INFORMATION ON VITAMIN B9 (METHYLFOLATE)

The glucosamine salt of (6S)-5-methyltetrahydrofolate and is structurally analogous to the reduced and active form of folic acid.

Folic acid and also food folate are not biologically active and need to be converted to the metabolically active 5-methyltetrahydrofolate (5-MTHF) through a multi-steps process where the enzyme methylenetetrahydrofolate reductase (MTHFR) owns a key role. Some individuals, due to their unique genetic patterns and expression, have polymorphic forms of this enzyme and do not produce adequate or effective MTHFR.

Methylenetetrahydrofolate reductase (MTHFR) is one of the most important enzymes in human physiology, deficiencies in production or function of this enzyme have been associated with increased risk of different diseases.

These defects related to MTHFR are very common, though they vary enormously between ethnic groups and regions. Emerging science of nutrigenomics indicates that MTHFR most often refers to a genetic mutation that inhibits the ability of the body to methylate (or convert folic acid from the food we eat into the metabolite we need, L-5-Methyltetrahydrofolate) so as some individuals cannot actually use folic acid.

Cutting edge scientific research is shed light how much the MTHFR polymorphism is implicated in chronic disease states and how folate nutrition may contribute to replace adequate methylation and overall health.

How it works:

The mechanism of action is related to the action of 5-methyltetrahydrofolate the active part of the proprietary ingredient.

5-methyltetrahydrofolate derives from tetrahydrofolic acid, through a series of metabolic reactions. Tetrahydrofolic acid acts as a coenzyme in several vital metabolic reactions participating in the transfer as acceptors and donors of various one-carbon fragments, involved in the biosynthesis of nucleotides purines and pyrimidines and in the metabolism of several important amino acids.

In concert with vitamin B12, folate coenzymes allow the conversion of the amino acid homocysteine into methionine. The lack of this conversion has been associated with various pathologies and diseases.

Conversion of tetrahydrofolic acid into 5-methyltetrahydrofolate is mediated by the action of the enzyme methylentetrahydrofolate reductase. In individuals with a genetic defect of the methylentetrahydrofolate reductase (MTHFR) this enzyme conversion is limited, consequently it will predispose these individuals to an increased risk for certain disease conditions.

Supplementation with 5-methyltetrahydrofolate is preferable to the one with folic acid, as it is immediately bioavailable to react with homocysteine to avoid the possibility to incur in hyperhomocysteinemia.

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