Statins weaken muscles by design
Posted by Henry Bauer on 2013/04/06
Muscle pain, rhabdomyalgia, is a common effect of statins. What statins can do to muscle caused Baycol (Bayer’s statin, cerivastatin) to be withdrawn from the market after many deaths from rhabdomyolysis, the physical breakdown of muscle. Statins affect muscles inevitably because the mechanism by which statins lower cholesterol production is the same mechanism that fuels energy production.
Statins reduce manufacture of cholesterol by inhibiting an enzyme, HMG-CoA reductase, which produces mevalonate on the way to making cholesterol. However, mevalonate is also a precursor to — among other things — Coenzyme Q10, CoQ10, ubiquinone. The latter is an essential part of the processes by which mitochondria, the energy-producing modules in every animal cell, do their work; the “ubi” in “ubiquinone” reflects that the substance is ubiquitous throughout the body. So lowering of energy, weakness, is a direct effect of statins, just as direct as the effect on cholesterol production. Muscle pain and muscle weakness, including weakness of the heart muscle, is not a “side” effect of statins, it’s a direct effect.
Here’s a pertinent story.
I had met T. a dozen years ago. We discovered many points of similarity in background, though he was a few years younger than me. We both swam regularly on weekday mornings, and became fairly regular partners at bridge. Like so many others, T. was on statins to lower his cholesterol.
He was quite competitive, including at swimming, and for several years he was always significantly faster than me. A few years ago, I began to be able to hold my own; even though my own pace was getting slower as I aged, he was slowing more and faster than I was.
About a year ago, T. slowed drastically, and about 6 months ago he stopped swimming altogether because it had become too strenuous for him. Neither his family physician nor his cardiologist mentioned that the statins he was taking might be a reason for his increasing weakness.
Two or three years ago, T.’s blood sugar had been regarded as being a bit high (which is another known “side” effect of statins). He was prescribed Avandia, but soon stopped taking it in view of unpleasant “side” effects (which are known to include risk of heart failure).
A couple of years ago, at a regular doctor’s visit, T.’s electrocardiogram showed an abnormality that was immediately diagnosed as atrial fibrillation. T. was prescribed coumadin, but when Pradaxa hit the market, T. was switched to that. At the next doctor’s visit, his cardiogram was normal, no sign of fibrillation. He was told that this could happen from this medication, something not to be found in the literature. What is to be found in the literature is that Pradaxa offers a significantly increased risk of heart attack. Anyway, T. was taken off it again when he couldn’t stand its gastric “side” effects.
Users of both Avandia and Pradaxa can sign up to join class-action lawsuits for damage done by the drugs.
A month ago T. became so weak that he was taken to hospital. A pacemaker was installed. He died a week later.
Such stories, “anecdotes”, are not supposed to be scientific evidence. T.’s death certificate just says congestive heart failure; indeed during his last two weeks of life he did suffer much fluid build-up in his legs, a typical symptom. I can’t help but believe, however, that T. was killed by many years of statin intake, possibly abetted by shorter periods on Avandia and Pradaxa — neither of which might have been prescribed had he not been taking statins with their known effects on blood sugar and heart muscle.
I think one may legitimately speculate about the number of deaths ascribed officially to heart failure without taking into account the medications that had been taken and which are known to carry risk of heart failure. Doctors trust, as they must, the information they receive from official sources, and from drug-company representatives who, after all, can tout only drugs that have been approved by the Food and Drug Administration. So when doctors treat someone for heart problems, including “high” cholesterol or “high” blood pressure or “high” blood sugar, and that person gets worse and dies, it is only natural to blame the underlying “heart disease” and not the drugs. I suggest that the death toll from prescription drugs is greatly under-reported for this sort of reason.
On a number of occasions, I talked to T. about CoQ10, but I don’t know whether he ever acted on my advice. I didn’t feel that I could nag him too persistently or try to supersede what he was being told by his doctors. I do know that none of them ever mentioned CoQ10 to him. Yet the fact that statins decrease production of CoQ10, and that the latter is an essential factor in energy production, has been very well known to medical science for a long time. That knowledge is even in the popular domain in such places as those health-testing booths in some stores. At my local Sam’s Club, the booth’s screen touts various supplements including CoQ10 which it describes as “particularly helpful” for people taking statins; a convenient euphemism for saying it’s essential, which might not be lawful since the machines are not licensed to practice medicine.
At any rate, it has long been well known that statins decrease the body’s production of CoQ10 and that supplemental CoQ10 can not only limit the damage done by statins but can also independently improve heart function; see for example the 1999 article, “Overview of the use of CoQ10 in cardiovascular disease” (BioFactors 9: 273-84), the 2003 review “The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications” (BioFactors 18: 101-11), and specifically about treating adverse effects of statins: “Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation”, BioFactors 25 (2005) 147-52. Principal authors on all those are Peter H. and Alena M. Langsjoen, who are associated with several Health Centers in Texas. But their insights and conclusions are shared widely among researchers, including those at drug companies. I’ll illustrate that with another story:
A. is an entrepreneurial scientist whom I have known very well indeed for a very long time. He has had an outstandingly distinguished career including election to more than one national academy. CoQ10 has been one of his special interests, he has supervised clinical trials on its use, and he has sought commercial backing to manufacture it in ways more efficient than current ones. Knowing that CoQ10 is invaluable for limiting damage from statins, he has proposed to drug companies that they partner with him to manufacture CoQ10 and to market it in combination with their statin as an obviously superior (and patentable, of course) product. At one company he was enthusiastically supported by the technical staff. But the deal could not be consummated because that company’s legal department ruled against it. Their grounds: Marketing such a product would show that the company had known that it was essential to take CoQ10 whenever using statin but had failed to include this advice or warning in its leaflets and advertisements. Thereby the company would be liable to lose out in law suits.
One can only wish devoutly that statin marketers will nevertheless lose some big lawsuits at some time in the future.
The pamphlets enclosed with statins, like the 22-page one for Merck’s Zocor, make no mention of CoQ10. The Merck leaflet does have some points of definite interest, though, for example:
“Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice”; in other words, as asserted in my earlier posting, one believes conclusions from clinical trials at one’s peril.
Because the below reactions are reported voluntarily from a population of uncertain size, it is generally not possible to reliably estimate their frequency or establish a causal relationship to drug exposure. The following additional adverse reactions have been identified during postapproval use of simvastatin: pruritus, alopecia, a variety of skin changes (e.g., nodules, discoloration, dryness of skin/mucous membranes, changes to hair/nails), dizziness, muscle cramps, myalgia, pancreatitis, paresthesia, peripheral neuropathy, vomiting, anemia, erectile dysfunction, interstitial lung disease, rhabdomyolysis, hepatitis/jaundice, fatal and non-fatal hepatic failure, and depression. There have been rare reports of immune-mediated necrotizing myopathy associated with statin use . . . . An apparent hypersensitivity syndrome has been reported rarely which has included some of the following features: anaphylaxis, angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, dermatomyositis, vasculitis, purpura, thrombocytopenia, leukopenia, hemolytic anemia, positive ANA, ESR increase, eosinophilia, arthritis, arthralgia, urticaria, asthenia, photosensitivity, fever, chills, flushing, malaise, dyspnea, toxic epidermal necrolysis, erythema multiforme, including Stevens- Johnson syndrome. There have been rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These cognitive issues have been reported for all statins. The reports are generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks)” [emphasis added].
That the reports may “generally” be “nonserious” will be of little comfort to those who experience these “side” effects in serious fashion and those whose symptoms do not resolve in the “median” period of 3 weeks — half of all those affected, which is what “median” signifies.
More generally, note how many different unpleasant effects have been reported. That suggests the reports are anything but rare. Recall too that competent analysts have speculated that adverse drug effects are under-reported by something like a factor of 10 (Betty Ann Bowser, “Certain antibiotics spur widening reports of severe side effects”, PBS Report, 16 June 2011).
Once again this posting is long enough, so I leave for another occasion a discussion of the other nasty things statins do besides weakening muscles.