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Life Extension Magazine
LEF Magazine May 1998

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Direct From JAMA


image Here is the abstract summarizing the study on the impact of vitamin B6 and folic acid on heart disease, as published in the Feb. 4, 1998, Journal of the American Medical Association. It is accompanied by a note from JAMA.

"Folate and Vitamin B6 From Diet and Supplements in Relation to Risk of Coronary Heart Disease Among Women." Eric B. Rimm, Sc.D.; Walter C. Willett, M.D., Dr.PH.; Frank B. Hu, M.D., Ph.D.; Laura Sampson, M.S.; Graham A. Colditz, M.B., B.S., Dr.PH.; JoAnn E. Manson, M.D., Dr.PH.; Charles Hennekens, M.D., Dr.PH.; Meir J. Stampfer, M.D., Dr. PH., JAMA. 1998;279:359-364

Context. Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6. However, prospective data relating intake of these vitamins to risk of coronary heart disease (CHD) are not available. Objective. To examine intakes of folate and vitamin B6 in relation to the incidence of nonfatal myocardial infarction (MI) and fatal CHD. Design. Prospective cohort study.

Setting and Patients. In 1980, a total of 80,082 women from the Nurses' Health Study with no previous history of cardiovascular disease, cancer, hypercholesterolemia, or diabetes completed a detailed food frequency questionnaire from which we derived usual intake of folate and vitamin B6. Main Outcome Measure. Nonfatal MI and fatal CHD confirmed by World Health Organization criteria.

Results. During 14 years of follow-up, we documented 658 incident cases of nonfatal MI and 281 cases of fatal CHD. After controlling for cardiovascular risk factors, including smoking and hypertension, and intake of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69 (95 percent confidence interval [CI]), 0.55-0.87 for folate (median intake, 696 µg/d vs. 158 µg/d) and 0.67 (95 percent CI, 0.53-0.85) for vitamin B6 (median intake, 4.6 mg/d vs. 1.1 mg/d). Controlling for the same variables, the RR was 0.55 (95 percent CI, 0.41-0.74) among women in the highest quintile of both folate and vitamin B6 intake, compared with the opposite extreme. Risk of CHD was reduced among women who regularly used multiple vitamins (RR=0.76; 95 percent CI, 0.65-0.90), the major source of folate and vitamin B6, and after excluding multiple vitamin users, among those with higher dietary intakes of folate and vitamin B6.

In a subgroup analysis, compared with nondrinkers, the inverse association between a high-folate diet and CHD was strongest among women who consumed up to 1 alcoholic beverage per day (RR=0.69; 95 percent CI, 0.49-0.97) or more than 1 drink per day (RR=0.27; 95 percent CI, 0.13-0.58).

Conclusion. These results suggest that intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women.

Editor's note. Although the separate pieces of the pathway that connect folate and vitamin B6 to coronary artery disease via homocysteine metabolism have been well studied in both laboratory and epidemiologic investigations, this article is the first to examine the entire pathway in an epidemiologic study. Using data from the Nurses' Health Study, the authors appear to confirm the hypothesis that increased intake of these nutrients may prevent coronary artery disease. However, as is the usual limitation of epidemiologic studies, the association needs further research to define the interactions that further delineate patients in whom the association is particularly strong. The interaction with alcohol intake is particularly intriguing, and if confirmed, may complicate the issue of establishing recommended daily nutrient intakes.

-David H. Mark, M.D., M.P.H.,
Contributing Editor



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