Diabetes & hyper-insulinemia as predictors of colorectal cancer risk
Diabetes and hyper-insulinemia as predictors of colorectal cancer risk in a prospective cohort of women
Women with diabetes are 1.5 times more likely to develop colorectal cancer than those who do not have the metabolic disorder, according to researchers at the University of Minnesota. The findings, they say, add to the complex body of evidence linking diet and colorectal cancer and also provide new evidence that furthers our understanding of the role of insulin in cancer promotion.
“Colorectal cancer and type II diabetes share a number of common factors, including obesity, so it is interesting to see the direct line between these two conditions,” said Andrew Flood, Ph.D., assistant professor in the Division of Epidemiology and Community Health at the University of Minnesota School of Public Health and the University of Minnesota Cancer Center “In general, the idea is that if elevated insulin levels create a biochemical environment conducive to cancer growth, it provides one mechanism by which diet and lifestyle can really influence cancer risk.”
With funding from the National Cancer Institute, Flood and his colleagues examined data from a massive screening study called the Breast Cancer Detection Demonstration Project, initiated at 29 centers throughout the United States in the 1970s. Flood’s team subsequently followed more than 45,000 study participants with no history of colorectal cancer or self-reported diabetes for eight years, (from 1987-1989 and from 1995-1998), to identify which of them subsequently developed colorectal cancer. According to their findings, women with diabetes had a greatly increased risk of developing colorectal cancer. “These results remained statistically significant even after controlling for all known and suspected confounding variables,” Flood said.
According to Flood, it is not exactly clear what aspect of diabetes is the underlying cause for this increased risk, but one hypothesis centers on the elevated concentration of insulin typically seen in people with type II diabetes. “In the early stages of the disease process, people become insulin resistant, meaning they must produce more and more insulin to regulate their blood sugar,” Flood said.
“Even after frank diabetes begins, insulin levels remain chronically elevated for extended periods before the pancreas can no longer supply the level of insulin the body demands,” Flood said. “If the elevated insulin is the problem, then pre-diabetics, who are also hyper-insulinemic, should also be at increased risk (for developing colorectal cancer).”
To test that idea, Flood and his colleagues re-analyzed the data, this time including women who were likely pre-diabetic at the beginning of the follow-up period. The idea, Flood says, is that these women were likely hyper-insulinemic at that stage. Surprisingly, the elevated risk, while still significant, had dropped slightly in comparison with that of known diabetics, Flood says.
According to Flood, this suggests that either the pre-diabetic women had not had elevated insulin long enough or intensely enough to increase risk as they observed in the diabetic women, or alternatively, something other than or in addition to hyper-insulinemia could explain the significant, increased risk for colorectal cancer they observed in people with diabetes.
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