The global market for statins has reached heart-stopping proportions, registering at almost $20 billion in 2012. In the US, one out of every four adults over the age of 45 is on statins, making these medications one of the leading types prescribed. The drugs work by lowering the liver’s production of low-density lipoproteins, also known as ‘bad’ cholesterol, which form the artery-clogging plaques that can lead to heart attack. But statins can cause significant side effects, ranging from sleeplessness to an increased risk of type 2 diabetes and potential liver damage.
One of the most common side effects is muscle pain and injury, which afflicts up to 38% of people taking statins. Now, researchers have hit upon a new gene variation that could explain why some individuals are less prone to this type of adverse reaction to such drugs.
The scientists themselves sound surprised at the discovery. “We weren’t focused on finding the cause of the muscle damage,” says Ronald Krauss, director of atherosclerosis research at Children’s Hospital Oakland Research Institute in California and lead author of the new study, which appears online today in Nature. “We were looking at cell lines from patients on statins to discover new gene variants and we found one that affects how the drug works.”
It’s not the first effort to look at statin side effect risks though the lens of genetics. Five years ago, researchers found that individuals on high doses of simvastatin—a statin marketed as Zocor by New Jersey-based Merck—who also carried a specific variant in the SLCO1B1 gene were fifteen times more likely to have muscle pain and injury, also known as myopathy. Based on these findings, which also correlated with markedly higher blood levels of a muscle damage biomarker, the US Food and Drug Administration set new guidelines recommending alternative medications for patients who need more than 40 milligram a day of simvastatin to lower their cholesterol.