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Dietary Antioxidants, Fruits, and Vegetables and the Risk of Barrett's Esophagus

Kubo, Ai, M.P.H., Ph.D.1; Levin, Theodore R., M.D.1; Block, Gladys, Ph.D.2; Rumore, Gregory J., M.D.1; Quesenberry, Charles P. Jr, Ph.D.1; Buffler, Patricia, Ph.D.2; Corley, Douglas A., M.D., Ph.D.1,3

American Journal of Gastroenterology: July 2008 - Volume 103 - Issue 7 - p 1614–1623
ORIGINAL CONTRIBUTION: ESOPHAGUS
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OBJECTIVE The present study evaluated the associations among antioxidants, fruit and vegetable intake, and the risk of Barrett's esophagus (BE), a potential precursor to esophageal adenocarcinoma.

METHODS We conducted a case–control study within the Kaiser Permanente Northern California population. Incident BE cases (N = 296) were matched to persons with gastroesophageal reflux disease (GERD) (GERD controls N = 308) and to population controls (N = 309). Nutrient intake was measured using a validated 110-item food frequency questionnaire. The antioxidant results were stratified by dietary versus total intake of antioxidants.

RESULTS Comparing cases to population controls, dietary intake of vitamin C and beta-carotene were inversely associated with the risk of BE (4th vs 1st quartile, adjusted odds ratio [OR] 0.48, 95% confidence interval [CI] 0.26–0.90; OR 0.56, 95% CI 0.32–0.99, respectively), and the inverse association was strongest for vitamin E (OR 0.25, 95% CI 0.11–0.59). The inverse trends for antioxidant index (total and dietary) and fruit and vegetable intake were statistically significant, while most total intakes were not associated with reduced risk. The use of antioxidant supplements did not influence the risk of BE, and antioxidants and fruits and vegetables were inversely associated with a GERD diagnosis.

CONCLUSION Dietary antioxidants, fruits, and vegetables are inversely associated with the risk of BE, while no association was observed for supplement intake. Our results suggest that fruits and vegetables themselves or associated undetected confounders may influence early events in the carcinogenesis of esophageal adenocarcinoma.

1Division of Research, Kaiser Permanente, Oakland, California; 2School of Public Health, University of California, Berkeley, Berkeley, California; and 3Department of Medicine and Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California

Reprint requests and correspondence: Ai Kubo, Division of Research, Kaiser Permanente, 2000 Broadway, Oakland, CA 94612.

CONFLICT OF INTEREST

Guarantor of the article: Ai Kubo, M.P.H., Ph.D.

Specific author contributions: Ai Kubo contributed to the reviews of the existing literature, statistical analyses, and the preparation of the manuscript; T.R. Levin and Greg Rumore conducted medical and pathology review; Charles Quesenberry and Gladys Block contributed to the statistical methods of the nutritional analysis; Patricia Buffler helped design the study; and Douglas Corley is a principal investigator of the case–control study and contributed to the statistical analyses and the preparation of the manuscript.

Financial support: The study is supported by grants K08DK002697 and RO1 DK63616 from the National Institutes of Health.

Potential competing interests: None.

Received December 4, 2007; accepted January 15, 2008.

© The American College of Gastroenterology 2008. All Rights Reserved.
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