Essential Nutrients in Carcinogenesis

Selwyn A. Broitman, Broitman, Selwyn A.

Observational and case-control epidemiologic data supported by experimental studies indicate that dietary cholesterol may contribute to colon tumorigenesis. A mechanism for this possible relationship is currently under investigation. Additional international epidemiologic data, although not uniformly consistent, indicate an inverse relationship between serum or plasma cholesterol levels and risk for colon cancer. This risk is greatest at serum cholesterol levels of less than 180 mg/dl. It has been suggested but not proven that individuals consuming diets high in dietary fat and cholesterol may have variations in cholesterol dynamics that account for lowered serum cholesterol levels and enhanced risk for colon cancer. Clinical evidence in both men and women indicates that age-sex-adjusted, low serum cholesterol levels may precede the detection of colon cancer by more than 5 years. Preclinical colon cancer is associated with a further decrease in serum cholesterol levels. It is not clear whether progression of the disease before metastatic spread results in continued lowering of serum cholesterol levels. In men with markedly elevated serum cholesterol levels who have been placed on cholesterol-lowering drugs such as clofibrate or cholestyramine, there was no evidence that such regimens increased the risk for colon cancer. It is possible that reductions in serum cholesterol associated with the use of these drugs are insufficient to lower cholesterol levels to a range associated with an increased risk for colon cancer.