The meteoric rise of GLP-1 receptor agonists like Ozempic (semaglutide) and Wegovy for weight management has revolutionised diabetes care and obesity treatment. However, recent clinical evidence has raised significant concerns about a potentially serious gastrointestinal complication: gastroparesis, commonly referred to as stomach paralysis. This condition represents a complex alteration in gastric motility that can profoundly impact patients’ quality of life and nutritional status.
Three major studies presented at Digestive Disease Week 2024 have shed new light on the relationship between semaglutide administration and gastroparesis development. The findings suggest that patients receiving GLP-1 therapy face a substantially elevated risk of developing this debilitating condition, with implications extending far beyond the typical nausea and vomiting associated with these medications. Understanding the mechanisms, clinical manifestations, and management strategies for Ozempic-induced gastroparesis has become crucial for healthcare providers navigating the growing landscape of incretin-based therapies.
Understanding gastroparesis as an ozempic side effect
Gastroparesis fundamentally represents a disorder of gastric neuromuscular function, characterised by delayed gastric emptying without mechanical obstruction. When examining the relationship between Ozempic and stomach paralysis, it’s essential to understand that this effect isn’t entirely unexpected given the drug’s mechanism of action. The condition manifests as impaired coordination between gastric smooth muscle contractions and neural control mechanisms, resulting in food remaining in the stomach for extended periods.
Recent epidemiological data reveals alarming statistics regarding gastroparesis incidence among GLP-1 users. Studies examining nearly 300,000 patients found that individuals taking semaglutide demonstrated a 66% increased likelihood of developing gastroparesis compared to control groups. Whilst the absolute risk remains relatively low at approximately 0.53% of treated patients, the clinical significance becomes apparent when considering the millions of individuals currently prescribed these medications globally.
GLP-1 receptor agonist mechanism and gastric motility impact
GLP-1 receptor agonists exert their therapeutic effects by mimicking endogenous incretin hormones, particularly glucagon-like peptide-1. These medications bind to GLP-1 receptors distributed throughout the gastrointestinal tract, including those located on gastric smooth muscle cells, enteric neurons, and vagal afferent fibres. The activation of these receptors initiates a cascade of intracellular signalling pathways that ultimately modulate gastric motility patterns.
The physiological slowing of gastric emptying represents one of the primary mechanisms through which GLP-1 agonists promote satiety and facilitate weight loss. However, this therapeutic gastric deceleration can progress beyond beneficial levels in susceptible individuals, culminating in pathological gastroparesis. Research conducted at Mayo Clinic demonstrated that patients receiving liraglutide experienced gastric emptying times extending to 70 minutes for half-meal clearance, compared to just four minutes in placebo groups.
Semaglutide-induced delayed gastric emptying pathophysiology
The pathophysiological mechanisms underlying semaglutide-induced gastroparesis involve complex interactions between neural, hormonal, and muscular components of gastric function. GLP-1 receptors expressed on gastric smooth muscle cells mediate direct inhibitory effects on contractile activity, whilst receptors on enteric neurons modulate the coordination of peristaltic waves. Additionally, central nervous system effects through hypothalamic GLP-1 receptors may contribute to altered gastric motility patterns.
Molecular studies have identified specific signalling pathways involved in GLP-1-mediated gastric dysfunction. The activation of adenylyl cyclase and subsequent elevation of cyclic adenosine monophosphate (cAMP) levels leads to protein kinase A activation, ultimately resulting in smooth muscle relaxation and decreased contractile force. Furthermore, GLP-1 receptor activation influences calcium channel function and intracellular calcium homeostasis, critical factors in gastric smooth muscle excitation-contraction coupling.
Vagal nerve function modulation by incretin mimetics
The vagal nervous system plays a pivotal role in coordinating gastric motility and emptying patterns. GLP-1 receptor agonists significantly influence vagal function through multiple mechanisms, including direct effects on vagal afferent fibres and modulation of central vagal control centres. These interactions can disrupt the normal coordination between gastric accommodation, antral contractions, and pyloric sphincter function.
Clinical observations suggest that patients with pre-existing vagal dysfunction may be particularly susceptible to developing severe gastroparesis when initiated on GLP-1 therapy. The concept of “unmasking” latent gastric motility disorders through incretin mimetic administration has gained increasing recognition among gastroenterologists specialising in motility disorders. This phenomenon may explain why some patients experience persistent gastroparesis symptoms even after medication discontinuation.
Dose-dependent gastric motor dysfunction patterns
Emerging evidence suggests a clear dose-response relationship between semaglutide administration and gastroparesis severity. Higher doses of GLP-1 receptor agonists correlate with more profound delays in gastric emptying and increased symptom severity. This relationship has important implications for clinical practice, as many patients require dose escalation to achieve optimal glycaemic control or weight loss outcomes.
Pharmacokinetic studies demonstrate that semaglutide’s extended half-life of approximately 165 hours contributes to sustained gastric motility suppression. Unlike shorter-acting GLP-1 agonists, the prolonged presence of semaglutide may lead to cumulative effects on gastric function, potentially explaining why some patients develop gastroparesis after months of apparently well-tolerated therapy. Understanding these temporal patterns is crucial for implementing appropriate monitoring strategies and early intervention protocols.
Clinical evidence of Ozempic-Associated gastric paralysis
The clinical evidence supporting the association between Ozempic and gastroparesis has grown substantially over recent years, driven by both formal research studies and real-world clinical observations. Multiple independent research groups have documented concerning patterns of gastroparesis development among patients receiving semaglutide therapy, with findings consistently demonstrating elevated risks compared to alternative treatment options.
The University of Kansas study, encompassing nearly 150,000 semaglutide-treated patients, revealed gastroparesis diagnosis rates of 0.53%, translating to approximately 750 affected individuals within their cohort. When compared to matched control groups not receiving GLP-1 therapy, this represented a statistically significant 66% relative risk increase . These findings have been corroborated by subsequent investigations utilising different patient populations and analytical methodologies, strengthening the evidence base for this association.
FDA adverse event reporting system database analysis
The FDA’s Adverse Event Reporting System (FAERS) database contains numerous reports of gastroparesis among patients receiving semaglutide therapy. Analysis of these reports reveals concerning patterns, including cases where gastroparesis symptoms persisted after medication discontinuation. The FDA has acknowledged receiving reports of stomach paralysis with both semaglutide and liraglutide, with some cases documented as “not recovered” at the time of reporting.
Regulatory authorities face challenges in establishing definitive causality due to the complex nature of gastroparesis aetiology and the presence of confounding factors such as underlying diabetes. However, the temporal relationship between medication initiation and symptom onset, combined with the known pharmacological effects of GLP-1 agonists on gastric motility, provides compelling evidence for a causal association. The FDA continues to monitor these reports whilst emphasising that benefits may outweigh risks for many patients requiring these medications for diabetes management or significant weight reduction.
Peer-reviewed studies on semaglutide gastroparesis incidence
Recent peer-reviewed publications have provided robust epidemiological evidence for increased gastroparesis risk among semaglutide users. The landmark study published in JAMA examined over 16 million patient records, identifying significant associations between GLP-1 receptor agonist use and severe gastrointestinal complications. This research demonstrated a 3.67-fold increased risk of gastroparesis among patients receiving these medications compared to those using alternative weight loss treatments.
The University Hospitals Cleveland study contributed valuable longitudinal data, tracking gastroparesis development over extended periods ranging from three months to two years. Their findings revealed that whilst gastroparesis incidence remained similar between treatment groups at three months, significant differences emerged from six months onwards, with the GLP-1 group demonstrating a 25% higher likelihood of developing gastroparesis at eighteen months. This temporal pattern suggests that prolonged exposure may be necessary for clinically significant gastroparesis to manifest in susceptible individuals.
Comparative risk assessment with dulaglutide and liraglutide
Comparative studies examining different GLP-1 receptor agonists have revealed varying gastroparesis risk profiles across this medication class. Research indicates that liraglutide users experience gastroparesis at rates of approximately 7 cases per 1,000 patients, whilst semaglutide demonstrates slightly higher incidence rates of 10 cases per 1,000 users. These differences may reflect variations in receptor binding affinity, pharmacokinetic properties, or dosing regimens between different agents.
Dulaglutide, another weekly GLP-1 receptor agonist, appears to have a somewhat lower gastroparesis risk profile compared to semaglutide, though direct head-to-head comparative studies remain limited. The molecular structure and specific receptor interaction patterns of different GLP-1 agonists may influence their propensity to cause severe gastric motility dysfunction. Understanding these comparative risks enables clinicians to make more informed decisions when selecting appropriate incretin-based therapies for individual patients, particularly those with pre-existing gastrointestinal concerns.
Case reports from mayo clinic and johns hopkins medical centres
Detailed case reports from leading medical institutions have provided valuable insights into the clinical presentation and natural history of Ozempic-induced gastroparesis. Mayo Clinic investigators documented cases involving patients who developed severe gastroparesis symptoms within months of initiating semaglutide therapy, with gastric emptying studies revealing profound delays in food clearance from the stomach.
One particularly illustrative case involved a 42-year-old patient who developed intractable vomiting and was found to have food remaining in her stomach from meals consumed several days previously. Gastric emptying scintigraphy revealed severe gastroparesis with less than 25% gastric emptying at four hours post-meal. Despite medication discontinuation, this patient experienced persistent symptoms requiring ongoing medical management with prokinetic agents and dietary modifications. Such cases highlight the potentially irreversible nature of gastroparesis in some individuals, emphasising the importance of early recognition and intervention strategies.
Gastroparesis symptom recognition and diagnostic protocols
Early recognition of gastroparesis symptoms in patients receiving Ozempic therapy is crucial for preventing progression to severe, potentially irreversible gastric dysfunction. The clinical presentation of semaglutide-induced gastroparesis often begins subtly, with symptoms that may initially be attributed to the expected gastrointestinal side effects of GLP-1 therapy. Healthcare providers must maintain heightened awareness of symptom progression patterns and implement systematic monitoring approaches to identify developing gastroparesis before it becomes debilitating.
The cardinal symptoms of gastroparesis include persistent nausea, recurrent vomiting, early satiety, postprandial fullness, and abdominal bloating. However, distinguishing these symptoms from typical GLP-1 side effects requires careful attention to temporal patterns and symptom severity. Gastroparesis-related symptoms typically persist or worsen over time, whereas standard GLP-1 side effects generally improve with continued therapy. Patients may describe vomiting food consumed several days previously, a pathognomonic sign of severe gastric stasis that warrants immediate clinical evaluation.
Diagnostic protocols for suspected gastroparesis should incorporate validated assessment tools and objective testing methodologies. The Gastroparesis Cardinal Symptom Index (GCSI) provides a standardised framework for symptom evaluation, whilst gastric emptying scintigraphy remains the gold standard for definitive diagnosis. This nuclear medicine study involves consuming a standardised meal containing radioactive tracers, followed by serial imaging to quantify gastric emptying rates over four hours. Normal gastric emptying should clear at least 90% of the meal contents within four hours, whilst gastroparesis is diagnosed when more than 10% remains.
Healthcare providers should implement systematic gastroparesis screening protocols for patients receiving long-term GLP-1 therapy, particularly those reporting persistent or worsening gastrointestinal symptoms beyond the initial treatment period.
Alternative diagnostic approaches include wireless motility capsule studies, which provide comprehensive assessment of gastrointestinal transit times throughout the entire digestive tract. This technology offers advantages over traditional scintigraphy by providing detailed information about gastric emptying, small bowel transit, and colonic function without radiation exposure. Additionally, upper gastrointestinal endoscopy may reveal retained food particles in the stomach, supporting the diagnosis of gastroparesis whilst excluding mechanical obstruction or other structural abnormalities.
Risk stratification protocols should identify patients at higher risk for developing severe gastroparesis complications. Factors associated with increased susceptibility include female gender, underlying diabetes mellitus, history of gastrointestinal surgery, concurrent medications affecting gastric motility, and pre-existing functional dyspepsia. Patients with multiple risk factors warrant more intensive monitoring and potentially alternative therapeutic approaches. Regular symptom assessment using standardised questionnaires, combined with periodic objective testing in high-risk individuals, can facilitate early detection and intervention before irreversible gastric dysfunction develops.
Risk stratification and patient vulnerability factors
Understanding patient-specific risk factors for developing Ozempic-induced gastroparesis is essential for implementing appropriate preventive strategies and monitoring protocols. Research has identified several demographic, clinical, and pharmacological factors that predispose individuals to severe gastric motility dysfunction when receiving GLP-1 receptor agonist therapy. These risk factors operate through various mechanisms, including baseline gastric function impairment, genetic polymorphisms affecting drug metabolism, and comorbid conditions that compromise gastric neuromuscular function.
Female patients demonstrate significantly higher gastroparesis risk compared to males, with studies indicating up to a two-fold increased susceptibility. This gender disparity may reflect hormonal influences on gastric motility, with oestrogen and progesterone fluctuations affecting gastric emptying rates. Additionally, women are more likely to have underlying functional gastrointestinal disorders that may predispose them to medication-induced gastroparesis. Age also plays a crucial role, with patients over 50 years demonstrating increased vulnerability due to age-related changes in gastric neuromuscular function and reduced adaptive capacity.
Pre-existing diabetes mellitus represents a particularly important risk factor, as diabetic gastroparesis shares pathophysiological mechanisms with medication-induced forms of the condition. Patients with longstanding diabetes, particularly those with evidence of diabetic neuropathy affecting other organ systems, face substantially elevated risks when initiated on GLP-1 therapy. The combination of underlying diabetic gastric dysfunction and pharmacologically-induced motility suppression can result in severe, potentially irreversible gastroparesis that proves challenging to manage even after medication discontinuation.
| Risk Factor | Relative Risk Increase | Clinical Considerations |
|---|---|---|
| Female Gender | 2.0x | Hormonal influences on gastric motility |
| Age >50 years | 1.5x | Reduced gastric adaptive capacity |
| Diabetic Neuropathy | 3.2x | Pre-existing gastric dysfunction |
| Prior GI Surgery | 2.8x | Altered gastric anatomy and innervation |
Genetic factors may also contribute to individual susceptibility patterns, with emerging research identifying polymorphisms in genes encoding GLP-1 receptors, gastric smooth muscle proteins, and neurotransmitter systems that influence gastroparesis risk. Pharmacogenomic testing may eventually enable personalised risk assessment and treatment selection, though such approaches remain investigational at present. Concurrent medications affecting gastric motility, including opioid analgesics, anticholinergic agents, and certain psychiatric medications, can synergistically increase gastroparesis risk when combined with
GLP-1 receptor agonists.
Previous gastrointestinal surgery, particularly procedures involving the stomach or vagus nerve, significantly increases gastroparesis susceptibility. Surgical interventions can disrupt normal gastric innervation patterns and alter anatomical relationships critical for coordinated gastric emptying. Patients with histories of fundoplication, gastric resection, or bariatric procedures require careful consideration before initiating GLP-1 therapy, as their baseline gastric function may already be compromised. The combination of surgical alterations and pharmacological motility suppression can precipitate severe gastroparesis that proves resistant to conventional management strategies.
Management strategies for ozempic-induced gastroparesis
The management of Ozempic-induced gastroparesis requires a comprehensive, multidisciplinary approach that addresses both the underlying pharmacological cause and the resulting gastric dysfunction. Treatment strategies must be individualised based on symptom severity, patient comorbidities, and the clinical necessity of continued GLP-1 therapy. Early intervention is crucial for optimising outcomes and preventing progression to irreversible gastric dysfunction that can significantly impact long-term quality of life.
The primary management decision involves determining whether GLP-1 therapy should be continued, modified, or discontinued entirely. This decision requires careful consideration of the original therapeutic indication, symptom severity, and availability of alternative treatments. For patients with severe gastroparesis symptoms, immediate medication discontinuation is often necessary, though recovery may be incomplete in some cases. Conversely, patients with mild symptoms may benefit from dose reduction strategies combined with symptomatic management, allowing continuation of beneficial metabolic effects while minimising gastric complications.
Symptom management protocols should address the multiple dimensions of gastroparesis, including nausea control, nutritional support, gastric motility enhancement, and prevention of complications such as dehydration and malnutrition. Antiemetic medications, particularly 5-HT3 receptor antagonists like ondansetron, provide effective nausea control without further compromising gastric motility. However, certain antiemetics such as promethazine should be avoided due to their anticholinergic effects that can worsen gastric stasis.
Prokinetic agent therapy with metoclopramide and domperidone
Prokinetic medications represent the cornerstone of pharmacological management for Ozempic-induced gastroparesis, with metoclopramide serving as the most commonly prescribed agent in many countries. Metoclopramide functions through dual mechanisms, acting as both a dopamine D2 receptor antagonist and a 5-HT4 receptor agonist, thereby enhancing gastric motility and coordination. The typical dosing regimen involves 10mg administered 30 minutes before meals and at bedtime, though doses may require adjustment based on symptom response and tolerance.
However, metoclopramide therapy carries significant limitations and potential risks that must be carefully considered. Long-term use is associated with tardive dyskinesia, an irreversible neurological complication characterised by involuntary movements. The FDA has issued black box warnings limiting metoclopramide use to 12 weeks duration except in exceptional circumstances. This temporal restriction poses challenges for managing chronic gastroparesis conditions that may persist beyond the acute medication-induced phase.
Domperidone offers an alternative prokinetic option with a more favourable side effect profile, particularly regarding central nervous system effects. Unlike metoclopramide, domperidone does not readily cross the blood-brain barrier, significantly reducing the risk of extrapyramidal side effects and tardive dyskinesia. However, domperidone availability varies by geographic region, with limited access in some countries due to cardiac safety concerns related to QT interval prolongation and potential arrhythmias in susceptible patients.
Erythromycin, a macrolide antibiotic with potent prokinetic properties, serves as an alternative option for acute gastroparesis management. The medication stimulates motilin receptors, triggering phase III migrating motor complexes that help clear the stomach of accumulated food particles. However, erythromycin’s effectiveness diminishes with prolonged use due to tachyphylaxis, limiting its utility for chronic management. Additionally, drug interactions and antibiotic resistance concerns restrict its long-term application.
Gastric electrical stimulation device implementation
Gastric electrical stimulation (GES) represents an advanced therapeutic option for patients with severe, medically refractory gastroparesis. This intervention involves surgical implantation of a device that delivers high-frequency electrical pulses to gastric smooth muscle, potentially improving symptoms and gastric emptying in selected patients. The Medtronic Enterra system, the most widely studied GES device, has received humanitarian device exemption status for gastroparesis treatment in cases where conventional therapies have proven inadequate.
Patient selection for GES requires careful evaluation by multidisciplinary teams including gastroenterologists, surgeons, and device specialists. Candidates typically have documented severe gastroparesis with gastric retention greater than 35% at four hours on scintigraphic testing, along with symptoms significantly impacting quality of life despite optimal medical management. The surgical implantation procedure involves laparoscopic placement of stimulation leads on the gastric serosa, connected to a pulse generator implanted in the abdominal wall.
Clinical outcomes with GES demonstrate variable effectiveness, with studies showing symptom improvement in 60-80% of patients, though gastric emptying normalisation occurs less frequently. The mechanism of benefit appears related to symptom modulation rather than direct enhancement of gastric motility, possibly through effects on gastric accommodation or visceral pain perception. Long-term follow-up data indicate sustained symptom improvement in many patients, though device-related complications including lead migration, infection, and battery depletion require ongoing monitoring.
Dietary modification protocols for delayed gastric emptying
Nutritional management plays a crucial role in gastroparesis treatment, with dietary modifications designed to optimise gastric emptying while maintaining adequate nutritional intake. The gastroparesis diet follows a graduated approach, progressing from liquid to solid foods based on symptom tolerance and gastric emptying capacity. During acute exacerbations, patients may require complete bowel rest with parenteral nutrition, while recovery phases allow gradual dietary advancement under careful supervision.
The cornerstone principles of gastroparesis dietary management include consuming frequent small meals, minimising high-fat and high-fibre foods, and emphasising easily digestible nutrients. Fat significantly delays gastric emptying and should be limited to less than 50 grams daily, distributed across multiple small portions. Insoluble fibre, found in raw vegetables and whole grains, can form bezoars in patients with severe gastric stasis and should be strictly avoided during acute phases.
Liquid nutrition supplements provide essential calories and nutrients while minimising gastric residue that could exacerbate symptoms. Specialised gastroparesis formulations contain pre-digested proteins, simple carbohydrates, and minimal fat content to optimise gastric emptying. However, the osmolarity of liquid supplements must be carefully considered, as hyperosmolar solutions can paradoxically delay gastric emptying through neural and hormonal feedback mechanisms.
Meal timing and positioning strategies can significantly impact symptom severity and gastric emptying rates. Patients should consume their largest meals earlier in the day when gastric motility tends to be most robust, while avoiding late evening meals that may remain in the stomach overnight. Post-meal positioning with the head elevated and slight right lateral positioning may facilitate gravitational gastric emptying and reduce reflux symptoms that commonly accompany gastroparesis.
Semaglutide dosage adjustment and discontinuation guidelines
The management of gastroparesis symptoms in patients receiving Ozempic often necessitates careful consideration of dosage modification or complete medication discontinuation. Clinical decision-making should incorporate symptom severity, therapeutic indication urgency, and availability of alternative treatments for the underlying condition. Mild gastroparesis symptoms may respond to dose reduction strategies, while severe cases typically require immediate medication discontinuation to prevent irreversible gastric dysfunction.
Dose reduction protocols should follow systematic approaches, typically involving 50% dose decreases with careful monitoring for both symptom improvement and maintenance of therapeutic benefits. Patients with diabetes mellitus requiring glycaemic control may benefit from temporary dose reduction while implementing alternative antidiabetic strategies. However, individuals using semaglutide primarily for weight management may require complete discontinuation if significant gastroparesis symptoms develop.
The timeline for medication discontinuation varies based on gastroparesis severity and individual patient factors. Mild cases may warrant a trial period of 2-4 weeks at reduced dosages, while severe symptoms necessitate immediate discontinuation. Given semaglutide’s extended half-life of approximately 165 hours, symptom improvement may not be apparent for 2-3 weeks following discontinuation. Patients should be counselled regarding this delayed recovery timeline to manage expectations and maintain compliance with supportive therapies.
Alternative therapeutic options should be explored for patients requiring discontinuation of GLP-1 therapy. Diabetic patients may benefit from SGLT-2 inhibitors, DPP-4 inhibitors, or insulin-based regimens, while those seeking weight management might consider lifestyle interventions, alternative pharmacotherapies, or bariatric surgical procedures. The selection of alternative treatments should account for individual patient characteristics, comorbidities, and previous treatment responses to optimise long-term outcomes.
Long-term prognosis and reversibility of gastric motor function
The long-term prognosis for patients who develop Ozempic-induced gastroparesis varies considerably, with recovery patterns influenced by multiple factors including symptom severity at presentation, duration of GLP-1 exposure, underlying patient characteristics, and timeliness of intervention. While many patients experience significant symptom improvement following medication discontinuation, complete recovery is not universal, and some individuals may develop persistent gastric dysfunction requiring ongoing management strategies.
Research examining gastroparesis reversibility following GLP-1 discontinuation provides both encouraging and concerning findings. The majority of patients demonstrate objective improvement in gastric emptying studies within 3-6 months of medication cessation, with gastric emptying times gradually returning toward baseline values. However, approximately 20-30% of patients continue to experience persistent symptoms and delayed gastric emptying despite prolonged medication withdrawal, suggesting potential for irreversible gastric neuromuscular changes in susceptible individuals.
Factors associated with incomplete recovery include advanced patient age, prolonged duration of GLP-1 therapy before symptom recognition, severe gastroparesis at presentation, and presence of underlying conditions predisposing to gastric dysfunction. Patients with diabetes mellitus face particular challenges, as distinguishing between medication-induced and diabetic gastroparesis can prove difficult, potentially complicating recovery assessment and long-term management strategies.
The window for optimal recovery appears to be within the first six months following medication discontinuation, emphasising the critical importance of early recognition and prompt intervention when gastroparesis symptoms develop in patients receiving GLP-1 therapy.
Long-term follow-up studies indicate that most patients who achieve symptom resolution maintain stable gastric function over extended periods, provided they avoid re-exposure to GLP-1 agonists or other medications known to impair gastric motility. However, some individuals may experience episodic symptom recurrence during periods of stress, illness, or dietary indiscretion, suggesting persistent vulnerability to gastric dysfunction even after apparent recovery.
The implications of persistent gastroparesis extend beyond immediate symptom management to encompass broader health considerations including nutritional status, medication absorption, quality of life, and healthcare utilisation. Patients with chronic gastroparesis require ongoing monitoring for complications such as malnutrition, vitamin deficiencies, and medication malabsorption that can significantly impact long-term health outcomes. Additionally, the psychological impact of chronic gastrointestinal symptoms should not be underestimated, with many patients experiencing depression, anxiety, and social isolation related to their condition.
Preventive strategies focusing on early symptom recognition and prompt intervention offer the best opportunity for optimising long-term outcomes. Healthcare providers should implement systematic monitoring protocols for patients receiving GLP-1 therapy, with particular attention to those identified as high-risk based on demographic and clinical characteristics. Patient education regarding gastroparesis symptoms and the importance of early reporting can facilitate timely diagnosis and intervention, potentially preventing progression to irreversible gastric dysfunction that significantly compromises long-term quality of life and health outcomes.