A study published recently in the Journal of Cachexia, Sarcopenia and Muscle raises concerns about a possible side-effect of long-term statin drug use: a significant decline in muscle mass and function.
The study assessed data from nearly 300,000 participants in the UK BioBank – approximately 260,000 non-statin users and nearly 40,000 statin users. (The UK Biobank is a prospective cohort of approximately half a million middle-aged and older participants across the United Kingdom. Baseline data collection occurred between 2006 and 2010, and included sociodemographic and lifestyle information, medical history, medication use, physical measurements, and biological samples.)
Researchers determined that compared to those who had never taken statins, continuous statin users displayed a 25% decline in grip strength and a 73% decline in appendicular lean mass, and this was irrespective of genetic susceptibility to statin response.
Compared to non-statin users, as a group, statin users were older (61 vs. 56 years), had a larger percentage of males (63% vs. 43%), had a higher BMI (29 vs. 27), and were more likely to have co-morbidities, such as diabetes or hypertension. However, even after adjusting for these and other factors, statin use was still associated with weaker grip strength and less appendicular lean mass. These measurements declined over time in non-statin users as well, but the decline was steeper among those continuously taking statins.
Several mechanisms were proposed as potentially influencing the decline in muscle mass and strength, such as reduction in isoprenoids and coenzyme Q10, which could contribute to mitochondrial dysfunction, inhibition of protein synthesis, and muscle atrophy. Additional mechanisms include increased apoptosis, disruption of calcium homeostasis and general myotoxicity (reflected by elevated creatine kinase levels). Researchers also speculated that beyond being directly harmful to muscle tissue, statins may aggravate insulin resistance and risk for type 2 diabetes, as well as accelerate aging and influence broader pathological outcomes. They noted, “These pathways suggest that statin- related muscle decline is not an isolated effect on muscle fibres, but part of a wider spectrum of metabolic disturbances.”