[Nutrition and cancer (author's transl)]

The problem of a relationship between nutrition and cancer has to be approached from two different points of view: 1. Direct effect of carcinogens present in foods or in food additives (direct carcinogenesis), 2. In-vivo synthesis of carcinogens caused by changes in metabolism due to altered dietary habits (indirect carcinogenesis). For the second mechanism, we have to make a distinction between the effects of nutritional deficiency and of nutritional excess. Some examples from animal experiments are presented. In man, possible relationships between nutrition and cancer are postulated mainly for tumors of the gastrointestinal tract and recently also for hormone-dependent cancers. Epidemiological evidence points to the major importance of the indirect way of carcinogenesis caused by specific nutritional deficiencies and excesses. Experimental studies in man are difficult to perform. Therefore, most hypotheses are based on statistical associations, and great caution is required in drawing inferences on causal relationships. Cancers of the upper and lower gastrointestinal tract epidemiologically behave in a different way, the former showing a marked decrease in most western countries, the latter a slight increase. The etiology of the cancers of the esophagus and stomach has still to be determined in spite of many hypotheses. Migrant studies show a major effect of environmental rather than genetic factors. Substantial differences in dietary habits between countries with high and low incidence of stomach cancer (Japan and United States) point to the importance of nutrition as an etiological factor with a high probability, but no specific dietary components have been identified so far. The same is true for cancer of the large bowel. Recent hypotheses suggest that dietary factors may relate to cancer of the colon by their effect on bile production and on the bacterial makeup of faeces which in turn might be transforming bile acids into active carcinogens. There is, however, disagreement about the specific dietary component responsible for this model of carcinogenesis. BURKITT stresses the importance of the lower consumption of dietary fiber, resulting in retarded bowel function and additional time for bacterial proliferation and degradation by bacteria of bile acids. WYNDER, on the other hand, explains the increased bile acid and neutral sterol excretion and microbial modification of these compounds with the high content of animal fat in the western diet. With hormone-dependent cancers (breast, endometrium, ovary, prostate), a correlation has been shown between body weight and height and breast cancer as well as between overweight and cancer of the endometrium. Which aspect of diet, if any, is responsible for changes in hormone metabolism, resulting in an increased risk of these cancers, is still to be proved. On the basis of current knowledge, it is extremely difficult to draw inferences for preventive action. Certainly, a cancer-preventing diet cannot be established...