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Discussion: Folate and Vitamin B12 Metabolism: Overview and Interaction with Riboflavin, Vitamin B6, and Polymorphisms

The folate-mediated one-carbon metabolic network is required for the synthesis of purine and thymidine nucleotides, and for the remethylation of homocysteine to methionine. Methionine is converted to S-adenosylmethionine which serves as a cofactor and methyl donor for numerous methylation reactions, including the methylation of DNA, RNA, proteins (including histones), and small molecules. Impairments in onecarbon metabolism, resulting from nutritional deficiencies or common single-nucleotide polymorphisms (SNP) in genes that encode folate-dependent enzymes, can affect genome synthesis and/or methylation, and thereby affect chromatin structure leading to wideranging effects on genome stability and expression. The mechanisms of folate-associated pathologies, including developmental anomalies, cancers, and neurodegenerative and vascular disorders, are unknown. They are multigenic, complex diseases resulting from imbalances in gene-nutrient interactions. Furthermore, the mechanism whereby increased folic acid intake prevents these pathologies is not known. Interventions based on association without mechanistic information are particularly vulnerable to unintended consequences, especially when the intervention achieves levels of intake that cannot be achieved in a healthy, food-based diet [1]. Emerging genomic criteria for establishing folate adequacy and upper limits