The Impact of Statins on Skeletal Muscle-Myalgia and Myopathy 

A particular interest in our lab has been the impact of statins on skeletal muscle. Statins are a class of cholesterol- lowering drugs that have been shown to greatly reduce the incidence and progression of cardiovascular disease. Given their safety and efficacy, statins are one of the most widely prescribed drug classes in the world. The most common side-effect of this drug is the development of myalgia and in severe cases, myopathy. These side-effects are the most common reason for prescription non-compliance and drug discontinuance of statins.


Muscle pain, also referred to as myalgia, has historically been a difficult entity to quantify. A primary reason underlying this fact is that muscle pain and muscle damage do not have to co-exist, and thus measures of muscle damage cannot be reliably used to assess pain. While myalgia can develop in response to injury, many clinical conditions exist where muscle pain is evident in the absence of clinically evident muscle damage. Individuals may present to a musculoskeletal disorders clinic with muscle damage in the absence of pain (ie myositis), muscle damage coupled with muscle pain, or muscle pain in the absence of muscle damage (ie statin myalgia or fibromyalgia).


In addition to myalgia, statin treatment can lead to the development of myopathy, or muscle damage. However, the mechanism by which this occurs is currently unknown. Statins have been shown to cause an increase in the production of mitochondrial reactive oxygen species (ROS) in skeletal muscle. These molecules can interact with proteins, lipids and DNA to impair cell signaling, increase inflammation and, ultimately, lead to cellular apoptosis. Whether or not patients with statin myopathy experience increases in ROS to an even greater extent than non-myopathic patients has yet to be determined. Therefore, our studies in this area hope to establish if increased ROS levels may provide a mechanism to explain the development of statin myopathy.