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Vitamin E intake, -tocopherol status, and pancreatic cancer in a cohort of male smokers

¹ From the Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health Human Services, Rockville, MD (RZS-S, SS-C, SW, and DA); the Department of Epidemiology, University of Michigan, Ann Arbor, MI (SS-C and DHG); the Departments of Environmental Health Sciences, Epidemiology, and Emergency Medicine, University of Michigan, Ann Arbor, MI (DHG); the Department of Health Promotion and Chronic Disease Prevention, National Public Health Institute, Helsinki, Finland (SM and JV); and the Genetics Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health Human Services, Rockville, MD (PT).

² Supported by the Intramural Research Program of the National Institutes of Health, Division of Cancer Epidemiology and Genetics, and the US Public Health Service contracts N01-CN-45165, N01-RC-45035, and N01-RC-37004 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services.

³ Reprints not available. Address correspondence to R Stolzenberg-Solomon, 6120 Executive Boulevard, Suite 320, Rockville, MD 20852. E-mail: rs221z{at}nih.gov.

Background: Evidence indicates that vitamin E has anticarcinogenic properties for gastrointestinal cancers; however, few studies have examined this with respect to exocrine pancreatic cancer.

Objective: The objective was to examine whether vitamin E intake and serum -tocopherol concentrations were prospectively associated with exocrine pancreatic cancer.

Design: We conducted a cohort analysis of prediagnostic vitamin E intake (4 tocopherols, 4 tocotrienols), serum -tocopherol concentrations, and pancreatic cancer in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of male Finnish smokers aged 50–69 y at baseline. During follow-up from 1985 to 2004 (maximum: 19.4 y; median: 16 y), 318 incident cases were diagnosed among cohort participants with complete serum samples (n = 29,092); 306 cases had complete dietary data (n = 27,111). Cox proportional hazards models adjusted for age, smoking history, history of diabetes mellitus, and/or serum cholesterol were used to calculate hazard ratios (HRs) and 95% CIs.

Results: Higher -tocopherol concentrations were associated with lower pancreatic cancer risk (highest compared with lowest quintile, HR: 0.52; 95% CI: 0.34, 0.80; P for trend = 0.03; continuous HR: 0.91; 95% CI: 0.84, 0.99). Polyunsaturated fat, a putative prooxidant nutrient, modified the association such that the inverse -tocopherol association was most pronounced in subjects with a high polyunsaturated fat intake (ie, >9.9 g/d; highest compared with lowest quintile, HR: 0.38; 95% CI: 0.20, 0.70; P for trend = 0.03; continuous HR: 0.86; 95% CI: 0.75, 0.97; P for interaction = 0.05 and 0.02, respectively). No associations were observed for dietary tocopherols and tocotrienols.

Conclusion: Our results support the hypothesis that higher -tocopherol concentrations may play a protective role in pancreatic carcinogenesis in male smokers.