Please note: The content of this post is my own, unless the technical terms is too hard to explain, then the content is copy and pasted. I am not a medical professional and thus the post is my point of view. But the content is science-based and credible. Just because it is a new science, does not necessarily make it quackery. Always consult your doctor first before trying a new treatment.
Do you want to see which genes are involved in influencing Homocysteine?
MTHFR C677T is the culprit. And if it is homozygous it is the worst.
We all have 2 MTHFR genes, one inherited from each parent. Some people have a genetic mutation in one or both of their MTHFR genes. People with mutations in one MTHFR gene are called “heterozygous” for the MTHFR mutation; if mutations are present in both genes, the person is said to be “homozygous” for the mutation.
The most common MTHFR mutation is called the MTHFR C677T mutation, or the “thermolabile” MTHFR mutation. Another common mutation is called MTHFR A1298C. To have any detrimental effect, mutations must be present in both copies of a person’s MTHFR genes. Having only one mutation, ie, being heterozygous, is, from a medical perspective, irrelevant. Even when 2 MTHFR mutations are present (eg, 2 C677T mutations, or one C677T mutation and one A1298C mutation), not all people will develop high homocysteine levels. Although these mutations do impair the regulation of homocysteine, adequate folate levels essentially “cancel out” this defect.
In an paper published by Dr Joseph Pizzorno, ND, Editor in Chief called “Homocysteine: Friend or Foe“, he list the following:
Genes Directly and Indirectly Involved in Homocysteine Metabolism
|MTHFR||Methylenetetrahydrofolate reductase||Conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate|
|CBS||Cystathionine-β-synthase||Condensation of homocysteine and serine to form cystathionine|
|MTR||Methyltetrahydrofolatehomocysteine methyltransferase||Remethylation of homocysteine to methionine|
|MTRR||Methionine synthase reductase||Reductive regeneration of cob(I)alamin cofactor required for the maintenance of MTR in a functional state|
|RFC1||Reduced-folate carrier||5-methyltetrahydrofolate internalization in cell|
|GCP2/FOLH1||Glutamate carboxypeptidase II||Polyglutamate converted to monoglutamate folate by action of the enzyme folylpoly-γ-glutamate-carboxypeptidase (FGCPI), an enzyme expressed by GCP2|
|ENOS||Endothelial nitric oxide synthase||Conversion of l-arginine to l-citrulline and nitric oxide synthase (NO)|
|TC2||Transcobalamine II||Transport of vitamin B12|
|SHMT1||Serine hydroxymethyltransferase I||Reversible conversion of serine and tetrahydrofolate to glycine and 5,10-methylenetetrahydrofolate|
|TYMS||Thymidylate synthase||5,10-methylenetetrahydrofolate and deoxyuridylate to form dihydrofolate and thymidylate|
|CTH||Cystathionine-γ-lyase||Hydrolysis of cystathionine to cysteine and α-ketoglutarate|
|MTHFD||Methylenetetrahydrofolate dehydrogenase||Conversion of 5,10-methylenetetrahydrofolate to 5,10-methenyltetrahydrofolate|
|MTHFS||Methenyltetrahydrofolate synthetase||Conversion of 5-formyltetrahydrofolate to 5,10-methenyltetrahydrofolate|
|APOE||Apolipoproteine E||Mediates the binding, internalization, and catabolism of lipoprotein particles|
|VEGF||Vascular endothelial growth factor||Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth|
|PON1||Paraoxonase I||Hydrolyzes the toxic organophosphorus. It also mediates an enzymatic protection of LDL against oxidative modification|
|BHMT||Betaine-homocysteine methyltransferase||In liver and kidney, it catalyses the conversion of betaine to dimethylglycine (DMG)|
|MAT1A||Methionine adenosyltransferase IA||Methionine to SAM by transfer of the adenosyl-moiety of ATP to the sulfur atom of methionine|
|AHCY||S-adenosy-l-homocysteine hydrolase||Hydrolysis of S-adenosy-l-homocysteine to adenosine and homocysteine|
|CBL||Cystathionine-β-lyase||Conversion of cystathionine to homocysteine|
|F5||Coagulation factor V||Cofactor for the factor Xa-catalyzed activation of prothrombin to the clotting enzyme thrombin|
|PAI1||Prothrombin activator inhibitor I||Inhibition of fibrinolysis by inhibiting the plasminogenactivator and t-PA|
We are complex beings, with complex systems.
Alex is currently taking Methyl Care from Metagenic:
|Ingredients||Amount Per Serving||% Daily Value|
|Serving Size||2 Capsules†|
|Servings Per Container||60|
|Vitamin B6 (as pyridoxine HCl)||25 mg||1,250%|
|Folate (as calcium L-5-methyltetrahydrofolate)††||800 mcg||200%|
|Vitamin B12 (as methylcobalamin)||1,000 mcg||16,667%|
|Zinc (as zinc citrate)||1.5 mg||10%|
|Manganese (as manganese citrate)||0.4 mg||20%|
|Molybdenum (as molybdenum glycinate)||15 mcg||20%|
|Betaine HCl||500 mg||*|
††As Metafolin®. Metafolin® is a registered trademark of Merck KGaA, Darmstadt Germany.
We need to do a homocysteine soon to see if any progress has been made in supporting his methylation cycle.
For now, this is the end of our MTHFR research, even though there is so much more.
Some of the resources used during my research: