Coenzyme Q 10 and statins: Biochemical and clinical implications

Abstract

Statins are drugs of known and undisputed efficacy in the treatment of hypercholesterolemia, usually well tolerated by most patients. In some cases treatment with statins produces skeletal muscle complaints, and/or mild serum CK elevation; the incidence of rhabdomyolysis is very low. As a result of the common biosynthetic pathway Coenzyme Q (ubiquinone) and dolichol levels are also affected, to a certain degree, by the treatment with these HMG-CoA reductase inhibitors. Plasma levels of CoQ 10 are lowered in the course of statin treatment. This could be related to the fact that statins lower plasma LDL levels, and CoQ 10 is mainly transported by LDL, but a decrease is also found in platelets and in lymphocytes of statin treated patients, therefore it could truly depend on inhibition of CoQ 10 synthesis. There are also some indications that statin treatment affects muscle ubiquinone levels, although it is not yet clear to which extent this depends on some effect on mitochondrial biogenesis. Some papers indicate that CoQ 10 depletion during statin therapy might be associated with subclinical cardiomyopathy and this situation is reversed upon CoQ 10 treatment. We can reasonably hypothesize that in some conditions where other CoQ 10 depleting situations exist treatment with statins may seriously impair plasma and possible tissue levels of coenzyme Q 10. While waiting for a large scale clinical trial where patients treated with statins are also monitored for their CoQ 10 status, with a group also being given CoQ 10, physicians should be aware of this drug-nutrient interaction and be vigilant to the possibility that statin drugs may, in some cases, impair skeletal muscle and myocardial bioenergetics.