Obesity and Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is defined as the reflux of gastric contents into the esophagus that causes troublesome symptoms, such as heartburn and regurgitation, and/or complications. Its estimated global prevalence is approximately 14%, although reported rates vary considerably depending on the population studied and the diagnostic criteria applied. Historically, GERD has been reported more frequently in North America and Europe than in East Asia; however, prevalence is increasing in many regions, and a simple distinction between “Western” and “Asian” populations is no longer sufficiently accurate. (PubMed)

Overweight and obesity are well-established risk factors for GERD. The association is dose dependent: the risk and severity of reflux symptoms generally increase with increasing body mass index. Abdominal or central obesity, reflected by an increased waist circumference, may be more relevant than BMI alone because visceral fat directly affects the pressure gradient between the abdominal cavity and the thorax. People with obesity have an approximately 1.2- to threefold higher risk of GERD symptoms and are also more likely to develop erosive esophagitis and other reflux-related complications.

Several mechanisms contribute to the association between obesity and GERD:

  1. Increased intra-abdominal pressure: Visceral adipose tissue increases intra-abdominal and intragastric pressure. This promotes the movement of gastric contents across the gastroesophageal junction into the esophagus, particularly after meals or when lying down.
  2. Impairment of the antireflux barrier: The lower esophageal sphincter and the surrounding crural diaphragm normally form a functional barrier against reflux. Obesity may impair this barrier and increase the pressure gradient across the gastroesophageal junction. Obesity has also been associated with more frequent transient lower esophageal sphincter relaxations, which are an important mechanism of reflux.
  3. Hiatal hernia: Obesity, particularly central obesity, is associated with an increased likelihood of hiatal hernia. Displacement of the gastroesophageal junction through the diaphragm disrupts the normal anatomical relationship between the lower esophageal sphincter and the crural diaphragm and can facilitate reflux. (NCBI)
  4. Altered gastric and esophageal function: Delayed gastric emptying, impaired esophageal clearance, increased meal volume and esophageal hypersensitivity may contribute in some patients. However, these abnormalities are not present in every person with obesity and GERD.
  5. Dietary and behavioural factors: Large meals, meals shortly before bedtime, smoking and individual trigger foods may worsen reflux symptoms. High-fat meals may delay gastric emptying and reduce lower esophageal sphincter pressure in some individuals. Alcohol, coffee, spicy foods and acidic foods do not affect all patients equally; therefore, broad and unnecessarily restrictive dietary exclusions are not generally recommended. Trigger foods should instead be identified individually. (PMC)
  6. Metabolic and inflammatory factors: Adipose tissue releases hormones, cytokines and other biologically active mediators that may affect gastrointestinal motility, mucosal sensitivity and inflammatory responses. These mechanisms may contribute to the relationship between visceral obesity and GERD, although their clinical significance is less clearly established than that of mechanical factors such as increased abdominal pressure. (PMC)

GERD commonly presents with heartburn and regurgitation. Other possible manifestations include upper abdominal or retrosternal pain, sleep disturbance, difficulty swallowing, chronic cough and hoarseness. Because these symptoms are not specific to GERD, alternative cardiac, pulmonary and gastrointestinal causes must be considered, particularly in patients with chest pain or predominantly extraesophageal symptoms. Long-standing or severe GERD may lead to erosive esophagitis, peptic strictures, gastrointestinal bleeding or Barrett’s esophagus. Barrett’s esophagus is associated with an increased risk of esophageal adenocarcinoma, although the absolute risk for an individual patient remains low. (PMC)

Management

Weight reduction should be recommended to patients with overweight or obesity and GERD. A reduction in body weight and waist circumference can improve heartburn and regurgitation and may reduce the need for acid-suppressive medication. Weight-loss interventions should combine an appropriate dietary strategy, regular physical activity and behavioural support.

Additional measures may include avoiding meals during the two to three hours before bedtime, stopping smoking, elevating the head of the bed in patients with nocturnal symptoms and avoiding individually identified trigger foods. Proton pump inhibitors are the most effective pharmacological treatment for frequent GERD symptoms and for healing erosive esophagitis. They are generally taken 30–60 minutes before a meal and should be used at the lowest dose that provides effective symptom control when long-term therapy is required. (PMC)

Patients with dysphagia, gastrointestinal bleeding, anemia, persistent vomiting, unexplained weight loss or chest pain require prompt medical assessment. Upper gastrointestinal endoscopy is generally indicated when alarm symptoms are present, when symptoms do not respond adequately to appropriate treatment or when there are multiple risk factors for Barrett’s esophagus. Ambulatory reflux monitoring may be required when the diagnosis remains uncertain. (PMC)

The choice of bariatric procedure is particularly important in patients with obesity and established GERD. Roux-en-Y gastric bypass can improve reflux and is generally the preferred bariatric procedure for suitable patients with severe GERD. Sleeve gastrectomy may cause new-onset GERD or worsen pre-existing reflux and should therefore be considered cautiously in patients with significant reflux disease or Barrett’s esophagus. The decision must be individualized after appropriate endoscopic assessment and multidisciplinary counselling. (PubMed)

References

  1. Katz PO, Dunbar KB, Schnoll-Sussman FH, Greer KB, Yadlapati R, Spechler SJ. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. American Journal of Gastroenterology. 2022;117(1):27–56. doi:10.14309/ajg.0000000000001538.
  2. Yadlapati R, Gyawali CP, Pandolfino JE, et al. AGA Clinical Practice Update on the Personalized Approach to the Evaluation and Management of Gastroesophageal Reflux Disease: Expert Review. Clinical Gastroenterology and Hepatology. 2022;20(5):984–994.e1. doi:10.1016/j.cgh.2022.01.025.
  3. Bischoff SC, Barazzoni R, Busetto L, et al. European Guideline on Obesity Care in Patients with Gastrointestinal and Liver Diseases: Joint ESPEN/UEG Guideline. Clinical Nutrition. 2022;41(10):2364–2405. doi:10.1016/j.clnu.2022.07.003.
  4. Eusebi LH, Ratnakumaran R, Yuan Y, Solaymani-Dodaran M, Bazzoli F, Ford AC. Global Prevalence of, and Risk Factors for, Gastro-oesophageal Reflux Symptoms: A Meta-analysis. Gut. 2018;67(3):430–440. doi:10.1136/gutjnl-2016-313589.
  5. Nirwan JS, Hasan SS, Babar ZUD, Conway BR, Ghori MU. Global Prevalence and Risk Factors of Gastro-oesophageal Reflux Disease: A Systematic Review with Meta-analysis. Scientific Reports. 2020;10:5814. doi:10.1038/s41598-020-62795-1.
  6. Wu JCY, Mui LM, Cheung CMY, Chan Y, Sung JJY. Obesity Is Associated with Increased Transient Lower Esophageal Sphincter Relaxation. Gastroenterology. 2007;132(3):883–889. doi:10.1053/j.gastro.2006.12.032.