Gastroesophageal reflux disease risk factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2] Asad Ullah Farooq, M.D.[[3]
Overview
Overview
Gastroesophageal reflux disease (GERD) results from the interaction of impaired antireflux mechanisms, increased reflux events, and reduced esophageal clearance. Risk factors include anatomic factors, physiologic abnormalities, lifestyle factors, medications, and demographic characteristics. The strongest established risk factors include obesity, hiatal hernia, smoking, and genetic predisposition. Other associated factors include pregnancy, scleroderma, sex-specific disease phenotypes, certain medications, dietary habits, and socioeconomic factors.[1][2]
Risk factors
Risk factors
Established risk factors
| Risk factor | Evidence |
|---|---|
| Obesity | One of the strongest modifiable risk factors for GERD. Increased abdominal pressure associated with obesity promotes gastroesophageal junction dysfunction, increases transient lower esophageal sphincter relaxations, and is associated with erosive esophagitis and Barrett esophagus.[1][2] |
| Hiatal hernia | Strongly associated with GERD by disrupting the normal anatomy of the gastroesophageal junction and impairing lower esophageal sphincter function.[1] |
| Smoking | Smoking increases GERD risk by reducing lower esophageal sphincter pressure, decreasing salivary bicarbonate secretion, and impairing esophageal acid clearance.[1][2] |
| Sex | Female sex is associated with a higher prevalence of GERD symptoms in population studies. However, male sex is associated with erosive esophagitis and Barrett esophagus, particularly more severe disease phenotypes. These differences likely reflect variation between symptom-based GERD and endoscopic disease manifestations.[1][4] |
| Pregnancy | Pregnancy increases GERD risk because of hormonal effects causing reduced lower esophageal sphincter tone and increased intra-abdominal pressure, particularly during later pregnancy.[1] |
| Scleroderma | Associated with GERD because of esophageal smooth muscle atrophy, impaired peristalsis, and lower esophageal sphincter dysfunction.[2] |
| NSAID use | Current NSAID use has been associated with an increased prevalence of GERD symptoms in observational studies.[1] |
| Race and ethnicity | Race and ethnicity are associated with differences in GERD phenotype and prevalence. White/Caucasian populations have been associated with a higher risk of erosive esophagitis compared with other racial groups (OR approximately 1.67); however, these findings may reflect differences in genetics, healthcare access, dietary patterns, and environmental exposures rather than race itself as a causal factor.[4] |
| Socioeconomic factors | Lower socioeconomic status has been associated with increased GERD prevalence in epidemiologic studies. Potential contributors include differences in obesity prevalence, diet, smoking exposure, healthcare access, and medication use. Socioeconomic status should be considered a contextual risk factor rather than a direct biologic cause of GERD.[2] |
Medication-related risk factors
Several medications may promote GERD by reducing lower esophageal sphincter pressure, delaying gastric emptying, or impairing esophageal clearance.[1][5]
Examples include:
- Anticholinergics
- Benzodiazepines
- Calcium channel blockers
- Theophylline
- Tricyclic antidepressants
- Progesterone and progestins
- Sildenafil
Clinicians should review medication lists in patients with new-onset or refractory GERD symptoms.[1][5]
Dietary and behavioral factors
Dietary factors are generally considered symptom triggers rather than independent causes of GERD. Individual responses vary considerably.[2]
Reported triggers include:
- Large meals
- High-fat meals
- Late evening meals
- Chocolate
- Coffee and caffeinated beverages
- Alcohol
- Carbonated beverages
- Peppermint
- Spicy food
- Citrus-containing foods
- Tomato-based foods
Behavioral factors associated with GERD include:
- Eating rapidly
- Eating between meals
- Lying down soon after eating
- Late-night eating
- Weight gain
Physical activity
The relationship between physical activity and GERD is complex. Moderate aerobic exercise appears to be associated with fewer GERD symptoms, whereas vigorous exercise involving increased intra-abdominal pressure, such as heavy weightlifting or stooped-position activities, may worsen reflux transiently during or after activity.[2]
Helicobacter pylori infection and GERD
Helicobacter pylori infection appears to be inversely associated with GERD, particularly reflux esophagitis. The proposed mechanism is reduced gastric acid secretion resulting from corpus-predominant gastritis.
A 2025 meta-analysis found that eradication of H. pylori was associated with increased GERD risk (pooled OR 2.01; 95% CI, 1.44-2.81). The association was stronger for reflux esophagitis specifically (OR 2.27; 95% CI, 1.57-3.29).[6]
However, this relationship demonstrates geographic heterogeneity. The inverse association between H. pylori and GERD appears stronger in East Asian populations than in Western populations, and several analyses have found minimal or no effect of eradication therapy on GERD symptoms in Western populations.[2][7]
The presence of GERD alone should not alter indications for H. pylori eradication when treatment is otherwise recommended.[8]
Clinical pearls
- Obesity, hiatal hernia, and smoking are among the strongest established modifiable risk factors for GERD.
- Most dietary factors function as symptom triggers rather than primary causes of GERD.
- Weight gain is associated with increased GERD risk, and smoking cessation may improve reflux symptoms.[9]
- Medication review should be considered in patients with new-onset or refractory GERD symptoms.
References
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Fass, R (2022). “Gastroesophageal Reflux Disease”. N Engl J Med. 387 (13): 1207–1216. doi:10.1056/NEJMcp2114026.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Richter, JE; Rubenstein, JH (2018). “Presentation and Epidemiology of Gastroesophageal Reflux Disease”. Gastroenterology. 154 (2): 267–276. doi:10.1053/j.gastro.2017.07.045.
- ↑ Maret-Ouda, J; Markar, SR; Lagergren, J (2020). “Gastroesophageal Reflux Disease: A Review”. JAMA. 324 (24): 2536–2547. doi:10.1001/jama.2020.21573.
- ↑ 4.0 4.1 4.2 Witarto, AP; Witarto, BS (2023). “Risk Factors and 26-Years Worldwide Prevalence of Endoscopic Erosive Esophagitis From 1997 to 2022: A Meta-analysis”. Sci Rep. 13: 15249. doi:10.1038/s41598-023-42636-7.
- ↑ 5.0 5.1 Dellon, ES; Shaheen, NJ (2010). “Persistent Reflux Symptoms in the Proton Pump Inhibitor Era: The Changing Face of Gastroesophageal Reflux Disease”. Gastroenterology. 139 (1): 7–13.e3. doi:10.1053/j.gastro.2010.05.016.
- ↑ Wang, H; Qu, Y; Lin, Y (2025). “Helicobacter pylori Infection and Eradication in Relation to Gastroesophageal Reflux Disease”. J Gastroenterol Hepatol. doi:10.1111/jgh.70009.
- ↑ Zamani, M (2021). “Systematic review with meta-analysis: association of Helicobacter pylori infection with gastro-oesophageal reflux and its complications”. Aliment Pharmacol Ther. 54 (8): 988–998. doi:10.1111/apt.16585.
- ↑ Maret-Ouda, J (2020). “Gastroesophageal Reflux Disease”. JAMA.
- ↑ Katz, PO; Dunbar, KB; Schnoll-Sussman, FH (2022). “ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease”. Am J Gastroenterol. 117 (1): 27–56. doi:10.14309/AJG.0000000000001538.
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