Barrett’s esophagus is a premalignant condition portending increased risk of esophageal adenocarcinoma. Given the significant morbidity and mortality of esophageal adenocarcinoma, identification of risk factors for Barrett’s esophagus and esophageal adenocarcinoma is crucial. There are a plethora of studies investigating the relationship of obesity with these pathologies. Recent studies reveal that this relationship may specifically be with central adiposity. Increased cell turnover and eventual carcinogenesis is likely precipitated by increased intragastric pressure but also is affected by the complex interplay of increased insulin resistance in patients with increased fat tissue. Further studies are warranted to evaluate if weight loss can decrease progression of Barrett’s esophagus.
Key points
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Barrett’s esophagus is characterized by metaplastic columnar epithelium in the distal esophagus. Esophageal adenocarcinoma can occur from dysplastic progression of Barrett’s esophagus.
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There is evidence that Barrett’s esophagus is more strongly related to central adiposity and waist-to-hip-ratio than overall obesity.
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Both obesity and the incidence of esophageal adenocarcinoma have increased significantly in the past three decades. Numerous studies have shown an association between obesity and esophageal adenocarcinoma.
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The mechanism by which obesity leads to carcinogenesis involves a complex interplay of inflammatory cytokines and hormones.
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Further studies are warranted to investigate whether weight loss can decrease the risk of Barrett’s esophagus and progression to esophageal adenocarcinoma.