In previous articles I have cited possible mechanisms of statin associated muscle damage from cell wall breakdown to fundamental changes in essential transcriptases.
By Duane Graveline, M.D., M.P.H.
Now we have we have a mechanism of statin action just reported that points directly at cholesterol lowering per se within the muscle fiber as the offending action and the vital changes of muscle structure occur with or without muscle symptoms and occur in most statin users!
In the Journal of Pathology 210: 94-102, 2006, Draeger A and others of the University of Bern, Switzerland report: Statin therapy induces ultrastructural damage in skeletal muscle in patients without myalgia.
Muscle pain and weakness are frequent complaints in patients treated with statins drugs, also known as HMG CoA reductase inhibitors. Many patients with myalgia have Creatine Kinase (CK) levels that are either normal or only marginally elevated and no obvious structural defects have been reported with myalgia only.
Draeger's group did skeletal muscle biopsies from statin treated and non-statin treated patients and examined them using electron microscopy and biochemical approaches. They reported clear evidence of skeletal muscle damage in statin treated patients despite their being asymptomatic. Although the degree of overall damage was minimal, it was the characteristic pattern of damage, including rupture of critical structures that caught the attention of the investigators.
These findings support the hypothesis that statin induced cholesterol lowering per se contributes to myocyte damage and suggests further that it is the specific lipid/protein organs of the skeletal muscle itself that renders it particularly vulnerable.
Was it only a decade ago that that the drug companies were reporting the possibility of up to 2% incidence of muscle damage when statins were used? Then along came the rhabdomyolysis deaths and reported real life myopathy levels much closer to 40% than to 2%, depending upon which team does the reporting. And now it seems that muscle effects might be universal.
Of course this depends upon the sensitivity of the tests being used. Does this remind you of the 100% incidence of cognitive damage in statin users, reported by Muldoon (if sufficiently sensitive testing is done) versus the negligible to no cognitive damage reported by other studies, even those using 80mg doses, based upon more casual observation? None are so blind as those who will not see.
Of course the problem here is one of awareness. With respect to cognitive function, we are not precise creatures. Rarely can we remember what we had for breakfast two days ago or your boss's spouse's name. Because of this natural tendency for forgetfulness we accept imprecision and a 5-10% cognitive loss might be barely noticeable in some. Similarly only athletes might notice a slight deterioration of skeletal muscle function, whereas most of us explain it away as old age or simple deconditioning.
The problem we face is in bringing this new information to the attention of prescribing physicians. As this study demonstrates some of statin damage is occurring in the absence of symptoms.
Does this mean they are not important? I think not.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor