Role of the Gastroenterologist in Managing Obesity

John K DiBaise; Amy E Foxx-Orenstein

Disclosures

Expert Rev Gastroenterol Hepatol. 2013;7(5):439-451. 

In This Article

Association of Obesity With GI Disorders

Obesity is also associated with a number of GI and hepatobiliary conditions (Box 1). Many of the GI diseases that are commonly seen in normal weight individuals are seen up to 2–3 times more commonly in those who are obese. Those with cancer and a BMI > 40 kg/m2 appear to have a higher mortality rate when compared to normal-weight individuals. Importantly, obesity is a modifiable risk factor for the disorders discussed below.

An increase of obesity and gastroesophageal reflux disease (GERD) in Western populations in the past 50 years suggests an association between the two conditions.[11] Indeed, studies examining the relationship between BMI and GERD have shown up to a 2.5-fold increase in the risk of regurgitation, erosive esophagitis and esophageal adenocarcinoma.[12] The distribution of body fat also seems to play a role. In a recent population-based, case-control study, waist circumference and waist–hip ratio were strongly associated with the presence of Barrett's esophagus, albeit in males only.[13] Another recent report also demonstrated an association of visceral fat and fat near the gastroesophageal junction with Barrett's, and with increased esophageal inflammation and high-grade dysplasia in Barrett's patients, independent of BMI.[14] Although not entirely clear, it is speculated that anatomic and physiologic obesity-related changes including reduced lower esophageal sphincter pressure, increased transient lower esophageal sphincter relaxation, presence of a hiatal hernia, increased intragastric pressure and presence of esophageal dysmotility may account for the increased prevalence of GERD and its complications in obese individuals.[15] Despite the apparent relationship between obesity and GERD, whether weight loss, particularly nonsurgical, and the means to achieve weight loss can resolve GERD symptoms in overweight and obese individuals remains unclear.[16] The outcomes and durability of fundoplication in the setting of severe obesity are not as good as those in patients who are not severely obese. As such, bariatric surgery, primarily the Roux-en-Y gastric bypass (RYGB) (see section below), has been suggested as a preferred surgical option in these patients.[17]

Obesity, the metabolic syndrome and rapid weight loss are modifiable risk factors of gallstone formation.[18] A BMI >30 kg/m2 is associated with about a threefold increase in risk of gallstone development, while a BMI > 45 kg/m2 is associated with a sevenfold increase in risk.[19] Obesity may disturb lipid and endogenous hormones metabolism and affect gallbladder motility, thereby increasing the risk of gallstones and gallbladder cancer.[20] Following bariatric surgery, weight loss of more than 25% of original weight postoperatively was found to be the only factor predictive of the development of gallstones and selection of patients for subsequent cholecystectomy, while traditional risk factors such as female gender, increased age and genetic traits were not predictive of symptomatic gallstone formation.[21]

Despite an increased prevalence of gallstones in obesity, there is no high-quality evidence supporting a higher incidence of gallstone pancreatitis in obese individuals. However, obesity, increased visceral fat in particular, has been associated with a higher incidence of pancreatitis complications and mortality.[22] In a recent report, overweight or obesity during early adulthood was associated with a greater risk of pancreatic cancer and a younger age of disease onset, while obesity at an older age was associated with a lower overall survival in patients with pancreatic cancer.[23] Obesity has also been associated with an increased risk of cholangiocarcinoma, although this is a less-established association.[24]

Obesity is associated with an increased risk of the spectrum of nonalcoholic fatty liver diseases (NAFLD) including simple steatosis, nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. Nonalcoholic fatty liver diseases has become one of the most common causes of liver disease worldwide and has been associated not only with obesity but also other features of the metabolic syndrome including insulin resistance, impaired glucose tolerance and dyslipidemia. Despite much investigation, the underlying mechanism and pathogenesis of NAFLD remain elusive. Population-based estimates for the prevalence of NAFLD range from 13% in Japan, where obesity is low, to 30% in the United States, including >90% in the super obese.[25] Nonalcoholic steatohepatitis is presumed to be the predisposing inflammatory state that links NAFLD with hepatic carcinogenesis, with 4–27% of nonalcoholic steatohepatitis cases transforming to hepatocellular carcinoma following the development of cirrhosis.[26] Importantly, there is evidence that obesity is associated with an increased risk of hepatocellular carcinoma independent of the presence of cirrhosis.[26,27] Because of the lack of other effective treatments, weight loss achieved through lifestyle modifications has been promoted as the standard treatment for NAFLD despite very little empiric evidence to support its effectiveness.[28]

Obesity is associated with an increased risk of colonic neoplasia. Obese persons have a higher risk of colon adenomas including advanced lesions compared to normal weight persons.[29] In particular, visceral adiposity and insulin resistance are risk factors for colonic adenomas. The presence of the metabolic syndrome carries a relative risk (RR) of 1.5 for all adenomas plus a twofold higher risk for advanced adenomas.[30] Moreover, increased BMI has been associated with lower quality bowel preparation, which could increase the polyp miss rate.[31] Considerable evidence also supports that excess body weight is an independent risk factor for colorectal cancer (CRC).[26] The overall RR of CRC is 1.4 for obese compared to normal weight,[32] with gender-specific variations at risk. A meta-analysis showed a stepwise increase in BMI of 5 kg/m2 associated with an RR for colon cancer of 1.2 (95% CI: 1.2–1.3) for men and a 1.09 (95% CI: 1.04–1.14) RR in women.[33] Increasing waist circumference and waist–hip ratio has also been associated with increased CRC risk. In a recent report, for each 10-cm increase in waist circumference, a 33% increased risk of CRC in males and 16% increase in females was seen.[34]

Obesity has been linked to a greater risk of complicated diverticulitis, recurrent episodes of diverticulitis and hospitalization for complications associated with diverticular disease.[35,36] In a cohort of more than 47,000 men followed prospectively for 18 years, a BMI >30 kg/m2 had an RR of 1.78 (95% CI: 1.08–2.94) for diverticulitis and 3.19 (95% CI: 1.45–7.00) for diverticular hemorrhage compared to a BMI <21 kg/m2.[37] Similar associations were seen using waist circumference and waist–hip ratio.

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