Dietary components that are implicated in pancreatic cancer exert their influence as factors for pancreatitis and diabetes mellitus. For example, excessive alcohol intake is associated with pancreatitis, which is a risk factor for pancreatic cancer . Similarly, excessive intake of simple carbohydrates exacerbates hyperglycemia in susceptible individuals, and diabetes is a risk factor for pancreatic cancer [32, 33].
Other than alcohol-related cirrhosis, carcinogenesis in the liver appears to be influenced only minimally by dietary constituents . Factors such as cirrhosis, HBV and aflatoxin contamination seem to exert more of an influence over carcinogenesis .
Multiple micronutrients including calcium [36-39], vitamin D , folate  and selenium  appear to have colorectal chemopre-ventive properties. Calcium decreases colon epithelial hyperprolifer-ation induced by bile and fatty acids , while vitamin D seems to modulate the effects of calcium. Folate is involved in the donation of methyl groups and the proper functioning of methyltetrahydro-folate reductase. Interestingly, it appears that folate supplementation in those individuals without cancer confers a protective effect; however, in those with neoplastic tissue, it may increase risk of cancer . Selenium enhances the peroxidation-inhibiting enzyme glutathione peroxidase and promotes coloncyte apoptosis, which may afford protection against colon carcinogenesis .
It has been suggested that high dietary fat intake may increase colon cancer risk. The proposed mechanism involves dietary fat-enhanced secretion of primary bile acids, which are converted to more cytotoxic secondary and tertiary bile acids by colonic bacteria . The correlation of dietary fat intake with cancer incidence is somewhat controversial . Although initial studies indicated a link between high dietary fat intake and cancer, more recently several epidemiologic studies have indicated a weak or no association [3, 43].
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