Molecular Epidemiology on insulin-like growth facto (IGF) and colorectal adenomas

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Etiological factors of colorectal adenomas were studied with special reference to insulin like growth factor (IGF) and related conditions. Frozen plasma samples of 3370 persons were used to measure IGF-I, IGFBP-3 and C-peptide, and genetic polymorphisms regarding folate, alcohol and bile acid metabolism were investigated in relation to colorectal adenoma risk. The metabolic syndrome, which is accompanied with sustained hyperinsulinemia, was strongly related to increased risk of colorectal adenomas. Glucose intolerance and high levels of C-peptide, a measure of hyperinsulinemia, were also associated with increased risk of adenomas, but neither IGF-I nor IGFBP-3 was associated with colorectal adenomas. Increased risk of colorectal adenomas associated with hyperglycemia or hyperinsulinemia is probably linked with a mechanism or mechanisms other than the IGF system. A folate-related genetic polymorphism, reportedly associated with colorectal cancer, was not related to colorectal adenomas. Nor was the ALDH2 polymorphism. However, a polymorphism of CYP7A1, an enzyme in the synthesis of bile acids, was associated with right-side colon adenomas, indicating that bile acids is linked with carcinogenesis in the right side colon. Smoking and alcohol use were both related to increased risk of colorectal adenomas, especially of distal adenomas. It was found that coffee was protective against diabetes mellitus, which is an important risk factor for colorectal adenomas. Smoking and alcohol use were related to deterioration in glucose tolerance. A dietary pattern representing high intake of dairy foods and fruits was found not only to be related to decreased risk of colorectal adenomas but also to be protective against glucose tolerance abnormality