Statins and Myoglobin: How Muscle Pain and Weakness Progress to Heart, Lung and Kidney Failure

Statin drug use has steadily increased over the last several decades, due to the widespread belief that cholesterol reduction is an important step in preventing heart disease. It is undeniable that statins are effective: they can decrease serum cholesterol levels from over 300 db/ml to well within the normal range in a matter of weeks. For a person who already has normal cholesterol levels, statins can drive their cholesterol down to levels not seen in nature. Statins have also been shown to reduce the relative risk of heart attacks in men in their 50's by as much as 30%, but, because heart attacks are relatively rare for this segment of the population, the absolute risk reduction is only on the order of 2%, a point that is often missed by the person being treated.

All drugs have potential side effects, and with any drug it's a matter of weighing the risk/benefit factors to decide whether the drug is warranted. Statin drugs have a remarkably diverse set of side effects, including cognitive and memory impairment, reduced libido, and muscle pain and weakness. The drug manufacturers claim that the incidence of side effects is relatively rare, but often side effects don't appear until after several months or even years into treatment. In many of these cases, it may not be obvious that the statin drug is the cause of the problem. This is especially true because these side effects can easily be attributed to increasing age. In fact, as I will show later, statin side effects can best be interpreted as an acceleration of the aging process.

In my view, statin drugs are never worth the risk of their side effects. Cholesterol is a vital nutrient, without which mammalian cells can not survive, and it is inconceivable to me that crippling the body's ability to synthesize cholesterol can ever be a good idea. In an excellent and highly informative review article published in 2009, Wainwright et al. [43] developed a strong argument that statin drugs, by depleting cholesterol, lead to a destabilization of cell membranes "from head to toe." This problem, in turn, increases risk to a long list of serious health conditions and diseases, including diabetes, multiple sclerosis, cognitive problems, hemorrhagic stroke, cancer, and even ALS (amyotrophic lateral sclerosis, also known commonly as Lou Gehrig's disease). Their arguments are backed up by references to 85 peer-reviewed journal publications. I have argued in previous essays that statins may increase the risk to Alzheimer's disease, as well as to sepsis, cancer, and heart failure.

The most commonly reported side effects to statin therapy are muscle pain and weakness. If left unchecked, these symptoms can progress to rhabdomyolysis (severe muscle damage) and kidney failure. Muscle weakness in the lungs can lead to breathing difficulties; in the heart it leads to heart failure. Statin users are reassured by their doctors that they can halt statin therapy if their liver and muscle enzymes rise too high. In practice, however, it's possible to suffer irreversible muscle damage (the problem does not go away after the statin therapy is stopped), and this can happen even when the enzyme levels are not above the normal range.

This essay will develop an argument for why, over time, a statin user may become increasingly weak, in some cases to the point of major disability. A key message is that muscles are forced to cannibalize themselves to acquire sufficient energy. But another factor is oxidative damage to muscle tissue, with subsequent disintegration of the cell walls. This is true not only for the skeletal muscles, but also for the respiratory muscles controlling breathing and the heart muscle. With continued abuse, the muscle cells disintegrate, and the debris travels in the blood stream to the kidneys, which can lead to kidney failure.

The rest of this essay will unfold as follows. In the next section, I will explain how statin drugs work, which will also show why they interfere with the synthesis not only of cholesterol but also of other essential biological substances involved in cell metabolism. The following section will present evidence that statins damage muscle cells. Sections 4 and 5 describe the biochemical pathways involved in assuring that muscles have enough energy to effect movement, especially during situations of stress such as extreme exercise. Section 6 describes the condition known as rhabdomyolysis, caused by extreme exercise but also by statin drugs, and the subsequent risk to kidney failure. Section 7 describes the role that myoglobin, a key protein found in muscle cells, plays in the disease process. After a section explaining how cholesterol protects cell membranes from oxidative damage, the four subsequent sections (sections 9-12) will be devoted to the repercussions of statin damage to the muscles, the heart, the lungs, and the pancreas, respectively. Finally, the conclusion section will summarize the essay and provide hints about my upcoming essay on ALS, a physically disabling neurodegenerative disease that is due not to muscle damage per se but to damage of the motor neurons in the spinal cord that transmit signals from the brain to the skeletal muscles.