The role of choline (via betaine) as a methyl donor suggests that insufficient maternal choline intake can exacerbate the effect of nutrient deficiencies (folate or vitamin B12) or polymorphisms (e.g., methylenetetrahydrofolate reductase, MTHFR) on hyperhomocysteinemia and the risk of adverse pregnancy outcomes. Here, MTHFR is linked to hyperhomocysteinemia.