Does Coenzyme Q10 Supplementation Mitigate Statin-Associated Muscle Symptoms?

Pharmacological and Methodological Considerations

Beth A. Taylor


Am J Cardiovasc Drugs. 2018;18(2):75-82. 

In This Article

Abstract and Introduction


Statin drugs markedly reduce low-density lipoprotein cholesterol and consequently the incidence of cardiac events. In approximately 5–10% of adults, these drugs are associated with a range of muscle side effects such as muscle pain, cramping and weakness. Reduction in mitochondrial coenzyme Q10 (CoQ10), or ubiquinone, has been proposed as a mechanism for these statin-associated muscle symptoms (SAMS), and thus various formulations of CoQ10 are marketed and consumed for the prevention and treatment of SAMS. However, data supporting the efficacy of CoQ10 are equivocal, with some studies showing that CoQ10 supplementation reduces the incidence and severity of SAMS and others finding no beneficial effects of supplementation. Methodological and pharmacological issues may confound interpretation of data on this topic. For example, many patients who report SAMS, such as those who have been enrolled in previous CoQ10 studies, may be experiencing non-specific (nonstatin-associated) muscle pain. In addition, the effectiveness of oral CoQ10 supplementation to increase mitochondrial CoQ10 in human skeletal muscle is not well established. This manuscript will critically evaluate the published data on the efficacy of CoQ10 supplements in the prevention and treatment of SAMS.


Approximately 30% of US adults have elevated low-density lipoprotein cholesterol (LDL-C), which doubles their heart disease risk.[1] Hydroxy-methyl-glutaryl (HMG) coenzyme A (CoA) reductase inhibitors or statins are the most effective medications for reducing LDL-C and reduce cardiac events by 20–44% in both coronary artery disease (CAD) patients[2] and in previously healthy subjects.[3] Statins are so effective that they are the most prescribed drugs in the USA and the world. The release of the 2013 American College of Cardiology and American Heart Association (ACC-AHA) guidelines for the treatment of cholesterol is likely to expand the use of statins. Comparing the recent 2013 ACC-AHA guidelines to the prior Third Adult Treatment Panel (ATP III) of the National Cholesterol Education Program guidelines suggests that the number of US adults eligible right now for statin therapy has increased from 43.2 million (37.5% of US adults) to 56.0 million (48.6%).[4] Much of this increase has occurred in older adults. According to the Centers for Disease Control, 26% of US adults > 40 years of age and 48% of adults > 75 years of age report using a cholesterollowering drug, with 93% of respondents using a statin.[1]

Statins are well-tolerated in most adults, with few serious adverse effects, but are frequently associated with mild muscle complaints, termed statin-associated muscle symptoms or SAMS, including myalgia, cramps and weakness. SAMS are widely perceived to be more prevalent in women and older adults, although data do not consistently support this perception.[5–8] Muscle side effects are a concern because they reduce medication compliance, decrease quality of life, reduce physical activity, muscle strength, and ability to perform activities of daily living, and result in preventable cardiac events.[9–15] The impact of SAMS is particularly relevant because, as stated earlier, increasing numbers of older adults are being prescribed statins. Older adults may already be vulnerable to muscle decrements associated with age, disease, and sarcopenia, and cannot afford to have additional impairments in strength, muscle activity, quality of life, and functional independence.

The effect of SAMS on statin compliance is particularly worrisome. The majority (~ 60%) of adults who discontinue statins report SAMS as the primary reason for statin nonadherence and discontinuation.[16] Patients stopping statins have a markedly increased risk of cardiovascular events.[12–15] Moreover, statin adherence is inversely associated with healthcare costs, as patients who are less adherent to statin therapy incur greater healthcare costs associated with a higher rate of cardiovascular events.[11,15] Furthermore, the cost of statin replacement medications, such as the new subtilisin/kexin rather than subtilisin kexin inhibitors, are so expensive that they threaten the financial health of insurance plans. Effective treatment strategies for SAMS will serve to increase the number of patients using these life-saving statins, thereby increasing statin adherence and reducing the costs of avoidable cardiovascular events and new, expensive, lipidlowering therapies.