Statin drugs are highly effective in lowering blood concentrations of LDL-cholesterol, with concomitant reduction in risk of major cardiovascular events. Statins, inhibitors of the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase enzyme, are widely used in clinical practice as first-line treatment for dyslipidaemia and in the prevention of cardiovascular disease (CVD) events.

Studies estimate that up to 50% of patients with cardiovascular disease stop taking their statin medications as directed. Many do so because of statin associated muscle symptoms (SAMS)—the onset of muscle aches, spasms, weakness and/or pain associated with statin therapy. 60% of people who stopped taking a statin cited muscle pain as the primary reason.


An association has been established between statin induced myopathy and variations in the SLCO1B1 gene. The SLCO1B1 gene codes for the organic anion transporter 1B1 responsible for the liver’s uptake and metabolism of statins. Inherited variations in the SLCO1B1 gene affect the function of this transporter. The presence of this common variant to SLCO1B1 results in a significantly decreased ability to take up statins by the liver, less effectiveness of the statin in lowering ‘bad’ LDL cholesterol levels, higher blood levels after dosing, and an increased risk of myopathy. Studies show that people who have inherited one or two copies of a specific SLCO1B1 variant are up to 4.5-fold and 17-fold increased risk respectively for developing significant myopathy due to statins.

Three SLCO1B1 genotypes have been identified and classified in terms of their effect on statin metabolism in the liver—normal (T/T), decreased (T/C), and markedly decreased (C/C):

  • The T/T genotype (valine/valine) is classified as normal statin metabolizers. These patients have a normal ability to metabolize statins. 
  • The T/C genotype (valine/alanine) is classified as a decreased statin metabolizer. These patients have a decreased ability to metabolize statins. They have up to a 4.5-fold increased risk for developing statin induced myopathy.
  • The C/C genotype (alanine/alanine) is classified as a markedly decreased statin metabolizer. These patients have a significantly decreased ability to metabolize statins. They have up to a 17-fold increased risk of developing myopathy on statin therapy.

Additionally, individuals carrying the T/C or C/C genotype are less responsive to statins for LDL-C lowering than those carrying the T/T genotype

SLCO1B1 genotyping help healthcare providers identify those patients who are at higher risk for statin induced myopathy due to a variation in their SLCO1B1 gene, and prescribe the right statin type and dose with the least probability of causing myopathy accordingly.

The benefits of SLCO1B1 genotyping are:

  1. Advanced identification of those patients who are at higher risk for statin induced myopathy
  2. Ability to prescribe the right drug type in the right dose according to a patient’s identified SLCO1B1 genotype.

Other factors associated with risk of statin induced myopathy such as diabetes, Creatine>1.0 mg/dL, hypothyroidism, use of calcium channel blockers, use of amiodorone, deficiencies of vitamin D and co-enzyme Q10, certain medications, age >65 years, female gender andphysical activityshoulde be considered.