Obesity and esophageal cancer: GERD, Barrett´s esophagus, and molecular carcinogenic pathways

Expert Rev Gastroenterol Hepatol. 2020 Jun;14(6):425-433. doi: 10.1080/17474124.2020.1764348. Epub 2020 May 22.

Abstract

Introduction: Increases in the rates of esophageal adenocarcinoma (EAC) have paralleled rises in the prevalence of overweight and obesity. Despite not being fully understood, obesity-related EAC seems to have different carcinogenic pathways.

Areas covered: This comprehensive review will thoroughly evaluate the current literature, describing the underlying mechanisms that help understanding the strong association between obesity and esophageal cancer.

Expert commentary: The risk of esophageal cancer among obese individuals could be partially explained by several factors: high prevalence of GERD; linear association between central adiposity and Barrett´s esophagus development; low levels of adiponectin and high levels of leptin that alter cell proliferation processes; insulin-resistant state that creates a tumorigenesis environment; and changes in the esophageal microbiota due to unhealthy dietary habits that promote carcinogenesis. In addition, a large proportion of obese patients are undergoing sleeve gastrectomy which can worsen GERD or cause de novo reflux, esophagitis, and Barrett´s metaplasia.

Keywords: Barrett´s esophagus; Obesity; Roux-en-Y gastric bypass; esophageal cancer; gastroesophageal reflux disease; sleeve gastrectomy.

Publication types

  • Systematic Review

MeSH terms

  • Adenocarcinoma / epidemiology
  • Adenocarcinoma / etiology
  • Adenocarcinoma / physiopathology*
  • Adipokines / physiology
  • Bariatric Surgery / adverse effects
  • Barrett Esophagus / etiology
  • Barrett Esophagus / physiopathology
  • Carcinogenesis
  • Diet
  • Esophageal Neoplasms / epidemiology
  • Esophageal Neoplasms / etiology
  • Esophageal Neoplasms / physiopathology*
  • Gastroesophageal Reflux / etiology
  • Gastroesophageal Reflux / physiopathology
  • Gastrointestinal Microbiome / physiology
  • Humans
  • Hyperinsulinism / etiology
  • Hyperinsulinism / physiopathology
  • Inflammation / etiology
  • Inflammation / physiopathology
  • Insulin Resistance / physiology
  • Obesity / complications
  • Obesity / diagnosis
  • Obesity / epidemiology
  • Obesity / physiopathology*
  • Risk Factors

Substances

  • Adipokines

Supplementary concepts

  • Adenocarcinoma Of Esophagus