Changes in esophageal physiology following weight loss interventions: a narrative review

Introduction

Obesity is prevalent worldwide, and more than half the world’s population will be overweight or obese by 2035 if current prevalence trends continue (1). Approximately 40% of the US population is overweight or obese according to the National Health and Nutrition Examination Survey (NHANES) for August 2021–August 2023, 10% of whom are morbidly obese (2), and 35 of the 50 US states have obesity prevalence rates ≥50% (3). Although prevalence is higher with older age and lower educational status, obesity is increasingly recognized in pediatric-age patients (2). Obesity is a risk factor for several chronic illnesses including coronary artery disease, chronic obstructive pulmonary disease, diabetes mellitus and colorectal cancer, contributing to an estimated $480.7 billion dollars in direct health care costs and an additional $1.24 trillion in indirect costs in 2016 alone (4).

Management of obesity involves weight loss. When diet and exercise fail, alternatives include pharmacologic therapy and invasive options. Among pharmacological agents, glucagon-like peptide-1 receptor agonists (GLP-1RAs) have recently gained popularity. When medical management fails, surgical and endoscopic interventions are often pursued. Laparoscopic adjustable gastric banding (LAGB) was introduced in the 1990s, but alternative bariatric surgical options of laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (RYGB), and endoscopic bariatric intervention including endoscopic sleeve gastroplasty (ESG) and intra-gastric balloons (IGB) are more commonly employed in the present day.

Both obesity and its management can alter foregut physiology. Medical, surgical and endoscopic management of obesity can be associated with adverse effects on esophageal physiology and pathophysiology, which are important for the treating physician to optimize the selection of intervention strategies and improving patient outcomes. Careful preoperative assessment and post-operative monitoring can help mitigate adverse events. Existing reviews have only partially addressed available evidence pertaining to esophageal physiologic changes following certain bariatric interventions (5,6); these are neither current nor comprehensive, and do not address medical weight loss options and all available bariatric interventions. This review describes foregut physiology and pathophysiology before and after medical, surgical and endoscopic interventions in obese individuals. We present this article in accordance with the Narrative Review reporting checklist (available at https://aoe.amegroups.com/article/view/10.21037/aoe-2026-1-0006/rc).

Methods

A comprehensive literature search was performed of online databases (PubMed and Google Scholar) from inception through December 31, 2025 for English language studies evaluating esophageal physiologic outcomes following bariatric interventions. Search terms included combinations of the following: “obesity”, “bariatric surgery”, “esophageal physiology”, “gastroesophageal reflux disease”, “sleeve gastrectomy”, “Roux-en-Y gastric bypass”, “endoscopic sleeve gastroplasty”, “gastric banding”, “intragastric balloon”, “GLP-1 receptor agonists”, “esophageal motility”, “high-resolution manometry”, “acid exposure time”, “pH monitoring”, “Barrett’s esophagus”, and “achalasia”. Relevant articles were also reviewed to identify additional resources. Since this is a narrative review, no formal systematic search protocol or framework was applied. Priority was given to randomized controlled trials (RCTs), prospective cohort studies, and systematic reviews. Case reports and case series were excluded except for novel endoscopic bariatric procedures with limited evidence. Studies that did not report esophageal physiologic or gastroesophageal reflux disease (GERD)-related outcomes were excluded. No formal study quality assessment was conducted (Table 1).

Physiologic esophageal metrics in obese individuals

Obesity increases intra-abdominal and intragastric pressures, but the relationship between obesity and esophageal sphincter physiology is complex and remains controversial (7-13). Some studies demonstrate compensatory esophageal physiologic changes to increased intraabdominal pressures, with higher body mass index (BMI) correlating with higher LES resting pressure (r=0.241, P<0.001), higher upper esophageal sphincter (UES) residual pressure (r=0.19, P<0.001), greater intra-bolus pressure (IBP) (r=0.249, P<0.001), and higher esophagogastric junction (EGJ) contractile integral (r=0.218, P<0.001) (Figure 1) (11). However, other studies have found the opposite results, with morbidly obese individuals showing lower LES pressures compared to non-obese individuals (15.1±4.9 vs. 10.5±5.4 mmHg, P<0.05), with obese individuals being twice as likely to have a defective LES [odds ratio (OR): 2.12, 95% confidence interval (CI): 1.63–2.75] (12,13). Yet other studies have shown equivocal results, with no changes in mean LES pressure, LES length, or peristaltic function among normal, overweight, and obese individuals (14). Transient LES relaxations (TLESRs) were increased in obese (7.3/hr) as compared to normal weight (2.1/hr) individuals, with a higher proportion of TLESRs associated with acid reflux in obese (63.5%) vs. normal weight (17.6%) individuals (14).

Figure 1 Changes in esophageal physiologic metrics and esophageal pathophysiology in obese individuals. Esophageal physiologic metrics change in response to increased intra-abdominal and intragastric pressures, primarily to reduce the impact of retrograde movement of gastric content or reflux from increased intra-abdominal pressure. LES resting pressure and diaphragmatic crural contraction increase to augment EGJ barrier function. Pathologic changes consist mainly of gastroesophageal reflux and its consequences when barrier function fails. A hiatus hernia can develop. Gastroesophageal reflux can manifest as esophageal symptoms (heartburn, regurgitation, esophageal chest pain, atypical symptoms), elevated esophageal acid exposure time, increased reflux episode counts, low mean nocturnal baseline impedance and/or erosive esophagitis. There is increased risk of GERD complications in obese individuals, including esophageal strictures, BE and EAC. BE, Barrett’s esophagus; EAC, esophageal adenocarcinoma; EGJ-CI, esophagogastric junction contractile integral; GERD, gastroesophageal reflux disease; LES, lower esophageal sphincter.

Reflux metrics can be abnormal in obese individuals irrespective of symptoms, with higher 24-hour acid exposure time (AET), lower mean nocturnal baseline impedance (MNBI), higher DeMeester score and higher total reflux episodes compared to non-obese individuals (11). Obese individuals have a higher incidence of reflux esophagitis (20.7% vs. 12.5%), Barrett’s esophagus (BE) (7% vs. 3.5%), GERD (38.33% vs. 16.86%), and hiatal hernia (18.5% vs. 15.3%) compared to the non-obese (Figure 1) (15). There is a marked increase in AET in higher BMI categories, with a positive association with symptom severity despite lower prevalence of esophageal motor disorders (16). For each unit increase in BMI, AET rises by 0.35% (95% CI: 0.42–0.46%) (17). Other studies have shown similar results in esophageal motility parameters and reflux episodes in obese compared to non-obese individuals (16,18-20).

Meta-analyses have shown increased risk of GERD symptoms, hiatus hernia, erosive esophagitis, and esophageal adenocarcinoma (EAC) in overweight and obese individuals compared to their normal BMI counterparts (21,22). Further, patients with central adiposity have a higher likelihood of erosive esophagitis [adjusted OR (aOR), 1.87; 95% CI: 1.51–2.31], BE (aOR, 1.98; 95% CI: 1.52–2.57) and EAC (aOR, 2.51; 95% CI: 1.54–4.06), compared to normal body habitus (23). For each 5 kg/m² increase in BMI, meta-analyses have shown a 6% increase in the risk of malignant progression (aOR, 1.06; 95% CI: 1.02–1.10; P<0.001; I²=0%) (24).

Impact of diet and exercise on esophageal physiology

Lifestyle modifications including calorie restriction, increased physical activity, and structured behavior change programs are typical initial recommendations for weight loss (25). Caloric restriction below maintenance requirements, substituting proteins and complex carbohydrates for energy sources, using fiber for satiation, and practicing mindful eating are initial dietary adjustments for weight loss (26). This is often combined with moderate intensity exercise that increases heart rate to 50–70% of maximum heart rate (27). Distal esophageal AET decreases with a calorie restricted diet when compared to a liberal diet (Table 2), but frequency of reflux symptoms does not necessarily decrease correspondingly (28,29). Once weekly physical activity is associated with decreased risk of GERD among obese individuals, but not in non-obese individuals (30). Active exercise such as intense running increases AET, intra-abdominal pressure, TLESRs, and reflux episodes, while reducing esophageal peristalsis, and basal LES pressure (31). Hiatus hernias can develop during exercise, and are more prevalent in power athletes and weight-lifters (32). However, despite increased reflux during exercise, the risk of erosive esophagitis is reduced with high intensity exercise over time in all BMI groups (33).

A large prospective study showed that physical activity is associated with a 25% reduction in EAC risk (34). Since then, two separate meta-analyses have demonstrated that physical activity reduces EAC risk by 32% and 21%, respectively (35,36). For every additional hour spent performing intermediate intensity physical activity, whole gut transit time decreased by 16.2% and colonic transit time by 25.5% when adjusted for age, sex, and body fat (37).

Thus, both the risk of objective GERD and GERD complications (erosive esophagitis, EAC risk) can be reduced with diet and exercise (Table 2).

Impact of weight loss medications on esophageal physiology

GLP-1RAs

GLP-1RAs have become popular medical options for weight loss refractory to diet and exercise. They mimic the action of endogenous incretin hormone GLP-1, which is released by the gut in response to food intake. They work by delaying gastric emptying, regulating appetite at a central level, and inhibiting glucagon secretion and glucose-dependent insulin secretion. These agents have been postulated to increase reflux burden (Table 2). A large retrospective matched cohort study of short-acting GLP-1RA showed modest increase in risk of erosive reflux disease [hazard ratio (HR) 1.21, 95%: CI: 1.11–1.33], esophageal stricture (HR 1.28; 95%: CI: 1.13–1.45), and BE (HR 1.50; 95%: CI: 1.16–1.94) (38). However, high-resolution manometry (HRM) patterns were normal in most patients treated with GLP-1RAs, and there was no association between specific agents and motor patterns (39). Prolonged gastric emptying and retained intragastric contents have raised concerns of aspiration in patients on GLP1-RA undergoing intubation or endoscopic intervention (40,41). While studies have shown conflicting results, gastric retention, and potential aspiration risk is reduced by prolonging fasting prior to endoscopy (42-44). Management of reflux disease and its complications can include acid suppression and lifestyle measures, reduction in GLP-1RA dose, slow dose escalation, and in severe cases, discontinuation of the agent (Table 2).

Other weight-loss medications

Pharmaceutical agents approved to promote weight loss include phentermine-topiramate, bupropion-naltrexone and orlistat. Phentermine is a sympathomimetic amine, commonly combined with topiramate, for augmentation of gamma aminobutyric acid (GABA) for central appetite suppression (45). This combination causes paresthesia, xerostomia, headache, dysgeusia and constipation, but no specific esophageal side effects are noted (46). Bupropion is a norepinephrine-dopamine receptor uptake inhibitor often used as an antidepressant and appetite suppressant. It is often combined with naltrexone for pro opiomelanocortin neuron stimulation that results in suppression of appetite and weight loss (45). Nausea, vomiting, headache and dizziness are side effects, but no esophageal consequences are reported (47). Orlistat is an intestinal lipase inhibitor, and blocks fat absorption in the small intestine (45). While the agent can cause oily diarrhea, steatorrhea and fecal urgency often leading to drug discontinuation, no esophageal symptoms or impact on esophageal physiology have been reported in the literature (48).

Impact of bariatric surgery on esophageal physiology

LSG

LSG is a restrictive bariatric procedure where as much as 80–85% of the stomach is resected along the greater curvature, effectively decreasing stomach volume and promoting early satiety. The EGJ and pylorus are preserved, but despite this, esophageal and EGJ function are impacted. A meta-analysis demonstrated an increase in AET of 2.1% [95% CI: 0.3–3.9] and DeMeester score of 8.6 [95% CI: 2.0–15.2] following LSG (49). Additionally, LES resting pressure and length decreased, with a mean difference of −2.8 [95% CI: −4.6 to −1.1] and −0.1 [95% CI: −0.2 to −0.02] mmHg, respectively, and the relative risk for erosive esophagitis after LSG was 2.3 (95% CI: 1.5–3.5) (49). Other studies have also reported significant reductions in intra-abdominal EGJ length, EGJ pressure, EGJ angle, and esophageal opening diameter, which, along with increased intragastric pressure, contribute to the likelihood of post-LSG reflux (Table 2) (50-52).

Long term data from a large cohort study with a 10-year follow-up showed that 65.1% of post-LSG patients developed reflux symptoms, with symptomatic patients showing significantly lower LES resting pressures as compared to the asymptomatic patient cohort (9.8±2.1 vs. 13.3±4.2 mmHg). Esophagitis was found in 29.4% patients and BE in 4.8% on endoscopy. Notably, duodenogastric reflux was reported in 31.8% of patients, highlighting bile reflux as an underappreciated contributor to post-LSG esophageal injury; more than half of the patients needed long-term proton pump inhibitor (PPI) therapy (53). Another meta-analysis, including over 20,000 patients, highlighted post-LSG GERD pooled incidence of 35% (95% CI: 30–41%), with subgroup analysis of clinical trials showing an incidence as high as 58% (95% CI: 39–75%) (54).

Post-LSG reflux is a pressure-driven phenomenon caused by structural and functional post-operative changes in the stomach and LES. The 70–80% reduction in gastric capacity leads to marked elevation in intragastric pressures, with studies showing pressure increases from 34 mmHg (21–45 mmHg) pre-operatively to 43 mmHg (32–58 mmHg) post-LSG when filled with saline (55). These elevated pressures are dynamically exacerbated during physiologic events. Swallow-induced intragastric hyperpressurization occurs in 77–90% of post-LSG patients (56,57), which acutely elevates gastro-esophageal pressure gradient by >10 mmHg and promotes reflux (57). This also fundamentally alters gastric emptying by creating a paradoxical emptying pattern: rapid early-phase gastric emptying immediately after meals, but slower late-phase emptying (2.5 vs. 1.4 mL/min) (58). Patients with >80% reduction in gastric capacity show the highest prevalence of symptomatic GERD, even though they have better weight loss outcomes (50,58). LSG also disrupts the angle of His, transforming it from an anti-reflux acute angle to a more obtuse angle that directly correlates with increased reflux episodes (50). Computational modeling confirms that wider His angles generate higher reflux flow, especially when the staple line starts directly from the pylorus without antral preservation (59). Surgical technique is crucial, with narrower bougie size associated with increased risk of regular PPI use post-LSG (60). Surprisingly, a greater distance of the pylorus from the resection line edge was associated with higher PPI use, which is in contrast to the computational study highlighting that not preserving antrum was associated with higher reflux (59,60). This can be explained by different definitions used for pyloric distance, study design (registry data vs. controlled computational model), and different outcomes measured (PPI use vs. reflux flow rate). Overall, the data on antral preservation and incidence of post-LSG GERD remains controversial, with studies showing beneficial effect of antral preservation, some showing the opposite, and others documenting equivocal results (61-64).

LSG also reduces intra-abdominal EGJ length with increase in esophageal opening diameter which contributes to LES incompetence (50). Studies show that the length of LES high-pressure zone, which functions as a mechanical barrier against reflux, decreases from 2.5 [interquartile range (IQR): 2.5–3] cm to 2 (IQR: 1.3–2.5) cm following LSG (65). As many as 26.6% of patients develop tubularized cardia herniation post-LSG, which is associated with isobaric hyper-pressurization of the proximal stomach that promotes reflux physiology (66). These factors, in combination, are responsible for increased GERD following LSG. In addition, an open and immobile pylorus has been detected in 82% of post-LSG patients, contributing to duodenogastric reflux, with studies showing bile presence in the gastric pouch in 39–68% of patients following LSG (67,68). This creates conducive environments for esophageal mucosal damage and BE (69).

Several studies have tried to pre-emptively identify patients at increased risk of post-LSG reflux. A 5-year prospective evaluation of esophageal physiology, preoperative HRM and 24-h esophageal pH monitoring showed that preoperative GERD symptoms as well as abnormal pH monitoring despite no symptoms were predictive of post-LSG reflux symptoms and GERD (70). A preoperative endoscopy can identify erosive esophagitis, BE, and hiatal hernia, which are additional markers that could predict post-LSG GERD (71).

While medical management can be attempted in patients with limited symptoms, conversion to RYGB is the most effective intervention for post-LSG GERD (Table 3) (72). A large retrospective cohort study including 4,400 patients showed that 80.1% of patients requiring revision for GERD had undergone LSG as their original procedure, and 84.4% of revisional surgeries were RYGB (73). A prospective study of PPI-refractory GERD post-LSG demonstrated LES incompetence and pathologic acid reflux in 97.4%, erosive esophagitis in 84.6% and BE 12.8% (74). Radiologic abnormalities, predominantly cardia dilation and hiatal hernia, were present in 90% of patients (74). These objective findings confirmed on endoscopy, manometry, 24-hour pH monitoring, and barium radiology support a structured pre-conversion workup to guide surgical decision making.

A retrospective study of consecutive LSG converted to RYGB for persisting GERD refractory to medical management reported 70% success in symptom control, with 60% of patients able to discontinue PPIs (75). Another retrospective study of 64 consecutive patients who underwent LSG to RYGB conversion with hiatal hernia repair showed improvement in reflux symptoms and early PPI discontinuation at 14-month follow-up, with sustained therapeutic benefits at 32 months (76). A retrospective study evaluating objective esophageal parameters after conversion from LSG to RYGB showed an improvement in DeMeester scores (70 pre-conversion to 34 post-conversion), total distal reflux episodes (43.8 vs. 19.1), total proximal reflux episodes (7.8 vs. 2.2), GERD clinical score (35.4 vs. 8.3) with no significant changes in HRM findings (77). This study also highlighted that shorter pre-conversion LES length (2.3 vs. 4.4 cm) was more likely to have persistently abnormal pH monitoring post conversion (77). Similarly, a prospective trial of LSG to one-anastomosis gastric bypass (OAGB) conversion showed improvement in gastric emptying time (34 min pre-conversion vs. 24 min post-conversion), post-prandial reflux events (39 vs. 26), total acid events (58.5 vs. 12) and bile stasis on endoscopy (72.7% vs. 40.9%) (78). Another study comparing RYGB with OAGB for post-LSG GERD showed 91.9% GERD resolution rates with RYGB vs. 77.4% with OAGB (P=0.03), with both showing equal improvement in GERD-health related quality of life (GERD-HRQL) scores (79).

Other invasive interventions explored consist of magnetic sphincter augmentation, antireflux mucosectomy, endoscopic radiofrequency therapy, and OAGB (80-83). Modified OAGB following LSG decreased number of postprandial reflux events [median 39 events (IQR: 13) pre-OAGB, to 26 (IQR: 7) post-OAGB], AET [(median 58.5 (IQR: 88) to 12 (IQR: 9.4), P=0.02], regurgitation scores (12±4.1 to 5.5±3, P=0.01), and reflux scores (37.1±15.7 to 16.8±12.6, P=0.003) with shorter operative time, better glycemic control, fewer early post-operative complication profile with comparable weight loss outcomes as compared to RYGB (78).

RYGB

RYGB is a restrictive and malabsorptive bariatric intervention for weight loss where a small gastric pouch is created and connected directly to the jejunum, bypassing much of the stomach and duodenum. RYGB disconnects the majority of the acid-forming stomach from the esophagus, making it ideal for obese patients with pre-operative GERD. Intragastric pressure in RYGB is lower than after LSG, leading to preservation or even improvement of LES resting pressure (49,84). On meta-analysis, RYGB is associated with significantly decreased objective GERD evidence (AET and DeMeester score), with no significant changes in esophageal motor function (Table 2) (49). Further, the relative risk of erosive esophagitis is lower after RYGB compared to LSG, 0.4 (95% CI: 0.2–0.8) post-RYGB vs. 2.3 (95% CI: 1.5–3.5), respectively (49). Prevalence of BE decreased from 2.7% to 1.4% post RYGB vs. increase from 0% to 3.6% post-LSG (49). Unlike post-LSG, esophageal motor parameters including distal contractile integral (DCI), integrated relaxation pressure (IRP), intraesophageal pressures, and bolus time clearance are typically preserved in RYGB (49,84-86).

Rare consequences of bariatric surgery in general and RYGB in particular include esophageal hypomotility and aperistalsis, including achalasia-like syndromes, through various mechanisms (Table 2) (71,87,88). A large multicenter cross-sectional study demonstrated that 12.4% of post-bariatric patients developed abnormal manometric patterns compared with 0% preoperatively (P=0.02), including achalasia in 7.2% and a distinct achalasia-like disorder termed post-obesity surgery esophageal dysfunction (POSED) in 5.2% (88). Although both conditions present with aperistalsis and dysphagia, POSED is characterized by increased gastric pressurization with aperistalsis, whereas achalasia results from impaired LES relaxation with elevated IRP (89). Both disorders show a time-dependent association, with increasing time since surgery independently associated with achalasia (12.5 vs. 5.8 years, P=0.02), POSED (15 vs. 5.8 years, P=0.02), and major motility disorders overall (6.6 vs. 4.9 years, P=0.01) (88). Regardless, both achalasia and POSED seem to respond symptomatically to therapies targeting the high-pressure zone, either LES or the gastrojejunal anastomosis (90). Peroral endoscopic myotomy (POEM) was superior in efficacy to laparoscopic Heller myotomy (LHM) in post-bariatric achalasia-like syndrome, with a clinical success rate of 93.8% and improvement in Eckardt scores (Table 2) (91). In contrast, LHM is associated with high dysphagia recurrence, reported in 67% of patients (92). Botulinum toxin injection or pneumatic dilation may provide temporary symptom relief, especially in refractory settings (90,91).

LAGB

LAGB is a bariatric procedure where a silicone band is tightened around the gastric fundus, effectively creating a small proximal pouch and thereby promoting early satiation (93). LAGB has a significant impact on esophageal motor physiology. An optimally adjusted LAGB results in a delay in transit of liquids and semisolids with increase in esophageal contractions (94). On HRM, there was a decrease in mean DCI and mean IBP following LAGB placement, both of which increased with stepwise increase in intraband pressure from 1 to 8 mL (95). Interestingly, volumes above 5 mL resulted in upward displacement of the LES with esophageal shortening (95).

Studies evaluating longitudinal esophageal motility 6 weeks and 6 months post-LAGB demonstrate significantly increased LES end-expiratory pressure both at 6 weeks and at 6 months, compared to the preoperative measurement (96). There was an increase in high-pressure zone length, with pouch formation associated with increased reflux symptoms (96). Even asymptomatic individuals have abnormal esophageal motility post-LAGB, similar to symptomatic individuals (97), although patients with abnormal preoperative esophageal motility experienced worsening GERD symptoms and esophageal dilation compared to those with normal esophageal motility undergoing LAGB (98). These findings emphasize the importance of evaluating baseline esophageal function and considering alternative bariatric procedures for patients with preexisting motility disorders (98).

A displaced LAGB has potential to create esophageal physiology similar to achalasia spectrum disorders. LAGB has been associated with abnormal esophageal motility such as hypercontractile esophagus, dilation, and aperistalsis (93,99,100). An achalasia-like pattern can result from iatrogenic esophageal dysmotility from LAGB, with impaired relaxation of the EGJ, increased intraluminal pressure, and subsequent esophageal dilation (Table 2) (101). Treatment primarily involves deflation of the band to relieve the obstruction. If symptoms persist, the LAGB may need to be removed (Table 2). Additional intervention in patients with persisting symptoms despite band removal consist of endoscopic dilation, or division of peri-esophageal fibrotic tissue that forms at the site of the band insertion (101,102).

ESG

ESG is a minimally invasive, organ-sparing, reversible endoscopic bariatric procedure where imbricating sutures are placed to reduce the stomach along the greater curvature, creating a tubular sleeve and effectively reducing gastric volume by 70% (103,104). ESG preserves gastric anatomy, fundal innervation, and the angle of His to limit disruption of EGJ, which translates to reduced reflux risk (105-107).

Since ESG preserves the gastric fundus, its sutures pull the gastric tissue and acutely angle the EGJ that can protect against reflux. The angle of His reduced from 62.2° to 59.6° in one report (108). Fundal preservation was emphasized and favored by 4 of 5 experts in a recent expert consensus (109). One study reported post-ESG mean gastric volume reduction of 30.2%, with 50% patients achieving >30% reduction; however, there was no control group for comparison (110). A computational comparison of stomach models showed a 77% reduction in stomach volume in LSG compared to 56% in ESG models (111). However, there are no studies in the literature currently that expand on HRM findings and pressure-volume relationships in patients undergoing ESG.

Current evidence indicates a favorable GERD profile following ESG in contrast to LSG. In a case-matched comparative study, ESG was associated with significantly lower incidence of new-onset GERD than LSG (1.9% vs. 14.5%, P<0.05) (Table 2) (106), complemented with greater total body weight loss at 6-month follow-up (23.6%±7.6% vs. 17.1%±6.5%, P<0.01) (106). Monthly validated questionnaire surveys over 52 weeks of follow-up in the MERIT trial demonstrated that GERD symptoms did not worsen following ESG compared to controls (107). In addition, a prospective study comparing foregut endoscopy and histopathology prior to as well as 6- and 12-months following ESG demonstrated significant improvement in mucosal as well as histopathological abnormalities (112). Recent prospective studies show that ESG improved both typical and atypical GERD symptoms and reduced PPI use from 38% to 20%, making it a preferred option in obese patients with concomitant GERD (113). However, objective esophageal physiologic data using reflux monitoring or contrast radiography are not available, and further research is needed. If reflux symptoms develop, medical management can be initiated.

IGBs

IGBs are space-occupying devices composed of silicone or polyurethane, which are filled with fluid (e.g., Orbera^®, ReShape^®) or gas (e.g., Obalon^®) (114) that are intended to fill intragastric space, thereby promoting satiety and potentially delaying gastric emptying (114). IGBs promote reflux, with rates ranging from 33.7% to 57.5% with Orbera fluid-filled balloons (115,116). High rates of GERD are also reported with other IGBs, including ReShape (54.5%) (117), Obalon (72.6%) (118), and Elipse (25%) (119). On objective esophageal physiologic testing, significantly higher DeMeester scores and delayed gastric emptying were found despite no change in LES pressures (120). If GERD develops and medical management is insufficient, balloon deflation and removal is an option (Table 2).

Other bariatric procedures

Vertical banded gastroplasty (VBG)

VBG, introduced in the 1980s as a purely restrictive operation, was initially popular but later abandoned due to high rates of late complications, including outlet stenosis, pouch dilation, and GERD (121). A prospective comparison of VBG and RYGB demonstrated significantly higher rates of symptomatic GERD (30% vs. 12.5%), abnormal 24-hour pH values (60% vs. 15%), and dysphagia (70% vs. 30%) in the VBG cohort at 1-year follow-up, despite minimal changes in esophageal motor physiology (121). Long-term weight loss was also inferior after VBG (46% vs. 70%), accelerating its decline (121).

Biliopancreatic diversion with duodenal switch (BPD-DS)

BPD-DS combines SG with pyloric preservation to reduce dumping but may increase intragastric pressures and worsen GERD (122,123). A 10-year long-term follow-up study reported de novo GERD incidence of 43.8% post BPD-DS (124). On meta-analysis, GERD improvement was more likely following RYGB than BPD-DS (OR 2.06, 95%: CI: 1.16–3.66), although de novo GERD incidence did not differ significantly (OR 1.05, 95%: CI: 0.50–2.23) (125). Despite metabolic efficacy, BPD-DS remains infrequently performed due to surgical complexity and nutritional risks (126,127).

One anastomotic gastric bypass (OAGB)

OAGB is a procedure where a single gastrojejunal anastomosis connects a long gastric pouch to a jejunal loop, bypassing the duodenum and proximal jejunum (128). There is no Roux limb in OAGB, and reflux of biliopancreatic secretions can occur into the gastric pouch with potential for distal esophageal exposure to bile (128). A randomized clinical trial limited to OAGB patients (the RYSA trial) showed 31.6% with bile reflux into the gastric pouch using bile reflux scintigraphy, with 2.6% having reflux to the esophagus, 15.8% of patients had microscopic esophagitis and 22.5% experienced reflux symptoms at 6 months (129). Another prospective study showed that after OAGB, 28.3% patients had esophagitis, 9.5% had BE, and 42.9% had bile in the gastric pouch but none had bile in the distal esophagus (130). Esophageal physiologic testing demonstrated no changes in LES pressures, decreased AET and DeMeester scores following OAGB compared to preoperative assessment (130).

Results from studies reporting incidence of de novo GERD after OAGB vary widely from 6% to 57%, depending on follow-up duration and diagnostic criteria used (131). The YOMEGA RCT comparing OAGB and RYGB demonstrated higher GERD rates following OAGB (41% vs. 18%) (132). Other studies have shown that OAGB can improve preexisting mild-moderate GERD, based on reduction in AET on ambulatory pH monitoring comparable to RYGB (133,134).

Studies evaluating mechanisms of GERD following OAGB demonstrate both acid reflux (30.2%) and bile reflux (27.9%) in symptomatic patients, with 11.6% having mixed reflux (135). Further, the presence of hiatal hernia before OAGB may predict an increased risk of de novo GERD, hence concurrent repair of hiatal hernia could be of value (136). Avoiding OAGB may be prudent in patients with advanced esophagitis or BE, and approximately 1.6% patients undergoing OAGB require revision surgery with conversion to RYGB the majority (137).

Single anastomosis duodeno-ileal bypass with sleeve gastrectomy (SADI-S)

SADI-S, first described in 2007, is a modification of BPD-DS, combining sleeve gastrectomy with single (rather than a double) duodeno-ileal anastomosis, bypassing majority of the small bowel (138). This procedure preserves the pylorus, which prevents complications of bile reflux in the gastric pouch unlike OAGB (139,140). A meta-analysis of 2,000 patients showed a pooled bile reflux incidence of only 1.23% with a pooled GERD incidence of 7.6% (4.8–21.4%), which is significantly lower than procedures like OAGB (140). Post SADI-S GERD outcomes have been heterogeneous, with studies showing resolution of pre-existing GERD in 53.2% patients, while other studies show de novo GERD post SADI-S in 3.6% of patients (141). Another cross-sectional study reported that the proportion of patients reporting reflux symptoms post SADI-S increased from 18.8% to 30.2% as follow-up duration extended from <2 years to >3 years follow-up (142). This may be related to the sleeve gastrectomy component in the SADI-S and BPD-DS procedures that increase intragastric pressures and predispose to GERD. A long-term follow-up study showed GERD symptoms in 35.3% of SADI-S patients and 20.7% of BPD-DS patients, but at >60-month follow-up, prevalence dropped to 23.8% and 15.8%, respectively (143). Also, out of 23 patients symptomatic before the procedure, only 8 remained symptomatic afterwards (143). Thus, even though pyloric preservation in these procedures lowers bile reflux burden as compared to OAGB, de novo GERD remains a clinically relevant concern due to the sleeve gastrectomy component. Longer follow-up studies with systematic endoscopic surveillance are needed before definitive conclusions in comparing BPD-DS and OAGB.

Sleeve gastrectomy with transit bipartition (SG-TB)

SG-TB, also called the “Santoro procedure” is another hybrid procedure that involves sleeve gastrectomy. This involves creating a gastro-ileal anastomosis with an entero-enteral anastomosis, connecting the duodenal limb to the ileal limb (144). Because of gastric sleeve creation that increases intragastric pressures, anti-reflux maneuvers are peformed concurrently, including hiatoplasty and cardioplication (145,146). A retrospective cohort study showed significantly lower incidence of GERD post SG-TB compared to LSG (7% vs. 29.0%, P<0.001) (147). Since the standard Santoro procedure involves two anastomoses, simplified variations have been explored including single anastomosis sleeve ileal (SASI) and single anastomosis sleeve jejunal (SAS-J) bypass. These procedures involve loop bipartition rather than transit bipartion, creating a loop anastomosis between the small bowel and gastric pouch (gastro-ileal in SASI and gastro-jejunal in SAS-J). This leads to decreased operative time and less post-operative complications. Short term follow-up studies show remission of GERD in 80–92% of the patients post SASI (148,149), with reduction over time to 25% at 4 years in long-term follow-up studies (150). SAS-J has shown GERD improvement in 89% of patients (151). Because of the absence of enteroenteric anastomosis, there is limited diversion of bile secretions to the stomach pouch, leading to increased bile acid reflux. Another 2-year follow-up study post SASI reported 5.3% of patients with bile reflux confirmed by endoscopy (148).

Data on novel endoscopic bariatric interventions remain limited. Nausea and vomiting rates of 39.4% were reported on meta-analysis following duodeno-jejunal bypass sleeve (DJBS) but assessment of GERD was not reported (104). Subsequent DJBS trials have focused on metabolic outcomes without evaluating GERD or esophageal physiology (152,153). Similarly, primary obesity surgery endoluminal (POSE) studies have reported postoperative nausea/vomiting without assessing GERD (154-156). One randomized trial found GERD in 8.1% of patients post-POSE vs. 4.5 % in the sham group (P=0.26) (157). There are no published data evaluating GERD incidence or esophageal physiology following Aspire Assist or small-bowel endoscopic bariatric therapies.

Clinical implications

The potential for esophageal physiologic changes and particularly the risk of GERD with bariatric interventions needs to be factored in while personalizing bariatric interventions to the individual patient. However, many of the esophageal consequences are identified after intervention has already taken place. These need to be recognized on the basis of presenting symptoms, investigated accordingly, and treated according to standard management paradigms (Table 3).

GERD is a common consequence of several bariatric interventions, and standard medical management with acid suppressive therapies constitutes the first approach when identified (158). Reduction in GLP-1RA dose, and rarely, discontinuation of the agent may be necessary when GERD develops. IGB may need deflation and removal if GERD is troublesome. For GERD following bariatric intervention such as LSG that persists despite medical management, mechanical intervention including magnetic sphincter augmentation and conversion to RYGB is sometimes needed. BE requires endoscopic surveillance according to current management guidelines (159).

When patients develop obstructive syndromes following bariatric intervention, standard evaluation includes endoscopy, barium radiography, manometry and functional luminal imaging probe studies. Anastomotic strictures may respond to endoscopic dilation. Achalasia-like syndromes may require botulinum toxin injection, which can be escalated to myotomy when necessary (160) (Table 3).

Limitations

Significant statistical heterogeneity exists in the meta-analysis cited in the review, which limits the precision of the pooled estimates. Although emphasis was placed on RCTs and prospective studies, retrospective studies are also cited for many novel procedures with limited data, which carry their own biases. Many of these studies had variable follow-up durations and used non-standard endoscopic procedures to diagnose esophageal pathologies. These outcomes are heavily dependent on individual operating interventionalists and surgeons, and difficult to standardize across institutes. GERD is defined inconsistently across studies, with some using symptom-based reflux, patient reported outcome instruments such as GERD questionnaire (GERD-Q) scores or PPI response, while others used standardized procedures such as ambulatory reflux monitoring. Lack of standardized esophageal endpoint reporting on HRM, ambulatory reflux monitoring, and endoscopy limits interpretation of results from cross-sectional studies. Similarly, bile acid reflux was defined variably, with some studies using scintographic studies, while others presenting histologic evidence of bile reflux with foveolar inflammation. Follow-up durations are variable across studies. This is important as short-term follow-ups might underestimate late complications post-procedure and overestimate improvement in GERD. This is especially true for pathologies such as BE, esophageal dysmotility, and achalasia-like syndromes, which are time-dependent phenomena. Moreover, many new interventions including SADI-S, OAGB and SG-TB have limited prospective data on outcomes and complications, and limited literature comparing one intervention with another.

Conclusions

Both medical and surgical bariatric interventions are associated with improved quality of life with durable weight loss, improved glycemic control, reduced cardiovascular risk, and reduced all-cause mortality in patients with obesity (161-164). However, a nuanced understanding of the benefits and limitations of each intervention is important to make appropriate management decisions based on the baseline comorbidities, anticipated risk and likelihood of benefit. Despite widespread use, data on long-term outcomes of bariatric interventions on esophageal symptoms and esophageal physiology are limited. An in-depth evaluation of post-intervention changes in esophageal physiological function is critically important for optimizing the selection of intervention strategies and improving patient outcomes. This review serves to inform the reader of esophageal physiologic changes and particularly the risk of GERD with bariatric interventions, which can be taken into consideration in personalizing the planning of bariatric interventions to the individual patient. Further prospective trials are needed to determine consequences of bariatric intervention so that informed decisions can be made while counseling patients and planning management.

Acknowledgments

Artificial intelligence tools were not used in the preparation of this manuscript.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://aoe.amegroups.com/article/view/10.21037/aoe-2026-1-0006/rc

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Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://aoe.amegroups.com/article/view/10.21037/aoe-2026-1-0006/coif). C.P.G. has received consultation fees from Medtronic, Phathom, Braintree, Alimentiv and Anaptys bio, and speaker fees from Carnot. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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