HOPE 2: can supplementation with folic acid and B vitamins reduce cardiovascular risk?

Iftikhar J Kullo

This article has no abstract so we have provided the first paragraph of the full text.

Homocysteine is a thiol-containing amino-acid intermediate that is formed during the metabolism of methionine, an essential amino acid. The observation that children and young adults with inborn errors of homocysteine metabolism developed arteriosclerosis raised the possibility that milder elevations in plasma homocysteine might predispose individuals to atherosclerotic vascular disease. Several studies, both prospective and retrospective, confirmed the association of serum homocysteine levels with cardiovascular events. Furthermore, homocysteine was shown to have oxidant, inflammatory, procoagulant and mitogenic effects in vitro, and cynomolgus monkeys fed a methionine-rich diet—causing them to develop hyperhomocysteinemia—were shown to have endothelial dysfunction.¹ Additional evidence came from studies showing an association between a methylenetetrahydrofolate reductase polymorphism and cardiovascular event rate.² Such Mendelian randomization studies are considered relatively robust to confounding and support a causal link between plasma homocysteine concentration and the risk of cardiovascular events.

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