TY - JOUR
T1 - Glycemic index, glycemic load, and the risk of pancreatic cancer among postmenopausal women in the women's health initiative observational study and clinical trial
AU - Simon, M. S.
AU - Shikany, J. M.
AU - Neuhouser, M. L.
AU - Rohan, T.
AU - Nirmal, K.
AU - Cui, Y.
AU - Abrams, J.
PY - 2010/12
Y1 - 2010/12
N2 - Background: Several reports have suggested that conditions associated with hyperinsulinemia and insulin resistance, such as diets high in carbohydrates, may influence the risk of pancreatic cancer, although results from prior studies have been mixed. Methods: We utilized data from the population-based women's health initiative (WHI) cohort to determine whether dietary factors that are associated with increased postprandial blood glucose levels are also associated with an increased risk of pancreatic cancer. The WHI included 161,809 postmenopausal women of ages 50-79, in which 332 cases of pancreatic cancer were identified over a median of 8 years of follow-up; 287 of these cases met the criteria for analysis. A validated 122-item food frequency questionnaire was used to estimate dietary glycemic load (GL), glycemic index (GI), total and available carbohydrates, fructose and sucrose. Baseline questionnaires and physical exams provided information on demographic, medical, lifestyle, and anthropometric characteristics. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between the exposures of interest and pancreatic cancer risk, with adjustment for potential confounders. Results: Dietary GL, GI, carbohydrates, fructose, and sucrose were not associated with increased risk of pancreatic cancer. The multivariable adjusted HR for the highest vs. the lowest quartile of GL was 0.80 (95% CI = 0.55-1.15, trend p = 0.31) and 1.13 (95% CI = 0.78-1.63, trend p = 0.94) for GI. The results remained negative when individuals with a history of diabetes were excluded. Conclusions: Our results do not support the hypothesis that dietary intake of carbohydrates is associated with increased risk of pancreatic cancer.
AB - Background: Several reports have suggested that conditions associated with hyperinsulinemia and insulin resistance, such as diets high in carbohydrates, may influence the risk of pancreatic cancer, although results from prior studies have been mixed. Methods: We utilized data from the population-based women's health initiative (WHI) cohort to determine whether dietary factors that are associated with increased postprandial blood glucose levels are also associated with an increased risk of pancreatic cancer. The WHI included 161,809 postmenopausal women of ages 50-79, in which 332 cases of pancreatic cancer were identified over a median of 8 years of follow-up; 287 of these cases met the criteria for analysis. A validated 122-item food frequency questionnaire was used to estimate dietary glycemic load (GL), glycemic index (GI), total and available carbohydrates, fructose and sucrose. Baseline questionnaires and physical exams provided information on demographic, medical, lifestyle, and anthropometric characteristics. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between the exposures of interest and pancreatic cancer risk, with adjustment for potential confounders. Results: Dietary GL, GI, carbohydrates, fructose, and sucrose were not associated with increased risk of pancreatic cancer. The multivariable adjusted HR for the highest vs. the lowest quartile of GL was 0.80 (95% CI = 0.55-1.15, trend p = 0.31) and 1.13 (95% CI = 0.78-1.63, trend p = 0.94) for GI. The results remained negative when individuals with a history of diabetes were excluded. Conclusions: Our results do not support the hypothesis that dietary intake of carbohydrates is associated with increased risk of pancreatic cancer.
KW - Glycemic index
KW - Glycemic load
KW - Pancreatic neoplasms
KW - Prospective cohort
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U2 - 10.1007/s10552-010-9632-4
DO - 10.1007/s10552-010-9632-4
M3 - Article
C2 - 20711806
AN - SCOPUS:78751574273
SN - 0957-5243
VL - 21
SP - 2129
EP - 2136
JO - Cancer Causes and Control
JF - Cancer Causes and Control
IS - 12
ER -