ABOUT STATIN RESPONSE

The muscle pain that made you give up on preventing heart disease — because the statin you were prescribed wasn't the one your genes could handle.

Whole genome sequencing identifies SLCO1B1 variants that determine which statins are safe and effective for you, enabling continued cardiovascular protection without myopathy risk.

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About this condition

Statin Response (SLCO1B1)

Statin-induced myopathy, characterized by muscle pain, weakness, and in severe cases rhabdomyolysis, occurs in approximately 0.5-1% of statin users and is the most common reason for statin discontinuation. However, genetic variants in SLCO1B1 identify patients at substantially elevated risk. SLCO1B1 encodes solute carrier organic anion transporter 1B1 (OATP1B1), which actively transports statins into hepatocytes, the site of their action. The SLCO1B1*5 variant (rs4149056, c.521T>C, p.Val174Ala) increases plasma concentration of simvastatin approximately 4-17-fold depending on carrier status, substantially increasing myopathy risk.

Heterozygous carriers of SLCO1B1*5 have approximately 4.5-fold increased risk of myopathy on simvastatin; homozygous carriers face approximately 16.9-fold increased risk. This risk is specific to simvastatin and atorvastatin (to a lesser degree); rosuvastatin and pravastatin are metabolized through different pathways and pose lower myopathy risk in SLCO1B1 variant carriers. Approximately 15% of European ancestry populations carry at least one SLCO1B1*5 allele, with frequency varying significantly by ancestry. The *5 variant reduces hepatic transporter function, decreasing hepatic uptake and permitting statins to accumulate in plasma and reach systemic tissues including muscle, leading to higher myopathy risk.

SLCO1B1 genotyping enables safe, continued statin therapy for patients with prior myopathy or at elevated genetic risk. A patient identified as SLCO1B1*5 heterozygous can safely use alternative statins including rosuvastatin or pravastatin, enabling continued cardiovascular risk reduction. For patients who are SLCO1B1*5 homozygous, simvastatin is contraindicated; alternative statins with different metabolism pathways are strongly preferred. Genotype documentation in the medical record ensures that simvastatin is not prescribed inadvertently and that future providers understand the individual's statin tolerance profile.

Gene locus
SLCO1B1 (12p12.1), HMGCR (5q13.3)

Standard panels may not include SLCO1B1, missing the #1 genetic cause of statin myopathy.

SLCO1B1 genotyping is recommended but not routine

The Clinical Pharmacogenetics Implementation Consortium (CPIC) published guidelines in 2012 recommending SLCO1B1 genotype-guided statin selection. However, many standard statin prescribing workflows do not include SLCO1B1 testing, even though the risk is substantial. Some pharmacogenomics panels include SLCO1B1, but single-gene panels and many standard lipid panels do not. For patients with prior statin-associated myopathy, genetic testing can identify the root cause and guide safe alternative statin selection. Whole genome sequencing captures SLCO1B1 and the full context of lipid metabolism genes, enabling comprehensive pharmacogenomic assessment.

Your statin choice determines whether you tolerate cholesterol therapy

A patient found to be SLCO1B1*5 heterozygous should avoid simvastatin; if a statin is clinically necessary, alternatives include rosuvastatin (CPIC recommends considering lower starting dose), pravastatin, or pitavastatin. If homozygous *5, simvastatin is contraindicated and alternative statins strongly preferred. For patients with prior statin-associated myopathy, SLCO1B1 genotyping identifies the genetic risk factor and enables safe alternative statin selection — often allowing lipid-lowering therapy to continue and cardiovascular protection to be maintained. Documented in the medical record, the genotype prevents future statin-related myopathy episodes and enables informed patient-provider discussion about lipid management options.

One test. A lifetime of answers.

One kit, sent to your home. Your entire genome sequenced at the clinical standard used for diagnostic decisions. 200+ physician-ready reports delivered to your Genome Manager in 6–8 weeks — permanent and updated as science advances.

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