Colon cancer prevention: today's challenge to biomedical scientists and clinical investigators.

Abstract

There is a general agreement that dietary factors, particularly dietary fat, significantly influence the pathagenesis of large bowel cancer. The following hypotheses on the etiology of colon cancer are suggested: 1)conversion of cholesterol and δ5−7-dehydrocholesterol, which are normally present in colonic contents and mucosa, to reactive metabolites that act as carcinogens, may be an important step in colon carcinogenesis; 2)dietary fat changes the concentration of bile acids and also the metabolic activity of colonic bacteria, which may produce tumorigenic compounds from bile acids; 3) mucosal and/or luminal conversion of cholesterol to its epoxide may be of etiologic significance; and 4) diet also influences mixed-function oxidases, which could play a role in modifying colon carcinogenesis. Today's challenges to biomedical scientists and clinical investigators involved in colon cancer are as follows: 1) the animal experimentor should design and effectively relate animal models to the human setting; 2) it should be found whether it is possible for the fecal constituents of an individual on an American diet to be made similar to those of individuals on a Japanese diet, and, if so, what degree of dietary modification is required?; 3) it should be found whether solitary polyps could be reduced in size by strict dietary modification; 4) regarding managerial preventive medicine, it should be decided whether it is recommended to reduce the fat and cholesterol content of our staple diet; and 5) with regard to individual preventive medicine, people should be aware of calorie excesses, and of the fat and cholesterol content of their diet from early in life onward.