Colon cancer genetics / edited by Patrick M. Lynch and Henry T. Lynch.

Date:
[1985]
Catalogue details

Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Colon cancer genetics / edited by Patrick M. Lynch and Henry T. Lynch. Source: Wellcome Collection.

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    6 COLON CANCER GENETICS researchers have resorted to less thorough and less accurate methods of obtaining dietary information, such as interviews or questionnaires. It is, therefore, not surprising that epidemiologic studies of specific dietary items have given conflicting results. Burkitt has emphasized that the distribution, both geographic and socioeconomic, of high-fat diets is almost the same as for low-fiber diets.^' In virtually all communities, 10 to 15% of the energy requirements are derived from protein and the remaining 85 to 90% come from fats and carbohydrates. Burkitt states that these two main sources of energy are reciprocally related, in that carbohydrate-rich diets are almost invariably fiber rich and high-fat diets are fiber poor. Studies by Antonis and Bersohn relate Burkitt's position to the potential role of dietary fats and bile acids in colon tumorigenesis.^^ These investigators presented evidence that reduc¬ ing the fat in a low-fiber diet or increasing the fiber in a high-fat diet would each decrease the fecal bile-acid concentration. A'^nitroso compounds in stools may have carcinogenic properties, and these have been reduced in stools by reducing fat intake or by adding large quantities of wheat bran to the daily diet.^^^® Mutagenic activity due to N- nitroso compounds was observed more frequently in feces from patients with colorectal cancer than in laboratory personnel. In addition to environmental factors such as high dietary intake of animal fats and proteins and low dietary intake of unrefined fiber, some other dietary factors correlate with the incidence of colon cancer. These include nonnutritive substances in food such as bacterial or fungal metabolites,''^ food additives such as nitrosamines and nitrosamides, and by-products arising from frying or barbecuing fish and meat.^ Indirect effects of diet may also be important in intestinal carcinogenesis. For example, diet can alter the metabolism of the intestinal microflora and the resulting altered bacterial-metabolic patterns can lead to either an increased or decreased conversion of procarcinogens to proximal carcino¬ gens.^ Dietary components may also influence the level of intestinal-epithe¬ lial microsomal-enzyme systems involved in the activation of carcinogens. If the risk of colorectal cancer is diminished by a vegetarian diet, it may be due to the excess of vegetables, not the absence of meat. Bjelke'^ suggests that vegetables in particular may have a protective effect against colorectal cancer. Case-control studies in Scandinavia and the United States showed the risk of colon cancer to be reduced by about 25% in men who ate large amounts of vegetables.Graham et al. also concluded that vegetables con¬ ferred protection against colon cancer.^ Experiments on the possible protective effect of dietary fiber on 1,2 dimethylhydrazine [DMH] injected animals have shown a significant bene- fit.2^^6.48 receiving DMH, the amount of stool bulk and the fiber con-
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