Breast, colorectal, and prostate cancer risk in the European Prospective Investigation into Cancer and Nutrition–Norfolk in relation to phytoestrogen intake derived from an improved database1234

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Background: The characterization of phytoestrogen intake and cancer risk has been hindered by the absence of accurate dietary phytoestrogen values.

Objective: We examined the risk of breast, colorectal, and prostate cancers relative to phytoestrogen intake on the basis of a comprehensive database.

Design: Demographic and anthropometric characteristics, a medical history, and 7-d records of diet were collected prospectively from participants (aged 40–79 y) in the European Prospective Investigation into Cancer and Nutrition–Norfolk (EPIC-Norfolk). Five hundred nine food items were analyzed by liquid chromatography–mass spectrometry/mass spectrometry, and 13C3-labeled internal standards were analyzed for isoflavones (genistein, daidzein, glycitein, biochanin A, and formononetin), lignans (secoisolariciresinol and matairesinol), and enterolignans from gut microbial metabolism in animal food sources (equol and enterolactone). From the direct analysis, values for 10,708 foods were calculated. Odds ratios (ORs) for breast (244 cases, 941 controls), colorectal (221 cases, 886 controls), and prostate (204 cases, 812 controls) cancers were calculated relative to phytoestrogen intake.

Results: Phytoestrogen intake was not associated with breast cancer among women or colorectal cancer among men. Among women, colorectal cancer risk was inversely associated with enterolactone (OR: 0.33; 95% CI: 0.14, 0.74) and total enterolignans (OR: 0.32; 95% CI: 0.13, 0.79), with a positive trend detected for secoisolariciresinol (OR: 1.60; 95% CI: 0.96, 2.69). A positive trend between enterolignan intake and prostate cancer risk (OR: 1.27; 95% CI: 0.97, 1.66) was attenuated after adjustment for dairy intake (OR: 1.19; 95% CI: 0.77, 1.82).

Conclusion: Dietary phytoestrogens may contribute to the risk of colorectal cancer among women and prostate cancer among men.

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1

From the MRC Centre for Nutritional Epidemiology in Cancer Prevention and Survival, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom (HAW, GGCK, AAM, and MAHL); the MRC Dunn Human Nutrition Unit, Cambridge, United Kingdom (GGCK); and the European Prospective Investigation into Cancer and Nutrition, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom (RNL and K-TK).

2

Portions of this manuscript were included in our report to the Food Standards Agency.

3

Supported by the Food Standards Agency (contract number T05028) and the Medical Research Council.

4

Address correspondence to HA Ward, MRC Centre for Nutrition and Cancer, Department of Public Health and Primary Care, Strangeways Research Laboratory, Wort’s Causeway, Cambridge, United Kingdom. E-mail [email protected].