Incidence rates for 27 cancers in 23 countries and mortality rates for 14 cancers in 32 countries have been correlated with a wide range of dietary and other variables. Dietary variables were strongly correlated with several types of cancer, particularly meat consumption with cancer of the colon and fat consumption with cancers of the breast and corpus uteri. The data suggest a possible role for dietary factors in modifying the development of cancer at a number of other sites. The usefulness and limitations of the method are discussed.

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Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices

All experimental studies in cancer are eventually aimed at limiting or curing the disease. When relationships have been established between environmental factors and the incidence of a particular disease, whether benign or malignant, evasive action can be taken before the actual causative agents or mode of action is understood. Cholera was evaded by the avoidance of sewage-contaminated water a century before the v. cholera was identified as the cause of the disease. Lung cancer can largely be avoided by abstinence from smoking cigarettes, although the carcinogenic mechanism whereby tobacco smoke causes cancer is not yet understood. A relationship can be demonstrated between certain bowel diseases and diet, and although this has not yet been shown to be causitive in the case of cancer, the relationship between an over-refined diet and diverticular disease can now be considered established. In view of the evidence, it seems justifiable to issue a warning against the removal of so much of the unabsorbable fiber from our food, and the associated over-ingestion of refined carbohydrates.

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Epidemiology of cancer of the colon and rectum

Insulin and insulin-like growth factor (IGF) axes are major determinants of proliferation and apoptosis and thus may influence carcinogenesis. In various animal models, modulation of insulin and IGF-1 levels through various means, including direct infusion, energy excess or restriction, genetically induced obesity, dietary quality including fatty acid and sucrose content, inhibition of normal insulin secretion and pharmacologic inhibition of IGF-1, influences colonic carcinogenesis. Human evidence also associates high levels of insulin and IGF-1 with increased risk of colon cancer. Clinical conditions associated with high levels of insulin (noninsulin-dependent diabetes mellitus and hypertriglyceridemia) and IGF-1 (acromegaly) are related to increased risk of colon cancer, and increased circulating concentrations of insulin and IGF-1 are related to a higher risk of colonic neoplasia. Determinants and markers of hyperinsulinemia (physical inactivity, high body mass index, central adiposity) and high IGF-1 levels (tall stature) are also related to higher risk. Many studies indicate that dietary patterns that stimulate insulin resistance or secretion, including high consumption of sucrose, various sources of starch, a high glycemic index and high saturated fatty acid intake, are associated with a higher risk of colon cancer. Although additional environmental and genetic factors affect colon cancer, the incidence of this malignancy was invariably low before the technological advances that rendered sedentary lifestyles and obesity common, and increased availability of highly processed carbohydrates and saturated fatty acids. Efforts to counter these patterns are likely to have the most potential to reduce colon cancer incidence, as well as cardiovascular disease and diabetes mellitus.

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Insulin, Insulin-Like Growth Factors and Colon Cancer: A Review of the Evidence

https://www.gastrojournal.org/article/0016-5085(84)90606-1/pdf

Intestinal flora in health and disease.

Some factors related to Westernization or industrialization increase risk of colon cancer. It is believed widely that this increase in risk is related to the direct effects of dietary fat and fiber in the colonic lumen. However, the fat and fiber hypotheses, at least as originally formulated, do not explain adequately many emerging findings from recent epidemiologic studies. An alternative hypothesis, that hyperinsulinemia promotes colon carcinogenesis, is presented here. Insulin is an important growth factor of colonic epithelial cells and is a mitogen of tumor cell growth in vitro. Epidemiologic evidence supporting the insulin/colon-cancer hypothesis is largely indirect and based on the similarity of factors which produce elevated insulin levels with those related to colon cancer risk. Specifically, obesity--particularly central obesity, physical inactivity, and possibly a low dietary polyunsaturated fat to saturated fat ratio--are major determinants of insulin resistance and hyperinsulinemia, and appear related to colon cancer risk. Moreover, a diet high in refined carbohydrates and low in water-soluble fiber, which is associated with an increased risk of colon cancer, causes rapid intestinal absorption of glucose into the blood leading to postprandial hyperinsulinemia. The combination of insulin resistance and high glycemic load produces particularly high insulin levels. Thus, hyperinsulinemia may explain why obesity, physical inactivity, and a diet low in fruits and vegetables and high in red meat and extensively processed foods, all common in the West, increase colon cancer risk.

Insulin and colon cancer

This is an epidemiological study of 107 patients with large bowel cancer and 307 control patients interviewed in Japan. Colon cancer is significantly less common in Japan, but rectal cancer is as common in Japan as it is in the United States. Japanese patients with cancer of the colon have a higher socioeconomic status than rectal cancer patients. Associated with the higher status is a more Western style diet. It is suggested that perhaps dietary fat influences the make-up of the bacterial flora and thus affects the pathogenesis of cancer of the colon. No significant relationship was found to medical and surgical diseases nor to the cholesterol and weight levels.

S. Ishikawa

Papers

Environmental factors of cancer of the colon and rectum II. Japanese epidemiological data