Niacin-induced hyperhomocysteinemia, an independent risk factor for arterial occlusive disease

Niacin (nicotinic acid) in its non-physiological dose level, is an effective broad-spectrum lipid-lowering agent. However, the hypolipidemic action of niacin could be potentially negated by its hyperhomocysteinemic effect. Since niacin is excreted predominantly as methylated pyridones, requiring methionoine as methyl donor, the niacin-induced h'yst accumulation in the body is thought to be a reflection of impaired remethylation and transsulfuration of h'yst. The niacin-associated hyperhomocysteinemia is also accompanied by biochemical evidence of vitamins B-6 and B-12, and folate, which are cofactors for the metabolism of h'yst. These untoward effects are reversed by administrations of the B-vitamins without affecting the hypolipidemic action of niacin. Furthermore, an addition of aspirin in the niacin treatment regimen, much of its cutaneous side effects can be alleviated. It seems probable that coronary heart disease can thus be better controlled by a combination of aspirin, niacin, and the B-vitamins as opposed to niacin alone.