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Departments of 1 Nutrition, 2 Epidemiology, and 3 Biostatistics, Harvard School of Public Health; 4 Department of Medicine, Channing Laboratory and 5 Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School; 6 Harvard Center for Cancer Prevention, Boston, Massachusetts; 7 Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota; 8 Divisions of Epidemiology and Biostatistics, Department of Environmental Medicine, New York University School of Medicine, New York, New York; 9 Center for Health Research, Loma Linda University School of Medicine, Loma Linda, California; 10 Department of Epidemiology, Maastricht University, Maastricht, the Netherlands; 11 Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, Minnesota; 12 Department of Social and Preventive Medicine, University at Buffalo, State University of New York, Buffalo, New York; 13 Department of Epidemiology, TNO Nutrition and Food Research Institute, Zeist, the Netherlands; 14 Division of Nutritional Epidemiology, National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; 15 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland; 16 Epidemiology and Surveillance Research, American Cancer Society, Atlanta, Georgia; 17 Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; and 18 Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York
Requests for reprints: Stephanie Smith-Warner, Harvard School of Public Health, Department of Nutrition, 665 Huntington Avenue, Boston, MA 02115. Phone: 617-432-4977; Fax: 617-432-2435.
Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food-frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer riskthe pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.74]. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% CI, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.
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