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http://howirecovered.com/my-genetics/
howirecovered.com
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rsID #
Risk Allele
CYP1A1*2C A4889G
rs1048943
TT
-/-
CYP1A1*4 C2453A
rs1799814
GG
-/-
CYP1A2 C164A
rs762551
AC
+/-
CYP1B1 L432V
rs1056836
CG
+/-
CYP1B1 N453S
rs1800440
TT
-/-
CYP1B1 R48G
rs10012
GG
-/-
5/6/2016 1:43 PM
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2 of 18
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DETOX
Gene & Variation
rsID #
Risk Allele
CYP2A6*2 A1799T
rs1801272
AA
-/-
CYP2C19*17
rs12248560
CC
-/-
CYP2C9*2 C430T
rs1799853
CC
-/-
CYP2C9*3 A1075C
rs1057910
AA
-/-
CYP2D6 S486T
rs1135840
GG
+/+
CYP2D6 T100C
rs1065852
GG
-/-
CYP2D6 T2850C
rs16947
AA
+/+
CYP2E1*1B G9896C
rs2070676
CC
-/-
CYP2E1*4 A4768G
rs6413419
GG
-/-
CYP3A4*1B
rs2740574
TT
-/-
CYP3A4*3 M445T
rs4986910
AA
-/-
CYPs are primarily membrane-associated proteins located either in the inner membrane of mitochondria or in
the endoplasmic reticulum of cells. CYPs metabolize thousands of endogenous and exogenous chemicals. Some
CYPs metabolize only one (or a very few) substrates, such as CYP19 (aromatase), while others may metabolize
multiple substrates. Both of these characteristics account for their central importance in medicine. Cytochrome
P450 enzymes are present in most tissues of the body, and play important roles in hormone synthesis and
breakdown including estrogen and testosterone synthesis and metabolism, cholesterol synthesis, and vitamin
D metabolism. Cytochrome P450 enzymes also function to metabolize potentially toxic compounds,
including drugs and products of endogenous metabolism such as bilirubin, principally in the liver.rs762551 (C)
allele is a slow metabolizer or of certain substrates including caffeine which means Im more stimulated by it than
most people.rs1056836 increases susceptibility to lung and breast cancer, blocks testosterone and inhibits
mitochondrial function.rs1135840 is involved in the metabolism of approximately 25% of all medications and most
psych meds including antipsychotics and antidepressants.
GPX3
rs8177412
TT
-/-
GSTM1
rs12068997
CC
-/-
GSTM1
rs4147565
GG
-/-
GSTM1
rs4147567
AA
-/-
GSTM1
rs4147568
TT
-/-
GSTM1
rs1056806
CC
-/-
GSTM1
rs12562055
TT
-/-
GSTM1
rs2239892
AA
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
GSTP I105V
rs1695
AG
+/-
GSTP1 A114V
rs1138272
CC
-/-
GSTP genes encode the Glutathione S-transferase P enzyme. Glutathione S-transferases (GSTs) are a family of
enzymes that play an important role in detoxification by catalyzing the conjugation of many hydrophobic and
electrophilic compounds with reduced glutathione. Mutations here will increase your need for glutathione and
importance of chelating out mercury.rs1695 influences asthma risk.
NAT1 A560G(?) (R187Q)
rs4986782
GG
-/-
rs1208
GG
+/+
rs1805158
CC
-/-
rs1799930
GG
-/-
rs1799931
GG
-/-
rs1801280
CC
+/+
NAT2 encodes N-acetyltransferases which are enzymes acting primarily in the liver to detoxify a large number of
chemicals, including caffeine and several prescribed drugs. The NAT2 acetylation polymorphism is important
because of its primary role in the activation and/or deactivation of many chemicals in the bodys environment,
including those produced by cigarettes as well as aromatic amine and hydrazine drugs used medicinally. In turn,
this can affect an individuals cancer risk.I have a particular combination of NAT2 polymorphisms rs1801280 (C)
+ rs1208 (G) which makes me a slow metabolizer. In general, slow metabolizers have higher rates of certain
types of cancer and are more susceptible to side effects from chemicals (known as MCS) metabolized by NAT2.
SOD2
rs2758331
AA
+/+
SOD2
rs2855262
CT
+/-
SOD2 A16V
rs4880
GG
+/+
SOD2 gene is a member of the iron/manganese superoxide dismutase family and may be one of the key
sources of my troubles. This protein transforms toxic superoxide, a byproduct of the mitochondrial electron
transport chain, into hydrogen peroxide and diatomic oxygen. In simpler terms, the more energy your
mitochondria produce, the more byproducts (also called free radicals) get produced. These toxic byproducts tear
up cell membranes and walls through a process called oxidative stress.Mutations in the SOD2 gene diminish
your ability to transform these toxic byproducts into harmless components. People with SOD2 polymorphisms
may not tolerate nitrates or fish oil well. Mutations in this gene have been associated with idiopathic
cardiomyopathy (IDC), sporadic motor neuron disease, and cancer.
Now what about SOD1 & 3? I dont know why it doesnt appear on this report but I was able to get some
information on it from Livewello and it looks like I am much better off there. Heres my SOD1 and SOD3 status.
Just for kicks, I decided to run SOD2 and I find it shows a much different picture than sterlings app: my SOD 2
on Livewello. Notice how it shows that I do have some working SOD2 genes!
5/6/2016 1:43 PM
My genetics
4 of 18
http://howirecovered.com/my-genetics/
DETOX
Gene & Variation
PON1 Q192R
rsID #
rs662
Risk Allele
C
+/-
***
TONGUE TIE / CLEFT PALATE
Gene & Variation
rsID #
Risk Allele
CTH S4031I
rs1021737
GT
+/-
IRF6
rs987525
AC
+/-
IRF6
rs861020
AG
+/-
RARA
rs7217852
AA
-/-
RARA
rs9904270
CC
-/-
TBX22
rs41307258
TBX22
rs28935177
***
ALLERGY/MOLD
Gene & Variation
rsID #
Risk Allele
HLA
rs7775228
TT
-/-
HLA
rs2155219
GT
+/-
***
IgE
Gene & Variation
rsID #
Risk Allele
FCER1A
rs2427837
AG
+/-
IL-13 C1112T
rs1800925
CC
-/-
DARC
rs2814778
TT
-/-
IL13
rs1295685
GG
-/-
CD14
rs2569191
CC
+/+
SOCS-1 -820G>T
rs33977706
CC
-/-
C3
rs366510
GT
+/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
FCER1A / OR10J2P
rs2494262
AA
+/+
FCER1A
rs2251746
CT
+/-
RAD50
rs2040704
AA
-/-
RAD50
rs2240032
CC
-/-
***
IgG
Gene & Variation
rsID #
Risk Allele
FCGR2A
rs1801274
AA
+/+
GSTM3 V224I
rs7483
CC
-/-
TNFRSF13B
rs4792800
AA
-/-
***
IgA
Gene & Variation
rsID #
Risk Allele
TRAF1
rs3761847
AG
+/-
IRF5
rs4728142
AA
+/+
IGF1R
rs2229765
AA
+/+
IFIH1 (HLA)
rs1990760
TT
-/-
HLA
rs9271366
AA
-/-
CFH
rs6677604
AG
+/-
HLA-DQA2
rs9275224
AG
+/-
MTC03P1
rs9275596
CT
+/-
rs9357155
GG
-/-
HLA-DPB2 / COL11A2P
rs1883414
AA
+/+
***
CLOTTING FACTORS
Gene & Variation
rsID #
Risk Allele
5/6/2016 1:43 PM
My genetics
6 of 18
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DETOX
Gene & Variation
rsID #
Risk Allele
CETP
rs1800775
AA
-/-
CYP4V2
rs13146272
AC
+/-
GP6
rs1613662
AA
-/-
ITGB3 T196C
rs5918
CT
+/-
KNG I598T
rs2731672
CT
+/-
NR1I2
rs1523127
AC
+/-
SERPINC1
rs2227589
CT
+/-
HRG
rs9898
CC
-/-
F12
rs1801020
AG
+/-
F11
rs2289252
CT
+/-
F11
rs2036914
CT
+/-
F10 113777509
rs3211719
AG
+/-
F7 A353G
rs6046
GG
-/-
F2 (Prothrombin 20210A)
i3002432
GG
-/-
F3 94997288
rs1324214
AA
+/+
F5 (Factor V Leiden)
rs6025
CC
-/-
F9 G580A
rs6048
***
METHYLATION
Gene & Variation
ACE Del16
rsID #
rs4343
Risk Allele
G
+/-
ACE (heterozygous mutation) converts Angiotensin I, a weak vasoconstrictor, into Angiotensin II, a powerful
vasoconstrictor, which can cause endothelial dysfunction, free radical stress, and stimulate the release of
aldosterone from the adrenal gland. Cofactors are zinc and chloride.High aldosterone wastes magnesium and
potassium, retains sodium, and stiffens the heart. Decreased potassium can lead to fatigue and decreased
energy production as cellular membrane activation especially in the brain and peripheral nervous system is
dependent upon sodium/potassium balance.In adults drug therapy and possibly flavonoids, hibiscus extract,
arginine and pomegranate can be used to block ACE and aldosterone. In kids, pay attention to electrolyte levels.
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
ADD1 G460W
rs4961
GG
-/-
ACAT1-02
rs3741049
GG
-/-
AGT M235T/C4072T
rs699
AA
-/-
AHCY-01
rs819147
CT
+/-
AHCY-02
rs819134
AG
+/-
AHCY-19
rs819171
CT
+/-
AHCY (various heterozygous mutations) SAMe is the key methyl donor generated from methionine; it is
metabolised to homocysteine by AHCY. A defect could create something of a bottleneck, lowering sulphate and
ammonia levels. This is not necessarily a bad thing if you have mutations along the transulfuration pathway (i.e.
the CBS enzyme), which would cause taurine levels to rise (with a corresponding decrease in glutathione).I dont
have this problem. Ordinary methylation support is fine in my situation, since this will keep the cycle spinning.
BHMT
rs16876512
CT
+/-
BHMT
rs6875201
AG
+/-
BHMT-02
rs567754
CC
-/-
BHMT-04
rs617219
AA
-/-
BHMT-08
rs651852
CT
+/-
BHMT R239Q
rs3733890
AG
+/-
BHMT (various heterozygous mutations) enzyme is responsible for converting homocysteine to methionine. It
does this by way of a short cut, bypassing the normal B12/methylfolate-dependent route.Mine is probably
working less optimally, which isnt a problem if I improve the status of my methylation cycle via the long route.
However, taking TMG (Betaine) may get this route functioning optimally.
CBS A13637G
rs2851391
CC
-/-
CBS A360A
rs1801181
GG
-/-
CBS C19150T
rs4920037
GG
-/-
CBS C699T
rs234706
GG
-/-
CBS N212N
rs2298758
GG
-/-
COMT
rs6269
GG
+/+
rs769224
GG
-/-
COMT H62H
rs4633
CC
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
COMT V158M
rsID #
rs4680
Risk Allele
A
-/-
COMT (one homozygous mutation) This gene helps break down dopamine and norepinephrine. A defect will
cause higher dopamine due to slower breakdown and is associated with ADD/ADHD. Defects will make you
more susceptible to dopamine fluctuations, therefore mood swings. People without COMT mutations are
generally more even tempered.My defect isnt on the V158M gene, which is the key enzyme for breaking down
dopamine. Those with mutations on this gene have to be careful with taking too many methyl donors.COMT must
be read along with VDR Taq note that my +/+ means I dont make much dopamine. Taking too many methyl
groups when you already have lots floating around (because your mutated gene isnt using them) can cause
mood swings, aggression, etc. This is one reason why some people struggle with mb12. I dont have this problem
because my COMT mutation is balanced by my VDR mutation.
DAO
rs2070586
GG
-/-
DAO
rs2111902
GT
+/-
DAO
rs3741775
AC
+/-
DHFR
rs1643649
TT
-/-
FOLR1
rs2071010
GG
-/-
FOLR2
rs651933
AG
+/-
FOLR3
rs7925545
AA
-/-
FOLR3
rs7926875
CC
-/-
FOLR Folate Receptor genes bind to folate and reduced folic acid derivatives and mediates delivery of
5-methyltetrahydrofolate to the interior of cells.
FUT2
rs492602
GG
+/+
FUT2
rs601338
AA
+/+
FUT2
rs602662
AA
+/+
FUT2 gene encodes the fucosyltransferase 2 enzyme which determines secretor status. Non-functional enzyme
resulting from a nonsense mutation in the FUT2 gene leads to the non-secretor phenotype. It has been shown
that non-secretor individuals show significantly reduced bifidobacterial diversity, richness, and abundance. This is
significant because intestinal microbiota plays an important role in human health.FUT2 has been called a robust
genetic predictor of vitamin B12 levels by Harvard researchers but so many genes are involved in B12 status I
cant make heads or tails of it yet.
G6PD
rs1050828
G6PD
rs1050829
GAD1
rs3749034
AA
+/+
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
GAD1
rs2241165
CC
+/+
GAD1
rs769407
CG
+/-
GAD1
rs2058725
TT
-/-
GAD1
rs3791851
CT
+/-
GAD1
rs3791850
GG
-/-
GAD1
rs12185692
CC
-/-
GAD1
rs3791878
GG
-/-
GAD1
rs10432420
AA
+/+
GAD1
rs3828275
CT
+/-
GAD1
rs701492
CT
+/-
GAD1
rs769395
AG
+/-
GAD2
rs1805398
GG
-/-
GAD these genes encode for glutamic acid decarboxylase which catalyzes the production of GABA.Glutamate
is the main excitatory neurotransmitter in the body and is essential for learning and short and long-term memory.
Glutamate is also the precursor to our primary calming neurotransmitter, GABA. GABA damps the propagation
of sounds so that a distinction can be made between the onset of sound and a background noise.Genomic
defects, viral illness, and heavy metals will compromise this balance, leading to excess glutamate, insufficient
GABA, excitotoxicity, and eventual neuron loss. Aluminum and lead also poisons this enzyme.Low GABA leads
to impaired speech, anxiety, aggressive behavior, poor socialization, poor eye contact, nystagmus, and
constipation. Glutamate excess does the same and also wastes glutathione and increases levels of TNF-alpha,
an inflammatory mediator that can produce gut inflammation.We can restore glutamate GABA balance by:
1. Addressing any CBS up regulation issues to decrease alpha-ketoglutarate production.
2. Decreasing intake of food precursors of glutamate (includes whey protein, gelatin, soy, peas, tomatoes,
parmesan cheese).
3. Supplementing with GABA
4. Copper inhibits conversion of glutamate to GABA by glutamate decarboxylase so avoid copper excess, or
better stated, an imbalance between copper and zinc.
5. Calcium is involved in glutamate toxicity, so supplement with magnesium to keep calcium in check.
6. Remove heavy metals with a chelating agent (toxicity due to mercury is aggravated by glutamate excess
they synergize to damage nerve cells).
7. Supplementing with Pycnogenol and grape seed extract.
GAMT
rs17851582
GG
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
GAMT
rs55776826
CC
-/-
GIF (TCN3)
rs558660
GG
-/-
MAO A R297R
rs6323
MAO A (heterozygous mutation) Monoamine oxidase A degrades serotonin, dopamine, epineprine, and
norepinephrine. This can result in swings in serotonin levels, and therefore mood swings.If youre affected, you
might want to reduce foods containing high levels of tryptophan. However, it is likely that, as methylation status
improves, serotonin fluctuations should also improve (based on improved levels of BH4).
MAT1A
rs72558181
CC
-/-
MTHFD1 C105T
rs1076991
CT
+/-
MTHFD1 G1958A
rs2236225
AA
+/+
MTHFD1L
rs11754661
GG
-/-
MTHFD1L
rs17349743
TT
-/-
MTHFD1L
rs6922269
GG
-/-
MTHFD1L
rs803422
GG
-/-
MTHFD This gene encodes a protein that possesses three distinct enzymatic activities related to folate. Recent
data shows choline requirements are increased by polymorphisms in the phosphatidylethanolamine
N-methyltransferase (PEMT) gene (i.e., 5465G->A; rs7946 and -744G->C; rs12325817) and in the
methylenetetrahydrofolate dehydrogenase (MTHFD1) gene (i.e., 1958G->A; rs2236225).Choline is a required
nutrient with roles in liver and brain function, lipid metabolism, and fetal development. Deficiency leads to liver
disease.
MTHFR 03 P39P
rs2066470
GG
-/-
MTHFR A1298C
rs1801131
TT
-/-
MTHFR A1572G
rs17367504
AA
-/-
MTHFR C677T
rs1801133
AG
+/-
rs2274976
CC
-/-
MTHFR
rs12121543
CC
-/-
MTHFR
rs13306560
CC
-/-
MTHFR
rs13306561
AA
-/-
MTHFR
rs1476413
CC
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
MTHFR
rs17037390
GG
-/-
MTHFR
rs17037396
CC
-/-
MTHFR
rs3737964
CC
-/-
MTHFR
rs4846048
AA
-/-
MTHFR
rs4846049
GG
-/-
MTHFR (heterozygous mutation) This enzyme has global effects for immune function, muscle metabolism,
neurochemical production and regulation, and detoxification.It is the enzyme most in vogue at the most for
analyzing because its responsible for converting inactive folate to active folate (i.e. methylfolate) and the +/defect is common.rs1801133 since your +/- is less efficient (operating at 65% of normal), your methylfolate
levels may be on the low side. It also suggests that you should stay away from folic acid and, perhaps, too much
dietary folate.
MTHFS
rs6495446
CC
+/+
MTHFS (homozygous mutation) MTHFS is the only enzyme known to catalyze a reaction with folinic acid. If
you have a deficiency in this enzyme, and you consume folinic acid (found in vegetables), it will build up in your
cells (this is from a note Rich wrote to Fred found here).The problem with this is that folinic acid normally acts as
a regulator of folate metabolism by inhibiting enzymes in this metabolism. In particular, it inhibits the serine
hydroxymethyltransferase (SHMT) enzyme, which normally is the main enzyme that converts tetrahydrofolate to
5,10 methylene tetrahydrofolate, which in turn is the substrate for making methylfolate.So, a deficiency in MTHFS
will allow folinic acid to rise inhibiting SHMT, which will lower 5,10 methylene tetrahydrofolate, and thus will also
lower production of methylfolate, which is needed by methionine synthase in the methylation cycle.This would
suggest that I need very high levels of methyl folate (and magnesium which is a cofactor).
MTR A2756G
rs1805087
AA
-/-
MTRR A66G
rs1801394
AG
+/-
MTRR H595Y
rs10380
CC
-/-
MTRR K350A
rs162036
AA
-/-
MTRR R415T
rs2287780
CC
-/-
MTRR-11 A664A
rs1802059
AG
+/-
MTRR
rs10520873
CT
+/-
MTRR
rs1532268
CT
+/-
MTRR
rs162049
AA
-/-
MTRR
rs3776467
AA
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
MTRR
rsID #
rs9332
Risk Allele
A
-/-
MTRR (homozygous mutation) Generates the Methyl-B12 used by MTR to convert 5-Methyl-THF into
Methionine. With mutation, Methyl-B12 generation is limited, diminishing MTRs ability to produce Methionine.
Homocysteine toxicity will occur along with impaired formation of S-Adenosyl Methionine (SAMe) and methylation
in general. Suggests inactive B12 supplements wouldnt work well for me. Supplement also with TMG
(trimethylglycine), phosphatidylserine, or phosphatidylcholine. Avoid dimethylglycine (DMG) which would actually
slow down the Homocysteine to Methionine conversion.
NOS1
rs3782206
CC
-/-
NOS2
rs2297518
GG
-/-
NOS2
rs2274894
TT
+/+
NOS2
rs2248814
AA
+/+
NOS3
rs1800783
TT
-/-
NOS3
rs1800779
AA
-/-
NOS3
rs3918188
AA
+/+
NOS3 G10T
rs7830
GG
-/-
NOS3 T786C
rs2070744
TT
-/-
NOS (some homozygous mutations) in a process dependent on BH4, NOS converts arginine into nitric oxide
and assists in ammonia detoxification. In the absence of BH4, NOS will convert Arginine into peroxynitrite or
superoxide, which are both bad free radicals.I may benefit from reducing protein intake, eating Yucca or butter
with meals, or supplementing with butyrate or BH4 to keep ammonia levels down. Thankfully, I dont have a CBS
upregulation, which would have an additive effect.
PEMT
rs4244593
GT
+/-
PEMT
rs4646406
AT
+/-
PEMT
rs7946
TT
-/-
PEMT This gene encodes an enzyme which converts phosphatidylethanolamine to phosphatidylcholine (the
most abundant mammalian phospholipid) by sequential methylation in the liver. Mutations may mean Id benefit
from supplementing choline or eating more eggs. Studies have recently shown that because of common genetic
polymorphisms, choline deficiency is a widespread problem. Men, postmenopausal women, and premenopausal
women with PEMT SNPs need to increase choline intake in the diet to offset elevated risk of liver dysfunction.
SHMT1 C1420T
rs1979277
AG
+/-
SHMT1
rs9909104
TT
-/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
rsID #
Risk Allele
SHMT2
rs12319666
GG
-/-
SHMT2
rs34095989
AG
+/-
SHMT Serine hydroxymethyltransferase (SHMT) is an enzyme which plays an important role in cellular
one-carbon pathways by catalyzing the reversible, simultaneous conversions of L-serine to glycine (retro-aldol
cleavage) and tetrahydrofolate to 5,10-methylenetetrahydrofolate (hydrolysis). This reaction provides the largest
part of the one-carbon units available to the cell. SHMT is a member of the PLP or P5P (B6) enzyme class. P5P
is needed by both mSHMT and cSHMT at all times to activate this enzyme. Dr. Yasko puts SHMT first of the first
priority mutations because it is a dead end pathway. If its blocked, it takes your folate and holds it there so you
wont get it converted into folinic or 5MTF. This means it steals this from the rest of the cycle. She also notes,
People with the SHMT and/or ACAT mutations sometimes have a greater tendency to experience gut dysbiosis
and imbalanced flora.
SLC19A1
rs1888530
CT
+/-
SLC19A1
rs3788200
AG
+/-
SLC19A1 The SLC19A1 gene encodes a transporter involved in folate and thiamine uptake and may play a
role in intracellular folate distribution [21].
TCN1
rs526934
AA
-/-
TCN2 C766G
rs1801198
CG
+/-
TCN the frailty genes. TCN1 and 2 are both B12-binding and transport proteins but TCN2 is the primary of the
two. Both deliver cobalamin to cells.
TYMS
rs502396
CC
+/+
TYMS A nasty cancer gene (the mutation). Thymidylate synthase catalyzes the methylation of deoxyuridylate
to deoxythymidylate using 5,10-methylenetetrahydrofolate (methylene-THF) as a cofactor. This function
maintains the dTMP (thymidine-5-prime monophosphate) pool critical for DNA replication and repair.
VDR Bsm
rs1544410
TT
+/+
VDR Bsm/Taq mediates an increase in dopamine production in response to Vitamin D (VDR is an abbreviation
for Vitamin D Receptor). The (+/+) form is less active, so you tend to be low in dopamine. Methyl status will be
low also, so you will be less sensitive to supplementation with methyl groups.I have (+/+), which read with my
normal V158M gene means that I have low vitamin D levels, poor tolerance to toxins and microbes, make less
dopamine and need and tolerate more methyl donors.
***
CELIAC DISEASE/GLUTEN INTOLERANCE
Gene & Variation
HLA
rsID #
rs2858331
Risk Allele
G
+/-
5/6/2016 1:43 PM
My genetics
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DETOX
Gene & Variation
HLA DQA1
rsID #
rs2187668
Risk Allele
T
-/-
***
THYROID
Gene & Variation
rsID #
Risk Allele
CTLA4
rs231775
AA
-/-
FOXE1
rs1867277
GG
-/-
FOXE1
rs7043516
AA
-/-
FOXE1
rs10984009
GG
-/-
***
EYE HEALTH
Gene & Variation
rsID #
Risk Allele
BCMO1
rs4889294
CT
+/-
BCMO1 R267S
rs12934922
AT
+/-
BCMO1 A379V
rs7501331
CC
-/-
***
MITOCHONDRIAL FUNCTION
Gene & Variation
rsID #
Risk Allele
ATP5g3
rs185584
AA
-/-
ATP5g3
rs36089250
TT
-/-
ATP5c1
rs2778475
AG
+/-
ATP5c1
rs1244414
CC
-/-
ATP5c1
rs1244422
CT
+/-
ATP5c1
rs12770829
CT
+/-
ATP5c1
rs4655
CT
+/-
COX5A
rs8042694
AG
+/-
COX6C
rs4626565
TT
-/-
5/6/2016 1:43 PM
My genetics
15 of 18
http://howirecovered.com/my-genetics/
DETOX
Gene & Variation
rsID #
Risk Allele
COX6C
rs7844439
CC
-/-
COX6C
rs4510829
GG
-/-
COX6C
rs1135382
GG
-/-
COX6C
rs7828241
AA
-/-
COX6C
rs12544943
AA
-/-
COX6C
rs4518636
TT
-/-
NDUFS3
rs2233354
TT
-/-
NDUFS3
rs4147730
AG
+/-
NDUFS3
rs4147731
GG
-/-
NDUFS7
rs2332496
AA
+/+
NDUFS7
rs7254913
AA
-/-
NDUFS7
rs1142530
TT
+/+
NDUFS7
rs7258846
TT
+/+
NDUFS7
rs11666067
AA
+/+
NDUFS7
rs2074895
AA
+/+
NDUFS7
rs809359
AA
-/-
NDUFS8
rs4147776
AA
-/-
NDUFS8
rs1122731
GG
-/-
NDUFS8
rs999571
GG
-/-
NDUFS8
rs2075626
TT
-/-
NDUFS8
rs3115546
TT
-/-
NDUFS8
rs1104739
AC
+/-
NDUFS8
rs1051806
CC
-/-
UQCRC2
rs6497563
CT
+/-
UQCRC2
rs4850
GG
-/-
UQCRC2
rs11648723
GG
-/-
5/6/2016 1:43 PM
My genetics
16 of 18
http://howirecovered.com/my-genetics/
DETOX
Gene & Variation
rsID #
Risk Allele
UQCRC2
rs12922362
AC
+/-
UQCRC2
rs2965803
CC
-/-
***
OTHER IMMUNE FACTORS
Gene & Variation
rsID #
Risk Allele
4q27 Region
rs6822844
GG
-/-
APOE
rs429358
TT
-/-
ATG16L1
rs10210302
CT
+/-
GSDMB
rs7216389
CT
+/-
HLA-DRB1
rs660895
AA
-/-
IL5
rs2069812
AG
+/-
IL-13
rs20541
GG
-/-
IL4R Q576R
rs1801275
AA
-/-
MeFV A744S
i4000409
CC
-/-
MeFV E148Q
rs3743930
CC
-/-
MeFV F479L
i4000403
GG
-/-
MeFV K695R
i4000407
TT
-/-
MeFV M680I
rs28940580
CC
-/-
MeFV M694I
rs28940578
CC
-/-
MeFV M694V
i4000406
TT
-/-
MeFV P369S
rs11466023
GG
-/-
MeFV R761H
i4000410
CC
-/-
STAT4
rs10181656
CG
+/-
TNF -308
rs1800629
GG
-/-
TNF -238
rs361525
AG
+/-
rs28940879
GG
-/-
5/6/2016 1:43 PM
My genetics
17 of 18
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DETOX
Gene & Variation
rsID #
Risk Allele
rsID #
Risk Allele
***
SULFONOTRANSFERASE
Gene & Variation
SULT1A1
rs35728980
TT
-/-
SULT1A1
rs1801030
TT
-/-
SULT1A1
rs1042157
NO CALL
SULT1A1
rs36043491
CC
-/-
SULT1A1
rs60749306
TT
-/-
SULT1A1
rs9282862
TT
-/-
SULT1A1
rs1042008
GG
-/-
SULT1A1
rs2925627
TT
-/-
SULT1A1
rs2925631
TT
-/-
SULT1A1
rs3020800
AA
-/-
SULT1A1
rs4149385
CC
-/-
SULT1A1
rs60701883
CC
-/-
SULT1A1
rs4149381
TT
-/-
SULT1A1
rs8057055
CC
-/-
SULT1A1
rs6498090
GG
-/-
SULT1A1
rs7193599
AA
-/-
SULT1A1
rs7192559
CC
-/-
SULT1A3
rs1059667
TT
-/-
SULT2A1
rs296366
CC
-/-
SULT2A1
rs296365
GG
-/-
SULT2A1
rs11569679
CC
-/-
SULT2A1
rs4149452
CC
-/-
SULT2A1
rs8113396
AA
-/-
5/6/2016 1:43 PM
My genetics
18 of 18
http://howirecovered.com/my-genetics/
DETOX
Gene & Variation
rsID #
Risk Allele
SULT2A1
rs2547242
TT
-/-
SULT2A1
rs2910393
CC
-/-
SULT2A1
rs4149449
CC
-/-
SULT2A1
rs2547231
AA
-/-
SULT2A1
rs4149448
AA
-/-
SULT2A1
rs11083907
GG
-/-
5/6/2016 1:43 PM