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June 26, 1996

Folate and Cardiovascular DiseaseWhy We Need a Trial Now

Author Affiliations

From the Channing Laboratory, Harvard Medical School and Brigham & Women's Hospital (Dr Stampfer), and the Departments of Epidemiology and Nutrition, Harvard School of Public Health (Drs Stampfer and Rimm), Boston, Mass.

JAMA. 1996;275(24):1929-1930. doi:10.1001/jama.1996.03530480071044

In this issue of The Journal, Morrison and colleagues1 provide important new information that fits neatly with the rapidly emerging area of homocysteine, folate, and cardiovascular disease. As comprehensively reviewed last year in JAMA,2 strong and remarkably consistent data have linked elevated levels of homocysteine with increased risk of cardiovascular diseases. The risk appears to be graded across the whole distribution of homocysteine levels and, if causal, would account for a substantial fraction of the incidence of these diseases. Elevated homocysteine levels can be reduced by even modest amounts of folate,3,4 providing a plausible mechanism for the remarkable findings of Morrison et al of a 69% increased risk of coronary mortality among those in the lowest quartile, as compared with highest quartile of serum folate. The findings are similar to previous studies using intermediate end points,5 as well as case-control data5 and preliminary prospective data