SLCO1B1 — statin-induced muscle pain risk
One copy of the SLCO1B1*5 reduced-function variant detected.
You have one working copy and one less-active copy of the SLCO1B1 gene.
Modestly increased risk of statin-induced myopathy (muscle pain or weakness), particularly with simvastatin at high doses. Other statins may be tolerated better.
You have a modestly higher risk of muscle pain or weakness from statins, especially simvastatin at higher doses. Other statins are usually easier to tolerate if you have this version.
What this means
SLCO1B1 is the transporter that takes statins from the bloodstream into liver cells, where they act. The *5 variant reduces transporter function, so more statin remains in circulation — and the higher systemic exposure is associated with muscle side effects. Effect is largest for simvastatin and lovastatin; smaller for atorvastatin; minimal for pravastatin and rosuvastatin, which use other transport routes.
SLCO1B1 is a protein that pulls statins out of your blood and into your liver, where they actually do their job lowering cholesterol. The *5 version of the gene makes a less-effective version of this protein, so more of the statin stays floating around in your blood instead of being cleared. Higher levels in your blood mean a higher chance of muscle pain or weakness — the most common reason people stop taking statins. The effect is biggest for simvastatin and lovastatin, smaller for atorvastatin, and minimal for pravastatin and rosuvastatin (which use different transporters). If you've ever had muscle problems on a statin, this is one of the more common genetic reasons why.
Caveats
- Statin side effects have many causes; SLCO1B1 status is one factor among several.
- Switching to a different statin often resolves muscle issues.
- This is one of the more genuinely actionable common pharmacogenetic variants.