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Folic acid supplements and fortified breakfast cereals can reduce homocysteine levels and ischemic heart disease risk

High levels of homocysteine in the blood have been confirmed as a major risk factor for ischemic heart disease and other vascular disorders. Increases in consumption of folate are known to reduce plasma homocysteine (tHcy). Dietary folates consist of a mixture of polyglutamated compounds of folic acid, in contrast to simple monoglutaed folic acid. Riddell et al., in a study in The American Journal of Clinical Nutrition, compared three approaches for their effectiveness in increasing the consumption of folates: folic acid supplementation, consumption of folic acid-fortified breakfast cereals, and increased consumption of folate-rich foods. They found that the cereal and supplements provided the best means of lowering plasma tHcy, while an increase in folate-rich foods yielded an insignificant reduction in tHcy.

Study participants included sixty-five free-living individuals ages 36-71 with elevated serum homocysteine concentrations. Prior to dietary intervention, the volunteers were asked to follow a fat-modified diet (30% of energy from fat) for two weeks. Thereafter, they were assigned either to a control group or to one of the three dietary intervention groups over a 12-week period: 600 mg of folic acid in tablet form each day; 600 mg folic acid per day from commercially available folic acid-fortified cereals; and increased consumption of folate-rich foods. While serum folate increased significantly in all three intervention groups, only the cereal group and the supplement group experienced significant decreases in tHcy, 24% and 21% respectively, potentially translating into 30-40% decreases in ischemic heart disease risk. In accounting for the lesser effectiveness of adding folate-rich foods to the diet, the authors point out that as little as 50% of naturally occurring folate maybe available from a mixed diet.

This study is the first to compare the effects of similar amounts of folate derived from different sources and its effect on homocysteine
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Contact: Beth M. Wettergreen
bmwettergreen@ucdavis.edu
530-754-7528
American Journal of Clinical Nutrition
29-May-2000


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