Now available from Gnosis, a chart that explains the folate metabolic pathway, from folic acid to active 5-methyltetrahydrofolate (5-MTHF)! Did you know that folic acid must be converted to an active form before it is used by the body?
Quatrefolic is the glucosamine salt of (6S)-5-methyltetrahydrofolate and is structurally analogous to the reduced and active form of folic acid, so Quatrefolic completely bypasses the conversion step and delivers a 'finished' folate that the body can immediately use without any kind of metabolism.
Impaired folic acid metabolism and MTHFR polymorphism
Methylenetetrahydrofolate reductase (MTHFR) is one of the most important enzymes in human physiology; deficiencies in the production or function of this enzyme have been associated with an increased risk of chronic disease states. Some individuals, because of their unique genetic patterns and expression, have polymorphic forms of this enzyme and do not produce adequate or effective MTHFR.
MTHFR converts folic acid/food folates into the activated form, (6S)-5-MTHF or 5-methyltetrahydrofolate. Genetic variations of this enzyme may impair MTHFR activity (by 55–70%) compared with a normal MTHFR enzyme. MTHFR polymorphisms are estimated to occur in up to 40% of the world population.
Based on the high prevalence of MTHFR genetic polymorphisms in the general population and concerns about reduced enzymatic activity, the worldwide scientific community is focusing its research in this area, recommending the use of folic acid supplementation — with the biological active form (6S)-5-methyltetrahydrofolate, such as Quatrefolic — to prevent folate-related pathology.
The debate about folic acid versus (6S)-5-MTHF also extends to consumers who are increasingly aware of the implications of MTHFR polymorphism in supporting their health. Consumers are also concerned about the potential clinical implications and adverse effects of high doses of folic acid related to the consumption of fortified foods.
Several studies have reported an increase in serum levels of unmetabolised folic acid (UMFA) levels since the implementation of folic acid fortification. A study published in 2014 clearly showed that 86% of the folic acid in the hepatic portal vein is unmetabolised, whilst almost all of the natural folate was converted correctly.
Variability in the presence or persistence of UMFA in the population suggests that it may be accumulated in the blood as a consequence of different conditions, such as impaired folic acid reduction to 5-methyltetrahydrofolate (genetic polymorphism) and the overdosing effect of uncontrolled folic acid intake.
