Diet, acetylator phenotype, and risk of colorectal neoplasia
1996
Roberts-Thomson, I.C. | Ryan, P. | Khoo, K.K. | Hart, W.J. | McMichael, A.J. | Butler, R.N.
Background Inherited or acquired differences in metabolic pathways that activate or inactivate dietary carcinogens may influence the risk of developing cancer. A polymorphism in N-acetyltransferase classifies people into fast and slow acetylators. This enzyme catalyses the formation of mutagenic products from foodstuffs, especially cooked meat and fish. Some data suggest that fast acetylators are at higher risk of colorectal cancer. We have studied the adenoma and cancer risk in relation to meat intake and acetylator status. Methods In a case-control study, we compared 110 patients with colorectal cancer, 89 patients with colorectal adenomatous polyps, and 110 controls. Acetylator status was assessed by the rate of acetylation of sulphamethazine given orally. Findings The fast-acetylator phenotype was associated with odds ratios of 1.1 (95% CI 0.6-2.1) and 1.8 (1.0-3.3) for adenoma and colorectal cancer, respectively. The highest risk occurred in the youngest fertile (<64 years) of cases (2.5 [0.7-9.4] and 8.9 [2.6-30.4], respectively). There was no difference between the sexes. The risk of adenoma or cancer increased with increasing intake of meat in fast but not in slow acetylators: covariate-adjusted odds of disease over three levels of meat consumption were 2.1 (0.9-4.7) for adenoma, 1.7 (0.9-3.5) for cancer, and 1.9 (1.0-3.7) for all tumours. Interpretation Our findings indicate that acetylator status modulates the risk of colorectal neoplasia associated with meat intake.
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