The case control study, presented at ASCO by Dr Stephen Gruber (University of Michigan, Ann Arbor), involved 1849 Israeli colorectal cancer patients (cases) and 1959 healthy controls matched for age, gender, and ethnic origins. The use of statins for at least five years was associated with a 51% reduction in the risk of colorectal cancer, with statins being used by 11.3% of controls and 5.8% of cases.

Gruber commented: "These observational data suggest that statins deserve further investigation in chemoprevention and therapeutic clinical trials." He added that the use of nonstatin cholesterol-lowering agents was not associated with reduced risk of colorectal cancer, suggesting that the protective effect was due to the statins rather than to the reduction in cholesterol. Gruber also noted that statins inhibit RAS and RhoA, two proteins that are potentially carcinogenic.

However, in a letter in this week's Lancet, Dr Bernard Nol (Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland) puts across a very different view.1

He notes that a previous article in the Lancet has suggested that myopathy and some other side effects of statins might be attributable to inhibition of selenoprotein synthesis.

He further points out that selenoprotein inhibition might heighten the risk of prostate and colon cancer and also trigger autoimmune diseases, more than 20 cases of which have been reported in patients treated with statins. "Further studies are, therefore, warranted to determine the long-term safety of these lipid-lowering agents," he concludes.