Professional Documents
Culture Documents
Company
Products
Opportunity
About Us
Contact
Join
Youngevity
Real Results
Time Freedom
Who We Are
Our Email
Today
QuackWatch Rebuttal
Townsend Letter
When you take on the A.M.A. and the various Pharmaceutical Giants, as has Dr. Wallach, you are bound to make some enemies.
One website in particular, QuackWatch, is especially vociferous in its denouncement of Dr.Wallach and all he stands for. To set
the record straight, we include the following rebuttal to the various charges and complaints contained on the QuackWatch
website, courtesy of Professor emeritus, Dr. G. N. Schrauser.
the obvious absence of a genetic defect. The monkeys were born in Yerkes Primate Research Center 14 by mother animals that
had been given extra doses of vegetable oil to treat a skin condition during pregnancy.
Wallach proposed on the basis of these findings that CF is an environmentally induced disease and suggested the CF could be
prevented and treated by selenium and other antioxidants. He conducted a survey of 120 families with one or more CF children
and concluded that the history and patient profile was consistent with an acquired environmental disease caused by a perinatal
deficiency of selenium, zinc and riboflavin, and CF can be exacerbated by diets which are also low in vitamin E and rich in
polyunsaturated fatty acids.
His work triggered the interest of a group of physicians who were looking for ways to help their CF patients. A few years later
these doctors were so impressed with Wallach's therapy that they awarded him the "Wooster Beach Gold Medal" in 1988 and
nominated him for a Nobel Prize in 1991. This nomination did not follow the prescribed procedure and was not recognized by the
Nobel Prize Committee. Critics now hold the mentioning of this nomination against him as any such nomination should be kept
strictly confidential. While this is true., it is actually a very minor point which should not be used to detract from his contribution.
To demonstrate the CF like pancreatic lesions develop in populations residing in regions naturally low in selenium, Wallach and
his wife, Ma Lan, M.D., a Chinese physician, traveled to China to conduct more research. In collaboration with researchers at
Harbin Medical University, Wallach showed that hitherto ignored pancreatic lesions occurred in 35% of 1700 documented cases
of Keshan disease (KSD), which is a cardiomyopathy occurring in low selenium regions of China. 15 In the meantime, other
researchers have drawn attention to the aberrant oxygen free radical activity and the low selenium and antioxidant status in cystic
fibrosis patients. 16 17 18 19
Although perinatal selenium and antioxidant vitamin deficiency is still not accepted as a cause of CF, it is agreed that selenium
deficiency my develop in CF children because of digestive malabsorption or after prolonged total parinateral nutrition. 20 21 22 A
case of cardiomyopathy in a CF patient which was caused by selenium deficiency has also been described.23 The therapy of CF
patients with selenium and antioxidant vitamins has since also been tested in a clinical trial. One German group 24 concluded: "In
cystic fibrosis (CF) patients the antioxidative balance is chronically disturbed. Free radicals were generated by bronchial-pulmonal
infection and additionally (there) exists a deficiency of antioxidative substances by enteral malabsorption especially (of) vitamin E
and selenium. For CF patients therefore we recommend a sodium selenite substitution therapy, best in combination with vitamin
E."
is now becoming a concern primarily in pregnancy. In a recent study with 20 pregnant women on self selected diets, positive
balance was observed only if a copper supplement was consumed. 33
Copper deficiency need not be caused solely by low dietary copper intakes; copper deficiency may be induced by dietary
components, notably fructose and ascorbic acid; some also consider excessive zinc as a possible risk factor. In all, rather than
being criticized, Wallach should be given credit for drawing attention to the important role of copper deficiency in the pathogenesis
of aneurysms.
The fact that copper influences the pigmentation of hair is well supported by observations with copper deficient animals.
Experiments conducted in the early 1930's showed that the fur of black coated rats turned gray when they were placed on a
copper deficient diet. Achromotrichia has been described in other species deficient in copper: rabbits, dogs and sheep. Copper is
known to be required for the transformation of tyrosine to melanin. In copper deficiency, the physical nature of hair is also
affected, it becomes brittle and crinkled because oxidative processes which give hair its normal elasticity require copper. 34 Other
factors contribute to the graying of hair, a deficiency of pantothenic acid, for example. Clinical studies of the effects of copper
supplementation on hair color in humans are lacking but Wallach does report one case in which gray hair regained pigmentation
in a woman after supplementing with copper. Wince copper is required for elastin and collagen biosynthesis, changes of elastic
connective tissues are expected to occur in copper deficiency. Since 75% of the typical diets in the United States furnish less than
the current daily requirement of 2mg of copper per day, 35 chronic copper deficiency thus could indeed contribute to hair
depigmentation and skin wrinkling, especially in women. In a recent study with 20 pregnant women on self selected diets, positive
balance was observed only if a copper supplement was consumed. 36
technique. On occasion, a serious case of constipation will cause a 'backache' from impacted stool or pressure from
gas Prevention includes proper lifting technique, strengthening exercises, proper nutrition including calcium (2000 mg) and
magnesium (800 mg), high fiber diets and eight glasses of water per day."
[4] L.C. Clark et al. The Nutritional Prevention of Cancer with Selenium 1983 1993. JAMA 276: 1957 1963.
[5] J.D. Beasley and J.J. Swift (1989): The Kellogg Report. The impact of Nutrition, Environment and Lifestyle on the Health of
Americans. The Institute of Health Policy and Practice, The Bard College Center, Annondale-on-Hudson, New York, 12502,
Library of Congress Catalog Card Number: 89-84263, p. 169.
[6] L.J. Goodman (1975) Longevity and mortality of American Physicians, 1969-1973. Milbank Memorial Fund Quarterly; Health
and Society 53(3): 353 375.
[7] Editorial, JAMA, 1902, issue of Oct. 25, p. 1053 4.
[8] G.M. Gould and W.L. Pyle,. Anomalies and curiosities of medicine. The Julian Press 1896, p. 380-381.
[9] K.B. Wells, C.E. Lewis, B. Leake, J.E. Ware, Jr. (1984). Do Physicians Preach what they Practice?" JAMA 252: 2846 2848.
[10] J.I. Rodale (1949), "The Healthy Hunzas." Rodale Press, Emmaus, PA, 1949.
[11] F.Silio, A. H. Laguna, L.e. Garcia, J.G. Guaman, M.S. Salvador (1966) Mineral composition of foods and drinking water from
Vilacabamba. In: Proc. Metal Ions in Biology and Medicine Vol. 4; Ph. Collery, J. Corbello, J.L. Domingo, J. D. Etienne, J.m.
Llobet eds. John Libbey Eurotext, Paris, 1996, pp 563-565.
[12] a: M. Salvador (1972) Vilacabamba, Tierra de Longevos. Caa de la Cultura Ecuatoriana, Quito, 1972 b: M. Salvador (1980) :
Aterosclerosis en Vilacabamba. Medicina y Ciencias biologicas XVI, 28.
[13] M. Williams-Sarkisian, B. Apisson: A diet for happy, healthy 100 years," German Edition, Die Kaukasus-Diat, Ullstein Verlag
Frankfurt, 1985.
[14] J.D. Wallach, B. Garmaise (1979): Cystic fibrosis A perinatal manifestation of selenium deficiency. In: Hemphill D.D. ed.,
Trace Substances in Environmental Health XIII, pp. 469 476.
[15] J.D. Wallach, Ma Lan, Wei Han Yu, Bo-Qi Gu, Feng Teng Yu and Roy F. Goddard (1990). Common denominators in the
etiology and pathology of visceral lesions of cystic fibrosis and Keshan Disease. Biol. Trace El. Res. 24: 189 205.
[16] P. Foucand, P. Therond, M. Marchand, F. Brion, F.F. Demelier, J. Navarro (1988). Selenium et vitamin E au cours de la
mucoviscidose. Arch. Fr. Pediatr. 45(6), 383 6.
[17] A.G. Thoman, V. Miller, A. Shenkin, G.S. Fell, F. Taylor (1994). Selenium and glutathione peroxidase status in pediatric
health and gastrointestinal disease. J. Pediatr Gastroent Nutr 19, 2: 213 219.
[18] B. Salh, K. Webb, P.M. Guyan, J.P. Day, D. Wickens, J. Griffin, J.M. Braganza, T.L. Dormand (1989), Clin. Chem. Acta 181
(1) 65-74.
[19] B.M. Winklhofer-Roob (1994): Oxygen free radicals and antioxidants in cystic fibrosis: the concept of an oxidant- antioxidant
imbalance. Acta. Paeditr Suppl. 395: 49 57.
[20] R.D. Watson, R.A. Cannon, G.S. Kurland, K.L. Cox, F.C. Frates (1985), Selenium responsive myositis during prolonged
home total parenteral nutrition in cystic fibrosis. JPEN J Parenteral Enteral Ntr. 9(1) 58 60.
[21] C. Dominguez, M. Llovera, E. Ruiz, V. Araujo, S. Linan, S. Gartner, N. Cobos, "Antioxidant trace elements, glutathione and
glutathione peroxidase in cystic fibrosis patients: relation to lipid peroxidation status. In: Proc. Conf. Metal Ions in Biology and
Medicine, Vol. 4; Ph. Collery, J. Corbello, J.L. Domingo, J.D. Etienne, J.M. Llobet eds., John Libbey Erotext, Paris, 1996, pp. 592
595.
[22] B. Dworkin, L.J. Newman, S. Berezin, W.S. Rosenthal, S.M. Schwarz, L. Leiss (1987). Low blood selenium levels in patients
with cystic fibrosis compared to controls and healthy adults. JPEN J. Parenteral and Enteral Nutr. 11(1) , 38 41.
[23] D.M. Volk, S.A. Cutliff (1986), Selenium deficiency and cardiomyopathy in a patient withcystic fibrosis. J.Ky. Med. Assoc. 84
(5) 222-4.
[24] E. Kauf, E. Janitzky, L. Vogt, K. Winnefeld, H. Dawczynski, M. Forberger, G. Jahreis, H. Vogel (1995). "The significance of a
selenotherapy in cystic fibrosis patients" Med. Klin. 90, Suppl. I, 41-45.
[25] E. Baasch (1966), Theoretische Uberlegungen zur Atiologie der Scierosis multiplex. Die Multiple Sklerose eine
Quecksilberallergie? Schweizer Archiv f. Neurologie, Neurochirurgie und Psychiatrie 98 (1) 1-19.
[26] E. Baasch, personal communication to author, 1995.
[27] Knolle and Gunther G. Knolle and B. Gunther (1967). Beitrag zur Atiologiehypothese: Amalgam und Multiple Sklerose. Schw.
Monatsschr. Zahnheilk. 77. 761- 776.
[28] T.H. Ingalis (1986): Triggers for multiple sclerosis. Lancet 2 (1986) 160.
[29] H. Visser (1995): Indikationed und Kontraindikationen der Amalgamfullung. In: Status quo and perspectives of amalgam and
other dental materials. L.T. Friberg and G.N. Schrauzer, eds. G. Thieme Verlag Stuttgart, New York, p.35.
[30] G.Q. Yang (1985), Keshan disease: an endemic selenium related deficiency disease. In: Trace Elements in Nutritional and
Children. R.K. Chandra, ed. Raven, New York, pp. 273-290.
[31] O.A. Levander and M.A. Beck (1997). Insights from Coxsackie B Virus induced myocarditis in mice deficient in selenium and
vitamin E. Biol. Trace El. Res. 56 (1) 5 21.
[32] H.L. Keil and V.E. Nelson (1931). The role of copper in hemoglobin regeneration and reproduction. J. Biol. Chem. 93: 49
[33] E.J. Underwood: Trace Elements in Human and Animal Nutrition., 3rd Ed., Academic Press, New York and London, 1971, pp
53 115.
[34] D.M. Danks, B.J. Stevens, P.E. Campbell, J.M. Gillespie, J. Walker-Smith, J. Blomfield and B. Turner (1972), Menke's kinky
hair syndrome. Lancet, 1: 1100 1102.
[35] L.M. Klevay and D.M. Medeiros (1966), Deliberations and Evaluations of the Approaches, Endpoints and Paradigms for
dietary recommendations about copper. J.Nutr. 126: 2419S 2419S.
[36] Taper L.J., et al. (1981), Zinc and copper retention in pregnant women. Fed. Proc. 40: 855.
[37] Current diagnosis and treatment, MA. Krupp, M.J. Chatton, S. Margen (1971), eds., Lange Medical Publications, Los Gatos,
Calif., pp. 329 330, and references cited therein.
[38] N.J. Greenberger and K. Isselbacher; Disorders of Absorption. In: Harrisons Principles of Internal Medicine, 6th Edition,
MacGraw-Hill Book Company, New York, pp. 1467 1484.
[39] J.H. Kellogg: Autointoxication or Intestinal Toxemia. 2nd Ed., The Modern Medicine publishing Co., Battle Creek, Michigan,
1922.
[40] K. Schwarz, D.B. Milne, and E. Vinyard (1970) Growth effect of tin compounds in rats maintained in a trace element
controlled environment. Biochim Biophys Res. Comm. 40, 22-29.
[41] K. Yokoi, M. Kimura and Y. Itokawa (1990), Effect of dietary tin deficiency on growth and mineral status in rats. Biol Trace E.
Res. 24: 223.
[42] R.A. Anderson (1997): "Nutritional factors influencing the glucose/insulin system: Chromium. J. Am. Coll. Clin. Nutr. 16: 404
410.
[43] S. Verma, M.C. Cam and J.H. McNeill (1998). Nutritionaly factors that can favorably influence the glucose/insulin system:
Vanadium. J.Am. Coll Nutr. 17 (1) 11-18.
[44] H.G. Preuss., T. Jarrell, R. Scheckenbach, S. Lieberman, R.A. Anderson (1998). Comparative effects of chromium, vanadium
and Gymnma on sugar induced blood pressure elevations in SHR. J. Amer. Coll. Nutr. 17 (21) 116 123.
[46] G.N. Schrauzer (1999), An evaluation of liquid vitamin and mineral technology. J. of Medicinal Foods, in press.
Top