Statin drugs are among the most frequently prescribed drugs in medicine. They are used to lower high levels of blood cholesterol, and secondarily to lower inflammation within blood vessel walls. Ironically, it's become clear recently that the primary preventive effect of statin drugs against the onset of cardiovascular disease (CVD) is their effect on lowering excess inflammation, rather than high blood cholesterol. The notion that lowering blood cholesterol alone is sufficient to prevent CVD is dubious at best, and simplistic. Cholesterol itself is an important substance produced in the liver. It's vital for cell membrane integrity, and serves as the raw material for a variety of hormones, all in the "steroid" category, which means that they are made using cholesterol as the precursor substance. These include testosterone, cortisol, estrogen, activated vitamin D, and others.
Despite the importance of cholesterol, most physicians who treat patients with high blood cholesterol levels will provide a prescription for a statin drug. While higher plasma cholesterol levels can be effectively managed through dietary and exercise modalities, many people aren't motivated enough to engage in these practices. As such, statin drugs are thought to offer an easy mode of protection against the onset of heart attacks and strokes. Again, this is a very dubious concept, since many other things can cause a heart attack or stroke besides an elevated plasma cholesterol level.
But, like any other drugs, statins are not side-effect free. Side effects related to the use of statins can include eye problems, liver abnormalities, and muscle breakdown. In regard to the latter, studies have shown that many people on statin drugs cannot produce any muscular progress from exercise because of an inhibitory effect induced by their statin use. The extent of this effect varies with dose, the specific statin drug used, and individual response to the drugs. This effect of statins on muscle function is known as myopathy, and is more likely to occur with certain statins, most notably simvastatin (Zocor) and mevastatin (Compactin). In contrast, another popular statin, provastatin (Pravachol) rarely causes myopathy.
The cause of statin-induced myopathy is generally attributed to an interference with the synthesis of coenzyme Q10, which is important in the function of mitochondria, local cell structures that, among other functions, produce energy and oxidize fat in muscle. Statins work by inhibiting an enzyme in the liver called HMB-COA-Reductase, which is the rate-limiting enzyme for cholesterol synthesis. But this enzyme is also involved in the same pathway that also produces COQ10, and by inhibiting this pathway, statins prevent the synthesis of Q10, which results in myopathy.
This suggests that anyone who is using statin drugs should also supplement their diet with pre-formed Q10. Despite this obvious solution to the statin/myopathy problem, most cardiologists do not often suggest that their patients on statins also use Q10 supplements. The reason for this is that some studies show that the myopathy side effect of the drugs is relatively rare. But the interference with muscle progress from exercise is far more common and subtle, and is often blamed on things other the statin drugs. Why doctors would be reluctant to suggest that patients on statins consider using Q10 supplements is strange, considering the low expense and side effect profile of Q10.
One study published two years ago found another solution to the statin-myopathy problem that isn't well-known. This study involved exposing isolated muscle cells first to statin drugs alone, then to cells exposed to statins, followed by exposure to insulinlike growth factor-1 (IGF-1). IGF-1 is an anabolic hormone, produced both in the liver under the aegis of growth hormone release, as well as directly in muscle. The local IGF-1 produced in muscle plays a primary role in promoting the activity of satellite cells, muscle stem cells required to repair and build muscle. In the new study, when muscle cells were exposed to statin drugs, the drugs reduced muscle proliferation an average of 50 percent. But when the muscle cells were then treated with IGF-1, all statin-induced negative effects on muscle were completely blocked.
While providing Q10 supplements to those on statin drugs would be the simplest solution to the statin-induced myopathy problem, it may not work for everyone. However, IGF-1 may be the ultimate solution to the problem. And you may not need to inject actual IGF-1 to get the benefits. IGF-1 is also significantly boosted by resistance exercise, as well as DHEA supplements. Indeed, various published studies have shown that initial muscle problems induced by exercise in people using statin drugs is often ameliorated within a short time after starting a resistance exercise program. My guess is that it's the IGF-1 from the exercise that is kicking in and thus preventing the excess muscle damage caused by the statin drugs.
Harfmann, BD, et al. IGF-1 protects against statin myotoxicity. Med Sci Sprts Ex 2011;43:372-373.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
