Cancer Prevention Program
Nearly two-thirds of adults in the United States are overweight or obese. One of the serious consequences of this obesity epidemic is the growing evidence that obesity increases risk for several common cancers. Hyperinsulinemia, and altered levels of adipocyte hormones, insulin-like growth factors and markers of inflammation often accompany obesity and may provide the mechanistic explanation for these observed associations of obesity with cancer. For example, IGF1 inhibits apoptosis and stimulates proliferation, and both insulin and leptin are mitogenic. On the other hand, obesity inhibits adiponectin, which is associated with both reduced inflammatory response and reduced cancer risk. Dietary patterns are related to the synthesis, metabolism, and distribution of these biomarkers. Diets can be characterized by their ability to influence the postprandial glucose response; e.g., diets rich in simple sugars and refined carbohydrates have a high glycemic index by producing a rapid rise in blood glucose, and meats, legumes and high-fiber foods have a low glycemic index. Despite the plethora of scientific papers suggesting that high-glycemic index foods or dietary patterns with a high glycemic load increase cancer risk, few intervention studies have evaluated whether these eating patterns influence biomarkers of cancer risk.
This study a randomized, controlled crossover feeding trial in 88 normal weight (BMI=18.5-29.9 kg/m2) and overweight/ obese men and women (BMI= 25.0-39.9 kg/m2). Participants will be randomized to eat either a low- or high-glycemic load diet for four weeks, followed by a four-week wash-out period, then cross-over to the other arm. Blood samples will be collected at the beginning and end of each diet period and assayed for insulin, glucose, IGF1, IGFBP3, leptin, adiponectin, C-reactive protein, serum amyloid A, interleukin-6 and plasma proteomic patterns. This study provides a rigorous test of common dietary patterns in humans and allows a direct test of diet-related mechanisms of obesity and biomarkers of carcinogenesis. By recruiting both lean and overweight/obese persons, we will be able to examine whether there is a differential response to the high- and low-glycemic load diets by BMI.
Contact: Yvonne Schwarz (206) 667-7804