Aaron P Thrift1, Jennifer R Kramer, Abeer Alsarraj, Hashem B El-Serag. 1. *Department of Population Health, Queensland Institute of Medical Research, Brisbane, Qld, Australia †Houston VA HSR&D Center of Excellence §Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center ‡Section of Health Services Research ∥Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX.
Abstract
GOAL: To evaluate whether the association between obesity and Barrett esophagus (BE) is due to total body fatness, abdominal obesity, or both. BACKGROUND: BE risk seems to be more strongly related to central obesity than total obesity. However, no studies have investigated the association between total obesity and BE using direct measures of total body fatness. STUDY: We conducted a case-control study among patients scheduled for elective esophagogastroduodenoscopy, and a sample of patients eligible for screening colonoscopy recruited from primary care clinics. BE cases were patients with specialized intestinal metaplasia, whereas controls had no endoscopic or histopathologic BE. All patients underwent a study esophagogastroduodenoscopy and had body measurements taken. Fat mass and fat-free mass were estimated from bioelectrical impedance analysis (BIA). We calculated odds ratios (OR) and 95% confidence intervals (95% CI) using multivariable logistic regression. RESULTS: There were 70 BE cases, 229 endoscopy controls, and 118 primary care controls. BMI and BIA-derived fat mass were highly correlated; however, we found no association between BMI, fat mass, and BE (vs. all controls: BMI, OR/1 SD=1.01; 95% CI, 0.76-1.34; fat mass, OR=1.02; 95% CI, 0.77-1.36). Waist-to-hip ratio was significantly associated with increased BE risk (vs. all controls: OR/1 SD=1.45; 95% CI, 1.03-2.04). We found similar results when we analyzed the control groups separately. CONCLUSION: Waist-to-hip ratio, but not fat mass or BMI, was associated with increased BE risk. This study provides strong evidence that BE is related to body size and composition through central adiposity and not through total body fatness.
GOAL: To evaluate whether the association between obesity and Barrett esophagus (BE) is due to total body fatness, abdominal obesity, or both. BACKGROUND: BE risk seems to be more strongly related to central obesity than total obesity. However, no studies have investigated the association between total obesity and BE using direct measures of total body fatness. STUDY: We conducted a case-control study among patients scheduled for elective esophagogastroduodenoscopy, and a sample of patients eligible for screening colonoscopy recruited from primary care clinics. BE cases were patients with specialized intestinal metaplasia, whereas controls had no endoscopic or histopathologic BE. All patients underwent a study esophagogastroduodenoscopy and had body measurements taken. Fat mass and fat-free mass were estimated from bioelectrical impedance analysis (BIA). We calculated odds ratios (OR) and 95% confidence intervals (95% CI) using multivariable logistic regression. RESULTS: There were 70 BE cases, 229 endoscopy controls, and 118 primary care controls. BMI and BIA-derived fat mass were highly correlated; however, we found no association between BMI, fat mass, and BE (vs. all controls: BMI, OR/1 SD=1.01; 95% CI, 0.76-1.34; fat mass, OR=1.02; 95% CI, 0.77-1.36). Waist-to-hip ratio was significantly associated with increased BE risk (vs. all controls: OR/1 SD=1.45; 95% CI, 1.03-2.04). We found similar results when we analyzed the control groups separately. CONCLUSION: Waist-to-hip ratio, but not fat mass or BMI, was associated with increased BE risk. This study provides strong evidence that BE is related to body size and composition through central adiposity and not through total body fatness.
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