Diet, nutrition, and cancer.
As the second leading cause of death in the United States, cancer is a major public health problem today. Cancer incidence varies worldwide and tends to change with migration. These epidemiological observations have led to the concept that environmental factors may be important in carcinogenesis. Diet and nutrition are receiving increased attention and the National Cancer Institute, as mandated by the Nation Cancer Act Amendments of 1974, is playing a major leadership role in expanding research efforts in the areas of environmental carcinogenesis, and nutrition in relation to cancer. The subject of diet, nutrition, and cancer is complex. Different types of cancer are not necessarily affected by dietary components in the same manner. Although the development of certain neoplasms may be repressed by specific dietary deficiencies, other types, particularly those of the liver and upper gastrointestinal tract, are actually augmented or potentiated by such deficienceis. In extrapolating results from animal experiments to humans, caution must be exercised because of possible differences in species response to the same dietary stimulus and because spontaneous tumors may react differently from experimentally-induced tumors. Diet and nutrition are viewed more appropriately as modifiers, rather than initiators, of tumorigenesis. Caloric intake, type and amount of fat, protein, amino acids, vitamins, minerals, fiber, and other dietary constituents have been studied in regard to their influence on the development of neoplasms. Dietary components may have opposing effects on tumorigenesis, i.e., protective and predisposing, and the consequence to the host will depend on the balance between these opposing forces. Studies conducted to date indicate that the modifying effect of diet and nutrition may be exerted through specific effects on 1) intestinal bacteria and substrates for bacterial metabolism, 2) microsomal mixed-function oxidase system, 3) endocrine system, 4) immunological system, 5) availability of metabolites for cell proliferations, and 6) rate of carcinogen transfer and duration of exposure to the carcinogen. More research is needed to elucidate the interaction between diet and each of these factors and to test the validity of the mechanisms proposed to explain such interactions. These studies will lead not only to a better understanding of carcinogenesis itself but also to a new understanding of the influence of diet on human physiology and metabolism.
D000818:Animals; D001205:Ascorbic Acid / Q000009:adverse effects / Q000627:therapeutic use; D001647:Bile Acids and Salts / Q000378:metabolism; D002784:Cholesterol; D004032:Diet / Q000009:adverse effects; D004041:Dietary Fats / Q000009:adverse effects; D004064:Digestive System / Q000473:pathology; D004734:Energy Metabolism; D005544:Forecasting; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications; D007422:Intestines / Q000382:microbiology; D009369:Neoplasms / Q000188:drug therapy / Q000209:etiology*; D009748:Nutrition Disorders; D009747:Nutritional Physiological Phenomena; D011134:Polysaccharides / Q000627:therapeutic use; D014801:Vitamin A / Q000009:adverse effects; D014802:Vitamin A Deficiency / Q000150:complications; D014803:Vitamin B Complex / Q000009:adverse effects; D014804:Vitamin B Deficiency / Q000150:complications
D001647:Bile Acids and Salts; D004041:Dietary Fats; D011134:Polysaccharides; D014801:Vitamin A; D014803:Vitamin B Complex; D002784:Cholesterol; D001205:Ascorbic Acid