Starting cholesterol medication often comes with mixed feelings. Many people know statins can lower the risk of heart attacks and strokes, yet stories about sore legs, heavy muscles or unexplained weakness create doubt.
For years, these symptoms were acknowledged but poorly explained, leaving patients unsure whether to continue treatment.New research now offers a clearer answer.
When protection comes with a cost
Statins are among the most prescribed drugs worldwide and are central to modern heart care.
Despite their benefits, muscle-related side effects remain one of the leading reasons people stop taking them.
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Until now, scientists lacked a precise explanation for how a heart-protective drug could disrupt muscle function.
Researchers from the University of British Columbia, in collaboration with the University of Wisconsin–Madison, have identified a specific molecular trigger.
Their findings, published in Nature Communications, suggest statins interfere directly with how muscle cells regulate calcium, a mineral essential for normal movement and strength.
A closer look inside muscles
Using advanced cryo-electron microscopy, the team examined how statins interact with a muscle protein known as the ryanodine receptor.
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This protein normally acts as a tightly controlled gate, releasing calcium only when muscles need to contract.
The researchers found that statins can force this gate to remain open. The result is a continuous calcium leak inside muscle cells, which can disrupt normal function and, in some cases, cause tissue damage.
The study focused on atorvastatin, one of the most widely used statins, but the mechanism may apply to others in the same drug class.
What this could change
Severe muscle injury is rare, but milder pain and fatigue affect many users and often lead to discontinued treatment.
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By pinpointing the cause, scientists may now be able to design safer statins that protect the heart without harming muscles.
Sources: ScienceDail and Nature
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