Gastroesophageal Reflux Disease

Some degree of gastric reflux is physiologic, does not cause any symptoms or esophageal injury, and does not require treatment.[1] Gastroesophageal reflux disease (GERD) is a syndrome of inappropriate backflow of gastric acid into the esophagus, which can result in inflammation and erosion of the esophageal mucosa. It is the most common upper gastrointestinal tract disorder in Western nations, affecting approximately 10-20% of the population, compared with less than 5% in Asia.

The pathophysiology involves defective lower esophageal sphincter function due to inappropriate sphincter relaxation. This condition may be exacerbated by alcohol intake, smoking, fatty foods, caffeine, chocolate, various medications (e.g., anticholinergics, calcium channel blockers), inadequate sphincter size or function, or abnormal sphincter position.

Symptoms include:

  • Heartburn (pyrosis). Typically described as a burning, retrosternal chest pain that radiates to the back, neck, or jaw. It lasts from minutes to hours, most commonly after meals, and is often exacerbated by recumbency and relieved by antacids. Because the pain may mimic cardiac ischemic pain (often described as crushing, related to exertion, involving shortness of breath and diaphoresis), a good description of the pain is medically useful.
  • Regurgitation. Patients typically have reflux of gastric content into the mouth or pharynx. Chronic reflux can result in severe sequelae, including erosion, ulceration, scarring, or stricture of the esophageal mucosa. Furthermore, a possible complication is the development of Barrett’s esophagus, in which metaplasia of the lower esophageal mucosa results in replacement of the squamous epithelium with columnar epithelium. Patients with Barrett’s esophagus are at high risk for developing esophageal adenocarcinoma.
  • Dysphagia. After longstanding reflux, esophagitis and strictures may occur, leading to difficulty swallowing.
  • Cough. A persistent, nonproductive cough is typically worse at night or in the early morning.
  • Hoarseness. Reflux of gastric acid irritates the larynx and vocal cords, causing the hoarseness.

Other symptoms may include hypersalivation, odynophagia (pain while swallowing), and nausea.

Risk Factors

Disorders and conditions that cause increased gastric pressure. Pregnancy and obesity (see Nutritional Considerations below) cause increased intra-abdominal pressure that is translated to the stomach. A meta-analysis involving more than 18,000 individuals revealed that overweight persons (BMI 25-29.9) had more than 50% greater risk for GERD, compared with those whose BMI was below 25. Obese individuals (BMI over 30) were at more than twice the risk.[2]

Diets high in refined carbohydrate. Diets high in refined carbohydrates (white bread and sweets) were associated with greater risk for GERD symptoms in a study of 7,124 participants in the German National Health Interview and Examination Survey.[3] Additional dietary factors are noted in Nutritional Considerations, below.

Diabetes. Diabetes mellitus can cause gastroparesis (which prolongs gastric emptying), resulting in increased gastric contents and gastric pressure. The increased pressure exerts abnormally high pressure on the lower esophageal sphincter and predisposes to reflux.

Hiatal hernia. In this syndrome, the stomach herniates upward through the diaphragm, displacing the lower esophageal sphincter from its anatomic position. As a result, the sphincter is often not functionally competent.

Disorders that result in esophageal dysmotility. Such disorders, which include scleroderma and Parkinson’s disease, can impair esophageal clearance of refluxed gastric acid.


Initial assessment should include a thorough history and physical examination to rule out a cardiac source of chest pain. Focused diagnostic testing may be necessary, including an EKG, chest x-ray, and blood tests that include cardiac enzymes.

In many cases, diagnosis can be made on the basis of the patient’s clinical response to a therapeutic trial using a proton pump inhibitor (e.g., omeprazole). A therapeutic trial of lifestyle changes (see Treatment, below), antacids, or histamine-2 (H2) blockers (e.g., ranitidine) may also be attempted, but these methods are less reliable for diagnostic purposes.

Upper GI endoscopy is the test of choice to diagnose esophagitis. It permits direct inspection of the inflamed mucosa and biopsy to rule out Barrett’s esophagus, malignancy, and infection. However, a negative examination does not distinguish between nonerosive GERD and functional dyspepsia.

Patients with Barrett’s esophagus require regular screening endoscopies to monitor for esophageal carcinoma.

According to guidelines issued by the American College of Physicians and the American Gastroenterological Association, endoscopy with biopsy should be performed at presentation for patients with dysphagia or symptoms that suggest malignancy and patients who have failed to improve after an empirical course of proton pump inhibitor (PPI) therapy.[4]

Further diagnostic testing may include the following:

Barium esophagram evaluates anatomical causes (e.g., hiatal hernia) and complications (e.g., strictures) of GERD.

24-hour pH monitoring correlates esophageal pH with symptom onset in order to diagnose reflux. It should be done in patients with no endoscopic evidence of mucosal damage. The pH monitoring should be performed after withholding PPI therapy for at least 7 days.

Esophageal manometry measures pressure within the esophagus to evaluate esophageal sphincter function and esophageal dysmotility. This method is not sufficiently sensitive to establish a diagnosis of GERD.


Lifestyle modification is often the initial therapy for mild-to-moderate disease. Weight loss, as described below, is an effective treatment, as is elevating the head of the patient’s bed by 6-8 inches.[5] Other commonly prescribed lifestyle changes have, as yet, little evidence to support their efficacy. These include dietary changes (see below), smoking cessation, avoiding postprandial recumbency (eating less than 2 hours before bed), and avoidance of tight-fitting clothing that increases intra-abdominal pressure.

Medications are usually effective for symptomatic relief.

Oral antacids, usually a combination of calcium carbonate or magnesium trisilicate, reduce exposure of the esophageal mucosa to gastric acid. These antacids may be preferable to aluminum-containing antacids due to the possible association between aluminum ingestion and dementia in later life.

Histamine-2 (H2) receptor blockers (e.g., ranitidine) are used for mild and intermittent symptoms. They decrease the secretion of acid by blocking the histamine H2 receptor on the gastric parietal cells. H2 blockers decrease the frequency and severity of symptoms as compared with antacids.

Sucralfate (aluminum sucrose sulfate) promotes healing and protects from further injury. It is most commonly used during pregnancy. Because it contains aluminum, concerns about the association with dementia in later life apply here, as they do for aluminum-containing antacids.

Alginates, derived from seaweed, forms a viscous gum within the stomach and reduces postprandial symptoms in individuals with mild reflux disease.[6],[7]

Proton pump inhibitors (PPIs) (e.g., omeprazole) are generally reserved for patients who fail H2 blocker therapy, have erosive esophagitis, or have frequent/severe symptoms. They work by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump (gastric acid inhibition).[8] They are usually taken daily, 30 minutes before the first meal of the day. Compared to H2 blockers, PPIs provide faster symptom relief and are more effective in healing erosive esophagitis. There are no major differences in efficacy between the different PPIs.

There are many concerns regarding prolonged use of PPIs such as hypochlorhydria, which predispose to infections with Clostridium difficile; malabsorption, primarily of magnesium and calcium, which may increase the risk of bone fractures; hypergastrinemia; gastric atrophy; acute interstitial nephritis; and malabsorption of iron and B12.[9],[10]

Patients with complications, recurrent or refractory esophagitis, strictures, or histological changes may require surgical interventions.

Fundoplication involves wrapping the distal end of the esophagus with the fundus of the stomach to restore the competence of the lower esophageal sphincter. It has approximately an 85% success rate in relieving symptoms and healing esophagitis.

Attaining or maintaining a healthy body weight may be helpful. As noted above, overweight individuals have a significantly increased risk for GERD.[11],[12],[13]

In addition, psychological distress, caused by either major life events or overt psychiatric disease, is associated with GERD symptoms.[14],[15],[16] Limited evidence suggests that stress-reduction techniques (e.g., relaxation training) may reduce symptoms in many persons.[17]

Nutritional Considerations

The causal role of dietary factors in GERD remains unsettled. It is noteworthy, however, that GERD is rarer in parts of Asia (approximately < 10%) and certain other countries than in the United States (approximately 25-30%), which may reflect differences in eating styles, food choices, and body weight.[18] The following factors appear to be associated with reduced GERD symptoms and can be used to tailor lifestyle interventions. Note, however, that the potential of these interventions is suggested mostly by observational studies and some small randomized control trials; they should be further tested in clinical trials especially in relation to overall dietary patterns.

Weight loss. As noted above, obesity is associated with a markedly increased risk of GERD. Weight loss may prevent or postpone the need for acid suppression medications.

Eating more fiber. Persons eating the most fiber have a 30% lower risk for GERD, compared with those who eat the least.[19] Fruit and high-fiber bread in particular have been associated with reduced risk.[3],[20]

Avoiding irritating foods. Although research is not abundant, available evidence indicates that fried, fatty, or spicy foods, raw onions, chocolate, peppermint, heavily salted foods, and carbonated beverages or drinks with high titratable acidity, such as citrus drinks and juices, may be associated with reflux and heartburn.[21],[22],[23],[24] In some cases, a higher percentage of calories coming from fat and the consumption of cholesterol-containing foods increases symptoms of reflux.[25] The digestion of fats, (from fatty meats, greasy or fried foods) requires the secretion of bile salt, which may cause dysfunction in lower esophageal sphincter.[26] Further, fat is high in calories and reducing intake may help with weight loss.

Eliminating coffee. Coffee reduces lower esophageal sphincter pressure, permitting gastroesophageal reflux.[27] Although studies have repeatedly shown that caffeine itself is not responsible for GERD, some evidence does indicate that decaffeination of coffee significantly reduces reflux.[28],[29] In addition, other compounds, such as those formed from roasting coffee, may trigger reflux indicating potential multifactorial associations.[30] There are many variables to control for (i.e., roasting process, presence of caffeine, consumption of it with or without food, etc.) making further research warranted to better tailor nutrition recommendations.[31],[32]

Avoiding alcohol. Compared with nondrinkers, alcohol consumers have at least double the risk of GERD.[33] Reflux symptoms may be more likely with regular consumption of spirits as opposed to beer and wine.[3]

Eating smaller meals. The total amount of food consumed during a meal appears to be related to reflux symptoms, perhaps because gastric distention triggers GERD symptoms.[34] Reducing meal size may therefore be a reasonable preventive strategy, particularly for patients who frequently experience delayed gastric emptying.[35],[36],[37],[38] Altering meal composition by reducing caloric density and percentage of fat may also reduce frequency and severity of symptoms.[39]

Avoid late night eating. Symptoms of GERD may be alleviated by avoiding late night eating. Patients should avoid going to bed less than 2 to 4 hours after consuming their last meal.

Vegetarian diet. A vegetarian diet may be protective against gastric reflux. A cross-sectional analysis of a group of Buddhist priests following a vegetarian diet were compared to a group of nonvegetarians matched for age and weight found that the nonvegetarian group had a significantly higher risk of esophageal reflux.[40] Antioxidants in plant-based foods may play a role in reducing free radicals that play a role in the pathogenesis of GERD. The combination of reducing animal products while consuming vegetables, fruits, legumes, and whole grains may help reduce symptoms of GERD.

Thickened feedings. Thickened feedings for children under 2 years of age reduce regurgitation severity and emesis frequency, although this does not lower the reflux index.[41]

To minimize risk of secondary complications, such as bone fractures when taking PPIs, it is helpful to note potential drug-nutrient interactions, as mentioned above.


See Basic Diet Orders chapter.

Avoid patient-specific food triggers or eliminate potential triggers (as described above) prospectively.

Smoking cessation.

Alcohol restriction.

Stress reduction.

What to Tell the Family

GERD is a common disorder that may be prevented or managed by maintaining a healthy weight, consuming a plant-based diet, avoiding mealtime overeating, and avoiding caffeine and irritating foods. In chronic cases, treatment may also involve antacid medications and occasionally even surgery to relieve symptoms and prevent erosive esophagitis.


  1. Richter JE. Typical and atypical presentations of gastroesophageal reflux disease. The role of esophageal testing in diagnosis and management. Gastroenterol Clin North Am. 1996;25(1):75-102.  [PMID:8682579]
  2. Corley DA, Kubo A. Body mass index and gastroesophageal reflux disease: a systematic review and meta-analysis. Am J Gastroenterol. 2006;101(11):2619-28.  [PMID:16952280]
  3. Nocon M, Labenz J, Willich SN. Lifestyle factors and symptoms of gastro-oesophageal reflux -- a population-based study. Aliment Pharmacol Ther. 2006;23(1):169-74.  [PMID:16393294]
  4. Kahrilas PJ, Shaheen NJ, Vaezi MF, et al. American Gastroenterological Association Medical Position Statement on the management of gastroesophageal reflux disease. Gastroenterology. 2008;135(4):1383-1391, 1391.e1-5.  [PMID:18789939]
  5. Kaltenbach T, Crockett S, Gerson LB. Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach. Arch Intern Med. 2006;166(9):965-71.  [PMID:16682569]
  6. Rohof WO, Bennink RJ, Smout AJ, et al. An alginate-antacid formulation localizes to the acid pocket to reduce acid reflux in patients with gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2013;11(12):1585-91; quiz e90.  [PMID:23669304]
  7. Poynard T, Vernisse B, Agostini H. Randomized, multicentre comparison of sodium alginate and cisapride in the symptomatic treatment of uncomplicated gastro-oesophageal reflux. Aliment Pharmacol Ther. 1998;12(2):159-65.  [PMID:9692690]
  8. Kahrilas PJ. Gastroesophageal reflux disease. JAMA. 1996;276(12):983-8.  [PMID:8805734]
  9. Howell MD, Novack V, Grgurich P, et al. Iatrogenic gastric acid suppression and the risk of nosocomial Clostridium difficile infection. Arch Intern Med. 2010;170(9):784-90.  [PMID:20458086]
  10. Yu EW, Bauer SR, Bain PA, et al. Proton pump inhibitors and risk of fractures: a meta-analysis of 11 international studies. Am J Med. 2011;124(6):519-26.  [PMID:21605729]
  11. Hampel H, Abraham NS, El-Serag HB. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med. 2005;143(3):199-211.  [PMID:16061918]
  12. Mathus-Vliegen EM, Tygat GN. Gastro-oesophageal reflux in obese subjects: influence of overweight, weight loss and chronic gastric balloon distension. Scand J Gastroenterol. 2002;37(11):1246-52.  [PMID:12465720]
  13. Fraser-Moodie CA, Norton B, Gornall C, et al. Weight loss has an independent beneficial effect on symptoms of gastro-oesophageal reflux in patients who are overweight. Scand J Gastroenterol. 1999;34(4):337-40.  [PMID:10365891]
  14. Naliboff BD, Mayer M, Fass R, et al. The effect of life stress on symptoms of heartburn. Psychosom Med. 2004;66(3):426-34.  [PMID:15184707]
  15. Stanghellini V. Relationship between upper gastrointestinal symptoms and lifestyle, psychosocial factors and comorbidity in the general population: results from the Domestic/International Gastroenterology Surveillance Study (DIGEST). Scand J Gastroenterol Suppl. 1999;231:29-37.  [PMID:10565621]
  16. Avidan B, Sonnenberg A, Giblovich H, et al. Reflux symptoms are associated with psychiatric disease. Aliment Pharmacol Ther. 2001;15(12):1907-12.  [PMID:11736721]
  17. McDonald-Haile J, Bradley LA, Bailey MA, et al. Relaxation training reduces symptom reports and acid exposure in patients with gastroesophageal reflux disease. Gastroenterology. 1994;107(1):61-9.  [PMID:8020690]
  18. El-Serag HB. Time trends of gastroesophageal reflux disease: a systematic review. Clin Gastroenterol Hepatol. 2007;5(1):17-26.  [PMID:17142109]
  19. El-Serag HB, Satia JA, Rabeneck L. Dietary intake and the risk of gastro-oesophageal reflux disease: a cross sectional study in volunteers. Gut. 2005;54(1):11-7.  [PMID:15591498]
  20. Nilsson M, Johnsen R, Ye W, et al. Lifestyle related risk factors in the aetiology of gastro-oesophageal reflux. Gut. 2004;53(12):1730-5.  [PMID:15542505]
  21. Rodriguez-Stanley S, Collings KL, Robinson M, et al. The effects of capsaicin on reflux, gastric emptying and dyspepsia. Aliment Pharmacol Ther. 2000;14(1):129-34.  [PMID:10632656]
  22. Rodriguez S, Miner P, Robinson M, et al. Meal type affects heartburn severity. Dig Dis Sci. 1998;43(3):485-90.  [PMID:9539641]
  23. Nebel OT, Fornes MF, Castell DO. Symptomatic gastroesophageal reflux: incidence and precipitating factors. Am J Dig Dis. 1976;21(11):953-6.  [PMID:984016]
  24. Herrera-López JA, Mejía-Rivas MA, Vargas-Vorackova F, et al. Capsaicin induction of esophageal symptoms in different phenotypes of gastroesophageal reflux disease. Rev Gastroenterol Mex. 2010;75(4):396-404.  [PMID:21169106]
  25. Shapiro M, Green C, Bautista JM, et al. Assessment of dietary nutrients that influence perception of intra-oesophageal acid reflux events in patients with gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2007;25(1):93-101.  [PMID:17229224]
  26. Newberry C, Lynch K. The role of diet in the development and management of gastroesophageal reflux disease: why we feel the burn. J Thorac Dis. 2019;11(Suppl 12):S1594-S1601.  [PMID:31489226]
  27. Thomas FB, Steinbaugh JT, Fromkes JJ, et al. Inhibitory effect of coffee on lower esophageal sphincter pressure. Gastroenterology. 1980;79(6):1262-6.  [PMID:7002705]
  28. Pehl C, Pfeiffer A, Wendl B, et al. The effect of decaffeination of coffee on gastro-oesophageal reflux in patients with reflux disease. Aliment Pharmacol Ther. 1997;11(3):483-6.  [PMID:9218070]
  29. Wendl B, Pfeiffer A, Pehl C, et al. Effect of decaffeination of coffee or tea on gastro-oesophageal reflux. Aliment Pharmacol Ther. 1994;8(3):283-7.  [PMID:7918922]
  30. DiBaise JK. A randomized, double-blind comparison of two different coffee-roasting processes on development of heartburn and dyspepsia in coffee-sensitive individuals. Dig Dis Sci. 2003;48(4):652-6.  [PMID:12741451]
  31. Shimamoto T, Yamamichi N, Kodashima S, et al. No association of coffee consumption with gastric ulcer, duodenal ulcer, reflux esophagitis, and non-erosive reflux disease: a cross-sectional study of 8,013 healthy subjects in Japan. PLoS ONE. 2013;8(6):e65996.  [PMID:23776588]
  32. Kang JH, Kang JY. Lifestyle measures in the management of gastro-oesophageal reflux disease: clinical and pathophysiological considerations. Ther Adv Chronic Dis. 2015;6(2):51-64.  [PMID:25729556]
  33. Rosaida MS, Goh KL. Gastro-oesophageal reflux disease, reflux oesophagitis and non-erosive reflux disease in a multiracial Asian population: a prospective, endoscopy based study. Eur J Gastroenterol Hepatol. 2004;16(5):495-501.  [PMID:15097043]
  34. Holloway RH, Hongo M, Berger K, et al. Gastric distention: a mechanism for postprandial gastroesophageal reflux. Gastroenterology. 1985;89(4):779-84.  [PMID:4029557]
  35. Emerenziani S, Zhang X, Blondeau K, et al. Gastric fullness, physical activity, and proximal extent of gastroesophageal reflux. Am J Gastroenterol. 2005;100(6):1251-6.  [PMID:15929753]
  36. Colombo P, Mangano M, Bianchi PA, et al. Effect of calories and fat on postprandial gastro-oesophageal reflux. Scand J Gastroenterol. 2002;37(1):3-5.  [PMID:11843031]
  37. Wu KL, Rayner CK, Chuah SK, et al. Effect of liquid meals with different volumes on gastroesophageal reflux disease. J Gastroenterol Hepatol. 2014;29(3):469-73.  [PMID:24712047]
  38. McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. Gastroenterology. 1981;80(2):285-91.  [PMID:7450419]
  39. Fox M, Barr C, Nolan S, et al. The effects of dietary fat and calorie density on esophageal acid exposure and reflux symptoms. Clin Gastroenterol Hepatol. 2007;5(4):439-44.  [PMID:17363334]
  40. Jung JG, Kang HW, Hahn SJ, et al. Vegetarianism as a protective factor for reflux esophagitis: a retrospective, cross-sectional study between Buddhist priests and general population. Dig Dis Sci. 2013;58(8):2244-52.  [PMID:23508985]
  41. Craig WR, Hanlon-Dearman A, Sinclair C, et al. Metoclopramide, thickened feedings, and positioning for gastro-oesophageal reflux in children under two years. Cochrane Database Syst Rev. 2004.  [PMID:15495056]
Last updated: December 10, 2020