Niacin in the treatment of dyslipidemia

I use niacin frequently in individuals with mixed dyslipidemia and/or who have not responded to other lipid-lowering agents. Niacin lowers triglyceride, LDL and lipoprotein(a); it is the most potent agent we have to raise HDL. Niacin has been said to be the ideal antihyperlipidemic agent, were it not for its side effects.

I have had only a few patients who could not tolerate prescription extended-release niacin (Niaspan, Abbott Laboratories). I minimize flushing by starting with 500 mg at bedtime and have the patient take nonenteric-coated 325 mg aspirin a half hour beforehand. I reassure patients that flushing will usually improve with time. I increase the dose by 500 mg per month based on response and tolerability, but never more than 2,000 mg per day.

One barrier, however, is that prescription extended-release niacin is expensive and not always covered by insurance because it contains a vitamin as the active ingredient. Some insurance providers will not pay for a vitamin, even if a prescription. Per Lexi-Drugs Online, one month of 2,000 mg Niaspan per day costs $253.92. This is an impossible expense for patients who do not have prescription coverage.

Many pharmacists recommend non-prescription sustained-release dietary supplement niacin (slow niacin) instead of prescription extended release for this reason. It is certainly much less expensive: only $30.36 per month for 2,000 mg day (same source as above).

However, non-prescription sustained-release dietary supplement niacin should not be considered equivalent to prescription extended-release niacin. This is not only because one is regulated by the FDA as a prescription drug and the other is not.

There is a very high rate of hepatotoxicity associated with sustained-release dietary supplement niacin, up to 52%. This has not been seen with dietary supplement immediate-release or prescription extended-release niacin. It is thought that this is caused by the extended-release niacin being metabolized by a low-affinity, high-capacity, conjugative pathway leading to nicotinuric acid. In contrast, sustained-release dietary supplement niacin appears to be metabolized by a high-affinity, low-capacity, oxidative pathway resulting in nicotinamide and other metabolites, some of which are hepatotoxic.

Patients should ideally be prescribed extended-release niacin. If this is not an option and dietary supplements must be used, then it should be immediate release and not sustained release. One problem with immediate-release niacin, however, is the very high rate of flushing which is intolerable for the majority of patients.

There is a non-prescription “no flush” niacin preparation: inositol hexanicotinate. However, no study has shown that it increases serum levels of niacin or beneficially affects lipids. The six molecules of niacin are so tightly bound to the inositol that it is not bioavailable. Thus, “no flush” niacin may well be considered to be “no effect.”

Am J Cardiol. 2007;99[suppl]:22C-31C.