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ORIGINAL RESEARCH COMMUNICATION |
1 From the Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA (LW, I-ML, SMZ, JEB, and HDS); the Department of Epidemiology, Harvard School of Public Health, Boston, MA (I-ML and JEB); the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA (JBB); and the Division of Aging, Department of Medicine, Brigham and Women's Hospital, Boston, MA (HDS). 2 Supported by research grants CA-047988, HL-43851, and HL-080467 from the National Institutes of Health, Bethesda, MD; a Research Scholar Grant from the American Cancer Society; and US Department of Agriculture Research Service under Cooperative Agreement no. 58-1950-4-401. 3 Reprints not available. Address correspondence to L Wang, Brigham and Women's Hospital, 900 Commonwealth Avenue East, Boston, MA 02215. E-mail: luwang{at}rics.bwh.harvard.edu.
Background: Flavonoids may protect against cancer development through several biological mechanisms. However, epidemiologic studies on dietary flavonoids and cancer risk have yielded inconsistent results.
Objective: We prospectively investigated the association between the intake of selected flavonoids and flavonoid-rich foods and risk of cancers in the Women's Health Study.
Design: A total of 3234 incident cancer cases were identified during 11.5 y of follow-up among 38,408 women aged
45 y. Intake of individual flavonols (quercetin, kaempferol, and myricetin) and flavones (apigenin and luteolin) was assessed from food-frequency questionnaires. Cox regression models were used to estimate the relative risk (RR) of total and site-specific cancer across increasing intakes of total and individual selected flavonoids and flavonoid-rich foods (tea, apple, broccoli, onion, and tofu).
Results: The multivariate RRs of total cancer across increasing quintiles of total quantified flavonoid intake were 1.00, 1.00, 0.93, 0.94, and 0.97 (P for trend = 0.72). For site-specific cancers, the multivariate RRs in the highest quintile of total quantified flavonoid intake compared with the lowest quintile were 1.03 for breast cancer, 1.01 for colorectal cancer, 1.03 for lung cancer, 1.15 for endometrial cancer, and 1.09 for ovarian cancer (all P > 0.05). The associations for the individual flavonoid intakes were similar to those for the total intake. There was also no significant association between intake of flavonoid-rich foods and the incidence of total and site-specific cancers.
Conclusion: Our results do not support a major role of 5 common flavonols and flavones or selected flavonoid-rich foods in cancer prevention.
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