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How Great Is the Hazard?

Peter W. F. Wilson, MD

JAMA. 2002;288:2042-2043.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In this issue of THE JOURNAL, 2 meta-analyses critically review the coronary heart disease (CHD) risks related to blood levels of homocysteine and a common variant of methylene tetrahydrofolate reductase (MTHFR), a gene that is known to be an important regulator of homocysteine metabolism.^1-2 The authors summarize data on the potential effects of this genetic variant and plasma homocysteine levels on CHD risk and conclude that the risks are increased modestly. While the authors do not recommend new approaches to evaluate persons at risk for CHD, the study findings do provide a perspective on how scientists assess the utility of newer biomarkers and genetic factors that may contribute to CHD risk.

The article on homocysteine levels by the Homocysteine Studies Collaboration concludes that the evidence of a link between higher homocysteine levels and CHD risk is weaker than previously reported in summary analyses, . . . [Full Text of this Article]

Author Affiliation: Boston University School of Medicine, Boston, Mass.

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