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  Vol. 154 No. 16, 22 August 1994 TABLE OF CONTENTS
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Diet and Breast Cancer Risk

Results From a Population-Based, Case-Control Study in Sweden

Lars Holmberg, MD; Eva M. Ohlander; Tim Byers, MD, PhD; Matthew Zack, MD, PHD; Alicja Wolk, PhD; Reinhold Bergström, PhD; Leif Bergkvist, MD, PhD; Erik Thurfjell, MD; Ake Bruce, PhD; Hans-Olov Adami, MD, PhD

Arch Intern Med. 1994;154(16):1805-1811.


Abstract

Background
We describe an epidemiologic analytical study of the relationship between current diet and breast cancer risk.

Method
The study design is a case-control analysis. Cases were recruited from a mammography screening program used within the national health care system; the control subjects were selected from subjects free of breast cancer in the same population. A total of 380 cases and 525 control subjects, frequency-matched for age, month of mammography, and county of residence, were identified. Of these, 265 cases and 432 control subjects were included in this analysis. Odds ratios for breast cancer in relation to food and nutrient intake were the main outcome measures.

Results
Exposure in the highest quartile of β-carotene intake gave an odds ratio of 0.6 (95% confidence interval, 0.4 to 1.0). No increased risk was noted with high fat intake. Breast cancer risk was associated with alcohol intake only when alcohol was analyzed in quartiles: odds ratio, 1.6 (95% confidence interval, 1.0 to 2.4) for the highest quartile of intake vs the lowest. Stratified analyses showed that a high fat intake might decrease the protective effect of β-carotene intake. Risks did not change appreciably with adjustment for total energy intake or known breast cancer risk factors.

Conclusions
As in most other studies, no strong risk factors for breast cancer have been identified in the current diet. The negative association between breast cancer risk and β-carotene intake may be supported by a plausible mechanism, but our finding concerning alcohol should be interpreted cautiously since there was no dose-response relationship and the biological mechanism for a threshold effect at very low levels of consumption is unclear.

(Arch Intern Med. 1994;154:1805-1811)



Author Affiliations

From the Cancer Epidemiology Unit (Drs Holmberg, Wolk, Bergström, and Adami) and Department of Surgery (Dr Holmberg), Mammography Unit, Department of Diagnostic Radiology (Dr Thurfjell), University Hospital and the National Food Administration, Uppsala, Sweden (Ms Ohlander and Dr Bruce); Division of Nutrition (Dr Byers), Division of Chronic Disease Control and Community Intervention (Dr Zack), National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Ga; Department of Statistics, Uppsala University (Dr Bergström); Department of Surgery, Central Hospital, Västeräs, Sweden (Dr Bergkvist); and Department of Epidemiology, Harvard School of Public Health, Boston, Mass (Dr Adami).



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