Pancreatic Cancer Linked to Available Carbohydrates and Glycemic Load
The authors investigated the associations of glycemic load, glycemic index, and carbohydrate intake with pancreatic cancer risk....
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High-carbohydrate diets have been linked to pancreatic cancer risk in case-control studies, but prospective studies have shown mostly null results. The authors investigated the associations of glycemic load, glycemic index, and carbohydrate intake with pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
Dietary intake was assessed by using a self-administered questionnaire. Between 1998 and 2006 (median follow-up = 6.5 years), 266 incident, confirmed pancreatic cancers were identified among 109,175 participants. Hazards ratios and 95% confidence intervals were adjusted for sex, smoking, body mass index, and total energy. Overall, elevated risks for pancreatic cancer were observed in the 90th versus 10th percentile of glycemic load (hazards ratio (HR) = 1.45, 95% confidence interval (CI): 1.05, 2.00), available carbohydrate (HR = 1.47, 95% CI: 1.05, 2.06), and sucrose (HR = 1.37, 95% CI: 0.99, 1.89) intake.
Higher dietary intakes of glycemic load, available carbohydrates, and sucrose were associated with greater risk of pancreatic cancer, while dietary glycemic index, starch, and fructose intakes were not associated with risk in this cohort. However, the positive associations observed for glycemic load, available carbohydrates, and sucrose were limited to the first 4 years of follow-up. No association was found for carbohydrate intake in the later follow-up period. Researcher also observed the reverse for total fat intake, particularly saturated fat, whereby an inverse association was observed in the earlier, but not later, follow-up period.
Although high glycemic load diets have a biologically plausible role in the development of pancreatic cancer, epidemiologic studies have shown consistent null results. In the Nurses' Health Study, a significant dose-response association for dietary glycemic load was observed only among women who were physically inactive and overweight (RR = 2.67, 95% CI: 1.02, 6.99). No statistically significant associations between glycemic load and pancreatic cancer were observed in subsequent prospective studies, including analyses restricted to physically inactive and/or overweight participants.
In conclusion, in this prospective study, an elevated risk of pancreatic cancer was associated with a high glycemic load and available carbohydrate intake only among participants with less than 4 years of follow-up. The association of total and saturated fat, in turn, was inversely associated with pancreatic cancer in the earlier, but not later, follow-up period. This finding suggests that participants who were diagnosed with incident pancreatic cancer earlier during follow-up may have been symptomatic at the time the food frequency questionnaire was completed, altering their diets to include more easily digestible carbohydrates and less fat. Future prospective studies examining recent diet and pancreatic cancer risk should consider the potential influence of preclinical disease on self-reported intake.
American Journal of Epidemiology. 2010;171(11):1174-1182.
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