Cite as: Archiv EuroMedica. 2026. 16; 4. DOI 10.35630/2026/16/Iss.4.05
Rumination syndrome is an underrecognized disorder of gut–brain interaction characterized by recurrent, effortless postprandial regurgitation resulting from maladaptive behavioral and gastrointestinal motor mechanisms. Although growing evidence has improved understanding of its epidemiology, pathophysiology, diagnosis, and management, the available data remain fragmented, and comprehensive reviews integrating current knowledge are limited.
To provide a comprehensive narrative review of the current evidence on the clinical presentation, diagnosis, and management of rumination syndrome, with particular emphasis on recent advances and their implications for clinical practice.
Relevant literature was identified through structured searches of PubMed and Google Scholar. The primary search covered studies published between January 2016 and 1 July 2026, with earlier key or foundational publications additionally included when relevant. Sources addressing clinical presentation, diagnostic criteria or diagnostic methods, non-pharmacological treatment, or pharmacological treatment were considered. Eligible sources included randomized controlled trials, prospective or retrospective clinical studies, observational studies, systematic reviews, clinical guidelines, relevant experimental research, and clinical trial registrations. Following title and abstract screening and full-text evaluation, 44 sources were included in the final narrative review.
Rumination syndrome is characterized by recurrent, effortless postprandial regurgitation, with clinical manifestations and disease severity differing according to age at symptom onset. Diagnosis is primarily based on clinical history and appropriate diagnostic criteria, including Rome IV in adults, Rome V in children and adolescents, and DSM-5. Postprandial high-resolution impedance manometry represents the reference standard for objective confirmation when required. Non-pharmacological interventions, particularly diaphragmatic breathing, together with biofeedback, behavioral therapy, patient education, and multidisciplinary management, represent the cornerstone of treatment. Pharmacological therapy has a limited adjunctive role. Baclofen currently has the strongest evidence among pharmacological agents, although the available evidence remains limited, while evidence supporting other medications is even less convincing.
Early recognition of the characteristic clinical presentation of rumination syndrome is essential for timely diagnosis and appropriate management. Diagnosis should be guided by age-appropriate criteria, with postprandial high-resolution impedance manometry providing objective confirmation when required. Behavioral interventions remain the mainstay of treatment, whereas pharmacological therapy has a limited adjunctive role. Earlier diagnosis and timely initiation of appropriate treatment may reduce unnecessary diagnostic investigations and improve clinical outcomes.
Keywords: rumination syndrome; disorders of gut–brain interaction; diaphragmatic breathing; diagnosis; behavioral therapy; Rome IV; Rome V; DSM-5; baclofen
Rumination syndrome is a functional gastrointestinal disorder classified among disorders of gut–brain interaction (DGBIs), characterized by recurrent, effortless regurgitation of recently ingested food, typically occurring 10–15 minutes after meals in the absence of nausea or retching [1]. The disorder is recognized in both the Rome IV criteria and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), highlighting its interdisciplinary nature and the close interplay between gastroenterological and psychiatric aspects [2,3]. Although historically considered a rare condition, growing evidence indicates that rumination syndrome is more common than previously recognized [4].
Globally, the prevalence of rumination syndrome is estimated at approximately 2.8%, indicating that it is relatively uncommon compared with other disorders of gut–brain interaction [5]. A large meta-analysis including 30 studies and 114,228 participants reported a prevalence of 0.4% among children and adolescents (0–18 years) and 3.7% among adults according to the Rome IV diagnostic criteria. Additional analyses based on the Rome III criteria and the Eating Disorders in Youth Questionnaire (EDY-Q) demonstrated a similar pattern, with an overall prevalence of 0.8% in the pediatric population compared with 3.0% in adults, regardless of the diagnostic criteria applied [6].
These findings suggest that earlier reports describing a relatively high prevalence of rumination syndrome in children may have reflected methodological limitations, selected study populations, and the use of older diagnostic criteria rather than a genuinely higher disease burden in the pediatric population [7].
Among adults, female sex, anxiety disorders, depression, a history of eating disorders such as anorexia nervosa or bulimia nervosa, higher body mass index (BMI), cigarette smoking, adherence to a gluten-free diet, and allergic rhinitis have been identified as independent factors associated with rumination syndrome [6,8–10]. In contrast, no significant association between sex and the prevalence of rumination syndrome has been observed in the pediatric population [6]. Current evidence indicates that rumination syndrome results from the interaction between altered gastrointestinal physiology and maladaptive learned behavioral mechanisms rather than structural gastrointestinal abnormalities [11].
The central pathophysiological event is an involuntary contraction of the anterior abdominal wall muscles occurring shortly after food intake, which leads to a marked increase in intra-abdominal pressure and reversal of the normal gastroesophageal pressure gradient [12,13]. This pressure change, together with transient relaxation of the lower esophageal sphincter (LES), facilitates the retrograde movement of gastric contents into the esophagus and oral cavity [2]. Postprandial gastric distension is considered one of the main triggers of abdominal wall contraction, suggesting an abnormal sensorimotor response within the upper gastrointestinal tract [14]. Increasing evidence also indicates that rumination represents a learned behavioral response, in which repeated subconscious contraction of the abdominal musculature in response to postprandial discomfort gradually becomes an automatic motor pattern, ultimately perpetuating the disorder [15,16].
Over the past decade, substantial progress has been made in understanding the epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of rumination syndrome. Nevertheless, the available evidence remains dispersed across studies addressing individual aspects of the disorder, while comprehensive reviews integrating current knowledge are limited. Given the growing recognition of rumination syndrome as a distinct disorder of gut–brain interaction and the expanding body of evidence regarding its clinical characteristics and management, an up-to-date synthesis of the available literature is warranted. Such a review may contribute to improving awareness of the disorder, facilitate its timely recognition, and support evidence-based clinical decision-making. However, important gaps remain in the current evidence, particularly regarding age-related differences in clinical presentation, the role of recently updated diagnostic criteria, the long-term effectiveness of behavioral interventions, and the place of pharmacological therapy in the management of rumination syndrome.
To provide a comprehensive narrative review of the current evidence on the clinical presentation, diagnosis, and management of rumination syndrome, with particular emphasis on recent advances and their implications for clinical practice.
Relevant literature was identified through structured searches of PubMed and Google Scholar. The primary search covered studies published between January 2016 and 1 July 2026, and the final search was completed on 1 July 2026. Earlier publications of particular relevance to the pathophysiology, diagnosis, and treatment of rumination syndrome were additionally included when they represented key or foundational evidence not adequately covered by more recent studies.
The principal search terms included "rumination syndrome", "rumination disorder", epidemiology, pathophysiology, clinical presentation, diagnosis, high-resolution impedance manometry, behavioral therapy, diaphragmatic breathing, biofeedback, baclofen, and treatment, combined with Boolean operators as appropriate. Studies were included if they addressed at least one of the predefined review domains: clinical presentation, diagnostic criteria or diagnostic methods, non-pharmacological treatment, or pharmacological treatment of rumination syndrome. Eligible sources included randomized controlled trials, prospective or retrospective clinical studies, observational studies, systematic reviews, clinical guidelines, relevant experimental research, and clinical trial registrations addressing the predefined review domains. Only English language sources were included.
Sources were excluded if they were unrelated to the review topic, lacked clinically relevant data, were duplicate reports, conference abstracts without full-text publication, or letters without original data.
The retrieved records underwent title and abstract screening, followed by full-text evaluation of potentially relevant studies. Following the selection process, 44 sources were included in the final review. As this was a narrative review, no formal systematic review methodology or risk of bias assessment was applied.
Rumination syndrome is characterized by recurrent, effortless regurgitation of recently ingested food in the absence of nausea or retching. Episodes typically begin within 10–15 minutes after meal consumption but may continue for up to 2 hours after eating, including following the ingestion of liquids alone. Regurgitation may recur multiple times during the same postprandial period, with the regurgitated material being rechewed, reswallowed, or expelled. However, the available literature does not identify factors determining which of these behaviors predominates in individual patients. The regurgitated material is typically undigested or only partially digested, retains the taste of recently ingested food, and is generally non-acidic, helping distinguish rumination syndrome from gastroesophageal reflux disease and vomiting. Episodes often cease spontaneously as gastric contents become progressively acidified during digestion [10,17].
Most patients do not report additional upper gastrointestinal symptoms, although some experience early satiety, postprandial fullness, or abdominal discomfort [18]. Clinical manifestations may differ according to the age at symptom onset. Children with early-onset disease generally exhibit milder symptoms despite more frequent regurgitation episodes, with lower rates of vomiting, weight loss, meal avoidance, and the need for enteral or parenteral nutritional support. Developmental delay, however, is reported more frequently in this group. In contrast, symptom onset during adolescence is more often associated with a more severe clinical course, coexisting anxiety and depressive disorders, greater dietary restriction, and more pronounced nutritional impairment [19].
The diagnosis of rumination syndrome is primarily based on clinical history. In adults, the Rome IV criteria remain an established diagnostic framework and require recurrent, effortless regurgitation of recently ingested food, typically occurring shortly after meals in the absence of retching, with symptoms persisting for at least 3 months and an onset at least 6 months before diagnosis. In addition, the Rome IV criteria include several supportive features that are not required for diagnosis but may increase diagnostic confidence and facilitate clinical differentiation. For children and adolescents, the recently published Rome V criteria provide the current pediatric diagnostic framework for rumination syndrome [17].
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), defines rumination disorder as repeated regurgitation of food persisting for at least 1 month. Unlike the adult Rome IV criteria, DSM-5 does not specify a temporal relationship between symptoms and meal consumption. The principal differences between the adult Rome IV criteria and DSM-5 are summarized in Table 1. Both diagnostic systems require that the symptoms cannot be better explained by another medical or psychiatric condition [6,21].
Table 1. Comparison of diagnostic criteria for rumination syndrome in adults according to Rome IV and DSM-5
| Criterion | Rome IV criteria [20,21] | DSM-5 criteria [21] |
| Core diagnostic criteria | 1. Persistent or recurrent regurgitation of recently ingested food into the mouth with subsequent spitting, remastication, or swallowing. 2. Regurgitation is not preceded by retching. | Repeated regurgitation of food, which may be reswallowed or spat out of the mouth. |
| Supportive criteria | 1. Effortless regurgitation events are usually not preceded by nausea. 2. Regurgitant contains recognizable food which may have a pleasant taste. 3. The process tends to cease when the regurgitated material becomes acidic. | Not defined. |
| Duration of symptoms | ≥3 months, with initial occurrence of symptoms ≥6 months prior to diagnosis. | ≥1 month. |
Differential diagnosis is primarily based on the characteristic pattern of regurgitation and associated symptoms. Rumination syndrome is distinguished by effortless, typically postprandial regurgitation without preceding nausea or retching, with recognizable and usually non acidic food. Gastroesophageal reflux disease is more commonly associated with acidic regurgitation, while achalasia and gastroparesis are more often accompanied by symptoms such as dysphagia, nausea, or abdominal discomfort. Gastric outlet obstruction should be considered when symptoms suggest impaired gastric emptying or mechanical obstruction. Eating disorders, particularly bulimia nervosa, may mimic rumination syndrome but are characterized by self induced regurgitation associated with concerns about body weight or body image [12,21,36].
The principal diagnostic criteria for rumination syndrome in children and adolescents according to Rome V are summarized in Table 2.
Table 2. Diagnostic criteria for rumination syndrome in children and adolescents according to Rome V [17]
| Criterion | Rome V criteria |
| Core diagnostic criteria | Repeated, seemingly effortless regurgitation of gastric contents that is reswallowed, rechewed, or expelled during or immediately after meals or ingestion of fluids. Regurgitation does not occur during sleep. |
| Additional requirements | Symptoms do not respond to standard management for gastroesophageal reflux disease or infant regurgitation. Symptoms cannot be fully explained by another medical condition. An eating disorder must be ruled out. |
| Duration of symptoms | Symptoms are present for at least 2 months, with onset after 3 months of age. |
The reference standard for objective confirmation of rumination syndrome is postprandial high-resolution impedance manometry (HRIM), which simultaneously assesses esophageal pressure and bolus transit, enabling identification of characteristic rumination episodes [22]. These episodes are characterized by a sudden increase in intragastric pressure, typically ≥30 mmHg (the R-wave), followed by transient relaxation of the lower esophageal sphincter and retrograde movement of gastric contents into the esophagus detected by impedance monitoring [23]. However, the conventional ≥30 mmHg intragastric pressure threshold may not capture all rumination episodes; Geysen et al. reported that this criterion failed to identify approximately 28% of episodes and proposed the gastro-sphincteric pressure gradient as an additional parameter to improve differentiation of rumination from gastroesophageal reflux and transient lower esophageal sphincter relaxations [24]. To maximize diagnostic yield, HRIM should be performed after ingestion of a meal known to provoke symptoms, followed by an adequately prolonged postprandial recording period. In selected cases, prolonged ambulatory HRIM monitoring may further increase the likelihood of capturing spontaneous regurgitation episodes. Complementary techniques, including abdominal wall electromyography and abdominal inductance plethysmography, may be used in specialized centers to demonstrate the coordinated muscular activity underlying rumination episodes [4].
Non-pharmacological management of rumination syndrome primarily consists of diaphragmatic breathing, biofeedback, behavioral therapy, patient education, relaxation techniques, and multidisciplinary behavioral programs [12,25]. Diaphragmatic breathing involves slow, controlled breathing with active diaphragmatic engagement, particularly during the postprandial period when regurgitation episodes most commonly occur. Its primary objective is to replace the maladaptive motor response with a competing physiological pattern, thereby reducing intra-abdominal pressure and preventing regurgitation [12,26]. By stabilizing the pressure gradient between the thoracic and abdominal cavities and limiting abrupt increases in intra-abdominal pressure caused by inappropriate abdominal wall contraction, diaphragmatic breathing interrupts the motor pattern responsible for regurgitation. In a prospective study of children with rumination syndrome, 23 patients with persistent symptoms underwent education regarding the pathophysiology of the disorder combined with diaphragmatic breathing training. Initial symptom resolution was observed in 82.6% of patients. However, 28.5% experienced symptom recurrence during follow-up [25,27,28]. In addition, studies evaluating autonomic nervous system activity have suggested that diaphragmatic breathing may increase postprandial vagal activity, providing a potential physiological explanation for its therapeutic effects [29].
Biofeedback may further enhance treatment by providing patients with real-time feedback on physiological parameters such as respiratory pattern and abdominal muscle activity, thereby facilitating voluntary control of the motor responses responsible for symptom generation [12,26]. In a randomized controlled trial, participants in the biofeedback intervention group demonstrated a mean 74% reduction in the number of rumination episodes after three therapy sessions, whereas no significant improvement was observed in the placebo group, 1%; p = 0.001. Furthermore, a significant reduction in the activity of the anterior abdominal wall and intercostal muscles (approximately 51–52%) was observed, indicating improved control of the abnormal motor pattern underlying symptom generation [30]. In a prospective study of 28 patients with rumination syndrome confirmed by manometry, biofeedback-guided control of abdominothoracic muscle activity reduced regurgitation episodes by 70% after three treatment sessions, with further improvement observed during 6 months of follow-up. At 6 months, 5 of 11 patients with available follow-up had completely suppressed rumination, while a further 2 patients achieved >95% improvement [31]. Patient education is also considered an important component of treatment, as understanding the behavioral nature of the disorder may improve adherence to therapy and reduce symptom-related anxiety. Behavioral therapy may provide additional benefit, particularly in patients with coexisting anxiety, depression, maladaptive coping strategies, or persistent symptoms despite diaphragmatic breathing [26]. Available clinical studies have generally reported favorable outcomes following behavioral therapy. In a retrospective study of 52 children and adolescents who received behavioral interventions, including diaphragmatic breathing, biofeedback, relaxation training, and/or cognitive behavioral therapy, rumination resolved completely in 29.6% of patients, and an additional 55.6% experienced clinical improvement, whereas symptoms remained unchanged in 12.9% [27,32]. In a large cohort study involving 247 children with rumination syndrome, the median age at symptom onset was 11 years, whereas the median age at diagnosis was 13 years, corresponding to a median diagnostic delay of 1 year.
The analysis demonstrated that patients with a longer interval between symptom onset and diagnosis were significantly less likely to achieve remission following behavioral therapy. Complete symptom resolution was achieved in 29% of patients, suggesting that earlier diagnosis and prompt initiation of behavioral therapy may improve the likelihood of favorable clinical outcomes [33]. Multidisciplinary treatment programs combining patient education, behavioral therapy, and individualized management strategies have also demonstrated promising long-term outcomes [34].
Baclofen is a gamma-aminobutyric acid type b (GABA-b) receptor agonist, which has the ability to cross the blood-brain barrier [35]. It is the pharmacological agent with the strongest evidence for the treatment of rumination syndrome. Its proposed mechanism of action involves increasing lower esophageal sphincter (LES) pressure and reducing the frequency of transient LES relaxations (TLESRs), thereby decreasing postprandial regurgitation [36]. In a randomised, double-blind, placebo-controlled, crossover trial, treatment with baclofen (10 mg three times daily) resulted in a significant reduction in the number of regurgitation event markers and rumination episodes compared with placebo. Baclofen treatment was also associated with a significant increase in LES pressure, a reduction in the frequency of TLESRs, and fewer reflux episodes. The most common adverse events were central nervous system–related, reflecting baclofen's ability to cross the blood–brain barrier, and included dizziness, vertigo, somnolence, confusion, weakness, and tremor [37]. Despite these encouraging findings, the evidence remains limited to a single randomised, controlled trial in adults. Further evidence is anticipated from a completed phase III, randomised, placebo-controlled, blinded trial evaluating the efficacy and safety of baclofen as an adjunct to behavioral therapy in paediatric patients with rumination syndrome; results have not yet been posted [38]. Unlike baclofen, tricyclic antidepressants (TCAs) do not directly affect the motor mechanisms of rumination syndrome. Their proposed benefit is attributed to modulation of the gut-brain axis through central pain modulation, reduced visceral hypersensitivity and effects on gastrointestinal sensorimotor function [39].
In a prospective observational study, treatment with a tricyclic antidepressant in combination with diaphragmatic breathing and relaxation therapy was associated with marked improvement in rumination symptoms. After a mean follow-up of 8.8 months, 90.9% of patients reported overall improvement in postprandial regurgitation symptoms, with a mean subjective symptom improvement of 68.9%, while 45.5% reported ≥80% overall symptom improvement. In addition, body weight stabilized or increased in 80.6% of patients who had experienced weight loss before treatment. However, as the study evaluated combination therapy without a control group, the independent efficacy of tricyclic antidepressants could not be determined [40]. Proton pump inhibitors (PPIs) and prokinetic agents have no established role in the treatment of rumination syndrome; available data suggest these medications have no effect on regurgitation frequency [14,21]. PPIs are frequently prescribed because patients are often initially misdiagnosed with gastroesophageal reflux disease; however, acid suppression does not address the underlying pathophysiology of rumination syndrome and generally fails to improve regurgitation symptoms [41]. Their use should therefore be limited to patients with concomitant gastroesophageal reflux disease or acid-related esophageal injury [14,21].
Despite substantial advances in the understanding of rumination syndrome, delayed diagnosis remains a significant clinical challenge with important implications for patient outcomes. Prolonged symptom duration has been associated with weight loss, malnutrition, dehydration, dental enamel erosion, halitosis, anxiety, fear of eating, social withdrawal, school absenteeism, and a marked reduction in quality of life [15,42,43]. These findings underscore that rumination syndrome should not be regarded as a benign functional disorder but rather as a condition that may substantially impair both physical health and psychosocial functioning if left unrecognized.
Interpretation of the available epidemiological evidence requires careful consideration of methodological differences between studies. Variations in diagnostic criteria, particularly between the Rome III, Rome IV and DSM-5 classifications, together with the use of alternative assessment tools such as the Eating Disorders in Youth Questionnaire (EDY-Q), may contribute to inconsistencies in reported prevalence estimates and diagnostic rates. These methodological differences limit direct comparisons across studies and highlight the need for greater standardization in future epidemiological research [6].
The considerable overlap between the clinical manifestations of rumination syndrome and those of other gastrointestinal and psychiatric disorders frequently complicates the diagnostic process. Recurrent regurgitation often prompts evaluation for gastroesophageal reflux disease, achalasia, gastroparesis, mechanical gastrointestinal obstruction, or eating disorders, particularly in the presence of alarm features. Consequently, many patients undergo extensive diagnostic investigations before the correct diagnosis is established.
Importantly, although additional testing is appropriate in selected patients to exclude alternative diagnoses, especially when alarm features are present, rumination syndrome is not a diagnosis of exclusion and can usually be identified based on a characteristic clinical history supported by the Rome IV criteria in adults, the Rome V criteria in children and adolescents, or the DSM-5 diagnostic criteria [4,17,21,44]. Improving awareness of this disorder among clinicians may therefore reduce unnecessary investigations, facilitate earlier diagnosis, and enable timely initiation of appropriate treatment.
Current evidence strongly supports a mechanism-based approach to the management of rumination syndrome. Recognition of the disorder as a learned behavioral motor dysfunction provides a clear rationale for prioritizing behavioral interventions over symptom-oriented pharmacological treatment. Diaphragmatic breathing remains the best-established therapeutic intervention and is widely regarded as the first-line treatment because of its simplicity, safety, and consistently favorable clinical outcomes [12,25]. Beyond diaphragmatic breathing, biofeedback, cognitive behavioral therapy, patient education, and multidisciplinary management may provide additional benefits, particularly in patients with persistent symptoms or psychiatric comorbidities. Given the multifactorial nature of rumination syndrome, integrating gastroenterological, nutritional, and psychological care may offer a more comprehensive therapeutic approach than isolated behavioral therapy alone. Furthermore, early recognition appears to be critical for achieving optimal outcomes, as delayed diagnosis may allow the maladaptive motor pattern to become increasingly established, potentially reducing the effectiveness of behavioral interventions.
Despite the encouraging results reported to date, the overall quality of evidence remains limited. Most published studies are retrospective or observational, include relatively small patient cohorts, and are characterized by heterogeneous treatment protocols, variable outcome measures, and limited long-term follow-up. Consequently, although current evidence consistently supports behavioral therapy as the standard of care, adequately powered randomized controlled trials with standardized treatment protocols and validated outcome measures are still required to determine the optimal treatment strategies, evaluate the durability of therapeutic benefits, and identify patient characteristics associated with the greatest likelihood of treatment response [11,12,15,18,25].
The limited role of pharmacological therapy further supports the concept that rumination syndrome is primarily a behavioral disorder rather than a pharmacologically responsive condition. Accordingly, medications should be considered adjunctive rather than primary treatment and reserved for patients with persistent symptoms despite appropriate behavioral therapy, those unable to engage in behavioral interventions, or individuals with coexisting gastrointestinal or psychiatric disorders that contribute to symptom burden. Among currently available agents, baclofen remains the only medication supported by evidence from a randomized controlled trial demonstrating a reduction in rumination episodes. In contrast, evidence supporting tricyclic antidepressants, proton pump inhibitors, prokinetic agents, and other neuromodulators remains limited. These medications are used primarily to address associated conditions or specific clinical circumstances rather than the underlying pathophysiology of rumination syndrome. Further high-quality randomized studies are needed to better define the role of pharmacological therapy and identify patients most likely to benefit from adjunctive medical treatment [14,21,37,38,40].
This narrative review has several limitations that should be acknowledged. First, the literature search was restricted to PubMed and Google Scholar and did not follow a formal systematic review methodology. Furthermore, the available evidence is characterized by substantial heterogeneity in study design, patient populations, diagnostic criteria, therapeutic interventions, and outcome assessment. Most published studies are retrospective or observational and include relatively small cohorts, limiting the overall quality of the evidence. Consequently, direct comparison of treatment outcomes across studies is challenging, and the current data do not allow definitive conclusions regarding the comparative effectiveness of the available therapeutic strategies for rumination syndrome.
Rumination syndrome is characterized by recurrent, effortless regurgitation of recently ingested food, typically occurring after meals, while clinical manifestations and disease severity may vary depending on the age at symptom onset.
Diagnosis is based primarily on a characteristic clinical history and appropriate diagnostic criteria: Rome IV in adults, Rome V in children and adolescents, and DSM-5. Postprandial high-resolution impedance manometry may be used when the diagnosis remains uncertain or objective confirmation is required.
Non-pharmacological approaches form the cornerstone of treatment, particularly diaphragmatic breathing, together with biofeedback, behavioral therapy, patient education, and, when appropriate, multidisciplinary management.
Pharmacological therapy has a limited adjunctive role. Among pharmacological agents, baclofen currently has the strongest evidence, although this evidence remains limited, while the evidence supporting other medications is even less convincing.
Earlier recognition of rumination syndrome and timely initiation of appropriate treatment may reduce unnecessary diagnostic investigations and improve clinical outcomes.
Conceptualization and methodology: Filip Chodań, Karol Kajda. Investigation and literature search: Filip Chodań, Olga Klimczak, Dagmara Laufer. Literature analysis: Karol Kajda, Estera Sośniecka, Adam Miler. Writing, original draft preparation: Filip Chodań, Karol Kajda, Olga Klimczak, Dagmara Laufer, Estera Sośniecka. Writing, review and editing: Karol Kajda, Adam Miler, Estera Sośniecka. Supervision: Filip Chodań.
All authors read and approved the final version of the manuscript and agree to be accountable for all aspects of the work.
No external funding was received for this study.
The authors declare no conflicts of interest.
Artificial intelligence tools, such as ChatGPT and other OpenAI systems, were used to support language refinement, structural improvement, and the development of certain text sections. All AI generated contributions were thoroughly reviewed and verified by the authors.