You may recall that years ago the drug companies wisely predicted that myopathy, defined as muscle inflammation, would be associated with the use of statins.
Unfortunately their prediction of an up to 2% incidence of muscle pain in statin users and prompt regression of discomfort with statin dosage reduction proved to be a masterpiece of understatement as we moved from ongoing drug company studies into the real world.
Then came Baycol®, removed by Bayer after 60 or more deaths from rhabdomyolysis. I have always regarded rhabdomyolysis as the most extreme form of muscle inflammation with muscle cell wall breakdown and release of cellular contents into the blood stream causing secondary kidney tubule blockage.
Despite Baycol's removal from the market, hundreds more rhabdomyolysis deaths from statins have been reported. Medwatch reports an average of 20 rhabdomyolysis death annually, just from Lipitor alone during the past 8 years.
Meanwhile a more objective look at muscle pain complaints would put the 2% drug company figure much closer to 20% in the real world and few athletes can take statins with impunity.
Previously I have mentioned two astronaut friends of mine with not a complaint in the world until they were placed on Lipitor® for modest cholesterol elevation (been there, done that - see my book, Lipitor®, Thief of Memory).
Within a few months muscle pain appeared, so my colleagues stopped their Lipitor only to find that the muscle pain persisted. Four years have now passed with persistence of their muscle pain problem and we can now entertain the diagnosis of permanent muscle pain triggered by statin use.
Whereas previously we were considering CoQ10 deficiency (among other things) now we are forced to consider such causes as mitochondrial mutation. How else does one get permanence?
And during this time study after study has been undertaken by the research community reporting the various mechanisms by which statins can damage muscle function. The most recent is the study by a group at the University of Alabama at Birmingham reporting that statins at higher doses may affect the ability of skeletal muscles to repair and regenerate themselves.
These scientists were examining the proliferative capacity of human satellite cells (SCs) in culture. The team used primary cell lines isolated from quadriceps muscle biopsies. SCs were mixed and grown for 48 hours with several concentrations of Zocor® plus the solvent DMSO (control.)
Special techniques were used to measure cell viability / reproducibility. Additionally the investigators determined the effects of varying concentrations of Zocor on satellite cells in different states of differentiation into true muscle cells. Higher doses of Zocor induced a strong, dose-dependent decrease in the viability of the satellite cells. Additionally, the viability was reduced by approximately half in differentiating cells (cells in which evolution to muscle cells was almost complete).
The team is now looking at effects in an older population where the adverse affects of statins would likely be under-reported because adults may not be able to distinguish between muscle pain related to a statin effect and a pain associated with the normal effect of aging. The researchers' words, not mine.
And all of this is in addition to ongoing research on selenium and muscle cell metabolism, CoQ10 and muscle cell function and the role of dolichols and glycoprotein / muscle metabolism - all established mechanisms by which statins may influence muscle function.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor