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

J.M. Genkinger*, D.J. Hunter, D. Spiegelman, K.E. Anderson, J.E. Buring, J.L. Freudenheim, R.A. Goldbohm, L. Harnack, S.E. Hankinson, S.C. Larsson, M. Leitzmann, M.L. McCullough, J. Marshall, A.B. Miller, C. Rodriguez, T.E. Rohan, A. Schatzkin, L.J. Schouten, A. Wolk, S.M. ZhangS.A. Smith Warner

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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 > or =30 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.
Original languageEnglish
Pages (from-to)757-762
JournalBritish Journal of Cancer
Volume94
Issue number5
DOIs
Publication statusPublished - 1 Jan 2006

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