This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wright, M. E. Articles by Leitzmann, M. F. Search for Related Content PubMed PubMed Citation Articles by Wright, M. E. Articles by Leitzmann, M. F. Related Collections Epidemiology Epidemiology: Nutritional Epidemiology

Supplemental and Dietary Vitamin E Intakes and Risk of Prostate Cancer in a Large Prospective Study

Divisions of ¹ Cancer Epidemiology and Genetics, ² Cancer Prevention, and ³ Cancer Control and Population Sciences, National Cancer Institute, NIH, DHHS, Bethesda, Maryland and ⁴ Department of Nutrition, Food Studies, and Public Health, New York University, New York, New York

Requests for reprints: Margaret E. Wright, Department of Pathology, College of Medicine, University of Illinois at Chicago, Room 130, 840 South Wood Street, Chicago, IL 60612. Phone: 312-996-9684; Fax: 312-996-4812. E-mail: mewright{at}uic.edu

Supplemental vitamin E (-tocopherol) has been linked to lower prostate cancer incidence in one randomized trial and several, although not all, observational studies. The evidence regarding dietary intake of individual vitamin E isoforms and prostate cancer is limited and inconclusive, however. We prospectively examined the relations of supplemental vitamin E and dietary intakes of -, ß-, -, and - tocopherols to prostate cancer risk among 295,344 men, ages 50 to 71 years and cancer-free at enrollment in 1995 to 1996, in the NIH-AARP Diet and Health Study. At baseline, participants completed a questionnaire that captured information on diet, supplement use, and other factors. Proportional hazards models were used to estimate relative risks (RR) and 95% confidence intervals (95% CI) of prostate cancer. During 5 years of follow-up, 10,241 incident prostate cancers were identified. Supplemental vitamin E intake was not related to prostate cancer risk (for >0-99, 100-199, 200-399, 400-799, and 800 IU/d versus never use: RR, 0.97, 0.89, 1.03, 0.99, and 0.97 (95% CI, 0.87-1.07) respectively; P_trend = 0.90). However, dietary -tocopherol, the most commonly consumed form of vitamin E in the United States, was significantly inversely related to the risk of advanced prostate cancer (for highest versus lowest quintile: RR, 0.68; 95% CI, 0.56-0.84; P_trend = 0.001). These results suggest that supplemental vitamin E does not protect against prostate cancer, but that increased consumption of -tocopherol from foods is associated with a reduced risk of clinically relevant disease. The potential benefit of -tocopherol for prostate cancer prevention deserves further attention. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1128–35)