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Niacin treatment increases homocysteine

IHN logo Researchers at the Eli Lilly Research Laboratories and the Oregon Health Sciences University have completed a study designed to determine whether it was the cholesterol-lowering drug colestipol or the niacin that caused the increase in homocysteine levels. Niacin (vitamin B3) has been used effectively to reduce elevated cholesterol levels. Niacin therapy is particularly desirable because it reduces the level of low-density lipoproteins (LDL - the "bad" cholesterol) and increases the level of high-density lipoproteins (HDL - the "good" cholesterol). A recent trial, which evaluated the effect of treating high cholesterol levels with both niacin and the cholesterol-lowering drug colestipol, found that the treated patients increased their blood plasma levels of homocysteine. High homocysteine levels have been associated not only with an increased risk for heart disease, but also with an increased risk for stroke, intermittent claudication, and hypothyroidism.

Their trial involved 52 patients with peripheral vascular (arterial) disease who were randomized to receive a placebo or up to 3000 mg/day of crystalline niacin for 48 weeks. At 18 weeks after the start of the study the average blood level of homocysteine had increased by 55 per cent (from 13.1 micromol/L to 21.1 micromol/L) in the niacin group. This increase is highly significant and according to other research corresponds to an increase in the risk of coronary artery disease of about 80 per cent. Of course, this increase in risk would be at least partially offset by the reduction in risk caused by the cholesterol reduction due to niacin therapy. The researchers point out that homocysteine levels can be effectively lowered by supplementation with folic acid and vitamin B6 and vitamin B12. They urge further studies to determine whether supplementation with these vitamins would be beneficial to patients undergoing long-term niacin therapy.
Garg, Rekha, et al. Niacin treatment increases plasma homocysteine levels. American Heart Journal, Vol. 138, December 1999, pp. 1082-87

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