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A 1-yr carcinogenicity bioassay was conducted in rats fed 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), simultaneously with AIN-76/ high-fat (HF) diet alone, or with 10% starch replaced with kumara, pineapple, coconut, or taro, prepared as for a human diet. All of the non-IQ treated control, kumara, pineapple, or taro but not coconut-fed rats survived to 1 yr. None of the IQ-fed animals survived to 1 yr and although there were minor survival time differences among the groups, none was statistically significant. At sacrifice, IQ/HF controls had tumors in the skin, Zymbal's gland, ear canal, oral cavity, liver, and small intestine, totaling 32 among 20 animals. Kumara-fed rats had a similar tumor distribution but no tumors in the ear or oral cavity, and a total of 27 tumors among 20 animals, whereas pineapple-fed rats showed a somewhat lower tumor incidence (23/20 animals), including no small intestine lesions. Unexpectedly, a higher tumor incidence, especially of skin tumors, was seen in coconut and taro-fed animals (35/20 and 41/20 animals, respectively). In particular, the incidence of malignant liver tumors and gastrointestinal tumors were significantly increased in the taro-fed group in comparison with the kumara group. [ABSTRACT FROM AUTHOR]

The dietary fiber (DF) hypothesis suggested that DF, as plant cell walls, protected against colorectal cancer. The implicit assumption in much historic literature was that the readily analyzed and quantified nonstarch polysaccharide (NSP) component was critical in cancer protection. However, the presence of polymeric phenolic components such as lignin or suberin has profound effects on the physicochemical properties of the cell walls and largely determines their physiological properties in humans. In certain groups of food plants, degradation of cell walls that contain neither lignin nor suberin releases ferulic acid and other hydroxycinnamic acids. These acids have antioxidant, antimutagenic, and other anticancer effects, including modulation of gene expression and immune response. Reexamination of literature on cancer protection suggests that plant cell walls containing significant amounts of phenolic components may be the most likely to protect against cancer. In the last 30 years, the definition of DF has been incrementally expanded to incorporate NSP extracted from plant cell walls and from sources other than plant cell walls, then resistant starch, and most recently nondigestible oligosaccharides. On the early definitions, increased consumption of DF could only be achieved by increasing the intake of whole grains, brans, or other food plant material that would increase the intake of plant cell walls containing significant amounts of phenolic components. However, the new definitions make it possible to increase "dietary fiber" without consuming any such materials. We suggest that this could have negative connotations for cancer risk in human populations. [ABSTRACT FROM AUTHOR]

Abstract: A high-fiber diet may protect against colon cancer because of the butyrate generated in the colon by bacterial fermentation of nonstarch polysaccharides. Butryrate can reverse neoplastic changes, at least in vitro, and resistant starch (RS) represents a source of butyrate in vivo. We examined the effects of replacing normal maize starch in the diet of rats with three preparations of RS on the amounts of starch, butyrate, and other short-chain fatty acids in the cecum. We examined the effects on fecal bulking and transit time, which have been suggested to protect against colon cancer. The RS preparations that we tested were potato starch, high-amylose maize starch, and an a-amylase- treated high-amylose maize starch. All had major effects on fecal weight and on the weight of the cecum but only slightly shortened transit times. All increased the amount of starch reaching the cecum and increased short-chain fatty acid production in the cecum; potato starch had the greatest effect and high-amylose maize starch the least. Potato starch, unlike high-amylose maize starch, enhanced the proportion of butyrate. Thus there were marked differences among sources of RS, even though these were all classified as RS2. The significance for colon cancer is discussed. [ABSTRACT FROM AUTHOR]