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The evidence on trial: cholesterol lowering and cancer
  1. A M Tonkin,
  2. A Forbes,
  3. S J Haas
  1. Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia
  1. Correspondence to Dr A M Tonkin, Cardiovascular Research Unit, Department of Epidemiology and Preventive Medicine, Monash University, Alfred Hospital, Melbourne, Australia 3004; andrew.tonkin{at}

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In an ideal world, medical care would be informed by a complete evidence base, implemented through supportive and appropriately funded systems and enacted by patients who, after being fully informed about the overall potential net benefits and any personal costs, complied with their recommended therapies.

The reality is in stark contrast. The evidence is usually incomplete, many governments do not “value” prevention, while the time pressures on professionals hinder their ability to deliver evidence-based care. In addition, the general population may be becoming increasingly sceptical about some aspects of medical treatments, particularly in relation to the ever-growing incidence of adverse events leading to product withdrawals. This is often because of cultural factors and, at times, the sensational reporting by media of any safety concerns, disproportionately to the benefits of a treatment. As a consequence, full compliance of patients with recommended therapies infrequently occurs.

The recently published Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study has again ignited controversy related to the possibility that cholesterol lowering may be associated with cancer.1 The question is a very important one. Cholesterol-lowering agents, particularly statins, are among the most commonly prescribed drugs, and their initiation may translate to potential exposure for 30 years or more. This article examines the scientific evidence base underlying such discussions and this topic in particular.

Seas study

Ezetimibe inhibits the intestinal absorption of cholesterol by binding to the Niemann–Pick CI-like 1 protein. The combination of ezetimibe and an HMG CoA reductase inhibitor (“statin”) is logical. This is because statins lower low-density lipoprotein (LDL) cholesterol by inhibition of cholesterol synthesis and upregulation of the hepatic LDL receptor which clears cholesterol from the vascular compartment, but at the same time, they increase the intestinal absorption of cholesterol.

In the double-blind controlled SEAS trial, 1873 patients with asymptomatic mild-moderate aortic stenosis and no …

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