LAUSR

1098 www.thelancet.com Vol 389 March 18, 2017 4 Dimmitt SB, Stampfer HG, Moran A, Scartozzi M, Warren JB. Statin dose based on limited evidence. J Am Coll Cardiol 2015; 65: 759–60. 5 LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med 2005; 352: 1425–35. from statins to comply with treatment. Although clearly valuable, there are now many effective treatments available for coronary prevention besides statins, such as weight loss and antihypertensive and antithrombotic therapy. Adverse effects from statins, for example cerebral haemorrhage, renal failure, and rhabdomyolysis, are doserelated and sometimes lethal. That toxicity might be reversible after statin cessation is unhelpful because the atheroma benefits would then cease to accrue. Many physicians do not appreciate that all of the reduced mortality and almost all of the reduction in coronary events conferred by statins are already evident at around effective dose 50 (ED50—ie, mean population dose known to reduce LDL to half of the maximum possible), which is only about 2 mg for atorvastatin. At doses higher than this, benefits plateau but adverse effects continue to increase up to 6-times with atorvastatin 80 mg daily, about 40-times ED50. We are not aware of any other drug treatment that has been shown to be necessary at such high doses. Higher doses increase the potential of interactions of statins with other drugs, with sometimes serious consequences. Proven, lower doses of statins are likely to be much better tolerated and accepted by patients.