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For many Americans, statins are a literal life saver. Doctors prescribe statins to patients of theirs with high levels of LDLs, commonly known as the “bad” cholesterol, to prevent cholesterol build-ups from becoming full-blown clogged arteries. By inhibiting the liver’s capacity to produce bad cholesterol, statins have proven invaluable to many suffering from dangerously elevated levels of LDLs.

However, statins are known to cause some really nasty side effects, including muscle soreness and myalgia, and whether a person will develop these nagging pains has heretofore been hit-or-miss. When these incurable muscle pains develop, patients tend to stop using statins, which puts them at a much higher risk of developing serious cardiovascular problems.

In a recent study, though, researchers from the University of Dundee have discovered a gene variation that seems to be highly correlated with a person’s development of side effects from statins. A gene that codes for the LILRB5 protein, which is involved in immune responses against an intruder, has been known to impact humans’ response to outside chemicals. The human immune system is incredibly complex — sometimes to the point of confusing the body itself. Sometimes, the immune system will attack either a perfectly benign but foreign molecule with full force, and still other times, the immune system will turn on itself, as is the case with autoimmune diseases like Alzheimer’s Disease.

The researchers in the study examined data from nearly 12,000 patients who had been prescribed statins and zeroed in on the markers of muscle damage in them. In people with two recessive versions of this gene, a variant called Asp247, statins caused a remarkably higher level of muscle pain and weakness. According to the study, “The same variant was previously linked to altered creatine phosphokinase enzyme levels, the authors noted, prompting speculation that it might contribute not only to general muscle aches but also statin-related muscle pain.”

More research is needed in the future to determine the full pathway of the gene, gene product, and adverse reaction to statins, but it’s a huge step for pharmacogenomics that we can correlate reactions to the same drug with the same genetic underpinnings. The next steps will be to determine how to account for the genes in prescribing the proper medication to prevent cardiovascular catastrophes.