Prevention of colorectal cancer: Diet, chemoprevention, and lifestyle

This article describes primary prevention of colon cancer (ie, interventions that do not involve the removal of diseased tissue or chemotherapy for known colon cancer). Although screenirig with ablation of adenomas has a significant impact on colon cancer [1], the logistics of screening are complicated [2-4]. These issues are addressed in accompanying articles. This article focuses on preventing the initiation and promotion of neoplastic growth, particularly with dietary measures. A goal of dietary epidemiology is to identify chemopreventive agents and strategies. The effects of diet are analyzed by observational approaches and experimental dietary, nutritional, or chemopreventive interventions. The adenomatous polyp or adenoma is an important surrogate endpoint for colon cancer [5-7]. The adenoma often remains indolent for years, so prevalence can be analyzed. The adenoma is common among older individuals, especially those more than 50 years old. As many as 30% to 50% of individuals older than 50 years of age harbor one or more adenomatous polyps [8]. The adenoma is usually asymptomatic and is generally discovered only during routine screening. The adenoma is the key premalignant lesion that leads to colon cancer [5,6]. Many, if not most, adenomas never progress to colon cancer, but most colon cancers emerge from adenomas (adenoma-to-carcinoma sequence). As the adenoma is more common than colon cancer and new adenomas develop in individuals who have had previous adenomas that were ablated, studies of interventions designed to prevent colon cancer usually analyze the adenoma as a surrogate marker. This strategy is based on preventing colon cancer by preventing adenomas. The weakness of this strategy is that the formation of adenomas does not guarantee that an individual is at increased colon cancer risk, but this weakness has not deterred investigators from studying the adenoma as a surrogate marker for human colon cancer. The proportion of colon cancer attributable to genetic syndromes-familial adenomatous polyposis and hereditary nonpolyposis colon cancer-seems to be small, so that screening for these two syndromes is unlikely to substantially reduce the incidence of colon cancer. Although these syndromes are powerful predictors of colon cancer, they are uncommon and contribute a relatively small proportion to the total colon cancer burden.