Send to

Choose Destination
Gastroenterology. 2007 Aug;133(2):403-11. Epub 2007 May 21.

Central adiposity and risk of Barrett's esophagus.

Author information

Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.



Aside from chronic reflux, the etiology of Barrett's esophagus (BE) remains largely unknown. This case-control study investigated body mass index (BMI), central adiposity, and cigarette smoking and risk of BE.


Washington residents newly diagnosed with specialized intestinal metaplasia on at least 1 of 4 esophageal biopsy specimens taken at community gastroenterology clinics (cases [n = 193]) were compared with matched population controls (n = 211). Case subgroups included those with any visible columnar epithelium (visible BE) and those with at least 2 cm of columnar epithelium (long-segment BE [LSBE]). Interviewers conducted personal interviews and took anthropometric measurements.


All measures of central adiposity were strongly related to BE risk, particularly for LSBE. For the high category of waist-to-hip ratio (WHR), the adjusted odds ratios were 2.4 (95% confidence interval [CI]: 1.4-3.9) for all cases, 2.8 (95% CI: 1.5-5.1) for visible BE, and 4.3 (95% CI: 1.9-9.9) for LSBE. In contrast, the associations with BMI were weaker. When BMI and WHR were modeled simultaneously, the associations with BMI were greatly attenuated, whereas those with WHR remained strong. Further adjustment for frequency of heartburn did not change these results. Cigarette smoking moderately increased risk but with no evidence of a dose-dependent response or increasing strength by case group.


These observations indicate the importance of identifying the mechanisms underlying obesity's role in BE and esophageal adenocarcinoma, and suggest that weight loss might be a fruitful approach to the prevention of these diseases.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center