9. The Evidence of Statin Damage to Muscles

Typically in America, if a person fails a stress test or suffers from a heart attack and then is found to have a blocked coronary artery, a stent will be introduced to correct the problem and high-dose statin therapy will be initiated, with the expectation that the drug will be needed for the rest of their life. The accepted belief today is that, no matter whether their cholesterol is already low, high-dose statin therapy will yield sufficient benefit to offset any side effects it might cause. At the same time, these patients are encouraged to spend up to an hour a day exercising on a treadmill, since exercise has been shown to be highly beneficial to heart disease prognosis. The exercise, in conjunction with the metabolic deficiencies induced by the statin drug, are a potentially lethal combination.

Typically, also, the patient is not alerted that a common side effect of statin drugs is muscle pain and muscle weakness. It is often the case that such symptoms don't appear immediately. In fact, it can sometimes be years before statin therapy leads to enough damage to cause obvious symptoms. By that time, the person may well believe that the pain and weakness are simply a consequence of getting older.

It has been widely claimed, and statin users seem to have embraced this concept, that, as long as you monitor your enzyme levels, you can simply terminate statin therapy if the enzymes get too high, and all will be well. However, judging from some of the sad stories that are showing up in comment pages all over the web, this has turned out not to be the case for some people.

An article published in July, 2009 [27] investigated the association between physical muscle damage and patients' complaints of muscle weakness or pain. Patients who reported weakness said, for example, that it was difficult to get up from a seated position without arm support. Those who reported pain generally said that it was worse after physical exercise. Only one out of 44 patients examined developed overt rhabdomyolysis, with the serum level of the muscle enzyme creatine kinase measured at 57,657 U/L. This patient required hospital treatment for management of his pain.

The authors were interested in investigating the extent to which muscle damage could be seen through muscle biopsy for these patients. They compared them with 20 patients who had never taken a statin drug. Twenty five of the 44 patients taking statins had clear muscle damage. None of the 20 controls had any evidence of damage. Other than the one patient with overt rhabdomyolysis, none of the others had muscle enzyme levels above the cut-off considered the upper level of "normal." For those patients with injuries, on average 10% of their fibers were injured. The authors concluded that the lack of elevated levels of creatine kinase does not rule out structural muscle injury.