If you live in the United States, and your doctor has identified that you are at high risk to heart attacks, he has likely prescribed a high dose statin even if your cholesterol levels are not high. You have likely also been put on a low-fat, low saturated fat diet, and you have been encouraged to work out on a treadmill every day.
My research indicates that, if you rigorously follow all of your doctor's advice, you will be facing severe muscle damage sooner or later. The statin drug's impact on the mitochondria and on the cell walls of the muscle cells is such that even modest exercise can lead to rhabdomyolysis. For some it will be obvious right away that the side effects are too damaging and the statin therapy must be terminated. For others, the damage will happen more insidiously, and will not become apparent until years after statin therapy was initiated. But often patients will find that the symptoms remain after the drug is stopped -- it will be too late to repair the muscle damage. Or, worse, they will develop kidney failure or heart failure as a consequence.
Statin drugs have many adverse side effects, but probably the most frequent complaints concern muscle pain and muscle weakness. In this essay, I have developed a physiological explanation for the mechanism responsible for this side effect. It is due to the fact that statins interfere with the synthesis of not only cholesterol, but also coenzyme Q10 and the dolichols. Statins also reduce the bioavailability to the cells of both fatty acids and all dietary antioxidants, due to the sharp reduction in serum levels of LDL, which delivers these essential nutrients to the cells.
Without sufficient coenzyme Q10, muscle cells suffer from an impaired ability to generate energy to fuel their contractions. They are forced to cannibalize their own proteins to survive. At the same time, powerful oxidative agents are generated which damage the myoglobin in the cell, rendering it both ineffective to transport oxygen and toxic to the cell wall. The oxidized myoglobin, known as "Ferryl myoglobin" is toxic to the fatty acids that are the main component of the cell wall. With insufficient cholesterol in the cell wall, the cell can't hold a charge, and this also causes it to waste energy. The lysosomes are unable to digest debris because they can't maintain a sufficiently acidic environment. The problem is further compounded by profound shortages of cholesterol, which would have offered further protection against oxidative damage to the fatty acids and ion leakage in the cell wall, the mitochondrial wall, and the lysosome wall. Eventually the cell disintegrates and the myoglobin is released into the blood stream. It makes its way to the kidneys, which try to dispose of it. But the Ferryl myoglobin is also toxic to the kidneys, which leads to severe kidney disease.
The low-fat diet and the exercise regime will both increase the likelihood that the statin drug will cause problems. Vigorous exercise increases the energy needs of the muscles, while the low-fat diet reduces even further the bioavailability of fatty acids to replace damaged cell walls. Furthermore, cell walls composed of unsaturated fats are more vulnerable to attack by the Ferryl myoglobin than those composed of saturated fats.
Because the heart is also a muscle, it also suffers from damage due to exposure to statins. This leads to a reduced likelihood of recovering from a diastolic heart attack, and an increased chance of developing heart failure. Damaged cells of the respiratory system lead to an increased risk of both pneumonia and interstitial lung disease, both of which are very dangerous for someone with a weak heart.
The JUPITER trial revealed that the treatment group had a 25% increased risk for diabetes, and I have explained above why this would be true. Diabetes is a significant risk factor for heart disease, so this outcome is disturbing, and one wonders whether the trial was terminated early to avoid making this number even worse. Dr. William Davis, a cardiologist who believes that statins should be a last resort in treating heart disease, has this to say about the JUPITER trial: "I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! 'You need Crestor! See, I told you it was genetic,' says the doctor after attending the nice AstraZeneca-sponsored drug dinner." ( Dr. Davis' Blog Post on JUPITER)
The news has just come out that even children are now being tested for high cholesterol, and it is being suggested that they should be put on a statin drug if they can not control their cholesterol levels (Children Taking Statins??). I find this news to be extremely disturbing, especially since none of the controlled statin trials have been conducted on children. We have no idea what negative consequences statin drugs might have on the developing nervous system of a child. However, it has been shown that statins can completely destroy the nervous system of an embryo .
A remarkable recent publication by Jeff Cable (December, 2009)  analyzes a set of 885 self-reported adverse effects of statin therapy by patients. Although the reports covered a wide range of known side effects of statins, including cognitive impairment, muscle pain and weakness, skin problems and sexual dysfunction, what was most disturbing was the large number of reports of severe neurological damage. Most distressing was the fact that there were a total of 17 reports of ALS with 2 additional reports related to motor neuron deterioration, which he counts together as 1 to give a total of 18. In ALS, nerve cells waste away or die, and can no longer send messages to muscles. This eventually leads to muscle weakening, twitching, and ultimately paralysis. As the disease progresses, swallowing and breathing become difficult. Most victims die within five years of diagnosis.
The author's comments related to neurological disorders and ALS are quoted here: "One fragment of information that was gained from the patient accounts is the apparent incidence of major neurodegenerative diseases which may well have been precipitated by statin therapy. ... The rarest of these conditions is ALS and yet in just 351 reports there were enough cases to have made the prediction (based upon incidence statistics) that an expected three million six hundred thousand accounts would have to be written before eighteen ALS/MND cases would have been revealed. This is such an astonishingly high number of cases to report within such a small participant group that it would be right to ask whether a fundamental error has been made. Absent any error it is also right to ask: What is really happening? What is the real risk posed by statin therapy?"
There is prior evidence from the literature implicating a relationship between statins and ALS -- a study of the FDA's adverse event reports  as well as a study showing that high cholesterol protects against ALS . My next essay will be on the subject of statin drugs' likely adverse effects on the nervous system: I will argue that statins increase risk not just to ALS but to multiple sclerosis, Parkinson's disease, and Alzheimer's.