CoQ10 and L-carnitine for Statin Myalgia?

James J DiNicolantonio


Expert Rev Cardiovasc Ther. 2012;10(10):1329-1333. 

In This Article

Statin Effects on CoQ10 Levels


A total of 34 patients were followed for 30 days to determine if CoQ10 blood concentrations were affected by atorvastatin.[7] Mean baseline blood concentrations of CoQ10 were 1.26 µg/ml. After 30 days of atorvastatin, blood concentrations of CoQ10 were significantly decreased by 49.2% (0.62 µg/ml; p < 0.001). The authors concluded that just a short exposure to atorvastatin caused a significant decrease in CoQ10 blood concentrations and that the decrease in blood CoQ10 levels may explain the myalgia and exercise intolerance associated with statin use. The authors also noted that it might a reasonable option to add CoQ10 to a patient on a statin, particularly if they are on atorvastatin.[7]


It has been postulated that hydrophilic statins may cause less myalgias compared with lipophilic statins because they do not undergo passive diffusion into tissues. Pravastatin, a hydrophilic statin, may be the optimal choice for eliminating statin-associated myalgias. Pravastatin is not metabolized by CYP3A4 and certain over-the-counter, and prescription medications can inhibit this enzyme, leading to an increase in statin concentrations and thus an increased risk for statin myalgias. Most of the time, myalgias in patients on a statin can be attributable to drug–drug or drug over-the-counter interactions. In this setting, pravastatin has an advantage over other statins since it is not metabolized by CYP3A4. Therefore, choosing pravastatin first or switching a patient who has started experiencing muscle pains on a different statin to pravastatin may be a reasonable option. Moreover, pravastatin seems to have the smallest effect regarding reducing CoQ10 levels in the body.[8–12]

Rosuvastatin: Case Report

Rosuvatatin is mainly metabolized by CYP2C9 and CYP2C19. It has been proposed that inhibition of rosuvastatin's intestinal metabolism can increase its concentrations in the body. This is logical considering that 90% of a rosuvastatin dose is excreted unchanged by the fecal route.[12] Grapefruit juice and pomegranate juice inhibit intestinal CYP3A4, and grapefruit juice also inhibits small bowel CYP3A5. A case report showed that a patient who started ingesting approximately 6 ounces of pomegranate juice twice weekly on rosuvastatin presented with a CK level of 138,030 U/l 3 weeks later.[12] Tropical fruit juices such as pomegranate juice may inhibit intestinal CYP2C9 or CYP2C19 and may need to be avoided if a patient is on rosuvastatin. It has been shown that muscle pains associated with statins are directly correlated with the dose. If the statin concentrations are increased, there is a greater chance that a patient will experience muscle pain. Many patients on statins also take concomitant verapamil or diltiazem. It might be a reasonable approach to switch these patients to a non-CYP3a4-metabolized statin such as pravastatin, rosuvastatin or fluvastatin or change verapamil/diltiazem to amlodipine if appropriate.[8–12]