Obesity is a growing medical and public health problem worldwide. The health implications of obesity include a wide spectrum of benign digestive diseases such as gastroesophageal reflux disease (GERD), Barrett’s esophagus (BE), erosive esophagitis, nonalcoholic fatty liver disease (NAFLD), gallstones, and pancreatitis and digestive organ cancers such as cholangiocarcinoma, hepatocellular carcinoma (HCC), pancreatic cancer, colorectal cancer (CRC), and esophageal cancer.
Obesity increases the prevalence of esophageal motility (i.e. movement) disorders. Esophageal transit time has been demonstrated to be prolonged in subjects with obesity. This is thought to be related to increased gastric and gastroesophageal junction resistance. Excess body weight produces higher intra-abdominal pressure and reduces lower esophageal sphincter pressure, predisposing obese individuals to GERD. Obesity is one of the known risk factors for developing erosive esophagitis. Barrett’s refers to the replacement of the normal squamous epithelium of the distal (lower) esophagus by specialized columnar epithelium. Barrett’s is usually a consequence of chronic GERD and predisposes one to adenocarcinoma of the esophagus. Several studies have shown an association between obesity, abdominal circumference and metabolic syndrome and Barrett’s esophagus. The incidence of esophageal adenocarcinoma is increasing. The molecular mechanisms linking obesity and esophageal adenocarcinoma have been investigated extensively and thought to be related to increased insulin and insulin like growth factors.
Gastric physiology and its neurohormonal regulation are altered in obesity. Higher BMI has been associated with greater fasting gastric volume and accelerated gastric emptying of solids and liquids. Obesity has been found to be a risk factor for erosive gastritis and gastric and duodenal ulcers. Obesity is considered a pro inflammatory and pro carcinogenic and is recognized as an important risk factor for cancer, including gastric cancer.
The prevalence of diarrhea in obese individuals is higher compared with normal weight controls. This is thought to be related to several mechanisms including bile acid diarrhea, accelerated colonic transit, increased mucosal permeability or intestinal inflammation. Medications used by obese individuals such as Metformin for diabetes or polycystic ovary syndrome also may cause diarrhea.
Colon and rectum:
Obesity is associated with a higher risk of developing diverticulosis. Several studies have documented an increased prevalence of adenomatous polyps with elevated BMI. Similarly, obesity is associated with an increased risk of adenoma recurrence.
Nonalcoholic Fatty Liver Disease has become the most prevalent chronic liver disease in the United States and the most frequent cause of increased transaminase levels (liver enzymes). Patients with NAFLD are at risk of progressive fibrosis and eventual cirrhosis. NAFLD confers increased risk of cardiovascular mortality and hepatocellular carcinoma.
Obesity has been well recognized for its strong association with gallstone disease, including cholelithiasis, cholecystitis, and cholesterolosis. Cholesterolosis is characterized by the accumulation of lipids in the mucosa of the gallbladder wall. It is a benign condition that is usually diagnosed incidentally during cholecystectomy or on ultrasonography.
Obesity and fat infiltration of the pancreas play a significant role in the endocrine pancreatic dysfunction that leads to the development of type 2 diabetes mellitus. Obesity is associated with more severe acute pancreatitis. Meta-analyses have reported an association between BMI and adenocarcinoma of the pancreas.