Everybody seems to know the importance of cholesterol and preventing heart disease. Although getting the ‘total cholesterol’ into a healthy range is a common goal for you and your doctor – it is mostly about two major component of the total cholesterol – the ‘good’ or HDL cholesterol and the ‘bad’ or LDL cholesterol. Up with the ‘good’ and down with the ‘bad’ is the slogan that applies.
The LDL cholesterol seems to accumulate in the heart vessel walls and contributes to local inflammation with formation and progression of atherosclerotic plaque. Dietary and medication therapies concentrate on lowered the circulating LDL in the blood stream. Lower LDL may cause less plaque progression and inflammation. Multiple published studies have shown that all of the ‘statin’ medications, in conjunction with lowering circulating LDL also reduce the future development of heart attacks (and even strokes) by about 30-40%. The HDL cholesterol works in a manner to ‘pick up’ (like a dump trunk) some of the LDL that has accumulated in the plaque and return it to the liver, where it is metabolized and excreted. The process of plaque development is a balance of LDL getting into the wall of an artery and the HDL trying to pick it up and take it back to the liver for processing.
Niacin (vitamin B3) has been known for years to lower circulating LDL (but NOT to the degree that statins do) and to increase circulating HDL (which statins in general do not do as consistently). A prescription Niacin (represented by the product Niaspan) was developed years ago and shown to slowly release Niacin into the body. Some years ago, a well known research study done in Seattle (the HATS trial) showed a 35% reduction in future heart attacks with a low dose statin – but a 70% reduction in heart attacks if the patient took BOTH a statin and Niaspan. That study seemed to indicate that lowering LDL and raising HDL provided a synergistic benefit. Unfortunately other similar trials failed to produce such spectacular results.
In a recent study, named AIM-HIGH and supported by the NIH, 3,314 individuals with known cardiovascular disease were first treated very aggressively with statins resulting in a major reduction in LDL levels and then were randomized to treatment with or without Niacin. During the 32-month follow-up period, there were 28 strokes (1.6%) in the Niacin group vs 12 strokes (0.7%) in the control group. But, nine of the strokes in the niacin group occurred after the drug had been discontinued. The safety monitoring board about a month ago then stopped the trial. A press conference on the ‘reasons’ to stop the trial resulted in sales for Niaspan plummeting in the next several weeks.
A press conference and the eventual rigorously reviewed publication of a scientific investigation are not the same thing. As a consequence, many experts in cholesterol management have unanswered questions about the data and are not willing to accept the ‘court of public press’.
Just the same, many of these experts suggest that they may have to at least think a bit harder about adding Niacin to a statin drug IF the LDL has already been reduced to a very low level (now considered to be <70 mg/dl). However, they all agree that if such an LDL goal cannot be attained in patients with known cardiovascular disease through diet and statins alone – they see no problems with adding on Niacin to assist lowering the LDL and potentially increasing the HDL.
The goal of lowering an individual’s risk to of plaque development and slowing down plaque progression is done with multiple angles of attack – proper diet, attaining a proper weight and body composition, regular aerobic and resistance training, and treating to appropriate cholesterol levels. The primary goal is to get the LDL cholesterol as low as possible and if that is achieved many experts suggest that adding Niacin may not provide added benefit; however, if the LDL goal cannot be achieved that adding on Niacin to assist with further lowering LDL (and perhaps raising HDL) is still quite clinically appropriate.
John A. Rumberger, PhD, MD, FACC
Director of Cardiac Imaging &
Director of the Lipid Management Program
The Princeton Longevity Center
