Folate is the generic term for the water-soluble B-complex vitamin that includes various chemical structures with similar biological activity. Folic acid, the common synthetic form of the vitamin, consists of three subunits: (1) a pteridine linked to, (2) para-aminobenzoic acid (PABA) which forms pteroic acid, and (3) glutamic acid (Combs, 2008). When one or more glutamic acid residues bond together, pteroylpolyglutamates are formed, and these represent the main cellular forms of folates in plants and animals (Combs, 2008). The oxidation state of the pteridine structure varies from the fully oxidized form (folic acid) to various levels of reduction (e.g., dihydrofolate, tetrahydrofolate, 5,10-methylene tetrahydrofolate; 5-methyltetrahydro-folate). While animal cells contain the necessary-enzymatic capacity to interconvert most folate species, they cannot synthesize the pteroic acid moiety, and are, therefore, dependent on an exogenous source of the pteroylglutamate (irrespective of oxidation state) in order to replace obligatory losses. Folate inadequacy limits one-carbon transfer reactions, thus limiting the ability of folate to serve as a substrate for the transfer of single carbon atoms in the metabolism of pyrimidines and purines (Fox and Stover, 2008), formate (Sokoro et al., 2008), and amino acids, including glycine, serine, and the sulfur amino acids methionine and homocysteine (Hcy) (House et al., 1999). The current review will focus on the recent advances in our understanding of folate nutrition, with speci c emphasis on the potential for folate to mitigate risk related to vascular disease.