Visceral Obesity and the Risk of Barrett’s Esophagus

Abstract

It still remains controversial whether simple obesity, as measured by the body mass index (BMI), is an independent risk factor for Barrett’s esophagus (BE). Recent studies have shown abdominal obesity, as defined by the waist circumference (WC) and the waist-to-hip ratio (WHR), to be a risk factor for BE, independent of the BMI, with the association between BMI and BE being no longer observed after adjustment for the WC and WHR. Moreover, visceral obesity, as directly measured by the surface area of the visceral adipose tissue (VAT) on abdominal CT images, has also been reported to have an association with the risk of BE. In addition to the mechanical effects of abdominal obesity, that is, increase of the intra- abdominal pressure by the large amount of adipose tissue, circulating factors secreted from the VAT, such as tumor necrosis factor-α, interleukin-6, leptin, and adiponectin, have also been proposed to be pathogenetically linked to BE and esophageal adenocarcinoma. Obesity is associated with the risk of BE, and this risk appeared to be mediated for the most part by abdominal obesity, especially visceral obesity. This raises several questions regarding the pathogenesis of obesity-related BE. Larger studies with prospective enrollment of patients are required for further examination of this issue.

Physical Activity and Sedentary Behavior in Relation to Esophageal and Gastric Cancers in the NIH-AARP Cohort

“…The predominant causal theory for the positive association between BMI with EA is that obesity increases the propensity for acid reflux via increasing intra-gastric pressure [27], distorting the lower esophageal sphincter [28,29], and increasing the likelihood for hiatal hernia [29,30]. An additional, non-mutually exclusive route of association that has been proposed is that visceral adiposity could affect risk of EA via systemic effects such as inflammatory cytokines or sex steroid hormones [29,31,32]. However, our models without adjustment for BMI were not materially different to the results presented herein.…”

Barrett Esophagus in Asia: Same Disease with Different Pattern

“…Abdominal obesity can explain, to some extent, the epidemiological features of BE and EAC. For example, body fat distribution tends more toward visceral obesity than simple obesity in groups at high risk of BE, such as Caucasians as compared with Asians, and men as compared with women 72,73…”

Role of adiponectin in obesity related gastrointestinal carcinogenesis

“…Low levels of serum adiponectin were associated with visceral obesity or being overweight and this constitutes an independent important risk factor for both BE and EA [74][75][76]. Further, investigations suggest that low plasma levels of adiponectin are linked with a greater risk of BE along with patients undergoing upper endoscopy [77,78] (Table 1).…”