Epidemiology

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Flavonoid intake and ovarian cancer risk in a population-based case-control study

  1. Margaret A. Gates1,2,†,*,
  2. Allison F. Vitonis3,
  3. Shelley S. Tworoger1,2,
  4. Bernard Rosner1,4,
  5. Linda Titus-Ernstoff5,
  6. Susan E. Hankinson1,2,
  7. Daniel W. Cramer2,3

Article first published online: 11 NOV 2008

DOI: 10.1002/ijc.24151

Issue

International Journal of Cancer

International Journal of Cancer

Volume 124, Issue 8, pages 1918–1925, 15 April 2009

Additional Information

How to Cite

Gates, M. A., Vitonis, A. F., Tworoger, S. S., Rosner, B., Titus-Ernstoff, L., Hankinson, S. E. and Cramer, D. W. (2009), Flavonoid intake and ovarian cancer risk in a population-based case-control study. Int. J. Cancer, 124: 1918–1925. doi: 10.1002/ijc.24151

Author Information

  1. 1

    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA

  2. 2

    Department of Epidemiology, Harvard School of Public Health, Boston, MA

  3. 3

    Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Boston, MA

  4. 4

    Department of Biostatistics, Harvard School of Public Health, Boston, MA

  5. 5

    Norris Cotton Cancer Center, Dartmouth-Hitchcock Medical Center, Lebanon, NH

  1. †

    Fax: +617-525-2008

*Channing Laboratory, 181 Longwood Avenue, Boston, MA 02115, USA

  1. †

    Fax: +617-525-2008

Publication History

  1. Issue published online: 12 FEB 2009
  2. Article first published online: 11 NOV 2008
  3. Manuscript Accepted: 24 OCT 2008
  4. Manuscript Received: 25 MAR 2008

Funded by

  • National Cancer Institute, National Institutes of Health. Grant Numbers: R01 CA054419, P50 CA105009, T32 CA009001, R25 CA098566

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Keywords:

  • flavonoids;
  • flavonols;
  • flavones;
  • diet;
  • ovarian cancer;
  • epidemiology

Abstract

Several recent studies have evaluated the association between dietary flavonoid intake and ovarian cancer risk, and all reported significant or suggestive inverse associations with certain flavonoids or flavonoid subclasses; however, most of these studies were small to moderate in size. We, therefore, examined this association in a large, population-based case-control study. We calculated intake of 5 common dietary flavonoids (myricetin, kaempferol, quercetin, luteolin, and apigenin), as well as total intake of these flavonoids, for 1,141 cases and 1,183 frequency-matched controls. We used unconditional logistic regression to estimate the relative risk (RR) of ovarian cancer for each quintile of flavonoid intake when compared with the lowest quintile. We did not observe an association between total flavonoid intake and ovarian cancer risk. The multivariable-adjusted RR for the highest versus lowest quintile of total flavonoid intake was 1.06 (95% confidence interval [CI] = 0.78–1.45). In analyses of each individual flavonoid, only intake of apigenin was associated with a borderline significant decrease in risk (RR, highest vs. lowest quintile = 0.79, 95% CI = 0.59–1.06; p-trend = 0.26), and this association was significant after adjustment for intake of the other 4 individual flavonoids (comparable RR = 0.72, 95% CI = 0.53–0.98; p-trend = 0.09). These results provide limited support for an association between flavonoid intake and ovarian cancer risk. However, given the findings of previous studies and the biologic plausibility of this association, additional studies are warranted. © 2008 Wiley-Liss, Inc.

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