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Epidemiology of Diet and Colon Cancer

For any particular cancer cell, was a researcher able to detect a mutation in any of the genes (oncogenes) associated with cancer  [Pg.907]

Would the mutation be expected to result in any change in the sequence of amino acids in the protein A change in a DNAbase can result in a change, or no change, in the amino acids. [Pg.907]

Would any component of the diet be expected to attack DNA and become attached to one of the nucleoside bases Would any constituent of the diet be expected to influence the normal process of methylation of cytosine residues on our DNA Could any component of the diet influence the concentration of hydrogen peroxide, or other forms of toxic oxygen, in the cell Is there any reason to believe that a particular cancer patient has a genetic defect in one of the DNA repair enzymes  [Pg.907]

An introduction to the terms and tools used to express and evaluate epidemiological data are presented here. One might consult Appendix C for definitions of various terms in epidemiology. [Pg.907]

A case-control study was designed to explore risk fadors for coloredal adenomas. Adenomas are precursors to 80-90% of all colorectal cancers. The study used 236 cases (with adenomas or polyps) and 409 controls (no adenomas) (Tseng et ah, 1996) (Table 11.2). All subjects were patients receiving colonoscopy exams. The subjects were not recruited from the general public. A month or so after the exam, the subjects were asked to fill out a food choice questionnaire. [Pg.907]

TABLE 11.2 Odds Ratios for Acquiring Adenoma and Associated Estimated Nutrient Intake [Pg.908]

By viewing the indicated food choices, and using tables of nutrients in foods, the researchers were able to estimate the daily intake of various nutrients, such as folate, vitamin C, calcium, and iron. The results for folate and vitamin C are shown separately for women and men in Table 11.2. The daily intakes for the nutrients were divided into four groups, as indicated. The risk for adenomas is expressed by a special term, called the odds ratio (OR) (see Appendix C). [Pg.908]

An OR of greater than 1,0 indicates that the indicated dietary practice is associated with an increased rale of adenoma. An OR of less than 1.0 means that the indicated dietary practice is associated with a decreased rate of adenoma. An OR that is greater than 2.0 or under 0.5 is considered to be impressive and convincing. An OR that is between 0.5 and 2.0 may be less convincing or, perhaps, confound ing. These values are not strict cutoff points. They might be considered to be fuzzy cutoff points. The fuzzy cutoff points of 0.5 and 2.0 apply to odds ratios. These fuzzy cutoff points also apply to another term, the risk ratio. [Pg.908]


Epidemiology of Diet and Colon Cancer Epidemiological Study of Colorectal Adenomas... [Pg.879]

While there are no epidemiologic data available on lipotropic factors and colon cancer in human populations, results of animal studies suggest a possible role for this class of nutrients (choline, methionine, vitamin and folate) in colon carcinogenesis (69). Table XVI lists results typical of those observed when rats are fed a diet high in fat, low in lipotropes and exposed to a colon carcinogen. [Pg.176]

Graham S, Dayal H, Swanson M, Mittelman A and Wilkinson G. 1978. Diet in the epidemiology of cancer of the colon and rectum. J Natl Cancer Inst 61 709-714. [Pg.41]

In conclusion, phytic acid forms soluble complexes with Ca2+ at intestinal pH under a variety of conditions and fails to inhibit Ca2 bioavailability to mice in our experimental system. Despite the hazard in direct extrapolation of results obtained with animals kept on a well-defined dietary regimen to humans consuming a complex diet, many elements of which affect Ca2+ bioavailability, our data demonstrate the need for a reevaluation of the putative antinutritional properties of dietary phytate. Our further contention that adequate levels of dietary phytate may actually be beneficial due to its food preserving properties and its protection against colonic cancer will warrant a prospective epidemiological human study designed to assess the longterm effects of dietary phytate on mineral bioavailability and inflammatory bowel diseases. [Pg.62]

A resurgence of interest in dietary fiber has been stimulated by epidemiological evidence of differences in colonic disease patterns between cultures with diets containing large quantities of fiber, and Western cultures having more highly refined diets. Many African countries, for example, are relatively free of diverticular disease, ulcerative colitis, hemorrhoids, polyps, and cancer of the colon Whereas most interest has focused on the beneficial role of dietary fiber, there is also concern that high fiber diets may cause disturbances in the absorption of nutrients such as minerals (see Mineral Nutrients) and vitamins. [Pg.617]

Wynder and Shigematsu (15) were the first to suggest that nutritional factors in general and specifically differences in fat intake may be responsible for the international variation in colon cancer incidence. Subsequent descriptive epidemiologic studies have found a strong positive association between colon cancer mortality or incidence in different countries and per capita availability in national diets of total fat (4,16) and of animal fat, estimated from food balance sheets. Such international correlations may be supportive of a hypothesis, but they should be interpreted with caution because the dietary data were based not on actual intake information but on food disappearance data. [Pg.126]

One hypothesis linking dietary fat to colon cancer is that cholesterol is converted to bile acids which act as promoters of carcinogenesis (58). Epidemiological studies have shown however, (38) that when beef consumption in the United States doubled (between 1940-1970) the incidence of colon cancer mortality was virtually unchanged. In addition, the incidence of colon cancer is the same in Seventh Day Adventists, who eat meat sparingly (59) and Mormons, who consume a conventional diet (60). [Pg.174]

A role for milk fat in cancer risk has not been examined adequately in epidemiological studies, because milk fat is not consumed as a single dietary item, but as a component of dairy products and dairy products also contain non-lipid components with anti-cancer potential (Parodi, 2001a, b). On the other hand, seven studies were found in the literature, where milk fat or butter diets were compared with diets containing equal amounts of polyunsaturated vegetable oils or margarine in animal models of colon, breast, and skin cancer. All seven studies showed that there was less tumor development with milk fat-based diets (Parodi, 2004). [Pg.631]


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