Folate
Homocysteine can be remethylated to methionine in two different ways – Folate is important for one pathway and choline for the other.
In the first case, homocysteine is methylated to methionine (addition of CH 3 groups) by the enzyme methionine synthase. For this process, methionine synthase requires methyl tetrafolate as a methyl group donor and cobalamin as a cofactor.In the second case, homocysteine is methylated by betaine homocysteine methyltransferase, which requires betaine as a methyl group donor. Betaine is an osmoregulator to which choline is irreversibly oxidized in the liver and kidney.
Choline deficiency, with correspondingly lower betaine formation, increases the need for methyl tetrafolate to methylate homocysteine and, accordingly, the need for dietary folate.Viewed differently, methyl groups, during folate deficiency, are increasingly used by choline and betaine for homocysteine remethylation, which in turn leads to an increased need for choline.
According to the European Food Safety Authority (EFSA) publication, Jacob and colleagues studied the effect of folate reserve depletion as well as the effect of folate saturation and its impact on choline status and in vivo methylation capacity in humans.
From this experiment, EFSA reports that adequate folate intake maintained plasma choline concentrations despite a low choline intake of 150-250 mg/day on average. Here, at both low folate and choline intakes, plasma free choline and phosphatidylcholine concentrations decreased, and total homocysteine concentrations increased.In addition, low folate intake was found to have a negative effect on plasma phosphatidylcholine concentrations at an “adequate” choline intake in several studies.