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Why We Need a Trial Now

Meir J. Stampfer, MD, DrPH; Eric B. Rimm, ScD

JAMA. 1996;275(24):1929-1930.

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

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 . . . [Full Text PDF of this Article]

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.

Footnotes
Reprints: Meir Stampfer, MD, DrPH, Channing Laboratory, 180 Longwood Ave, Boston, MA 02115.

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