Nutritional factors and colon cancer

Abstract

During the last 2 decades, substantial progress has been made in understanding the relationship between dietary constituents and the development of colon cancer in man. Unlike studies of cancer among smokers and nonsmokers, nutritional epidemiologic studies are confronted with the inherent difficulty of assessing reasonably precise exposures. The lack of consistency between international correlation studies and case-control studies does not necessarily negate a dietary etiology of colon cancer because these inconsistencies may have arisen, at least in part, from methodological limitations. Some of these deficiencies in epidemiological studies of diet and cancer have been corrected; recent case-control studies demonstrated that high dietary fat is a risk factor for colon cancer development and that an overall increase in intake of foods high in fiber might decrease the risk for colon cancer. The results of epidemiologic studies may be assumed to present conservative estimates of the true risk for cancer associated with diet. The populations with high incidences of colon cancer are characterized by high consumption of dietary fat, which may be a risk factor in the absence of factors that are protective, such as whole-grain cereals and of other high fiber. Laboratory-animal model studies have shown that certain dietary lipids and fibers influence tumorigenesis in the colon. The data of metabolic epidemiological and laboratory-animal model studies are sufficiently convincing with respect to the enhancement of colon cancer by type of fat and protection by certain dietary fibers.

Omega‐3 fatty acids in colorectal cancer prevention

“…[33][34][35][36] Studies conducted in our laboratory and those of others have consistently demonstrated that diets high in beef tallow, lard and corn oil (20 -23% in the diet) significantly increased chemically induced colon carcinogenesis in F344 and Sprague-Dawley rats as compared to diets low (5%) in these fats. 11,[33][34][35][36][37][38] Additional studies conducted in our laboratory also demonstrate that male F344 rats fed diets containing 20% lard or 20% corn oil rich in n-6 PUFAs were more susceptible to 1,2-dimethylhydrazine-induced colon carcinogenesis compared with those fed diets containing 5% lard or 5% corn oil. 38 Deschner et al 39 demonstrated that dietary n-3 PUFAs (fish oil) inhibits methylazoxymethanol (metabolite of azoxymethane)-induced focal areas of dysplasia and colon tumors, whereas n-6 PUFAs (corn oil) enhance colon tumorigenesis in rats.…”

“…11,40 These studies provided evidence in preclinical models that diets containing high amount of saturated fat of animal origin or n-6 PUFAs had a greater colon tumor-enhancing effect than diets low in such fatty acids, whereas diets high in n-3 PUFAs had no such enhancing effect Further studies in our laboratory have evaluated the modulating effects of high dietary corn oil and safflower oil rich in n-6 PUFAs, olive oil high in monounsaturated fatty acid oleic acid, coconut oil high in medium-chain fatty acids such as lauric acid and fish oil during the postinitiation stage of AOM-induced colon carcinogenesis in male F344 rats. 14,37,38,41 Animals fed diets containing high corn oil or safflower oil (23.5%) had a higher incidence of colon tumors than did those fed diets low in fat (5%). By contrast, diets high in coconut oil, olive oil or menhaden fish oil had no such colon tumor-enhancing effect.…”

“…Several studies indicate that diets high in saturated fatty acids (beef tallow and lard) and n-6 PUFAs (corn oil or safflower oil) increase the concentration of colonic luminal secondary bile acids, including deoxycholic acid and lithocholic acid, whereas dietary fish oil high in n-3 PUFAs had no such enhancing effect. 37 Metabolic epidemiologic studies demonstrated that populations who are on typical Western diet and at high risk for colon cancer excrete high levels of secondary bile acids. 50,51 Secondary bile acids have been shown to stimulate protein kinase C (PKC) in a manner similar to phorbol esters, induce cell proliferation and ornithine decarboxylase activity, a rate-limiting enzyme in polyamine biosynthesis, and act as promoters in colon carcinogenesis.…”

Deoxycholate induces DNA damage and apoptosis in human colon epithelial cells expressing either mutant or wild-type p53

“…The risk of colon cancer is increased by diets high in fat [4], although this is not always the case [5]. Nevertheless, it is generally thought that high fat diets have cancer-promoting effects by way of bile acids or their salts [6].…”

Intestinal expression of mutant and wild‐type progastrin significantly increases colon carcinogenesis in response to azoxymethane in transgenic mice

“…Several dietary and hormonal factors modulate the proliferative potential of the colonic epithelium; among these factors is the peptide hormone gastrin. [3][4][5] The gastrin gene is expressed by enteroendocrine (G) cells in the antrum of the stomach. Gastrin gene products (called gastrins) are processed by endopeptidases within G cells; these endopeptidases convert the full-length precursor peptide (PG) into a glycine-extended gastrin (G-Gly).…”