Homocysteine and cardiovascular risk

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Abstract
The homocysteine theory of atherosclerosis, based originally on the presence of cardiovascular disease (CVD) in those with inborn errors of homocysteine metabolism (1), has in recent times had a few reversals. These relate principally to the pattern that has emerged from many studies. Although virtually all the retrospective and most of the prospective case-control studies showed associations between even modest elevation of plasma total homocysteine (tHcy) and CVD, several large and apparently well-conducted prospective studies did not find this association. Furthermore, the presence of the so-called thermolabile polymorphism of the gene for the folate-dependent enzyme methylene tetrahydrofolate reductase (MTHFR), which is known to be associated with elevated tHcy, does not appear to carry a higher risk of CVD. These issues are addressed in 2 Perspectives in this issue of the Journal from opposite standpoints by 2 groups at the forefront of research in this area.

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