OBJECTIVES: A history of type 2 diabetes is one of few consistent risk factors for pancreatic cancer. Potentially modifiable factors related to fasting insulin and glucose concentrations may influence pancreatic cancer risk. METHODS: Multiple linear regression models were used to identify anthropometric, clinical, behavioral, and dietary factors associated with fasting insulin and glucose in a subcohort of non-diabetics in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (n = 366). Hazards ratios (HRs) and 95% confidence intervals (CIs) were calculated among the larger cohort (n = 27,035). RESULTS: During follow-up (median 16.1 years), 305 participants developed pancreatic cancer. Fasting insulin and/or glucose were positively associated with body mass index (BMI), height, and dietary total and saturated fat and inversely associated with serum high-density lipoprotein cholesterol (HDL) and dietary available carbohydrates, sucrose, and alcohol. Comparing highest to lowest quintiles, total fat (HR = 1.54, 95% CI 1.05-2.25, p-trend = 0.01) and saturated fat (HR = 1.38, 95% CI 0.97-1.98, p-trend = 0.06) were positively associated and available carbohydrates (HR = 0.63, 95% CI 0.44-0.90, p-trend = 0.01), particularly sucrose (HR = 0.62, 95% CI 0.43-0.89, p-trend = 0.09), were inversely associated with risk of pancreatic cancer. BMI, HDL, height, and alcohol were not associated with pancreatic cancer risk. CONCLUSION: Dietary fat is associated with higher fasting insulin concentrations and may increase pancreatic cancer risk in smokers.
RCT Entities:
OBJECTIVES: A history of type 2 diabetes is one of few consistent risk factors for pancreatic cancer. Potentially modifiable factors related to fasting insulin and glucose concentrations may influence pancreatic cancer risk. METHODS: Multiple linear regression models were used to identify anthropometric, clinical, behavioral, and dietary factors associated with fasting insulin and glucose in a subcohort of non-diabetics in the Alpha-Tocopherol, Beta-CaroteneCancer Prevention Study (n = 366). Hazards ratios (HRs) and 95% confidence intervals (CIs) were calculated among the larger cohort (n = 27,035). RESULTS: During follow-up (median 16.1 years), 305 participants developed pancreatic cancer. Fasting insulin and/or glucose were positively associated with body mass index (BMI), height, and dietary total and saturated fat and inversely associated with serum high-density lipoprotein cholesterol (HDL) and dietary available carbohydrates, sucrose, and alcohol. Comparing highest to lowest quintiles, total fat (HR = 1.54, 95% CI 1.05-2.25, p-trend = 0.01) and saturated fat (HR = 1.38, 95% CI 0.97-1.98, p-trend = 0.06) were positively associated and available carbohydrates (HR = 0.63, 95% CI 0.44-0.90, p-trend = 0.01), particularly sucrose (HR = 0.62, 95% CI 0.43-0.89, p-trend = 0.09), were inversely associated with risk of pancreatic cancer. BMI, HDL, height, and alcohol were not associated with pancreatic cancer risk. CONCLUSION: Dietary fat is associated with higher fasting insulin concentrations and may increase pancreatic cancer risk in smokers.
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