'obvious', then one need not resort to in-depth
detective work of questionable validity on 'paleolithic' diets to conclude the deleterious effects of most
"modern" foods. A considerable body of literature exists in nutritional research, which clarifies the nature of
many of the more harmful "new" foods (e.g., Trans-fatty acids and refined carbohydrates). As for fatty meats
and dairy products, valid inferences cannot be drawn within our cultural matrix with the current information.
To make definitive statements regarding these latter foods' effects in our culture, it would be necessary to
partial out the variance contributed by modern agricultural and preparation methods. Cross-cultural studies
suggest that these food categories require a more sophisticated analysis with regard to their place in human
nutrition than the dichotomous thinking often displayed in nutritional circles. 2. Loren Cordain stated: "The
information that has been garnered by ethnologists and anthropologists has value and provides insight into
what the components of the completely aboriginal diet would have been prior to contact and acculturation."
It is true that available data on macronutrient ratios among aboriginal peoples provide interesting
anthropological information. However, there appears to be little information in anthropological works on
micronutrient ratios among aboriginal peoples, which is at least as critical in understanding dietary effects as
macronutrient information. Furthermore, it is unclear how aboriginal nutritional practices have much
relevance for current psychosocial conditions, which include requirements for sustained attention under low
motor activity levels (e.g., school), as well as coping with a panoply of relatively new environmental toxins.
Oriental cultures have known for millennia that dietary needs vary according to activity levels. For example
in most spiritual traditions from the Indian subcontinent, China and Japan, a high carbohydrate, low fat, low
protein diet with few animal foods has been considered most ideal for contemplative practices.
3. With regard to Loren Cordain's statement that the "reported longevity of Hunzas and Vilcambas may have
a genetic component which is independent of environmental factors, " some evidence suggests that peoples
in contiguous areas to that of the Hunzas share a similar genetic history, but have a considerably different
nutritional pattern, as well as less favorable pathology profiles and longevity rates(1).
4. With regard to Loren Cordain's statement about "Harman's classic free radical theorygenerally accepted as
a contributor to the aging process by most nutritionists and gerontologists, " a number of points need to be
made. First, free radical theory is only one of at least six major theories of aging, and is by no means
accepted by all researchers as a causal factor in aging (2). The inclusion of antioxidants in the diet, which
scavenge free radicals, has been found to improve aging biomarkers such as tissue age pigments (3).
However, in rodent studies, the administration of free radical scavengers has not unequivocally prolonged
maximum life span (4, 5, 6). For a review of survival curves from populations administered antioxidants, see
Walford, 1986, p.389 (4). Although there is considerable evidence that free radicals are associated with
tissue damage, it is not clear whether they exert a causal influence (7, 6). Weindruch and Walford (6)
contend that caloric restriction is the only known method of prolonging maximum life span. Finch (8) states
that "caloric restriction is the only known environmental means to alter the acceleration of mortality
rate(MRDT) in any mammal." Harman (9) points out that although average life span of mice has been easily
increased with antioxidant treatment, "the increases were not accompanied by any certain extensions of
maximum life spans." Loren may wish to read in the article he referenced (Harman, 9, p. 7127) that "the
question remains, now as in 1954: are free radical reactions the sole cause of aging, the major cause, or a
minor contributor to the process?" It seems that aging is most likely a dialectical multi-factorial process, and
thus not approachable by a reductionist analysis. Rather, it may resemble a fractal surface where a higher
order dimension is greater that the sum of its components.
5. With regard to Loren's point 6, in which he states that "most nutritionists would agree that diets high in
fruits and vegetables such as the 'paleodiet' would be healthful not only during the reproductive years, but
also during the post-reproductive years, " the issue of quantity of food intake also seems germane to
longevity. A study by Ross and Bras (10) is illustrative of the point made in my November letter that perhaps
the paleolithic diet was "evolutionarily selected because it was the most effective to develop the human form
for the first two decades of life with the goal of effective reproduction." Ross and Bras found that rats given
the opportunity to self select food types and quantities chose to maximize body growth, development and
most likely fecundity rates, at the expense of individual health and survival. This ad lib group also
experienced a significantly higher rate of tumor growths and other pathologies.
11/46 (1999)
6. As to Loren's Santayana quote, "Those who cannot remember the past are condemned to repeat it, " one
could as easily apply this statement in a different direction than intimated by Loren. We might consider this
quote as an admonition to "20th century man and his fledgling science" that paleolithic man's "eons of
evolutionary experience that is still far wiser than the mind" of contemporary man, eventuated in the
abandonment of the hunter-gatherer lifestyle and diet in favor of agricultural practices.
In reply to Sally Fallon and Mary Enig's points:
1. Sally and Mary stated that "the greatest longevity among inhabitants of Soviet Georgia is found in those
who consume the most meat and fat." It appears that such a conclusion is questionable in that we now know
that it is difficult to ascertain birth dates due to faulty or absent record keeping and dissimulation for cultural
reasons (11).
2. Sally and Mary stated: "No good studies have shown that calorie restriction contributes to a longer life in
humans." First, at the risk of belaboring the obvious, much of our biomedical knowledge has been obtained
from animal research. Specific small- scale physiological processes are not always applicable to cross
species comparisons. For example, primates are incapable of vitamin C synthesis, while most rodents have
this capability. Large-scale general physiological processes, on the other hand, can often be extrapolated
from one species to another (e.g., immune system functioning among mammals). Dietary restriction
decelerates aging in a variety of poikilotherms (12, 13, 14) and homeotherms (6). Although this is not
definitive proof that the same results would be found in a human population, it seems that similar results
would be found with a high degree of probability. A second area which may provide suggestive evidence
regarding human longevity, is cross-cultural studies. Remaining cognizant of the aforementioned difficulties
in establishing accurate birth records, the apparent longevity of the Hunzas may be associated with a low
daily caloric intake: an estimated average of 1900 calories per day (15). In Okinawa, where accurate birth
records have been kept since the latter part of the 19th century, the calorie intake of school children is only
62% of what is recommended for Japan and the longevity incidence appears to be the highest in the world
(16).
3. Sally and Mary stated: "The Framingham study found that those who consumed the greatest number of
calories weighed the least, had the lowest serum cholesterol and were the most physically active." This study
is flawed in a number of respects and makes the above statement difficult to interpret. The percentage of
nicotine users in the most overweight group of the original Framingham study was 55% while over 80%
users in the most underweight group (17). The possible effects of this contaminating variable difference
between groups makes it difficult to link caloric intake levels with reliable biomarkers or increased life span.
Physical activity levels have not been found to be consistently related to longevity. A National Institute of
Aging study found that in rats fed ad lib, exercise increased longevity while decreasing it in the very
extended life spans of calorie restricted rats (18). Furthermore, Sally and Mary have pointed out many times
that cholesterol is a 'bogus issue' and of no relevance to coronary heart disease, and thus to longevity.
4.Sally and Mary stated: "Animal studies showing reduced numbers of tumors in animals on restrictedcalorie diets also found that the restricted-calorie groups had larger and more virulent tumors than those on
non-restricted diets." In the Ross and Bras (19) and Ross (20) studies, those rats on dietary restriction
showed about one-half the total number of tumors as controls, while showing an increase in skin carcinomas.
The incidence of skin carcinoma, however, was small in both control and experimental groups (Figures 1 and
2, Ross & Bras, 19). Furthermore, the degree of dietary restriction in these studies was greater than most
other studies (approximately 30% ad lib), and may be a case of malnutrition rather than calorie restriction
with adequate nutrition. It is also noteworthy that the onset age of these carcinomas in the dietary restricted
animals was consistently later in their lives than found in the ad lib animals. Under conditions of less
restriction of calorie intake, these tumor growth results are usually not found (21, 6).
General Comments:
12/46 (1999)
It appears that in the Paleo Diet writings and in the Price-Pottenger Foundation literature, there is an
underlying assumption that the ancient and aboriginal ways of eating are closer to the heart of dietary
wisdom, that is, are somewhat more consistent with 'natural law'. This assumption seems to a large extent
dependent on a inference from observations of the statistical frequency of eating patterns in populations to an
imperative regarding how human beings 'ought' to eat. Although these writings are informed by research in
the biological sciences, the primary impetus and direction seem to arise from findings in paleontology and
anthropology. This could be seen as a case of the 'naturalistic fallacy' where a leap is made from an 'is'
statement to an 'ought' statement. This issue is complex and requires considerably more discussion than is
suitable for this particular forum. Suffice it is to point out that many 'natural' practices by our pre-civilized
ancestors and present day aboriginal peoples fall far short of Loren's "far wiser than the mind of 20th century
man" criterion. Paleo adepts and Price-Pottenger writers in particular should take note that primitive 'natural'
eating practices such as eating animal flesh raw (including human) has often proved disastrous. Kuru, a TSE
disease among the Fore people of New Guinea, was transmitted by the 'natural' aboriginal practice of
honoring close relatives by eating them after they died (22). In another area of the world, evidence from the
ancient Americas has shown that the assumption of the evolution of parasites subsequent to developed
agriculture and livestock domestication, was wrong (23). Mummy remains from the Chinchorro, a tribe from
northern coastal Chile between 550 to 500 B.C., show that they were infested with a sea lion tapeworm
(D.pacificum), resulting in pernicious anemia, leading to porous skeletons, weakness and death. These
peoples, like many other aboriginal peoples, enjoyed the 'natural' practice of eating their sea food raw.
Despite what modern day Rousseauians would like to believe, not all things that are untainted by civilization
are good.
Sincerely,
Brian J. MacLean Ph.D. Psychologist
References
1. Hoffman, J.M. Hunza . New Win Publishing Co., 1997. 2. Pryor W.A. The free-radical theory of aging
revisited: a critique and a suggested disease-specific theory. In Warner, H.R., Butler, R.N., Sprott, R.L., and
Schneider, E.L. (Eds.): Modern Biological Theories of Aging. New York, Raven Press, 1987. 3. Tappel,
A.L., Fletcher, B. and Deamer, D. Effects of antioxidants and nutrients on lipid peroxidation fluorescent
products and aging parameters in the mouse. J. Gerontology, 28:415, 1973. 4. Walford, R.L. The 120-Year
Diet. New York, Simon and Schuster, 1986. 5. Hiramoto, R.N., Ghanta, U.K., and Soong, S. Effect of
thymic hormones in immunity and life span. In Goidl, E.A. (Ed.): Aging and the Immune Response. New
York, Marcel Dekker, Inc., 1987, pp.177-198. 6. Weindruch, R., and Walford, R.L. The Retardation of
Aging and Disease by Dietary Restriction. Charles Thomas Publisher, Springfield, Illinois, 1988. 7.
Halliwell, B. and Grootveld, M. The measurement of free radical reactions in humans. FEBS Lett, 213:9,
1987. 8. Finch, C.E. Longevity, Senescence and the Genome. University of Chicago Press, 1990. 9. Harman,
D. The aging process. Proc. Natl. Acad. Sci. U.S.A. 78:7124, 1981. 10. Ross, M.H., and Bras, G. Dietary
preference and diseases of age. Nature, 250:263, 1974. 11. Medvedev, Z.A. Caucusus and Atlay Longevity:
A Biological or Social Problem. The Gerontologist, 14:381, 1974. 12. Comfort, A. Effect of delayed and
resumed growth on the longevity of a fish (Lebistes reticulatus, Peters) in captivity. Gerontologia, 8:150,
1963. 13. Reimers, N. A history of a stunted brook trout population in an alpine lake: A life span of 24 years.
California Fish and Game, 65:196, 1979. 14. Walford, R.L. Maximum Life Span. New York, Norton, 1983.
15. Leaf, A. National Geographic, 143:93, 1973. 16. Kagawa, Y. Impact of westernization on the nutrition of
Japanese: changes in physique, cancer, longevity, and centenarians. Prev Med, 7:205, 1978. 17. Castelli,
W.P. Cited by Wall Street Journal, Dec, 1, 1982, p.32. 18. Goodrick, C.L. The effect of exercise on survival
of food-restricted and non-restricted mice. Cited by Science News, Dec1, 1979, p. 375. 19. Ross, M.H., and
Bras, G. Influence of protein under- and overnutrition on spontaneous tumor prevalence in the rat. J. Nutr.,
103:944, 1973. 20. Ross, M.H. Nutrition and longevity in experimental animals. In Winick, M. (Ed.),
Nutrition and Aging. New York, Wiley, 1976 pp. 43-57. 21. Ross, M.H. Nutritional regulation of longevity.
In Behnke, J.A., Finch, C.E. and Moment, G.B. (Eds.), The Biology of Aging. New York, Plenum Press,
1978, pp. 173-189. 22. Prusiner, S. The Prion Disease. Scientific American, Jan. 1995, pp. 48-57. 23.
Pringle, H. The sickness of mummies. Discover, Dec. 1998, pp. 74-83.
PALEODIET Archives
Subject: Response to Loren Cordain and Sally Fallon & Mary Enig
From: Dean Esmay
Reply-To:
13/46 (1999)

Date: Fri, 5 Mar 1999 11:12:49 -0500
A few comments:
First, I am not comfortable this creeping use of the term "paleodieters" that we see here and there used in
reference to members of this symposium (not just in Brian's message--I've seen it used in other submissions
to this list). The term implies either that people on this list are specifically eating a certain way, or that there
is some sort of monolithic point of view on the issues discussed here. Neither is the case. This is a silly word
and I'd like to see it go away.
I am also not sure who "modern-day Rousseauians" is supposed to be referring to. The inference I draw is
that if one holds to the theory that an animal will probably be healthiest eating the foods it evolved to eat,
one holds to an anti-civilization creed. I hope that inference is incorrect, as that would be both a non-sequitur
and an unprovoked ad-hominem attack. It would also be factually incorrect, since more than one scientist
who's written on the issue of evolutionary diets have acknowledged the tremendous advances modern
civilization has brought to human health and well-being. Including more than one member of this group.
As for research, just to add fuel to discussion, I thought I'd mention that Brian and others may wish to
examine the Georgia Centerarian study (1), which amongst other things showed that on average, Americans
who live past the age of 100 tend to avoid calorie-restricted diets. They also tend to eat generous amounts of
fatty and cholesterol-ridden foods, and to ignore medical advice on healthy diets. They also tend to eat
generous amounts of cereal grains and dairy products.
Correlation is not causation. But it's interestind that a study like this can so easily fly in the face of so many
different theories espoused both here and elsewhere.
(1) Johnson, MA, The Georgia centenarian study: Nutritional patterns of centenarians, International Journal
of Aging and Human Development, 1992;34(1):57-76.
Russell (1872-1970)
PALEODIET Archives
Subject: Response to Dean Esmay
Reply-To:
Date: Fri, 5 Mar 1999 11:45:55 -0800
Thanks to Dean for pointing out a term which seems to require further clarification. The term 'Roussouians'
was used not to describe particular people as much as a tendency, often implicit, that I have noted in the
thinking of a variety of nutritional schools. Nor is the term necessarily pejorative, but often seems to be an
ideological obstacle to obtaining a more complete picture. For example, in many vegetarian writings we find
musings and longings for a 'Golden Age' when the human diet was 'pure' prior to the 'Fall.' This is evident in
the Macrobiotic literature where the goal is to reach a 'balance' which was presumably attained in 'primordial'
times by 'proper' eating habits. In the Paleo Diet and Price-Pottenger writings, the thrust seems
overwhelmingly weighted towards extolling the virtues of ancient and aboriginal nutritional patterns with
little attention given to possible drawbacks of these eating patterns. However, as I pointed out in my last
submission, I recognize that 'these writings are informed by research in the biological sciences.' On the other
hand, perhaps I have missed a discussion of possible negative aspects of what appears to be understood as
constituting the broad outlines of these dietary regimens. If so, I would be most appreciative of references to
correct possible misconceptions.
I tend to agree with Dean that 'Paleodieters' is an inappropriate rubric to describe those who are investigating
and adhering to a 'paleolithic' nutritional regimen. As I pointed out in my letter in November, 1998, the
'available information on Paleolithic peoples is so scanty that it seems specious to believe that one can follow
their nutritional practices with more than a modicum of accuracy.' Thus, to believe that one is a 'Paleodieter'
is at best, a loose approximation. However, it is understandable that writers on the Symposium List would
use the term 'Paleodieters' since the address is 'Archives of PALEODIET.' Perhaps the address 'Archives of
NONMONOLITHIC PALEODIET' would be more instructive for lay writers like myself.
Respectfully,
14/46 (1999)
B. MacLean Ph.D. Clinical Psychologist
PALEODIET Archives
Subject: Response to Dean Esmay
From: Dean Esmay
Reply-To:
Date: Sun, 7 Mar 1999 15:35:40 -0500
The name of this list is "The Paleolithic Diet & Exercise Symposium, " which is shortened to "The
Paleolithic Diet Symposium" on our web page
(http://maelstrom.stjohns.edu/CGI/wa.exe?A0=paleodiet&D=&F=&H=&O=&S=&T=). I don't see why an
email address would be mistaken for a name, but I'll talk to Don about clarifying it.
If evidence of negative effects of hunter/gatherer diets is to be had, I'd quite like to know about it. Any
references or research or direct experience to that effect is welcome here. We've been too quiet of late, and
any discussion which includes verifiable data is valuable.
PALEODIET Archives
Subject: Negative dietary practices
Reply-To:
Date: Mon, 8 Mar 1999 13:20:33 -0800
Dean wrote:
"If evidence of negative effects of hunter/gatherer diets is to be had, I'd quite like to know about it. Any
references or research or direct experience to that effect is welcome here. We've been too quiet of late, and
any discussion which includes verifiable data is valuable."
I have no data, just a general comment. One would expect instances of negative effects of H/G (or other)
diets, but to the extent that the "negative" practices constrain the survival of the group and are discovered as
such, one would expect such practices to be selected out over time.
It seems that many dietary practices have mixed effects, and it takes time for a group to sort those out -especially if they lack a scientific method, which tends to reduce the amount of trial and error that has been
in use for most of human evolution. (Though it is amazing that H/G people figured out so much about
various foods and how best to prepare them -- without the help of cookbooks!)
For example, it may be that modern civilization is on the verge of discovering that heavy use of grains and
dairy products is perhaps, on balance, not such a good idea after all. (It will be interesting to see what the
impact will be of Loren Cordain's upcoming article on problems with human grain consumption -- please
alert us when it appears, Loren)
I recall that in Woody Allen's movie from the 1970s, "Sleeper, " the guy wakes up in the distant future and
the medical team tells him that all his friends have been dead for 200 years. Woody responds, "But they all
ate organic brown rice!" Little did we know back in 1975 how harmful that might be! They also let him
know that items like chocolate are now known to be very healthful for people!
Yours truly, Steve Meyers
PALEODIET Archives
Subject: Conference Announcement (fwd)
Reply-To:
Date: Fri, 12 Mar 1999 11:54:41 +0000
15/46 (1999)
---------Forwarded message
---------Date: Wed, 10 Mar 1999 14:55:13 GMT From: Ms HB BRICKLEY To: Subject: Conference Announcement
Announcement & Call For Papers First Annual Conference of The British Association of Biological
Anthropology & Osteoarchaeology.
10th-12th September 1999, The University Of Birmingham.
The association is aimed at all individuals interested or working in any related field at any level, be it
funerary archaeology, osteoarchaeology, physical anthropology or human evolution. The assocaition aims to
provide a forum for the exchange of ideas and information, and to improve standards in all aspects of the
study of the biology of past and present peoples within their cultural context.
Conferemce sessions are: Aspects of the planning, recovery, analysis and conservation of human remains.
Ethics and Repatriation. Human Reproduction and Growth.
For conference details and booking contact: Dr Megan Brickley, Department of Ancient History &
Archaeology, University of Birmingham, Edgbaston, Birmingham B15 2TT. Tel. 0121 414 5497.
For more information on the association and membership details contact Dr Linda O'Connell, School of
Conservation Sciences, University of Bournemoth, Dorset House, Talbot Campus, Fern Barrow, Poole,
Dorset BH12 5BB. Tel: 01202 595 178.
Dr Megan Brickley Department of Ancient History & Archaeology University of Birmingham Edgbaston
Birmingham B15 2TT
Tel. 0121 414 7964 Fax. 0121 414 3595
========================================================================= Dr.
=========================================================================
PALEODIET Archives
From: Jacques Laurin
Reply-To:
Date: Mon, 15 Mar 1999 06:19:04 +0000
Steve Meyers wrote :
> It seems that many dietary practices have mixed effects, and it takes time for a group to sort
> those out -- especially if they lack a scientific method, which tends to reduce the amount of
> trial and error that has been in use for most of human evolution. (Though it is amazing that H/G
> people figured out so much about various foods and how best to prepare them -- without the help of
> cookbooks!)
Is there any scientific evidence supporting the human trial and error theory in hunting gathering times? I
would really enjoy sources. I wonder how the rest of the living things manage the lack of scientific method
...and cookbooks?
Yours truly Jacques Laurin
PALEODIET Archives
Subject: Re: Cereal Grain Article Citation
From: Loren Cordain
Reply-To:
Date: Mon, 15 Mar 1999 14:34:41 -0700
In the last paleodiet digest, Steve Meyers inquired about the publication date of my review article on cereal
grains. As far as I am aware, the article will be published in April (next month), and the citation will be:
16/46 (1999)
Cordain L. Cereal grains:Humanity's double edged sword. World Review of Nutrition and Dietetics
1999;84:000-000 (I dont have page numbers yet).
Also scheduled for publication in this same issue is a detailed and up to date version of Jennie Brand-Miller's
theory of the "Carnivore Connection" in which she further delineates how pre-agricultural humans were
adapted to a diet high in protein and low in carbohydrate.
Readers may also be interested in a letter which Jennie, Neil Mann and I published in Diabetologia (Cordain
L, Brand-Miller J, Mann N. Scant evidence of periodic starvation among hunter-gatherers. Diabetologia
1999;42(3):383-84.) which challenges J.V. Neel's commonly accepted theory regarding the selection
pressures for the evolution of a "thrifty genotype" in pre-agricultural humans. By the way, the basis for this
article developed from discussions we have had on this listserve. This letter can be directly downloaded in
pdf format from the following website:
http://link.springer.de/link/service/journals/00125/tocs/t9042003.htm
Cordially,
Loren
PALEODIET Archives
Reply-To:
Date: Tue, 16 Mar 1999 04:21:21 +0000
Loren Cordain wrote
> This letter can be directly downloaded in pdf format from the following website:
> http://link.springer.de/link/service/journals/00125/tocs/t9042003.htm
It needs a password to access those .pdf files. J.L.
PALEODIET Archives
Subject: Life span estimates
Reply-To:
Date: Sat, 24 Apr 1999 14:07:56 -0700
In reference to Dean's recent posting, here is the main point:
THE idea that our ancestors died very young may be a myth based on a statistical error, according to a team
of British archaeologists. They say a bias in the methods used for analysing human bones can underestimate
the true age of death by as much as 30 years.
It will be interesting to see what other archaeologists think about this (unlike the typical coverage in say,
Science, in this article there was not any comment by the "skeptics"); perhaps one of you on this list could
comment and perhaps keep us posted of developments?
Steve Meyers
PALEODIET Archives
Subject: Lectins
From: Dean Esmay
Reply-To:
Date: Sat, 24 Apr 1999 15:49:32 -0400
17/46 (1999)
A member who prefers to remain anonymous forwarded these interesting pages to me. I thought I'd forward
them on to you all.
http://www.cryst.bbk.ac.uk/research/lectin/lectin.html http://www.vectorlabs.com/Lectins/Ldescript.html
PALEODIET Archives
Subject: Ethnobotany symposium
From: Dean Esmay
Reply-To:
Date: Sat, 24 Apr 1999 15:54:36 -0400
Recently receieved in email, a call for papers. This appears to have been translated from Spanish and in parts
the language is a little rough.
DOC 012 INTERNATIONAL SYMPOSIUM ETHNOBOTANY MEDICINAL PLANTS, FOLK
TRADITIONS, HISTSORY, PHARMACOLOGY Under auspices Universidad para La Paz, Costa Rica,
Set., 14-18, 1999
GuideIines for authors
1. Deadline for manuscripts: 28 May, 1999.
2. Manuscript Length and Preparation Max. 30 pages of 30 lines each (~ 20%) typed on standard-size (8.5 x
11 inches) paper using 1.5 line spacing.
3. Title As clearer, appealing and short, as possible.
4. Structure Introduction: approx. 10 lines) Should not be a summary Conclusion: approx. 10 lines} of the
text Body of text clearly structured using subheadings (easier to read).
5. Contents The text should be written specially for this publication and be understandable without
consultation of further literature.
6. Historical dates Persons; date of birth and death. Historical events: exact date(s) or, where not possible, the
year(s).
7. Style and nature of text Informative, stimulating text, possibly incorporating latest research findings; of
high standard but accessible to the general public.
8. Source languape Contributions may be written in the language of the author's choice, but should
preferably be in his or her mother parole.
9. Ilustrations At least 4-6 illustrations (if both landscape and portrait format) should be submitted per
contribution. Illustration copy delivered by authors wiIl be mailed back to them after printing. Authors have
to supply their own illustrations. Copies are requested for later printing of Memories.
10. References A maximum of 10-15 references per contribution, in alphabetical order. Three examples of
references follow.
Reference to a book Gleason J. B.et al (1998): Psycholinguistics. Harcourt Brace College Publishers, Texas
Reference to a chapter in a book: Erwin-Tripp S.(1998): Conversational Discourse Chapter 6, pp., 238-270 in
Psycholinguistics, loc. cit.
Reference to a chapter in a Journal article Binder-Fritz Ch. (1999): Western Medicine Alone Does Not Cure
Maori Sickness. Pp., 4-13,
Febr., 1999, Vol 1, Nr 2, Viennese Ethnomedicine Newsletter. University of Vienna, Austria.
11. lndex If possible Contributions should be indexed.
12.Editing The Organisers of the Conference keep the right to edit all texts and have consult from experts
where needed.
13. Translations The publication will appear in English, and Spanish. No translation will be done of original
works. The publication will be effective according to the the original contributions.
14. Curriculum Vitae Authors are requested to submit a short Curriculum Vitae, specifying publications and
academic titles. Full addresses, incluidng e-mail will be delivered with CV. End Papers guidelines
Ethnobotany Symposium RCHC Sunday, April 18, 1999
PALEODIET Archives
Subject: Meat-eating ancestors in the news
From: Dean Esmay
Reply-To:
18/46 (1999)

Date: Sat, 24 Apr 1999 15:56:49 -0400
There seems to be a lot of this in the news lately:
http://www.abcnews.go.com/sections/science/DailyNews/hominid990422.html
PALEODIET Archives
Subject: Re: lectins
Reply-To:
Date: Sun, 25 Apr 1999 03:15:32 -0400
For those who are interested in lectins another article:
Freed, DLJ (1999). Do dietary lectins cause disease? British Medical Journal 318:1023-1024.
http://www.bmj.com/cgi/content/full/318/7190/1023
A more detailed information about Australopithecus garhi and earliest evidence of animal butchery from
University of California, Berkeley, Press Release:
http://www.urel.berkeley.edu/urel_1/CampusNews/PressReleases/releases/4-19-1999z.html
PALEODIET Archives
Subject: D'Adamo on lectins
From: Todd Moody
Reply-To:
Date: Mon, 26 Apr 1999 09:38:11 -0400
Since Dean has recently posted some URLs related to lectins, I thought I'd add this one:
http://www.dadamo.com/literature/lrc.htm
This is Peter D'Adamo's web site and a lenthy essay by him about lectins. On the same page, further down, is
some interesting material about ABO-specific differences in alkaline phosphatase secretion and its possible
relevance to fat digestion.
Todd Moody
PALEODIET Archives
Subject: Re: Paleodiet concept on Dateline NBC
From: Loren Cordain
Reply-To:
Date: Mon, 26 Apr 1999 10:30:15 -0600
To interested readers;
Dateline NBC recently interviewed me on the "paleodiet" concept and will be airing the interview either
tonight (Monday, April 26) or Wednesday, April 28.
Cordially,
Loren
PALEODIET Archives
Subject: More PaleoPress
From: Arthur De Vany
19/46 (1999)
Reply-To:
Date: Mon, 26 Apr 1999 12:45:57 -0700
Coterminous with Loren Cordain's appearance on Dateline NBC will be an article on Evolutionary Fitness
and Diet to appear in Women's Health and Fitness (this month's issue I am told). In addition, one episode of a
PBS TV series called Closer to the Truth will feature Roy Walford (the UCLA scientist who exposes under
eating) and myself, along with geneticists and doctors discussing diet and fitness. The Closer to the Truth
series will air in the top 25 PBS markets starting next fall.
Walford eats a near-Paleo diet, nutrient dense, low calorie food and does body building to retain muscle
mass. This is similar to Evolutionary Fitness, except that in Evolutionary Fitness dietary restriction is
episodic rather than uniform. And, overall there is only moderate restriction in an evolutionary eating
pattern.
Dr. Walford did not answer my question to my satisfaction. It is that too few of the caloric restriction studies
have considered episodic restrictions, such as a paleolithic hg might have experienced, and all that I am
aware of have an ad libitum-fed control. Comparing a rat that is pigging out with one whose diet is restricted
may demonstrate that overeating is poor health practice (which it is).
On the age of ancestors; it is well-known that the incidence of extreme events, such as living to very old age,
is a function of the size of the sample. Modern humans comprise a large sample and, hence the upper tail
probabilities reasonably well match the theoretical distribution. But, for paleo ancestors, the samples are
extremely small. As sample size grows, so too will the upper tail frequencies. Current estimates of age
distributions among ancestors are plagued with the small sample problem and such estimates will continue to
reach upward as the size of the sample grows.
There is no unitary cause of death and the age of the oldest (modern and paleolithic) human will continue to
creep up as we record more data, and this independent of advances in health or any other changes. The upper
tail of the theoretical Gompertz curve (log survival rate, linear age) of survival is unbounded, implying there
is no finite limit to age and that the variance of the distribution and the extreme events in the upper tail will
drift upward with sample size. That is exactly what is seen in animal populations as the number of subjects
correctly age dated expands.
-- Arthur De Vany Department of Economics and Institute for Mathematical Behavioral Sciences University
of California Irvine, CA 92697-5100 http://www.socsci.uci.edu/econ/personnel/devany/devany.html 949824-5269
PALEODIET Archives
Subject: Broadcasting paleodiet, life span
Reply-To:
Date: Thu, 29 Apr 1999 22:21:31 +0200
Parts/Attachments:
At 13.38 -0600 99-04-28, Loren Cordain wrote:
> My scheduled interview on dateline for this evening has been postponed because of the increased
> coverage of the Columbine High School tragedy - will let you know when it is re-scheduled. Mine
> was however not postponed - the best known and most respected scientific radio program in Sweden
> today sent a 20 minutes interview with me on the concept Geneva of paleodiet in the prevention of
> cardiovascular disease and diabetes. I would like to comment on life span in past populations but
> I have too little time at the moment. To put it short, age estimates from human bones are very
> uncertain indeed above the age of 40. Even a complete skeleton from someone who is supposed to
> have died at the age of 50 could well have passed 80 years of age.
1. Arcini Caroline (1999). Health and disease in early Lund: Osteo-pathologic studies of 3, 305 individuals
buried in the first cemetery area of Lund 990-1536 [PhD Thesis].
2. Isan, M. Y., Kennedy, K. A. R. (1989). Reconstruction of life from the skeleton. New York, Wiley-Liss.
20/46 (1999)
3. Saunders, S. R. and M. A. Katzenberg (1992). Skeletal biology of past peoples: research methods. New
York, Wiley-Liss.
PALEODIET Archives
Subject: 2.34 million year old tool "factory"
From: Dean Esmay
Reply-To:
Date: Sat, 8 May 1999 11:08:11 -0400
I notice that the above-mentioned article about the dig in Kenya found fish bones among the fauna
apparently processed with stone tools at the site.
If I'm not mistaken, this may be the earliest evidence of fish consumption by humans to date. Although the
fish bones were less than 1% of the fauna remains found at the site, they were clearly there, along with other
aquatic animals. (see http://www.nature.com/server-java/Propub/nature/399057A0.table-1) -=It was said that when people heard Cicero speak they said, "What a clever fellow is Cicero, " but when they
heard Demosthenes speak they said, "Let us march against Philip."
PALEODIET Archives
Subject: Re: 2.34 million year old tool "factory"
Reply-To:
Date: Sat, 8 May 1999 10:32:22 -0500
Dean Esmay writes:
> I notice that the above-mentioned article about the dig in Kenya found fish bones among the fauna
> apparently processed with stone tools at the site. If I'm not mistaken, this may be the earliest
> evidence of fish consumption by humans to date. Although the fish bones were less than 1% of the
> fauna remains found at the site, they were clearly there, along with other aquatic animals. (see
> http://www.nature.com/server-java/Propub/nature/399057A0.table-1)
Note that there is a qualifying statement in the text of the paper (p.59) which says:
The fragmentation and the distribution of the fossils within the presumably short sequence of LA2C point to
natural accumulation. The bones, which are encrusted and poorly preserved, show no evidence of anthropic
action. However, the tortoise bones and ostrich-egg fragments are more closely associated with the lithic
artefacts; their systematic presence in both Lokalalei sites may show a possible hominid collecting strategy.
Also, the deposits occurred in an ancient floodplain, so one would (presumably) expect there to be some fish
bones regardless of human activity.
--Ward Nicholson
PALEODIET Archives
Subject: Re: Dateline NBC
From: Loren Cordain
Reply-To:
Date: Sat, 22 May 1999 14:09:12 -0600
Here we go again. I got a call from the producers of Dateline NBC and the piece that they did on my research
on paleodiets is supposed to air this Monday (May 24) night. Hopefully, it will not be pre-empted again.
Cordially,
Loren
21/46 (1999)
PALEODIET Archives
Subject: Re: An interesting issue of World Review of Nutrition and Dieteti cs
From: Loren Cordain
Reply-To:
Date: Tue, 15 Jun 1999 09:49:53 -0600
There has been quite a lull in the activity of this listserve - perhaps we're all getting talked out. Anyway, for
those that may be interested, my cereal grain manuscript has finally come into print along with two very
important articles concerned with the paleodiet concept in the most recent issue of the World Review of
Nutrition and Dietetics. The articles in this issue (entitled: Evolutionary Aspects of Nutrition and Health.
Diet, Exercise, Genetics and Chronic Disease) are as follows:
1. Neel, J.V.: When Some Fine Old Genes Meet a 'New' Environment 2. Cordain, L.: Cereal Grains:
Humanity's Double-Edged Sword 3. Brand-Miller, J.C.; Colagiuri, S.: Evolutionary Aspects of Diet and
Insulin Resistance 4. Chen, J.D.: Evolutionary Aspects of Exercise 5. Simopoulos, A.P.: Genetic Variation
and Nutrition
Note that author J.V. Neel is the originator of the so called "Thrifty Genotype Hypothesis", perhaps one of
the most orienting concepts in nutritional and biomedical anthropology (1) . Also, note that Jennie Brand
Miller's classic "Carnivore Connection" hypothesis (2) has been updated and revised in her article in this
issue of World Review of Nutrition and Dietetics. Artemis Simopoulos, M.D., is to be commended for
putting together such an important and timely compilation of articles showing how humanity's genetic
makeup has been directly influenced by nutritional selective pressures and how our present day diet may be
discordant with our stone age genome. Interested readers can obtain this issue at this website:
http://www.karger.ch/bookseries/wrund/wrund084.htm
Cordially,
Loren
References
1962;14:353-62. 2. Brand Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the
evolution of NIDDM. Diabetologia 1994;37:1280-86.
PALEODIET Archives
Subject: "New" hypothesis
From: Dean Esmay
Reply-To:
Date: Fri, 25 Jun 1999 14:54:42 -0400
Submitted by one of our archaeologist friends:
--http://www2.ari.net/rjohnson/articles/VOLCANO.UIL.html
CHAMPAIGN, Ill. -- A new hypothesis about recent human evolution suggests that a horrific "volcanic
winter" 71, 000 years ago, followed by the coldest 1, 000 years of the last Ice Age, brought widespread
famine and death to modern human populations around the world. The abrupt "bottleneck, " or decrease, in
our ancestors' populations, in turn, brought about the rapid "differentiation" -- or genetic divergence -- of the
surviving population.
-="You've got to keep fighting. You've got to risk your life every six months to stay alive." --- Elia Kazan
PALEODIET Archives
22/46 (1999)
Subject: Re: "New" hypothesis

Reply-To:
Date: Tue, 29 Jun 1999 09:38:44 +0100
On Fri, 25 Jun 1999, Dean Esmay wrote:
> Subject: "New" hypothesis
> Submitted by one of our archaeologist friends:
> --> http://www2.ari.net/rjohnson/articles/VOLCANO.UIL.html
Not so new - for those who want the full details, it was published about a year ago as:
Ambrose, SH (1998) Late Pleistocene human population bottlenecks, volcanic winter and the differentiation
of modern humans. Journal of Human Evolution 34 623-651
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Bottleneck
From: M E Wood
Reply-To:
Date: Wed, 30 Jun 1999 10:02:40 +1200
It is good to get the reference for the Late Pleistocene human population bottlenecks. It is very useful if one
has access to academic journals in the print medium. However not every one all over the world can find the
same journals in libraries. Not everyone has libraries! I often wonder if the academic community is taking
full advantage of the new technology? The idea of the World Wide Web conceived by Tim Berners Lee was
for very a different means of publishing ideas.
http://wwwinfo.cern.ch/pdp/ns/ben/TCPHIST.html
Many articles which actually do appear on the WWW are still facsimiles of print media especially from
universities and similar institutions
There are footnotes and bibliographies, even. All the references are to printed books and journals. This is a
new medium. Instead of articles transferred in total there should be linked pages. You can see the same
unimaginative things happening as the publishers take over e magazines. This new medium needs a total
rethink about spreading of knowledge but I fear the dead hand of the academic publishing house will stifle it.
M E Wood
PALEODIET Archives
Subject: Cooking: another aspect
Reply-To:
Date: Mon, 19 Jul 1999 17:49:12 -0400
Most of us like the smell and the taste of fried or grilled meat (potatoes ...hmmh). Obviously this preference
has something to do with substances, that are produced during the Maillard reaction. But chemical analyses
do not explain why we like these substances. Are we only imprinted to mothers steaks or does this reflect an
adaptational process, fixed in our genes? Have our nutritional preferences changed to cooked and fried foods
as an adaptation to a long hominid use of fire?
23/46 (1999)
I do not think so. Many animals like fried food too (just a personal observation; sorry, no references....). The
reason could be the production of opiate-like substances during the browning process. This hypothesis is
supported by the findings of a new study: Exploring the Maillard reaction, Wang et al. detected two novel
substances belonging to the class of DF-Carbolines. DF-Carbolines are psychoactive alkaloids and can be
found in tobacco, in the hallucinogenic beverage ayauasca and some are produced in the organism after
consumption of alcohol.
Reference: Mingfu Wang, Yi Jin, Jiangang Li, & Chi-Tang Ho (1999). Two novel DF-Carboline compounds
from the Maillard reaction between xylose and tryptophan. Journal of Agricultural and Food Chemistry
47:48-50
PALEODIET Archives
Subject: Cooking or not cooking
Reply-To:
Date: Sun, 18 Jul 1999 11:37:04 -0400
Hello
I would appreciate comments on this text about the problems of cooking.
"Through the working of natural selection, each species adapts to the conditions of its habitat. Such
adaptation, however, takes many generations ; the genetic code changes very slowly over time (less than 1 %
in the six million years since our forebears diverged from the chimpanzees). The practice of cooking is quite
recent in relation to the biological time scale, each new alimentary challenge introduced by intelligent
artifice may pose a new metabolic problem and entail pathological consequences. For any culinary artifice,
there is a reason to ask :
whether a genetic adaptation has been or would have been necessary whether such adaptation is possible
whether it has had time to occur
This issue, apparently ignored by medical research, is quite critical, being at the very heart of the world
health problem. The prognosis in any illness depends inevitably on nutrition. Therefore the illness depends
on nutrition (even if one is ignorant of its mechanisms). It is helpful, then, to pose the problem of adaptation
before plunging blindly into a quest for therapeutics that risk missing the point, that in fact remain unavailing
in the face of various diseases. Three quarters of the population die of neoplastic or cardiovascular diseases,
which are not necessarily preordained by nature.
Non-original foods introduce molecules into the organism to which the enzymes, programmed by the genetic
code, have no reason to be adapted. These "non-original molecules" may be created in chemical reactions
induced by cooking, or may come from foods not in the original alimentary spectrum of humans (such as
animal milk). It will be impossible for some of these to be metabolized normally ; instead, blocked at some
stage of transformation, they will accumulate in the organism, provoking a gradual culinary intoxination.
They will be found in the circulating fluids (blood, lymph) or stored within the cells or in the interstitial
spaces (amylose), in fatty deposits, or even integrated into cell and tissue structures (membranes, collagen,
joints, dentin, etc...)
Contemporary studies of metabolism have not yet given much consideration to these abnormal molecules,
whose transformations constitute an anomolous, or "paradoxical" metabolism (= processes not provided for
by the genetic code, which we call "parabolism"). Some of these substances could provoke all kinds of
disorders (as many disorders as there are classes of substances and functions in the organism). In other
words, the culinary intoxination will give rise to a "molecular pathology" which could constitute the cause in
whole or in part of numerous illnesses.
The notion of intoxication as conceived by medical science refers either to chemical substances or to
alimentary intoxication due to accidental contamination, fermentation, surfeit, or any intolerance ; and in
pathological cases, to an excess of the waste products of normal metabolism. Fringe medicine gives more
weight to the alimentary factor than does conventional thinking, but at present neither seems to have
distinguishe clearly between original toxins and non-original toxins.
24/46 (1999)
In fact, certain molecules present in original foods are toxic, as are certain by-products of metabolism : these
substances, however, have existed all the time, so that the programming of our genetic code provides for
their elimination through normal channels (= detoxication). The same cannot be said of molecules that
deviate from this programming, which must be eliminated by various unexpected mechanisms (deviant
channels) and over much longer periods of time."
Thank you for your time Jacques Laurin
PALEODIET Archives
Subject: Re: Cooking or not cooking
Reply-To:
Andrew Millard
Date: Tue, 20 Jul 1999 09:47:57 +0100
On Mon, 19 Jul 1999, Jacques Laurin wrote:
> I would appreciate comments on this text about the problems of cooking. "Through the working of
> natural selection, each species adapts to the conditions of its habitat. Such adaptation, however,
> takes many generations ; the genetic code changes very slowly over time (less than 1 % in the six
> million years since our forebears diverged from the chimpanzees). The practice of cooking is quite
> recent in relation to the biological time scale, each new alimentary challenge introduced by
> intelligent artifice may pose a new metabolic problem and entail pathological consequences.
I'm not convinced that alimentary change is that much of a challenge. For one thing the 1% change is across
the entire genome and we don't know the percentage difference in the minority of the genome which is
coding and this is the important figure in terms of adaptive difference. Secondly the gorilla diverged from
humans and chimpanzees at about the same time, but the three species have very different diets, body sizes
(including extent of sexual dimorphism), mating patterns, etc, and all those differences presumably have a
genetic basis within the 1% difference.
> For any culinary artifice, there is a reason to ask : whether a genetic adaptation has been or
> would have been necessary
OK
> whether such adaptation is possible whether it has had time to occur
I don't think we can necessarily expect to answer this, we know so little about the genetic basis of differences
in diets that we can hardly begin to guess what isn't possible. Given the differences already present between
species, it seems likely that given enough time most things are possible. But at present we can't predict a
priori how much time is enough.
> This issue, apparently ignored by medical research, is quite critical, being at the very heart of
> the world health problem. The prognosis in any illness depends inevitably on nutrition. Therefore
> the illness depends on nutrition (even if one is ignorant of its mechanisms). It is helpful, then,
> to pose the problem of adaptation before plunging blindly into a quest for therapeutics that risk
> missing the point, that in fact remain unavailing in the face of various diseases. Three quarters
> of the population die of neoplastic or cardiovascular diseases, which are not necessarily
> preordained by nature.
According tothe World Health Organization "World Health Report 1999" Appendix on mortality
(http://www.who.int/whr/1999/en/pdf/mortality.pdf) Mortality in WHO member countries in 1998 is
estimated at: Communicable diseases, maternal and perinatal 30.5% conditions and nutritional deficiencies
Noncommunicable conditions 58.8% To which neoplasms contribute 13.6% and cardiovascular diseases
30.9% Injuries 10.7%
Thus 44.5% of the world population die of neoplastic or cardiovascular disease - hardly three-quarters!
However, many of the other non-communicable causes have a dietary component in their etiology, eg
diabetes, asthma.
> Non-original foods introduce molecules into the organism to which the enzymes, programmed by the
> genetic code, have no reason to be adapted. These "non-original molecules" may be created in
> chemical reactions induced by cooking, or may come from foods not in the original alimentary
> spectrum of humans (such as animal milk). It will be impossible for some of these to be
> metabolized normally ; instead, blocked at some stage of transformation, they will accumulate in
> the organism, provoking a gradual culinary intoxination. They will be found in the circulating
25/46 (1999)
> fluids (blood, lymph) or stored within the cells or in the interstitial spaces (amylose), in fatty
> deposits, or even integrated into cell and tissue structures (membranes, collagen, joints, dentin,
> etc...)
They may get into tissue structures but the collagens are a set of protein molecules with a specific structure other molecules cannot get into them. One or more examples would help your argument here: one might
naively suppose that all ingested proteins are denatured in the digestive system, and all are then hydrolysable
by enzymes - so what is there in animal milk that gets into the body? The substance which springs to mind as
fitting your description is lead, which accumulates over a lifetime because humans have no excretion
mechanism for it.
(Rest deleted - I can't comment on it)
Andrew Millard
========================================================================= Dr.
=========================================================================
PALEODIET Archives
From: Randall Collura
Reply-To:
Date: Tue, 20 Jul 1999 10:23:20 -0400
Jacques Laurin wrote:
> Such adaptation, however, takes many generations ; the genetic code changes very slowly over time
> (less than 1 % in the six million years since our forebears diverged from the chimpanzees). The
> practice of cooking is quite recent...
It's not the genetic code that's changing here but the DNA sequences that regulate the expression of and code
for proteins (i.e. enzymes). The often quoted 1% or 2% figure between humans and chimpanzees is an
average (of single copy, coding DNA) with some genes being identical and others being more divergent (see
Sibley and Ahlquist 1987). Also, not all DNA base changes are equivalent; a single base change that results
in an amino acid replacement in the active site of an enzyme can drastically alter or diminish function while
many changes in other parts of the molecule may have only a slight effect.
> there is a reason to ask : whether a genetic adaptation has been or would have been necessary
If cooking creates novel compounds that are otherwise not found then perhaps genetic changes would be
required. If cooking only alters the availability of compounds that are naturally present (by destroying some
and making others more available) then no. (This IS an active area of anthropology research.)
> whether such adaptation is possible
Sure it's possible.
> whether it has had time to occur
This depends on the selection pressure. If there is a lot of selection pressure then changes can occur quite
rapidly in evolutionary time (see Messier and Stewart 1997).
> chemical reactions induced by cooking, or may come from foods not in the original alimentary
> spectrum of humans (such as animal milk).
Infants ARE supposed to consume animal (human) milk and are adapted to digest it.
> In other words, the culinary intoxination will give rise to a "molecular pathology" which could
> constitute the cause in whole or in part of numerous illnesses.
COULD, perhaps but this is just speculation. It's just as likely that any new molecules created by cooking
would be metabolized by the enzymes that have evolved over millions of years to deal with all kinds of biomolecules. Just because a specific compound is new doesn't necessarily mean it can't be processed. Also, it
seems that cooking would be more likely to break down existing molecules rather than create new ones. I'm
frankly far more concerned with the multitudes of synthetic chemicals that have been introduced into our
food and environment over the last 100 years.
Randall Collura
26/46 (1999)
Sibley, C. G. and J. E. Ahlquist (1987). "DNA hybridization evidence of hominoid phylogeny: results from
an expanded data set." J Mol Evol 26(1-2): 99-121.
Messier, W. and C. B. Stewart (1997). "Episodic adaptive evolution of primate lysozymes." Nature
385(6612): 151-4.
_______________________________________________________________________ Randall Collura
Phone - (617) 495-8323 Harvard/Anthropology Fax - (617) 496-8041 Peabody Museum 11 Divinity Ave.
Email - Cambridge, MA 02138
WWW - http://www.fas.harvard.edu/~collura/index.html
_______________________________________________________________________
PALEODIET Archives
Subject: Fire and adaptation to cooking
Reply-To:
Date: Tue, 20 Jul 1999 23:15:26 -0700
There is a nice discussion of fire and cooking in human evolution by Ward Nicholson at:
http://www.beyondveg.com/nicholson-w/hb/hb-interview2a.shtml
Steve Meyers
PALEODIET Archives
Subject: Raw vs cooked food
Reply-To:
Date: Tue, 20 Jul 1999 23:22:30 -0700
There is also a lengthy and quite interesting investigation of the science on raw vs. cooked food at:
http://www.beyondveg.com/tu-j-l/raw-cooked/raw-cooked-1a.shtml
Steve Meyers
PALEODIET Archives
Subject: Cooking or not cooking and potential genetic defect
From: Luc De Bry
Reply-To:
Date: Wed, 21 Jul 1999 15:13:58 +0200
Cooking or not cooking and potential genetic defect, in response to
Date: Sun, 18 Jul 1999 11:37:04 -0400 From: Jacques Laurin Subject: Cooking or not cooking
... (snipped for space reason)
For any culinary artifice, there is a reason to ask :
> whether a genetic adaptation has been or would have been necessary whether such adaptation is
> possible whether it has had time to occur
In order to become able to cook, humans must have learnt to overcome natural animal fears from the fire. It
suggests that the differentiation, rise and spread of the human species may be due to a genetic defect causing
the suppression of instinctive fears from the fire. Thus, one should perhaps replace traditional search for the
so-called superior gene by a search for the missing instinct and/or gene, or at least for the missing gene
expression.
> This issue, apparently ignored by medical research, is quite critical, being at the very heart of
> the world health problem.
27/46 (1999)
It is not ignored. It is part of research among others about the Maillard reaction (see ref. below). Although
British brewers would argue that Ling (1911) was first, the original most cited work dates back to a 1913
landmark book of Dr. Louis-Camille Maillard of France. Maillard symposii are now held every four years.
Scientists of both medical and food research participate. The last symposium was held at London in 1997, at
the Royal College of Physicians, opposite the corner of Regent's Park.. The EU sponsors a Maillard program
throughout Europe. The next and 7th. symposium is due to be held in Japan in 2001. The major world health
problem is caused by over-cooking. But who wants to eat burnt foods anyway?
... (snipped)
> chemical reactions induced by cooking,
Advanced Maillard reaction products or burnt products may indeed cause some toxicity and mutagenic and
carcinogenic reactions. Well conducted Maillard reaction is a prerequisite to detoxify natural and powerful
anti-nutritional factors contained in all seeds. Without this mastering of the Fire Technology, there would be
no point spending time and energy at growing toxic grains and beans, such as wheat and barley, soybeans,
cocoa beans, etc. The Maillard reaction is also naturally occuring in the human body. It is associated to
ageing, cataracts, diabetes, etc.
Furthermore, the Maillard reaction involves a number of oxido-reductions. The same reaction was apparently
also present at the origins of Life. A number of cooking-derived and Maillard-generated anti-oxidants and
other compounds have useful nutritional and health properties.
Without it, there would probably be neither life nor humans. With too much of it, life and humans age to
their ends. The Maillard reaction gave us life. The Maillard reaction maintains life. The Maillard reaction
takes our lives back. The Bible says something like (excuse my poor English): "you are dust and you will be
dust again".
A few recent references:
Maillard Reactions in Chemistry, Food, and Health by Theodore P. Labuza, Gary A. Reineccius Hardcover
(December 1994) Royal Society of Chemistry; ISBN: 0851868029
The Maillard Reaction : Consequences for the Chemical and Life Sciences Raphael Ikan(Editor), Raphael
Akan (Editor); Paperback - 228 pages (September 1996) John Wiley & Sons; ISBN: 0471963003
The Maillard Reactions in Foods and Medicine Special Publication (Royal Society of Chemistry), 223) J.
O'Brien(Editor); Hardcover (August 1998) Royal Society of Chemistry; ISBN: 0854047336
Regards,
Luc -- Luc De Bry, Ph.D., Head of Research Department GENERAL BISCUITS BELGIE De BeukelaerPareinlaan, 1 B-2200 Herentals - Belgium
Tel 32 (0)14 24 14 32 Fax 32 (0)14 24 10 25 Email:
An Operating Company of http://www.danonegroup.com
Home email :
PALEODIET Archives
Subject: Raymond Hames at U. of Nebraska
From: Dean Esmay
Reply-To:
Date: Mon, 26 Jul 1999 11:56:20 -0400
Here are some interesting web links.
TOPICS IN HUNTING AND GATHERING
http://www.unl.edu/rhames/courses/forout97.htm
This is an extensive course description for a class at the University of Nebraska on hunter/gatherer lifestyles.
The instructor is one Raymond Hames. Hunters and Gatherers Anthropology is a course taught by Raymond
Hames at U. of Nebraska. Includes lecture notes on the book The Foraging Spectrum which outlines the
important research issues, theory, and problems in hunter-gatherer research.
Hames also has a web page full of interesting links and information at:
http://www.unl.edu/rhames/courses/kelly5_end.htm
28/46 (1999)
PALEODIET Archives
Subject: Cordain/Crayhon Interview
From: "William Thornton, DC"
Reply-To:
Date: Mon, 26 Jul 1999 23:32:33 -0700
Dr. Cordain,
Superb interview. A few questions for clinical applications:
1. RE: unleavend bread. Would the problems associated with this food be mitigated (and to what degree) by
SPROUTING the grains and making an unleaved bread?
2. RE: "Foods which yield a net acidic load mainly as sulfates... Foods which cause a net acid excretion
include meat, fish, cheeses and grains. Excess dietary protein can adversely affect bone." What then is the
effect of supplemental sulfur, as MSM (Methyl-Sulfonyl-Methane), for the symptoms of arthritis? Are we
merely adding to the acid burden in the body with MSM, resorbing more bone? High sulfur vegetables
(cabbage, kale, asparagus, etc), do these benefit the body by providing sulfur for healthy hair, nails,
connective tissue as claimed by nutrition books?
On a clinical note, the validity of your thesis in favor of the paleo diet has been borne out in the application
of a paleo diet with many of my patients who suffer from insulin-resistance syndrome. Many years as
vegetarians (really as "grain-arians", considering the amount of grain so-called vegetarians eat) has led to
serious deficiencies and symptomology. Only in these past few years (upon learning of the paleo diet
approach, from Eaton, Eades, Sears and yourself) have I been able to turn things around by strictly adhering
to a near-zero grain diet. In addition, because of their insulin resistance, these patients must also restrict their
intake of fruits, as well.
In considering the value of paleopathology/paleobiology, I am reminded of the sign hanging over the door in
cadaver dissection-anatomy lab at med school, written in Latin, it translates to: "The Dead Teach The
Living." There is much to learn from those who have come before us, lived, died and now provide testimony
to their lifestyles in the remnants of their physical bodies.
Thank you for your enlightening and vital work in this area.
William Thornton, DC
PALEODIET Archives
Reply-To:
Date: Fri, 30 Jul 1999 05:17:23 -0400
I would like to thank you all for your time, this was really enlightning. There are few minor points I would
like to address in order to clarify my thoughts on the subject.
> I'm not convinced that alimentary change is that much of a challenge. For one thing the 1% change
> is across the entire genome and we don't know the percentage difference in the minority of the
> genome which is coding and this is the important figure in terms of adaptive difference. Secondly
> the gorilla diverged from humans and chimpanzees at about the same time, but the three species
> have very different diets, body sizes (including extent of sexual dimorphism), mating patterns,
> etc, and all those differences presumably have a genetic basis within the 1% difference. ...we
> know so little about the genetic basis of differences in diets that we can hardly begin to guess
> what isn't possible. Given the differences already present between species, it seems likely that
> given enough time most things are possible. But at present we can't predict a priori how much time
> is enough.
29/46 (1999)
If we have the right to hope for a future adaptation to the new proteins of wheat, corn or cow's milk, it seams
to me that it is a different story when we are talking about cooked food. Many new chemical species
generated by the action of cooking, isomers for instance, differ too much from the natural molecules to
expect our digestive enzymes to be active on them. Do we know what happens to the isomers that go through
the intestinal barrier? I guess that at best, they are unusable but in many cases, they are probably dangerous.
...so what is there in animal milk that gets into the body?
In general, there is certainly no problem with human female milk but cow's milk seems to be a different
story. Although Boudet (1993), Andre (1983) did excellent general reviews and Seignalet (1996) a detailed
analysis on the differences between human and cow's milk and the risks linked to it`s consumption (all in
french), I would appreciate comments on these already translated excerpts from : What milk to feed a
newborn baby? by Professor J. Lestradet, in Journal of Nutrition and Diet (Cahiers de nutrition et de
dittique), March 1982.
Any kind of milk other than mothers milk, used in an unaltered state, will cause major disruptions.
Differences between types of milk are fundamental. As a matter of fact, there is twice as much lactose in
human milk as in cows milk, and it is known that lactose is vital for brain growth, which is twice as quick in
a baby as in a calf". The writer notes that ... "Romulus and Remus couldnt possibly have been suckled by a
she-wolf since there is nine times as much protein in its milk as in human milk. Such a high intake of protein
would quickly have proved lethal, since the liver and kidneys, which excrete uric acid, would have been
grossly overworked. Such an overload is already at work with cows milk in which there is three times as
much protein as in human milk. It is to be noted that the liver and kidneys of a bottle-fed child are 30%
larger than the very same organs in a breast-fed child. Cows milk doesnt address calcium absorption better
than human milk, although it contains three times as much calcium. Cows milk contains five times as much
phosphate as human milk, and this causes two-thirds of the calcium to be retained in the gut_the result being
that a bottle-fed child tends to have low blood calcium. Further, cows milk, whether formulated or not,
contains iron and this enhances the growth of pathogenic bacteria. Using partly skimmed spray-dried milk,
one is going the other way and setting up an iron deficiency in the newborn, which is, additionally, worsened
since cows milk protein irritates the digestive tract and causes microscopic bleeding. As for salt, which
cows milk is three times as high in, it is known to cause water retention and high blood pressure. There are
grounds for thinking that starting a child out on too much salt could well account for some cases of adult
high blood pressure."
Many other worth mentionning points, like the absence of gynolactose and gammalinolenique acid and the
presence of betalactoglobuline etc. in cow`s milk, are absent from these excerpts but as a starting point, I
guess this is enough...
Luc De Bry wrote:
> Advanced Maillard reaction products or burnt products may indeed cause some toxicity and mutagenic
> and carcinogenic reactions. Well conducted Maillard reaction is a prerequisite to detoxify natural
> and powerful anti-nutritional factors contained in all seeds. Without this mastering of the Fire
> Technology, there would be no point spending time and energy at growing toxic grains and beans,
> such as wheat and barley, soybeans, cocoa beans, etc. The Maillard reaction is also naturally
> occuring in the human body. It is associated to ageing, cataracts, diabetes, etc.
> Furthermore, the Maillard reaction involves a number of oxido-reductions. The same reaction was
> apparently also present at the origins of Life. A number of cooking-derived and Maillard-generated
> anti-oxidants and other compounds have useful nutritional and health properties.
> Without it, there would probably be neither life nor humans. With too much of it, life and humans
> age to their ends. The Maillard reaction gave us life. The Maillard reaction maintains life. The
> Maillard reaction takes our lives back. The Bible says something like (excuse my poor English):
> "you are dust and you will be dust again".
Correct me if I'm wrong but isn't there more to cooking then Maillard reactions? As described by Cuq and
Lorient (1992) (excuse my poor english translation) Cooking has multiple consequences (in short): Modification of the spatial structure - Modification of the lateral chains of the amino acids residues Interaction between many proteins - Interaction between proteins and glucides reducer (Maillard reactions) Hydrolysis of the peptidic - Isomer formation - Interaction between proteins and lipoids (multiple and
complex) leading to the production of free radicals - Interaction between proteins and polyphenols.
Comments?
Jacques Laurin
References:
Boudet, M. "Le lait maternel : production et constitution." Bulletin AMKI, 1993a, no 5, 3-8.
30/46 (1999)
Andre, G. "Dietetique de l'enfant.", 1 vol., Masson, Paris, 1983, 276 pages.

Seignalet, Dr. J. "L'alimentation ou la troisieme medecine.", Collection Ecologie humaine, Francois-Xavier
de Guibert, 1996, 452 p.
Cuq, J.L. et Lorient, D., "Influence de traitements technologiques sur la valeur nutritionnelle des protines
alimentaires.", in "Aspects nutritionnels des constituants des aliments. Influence des technologies.", 1 vol.,
Lavoisier Tec et Doc, Paris, 1992, 41 pages.
PALEODIET Archives
Subject: gluten and breast milk
From: Mary
Reply-To:
Date: Sat, 31 Jul 1999 15:30:00 -0700
On the gluten (celiac) list, many say that if a breast feeding mother eats gluten and casein, they will be
present in the breast milk.
On the other hand, I had a breast feeding expert email me that gluten and casein do NOT get into the
mother's milk.
Does anyone know?
PALEODIET Archives
Subject: Protein and risk of heart disease
Reply-To:
Date: Sat, 31 Jul 1999 18:30:50 -0700
The latest issue of Am Jour Clin Nutrition reports Harvard study showing higher protein intake associated
with reduced risk of heart disease among women. This may be first prospective cohort study showing such
an effect.
From Abstract:
Results: We examined the association between dietary protein intake and incidence of ischemic heart disease
in a cohort of 80082 women aged 3459 y and without a previous diagnosis of ischemic heart disease, stroke,
cancer, hypercholesterolemia, or diabetes in 1980. Intakes of protein and other nutrients were assessed with
validated dietary questionnaires. We documented 939 major instances of ischemic heart disease during 14 y
of follow-up. After age, smoking, total energy intake, percentages of energy from specific types of fat, and
other ischemic heart disease risk factors were controlled for, high protein intakes were associated with a low
risk of ischemic heart disease; when extreme quintiles of total protein intake were compared, the relative risk
was 0.74 (95% CI: 0.59, 0.94). Both animal and vegetable proteins contributed to the lower risk. This inverse
association was similar in women with low- or high-fat diets.
Conclusions: Our data do not support the hypothesis that a high protein intake increases the risk of ischemic
heart disease. In contrast, our findings suggest that replacing carbohydrates with protein may be associated
with a lower risk of ischemic heart disease. Because a high dietary protein intake is often accompanied by
increases in saturated fat and cholesterol intakes, application of these findings to public dietary advice should
be cautious.
[but pointing in a Paleodiet direction...]
For full text of article:
http://www.ajcn.org/cgi/content/full/70/2/221
Steve Meyers
PALEODIET Archives
Subject: Re: gluten and breast milk
From: Don Wiss
Reply-To:
31/46 (1999)

Date: Sat, 31 Jul 1999 18:50:07 -0400
Mary asked:
> On the gluten (celiac) list, many say that if a breast feeding mother eats gluten and casein,
> they will be present in the breast milk. On the other hand, I had a breast feeding expert email me
> that gluten and casein do NOT get into the mother's milk.
I don't know what you mean by a breast feeding expert. You mean someone expert in the techniques of
breast feeding? The reason people on the celiac list state what they do is this has been researched. Below is
just one of two articles written by Dr. Reichelt and on the web. He has been researching the impact of gluten
and casein intolerance on certain individuals with developmental delays. A collected set of his postings to the
net has been put up at:
http://www.panix.com/~donwiss/reichelt.html
From: (Kalle Reichelt) Date: 09/28/95 08:23:24 AM Subject: dietary proteins in mothers milk
Hi. It has been clearly established that bioactive and significant amounts of protein and peptides are taken up
from the gut (1, 2). It is therefore not suprising that the same proteins can be measured in mothers milk (3-6).
This has been done by immunological technique and also demonstration that the proteins are not fragments
of the precursors by electrophoresis on acrylamide gels. Gliadin proteins see ref 6. That this mechanism may
have serious consequences is illustrated by the many papers relating peptide fragments of milk proteins and
the induction of antibodies that destroy the beta-cells (insulin producing cells) and cause diabetes mellitus (79). Certain epilepsy is also related to gluten (10).
References: 1: Gardner MLG (1994) Absorption of intact proteins and peptides. in Physiol of gastrointestinal
Tract 3rd edit (edit: LR Johnson) Raven press, NY pp1795-1820. 2: Gardner MLG and Stffens K-J
(eds)(1995) Absorption of orally adminsitered enzymes. Springer Verlag, Berlin, Heidelberg. 3: AxelssonI et
al (1986) Bovine bveta-lactoglobulin in human milk. Acta Paed Scand 75: 702-707. 4: Kilshaw PJ and Cant
AJ (1984) The passage of maternal dietary protein into human breast milk. Int Arch Allergy and Appl
Immunol 75:8-15. 5; Stuart Ca et al (1984) Passage of cow's milk protein in breast milk. Clin Allergy 14:
533-535. 6: Troncone R et al (1987) Passge of gliadin into human breast milk. Acta paediat Scand. 76: 453456. 7: Karjalainen J et al (1992) Bovine albumin peptide as possible trigger of insulin-dependent diabetes
mellitus. New Eng J Med 327: 302-307. 8: Martin JM et al (1991) Milk protein in the etiology of insulindependent diabetes mellitus (IDDM) Ann Med 23: 447-452. 9: Virtanen SM et al (1994) Diet, cow's milk
protein antibodies and the risk of IDDM in Finnish children. Diabteologica 37: 381-387. 10: Gobbi G et al
(1992) Coeliac disease, epilepsy and cerebral calcifications. The Lancet 340: 439-443.
All the best Cheers
TINY
K. Reichelt Pediatric Research Institute N-0027 Oslo, Norway Tel: +47 22 86 90 45 Fax: +47 22 86 91 17 Email:
PALEODIET Archives
Subject: Gain or loss?
Reply-To:
Date: Sun, 1 Aug 1999 21:44:48 -0400
Here are excerpts of an old article I found quite interesting.
32/46 (1999)
When an animal eats, it acts like a computer; that is, the most sophisticated kind of computer, that could
choose the best quality foods in the right amounts, better than an expert dietitian ever could. Conversely,
man is like a broken-down computer, which compels him to eat anything, anyhow, and which sometimes
leads him to obesity or alcoholism .... Food, according to its chemical composition, is broken down into fats
(glycerides), sugars (saccharides), and proteins (nitrogenous food such as eggs, grains, meat, and fish)....
When it makes its choice, an animal is able to pick the foods it needs to balance input against output
accurately from the relevant nutrients. An American, Professor Richter, was the first to demonstrate that rats
were remarkably able when it came to selecting from a range of foods the appropriate amounts of protein,
vitamins, and mineral salts necessary for their continued health. Even better, rats can change their minds,
when their internal balance is experimentally tampered with. In this way, rats automatically increase their
salt intake after removal of their adrenal glands; they will eat fats over sugars once they have been turned
into diabetics; they select whatever vitamin they happen to be deficient in.... This is most striking in
chickens.... Chickens pick the amount and kind of food they require solely on the basis of the needs of the
egg they lay daily.... When producing egg white, the chicken only eats whole, high protein food. When the
egg is taking up water, the hen drinks plentifully. Finally, when the shell is forming, the hen goes for
calcium. One might imagine that that was due to circadian rhythm. Not so at all, since when chickens are
raised from birth in constant light that is, when they don't experience nighttime, their eating cycles remain
unchanged. Further proof would be contributed from chickens that do not or no longer lay, or even from
roosters. In the foregoing, there is no staggered intake of protein, calcium, or water. What's more, given that
fowl can make up for the loss (incurred through laying its eggs, a case in point) by relevantly adjusting the
quality of their food, they can also balance their diet, which man can't do.
Are all the primates, except man, able to do that? "Man not being able to "naturally" balance it`s diet", Is that
a preconception or a proven fact? Is all this in relation with "the production of opiate-like substances during
the cooking process"? Are there any other reasons? Are there any recent papers on the subject?
Thanks Jacques Laurin
References:
Marching orders straight from the organs, Science et Vie (Science and Life) n 729, June 1978.
PALEODIET Archives
Subject: Spices
From: Todd Moody
Reply-To:
Date: Mon, 2 Aug 1999 14:50:44 -0400
I'd like to invite some comments on the question of human adaption to spice herbs.
First, let me set this up. I'm accepting as a premise the proposition that the less exposure a population has had
to a given food, the less likely that population is to be well adapted to it. This, I take it, is the basic premise
of attempts to emulate or implement paleolithic diets in the modern world, for health purposes. It implies a
second premise, namely that lack of adaptation to a food makes it more likely to cause health problems.
Now, there appears to be general agreement that paleolithic humans didn't eat *much* in the grain and dairy
categories, but they might have eaten small amounts of each. For example, raw "green" wheat kernels are
edible for a short time, before they fall off the stalks. The rennet-fermented cheese in the stomach of a young
killed animal would also have been eaten occasionally. But, as I understand it, these foods would have been a
very small part of any paleolithic diet.
Optimal foraging theory indicates that hunter-gatherers will always favor calorically denser foods when they
can get them, and certainly avoid foods that require more energy to gather than they actually provide.
This brings us to my question. The various spice herbs are mostly vanishingly low in calories, and are
pungent enough in taste that it seems doubtful that anyone would eat very much of them at a time anyway.
Many spices have potent health-promoting effects, it seems, because of antioxidants and other ingredients
present in them, but prehistoric humans wouldn't have known of that. Indeed, it's hard to see why they would
have bothered with these plants at all. If that is correct, the contribution of these plants to their diet would
have been at least as negligible as that of grains or dairy foods. Therefore we shouldn't be very well adapted
to them. Nevertheless, they seem to be good for us.
What is the explanation?
Todd Moody
33/46 (1999)
PALEODIET Archives
Subject: Re: Spices
Reply-To:
Date: Tue, 3 Aug 1999 10:12:41 -0400
Todd Moody wrote :
> This brings us to my question. The various spice herbs are mostly vanishingly low in calories, and
> are pungent enough in taste that it seems doubtful that anyone would eat very much of them at a
> time anyway. Many spices have potent health-promoting effects, it seems, because of antioxidants
> and other ingredients present in them, but prehistoric humans wouldn't have known of that. Indeed,
> it's hard to see why they would have bothered with these plants at all. If that is correct, the
> contribution of these plants to their diet would have been at least as negligible as that of
> grains or dairy foods. Therefore we shouldn't be very well adapted to them. Nevertheless, they
> seem to be good for us. What is the explanation?
I would like to make a parallel between your interrogation and 2 articles, one in "Natural History" and the
other one in "Equinox" about muriquis and chimpanzees "playing doctor with nature's drugs".
In the Natural History 1993 article, Karen B. Strier writes : "...During the same critical time of year (mating
season), muriquis also alter their behavior by making speedy excursions away from the central part of the
forest, where they usually hang out, to the periphery, where the forest gives way to surrounding pasture.
Once there, they leap across gaps in the canopy to reach the fruit of another species of legume, Enterolobium
contortisiliquum, whose common name is monkey ear. Uncharacteristically, both male and female muriquis
abandon the monkey ear trees long before the fruits are depleted, suggesting that they only need a taste to be
satisfied. What they are seeking in these fruits is unknown, but monkey ear fruits contain stigmasterol, a
steroid used in laboratory synthesis of progesterone..."
In the 1994 Equinox article, Michael McRae writes : "...Primatologist Michael Huffman ...is in the vanguard
of an emerging field that goes by the imposing name of zoopharmacognosy (the science of animal self
medication with plants and other natural substances). Of the approximately 200 plant species in the
chimps'diet at Mahale, Huffman believes that 14 (including Aspilia mossanbicensis, a relative of the
sunflower that is widely used in bush medicine in Africa) are eaten not for taste or nourishment but chiefly
for medicinal benefit..." and further "...Bitterness may be how chimps determine dosage, a signal from the
plant or insect that says, "Don't eat me!"..."
Hope this helps... Is there a primatologist or a zoopharmacognosist(?) in this list? I would be very interested
in further readings on the subject. Any suggestions?
Jacques Laurin
References Strier, K.B. (1993). "Menu for a monkey." Natural History vol.102 No.3: 34-42. McRae, M.
(1994). "Creature Cures." Equinox vol.75: 46-55
PALEODIET Archives
Subject: Re: PALEODIET Digest - 1 Aug 1999 to 3 Aug 1999 (#1999-46)
Reply-To:
Date: Tue, 3 Aug 1999 19:29:31 EDT
Jaques and the list,
<<Are all the primates, except man, able to do that? "Man not being able to "naturally" balance it`s diet", Is
that a preconception or a proven fact? Is all this in relation with "the production of opiate-like substances
during the cooking process"? Are there any other reasons? Are there any recent papers on the subject?
This is a very interesting topic. I think that the premise that man cannot balance its diet "naturally" comes
from watching nineteenth and twentieth century man. We don't have any people left who are living lives
totally unaffected by the twentieth century.
34/46 (1999)
Certainly our cultures have affected us. Acculturation might be responsible for this phenomenon of people
not eating a natural diet. The western cultures have had many millenia of acculturation, as have many
oriental cultures. Once a culture adopts agriculture, the elite have preferential access to the crops -- even if
this results in poor health. Sorry, I don't have any references to cite, although i've seen discussions in some
nutrition texts about oriental cultures. Their elite people, who ate white (polished) rice, had relatively poor
health, while poorer people in the society ate unpolished brown rice and had much better health because they
were consuming the B vitamins that the elite had polished off. As an anthropologist, I think it is culture that
results in this type of behavior. So, perhaps one question that we should ask is: "is cultural pressure strong
enough to overcome instinctual eating patterns in humans?" I would argue yes, it is -- particularly over long
periods of time.
Linda Scott Cummings, Ph.D. Paleo Research
PALEODIET Archives
Subject: Re: Gain or loss?
Reply-To:
Date: Wed, 4 Aug 1999 23:49:54 -0400
Linda Scott Cummings wrote :
> As an anthropologist, I think it is culture that results in this type of behavior. So, perhaps one
> question that we should ask is: "is cultural pressure strong enough to overcome instinctual eating
> patterns in humans?" I would argue yes, it is -- particularly over long periods of time.
Considering that some non human primates have the ability to use and even make tools, would it be
exaggerate to consider the mastery of fire as "the" prime factor of human originality? Then fire is still only
another tool until it is used to process something. Processing implies changing the nature of the thing that is
being processed, right? Cooking, for instance, changes the nature of the food on a molecular level. Amongst
other things, could the new molecules generated by cooking stimulate the brain (how can I say that) in a new
and not necessarily adapted way? Could cooking be "the" point of rupture between natural (or innate)
behavior and, what we call, cultural behavior, overcoming instinctual eating patterns by the same token?
Here's a small excerpt from an interesting and disturbing book "La Guerre du Cru" that may shed some light
on the consequences of this event (cooking) : "...For a baby, the intensity of taste bud gratification and
frustration... is very important. Imagine a baby eating pineapple: The first slice tastes great, and the second
stings his tongue, whereas, with cookies, the second one is as good as the first, and likewise for the third and
the fourth, and his enjoyment always remains the same. He will reinforce himself in the belief that every one
of his predictions must come true and the outside world must somehow cater for his yearning. Learning with
raw food, on the other hand, might bear in on him that reality is hard to foretell and that any impression of
taste is basically built-in, and, also, like any kind of flavor, any kind of knowledge is always temporary..."
Does all this make sense to you? Any thoughts? Any scientific readings on the subject? By the way, please
tell me if I'm overly simplistic or simply being delirious.
Jacques Laurin
Reference Burger, G.C. "La Guerre du Cru." Roger Faloci Editeur, Paris, 1985, 221 pages.
PALEODIET Archives
Subject: Acculturation
From: Dean Esmay
Reply-To:
Date: Sun, 8 Aug 1999 15:40:21 -0400
The suggestion that cultural pressures exert a change on our diet, and may explain unhealthy eating patterns,
at a certain level this seems unsatisfactory. There is almost indisputably some influence from culture (for
example, most Americans have a strong aversion to eating insects, which are popular in many other
cultures). But can this be the primary explanation for bad eating patterns?
35/46 (1999)
Certainly, if homo sapiens has any innate instinctive or biochemical drive toward eating a certain way, then
we would probably expect to see that most cultures would drive the most powerful members of a society to
eat the most healthy foods. Apparently such a drive does not exist, or if it does it's easily overridden.
On the other hand, the idea that any animal species knows "instinctively" how to eat right strikes me as
questionable. I have seen many domesticated animals who are quite fat and sluggish. Relatives of mine have
a dog, it's a small dog that should weigh no more than 15-20 pounds but weighs easily twice this and can
barely manage to navigate stairs. I see no reason to think that other species really have an instinct to perfectly
eat exactly the right things whenever possible and to never eat "wrong."
Human beings, in my experience, eat foods which taste good to them. Do we have to be taught to be attracted
to highly sweet or very rich foods? Did we as children need to be "taught" to like candy? Why does every
culture on the planet seem to snap up foods common to the western world, such as candies, white breads, etc.
as saon as it's available to them? Is it because some psychological factor has them wanting to emulate us? Or
is it possible that sweet, fatty, calorie-dense, easy-to-obtain, easy-to-prepare foods in general are pleasing to
most any animal?
If bad eating habits are entirely socially derived, then we would also expect that changing social attitudes
would show effective improvements in health, yes?
PALEODIET Archives
From: Ben Balzer
Reply-To:
Date: Mon, 9 Aug 1999 15:13:26 +1000
> Date: Wed, 4 Aug 1999 23:49:54 -0400
> From: Jacques Laurin Subject: Re: Gain or loss?
> Linda Scott Cummings wrote :
> As an anthropologist, I think it is culture that results in this type of behavior. So, perhaps one
> question that we should ask is: "is cultural pressure strong enough to overcome instinctual eating
> patterns in humans?" I would argue yes, it is -- particularly over long periods of time.
> Considering that some non human primates have the ability to use and even make tools, would it be
> exaggerate to consider the mastery of fire as "the" prime factor of human originality? Then fire
> is still only another tool until it is used to process something. Processing implies changing the
> nature of the thing that is being processed, right? Cooking, for instance, changes the nature of
> the food on a molecular level. Amongst other things, could the new molecules generated by cooking
> stimulate the brain (how can I say that) in a new and not necessarily adapted way? Could cooking
> be "the" point of rupture between natural (or innate) behavior and, what we call, cultural
> behavior, overcoming instinctual eating patterns by the same token?
Many other factors influence behaviour. For example, low-level lead exposure has long been known to affect
intelligence. Research shows even stronger adverse effects of lead on behaviour, with enormous increases in
antisocial and delinquent behaviour. (Needleman's 1996 paper is especially disturbing). Breastfeeding has
been shown to have a positive effect on IQ, so one must presume that childhood nutrition will also have an
effect. How that relates to effects on behaviour is difficult to say, but if our experiences with lead are any
guide, the effects of nutrition on behaviour may be stronger than those on IQ.
Drawing on from this, antinutrients in Neolothic foods have adverse effects on neurodevelopment, they can
be expected to have particularly large effects on behaviour. This would be combined with the effects that
lead has on us (we've all been exposed tom substantial amounts of lead. Fortunately the USA is addressing
the problem, but the response is slow elsewhere).
It would be interesting to think that paleolithic man mightn't be the homicidal maniac that Neolithic tends to
be (but perhaps they were worse).
Dr. Ben Balzer
References Needleman, Herbert L. et al, "Bone Lead Levels and Delinquent Behavior, " JOURNAL OF THE
AMERICAN MEDICAL ASSOCIATION Vol. 275, No. 5 (February 7, 1996), pgs. 363-369.
Rachel's health and Environment Weekly http://www.monitor.net/rachel/rehw-index.html issues 529, 318,
294, 214, 189, 3
36/46 (1999)
Alan L. Mendelsohn, Benard P. Dreyer, Arthur H. Fierman, Carolyn M. Rosen, Lori A. Legano, Hillary A.
Kruger, Sylvia W. Lim, and Cheryl D. Courtlandt "Low-Level Lead Exposure and Behavior in Early
Childhood" Pediatrics 1998; 101: e10. http://intl.pediatrics.org/content/vol101/issue3/
PALEODIET Archives
Reply-To:
Date: Fri, 13 Aug 1999 14:57:15 +0100
On Fri, 30 Jul 1999 Jacques Laurin wrote:
> If we have the right to hope for a future adaptation to the new proteins of wheat, corn or cow's
> milk, it seams to me that it is a different story when we are talking about cooked food. Many new
> chemical species generated by the action of cooking, isomers for instance, differ too much from
> the natural molecules to expect our digestive enzymes to be active on them. Do we know what
> happens to the isomers that go through the intestinal barrier? I guess that at best, they are
> unusable but in many cases, they are probably dangerous.
Do these molecules really differ so much that there are no chances of digesting them? Cooked food rots quite
nicely, which means that bacteria and other organisms are degrading these compounds - surely similar
mechanisms could develop in other species?
Andrew Millard wrote
> ...so what is there in animal milk that gets into the body?
All the things you listed in reply are either present in different proportions or absent from human milk: what
is in animal milk that is not in human milk and enters the body from the gut?
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Spices
Reply-To:
Date: Fri, 13 Aug 1999 15:13:24 +0100
On Mon, 2 Aug 1999 Todd Moody
> I'd like to invite some comments on the question of human adaption to spice herbs.
> ......snip....... Optimal foraging theory indicates that hunter-gatherers will always favor
> calorically denser foods when they can get them, and certainly avoid foods that require more
> energy to gather than they actually provide.
This simply illustrates that optimal foraging theory is not everything. Drinking water requires more calories
to collect than it gives but no one expects humans not to drink! More seriously, humans like to exhibit what
archaeologists know as "conspicuous consumption", using resources in a fashion that indicates you have
resources to spare.
> This brings us to my question. The various spice herbs are mostly vanishingly low in calories, and
> are pungent enough in taste that it seems doubtful that anyone would eat very much of them at a
> time anyway. Many spices have potent health-promoting effects, it seems, because of antioxidants
> and other ingredients present in them, but prehistoric humans wouldn't have known of that.
Why shouldn't prehistoric people have been good herbalists? Modern hunter-gatherer and "primitive"
populations are being tapped for their knowledge of herbal/natural/traditional remedies which western
pharmaceutical companies may be able to exploit.
> Indeed, it's hard to see why they would have bothered with these plants at all. If that is
37/46 (1999)
> correct, the contribution of these plants to their diet would have been at least as negligible as
> that of grains or dairy foods. Therefore we shouldn't be very well adapted to them. Nevertheless,
> they seem to be good for us. What is the explanation?
I suspect the answer is that we are not adapted to consuming large amounts of them. For example, people
have been using tobacco, coca, opium poppies and other narcotics in small quantities for at least several
millennia. Chewing coca leaves to feel good does little harm, but taking large quanitites of crack cocaine
does much harm to a person. Feeling good on a few coca leaves propabbly helps one deal with the stresses of
life in a way that optimal foraging theory doesn't account for. Similarly I guess the plant that produces
quinine is worth eating if you have malaria but not worth bothering with otherwise.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Cooked vegetables
From: Dean Esmay
Reply-To:
Date: Sun, 15 Aug 1999 14:55:50 -0400
Submitted by Douglas in Pittsburgh:
"This is a preview of an article to be published in Current Anthropology in December. it apparently suggests
that the consequences of cooking vegetables outweigh the consequences of cooking meat, not just
nutritionally but socially as well.
http://cnn.com/HEALTH/diet.fitness/9908/11/science.cooking.reut/
"
This is a popular (Reuters) account of a paper due to be published in Current Anthropology later this year.
As it's a popular account we can probably expect the story to be rather shallow on details. It's also interesting
that these scientists have chosen to speak to the press even before their paper is published. I'm not sure that's
a good sign. But the article is interesting.
Thanks to Douglas for sending it along.
PALEODIET Archives
Subject: Cooking veggies and human evolution
Reply-To:
Date: Sun, 15 Aug 1999 17:50:46 -0700
The argument put forward for the role of cooking plant food in human evolution seems rather speculative.
The connection between cooking vegetables and increased body size does have a certain logic to it, but how
strong is the evidence for such cooking?
"We strongly suspect hominids began using fire about 1.9 million years ago, when Homo erectus appeared, "
he added. He said colleagues working in Kenya have recently contacted his team and said they have
evidence that humans were controlling fire that long ago. The most recent accepted evidence puts fire use at
just 200, 000 to 500, 000 years ago."
That is not exactly highly verified information!
Some of the other claims are rather dubious.
"Learning how to cook probably also allowed humans to develop their unique monogamous society, the
researchers reported" -This is a very strange claim, since many human cultures cook and also practice polygamy!
"Modern humans share food, but apes don't, " Laden said. "This is a transition between apelike behavior and
humanlike behavior."
38/46 (1999)
This statement is not correct, though the "sharing" of meat by chimps is perhaps not "voluntary." (see:
Stanford, C. Chimpanzee hunting behavior and human evolution, American Scientist, May/June 1995)
Steve Meyers
Staff Scientist Lawrence Berkeley National Laboratory Berkeley, CA E-mail:
PALEODIET Archives
Subject: Cooking veggies and human evolution
From: Ray Audette
Reply-To:
Date: Tue, 17 Aug 1999 03:41:49 -0500
> "We strongly suspect hominids began using fire about 1.9 million years ago, when Homo erectus
> appeared, " he added
This is also the time that many other species increased in size to take advantage of vast areas of steppetundra. These species were collectively known as the Pleistocene Megafauna. Hominids had to evolve into a
mega form to take advantage of this new enviroment. Game of all kinds existed in this enviroment in
densities unknown in historical times and far surpassing the original tropical grassland enviroment of the
original hominids.
> "Learning how to cook probably also allowed humans to develop their unique monogamous society,
> the researchers reported" -Lifetime monagamy developed in responce to economic conditions brought about by the invention of the
plow according to a Scientific American article intittled "High Fertility in Sub-Saharan Africa". In the
aproximately 5% of human cultures (of over 3, 000 studied by anthropologists) that practice lifetime
monagamy, plow based agrairian cultures predominate. Because of tetse flys, Tropical Africa remained
pologamous.
> "Modern humans share food, but apes don't, " Laden said. "This is a transition between apelike
> behavior and humanlike behavior."
Sharing, like many other "humane" practices exist in Nature only in carnivores who hunt in packs.
Herbavores don't behave in this manner. This is what makes dogs and Harris Hawks (the only birds of prey
that hunt in packs) such pleasant hunting companions.
Ray Audette Author "NeanderThin"
PALEODIET Archives
Subject: re. Cooking vegetables and Fallacious Reasoning
From: Don and Rachel Matesz
Reply-To:
Date: Tue, 17 Aug 1999 09:39:16 -0500
--- Don and Rachel Matesz Next Generation Nutrition. (419) 476-2967
Wrt the article on cooked vegetables "Early humans got smart by cooking veggies, study says": This idea
that we got smart by cooking vegetables, not by hunting and meat eating, may be politically correct, but it is
illogical and biochemically incredible. Here are my reasons:
1) Cooking is a highly sophisticated behavior that requires intelligence not had by any other primate. No
non-human primate cooks. Our closest primate relatives, the chimps, do hunt. Therefore, hunting definitely
preceded cooking. The "advance" from eating everything raw to using fire for cooking had to wait for
improvements in brain capacity, hand eye coordination, manual dexterity, etc. In other words, cooking could
not have become common activity for man until after his nervous system had developed beyond that of the
chimps. Hence, cooking must have come after man became "smart"--in other words, man did not become
"smart" by cooking, he started cooking after becoming "smart".
2) Further, there is not enough of essential fatty acids in cooked vegetables to support development of a more
sophisticated nervous system or brain. The omega-6 EFA arachidonic acid (AA) and the omega-3 EFA
docosahexaenoic acid (DHA) are of prime importance as structural materials of the brain.
39/46 (1999)
To the best of my knowledge, there are no vegetable sources of AA (Whitney and Rolfes, Understanding
Nutrition, West Publishing Co, 1993, pp. 140-142), but land animal meats are rich in this fat. Land
vegetables do not provide significant amounts of DHA. Most have no DHA, but Simopoulos et al suggest
that buttercrunch lettuce and mustard greens supply .001 mg DHA per g, and red leaf lettuce supplies .002
mg DHA per g (Simopoulos AP, w-3 Fatty acids in Growth and Development and in Health and Disease,
Part I, Nutrition Today, March/April 1988). This is compared to salmon, for example, which contains 6 mg
DHA per g, and land animal brains, which are approximately 60% fat, approx 40% of that fat being DHA.
It is generally accepted that although humans can produce some AA from linoleic acid found in vegetables
(mostly seeds), and some EPA or DHA from linolenic acid found in vegetable sources, HOWEVER "The
converson process is slow, so the most effective way to sustain body stores of arachidonic acid, EPA, and
DHA is to obtain them directly from foods." (Whitney and Rolfes, Understanding Nutrition, West Publishing
Co, 1993, pp. 141)
Greens do provide alpha-linolenic acid (ALA), which some animals can convert to DHA, but various studies
have shown that modern humans have little or no ability to achieve this conversion. For example, I have
been informed (I have not yet read the entire study myself) that a study recently published in the Am J Clin
Nutr (1999; 69: 872-82) compared the biological value vegetable source ALA and fish source EPA and DHA
and concluded: "Because such small amounts of EPA and other long chain Omega-3 PUFAs are produced
after ALA-rich diets, it is clear that the 2 main sources of Omega-3 PUFAs (plants and fish) do not have
equivalent biological effects in humans."
This research supports previous studies (cited by professor Michael Schmidt, Smart Fats, North Atlantic
Books 1997, pp. 48-49) that have shown that long term vegetarians have low blood levels of DHA compared
to omnivores (Agren JJ et al. Fatty acid composition of erythrocyte, platelet, and serum lipids in strict
vegetarians, Lipids 1995; 30 (4): 365-69), that infants born of vegetarian mothers have lower blood levels of
DHA compared to infants born of omnivores (Reddy S et al, The influence of maternal vegetarian diet on
essential fatty acid status of the newborn, Eur J Clin Nutr 1994; 48: 358-68), and that the DHA levels of
breast-fed infants of vegetarian mothers are only about one-third of the levels found in breast-fed infants of
mothers who consumed meat and vegetables (Sanders TAB, Reddy S, The influence of a vegetarian diet on
the fatty acid composition of milk and the esential fatty acid status of the infant, J Pedeatr 1992; 120: s7177).
Other primates are incapable of producing much DHA from ALA. Monkeys require DHA as proven by the
fact that monkey infants deprived of DHA lose visual acuity. (Crawford and Marsh, Nutrition and Evolution,
Keats 1995, p. 128)
In fact, there is no known mammal that is capable of making enough AA from LA or DHA from ALA to
produce a large brain. Thus, in their book Nutrition and Evolution (Keats 1995) professors Crawford and
Marsh observe "it is consistently true over the whole range of species that carnivores are cleverer than their
prey" (p. 129) and "The paleontological evidence tells us that throughout evolution the brains of the
carnivores have consistently been in advance of the corresponding herbivores." (p. 130) This is in spite of the
fact that herbivores consume large amounts of green leaves rich in ALA and perhaps containing tiny
amounts of DHA.
I suggest to all reading the excellent examples Crawford and Marsh provide showing the vast difference
between herbivore and carnivore anatomy, physiology and behavioral capacities, and relating those
differences to differences in EFA intake. The general rule, to which there are no known exceptions: All
animals having large brains, sophisticated nervous and vascular systems, and a capacity for complex
intelligent behavior are carnivores or omnivores, and must be in order to obtain sufficient EFAs for building
their large brains, sophisticated nervous and vascular systems.
So there is no reason to believe that early man had any ability to make large amounts of DHA out of the
alpha-linolenic acid (ALA) found in green leaves. Furthermore, it has been estimated that even in the best of
ALA converters, it takes 10 grams of ALA to produce just one gram of DHA. The absolute amount of ALA
in green leaves is very small, on average less than one half gram per 100 gram portion, so literally enormous
amounts of green leaves would have to be eaten to get significant amounts of DHA. Mankind simply does
not have the kind of gut needed to process that amount of greens. Finally, both ALA and DHA are heatlabile, so cooking greens would have destroyed much of the value of any omega-3 fats.
3) The authors of this "research" say "We don't see meat as a high energy food source. It has to be (a) high
energy food source to explain this doubling of body size." If they don't see meat as a high-energy food source
and think that cooked vegetables are high-energy foods, I suggest that they try living on nothing but cooked
vegetables for a few weeks. Here are some facts:
Energy value for one cup portions (one cup of raw meat is approximately 8 - 9 ounces):
40/46 (1999)
Food Calories
Cabbage, cooked 32 Kale, cooked 40 Broccoli, cooked 50 Pumpkin, cooked 50 Onions, cooked 60 Carrots,
cooked 70 Winter squash, cooked 110 Sweet potato, boiled and mashed 364
Nuts, raw 933
Eggs, eight medium raw 640
Wild game, raw, lean only 232 (Average, taken from Eaton, et al Paleolithic Prescription)
Beef brains, raw 392
Animal fat, raw 1840 (This would represent marrow, storage fat, etc.)
From these figures it is hard to understand how the authors of the "study" in question could conclude that
cooking vegetables gave early man access to "high energy" foods. My guess is that the authors have not
looked at energy density in terms of volume, i.e. calories per cup, but have been misled by looking only at
calories per gram. If you look at calories per cup, the only vegetable that on a cup for cup basis comes near
to the energy value of wild game lean meat is the tuber sweet potato. A hunter gatherer would have to eat
two cups of cooked winter squash, over three cups of cooked carrots, nearly four cups of cooked onions, or
nearly six cups of cooked green leafy vegetables to equal just one cup of raw lean meat.
Brains are higher in fat, so they are almost twice as energy dense as lean meat; the fat content of brains is not
affected by feeding practices--the brains of wild game are just as rich in fat as are the brains of domesticated
cattle. Further, the EFA profiles of brains of all species so far studied are identical (Crawford and Marsh,
Nutrition and Evolution, p. 125)
Eggs also are much more energy dense than vegetables--and wild bird's eggs are also rich in both AA and
DHA compared to vegetables (they are in there as the building blocks for the nervous system of the bird).
Further, it is known that not only aboriginal people but also chimpanzees eat raw brains and eggs when they
can get them. So we don't have to guess that maybe early man ate those things--it would be odd if he didn't.
Now take a look at nuts--which are mostly fat-- and animal fat--THERE IS THE ENERGY DENSITY
REQUIRED! Again, it is known that both chimps and aboriginal people eat marrow and kidney fat. But
"primitive" people eat more meat and more fat than chimps.
The idea that cooking vegetables was the key to a high energy density diet is absurd. The easiest way for a
land locked primate to get a high energy density diet is to EAT BRAINS AND MARROW FAT. These
foods are also the best for increasing intake of linoleic acid, EPA, DHA, and other fats needed for
development and maintenance of sophisticated eyes, brain, nervous and vascular systems.
If you discard the preconception that our ancestors were land-locked, there are other sources of the required
fats. At the shoreline, a primate can get a high energy density diet by eating SEA MAMMALS AND/OR
FATTY FISH. Professors Crawford and Marsh make a good case (in Nutrition and Evolution) for the theory
that early man was a consumer of sea foods rich in fats, along with land animal fats (brains and marrow).
But eating brains and marrow fat is politically incorrect these days. With all the popular hysteria about the
dangers of eating organ meats and fat, who is going to publish a head-line stating that "EARLY MAN
DEVELOPED A BIG BRAIN BY EATING BRAINS AND FAT, STUDY SAYS"?
This is one of the worst examples of junk reporting and junk science we've seen in a while. By presenting
this half-baked politically correct supposition to the public before the scientific community has an
opportunity to comment upon it, the authors of this supposed research will be patted on the back, and their
"conclusions" will be by many laymen accepted as "fact"--after all, it is very unlikely that Reuters will in a
few days publish with bold headlines all of the logical and biochemical objections I or any one else will have
to their mistake.
Don Matesz
PALEODIET Archives
Subject: Re: Cooking veggies and human evolution
From: Don and Rachel Matesz
Reply-To:
Date: Sun, 19 Sep 1999 17:41:54 -0400
--- Don Matesz Next Generation Nutrition. (419) 476-2967
Ray Audette wrote on "Cooking veggies and human evolution":
> This is also the time that many other species increased in size to take advantage of vast areas of
> steppe-tundra. These species were collectively known as the Pleistocene Megafauna. Hominids had to
41/46 (1999)
> evolve into a mega form to take advantage of this new enviroment.
I am pretty sure Ray did not mean this the way it reads. The species in question did not "increase in size [in
order] to take advantage of vast areas of steppe-tundra", they increased in size BECAUSE they took
advantage of the resources of those areas. The increase in size was not intentional (Hey, lets increase in size
then we can take advantage of these vast areas....), but was a natural consequence of taking advantage of the
increased nutrients available from those areas.
In my post April 17 1999 I wrote:
> Brains are higher in fat, so they are almost twice as energy dense as lean meat; the fat content
> of brains is not affected by feeding practices--the brains of wild game are just as rich in fat as
> are the brains of domesticated cattle. Further, the EFA profiles of brains of all species so far
> studied are identical (Crawford and Marsh, Nutrition and Evolution, p. 125)
To clarify, although the %fat content of brains is fixed, the EFA content actually is variable within limits
based on the food the animal eats. For example, on a DHA-rich diet, human have more DHA in their cerebral
neurons than on a DHA poor diet, although the total fat content of the brain will remain the same. According
to professor Michael Schmidt, Dr. C.D. Stubbs has stated "when cells are deprived of sources [of DHA] in
the diet the cell wil tend to produce the neraest fatty acid (in terms of unsaturation and chian length) that is
possible, even if the faty acid is from the omega-6 series." The nearest "substitute" for DHA is DPA (omega6), which is far inferior to DHA with regard to neural activity. (Stubbs CD, The structure and function of
docosahexaenoic acid in membranes, in Sinclair A, Gibson R, eds, Essential Fatty Acids and Eicosanoids,
Champaign Ill, American Oil Chemists' Society 1992: 116 cited in Schmidt M, Smart Fats, North Atlantic
Books, 1997, p. 47).
Since it seems that some would like to take issue with it, I would like to drive home the point that as a matter
of fact, not all animals make AA and DHA from vegetable precursors, and of those that do, the amount they
make is insufficient to support development of a sophisticated nervous system. There are some animals,
including humans, who are incapable of converting the "precursors" into the longer chains in amounts
required for nervous system development, maintenance and health. I quote from Nutrition and Evolution
(Keats, 1995) Marsh and Crawford, who has done much of the relevant research:
"Were all species able to make the neural fatty acids from the starting point in plants? In all small mammals
like mice, rats and tree shrews, there was evidence of ample conversion. However, in the large herbivores
like cows, buffaloes and giraffes, which eat leaves and seeds, we could find plenty of the original linoleic
and alpha-linolenic acids in their tissues, but the conversion process to the neural fatty acids was not
completed; it seemed to peter out. The production of the most polyunsaturated fatty acid, docosahexaenoic
acid (22:6, n-3) was most affected. The tissues of the large herbivores accumulated only small amounts of
these neural fatty acids, whereas the big cats which ate them had many more.
"This was interesting because carnivores have more sophisticated nervous systems and presumably a higher
demand for neural fatty acids. Were they perhaps better at making them? Surprisingly, we found the
opposite. John Rivers and Andrew Sinclair reported another peculiarity of cats in 1975: cats did not convert
plant EFAs into neural fatty acids (Rivers, Sinclair & Crawford, 1975). Others have found that this same
principle operated in carnivorous fish. This inability is similar to the inability of the cat to make vitamin A
from the carotenoids in plants. It relies on the efforts of its prey!
"Once again the economy of this method is clear. The process of building up these long-chain fatty acids is
tedious. Any animal that can bypass even a part of it can switch off the mechanism, save on effort and time
and possibly on genetic 'disk space'. The same argument applies as with vitamin A: the direct supply of
preformed nerual fatty acids could alow the development of biological systems dependent on or stimulated
by these nutrients.
"The ready availability of preformed neural acids and vitamin A in the flesh the carnivores eat offers
nutrients needed specifically to suport more sophisticated brains, nervous and optical systems. They can
afford the luxuries of widely adjustable irises in their eyes, along with the nerves and central control systems
they demand. The herbivores cannot." (Nutrition and Evolution, p. 126 - 128)
In short--by skipping the step of making all the neural fats from scratch, humans like other carnivores are
able to divest themselves of biological investments in the hard- and softwares required for producing neural
fats from 'scratch', and instead invest their biological resources in making new structures from neural fats-'hardwares' like the kinds of supersensitive eyes, peripheral nerves, and cerebral developments that allow me
to type this post.
Don Matesz
42/46 (1999)
PALEODIET Archives
Subject: An introduction and questions
From: "Steve McBride, DVM"
Reply-To:
Date: Sun, 19 Sep 1999 17:23:06 -0400
Greetings:
I just wanted to briefly introduce myself. I am a veterinarian in private practice that has been recently
introduced to the subject of paleonutrition. My undergraduate education is in physics and biology at Notre
Dame University and my DVM is from Michigan State University. I have broadened my interest in nutrition
from primarily that of our canine and feline friends, to human nutrition. I stumbled across this current forum
after reading NeanderThin by Ray Audette and doing some research on the internet. I am familiar with
movements in pet circles to return to their native diets (BARF diet -- bones and raw foods) and found it
enlightening that so much good research has been done in this direction in human nutrition. In particular,
writings by Loren Cordain, Ph.D., have provided good scientific backing for many of the ideas being
promoted. My thanks to him.
Now, two questions:
1. In veterinary medicine, worsening of renal disease has been linked with the phosphorus content of diets. It
used to be thought it was the protein content, based on studies in rats and man. Can anyone point me to data
that disputes protein as an aggravator of renal disease in man? As far as I am aware, the jump from protein to
phosphorus content has not been established in human nutrition.
2. In one of his articles, Loren Cordain alludes to the use of slow methods of cooking as being practiced in
primitive societies, then suggests using a crockpot to mimic this (good for tenderizing tough meats). Does
such long exposure to heat and moisture not cause a significant decay in nutritional value? How does it
compare to other forms of cooking. In the production of pet foods, supplements have to be added back to the
formulation after it is processed. Now I realize that they use extreme conditions to produce things like dry
kibble, but the principle still applies.
Thanks in advance for your answers,
Steve McBride
PALEODIET Archives
Subject: Cancer & Insulin resistance
From: Dean Esmay
Reply-To:
Date: Sun, 19 Sep 1999 18:17:09 -0400
An interesting page recommended by Allen E. Gale:
http://home.infospace.com/cancer10
PALEODIET Archives
Subject: Re: High protein diets and renal disease.
From: Loren Cordain
Reply-To:
Date: Mon, 20 Sep 1999 16:36:38 -0600
43/46 (1999)
In response to Steve McBride's question regarding high protein diets and renal disease: In the UK, the
Department of Health (1) concluded that "whilst in no case is there conclusive evidence of harmful effects of
excessive intakes of dietary protein in healthy people, there is firm evidence that excessive dietary protein
contributes to deterioration of renal function in patients with renal disease by increasing intraglomerular
pressure and glomerular filtration rate" (2-4). A number of recent studies (5-7) support the concept that
elevated protein intake in normal subjects does not impair kidney function. High protein diets have recently
been shown to be associated with reductions in blood pressure (8-10) and in breast cancer (11) and ischemic
heart disease risk (12). Further, a recent trial involving high protein diets showed that they were more
effective than high carbohydrate diets in weight loss diets while producing a more favorable blood lipid
profile (13).
Loren
REFERENCES
1. Department of Health (1991) Dietary Reference Values for Food Energy and Nutrients for the United
Kingdom. Report on Health and Social Subjects no. 41. London: H.M. Stationery Office. 2. Brenner BM.,
Meyer TW. & Hostetter TH. (1982)Dietary protein intake and the progressive nature of kidney disease: the
role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis
in aging, renal ablation, and intrinsic renal disease. New England Journal of Medicine 307, 652-659. 3.
Rudman D. (1988)Kidney senescence ; a model for aging. Nutrition Reviews 46, 209-214. 4. Wiseman MJ.,
Hunt R., Goodwin A., Gross JL., Keen H. & Viberti GC. (1987)Dietary composition and renal function in
healthy subjects. Nephron 46, 37-42. 5. Brandle E., Sieberth HG. & Hautmann RE. (1996)Effect of chronic
dietary protein intake on the renal function in healthy subjects. European Journal of Clinical Nutrition 50,
734-740. 6. Kimmel PL., Lew SQ. & Bosch JP. (1996)Nutrition, ageing and GFR: is age-associated decline
inevitable? Nephrology Dialysis and Transplantation 11, Suppl. 9, 85-88. 7. Walser M. (1992)The
relationship of dietary protein to kidney disease. In Dietary Proteins in Health and Disease, pp. 168-178[GU
Liepa, editor]. Washington, DC: American Oil Chemists Society. 8. Stamler J., Elliott P., Kesteloot H.,
Nichols R., Claeys G., Dyer AR. & Stamler R. (1996b)Inverse relation of dietary protein markers with blood
pressure. Findings for 10, 020 men and women in the INTERSALT Study. INTERSALT Cooperative
Research Group. INTERnational study of SALT and blood pressure. Circulation 94, 1629-1634. 9.
Obarzanek E., Velletri PA. & Cutler JA. (1996)Dietary protein and blood pressure. Journal of the American
Medical Association 275, 1598-1603. 10. He J et al. Effect of dietary fiber and protein on blood pressure: a
review of epidemiologic evidence. Clin Exp Hypertens 1999;21:785-96. 11. Holmes MD et al. Dietary
factors and the survival of women with breast carcinoma. Cancer 1999;86:826-35. 12. Hu FB et al. Dietary
protein and risk of ischemic heart disease in women. Am J Clin Nutr 1999;70:221-7. 13. Skov AR.
Randomized trial on protein vs carbohydrate in adlibitum fat reduced diet for the treatment of obesity. Int J
Obesity 1999;23:528-36.
Loren Cordain, Ph.D., Professor Department of Health and Exercise Science Colorado State University Fort
PALEODIET Archives
Subject: Re: Cooking vegetables and Fallacious Reasoning
From: Gary Ditta
Date: Sun, 10 Oct 1999 17:22:57 -0400
I found Steve Matesz's post about the fallacious reasoning behind the cooked vegetables article to be quite
interesting. Nevertheless, I'm having a hard time digesting (pardon the pun) Marsh and Crawford's
"...general rule, to which there are no known exceptions: All animals having large brains, sophisticated
nervous and vascular systems, and a capacity for complex intelligent behavior are carnivores or omnivores,
and must be in order to obtain sufficient EFAs for building their large brains, sophisticated nervous and
vascular systems."
44/46 (1999)
Although "man" is indeed an omnivore, it is also clear that human individuals (and large classes of humans:
e.g. Hindus) are quite capagle of living and reproducing on a vegetarian diet. Biochemical differences might
exist between the brains/nervous systems of vegetarians and non-vegetarians, but unless compelling
arguments can be advanced showing a functional detriment at the level of evolutionary fitness for
vegetarians, lower level arguments (e.g. DPA predominates in the brains of vegetarians and is far inferior to
DHA with regard to neural activity) would seem to be either irrelevant or to indicate that the current
biochrmical knowledge base is inadequate.
Gary Ditta
PALEODIET Archives
Subject: Intact frozen mammoth
From: Dean Esmay
Date: Sun, 10 Oct 1999 17:40:09 -0400
Loren sent me this interesting URL a few days ago, I'm just getting 'round to catching up on my old email.
http://www.discovery.com/exp/mammoth/dispatch.html
It's not really directly related to our list subject, but it's a fascinating and exciting discovery that I suspect
most of our members would enjoy reading about. I also find myself wondering if in a decade or three I might
not be able to order wooly mammoth steak from my favorite restaurant. An amusing thought, anyway.
PALEODIET Archives
Subject: Renal disease/Nutrient losses in cooking
Date: Sun, 10 Oct 1999 17:44:49 -0400
Steve McBride asked two questions which I can help answer:
1. Can anyone point me to data that disputes protein as an aggravator of renal disease in man?
My understanding of this issue is that dietary protein does not CAUSE renal disease but that in the presence
of renal disfunction (as often occurs as a complication of diabetes), some experts believe that high protein
diets will aggravate it. However, when put to the test, there is conflicting evidence. A point of difference is
the definition of high vs low protein diets. I'm sorry I don't have time at present to give you the references. It
is a regular subject in the Diabetes journals.
2. Does such long exposure to heat and moisture not cause a significant decay in nutritional value? How does
it compare to other forms of cooking?
Long exposure to heat and water will adversely affect the heat labile vitamins such as vitamin C and thiamin.
There is not much vitamin C left if you cook any chopped vegetable for a long time. A high proportion of the
water-soluble vitamins, even if stable to heat, end up in the cooking water (which may be thrown away). On
the other hand, heat will increase the bioavailability of some nutrients such as starch, the carotenoids and
niacin.
I think it's arguable that hunter-gatherers always used slow methods of cooking. Australian Aborigines used
hot ashes and cooking times could be very short. The cooking time depended on the size of the animal. They
rarely boiled anything in water.
Best wishes Jennie Jennie Brand Miller PhD Associate Professor in Human Nutrition Department of
Biochemistry G08 University of Sydney NSW 2006 Australia Phone: (61 2) 9351 3759 Fax: (61 2) 9351
6022
PALEODIET Archives
Subject: Re: Cordain interview in Australia
From: Loren Cordain
Date: Fri, 15 Oct 1999 12:09:47 -0600
45/46 (1999)
Many thanks to Jenny Brand Miller, Neil Mann, the Nutrition Society of Australia, the Dieticians
Association of Australia and the Meat and Livestock Association of Australia for inviting me to speak on the
"Paleodiet" concept in Australia. The local media did quite a blitz on my visit, and one of the interviews can
be found at:
http://www.abc.net.au/worldtoday/s57024.htm
Cordially,
Loren
46/46 (1999)
PALEODIET Archives
Subject: New moderator of Paleodiet - revival of the list
From: Dan Petersson
Reply-To:
Date: Wed, 2 Feb 2000 07:35:37 +0100
The Paleodiet list has been very quiet lately, which probably has prompted some of you to wonder if it has
silently passed away. This is not the case. Due to other commitments, Dean Esmay has not been able to
actively moderate the Paleodiet list the past months, which has caused some lag. After discussions between
him and co-owners Loren Cordain, Staffan Lindeberg, and Don Wiss, it was decided that I should assume
the responsibility of the daily management of the list. As list creator, Dean Esmay will retain a moderator
emeritus role. There will certainly be more than one time that I will run to him for help, as well as to the
other list-owners. However, the day-to-day technicalities such as approval of contributions to the list will be
handled by me.
As a short introduction, I am a last-year medical student at Lund University in Sweden. My interest in the
paleolithic diet and an evolutionary view on medicine was sparked - as perhaps for a few others on this list by Randolph Nesse's and George Williams' book "Evolution and Healing", and was further fuelled by my
encounter with Staffan Lindeberg. Researchwise, I am hoping to at some point do a follow-up study of
Staffan's study of cardiovascular disease amongst Trobriand Islanders on Kitava, in which I would like to
study urbanised Trobriand Islanders. Thus I am interested in any and all experiences of migrant studies.
In the past, this list has served as a forum for spirited academic debate. It is my sincere hope that this will
shortly be true once again.
Let us revive the Paleodiet mailing list!
Regards, Dan Petersson
PALEODIET Archives
Subject: intelligence; evolution
From: Dick Dawson
Reply-To:
Date: Sat, 5 Feb 2000 17:21:29 -0500
On Ben Balzer's email:
I read the core point that competing intelligence of a species is a factor in selection for gain in intelligence.
I must add: I've read that some sociologists claim actual fertility of our highest mental level functioning
citizens is lower than average. We note that professional workers tend to have smaller numbers of children
than average.
Dick web: use either (same server): http://top.syr.edu/~ddawson http://unixweb.syr.edu/~ddawson
[..]
Was the stress other carnivores? No. No other animal was a real threat to a band of humans (and dogs). It
certainly wasn't a hole in the ozone layer.
The stress was, quite simply, OTHER HUMANS.
The fact that we are homicidal is the underlying stress that caused our intelligence to keep on evolving: there
is a survival advantage in being smarter than the next human. The evolutionary force was not being better
able to survive the environment, it was in being better able to survive attack from other humans.
[..]
Perhaps competitive is the point, 'homicidal' might be 1 avenue of competition. Modern wild carnivore
studies show considerable homicidal behavior: lions kill cheetah cubs, new lion males kill young cubs of
previous pride lions, lions & hyena kill each others' cubs etc. Carnivores rarely or never eat cubs they kill:
the behavior is competition, not feeding. Also new family boss male gorilla often kill young offspring of
replaced males. All this perhaps selects for the genetic material of the new males; keeps the probably
genetically transmitted instinct alive in the gene pool.
Napoleon Chagnon's studies among the Yanomamo pretty much fit this model. Some modern
deconstructionists have discredited Chagnon; I suspect he's right. _L_A_Times_ had an article on Chagnon
recently.
1/23 (2000)
Dick
PALEODIET Archives
Subject: Re: PALEODIET Digest - 2 Feb 2000 to 5 Feb 2000 (#2000-2)
From: Todd Moody
Reply-To:
Date: Sat, 5 Feb 2000 20:38:40 -0500
On Sat, 5 Feb 2000, Automatic digest processor wrote:
> Was the stress other carnivores? No. No other animal was a real threat to a band of humans (and
> dogs). It certainly wasn't a hole in the ozone layer. The stress was, quite simply, OTHER HUMANS.
> The fact that we are homicidal is the underlying stress that caused our intelligence to keep on
> evolving- there is a survival advantage in being smarter than the next human. The evolutionary
> force was not being better able to survive the environment, it was in being better able to survive
> attack from other humans.
It's an interesting theory, Ben, but I think it's question-begging. We are certainly not the first, nor the last,
species to be successful enough to have to compete amongst ourselves for resources. What you are
overlooking is that what made the next human so fearsome was precisely his intelligence. So we end up with
the circular explanation that we are intelligent because we are homicidal and homicidal because we are
intelligent (and need to defend ourselves against our own kind). This points to a kind of cognitive "arms
race" that has pushed human intelligence beyond the envelope that is normal on this planet. But the fact that
this has occurred only once should make us skeptical. Since, we are told, convergent evolution is supposed to
be the rule, why aren't there other species that have achieved full sapience? The explanation, to be
convincing, will have to point to circumstances that humans (or proto-humans) and only humans have had to
contend with in their evolutionary struggle.
Todd Moody
PALEODIET Archives
Subject: Re: PALEODIET Digest - 2 Feb 2000 to 5 Feb 2000 (#2000-2)
Reply-To:
Date: Sun, 6 Feb 2000 11:26:08 +0200
Re: 1. The terrible truth about intelligence (updated 4 Feb 2000)
Just a thought to add to your concept: A local doctor, here in South Africa, holds the theory that one of the
stressors in urban life is the presence of straight lines in abundance. His reasoning is that the only creatures
that make straight lines are other human beings, and the only real threats to us are other human beings,
therefore the presence of straight lines are an automatic, subliminal stressor. His advice is to get out into the
bush as often as possible!
Mandi Smallhorne Editor, PhysioForum
PALEODIET Archives
Subject: Intelligence
From: M E Wood
Reply-To:
Date: Sun, 6 Feb 2000 16:01:54 +1300
2/23 (2000)
If a mere lurker may suggest. We don't know there wasn't an ozone hole in the past! Volcanoes can cause
some depletion in ozone and volcanoes have been very active in some parts of the period of human
development. There has been global warming and cooling. Some very cold periods which were coterminous
with drought conditions which suggest changes in vegetation and therefore in the distribution of herd
animals. There are sites which deal with vegetational change, my favourite is Jonathan Adams'
http://www.esd.ornl.gov/projects/qen/nerc.html This could result in humans either competing for scarcer
resources or scattering further a field. M E Wood (Prehistoric Archaeology, U Edinburgh) New Zealand
PALEODIET Archives
Subject: Dairy and CHD
From: Todd Moody
Reply-To:
Date: Wed, 9 Feb 2000 14:31:29 -0500
Seely's research [1, 2] found a strong correlation between milk intake and heart disease, but interestingly that
correlation was not present for cheese, considered separately from dairy intake as a whole. I am wondering if
this could be because cheese is relatively high in dairy fat, which is a source of conjugated lineoleic acid.
CLA apparently has anti-atherogenic (and anti-carcinogenic) properties. But if that is so, wouldn't the
protective effect be even stronger for butter?
Todd Moody
[1] Med Hypotheses 1981 Jul;7(7):907-18
Diet and coronary disease: a survey of mortality rates and food consumption statistics of 24 countries.
Seely S
Direct, linear and reasonably accurate correlation has been found between coronary heart disease (CHD)
mortality rates and the consumption of unfermented milk proteins--namely the protein content of all dairy
products with the only important exception of cheese--in a study of male mortality rates and food
consumption statistics of 24 countries. Thus in Finland, with the highest CHD mortality amongst these
countries, the consumption of unfermented mile proteins is also higher than in the other countries, 30.4
g/day, corresponding to the protein content of 0.85 l of whole milk. In Germany, Yugoslavia and Japan male
CHD mortality is approximately a half, a quarter and a tenth of that in Finland. So is the consumption of
milk proteins, 14.1, 8.1 and 2.5 g respectively. Multivariate analysis on the combined effect of milk proteins
and other possible atherogenic agents, like sugar, saturated fats and cigarette smoking, is performed, the
results tending to confirm the leading role of milk proteins, attributing only an adjuvant effect to co-factors.
Possible theoretical interpretation of the results is briefly discussed.
UI: 82035315
[2] Int J Cardiol 1988 Aug;20(2):183-92
Diet and coronary arterial disease: a statistical study.
Seely S
Department of Cardiology, University of Manchester, Royal Infirmary, U.K.
Statistical analysis comparing mortality rates from coronary arterial disease with food consumption in 21
countries belonging to the Organisation of Economic Cooperation and Development is presented. In a
preliminary process correlation coefficients are calculated for coronary mortality and all food items
appearing in statistics collected for food consumption as well as for some combinations of food items. The
highest correlations obtain with oats, milk proteins (other than the protein content of cheese), milk fats and
sugar. These items are investigated in greater detail with respect to mortality from coronary arterial disease
in males and females in various age groups and for various time intervals between the dates of mortality and
statistics for food consumption. Correlations tend to increase in the older age groups and with longer time
intervals. The highest correlation coefficient found is 0.94 for deaths due to coronary arterial disease for
males in the 65-74 age group with the combined consumption of oats and milk proteins.
PMID: 3209250, UI: 89092491
[3] Proc Soc Exp Biol Med 2000 Jan;223(1):8-13
Mechanisms of action of conjugated linoleic acid: evidence and speculation.
Pariza MW, Park Y, Cook ME
3/23 (2000)
Conjugated linoleic acid (CLA) has been shown to inhibit carcinogenesis and atherosclerosis, enhance
immunologic function while protecting against the catabolic effects of immune stimulation, affect body
composition change (reducing body fat gain while enhancing lean body mass gain), and stimulate the growth
of young rats. We discuss possible biochemical mechanisms that underlie these physiological effects. We
emphasize the importance of considering the effects, both individually and combined, of the two CLA
isomers (cis-9, trans-11 CLA and trans-10, cis-12 CLA) that have been shown to exhibit biological activity
and which appear to exert their effects via different biochemical mechanisms.
PMID: 10632956, UI: 20098757
PALEODIET Archives
Subject: Moderator's note
From: Dan Petersson
Reply-To:
Date: Fri, 11 Feb 2000 20:50:06 +0100
In my ambition to stimulate discussion, I fear some posts have been accepted which perhaps should not have
been. To be more specific, the thread on the evolution of intelligence initiated by Ben Balzer has been too
speculative in tone for this forum. To avoid this escalating into something that could harm the general tone of
this list, no further posts in that thread will be published. If anyone has any suggestions where that discussion
could continue, I will forward them to the list.
These problems have been caused by too much permissiveness on my part. I hope all of you will have
patience with my first fumbling steps as moderator.
Regards, Dan Petersson Moderator
PALEODIET Archives
Subject: Cardiac Operation Update
From: Charles Hunt
Reply-To:
Charles Hunt
Date: Thu, 2 Mar 2000 12:56:06 -0800
Dear Family, Friends and Associates,
Thank you so much for your love and support going into this unexpected emergent situation with my heart
last week. I don't have the words to adequately express my gratitude for all the kindnesses you sent. It has
really, really helped~
On the healing front, I'm back from UCLA Medical Center and on the mend back at home now after surgery
last Friday... also off the narcotic pain killers so I can put two words together again without slurring and
finally answer your e-mails...can't drive for 2 weeks and have to hold off on weightlifting for 6 weeks while
all my new parts settle in and lock down...
In Brief:My heart has a rather big electrical problem from a birth defect that has grown much worse and can
cause sudden death (of which I've had some very close calls as of late) so it needed an electrical solution to
keep me on the planet....
so, what I've got installed now is a 'difribulator/pacemaker' that's very sophisticated... it can "jumpstart" me if
I have a sudden death event, or "pace me" if I get close to one in the hope that it won't have to give me the
"big jolt"...
Honestly, it'll take some getting used to physically & emotionally... but I think it'll come in handy for
warming coffee or the next time my car won't start!.... ;)
"Electric" Charles Author, Charles Hunt's Diet Evolution: "Eat Fat and Get Fit!"
original notice: Dear Family, Friends and Associates,
> I've started having a bunch of abnormal heart arrhythmias in the last 6 months that put me at a
> big risk for sudden death. Seems my heart birth defect IHSS (Idiopathic Hypertrophic Subaortic
> Stenosis), which knocked me down when I was 24, has worsened quite a bit. I had a long arrhythmia
> last week while sitting on a couch visiting with a friend that was recorded on a digital monitor I
> was wearing. Seems I scared the Dr's really good with that one, so they're going to implant a
4/23 (2000)
> defribulator to shock me from the inside if my heart goes into this abnormal rhythm, or pace it
> (pacemaker)if it goes too slow. They actually wanted me in the hospital already for the procedure,
> but I was too overwhelmed at first with it all and wanted to talk with them more (later today). I
> go in Friday for the implant and should come home sometime Saturday. Guess that means I'll have to
> give up the nude book cover shots...;) I think I'll be back on line later next week~ Till then,
> you rascals stay out of trouble!
> Charles
> Author, Charles Hunt's <http://www.charleshunt.com
> Diet Evolution
PALEODIET Archives
Subject: From: Luis Alberto Vargas
Reply-To:
Date: Tue, 7 Mar 2000 17:50:26 -0600
This is a question from Instituto de Investigaciones Antropologicas in Mexico City. Our archaeologists are
studying ancient floors from Teotihuacan, some of them are made of dirt and others of stucco. So far they
have been able to identify food remains by analyzing remains of seeds, pollen, phytolites, and some
inorganic indirect tracers such as phosphorus. They are now planning to simulate ancient house floors and
see how food remains are preserved, and how their remains can be identified. Has any of you done similar
studies, or have an idea of other remains that should be sought?
PALEODIET Archives
Subject: Plant Animal Subsistence Ratio study
From: Ben Balzer
Reply-To:
Date: Wed, 29 Mar 2000 09:01:40 -0500
I would like to bring to your attention the publication of the following paper in the American Journal of
Clinical Nutrition in March 2000. I believe it is an important milestone in paleolithic/hunter-gatherer
nutrition, and recommended it to all interested parties. (The moderator may prefer to approach Professor
Cordain for comment).
Loren Cordain, Janette Brand Miller, S Boyd Eaton, Neil Mann, Susanne HA Holt, and John D Speth Plantanimal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets Am J Clin
Nutr 2000;71:682-692. http://www.ajcn.org/content/vol71/issue3/
Also in this issue see:
Editorial: Katharine Milton Hunter-gatherer dietsa different perspective Am J Clin Nutr 2000;71:665-667.
Book Review: Noel W Solomons Evolutionary Aspects of Nutrition and Health: Diet, Exercise, Genetics and
Chronic Disease, Am J Clin Nutr 2000;71:854-855.
Ben Balzer
Dr. Ben Balzer Beverly Hills Medical Service 109 Morgan St Beverly Hills 2209 NSW AUSTRALIA Tel+
61 2 9502 3355, Fax +61 2 9502 4243
PALEODIET Archives
Subject: Science article
From: Liza May
Reply-To:
Date: Fri, 12 May 2000 09:17:45 -0400
Earliest Pleistocene Hominid Cranial Remains from Dmanisi, Republic of Georgia: Taxonomy, Geological
Setting, and Age
5/23 (2000)
Leo Gabunia, Abesalom Vekua, David Lordkipanidze, Carl C. Swisher III, Reid Ferring, Antje Justus,
Medea Nioradze, Merab Tvalchrelidze, Susan C. Antn, Gerhard Bosinski, Olaf Jris, Marie-A.-de Lumley,
Givi Majsuradze, and Aleksander Mouskhelishvili
Science May 12 2000: 1019-1025.
-- Liza May, M.S. Email: phone:(301)261-0555 fax:(410)451-6105
PALEODIET Archives
Subject: Paleodiet Tocopherols
From: Dan Petersson
Reply-To:
Date: Tue, 23 May 2000 10:45:43 +0200
Moderator's note: message from Michael J Rae,
All:
There's been a fair amont of research over the last few years into the absorption and retention of members of
the vitamin E complex. The "alpha-tocoherol transfer protein" is an hepatic mechanism whereby the body
conserves a-tocopherol preferrentially by incorporating it actively into LDL; not only are other tocoperols
not conserved by ATTP, but gamma tocopherol is actually prefe-rentially excreted as well, as part of a blood
pressure regulating measure (the metabolite, LLU-alpha, into which g-toco is degraded before excretion is a
natriuretic factor).
There has been some speculation that the a-toco conservation might reflect a relative lack of this member of
the E complex in the paleolithic diet, so that deliberate conservation was necessary in the face of competition
from other tocos at the level of absorption. the modern typical N American diet does indeed contain much
more g-toco than a-; however, the typical Euroean diet actually has more a-.
So: has anyone done any research, or seen any research, or would anyone consider DOING research, to
investigate the relative proportions of the tocopherols in the Paleodiet, via hunter-gatherer diets eg?
Thanks!
-Michael
Reference Brigelius-Flohe R, Traber MG. Vitamin E: function and metabolism. FASEB J 1999
Jul;13(10):1145-55
Get your FREE Email at http://mailcity.lycos.com Get your PERSONALIZED START PAGE at
http://my.lycos.com
PALEODIET Archives
From: John Macgregor
Reply-To:
Date: Wed, 24 May 2000 15:19:37 +1000
I'm a science journalist - and am presently writing an article for New Scientist on paleolithic exercise
patterns. (I.e. the types, duration, intensity and frequency of movement to which we are now adapted.) I have
enlisted the help of Loren Cordain and Art De Vany, have read their papers, and have combed the archives but if any of you have things you want to bring to my attention on this subject, they would be welcome.
You may also want to comment on my speculation/question re whether hunt frequencies, territorial ranges
and therefore exercise levels may have fallen with the advent of fire (~125 KYA+), because cooked food
'keeps' longer than uncooked.
You can email me at .
Cordially
John Macgregor
phone & fax: 61 2 6680 5509
PALEODIET Archives
6/23 (2000)

Reply-To:
Date: Tue, 30 May 2000 20:24:35 EDT
In a message dated 5/23/00 3:01:18 PM EST, writes:
<< So: has anyone done any research, or seen any research, or would anyone consider DOING research, to
investigate the relative proportions of the tocopherols in the Paleodiet, via hunter-gatherer diets eg?
> Michael,
I'd be interested in collaborating on some Paleodiet research. I have some good records of regional Paleodiets
(remember they are different by regions). For native foods I don't know where to get information regarding
proportions of tocopherols, but I do have a pretty good idea about lots of the plants consumed in various
parts of North America. I'd prefer to start there because I have better data.
Linda Scott Cummings, Ph.D. Paleo Research
PALEODIET Archives
Subject: Re: Paleo Tocopherols/Tocotrienols
From: Michael J Rae
Reply-To:
Date: Mon, 5 Jun 2000 16:42:33 -0700
On Mon, 5 Jun 2000 16:00:36
> From: Linda Scott Cummings
> In a message dated 5/23/00 3:01:18 PM EST,
> writes:
> So: has anyone done any research, or seen any research, or would anyone consider DOING
> research, to investigate the relative proportions of the tocopherols in the Paleodiet, via
> hunter-gatherer diets eg? Michael, I'd be interested in collaborating on some Paleodiet research.
If you are suggesting a collaboration with ME, I'm afraid I'm not a researcher, academic or otherwise,
although I'd be more than happy to go digging and processing data if you can suggest where I should go dig!
I might also be able to get some raw data from an aquaintance of mine who DOES do E research.
I have some good records of regional Paleodiets (remember they are different by regions). I'd prefer to start
[in North America] because I have better data.
Even the most tentative and preliminary of reports would be better than nada.
Thanks for your interest in the topic! Let me know if you proceed, and how I can help.
-Michael
Send FREE Greetings for Father's Day--or any day! Click here:
http://www.whowhere.lycos.com/redirects/fathers_day.rdct
PALEODIET Archives
Subject: Re: PALEODIET Digest - 24 May 2000 to 5 Jun 2000 (#2000-12)
From: Kerin O'Dea
Reply-To:
Date: Wed, 7 Jun 2000 20:13:48 +1000
I wish to notify a change of address. From tomorrow my new email address is: Regards Kerin O'Dea
Automatic digest processor wrote:
> 1. PALEODIET Digest - 15 May 2000 to 23 May 2000 (#2000-10)
>
------------=-=-=-=-=-=-=- IMPORTANT NOTICE -=-=-=-=-=-=-------------Paleolithic Diet Symposium List
7/23 (2000)
> ** Make sure you have a subject line that reflects your topic **
>
---------------------------------------------------------------------> Date: Tue, 30 May 2000 20:24:35 EDT
> From: Linda Scott Cummings Subject: Re: PALEODIET Digest - 15 May 2000 to 23 May 2000 (#200010)
> In a message dated 5/23/00 3:01:18 PM EST,
> writes:
> So: has anyone done any research, or seen any research, or would anyone consider DOING
> research, to investigate the relative proportions of the tocopherols in the Paleodiet, via
> hunter-gatherer diets eg? Michael, I'd be interested in collaborating on some Paleodiet research.
> I have some good records of regional Paleodiets (remember they are different by regions). For
> native foods I don't know where to get information regarding proportions of tocopherols, but I do
> have a pretty good idea about lots of the plants consumed in various parts of North America. I'd
> prefer to start there because I have better data.
> Linda Scott Cummings, Ph.D.
> Paleo Research
>
-----------------------------> End of PALEODIET Digest - 24 May 2000 to 5 Jun 2000 (#2000-12)
>
**************************************************************
-___________________________________________________
Kerin O'Dea Professor and Head, Centre for Population Health and Nutrition Monash Institute of Public
Health Research, Monash University Monash Medical Centre 246 Clayton Road Clayton VIC 3168 Australia
Tel: +61 3 9594 5510 Fax: +61 3 9594 5509 http://www.monash.edu.au/
PALEODIET Archives
Subject: carbohydrates
From: Sean Mcbride
Reply-To:
Date: Fri, 9 Jun 2000 01:51:56 -0400
I am a bit confused about the whole carbohydrate issue. It appears that most hunter-gatherers utilised some
form of concentrated carbohydrate, whether it be yams, seeds, rootstarch or whatever. (The arctic peoples
used fat as an alternative since carbohydrate was scarce, as did the people of Pacific Northwest America).
There seem to be four reasons for including carbohydrate resources in the human diet. One is to counteract
(offset might be a better word) high levels of protein from animal resources (if animal resources are
abundant). The second reason is to spare protein from being converted into energy which is an inefficient
process and deprives the body of protein for maintenance and repair (Vayda 1987, Speth and Spielmann
1983). The third reason is that the brain uses glucos e from carbohydrate preferentially over other foods. The
final reason is to provide calories in the absence of animal resources by which I mean that if other food
resources are unavailable (e.g. mammals, fish, insects etc)people will concentrate on supplying their energy
needs from carbs.
8/23 (2000)
It seems to me that if the brain uses carbohydrate preferentially then the Inuit are operating (successfully) on
an inefficient process . I've forgotten the process but i believe there is another way of feeding the brain if
they lack carbohydrate in their diet. If there is a limit to the amount of protein we can consume, and if wild
animals in the temperate regions contain low percentages of fat, then it would seem that we would have to
consume fairly rich carbohydrates (concentrated?)in order to live healthily. Gould (1966), for example,
observed that a 97-lb (44kg) kangaroo yielded only 4 ounces (114g 9 of removable fat. Eating animals like
this would surely lead to protein toxicity given the imbalance of protein to fat in the absence of carbohydrate.
Fruit and vegetables provide carbohydrate, and so do tubers, grains, and a variety of nut seed resources.
However, since all the Australian Aboriginal groups I have looked at have utilised one or more staples that
are basically a starch food, can anyone explain to me why the use of these concentrated carbohydrates was so
widespread?. Especially when the palaeodiet that is generally proposed on this list seems to be low in these
types of carbohydrate.
Also, since their appears to be a high prevalence for fat amongst hunter-gatherers does that mean that we
have an evolutionary need to eat higher levels of fat or does it reflect the lack of fat in the environment in
temperate/tropical regions? We seem to have been hardwired for sweetness hence an interest in f ruit, honey
etc but fat is not sweet. Carbohydrates, although not tasting sweet convert fairly readily to sugars I believe.
Might that be a reason for the widespread use of them, if they fulfill some sort of sweetness criteria?
Or, is the consumption of starchy carbohydrates simply the result of human groups requiring more and more
energy due to population increases, environmental changes or whatever, and having to turn to starchy carbs
as a necessity to maintain their energy requirements. After all, many of the carbs used by hunter-gatherers
require large amounts of manual labour to separate the starch from the plant or to rid the starch of toxins or
both.Which brings up the question of 'Why bother' unless you had to?
I would really appreciate any feedback that might clear up my confusion on these issues.
Thanks
Sean McBride University of Queensland
Gould, R. A. (1981). Food sharing in Australia and California. Omnivorous Primates:Gathering and Hunting
in Human Evolution. R. S. O. Harding and G. Teleki. New York, Columbia University Press.
Speth, J. K. and K. R. Spielmann (1983). Energy source, protein metabolism, and hunter-gatherer
subsistence strategies. Journal of Anthropological Archaeology 2(1): 1-31.
Vayda, A. P. (1987). Explaining what people eat: A review article. Human Ecology 15(4): 493-510.
PALEODIET Archives
Subject: Re: Response to Sean McBride's Carbohydrate Question
From: Loren Cordain
Reply-To:
Date: Fri, 9 Jun 2000 16:29:03 -0600
9/23 (2000)
Sean poses many good questions in his recent post, and I believe that the answers to quite a few of these can
be found in our most recent paper (1) as well as in my colleague, Jennie Brand-Miller's classic Carnivore
Connection paper (2). In the absence of carbohydrate, liver and kidney are the main organs that can
synthesize glucose (gluconeogenesis) from either glucogenic amino acids or glycerol, a product of adipose
tissue metabolism. Inuit and other native populations that eat little or no carbohydrate must rely upon
gluconeogenesis for glucose as substrate for brain and nervous tissue metabolism. Besides the brain and
nervous tissue other tissues (erythrocytes, and fetus) also require glucose. Glucose is required in adipose
tissue as a source of glyceride-glycerol, and it probably plays a role in maintaining the level of intermediates
of the citric acid cycle in many tissues. It is clear that even under conditions where fat may be supplying
most of the caloric requirement, there is always a certain basal requirement for glucose. Finally, glucose is
the only fuel that will supply energy to skeletal muscle under anaerobic conditions. The evolutionary
selection for peripheral insulin resistance in the muscles then is a mechanism by which glucose can be
efficiently conserved and routed to brain and fetus - hence providing increased survival value when there is
little carbohydrate in the diet (2). As early hominids migrated from the tropics to higher latitudes during the
Paleolithic (3) and became increasingly dependent upon animal foods, it is quite likely that they would have
been forced to reduce their carbohydrate intake because of the seasonal availability of plant foods that can be
eaten and physiologically digested by non-fire using hominids. Hence, peripheral insulin resistance which
once had positive survival in a carbohydrate poor environment for our ancient ancestors, now represents a
liability in modern humans because it increases the likelihood of susceptibility to a number of chronic
diseases (hypertension, type II diabetes, obesity, dyslipidemia and coronary heart disease) (2). Because there
is a physiologic protein ceiling that has been quantified (1), then unlimited consumption of protein from very
lean or small animals is also not possible. If carbohydrate is unavailable or scarce, as it is at higher latitudes
particularly during winter and early spring, then the only solution is to eat more fat. As we have shown (1)
larger species of mammals contain relatively more fat than smaller species, hence early humans living in
carbohydrate poor environments would have preferentially preyed upon larger animal species. This principal
would have held true for modern hunter-gatherers (Cro Magnon) living in Europe and North America
(PaleoIndians). Its does not seem coincidental that megafauna extinctions occurred roughly the same time
modern human numbers dramatically increased on both of these continents. In more southernly latitudes
where carbohydrate was available, megafauna persisted into modern times because there was another dietary
solution to the protein ceiling. Once megafauna became extinct, human populations must have also declined
because the protein ceiling prevented the consumption of the available calories from small animals (1). The
adoption of agriculture (i.e. cereal grain domestication) abrogated the physiological protein ceiling because
cereal carbohydrate effectively dilutes the high protein content of small or lean animals depleted of fat.
Cereals can be stored overwinter without decomposing thereby allowing neolithic humans the ability to eat
all sized animal regardless of their fat content, even when body fat stores are depleted. By abrogating the
protein ceiling, cereal grains permitted more people to live on a square acre of land, becaue more of the
available biomass (in addition to the cereal grain itself) could now be consumed. Hence, humans adopted
agriculture, because in Sean's own words, "they had to".
Cordially,
Loren
1. Cordain L, Brand Miller J, Eaton SB, Mann N, Holt, Speth JD. Plant-animal subsistence ratios and
macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr 2000;71:682-92. 2.
Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM.
Diabetologia 1994 37:1280-6. 3. Gabunia L, Vekua A, Lordkipanidze D, Swisher CC 3rd, Ferring R, Justus
A, Nioradze M, Tvalchrelidze M, Anton SC, Bosinski G, Joris O, Lumley MA, Majsuradze G,
Mouskhelishvili A. Earliest Pleistocene hominid cranial remains from Dmanisi, Republic of Georgia:
taxonomy, geological setting, and age. Science 2000;288(5468):1019-25.
Collins, CO 80523 tel: (970) 491-7436 fax: (970) 491-0445 email:
PALEODIET Archives
Subject: Article on Neanderthal diet
From: Dan Petersson
Reply-To:
10/23 (2000)
Date: Thu, 15 Jun 2000 11:35:16 +0200

Richard Keene and Bob Avery have brought to my attention an upcoming article in the June 20 issue of the
Proceedings of the National Academy of Sciences:
Michael P. Richards, Paul B. Pettitt, Erik Trinkaus, Fred H. Smith, Maja Paunovic, and Ivor Karavanic;
Neanderthal diet at Vindija and Neanderthal predation: The evidence from stable isotopes
It might be of interest to the participants of this list. The abstract, which can be read at:
http://www.pnas.org/cgi/content/abstract/120178997v1
as well as media reports on the article have presented the article as evidence of a maily carnivorous diet
among the Neanderthals.
/Dan
PALEODIET Archives
Subject: fat and carbs
From: Sean Mcbride
Reply-To:
Date: Wed, 12 Jul 2000 01:00:22 -0400
Thanks Loren for your detailed reply to my question regarding carbohydrates. I apologise for the delay in
replying. Your response clarified a question for me. As I stated in my last post, Gould (1966), observed that a
97-lb (44kg) kangaroo yielded only 4 ounces (114g)of removable fat. Assuming for the sake of argument
that the useable carcass is around 65% of the total weight (Cordain et al. 2000:685)(although I suspect a
kangaroo would produce a higher useable weight than an ungulate). So, we're looking at about 29kg of meat
with 114g of fat. It would be unlikely for one individual to consume an entire Kangaroo, so let us say it is
shared between 10 people, providing around 3kg of meat and 11g of fat per person (assuming it was divided
equally which it probably would not be).
If (as the Angmagssalik eskimos seem to prefer [Speth 1989:334])a reasonable mix of fat to protein is half half (although Steffansson guggests one pound of fat to 6-7 lbs of lean meat for pemmican), then the
example above is way out of kilter in terms of too much protein and not enough fat. This diet would need to
be supplemented by carbohydrates in the form of fruit or starch. Since in my experience of Australian bush
fruits many of them are not particularly high in sugars (although Jenny would know better than I about
this)this would tend to indicate a need for starchy carbs.
Relating this back to palaeodiet - even hunting megafauna with an increase in fat due to their increased size
early peoples would still have had to have used carbohydrate sources to offset the high protein levels. Since a
number of authors suggest that carbohydrate was scarce in these environments the q uestion becomes "What
then did they eat" was it carbohydrates or were they adapted to gluconeogenesis.
I hope this makes sense and would appreciate any comments
Cheers
Sean McBride
Cordain, L., J. Brand-Miller, S. B. Eaton, N. Mann, S.H.A. Holt and J.D. Speth 2000 Plant-animal
subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American
Journal of Clinical Nutrition 71:682-692.
Gould, R.A. 1966 Notes on hunting, butchering and sharing among the Ngatatjara and their neighbours in the
Western Australian desert. Kroeber Anthropological Society Papers 36:41-63.
Speth, J.D. 1989 Early hominid hunting and scavenging: The role of meat as an energy source. Journal of
Human Evolution 18:329-343.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
From: Melissa Darby
Reply-To:
Melissa Darby
Date: Fri, 14 Jul 2000 14:44:21 -0700
11/23 (2000)
I have postulated that in the Northern Hemisphere (North America, Siberia, Northern Europe) as the ice
sheet was retreating there were considerable wetlands that supported Sagittaria latifolia- an emergent wetland
plant spread by waterfowl and known as a pioneering plant because it was one of the first to colonize these
areas. It grows as a monoculture, and can take over a wetland. On the lower Columbia River, and in the
Mississippi delta there are places where there is no other plant except S.latifolia for hundreds of acres. This
is the model I suggest existed ca. 10, 000 b.p. in the shallow lakes, ponds, streamsides, wetlands that were
present draining the water from the icesheet.
The plants would also support grazing megafauna because wetlands (even in cold climates) are highly
productive re calories/biomass per sq meter. The tuber tastes like a potato, cooks as fast or faster than a
potato and does not need to be processed with stone tools, nor is it associated with fire cracked rock, it can be
baked in hot ashes i.e. it is hard to find in the archaeological record. It was available/harvestable from early
fall to mid-spring when plant foods are generally considered to be scarce, and was very cost effective to
harvest. It dries well, and can be stored for long periods of time. It has been recovered in paleo sites in
Poland, and in caves in the Great Basin. Pollen studies support my hypothesis. My thesis is available upon
request. Melissa Darby
-----Original Message----- From: Automatic digest processor To: Recipients of PALEODIET digests Date:
14 July, 2000 1:00 PM Subject: PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
> 1. fat and carbs
> ------------=-=-=-=-=-=-=- IMPORTANT NOTICE -=-=-=-=-=-=-------------> ** Make sure you have a subject line that reflects your topic **
> ---------------------------------------------------------------------> Date: Wed, 12 Jul 2000 01:00:22 -0400
> From: Sean Mcbride Subject: fat and carbs
> Thanks Loren for your detailed reply to my question regarding carbohydrates. I apologise for the
> delay in replying. Your response clarified a question for me. As I stated in my last post, Gould
> (1966), observed that a 97-lb (44kg) kangaroo yielded only 4 ounces (114g)of removable fat.
> Assuming for the sake of argument that the useable carcass is around 65% of the total weight
> (Cordain et al. 2000:685) (although I suspect a kangaroo would produce a higher useable weight than
> an ungulate). So, we're looking at about 29kg of meat with 114g of fat. It would be unlikely for
> one individual to consume an entire Kangaroo, so let us say it is shared between 10 people,
> providing around 3kg of meat and 11g of fat per person (assuming it was divided equally which it
> probably would not be).
> If (as the Angmagssalik eskimos seem to prefer [Speth 1989:334])a reasonable mix of fat to protein
> is half -half (although Steffansson guggests one pound of fat to 6-7 lbs of lean meat for
> pemmican), then the example above is way out of kilter in terms of too much protein and not enough
> fat. This diet would need to be supplemented by carbohydrates in the form of fruit or starch.
> Since in my experience of Australian bush fruits many of them are not particularly high in sugars
> (although Jenny would know better than I about this)this would tend to indicate a need for starchy
> carbs. Relating this back to palaeodiet - even hunting megafauna with an increase in fat due to
> their increased size early peoples would still have had to have used carbohydrate sources to
> offset the high protein levels. Since a number of authors suggest that carbohydrate was scarce in
> these environments the question becomes "What then did they eat" was it carbohydrates or were they
> adapted to gluconeogenesis.
> I hope this makes sense and would appreciate any comments
> Cheers
> Sean McBride
> Cordain, L., J. Brand-Miller, S. B. Eaton, N. Mann, S.H.A. Holt and J.D.
> Speth
> 2000 Plant-animal subsistence ratios and macronutrient energy estimations
> in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition
> 71:682-692.
> Gould, R.A.
12/23 (2000)
> 1966 Notes on hunting, butchering and sharing among the Ngatatjara and
> their neighbours in the Western Australian desert. Kroeber Anthropological
> Society Papers 36:41-63.
> Speth, J.D.
> 1989 Early hominid hunting and scavenging: The role of meat as an energy
> source. Journal of Human Evolution 18:329-343.
> -----------------------------> End of PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
> ***************************************************************
PALEODIET Archives
Subject: Re: PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
From: Barry Groves
Reply-To:
Barry Groves
Date: Sat, 15 Jul 2000 09:26:18 +0100
There is an apparent error in Sean's reasoning on the weight of fat in a kangaroo -- and for that matter other
animals. Archaeology has determined that, in Eurasia, through the discovery of smashed long bones and
broken skulls, palaeolithic hunters' preferred food was the animals' brains and bone marrow. These are both
very high in fats.
I don't know how much fat, by weight, there is in a kangaroo's brain and total marrow, but I am sure it is a
great deal more than 4 ounces. If this is taken into consideration, the figures will be very different from the 4
ounces per 97 lbs that Gould (1966) measured. Although probably not as high a percentage as Stefansson's 1
in 6-7, it will still be a considerable amount. It should not be forgotten that Australian Aborigines also
consume other sources of protein/fats e.g. fat grubs.
I hope this helps
Barry Groves
----- Original Message ----- From: "Automatic digest processor" To: "Recipients of PALEODIET digests"
Sent: Friday, July 14, 2000 9:00 PM Subject: PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
> 1. fat and carbs
>
>
---------------------------------------------------------------------> Date: Wed, 12 Jul 2000 01:00:22 -0400
> From: Sean Mcbride Subject: fat and carbs
> Thanks Loren for your detailed reply to my question regarding carbohydrates. I apologise for the
> delay in replying. Your response clarified a question for me. As I stated in my last post, Gould
> (1966), observed that a 97-lb (44kg) kangaroo yielded only 4 ounces (114g)of removable fat.
> Assuming for the sake of argument that the useable carcass is around 65% of the total weight
> (Cordain et al. 2000:685)(although I suspect a kangaroo would produce a higher useable weight than
> an ungulate). So, we're looking at about 29kg of meat with 114g of fat. It would be unlikely for
> one individual to consume an entire Kangaroo, so let us say it is shared between 10 people,
> providing around 3kg of meat and 11g of fat per person (assuming it was divided equally which it
> probably would not be).
> If (as the Angmagssalik eskimos seem to prefer [Speth 1989:334])a reasonable mix of fat to protein
> is half -half (although Steffansson guggests one pound of fat to 6-7 lbs of lean meat for
> pemmican), then the example above is way out of kilter in terms of too much protein and not enough
> fat. This diet would need to be supplemented by carbohydrates in the form of fruit or starch.
13/23 (2000)
> Since in my experience of Australian bush fruits many of them are not particularly high in sugars
> (although Jenny would know better than I about this)this would tend to indicate a need for starchy
> carbs. Relating this back to palaeodiet - even hunting megafauna with an increase in fat due to
> their increased size early peoples would still have had to have used carbohydrate sources to
> offset the high protein levels. Since a number of authors suggest that carbohydrate was scarce in
> these environments the question becomes "What then did they eat" was it carbohydrates or were they
> adapted to gluconeogenesis.
> I hope this makes sense and would appreciate any comments
> Cheers
> Sean McBride
> Cordain, L., J. Brand-Miller, S. B. Eaton, N. Mann, S.H.A. Holt and J.D.
> Speth
> 2000 Plant-animal subsistence ratios and macronutrient energy estimations
> in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition
> 71:682-692.
> Gould, R.A.
> 1966 Notes on hunting, butchering and sharing among the Ngatatjara and
> their neighbours in the Western Australian desert. Kroeber Anthropological
> Society Papers 36:41-63.
> Speth, J.D.
> 1989 Early hominid hunting and scavenging: The role of meat as an energy
> source. Journal of Human Evolution 18:329-343.
>
-----------------------------> End of PALEODIET Digest - 15 Jun 2000 to 14 Jul 2000 (#2000-16)
>
***************************************************************
>
PALEODIET Archives
Subject: Re: PALEODIET Digest - 14 Jul 2000 to 16 Jul 2000 (#2000-17)
From: s338048
Reply-To:
Date: Wed, 19 Jul 2000 08:52:36 +1000
Thanks to Melissa Darby and Barry Groves for raising some interesting points in their replies. I am curious
as to whether Sagittaria latifolia is easily digested without cooking and what sort of calorie returns are
available. If it is not possible to provide enough fat from temperate and tropical animals without resorting to
carbs then perhaps we should be looking for similar plants to S. latifolia around the world that could have
provided these carbs.
In response to Barry Groves his comments about the fat in the brain are probably valid in that use of the
brain and marrow would have increased the fat availability. I don't remember if Gould (1966) included fat
from the brain in his estimate. I suspect not. In Gould (1980:193) he mentions people of the Western Desert
"breaking up or pounding carcasses in order to obtain every last scrap of edible material" so they were
probably getting at the bone marrow as well. However, many years ago I brain tanned a Kangaroo skin using
Kangaroo brain and I vaguely remember that the brain was not very large (smaller than a closed fist). The
energy return from fat is around 38kJ/g, and carbohydrate and protein both return around 17kJ/g. Even with
double the energy return from fat I'm not convinced that there is enough fat on these animals to compensate
for the protein quantity. Perhaps someone has figures on total fat contents from animals (including brain and
marrow). As Barry points out they ate other fat resources e.g. insects.
However, it appears that all Aboriginal groups that I have investigated had a carbohydrate staple. This could
simply reflect the fact that animal resources were becoming scarcer in more recent times. Although, if one
believes that early people were mainly exploiting large animals with sufficient fat and the absence or low
levels of carbohydrate then perhaps gluconeogenesis was the norm for earlier people. It seems more likely to
me that they were exploiting some form of carbohydrate such as the S.latifolia as suggested by Melissa
14/23 (2000)
Cheers
Sean McBride
Gould, R.A. 1966 Notes on hunting, butchering and sharing among the Ngatatjara and their neighbours in the
Western Australian desert. Kroeber Anthropological Society Papers 36:41-63.
Gould, R.A. 1980 Living Archaeology. Cambridge University Press, Cambridge.
----------
PALEODIET Archives
Subject: Re: caloric requirements
From: Melissa Darby
Reply-To:
Melissa Darby
Date: Fri, 21 Jul 2000 18:11:01 -0700
Regarding calories expended and gained during foraging for Sagittaria latifolia.
I have calculated that the return on harvesting Sagittaria latifolia is 1 calorie expended for 18 gained.
The tubers float when one wades around in the soft mud and agitates its. This ability to float assists
waterfowl when they graze, and also assisted human populations when they gathered this plant in North
America. In October while treading in the silty mud in a S.latifolia patch in water just above my knees, 113
tubers were released from the substrate and floated to the surface within a thirty minute time period. Keely
has calculated that there are 3.6 calories per dry gram of wapato (Keely 1980). During this trial, I collected 1,
505 grams (fresh) of wapato. Since the dry weight of wapato is about half the weight of fresh tubers, there
was caloric net of 2, 709 calories of energy. My expenditure of calories I calculate was the same as riding a
bike at a moderate pace at about 300 calories an hour. Of course if the harvester has to break through ice to
harvest it, or harvest in deep cold water the cost effectiveness goes down.
Eating the tubers raw is ok, and there is ethnohistoic data that they were eaten raw though usually cooked;
but they not as tasty. I don't know if all the carbs are available uncooked.
I agree with you that we should be looking at plants such as these. Some plant foods require little processing;
stone tools are not associated with their use. I think we should be also looking at that old paradigm that stone
tools as indicators of the intensification of plant use, and amend it.
Thanks
Melissa Darby
Keely, Patrick Byron
1980 Nutrient Composition of Selected Important Plant Foods of the Pre-Contact Diet of the Northwest
Native American Peoples. M.S. Thesis, University of Washington, Nutritional Sciences and Textiles Dept.
Kubiak-Martens, L.
1996 Evidence for possible use of plant foods in Palaeolithic and Mesolithic diet from the site of Calowanie
in the central part of the Polish Plain. Vegetation History and Archaeobotany (1996) 5:33-38.
-----Original Message-----
PALEODIET Archives
Subject: Re: Kangaroo fat and protein poisoning
From: Loren Cordain
Reply-To:
Date: Sun, 6 Aug 2000 13:24:45 -0600
15/23 (2000)
I'd like to respond to Sean McBride's post of July 14th regarding kangaroo fat and the physiological protein
ceiling. Gould's (1) observation that a 97 lb (44 kg) kangaroo yielded only 4 ounces (114 g) of removable fat
would not give the true picture of the total carcass fat because it doesnt account for endogenous, nondissectable structural and storage fat. Additionally, fat given by weight rather than by energy for wild animal
carcasses is misleading because it doesn't adequately reveal the carcass protein/fat relationships. It is possible
to mathematically re-arrange the Pitts and Bullard regression (2) and solve for % body fat from body weight
rather than FFM such that (log % body fat = 0.357 + 0.177 x (log body wt (g); r =0.75; SEE = 0.27). So, a 44
kg kangaroo would be predicted to have 8.2% body fat by weight (360.8 g) if one were to homogenize the
entire carcass and chemically extract the total lipid mass. If one subtracts the amount of fat that Gould was
able to dissect (114 g) from the predicted total carcass fat (360.8 g), the remaining figure (246.8 g) represents
the predicted non-dissectable lipid. The endogenous non-dissectable lipid in the tissues of wild animals
averages 2.1 % by weight for muscle, 3.8 % for liver, 9.3% for brain, 51% for marrow and 82.3 % for
subcutaneous storage fat (3). Hence, the residual fat (~ 250 g) that Gould was not able to extract lies
primarily as structural lipid in muscle and other organs. Additionally storage triglyceride would be present in
marrow (it is unclear if Gould used marrow in his estimates). Using the 3rd order polynomials that we have
developed (4), it is possible to now examine the true energetic relationships between fat and protein in our 44
kg kangaroo in light of the physiologic protein ceiling. The total carcass food by energy would be 46% fat
and 54% protein. Since the maximal protein ceiling in humans averages about 35% of total energy (4), then
most of the kangaroo edible carcass could be consumed, providing the fat were divided evenly and that just a
small amount of carbohydrate from plant food were available. Fat can even be extracted from non-edible
portions (cancellous bone tissues) of the carcass by boiling them. Also, remember that the protein ceiling is
an absolute number (i.e. grams of protein, not % total calories) - consequently, high amounts of protein could
be eaten for a number of consequtive days, as long as either a fat or carbohydrate source were eventually
found to make up the caloric deficiency that was dictated by the excessive lean meat. Only when lean meat is
the sole available food source day after day will symptoms of protein toxicity emerge. Human's living at
northern latitudes preferentially hunted megafauna because these beasts contained both absolutely and
relatively more fat. Hence, at northern latitudes wherein carbohydrate (plant food) sources are seasonally
restricted, the fat obtained from larger mammals was sufficient to dilute the lean protein from muscle tissues.
The fossil record shows that the worldwide extinction of animals that took place at the end of the Pleistocene
occurred primarily in animals over 100 kg (220 lbs) (5). Using the Pitts and Bullard regression (2), a 220 lb
mammal would be expected to have about 15% body fat. Applying our cubic regressions (4) to this value, a
220 lb mammal would have 60 % of its total body energy as fat and 40% as protein. The protein value then is
very close to maximal protein ceiling (also 40 % of energy) -- hence it is not surprising that the "cutoff"
values for megafauna extinction (100 kg) corresponds almost exactly to the value for the maximal
physiological protein ceiling in humans. In animals weighing less than 100 kg, the entire carcass cannot be
consumed unless there is a carbohydrate source, whereas in animals weighing more than 100 kg, the entire
carcass can be eaten with no worry about protein toxicity and with no need to find a carbohydrate source.
REFERENCES 1. Gould RA. Notes on hunting, butchering and sharing among the Ngatatjara and their
neighbours in the Western Australian desert. Kroeber Anthropological Society Papers 1966;36:41-63. 2. Pitts
GC, Bullard TR. Some interspecific aspect of body composition in mammals. In: Body composition in
animals and man. Washington D.C.: National Academy of Sciences, 1968:45-70. (Publication 1598). 3.
Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African
hominids: evolutionary implications for human brain development. World Rev Nutr Diet, in press. 4.
Cordain L, Brand Miller J, Eaton SB, Mann N, Holt SHA, Speth JD. Plant-animal subsistence ratios and
macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr 2000;71:682-92.
1991;66:453-562.
PALEODIET Archives
Subject: Re: PALEODIET Digest - 22 Jul 2000 to 6 Aug 2000 (#2000-20)
From: s338048
Reply-To:
16/23 (2000)
Date: Mon, 7 Aug 2000 11:49:58 +1000

I'd like to thank Loren Cordain for clearing up this issue of the fat and protein content of Kangaroo. I for one
have been confused about the issue of whether it was weight or percentage of energy returned that was most
important.
Sean McBride
---------> From: Automatic digest processor To: Recipients of PALEODIET digests Subject: PALEODIET Digest
- 22 Jul 2000 to 6 Aug 2000 (#2000-20)
> Date: Monday, August 07, 2000 6:00 AM
> 1. Kangaroo fat and protein poisoning
>
>
---------------------------------------------------------------------> Date: Sun, 6 Aug 2000 13:24:45 -0600
> From: Loren Cordain Subject: Re: Kangaroo fat and protein poisoning
> I'd like to respond to Sean McBride's post of July 14th regarding kangaroo fat and the
> physiological protein ceiling. Gould's (1) observation that a 97 lb (44 kg) kangaroo yielded only
> 4 ounces (114 g) of removable fat would not give the true picture of the total carcass fat because
> it doesnt account for endogenous, non-dissectable structural and storage fat. Additionally, fat
> given by weight rather than by energy for wild animal carcasses is misleading because it doesn't
> adequately reveal the carcass protein/fat relationships.
> It is possible to mathematically re-arrange the Pitts and Bullard regression (2) and solve for %
> body fat from body weight rather than FFM such that (log % body fat = 0.357 + 0.177 x (log body wt
> (g); r =0.75; SEE = 0.27). So, a 44 kg kangaroo would be predicted to have 8.2% body fat by weight
> (360.8 g) if one were to homogenize the entire carcass and chemically extract the total lipid
> mass. If one subtracts the amount of fat that Gould was able to dissect (114 g) from the predicted
> total carcass fat (360.8 g), the remaining figure (246.8 g) represents the predicted
> non-dissectable lipid. The endogenous non-dissectable lipid in the tissues of wild animals
> averages 2.1 % by weight for muscle, 3.8 % for liver, 9.3% for brain, 51% for marrow and 82.3 %
> for subcutaneous storage fat (3). Hence, the residual fat (~ 250 g) that Gould was not able to
> extract lies primarily as structural lipid in muscle and other organs. Additionally storage
> triglyceride would be present in marrow (it is unclear if Gould used marrow in his estimates).
> Using the 3rd order polynomials that we have developed (4), it is possible to now examine the true
> energetic relationships between fat and protein in our 44 kg kangaroo in light of the physiologic
> protein ceiling. The total carcass food by energy would be 46% fat and 54% protein. Since the
> maximal protein ceiling in humans averages about 35% of total energy (4), then most of the
> kangaroo edible carcass could be consumed, providing the fat were divided evenly and that just a
> small amount of carbohydrate from plant food were available. Fat can even be extracted from
> non-edible portions (cancellous bone tissues) of the carcass by boiling them. Also, remember that
> the protein ceiling is an absolute number (i.e. grams of protein, not % total calories) > consequently, high amounts of protein could be eaten for a number of consequtive days, as long as
> either a fat or carbohydrate source were eventually found to make up the caloric deficiency that
> was dictated by the excessive lean meat. Only when lean meat is the sole available food source day
> after day will symptoms of protein toxicity emerge.
> Human's living at northern latitudes preferentially hunted megafauna because these beasts
> contained both absolutely and relatively more fat. Hence, at northern latitudes wherein
> carbohydrate (plant food) sources are seasonally restricted, the fat obtained from larger mammals
> was sufficient to dilute the lean protein from muscle tissues. The fossil record shows that the
> worldwide extinction of animals that took place at the end of the Pleistocene occurred primarily
17/23 (2000)
> in animals over 100 kg (220 lbs) (5). Using the Pitts and Bullard regression (2), a 220 lb mammal
> would be expected to have about 15% body fat. Applying our cubic regressions (4) to this value, a
> 220 lb mammal would have 60 % of its total body energy as fat and 40% as protein. The protein
> value then is very close to maximal protein ceiling (also 40 % of energy) -- hence it is not
> surprising that the "cutoff" values for megafauna extinction (100 kg) corresponds almost exactly
> to the value for the maximal physiological protein ceiling in humans. In animals weighing less
> than 100 kg, the entire carcass cannot be consumed unless there is a carbohydrate source, whereas
> in animals weighing more than 100 kg, the entire carcass can be eaten with no worry about protein
> toxicity and with no need to find a carbohydrate source.
>
> REFERENCES
> 1. Gould RA. Notes on hunting, butchering and sharing among the
> Ngatatjara and their neighbours in the Western Australian desert. Kroeber
> Anthropological Society Papers 1966;36:41-63.
> 2. Pitts GC, Bullard TR. Some interspecific aspect of body composition
> in mammals. In: Body composition in animals and man. Washington D.C.:
> National Academy of Sciences, 1968:45-70. (Publication 1598).
> 3. Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy
> density of foods available to African hominids: evolutionary implications
> for human brain development. World Rev Nutr Diet, in press.
> 4. Cordain L, Brand Miller J, Eaton SB, Mann N, Holt SHA, Speth JD.
> Plant-animal subsistence ratios and macronutrient energy estimations in
> worldwide hunter-gatherer diets. Am J Clin Nutr 2000;71:682-92.
> 5. Stuart AJ. Mammalian extinctions in the late pleistocene of
> northern eurasia and north america. Biol Rev 1991;66:453-562.
>
> Loren Cordain, Ph.D., Professor
> Department of Health and Exercise Science
> Colorado State University
> Fort Collins, CO 80523
> tel: (970) 491-7436
> fax: (970) 491-0445
> email:
> http://www.colostate.edu/Colleges/CAHS/ess/cordain.htm
>
-----------------------------> End of PALEODIET Digest - 22 Jul 2000 to 6 Aug 2000 (#2000-20)
>
**************************************************************
PALEODIET Archives
Subject: Re: kangaroo fat and eskimo diet
From: s338048
Reply-To:
Date: Fri, 11 Aug 2000 18:14:19 +1000
In Loren Cordains extremely interesting most recent post he states:
"In animals weighing less than 100 kg, the entire carcass cannot be consumed unless there is a carbohydrate
source, whereas in animals weighing more than 100 kg, the entire carcass can be eaten with no worry about
protein toxicity and with no need to find a carbohydrate source."
18/23 (2000)
With regards the eskimo (last i heard they preferred eskimo to Inuit but I could be wrong), given that they
didn't need a carbohydrate source, to supply glucose for the brain and CNS I assume they would rely on
gluconeogenesis.I'm curious as to how easily the body can switch from fuel source to fuel source? If the
eskimo are using ketone bodies for energy how easily would they switch to say a diet that started to include
berries (e.g. in southwest Alaska). I believe a switch from a mixed diet to a meat diet "leads to asymptomatic
ketosis and ketonuria" which diminish as the body adapts to using the ketone bodies (Draper 1977:312).
Does anyone know if there is any effect going the other way?
It is interesting that there is a sucrase deficiency among some Eskimo leading to the inability to digest
sucrose in the intestine (Draper 1977:313). In the more tropical and temperate regions the diet would be
more varied and given our evolutionary desire for sweet things (especially fruit) people in these regions are
obviously able to digest sucrose.
Given that variety in the diet is often considered important by hunter-gatherers I guess my main question is
whether simply because people did not require a carbohydrate source when consuming 100kg+ animals
would they still have sought them out?. My feeling is that they would (especially fruits and honey for taste
and variety sake) but Lorens post does indicate that once the big animals became scarce greater carbohydrate
supplies (tubers, roots etc) would have been sought out if fruit and honey were not .
Sean McBride
Draper, H.H. 1977 The Aboriginal Eskimo diet in modern perspective. American anthropologist 79 (2):309316
PALEODIET Archives
Subject: Re: Corrections to Kangaroo fat
From: Loren Cordain
Reply-To:
Date: Thu, 17 Aug 2000 12:38:51 -0600
In my recent post regarding the total amount of body fat in a 44kg kangaroo, I erroneously reported the total
amount of body fat predicted by the Pitts and Bullard regression (1). A 44kg kangaroo with a predicted body
fat of 8.2% would have 3608 g of total fat, not 360.8 g. Hence, the difference between the total predicted fat
and the amount actually dissected would be (3608 g -113 g) 3, 495 g. This figure represents the nondissectable fat that is bound in cell membranes in various organs and tissues. However, it is unlikely that a 44
kg kangaroo with only 113 g of dissectable fat would have this much non-dissectable structural fat bound to
tissues and organs. Hence, the Pitts and Bullard equation almost certainly overestimates the total amount of
body fat in this kangaroo. Total body fat can also be estimated by knowing the various weights of the major
tissues and their relative fat percent and then summing these values. Here's a table of estimated values for
this 44 lb kangaroo:
Tissue % carcass wt. Organ wt. (g) %fat total fat (g) muscle 0.50 22, 000 0.02 440 bones 0.13 5720 .03 172
liver, organs 0.075 3300 0.04 132 washed GI tract 0.06 2640 0.02 53 blood 0.012 526 0.02 11 marrow 0.004
176 0.51 90 brain 0.0014 62 .093 6 skin 0.13 5720 0.10 572 storage fat 0.0026 114 0.82 94 GI contents, hair,
nails etc 0.085 3740 na na Total 1.00 44000 na 1568
Consequently, in all likelihood this particular 44 kg kangaroo would have a total body fat content of about
3.6% by weight if total carcass analysis were done via chemical extraction. With 3.6 % body fat, our 3rd
order polynomial equations (2)show that an animal with 3.6% body fat by weight would have 27% fat by
energy and 73 % protein by energy. Note that traditional Aborigines would have singed the hair from the
hide and eaten the skin, a rich source of fat. Even still, the protein content of this lean kangaroo would have
caused protein toxicity, if a carbohydrate (plant food source) were not available to dilute (in effect) the
excessive protein in this animal's body.
PALEODIET Archives
Subject: Paleo infant feeding
From: Andre' Briend
19/23 (2000)
Reply-To:
Date: Tue, 29 Aug 2000 09:56:46 +0200
Dear all,
First a few words to introduce myself.
I am a MD (Paris) with a PhD in nutrition, working for the last 20 years + on problems of infant and child
feeding in developing countries. I am now involved in the development of foods for treatment / prevention of
child malnutrition.
I became interested in paleo diet after reading several papers on the subject (discussing mainly its
implications on prevention of chronic diseases related to affluence in adults) which also led me to question
the "traditional" approach to feeding children. It is widely believed that children aged 4 to 6 months should
receive in addition to breast milk (or to whatever is used as a milk substitute) a porridge, which is usually
prepared by boiling cereal flour with some animal milk. Yet, cereals, animal milk, and utensil to boil them
are recent in human evolution. I never heard of any animal preparing porridge for feeding the young.
I never liked the idea of feeding children with porridges. Bacteria easily contaminate porridges if not
consumed just after cooking. Porridges have a low energy density. They have a high phytate content. If milk
is not added, they are grossly lacking key nutrients (Ca, Mg, Zn, Fe...). Even if milk is added, they do not
contain enough absorbable iron to prevent anaemia, one of the leading problems in child nutrition throughout
the world.
In poor countries, efforts have been made to prepared low cost weaning food, (or complementary food, to be
politically correct and avoid confusion with cessation of breast feeding) which are cheap copies of the
western "milk with cereal" infant foods. Results are disappointing.
I suspect paleo diet thinking could help to generate new thinking for child nutrition in developing countries.
The idea would not be to ask people to move back to the forest and hunt wild animals, but to provide a target
for designing complementary foods. This might be more adapted than present attempts to copy western
infant foods.
As a newcomer to this mailing list, I am surprised to find hardly any reference to problems of infant child
feeding in the archives of the forum. Is this debated elsewhere? Or did I miss some important reference or
book on the subject, which would illuminate me? (I do not know how to search through the anthropological
litterature).
Anybody interested in sharing ideas on this topic?
Andr
Andr Briend, MD, PhD tel : 33-1-53 01 80 36 CNAM - ISTNA fax : 33-1-53 01 80 05 5 rue du Vertbois,
75003 Paris, France
PALEODIET Archives
Reply-To:
Date: Tue, 29 Aug 2000 18:28:57 EDT
Andre',
Some thoughts on Paleo infants and food. These are generated from my experience as a mother and my
perceptions, as well as a look at early Christian human feces from the Sudan.
First, my daughter was breast fed for 2 years. For the first ear she had almost no other food because she
would not eat anything else. I did not buy canned baby food, but rather just ground up what we ate. We never
did try porridge or cereals. Fruits were good and some vegetables were OK. Finely ground meat was also
pretty good. As she ate more after her first year she ate more of the same types of things, never eating
"traditional" baby foods. I would not be surprised if Paleo mothers fed their infants pre-chewed foods that
they were eating. Therefore, the foods would vary with geography. I just can't imagine that any other special
preparations were made. Mothers probably watched what their babies and young children liked and ate well
and tried to give them more of what worked.
20/23 (2000)
My look at human feces from a population of early Christians living along the Nile River about 1400 years
ago indicates that the infants and small children ate what the adults ate. This is not really ancient, but at least
is not a modern population. As for age at weaning, look at physical anthropology studies. There is a lot of
mortality at the transition from breast feeding to eating adult foods in the prehistoric and historic records.
Presumably largely from weanling diarrhea. Perhaps something could be added to the diet to get the proper
bacteria into the system, such as yoghourt.
I would say look to the diet of the adults and ask what is nutritious, what lends itself to a bit of processing,
and what can be done to transition the digestive tract into working well with these foods, and experiment
from there. I believe that weaning probably did not occur until 2 years of age or more for many groups, so
there might be opportunity to encourage going back to this practice and making certain that mothers have
adequate diets to sustain quality nursing for 2 years.
Hope some of these thoughts help. Perhaps many are things that you have already tried.
Regards, Linda Scott Cummings, Ph.D. Paleo Research 15485 W. 44th Ave. Golden, CO 80403 USA (303)
277-9848
PALEODIET Archives
Subject: Re: Paleo Infant feeding
Reply-To:
Date: Wed, 30 Aug 2000 15:02:00 +0100
On Tue, 29 Aug 2000, Andre' Briend wrote:
> As a newcomer to this mailing list, I am surprised to find hardly any reference to problems of
> infant child feeding in the archives of the forum. Is this debated elsewhere? Or did I miss some
> important reference or book on the subject, which would illuminate me? (I do not know how to
> search through the anthropological litterature). Anybody interested in sharing ideas on this topic?
The first book to read is
Breastfeeding: biocultural perspectives (ed. P. Stuart-Macadam and K. A. Dettwyler), Aldine de Gruyter.
1995.
which includes chapters on breastfeeding in prehistory and a comparative study of primate weaning ages.
There is one study comparing prehistoric agriculturalists and hunter-gatherers (1) which showed that there
was no difference in the age of weaning, contrary to the hypothesis that the introduction of gruels enabled
earlier weaning and therefore contributed to increased birth rates in agriculturalist societies. But this is the
only prehistoric hunter-gatherer population on which we have data on the age of weaning. Our techniques for
determining age of weaning are still not good enough to say very much about the actual ages (2). Bearing
this in mind, the present data suggest that hunter-gatherer weaning occurred at similar ages to agriculturalist
weaning. Ethnographic evidence (summarised in the book cited above) suggests that babies were fed with
pre-chewed adult food.
Andrew
(1) Fogel M. L., Tuross N., Johnson B. J. and Miller G. (1997) Biogeochemical record of ancient humans.
Org. Geochem. 27, 275-287.
(2) Millard AR (in press, 2000) A model for the effect of weaning on nitrogen isotope ratios in humans, pp.
51-59 in Goodfriend GA, Collins MJ, Fogel ML, Macko SA, & Wehmiller JF (eds) Perspectives on aminoacid and protein geochemistry. New York, Oxford University Press.
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Paleo infant feeding
Reply-To:
21/23 (2000)
Date: Thu, 31 Aug 2000 07:29:13 +1000

Dear Andre,
I have an interest in the subject because the young infant's dependence on exogenous Fe is very high. It
provides another argument to support the hypothesis that meat must have played an important role in
paleolithic diets. There must have been more than enough meat if even infants got to share the spoils.
It has always struck me as odd that cereals are recommended as the infant's first food (apart from human
milk), yet they need to iron fortified to make them suitable. Whenever I bring up this topic of discussion with
my colleagues, I get the argument that meat is scarce in developing countries and not environmentally sound.
Organ meat and the flesh of newly killed animals would have been virtually sterile and an almost complete
source of nutrients. Even vitamin C would have come from liver and muscle. I am not sure about calcium
intake - is bone marrow a good source of calcium or not?
Cheers Jennie
Jennie Brand-Miller PhD Associate Professor in Human Nutrition Department of Biochemistry G08
University of Sydney NSW 2006 Australia Phone: (61 2) 9351 3759 Fax: (61 2) 9351 6022 Website:
http://www.biochem.usyd.edu.au/staff/brandmiller/index.html
PALEODIET Archives
Subject: Paleo Infant Food
From: Ray Audette
Reply-To:
Date: Wed, 30 Aug 2000 16:01:02 -0500
VilhjalmurStefansson talks of the feeding of Inuit infants and children in several of his books. Their
traditional children's food was fish-head soup. The heads of Arctic fish have large fat deposits so this food is
very caloriticly dense. My own son Gray-Hawk (now 5) weaned himself after his first year and would eat
almost nothing but pemmican for about a year after that.
New cheaper sources of animal fat and protein would have to be found to make such foods available to third
world children. New methods of vacuum harvesting of termite mounds may make this possible. It has been
estimated that there are about 900 lbs. (400 Kilos) of termites for every human on earth.
Ray Audette Author "NeanderThin" http://www.neanderthin.com
PALEODIET Archives
From: Andre' Briend
Reply-To:
Date: Fri, 1 Sep 2000 10:22:30 +0200
Dear Jenny,
Thanks for your comments to my post.
I agree with you that it does not make sense to recommend cereals as first complementary infant food, since
it has a high phytate content which prevents absorption of non heme iron. Babies unfortunately do not have
in their gut the phytase needed to eat a high cereal diet. This is in contrast with the rat who apparently is
more adapted than us to cereals (1) . This may explain the very high prevalence of anaemia in children world
wide in most societies, with the only exception of those using iron fortified infant cereals and infant milk
formulas.
No doubts, meat would make more sense as first infant food. Unfortunately, it is indeed usually quite
expensive in developing countries.
Caclium of course is in low in meat, but we are talking about children receiving breast milk and receiving
their calcium supply from their mother. In non milk eating society, the mother, as other adults, usually gets
its calcium from leaves and from animal bones. I do not know about the calcium content of bone marrow. I
guess it must be low in calcium but quite high in iron.
22/23 (2000)
1- Iqbal TH, Lewis KO, Cooper BT. Phytase activity in the human and rat small intestine. Gut. 1994
Sep;35(9):1233-6.
Best regards,
Andr
Andr Briend, MD, PhD tel : 33-1-53 01 80 36 CNAM - ISTNA fax : 33-1-53 01 80 05 5 rue du Vertbois,
75003 Paris, France
23/23 (2000)
PALEODIET Archives
Subject: changes in human height
From: Ed Jacobson
Reply-To:
Date: Mon, 10 Sep 2001 17:10:30 -0500
As I understand, pre-agricultural man was taller than modern man. I understand that the transition to
agriculture is largely responsible for this, with the three important factors being: 1) the mineral blocking
effects of the phytates in grains; 2) the decrease in animal protein and bone building vitamins A and D that
are found in animal fats; and 3) decrease in calories consumed per person as the population grew (including
periodic famine due to lack of reliable harvests). In the last 100 years, at least in Western societies, we have
recovered much of that height. Why? 1) Are we eating more or less animal protein than 100 years ago? Mary
Enig and Sally Fallon assert that we are eating LESS animal FATS; is the opposite true for animal protein,
i.e., are we eati ng more lean beef and chicken and cooking less and less with butter and lard? 2) Is the
increase in height due to the refinement of our grains, which strips them of their phytate content? If so, what
does this say about recommendations that we eat more whole grain products? 3) Is the increase in height due
to the hormones injected into animals, as many vegetarians have suggested? Is there evidence that these
hormones are present in sufficient amounts in store bought meat to have a physiological effect? Do these
hormones survive the digestion process? My understanding was that hormones are proteins, and like most
proteins, they are broken down into their constituent amino acids during the digestion process. How then can
they have an effect on humans? Do they slip through the gut wall? Aren't these "leaks" in the gut wall due to
ingestion of whole grains? Is it not true that these hormones would h ave to be COMPLETELY undigested,
i.e., if part of their structure had been cleaved off, they would not bind to the receptor site? 4) In "African
Exodus", Chris Stringer and Robin McKie state that human height has decreased steadily over the last 10,
000 years. In places where agriculture was adopted, there was a dramatic drop off, but in other places, there
was still a dropoff, albeit a more gradual one. For example, the average height of Australian Aboriginee
males has decreased from 5'10" to 5'6" in the last 10, 000 years, despite lack of contact with agriculture. Is
this due to the change in lifestyle and eating patterns that has occurred in the last 10, 000 years due to the last
Pleistoceine extinction? Could there have been a dropoff in animal foods and a decline in calories in general
in the last 10, 000 years amongst hunter-gatherers that accounts for this decline in stature and robust icity? In
Nutrition and Physical Degeneration, Weston Price states that for those aborigines living in the areas of the
most abundant animal foods, particularly sea foods, "their stature was large and well formed".
1/1 (2001)
PALEODIET Archives
Subject: High protein
From: Todd Moody
Reply-To:
Date: Fri, 2 Aug 2002 07:38:07 -0400
This list has been quiet. I have a question about the following assertion, "The coastal diet composition was
nearly all animal foods, mostly seafood with some birds and kangaroo, and was approximately 80% protein,
20% fat, and less than 5% carbohydrate." It is based on the following research: O'Dea K (1984) "Marked
improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary
reversion to traditional lifestyle." Diabetes, vol. 33, no. 6 (Jun.), pp. 596-603.
What surprises me is the claim that the diet of the coastal aborigines is 80% protein. I've never heard of a diet
this high in protein, and had the idea that it could not be tolerated. Comments?
Todd Moody
PALEODIET Archives
Subject: Re: PALEODIET Digest - 11 Sep 2001 to 8 Aug 2002 (#2002-1)
From: "Balzer, Ben"
Reply-To:
Date: Tue, 20 Aug 2002 16:17:09 +1000
Todd, I have heard that the dietary protein ceiling is due to the limit on the body's ability to produce urea. I
think the estimates may be flawed because muscle meat and organ meats behave differently. eg Liver
contains high levels of many vitamins which may be needed to metabolise protein. I would hypothesise that
the protein ceiling is higher on organ meat-rich diets than on muscle meat diets, and would like to discuss
this on the list. I would like to know any evidence that feeding trials to determine the upper limit of protein
considered the relevance of organ meats.
I also hypothesise that O'Dea's estimates may be correct if the Aboriginal diets were rich in organ meatswhich other data suggest they are.
While I can accept that there is a metabolic ceiling on urea production, there are other important constraints
on the utilisation of meat as a food. Let us consider 2 true carnivores- lions and dogs.
Lions and dogs cannot live on steak (muscle meat) alone.
Weston Price (N+PD) reports that lions could not breed in captivity when fed on steak alone. In the early
1900's Lions used to cost $4000. When it was realised that in the wild, the liver is the first thing they eat,
liver was added with excellent results, such that they bred easily and they cost a mere $40.
Crawford and Marsh (Nutrition and Evolution) report lions in Africa fed on steak alone suddenly becoming
cripples due to spinal collapse from osteomalacia due to high Po4/Ca ratio. The solution then was meaty
bones such as ribs that the lions could crush (unable to crush the larger bones). Thus they reinvented Price's
wheel to some degree (I know for sure that Marsh has read Price and I presume Crawford has too).
Ina Billinghurst (Give Your Dog a Bone (A Paleo Diet for dogs) www.drianbillinghurst.com) reports dogs
cannot thrive on steak but do extremely well on a diet of steak, organ meats and raw meaty bones.
On an empirical basis, organ meats become essential for high protein diets for carnivores. Thus, if dogs and
lions cannot live on steak alone, how would one expect an omnivore to do well on it? Thus, I think that all
high protein diets for humans probably need the addition of organ meats.
Why should this be so? There are several obvious reasons, but I prefer to simplistically stick to the empirical
evidence. I think that Weston Price presented buckets of good empirical evidence and in a way it's a shame
that we have had to wait until we have evidence at the molecular level to prove that he was right. The
empirical animal evidence is also important.
Liver is a storage depot for vitamins and minerals, and this is probably crucial. These may provide necessary
co-factors for the digestion of protein, production of urea etc. It is a good source of essential fatty acids
omega 3 and 6. It is an excellent source of many biochemical including glutathione lipoic acid biotin etc etc.
1/14 (2002)
"Standard" high protein diets eg Atkins, Scarsdale do not have a formal source of vitamin A or sufficient
omega 3 fats, unless one stumbles onto fish (omega 3 and 6), pink fish (vitamin A). They also have a low
calcium/phosphorus ratio unless one consumes small bones, or eats marrow. Salmon and some other foods
are high in calcium. Fruit and vegetables also supply calcium. Acid load is high in these diets but again is
ameliorated by fruit and vegetables, and also by most mineral waters (bicarbonate content varies greatly- eg
Evian is quite high and will neutralise quite a lot of acid).
Thus, I believe most high protein diets are not viable unless one includes organ meats, including liver, and
preferably marrow too.
Ben Balzer
PALEODIET Archives
From: Alexis Willett
Reply-To:
Date: Wed, 28 Aug 2002 15:41:18 +0100
Dear All,
As regards the discussion on the effects of high protein diets, I would just like to draw your attention to the
current debate on the online version of the British Medical Journal at the following address:
http://bmj.com/cgi/content/full/325/7361/408/d
The pro's and con's of high protein diets and their physiological implications are being wrangled by
researchers and physicians alike.
Alexis Willett.
Nutrition and Bone Health Research MRC Human Nutrition Research Elsie Widdowson Laboratory
Fulbourn Road Cambridge CB1 9LR Telephone: 01223 426356
PALEODIET Archives
From: Edward Thompson
Reply-To:
Date: Wed, 28 Aug 2002 17:28:20 -0500
Response to 28 Aug 2002 post regarding current debate over high protein diets:
With regard to the renal acid load (along with the corresponding increase in urinary calcium excretion) that
has been oberved in trials investigating high protein diets, a pivotal confounding variable (potassium intake)
has been postulated to explain most of the variance in outcome (ie. a high potassium intake reduces proteininduced renal net acid excretion). Source:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
cmd=Retrieve&db=PubMed&list_uids=9734733&dopt=Abstract
Under an a priori assumption of the validity of the simple, modifiable, nutritional r elationship outlined in the
article above (between potassium, protein, and renal net acid excretion), this "revelation" would be in
accordance with an evolutionary hypothesis of optimal human nutrition because paleolithic-type diets were
thought to provide approximately 2-4 times as much potassium as modern "Western-type" diets now provide.
Using the equation identified by the investigators in the link above, it may be reasonable to attempt to
modify the ratio of 'potassium-to-protein' in order to meet, or exceed, about 40 mg dietary potassium for
every gram of protein ingested. If this relationship between dietary potassium, protein, and renal net acid
excretion holds for the majority of the population, then this simple modification has the potential to reverse
most of the negative, physiology-based concerns regarding high protein diets (most of which concern renal
dynamics).
2/14 (2002)
Other con cerns (e.g. the fatty acid profile of the protein foods consumed) would not necessarily be
addressed by this simple nutritional algorithm, however, so it would not necessarily provide individuals a
"free pass" to consume as much protein as is desired. If the current debate on high protein diets is to be
productive, then the relationship between dietary potassium, protein, and renal net acid excretion must be
included in future discussions. Further investigation of this relation is also warranted, in order to unveil the
renal dynamics associated with high protein diets and to stratify the potential effects in the population at
large, including those with altered renal function (ie. renal diseases).
Ed Thompson
PALEODIET Archives
Subject: Reply to B Balzer - Re: Organ meats & the physiologic protein ceiling
Reply-To:
Date: Wed, 28 Aug 2002 21:58:27 -0500
Ben,
I am interested in your proposed concept regarding organ meats and the dietary protein ceiling. It is my
understanding that urea formation is the limiting physiological factor (as you had mentioned earlier). If urea
formation was at its maximum, additional protein channeling into catabolic pathways would theoretically
yield an increase in ammonia production (neurotoxic). It is also my understanding that the only way to
curtail urea formation, at least in a physiological sense, is to curtail net protein catabolism. This would
require a close match between dietary protein intake and anabolism/maintenance of tissue proteins (protein
deposition into tissues, such as muscle mass, or even as an increase/maintenance of metabolic enzymes).
If, however, organ meats were substituted for "muscle meats", how might this "ceiling" be raised? Are you
proposing that there might be a mechanism for:
-increased hepatic capacity for urea formation?
-decreased ammonia toxicity (due to body compartment channeling or improved ammonia
metabolism/excretion)?
-increased anabolism (increased protein accretion at the tissue/enzyme level)?
These 3 mechanisms seem to be the only ones that are plausible. However, I would not presume to preclude
the fact that you may indeed have a fourth mechanism in mind. The arguments that I've seen in journal
articles imply that fat intake must be high enough to limit protein intake to about 35-40% or less of total
energy intake (or suffer the metabolic consequences of an ammonia burden). They have n ot forwarded a
specific argument (beyond increasing the contribution of fat to the protein in found in meats) for organ
meats. Would you please elaborate on a mechanism for an "organ meat- induced" increase in dietary protein
tolerance?
Ed Thompson
PALEODIET Archives
From: "Balzer, Ben"
Reply-To:
Date: Thu, 29 Aug 2002 07:31:21 +1000
This is exactly the point of my previous post- that high protein diets are usually poorly designed. My reading
of the Atkins diet is that any source of omega 3 fats, vitamin A or B-vitamins is purely accidental (leaving
out the "Atkins vitamin supplements"). No attempt is made to mitigate the potential renal acid load. Thus
these (Atkins style) diets are preordained to failure. If they would kill a brown dog, we cannot recommend
them for humans. I believe that high protein diets are viable but need to follow the rules of wild carnivoresi.e. to include organ meats and meaty bones as sources of omega 3 vitamin A B-vitamins and calcium.
3/14 (2002)
Acid load can be ameliorated by inclusion of fruit and vegetables (discouraged on Atkins diet) or by the
inclusion of high bicarbonate mineral waters (e.g. Evian is very high in bicarbonate). Natural river waters are
also high in bicarbonate- about 1/4 of Evian's level). Discussion of the acid load of natural waters is an
important issue which I would like to take up on this list and also at acidbasebone nutrition group To
subscribe click mailto:
Ben Balzer
http://bmj.com/cgi/content/full/325/7361/408/d
The pro's and con's of high protein diets and their physiological implications are being wrangled by
researchers and physicians alike.
Alexis Willett.
PALEODIET Archives
Subject: High protein diets
From: Tamsin O'Connell
Reply-To:
Date: Thu, 29 Aug 2002 15:35:29 +0100
Dear all,
I have two lines of contribution to the discussion on high protein diets, in which I have tried to summarize
what is in some of the literature.
Firstly, from a metabolic point of view, is there a maximum limit on protein intake by the body? If one
considers the physiological outcome of eating protein, Ben Balzer is right in that it is the body's rate of
production of urea that is the primary limiting factor. Excess intake of nitrogen leads in a short space of time
to hyperammonaeia, which is a build up of ammonia in the bloodstream, and this is toxic to the brain. To
avoid ammonia build-up, nitrogen must be excreted as urea in mammals, and urea is produced in the liver.
Urea production requires oxygen, in a ratio of one mole of oxygen to one mole of amino acid nitrogen.
Estimates of oxygen consumption by the human liver are somewhat lacking, but extrapolating from in vitro
and animal studies, the liver of a 73kg man would use between 2 and 5 moles of oxygen per day. So if the
liver did nothing else but produce urea, a 73 kg man could process 2 to 5 moles of amino acid nitrogen a day,
which is 28 to 70g of N which is equivalent to 175 to 438 g of protein a day (figures from McGilvery, 1983,
p791). This is if the liver ONLY produced urea. But as it has other important functions, these values can be
considered as extreme upper limits, and a more realistic limit would be half this. Incidentally 175 to 438 g of
protein a day for the mythical 73kg man equates to 2.3 to 6 g/kg body weight/day, which compares to typical
UK intake of 1.2 g/kg body weight/day. An intake of 175 to 438 g of animal protein a day would generate
3.1 to 7.9MJ of energy.
4/14 (2002)
Now turning to whole organism studies, be they lions, dogs or humans. I would suggest that when most
people think of an animal eating a carnivorous diet, they tend to think of it as being a protein-based one. This
is false. A carnivorous diet is more fat than protein, and with little or no carbohydrate. I consider that this is
why lions fare better on a diet high in organ meats than one with lots of steak: it is not the prevalence of
vitamins, minerals, essential fatty acids etc in organ meats that makes them a better source of food but fat in
general. There is much anecdotal evidence in the literature that humans can survive on a purely animal
product diet, but only if it is high in fat. Speth et al (Speth & Spielmann 1983; Speth 1987) discuss this, as do
Noli & Avery (1988). The general pattern appears to be that a lean meat diet leads to nausea in 3 days,
symptoms of starvation and ketosis in 7-10 days, severe debilitation in 12 days and possibly death in weeks.
Perhaps one of the best documented study is that of the Arctic explorer, Vilhjamur Stefannson and some
contemporaries (see McClelland et al 1930-31). They ate an animal meat diet for more than a year to see
whether such a diet could be healthy. Everything was fine until they were asked to eat only lean meat.
McClelland wrote: 'At our request he began eating lean meat only, although he had previously noted, in the
North, that very lean meat sometimes produced digestive disturbances. On the third day nausea and diarrhea
developed. When fat meat was added to the diet, a full recovery was made in two days. This disturbance was
followed by a period of persistent constipation lasting 10 days. The subject had a craving for calf brain, of
which he ate freely. (Calf brain is 9g of lipid and 11g of protein per 100g.) On March 12, poor appetite,
nausea, and abdominal discomfort were present and a second milder attack of diarrhea occurred which
responded quickly to a proper proportionment of lean and fat meat.' When one looks in the literature at
typical modern diet compositions from 'western' populations to hunter-gatherers, most derive 12 to 25% of
their energy from protein, and the maximum (Canadian and Greenland Eskimos) is 45% (see Ulijaszek &
Strickland, 1993, table 3.8), again suggesting that the optimum 'carnivorous' diet has to be higher in energy
(fat/carbohydrate) than in protein.
I would also argue is that when discussing high protein diets, one must be careful to clarify whether it is a
high absolute consumption of meat (limited by urea production probably to an absolute max of 6g/kg body
weight/day) or high proportion of protein relative to carbohydrate and lipid (limited to probably about 40%
max of calorific intake). Otherwise one can get into a tangle. It is particularly noticeable when reading about
modern 'fad' diets that are presented as 'high-protein' that it is rarely indicated whether the diet means
consumption of large quantities of protein or a lot of protein relative to other macro-nutrients.
Hope some of this is useful,
Tamsin O'Connell
Refs
McClelland et al (1930-1931) 'Clinical Calorimetry: XLV, XLVI, XLVII. Prolonged Meat Diets......'
J.Biol.Chem. 87:651, 87:669, 93:419 McGilvery, (1983) A Functional Approach to Biochemistry, 3rd
edition, p791. Noli & Avery, (1988) 'Protein poisoning and Coastal Subsistence' J.Archaeol.Sci. 15:395-401
Speth & Spielmann, (1983) 'Energy source, protein metabolism, and hunter-gatherer subsistence strategies'
J.Anthr. Archaeol. 2:1-31 Speth, (1987) 'Early Hominid Subsistence Strategies in Seasonal Habitats'
J.Archaeol.Sci. 14:13-29 Ulijaszek & Strickland, (1993) Nutritional Anthropology
----------------------------------Dr Tamsin O'Connell Research Laboratory for Archaeology University of Oxford 6 Keble Road, Oxford,
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
Subject: Re: O'dea K 1984 report on aboriginal protein intake
Reply-To:
Date: Thu, 29 Aug 2002 16:16:56 -0500
Short reply: It seems that the figure posted for protein intake of this aboriginal group (80% of dietary energy
coming from protein) is an overestimate.
Long reply: After viewing the abstract (originally mentioned by Todd Moody) regarding protein intake, it
appears that concerns over the macronutrient profile being incompatible with human metabolism seem
premature. The abstract- (copy & paste the following):
5/14 (2002)
-mentions that 64% of the total energy intake was provided by "animal food" (which itself may be up to 80%
protein and 20% fat), bu t this leaves 36% of the energy in the diet provided by plant foods, which would
bring the relative contribution of energy from protein down, perhaps to a level that is metabolically
manageable (but still high at around 60%!).
Another confounder, however, is the reported value for total energy intake, which was only 1200
kcal/person/day. At 1200 kcal and 60% protein, only 180 grams (720 kcal) of protein would be consumed,
which is well within estimates (for a mean body wt of about 80 kg, reported by O'Dea) of the physiologic
protein ceiling which has been worked out by Cordain et al (Am J Clin Nutr 2000 Mar;71(3):682-92) to be
around 3+ g/kg bdy wt).
Ed Thompson
PALEODIET Archives
From: Todd Caldecott
Reply-To:
Date: Sun, 1 Sep 2002 10:26:22 -0600
Hi all,
this appears to be a very quiet list, so its nice to see a little action.
i wonder to what extent concurrent vegetable consumption limits the production of urea and nitrogenous
wastes, or acts in other ways to mediate the effect of a high protein diet. it seems to me that with the
burgeoning popularity of the paleolithic diet, or in diets that share similar principles, i.e. Atkins etc, there is
an undue emphasis upon animal protein. For e.g. I know that the coastal first nations people of british
columbia (salish, haida, tlingit etc.) consumed an enormous diversity of vegetation, much greater that what is
typically consumed today in NA, along with a high protein, high fat diet. It seems to me that if we want a
more complete analysis of the problem we need to look at a lot more than just the major macronutrients. For
some reason the vegetables always get left out of the equation, despite the admonitions of mothers all over
the world.
Personally, my interest is in the clinical usage of paleolithic diet, and i have consistently seen a need for high
(non-starchy) vegetable consumption in high protein diets in most individuals. In most of the literature in
natural medicine this is phrased in terms of acid vs. alkaline, and we have found that a higher ratio of
vegetation to protein seems to prevent some the problems associated with the acidic effects of a high
protein/low CHO diet and can be therapeutic (e.g. gout). And, as I am also a clinical herbalist, I utilize a
wide variety of medicinal plants that contain an incredible diversity of constituents that can have a variety of
activities on metabolic function, for e.g. enhancing liver detoxification, hepatoprotection etc. Many of these
herbs of course were certainly harnessed by our paleolithic forebears. Now I haven't seen any studies that
have looked at the ornithine cycle and the effect of certain vegetables or herbs specifically, but i think it
might be worthy of investigating.
> Ben,
> I am interested in your proposed concept regarding organ meats and the dietary protein ceiling. It
> is my understanding that urea formation is the limiting physiological factor (as you had mentioned
> earlier). If urea formation was at its maximum, additional protein channeling into catabolic
> pathways would theoretically yield an increase in ammonia production (neurotoxic). It is also my
> understanding that the only way to curtail urea formation, at least in a physiological sense, is
> to curtail net protein catabolism. This would require a close match between dietary protein intake
> and anabolism/maintenance of tissue proteins (protein deposition into tissues, such as muscle
> mass, or even as an increase/maintenance of metabolic enzymes). If, however, organ meats were
> substituted for "muscle meats", how might this "ceiling" be raised? Are you proposing that there
> might be a mechanism for: -increased hepatic capacity for urea formation? -decreased ammonia
> toxicity (due to body compartment channeling or improved ammonia metabolism/excretion)?
> increased anabolism (increased protein accretion at the tissue/enzyme level)?
> I would also argue is that when discussing high protein diets, one must be careful to clarify
> whether it is a high absolute consumption of meat (limited by urea production probably to an
6/14 (2002)
> absolute max of 6g/kg body weight/day) or high proportion of protein relative to carbohydrate and
> lipid (limited to probably about 40% max of calorific intake). Otherwise one can get into a
> tangle. It is particularly noticeable when reading about modern 'fad' diets that are presented as
> 'high-protein' that it is rarely indicated whether the diet means consumption of large quantities
> of protein or a lot of protein relative to other macro-nutrients.
> **************************************************************
Todd Caldecott www.wrc.net/phyto/phyto.html
PALEODIET Archives
From: "Balzer, Ben"
Reply-To:
Date: Tue, 3 Sep 2002 22:52:27 +1000
Ed, I am proposing that organ meats can increase the hepatic capacity for urea formation- by the provision of
vitamin and mineral co-factors for the production of urea. (This is analogous to the situation of the
metabolism of carbohydrates- it is sometimes mentioned that fruits contain sufficient thiamine to enable to
metabolism of their carbohydrate, whereas pure sucrose does not). It should be possible to test this
proposition with simple feeding trials. It really depends on which vitamins and minerals are required in
which quantities to metabolise protein. One then can look at their dietary sources. Liver, for example plays a
major metabolic role as a store for vitamins and minerals and so provides large quantities.
Perhaps they could increase ammonia excretion by providing co-factors for that process too.
I have demonstrated some critical differences below with USDA figures
http://www.nal.usda.gov/fnic/foodcomp/ for lamb liver and lamb leg- You will observe that liver has
significantly higher levels of Iron Phosphorus Copper, Manganese, Selenium, Vitamin C, total ascorbic acid
Thiamin Riboflavin Niacin Pantothenic acid Vitamin B-6 Folate, B12 and Vitamin A. Liver is often
mentioned as a source of other nutrients such as biotin, alpha lipoic acid, glutathione, and Co-Q10 (though I
do not know their bioavailablity).
I propose that some or all of these vitamins are required to metabolise dietary protein. This in turn explains
much of the reason why carnivores require organ meats in their diets. High protein diets of dogs and lions are
high in organ meats and thus would be high in the above vitamins. Traditional hunter gatherer diets may be
similarly high in organ meats(comments?)(NB organ meats were significant in ref 1).
I do not know if the PRAL (potential renal acid load) of organ meats differs from that of muscle meats. The
PRAL is determined by the metabolic fate of the food.
The other factors I mentioned (alkaline load from fruit vegetables and natural waters, essential fatty acids,
other vitamins not required for protein metabolism) would also contribute to the healthfulness of the diet.
Ben Balzer
> Are you proposing that there might be a mechanism for: -increased hepatic capacity for urea
> formation? -decreased ammonia toxicity (due to body compartment channeling or improved ammonia
> metabolism/excretion)?
> -increased anabolism (increased protein accretion at the tissue/enzyme level)? DATA lamb liver and
lamb leg- Note that this data does not specify whether it was grain fed or pasture fed (nor did beef liver,
which I would presume was grain fed in the USA). I am not aware of US lamb feeding practices.
References: 1. Cordain L, Brand Miller J, Boyd Eaton S, Mann N, Holt SHA, and Speth JD Plant-animal
subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets Am J Clin Nutr
2000;71:68292.
7/14 (2002)
USDA: Lamb, variety meats and by-products, liver, raw rawNDB No: 17199 Nutrient Units Value per100
grams ofedible portion SampleCount Std.Error Proximates Water g 71.37 17 0.201 Energy kcal 139 0
Energy kj 582 0 Protein g 20.38 1 Total lipid (fat) g 5.02 1 Ash g 1.44 1 Carbohydrate, by difference g 1.78
0 Fiber, total dietary g 0.0 0 Minerals Calcium, Ca mg 7 1 Iron, Fe mg 7.37 1 Magnesium, Mg mg 19 1
Phosphorus, P mg 364 1 Potassium, K mg 313 1 Sodium, Na mg 70 1 Zinc, Zn mg 4.66 8 0.375 Copper, Cu
mg 6.979 520 0.228 Manganese, Mn mg 0.184 13 0.028 Selenium, Se mcg 82.4 13 7.680 Vitamins Vitamin
C, total ascorbic acid mg 4.0 1 Thiamin mg 0.340 1 Riboflavin mg 3.630 1 Niacin mg 16.110 1 Pantothenic
acid mg 6.130 1 Vitamin B-6 mg 0.900 1 Folate, total mcg 230 4 19.068 Folic acid mcg 0 0 Folate, food mcg
230 4 19.068 Folate, DFE mcg_DFE 230 0 Vitamin B-12 mcg 90.05 19 5.464 Vitamin A, IU IU 24612 2
Retinol mcg 7391 2 Vitamin A, RAE mcg_RAE 7391 2 Lipids Fatty acids, total saturated g 1.940 0 14:0 g
0.050 21 16:0 g 0.680 21 18:0 g 1.120 21 Fatty acids, total monounsaturated g 1.050 0 16:1 undifferentiated
g 0.130 21 18:1 undifferentiated g 0.920 21 Fatty acids, total polyunsaturated g 0.750 0 18:2 undifferentiated
g 0.320 21 18:3 undifferentiated g 0.070 21 20:4 undifferentiated g 0.360 21 Cholesterol mg 371 4 43.495
Amino acids Tryptophan g 0.236 6 Threonine g 0.882 6 Isoleucine g 0.878 6 Leucine g 1.665 6 Lysine g
1.102 6 Methionine g 0.442 6 Cystine g 0.214 6 Phenylalanine g 0.910 6 Tyrosine g 0.727 6 Valine g 1.122 6
Arginine g 1.143 6 Histidine g 0.479 6 Alanine g 1.022 6 Aspartic acid g 1.758 6 Glutamic acid g 2.198 6
Glycine g 0.985 6 Proline g 0.974 6 Serine g 0.878 6 Lamb, domestic, leg, sirloin half, separable lean only,
trimmed to 1/4" fat, choice, rawNDB No: 17021 Nutrient Units Value per100 grams ofedible portion
SampleCount Std.Error Proximates Water g 73.57 32 0.470 Energy kcal 134 0 Energy kj 561 0 Protein g
20.55 32 0.328 Total lipid (fat) g 5.08 32 0.221 Ash g 1.07 32 0.011 Carbohydrate, by difference g 0.00 0
Fiber, total dietary g 0.0 0 Minerals Calcium, Ca mg 7 32 0.465 Iron, Fe mg 1.83 32 0.094 Magnesium, Mg
mg 27 32 1.196 Phosphorus, P mg 189 16 4.452 Potassium, K mg 284 32 14.399 Sodium, Na mg 64 32
2.551 Zinc, Zn mg 3.77 32 0.173 Copper, Cu mg 0.132 32 0.006 Manganese, Mn mg 0.024 0 Selenium, Se
mcg 23.4 0 Vitamins Vitamin C, total ascorbic acid mg 0.0 0 Thiamin mg 0.140 16 0.007 Riboflavin mg
0.250 16 0.015 Niacin mg 6.330 16 0.303 Pantothenic acid mg 0.740 16 0.017 Vitamin B-6 mg 0.170 0
Folate, total mcg 24 16 1.354 Folic acid mcg 0 0 Folate, food mcg 24 16 1.354 Folate, DFE mcg_DFE 24 0
Vitamin B-12 mcg 2.76 16 0.149 Vitamin A, IU IU 0 0 Retinol mcg 0 0 Vitamin A, RAE mcg_RAE 0 0
Vitamin E mg_ATE 0.240 0 Tocopherol, alpha mg 0.24 0 Lipids Fatty acids, total saturated g 1.820 0 10:0 g
0.010 373 12:0 g 0.010 373 14:0 g 0.130 373 16:0 g 0.990 373 18:0 g 0.600 373 Fatty acids, total
monounsaturated g 2.040 0 16:1 undifferentiated g 0.150 373 18:1 undifferentiated g 1.850 373 Fatty acids,
total polyunsaturated g 0.460 0 18:2 undifferentiated g 0.350 373 18:3 undifferentiated g 0.070 373 20:4
undifferentiated g 0.050 373 Cholesterol mg 66 16 1.602 Amino acids Tryptophan g 0.240 0 Threonine g
0.880 0 Isoleucine g 0.991 0 Leucine g 1.598 0 Lysine g 1.815 0 Methionine g 0.527 0 Cystine g 0.245 0
Phenylalanine g 0.837 0 Tyrosine g 0.691 0 Valine g 1.109 0 Arginine g 1.221 0 Histidine g 0.651 0 Alanine
g 1.236 0 Aspartic acid g 1.809 0 Glutamic acid g 2.982 0 Glycine g 1.004 0 Proline g 0.862 0 Serine g 0.764
0
PALEODIET Archives
Reply-To:
Date: Tue, 3 Sep 2002 22:57:01 -0500
Ben,
It appears that there is animal evidence in support of the concept of micronutrient-induced alterations in the
capacity for urea synthesis. Rates of urea synthesis have been observed to depend on, but may not be limited
to, vitamin A [1], biotin [2] and, in diseased-states, carnitine [3].
Interestingly, with regard to biotin and carnitine at least, effects are noted at the level of gene expression for
urea cycle enzymes. As vitamin A is quite active at the gene level, a change in gene expression (although not
reported in the study cited) may indeed explain its affects on urea synthesis, as well.
It would be insightful to measure the differential intake of these 3 regarding organ meats vs "muscle meats"
(and whether this "difference" would be predicted to significantly alter rates of urea synthesis in the
population at large).
Ed Thompson
8/14 (2002)
References: [1] John A, Sivakumar B. Effect of vitamin A deficiency on nitrogen balance and hepatic urea
cycle enzymes and intermediates in rats. J Nutr 1989 Jan;119(1):29-35
[2] Maeda Y, Kawata S, Inui Y, Fukuda K, Igura T, Matsuzawa Y. Biotin deficiency decreases ornithine
transcarbamylase activity and mRNA in rat liver. J Nutr 1996 Jan;126(1):61-6
[3] Horiuchi M, Kobayashi K, Tomomura M, Kuwajima M, Imamura Y, Koizumi T, Nikaido H, Hayakawa
J, Saheki T. Carnitine administration to juvenile visceral steatosis mice corrects the suppressed expression of
urea cycle enzymes by normalizing their transcription. J Biol Chem 1992 Mar 15;267
PALEODIET Archives
Subject: Reply to Ben Balzer - lions & dogs / protein ceiling
From: Roland Rohde
Reply-To:
Date: Fri, 6 Sep 2002 08:12:58 +0200
Ben,
the $4000 lion story is a nice one.
Anyway I would very strongly support the concept of liver as an essential nutrient for man, too. There surely
are many vitamins and trace elements contained in liver that make it a complement to meat (and milk in
babies). And there are continuously discovered new vitamin-like constituents, like the RXR-receptor
hormone phytanic acid [1, 2].
But there is one component that alone makes liver essential for man under paleolithic conditions: copper.
Before science was pushed onto the slippery greasy road, there has been much work on copper and
arteriosclerosis. You can look for Klevay, Leslie M, in medline and take his papers as a starting point. It
could be shown that copper deficiency leads to arteriosclerosis in many animals, because the copper
dependent integrity of the internal elastic lamina (IEL), a thin elastic layer that is separated by only one
endothelial cell layer from blood, is crucial for the development of intimal thickening. I can confirm this
notion completely from my own experiences. We are developing coronary stents. One unsolved problem
with these devices is the development of restenosis. In many experimental setups 80% of the restenosis is to
be explained by the way, the stent tortures the IEL. The IEL is a protein polymer, polymerized from
monomers that are secreted by the surrounding cells. But the polymerizing enzyme, lysyl oxidase (LOX),
contains copper and its production depends on copper supply [3]. Copper is needed for many biochemical
reactions, e.g. for the necessary jodide-oxidation in the thyroid gland (EC 1.11.1.8, think of the thyroxin
dependency of cholesterol metabolism!) and the iron utilization for heme-production. Milk produkts are free
of copper (and iron). So babies cannot thrive on milk if they have used up the maternal iron and copper
deposits in their liver, especially if already the mother was copper deficient. This is experimentally proven in
rodents [4]. Meat is copper deficient, too. Rodents become copper deficient if fed with meat as the sole
copper source. Safe copper intake is 1, 5-3 mg [5], but many western people have less than 1 mg a day. But
where does one get even this much from? Most foods are poor in copper. Only some invertebrates (possibly
because of their hemocyanine-copper containing blue blood) and some nuts (cocoa) contain enough of it, and
- liver. But where did our hand-ax throwing ancestors get their cocoa or shellfish from, living near the glacial
edge a million years ago? The only reliable copper source, at all times and at all places humans could
survive, was liver. Especially that of lambs and other ruminants. Do you remember that key scene in "Dances
with Wolves?" After a long period of famine the bisons came back and the first thing, the red man took out
of the first bison was the liver, offering it to the white man as a sign of esteem. There is at least one
multicenter study (FOODCUE) on its way to look for copper effects [6].
What the protein ceiling discussion concerns, it is quite usual for bodybuilders to eat 5g/KgBW protein
together with very low fat, e.g. 50% of calories. Look at the end of the table at
http://www.gunters.net/Diets/DietsFsetG.htm
Prot: 619, 8 g, 52% Carb: 412 g, 35% Fat: 69 g, 13%
kcal: 4823.
This is not unusual for a top body builder (m = 134 kg, essentially muscle
http://www.gunters.net/Diets/DiaryMrO2001G.htm).
But liver seems not a very typical foodstuff for body builders.
[1] McCarty M, The chlorophyll metabolite phytanic acid is a natural rexinoid--potential for treatment and
prevention of diabetes. Med Hypotheses 2001 Feb;56(2):217-9.
9/14 (2002)
[2] Heim M, Phytanic acid, a natural peroxisome proliferator-activated receptor agonist, regulates glucose
metabolism in rat primary hepatocytes. FASEB J 2002 Mar 26.
[3] Rucker RB, Copper, Lysyl oxidase, and extracellular matrix protein cross-linking. Am J Clin Nutr
1998;67(suppl):996S-1002S.
[4] Hunsaker HA, Marginal copper deficiency in rats; Atherosclerosis, 51(1984):1-19.
[5] Klevay LM, Lack of a RDA for copper may be hazardous to your health. J Am Coll Nutr
1998;17(4):322-326.
[6] Turley E, Copper supplementation in humans .... FreeRadBiolMed 2000, 29(11): 1129-34.
roro
NNNN NNNN roland rohde, md, +49 (511) 906 35- Tel -03 FAX -69 NN N NN mailto: NN N NN NN
Leibniz Research Labs for Biotechnology NN N NN and Artificial Organs (LEBAO) NN N NN NN NN
Hannover Medical School (MHH) NN http://www.mh-hannover.de NN LEBAO Department of
Cardiovascular Surgery
PALEODIET Archives
Subject: Reply to Ed Thompson: potassium / acid load
From: Roland Rohde
Reply-To:
Date: Fri, 6 Sep 2002 08:25:09 +0200
Ed,
I've some comments on the potassium (K+) and acid/base discussion.
One of the first lessons every medical student has to learn is about the sensitivity of the blood K+ -level. The
correct function of many physiologic systems severely depends on it, especially the rhythm of the heart
contraction. If he doesn't, he will have to learn it the hard way: you can kill a laboratory animal (or a patient)
very efficiently and fast by carelessly playing around with K+ - containing infusions. Another clinical
experience is that the only reliable method to bring a high K+ -level down is a slow infusion of insulin (if
necessary plus glucose). This even works if the patient is diabetic! If he is not, a pure glucose infusion will
do, because this slowly raises the patients own insulin production. Now imagine what happens, if somebody
with a normal or even low K+ blood level gets a long lasting glucose infusion from his gut, let us assume
from white bread with butter and honey, that is not accompanied by an adequate amount of K+. Keep in
mind that 98% of the K+ is inside of our cells and that the K+ content of the extracellular space may only
change by about half a gram (contained in 150 g of lean meat) without severe consequences. Right! This
sounds like an emergency situation for some of our electrolyte watchdogs! And now imagine this happens
three or more times a day, 40 years long! Most likely, the controller will give it up some day and care for the
correct K+ level instead of glucose disposal. There's at least one prospective study that shows a low K+
intake as one risc factor for diabetes [1]. Let me mention some well accepted facts, that can be found in
every pharmacology or physiology/biochemistry textbook.
i) The insulin sensitivity/resistance of the insulin target cells, especially muscle cells, strongly depends on
their K+ -content. K+ -uptake is not only needed for glucose storage as glycogen but also for the activation
of many glycolytic enzymes. E.g., the insulin resistance seen after the therapy with certain diuretics
(thiazides) is caused by their K+ -wasting properties. K+ -deficiency is always an intracellular one (98% of
the stock). (For a clinical example, see [2].)
ii) The insulin secretion of the pancreatic beta-cell strongly depends on its K+ -content. The K+ -level is the
common final path of many metabolic and regulatory mechanisms leading to the secretion of insulin. During
the last ten years, the receptors (look for SUR1, Kir6.x in medline) of the sulfonylurea class of oral
antidiabetics have been identified as an inhibitor of ATP-dependent K+ -releasing membrane pores. The so
called "persistent hyperinsulinemic hypoglycemia of infancy" has been proven to be caused by a mutation in
the genes coding for these pores leading to high K+ and thus uncontrollable high insulin levels [3]. This state
can be bettered by agents, that lower the K+ in the beta-cell.
Needless to say, that many metabolic disorders (like hypertension [4]) are characterized by K+ -deviations
and that for many diseases, insulin resistance is a common feature or a risc indicator/factor.
10/14 (2002)
Man is specialised on food that contains mainly intracellular substances. So one should await that the insulin
actions on all these components, like amino acids, glucogenetic equivalents, K+, phosphate [5], magnesium,
are tied together very closely. As protein is converted to glucose in a 7:4 relation and 21g protein is
accompanied by about 360 mg K+ in meat, we should ingest about 360 mg for every 12g glucose. Or more
than 10g for 360 g carbs (western diet: 2-4g).
But even if we eat paleo-style, we possibly are not free to feast solely on blueberrys or bone marrow! Insulin
has not only anabolic properties. It promotes the catabolism of energy by stimulation of glycolysis and thus
supports heat production and physical activity. For our medical grandfathers in the pre-insulin era a lowenergy diet was one of the few therapeutical options to treat diabetes, i.e. the lack of insulin action as we call
it today. In a diet, where "food intake" and not "glycemic load" triggers insulin, energy intake could be
another parameter that is tied to K+. A 40% / 60% protein-fat relation from meat would mean 6g K+ in 3000
kcal.
An important additional factor for the cellular K+ -content is the blood pH. If blood becomes more acidic,
this leads to a H+ -shift from blood to cells and a reverse K+ -shift. The K+ shifted to the extracellular space
is excreted by the kidneys and thus lost. In a low carb diet, this danger always is present (Ketosis! See
recently [6]). This is not a question of acid-base-balance! Additional 100g protein contains additional 16g
nitrogen = 1, 14 mol that could be excreted as positively charged ammonia instead of neutral urea by the
kidneys, sparing 1, 14 * 39g = 45g K+, if necessary! A person eating 280 g of protein instead of 80g
theoretically may excrete 2280 mVal more basic equivs as NH4+. This is often not considered by those acidbase-balance people. Protein is the most basic nutrient one can find!
There is another side aspect of this. Protein is a very good buffer. If you eat something very basic (like
potash or soda) or a good buffer (like protein) your stomach will have to secrete many H+ (and Cl-) -ions to
make its content acid. These ions are drawn from the blood, making blood more basic which is followed by a
H+ shift from cells to blood. The following K+ -shift into the cells lowers blood K+ -levels, preparing the
blood for the uptake of ingested K+, renders the beta-cells more sensitive for scretion stimuli, and makes
muscle cells more insulin sensitive. All this happens before anything enters the gut!
Our veggie-friends always insist on how good they feel if they eat only fruits and vegetables. Why shouldn't
we believe them? But let's do a rational analysis. We all know that vegetables are not those vitamin bombs
(besides of C) they are thought to be. And even the invention of the vitamin pill has not brought mankind to
olympic hights of healthiness, beauty and power. And trace elements are surely important but very
inconsistently found in different plants and very dependent on their availability in the soil. So everything
boils down to high sugar and kationic mineral content (like Mg++ and K+, potash). The combination sugar /
K+ seems to make people feel well. What can a paleo-dieter do to stay K+ -replete?
i) Avoid metabolic acidosis. ii) About 2g K+ in 1000 kcal plus additional 3g for every 100 g carbs. iii) The
K+ must be present in the meals.
[1] Colditz, Am J Clin Nutr 1992 May;55(5):1018-23 [2] Tourniaire J, IS 0338-1684, Diabete Metab 1988
Dec;14(6):717-20 [3] Reis, Diabetes Metab 2002 Feb;28(1):14-9 [4] Resnick, Hypertension 2001 Sep;38(3
Pt 2):709-12 [5] Lind, Am Heart J 2001 Oct;142(4):720-4 [6] Westman, Am J Med 2002 Jul;113(1):30-6)
roro
NNNN NNNN roland rohde, md, +49 (511) 906 35- Tel -03 FAX -69 NN N NN mailto: NN N NN NN
Leibniz Research Labs for Biotechnology NN N NN and Artificial Organs (LEBAO) NN N NN NN NN
Hannover Medical School (MHH) NN http://www.mh-hannover.de NN LEBAO Department of
Cardiovascular Surgery
PALEODIET Archives
Subject: Introduction
From: Todd Moody
Reply-To:
Date: Tue, 10 Sep 2002 08:03:40 -0400
Some members of this list are aware that I am the new moderator, but for those who do not know it, this is a
brief introduction.
11/14 (2002)
Unlike just about everyone else on the list, I do not have any credentials in the relevant areas of nutrition,
physiology, anthropology, etc. My Ph.D. is in philosophy, which I teach at St. Joseph's University in
Philadelphia. As far as the subject-matter of the list is concerned, I am strictly an auto-didact. As moderator,
my only claim to competence is that I have some understanding of what is and isn't professional-level
discourse.
The Paleodiet list is intended for professional-level discussion among researchers, and that is the principle
that I shall try to adhere to as moderator. This means that the standards are somewhat more formal than on
the many "chat" lists that exist, and the volume is consequently somewhat lower. I will normally not forward
informal "from the hip" comments to the list. I have nothing against that kind of conversation; it's just not my
understanding of what this list is about.
On the other hand, Paleodiet is not, and cannot be, a peer-reviewed scholarly journal or a substitute for one.
So it's somewhere in between a journal and an informal discussion list. It's a place where researchers can try
out ideas and get feedback. Messages on Paleodiet will normally be supported by references to the
appropriate scientific literature. This is how the list has been run in the past, and this is how I shall attempt to
continue to do it.
So that's my pitch. I hope it works out.
Todd Moody
PALEODIET Archives
Subject: Re: Reply to Ed Thompson: potassium / acid load
Reply-To:
Date: Tue, 10 Sep 2002 23:36:00 -0500
Roland,
My understanding of your reply to my posting (about dietary potassium, dietary protein, and renal acid load)
seems to do 2 things:
1. To negate the perceived importance of the protein/potassium ratio [which you seem to do by arguing that
protein does not induce a net acid load]
2. To implicate a new dietary ratio (ie. carbohydrate/potassium or carbohydrate/cations) to be of primary
functional importance in maintaining human health [which you seem to do by arguing that carbohydrate
intake in the context of a subclinical potassium deficiency may be at the root of most (all?) of the modernday diet-related metabolic disorders that have surfaced as public health concerns in the past century or so primarily due to diet-induced insulin resistance]
While you may be found to be entirely correct in these 2 seperate postulations, will you please respond to the
following concerns which surface when your post is subjected to the scrutiny of critical analysis?
First, with regard to point #1 from above (that protein does not induce a net acid load), I understand that, at
least in theory, protein might be thought of as being alkaline to the human body (by providing an excess of
ammonia). Still, empirical observations have quantified a renal acid load following increases in dietary
protein [1, 2]. Can/will you provide any reasoning for these observations (as they directly contradict the
"protein doesn't induce a net acid load" argument)?
And secondly, with regard to point #2 from above (that the dietary carbohydrate/cation r atio is the pivotal
dietary factor implicated in the recent rise of insulin resistance in Western populations): How do you explain
other 'competing' theories that seem to have data supporting them, such as a dose-response effect of the longchain omega-3 polyunsaturated fatty acids on insulin sensitivity in the animal model [3] which, I must admit
however, has not been conclusively substantiated in humans [4]?
Ed Thompson
References:
[1] Remer T, Manz F. Estimation of the renal net acid excretion by adults consuming diets containing
variable amounts of protein. Am J Clin Nutr 1994 Jun;59(6):1356-61
[2] Manz F, Remer T, Decher-Spliethoff E, Hohler M, Kersting M, Kunz C, Lausen B. Effects of a high
protein intake on renal acid excretion in bodybuilders. Z Ernahrungswiss 1995 Mar;34(1):10-5
[3] Somova L, Moodley K, Channa ML, Nadar A. Dose-dependent effect of dietary fish-oil (n-3)
polyunsaturated fatty acids on in vivo insulin sensitivity in rat. Methods Find Exp Clin Pharmacol 1999
May;21(4):275-8
12/14 (2002)
[4] Vessby B. Dietary fat and insulin action in humans. Br J Nutr 2000 Mar;83 Suppl 1:S91-6
PALEODIET Archives
Subject: Re: Reply to Ed Thompson: potassium / acid load
From: Roland Rohde
Reply-To:
Date: Thu, 12 Sep 2002 13:35:48 +0200
Ed,
nothing could be farther from me than separating protein from potassium. In fact, I used their ratio for my
calculations. Nor dit I want to establish new dietary ratios. What I simply wanted to show is that it's not
necessary to explain the deleterious effects of potassium deficiency by acid/base calculations. Actually they
are physiologically not very relevant, to say the least.
The kidneys (and the lungs, CO2) are responsible for the acid/base balance. Most relevant is the question,
wether the excreted acids can be compensated by an appropriate amount of bases to keep the pH-value in a
"normal" range. Whether these bases are fixed or more volatile is not so important. In case of protein it's
pretty clear that it always brings more potential NH4+ with it than is needed to compensate for the sulphur
content. By the way, your literature [2] explicitely confirms this. I cite from the abstract:
"In the bodybuilders renal ammonium excretion was higher at any given value of urine pH than in the
controls. In a regression analysis protein intake proved to be an independent factor modulating the ratio
between urine-pH and renal ammonium excretion.The concomitant increase of renal net acid excretion and
maximum renal acid excretion capacity in periods of high protein intake appears to be a highly effective
response of the kidney to a specific food intake leaving a large renal surplus capacity for an additional renal
acid load."
A newer one [1] from the same author:
Further analyses of the interrelation between diet and acid-base status revealed that increasing protein intake
(despite its potential to increase NAE) also significantly improves the capacity for renal net acid excretion by
stimulating urinary ammonium excretion. ... protein itself moderately improves the renal capacity to excrete
net acid by increasing the endogenous supply of ammonia which is the major urinary hydrogen ion
acceptor."
As everything that we ingest has to pass our vascular system before it is metabolized within the cells, I
further tried to direct your attention to the well known fact that K+ is one of the most critical food
constituents, critical for the appropriate function of many excitable organs, like the heart. A high potassium
concentration (in the blood, not in the cells) can kill you within one single heart beat. This ion is closely tied
to glucose metabolism, a substance that in a paleolithic diet is mainly a metabolic intermediate sourcing from
and stoichiometrically coupled to protein uptake. Carbs as the essentally new neolithic nutritional factor can
thus disturb this delicate electrolyte balance. The 10g K+ per 100g carb ratio is merely a theoretical one and
was mentioned to get an idea of the K+ gap in western diets if we assume a stoichiometric relation between
cellular K+- and glucose-uptake, independently of the glucose source (food or gluconeogenesis). Grain is
especially deleterious, because it is accompanied by about only 0, 6 grams of K+ per 100g starch, even if one
eats all parts of the grain. White flour has even half of that, i.e. 3% of what it should have. It's a little bit
strange that many of the mentioned K+ -facts are well accepted in classical medical sciences like
pharmacology, intensive care medicine, and anesthesiology because they are relevant for the survival of their
patients. But there seem to be no consequences for every day life of the general population. Many
nutritionists talk about the "empty calories" of sugar and fat. But they are not aware of the emptiness of grain
and even many fruits in this respect. Assuming that man is so very strongly adapted to meat that he will not
really thrive on a diet that is composed very differently, a K+ -imbalance could well be one possible
additional factor for diabetes and other diseases. One factor, not the sole one and not even necessarily the
pivotal one.
13/14 (2002)
Especially the omega-3 connection is very promising. The cited paper [3] is in so far not untypical as it uses
not a pure omega-3 fatty acid but fish oil, that surely contains a lot of other active metabolites, like vitamins
A and D. In my recent posting "lions & dogs" you can find two papers [4, 5] about phytanic acid (PA). This
is a new star on the fatty acid scene. It is already proven to positively influence the glucose metabolism [5] in
rat liver cells. It acts as a vitamin-hormone, very similar to vitamin A [literature in 4]. And it is hormonally
necessary as a coactivation partner for the so called ppar-receptors that mediate the effects of many of those
fatty acids like omega-3. It is most exciting that PA not only is ocurring in the same fats that have good
omega-3/6 ratios, fish oil [6] and the fat of grass fed animals, it even comes from the same primary sources,
namely grass or algae that contain chlorophyll. Even nematodae and insects have receptors for it!
There is no contradiction between potassium and fatty acids as causative factors in diabetes development.
Diseases like diabetes can't be monocausal from a non-paleo point of view, otherwise we would know the
cause since a long time.
Roland
[1] Remer, T. Influence of nutrition on acid-base balance--metabolic aspects. Eur J Nutr 2001 Oct;40(5):21420
[2] Manz F, Remer T, Decher-Spliethoff E, Hohler M, Kersting M, Kunz C, Lausen B. Effects of a high
protein intake on renal acid excretion in bodybuilders. Z Ernahrungswiss 1995 Mar;34(1):10-5
[3] Somova L, Moodley K, Channa ML, Nadar A. Dose-dependent effect of dietary fish-oil (n-3)
polyunsaturated fatty acids on in vivo insulin sensitivity in rat. Methods Find Exp Clin Pharmacol 1999
May;21(4):275-8
[4] McCarty M, The chlorophyll metabolite phytanic acid is a natural rexinoid--potential for treatment and
prevention of diabetes. Med Hypotheses 2001 Feb;56(2):217-9.
[5] Heim M, Phytanic acid, a natural peroxisome proliferator-activated receptor agonist, regulates glucose
metabolism in rat primary hepatocytes. FASEB J 2002 May;16(7):718-20
[6] Ratnayake WM, Olsson B, Ackman RG. Novel branched-chain fatty acids in certain fish oils. Lipids
1989 Jul;24(7):630-7.
roro
14/14 (2002)
PALEODIET Archives
Subject: Sciam Human Evolution Special
From: "Balzer, Ben"
Reply-To:
Date: Mon, 4 Aug 2003 10:44:17 +1000
http://www.sciam.com/special/toc.cfm?issueid=11&sc=rt_nav_list
Scientific American have a special on human evolution which has something to offend just about everybody.
There are article on many aspects including diet, childbirth etc. I haven't read much of it yet, but thought I'd
post it up as it won't be on the news stands much longer.
The article on "if humans were built" to last focuses on the (totally incorrect) assumptions of western
medicine that diseases like osteoporosis and osteoarthritis are inevitable (and presumably of genetic origin).
Indeed I thought the paleopathological evidence was clear that osteoarthritis was rare (aside from in a spear
throwing elbow or next to a fracture), and that osteoporotic fractures were only found in Inuit (which may
relate to their extreme diet). I hope one day that this article may be used by medical historians to show how
blinkered thinking was in our day.
Dr Ben Balzer 109 Morgan St Beverly Hills 2209 NSW Australia Tel (02) 95023355 Fax (02) 95024243 Int'l
prefix(+612)
PALEODIET Archives
Subject: Re: Sciam Human Evolution Special
Reply-To:
Date: Thu, 7 Aug 2003 11:18:32 -0500
Parts/Attachments:
text/html (56 lines)
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PALEODIET Archives
Reply-To:
Date: Fri, 8 Aug 2003 15:28:06 -0500
2nd attempt (1st version muddled) ...
Ben,
Thanks for posting this. I read some of this article, but got sick to my stomach [from it]! You are [so] right
about them being so wrong!
Sometimes I cannot believe how the activity that we call "science" can be so entrenched with commercial
interests and how individual scientists must be corrupted (or at least corruptible) in order to appear so
intellectually dishonest! I mean: What does it take to state ANY confidence in a notion that "potatoes, etc"
(read: carbohydrates) are the dietary change that enlarged our brain?! I cannot BELIEVE the lack of any talk
of fatty acids in this article! It should be a crime to leave those out of the article!
Those in the future will look back at this article (realizing the known science that was omitted) and say that
we were so dishonestly greedy at one time that we didn't reasonably care about truth & understanding.
Ed
1/61 (2003)
PALEODIET Archives
From: Nina Planck
Reply-To:
Date: Fri, 8 Aug 2003 15:59:28 -0400
Thank you for alerting me to this.
I am beginning to work in earnest on two parts of my book, one on soy and the other on teh cholesterol
hypothesis. If you would like to steer me toward other reseach, researchers, or experts, I'd love to know
about them.
It's called REAL FOOD, for Harper Collins next year, and it's about - well, here's the intro again.
best wishes, Nina Planck
-------Original Message------From: "Balzer, Ben" Sent: 08/03/03 08:44 PM To: Subject: Sciam Human Evolution Special
> http://www.sciam.com/special/toc.cfm?issueid=11&sc=rt_nav_list
Scientific American have a special on human evolution which has something to offend just about everybody.
There are article on many aspects including diet, childbirth etc. I haven't read much of it yet, but thought I'd
post it up as it won't be on the news stands much longer.
The article on "if humans were built" to last focuses on the (totally incorrect) assumptions of western
medicine that diseases like osteoporosis and osteoarthritis are inevitable (and presumably of genetic origin).
Indeed I thought the paleopathological evidence was clear that osteoarthritis was rare (aside from in a spear
throwing elbow or next to a fracture), and that osteoporotic fractures were only found in Inuit (which may
relate to their extreme diet). I hope one day that this article may be used by medical historians to show how
blinkered thinking was in our day.
prefix(+612)
>
NINA PLANCK Director GREENMARKET 212 477 3220 Ext 21 130 East 16th St NY NY 10003
PALEODIET Archives
From: Dean Esmay
Reply-To:
Date: Mon, 11 Aug 2003 10:32:12 -0400
We have to be careful about generalizing about the Inuit, however. They led a generally more physically
gruelling existence than many other hunter/gatherers: kayaking tends to compress vertebrae, running and
jumping and generally hunting on frozen tundra or ice tends to be harder on the legs, hips, and back, falls
tend to be more damaging, and so on. A lot of the increase of compression fractures and osteoarthritis may
be due to a harder lifestyle, not necessarily the extremes of the diet. Or of course it could be the diet, or could
be some of both. But it's not safe to assume, and I don't think anyone's done the research to definitively
answer that question.
PALEODIET Archives
Subject: Draft of my "Letter to the Editor" sent to Scientific American
Reply-To:
Date: Tue, 19 Aug 2003 12:18:11 -0500
Comments on the following draft (already sent; waiting for editor's reply) are welcome.
---------begin draft----------LETTER TO THE EDITOR (Scientific American magazine):
2/61 (2003)
An Unscientific American?
On the surface of it, and from the standpoint of informing public health policy and/or research direction, the
article by Leonard ("Food for Thought") published in the 'Human Evolution' Special Edition issue appears to
be strikingly uninformative. This perception is perhaps best illustrated and verified by a take-away message
from the article that appears as a bullet point on page 65:
"The health concerns of the industrial world, where calorie-packed foods are readily available, stem not from
deviations from a specific diet but from an imbalance between the energy we consume and the energy we
expend."
My response: All hail the supreme Energy Balance Equation! For 'tis the cal'ries-in-minus-cal'ries-out that
doth endow a man his heretofore claim to health! Human health is just THAT simple to summarize and the
'masses' MUST now concur with this epiphany, no matter how incongruent it is with the growing body of
medical and scientific evidence on the matter!
Conceding the point that being overweight is indeed a crucial detriment to health, I must nevertheless charge
Mr. Leonard with the error of taking quite a myopic viewpoint regarding this one aspect of health/risk.
Apparently Mr. Leonard is unaware (or unconcerned?) with recent scientific advances in knowledge
regarding a cause-and-effect relationship noted between PARTICULAR eating patterns, regardless of
changes in bodyweight, and particular HEALTH OUTCOMES (no - not just "biomarkers" of "health" or
"risk" - but real-life "health outcomes").
Of all the "health outcomes" measured, mortality is the hardest to dispute (only a severe skeptic would deny
that someone cold and no longer breathing is still available for "follow up"!). A case in point would be the
notable reduction in all-cause mortality (from fish oil supplementation) in the GISSI-Prevention Trial1, a
trial involving over 11, 000 people with coronary heart disease.
As a validation of the power of the specific food component tested here (fish oil), the reduction in mortality
that was found in the trial, which was already evident by the 3-month mark, was also independent of both
baseline diet AND concurrent drug therapy. And it is this kind of finding that has led to the production of
prescription "fish oil" capsules (e.g. Omacor) approved for the secondary prevention of myocardial
infarction.
I will leave aside the evolutionary issue of the necessary surplus of particular long-chain polyunsaturated
fatty acids (e.g. DHA) that is required for brain development in humans, and simply offer up another
example/validation of discernable evidence of benefit from a recent clinical trial. The trial in question2
assessed the effect of altering maternal intake of fish oil on a subsequent measure of the child's intelligence
at 4 years of age. The point estimate showed a 3-4% difference (increase) in 4-year-old intelligence
(Kaufman Assessment Battery for Children) that reached statistical significance.
Carrying this issue of the "surplus of particular fatty acids required by the human brain" to its logical
extension, to find that carbohydrate intake (potatoes, etc) was the only theory offered up to explain the
evolution of the human brain is no less than amusing. One is tempted to ask whether Mr. Leonard feels
restraint or pressure (ie. is "under duress") from the corporate interests of agribusiness, or if he is perhaps in
cahoots with them to advance interests of his own. My query on this particular issue of honest reporting,
although stated frankly, is admittedly baseless and without any substantial weight of argument. My
inclination to be so bold here and to throw such an idea out into this forum is really a ploy to elevate
awareness of the fact that billions of dollars change hands annually in the food industry; and that relatively
empty summations regarding nutrition science ought to be questioned (as nothing "sells" products like public
confusion combined with the pervasive, misleading, authoritative advertisements that we are bombarded
with).
Regardless of Mr. Leonard's reply on this query (which I can imagine would be more than subtle), I must
elaborate that the preventable medical costs expected to result from changes in diet and lifestyle would add
up to a sum greater than the initial cost of the diet and lifestyle changes made (on a whole). In other words,
we should expect a net monetary gain for society as a whole, even if particular individuals and particular
food corporations bear a disproportionately large portion of this initial cost (and EVENTUALLY this will
turn PROFITABLE for the corporations that instigate the technology required to bring the low-technology "evolutionary" - foods back to market). There are already a number of promising, low-cost modifications of
diet and lifestyle available to us: such as vigorous exercise and an ample intake of fruits, vegetables, lean
meats, and fish (baked or broiled, but not fried).
Reference: 1. Marchioli R, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids
after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della
Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105(16):1897-903.
3/61 (2003)
2. Helland IB, Smith L, Saarem K, Saugstad OD, Drevon CA. Maternal supplementation with very-longchain n-3 fatty acids during pregnancy and lactation augments children's IQ at 4 years of age. Pediatrics.
2003 Jan;111(1):e39-44.
Edward Thompson Health & Exercise Sciences Globe College, MN Email:
--------------end draft----------------Again, comments (either pro OR con) are welcome.
Ed
PALEODIET Archives
Subject: Re: Draft of my "Letter to the Editor" sent to Scientific American
From: Keith Thomas
Reply-To:
Date: Tue, 19 Aug 2003 16:49:12 -0500
On Tue, 19 Aug 2003 12:18 Edward Thompson
> Comments on the following draft ... are welcome. Ed, I'm sure you enjoyed writing it! I hope the
> length doesn't - on its own - rule it out. A case in point would be the notable reduction in
> all-cause mortality (from fish oil supplementation) in the GISSI-Prevention Trial1, a trial
> involving over 11, 000 people with coronary heart disease.
Perhaps one example of fish oil and one example from another, quite different area, might have been more
effective that two concerning fish oil.
> One is tempted to ask whether Mr. Leonard feels restraint or pressure (ie. is "under Eduress")
> from the corporate interests of agribusiness, or if he is perhaps in cahoots with them to advance
> interests of his own.
Good point. There are corporate interests that exert direct pressure (these are well illustrated in the Enig and
Fallon paper "The Oiling of America". But the real problem is more pervasive - cultural hegemony quietly
rules out of question a serious approach to prevention rather than treatment.
I am dismayed when I see so often serious articles, even in the top end popular media, about the perils from
diabetes, obesity, sedentism etc. The articles point to rapidly increasing incidence of pathologies and the
implications for individuals, health systems, insurance, paying for retired baby-boomers etc. But the articles
almost always end with a nudge and a wink, to the effect that doing away with fries or exercising more for
the rest of our lives is just too hard. It is as if we were on a moving pathway to years of pain and disability,
but that the ride is so much fun today that we can't bear to get off or think about tomorrow. What
evolutionary survival trait, I ask myself, is now responsible for this bizarre phenomenon?
The option we resort to is that promised by big pharma.
Perhaps Leonard's article is not the one in which the start should be made to advocate Paleo lifestyle
changes, such as those you advocated, but I'm still waiting for a serious article that will do this AND
succeed.
Keith
PALEODIET Archives
From: Bob Avery
Reply-To:
Date: Tue, 19 Aug 2003 23:13:41 -0400
Edward,
> Comments on the following draft (already sent; waiting for editor's reply) are welcome.
My take upon initial reading? Too verbose and polemical to get published, but good luck! I estimate that you
could have made the salient points in about 1/4-1/3 of the space. Editors love brevity.
Bob Avery
?!
4/61 (2003)
PALEODIET Archives
Reply-To:
Date: Wed, 20 Aug 2003 16:16:41 -0500
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Reply-To:
Date: Thu, 21 Aug 2003 12:17:14 +0100
I must admit to be slightly stunned at reading Ed Thompson's response to William Leonard's article in
Scientific American, which appears to be a massive over-reaction to what I felt was a pretty well-balanced
article. [I have to admit here to not having read the article as it appears in the recent Human Evolution
special, but as it first appeared in SciAm in Dec 2002, but as the Dec02 version has exactly the same title,
and the same quoted bullet point by ET, I assume it has much the same thrust.]
In response to Leonard's statement that "The health concerns of the industrial world, where calorie-packed
foods are readily available, stem not from deviations from a specific diet but from an imbalance between the
energy we consume and the energy we expend." ET somewhat sarcastically states "All hail the supreme
Energy Balance Equation! For 'tis the cal'ries-in-minus-cal'ries-out that doth endow a man his heretofore
claim to health! Human health is just THAT simple to summarize and the 'masses' MUST now concur with
this epiphany, no matter how incongruent it is with the growing body of medical and scientific evidence on
the matter!"
I am afraid that yes for a lot of people, it really is that simple. In a world where 200million people are obese,
with all the consequent health risks that this entails, and with an increasingly sedentary lifestyle in the
developed world, taking in any amount of essential fatty acids and fish oils is not going to do as much for
you as adjusting one's energy balance: eating less or exercising more as a first step to improving health will
do more good as a whole for individuals AND for society than specific dietary changes.
That is not to say that I disagree that diet composition should ALSO be improved for certain groups or
individuals. But for an educated individual (as I assume) in this field such as ET to respond in such a manner
is not appropriate. An awful lot of overweight people are searching for a 'quick fix' which they will fail to
find. Until the message is clear that most people will never be able just to eat as much as they want and stay
as thin as they like, then the growing trend of increasing obesity will continue, while people desperately turn
to pharmaceuticals or quack diets. The irony of ET's response is that at the end of the letter, he seems to
concur with what I have just written in saying "I must elaborate that the preventable medical costs expected
to result from changes in diet and lifestyle would add up to a sum greater than the initial cost of the diet and
lifestyle changes made (on a whole)... There are already a number of promising, low-cost modifications of
diet and lifestyle available to us: such as vigorous exercise and an ample intake of fruits, vegetables, lean
meats, and fish (baked or broiled, but not fried)." Trouble is that this good and sensible point is lost in the
verbosity of the whole.
One has to ask if ET has something against Leonard, especially given what he writes about the pressures of
agribusiness, when Leonard is well known for being an eminent nutritional anthropologist with a long
history of good and solid research in this area?
yours,
5/61 (2003)
Tamsin O'Connell
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Fri, 22 Aug 2003 06:50:00 +0100
Tamsin O'Connell said:
> I am afraid that yes for a lot of people, it really is that simple. In a world where 200million
> people are obese, with all the consequent health risks that this entails, and with an increasingly
> sedentary lifestyle in the developed world, taking in any amount of essential fatty acids and fish
> oils is not going to do as much for you as adjusting one's energy balance: eating less or
> exercising more as a first step to improving health will do more good as a whole for individuals
> AND for society than specific dietary changes.
I have to disagree with Tamsin as weight isn't about calories and energy balance; it is far more about
constituents of diet. For example: In a trial of different diets in 1932 by Drs Lyon and Dunlop in the
Edinburgh Hospital, Scotland, overweight patients on 1, 000 calorie diets lost an average of 49g a day on a
high carb, low fat diet, but over 4 times that amount, 205g, on a low-carb, high-fat diet. Kekwick and Pawan
also showed that a diet high in fats and low in carbs was better for weight loss at the Middlesex Hospital,
London, England, in 1956. Some patients on a 1, 000 calorie low fat diet composed mainly of carbs, actually
put weight on, while on a 2, 600 calorie, low carb, high fat diet, the same patients lost weight.
Lyon D M, Dunlop D M. The treatment of obesity: a comparison of the effects of diet and of thyroid extract.
Quart J Med. 1932; 1: 331. Kekwick A, Pawan G L S. Calorie intake in relation to body-weight changes in
the obese. Lancet. 1956; ii: 155.
Think about lions. How many do you see rushing all over the veldt getting lots of exercise? They don't count
calories either. Yet you will never see an overweight lion in its natural habitat, no matter how abundant its
food supply. Why? Because they eat what is natural to them. We don't -- for we too are a carnivorous
species. And therein lies the problem.
Barry Groves, PhD Author of "Eat Fat, Get Thin!" http://www.second-opinions.co.uk
PALEODIET Archives
Reply-To:
Date: Fri, 22 Aug 2003 11:20:50 -0500
> Overweight lions will fail to catch food even if it is abundant, and then they will become thinner
> lions. One might equally ask how many fat koalas does one see? None and they are vegetarian, move
> slowly and have an abundant food supply. Just because another species is not seen to be
> over-weight does not make it a good analogue for humans. What evidence is their that humans are
> carnivores rather than omnivores?
6/61 (2003)
Not carnivores, necessarily, but there's evidence that we evolved on a meat-heavy diet virtually devoid of
grains, beans, and other concentrated carb foods. An article in The American Journal of Clinical Nutrition in
March, 2000, reported on a multi-university, multi-national study of hunter-gatherer diets, both from
paleoanthropological evidence, and study of the few remaining hunter-gatherer groups, and concluded that
hunter-gatherers generally get over half their calories from animal foods, with the rest coming primarily from
vegetables. It specifically said that "protein was elevated at the expense of carbohydrates." -- Dana
Carpender
PALEODIET Archives
Reply-To:
Date: Fri, 22 Aug 2003 11:51:01 -0600
Hello all,
FWIW I use dietary strategies in my daily practice as a clinician and from my experience a diet high in
carbohydrates, whether from cereals and grains OR fruits ends up having the same effect in promoting
insulin resistance and hyperinsulinemia. Fruit has certainly always been an important part of the human diet
but with two important caveats:
1) fruit was only consumed in limited amounts during specific periods of time, at least in temperate
populations. In my part the world for e.g., in Alberta, Canada, good luck to you to try to grow any kind of
fruit at all, and if you do, the season is extremely short; 2) most fruit available today is the modern
hybridized version of ancestral fruits, the latter of which have an overall higher fiber content and usually
more seeds, containing additional sources of proteins and fats (e.g. the Saskatoon or Serviceberry
[Amelanchier alnifolia], that despite being an important food for First Nations and early pioneers, most
modern folks find them too mealy). This latter point also applies to the modern hybrized versions of many
vegetables, e.g. the carrot (Daucus carota), which bears little similarity to the sweet, fleshy orangey-pink
version of today
as for eating raw foods, I think it might be interesting to note that in the ancient systems of medicine,
including Ayurveda and TCM, raw foods are avoided because they are considered to be difficult to digest.
This perspective is certainly borne out in my clinical experience, in which I will emphasize a diet rich in
quality animal proteins along with above-ground steamed vegetables, and when patients follow this, I can
almost always suspend any additional therapy. Despite Gandhi's admonishment for folks to "chew their juice
and juice their food, " most modern folk don't chew their food all that well, reducing to a substrate that can
then be acted upon by chemical means, and given the lack of cellulase produced in the human GIT, all those
crunchy raw foods pretty much pass through the GIT undigested, and are at best a source of prebiotics.
On Thursday, August 21, 2003, at 06:16 PM, Bob Avery wrote:
> Tamsin,
> Until the message is clear that most people will never be able just to eat as much as they want
> and stay as thin as they like, then the growing trend of increasing obesity will continue If one
> eats only uncooked fruits and veggies, one can accomplish just that. It's been proven over and
> over. You will probably even get thinner than you like! (:-)
> Bob Avery
> ________________________________________________________________
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400 - 1228 Kensington Rd. NW Calgary, AB T2N 5P6 CANADA tel: (403) 270-0891 ext 315 fax: (403)
283-0799 email: http://www.wrc.net/phyto
*******************************************
7/61 (2003)
PALEODIET Archives
From: Todd Moody
Reply-To:
Date: Fri, 22 Aug 2003 12:52:28 -0400
> But both these studies are on diets of average to low calories compared to recommended adult
> intakes. What's the difference in weight gain between people on, say, 4000-calorie and
> 1000-calorie diets? It's not surprising that at constant calories the composition of the diet can
> make a difference, but reducing calories has an effect too. It seems incredible to me that adults
> on a 1000-calorie diet could gain weight, as their metabolic expenditure ought to exceed this with
> even a modest amount of activity, and if the energy is not coming from burning of body reserves,
> then our fundamental understanding of where biological systems get their energy from is in doubt.
The thing that has not been sufficiently studied, in my opinion, is not simply weight loss on isocaloric diets
of varying macronutrient ratios, but changes in body composition. That said, however, there are studies that
suggest that lower carbohydrate diets preserve lean body mass and favor fat loss, in comparison with higher
carb diets of comparable energy content. For example, the small study done by Charlotte Young in the early
1970s showed exactly this effect. All consumed 1800 kcal/day. All consumed 115g/day of protein. Only the
fat and carb content was varied. Those eating the most fat (133g/day) and least carb (30g) lost more body fat
and less LBM than those getting more carb (104g/day) and less carb (103g/day). There was also a modest but
significant difference in total weight loss.
This was a small study. There need to be more studies like this. But I think recent studies that have been
done (finally) on lowcarb diets tend to confirm Young's results (e.g., Layman's study).
From the standpoint of the obesity problem, these findings are tremendously important. Weight loss that
involves a significant loss of LBM is very likely to result in rebound weight gain, due to the ensuing drop in
metabolic rate.
In support of Barry Groves' opinion that humans have differentiated themselves from other primates by
becoming largely carnivorous, I recommend Craig Stanford's book The Hunting Apes: Meat Eating and the
Origins of Human Behavior. Stanford's emphasis is not nutritional, but he makes a very strong case for the
claim that our species has, of necessity, followed an adaptational trajectory of increasing carnivory.
Todd Moody
_____________________
Charlotte Young, Weight Loss on 1800 kcal Diets varying in Carbohydrate Content. Am J of Clin Nut 1971
290-6.
Craig B. Stanford, The Hunting Apes: Meat Eating and the Origins of Human Behavior. Princeton
University Press, 2001.
PALEODIET Archives
Reply-To:
Date: Fri, 22 Aug 2003 17:12:26 +0100
On Fri, 22 Aug 2003, Barry Groves wrote:
> I have to disagree with Tamsin as weight isn't about calories and energy balance; it is far more
> about constituents of diet. For example: In a trial of different diets in 1932 by Drs Lyon and
> Dunlop in the Edinburgh Hospital, Scotland, overweight patients on 1, 000 calorie diets lost an
> average of 49g a day on a high carb, low fat diet, but over 4 times that amount, 205g, on a
> low-carb, high-fat diet. Kekwick and Pawan also showed that a diet high in fats and low in carbs
> was better for weight loss at the Middlesex Hospital, London, England, in 1956. Some patients on a
> 1, 000 calorie low fat diet composed mainly of carbs, actually put weight on, while on a 2, 600
> calorie, low carb, high fat diet, the same patients lost weight.
8/61 (2003)
But both these studies are on diets of average to low calories compared to recommended adult intakes.
What's the difference in weight gain between people on, say, 4000-calorie and 1000-calorie diets? It's not
surprising that at constant calories the composition of the diet can make a difference, but reducing calories
has an effect too. It seems incredible to me that adults on a 1000-calorie diet could gain weight, as their
metabolic expenditure ought to exceed this with even a modest amount of activity, and if the energy is not
coming from burning of body reserves, then our fundamental understanding of where biological systems get
their energy from is in doubt.
Did these studies control for the activity levels and energy expenditure of the patients?
> Think about lions. How many do you see rushing all over the veldt getting lots of exercise? They
> don't count calories either. Yet you will never see an overweight lion in its natural habitat, no
> matter how abundant its food supply. Why? Because they eat what is natural to them. We don't -> for we too are a carnivorous species. And therein lies the problem.
Overweight lions will fail to catch food even if it is abundant, and then they will become thinner lions. One
might equally ask how many fat koalas does one see? None and they are vegetarian, move slowly and have
an abundant food supply. Just because another species is not seen to be over-weight does not make it a good
analogue for humans. What evidence is their that humans are carnivores rather than omnivores?
Andrew Millard
========================================================================= Dr.
Durham. DH1 3LE. United Kingdom. Fax: +44 191 334 1101 http://www.dur.ac.uk/a.r.millard/
=========================================================================
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Sat, 23 Aug 2003 08:53:13 +0100
> But both these studies are on diets of average to low calories compared to recommended adult
> intakes. What's the difference in weight gain between people on, say, 4000-calorie and
> 1000-calorie diets? It's not surprising that at constant calories the composition of the diet can
> make a difference, but reducing calories has an effect too. It seems incredible to me that adults
> on a 1000-calorie diet could gain weight, as their metabolic expenditure ought to exceed this with
> even a modest amount of activity, and if the energy is not coming from burning of body reserves,
> then our fundamental understanding of where biological systems get their energy from is in doubt.
> Did these studies control for the activity levels and energy expenditure of the patients?
I hope you will bear with me as the following is rather long.
That high-energy diets work better for weight loss has often been puzzling, and it has proved very difficult
for dieticians and doctors to accept them because, on the face of it, they appear to challenge the laws of
physics. But there are several reasons why they do not.
All carbohydrate -- sugars and starches -- contains energy to the value of four calories per gram and that fat
has nine calories per gram.
The calorie is a unit of heat. The way the energy content of a food is determined is by burning it in a device
called a 'bomb calorimeter' and measuring the amount of heat it gives off.
If we take a gram of carbohydrate and burn it in this way, we get an energy value of 4.2 calories, or more
correctly kilocalories (kcals). If we do the same with protein, we get a figure of 5.25 kcals. But we must
deduct one calorie because we know that a gram of protein does not oxidise readily and gives rise to urea and
other products to this value which are excreted and which must be subtracted. That gives a final figure for
protein of 4.25 kcals. And if we burn a gram of fat in the bomb calorimeter we get 9.2 kcals.
These figures are then rounded to the nearest whole number: 4, 4 and 9 respectively, and are used in calorie
charts to indicate the energy values of foodstuffs and, thus, to allow slimmers to measure the amounts that
they may eat. But there are two basic flaws in using these figures to determine the amounts of food we
should eat.
9/61 (2003)
THE FIRST FLAW The more obvious flaw in the argument is that our bodies do not burn these foods in the
same way that they are burned in a bomb calorimeter. If they did, we would glow in the dark. In fact the
digestive process is quite inefficient so that all we eat is not even absorbed by the body, let alone used by it.
The chemical process, whereby the blood sugar, glucose, is oxidised in the body to provide energy, gives rise
to carbon dioxide that leaves the body via the lungs as we breathe. Clinicians measure energy use by getting
their subjects to exercise on a treadmill or an exercise bike and measuring the amount of oxygen breathed in
and the amount of carbon dioxide breathed out. But if you are going to equate energy intake with energy
expenditure, you can only do it if all the carbon leaves the body in this way. But it doesn' t. In fact, only
about half is exhaled as carbon dioxide, the other half is excreted in sweat, urine and faeces as energycontaining molecules: urea, lactates and pyruvates, the energy values of which must be deducted from the
original food intake. All of these can vary from time to time and they also vary with the types of food eaten.
We know, for example, that if a lot of fat is eaten, it puts ketones into the urine. And we know that the value
of a gram of ketones derived from fat is roughly four calories. So, in this case, nearly half the energy from fat
goes, not into providing the body with energy, but down the toilet.
THE SECOND FLAW Nutritionists frequently liken eating food to putting petrol in a car -- simply treating
food as fuel. But this concept is quite wrong. Unlike the car, your body has the ability to repair and renew
itself, for which it uses proteins, fats and other nutrients found in food. The second and more important flaw
in the argument, therefore, is that your body does not use all the food it has available merely to provide
energy.
All edible carbohydrates have but one purpose: to supply calories that your body can use for energy.
Counting them might have some point, as they do nothing else. But while the body can use proteins and fats
to provide energy, they do very much more -- in ways that do not involve the production of energy.
Body cells are in a constant state of death and rebirth. No matter how many birthdays you have had, very
little of you is more than eight years old. The primary function of dietary proteins is used in this process: for
the manufacture and repair of skin, blood and other body cells; to make hair and finger- and toe-nails. The
amount of protein needed for this purpose is generally accepted to be about one gram per kilogram of lean
body weight. As meats contain approximately 23 grams of protein per 100 grams, a person weighing, say, 70
kg (11 stones) needs to eat about 300 g (11 oz) of meat, or its equivalent, every day just to supply his basic
protein needs. Even eating lean chicken this would contain some 465 calories. These calories are not used to
supply energy, they contribute nothing to the body's calorie needs and so must be deducted if you are
counting calories.
Much of the fat we eat is also used to provide materials used by the body in processes other than the
production of energy: the manufacture of bile acids and hormones, the essential fatty acids for the brain and
nervous system, and so on. All these must be deducted as well.
Thus trying to determine, from food intake and energy expenditure, how much excess energy your body will
store as fat will give a completely wrong answer unless these other factors are known and allowed for. But
how do you measure these? The simple answer is: you can't. There is no point, therefore, in trying. And
calorie counting, which is the foundation of practically every modern slimming diet is a complete waste of
time.
Andrew wrote:
> Overweight lions will fail to catch food even if it is abundant, and then they will become thinner
> lions. One might equally ask how many fat koalas does one see? None and they are vegetarian, move
> slowly and have an abundant food supply. Just because another species is not seen to be
> over-weight does not make it a good analogue for humans. What evidence is their that humans are
> carnivores rather than omnivores?
You are quite right that I could have looked at another species, because ALL animals in their natural habitat
are a normal weight. But, then, all of them consume a diet that is natural to them without anyone having to
tell them what, when and how much to eat.
The evidence for our being carnivores is contained within us: our gastrointestinal tract. As biochemistry
textbooks are not the easiest books to read, see Walter Voegtlin's book, "The Stone Age Diet", published in
1976, for a masterful treatise on the subject.
Barry Groves http://www.second-opinions.co.uk
PALEODIET Archives
From: Liza May
10/61 (2003)
Reply-To:
Date: Sat, 23 Aug 2003 10:59:15 -0400
Public release date: 21-Aug-2003 Contact: Steve Bradt 215-573-6604 University of Pennsylvania
Smaller food portions may explain the 'French paradox' of rich foods and a svelte population
PHILADELPHIA -- The "French paradox" -- the perplexing disconnect between France's rich cuisine and
slender population -- can be explained in part by portions that are significantly smaller in French restaurants
and supermarkets than in their American counterparts. So say researchers at the University of Pennsylvania
and CNRS in Paris, who compared the size of restaurant meals, single-serve foods and cookbook portions on
both sides of the Atlantic.
"The French paradox is only a paradox if one assumes that dietary fat is the major cause of obesity and
cardiovascular disease, " said Paul Rozin, professor of psychology at Penn and lead author of a paper in the
September issue of the journal Psychological Science. "However, recent studies suggest that the importance
of fat intake as a risk factor has been greatly exaggerated.
While the French eat more fat than Americans, they probably eat slightly fewer calories, which when
compounded over years can amount to substantial differences in weight."
The French paradox has long stymied American dieters and scientists, puzzled by the ability of the French to
remain trim while downing buttery croissants, creamy brie and decadent pastries. Just 7 percent of French
adults are obese, as compared with 22 percent of Americans, and the mortality rate from heart disease is
significantly lower in France.
Rozin and his colleagues weighed portions at 11 comparable pairs of eateries in Paris and Philadelphia,
including fast-food outlets, pizzerias, ice cream parlors and a variety of ethnic restaurants. They found the
mean portion size across all Paris establishments was 277 grams, compared to a mean in Philadelphia of 346
grams -- 25 percent more than in Paris.
In just one of the 11 comparisons, between Hard Rock Cafes in both cities, were the Parisian portions larger.
Three other international restaurant chains consistently served larger portions in the U.S., and Philadelphia's
Chinese restaurants served meals that were on average 72 percent heftier than those served by Chinese
restaurants in Paris.
The researchers also examined references to portion size in Philadelphia and Paris editions of the 2000 Zagat
restaurant guide. Serving sizes were not only mentioned roughly three times as frequently in reviews of
Philadelphia restaurants, but, of these mentions, fully 88 percent described large portions, compared to just
52 percent in Paris.
"Many studies have shown that, if food is moderately palatable, people tend to consume what is put in front
of them and generally consume more when offered more food, " Rozin said. "Much discussion of the 'obesity
epidemic' in the U.S. has focused on personal willpower, but our study shows that the environment also plays
an important role and that people may be satisfied even if served less than they would normally eat."
Extending their approach to single-serve foods sold in supermarkets, Rozin and colleagues found 14 of 17
items studied were larger in American stores. For example, a candy bar sold in Philadelphia was 41 percent
larger than the same product in Paris, a soft drink was 52 percent larger, a hot dog was 63 percent larger and
a carton of yogurt was 82 percent larger.
Rozin's co-authors on the Psychological Science paper are Kimberly Kabnick and Erin Pete at Penn, who
conducted the work as part of their senior Psychology Honors thesis, and Claude Fischler and Christy
Shields at CNRS. Their work was sponsored by the National Institute on Drug Abuse.
PALEODIET Archives
From: John Fletcher
Reply-To:
Date: Mon, 25 Aug 2003 15:24:40 +0100
Perhaps the fact that the French eat more slowly is also a factor? Dr John Fletcher Reediehill Farm,
Auchtermuchty, Fife KY14 7HS Scotland Tel (44) 1337 828369 Fax (44) 1337 827001
www.fletcherscotland.co.uk e-mail:
11/61 (2003)
PALEODIET Archives
Subject: Reply to Tamsin
Reply-To:
Date: Tue, 26 Aug 2003 12:10:02 -0500
Reply to Tamsin (see below for my response to some points made)
Tamsin: I am afraid that yes for a lot of people, it really is that simple. In a world where 200million people
are obese, with all the consequent health risks that this entails, and with an increasingly sedentary lifestyle in
the developed world, taking in any amount of essential fatty acids and fish oils is not going to do as much for
you as adjusting one's energy balance: eating less or exercising more as a first step to improving health will
do more good as a whole for individuals AND for society than specific dietary changes.
Ed: Tamsin, you bring up a good point about COMPARISON of variables (ie. What weighs heavier in
influencing outcomes, energy balance or diet quality?), but I have to ask you: How did 200 million of us
become obese? Was it a pure lack of will-power, or did the food industry have something to do with it? Are
there ways that food scientists have capitalized on human physiology to create foods that encourage
consumption, or not?
Continuing with this line of thinking, a telling string of questions might be: What is caffeine doing in Cocacola? What was the original ingredient in COCA-cola? Have cola companies been able to move into even
primary schools now with their soda pop machines? Has this now largely replaced milk/juice consumption?
In short, what role has industry played in this centurys over-consumption by the public (a public who has for reasons which this key article could have resolved - become cynical regarding nutrition
knowledge/advice)?
Also, apparently my research examples showing diet QUALITY (increased omega-3 fat consumption)
affecting human lives in a quantitative way (surviving heart disease) and possibly also in a qualitative way
(possibly affecting intelligence) failed to persuade you that diet quality is a major issue. If the 2 examples
that I gave are not convincing enough, then I will believe that this discussion was over before it began
(which, I feel, is unfortunate).
Tamsin: Until the message is clear that most people will never be able just to eat as much as they want and
stay as thin as they like, then the growing trend of increasing obesity will continue, while people desperately
turn to pharmaceuticals or quack diets.
Ed: Tamsin, this goes back to my earlier point about the food industry using human physiology to drive up
consumption which, when combined with perpetuated public confusion that stems from those in the know
who prefer not to inform the public about the details regarding human nutrition and satiety, leads to our
predicament.
I concur that the human will is not an entirely robust bed-rock that can be relied upon to stem overeating
(many will overeat, even if you show them how to manage food intake, satiety mechanisms, etc), but you are
calling for a denial of human weakness (ie. the public just needs to be disciplined more, or suffer) and I am
calling for education of the public.
In short, I believe that I am being more realistic and that you are evading a critical issue. So, it seems that we
both believe that the other is evading something. Now we just have to figure out which of our competing
views is the more rational one.
Tamsin: One has to ask if ET has something against Leonard, especially given what he writes about the
pressures of agribusiness, when Leonard is well known for being an eminent nutritional anthropologist with
a long history of good and solid research in this area?
Ed: I have nothing personally against Leonard. I have to admit that I did research Leonards numerous
publications (and I was awful scared to find out that he is indeed eminent!). The reason that I did not let this
interfere with my response is that I recognized that my fear (of strongly disagreeing with someone eminent)
was irrational, no matter how strongly felt its very roots stem from the logical fallacy of the Appeal to
Authority.
Ed
PALEODIET Archives
Subject: [Fwd: RE: Draft of my "Letter to the Editor" sent to Scientific American]
12/61 (2003)
From: Todd Moody

Reply-To:
Date: Tue, 26 Aug 2003 14:35:26 -0400
Perhaps the French eating more organ meats and root vegetables is part of their better health. Also for the
Greeks. Organ meats and root vegetables are strongly featured in hunter gatherer diets- I strongly encourage
them as firstly I suspect they are important to good health and secondly I don't like Paleo diets being diets of
exclusion- if one concentrates too much on what NOT to eat one gets monotony, so these give us some room
to broaden the diet (even if many people find turnips and liver unappetising, that is their freedom to choose).
I was never able to find the antioxidant levels of root vegetables despite a thorough search. The lacklustre
reputation of root vegetables may have left them unfairly ignored by the biochemists.
As for eating more slowly, it seems to me that the French Greeks and Italians talk a lot more whilst eating
(dare I say using their hands to gesticulate might further slow things a bit). Has anyone seen any research on
whether talking during meals is correlated (positively or negatively) with overweight?
Ben Balzer
PALEODIET Archives
Subject: Re: Reply to Tamsin
From: Liza May
Reply-To:
Date: Tue, 26 Aug 2003 16:10:44 -0400
Edward Thompson wrote:
> What weighs heavier in influencing outcomes,
> energy balance or diet quality?), but I have to ask you: How
> did 200 million of us become obese? Was it a pure lack of
> will-power, or did the food industry have something to do
> with it? Are there ways that food scientists have
> capitalized on human physiology to create foods that
> encourage consumption, or not?
It's a combination of many factors Edward. Lagging adaptation to modern foods, human nature re eating and
addictions, quality and availability of food available, advertising, exercise/overwork/sleep patterns.
Liza
PALEODIET Archives
Reply-To:
Date: Tue, 26 Aug 2003 17:20:00 +0100
On Sat, 23 Aug 2003, Barry Groves wrote:
> Andrew Millard wrote:
> It seems incredible to me that adults on a 1000-calorie diet could gain weight, as their metabolic
> expenditure ought to exceed this with even a modest amount of activity, and if the energy is not
> coming from burning of body reserves, then our fundamental understanding of where biological
> systems get their energy from is in doubt. Did these studies control for the activity levels and
> energy expenditure of the patients? I hope you will bear with me as the following is rather long.
13/61 (2003)
It is long, but it does not answer my questions. That calories are measured in a bomb calorimeter is only
tangentially relevant: the calorimeter is very efficient at extracting energy from the food and thus the
measurement provides an upper bound on what the human body can extract from its food. So, how does
someone on a 1000 calorie diet, but who must be extracting less than this from the diet, gain weight even if
they lie in bed all day? (Human adults' basal metabolic rate is 70-80 Watts depending on sex and age, so the
minimum kilocalories required per day is about 3600*24*75/4200=1542.)
> In fact the digestive process is quite inefficient so that all we eat is not even absorbed by the
> body, let alone used by it.
True, though this is not what you say on your website http://www.secondopinions.co.uk/carn_herb_comparison.html where human and wolf digestive efficiencies are given as an
amazing 100%!
I also take issue with the following:
> Body cells are in a constant state of death and rebirth. No matter how many birthdays you have
> had, very little of you is more than eight years old. The primary function of dietary proteins is
> used in this process: for the manufacture and repair of skin, blood and other body cells; to make
> hair and finger- and toe-nails. The amount of protein needed for this purpose is generally
> accepted to be about one gram per kilogram of lean body weight. As meats contain approximately 23
> grams of protein per 100 grams, a person weighing, say, 70 kg (11 stones) needs to eat about 300 g
> (11 oz) of meat, or its equivalent, every day just to supply his basic protein needs. Even eating
> lean chicken this would contain some 465 calories. These calories are not used to supply energy,
> they contribute nothing to the body's calorie needs and so must be deducted if you are counting calories.
But only the skin hair and nails are excreted as protein (plus excretion in breastmilk). The other body cells'
protein is broken down and recycled within the body or excreted as urea, so the protein intake required for a
protein mass-balance is not as much as you say, or you have listed too many tissues as protein outputs.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: [Fwd: RE: Draft of my "Letter to the Editor" sent to ScientificAmerican]
Reply-To:
Date: Tue, 26 Aug 2003 17:49:01 -0500
Todd Moody wrote:
> Perhaps the French eating more organ meats and root vegetables is part of their better health.
> Also for the Greeks. Organ meats and root vegetables are strongly featured in hunter gatherer
> diets- I strongly encourage them as firstly I suspect they are important to good health and
> secondly I don't like Paleo diets being diets of exclusion- if one concentrates too much on what
> NOT to eat one gets monotony, so these give us some room to broaden the diet (even if many people
> find turnips and liver unappetising, that is their freedom to choose). I was never able to find
> the antioxidant levels of root vegetables despite a thorough search. The lacklustre reputation of
> root vegetables may have left them unfairly ignored by the biochemists.
Have you tried the USDA nutrient database? It doesn't cover things like lycopene, but it certainly lists the
antioxidant vitamins and minerals.
ITA about organ meats. I had a debate on a totally non-nutrition-related newsgroup recently because one of
the posters came up with the old canard about liver being unhealthy because it's "the filter of the body" -- as
if livers were like oil filters, and all the toxins just stayed in them. I try to work liver in fairly frequently, and
need to start eating kidneys again; I grew up eating them and always liked them. I mean, liked them as in,
"Oh, goody, kidneys for dinner!!" rather than, "Oh, okay, I'll eat them..."
Haven't tried sweetbreads, but I suppose I should; I bet I'd like them. I do worry about brain, what with CJD
and all that. Oh, and marrow is arguably the most delicious substance on the planet. Hot lamb marrow,
mmmmmm...
14/61 (2003)
Of course, we could all just eat a lot of cheap luncheon meat, liverwurst, and chorizo. Isn't that where most
organ meats go nowadays? The chorizo at my grocery store has "salivary and lymph glands" listed as the
primary ingredient. Mighty tasty, too. -- Dana W. Carpender
PALEODIET Archives
Subject: French Paradox
From: Don Wiss
Reply-To:
Date: Tue, 26 Aug 2003 19:37:35 -0400
When people look for reasons for the French Paradox they look for what they are adding to their diet to get
protective benefits. Todd Moody suggests they are eating more organ meats and root vegetables. Recent
news article suggest it comes from their drinking red wine. This focus on what to add probably comes from a
marketing mentality. If we can just find what it is we can sell it to everybody else.
I, on the other hand, have the theory that it comes from what they don't eat. So my theory is the paradox
comes from their consuming less trans fats. They use real butter, not margarine. They tend not to deep fry
foods. French fries are pan fried in oil. In general they eat real foods, not fake ones. Does this makes sense to
anyone else?
Don.
PALEODIET Archives
Subject: Re: French Paradox
From: Jerry Stegenga
Reply-To:
Date: Wed, 27 Aug 2003 09:39:18 EDT
In a message dated 8/27/2003 9:18:52 AM Eastern Daylight Time, writes: In general they eat real foods, not
fake ones. Does this makes sense to anyone else? Yes, It has long been my opinion that manufactured
(processed) foods have been our downfall. These foods include all dairy products, all grain products - - -any
food that would not exist in nature without mans intervention. JerrySteg
PALEODIET Archives
From: matesz
Reply-To:
Date: Wed, 27 Aug 2003 09:54:08 -0400
Don Wiss wrote:
> I, on the other hand, have the theory that it comes from what they don't eat. So my theory is the
> paradox comes from their consuming less trans fats. They use real butter, not margarine. They tend
> not to deep fry foods. French fries are pan fried in oil. In general they eat real foods, not fake
> ones. Does this makes sense to anyone else?
Yes, I agree.
Don
PALEODIET Archives
Reply-To:
15/61 (2003)
Date: Wed, 27 Aug 2003 10:54:22 -0500

Don Wiss wrote:
> When people look for reasons for the French Paradox they look for what they are adding to their
> diet to get protective benefits. Todd Moody suggests they are eating more organ meats and root
> vegetables. Recent news article suggest it comes from their drinking red wine. This focus on what
> to add probably comes from a marketing mentality. If we can just find what it is we can sell it to
> everybody else. I, on the other hand, have the theory that it comes from what they don't eat. So
> my theory is the paradox comes from their consuming less trans fats. They use real butter, not
> margarine. They tend not to deep fry foods. French fries are pan fried in oil. In general they eat
> real foods, not fake ones. Does this makes sense to anyone else?
Yes. Also the fact that they eat remarkably less sugar than Americans do (or than the English and Scots do,
for that matter.)
Of course, there's no reason why there has to be *one* factor. Multifactorialism is pretty darned common, I
believe.
-- Dana
PALEODIET Archives
Subject: Organ Meats (was: RE: Draft of my "Letter to the Editor" sent to ScientificAmerican]
From: Liza May
Reply-To:
Date: Wed, 27 Aug 2003 12:01:08 -0400
Dana W. Carpender wrote:
> I had a debate on a totally non-nutrition-related newsgroup recently because one of the posters
> came up with the old canard about liver being unhealthy because it's "the filter of the body" -> as if livers were like oil filters, and all the toxins just stayed in them.
Certain toxins do tend to accumulate in the liver, however, so it is wise to be aware if there is some specific
agent you'd like to avoid.
> Oh, and marrow is arguably the most delicious substance on the planet. Hot lamb marrow, mmmmm...
My favorite too, but I prefer it raw, when it is dense and creamy like butter. Cooking makes it too gelatinous
for me.
Liza
PALEODIET Archives
Subject: humans and obesity
Reply-To:
Date: Wed, 27 Aug 2003 12:45:19 +0100
Just want to say everyone, that after a long silence on the Palaeolithic Diet symposium, what a great
discussion this is. Have decided that I am going to reply to lots of points raised by different people in two
emails, separated by subject, as otherwise we are getting longer and longer messages with things copied in. I
shall reply to Ed Thompson's more specific email re his and my views in another, so everyone can skip that if
too bored or not enough time!
So, this posting concerns obesity. Ed Thompson suggests that I think the current increase in obesity is due to
lack of willpower, whereas he has his suspicions of the conspiring food industry. In a way I do think it
related to willpower, but totally unavoidable as it is an age old drive to eat more, as I go with the 'thrify gene'
theory that humans throughout all evolution have struggled against starvation, and therefore we have been
genetically selected to be on the plump side - gain weight easily in times of plenty, so there is a reserve in
times of hardship. For a great, if v personal view of recent selection pressures such as documented famines,
see: Prentice, A. M. (2001). Fires of life: the struggles of an ancient metabolism. Nutrition Bulletin 26: 1327. A thought-provoking read.
16/61 (2003)
I don't think we can blame the food industry, because all they are doing is capitalising on a natural urge. We
are programmed to prefer energy dense foods, and this programming came about long before the food
industry happened. Look at the goddess figurines from Neolithic Catal Huyuk in Turkey (6000BC) - they are
hugely fat. Fat has been recognised and worshipped as desirable for a long time in human culture and
society, until very recently when all of a sudden there was no shortage of foods to balance out our desire to
eat. This desire for energy-dense foods is also why people will never be able to eat as much as they like and
be as thin as they like, despite what Bob Avery says. Because what he overlooked in his comment that we
would be fine if we all ate only raw veggies, is that when people want to eat as much as they like, they want
to eat as much as they like OF FOODS THAT THEY LIKE. I would venture that most people would think
that eating only raw veggies isn't that much more palatable than cutting back.
Thinking about human weight and whether we are the only species that struggle. Barry Groves says that 'all
animals in their natural habitat are a normal weight.' That point is one that most animal researchers would
debate. Some can often be severely underweight. The mechanism for controlling animal weight in the natural
habitat is not simply natural satiety, although that will play a part. There can be an oscillation in weight of an
individual, as Andrew Millard pointed out in the case of an overweight lion that cannot catch its food, so
starves until it is thin enough to be fast enough to catch it. Or there can be changes in the population size and
structure resulting in the most number of (just) reproducing individuals, who are not necessarily in prime
individual health. The latter point has been amply demonstrated in the red deer on Rum: Tim Clutton-Brock
et al.'s work that a season of plenty leads to fatter deer in the very short term but then greater reproductive
success which will use up all the reserves. A similar thing has been observed in feral donkeys in Australia,
where after culling of a population to provide more grazing per individual and improve individual fitness, the
population rebounded in size very quickly, growing at 20% a year, and with far greater survival of neonates,
to get back to the original density. Both studies are detailed in a v good book: White, T. R. C. (1993). The
inadequate environment. Nitrogen and the abundance of animals. Berlin, Springer Verlag.
On the flip-side, we are not the only animals that will be obese if given the chance. Robert Sapolsky's famous
study of a olive baboon troop in the Masai Mara, whom he wrote about as 'junk food monkeys', completely
abandoned their usual diet when they discovered that they could feast to their hearts' content on garbage from
the national park buildings. Despite that they matured earlier and had a wonderful time with endlessly
available food, they also became obese, cholesterol (LDL) rose, and they all finally got a nasty dose of
bovine TB. I know that one can hold up hands in horror and say humans were responsible for the waste, but
the baboons CHOSE to eat this food, because it was an easy life. We humans do much the same.
Next mail: carnivore or omnivore??
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
Subject: humans: carnivores or omnivores
Reply-To:
Date: Wed, 27 Aug 2003 12:50:16 +0100
So, the old chestnut: are humans adapted to be carnivores or omnivores? I have to conclude, looking at all
the evidence, that I believe that we are definitely omnivores. My responses to the number of points made are
below.
17/61 (2003)
1. Gut shape etc Our gut is NOT that of a carnivore (pace Barry Groves) or herbivore (folivore) in terms of
proportion. For the best discussion of this area, see work by Katharine Milton, with an excellent essay in the
fantastic book by Harris and Ross (1987). Food & Evolution: Towards a Theory of Human Food Habits. The
most similar guts in proportion and structure (most gut volume in small intestine) are the New World
capuchin monkeys, and also baboons. Both of these species consume high-quality, energy-dense foods,
which are not meat, but sugary fruits and protein-rich and lipid-rich seeds. Animal meat and fat is an energydense food, but it's not the only one. But Milton also makes the point that the gut is a very plastic organ, with
animal studies showing that a change in diet (incr energy requirements, decr diet quality) can result in a
change in gut proportion. So the human gut as is could be a relatively recent development. Also worth
saying, as Milton does, that the gut is very ancestrally derived, so there is not an immediate correlation with
gut and diet: eg a cecum usually indicates a diet high in plant foods, but both the hippo and the giant panda
lack a cecum and they are strongly herbivorous.
Following on from Todd Moody's mention of Craig Stanford's point that humans have, of necessity,
followed an adaptational trajectory of increasing carnivory, it may be that we are adapted to energy-dense
foods, that were originally fruits and seeds etc, but as our abilities with tools and social organisation (hunting
in groups) developed, we replaced one energy dense food that was time-consuming to gather and each
individual had to do themselves with another that was easier and quicker to get. Optimal foraging theory.
2. Ethnographic evidence for hunter-gatherer diets. Dana Carpender cites Cordain et al.'s article in Am. J.
Clin. Nutr., March, 2000, to provide 'evidence that we evolved on a meat-heavy diet virtually devoid of
grains, beans, and other concentrated carb foods.' I have one slight caveat that using ethnographic evidence
of HG diets as an example of how we used to live can be dangerous, as HGs have been marginalised by
developing societies for several centuries at least, and so what is representative in historical sources MAY
not be representative of Palaeolithic and Mesolithic populations. But further than that, I take issue with the
point that we have evolved on a hunter-gatherer diet, as hunting and gathering as we now think of it in a
socially developed society is a relatively recent thing in human evolution. We did an awful lot of eating and
evolving as early hominids (Australopithecus, early Homo), and so many of our dietary evolutions and
adaptations precede Homo sapiens sapiens society. Cordain et al, from my reading of their excellent article,
do not suggest that a meat-rich ( > 50% energy) is the diet we humans evolved on, just what most huntergatherers have eaten recently. They also make the point quite clearly that no single diet represents all huntergatherer societies, which suggests to me that we are well adapted to a varied diet, similar to other
omnivorous primates, and dissimilar to carnivores such as felids, or folivores, who both have a much
narrower diet composition.
3. Fossil evidence The palaeontological and archaeological evidence is of course inconclusive, given the
small number and fragmentary quality of remains over the last 5Myr. However, the dependence on meat is
thought to be a relatively recent development. Based on dental wear, most Australopithecus are thought to
have a wide ranging diet varying between fruits and leaves (A. africanus) to tougher, more fibrous foods (A.
robustus). Stable isotope analysis provides some clue that Australopithecus was firmly adapted to the
grassland. Only coming into the Palaeolithic is the dependence on animal resources increased (H
neandertalensis and H sapiens), and one could certainly argue that in the colonisation of Europe, that is an
adaptation to a colder environment, where availability of suitable plant foods is reduced.
4. Physiological adaptations Finally, physiologically, we still carry many of the traits that evolved from our
primate ancestry, such as an inability to synthesise Vitamin C, very rare among non-primate mammals. This
suggests that at some point, we ate so much that we didn.t need to make it. So fruit must have been an
important part of our diet for long enough to lose that synthetic ability. Todd Caldecott also makes a good
point that fruits as we eat them now do now necessarily bear much resemblance to wild fruits, being lower in
fibre and higher in sugar. This is also true for wild vs farmed animals. So just eating what on the surface may
appear to be a traditional diet may not be what it would have been 1000's of years ago.
Think that's enough for now! Off to have my well-balanced lunch of animal and plant protein, fat and
carbohydrate, all in moderation.
Tamsin
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
18/61 (2003)

From: Barry Groves
Reply-To:
Date: Wed, 27 Aug 2003 15:41:17 +0100
Andrew: So, how does someone on a 1000 calorie diet, but who must
> be extracting less than this from the diet, gain weight even if they lie in bed all day? (Human
> adults' basal metabolic rate is 70-80 Watts depending on sex and age, so the minimum kilocalories
> required per day is about 3600*24*75/4200=1542.)
Good question. In being brief I have misrepresented the facts slightly. There was only one patient who put on
weight. This was due to water retention during her menstrual cycle. But others maintained their weight on 1,
000 kcal, high-carb diets for short periods. Why they didn't lose is unclear from the data.
Andrew:
> In fact the digestive process is quite inefficient so that all we eat is not even absorbed by the
> body, let alone used by it. True, though this is not what you say on your website
> http://www.second-opinions.co.uk/carn_herb_comparison.html where human and wolf digestive
> efficiencies are given as an amazing 100%!
Voigtlin states: "The coefficient of digestion is the percentage of ingested food that is digested, absorbed,
and utilized by the animal. It is a measure of nutritive efficiency and, in the carnivore EATING ITS
NATURAL DIET of meat and fat, the coefficient approaches 100%." (emphasis mine).
Much of what we eat today is *not* natural to us as a species. A proportion of this will pass undigested
through the gut. Even herbivores waste around 50% of their intake through imperfect digestion and
absorption. As we are not herbivores, it would not be unreasonable to assume that our gut is at least as
inefficient at processing such material, particularly if it is eaten in the raw state.
Andrew:
> But only the skin hair and nails are excreted as protein (plus excretion in breastmilk). The other
> body cells' protein is broken down and recycled within the body or excreted as urea, so the
> protein intake required for a protein mass-balance is not as much as you say, or you have listed
> too many tissues as protein outputs.
Much of the gut mucosa is replaced every three days. Are those cells reabsorbed? I reiterate that 1g per kg
lean body weight is the accepted figure for dietary protein intake if from animal sources; 1.5g if from plant
sources. If you know otherwise, please give me a reference. Although, having asked that, these figures will
probably have been revised downward recently as 'healthy eating' insists that we eat less meat and more
flour, so I wouldn't put too much trust in them.
PALEODIET Archives
Subject: Re: humans and obesity
Reply-To:
Date: Wed, 27 Aug 2003 19:09:28 -0400
Tamsin O'Connell wrote:
> [...] I don't think we can blame the food industry, because all they are doing is capitalising on
> a natural urge. We are programmed to prefer energy dense foods, and this programming came about
> long before the food industry happened. Look at the goddess figurines from Neolithic Catal Huyuk
> in Turkey (6000BC) - they are hugely fat. Fat has been recognised and worshipped as desirable for
> a long time in human culture and society, until very recently when all of a sudden there was no
> shortage of foods to balance out our desire to eat. Correct me if I'm wrong, but no matter the
> availability, I don't think you can get fat on a Paleolithic diet (excluding cereals and milk
> products). The possibility to get fat (amongst other) is a Neolithic novelty. This desire for
> energy-dense foods is also why people will never be able to eat as much as they like and be as
> thin as they like, despite what Bob Avery says. Because what he overlooked in his comment that we
> would be fine if we all ate only raw veggies, is that when people want to eat as much as they
19/61 (2003)
> like, they want to eat as much as they like OF FOODS THAT THEY LIKE. I would venture that most
> people would think that eating only raw veggies isn't that much more palatable than cutting back.
> [...] On the flip-side, we are not the only animals that will be obese if given the chance. Robert
> Sapolsky's famous study of a olive baboon troop in the Masai Mara, whom he wrote about as 'junk
> food monkeys', completely abandoned their usual diet when they discovered that they could feast to
> their hearts' content on garbage from the national park buildings. Despite that they matured
> earlier and had a wonderful time with endlessly available food, they also became obese,
> cholesterol (LDL) rose, and they all finally got a nasty dose of bovine TB. I know that one can
> hold up hands in horror and say humans were responsible for the waste, but the baboons CHOSE to
> eat this food, because it was an easy life. We humans do much the same.
If I understand this common behavior well, humans and baboons are behaving like addicts as soon as they
eat foodstuff that was never part of their natural (original) environment.
Jacques Laurin
PALEODIET Archives
Subject: Re: humans and obesity
From: Bob Avery
Reply-To:
Date: Wed, 27 Aug 2003 22:32:44 -0400
Tamsin,
I wasn't going to speak further, but since this post appears to have been directed at me, I will elaborate.
> This desire for energy-dense foods is also why people will never be able to eat as much as they like and
be as thin as they like, despite what Bob Avery says.
And I still disagree with you. I've seen countless examples. It's what you eat, not how much you eat, that
counts most.
> Because what he overlooked in his comment that we would be fine if we all ate only raw veggies, is that
when people want to eat as much as they like, they want to eat as much as they like OF FOODS THAT
THEY LIKE.
"Likes" are malleable and formed largely by habit. New habits can be learned.
This seems to apply in all areas of life, not just diet. Aren't choices of recreational activities determined more
by habit than by genetic imperative? It seems fashionable these days to blame most human miseries on
genetics when environment is by far the larger determining influence of the two.
> I would venture that most people would think that eating only raw veggies isn't that much more palatable
than cutting back.
I would venture to agree with you, but most people have never given them a fair trial. After an
acclimatization period, they can be much more enjoyable than the former "likes" ever were. I know; I've
been there. For 45 years, I made poor eating choices due to ignorance and habit. I'll now choose fresh,
organic peaches and broccoli over chocolate cake any day (though my former poor choices weren't quite
THAT poor).
Of course, the quality of the produce is hugely relevant too. Much of what's for sale these days isn't worth
eating, I'll grant you.
> 'junk food monkeys', completely abandoned their usual diet when they discovered that they could feast to
their hearts' content on garbage from the national park buildings.
> they also became obese
Exactly illustrative of the problem humans face! That cooked, highly refined and processed commercial junk
is what makes us fat, not our natural foods as obtainable in our natural habitats.
Sure, the artificial, processed stuff is addictive -- it's meant to be -- but it only tastes "better" to warped
tastebuds. The animals first eat it as a matter of expediency, and then they get hooked on it, just as a cocaine
addict does with cocaine or a tobacco addict with nicotine.
Many recovered nicotine addicts can't stand the smell of tobacco smoke any more than nonsmokers can, yet
they wallowed in smoky bars and pool halls formerly and appeared to enjoy the smoke. Why is that?
20/61 (2003)
Anyone here ever get hooked on sodium chloride, where everything you eat had to be heavily salted to "taste
good"? And then had the opposite experience of giving up salt completely and after an adaptation period
gradually rediscovering the delicious, delicate flavors of the pure, unadulterated foods in their natural,
unspiced state? Which ultimately tastes better? I've been on both sides of that fence, but it's easy to guess
which side I eventually came down on.
None of this adulterated food eating is a genetic imperative. For most humans, it's a conscious choice, albeit
one heavily influenced by media misinformation and prior cultural conditioning begun almost from the
moment of birth. (Ever noticed how babies first being indoctrinated with processed, adulterated "baby foods"
spit them out repeatedly until they become hooked on them? We do have natural instincts that warn us away
from that stuff, but they become overwhelmed by cultural conditioning at a very early age.)
BTW, I am far from obese, most would say underweight, and have no need of counting calories to remain
that way because satiety mechanisms work very well when natural, unprocessed and unadulterated foods are
eaten.
By contrast, before I started eating this way, I had developed the so-called "middle age spread, " with
protruding waistline and double chin. Those are long gone now. My genes are as "thrify" as anyone else's
when they are abused with poor food choices.
I'm one living example, but only one of many, of what I'm talking about. Perhaps you still disagree (not
having personally experienced both ways of eating for any length of time), but I think it's far easier to learn
to make better food choices than it is to count calories and portion sizes, and it makes for a much more
enjoyable eating experience in the long run. In the short run, any change from the customary will be
uncomfortable. That's the nature of biological organisms and their homeostatic adaptation mechanisms.
> Despite that they matured earlier and had a wonderful time with endlessly available food, they also
became obese, cholesterol (LDL) rose, and they all finally got a nasty dose of bovine TB.
"Despite" is the wrong word and shows the cultural bias of the researcher.
This early maturation is a pretty universal sign of degeneration. The "common wisdom" has it that the
continuing decline in the age of human puberty in Western cultures over the past century, especially in the
US, is due to better nutrition, when in fact it is due to the exact opposite cause.
My young nephew undertook a cleverly considered science project for an elementary school biology class.
Not knowing what the result would be, he raised two groups of common beetles in aquariums on ad libidum
feedings of identical foods, the only difference being that one group had its drinking water spiked with
caffeine. The result of the experiment was that the caffeinated beetles became much more active than the
controls (one might say hyperactive), grew faster, matured sooner, reproduced earlier -- and DIED earlier!
Those of you who are home gardeners or farmers will recognize the old farmers' aphorism, "The stressed
plant goes first to seed."
Yes, under physiological stress, biological organisms mature and reproduce at earlier ages. It applies to
plants, insects, animals, and humans alike.
Probably Nature's way of saying, "Hey, this organism isn't going to last very long! We'd better hurry up and
get it reproducing ASAP before it keels over."
> I know that one can hold up hands in horror and say humans were responsible for the waste, but the
baboons CHOSE to eat this food, because it was an easy life. We humans do much the same.
Alas! Would that we humans were more intelligent and farsighted than baboons! This world would be a
much better place.
Bob Avery
PS I would like to thank the moderator for allowing some discussion here for a change. It's nice to see the list
coming to life again.
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Thu, 28 Aug 2003 07:33:12 +0100
Yes, Don, I am sure you are right.
21/61 (2003)
It may also be related to the way they eat. I have listed a number of differences below, but perhaps the most
significant difference may be that meals around the Mediterranean aren't eaten on the run, under stress. (The
various differences below are to be read together -- Mediterranean 1 with British 1, and so on)
Mediterranean Eating Pattern 1. The average Mediterranean diet comprises natural, unprocessed meat,
vegetables and fruit, which are usually bought fresh daily. 2. Meat plays an important part in the diet, 3.
Meals are taken slowly, without hurrying. Lunch usually takes up to two hours -- and is followed by a siesta.
4. Fats eaten are butter, olive oil and unprocessed animal fats 5. Over 60 percent of energy intake is before
2.00 pm 6. Wine (believed to be protective againt heart disease), is drunk during meals as part of that meal.
British Eating Pattern 1. The average British diet is composed of packaged, highly processed foods, high in
concentrated carbohydrates, hydrogenated vegetable oils and chemical additives. 2. We are told to eat less
meat 3. Food is rushed. Lunches are eaten on the run or combined with work. Often, they are junk food
snacks. 4. Fats eaten are highly processed margarines, low fat fat substitutes, and hydrogenated vegetable
oils. 5. The largest meal is eaten in the evening 6. Beer, wines and spirits are drunk in the evening after the
evening meal.
----- Original Message ----- From: "Don Wiss" To: Sent: Wednesday, August 27, 2003 12:37 AM Subject:
French Paradox
> When people look for reasons for the French Paradox they look for what they are adding to their
> diet to get protective benefits. Todd Moody suggests they are eating more organ meats and root
> vegetables. Recent news article suggest it comes from their drinking red wine. This focus on what
> to add probably comes from a marketing mentality. If we can just find what it is we can sell it to
> everybody else. I, on the other hand, have the theory that it comes from what they don't eat. So
> my theory is the paradox comes from their consuming less trans fats. They use real butter, not
> margarine. They tend not to deep fry foods. French fries are pan fried in oil. In general they eat
> real foods, not fake ones. Does this makes sense to anyone else?
> Don.
PALEODIET Archives
From: Reply-To:
Date: Sun, 31 Aug 2003 11:58:20 EDT
Don,
I gave a talk for a conference organized by Dr. George Mann's Veritas Society in November 1991, and then
wrote the chapter for George Mann's book of this conference, which was published in 1993 in the UK. The
data for fat intake in France match your understanding completely. Less trans in the diet, more animal fat in
the diet, and the French regulations do not allow frying in partially hydrogenated fats or for that matter deep
frying in either soy or canola oils.
Mary Enig
PALEODIET Archives
From: jean-louis tu
Reply-To:
Date: Mon, 1 Sep 2003 09:14:04 +0200
As I live in France and I've spent one year in the United States, I think I am in a good position to compare
both diets and eating patterns:
1. Breakfast: mainly consists of bread, butter and jam. Although none of these foods are part of a Paleolithic
diet, breakfast is usually much lighter (in terms of calories) than the average American breakfast.
2. Main meals: usually meat, grains, vegetables, cheese. Fruit or cake for dessert. Usually, meals are more
varied than in the US, especially since we eat real meals (i.e. more whole foods) at lunch instead of
sandwiches.
22/61 (2003)
3. Drinks: it is true that French people drink more red wine, which is supposed to help prevent cardiovascular
disease, but we drink wine mainly in social occasions (and not so often at home). On the other hand, I think
the main difference with Americans is that we consume far less soft drinks and more water instead.
4. Between meals: we tend to eat less junk food.
5. Fat: we eat less hydrogenated fat. Compare the list of ingredients on a package of American food and on a
package of French food and you'll be convinced. Concerning oil, it is true that some olive oil is consumed,
but that's mainly in the South of France (at most 1/4 of the population).
6. Packaged foods are usually less processed in France than in the US (compare the length of lists of
ingredients).
7. Portion sizes: VERY significantly smaller in France (order a piece of pizza or a meal in a Chinese
restaurant in both countries and you'll see the difference).
8. Organ meats: we do eat some (pt), but not so much and not so often.
P.S. When I say "we" in the text above, I am actually not including myself since my diet is mainly raw Paleo.
PALEODIET Archives
Reply-To:
Date: Tue, 2 Sep 2003 13:21:28 -0600
On Monday, September 1, 2003, at 01:14 AM, jean-louis tu wrote:
> As I live in France and I've spent one year in the United States, I think I am in a good position
> to compare both diets and eating patterns: 1. Breakfast: mainly consists of bread, butter and jam.
> Although none of these foods are part of a Paleolithic diet, breakfast is usually much lighter (in
> terms of calories) than the average American breakfast.
Hi Jean-Louis
Is this traditional for the French, all over France and not just urban centers? What might a typical "farm"
breakfast be? In many places this was a hardy meal, something along the line of steak and eggs. In fact, I
think the idea of a "sweet" breakfast is a relatively modern innovation, and one that is not seen in many
traditional cultures, whether it was rich in animal protein or not (e.g. idlis and sambar in South India, beans
and tortilla in S. America etc.)
> 3. Drinks: it is true that French people drink more red wine, which is supposed to help prevent
> cardiovascular disease, but we drink wine mainly in social occasions (and not so often at home).
I seriously doubt that the wine issue alone makes a significant impact upon CVD prevention. Rather, I think
it might be wiser the broad array of vegetables in the traditional diet, from garlic and shallots, rampion and
mustard greens, edible flowers and culinary herbs, as well as free-range grass fed animal meat and viscera
etc. ALL of which are incredibly high in macro-trace minerals, water/fatsoluble vitamins, antioxidants etc,
etc.
Some cultures consider vegetables like garlic as both a food and medicine. Garlic is only the most familiar
example. Chosen somewhat randomly, another vegetable, Benincasa hispida (Kushmanda), a gourd in the
Curcubitaceae, is used in the cuisine of both India and China and has scientifically validated beneficial
effects upon memory and learning, ulcers and bronchospasm - of course the Indians and the Chinese have a
far more sophisticated understanding of its benefits, and has been recorded in the materia medica of India for
some 3000 years. The point is, most traditional cultures had a way to take care of themselves that was based
on empirical folkloric knowledge, easily accessible, growing in abundance in family gardens and in the wild.
Got a cold and flu? a ancient Chinese home remedy is a nice shitake mushroom broth with ginger and green
onion - all of which have demonstrated antiviral and immunomodulating properties. Anyway, it should be
clear that the extreme prevalence of CVD and autoimmune dz in the West are simultaneous with a loss of
traditional knowledge and practices. Wine consumption if anything has probably increased in prevalence in
NA, which hasn't affected the incidence of CVD at all. The to wine, as another potential source of CHOs, is
in moderation
> On the other hand, I think the main difference with Americans is that we consume far less soft
> drinks and more water instead.
23/61 (2003)
This is a huge problem in the states - it used to be a treat to go downtown to hang out at the local soda
fountain. Its amazing how dull we've become, and allowed what was previously exotic become the norm,
only to observe the effects on homeostatic mechanisms
Todd Caldecott, Cl.H., AHG Clinical Herbalist Wild Rose Clinic
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PALEODIET Archives
Subject: Humans are Meat Eaters
From: Liza May
Reply-To:
Date: Wed, 3 Sep 2003 16:42:21 -0400
Meat eating is an old human habit
19:00 03 September 03
Humans evolved beyond their vegetarian roots and became meat-eaters at the dawn of the genus Homo,
around 2.5 million years ago, according to a study of our ancestors' teeth.
In 1999, researchers found cut marks on animal bones dated at around 2.5 million years old. But no one
could be sure that they were made by meat-eating hominids, because none appeared to have suitable teeth.
Now an analysis by Peter Ungar of the University of Arkansas has revealed that the first members of Homo
had much sharper teeth than their most likely immediate ancestor, Australopithecus afarensis, the species
that produced the famous fossil Lucy.
What sharp teeth you have... Eating meat requires teeth adapted more to cutting than to grinding. The ability
to cut is determined by the slope of the cusps, or crests. "Steeper crests mean the ability to consume tougher
foods, " Ungar says. He has found that the crests of teeth from early Homo skeletons are steeper than those
of gorillas, which consume foods as tough as leaves and stems, but not meat.
Ripe fruit
But the crests of teeth from A. afarensis are not only shallower than those of early Homo, they are also
shallower than those of chimpanzees, which consume mostly soft foods such as ripe fruit, and almost no
meat.
"Ungar shows that early Homo had teeth adapted to tougher food than A. afarensis or [chimpanzees]. The
obvious candidate is meat, " says anthropologist Richard Wrangham of Harvard University.
Ungar used a laser to scan each tooth and mapped the surface as though it were a landscape, using a
geographic information system, he told a symposium on diet and evolution at the University of Arkansas in
August.
He had to find a way to compare teeth already worn by use, because unworn teeth are extremely rare in
fossils. In a previous study on the teeth of gorillas and chimps, he validated the technique by showing that
the differences between species' teeth remain constant however much they are worn down (Proceedings of
the National Academy of Sciences, vol 100, p 3874).
Short: http://tinyurl.com/m519
Long: http://www.newscientist.com/news/news.jsp?id=ns99994122
PALEODIET Archives
Subject: dietary ratios
Reply-To:
Date: Thu, 11 Sep 2003 13:46:14 -0600
Hello folks, i was reviewing Cordain's food pyramid:
24/61 (2003)
http://www.paleofood.de/ENGPaleo/ENGPyramids/engpyramids.html
and contemplating the impact upon patient health and compliance, I thought that it would be interesting and
helpful to get your feedback upon what y'all think of what proportions of different foods should comprise of
the diet. Because most folks don't pay all that much attention the specific caloric content of their diet, and nor
do most actually weigh out the foods they eat, I usually recommend dietary components in basic proportions
(i.e portions of the proverbial pie): it makes it easier for patients to actual visualize what to eat. According to
Cordain's food pyramid, meats make up 56-64% of the total caloric intake, which obviously contains some
admixture of fat and protein depending upon the protein source. Compared to the (non-starchy) vegetable
intake, which have an alkalizing effect on pH and supply a whole host of vitamins and antioxidant
compounds but provides little in the way of actual calories, the meat proportion may be less in my diet as
compared to Cordain, or it may be fairly close: there are obviously several variables to take into account
here. Also, because in temperate regions vegetation is available for a much longer portion of the year than
actual fruits, this is reflected in the proportion of fruit to vegetable intake I describe below:
30% meats 40% (non-starchy) vegetables 15% fats (above that contained in meats, e.g. olive oil, butter,
coconut oil etc) 15% carbohydrate, i.e. temperate fruits (in summer/fall) or starchy vegetables (in winter, not
potatoes).
I will also allow some whole grains (e.g. rice, oatmeal, barley, but not flour) for non-sensitive folks in the
CHO portion simply because most people will not give them up entirely unless the condition requires it (e.g.
CVD, diabetes, autoimmunity), and there may be some additional benefit as a source of fiber to maintain the
GI ecology. Although most patients make a "best effort" to achieve the above, in some cases its pretty hard
to determine what exactly they are eating day in and day out (without extensive reporting), so I often gage
successful implementation upon a reduction in symptoms (e.g. GI distress, skin conditions, BP etc.) I realize
that most of you are not clinicians, and therefore may not have any experience in implementing dietary
changes in others, but even still, I would be interested to hear how your thoughts or practices compare with
the above.
Of course it is impossible to eat completely in a paleolithic fashion, and given that most don't live in a
paleolithic environment (i.e. most of us live in a semi-tropical indoor environment for much of our lives), I
have modified the diet to reflect this as well, as well as my knowledge of dietary practices in traditional
Chinese and Indian (Ayurvedic) medicine.
Thanks for your thoughts...
*******************************************
*******************************************
*******************************************
PALEODIET Archives
Subject: Re: dietary ratios
From: matesz
Reply-To:
Date: Fri, 12 Sep 2003 12:50:09 -0400
A major problem with prescribing dietary ratios using percentage of calories is that meat and fat are up to 45
times more calorically dense than vegetables and fruits.
Consequently, meat and fat can supply more than 50% of calories in a diet while being less than 30% of the
weight.
Example:
100 g of beef brisket (182 cal) 114 g of sweet (or white) potato (120 cal) 100 g of broccoli (31 cal) 100 g of
blueberries (65 cal) 10 g of butter (72 cal) 12 g of whipped cream (unsweetened) (36 cal)
Total mass = 436 g Total calories = 506 Protein = 38 g Carb = 47 g Fat = 19 g
Percent calories from meat and fat = 57% Percent calories from vegetables and fruits = 43%
Dr. Cordain's Am J Clin Nutr article states that wherever possible hunter-gatherers consumed 45-65% of
energy from animal food. Conversely that means 35-55% from plants. This menu is right there.
25/61 (2003)
Percent mass from meat and fat = 28% Percent mass from plants = 72%
So is this meal, or the hunter-gatherer diet, meat-based or plant-based? Both! Meat/fat based by calories,
plant-based by weight.
Protein = 30% Carb = 37% Fat = 34% (Sum not = 100 due to rounding)
72% of mass is plants but protein is 30% of calories! Note that the inclusion of a starchy vegetable and a fruit
in the same meal does not produce an excessive carb load. Cordain's team estimated "the most plausible
percentages of total energy [in hunter-gatherer diets] would be 19-35% protein, 22-40% carbohydrate, and
28-58% fat." Again this menu is right on.
Remember the example I've given supplies only 506 calories. Add 10 more grams of fat or oil and the meal
is 446 g, 596 calories, 29 g fat, 44% of calories from fat, 31% carbohydrate, and 26% protein. Now 70% of
calories come from protein and fat, only 31% from carbs, but by weight it is still 70% plant foods.
Also, Cordain's team estimated that "fruit represented 41% of the total number of food items, seeds and nuts
represented 26%, and underground storage structures of plants (roots, tubers, and bulbs) represented 24%" of
plant foods eaten by hunter-gatherers. That means fruits, roots, tubers, and bulbs made up 65% of plant foods
eaten by hunter-gatherers. That's why my example includes a tuber and a fruit, together making two-thirds of
the weight of the plant food in the menu.
Cordain's team emphasized: "By and large, plant-food items with the greatest ratio of energy capture to
energy expenditure would have provided most of the daily plant-food energy of world-wide huntergatherers." In other words, they preferred fruits, roots, tubers, and bulbs to leaves and other low carbohydrate
plants by a wide margin.
So I don't think you can exclude or limit those foods and emphasize non-starchy vegetables and say you are
following the hunter-gatherer example. Besides, as my examples show, these can be included without
providing any overload of carbohydrate.
Also, Sebastian et al have calculated that 87% of hunter-gatherer diets were net base producing. If you do the
calculations (which I have in our forthcoming book, The Garden of Eating), to achieve a net base-producing
diet, it is necessary for fruits and vegetables to form more than 65% of the diet by weight. Which means, if
you include any grains, and want to maintain an alkaline residue, the grains have to replace some meat, not
some vegetables or fruits.
Todd Caldicott wrote:
"most [of us] don't live in a paleolithic environment (i.e. most of us live in a semi-tropical indoor
environment for much of our lives), I have modified the diet to reflect this as well, "
You may be interested to learn that traditional Eskimos kept their dwellings pretty warm. In his Harper's
article "Adventures in Diet", Stefansson wrote that in midwinter the Eskimo family he lived with "burned
seal or whale oil" for cooking and heating. "The temperature at night was round 60 degrees F, " but when the
fires were stoked during the day, after they returned from a day of fishing, "we came home to a dwelling so
heated by the cooking that the temperature would range from 85 to 100 degrees F, or perhaps even higher-more like our idea of a Turkish bath than of a warm room. Streams of perspiration would run down our
bodies, and the children were kept busy going back and forth with dippers of cold water, of which we
naturally drank great quantities."
Thankfully people don't have to weigh all their food to get the right ratio; if you simply eat about three plant
food portions for each animal food portion, the weight ratio is satisfied. More insights, practical tips and
more than 250 recipes are provided in our forthcoming book The Garden of Eating: The Definitive Guide to
Practicing a Produce-Dominated Diet.
Don Matesz
Thankfully, people don't have to weigh all their food -- --- Don and Rachel Matesz
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Tue, 16 Sep 2003 07:06:59 +0100
Don Matesz wrote
> A major problem with prescribing dietary ratios using percentage of calories is that meat and fat
> are up to 45 times more calorically dense than vegetables and fruits.
26/61 (2003)
This is a good point, particularly as it tends to refute Cordain's ratios. While our ancestors may have eaten
sufficient plant material to supply 35-55% of their calories from plant foods before the advent of the Ice
Ages, there is no way they could have done so during them. With long cold winters and short cool summers,
for most of the year there would have been very little plant material to eat. Thus I do not accept Cordain's
ratios during the last 2.5 million years. And that is the time when 99.9% of our present genetic makeup
would have been formed.
> Percent mass from meat and fat = 28%
> Percent mass from plants = 72%
While there would have been regional differences in climate and food supply, which today are expressed in
racial differences in patterns of such diseases as obesity, diabetes and coronary heart disease, these could not
have been as great as to have provided such a large proportion of plant material to constitute 72% mass
during the Ice Ages, even if a hominid stomach was able to hold such a large volume, which I doubt. And
even if such uncooked material could have been digested. We have no dietary enzymes or micro-organisms
that will do the job today. If we had them then, why don't we now?
No, under these circumstances, I believe that ratios based on Cordain's hypotheses are unreliable and
untenable.
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Sat, 13 Sep 2003 16:12:36 +0100
Hi all
I take a very different route, although I too recommend in ratios. In my case, as it is far healthier for fat to be
the major source of fuel as it was in palaeolithic times and in more recent primitive cultures, I recommend
10-15% of calories from carbs, mainly from fresh green and yellow veges, 15-25% of calories from good
quality animal proteins, and 60-70% of calories from fats, again mainly from animal sources.
Although I don't rule out any foods completely, I do believe that grains are not at all healthy, being
responsible for a whole range of conditions from coeliac disease to asthma to eczema. I would particularly
avoid wholegrains because of their phytate content. Many studies in Canada and elsewhere have indicted
wholegrains as causes of a wide range of deficiency diseases, see below. For example, more iron was
absorbed from white bread than from wholemeal bread, even though the wholemeal bread contained 50%
more. (Kelsay 1978 below)
Moynahan EJ. Nutritional hazards of high-fibre diet. Lancet. 1977; i: 654-5.; Kelsay JL. A review of
research on effect of fibre intake on man. Am J of Clin Nutr. 1978; (31): 142.; Turnlund JR et al. A Stable
isotope study of zinc absorption in young men: effects of phytate and alpha-cellulose. Am J Clin Nutr 1984;
40: 1071-77.; Bindra GS, Gibson RS. Iron status of predominantly lacto-ovo vegetarian East Indian
immigrants to Canada: a model approach. Am J Clin Nutr 1986; 44: 643-52. Southgate DAT. Minerals, trace
elements and potential hazards. Am J Clin Nutr 1987; 45: 1256-66. Clements MR. The problem of rickets in
UK Asians. J Hum Nutr & Dietet 1989; 2: 105-16. Hallberg L, et al. Phytates and the inhibitory effect of
bran on iron absorption in man. Am J Clin Nutr. 1987; 45(5): 988. Balasubraminian R, et al. Effect of wheat
bran on bowel function and fecal calcium in older adults. J Am Coll Nutr. 1987; 6(3): 199. Hallfisch J, et al.
Mineral balances of men and women consuming high fibre diets with complex or simple carbohydrate. J
Nutr. 1987; 117(2): 403.
to mention just a few.
Barry Groves, PhD http://www.second-opinions.co.uk
----- Original Message ----- From: "Todd Caldecott" To: Sent: Thursday, September 11, 2003 8:46 PM
Subject: dietary ratios
> Hello folks, i was reviewing Cordain's food pyramid:
> http://www.paleofood.de/ENGPaleo/ENGPyramids/engpyramids.html and contemplating the impact
> upon patient health and compliance, I thought that it would be interesting and helpful to get your
> feedback upon what y'all think of what proportions of different foods should comprise of the diet.
> Because most folks don't pay all that much attention the specific caloric content of their diet,
27/61 (2003)
> and nor do most actually weigh out the foods they eat, I usually recommend dietary components in
> basic proportions (i.e portions of the proverbial pie): it makes it easier for patients to actual
> visualize what to eat. According to Cordain's food pyramid, meats make up 56-64% of the total
> caloric intake, which obviously contains some admixture of fat and protein depending upon the
> protein source. Compared to the (non-starchy) vegetable intake, which have an alkalizing effect on
> pH and supply a whole host of vitamins and antioxidant compounds but provides little in the way of
> actual calories, the meat proportion may be less in my diet as compared to Cordain, or it may be
> fairly close: there are obviously several variables to take into account here. Also, because in
> temperate regions vegetation is available for a much longer portion of the year than actual
> fruits, this is reflected in the proportion of fruit to vegetable intake I describe below: 30%
> meats 40% (non-starchy) vegetables 15% fats (above that contained in meats, e.g. olive oil,
> butter, coconut oil etc) 15% carbohydrate, i.e. temperate fruits (in summer/fall) or starchy
> vegetables (in winter, not potatoes).
> I will also allow some whole grains (e.g. rice, oatmeal, barley, but not flour) for non-sensitive
> folks in the CHO portion simply because most people will not give them up entirely unless the
> condition requires it (e.g. CVD, diabetes, autoimmunity), and there may be some additional benefit
> as a source of fiber to maintain the GI ecology. Although most patients make a "best effort" to
> achieve the above, in some cases its pretty hard to determine what exactly they are eating day in
> and day out (without extensive reporting), so I often gage successful implementation upon a
> reduction in symptoms (e.g. GI distress, skin conditions, BP etc.) I realize that most of you are
> not clinicians, and therefore may not have any experience in implementing dietary changes in
> others, but even still, I would be interested to hear how your thoughts or practices compare with
> the above. Of course it is impossible to eat completely in a paleolithic fashion, and given that
> most don't live in a paleolithic environment (i.e. most of us live in a semi-tropical indoor
> environment for much of our lives), I have modified the diet to reflect this as well, as well as
> my knowledge of dietary practices in traditional Chinese and Indian (Ayurvedic) medicine. Thanks
> for your thoughts...
> Todd Caldecott, Cl.H., AHG
> Clinical Herbalist
> Wild Rose Clinic
PALEODIET Archives
Subject: Meat Bias dietary ratios
From: M Darby
Reply-To:
Date: Tue, 16 Sep 2003 20:29:58 -0700
re: " With long cold winters and short cool summers, for most of the year there would have been very little
plant material to eat." Barry Groves
Sagittari latifolia (wapato) is a wetland plant that produces a tuber that was and is available and harvestable
from about now (September) through April in the Northwest part of the US. This plant was prolific during
the last Ice Age in North America, the North American Great Basin, Siberia and Northern Europe according
to pollen data. It is a 'pioneering' species of wetland plant that occupied newly open areas as the ice receded.
It is spread rapidly by waterfowl eating the seed heads and redepositing them in new locations. So,
paleolithic people had a good source of carbohydrates available to them. Other species who may have taken
advantage of this carbohydrate include: waterfowl, beaver, muskrat and perhaps Mammoth (who may have
eaten the dense above ground biomass in the wetlands).
This tuber is prolific, with a harvest net of approximately 5, 418 kcal per hour in my experiments. I harvested
it out of a pond where the water was knee-high. Hourly gathering yields of camas were similar, 5, 279 kcal,
however Sagittaria tubers are harvestable in fall and spring (and all winter in shallow ice free mud flats and
lakes though cost effectiveness drops in deeper, colder water). The tubers can be dried, stored fresh in a cool
place, or cooked fresh. They are done within ten minutes in hot ashes, do not need long cooking times or
stones for long oven cooking, do not need processing in order to be palatable (i.e. grinding, mashing).
28/61 (2003)
Long cold winters and short cool summers would limit the productivity that is seen now in the Northwest,
but no one can say that during the last ice age people in North America, Siberia, Northern Europe would
have had no access to a high carbohydrate plant material to eat during the winter. Melissa Darby
PALEODIET Archives
From: Bob Avery
Reply-To:
Date: Wed, 17 Sep 2003 00:38:14 -0400
Barry,
> And even if such uncooked material could have been digested. We have no dietary enzymes or
> micro-organisms that will do the job today. If we had them then, why don't we now?
I have them. Uncooked fruits and veggies, nuts and seeds make up the vast preponderance of my diet and
have done so for 10 years now. If I didn't have the enzymes to digest them, I'd be long gone by now. Even
the occasional animal parts I consume are taken raw.
Is there any proof that all or most of the Earth was ever covered in ice?
Some people think that "ice ages" are a misnomer, that what really happens is that the Earth tilts and slips on
its axis periodically as ice accumulates on the poles and makes the globe topheavy, so that what you end up
with is parts that used to be warm getting iced over and other parts that used to be polar getting warmed up.
Does anyone really know what was going on here millions of years ago?
Bob Avery
?!
PALEODIET Archives
Subject: Dietary ratios: Still valid?
From: Ed Blonz
Reply-To:
Date: Wed, 17 Sep 2003 07:55:00 -0700
If we accept that "you are what you eat (and absorb)" this makes ratios are questionable value given the fact
that the diet of the now-domesticated animals has changed radically. Beneficial lipids and minor excipients
in the muscle, bone and fat of wild grazing animals are no longer there, having been replaced by uniformity
born of a grain-based finishing diet.
____________________________
Ed Blonz, Ph.D. Website: http://blonz.com
PALEODIET Archives
Reply-To:
Date: Wed, 17 Sep 2003 13:14:27 +0100
On Tue, 16 Sep 2003, Barry Groves wrote:
> While our ancestors may have eaten sufficient plant material to supply 35-55% of their calories
> from plant foods before the advent of the Ice Ages, there is no way they could have done so during
> them. With long cold winters and short cool summers, for most of the year there would have been
> very little plant material to eat.
29/61 (2003)
Whilst global ice-age climates would have been cooler than today, the earth's position relative to the sun was
very little different to today, so growing seasons were longer then than now for the same mean temperature.
There is likely to have been plenty of plant material in those parts of the world where humans resided.
Alfano et al (2003) show by comparison of biome simulations and pollen data that temperate grasslands and
forests dominated the landscape of southern Europe (Iberia-Italy-Balkans) in oxygen isotope stage 3. The
availability of plant foods would probably exceed that of northern Europe today, given longer growing
seasons. Present-day tropical and sub-tropical areas had different plant communities in many places to those
they have today, but outside of the expanded deserts plant *productivity* is likely to have been similar.
Given that genetic evidence shows that until relatively recently the majority of humans ancestral to modern
people lived in sub-Saharan Africa (Relethford & Jorde 1999), the influence of reduced plant availability in
ice-age northern Eurasia on human evolution is likely to be fairly small. Even more so when one considers
that there is no evidence for modern humans in this area until after 50, 000 years ago.
> Thus I do not accept Cordain's ratios during the last 2.5 million years. And that is the time when
> 99.9% of our present genetic makeup would have been formed.
This cannot be true. We share about 95% of our genetic make-up with chimpanzees (Britten 2002), from
which our species diverged at least 6-7 million years ago. Only a very small proportion of our genetic makeup can have evolved in the last 2.5 million years, albeit that important part which distinguishes us from other
species.
References
Alfano MJ, Barron EJ, Pollard D, Huntley B & Allen JRM (2003) Comparison of climate model results with
European vegetation and permafrost during oxygen isotope stage three. Quaternary Research 59 97-107
Britten RJ (2002) Divergence between samples of chimpanzee and human DNA sequences is 5% counting
indels. Proceedings of the National Academy of Sciences 99 13633-13635.
Relethford JH & Jorde LB (1999) Genetic evidence for larger African population size during recent human
evolution. American Journal of Physical Anthropology 108 251-260.
Andrew
======================================================================== Dr.
=========================================================================
PALEODIET Archives
From: matesz
Reply-To:
Date: Wed, 17 Sep 2003 15:35:36 -0400
-- --- Barry Groves wrote:
> Percent mass from meat and fat = 28%
> Percent mass from plants = 72%
> While there would have been regional differences in climate and food supply, which today are
> expressed in racial differences in patterns of such diseases as obesity, diabetes and coronary
> heart disease, these could not have been as great as to have provided such a large proportion of
> plant material to constitute 72% mass during the Ice Ages, even if a hominid stomach was able to
> hold such a large volume, which I doubt.
This is a perfect example of the confusion I was trying to clarify. A percentage of mass is not a mass nor a
volume. A diet could have a high proportion of mass from plants, but that may not actually be an
inordinately large volume or mass of plant food. My example was intended to show that to be the case. It
contained one small sweet potato and about one cup each of broccoli and blueberries.
As I recall, Dr. Groves recommended something like 20% protein, 60% fat, and 20% carbohydrate, from
non-starchy green and yellow vegetables. If he meant percentages by calories an example meal would be:
100 g of beef brisket 35 g of butter 130 g of boiled kale (1 cup) 117 g of roasted carrots (1 cup)
Here's the analysis:
Total calories=587 Macronutrients: 23 g CHO, 39 g Fat, 36 g Protein Percent of calories: Carb=16%,
Fat=60%, Prot=25%
30/61 (2003)
Total weight: 382 g (0.84 lb.) Percent weight from animal matter: 35% Percent weight from plant matter:
65%
Here you can see that if you restrict plant matter to green and yellow vegetables, about two-thirds of the
mass of the meal will have to be plant matter to obtain approximately 16% of calories from carbohydrates.
Four of those meals would provide 2348 calories.
If you add 65 g more butter to this meal to raise it up to 1055 calories, at that point fat will provide 78% of
energy, protein 14%, and CHO only 9% of calories but of the total 447 g of food, 247 g or 55% will still be
plant matter.
Whether a hominid stomach could hold 447 grams of food I don't know. But the gut capacity of hominids 2.5
million years ago is immaterial. Cordain's figures are based on documents of recent hunter-gatherers, not
speculations about hominids 2.5 million years ago. I regularly eat meals of the type I outlined in my previous
post and know for certain that a modern human can easily consume meals of such proportions without any
digestive discomfort.
Moreover, even though Eskimos could have lived on a 100% meat and fat diet, Weston Price reported that
they sought out whatever plant foods they could get in season, and preserved some plant foods (in fat) for the
winter. If man is designed to be a pure carnivore, why would Eskimos do that?
Dr. Groves wrote: "And even if such uncooked material could have been digested. We have no dietary
enzymes or micro-organisms that will do the job today. If we had them then, why don't we now?"
Who specified uncooked? Not I. Humans--and here I mean modern homo sapiens sapiens-- cook foods, both
meat and vegetables. This is as true of recent hunter-gatherers as of civilized man.
Cooking effectively opens plant cell walls to allow our digestive system to assimilate plant nutrients. It
reduces plant food volume and eliminates the need for fiber-digesting enzymes or microbes. Moreover meat
also is much more digestible after cooking. Cooked meat is much easier to chew and cooking denatures the
proteins more completely than the stomach's HCl, rendering the proteins much more vulnerable to hydrolysis
by our digestive enzymes.
I know of no evidence indicating that any known modern human tribe ever maintained itself on an all raw
food diet. Stefansson reported that even the Eskimos ate much of their food cooked.
In fact, Dr. Richard Wrangham of Harvard has written: "Dental reduction that accompanied the evolution of
Homo ergaster implies that a new and softer fallback food was then adopted. It seems unlikely to have been
raw meat, because raw meat is difficult to chew and is an improbable fallback food. Cooked plant food, on
the other hand, is a viable fallback food for early humans because it fits the changes in digestive anatomy
and solves the ecological problems of surviving periods of food scarcity. Living humans appear unable to
live on a diet of raw food in the wild, and the fossil record suggests that the time when adaptation to a diet of
cooked food began was with Homo ergaster, potentially accounting for various changes in anatomy and lifehistory. This analysis suggests that cooking is a core adaptation in permitting humans to use large amounts of
energy despite a digestive apparatus adapted to soft and easily digestible foods."
I am informed Homo ergaster emerged approx. 1.9 million y.a. If connected to modern homo sapiens sapiens
that would represent some 63, 000 generations.
Don
PALEODIET Archives
Subject: Re: Draft of my "Letter to the editor" sent to Scientific American
From: "Balzer, Ben"
Reply-To:
Date: Thu, 18 Sep 2003 08:12:35 +1000
Scientific American 2003 Human Evolution Special Re: Food For Thought William R Leonard
Short version: Leonard raises some interesting points about evolutionary theory. He certainly has succeeded
in giving us food for thought but he has left me with an intellectual stomach ache. His discussion of various
aspects of bioenergetics was very enlightening but he leaps to a number of unjustified conclusions about the
effect of diet on the health of modern man.
He gives examples at length, but I think the principle he is driving at could be stated as the carrying capacity
of an area of land for a species is directly related to the amount of energy the species can procure from the
land. Leonard attempts to refute the role of other dietary factors in human health and thus leap to the
convenient but unjustified conclusion that excess energy intake is the cause of diseases of civilisation.
31/61 (2003)
On the last page he indicates he views the human as a great garbage-guts capable of eating anything and
inter-converting it at will. He correctly asserts our species was not designed to subsist on a single optimal
diet. What is remarkable is the extraordinary variety of what we eat and attributes this dexterity to evolution.
One is then left to subliminally insert an unwritten dogma of modern science- that evolution is always perfect
(to do otherwise would presumably be to become a heretic or a flat-Earther) and ipso facto we must be
perfectly suited to all these diets. More dangerously, Leonard implies that if we are suited to so many diets,
then we must be suited to virtually every diet.
However over 99.5% of our evolution was moulded entirely under the influence of the Paleolithic food
groups, present since time immemorial, (and still eaten by modern hunter-gatherers), and not under the
influence of the Neolithic food groups of grains beans, potatoes, and more recently of alcohol, sugar, salt,
MSG, and a large variety of other foods and substances. Thus Leonard has presented no evidence to justify
the hypothesis that we have evolved to eat the Neolithic food groups with impunity. Therefore to bundle off
our health problems as being entirely due to bioenergetic factors is unjustified.
He also overlooks the physiological impact of diet- there are undeniable physiological effects from omega
6/3 balance, trans fats, glycemic load, and acid-base balance etc, that go far beyond the impact of the energy
intake and expenditure. Furthermore, diseases of modern man go far beyond mere obesity, and most cannot
be explained by energy balance, although this makes a contribution in many, particularly in conjunction with
elevated levels of insulin and free IGF-1.
Compared to modern diets of equal energy, hunter gatherer diets tend to have much higher vitamin and
mineral levels, more omega-3 fat, less omega-6, no trans-fat, low salt, negative acid load, more protein, less
carbohydrate, more antioxidants, far more phytosterols etc. These attributes make them much less likely to
cause disease. Neolithic foods generally introduce changes that are acknowledged as unhealthful. Many socalled advances of modern nutritional science have done nothing more than reverse-engineer features of
Paleolithic diets.
Diet has many dimensions, and all are important. There are very generous inbuilt evolutionary tolerances to
variation in many of these dimensions, as Leonard clearly recognises. But once the boundaries of
evolutionary tolerance are exceeded, health must be affected. This is the basis of modern discussions on this
list. This is corroborated by the absence of many common Western diseases in scientifically studied
populations who eat Paleolithic food groups i.e. hunter-gatherer populations. Energy may be the most
important of these dietary dimensions in evolutionary theory, but this does not excuse one from ignoring the
impact of other dietary factors on the health problems of modern man.
Neolithic farmers have managed to dominate the world and nearly eliminate hunter-gatherers, partly or
entirely because of their bioenergetic advantages. But they have paid a terrific cost in terms of disease
burden, and many of these diseases are due to the quality of the food rather than the quantity of energy.
Yours faithfully Ben Balzer Dr Ben Balzer General Practitioner Beverly Hills Medical Service 109 Morgan
St Beverly Hills 2209 NSW Australia Tel (02) 9502 3355 Fax (02) 9502 4243 Int'l prefix (+612)
Further reading: 1. Cordain, Loren. Cereal Grains, Humanity's Double Edged Sword. PDF available from
www.thepaleodiet.com 2. Cordain, Loren. The Paleo Diet. 3. Liener, Irvin, ed. Toxic Constituents of Plant
Food Substances, 2nd ed 1980 Academic Press- See Introduction 4. Diamond, Jared, Guns Germs and Steel
Long Version (Insert at SNIP above)
He is quick to point out that the success of our species has been greatly assisted by the large variety of
foodstuffs (and therefore energy) in our diets- being not merely omnivorous but also eating a very large
variety of plant foodstuffs. He also points to our ability to use tools to eat the brain and marrow of prey- a
wonderful bonus of energy for little extra effort- energy that is mostly wasted by other carnivores. Digging
for roots provides another source of energy. The use of fire for cooking can increase the energy yield of
many plants and also make some toxic roots/tubers edible (eg potatoes), and similarly make some toxic seeds
edible(cereal grains and lentils/beans). Liener 1980 concludes that the cooking of toxic plants doubled the
available plant food energy available to a forager. Farming goes even further to increase available food
energy enormously (10-100 times according to Jared Diamond) by removing inedible species from the land.
I would agree that the procurement of energy is easily the single most important role of diet for all species.
All else in diet is secondary. Seasonal variation is also critical and earlier correspondence on this list
confirms that winter starvation has been an important bottleneck for our species. By crude example, I think
Leonards view would imply that in a forest if the chimps all ate bananas and the forest could support one
hundred chimps- that if they learnt to also eat apples then the forest could support two hundred chimps
(assuming the apples could supply as much energy as the bananas).
32/61 (2003)
Leonard further points out that bipedal locomotion is energetically efficient, and reduces energy
consumption, and clearly this will assist to increase the carrying capacity of the land for the species. Perhaps
some of the energy requirements of our large brain are directly offset by the energy savings of bipedal
locomotion- large parts of the brain being devoted to balance and locomotion. While our large brain may
consume 25-30% of resting energy needs, bipedalism saves energy. It seems likely bipedalism is dependent
upon a larger brain, and that even larger brains probably are required for even better balance and locomotion.
Leonard states that bipedalism was immediately followed by an expansion of the brain. Given the large
amount of energy the brain devotes to balance and locomotion, perhaps the energy expended by intellectual
and abstract thought isnt as big as one might assume- besides which planning and cunning etc can save
much energy, particularly when hunting, and so can be justified on bioenergetic grounds in their own right.
One is left wondering whether the brain evolved because it was efficient and gave us a competitive
advantage or whether merely our energetic prowess made sufficient energy available to splurge on more
brain matter
There are limits on the energy equation for success of a species. If our success depends (as it has for over 10,
000 years) upon the cooking of toxic plants in order to detoxify them (e.g. grains, beans, potatoes), we must
obtain wood for fires. Obtaining wood can be environmentally destructive and reduce the carrying capacity
of the land for our species. I presume that the work required to obtain wood and cook has been included in
discussions of optimal foraging theory.
If a species causes significant environmental destruction, the carrying capacity can decrease. An example of
this is the elephant whose tree destroying activities are so environmentally destructive that culling programs
are needed. Farming may increase available food energy but sustainability needs to be considered.
Leonard uses humans large day range of foraging to explain their rapid spread. Their immense success in
procuring energy and locomotive efficiency would seem better reasons.
In the area of brain evolution, Leonard has concentrated on energetics, including a discussion of
Wranghams hypothesis that the energy from tubers made sufficient energy available to splurge on more
brain matter. There is no direct discussion of the role of micronutrients in brain evolution, which many
workers see as critical. The issues of energetics are important and perhaps micronutrients are better
considered another day. The article was really about energetics and evolution rather than
PALEODIET Archives
Reply-To:
Date: Thu, 18 Sep 2003 10:57:42 -0600
> "most [of us] don't live in a paleolithic environment (i.e. most of us live in a semi-tropical
> indoor environment for much of our lives), I have modified the diet to reflect this as well, " You
> may be interested to learn that traditional Eskimos kept their dwellings pretty warm. In his
> Harper's article "Adventures in Diet", Stefansson wrote that in midwinter the Eskimo family he
> lived with "burned seal or whale oil" for cooking and heating. "The temperature at night was round
> 60 degrees F, " but when the fires were stoked during the day, after they returned from a day of
> fishing, "we came home to a dwelling so heated by the cooking that the temperature would range
> from 85 to 100 degrees F, or perhaps even higher--more like our idea of a Turkish bath than of a
> warm room. Streams of perspiration would run down our bodies, and the children were kept busy
> going back and forth with dippers of cold water, of which we naturally drank great quantities."
the caveat here is that the Inuit spent most the day outside in contrast, even people in very northerly latitudes
tend to spend _all day_ inside, the only time they are outside is walking out to their car, etc. even though we
know the indoor environment to be up to 5 -6 times more toxic hence an even greater need for vegetables,
particularly those rich in sulfur compounds (e.g. garlic), indoles (e.g. cruciferous vegetables), b-vitamins (in
part derived from commensal bacteria, which subsist on dietary fiber), vitamin C (citrus, capsicums etc.) and
various minerals (particularly dense in culinary herbs) needed for phase I and II hepatic detoxification
Todd Caldecott http://www.wrc.net/phyto
PALEODIET Archives
33/61 (2003)

Reply-To:
Date: Thu, 18 Sep 2003 11:00:25 -0600
On Saturday, September 13, 2003, at 09:12 AM, Barry Groves wrote:
> Hi all I take a very different route, although I too recommend in ratios. In my case, as it is far
> healthier for fat to be the major source of fuel as it was in palaeolithic times and in more
> recent primitive cultures, I recommend 10-15% of calories from carbs, mainly from fresh green and
> yellow veges, 15-25% of calories from good quality animal proteins, and 60-70% of calories from
> fats, again mainly from animal sources.
but what does this look like in terms of proportions? The calorie-model is inefficient for most people to
determine dietary ratios - its far to reductionist for something as innate as eating...
Todd Caldecott http://www.wrc.net/phyto
PALEODIET Archives
Subject: Re: Dietary ratios: Still valid?
Reply-To:
Date: Thu, 18 Sep 2003 11:45:06 -0500
Ed Blonz wrote:
> If we accept that "you are what you eat (and absorb)" this makes ratios = are questionable value
> given the fact that the diet of the now-domesticated animals has changed radically. Beneficial
> lipids and minor excipients = in the muscle, bone and fat of wild grazing animals are no longer
> there, = having been replaced by uniformity born of a grain-based finishing diet.=20
Am I right in my understanding that much of Europe favors grass-fed meat? Wish we could get it here...
Hmm. I'm buying six acres. Perhaps I should run a cow every summer?
-- Dana W. Carpender Howard Dean For President Take Back the Democratic Party! Take Back America!
http://www.deanforamerica.com
PALEODIET Archives
From: Bob Avery
Reply-To:
Date: Thu, 18 Sep 2003 22:56:28 -0400
Don,
> Moreover meat also is much more digestible after cooking.
I have to disagree with you there. The simple fact that eating cooked meat produces body odors and
putrefactive stool odors while eating raw meat does not should be sufficient to contradict that statement.
> Cooked meat is much easier to chew and cooking denatures the proteins more completely than the
stomach's HCl,
And therein lies the problem, since digestion is a carefully regulated and controlled process of enzymatic
activity yielding recognizable (to our body cells) end products, whereas the destruction wrought by heat is
uncontrolled and produces many noxious compounds our bodies are not equipped to deal with. Those that
have been tested on laboratory animals have been shown to be carcinogenic.
This applies equally to the delicate fat contents of the meat as well as to the protein contents. There is no
biochemical equivalence between digestive catabolism and heat degradation.
I don't know about you, but every time I used to eat cooked eggs, my stools would reek of sulfur (hydrogen
sulfide?), but no such putrefactive odors occur after I eat a raw egg.
34/61 (2003)
> I know of no evidence indicating that any known modern human tribe ever maintained itself on an all
raw food diet. Stefansson reported that even the Eskimos ate much of their food cooked.
I don't know of any such tribes either, but I know of individuals such as myself who do so, and with superior
health results to show for it.
> Cooked plant food, on the other hand, is a viable fallback food for early humans because it fits the
changes in digestive anatomy and solves the ecological problems of surviving periods of food scarcity.
What's likely to "fall back" are your gum lines when you eat it. In 10 years of all raw, I have had NO new
cavities or any increase in periodontal disease, yet my teeth are full of existing holes from my prior cooked
diet. I believe that cooked food is the primary cause of dental caries, which is certainly not a natural
occurrence.
> Living humans appear unable to live on a diet of raw food in the wild
This would be an astounding finding were it true, considering that 100% of all other Earth creatures are able
do so, and at the cellular level, our biological needs are much the same as for any other life form.
Bob Avery
?!
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Fri, 19 Sep 2003 07:41:59 +0100
Bob Avery said
> Is there any proof that all or most of the Earth was ever covered in ice?
Is there any doubt? When there was so much water stored in ice that sea levels were low enough for animals
and humans to walk between what is now mainland Europe and the British Isles, then I submit that the whole
globe must have been considerably cooler than it is today.
I thank Melissa Darby for the information about Sagittari latifolia (wapato). This is a plant I don't know. I
would like to know more: what is its amino acid profile, for example? Could it have been used as a staple
source of the nutrients the body needs for any length of time?
I take Don's point about ratios -- if the plant foods are cooked. The question now is: when did cooking
become universal?
Homo erectus began to appreciate the value of fire around 350, 000 years ago. Although hearths have been
discovered that are 100, 000 years old, these are very rare. European Neanderthal coprolites from around 50,
000 years ago, before their use of fire, contain no plant material. (Bryant V M, Williams-Dean G. The
Coprolites of Man. Scientific American, January 1975.)
It seems that it was not until Cro-Magnon's colonisation of Europe, some 35, 000 years ago, that hearths
became universal. Even then the evidence suggests that they were not used for cooking plants but merely for
warmth. This is really too recent in our history for any big change in genetic makeup, surely?
Yes, Dana, we in Europe do eat grass-fed ruminants, although there may be some grain based feed
introduced during winter months. We wouldn't give you a thank-you for wholly grain-fed animals.
PALEODIET Archives
Reply-To:
Date: Fri, 19 Sep 2003 10:15:03 -0500
Bob Avery wrote:
> Don,
> I know of no evidence indicating that any known modern human tribe ever maintained itself on an
> all raw food diet. Stefansson reported that even the Eskimos ate much of their food cooked. I
35/61 (2003)
> don't know of any such tribes either, but I know of individuals such as myself who do so, and with
> superior health results to show for it. Cooked plant food, on the other hand, is a viable fallback
> food for early humans because it fits the changes in digestive anatomy and solves the ecological
> problems of surviving periods of food scarcity. What's likely to "fall back" are your gum lines
> when you eat it. In 10 years of all raw, I have had NO new cavities or any increase in periodontal
> disease, yet my teeth are full of existing holes from my prior cooked diet. I believe that cooked
> food is the primary cause of dental caries, which is certainly not a natural occurrence.
Data point: I have been eating a low carb diet, pretty much balanced between meat, poultry, eggs, low carb
vegetables, and nuts and seeds, with almost all cooked proteins, more raw veg than cooked, but certainly
some cooked veg, for 8 years now. I, too, have superb health to show for it. I also have no new cavities, nor
any gum disease, though I had none before, either. (I have never had a cavity, never had more than transient
gum disease, and that as a sugar addicted kid, never had braces, still have all four wisdom teeth. Cheap
mouth!)
However, my husband, who eats pretty much the same as I, did indeed have teeth that were rotting away
before -- and has had not a single new cary since going low carb 8 years ago. His blood work and health are
stellar, as well.
-- Dana
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Sat, 20 Sep 2003 20:24:29 +0100
> Moreover meat also is much more digestible after cooking.
No, it isn't.
At first, all our food, whether from animal or vegetable sources, was eaten raw. Now cooking food has
become a way of life. Most people in Western society today would not eat uncooked meat. As possible
pathogens would not be killed, it may be unwise to eat raw meat. But, while boiling parallels the first stages
of digestion, and may be helpful in that process, over-cooking in a way that chars food can present the
digestive processes with food that it has more difficulty digesting.
In 1838, in Canada, Dr. William Beaumont performed a remarkable series of experiments on a man named
Alexis St. Martin. St. Martin had an opening in the front wall of his stomach from a gunshot wound. Even
after the wound had healed, there remained a small opening through which the mucous membrane of his
stomach could be seen and, through which, substances could be introduced into the stomach or removed
from it. Dr. Beaumont was able to introduce foodstuffs through the opening and observe the rate of
digestion. By so doing, he found that raw beef digested in two hours, well done boiled beef in three hours but
well done roast beef took four hours. Similarly, raw eggs were digested in one-and-a-half hours but hardboiled eggs took three-and-a-half hours.
In contrast, the cellulose which envelops cereal grains, and which is the major constituent of all vegetable
cell walls, was not broken down at all by the digestive juices. Beaumont found that unless they were ruptured
in some way, their contents passed right through the body without the body deriving any nutritional benefit
from them. Cooking and chewing were both thought to accomplish this task. But the billions of plant cells
are microscopically small. Chewing might rupture some of the cell walls but it would be a very small
percentage of the total, and very wasteful.
There is then the problem of the starch molecule itself: cooking is the only means of breaking down starches
so that we can digest them. As a consequence, all vegetable matter, and particularly cereals and other starchy
root vegetables need not only to be cooked, but also to be well cooked, before they can be digested.
> I don't know about you, but every time I used to eat cooked eggs, my stools would reek of sulfur
> (hydrogen sulfide?), but no such putrefactive odors occur after I eat a raw egg.
I always eat eggs cooked (in a variety of ways (because of the possibility of salmonella) and I eat several
extra large eggs every day. My stools have little or no smell. They also leave me quite cleanly so that no
paper is needed, although I always use one piece to confirm this.
> Living humans appear unable to live on a diet of raw food in the wild.
36/61 (2003)
Not true. There are many foods that can be eaten raw. As Bob says all foods from animal sources can be
eaten raw, as can many fruits and other plant foods, although that may be somewhat wasteful.
> What's likely to "fall back" are your gum lines when you eat it. In 10 years of all raw, I have
> had NO new cavities or any increase in periodontal disease, yet my teeth are full of existing
> holes from my prior cooked diet. I believe that cooked food is the primary cause of dental caries,
> which is certainly not a natural occurrence.
Certainly my gums and teeth were not good at the time I started to eat a low-carb diet in 1962 when I was 26
years old. Since then I have had to have very little work done. Now age 67 I still have all my own teeth and
my dentist always remarks how good my teeth and gums are.
PALEODIET Archives
Subject: ice and fire
Reply-To:
Date: Mon, 22 Sep 2003 10:45:06 +0100
On Fri, 19 Sep 2003, Barry Groves wrote:
> Bob Avery said
> Is there any proof that all or most of the Earth was ever covered in ice? In short: No. Is there
> any doubt? When there was so much water stored in ice that sea levels were low enough for animals
> and humans to walk between what is now mainland Europe and the British Isles, then I submit that
> the whole globe must have been considerably cooler than it is today.
Major glaciations have occurred during the Pleistocene (1.8 million to 10, 000 years ago), before that there
were cyclical temperature variations but any glaciations were much smaller. During the Pleistocene the
majority of the earth was never covered in ice. Ice sheets and glabal temperatures fluctuated, with some
periods actually warmer than the present. At their maximum extent ice sheets extended as far south as the
river Thames and northern Germany in Europe, with additional major ice caps in the Alps, southern Andes
and parts of East Asia.
At the last glacial maximum (LGM) global average temperature was about 5 degrees C below today, but
there were massive variations in this decrease across the globe:
Zone greatest decrease in mean temperature (oC) northern temperate 7 Equatorial 3 Southern temperate 3
There were of course local variations on the averages, with parts of Britain 20 degrees below today's average.
(Mostly summarised from pp45-46 of Roberts, N (1989) The Holocene: an environmental history.
Blackwell: Oxford)
> I take Don's point about ratios -- if the plant foods are cooked. The question now is: when did
> cooking become universal?
This is a very hard question to answer. I and some colleagues have spent several years trying to devise
methods for detecting bone that has been cooked. All the chemical signs of cooking that we can find also
occur at a much slower rate in the decay processes which occur after burial. (e.g. Roberts SJ, Smith CI,
Millard A & Collins M 2002 The taphonomy of cooked bone: characterising boiling and its physicochemical effects, Archaeometry 44(3) 485-494.) One can find and identify burnt materials relatively easily,
and although burning is not cooking, this is about the best we can do.
> Homo erectus began to appreciate the value of fire around 350, 000 years ago.
I think this must be a reference to the deposits at Zhoukoudien (the "Peking Man" site), which have now
been shown to be waterlain deposits rather than ashes (Weiner S, Xu QQ, Goldberg P, Liu JY, Bar-Yosef O
Evidence for the use of fire at Zhoukoudian, China Science 281 251-253). If there is any other evidence for
ash quite this early I'd like to hear about it.
> Although hearths have been discovered that are 100, 000 years old, these are very rare. European
> Neanderthal coprolites from around 50, 000 years ago, before their use of fire, contain no plant
> material. (Bryant V M, Williams-Dean G. The Coprolites of Man. Scientific American, January 1975.)
37/61 (2003)
But ash deposits do form the major consituents of many cave sediments, e.g Kebara, Hayonim and Tabun in
Israel, with dates going back over 200, 000 years, indicate prolonged use of fire but without any surviving
hearth structures. This use of fire is not unequivocally associated with a particular hominid species, but
appears to predate the speciation that led to modern humans, and it is therefore within an appropriate
timescale for evolution of a gut dependent on cooked foods. Neanderthals are unlikely to have contributed
significantly to the modern human gene-pool, so the contents of their coprolites are less relevant than they
might othewise be.
> It seems that it was not until Cro-Magnon's colonisation of Europe, some 35, 000 years ago, that
> hearths became universal. Even then the evidence suggests that they were not used for cooking
> plants but merely for warmth. This is really too recent in our history for any big change in
> genetic makeup, surely?
It seems to me that the actions of Cro-Magnon people may not be indicative of the majority of our ancestry.
They were living in a marginal environment and genetic studies of modern European mitochrondrial DNS
suggest that the majority of ancestors of modern Europeans entered Europe after the LGM - presumably
from areas where the technology and hearth-usage were different.
Andrew
========================================================================= Dr.
=========================================================================
PALEODIET Archives
Subject: Re: Meat in the Human Diet
Reply-To:
Date: Mon, 22 Sep 2003 13:17:14 -0600
Dear Bob,
I'm sorry I haven't the time to do a full critique of the piece but there are many holes in it. The physiology
argument is old and perhaps someone can invite the author to beyond the law of the excluded middle and
embrace his fuzziness: we are omnivores, not ruminants and not carnivores. The evidence of this to my mind
is the fact that we are still here, unlike our less adaptable hominid cousins.
> His Aberrant Behavior Ruins His Potency Eating meat diminishes sexual performance and
> masculinity.
> The male hormone testosterone that determines sexual development and interest has been found to be
> 13 % higher in vegans (a strict plant diet no animal products of any kind) than in meat-eaters. 18
the abstract continues that the elevations in T were "...offset by higher sex hormone binding globulin, and
there were no differences between diet groups in free testosterone, androstanediol glucuronide or luteinizing
hormone."
but anyway, when is one study proof of anything? another study found no statistical difference:
Key TJ, Roe L, Thorogood M, Moore JW, Clark GM, Wang DY. Testosterone, sex hormone-binding
globulin, calculated free testosterone, and oestradiol in male vegans and omnivores. Br J Nutr. 1990
Jul;64(1):111-9.
and another study contradicts the author's findings:
Raben A, Kiens B, Richter EA, Rasmussen LB, Svenstrup B, Micic S, Bennett P. Serum sex hormones and
endurance performance after a lacto-ovo vegetarian and a mixed diet. Med Sci Sports Exerc. 1992
Nov;24(11):1290-7.
selective scientific reasoning - pretty standard fair actually. First the belief, then the hypothesis, and then
selective reasoning based on lower order logistics.
> Meat-eaters are likely to become impotent because of damage caused to the artery system that supplies
> their penis with the blood that causes an erection. 19 Erectile dysfunction is more often seen in men
> with elevated cholesterol levels 20 and high levels of LDL "bad" cholesterol 21 both conditions
> related to habitual meat-eating.
38/61 (2003)
this is a rehash of a long tired argument. The author proves nothing, and the conclusion he draws about meat
eating aren't related to the actual findings re: dyslipidemia, and nor do they correspond with my clinical
experience, where by implementing a low CHO diet ends up reducing cholesterol, LDL and triglycerides. In
the latter case Gerald Reaven states that serum insulin levels more or less parallel triglyceride levels in the
syndrome X pattern, which is assoc. with impotence.
I generally find that vegans who have switched back to eating a little meat immediately feel more
"grounded" and have an enhanced ability to focus and concentrate, and are generally less sensitive (to drugs,
toxins) and to other people. In Ayurvedic medicine meat is considered to be tamasic, the energy of inertia,
darkness and heaviness, and thus vegetarian diets are recommended in some yogic traditions to loosen up
one's attachment, to embrace spiritual energies and move beyond the confines of physicality. This of course
is all very well is one is planning on leaving the life of the "householder, " but for the rest of us schmucks
stuck in samsara we need a some inertia to simply be effective in life. IMHO those idealists who become
vegans are exactly those that need to eat more meat, and for those who only visit that salad bar as an excuse
to get more blue-cheese salad dressing, bacon bits and jello are those that need more vegetables in their life.
On Saturday, September 20, 2003, at 09:08 PM, Bob Avery wrote:
> This article poses some interesting challenges to the paleodiet nutritional theory, based
> primarily on comparative anatomy and physiology.
> http://www.nealhendrickson.com/mcdougall/030700pumeatinthehumandiet.htm Comments anyone?
> Bob Avery
> Todd Caldecott, Cl.H., AHG Clinical Herbalist Wild Rose Clinic
*******************************************
*******************************************
*******************************************
PALEODIET Archives
From: Bob Pastorio
Reply-To:
Date: Mon, 22 Sep 2003 18:26:59 -0400
Bob Avery wrote:
A bit more spin than serves the seeker of fact. The effort to create a correspondence and close parallel with
other primates falls apart when the fact that we are tool users with complex language skills is factored in.
Looking at human dentition and noting that it isn't like wolves or lions is a moot discussion point when the
fact of cooking enters the picture. We don't need teeth like carnivores. Likewise that our hands are designed
for picking plants rather than tearing apart meat. Our hands are designed for holding tools that tear apart
meat. We don't need claws.
Humans are unique in that we, more than any other creatures, can change our environments to suit our
strengths and to minimize our weaknesses. I have no fur so I wear clothing. I can't run faster or further than a
horse so I drive something - be it animal or mechanical.
All of which makes direct comparisons with other earthly denizens a bit of a strain. Talking about the
diseases we're subject to that are relatively new in human history has also to include the facts that we live
longer and diagnose better than ever before. The logic is stretched in many places. He says there's a "proper"
diet for dogs, cats, horses, each kind of bird and that presupposes that there's a proper diet for humans. Too
much of this sort of seeming wishful thinking. Some interesting points, but largely too much of a reach.
Pastorio
PALEODIET Archives
39/61 (2003)
Subject: Organ Meats

From: "Balzer, Ben"
Reply-To:
Date: Mon, 22 Sep 2003 21:20:13 +1000
Resent as it got lost in cyberspace
Dana
I tell people the liver is the "juicer" rather than the filter. Physiologically it certainly has both roles and
"juicer" sounds nicer and helps explain its huge content of mineral vitamins and other micronutrients. The
toxin aspect makes it particularly important to look at the farming method and pasture fed will be much
superior (esp. if organic). Grain fed meat requires more antibiotics and other chemicals and also is more
prone to liver abscesses etc, and it has an inferior profile of vitamins minerals and other nutrients (see e.g.
www.eatwild.com)
As for the brain and mad cow disease, well now you've got me started. One of the first proven prion brain
diseases was kuru in the New Guinea highlands. This was proven to be due to the ritual eating of the brains
of deceased relatives. Cessation of this practice has stamped out kuru. Thus it is entirely predictable that
when agricultural economists decided to feed cows the brains of their own deceased relatives, that they had
created an opportunity for a prion disease to enter the cycle, and be concentrated upwards, exponentially
affecting more cows. In due course this has happened. Nature has many potential life cycles that various
pests can enter, and it is clearly important to examine in great detail the consequences of any changes to the
natural feeding and breeding cycles, from the point of view of ensuring that one does not create an
opportunity for a pathogen.
The silver lining of the mad cow cloud would have to be the short life span of the mad cow disease.
Fortunately is was rapid enough to show up in the short life span of a cow (albeit they have a small brain).
On the speculative side, one can only imagine the cataclysmic effect had the prion had a longer life cyclethat of kuru is over 20 years- in which case the cows would never have gotten sick prior top slaughter. If that
were the case, then humans could have been infected without ever realising the source. It remains to be seen
if there is only one cow prion- if a longer cycle prion had already entered the cycle, it might still be
incubating.
Fortunately it appears that most Australian beef comes from non-cannibalistic sources :-).
Ben Balzer
Dr Ben Balzer 109 Morgan St Beverly Hills 2209 NSW Australia Tel (02) 9502 3355 Fax (02) 9502 4243
Int'l prefix (+612)
PALEODIET Archives
Subject: Re: scientific proof, teeth, health claims etc
From: Todd Moody
Reply-To:
Date: Tue, 23 Sep 2003 10:33:55 -0400
Tamsin O'Connell wrote:
> Dear all, Much as I enjoy the lively discussion going on, can I just suggest that we all move away
> from the 'individual as proof of a theory' idea?
I'm going to use this suggestion as an opportunity to issue a gentle reminder that this list is meant to occupy a
niche somewhere in between an academic journal (which it cannot be) and a chat list (which it could). What
we want to do here is share our research, challenge each others' ideas, and so forth. Ideally, those doing
scholarly work in the relevant fields will benefit by the exchanges, and the rest of us will be edified. For this
reason, posts of a purely anecdotal nature are to be avoided, and I will make an effort to restrict them. That
doesn't mean that anecdotes are forbidden on this list, but if present they should be used as a supplement to
actual research that is adduced, rather than the whole content of a message.
I will also hold back messages that consist of just a line or two of "rejoinder" to a longer quoted message.
40/61 (2003)
The point is by no means to stifle discussion. This list has been dormant for a while and the recent and
current discussions are excellent. I also don't want to give the impression that only the publishing scholars
are welcome to post messages. But any one of us can, with a bit of effort, do a bit of digging and be a
"scholar" for purposes of this list.
That's all. Carry on.
Todd Moody listop
PALEODIET Archives
From: matesz
Reply-To:
Date: Tue, 23 Sep 2003 10:38:48 -0400
> In 1838, in Canada, Dr. William Beaumont performed a remarkable series of experiments on a man
> named Alexis St. Martin. St. Martin had an opening in the front wall of his stomach from a gunshot
> wound. Even after the wound had healed, there remained a small opening through which the mucous
> membrane of his stomach could be seen and, through which, substances could be introduced into the
> stomach or removed from it. Dr. Beaumont was able to introduce foodstuffs through the opening and
> observe the rate of digestion. By so doing, he found that raw beef digested in two hours, well
> done boiled beef in three hours but well done roast beef took four hours. Similarly, raw eggs were
> digested in one-and-a-half hours but hard-boiled eggs took three-and-a-half hours.
Before Todd Moody posted, I was about to ask how this constitutes scientific evidence.
We have one study.
Performed on one man.
The man had a gunshot wound in his stomach.
Substances were introduced to his stomach through the hole in it, not via chewing and swallowing.
Consequently, this study can't tell us much about normal digestion.
Besides being (to my knowledge) uncorroborated, it has these flaws:
The sample size too small.
The subject had major damage to the organ being studied, so it won't necessarily give an accurate account of
what happens in an undamaged stomach.
Skipping the mastication further distances this study from digestion in normal humans.
Moreover, this study seems focussed only on measuring how long each item remained in the stomach. Very
little actual digestion occurs in the stomach. That the raw food was passed to the small intestine more quickly
does not mean it was more thoroughly digested, or that more nutrients were assimilated from the raw than
from the cooked.
This study didn't examine what happens after the stomach, in the small intestine, where most digestion
occurs. The raw food might spend half as much time in the stomach and twice as much time in the small
intestine, compared to cooked food. In the end then there'd be no difference.
Another possibility is the raw food is passed through so quickly there is reduced assimilation. If that were so
then you have to eat more raw food than cooked to get the same nutrition.
Passing quickly isn't necessarily always good sign. If you eat a poison it may pass quickly also--you get
diarrhea as a result. Faster movement thus may represent the body rejecting the food.
Enough said. I'm not making conclusions, just pointing out that this study has many flaws and the
conclusions often drawn do not follow inexorably.
Don
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Tue, 23 Sep 2003 11:00:21 +0100
41/61 (2003)
Hi Bob
There are both truths and truths that are misinterpreted in this article. I haven't time to comment on every
point. However, here are justa few:
Article "A traditional Arctic Eskimo, living in a subfreezing climate, could expend 6000 calories and more a
day just to keep warm and hunt for food. The high-fat animal food sources - fish, walrus, whale, and seal from his local environment were the most practical means of meeting the demands of those rigorous
surroundings. Modern Eskimos living in heated houses and driving around in their climate-controlled SUVs,
still consuming a high-meat diet, have become some of the fattest and sickest people on earth."
The traditional Actic Eskimo, actually lives in a very warm environment when at home. Their igloos,
according to Weston Price and Stefannson, are maintained at such high temperatures that the are usually
nude within them. The also spend up to eight months during the winter not hunting and rarely venturing
outside, yet suffer no ill health. What the article doesn't say about the "modern" Eskimos is that their diet was
changed dramatically by trading with Europeans. Their diet now contains large quantities of "healthy" wheat
and other cereals, potatoes, etc. It is that which is the cause of the decline in their health.
Article "Most apes living today eat essentially as vegetarians - consuming a diet composed of the fruits,
leaves, flowers, and bark, with sporadic consumption of very small amounts of insect material (like termites)
and less commonly, small animals."
Has the writer observed chimanzees killing and eating colobus monkeys? Meat plays a far greater part in a
chimapzee's diet than the writer credits.
On teeth, the article makes out that our teeth are designed to cope with plant foods. I defy anyone to clench
their teeth together and then move their jaws sideways to "grind" in the way that herbivores do.
Article "From our lips to our anus our digestive system has evolved to efficiently process plant foods."
Even a herbivore's digestive system is only about 50% efficient. When eating meats and fats, our digestion is
over 90% efficient, when eating raw veg it is far less that a herbivore's. No mammal produces any dietary
enzymes that will break down and digest the cellulose that forms plant cell walls. Until cell walls are
ruptured, the cells' contents are not available to the digestion.
Herbivores use bacteria and other organisms to do the job for them. The process is a fermentative one and all
herbivores are classed by where in their gut this fermentation takes place. Ruminants -- sheep, cattle, etc -with their 4 stomachs which contain the necessary organisms are known as foregut fermenters and those
whose caecums and colons contain the organisms -- horses, gorillas, chimps, etc -- are known as hindgut
fermenters. But wherever the fermentation takes place, nutrients released by this fermentation process are
absorbed.
Our gut is pretty sterile except for our colons. We do harbour bacteria here and in many people these are
fermentative. However, our colons are built to extract and conserve water, they are not designed to absorb
proteins, fats, sugars, vitamins, etc. In other words we do not absorb nutrients via a fermentative process.
And as we have no cellulose digesting enzyme either, we cannot be ideally suited to a raw veg diet.
If we take this one step further and compare our colons with those of our nearest relatives we find that our
colon/caecum accounts for around 20% of our gut's total volume, whereas the colons of the fermentative
chimps and gorillas is more than 50% of the total volume.
Article "The stomach juices of a meat-eating animal are very concentrated in acid. The purpose of this acid is
to efficiently break down the muscle and bone materials swallowed in large quantities into the stomachs of
meat-eaters. Digestion of starches, vegetables and fruits is accomplished efficiently with the much lower
concentrations of stomach acid found in the stomachs of people, and other plant-eaters."
This is mostly true. Meat eaters do have much stronmger HCl than plant eaters. But the acidity of our HCl is
not as weak as the article says, it is strong as in the carnivores. pH is about 1.5.
Article "The human intestine is long and coiled, much like that of apes, cows, and horses. This configuration
makes digestion slow, allowing time to break down and absorb the nutrients from plant food sources. The
intestine of a carnivore, like a cat, is short, straight, and tubular. This allows for very rapid digestion of flesh
and excretion of the remnants quickly before they putrefy (rot). . . . Overall, the intestines of meat-eaters are
noticeably simpler than ours."
Our gut is a simple tube with a bulge (stomach) at its beginning -- exactly the same as all carnivores. Its total
length is approximately 5 times body length. That of the big cats is approximately 7 times body length. The
gut of a herbivore, by contrast is some 27 times body length and, in the ruminants, much more complex. In
our nearest relatives, it is also a similar length and, as I have already mentioned, it differs markedly in that
apes' colons are much bigger than ours.
In other words, our gut, in terms of length and complexity is even more "carnivore" than the big cats.
42/61 (2003)
There are some anomalies. It is true that we have alpha amylase in saliva, which is used to digest starches.
But this action only happens before the starch reaches the stomach as the action is killed by the digestive
juice. We also have several enzymes to digest starch and the various sugars, which are used in our small
intestine. They must be there for a purpose and that purpose is to deal with carbohydrates. This could make
us omnivores, except for the still vexed question of how to get into plant cells to allow those enzymes to
digest the starches and sugars.
Could chewing be the answer? It's not likely as a sheep with its continual chewing, fermentation,
regurgitation, more chewing and more fermentation only manages to gigest about half the contents. We do
not even have that facility.
So, all in all, I believe that we are really not at all well suited to a diet wholly of vegetation.
Oh, by the way, animal products -- meat, fat, cholesterol -- have never been shown to cause either heart
disease or cancers or, as far as I am aware, any other disease (except from infected produce or man-made
chemical pollution). Only processed plant material has.
----- Original Message ----- m From: "Bob Avery" To: Sent: Sunday, September 21, 2003 4:08 AM Subject:
Meat in the Human Diet
> Bob Avery
PALEODIET Archives
Subject: Re: Organ Meats
From: Dick Bird
Reply-To:
Date: Tue, 23 Sep 2003 11:09:54 +0100
I am not sure if I buy this one. Suppose that there was an epidemic of measles in New York. Would we
conclude that this was because New Yorkers were eating one anothers' brains? Yet we jump to this
conclusion in New Guinea because two stories, the story about cannibalism and the story of prion
transmission, fit neatly together, and the cause of mad cow disease (bovine spongiform encephalopathy, or
BSE) and its human equivalent, variant CJD, has thus apparently been identified.
Cannibalism as an explanation is suspect because ritual cannibalism (as opposed to survival cannibalism) so
often, if not always, turns out to be a fabrication (see Arens "The Man-Eating Myth Anthropology and
Anthropophagy" circa 1978.)
The prion transmission hypothesis was suspect for a long time but was adopted finally before even one in
vitro experimental demonstration of its workability as a means of transmission. Prions are peculiar entities;
they carry just enough information to do the job required of them but they are small enough to get through
the blood/brain barrier which would normally protect us. So in a sense they had to exist if the blame for
vCJD was to be laid at the door of poor feeding methods. I can't remember how many thousands of cattle
were sacrificed in the UK, the worst hit country for BSE, but it was reminiscent of biblical times. When the
purge was over we were pronounced whole again but only very slowly and reluctantly were we allowed to
once again export meat to continental Europe.
The trouble with thinking you have found the criminal when you haven't is that he may still be at large and
liable to strike again. There are other hypotheses of BSE, and its human analog. One was based on the fact
that VCJD sufferers were often farmers, veterinarians and the like, or in a few cases worked in garden
centres. The common factor in these people was exposure to organophosphates, which is often of course true
of cows as well.
Dick Bird
-----Original Message----- Ben Balzer said
43/61 (2003)
As for the brain and mad cow disease, well now you've got me started. One of the first proven prion brain
diseases was kuru in the New Guinea highlands. This was proven to be due to the ritual eating of the brains
of deceased relatives. Cessation of this practice has stamped out kuru. Thus it is entirely predictable that
when agricultural economists decided to feed cows the brains of their own deceased relatives, that they had
created an opportunity for a prion disease to enter the cycle, and be concentrated upwards, exponentially
affecting more cows. In due course this has happened.
PALEODIET Archives
Subject: scientific proof, teeth, health claims etc
Reply-To:
Date: Tue, 23 Sep 2003 11:37:56 +0100
Dear all,
Much as I enjoy the lively discussion going on, can I just suggest that we all move away from the 'individual
as proof of a theory' idea?
Bob Avery writes:
> What's likely to "fall back" are your gum lines when you eat it. In 10 years of all raw, I have
> had NO new cavities or any increase in periodontal disease, yet my teeth are full of existing
> holes from my prior cooked diet. I believe that cooked food is the primary cause of dental caries,
> which is certainly not a natural occurrence.
Barry Groves writes:
> Certainly my gums and teeth were not good at the time I started to eat a low-carb diet in 1962
> when I was 26 years old. Since then I have had to have very little work done. Now age 67 I still
> have all my own teeth and my dentist always remarks how good my teeth and gums are.
Taken as generalisations (raw food diets don't give you caries, low-carb diets don't give you caries) these two
statements could be taken by some readers to be contradictory. But the fact is that caries, gum disease, in fact
all dental health is a multi-factorial problem. And some individuals may have good teeth on a rubbish diet
and vice versa. If we are to approach all (palaeo)diet scientifically, then we must look at larger scale research
than that on an individual.
'One swallow does not a summer make', and a finding based on a single individual does not prove a scientific
theory. Can I make a plea for us all to try to take a more systematic approach?
ON the archaeological evidence, caries generally increases with increasing agriculturalisation in the
neolithic, but the evidence is equivocal in some areas. Overall, most archaeologists believe it is the
increasing starchy content of the diet that results in caries, but this can be moderated by a number of other
factors.
Tamsin
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
Subject: Bones from French cave show Neanderthals, Cro-Magnon hunted same prey
From: Liza May
Reply-To:
Date: Tue, 23 Sep 2003 12:57:18 -0400
Public release date: 22-Sep-2003 Contact: Joel Schwarz 206-543-2580 University of Washington
Bones from French cave show Neanderthals, Cro-Magnon hunted same prey
44/61 (2003)
A 50, 000-year record of mammals consumed by early humans in southwestern France indicates there was
no major difference in the prey hunted by Neanderthal and Cro-Magnon, according to a new study. The
paper, published in the online Journal of Archaeological Science, counters the idea proposed by some
scientists that Cro-Magnon, who were physically similar to modern man, supplanted Neanderthals because
they were more skilled hunters as a result of some evolutionary physical or mental advantage.
"This study suggests Cro-Magnon were not superior in getting food from the landscape, " said lead author
Donald Grayson, a University of Washington professor of archaeology. "We could detect no difference in
diet, the animals they were hunting and the way they were hunting across this period of time, aside from
those caused by climate change.
"So the takeover by Cro-Magnon does not seem to be related to hunting capability. There is no significant
difference in large mammal use from Neanderthals to Cro-Magnon in this part of the world. The idea that
Neanderthals were big, dumb brutes is hard for some people to drop. Cro-Magnon created the first cave art,
but late Neanderthals made body ornaments, so the depth of cognitive difference between the two just is not
clear."
The study also resurrects a nearly 50-year-old theory first proposed by Finnish paleontologist Bjrn Kurtn
that modern humans played a role in the extinction of giant cave bears in Europe. Cro-Magnon may have
been the original "apartment hunters" and displaced the bears by competing with them for the same caves the
animals used for winter den sites.
Grayson and his colleague, Francoise Delpech, a French paleontologist at the Institut de Prehistoire et de
Geologie du Quanternaire at the University of Bordeaux, examined the fossil record left in Grotte XVI, a
cave above the Ceou River, near its confluence with the Dordogne River. The cave has a rich, dated
archaeological sequence that extends from about 65, 000 to about 12, 000 years ago, spanning the time when
Neanderthals flourished and died off and when Cro-Magnon moved into the region. Neanderthals
disappeared from southwestern France around 35, 000 years ago, although they survived longer in southern
Spain and central Europe.
The researchers were most interested in the transition from the Middle to Upper Paleolithic, or Middle to
Late Stone Age.
Neanderthals occupied Grotte XVI as far back as 65, 000 years ago, perhaps longer. Between 40, 000 and 35,
000 years ago, people began making stone tools in France, including at Grotte XVI, that were more like
those later fashioned by Cro-Magnon. However, human remains found with these tools at several sites, were
Neanderthal, not Cro-Magnon. Similar tools but no human remains from this time period were found in
Grotte XVI and people assumed to be Cro-Magnon did not occupy the cave until about 30, 000 years ago.
The researchers examined more than 7, 200 bones and teeth from large hoofed mammals that had been
recovered from the cave. The animals - ungulates such as reindeer, red deer, roe deer, horses and chamois
were the most common prey - were the mainstay of humans in this part of the world, according to Grayson.
He and Delpech found a remarkable dietary similarity over time. Throughout the 50, 000-year record, each
bone and tooth assemblage, regardless of the time period or the size of the sample involved, contained eight
or nine species of ungulates, indicating that Neanderthals and Cro-Magnon both hunted a wide variety of
game.
The only difference the researchers found was in the relative abundance of species, particularly reindeer,
uncovered at the various levels in Grotte XVI. At the oldest dated level in the cave, reindeer remains
accounted for 26 percent of the total. Red deer were the most common prey at this time, accounting for
nearly 34 percent of the bones and teeth. However, as summer temperatures began to drop in Southwestern
France, the reindeer numbers increased and became the prey of choice. By around 30, 000 years ago, when
Cro-Magnon moved into the region, reindeer accounted for 52 percent of the bones and teeth. And by around
12, 500 years ago, during the last ice age, reindeer remains accounted for 94 percent of bones and teeth
found in Grotte XVI.
Grayson and Delpech also looked at the cut marks left on bones to analyze how humans were butchering
their food. They found little difference except, surprisingly, at the uppermost level, which corresponds to the
last ice age.
"It is possible that because it was so cold, people were hard up for food, " Grayson said. "The bones were
very heavily butchered, which might be a sign of food stress. However, if this had occurred earlier during
Neanderthal times, people would have said this is a sure sign that Neanderthals did not have the fine handeye coordination to do fine butchering."
In examining the Grotte XVI record, the researchers also found a sharp drop in the number of cave bears
from Neanderthal to Cro-Magnon times.
45/61 (2003)
"Cave bears and humans may have been competing for the same living space and this may have led to their
extinction, " Grayson said. He added that it is not clear if the decline and eventual extinction of the bears was
driven by an increase in the number of humans or increased human residence times in caves, or both.
"If we can understand the extinction of any animal from the past, such as the cave bear, it gives us a piece of
evidence showing the importance of habitat to animals. The cave bear is one of the icons of the late
Pleistocene Epoch, similar to the saber tooth cats and mammoths in North America. If further study supports
Kurtn's argument, we finally may be in a position to confirm a human role in the extinction of a large
Pleistocene mammal on a Northern Hemisphere continent."
### For more information, contact Grayson at (206) 543-5587 or grayson at u.washington.edu or Delpech at
033-05-56-84-8890 or
PALEODIET Archives
Reply-To:
Date: Tue, 23 Sep 2003 17:25:42 -0600
> Oh, by the way, animal products -- meat, fat, cholesterol -- have never been shown to cause either
> heart disease or cancers or, as far as I am aware, any other disease (except from infected produce
> or man-made chemical pollution). Only processed plant material has.
> Barry Groves
> http://www.second-opinions.co.uk
Hi Barry
what do you think about the correlation drawn by several studies, between a diet high in saturated fat and
increased beta-glucuronidase activity, which leads to the (re)absorption of hormones and toxins in the bile,
which in turn, is a caustive factor for disease, e.g. breast cancer? This is an oft cited reason to decrease
dietary fat and increase fiber. I know this isn't a fair question because most research doesn't look at a high fat
diet per se, only fat and fiber in greater or lesser volumes.
1: Goldin BR, Adlercreutz H, Gorbach SL, Warram JH, Dwyer JT, Swenson L, Woods MN. Estrogen
excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med. 1982 Dec
16;307(25):1542-7. PMID: 7144835 [PubMed - indexed for MEDLINE]
2: Domellof L, Darby L, Hanson D, Mathews L, Simi B, Reddy BS. Fecal sterols and bacterial betaglucuronidase activity: a preliminary metabolic epidemiology study of healthy volunteers from Umea,
Sweden, and metropolitan New York. Nutr Cancer. 1982;4(2):120-7. PMID: 6298751 [PubMed - indexed for
MEDLINE]
3: Indira M, Vijayammal PL, Menon PV, Kurup PA. Effect of dietary fiber on intestinal bacterial betaglucuronidase activity in chicks fed a cholesterol-containing diet. Cancer. 1980 Dec 1;46(11):2430-2. PMID:
6254631 [PubMed - indexed for MEDLINE]
4: Reddy BS, Hanson D, Mangat S, Mathews L, Sbaschnig M, Sharma C, Simi B. Effect of high-fat, highbeef diet and of mode of cooking of beef in the diet on fecal bacterial enzymes and fecal bile acids and
neutral sterols. J Nutr. 1980 Sep;110(9):1880-7. PMID: 7411244 [PubMed - indexed for MEDLINE]
5: Reddy BS, Hedges AR, Laakso K, Wynder EL. Metabolic epidemiology of large bowel cancer: fecal bulk
and constituents of high-risk North American and low-risk Finnish population. Cancer. 1978
Dec;42(6):2832-8. PMID: 728877 [PubMed - indexed for MEDLINE]
6: Hambly RJ, Rumney CJ, Fletcher JM, Rijken PJ, Rowland IR. Effects of high- and low-risk diets on gut
microflora-associated biomarkers of colon cancer in human flora-associated rats. Nutr Cancer.
1997;27(3):250-5. PMID: 9101554 [PubMed - indexed for MEDLINE]
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46/61 (2003)
PALEODIET Archives
From: Barry Groves
Reply-To:
Date: Wed, 24 Sep 2003 11:31:01 +0100
Hi Todd
The problem with these studies is that modern clinical trials are conducted in the wrong context -- that of a
'healthy', processed-carbohydrate, relatively low-fat diet. The addition of fibre to diet might mitigate the
effects of such diets but don't address the causes. There are also contradictory studies in the modern
literature, which show low levels of cancer in peoples with a low-fibre, high meat intake, and increases of
cancers with increasing dietary fibre. There are also "paradoxes":
1. Lyon JL, Gardner JW, et al . Low cancer incidence and mortality in Utah. Cancer 1977; 39: 2608 2.
Dietary studies of cancer of the large bowel in the animal model . In Vahouny GV, Kritchevsky D (Eds).
Dietary Fibre: Basic and Clinical Aspects . Plenum, New York. 1986. p 469 3. Wasan HS, Goodlad RA.
Fibre-supplemented foods may damage your health. Lancet 1996; 348: 319-20. 4. Fuchs CS, et al . Dietary
Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New Engl J Med 1999; 340: 169-176,
223-224. 5. Smith-Warner SA, et al. Intake of Fruits and Vegetables and Risk of Breast Cancer: A Pooled
Analysis of Cohort Studies. JAMA . 2001; 285: 769-776. 6. Tokudome S, Nagaya T, Okuyama H, et al.
Japanese versus Mediterranean Diets and Cancer. Asian Pac J Cancer Prev. 2000;1(1):61-66.
To get the right answers we need to look at older epidemiological studies: those of Weston Price, Stefansson,
McCarrison, Boyd Orr, et al, on such peoples as the Maasai, Watusi, Berbers, Marsh Arabs, Neurs, Nagas,
Inuit, etc. (Unfortunately, these peoples are much more difficult to study now as the diets of many have been
adulterated by contact with Western society.) If we look at this evidence, we find no relation between
saturated fat intake or meat intake and any cancers.
I don't tend to rely on animal studies as, although there are many similarities between us and other mammals,
when it comes to diet there are significant confounding factors.
----- Original Message ----- From: "Todd Caldecott" To: Sent: Wednesday, September 24, 2003 12:25 AM
> Oh, by the way, animal products -- meat, fat, cholesterol -- have never been shown to cause either
> heart disease or cancers or, as far as I am aware, any other disease (except from infected produce
> or man-made chemical pollution). Only processed plant material has.
> Barry Groves
> http://www.second-opinions.co.uk
>
> Hi Barry
> what do you think about the correlation drawn by several studies, between a diet high in saturated
> fat and increased beta-glucuronidase activity, which leads to the (re)absorption of hormones and
> toxins in the bile, which in turn, is a caustive factor for disease, e.g. breast cancer? This is
> an oft cited reason to decrease dietary fat and increase fiber. I know this isn't a fair question
> because most research doesn't look at a high fat diet per se, only fat and fiber in greater or
> lesser volumes. 1: Goldin BR, Adlercreutz H, Gorbach SL, Warram JH, Dwyer JT, Swenson L, Woods
MN.
> Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med.
> 1982 Dec 16;307(25):1542-7. PMID: 7144835 [PubMed - indexed for MEDLINE] 2: Domellof L, Darby
L,
> Hanson D, Mathews L, Simi B, Reddy BS. Fecal sterols and bacterial beta-glucuronidase activity: a
> preliminary metabolic epidemiology study of healthy volunteers from Umea, Sweden, and metropolitan
> New York. Nutr Cancer. 1982;4(2):120-7. PMID: 6298751 [PubMed - indexed for MEDLINE] 3: Indira
M,
> Vijayammal PL, Menon PV, Kurup PA. Effect of dietary fiber on intestinal bacterial
> beta-glucuronidase activity in chicks fed a cholesterol-containing diet. Cancer. 1980 Dec
> 1;46(11):2430-2. PMID: 6254631 [PubMed - indexed for MEDLINE] 4: Reddy BS, Hanson D, Mangat
S,
47/61 (2003)
> Mathews L, Sbaschnig M, Sharma C, Simi B. Effect of high-fat, high-beef diet and of mode of
> cooking of beef in the diet on fecal bacterial enzymes and fecal bile acids and neutral sterols. J
> Nutr. 1980 Sep;110(9):1880-7. PMID: 7411244 [PubMed - indexed for MEDLINE] 5: Reddy BS,
Hedges AR,
> Laakso K, Wynder EL. Metabolic epidemiology of large bowel cancer: fecal bulk and constituents of
> high-risk North American and low-risk Finnish population. Cancer. 1978 Dec;42(6):2832-8. PMID:
> 728877 [PubMed - indexed for MEDLINE] 6: Hambly RJ, Rumney CJ, Fletcher JM, Rijken PJ,
Rowland IR.
> Effects of high- and low-risk diets on gut microflora-associated biomarkers of colon cancer in
> human flora-associated rats. Nutr Cancer. 1997;27(3):250-5. PMID: 9101554 [PubMed - indexed for
MEDLINE]
>
> Todd Caldecott, Cl.H., AHG
PALEODIET Archives
Subject: Re: scientific proof, teeth, health claims etc
Reply-To:
Date: Wed, 24 Sep 2003 13:37:26 -0600
> ON the archaeological evidence, caries generally increases with increasing agriculturalisation in
> the neolithic, but the evidence is equivocal in some areas. Overall, most archaeologists believe
> it is the increasing starchy content of the diet that results in caries, but this can be moderated
> by a number of other factors.
I would be interested to hear of any research that examines the relationship between vitamin D3 status and
risk of caries (and if D3 is in fact what Price refers to as "activator X" in his text "Nutrition and Physical
Degeneration"). Certainly the D3 content of our diet has declined over the last few years, and activated
ergosterol appears not be as biologically active as thought. For that matter, what do y'all think is an
appropriate dosage range for D3. According to two recent papers D3 supplementation should be increased to
upwards of 1000 IU daily, all year long, for folks in temperate climes.
Veith, R. 2001. Vitamin D Nutrition and its Potential Health Benefits for Bone, Cancer and Other
Conditions. Journal of Nutritional & Environmental Medicine. 11, 275291 Zittermann, A. 2003. Vitamin D
in preventive medicine: are we ignoring the evidence? British Journal of Nutrition. 89, 552572
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PALEODIET Archives
Reply-To:
Date: Wed, 24 Sep 2003 14:12:51 +0100
Hi, a quick response to Barry repeating a number of points that I made on the list a few months ago.
> On teeth, the article makes out that our teeth are designed to cope with plant foods. I defy
> anyone to clench their teeth together and then move their jaws sideways to "grind" in the way that
> herbivores do.
48/61 (2003)
Herbivores that grind their plant foods with their teeth in that sideways motion are usually folivores, that is
they eat leaves with a high cellulose and often silica content. There are many foods of plant origin that do not
require grinding to be palatable, ie fruits, tubers, shoots. Not all herbivores need grinding teeth, ie a number
of primates.
> If we take this one step further and compare our colons with those of our nearest relatives we
> find that our colon/caecum accounts for around 20% of our gut's total volume, whereas the colons
> of the fermentative chimps and gorillas is more than 50% of the total volume.
Yes, but as I have said before, primates that eat 'high quality' energy dense plant foods have similar gut and
colon/caecum proportions to us, eg baboons and capuchin monkeys. Not all primates/chimps/apes are
fermenters.
> Our gut is a simple tube with a bulge (stomach) at its beginning -- exactly the same as all
> carnivores. Its total length is approximately 5 times body length. That of the big cats is
> approximately 7 times body length. The gut of a herbivore, by contrast is some 27 times body
> length and, in the ruminants, much more complex. In our nearest relatives, it is also a similar
> length and, as I have already mentioned, it differs markedly in that apes' colons are much bigger
> than ours. In other words, our gut, in terms of length and complexity is even more "carnivore"
> than the big cats.
The 'simple tube' is not an accurate description of the human gut. The proportions for humans are approx:
20% stomach, 60-65% small intestine, 1-3% caecum, 20-ish% colon, very different to carnivores (to be
specific the order Carnivora) in the small intestine part. But not all herbivores have similar gut proportions.
Some have aspects of their guts similar to carnivores (eg no caecum), yet are definite herbivores - eg hippos.
I feel Barry is being rather simplistic in his division of gut type and correlation with dietary group. We are
not more similar to carnivores than we are to herbivores, for the reason that there is a lot of variation
throughout the mammalian kingdom. For an excellent discussion of this whole subject, complete with very
comprehensive and comprehensible diagrams, see Stevens, C. E. and I. D. Hume (1995). Comparative
physiology of the vertebrate digestive system. Cambridge, Cambridge University Press.
I hesitate to say this, as I do not want to be offensive, but I venture that Barry would rather that this simple
division of carnivore/herbivore does hold up, as it appears from his prior postings that he would rather that
we as humans are incontrovertibly carnivore. I have no problem with this attitude towards human diet, unless
the individual holding it twists the science to suit their opinion.
Tamsin
OX1 3QJ, UK tel:01865-283641 fax:01865-273932
-----------------------------------
PALEODIET Archives
Subject: Study: Same molecule in meat, milk, tumors
From: Liza May
Reply-To:
Date: Tue, 30 Sep 2003 15:19:07 -0400
WASHINGTON (Reuters) --A non-human molecule found in red meat and milk makes its way into the
human system when eaten -- and seems to build up especially in tumors, U.S. researchers reported on
Monday.
The compound, called sialic acid, is found on the surfaces of animal cells but is not found in people, and may
be one reason why animal-to-human organ and tissue transplants do not work well. Animals have a version
called Neu5Gc, while humans carry Neu5Ac.
But researchers at the University of California San Diego found it does show up in the human body, and
showed it can be absorbed from eating red meat and milk.
They also showed that the body produces an immune response against the molecule.
Dr. Ajit Varki and colleagues, reporting in the Proceedings of the National Academy of Sciences, say it is
too soon to make any recommendations based on their findings.
"Of course, there are already existing recommendations that people should not consume too much food
containing saturated fats, such as dairy products and red meats, " Varki said in a statement.
49/61 (2003)
"The highest amount [of Neu5Gc] was found in lamb, pork, and beef [so-called 'red meat'], " the researchers
wrote. Levels were very low or undetectable in poultry and fish, vegetables and hen's eggs.
Varki, who is not a vegetarian, noted that many studies have linked a diet rich in meat and milk with cancer,
heart disease and other diseases.
Autoimmune diseases "The small amounts of Neu5Gc in normal tissues also raise the possibility that antiNeu5Gc antibodies are involved in autoimmunity, " the researchers said.
Autoimmune diseases occur when the body mistakenly attacks healthy tissue and include type-1 or juvenile
diabetes and some types of arthritis. "In this regard, it is interesting that vegetarian diet has been suggested to
improve rheumatoid arthritis, " they wrote.
http://tinyurl.com/p7t2
PALEODIET Archives
Subject: Re: Study: Same molecule in meat, milk, tumors
From: matesz
Reply-To:
Date: Tue, 30 Sep 2003 17:57:40 -0400
Liza:
Why did you leave out this part?:
[Snip]
But much research has focused on the fat content of animal fat or byproducts of cooking meat as the cause of
disease.
Varki's collaborator Dr. Elaine Muchmore developed an antibody -- an immune system targeting protein -that would hook onto Neu5Gc. The team found Neu5Gc in human tumor samples and to a much lower
degree in healthy tissue.
More tests showed that most people had made their own antibodies that recognized Neu5Gc, and thus could
potentially initiate an inflammatory immune response.
Varki and two colleagues drank Neu5Gc purified from pork sources, and the molecule showed up in their
urine, blood, hair and saliva.
"We need to find out if there is any association between the presence of Neu5Gc and/or the anti-Neu5Gc
antibodies with any disease, " Varki said. "This will require large-scale population studies."
In some cases the human immune response was similar to that seen when people are exposed to another
animal molecule, this one a cell surface molecule called alpha galactose.
Varki noted that the molecule is almost certainly not immediately toxic to people.
"Meat eating has certainly been a feature of human ancestors for many hundreds of thousands of years, " he
said.
"Thus, it is indeed possible that humans have developed some kind of tolerance or indifference to Neu5Gc.
However, most humans are continuing to make antibodies against Neu5Gc."
It could be that the damage only builds up over years -- and that as people live longer, the consequences
make themselves felt.
"However, we are now living longer and the question arises whether the gradual accumulation of Neu5Gc
and the simultaneous presence of antibodies against could be involved in some diseases of later life, " he
said.
[snip]
Basically, the research is interesting but inconclusive. However, snipping it where you did seemed designed
to play up the case against meat and down-play the uncertainties the researchers expressed.
Tumors contain a lot of molecules. As they said, large scale studies and research on possible mechanisms
would have to be done to show any firm causitive link between this Neu5Gc and cancer. So far its just a
tenuous link and speculation.
The authors make the common mistake of assuming that all people in the past lived shorter lives than we do.
They like others confuse average life expectancy, which is reduced by early deaths, and actual individual life
spans.
Socrates, Plato, and Aristotle all lived past 70, more than 2000 years ago. Socrates you know may have lived
longer but was put to death.
In the McDougall article that was discussed here last week the same mistake. To distill it:
50/61 (2003)
The average life expectancy is based on averaging all deaths. So if you have 5 people die in their first year of
life (infections), 5 die at an average age of 35 from hunting accidents, and 5 live to 70, the average life
expectancy of this group will be calculated to be 35 years of age. Yet 33% of the people lived to 70. This is
an oversimplification of how stats are misunderstood to make it look like all pre-industrial people died at 35.
McDougall made the more remarkably misguided statement that you only have to live to 20 to reproduce. If
he means just popping out a baby he has an incomplete view of reproduction. Most people understand that
infants are not self-sufficient. In fact, it takes about 16 years to truly reproduce oneself in a child, i.e. get
him/her to the point of true self-sufficiency. Because of the long dependency period in humans, I find it
difficult to imagine any human group surviving long if all members died at 30 or so.
Weston Price and Stefansson searched for cancer among primitives without success although many ate large
amounts of animal products and lived to advanced ages (as documented by the photos in Price's book).
Moreover, U.S. cancer rates have skyrocketed since 1900 in America, but average red meat consumption has
actually slightly declined according to USDA figures. These researchers are suggesting poultry is safer, but
over the past century in the U.S. chicken consumption has gone up. And these days cancer is growing in
prevalence in young people, so the meat+aging hypothesis seems to be leaking from the start.
Don
PALEODIET Archives
From: Dick Bird
Reply-To:
Date: Wed, 1 Oct 2003 12:01:42 +0100
A letter in last week's Nature gives evidence that in the British Isles there was a sharp switch between fish
eating and meat eating in about 5 000 BP. Analysis of C13 content in bones has shown a wide range of
values in remains before this date but a very narrow one (corresponding to the meat diet) which cuts in
afterwards. The authors speculate that this was the beginning of herding.
"Marine foods seem for whatever reason to have been comprehensively abandoned from the beginning of the
Neolithic in Britain"
Nature 25 Sept 2003: v425, p366 "Sharp Shift in Diet at Onset of Neolithic" Richards Shulting & Hedges.
The implication seems to me to be that commercial factors conditioned diet then, as now!
Dick Bird
PALEODIET Archives
Reply-To:
Date: Tue, 30 Sep 2003 22:56:01 -0500
Liza,
The article on sialic acid, which purports to explain the probable adverse effects of meat consumption, is
somewhat misleading (against the backdrop of controlled observations regarding these postulated adverse
effects). The quote that I will "pick on" is the following:
"Varki, who is not a vegetarian, noted that many studies have linked a diet rich in meat and milk with cancer,
heart disease and other diseases."
The part that I will "pick on" is cancer, using 3 highly-relevant studies:
Study #1: A reduction in the status of meats from a probably causal status in colorectal cancer down to
something regarded as possibly causal, but not longer regarded as probably causal (research indicates that it
is no longer to be considered a probable cause):
"the relationship between meats in general and colorectal cancer now looks weaker than the 'probable' status
it was judged to have by the WCRF in 1997."
Truswell AS. Meat consumption and cancer of the large bowel. Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S1924.
51/61 (2003)
Study #2: A nonsignificant increase in breast cancer risk in vegetarians (when adjusted for intake of
vegetables and pulses):
"Adjustment for intake of vegetables and pulses reverted the odds of breast cancer in lifelong vegetarians
relative to lifelong meat-eaters (OR=1.04; 95% CI=0.65-1.68) and attenuated the quartile-specific estimates
for meat intake, whereas the inverse trends in the odds of breast cancer with intake of vegetables and pulses
remained after adjustment for type of diet or meat intake."
Dos Santos Silva I, Mangtani P, McCormack V, Bhakta D, Sevak L, McMichael AJ. Lifelong vegetarianism
and risk of breast cancer: a population-based case-control study among South Asian migrant women living in
England. Int J Cancer. 2002 May 10;99(2):238-44.
Study #3: A nonsignificant increase in the overall death rate in vegetarians:
"Comparing vegetarians with nonvegetarians within each cohort, the death rate ratios (DRRs), adjusted for
age, sex and smoking, were 1.03 (0.95, 1.13) in the Health Food Shoppers Study, 1.01 (0.89, 1.14) in the
Oxford Vegetarian Study, and 1.05 (0.86, 1.27) in EPIC-Oxford."
Key TJ, Appleby PN, Davey GK, Allen NE, Spencer EA, Travis RC. Mortality in British vegetarians: review
and preliminary results from EPIC-Oxford. Am J Clin Nutr. 2003 Sep;78(3 Suppl):533S-538S.
Liza, while all that these 3 studies actually show is "statistical equivalence", this boring fact DOES indeed
say something. It invalidates the reasoning of those who would attempt to maintain that meats are a probable
cause of disease and early death in humans. In other words, and using evidence-based reasoning: one must
conclude that the weight of evidence on the matter, while not conclusive, IS conclusive that meat is NOT the
"health hazard" various PhDs have maintained up to now.
So, let's make sure to take the: "many studies have linked a diet rich in meat and milk with cancer, heart
disease and other diseases" quote in context of the totality of scientific evidence (and realize that it is
misleading).
Note: Regarding milk consumption, I would have to say that it appears "guilty as charged" regarding prostate
cancer (a "probable" cause).
Ed
PALEODIET Archives
From: Liza May
Reply-To:
Date: Wed, 1 Oct 2003 12:09:38 -0400
Edward Thompson wrote on Tuesday, September 30, 2003 11:56 PM:
> The article on sialic acid, which purports to explain the probable adverse effects of meat
> consumption, is somewhat misleading (against the backdrop of controlled observations regarding
> these postulated adverse effects). ... one must conclude that the weight of evidence on the
> matter, while not conclusive, IS conclusive that meat is NOT the "health hazard" various PhDs have
> maintained up to now.
Ed, I agree! I am aware of the data you've cited, and much more. I posted the article only because I thought
list members in other areas of the world might find interesting what is appearing in leading media here in the
U.S. Liza
PALEODIET Archives
From: Liza May
Reply-To:
Date: Wed, 1 Oct 2003 15:00:44 -0400
matesz wrote on Tuesday, September 30, 2003 5:58 PM:
> Why did you leave out this part?:
> [Snip]
> But much research has focused on the fat content of animal
52/61 (2003)
> fat or byproducts of cooking meat as the cause of disease.

> Varki's collaborator Dr. Elaine Muchmore developed an
> antibody -- an immune system targeting protein -- that would
> hook onto Neu5Gc. The team found Neu5Gc in human tumor
> samples and to a much lower degree in healthy tissue.
Don,
I did not post the full article because Reuters articles specifically state the following:
" Copyright 2003 Reuters. All rights reserved. This material may not be published, broadcast, rewritten, or
redistributed. "
... and we are a public forum.
I included the opening paragraphs of the piece, and the url for those interested in reading the entire piece,
which is common practice in groups like this.
Liza
PALEODIET Archives
Subject: Vitamin D
From: Bob Avery
Reply-To:
Date: Thu, 2 Oct 2003 23:11:42 -0400
There are several important, only recently understood, and not yet widely appreciated, points to be made
about vitamin D: Healthy/desirable levels are much higher than was thought. Laboratory reference ranges for
25-hydroxyvitamin D (25(OH)D) are still stated at around 40-100 nmol l-1. But people who live in
equatorial regions, and spend much of their days in the sunlight (farmers and lifeguards, for instance),
consistently show levels over 100 nmol l-1, and even above 200 nmol l-1. Because humanity evolved in such
an environment, it is clear that the vitamin D exposure that parallels the Stone Age diet, as the environment
in which humanity evolved, was much higher than the levels we have now come to regard as normal. Yet
vitamin D deficiency is widespread in developed countries, and food fortification is disappointing as a
solution to this. http://www.mult-sclerosis.org/news/Jan2002/FullTextVitaminDReassessment.h tml
?!
PALEODIET Archives
Subject: New road reveals Stone Age site
From: Liza May
Reply-To:
Date: Mon, 6 Oct 2003 23:15:16 -0400
Archaeologists believe they may have stumbled upon a major Stone Age site - on the route of a new bypass.
The site dates back between 250, 000 and 300, 000 years and may even provide evidence of one of the
earliest uses of fire.
Archaeologists discovered a range of items at the location in Harnham, near Salisbury in Wiltshire, including
44 "very rare" flint hand axes - the earliest form of tool used by man.
Yet the dig was only organised after the county council unveiled plans to build a relief road for the village.
One of the most exciting discoveries on the site has been evidence of charcoal - which could point to an early
use of fire.
Full text:
http://tinyurl.com/pyzn
PALEODIET Archives
Subject: Raw vs Cooked
From: Liza May
Reply-To:
53/61 (2003)

Date: Tue, 7 Oct 2003 14:18:07 -0400
Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):35-46
'Cooking as a biological trait'
Wrangham R, Conklin-Brittain N.
Department of Anthropology, Harvard University, Peabody Museum, 11 Divinity Avenue, MA 02138,
Cambridge, USA
No human foragers have been recorded as living without cooking, and people who choose a 'raw-foodist'
life-style experience low energy and impaired reproductive function. This suggests that cooking may be
obligatory for humans. The possibility that cooking is obligatory is supported by calculations suggesting that
a diet of raw food could not supply sufficient calories for a normal hunter-gatherer lifestyle. In particular,
many plant foods are too fiber-rich when raw, while most raw meat appears too tough to allow easy chewing.
If cooking is indeed obligatory for humans but not for other apes, this means that human biology must have
adapted to the ingestion of cooked food (i.e. food that is tender and low in fiber) in ways that no longer allow
efficient processing of raw foods. Cooking has been practiced for ample time to allow the evolution of such
adaptations. Digestive adaptations have not been investigated in detail but may include small teeth, small
hind-guts, large small intestines, a fast gut passage rate, and possibly reduced ability to detoxify. The
adoption of cooking can also be expected to have had far-reaching effects on such aspects of human biology
as life-history, social behavior, and evolutionary psychology. Since dietary adaptations are central to
understanding species evolution, cooking appears to have been a key feature of the environment of human
evolutionary adaptedness. Further investigation is therefore needed of the ways in which human digestive
physiology is constrained by the need for food of relatively high caloric density compared to other great
apes.
PMID: 14527628
PALEODIET Archives
From: Roland Rohde
Reply-To:
Date: Wed, 8 Oct 2003 03:33:28 -0500
Liza,
it's a well known fact that milk sugar (lactose) is not simply any sugar. Actually it causes baby's gut to
become leaky for some of the valuable milk constituents that are provided by mother's glands and that should
not be digested (hormones like IGF1) or got lost (like the calcium from mummy's bones).
Pastoral tribes like the Samburu and the Masai know this well. They never mix milk and meat. This rule is
the origin of the appropriate jewish kashrut. It's not unlikely that our gut becomes leaky for many
immunogenic food constituents (e.g. Neu5Gc) if we drink not fermented milk or -even worse- drink it
together with meat. But today, you can find milk sugar as an additive in many prepared meat products.
> "Of course, there are already existing recommendations that people should not consume too much
> food containing saturated fats, such as dairy products and red meats, " Varki said in a statement.
Statements like these seem to be pretty outdated. Not only is the theory of the beneficial vegetable fats
completely paradoxified by the facts, e.g. the masai, the french, the israelis, in this order. As it becomes clear
that polyunsaturated fats are toxic in higher amounts, they try to switch to the so called 'mediterranean diet'
rich in monounsaturates as they are present in olive oil, like it is grown and used in Israel, a mediterranean
country and world champion in the rate of heart disease.
There is considerable scientific evidence that at least the saturated fatty acid stearic acid is sort of semiessential for man. I don't want to bore you. Literature or discussion on request.
Roland
PALEODIET Archives
54/61 (2003)
Reply-To:
Date: Wed, 8 Oct 2003 12:58:12 -0600
Roland,
I would be very interested to see the data that lactose enhances GI permeability
best.. Todd Caldecott
On Wednesday, October 8, 2003, at 02:33 AM, Roland Rohde wrote:
> Liza,
> it's a well known fact that milk sugar (lactose) is not simply any sugar. Actually it causes
> baby's gut to become leaky for some of the valuable milk constituents that are provided by
> mother's glands and that should not be digested (hormones like IGF1) or got lost (like the calcium
> from mummy's bones). Pastoral tribes like the Samburu and the Masai know this well. They never mix
> milk and meat. This rule is the origin of the appropriate jewish kashrut. It's not unlikely that
> our gut becomes leaky for many immunogenic food constituents (e.g. Neu5Gc) if we drink not
> fermented milk or -even worse- drink it together with meat. But today, you can find milk sugar as
> an additive in many prepared meat products. "Of course, there are already existing recommendations
> that people should not consume too much food containing saturated fats, such as dairy products and
> red meats, " Varki said in a statement. Statements like these seem to be pretty outdated. Not only
> is the theory of the beneficial vegetable fats completely paradoxified by the facts, e.g. the
> masai, the french, the israelis, in this order. As it becomes clear that polyunsaturated fats are
> toxic in higher amounts, they try to switch to the so called 'mediterranean diet' rich in
> monounsaturates as they are present in olive oil, like it is grown and used in Israel, a
> mediterranean country and world champion in the rate of heart disease. There is considerable
> scientific evidence that at least the saturated fatty acid stearic acid is sort of semi-essential
> for man. I don't want to bore you. Literature or discussion on request.
> Roland
> Todd Caldecott http://www.wrc.net/phyto
PALEODIET Archives
From: matesz
Reply-To:
Date: Wed, 8 Oct 2003 19:28:34 -0400
> There is considerable scientific evidence that at least the saturated fatty acid stearic acid is
> sort of semi-essential for man. I don't want to bore you. Literature or discussion on request.
> Roland
I would be interested in knowing what literature supports this and also under what conditions would stearic
acid become essential. For it appears to me people produce buckets of it.
Don
PALEODIET Archives
From: Roland Rohde
Reply-To:
Date: Fri, 10 Oct 2003 11:04:22 -0500
> I would be very interested to see the data that lactose enhances GI permeability
Todd,
that lactose does something special with our gut must have been known for a long time because I saw this
mentioned in textbooks from the sixties (without citations). But there are newer ones, too.
55/61 (2003)
An experimental paper [1] concludes "These and other data indicated that lactose is not interacting directly
with Ca++ in solution but is interacting with the absorptive cells of the intestine to increase their
permeability to Ca++."
There just was an interesting letter in the Journal of Pediatrics [2]. It should bee freely accessible online and
has some citations. If you shouldn't be able to find/read it, here are some of them: [3-5].
The paper [6] shows that lactose is not the only enhancing factor in milk.
Not every mineral uptake is enhanced [7, 8], and not only minerals are affected [9, 10].
The uptake of intact IGF1 is another established fact [11, 12].
I even remember an article showing that in humans, the blood levels of IGF-1 after milk ingestion are
elevated. Sorry, I lost the citation (somewhere on my HD). Perhaps someone else knows it.
A close look at the original article [13] about that sialic acid (Neu5Gc) raises some questions.
(i) The test persons avoided animal foods two days before the start of the experiment and even avoided
shampoos potentially containing Neu5Gc.(Good!) Then they were given ~150mg Neu5Gc and continously
fruit juice and soymilk at a constant rate for 6 h. But as many foods of non-animal origin contain milk sugar
as an additive (possibly in the preexperimental period) and even other sugars influence the uptake of
nutrients [10] the Neu5Gc-uptake could have been sustained as well. If there was a mild bowel inflammation
in some of the test persons caused by our western diet it might have persisted. The guts of the volunteers
should have been given a little more time to adapt and a nutrition that heals inflammatory gut diseases.
(ii) The same authors made it likely [14] that the loss of the gene responsible for Neu5Gc-formation in
humans took place just before the human brain startet to grow (and prey became the main food source). They
even suspect that this was a prerequisite for brain expansion in humans because Neu5Gc-concentrations are
always low in the brain even in animals with high tissue levels of it. Neu5Gc seems to be well incorporated
in surface antigens of many human epithelial tissues after resorption [13]. As such surface antigens are most
likely involved in the recognition of our "self" and in cellular communication this should happen under
strong genetic control and not by chance. And as Neu5Gc must have some function in animals, we have to
ask wether human tissues need it, too, at least in small amounts, making it an essential nutritional factor and
humans dependent on meat (like with B12). Possibly, humans survived the loss of this sialic acid only
because they had food sources. That it is found especially in tumor cells could even mean that these cells
switched off their control systems because the couldn't otherwise get enough of it. There is not a single
aspect that supports a possible carcinogenicity of Neu5Gc.
(iii) Even the presence of antibodies against Neu5Gc-containing polysaccharides (pure Neu5Gc cannot be
immunogenic) doesn't mean much. It could simply be the consequence of a leaky gut permitting the uptake
of complex immunogenic substances thus leading to a mild form of "serum sickness" [like mentioned in 13].
If they were directed against the Neu5Gc-containing human antigens, they should have been extracted by our
tissues [15]. There is a wide range of the measured antibody titers and they are small, not like with the titers
against the xenoantigen Gal-alpha1, 3Gal. Their Fig. 6 has different scale factors for both antibody-axes. All
Neu5Gc-titers are below the Gal-titers! A reaction between such antibodies and our tissues would be some
sort of autoimmune reaction. A leaky gut could lead to the formation of crossreacting autoantibodies. But
there are many epitopes in our nutrition which could do that under leaky gut-conditions, even in vegetables.
roland
[1]Armbrecht, HJ, Wasserman RH. Enhancement of Ca++ uptake by lactose in the rat small intestine. J Nutr
1976 Sep;106(9):1265-71.
[2]J Pediatr 2003 Jun;142(6):737-8.
[3]Lengeman, FW. The site of action of lactose in the enhancement of calcium utilization. J Nutr 1959; 69:
537-546.
[4]Ziegler EF, et. al. Lactose enhances mineral absorption in infancy. J Pediatr Gastroenterol Nutr 1983; 2:
288-294.
[5]Moya M, et. al. Short-term polycose substitution for lactose reduces calcium absorption in healthy term
babies. J Pediatr Gastroenterol Nutr 1992; 14: 57-61.
[6]Camara-Martos F, et. al. Influence of dietary factors on calcium bioavailability: a brief review. Biol Trace
Elem Res 2002 Oct;89(1):43-52.
[7]Abrams SA, et. al. Calcium and zinc absorption from lactose-containing and lactose-free infant formulas.
Am J Clin Nutr 2002 Aug;76(2):442-6.
[8]Beynen AC, et. al. Magnesium balance in adult cats fed a dry food rich in lactose. J Anim Physiol Anim
Nutr (Berl) 2003 Aug;87(7-8):245-50.
[9]Lane RH, et. al. IGF alters jejunal glucose transporter expression and serum glucose levels in immature
rats. Am J Physiol Regul Integr Comp Physiol 2002 Dec;283(6):R1450-60.
56/61 (2003)
[10]Play B, et. al. Glucose and galactose regulate intestinal absorption of cholesterol. Biochem Biophys Res
Commun 2003 Oct 17;310(2):446-51.
[11]Philipps AF, et.al. Absorption of milk-borne insulin-like growth factor-I into portal blood of suckling
rats. J Pediatr Gastroenterol Nutr 2000 Aug;31(2):128-35.
[12]Buts JP. Bioactive factors in milk Arch Pediatr 1998 Mar;5(3):298-306.
[13]Ahead of print. Tangvoranuntakul P, et. al. Human uptake and incorporation of an immunogenic
nonhuman dietary sialic acid. PNAS 2003 Oct 14; 100: 12045-50.
[14]Chou HH, et. al. Inactivation of CMP-N-acetylneuraminic acid hydroxylase occurred prior to brain
expansion during human evolution. PNAS 2002 Sep 3;99(18):11736-41.
[15] Macchiarini P, et.al. Evidence of human non-alpha-galactosyl antibodies involved in the hyperacute
rejection of pig lungs and their removal by pig organ perfusion. J Thorac Cardiovasc Surg 1998
Nov;116(5):831-43.
PALEODIET Archives
From: Roland Rohde
Reply-To:
Date: Mon, 13 Oct 2003 11:31:27 -0500
> ... people produce buckets of it. [of stearic acid. roro]
Don,
they do. But something eats it up at once. This something is called StearoylCoA-Desaturase (SCD-1) and
transforms a supposedly bad guy (saturated stearic acid, SA) into a good one ('mediterranean' oleic acid,
OA). Did you ever think about why the adipose tissue of starch-fed animals like pigs (and of many humans)
contains a lot of OA, much palmitic acid and only small amounts of SA?
In mammals, OA synthesis is performed in three steps. An enzyme complex called fatty acid synthase (FAS)
at first makes a palmitic acid from carbs or amino acids as primary source. It stops at a chain length of 16
carbons. The n a separate enzyme, Long Chain Elongase [1] (LCE), adds two more carbons resulting in SA.
And, finally, a cis-doublebond is inserted in the middle by SCD-1. Therefore, the lots of OAs in adipose
tissue of animals with negligible fat intake have to pass the SA-step. The relative activities of LCE and SCD1 are critical for the SA-content not only of the fat cells but of cell membranes, too. The group of James
Ntambi in Madison, WI, worked more than 15 y about the SCD-1 enzyme [2] and found out some strange
properties.
First, the SCD-1 product OA has well known indispensable metabolic functions similar to it's precursor SA.
Virtually every cell is able to synthesize them and thus they cannot be essential in the strict meaning, of
course. A loss of this capability would most likely make us die before birth. But in spite of being one of the
most abundant nutrients, OA from the meals or just from our stores cannot be reused in some metabolic
processes like lipoprotein assembly [3] and cholesterol/wax-ester formation [4]. It has to be built de novo by
SCD-1 from SA! This makes SCD-1 an extremely important control point of our metabolism and results in a
continuous need for SA. And that's not all. SCD-1 knockout mice don't get fat even if they are fed a fatty
chow. This is not because they eat less. They burn more fat [2, 5, 6]!
This canonly be explained in two ways. Wherever the metabolic target may be, either the diminished
availability of SA or the formation of an OA-compound makes mice fat. It was made probable [2, 5] that one
of these targets is the combustion control of the mitochondria in muscle, liver, and other organs. SA
stimulates the fat combustion maximally if compared to other fatty acids and SCD-1 attenuates burning by
transforming it locally into the less activating OA and by supporting fatty acid synthesis [7, 8, 9]. This makes
much sense! SCD-1 is one of the most strongly induced enzymes in lipogenic states [10], something many
people don't like very much to be in and that should not be present in a paleodiet. In such a state, it
seemsmetabolically reasonable to spare fats by lowering their combustion first before starting their
production. If the burning of energy has to be sustained, cells could directly burn the carbs.
57/61 (2003)
But there is one situation where these mechanisms have to be overridden: if there is a lack in metabolically
needed SA. As the two SA-forming enzymes FAS and especially the rate limiting LCE [11] (that apparently
can use external or stored palmitic acid) both are lipogenic enzymes [10], a lipogenic state has to be induced
whatever the nutritional status may be. Even on a weight reduction diet. A diet rich in fat but low in SA will
result in fuelling of dietary fat into our st ores and additional SA/OA production. If SA supply is low, a diet
rich in carbs might even be better because the body has only to produce as much fat as is needed for the
mentioned metabolic processes.
But in a non-lipogenic fatty diet, SA becomes really somehow essential. There are classical studies showing
the nutritional advantages of SA [12, 13]. Obese or insulin resistant people have high blood levels of fatty
acids. Why shouldn't our liver and muscles be able to use an abundant fat supply from the stores for
lipoprotein production or heating [14], respectively, like at the time when we lost our fur? If we consider the
papers [2], [5], and [20], an obvious explanation would be a wrong composition of the fatty acid stream from
adipose tissue. Indeed, low SA content of our fat cells (and cell membranes) was identified as a risc factor(s)
[15].
A low SCD-1 activity st rongly enhances insulin sensitivity [16]. So an important process could be the
induction of a vitious cycle: Low SA supply would cause insulin resistance to induce a lipogenic state by
increase of insulin production and thus to rise the SA-production. But as SCD-1 is the most strongly induced
lipogenic enzyme [10], the situation could become even worse because of enhanced SA-desaturation.
Especially the intake of fructose containing sugars could be deleterious as fructose directly induces
additional SCD-1 [19] without involving the insulin-axis.
A diet rich in fructose/fat and poor in SA seems to be ideal to get fat.
Additionally is there evidence that one metabolic SA-sensor is a so called orphan receptor named
HNF4alpha [17, 18]. If this receptor has a mutation in its lipid recognizing domain, an inheritable form of
diabetes occurs [18]. One can imagine what happens if the natural ligand of HNF4a is lacking.
HNF4a seems even to be involved in the important metabolic switch mechanisms acting during weaning. As
human milk fat is low and the fat of grass fed ruminants (and elephants/mammoths, glacial adult food) is rich
in SA from their gut bacteria one can construct a path from the fat type consumed to the fine tuning of the
metabolic point of work. But that is another story.
Fats can be categorized in four groups in respect to their SA content. (i) Most vegetable oils and fats are very
low in SA. (ii) A few have very high SA contents (30-40%) but they are exotic or expensive: shea butter,
cupu assu and cocoa butter. (Be aware of the fructose/saccharose [19] in black chocolate!). (iii) Fats of nonruminants, especially carb-fed, contain around 10%, like milk fat of cows. The milk fats of other animals
(camels? buffalos?) possibly contain more. (iv) Fat depots of ruminants contain around 20%. Thus a
paleolithic diet with 60-70% fat should have supplied at least 12-14 kcal% SA.
I must admit that the quoted arguments are no definitive proofs. But most of the cited papers are not that kind
of greasy woodoo but rock solid biochemistry.
Roland
[1] Moon YA, et. al. Identification of a mammalian long chain fatty acyl elongase regulated by sterol
regulatory element-binding proteins. J Biol Chem 2001 Nov 30;276(48):45358-66.
[2] Ntambi, JM, et. al. Recent insights into stearoyl-CoA desaturase-1. Curr Opin Lipidol 2003
Jun;14(3):255-61.
[3] Miyazaki, M, et. al. A lipogenic diet in mice with a disruption of the stearoyl-CoA desaturase-1 gene
reveals a stringent requirement of endogenous monounsaturated fatty acids for triglyceride synthesis. J Lipid
Res 2001 Jul;42(7):1018-24.
[4] Miyazaki C M, et. al. Targeted disruption of stearoyl-CoA desaturase1 gene in mice causes atrophy of
sebaceous and meibomian glands and depletion of wax esters in the eyelid. J Nutr 2001 Sep;131(9):2260-8.
[5] Cohen, Paul Role for stearoyl-CoA desaturase-1 in leptin-mediated weight loss. Science 2002 Jul
12;297(5579):240-3.
[6] Ntambi JM, et. al. Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity. Proc Natl
Acad Sci U S A 2002 Aug 20;99(17):11482-6.
[7] Lunzer, MA, et. al. Inhibition of rat liver acetyl coenzyme A carboxylase by long chain acyl coenzyme A
and fatty acid. Modulation by fatty acid-binding protein. J Biol Chem 1977 Aug 10;252(15):5483-7.
[8] McGee, R, et. al. Fatty acid biosynthesis in Erlich cells. The mechanism of short term control by
exogenous free fatty acids. J Biol Chem 1975 Jul 25;250(14):5419-2 5.
[9] Goodridge, AG, et. al. Regulation of fatty acid synthesis in isolated hepatocytes prepared from the livers
of neonatal chicks. J Biol Chem 1973 Mar 25;248(6):1924-31.
58/61 (2003)
[10] Horton, JD, et. al. Combined analysis of oligonucleotide microarray data from transgenic and knockout
mice identifies direct SREBP target genes. Proc Natl Acad Sci U S A 2003 Sep 25;.
[11] Marcelo, CL, et. al. Fatty acid metabolism studies of human epidermal cell cultures. J Lipid Res 1993
Dec;34(12):2077-90.
[12] Bonanome, A Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels. N Engl J Med
1988 May 12;318(19):1244-8.
[13] Newbold HL Reducing the serum cholesterol level with a diet high in animal fat. South Med J 1988
Jan;81(1):61-3.
[14] Bavenholm, PN, et. al. Insulin resistance in type 2 diabetes: assoc iation with truncal obesity, impaired
fitness, and atypical malonyl coenzyme A regulation. J Clin Endocrinol Metab 2003 Jan;88(1):82-7.
[15] Yli-Jama, P, et. al. Serum free fatty acid pattern and risk of myocardial infarction: a case-control study.
J Intern Med 2002 Jan;251(1):19-28.
[16] Rahman, SM, et. al. Stearoyl-CoA desaturase 1 deficiency elevates insulin-signaling components and
down-regulates protein-tyrosine phosphatase 1B in muscle. Proc Natl Acad Sci U S A 2003 Sep
16;100(19):11110-5.
[17] Navas, MA, et. al. Functional characterization of the MODY1 gene mutations HNF4(R127W),
HNF4(V255M), and HNF4(E276Q). Diabetes 1999 Jul;48(7):1459-65.
[18] Dhe-Paganon, S, et. al. Crystal structure of the HNF4 alpha ligand binding domain in complex with
endogenous fatty acid ligand. J Biol Chem 2002 Oct 11;277(41):37973-6.
[19] Waters, KM, et. al. Insulin and dietary fructose induce stearoyl-CoA desaturase 1 gene expression of
diabetic mice. J Biol Chem 1994 Nov 4;269(44):27773-7.
[20] Jen, KL, et. al. Differential effects of fatty acids and exercise on body weight regulation and metabolism
in female Wistar rats. Exp Biol Med (Maywood) 2003 Jul;228(7):843-9.
PALEODIET Archives
Subject: New Clue on Which Came First, Tools or Better Diets
From: Liza May
Reply-To:
Date: Mon, 27 Oct 2003 09:48:25 -0500
New Clue on Which Came First, Tools or Better Diets By JOHN NOBLE WILFORD
Published: October 21, 2003
The discovery in Ethiopia of stone tools almost 2.6 million years old could help resolve a debate over human
brain size, diet and toolmaking.
On a hillside in the badlands of Ethiopia, an ancestral home of the human family, an international team of
scientists has uncovered the earliest known stone tools to be found mixed with fragments of fossilized animal
bones. The scientists think the material, almost 2.6 million years old, is the strongest evidence yet that the
primal technology was used to butcher animal carcasses for meat and marrow.
The discovery could go a long way toward resolving a debate in paleoanthropology: which came first, a
significant advance in the brain that enabled human ancestors to make tools, or the toolmaking ability that
led to an enriched diet and then an evolutionary change in the brain?
"I believe the use of stone tools came first and the larger brain came later with a more substantial meat diet, "
Dr. Sileshi Semaw, the leader of the discovery team, said last week by telephone.
The findings are described in the current issue of The Journal of Human Evolution. Dr. Semaw, principal
author of the report, is a paleoanthropologist who is a research associate at the Center for Research Into the
Anthropological Foundations of Technology at Indiana University.
The age of the stone tools was no surprise, the researchers said. Working in the same region a decade ago,
Dr. Semaw found similar cobbles flaked for use in scraping and cutting at sites of about the same age. The
cobbles were hailed as the earliest known artifacts created by distant human relatives, known as hominids.
Nor was it startling to find animal bones with cut marks, presumably made by the sharp edges of butchering
tools. Similar fossilized bones with stone-tool cut marks had been excavated at a site 50 miles away, but
without any associated artifacts. Never before, the researchers said, had stone artifacts and animal bones
been found together at a single site from this early time in human evolution.
59/61 (2003)
In the journal report, Dr. Semaw's group said the discovery near the bank of a branch of the Gona River, in
the Afar region of Ethiopia, had provided "the oldest known archaeologically documented associations
between artifacts and broken faunal elements, " or animal bones.
Another member of the team, Dr. Michael J. Rogers of Southern Connecticut State University in New
Haven, said in an interview that the stone tools and the animal bones, probably from ancestors of wildebeests
and zebras, had been unquestionably associated with each other.
"What's important, " Dr. Rogers said, "is that this suggests that early stone-tool use was responsible for much
of the expansion of hominid diet from mostly plants to more meat and marrow."
Dr. Rogers, a paleoanthropologist, came upon the most revealing site three years ago while searching the arid
hills for fossils or artifacts. Several sharp flakes of rock caught his eye. They were no more than an inch or
two long, he said, and they were different from any other rock on the surface. They looked as if they had
recently eroded out of the hill.
"We got a little bit excited, " Dr. Rogers said, and soon he and colleagues began excavating and uncovered
some of the cobbles from which the flakes had been broken. Then they began finding bones, including rib
and limb fragments. At another site a few yards away, discovered by Dr. Jay Quade of the University of
Arizona, the excavators found several bones with distinct cut marks.
The quality of the tool workmanship impressed the researchers. "The flakes are amazingly well struck and
look much the same as tools made a million years later, " Dr. Rogers said.
No hominid fossil bones have been found at the sites, so it is impossible to tell who the toolmakers were. The
researchers said that they were probably members of the 2.5-million-year-old species named
Australopithecus garhi, which lived in Ethiopia and was identified in 1999 by Dr. Tim D. White of the
University of California at Berkeley.
Dr. White said the new research provided more evidence that "a dietary and technological threshold had been
crossed" by 2.6 million years ago.
http://www.nytimes.com/2003/10/21/science/21TOOL.html
PALEODIET Archives
Subject: High Carb and Liver Disease
From: Liza May
Reply-To:
Date: Tue, 28 Oct 2003 14:37:26 -0500
BOSTON (Reuters Health) Oct 27 - The high-carbohydrate, low-fat diet often recommended for morbidly
obese patients with fatty liver disease is associated with increased liver inflammation, physicians at Johns
Hopkins Medical Institutions report.
Conversely, high fat diets were associated with a lower risk for inflammation, according to study results
presented at the 54th Annual Meeting of the American Association for the Study of Liver Diseases.
Dr. Jeanne M. Clark, assistant professor of medicine, said in an interview that the results are hypothesisgenerating and point out the need for a prospective study. "But meanwhile, once again we are faced with
results that suggest we need to be very cautious in our dietary recommendations, " she said.
It appears, Dr. Clark said, that recommending low-fat diet in morbidly obese patients could "worsen nonalcoholic fatty liver disease."
[SNIP]
http://tinyurl.com/sqhh
http://www.medscape.com/viewarticle/463483
PALEODIET Archives
Subject: Re: High Carb and Liver Disease
From: Ben Balzer
Reply-To:
Date: Wed, 29 Oct 2003 19:48:51 +0800
60/61 (2003)
This is consistent with the known association of NASH/FLD with hyperinsulinaemia/ insulin resistance
syndrome. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
It is also associated with oxidative stress . Paleo diets have far more antioxidants than high carb diets.
Dr Ben Balzer
Quoting Liza May :
> BOSTON (Reuters Health) Oct 27 - The high-carbohydrate, low-fat diet often recommended for
> morbidly obese patients with fatty liver disease is associated with increased liver inflammation,
> physicians at Johns Hopkins Medical Institutions report. Conversely, high fat diets were
> associated with a lower risk for inflammation, according to study results presented at the 54th
> Annual Meeting of the American Association for the Study of Liver Diseases. Dr. Jeanne M. Clark,
> assistant professor of medicine, said in an interview that the results are hypothesis-generating
> and point out the need for a prospective study. "But meanwhile, once again we are faced with
> results that suggest we need to be very cautious in our dietary recommendations, " she said. It
> appears, Dr. Clark said, that recommending low-fat diet in morbidly obese patients could "worsen
> non-alcoholic fatty liver disease."
> http://tinyurl.com/sqhh
> http://www.medscape.com/viewarticle/463483
61/61 (2003)
PALEODIET Archives
Subject: Omega-6 FAs and diabetic blindness
From: Roland Rohde
Reply-To:
Date: Wed, 25 Feb 2004 09:03:36 -0500
Hi,
I would like to direct the attention of the l ist members to a paper (1) that closes a crucial gap in our
understanding of the sequence of metabolic events finally resulting in diabetic blindness.
There is growing evidence that an accumulation of omega-6 fatty acids and especially their elevated
blood levels (free fatty acids, FFAs) are causative factors in the development of endothelium
dependent vascular diseases (1, 2).
The paper (1) convincingly shows that these FFAs in concentrations actually present in the blood of
diabetics (literature in 1) and persons with a high cardiovascular risc (2) specifically induce the
expression of certain endothelial surface molecules. The enhanced expression of these factors is a well
known starting point for the attachment of blood cells ('leukocyte rolling') which are responsible for
the induction and perpetuation (3) of inflammatory processes resulting in atheroslerosis.
As FFAs are not only elevated in diabetes but in many high-risk states like obesity, stress, and insulin
resistance, too, the omega-6 content of the adipose tissue could be responsible for the high blood
levels as these fats are always primarily released.
Diabetics are not only unable to keep their blood glucose levels low. The increase of the FFAs is often
more severe and precedes the increase of glucose. Additionally, the diabetic liver is unable to extract
and adequately metabolize omega-6 acids thus leading to high blood levels and consecutively to
diabetic retinopathy and blindness (1).
The actions of omega-6 FAs are in part dependent on their enzymatic conversion into hormonally
active hydroxy acids (1). One receptor that is activated by these hormones (4) is the receptor for the
thiazolidinedione class of antidiabetic drugs. A well known adverse effect of these drugs is weight
gain. The increase of omega-6 consumption in westernized populations could to some extent be
responsible for the obesity epidemic.
Since about 100 years pathologists knew that the deposition of so called amyloid in pancreatic islets is
typical for human, feline, and simian diabetes. Amyloid is an aggregation product of the hormone
amylin which is stoichiometrically cosecreted with insulin. One of the best inducers of amyloid
deposition are omega-6 FFAs (5, for Alzheimer-amyloid see 6).
A very interesting reading in this context is the the paper of Staffan, Loren, et. al. (7), highlighting a
principal difference between the nutrition in Kitava and Sweden. The intake of polyunsaturated
omega-6 and monounsaturated fats in Kitava is very low (not more than 2% each compared to 16%
mono and 5% poly in Sweden), while the intake of carbs is very high (70%). But vascular risk and
body weight are both very low, in spite of low protein intakes.
Such a diet is not very 'paleo' and points to the possible role of omega-6 uptake. It could even be more
important than consumption of carbs.
Omega-6 FAs disturb and interfere with delicate hormonal control systems (prostaglandins,
leukotrienes, lipoxins, hydroxy-FAs, omega-3-FA interconversion) and are merely one enzymatic
(lipogygenase-) step away from hormonally active substances.
roland
(1) Chen W, et. al.: Dyslipidemia, but not hyperglycemia, induces inflammatory adhesion molecules in
human retinal vascular endothelial cells. Invest Ophthalmol Vis Sci. 2003 Nov;44(11):5016-22.
(2) Yli-Jama P, et. al.: Serum free fatty acid pattern and risk of myocardial infarction: a case-control
study. J Intern Med. 2002 Jan;251(1):19-28.
(3) Ross R.: Atherosclerosis--an inflammatory disease. N Engl J Med. 1999 Jan 14;340(2):115-26.
(4) Shankaranarayanan P, et. al.: IL-4 induces apoptosis in A549 lung adenocarcinoma cells: evidence
for the pivotal role of 15-hydroxyeicosatetraenoic acid binding to activated peroxisome proliferatoractivated receptor gamma transcription factor. J Immunol. 2003 Jan 15;170(2):887-94.
1/13 (2004)
(5) Ma Z, Westermark GT. et. al.: Effects of free fatty acid on polymerization of islet amyloid
polypeptide (IAPP) in vitro and on amyloid fibril formation in cultivated isolated islets of transgenic
mice overexpressing human IAPP. Mol Med. 2002 Dec;8(12):863-8.
(6) Wilson DM, et. al.: Free fatty acids stimulate the polymerization of tau and amyloid beta peptides.
In vitro evidence for a common effector of pathogenesis in Alzheimer's disease. Am J Pathol. 1997
Jun;150(6):2181-95.
(7) Lindeberg S, et. al.: Determinants of serum triglycerides and high-density lipoprotein cholesterol in
traditional Trobriand Islanders: the Kitava Study. Scand J Clin Lab Invest 2003;63(3):175-80.
PALEODIET Archives
Subject: Re: Omega-6 FAs and diabetic blindness MSG
From: "Balzer, Ben"
Reply-To:
Date: Fri, 27 Feb 2004 10:59:17 +1100
Roland That is very interesting. There is some evidence that omega 6 fats are harmful in macular
degeneration too, according to expert opinion (Prof P Beaumont, Macular degeneration foundation
Australia).
Another mechanism that is relevant to the interest of the list is glutamate excitotoxicity. Dietary MSG
is related to this.
Raito http://www.scientific-com.com/AJO/backissues/v1n2/article/ This paper indicates that glutamate
stimulates nerve cells to death (apoptosis to be precise) in glaucoma, and that glaucoma patients have
higher levels of glutamate in the intraocular fluid (due to damaged retina). Thus a vicious cycle is set
up wherein the damaged retina becomes leaky and permits the increased entry of glutamate from
plasma. This glutamate then causes apoptosis, thus exacerbating the visual loss. One would anticipate
similar, if not worse, leakiness in the diabetic eye.
While there is no mention of dietary MSG in Rait's paper, Blaylock documents well that humans
absorb MSG well (better than lab animals- I think around 7 times the elevation rats get on equivalent
dosages) and it causes large spikes in serum glutamate level. It would be logical to see if dietary MSG
restriction could benefit patients with glaucoma and other eye diseases especially macular
degeneration. Drugs that block glutamate (eg memantine) slow down cell loss from glaucoma and
large trials are underway with this drug, but I can't find any evidence of simple use of low MSG diets
being used (please let me know if they are).
Russell Blaylock's Excitotoxins makes it clear that MSG has undesirable excitotoxic effects on
nervous tissue, especially in situations where the blood brain barrier is leaky or non-existent (eg
periventricular area, neurohypophysis, damaged retina & foetal brain)
http://news.bbc.co.uk/1/low/health/2352709.stm is a media article about dietary MSG damaging the
rat retina, and also implicating MSG in the high level of normal tension glaucoma in Asian
populations.
Pubmed has indexed a number of papers linking glutamate to cell loss in glaucoma.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Index&DB=PubMed
Ben Balzer
> -----Original Message----> From: Paleolithic Diet Symposium List
> [mailto:]On Behalf Of Roland Rohde
> Sent: Thursday, 26 February 2004 1:04 AM
> To:
> Subject: Omega-6 FAs and diabetic blindness
>
> Hi,
> I would like to direct the attention of the l ist members to a paper (1) that closes a crucial gap
> in our understanding of the sequence of metabolic events finally resulting in diabetic blindness.
> There is growing evidence that an accumulation of omega-6 fatty acids and especially their
2/13 (2004)
> elevated blood levels (free fatty acids, FFAs) are causative factors in the development of
> endothelium dependent vascular diseases (1, 2). The paper (1) convincingly shows that these FFAs
in
> concentrations actually present in the blood of diabetics (literature in 1) and persons with a
> high cardiovascular risc (2) specifically induce the expression of certain endothelial surface
> molecules. The enhanced expression of these factors is a well known starting point for the
> attachment of blood cells ('leukocyte rolling') which are responsible for the induction and
> perpetuation (3) of inflammatory processes resulting in atheroslerosis. As FFAs are not only
> elevated in diabetes but in many high-risk states like obesity, stress, and insulin resistance,
> too, the omega-6 content of the adipose tissue could be responsible for the high blood levels as
> these fats are always primarily released. Diabetics are not only unable to keep their blood
> glucose levels low. The increase of the FFAs is often more severe and precedes the increase of
> glucose. Additionally, the diabetic liver is unable to extract and adequately metabolize omega-6
> acids thus leading to high blood levels and consecutively to diabetic retinopathy and blindness
> (1). The actions of omega-6 FAs are in part dependent on their enzymatic conversion into
> hormonally active hydroxy acids (1). One receptor that is activated by these hormones (4) is the
> receptor for the thiazolidinedione class of antidiabetic drugs. A well known adverse effect of
> these drugs is weight gain. The increase of omega-6 consumption in westernized populations could
> to some extent be responsible for the obesity epidemic. Since about 100 years pathologists knew
> that the deposition of so called amyloid in pancreatic islets is typical for human, feline, and
> simian diabetes. Amyloid is an aggregation product of the hormone amylin which is
> stoichiometrically cosecreted with insulin. One of the best inducers of amyloid deposition are
> omega-6 FFAs (5, for Alzheimer-amyloid see 6). A very interesting reading in this context is the
> the paper of Staffan, Loren, et. al. (7), highlighting a principal difference between the
> nutrition in Kitava and Sweden. The intake of polyunsaturated omega-6 and monounsaturated fats
in
> Kitava is very low (not more than 2% each compared to 16% mono and 5% poly in Sweden),
while the
> intake of carbs is very high (70%). But vascular risk and body weight are both very low, in spite
> of low protein intakes. Such a diet is not very 'paleo' and points to the possible role of omega-6
> uptake. It could even be more important than consumption of carbs. Omega-6 FAs disturb and
> interfere with delicate hormonal control systems (prostaglandins, leukotrienes, lipoxins,
> hydroxy-FAs, omega-3-FA interconversion) and are merely one enzymatic (lipogygenase-) step
away from hormonally active substances.
> roland
> (1) Chen W, et. al.: Dyslipidemia, but not hyperglycemia, induces inflammatory adhesion
molecules
> in human retinal vascular endothelial cells. Invest Ophthalmol Vis Sci. 2003 Nov;44(11):5016-22.
> (2) Yli-Jama P, et. al.: Serum free fatty acid pattern and risk of myocardial infarction: a
> case-control study. J Intern Med. 2002 Jan;251(1):19-28.
> (3) Ross R.: Atherosclerosis--an inflammatory disease. N Engl J Med. 1999 Jan 14;340(2):115-26.
> (4) Shankaranarayanan P, et. al.: IL-4 induces apoptosis in A549 lung adenocarcinoma cells:
> evidence for the pivotal role of 15-hydroxyeicosatetraenoic acid binding to activated peroxisome
> proliferator-activated receptor gamma transcription factor. J Immunol. 2003 Jan 15;170(2):887-94.
> (5) Ma Z, Westermark GT. et. al.: Effects of free fatty acid on polymerization of islet amyloid
> polypeptide (IAPP) in vitro and on amyloid fibril formation in cultivated isolated islets of
> transgenic mice overexpressing human IAPP. Mol Med. 2002 Dec;8(12):863-8.
> (6) Wilson DM, et. al.: Free fatty acids stimulate the polymerization of tau and amyloid beta
> peptides. In vitro evidence for a common effector of pathogenesis in Alzheimer's disease. Am J
> Pathol. 1997 Jun;150(6):2181-95.
> (7) Lindeberg S, et. al.: Determinants of serum triglycerides and high-density lipoprotein
> cholesterol in traditional Trobriand Islanders: the Kitava Study. Scand J Clin Lab Invest
> 2003;63(3):175-80.
3/13 (2004)
PALEODIET Archives
Subject: Re: Omega-6 FAs and diabetic blindness MSG
From: Roland Rohde
Reply-To:
Date: Tue, 2 Mar 2004 08:05:15 -0500
Ben,
this is nice complementary information. The Rait article underscores the relevance of a reduced retinal
blood flow. The current theory says that in the small retinal vessels the (possibly omega-6 triggered)
adherence of a single leukocyte (nice photos in 1) may trigger the complete sequence of events leading
to stop of flow and endothelial apoptosis.
Prof. Beaumont probably refers to a case-control study (2) and a prospective study (3) showing that
(2)"...Higher vegetable fat consumption was associated with an elevated risk for AMD(age-related
macular degeneration). After adjusting for age, sex, education, cigarette smoking, and other risk
factors, the odds ratio (OR) was 2.22 .... for persons in the highest vs those in the lowest quintiles of
intake (P for trend, .007). The risk for AMD was also significantly elevated for the ... intake of
monounsaturated (OR, 1.71) and polyunsaturated (OR, 1.86) fats (Ps for trend, .03 and .03,
respectively). Higher consumption of linoleic acid was also associated with a higher risk for AMD (P
for trend, .02). Higher intake of omega-3 fatty acids was associated with a lower risk for AMD among
individuals consuming diets low in linoleic acid, an omega-6 fatty acid (P for trend, .05; P for
continuous variable, .03). Similarly, higher frequency of fish intake tended to reduce risk for AMD
when the diet was low in linoleic acid (P for trend, .05). Conversely, neither omega-3 fatty acids nor
fish intake were related to risk for AMD among people with high levels of linoleic acid intake."
and
(3)"...Higher total fat intake increased the risk of progression to the advanced forms of AMD, with a
relative risk (RR) of 2.90 ..., after controlling for other factors (P trend =.01). Animal fat intake was
associated with a 2-fold increased risk of progression (RR, 2.29 ...), although the trend for increasing
risk with higher animal fat intake was not significant (P=.09). Higher vegetable fat intake had a
stronger relationship with increased risk of AMD progression with an RR of 3.82 ... (P trend =.003).
Saturated, monounsaturated, polyunsaturated, and transunsaturated fats increased the likelihood of
progression (RR, 2.09 and P trend =.08; RR, 2.21 and P trend =.04; RR, 2.28 and P trend =.04; RR,
2.39 and P trend =.008, respectively). Higher fish intake was associated with a lower risk of AMD
progression among subjects with lower linoleic acid intake. Processed baked goods, which are higher
in some of these fats, increased the rate of AMD progression approximately 2-fold, and nuts were
protective.
It is of note that in the paper (3) patients were excluded who ever had a diagnosis of cancer. As cancer
is related to the omega-6 intake, too, this might have even weakened the significances.
Furthermore, all animal fat related variables (saturated fats, high fat dairy, meat) lost their
significances after controlling for vegetable fats and other variables while the significances of
vegetable fats rose after controlling for animal fat.
And we should not forget the omega-6 content of grain fed pork and poultry, accounting for a major
part of western animal fat intake and thus possibly leading to p-values close to significance (e.g. that
0.09 and 0.08 for animal and saturated fat, respectively).
The authors state that nut intake is possibly protective because of other constituents and significance
became borderline after controlling for other variables.
These studies together with the Chen (and Lindeberg) study (ref. in my february-posting) show again
that the omega-6 FAs have to be considered as one of the major neolithic nutrients as far as
pathogenetic processes are concerned. Many diseases of civilization have a long history. Even the
ancient egypts knew many of them. But a diet consisting basically of whole-grain products (like in
egypt) is not so different from what grain-fed animals consume. Comparable adipose tissue contents of
omega-6 acids can be assumed *especially* if the absolute fat consumption is low and consists mainly
of germ oils or other fats with a high omega-6 fraction.
roland
4/13 (2004)
(1) Joussen AM, Murata T, Tsujikawa A, Kirchhof B, Bursell SE, Adamis AP. Leukocyte-mediated
endothelial cell injury and death in the diabetic retina. Am J Pathol. 2001 Jan;158(1):147-52.
(2) Seddon JM, Rosner B, Sperduto RD, Yannuzzi L, Haller JA, Blair NP, Willett W. Dietary fat and
risk for advanced age-related macular degeneration. Arch Ophthalmol. 2001 Aug;119(8):1191-9.
(3) Seddon JM, Cote J, Rosner B. Progression of age-related macular degeneration: association with
dietary fat, transunsaturated fat, nuts, and fish intake. Arch Ophthalmol. 2003 Dec;121(12):1728-37.
PALEODIET Archives
Subject: Nature slimming feature
Reply-To:
Date: Wed, 17 Mar 2004 20:26:39 +0000
Interesting, but tantalising in places Nature feature on scientific studies of slimming. It's pretty
equivocal about any advantage of low-carb diets over high-carb diets for weight loss.
> Science of dieting: Slim pickings The dieting industry is a massive money-spinner. Yet across the
> developed world, waistlines continue to expand. In this free feature, Declan Butler examines the
sparse
> evidence behind the claims made for leading diet plans. http://info.nature.com/cgi> bin24/DM/y/eOOC0BfdPV0Ch0JvN0Al
Andrew
=========================================================================
Dr. Andrew Millard Department of Archaeology, University of Durham, Tel: +44 191 334 1147 South
Road, Durham. DH1 3LE. United Kingdom. Fax: +44 191 334 1101 http://www.dur.ac.uk/a.r.millard/
=========================================================================
PALEODIET Archives
Subject: "Side effects" of dieting
Reply-To:
Date: Wed, 24 Mar 2004 10:20:02 +0200
A recent Nature article (18 March) refers to concerns about safety of low-carb diets: 'One recent
review of the safety of low-carbohydrate diets reeled off an alarming list of potential problems:
"Complications such as heart arrhythmias, cardiac contractile function impairment, sudden death,
osteoporosis, kidney damage, increased cancer risk, impairment of physical activity and lipid
abnormalities can all be linked to long-term restriction of carbohydrates in the diet."'
Is anybody on the list able to point me in the direction of any similar review naming possible
complications from the 'standard' diet - low-fat, high-carb?
Mandi Smallhorne South Africa Tel: 27 11 672-3555 Fax: 27 11 674-3804 Cell: 082 881-8270
PALEODIET Archives
Subject: Re: "Side effects" of dieting
From: Bob Pastorio
Reply-To:
Date: Wed, 24 Mar 2004 12:08:06 -0500
Mandi Smallhorne wrote:
> A recent Nature article (18 March) refers to concerns about safety of = low-carb diets: =20 'One
5/13 (2004)
> recent review of the safety of low-carbohydrate diets reeled off an = alarming list of potential
> problems: "Complications such as heart = arrhythmias, cardiac contractile function impairment,
> sudden death, = osteoporosis, kidney damage, increased cancer risk, impairment of = physical
> activity and lipid abnormalities can all be linked to long-term = restriction of carbohydrates in
> the diet."'
These are the standard criticisms of low-carb dieting. Most don't have much research support.
> Is anybody on the list able to point me in the direction of any similar = review naming possible
> complications from the 'standard' diet - low-fat, = high-carb?
There's a newsgroup called <alt.support.diet.low-carb
> that has a FAQ that includes a lot of direct, anecdotal and other kinds of information, and links to
way too much other stuff, including medical material. It's unabashedly pro lo-carb but, keeping that in
mind, it's still worth the ride. <http://www.grossweb.com/asdlc/faq.htm
Pastorio
> Mandi Smallhorne
> South Africa
> Tel: 27 11 672-3555
> Fax: 27 11 674-3804
> Cell: 082 881-8270
>
PALEODIET Archives
Subject: Re: Side effects of dieting
From: ""
Reply-To:
Date: Wed, 24 Mar 2004 12:44:16 -0500
I don't have access to the Nature article, but on the face of it these concerns seem ridiculous. Perhaps
they hold for some extreme (perhaps those very high saturated fat, zero vegetable) lo-carb diets, with
extreme ketosis for very long terms. On the contrary, I associate heart arrhythmias and heart muscle
problems with low calorie high carb diets, which are known to casue weight loss in part by attacking
muscle, including heart muscle, tissue: e.g., the dangers of death from prolonged fasting (even "juice"
fasting).
I'm interested to hear from our more scholarly list members.
John Blank, L.Ac.
Original Message:
----------------From: Mandi Smallhorne Date: Wed, 24 Mar 2004 10:20:02 +0200 To: Subject: "Side effects" of
dieting
A recent Nature article (18 March) refers to concerns about safety of = low-carb diets: =20 'One recent
review of the safety of low-carbohydrate diets reeled off an = alarming list of potential problems:
"Complications such as heart = arrhythmias, cardiac contractile function impairment, sudden death, =
osteoporosis, kidney damage, increased cancer risk, impairment of = physical activity and lipid
abnormalities can all be linked to long-term = restriction of carbohydrates in the diet."'
Is anybody on the list able to point me in the direction of any similar = review naming possible
complications from the 'standard' diet - low-fat, = high-carb?
Mandi Smallhorne South Africa Tel: 27 11 672-3555 Fax: 27 11 674-3804 Cell: 082 881-8270
-------------------------------------------------------------------mail2web - Check your email from the web at http://mail2web.com/ .
PALEODIET Archives
6/13 (2004)
Reply-To:
Date: Thu, 25 Mar 2004 11:52:01 -0500
Bob Pastorio wrote:
> Mandi Smallhorne wrote:
> A recent Nature article (18 March) refers to concerns about safety of = low-carb diets: =20 'One
> recent review of the safety of low-carbohydrate diets reeled off an = alarming list of potential
> problems: "Complications such as heart = arrhythmias, cardiac contractile function impairment,
> sudden death, = osteoporosis, kidney damage, increased cancer risk, impairment of = physical
> activity and lipid abnormalities can all be linked to long-term = restriction of carbohydrates in
> the diet."'
> These are the standard criticisms of low-carb dieting. Most don't have much research support. Is
> anybody on the list able to point me in the direction of any similar = review naming possible
> complications from the 'standard' diet - low-fat, = high-carb?
> There's a newsgroup called <alt.support.diet.low-carb that has a FAQ that includes a lot of
> direct, anecdotal and other kinds of information, and links to way too much other stuff, including
> medical material. It's unabashedly pro lo-carb but, keeping that in mind, it's still worth the
> ride. <http://www.grossweb.com/asdlc/faq.htm
Well, and years ago, when I had first started low carbing, and was dazzled by the results, I was also
taking Argumentation and Debate at the local University. I had to do a scientific argument, so of
course I did low carb dieting. I was required to argue both sides, so I spent *hours* searching PubMed
for any evidence that those 6-11 servings of grain per day were good for *anything* -- I ran
"carbohydrate hypertension" "carbohydrate atherosclerosis" "carbohydrate NIDDM, " etc, etc, etc. I
found some evidence that if you're going to eat all that starch, you'd do best to limit fats. But I found
*nothing* to convince me there was *any* benefit to eating all that carbohydrate in the first place.
Dana (8 1/2 years low carbing, and still alive and healthy, thank you.)
PALEODIET Archives
From: matesz
Reply-To:
Date: Fri, 26 Mar 2004 10:47:42 -0400
Dana Carpender wrote:
I was required to argue both sides, so I spent
> *hours* searching PubMed for any evidence that those 6-11 servings of grain per day were good
for
> *anything* -- I ran "carbohydrate hypertension" "carbohydrate atherosclerosis" "carbohydrate
> NIDDM, " etc, etc, etc. I found some evidence that if you're going to eat all that starch, you'd do
> best to limit fats. But I found *nothing* to convince me there was *any* benefit to eating all
> that carbohydrate in the first place.
> Dana (8 1/2 years low carbing, and still alive and healthy, thank you.)
One problem with this research approach: you used carbohydrate, not types of foods or specific foods,
to drive your search (at least as you presented it here).
You could come up with nothing using this approach, but if you searched using classes of food or
specific foods that happen to be rich in carbohydrate you could find different results.
Examples would be:
"fruit hypertension" "fruit atherosclerosis" "fruit IHD"
"vegetables hypertension" "sweet potatoes hypertension"
"whole grains atherosclerosis" "whole grains hypertension" "whole grains IHD" "whole grains
NIDDM"
I just searched medline with "whole grains and NIDDM".
7/13 (2004)
This way I found studies linking whole grains with reduced all cause mortality, reduced insulin levels,
and reduced risk of diabetes, IHD, ischemic stroke, just in the first ten items retrieved.
Don
PALEODIET Archives
Subject: I a humble member of the list
From: ME Wood
Reply-To:
Date: Fri, 26 Mar 2004 12:56:23 +1200
Dear List I have suddenly started getting the list again. I don't know if it is of interest but since I have
food sensitivities which make it advisable I don't eat grains or potatoes or related roots. I haven't for a
long time now. My doctor thinks I am young looking and basically very healthy.(recently became
66yrs old)
I have worked on the basis that I may be short of monoamine oxidase B and take the precautions
which someone who had MAO inhibited would take.
I don't know if this is any particular interest to any one.
I joined the group as a person who trained in Prehistoric Archaeology (Edinburgh)and so was
interested in palaeolithic diet.
M E Wood
PALEODIET Archives
Subject: Re: Thyroid as an iodine source in hunter gatherers
From: Liza May
Reply-To:
Date: Mon, 17 May 2004 12:06:54 -0400
Very interesting topic Ben. I would like to be kept informed of what you might discover on this, if you
are able to learn something from sources other than this list. May I ask you to keep me posted?
Thanks, Liza
~~~~~~~~~~
Liza May, M.S. Clinical Nutrition Phone: 301-261-0555 Fax: 410-451-6105 Email: 1153 Route 3
North #41 Gambrills, MD 21054 USA
> [mailto:] On Behalf Of Balzer, Ben
> Sent: Monday, May 17, 2004 4:30 AM
> To:
> Subject: Thyroid as an iodine source in hunter gatherers
> Dear All
> I enquire whether members of the list might have any information as to whether any hunter
> gatherers have been documented to consume the thyroid gland of prey. Iodine has the most
profound
> effect of any single factor on IQ- iodine deficiency reduces IQ an average of 13.5 or 15 points
> depending on which authority one reads. This is sufficient to triple the number of children with
> mild developmental delay and increase 7 fold those with severe developmental delay (by simple
> consideration of leftward displacement of the IQ curve by 15 points).
> http://www.who.int/nut/idd.htm Iodine deficiency affects over 740 million people worldwide and
it
> is a major priority of the WHO http://www.who.int/nut/idd.htm Unfortunately, none of the studies
> on IQ and omega 3 have been controlled for iodine (Simopoulos, A. Personal communication).
8/13 (2004)
> Accordingly, identification of dietary sources of evolution during evolution is important. Iodine
> has been singled out as a factor that supports the aquatic ape hypothesis that our evolution
> occurred on the seashore, see allserv.rug.ac.be/~mvaneech/Cunnane.html (A SHORE-BASED
DIET
> RICH IN ENERGY AND 'BRAIN-SPECIFIC' NUTRIENTS MADE HUMAN BRAIN
EVOLUTION POSSIBLE). An alternative
> source of iodine available to carnivores is the thyroid gland of prey. Indeed under-trained
> butchers sometimes give exogenous transient thyrotoxicosis to their customers by including
thyroid
> in their hamburger mince ("hamburger thyrotoxicosis).
> www.mja.com.au/public/issues/180_10_170504/letters_1705 04_fm-4.html Other sources come to
> mind- Weston Price documented the woman from African highlands who travelled to the Nile to
get
> plants and burn them in order to keep the ashes and bring them home for her children to eat to
> prevent goitre (she had a very large one). I can't find any data on brain's content of iodine but
> wouldn't be surprised if this had some too). The coastal treks of pacific islanders could have
> provided iodine as well as long chain omega 3 fatty acids.
> Ben Balzer
> Dr Ben Balzer
> 109 Morgan St
> Beverly Hills 2209
> NSW Australia
> Tel (02) 95023355 Fax (02) 95024243 Int'l prefix(+612)
>
PALEODIET Archives
Subject: thyroid as an iodine source in hunter gatherers
From: D Dawson
Reply-To:
Date: Mon, 17 May 2004 17:33:08 -0400
Ben wrote:
> I enquire whether members of the list might have information as to whether any hunter gatherers
> have been documented to consume the thyroid gland of prey. Iodine has the most profound effect
of
> any single factor on IQ: iodine deficiency reduces IQ an average of 13.5 or 15 points
Would this be signficant as some direct effect of iodine on brain function or as an agent for sufficient
thyroid activity? I believe hypo thyroid is often associated with decreased mental fuction and chronic
fatigue.
Dick 128.230.208.14/~ddawson 128.230.208.46/~ddawson
PALEODIET Archives
Subject: Thyroid as an iodine source in hunter gatherers
From: "Balzer, Ben"
Reply-To:
Date: Mon, 17 May 2004 18:29:58 +1000
Dear All I enquire whether members of the list might have any information as to whether any hunter
gatherers have been documented to consume the thyroid gland of prey.
9/13 (2004)
Iodine has the most profound effect of any single factor on IQ- iodine deficiency reduces IQ an
average of 13.5 or 15 points depending on which authority one reads. This is sufficient to triple the
number of children with mild developmental delay and increase 7 fold those with severe
developmental delay (by simple consideration of leftward displacement of the IQ curve by 15 points).
http://www.who.int/nut/idd.htm
Iodine deficiency affects over 740 million people worldwide and it is a major priority of the WHO
http://www.who.int/nut/idd.htm
Unfortunately, none of the studies on IQ and omega 3 have been controlled for iodine (Simopoulos, A.
Personal communication).
Accordingly, identification of dietary sources of evolution during evolution is important. Iodine has
been singled out as a factor that supports the aquatic ape hypothesis that our evolution occurred on the
seashore, see http://allserv.rug.ac.be/~mvaneech/Cunnane.html (A SHORE-BASED DIET RICH IN
ENERGY AND BRAIN-SPECIFIC NUTRIENTS MADE HUMAN BRAIN EVOLUTION
POSSIBLE).
An alternative source of iodine available to carnivores is the thyroid gland of prey. Indeed undertrained butchers sometimes give exogenous transient thyrotoxicosis to their customers by including
thyroid in their hamburger mince ("hamburger thyrotoxicosis).
http://www.mja.com.au/public/issues/180_10_170504/letters_170504_fm-4.html
Other sources come to mind- Weston Price documented the woman from African highlands who
travelled to the Nile to get plants and burn them in order to keep the ashes and bring them home for
her children to eat to prevent goitre (she had a very large one). I can't find any data on brain's content
of iodine but wouldn't be surprised if this had some too). The coastal treks of pacific islanders could
have provided iodine as well as long chain omega 3 fatty acids.
Ben Balzer Dr Ben Balzer
> 109 Morgan St Beverly Hills 2209 NSW Australia Tel (02) 95023355 Fax (02) 95024243 Int'l
prefix(+612)
PALEODIET Archives
From: Roland Rohde
Reply-To:
Date: Tue, 18 May 2004 09:22:52 -0500
Ben,
I assume they will have consumed the thyroid gland because they didn't have so extensive histologic
knowledge. (Like some butchers?)
The link between iodine and omega-3, or better DHA (docosahexaenoic acid), is very substantial,
indeed. Thyroid hormone acts through the thyroid hormone receptor (THR).THR needs (like the
vitamin D-receptor) the so called retinoic X receptor (RXR) as partner to take effect. The natural
ligand of the RXR is - n o t - retinoic acid, but DHA. DHA is essential for man, in contrast to the other
omega-3 fish oil acid, EPA, which can be synthesized of vegetable omega-3 acids like linolenic acid.
One of the best known sources of DHA is brain. About one third of th e brain lipids consists of
DHA.Vegetables are devoid of DHA.
It is likely that goitre, which is endemic especially in alpine regions, is not only caused by the lack of
iodine in these regions far from the sea level, but by a lack of DHA containing fatty fish, too. But this
problem should not apply to brain consuming hunters. As animals tend to concentrate iodine from
their environment, at least if they are able to survive under such harsh conditions, a lack of iodine
shouldn't be a problem for hunters either.
roland
PALEODIET Archives
10/13 (2004)
From: Kerin O'Dea

Reply-To:
Date: Wed, 19 May 2004 08:19:35 +0930
My experience with Aboriginal hunter gatherers in Australia is that all internal organs were consumed
(except the large intestine, contents of the small intestine and gall bladder). Regards kerin O'Dea
-----Original Message----- From: [mailto:]On Behalf Of Liza May Sent: Tuesday, 18 May 2004 9:18
PM To: Subject: Re: Thyroid as an iodine source in hunter gatherers
Original Recipients:To:
Very interesting topic Ben. I would like to be kept informed of what you might discover on this, if you
are able to learn something from sources other than this list. May I ask you to keep me posted?
Thanks, Liza
~~~~~~~~~~
Liza May, M.S. Clinical Nutrition Phone: 301-261-0555 Fax: 410-451-6105 Email: 1153 Route 3
North #41 Gambrills, MD 21054 USA
> Sent: Monday, May 17, 2004 4:30 AM
> To:
> Subject: Thyroid as an iodine source in hunter gatherers
> Dear All
> I enquire whether members of the list might have any information as to whether any hunter
> gatherers have been documented to consume the thyroid gland of prey. Iodine has the most
profound
> effect of any single factor on IQ- iodine deficiency reduces IQ an average of 13.5 or 15 points
> depending on which authority one reads. This is sufficient to triple the number of children with
> mild developmental delay and increase 7 fold those with severe developmental delay (by simple
> consideration of leftward displacement of the IQ curve by 15 points).
> http://www.who.int/nut/idd.htm Iodine deficiency affects over 740 million people worldwide and
it
> is a major priority of the WHO http://www.who.int/nut/idd.htm Unfortunately, none of the studies
> on IQ and omega 3 have been controlled for iodine (Simopoulos, A. Personal communication).
> Accordingly, identification of dietary sources of evolution during evolution is important. Iodine
> has been singled out as a factor that supports the aquatic ape hypothesis that our evolution
> occurred on the seashore, see allserv.rug.ac.be/~mvaneech/Cunnane.html (A SHORE-BASED
DIET
> RICH IN ENERGY AND 'BRAIN-SPECIFIC' NUTRIENTS MADE HUMAN BRAIN
EVOLUTION POSSIBLE). An alternative
> source of iodine available to carnivores is the thyroid gland of prey. Indeed under-trained
> butchers sometimes give exogenous transient thyrotoxicosis to their customers by including
thyroid
> in their hamburger mince ("hamburger thyrotoxicosis).
> www.mja.com.au/public/issues/180_10_170504/letters_1705 04_fm-4.html Other sources come to
> mind- Weston Price documented the woman from African highlands who travelled to the Nile to
get
> plants and burn them in order to keep the ashes and bring them home for her children to eat to
> prevent goitre (she had a very large one). I can't find any data on brain's content of iodine but
> wouldn't be surprised if this had some too). The coastal treks of pacific islanders could have
> provided iodine as well as long chain omega 3 fatty acids.
> Ben Balzer
> Dr Ben Balzer
> 109 Morgan St
11/13 (2004)
> NSW Australia

PALEODIET Archives
Subject: Re: thyroid as an iodine source in hunter gatherers
Reply-To:
Date: Wed, 19 May 2004 16:51:40 -0500
D Dawson wrote:
> Ben wrote:
> I enquire whether members of the list might have information as to whether any hunter gatherers
> have been documented to consume the thyroid gland of prey. Iodine has the most profound effect
> of any single factor on IQ: iodine deficiency reduces IQ an average of 13.5 or 15 points
> Would this be signficant as some direct effect of iodine on brain function or as an agent for
> sufficient thyroid activity? I believe hypo thyroid is often associated with decreased mental
> fuction and chronic fatigue.
As a person who swallows 3/4 of a grain of Armour thyroid every morning because of a hypothyroid
condition, I can attest to the decreased mental function and fatigue. I went to NYC on business last fall
and forgot my thyroid meds. By two days in I was tired, by four days in I was barely alive, not to
mention dizzy. I felt like I was looking at the world from the bottom of a well I was far too tired to
climb out of. It was horrible, and I found myself thinking of all the poor folks who were hypothyroid
before there was any medical understanding of the problem. They became myxedemic cretins, and no
doubt sat, blob-like, in a corner for most of their lives.
BTW, I took my BP at the grocery store on my way home -- 90/47. No wonder I was dizzy. If
civilization as we know it ever collapses, I'll have to take to devouring the raw thyroid glands of
rabbits and squirrels on a daily basis.
Dana
PALEODIET Archives
Subject: Re: FW: Rabbit starvation and biochemical tests
From: Ed Thompson
Reply-To:
Date: Tue, 27 Jul 2004 13:23:53 -0500
Ben,
I'd suggest to merely use the value that most determines physiological consequence: ammonia. Here
are 2 relevant excerpts:
1. For levels ...
"Ammonia levels above 200 micromol/l are usually caused by inherited metabolic diseases and it is
essential to make a diagnosis for genetic counselling, even if the patients die. The aim of treatment is
to lower the ammonia concentrations as fast as possible. Sodium benzoate, sodium phenylbutyrate and
arginine can exploit alternative pathways for the elimination of nitrogen but haemodialysis or
haemofiltration should be instituted if ammonia concentrations are 500 micromol/l or if they do not
fall promptly. Long-term management involves drugs, dietary protein restriction and use of an
emergency regimen during illness. Severe hyperammonaemia is usually associated with irreversible
neurological damage, particularly if levels have been above 800 micromol/l for 24 hours ..."
Leonard JV, Morris AA. Urea cycle disorders. Semin Neonatol. 2002 Feb;7(1):27-35.
2. And one for relevant interventions ...
12/13 (2004)
"In a patient with a presumed inherited metabolic disorder, the aim of therapy should be to normalize
blood ammonia levels. Recent experience has provided treatment guidelines that include minimizing
endogenous ammonia production and protein catabolism, restricting nitrogen intake, administering
substrates of the urea cycle, administering compounds that facilitate the removal of ammonia through
alternative pathways, and, in severe cases, dialysis therapy."
Mathias RS, Kostiner D, Packman S. Hyperammonemia in urea cycle disorders: role of the
nephrologist. Am J Kidney Dis. 2001 May;37(5):1069-80.
Ed
13/13 (2004)
PALEODIET Archives
Subject: Re: Mailing List Changes
From: Liza May
Reply-To:
Date: Mon, 17 Oct 2005 11:08:27 -0400
I would like to see the list continue in some form. And thank you, Ben, for looking into the options. Liza
May, M.S.
> Sent: Monday, October 17, 2005 5:16 AM
> To:
> Subject: Mailing List Changes
> Dear Paleodiet Listowner and fellow members,
> As maelstrom will close its mailing list service in January, I would like to offer an alternative
> free service for you. I have recently investigated mailing list software for Trevor Beard and the
> low salt crowd with a satisfactory conclusion. Mailman software is pretty much the universal
> standard for university mail lists now. Major-domo is going out. I have a couple of other web
> lists now on a Mailman server and it is satisfactory but does not have a search option. The admin
> interface is simple to use. I am getting the service free of charge from some Aussie medical
> computing experts. The low salt list works well but we're just going along slowly. Non-commercial
> lists are welcome. The server is in Germany. I will try to find out about search facilities. I
> suppose a Google window might be set up. (these are can-do guys). Alternatively, Professor Cordain
> may be able to get a mailman list set up at Colostate. A Google search shows it is in use there in
> some departments, but it depends on his department's IT people. It is simple to create lists once
> it is installed. If you are an IT addict you can set up Mailman on any server that copes with
> Linux. It is free. That is beyond my current tinkerage level. Also there are expensive commercial
> services that charge per email (eg 400 members times 100 posts= 40, 000 messages charged). So
> please let me know if you want a new list set up. The listowner can be anyone whom you care to
> nominate. I am happy to participate as a co-administrator for a short time if you wish as I have
> experience with the interface.
> Dr Ben Balzer
> 109 Morgan St
> NSW Australia
>
PALEODIET Archives
Subject: Mailing List Changes
From: "Balzer, Ben"
Reply-To:
Date: Mon, 17 Oct 2005 19:16:00 +1000
Dear Paleodiet Listowner and fellow members,
As maelstrom will close its mailing list service in January, I would like to offer an alternative free service for
you.
1/4 (2005)
I have recently investigated mailing list software for Trevor Beard and the low salt crowd with a satisfactory
conclusion. Mailman software is pretty much the universal standard for university mail lists now. Majordomo is going out. I have a couple of other web lists now on a Mailman server and it is satisfactory but does
not have a search option. The admin interface is simple to use. I am getting the service free of charge from
some Aussie medical computing experts. The low salt list works well but we're just going along slowly.
Non-commercial lists are welcome. The server is in Germany. I will try to find out about search facilities. I
suppose a Google window might be set up. (these are can-do guys).
Alternatively, Professor Cordain may be able to get a mailman list set up at Colostate. A Google search
shows it is in use there in some departments, but it depends on his department's IT people. It is simple to
create lists once it is installed. If you are an IT addict you can set up Mailman on any server that copes with
Linux. It is free. That is beyond my current tinkerage level. Also there are expensive commercial services
that charge per email (eg 400 members times 100 posts= 40, 000 messages charged).
So please let me know if you want a new list set up. The listowner can be anyone whom you care to
nominate. I am happy to participate as a co-administrator for a short time if you wish as I have experience
with the interface.
prefix(+612)
PALEODIET Archives
From: Don Wiss
Reply-To:
Date: Mon, 17 Oct 2005 22:24:10 -0400
At 11:08 AM 10/17/2005 -0400, you wrote:
> I would like to see the list continue in some form.
This list will continue in the same form at www.icors.org. It will still be Listserv software. Old archives will
be restored. The only change will be the address will change from maelstrom to icors.
Don.
PALEODIET Archives
From: "Balzer, Ben"
Reply-To:
Date: Tue, 18 Oct 2005 08:39:12 +1000
Dear All it appears some moves are already afoot to move maelstrom lists to http://www.icors.org/ with
archive preservation. It's not clear which software will be running the email lists. Please monitor this
situation and if you need an alternative please let me know. I suggest that the listowner downloads an archive
of members details. Ben
At 06:52 PM 10/17/2005 +1000, you wrote:
> As you know, maelstrom are closing their lists. I suppose this affects your lists.
Hi Ben,
We plan to move all the active lists to a new Listserv run by ICORS, which is being set up to handle all the
maelstrom lists. It will have the latest Listserv software and enough space that we can restore the old
archives. See:
http://www.icors.org/
Don.
> [mailto:]On Behalf Of Liza May
> Sent: Tuesday, 18 October 2005 1:08 AM
> To:
2/4 (2005)
> Subject: Re: Mailing List Changes

>
> I would like to see the list continue in some form.
> And thank you, Ben, for looking into the options.
> Liza May, M.S.
>
> Sent: Monday, October 17, 2005 5:16 AM
> To:
>
> free service for you. I have recently investigated mailing list software for Trevor Beard and the
> low salt crowd with a satisfactory conclusion. Mailman software is pretty much the universal
> standard for university mail lists now. Major-domo is going out. I have a couple of other web
> lists now on a Mailman server and it is satisfactory but does not have a search option. The admin
> interface is simple to use. I am getting the service free of charge from some Aussie medical
> computing experts. The low salt list works well but we're just going along slowly. Non-commercial
> lists are welcome. The server is in Germany. I will try to find out about search facilities. I
> suppose a Google window might be set up. (these are can-do guys). Alternatively, Professor Cordain
> may be able to get a mailman list set up at Colostate. A Google search shows it is in use there in
> some departments, but it depends on his department's IT people. It is simple to create lists once
> it is installed. If you are an IT addict you can set up Mailman on any server that copes with
> Linux. It is free. That is beyond my current tinkerage level. Also there are expensive commercial
> services that charge per email (eg 400 members times 100 posts= 40, 000 messages charged). So
> please let me know if you want a new list set up. The listowner can be anyone whom you care to
> nominate. I am happy to participate as a co-administrator for a short time if you wish as I have
> experience with the interface.
> Dr Ben Balzer
> 109 Morgan St
> NSW Australia
PALEODIET Archives
From: Dick Bird
Reply-To:
Date: Thu, 3 Nov 2005 19:48:32 -0000
Paleodiet is one of the best lists I have ever belonged to. I would very much like to see it continue in some
form, and would contribute as and when I am able.
Dick
Dr R J Bird Visiting Scholar Northumbria University
> Sent: 17 October 2005 10:16
> To:
3/4 (2005)
> free service for you. I have recently investigated mailing list software for Trevor Beard crowd
> with a satisfactory conclusion. Mailman software is pretty much the universal standard for
> university mail lists now. Major-domo is going out. I have a couple of other web lists now on a
> Mailman server and it is satisfactory but does not have a search option. The admin interface is
> simple to use. I am getting the service free of charge from some Aussie medical computing experts.
> The low salt list works well but we're just going along slowly. Non-commercial lists are welcome.
> The server is in Germany. I will try to find out about search facilities. I suppose a Google
> window might be set up. (these are can-do guys). Alternatively, Professor Cordain may be able to
> get a mailman list set up at Colostate. A Google search shows it is in use there in some
> departments, but it depends on his department's IT people. It is simple to create lists once it is
> installed. If you are an IT addict you can set up Mailman on any server that copes with Linux. It
> is free. That is beyond my current tinkerage level. Also there are expensive commercial services
> that charge per email (eg 400 members times 100 posts= 40, 000 messages charged). So please let me
> know if you want a new list set up. The listowner can be anyone whom you care to nominate. I am
> happy to participate as a co-administrator for a short time if you wish as I have experience with
> the interface.and the low salt
> Dr Ben Balzer
> 109 Morgan St
> NSW Australia
4/4 (2005)

Paleodiet List 1997 2005

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PALEOLITHIC DIET SYMPOSIUM LIST(1997-2005)

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Best Wishes, Ron Hoggan Calgary, Alberta, Canada

From: (Ron Hoggan)

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

From: Staffan Lindeberg

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Date: Fri, 28 Mar 1997 11:36:14 -0800

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

My, what a lot to absorb.

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

From: Dean Esmay

Date: Tue, 1 Apr 1997 00:23:15 -0800

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Subject: The paleolithic diet

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Kevin Tisdel writes:

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

The only data I know

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Date: Sun, 27 Apr 1997 23:34:22 +0200

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List

Paleolithic Diet Symposium List