Current guidelines for the prevention of CAD (coronary artery disease) focus on lowering LDL-C levels, although recently there has been a lot of interest in HDL-C as a secondary target of therapy. High levels of LDL-C appear to be strongly correlated to an increased risk of CAD because LDLs are intimately linked to oxidative and inflammatory processes in the arterial wall. Raising HDL-C levels might also afford opportunities to lower this risk, especially in patients with pre-existent atherosclerosis. HDL-C is protective against atherosclerosis, largely due to its function of reverse cholesterol transport as well as its role in fibrinolysis, antioxidant functions and reduction of platelet aggregability (clumping).
Niacin (nicotinic acid) is the most potent HDL-C raising agent currently on the market, followed by fibrates. Niacin can be purchased over the counter. Niacin lowers the levels of all three atherosclerotic lipoproteins--VLDL, LDL and Lp(a), and in addition it raises HDL-C more than any other pharmacologic agent presently available. It inhibits fat-mobilizing lipolysis in adipose tissue, leading to a lowering of free fatty acids, which has many metabolic implications. Recently, a nicotinic acid receptor has been identified, and the drug has been found to stimulate the expression of the ABCA 1 membrane cholesterol transporter. Lipid-modifying monotherapy with the use of pharmacologic agents known as statins (which help to lower LDL-C) may be potentiated by the use of niacin as well.
You will no doubt hear more about this wonder drug in the future.