Impact of obesity on Barrett’s esophagus and esophageal adenocarcinoma

The incidence of obesity and esophageal adenocarcinoma (EAC) has significantly increased in the past 3 decades, with several studies demonstrating an association between obesity and the development of Barrett’s esophagus (BE) and EAC. Recent data suggest that BE is more strongly associated with central obesity as compared with overall obesity. The mechanism in which central obesity leads to carcinogenesis is via both gastroesophageal reflux disease (GERD)-dependent and independent pathways. Central obesity results in an increase in abdominal pressure and development of a hiatal hernia that increases the risk of GERD and development of BE. In the GERD-independent pathway, there is an alteration in cell proliferation through the carcinogenic effects of high leptin and low adiponectin levels, hyperinsulinemia and insulin-resistant environment, presence of growth factors, and altered esophageal microbiota due to unhealthy diet. Furthermore, bariatric surgeries such as sleeve gastrectomy can cause worsening GERD and thereby increase the risk of BE. Herein, we summarize the existing data on the increased evidence of BE and EAC risk in obesity and the current literature regarding the underlying mechanisms associated with central obesity, BE, EAC, as well as the role of surgery to modulate these risks.