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Eur J Epidemiol. 2017 Nov;32(11):1007-1017. doi: 10.1007/s10654-017-0301-8. Epub 2017 Sep 1.

Dietary sugar/starches intake and Barrett's esophagus: a pooled analysis.

Author information

1
Department of Epidemiology, University of North Carolina at Chapel Hill, 135 Dauer Drive, CB# 7435, Chapel Hill, NC, 27599-7435, USA. nanl@live.unc.edu.
2
Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.
3
Department of Epidemiology and Biostatistics, University of South Carolina, Columbia, SC, USA.
4
Division of Epidemiology, University of California, Berkeley, Berkeley, CA, USA.
5
Department of Epidemiology, University of North Carolina at Chapel Hill, 135 Dauer Drive, CB# 7435, Chapel Hill, NC, 27599-7435, USA.
6
Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
7
Division of Research and San Francisco Medical Center, Kaiser Permanente, Northern California, Oakland, CA, USA.
8
Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.

Abstract

Barrett's esophagus (BE) is the key precursor lesion of esophageal adenocarcinoma, a lethal cancer that has increased rapidly in westernized countries over the past four decades. Dietary sugar intake has also been increasing over time, and may be associated with these tumors by promoting hyperinsulinemia. The study goal was to examine multiple measures of sugar/starches intake in association with BE. This pooled analysis included 472 BE cases and 492 controls from two similarly conducted case-control studies in the United States. Dietary intake data, collected by study-specific food frequency questionnaires, were harmonized across studies by linking with the University of Minnesota Nutrient Database, and pooled based on study-specific quartiles. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for age, sex, race, total energy intake, study indicator, body mass index, frequency of gastro-esophageal reflux, and fruit/vegetable intake. In both studies, intake of sucrose (cases vs. controls, g/day: 36.07 vs. 33.51; 36.80 vs. 35.06, respectively) and added sugar (46.15 vs. 41.01; 44.18 vs. 40.68, respectively) were higher in cases than controls. BE risk was increased 79% and 71%, respectively, for associations comparing the fourth to the first quartile of intake of sucrose (ORQ4vs.Q1 = 1.79, 95% CI = 1.07-3.02, P trend = 0.01) and added sugar (ORQ4vs.Q1 = 1.71, 95% CI = 1.05-2.80, P trend = 0.15). Intake of sweetened desserts/beverages was associated with 71% increase in BE risk (ORQ4vs.Q1 = 1.71, 95% CI = 1.07-2.73, P trend = 0.04). Limiting dietary intake of foods and beverages that are high in added sugar, especially refined table sugar, may reduce the risk of developing BE.

KEYWORDS:

Added sugar; Barrett’s esophagus; Diet; Sweetened desserts/beverages

PMID:
28864851
PMCID:
PMC6331010
DOI:
10.1007/s10654-017-0301-8
[Indexed for MEDLINE]
Free PMC Article

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