Epidemiology

British Journal of Cancer (2006) 94, 757–762. doi:10.1038/sj.bjc.6603020 www.bjcancer.com
Published online 21 February 2006

Alcohol intake and ovarian cancer risk: a pooled analysis of 10 cohort studies

Institution where work was performed: Harvard School of Public Health, Boston, MA, USA

J M Genkinger1, D J Hunter1,2,3, D Spiegelman2,4, K E Anderson5, J E Buring2,6, J L Freudenheim7, R A Goldbohm8, L Harnack5, S E Hankinson2,3, S C Larsson9, M Leitzmann10, M L McCullough11, J Marshall7, A B Miller12, C Rodriguez11, T E Rohan13, A Schatzkin10, L J Schouten14, A Wolk9, S M Zhang2,6 and S A Smith-Warner1,2

  1. 1Department of Nutrition, Harvard School of Public Health, Boston, MA, USA
  2. 2Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA
  3. 3Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
  4. 4Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA
  5. 5Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN, USA
  6. 6Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
  7. 7Department of Social and Preventive Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA
  8. 8Department of Food and Chemical Risk Analysis, TNO Quality of Life, Zeist, The Netherlands
  9. 9Division of Nutritional Epidemiology, National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden
  10. 10Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA
  11. 11Epidemiology and Surveillance Research, American Cancer Society, Atlanta, GA, USA
  12. 12Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
  13. 13Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA
  14. 14Department of Epidemiology, NUTRIM, Maastricht University, Maastricht, The Netherlands

Correspondence: Dr JM Genkinger, E-mail: pooling@hsphsun2.harvard.edu

Received 17 November 2005; Revised 16 January 2006; Accepted 30 January 2006; Published online 21 February 2006.

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Abstract

Alcohol has been hypothesized to promote ovarian carcinogenesis by its potential to increase circulating levels of estrogen and other hormones; through its oxidation byproduct, acetaldehyde, which may act as a cocarcinogen; and by depletion of folate and other nutrients. Case–control and cohort studies have reported conflicting results relating alcohol intake to ovarian cancer risk. We conducted a pooled analysis of the primary data from ten prospective cohort studies. The analysis included 529 638 women among whom 2001 incident epithelial ovarian cases were documented. After study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then were pooled using a random effects model; no associations were observed for intakes of total alcohol (pooled multivariate RR=1.12, 95% CI 0.86–1.44 comparing greater than or equal to30 to 0 g day-1 of alcohol) or alcohol from wine, beer or spirits and ovarian cancer risk. The association with alcohol consumption was not modified by oral contraceptive use, hormone replacement therapy, parity, menopausal status, folate intake, body mass index, or smoking. Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. This pooled analysis does not support an association between moderate alcohol intake and ovarian cancer risk.

Keywords:

alcohol, ovarian cancer, pooled analysis