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One carbon metabolism is fundamental in providing sufficient methionine for optimal foetal development and pregnancy outcome. The methionine synthase (MS) and betaine:homocysteine methyltransferase (BHMT) pathways intersect in the methionine cycle and are key determinants of methionine synthesis. Folate and cobalamin drive the MS pathway and betaine, dietary or as a result of choline oxidation, drives the BHMT pathway. Cell, animal and human studies consistently show that these pathways interact. Globally, methionine synthesis depends initially on the MS pathway, but growing evidence shows that the BHMT pathway is stimulated or at least enhanced when the MS pathway is performing suboptimally or is metabolically stressed. This has been observed in developing embryos, in adults subjected to a methionine load test, in adults with suboptimal status in folate or other B vitamins and during pregnancy. BHMT activity, both in the mother and in the fetus, increases as pregnancy progresses and is greater when folate status is low. The converse applies when folate status is replete and betaine is spared. The phosphatidylethanolamine N-methyltransferase pathway for phosphatidylcholine synthesis is preferred over choline usage by the choline oxidation pathway during pregnancy.

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