FVL: Factor V Leiden. When factor V is found heterozygous, the odds of FVL’s having a clotting event in their lifetime is much greater than the someone without this mutation. Factor V Leiden is sometimes called Activated Protein C Resistance because this mutation leads to protein C resistance.
When pregnant, the uterus is fed with capillaries. So miscarriage is related to this particular mutation.
Remember, this is a gene where you will rarely see someone homozygous because it is usually not caught before a major clotting event occurs.
FVL can be serious even when heterozygous. So when someone knows that he or she has FVL, it is best for them to have their physician run platelets, C reactive protein and fibrinogen.

FVL is easily manageable.

These people are at higher risk of developing DVT especially when on hormone therapy or birth oral birth control.

Speak with your practitioner if you have any concerns.


F2 (Prothrombin 20210A) : Like FVL, it is extremely rare to find someone homozygous. Heterozygous people are at higher risk of developing a clotting event some time in their life when not monitored.

The F2 gene provides instructions for making a protein called prothrombin (also called coagulation factor II).

This gene is also related to miscarriage as the uterus is fed with capillaries.

Thrombin is also thought to be involved in cell growth and division (proliferation), tissue repair, and the formation of new blood vessels (angiogenesis).

2-5% of Caucasians and 0.3 percent of African Americans are heterozygous for G20210A.

It is important to be monitored throughout your lifetime if you have this mutation.

These people are at higher risk of developing DVT especially when on hormone therapy or birth oral birth control.


FUT2: The 3 major FUT2 genes that seem to cause problems are FUT2 A12190G, FUT2 G12447A and FUT2 G12758A. When these three SNPs are homozygous, these people cannot make H antigen.
Why is H antigen important?

The specificity of the H antigen is determined by the sequence of oligosaccharides. Almost everyone to date who has been diagnosed with ulcerative colitis and Crohn’s disease are homozygous for these three particular mutations. These three FUT2’s play a huge role in autism.

FUT2’s catalytic activity is GDP-beta-L-fucose + beta-D-galactosyl-(1->3)-N-acetyl-beta-D-glucosaminyl-(1->3)-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1)-ceramide = GDP + alpha-L-fucosyl-(1->2)-beta-D-galactosyl-(1->3)-N-acetyl-beta-D-glucosaminyl-(1->3)-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1)-ceramide.

FUT2 is involved in protein glycosylation.

More or less, if you are lacking the ability to produce H antigen in the gut, your probiotics will not have anything to stick to in the gut.

I normally do not recommend products and I am not affiliated with Klaire Labs in any way but they do have a prebiotic called Galactomune that contains galactooligosacchrides and beta-glucan. These are essential for anyone with the above FUT2’s homozygous in order for probiotics to stick to their gut and be utilized.
Another thing that we see quite often in these homozygouse FUT2’s is hyperoxaluria when a prebiotic containing galactooligosacchrides and beta-glucan is not administered daily. It is nearly next to impossible to heal the gut of these people without these type of prebiotics.
Next, most of the probiotics that they are missing in the gut have to do with breaking down oxalates. Again I do not normally recommend certain probiotics and I am not affiliated or do I get paid for promoting the following companies. It is best to wait about 12 weeks before starting Bravo yogurt in order to have the prebiotics in place. Bravo contains all essential probiotics in order to remove oxalates from the gut and to jump start sulfation in the gut. One product that can be started with Galactomune until you have the prebiotic in place for a few months is Jarro-Dophilus EPS. It does contain a handful of essential probiotics that are needed to remove oxalates but not all of them. Unfortunately Bravo holds the patent on many of the probiotics needed to remove oxalate from the body.

Since poor producers of H antigen already have issues maintaining a healthy gut flora because of their lack of prebiotic production, it is obvious that GMO’d Roundup Ready glyphosate which destroys the shikimate pathway of our gut microbiome is not healthy at all for anyone and especially for these individuals.


MTHFR: MTHFR requires folate, NADPH, SAMe and FAD.
MTHFR is one of the final steps in methylation.
It can play a huge role in miscarriage. When the blood is folate deficient, red blood cells become oddly shaped and the uterus is fed with capillaries. Also when the body is NADPH deficient due to G6PDD which is the most common enzyme deficiency in the world, red blood cells literally start exploding.

Things to look out for if someone is folate deficient or high or low in homocysteine:
Do they have DHFR and are having trouble converting folic into folate?
Do they have MTHFS homozygous and MTHFD1L mutations and are consuming folinic acid?
Do they have hyperoxaluria which shuts off methionine synthase where MTHFR resides?

Do they have have G6PD deficiency (400 million people do)?


G6PD: I like to call G6PD the “Mother SNP” of the Pentose Phosphate Pathway (PPP). This pathway controls the production of NADPH.
What happens when the PPP is not working like it should because of G6PD deficiency?

  • Your red blood cells explode
  • Your reduced glutathione has oxidative damage
  • Your ferritin increases
  • CFS/ME due to mitochondrial dysfunction
  • Cannot make PAPs
  • Cannot make ATP
  • Shut off the citric acid cycle
  • Shutdown of Phase I liver detox where CYP450’s reside
  • Circadian rhythm is compromised
  • Redox signaling becomes impaired
  • EMF sensitivity sets in
  • Higher risk for hemolytic anemia
  • Higher risk for POTS (10% of people with POTS are G6PDD)
  • Higher risk for lupus
  • Higher risk of being injured by a fluoriquinolone

You can learn more about drugs and food to avoid if you are diagnosed with an actual G6PD deficiency at www.g6pddeficiency.org


APOE 2 and 4: Known as the Alzheimer gene. Two of the biggest things that our governments worldwide have seen is that most people with Alzheimer’s seem to have elevated A1C and elevated homocysteine. Why are they not telling us this but making more drugs?

I like to call APOE’s “grain brains”. We do see that their omega 3’s and 6’s are not balanced.

Another thing that many APOE’s have in common that do end up with dementia are metals. Mercury amalgam fillings, aluminum and mercury on the brain.


VDR: When the vitamin D receptor gene is impaired, this can lead to many health problems. Vitamin D hormone is needed to break down into GcMAF which is then needed to attack stealth pathogens, viruses and cancer cells.

Did you know that you can only get sulfated D from the sun between 8am and noon?
Many chronically ill do not get out of the bed to get sulfated D from the sun. Also many chronically ill people are low on GcMAF because they are low on D3 which needs to be sulfated and and broken down into GcMAF. Ever wondered why most people with cancer are D deficient? Because GcMAF which is one billionth of a gram in the blood is crucial. GcMAF has six attacks on cancer including the cannabinoid pathway. That is why many who do CBD oils have shrunk their tumors.
We also see that many people with viral overloads, autism, cancer and lyme are GcMAF deficient. They may even have D levels close to 100 but they are not sulfating their D3 because of the following:

  • Eating GMO’d Roundup ready foods. Glyphosate converts into glyoxylate. Oxalates share the same transport system as sulfation. I call it oxalates “hogging” up the transport system. This causes poor sulfation of D3 where it cannot sulfate D3 into GcMAF.
  • Zinc is needed to sulfate D3
  • DAO is needed to sulfate D3
  • Lysine is needed to sulfate D3
  • P5P is needed to sulfate D3
  • B6 is needed to sulfate D3


GAD: GAD is needed to convert the excitotoxin glutamate into the calming neurotransmitter GABA.

Did you know that most heroin users and alcoholics are not converting their glutamate into GABA? Heroin and alcohol temporarily make GABA.

GAD’s cofactor is P5P. B6 converts into P5P on most people. P5P is lysine dependent. Makes you question if B6 toxic people are lysine deficient because many B6 toxic people have hyperoxaluria and P5P as well as lysine are needed to convert glutamate into GABA in order to sulfate D3 into GcMAF.
See the domino effect yet?


COMT:  COMT V158M +/+ and COMT H62H +/+ along with VDR Bsm -/- makes for a storm of catecholamines. These people have issues breaking down epinephrine, norepinephrine, dopamine and estrogens.
With that when they are given high dose methyl donors such as methyl b12, methylfolate, trimethylglycine and caffeine, you can cause a huge storm of anxiety and panic.

These people when chronically ill also tend to have high cortisol levels.

IV niacin only (not a cheap mix of niacin with amino acids added) sometimes help these people calm down their catecholamine activity.

COMT’s catalytic activity is S-adenosyl-L-methionine + a catechol = S-adenosyl-L-homocysteine + a guaiacol. And COMT’s cofactor is magnesium. Makes you wonder why some people feel calmer after taking an epsom bath or a magnesium supplement.




Coming in the near future to MTHFR Support:

  • The glyoxylate pathway
  • The iron metabolism pathway
  • The thiamine pathway
  • More videos next to the SNPs
  • 2nd edition SNPbit Conpendium (Cynthia Smith) www.lifezonewellness.com
  • More diagrams (Cynthia Smith) www.lifezonewellness.com
  • Autoimmune variant report


If you would like to know more about these SNPs, you can run your data from 23andme or DNAancestry through our variant report at www.mthfrsupport.com .

If you would like to learn more about SNPs on your variant report you can order our SNPbit Conpendium.