FOLIC ACID ROLE IN LOWERING HOMOCYSTEINE LEVELS
This article was originally published in The Tan Sheet
FOLIC ACID ROLE IN LOWERING HOMOCYSTEINE LEVELS indicates a potential use for preventing heart attacks, Meir Stampfer, MD, Harvard School of Medicine, suggested at the Council for Responsible Nutrition's annual conference on Sept. 22. Stampfer reported that an analysis of blood samples from participants in the Health Professionals Follow-Up Study revealed higher levels of homocysteine in heart attack patients than in controls. "In most cases," Stampfor reported, "our study indicates that men with high homocysteine levels can have those levels normalized with folate supplements." The "corollary," he continued, is that folate supplementation has the "potential impact . . . to reduce risk of heart disease through this mechanism." Stampfer reported that people with homocysteine levels at the top 5% had an excess risk of myocardial infarction that was "quite substantial." He noted that the risk of MI was "more than three- fold higher" for individuals whose homocysteine levels were at the highest 5% versus individuals with normal levels. "The three main co-factors for metabolism of homocysteine are vitamin B, vitamin B and folate," Stampfer said. "In particular," he noted, "our findings indicate that high levels of folate supplements [between 400 mcg and 800 mcg] are very effective in reducing high levels of homocysteine." "We've established that high homocysteine is a risk factor; we've established that folate can reduce homocysteine levels. What's missing is to show that if you lower the level, you indeed lower the risk," Stampfer said. Stampfer's findings are based on blood samples from about two- thirds of the 39,910 men participating in the Health Professionals Follow-Up Study that are being analyzed by his research group for predictors of cancer and heart disease risk under a National Cancer Institute grant ("The Tan Sheet" May 24, p. 10). Stampfer said his group was able to identify 271 incidences of myocardial infarction that occurred in the five years after the Health Professionals Follow-Up Study and 271 matched controls who had remained free of a cardiac event and were similar in age and smoking habits. Acknowledging that the difference in mean homocysteine levels between cases and controls appears to be minor, Stampfer declared that, "in fact, it is a statistically significant difference, with the cases having a significantly higher level of homocysteine than the controls." He pointed out that individuals born with a genetic defect that allows homocysteine to increase to very high levels generally die from cardiovascular disease in their teens or younger. Calling for further studies, particularly in women, Stampfer reported that his group is attempting to replicate the homocysteine findings in women using blood samples obtained from participants in the Nurses' Health Study. "The second thing we need," he added, "are . . . randomized, placebo-controlled trials giving folate or placebo" to individuals with high homocysteine levels.
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