Vladutiu and others recently demonstrated the surprising finding of an increase in the frequency of genetic carriers for metabolic muscle diseases in patients with severe statin myopathy.
In a series of 136 patients with statin myopathy, 10% had mutations causing one of the following metabolic muscle diseases compared with only 3% in a statin-tolerant control group (p=0.04). An increase was found in the carrier frequency of myophosphorylase deficiency, also known as McArdle disease, that was 20-fold higher in patients with statin myopathies compared to statin-tolerant controls.
The number of carriers for CPT II deficiency among statin myopathy patients was increased 13-fold. The actual number of mutations for these disorders among patients with statin myopathy was increased 4-fold over controls (p<0.0001). It is clear that carriers for certain metabolic muscle diseases appear to be increased among individuals who develop statin myopathy and many of them were never symptomatic before taking statins.
Even in the absence of carrier states there is a certain risk of severe muscle inflammation when statins are used. It is somehow in the biochemical nature of the statins. In the statin known as Baycol®, manufactured by Bayer, this tendency for muscle inflammation was particularly extreme resulting in nearly one hundred rhabdomyolysis deaths before being removed from marketing in 2004. However the tendency remains with use of other statins and there is little public or professional awareness that hundreds of cases of severe muscle inflammation still occur annually contributing to 20 deaths in each of the past 5 years just from Lipitor® alone. When known carrier frequency for metabolic myopathies are added to the purely statin associated numbers the results can be surprising.
Imagine the problems statin users in the United Kingdom face each day with over the counter availability of statin drugs, rarely suspecting they may be carrying one of more abnormal genes that when combined with statins will result in serious and even lethal muscle inflammation. There already is a degree of risk for statin associated muscle inflammation when one is free of these predisposing genetic characteristics but for genetic carriers of these abnormal traits the risk appears to be compounded.
Most investigators speculate that interference with cholesterol metabolism, by statin drug interference of the mevalonate pathway, disrupts the mitochondrial membrane, in which cholesterol is a necessary component. I have stated many times before that all statins are reductase inhibitors and as such inevitably inhibit the synthesis of CoQ10, a vital component of cell wall membrane presenting another mechanism, that of CoQ10 deficiency, for mitochondrial membrane failure.
Needless to say mechanisms for statin damage abound, prompting one admitted statin basher to email me:
"Sounds like 'blame the patient' again. It's not the statins; it's the genetic inferiority of the 'mutant' patient. And it's not the doctors' fault that the patient might be crippled and disabled for the rest of their lives, either, because routine screening is "not cost effective or widely available and may not make sense on a population level."
One wonders as I plow through study after study of statin mechanisms of damage.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor