Vladutiu and others recently demonstrated the surprising frequency of genetic carrier state for metabolic muscle diseases. Naturally, when one of these unsuspecting carriers is prescribed statins, muscle damage of varying degrees can be expected to result.
In her series of 132 patients with statin myopathy. 36% had at least one genetic abnormality and 30% had more than one abnormality. Vladutiu reported the increase in carrier frequency of myophosphorylase deficiency was 20-fold in patients with statin myopathies compared to normal controls (p<0.0001).
Similarly, carnitine palmitolytransferase (CPT II) deficiency was 11 times higher in statin myopathy patients compared to normal controls (p<0.0001). This means that the rate of statin myopathy can be expected to be 10 to 20 times more common in those with underlying and usually unsuspected genetic metabolic abnormalities.
Imagine the problems statin users in the United Kingdom are encountering with over the counter availability of statin drugs, little suspecting they may be carrying one of more abnormal genes that when combined with statins will result in serious muscle inflammation.
There already is a substantial 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 is greatly 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.
Readers may recall 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."
Are we apologizing for statins? One wonders as reason after reason for statin damage is discovered.
"Clearly professional athletes are among the mutants whose fault it is that statins disable, as they are explicitly precluded. Because they are more likely to be harmed or because they have ready access to high priced lawyers and can demonstrably and easily show economic harm from statin disability?"
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
