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Department of Health Sciences Research, Mayo Clinic and Mayo Clinic Cancer Center, Rochester, Minnesota 55905 [T. A. S., R. A. V., J. R. C., C. M. V., J. E. O., V. S. P.]; Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois 60611 [S. M. G.]; Division of Research, Kaiser Permanente, Oakland, California 94611 [L. H. K.]; and Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota 55454 [A. R. F.]
Alcohol intake is an established risk factor for breast cancer, but the underlying mechanism remains unknown. Four recent studies have described interactions of alcohol and low folate intake. We examined this interaction on the risk of postmenopausal breast cancer stratified by tumor receptor status for estrogen (ER) and progesterone (PR). The Iowa Women’s Health Study is a prospective cohort study of 34,393 at-risk women. Alcohol use and folate intake from diet and supplements were estimated at baseline in 1986 through a semiquantitative food frequency questionnaire. Through 1999, 1,875 cases of breast cancer were identified through linkage to the Iowa Surveillance, Epidemiology, and End Results registry. Compared with nondrinkers with folate intakes above the 50th percentile, women with low folate and high alcohol were at 1.43-fold greater risk (1.02–2.02). When stratified by tumor receptor status for ER or PR, the risks for low folate/high alcohol were 2.1 (1.18–3.85), 1.0 (0.76–1.42), 1.2 (0.88–1.70), and 1.2 (0.69–2.02) for ER-, ER+, PR+, and PR- tumors, respectively. Because the results were limited primarily to ER- tumors, one plausible interpretation of these data is that alcohol influences breast cancer through its metabolite, acetaldehyde, rather than through effects on ER levels and receptor-mediated pathways.
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