Is Obesity Associated with Barrett’s Esophagus and Esophageal Adenocarcinoma?

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Key points

  • Barrett’s esophagus is characterized by metaplastic columnar epithelium in the distal esophagus. Esophageal adenocarcinoma can occur from dysplastic progression of Barrett’s esophagus.

  • There is evidence that Barrett’s esophagus is more strongly related to central adiposity and waist-to-hip-ratio than overall obesity.

  • 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

Barrett’s esophagus

Barrett’s esophagus is characterized by the replacement of squamous mucosa in the distal esophagus with metaplastic columnar epithelium as a result of chronic exposure of the distal esophagus to acidic gastric contents. Barrett’s esophagus can progress to low-grade dysplasia and high-grade dysplasia before ultimately terminating in EAC seen in Fig. 1. However, this pathway is not obligatory.4 Nevertheless, Barrett’s esophagus is associated with a 40-fold increase in the risk of EAC over the

Obesity and Barrett’s esophagus

Epidemiologic studies have revealed that the mean body mass index (BMI) is higher in patients with Barrett’s esophagus than the general population.6 Follow-up cross-sectional studies have demonstrated a significant relationship between Barrett’s esophagus and obesity.7 Additionally, it has been shown that increased BMI is associated more strongly with long-segment than short-segment Barrett’s esophagus.6 Therefore, obesity may be a risk factor for Barrett’s metaplasia and a possible factor in

Obesity and esophageal adenocarcinoma

The incidence of EAC has increased a staggering 600% over the last 30 years.11 At the same time, the worldwide prevalence of obesity has also increased. Fig. 3 shows the trends in incidence of EAC and in obesity prevalence. Given the increase in obesity and EAC in the past several decades, numerous studies have examined this relationship. A study based on registry data examined the increase in EAC in the United States, Spain, and the Netherlands. There was a significant increase in all three

Mechanism of carcinogenesis

A logical mechanism for the relationship between obesity, Barrett’s esophagus, and EAC is the pathway of GERD. Obesity causes increased intra-abdominal pressure and an increased risk of hiatal hernia. When pressure and distention in the stomach increase, transient lower esophageal sphincter relaxations are triggered; this facilities the retrograde movement of gastric contents into the distal esophagus. As seen in Fig. 4, increased intragastric pressure and decreased intraesophageal pressure can

Dietary impact

There have been many studies on the role of diet in Barrett’s esophagus and EAC. Dietary nitrites have been identified and publicized as a potential risk factor for many types of malignancy.24 They are found naturally in high quantities in green leafy vegetables and are often added to processed meats. Nitrites are converted into nitrous oxide in the presence of gastric acid, and in the epithelium of esophagus can lead to the production of N-nitroso products, which are potential carcinogens.

Summary

Barrett’s esophagus, EAC, and obesity have all increased dramatically over the past several decades. Based on current data, generalized and central obesity are risk factors for Barrett’s esophagus and general obesity is a risk factor for EAC. BMI is not applicable to every patient and abdominal obesity specifically may play a more important role. Given that men have a higher prevalence of central obesity than women; this finding may account for the gender disproportionate incidence of Barrett’s

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  • Cited by (8)

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    Disclosure Statement: The author has nothing to disclose.

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