Management of constipation: A narrative review of evolving strategies and methodological challenges

Abstract

Constipation is a common multifactorial gastrointestinal disorder with a significant impact on quality of life, healthcare utilization, and economic burden. It encompasses a spectrum of symptoms, including infrequent bowel movements (fewer than three per week), lumpy or hard stools (Bristol Stool Form Scale 1 or 2), straining, difficult stool passage, a sense of incomplete evacuation, etc. When no organic cause is identifiable, the condition is labeled as functional constipation. Pharmacological management of constipation has been extensively explored, with several new therapies added to the armamentarium in the last decade. However, its management remains challenging due to heterogeneous etiologies, varied diagnostic approaches, and the broad spectrum of therapeutic options. This narrative review summarizes contemporary strategies for the management of constipation, encompassing lifestyle and dietary modifications, pharmacological therapies, behavioral interventions, and surgical options for refractory cases. Traditional laxatives continue to form the mainstay of treatment, but newer agents such as prosecretory drugs, serotonergic agonists, and bile acid modulators have expanded therapeutic possibilities, offering targeted mechanisms and improved tolerability. Non-pharmacological approaches, including biofeedback for pelvic floor dysfunction and neuromodulation techniques, provide effective alternatives in selected patients. Despite these advances, substantial methodological variability exists in clinical trials, including differences in diagnostic criteria, endpoints, and follow-up durations, limiting the generalizability of findings. A more standardized framework for defining outcomes and assessing long-term efficacy is needed to strengthen evidence-based practice. Ultimately, the management of constipation requires an individualized approach that integrates symptom severity, underlying pathophysiology, patient preference, and availability of resources. Newer research is focused on tailoring treatment to special groups of patients with refractory constipation, surgical modalities for patients with neurogenic bowel, and microbiome modulation using artificial intelligence.

Key Words: Constipation; Gastrointestinal motility disorders; Irritable bowel syndrome; Defecation disorders; Colonic transit; Pelvic floor disorders; Prokinetic agents; Disorders of gut-brain interactions

Core Tip: Chronic constipation is a heterogeneous disorder encompassing distinct pathophysiologic phenotypes, including normal-transit constipation, slow-transit constipation, defecatory disorders, and a broad range of secondary organic causes. Failure to recognize these subtypes contributes to suboptimal treatment responses and inconsistent outcomes in both clinical practice and trials. Accurate diagnosis requires a structured, stepwise approach integrating careful history, targeted physical examination, and selective use of physiologic and imaging investigations. Management should be phenotype-driven, combining lifestyle measures, pharmacologic therapy, and pelvic floor-directed interventions when appropriate. Emphasizing mechanism-based evaluation and individualized treatment strategies is essential to improve long-term outcomes and reduce unnecessary therapeutic escalation.

INTRODUCTION

Constipation is a multifactorial gastrointestinal disorder that encompasses a spectrum of symptoms, including infrequent bowel movements (fewer than three per week), lumpy or hard stools (Bristol Stool Form Scale [BSFS] 1/2), straining, difficult stool passage, and a sense of incomplete evacuation, which collectively affect clinical outcomes, daily comfort, and overall well-being[1,2]. There have been various criteria proposed to diagnose constipation, resulting in heterogeneity in prevalence estimates, which range from 10.1% to 20%[3,4]. This prevalence is higher in the geriatric population, possibly due to polypharmacy, aging effects, etc.[5,6].

Beyond numbers and trends, constipation has detrimental effects on quality of life and causes significant physical and psychological distress[7]. It is important to understand that constipation is not a single entity; rather, it is an umbrella term encompassing multiple subtypes. The classification of constipation has been expanded in a section below, but it is important to note that each subtype is characterized by distinct pathophysiological mechanisms and clinical presentations[8,9]. Differentiating these patterns is crucial, as treatment varies across subtypes, as expanded upon in later sections.

Despite the availability of structured patient-centered diagnostic tools such as the BSFS, symptom-based classification systems (Rome IV criteria), variability exists in symptom reporting and clinical decision-making. Although instruments such as the BSFS and Wexner Score aid in symptom recognition and stratification, differences in reporting and outcome measures persist, which complicate diagnosis and treatment selection. The quality of evidence remains inconsistent, with clinical trials lacking uniformity in design and outcome measures. Hence, many patients remain symptomatic despite multiple interventions.

Thus, the high prevalence, variable burden, and evolving treatment with individual variability warrant a comprehensive yet critical narrative review of the diagnostic challenges and therapeutic hurdles encountered in the treatment of functional constipation (FC). This narrative review aims to address the need for a comprehensive summary of current best practices for managing chronic constipation in adults. It is against this backdrop that existing and emerging therapies for constipation in adults offer new opportunities for personalized care.

METHODOLOGY

Evidence was synthesized on the epidemiology, pathophysiology, diagnostic evaluation, treatment methods, and methodological gaps and challenges associated with constipation in adults. A comprehensive literature search was conducted using PubMed and Scopus using predefined search strings that focused on lifestyle interventions, pharmacologic therapies, laxative categories, microbiome modulation, standardization in care, and methodological considerations in constipation research. The primary search covered papers from 2010 to 2025, with earlier pivotal trials and studies included when deemed essential for the clinical context. The search strategy used both Medical Subject Headings terms and free text related to the topics. The literature search was conducted using the terms “constipation” and “functional constipation” in combination with key management-related words including “lifestyle intervention”, “dietary fiber”, “laxatives”, “polyethylene glycol”, “lubiprostone”, “linaclotide”, “prucalopride”, “biofeedback”, “neuromodulation”, and “surgical intervention”.

Randomized controlled trials, studies on adult populations, systematic reviews and meta-analyses, clinical guidelines and consensus statements, and landmark studies of pharmacologic therapies were included. Non-English articles, case reports, and exclusive pediatric studies, unless relevant to the pathophysiology of constipation, were excluded. Records were initially screened by title and abstract for relevance, followed by full-text assessment. Evidence was selected and synthesized in a narrative manner, with prioritization given to international guidelines and consensus statements, high-quality systematic reviews, and randomized controlled trials, while observational studies were used to contextualize epidemiology, practice principles, and safety data. The results were organized thematically according to the headings below.

CLASSIFICATION OF CONSTIPATION

Constipation has been broadly classified into two major subtypes: (1) Primary; and (2) Secondary constipation, depending upon the underlying pathophysiological mechanism.

It may arise as a primary (functional) disease or as a secondary condition due to medications, systemic diseases, neurological conditions, or structural abnormalities. Primary constipation can be due to colonic motility and transit abnormalities, defecatory dysfunction, neuroenteric and hormonal regulations, microbiota, gut-brain axis, etc. Primary/FC has been further subdivided into subtypes: Slow-transit constipation (STC), normal-transit constipation (NTC), and defecatory (pelvic floor) dysfunction or dyssynergic defecation.

Secondary causes of constipation are often completely reversible upon removing the causative factor. Commonly, medications such as anticholinergics, antipsychotics, calcium channel blockers, iron supplements, and antihistamines impair motility or reduce secretion. Endocrine and metabolic disorders such as hypothyroidism, hypercalcemia, diabetes, and pregnancy can also alter neuromuscular and hormonal regulation. Neurological causes (Parkinson’s disease, multiple sclerosis, spinal cord lesions) may impair anorectal coordination or reduce parasympathetic activity. Finally, structural abnormalities, including rectoceles, strictures, and post-surgical anatomical changes, should be considered when symptoms are refractory or accompanied by alarm features. Opioid-induced constipation (OIC) has a distinct pathophysiology rooted in peripheral μ-opioid receptor activation, which decreases propulsive motility and increases fluid absorption[10]. The classification and etiologies of constipation have been summarized in Table 1.

Table 1 Classification and etiologies of constipation.

Category	Subtype	Causes	Key features
Primary (functional) constipation	Normal-transit constipation	Associated with irritable bowel syndrome-constipation predominant, stress, and visceral hypersensitivity. Low fiber and fluid intake. Sedentary lifestyle	Normal colonic transit time, but patient feels constipated due to perceived difficulty. Reduced bulk of stool. Weaker colonic stimulation. Dry stools
	Slow-transit constipation	Colonic neuropathy. Colonic myopathy. Possible association with eating disorders. Altered serotonin levels	Delayed colonic transit time due to impaired colonic motility. Predominant in young women. Reduced high-amplitude propagated contractions
	Defecatory disorders (pelvic floor dysfunction/outlet obstruction)	Dyssynergic defecation (inappropriate pelvic floor contraction). Impaired rectal propulsive forces. Obstructed defecation syndrome. Structural abnormalities (rectocele, rectal prolapse, excessive perineal descent)	Failure of anorectal coordination. Difficult or blocked evacuation
Secondary (organic) constipation	Systemic/metabolic/endocrine	Diabetes mellitus. Dehydration. Amyloidosis. Uremia. Chronic kidney disease. Pregnancy. Hypercalcemia. Hypokalemia. Hypothyroidism	Systemic or metabolic slowing of the GI tract
	Neurologic	Parkinson’s disease. Multiple sclerosis. Spinal cord injury. Stroke. Hirschsprung disease. Autonomic neuropathies	Due to impaired neural control of bowel movements and defecation
	Structural/mechanical	Colonic strictures (ischemia, radiation induced, inflammatory). Colorectal cancer. Anal fissures (pain leading to stool retention). Megacolon	Mechanical obstruction or pain-related stool withholding
	Medication-induced	Opioids. Anticholinergics (TCAs, antihistamines). Calcium channel blockers. Iron supplements. Calcium or aluminum containing antacids. Antipsychotics/anticonvulsants (gabapentin, pregabalin). Diuretics (due to dehydration)	Common and most important cause. Due to motility or increased water absorption of water or reduced secretions

GI: Gastrointestinal; TCA: Tricyclic antidepressant.

PATHOPHYSIOLOGY OF CONSTIPATION

The pathophysiology of constipation is explained by multiple mechanisms involving disturbances in colonic motility, evacuation mechanics, neuroenteric regulation, and the microbiota-gut-brain axis. It is imperative to understand these processes to accurately phenotype patients and offer targeted therapy. Figure 1 offers a succinct overview of the etiological framework of constipation. The pathophysiology of constipation varies with the underlying etiology.

Figure 1 Etiology of constipation. Overview of the major pathophysiologic contributors to chronic functional constipation, including neurologic, behavioral, psychological, dietary, medication-related, structural, metabolic, and microbiome-associated factors. The figure illustrates the multifactorial and often overlapping mechanisms underlying symptom development. ADHD: Attention-deficit hyperactivity disorder.

Colonic motility and transit abnormalities

Colonic motility plays a key role in normal stool movement through the intestine. Transit in the colon depends on coordinated segmented motility and high-amplitude propagating contractions (HAPCs). This propels the luminal contents from the colon to the rectum. In the STC subtype, both the frequency and amplitude of HAPCs are reduced, leading to decreased motility. This can be attributed to abnormalities in cholinergic pathways, interstitial cells of Cajal dysfunction, and colonic neuromuscular incoordination. These factors play a key role in the reduction of contractility and motility[11,12]. Thus, this variant is often associated with a blunted response to meals and pharmacological bulking agents, further complicating treatment options[13].

Manometric and scintigraphic studies further prove this as they show delays in segmental transit, suggesting the involvement of intrinsic neural or smooth-muscle dysfunction[14]. In contrast to STC, the NTC subtype has normal physiological transit, despite a similar symptom profile. Thus, knowing the subtype guides the underlying pathophysiological process and choosing appropriate management, following the principles of precision medicine.

Defecatory (pelvic floor) dysfunction

Defecatory disorders, including dyssynergic defecation, account for close to half of all cases of constipation. This is reflective of how the problem often lies not in the transit, but in the mechanics of evacuation. These conditions arise when the pelvic floor and abdominal muscles fail to coordinate effectively. This ultimately leads to inadequate rectal propulsive force and impaired puborectalis muscle relaxation. This results in a cycle of stool retention, incomplete evacuation, and compensatory straining or digital maneuvers to evacuate stools[15]. Diagnosing these disorders requires objective confirmation, with anorectal physiology tests and balloon expulsion tests serving as key tools for this diagnosis to be made[15,16].

Neuroenteric regulation and autonomic dysfunction

Another major contributor to constipation is dysregulation of neural control mechanisms that govern motility and evacuation. Autonomic dysfunction can manifest as sympathetic overactivity or parasympathetic insufficiency, which slows transit and reduces rectal evacuation[17]. Enteric neuropathies, whether primary or secondary to systemic diseases such as diabetes and Parkinson’s, can impair excitatory signaling and disrupt peristalsis. Hormonal factors add a layer of complexity, where serotonin (5-HT), peptide YY, and glucagon-like peptide-1 slow transit while ghrelin and motilin increase motility. Dysregulation of these pathways, including reduced mucosal 5-HT availability or altered receptor expression, has been observed in chronic constipation[18]. These mechanistic insights highlight the success of targeted therapies like 5-HT4 agonists, which are effective in restoring motility signaling.

Microbiota and gut-brain axis

Altered gut microbiota composition has increasingly been recognized as a pathophysiological mechanism for constipation. Many patients show characteristic shifts, including reduced bifidobacteria, decreased butyrate-producing species, and shifts in Firmicutes/Bacteroidetes ratios[19,20]. Microbial metabolites are believed to shape motility and sensory function through several mechanisms; variations in short-chain fatty acid profiles, bile acid transformation, and microbial neurotransmitter synthesis all influence colonic motility and visceral sensation. Butyrate, in particular, enhances smooth muscle contractility and intestinal secretion, and its deficiency may directly promote slow transit. The microbiota-gut-brain axis plays into this causation, as microbial metabolites interact with vagal pathways, immune mediators, and enteroendocrine cells, modulating both motor and sensory functions[21]. These interactions explain the substantial interpatient variability observed in symptom patterns and treatment responses (Figure 2).

Figure 2 Treatment options for constipation in adults. Summary of available treatment modalities for chronic functional constipation, including lifestyle and dietary interventions, over-the-counter laxatives, prescription pharmacologic therapies, and emerging nonpharmacologic strategies. Treatment selection is guided by symptom severity, prior treatment response, and suspected underlying pathophysiology. IBAT: Ileal bile acid transporter.

DIAGNOSIS AND SCREENING

Patients with constipation present with general nonspecific symptoms such as hard, lumpy stools, a sensation of incomplete bowel evacuation, bloating, the need for digital evacuation maneuvers, or reduced stool frequency[1]. If no significant abdominal pain is present, the patient is most likely to have FC, whereas if pain is a predominant symptom, the patient is most likely to have irritable bowel syndrome with constipation (IBS-C)[22,23].

The Rome IV framework encompasses symptom-based clusters across several disorders of gut-brain interaction, with specific criteria established for each disorder. The Rome IV criteria for FC includes the presence of at least two or more of six symptoms in criterion 1 for the last 3 months, with symptom onset at least 6 months prior to diagnosis[24]. The criteria are summarized in Table 2.

Table 2 Rome IV diagnostic criteria for functional constipation (diagnosis requires the presence of at least two or more of six symptoms in criteria 1 for the last 3 months, with symptom onset at least 6 months prior to diagnosis).

No.	Criterion
1	Must include two or more of the following: (1) Straining during > 25% of defecations; (2) Lumpy or hard stools > 25% of defecations (Bristol Stool Form Scale 1 or 2); (3) Sensation of incomplete evacuation > 25% of defecations; (4) Sensation of anorectal obstruction/blockage > 25% of defecations; (5) Manual maneuvers to facilitate > 25% of defecations (digital evacuation, support of the pelvic floor); and (6) Fewer than three spontaneous bowel movements per week
2	Loose stools are rarely present without the use of laxatives
3	Insufficient criteria for irritable bowel syndrome

While the diagnosis of FC/IBS-C is made largely through reliance on patient history, per abdominal examination helps rule out abdominal masses implicated in causing constipation. The digital rectal examination (DRE) plays an important role in identifying pelvic floor dyssynergia; excludes alarm symptoms; and reveals polyps, hemorrhoids, excoriations, fissures, and rectal prolapse[8,25]. DRE identifies pelvic floor dyssynergia with 87% specificity and 75% sensitivity when measured against standard manometry[26,27]. Another aspect to note on examination is the sphincter tone and incontinence[28].

It is important to assess for ‘alarm’ symptoms that may point towards an organic etiology, such as colon cancer[29,30]. The presence of any of these symptoms prompts further workup to exclude organic causes of constipation from FC[31]. Table 3 summarizes the alarm symptoms.

Table 3 Alarm symptoms in patients with constipation.

Symptoms
Unintentional weight loss (more than 10% in 3 months)
Blood in stools
Family history of colorectal cancer or inflammatory bowel disease
New-onset symptoms after 50 years of age
Rectal tenesmus
Iron deficiency anemia
Jaundice
Cachexia
Positive fecal occult blood test

If the patient presents with alarm symptoms like significant weight loss, hematochezia, or abdominal pain, it is recommended to err on the side of caution and perform a colonoscopy[32]. There is some merit in considering a colonoscopy in patients with signs of constipation who are younger than the screening age, due to the increasing incidence of early-onset colorectal cancer[33].

Routine laboratory assessment is not recommended in patients without alarm symptoms, according to the American College of Gastroenterology. Objective assessments for constipation are useful in patients who may have metabolic diseases causing constipation. Lab workup in this case includes thyroid-stimulating hormone, serum glucose, creatinine, and serum calcium[34]. Diagnosis should be individualized based on symptoms. Table 2 reiterates the key aspects of a thorough history and physical examination, and the utility of certain laboratory investigations, structural evaluation of the intestines.

Advanced testing is usually reserved for patients who have intractable chronic constipation that is not responsive to first-line measures and laxatives. This includes testing colonic transit time, anorectal manometry, the balloon expulsion test, and radiographic studies of the colon[35]. Figure 3 and Table 4[36-44] outline the workflow and various diagnostic modalities that are beneficial in diagnosing slow transit constipation, NTC, functional defecation disorders, and structural abnormalities.

Figure 3 Workflow in diagnosing and treating functional constipation in adults. Proposed clinical algorithm for the evaluation and management of chronic functional constipation, beginning with exclusion of secondary and organic causes, followed by empiric therapy and escalation based on treatment response. Physiologic testing, including colonic transit studies and anorectal function testing, is incorporated to distinguish normal-transit constipation, slow-transit constipation, and defecatory disorders, thereby guiding targeted therapy. CTT: Colonic transit time; FED: Fecal evacuation disorder; IBS-C: Irritable bowel syndrome with constipation.

Table 4 History and assessment in patients with constipation.

Diagnostic tool	Technique	Utility	Limitations
History and physical examination (including DRE)	Detailed bowel history, which includes frequency, stool form (Bristol chart), straining, sensation of blockage, and incomplete evacuation. Review of fluid, dietary intake, and activity. History of medication use. History of comorbidities (thyroid disease, diabetes, neurologic disorders. Digital rectal examination-Assess the anal tone, voluntary squeeze, pelvic floor relaxation during simulated defecation, and for the presence of stool, hemorrhoids, rectocele[8]	Used to identify secondary causes. DRE can strongly indicate dyssynergic defecation by detecting paradoxical anal sphincter contraction and inadequate pelvic floor contraction[34]. Identifies fecal retention or impaction, anorectal fissures, strictures, masses, or pain-avoidant behavior	It is a highly subjective tool. Dependent on the clinician’s expertise. DRE has low sensitivity for subtle pelvic floor lesions[26]. Cannot diagnose slow-transit constipation. Cannot identify structural lesions higher in the colon
Laboratory evaluation	Blood tests like CBC, TSH, serum calcium, glucose, electrolytes, serum creatinine, etc.[25,34]	Used to identify endocrine or metabolic causes of constipation[8]. It also helps to rule out systemic disease mimicking constipation	Cannot identify the type of constipation (e.g., slow transit vs pelvic floor dysfunction)[27]
Colonoscopy and sigmoidoscopy	Endoscopic evaluation of colonic mucosa with the ability to biopsy[32]	Very useful tool in the presence of alarm symptoms like bleeding per rectum, anemia, weight loss, age > 50 with new onset symptoms, and family history of colorectal cancer[31]. Used to detect neoplasia (polyps, colorectal cancer), strictures, IBD, and solitary rectal ulcer syndrome[31]	Cannot diagnose functional constipation. Normal in most cases of chronic idiopathic constipation[26]. Invasive procedure. Requires patient preparation
Radiographic imaging	Plain abdominal X-ray (KUB)-simple supine radiograph[34]	Detects colonic dilation, megacolon, fecal loading or obstruction[31]	Correlates poorly with the severity of symptoms. Adds limited diagnostic value[26]. Cannot differentiate motility disorders
	CT abdomen/CT colonography-Imaging with contrast (IV or oral) or air insufflation for colonography[8]	Used to identify mechanical obstruction, tumors, volvulus, and strictures[8]. Helpful in identifying complications of constipation, stercoral colitis, and perforation	Radiation exposure. Cannot be used to diagnose functional constipation[26]. Cannot give information about motility
Colonic transit studies	Radiopaque marker test[35]. Patient ingests capsules containing makers. Abdominal X-rays are taken on day 3 and day 5. Distribution pattern is analyzed for segmental or global delay	Gold standard for diagnosing slow transit constipation[8]. Helps to distinguish between normal transit, colonic inertia (severe delay) and segmental delay (often left colon). Helps to distinguish slow transit constipation from pelvic floor dyssynergia	Requires multiple visits over days. Radiation exposure. Does not assess pelvic floor coordination directly. Interpretation requires experience[26]
	Scintigraphic colonic transit studies[35]. Patient eats a radiolabeled meal, and serial gamma camera images track transit through the GI tract	Provides more detailed regional motility mapping. Measures gastric, small bowel, and colonic transit	Costly and limited availability. Radiation exposure
	Wireless motility capsule (smart pill). Patient swallows a capsule that records pH, temperature, and pressure of the tract as it moves. Data are transmitted to the external receiver	Measures segmental transit times-gastric emptying time, small bowel transit, colonic transit. Useful in suspected cases of generalized dysmotility. Can distinguish between global motility disorders and isolated constipation	Expensive. Should not be used if there are strictures or obstructions. Limited availability. Cannot assess pelvic floor mechanics
Anorectal function studies	Anorectal manometry[36]. A high-resolution catheter is inserted into the rectum, which measures resting and squeeze pressures, recto anal inhibitory reflex, rectal compliance, and simulated defecation dynamics	Primary diagnostic tool for dyssynergic dysfunction[38]. Helps to detect paradoxical anal sphincter contraction, inadequate propulsive forces, and sensory deficits. Helps in tailoring biofeedback therapy	Cannot identify structural abnormalities like rectocele, prolapse, etc. Not standardized[38]. Cannot measure transit. Requires experienced and trained personnel
	Balloon expulsion test. Balloon filled with water in rectum and patient attempts to expel it in less than 1-2 minutes	A simple screening test for outlet obstruction. Highly specific when abnormal	Not sensitive. Normal result doesn’t exclude dyssynergia[40]. Does not distinguish the exact type of pelvic floor disorder
	Defecography[40]. Contrast paste is inserted into the rectum, and patient tries to defecate under fluoroscopy	It can be used to visualize structural abnormalities, such as rectocele, internal intussusception, external prolapse, megarectum, and perineal descent	Radiation exposure. Does not evaluate physiology. Very uncomfortable procedure
	MRI defecography. Gel is inserted into rectum and pelvic MRI is performed during rest, squeeze, and defecation phases	It has better soft tissue resolution. Helps in detecting pelvic floor dyssynergia, multi-compartment organ prolapses, and rectocele[41]. No radiation exposure	Expensive. Limited availability. Difficult for patients to defecate in an MRI environment
Endoanal ultrasound	A high-frequency probe is inserted into anal canal[42]	Can identify sphincter defects. Helpful in identifying postpartum sphincter injury or suspected trauma	Not useful for most cases of constipation. Provides very little functional information
Rectal biopsy	Suction or full-thickness biopsy to identify ganglion cells	Definitive diagnostic tool for Hirschsprung disease[43]. Can also identify chronic intestinal pseudo-obstruction with neuropathic or myopathic features	Invasive. Not usually indicated in adults unless there is severe and unexplained megacolon
Psychosocial and behavioral assessment	Evaluate for anxiety, depression, eating disorders, trauma, and abuse history[44]	Can be useful to identify behavioral contributors to constipation[44]. Important tool of assessment in IBS-C and functional GI disorders	It is a very subjective tool. Cannot diagnose primary motility disorders. Requires patient cooperation

CBC: Complete blood count; CT: Computed tomography; DRE: Digital rectal examination; GI: Gastrointestinal; IBD: Inflammatory bowel disease; IBS-C: Irritable bowel syndrome with constipation; KUB: Kidneys, ureters, and bladder (plain abdominal radiograph); MRI: Magnetic resonance imaging; TSH: Thyroid-stimulating hormone.

This exhaustive workup is done systematically to ensure that patients are diagnosed with maximum accuracy, as a lot of patients are otherwise lost to follow-up. Ultimately, once constipation is evaluated, patients with FC benefit from a combination of nonpharmacologic and pharmacological management.

MANAGEMENT OF CONSTIPATION

Nonpharmacologic management

Nonpharmacologic management involves patient education about diet, fiber intake, fluid intake, physical activity, and recognizing external disease processes that may cause or exacerbate constipation. Dietary interventions are a cornerstone of constipation care, with new data improving our understanding of fiber, micronutrients, and the role of the gut-brain axis in constipation.

Dietary fiber

Dietary fiber helps relieve constipation by retaining water to increase stool bulk, mechanically stimulating the colonic mucosa, accelerating intestinal transit, and beneficially modulating the gut microbiome, thereby promoting more regular and effective bowel movements[35,45].

A 2012 meta-analysis of five studies showed that fiber intake increased stool frequency but did not demonstrate a significant difference in stool consistency, laxative use, treatment success, or painful defecation[46]. Christodoulides et al[47] published a systematic review with meta-analysis put forth results from seven trials which demonstrated that fiber is moderately effective in increasing stool frequency (standardized mean difference [SMD] = 0.39; 95% confidence interval [CI]: 0.03-0.76; P = 0.03), but also causes gastrointestinal side effects (flatulence; SMD = 0.56, 95%CI: 0.12-1.00; P = 0.01). A 2022 systematic review and meta-analysis of various randomized controlled trials (RCTs) continued to support the notion that dietary fiber improves constipation, although it increases flatulence[48].

Soluble fibers, such as psyllium and inulin, dissolve in water to form a gel that increases stool water content, softens stools, and can accelerate colonic transit while promoting beneficial shifts in the gut microbiota, whereas insoluble fibers, like cellulose, hemicellulose and lignin, remains largely intact, adds bulk to stool, mechanically stimulates intestinal motility, and helps shorten transit time, all of which contribute to relief from constipation[49]. Wheat bran has also been shown to improve defecation frequency and transit time[50].

Among patients with end-stage renal disease on hemodialysis, higher dietary fiber was associated with reduced constipation symptoms without adversely affecting electrolyte levels[51]. The recommended fiber intake for adults sits at 25-30 g per day, although there is no consensus on the exact values[52]. For clinicians recommending fiber, practical guidance continues to emphasize titration, osmotic properties of fiber, and tolerability considerations[53].

Fluid and other dietary interventions

Foods that are associated with decreased odds of constipation are whole fruits, vegetables, greens and beans, whole grains, protein-rich foods, seafood, and plant proteins[54,55]. A higher sodium intake was shown to increase the odds of constipation (P < 0.05)[54]. Per the same study, a higher adherence to the Healthy Eating Index-2015, which is an indicator of dietary quality, was reflected in lower rates of constipation[54]. Combined micronutrient approaches are also evolving. Research has shown that magnesium oxide combined with inulin has led to favorable shifts in short-chain fatty acid production and gut microbiota, suggesting that titrating micronutrients has a role to play in striking a balance in the gut[56].

An intuitive response to patients with constipation is to try and increase fluid intake to prevent excessive water absorption in the colon and stimulate colonic motility. A study done in adults with chronic constipation revealed that higher mineral water intake (0.5-1 L/day) was associated with a greater overall “response to treatment” in adults with chronic constipation relative to low mineral water (relative risk = 1.47). The authors also noted that this intake did not significantly change stool frequency or improve specific constipation symptoms[57].

Other lifestyle interventions

Other factors independently influencing FC in adults are physical activity, mental health, and other disease processes. Physical activity exerts modest but consistent benefits on gastrointestinal motility. Studies have shown that aerobic activity improves transit time and stool frequency, although intense training may exert counterproductive effects in some individuals[58]. Depressive symptoms, unhealthy dietary patterns, and a history of smoking were shown to be significant contributors to constipation (P < 0.05) in middle-aged adults[59]. External disease processes, such as diabetes, also affect manifestations of constipation. In adults with type 2 diabetes, women reported higher constipation prevalence, which was explained in part by differences in physical activity and diet[60]. Other lifestyle metrics that indicate cardiovascular health, such as smoking status, blood pressure, and cholesterol, are also indicators of gut health and bowel motility. This reflects the common interplay between diet quality, activity, and metabolic health[61].

To summarize, reinforcing diet, hydration, and physical activity as first-line strategies is a reasonable approach to treating constipation.

Medical therapy for constipation

Medical therapy is the mainstay of treatment for constipation when symptoms are not resolved with a change in diet and lifestyle. The medications used generally target either intestinal motility, increasing stool bulk or water content, or modulate fluid secretion within the gut. The major therapeutic classes include bulk-forming agents, osmotic laxatives, stimulant laxatives, intestinal secretagogues, prokinetic/colokinetic agents, and ileal bile acid transporter inhibitors, with each class targeting distinct pathophysiological pathways[62].

Fibers or bulk-forming agents like psyllium and methylcellulose increase stool bulk and water content, as well as promote regularity in stools. Osmotic laxatives are polyethylene glycol, lactulose, and magnesium salts[63]. In both adult and geriatric populations, osmotic and bulk laxatives form the backbone of therapy. Therapy in geriatric populations is a delicate balance among safety, drug interactions, and polypharmacy[64].

Intestinal secretagogues include chloride channel activators such as lubiprostone and guanylate cyclase-C analogs like linaclotide and plecanatide. Tenapanor is a first-in-class inhibitor of the gastrointestinal sodium/hydrogen exchanger isoform 3 that increases intestinal fluid secretion and improves symptoms of IBS-C. It increases complete spontaneous bowel movements and reduces abdominal pain and bloating[65]. Prokinetic/colokinetic agents such as prucalopride, a serotonin receptor (5HT-4) agonist, have been shown to improve motility and reduce colonic transit time[66,67]. Prucalopride has demonstrated consistent efficacy and safety across populations with chronic constipation, including improved motility and reduced colonic transit time. These are relatively newer agents and are used if first-line therapy fails. Elobixibat is another emerging treatment option that acts by inhibiting the ileal bile acid transporter, thereby increasing colonic bile acids and accelerating colonic transit[68,69].

Stimulant laxatives include medications such as senna and bisacodyl. This class of drugs ultimately increases bowel motility and peristalsis. Stimulant laxatives remain effective short-term first-line agents but should be used judiciously: Chronic misuse is associated with cathartic colon, mucosal changes, and psychopathology, particularly in eating disorders[70]. Magnesium salts continue to be utilized but require caution, due to the risk of hypermagnesemia[71].

For OIC, preventive regimens such as including a stimulant laxative with a stool softener are underutilized despite evidence supporting scheduled laxatives and peripherally acting μ-opioid antagonists in palliative settings[72-74].

An important diverging point in the treatment of chronic constipation is when a patient is diagnosed as having NTC, STC, and dyssynergic defecation. While STC is managed with medications that improve colonic motility, NTC is mainly managed similar to IBS-C, and dyssynergic defecation is managed with biofeedback therapy[8].

MANAGEMENT OF DYSSYNERGIC DEFECATION

Pelvic floor retraining and biofeedback

Dyssynergic defecation is an underdiagnosed contributor to constipation. Biofeedback therapy involves developing neuromuscular training and visual and verbal feedback. A probe and sensors are used to train patients to coordinate pelvic floor muscle contraction. It has emerged as a promising first-line modality to treat patients with dyssynergic defecation. Research has demonstrated its superiority over laxatives alone in improving coordination, reducing straining, and enhancing the quality of life as outlined in Table 5[75-85]. Observational studies have shown that there is sustained improvement in abdominal symptoms following structured biofeedback programs[86]. Recent advances include fecal microbiota transplantation along with biofeedback. Although this has shown early promise, the data remain preliminary[87,88].

Table 5 Pharmacological management of constipation.

Drug class/agent	Mechanism of action	Key clinical trials	Guideline-directed management (AGA/ACG, NICE[65,66])
Bulk-forming laxatives. Psyllium (ispaghula husk)	Soluble fiber-absorbs water-stimulates peristalsis	Multiple RCTs show psyllium superior to placebo for stool frequency and consistency. Studies show that psyllium is superior to docusate for stool frequency and consistency[75]. Double-blind RCT concluded that psyllium improved stool output significantly in chronic idiopathic constipation[76]	First-line therapy for mild constipation. Mainly used for patients with low fiber intake
Osmotic laxatives	Polyethylene glycol (PEG 3350). It is a non-absorbable polymer that retains water and increases bulk of stools and accelerates transit	Various RCTs showed that PEGs have significantly improved frequency and form of stools when compared to placebo[75]. Cochrane meta-analysis comparing PEG vs Lactulose indicated PEG to be more effective and better tolerated[77]	First line of therapy after fiber for CIC. It is the preferred osmotic laxative. Safe long-term use profile. Useful in patients needing a predictable effect
	lactulose. It is a non-absorbable disaccharide which is hydrolyzed by the colonic bacteria into short-chain fatty acids, which stimulate peristalsis by exerting an osmotic effect and stool acidification	Study showed that patients with FC taking lactulose in combination with PEG exhibited better symptom relief[78]	Use only if PEG is not tolerated by the patient or is unavailable
	Magnesium salts (hydroxide, citrate). They act by stimulating CCK release and exert an osmotic effect, which increases motility	Limited modern-day high-quality trials, but older RCTs demonstrate efficacy	Mainly useful in acute conditions for rapid relief especially in young adults
Stimulant laxatives	Senna (sennosides). Anthraquinone derivatives are converted into active metabolites that stimulate the myenteric plexus and increase peristalsis and secretion	RCT in chronic constipation showed improved stool frequency when compared to placebo[79]	The second line of therapy if osmotic laxatives are inadequate. Good choice for rescue therapy
	Bisacodyl. It is a diphenylmethane derivative that stimulates colonic propulsion and secretion via activation of enteric neural pathways	Studies showed its effectiveness in spontaneous bowel movements and improved stool consistency[80]. FDA-approved trials showed superiority to placebo in both acute and chronic constipation	Effective for short-term use or as a rescue agent. Usually reserved for refractory constipation
Stool softeners	Docusate sodium. It acts as a surfactant and reduces surface tension and allowing water penetration into the stool	Evidence showed limited efficacy. RCTs have indicated that docusate is not superior to psyllium or PEG	Reserved for postoperative use or when straining must be avoided (e.g., anorectal disease), but not recommended for CIC
Serotonergic agonists	Prucalopride. Highly selective 5-HT4 agonist. Stimulates enteric neurons, enhancing acetylcholine release and coordinated colonic peristalsis, thereby accelerating colonic transit and increasing spontaneous bowel movements	Prucalopride 2 mg and 4 mg administered daily significantly increased the proportion of patients achieving ≥ 3 spontaneous complete bowel movements per week compared to placebo[81]. RCTs in the Asia-Pacific region demonstrated Prucalopride 2 mg once daily significantly improved bowel movements and symptoms vs placebo over 12 weeks[82]	Second-line drug with proven efficacy. Especially useful in slow transit constipation and colonic inertia
Secretagogues	Lubiprostone. Chloride channel activator and guanylate cyclase-c agonist. Activates ClC-2 chloride channels on intestinal epithelium and increases chloride-rich fluid secretion; it softens stool and increases transit	RCT reported significant increase in spontaneous bowel movements (SBMs) in week 1 in patients with CIC[83]. Chronic constipation Phase 3 trials showed improved stool consistency and decreased straining	Mainly used as a second agent after failure of fiber/PEG. Indicated for CIC and IBS-C (women)
	Linaclotide. Acts as an agonist of GC-C, increasing cGMP, which activates CFTR, causing increased chloride and bicarbonate secretion leading to increased intestinal fluid and decreased visceral pain	RCTs for CIC showed improved CSBM frequency and stool consistency[84]. Long-term open-label trial showed sustained efficacy	Preferred secretagogue for CIC and IBS-C when OTC measures are not effective. Has strong evidence for pain reduction too
	Plecanatide. It acts as a uroguanylin analog, causing pH-sensitive GC-C activation and increased chloride secretion and motility	RCTs demonstrated increased CBSMs vs placebo, with excellent tolerability in patients with CIC[79]	Second-line therapy for CIC and IBS-C after unsuccessful OTC therapy. Excellent safety profile in older adults
IBAT inhibitor	Elobixibat. Inhibits bile acid absorption in ileum, increasing their delivery to the colon. Enhances colonic fluid secretion and motor activity to accelerate transit and improve spontaneous bowel movements	RCTs demonstrated significant increase in spontaneous bowel movements and improved stool consistency[68,69]	Good modality to treat chronic constipation. Excellent safety profile in elderly, and those with comorbidities

ACG: American College of Gastroenterology; AGA: American Gastroenterological Association; CCK: Cholecystokinin; CFTR: Cystic fibrosis transmembrane conductance regulator; cGMP: Cyclic guanosine monophosphate; CIC: Chronic idiopathic constipation; CSBM: Complete spontaneous bowel movement; FDA: United States Food and Drug Administration; GC-C: Guanylate cyclase-C; IBAT: Ileal bile acid transporter; IBS-C: Irritable bowel syndrome with constipation; NICE: National Institute for Health and Care Excellence; OTC: Over-the-counter; PEG: Polyethylene glycol; RCT: Randomized controlled trial.

EMERGING TREATMENT OPTIONS

Neuromodulation and electrical stimulation

Neuromodulatory therapies are being explored in refractory constipation. Here, the sacral nerve is stimulated, which may assist in fecal incontinence and slow transit constipation. Sacral neuromodulation systems, such as Axonics, have shown benefit in urinary as well as fecal dysfunction, including in cases of severe constipation that were unresponsive to conservative measures[89]. Electrical stimulation therapies continue to evolve and may be worth considering as adjunctive therapy in patients who do not benefit from biofeedback therapy[90]. As colorectal surgery techniques evolve, there may be improved understanding and planning for neuromodulation in complex patients[91,92].

Transanal irrigation and structured bowel programs

Transanal irrigation (TAI) is the process by which water is introduced into the rectum through the anus to assist bowel movements in patients with neurogenic bowel dysfunction. This process helps in regularizing bowel movements in this group of patients. Current research supports TAI as part of multimodal management for spinal cord injury, as it has reduced constipation and enhanced quality of life[93]. Pediatric studies provide long-term evidence of safety, adherence, and microbiota modulation in chronic neurogenic constipation[94-97].

Organizational structure strongly influences the adoption of nonpharmacologic bowel programs, and implementing a structured approach could benefit adult FC[98].

Other nonpharmacological interventions

Acupuncture has gained renewed interest, with meta-analyses demonstrating significant improvements in stool frequency and global symptoms in FC[99,100]. This ties in with traditional Chinese medicine, which categorizes constipation into excessive and deficient patterns, and takes into account the appearance of the tongue, pulse, and patient symptoms. Here, acupuncture is used with a treatment principle of purgation[101].

Broader assessments of neurogenic bowel burden highlight the complexity of managing constipation alongside fecal incontinence in neurologic and spinal disorders using nonpharmacological interventions.

Surgical and complex care

Surgical treatment of constipation is reserved for refractory constipation due to colonic inertia, anatomical abnormalities, or severe structural disease. Advances in three-dimensional printing have improved surgical planning and neuromodulation placement in intractable constipation[92]. Multidisciplinary colorectal and pelvic malformation units highlight the importance of coordinated care for complex constipation and dysmotility, integrating surgical, medical, and rehabilitative expertise[102]. Rectal obstruction, which describes impaired evacuation of stool due to functional or structural abnormalities at the level of the rectum, such as rectocele, strictures, rectal prolapse, or the anal canal. While initial management of rectal obstruction includes stool consistency optimization and pelvic floor therapy, definitive management requires targeted surgical intervention.

Rare case reports such as those of ileal lipomas illustrate the need for careful screening for structural pathology in refractory constipation presentations[103]. Figure 3 presents a consolidated overview of treatment options and the sequence in which they may be introduced in the management of patients who present with constipation.

METHODOLOGICAL CHALLENGES TO DIAGNOSING CONSTIPATION

Diagnosing constipation remains challenging due to the heterogeneity of diagnostic methods used across clinical and research settings[2]. Table 6 enlists the important methodological challenges clinicians and researchers face in managing constipation.

Table 6 Methodological challenges in constipation research and treatment.

Domain	Methodological challenges
Heterogeneity of constipation phenotypes	Many studies fail to categorize participants by subtype, leading to heterogeneous study populations, weak treatment effects, and difficulty in comparing trials
Diagnostic heterogeneity	ROME IV criteria exclude patients with abdominal discomfort (not pain) from the IBS-C category, leading to internal shift of patients from the IBS-C category to FC category. Variable classification in different studies leads to conflict in inclusion criteria, variability in symptom severity, and confounded treatment outcomes
Excess reliability on subjective symptom reporting	Difficult to standardize across various populations
Lack of universal biomarkers for identifying colonic motility patterns, pelvic floor dyssynergia, gut sensory abnormalities, and neuroenteric dysfunction	Hinders objective diagnosis and classification
Variance in diagnostic tools across centers	Limits comparability across different studies and complicates meta-analysis
Variability in outcome measures across trials	Rapidly evolving endpoints make historical comparisons difficult
Placebo response is high, as constipation trials often show 25%-40% placebo response for CSBM improvements	Needs larger sample sizes to demonstrate drug efficacy and complicates understandability
Short duration of many trials	Constipation is usually a chronic condition, but most of the trials are conducted for few months only. Long-term efficacy, tolerance, and safety remain uncertain in many therapies
Underrepresentation of special populations like children, elderly, pregnant women, and patients with neurological disabilities	Limits generalizability
Difficulty differentiating cause and consequence	Domination of cross-sectional designs; only a few longitudinal studies exist
Cross-cultural differences in symptom interpretation	Affects global trial reproducibility
Regulatory differences across different regions. FDA, EMA, and Asian regulatory agencies require different endpoints, PRO instruments, and trial durations	Development of new drugs must navigate through incoherent methodological standards
Limited integration of multidimensional techniques. Optimal study design requires combining motility testing, sensory testing, neuroimaging, microbiome analysis, and psychological assessment	Limited mechanistic depth as most clinical trials tend to use only one or two modalities

CSBM: Complete spontaneous bowel movement; EMA: European Medicines Agency; FC: Functional constipation; FDA: Food and Drug Administration; IBS-C: Irritable bowel syndrome with constipation; PRO: Patient-reported outcome; ROME IV: Rome IV diagnostic criteria for functional gastrointestinal disorders.

The diagnostic criteria for IBS-C has evolved over time[103]. For instance, Rome IV requires abdominal pain (rather than discomfort) for IBS diagnosis; and the subclassification to IBS-C in Rome IV is now based on the proportion of symptomatic stools as opposed to all stools in Rome III[104,105]. Studies comparing Rome III vs Rome IV criteria report differing prevalence of IBS-C[105,106]. Furthermore, relying on symptom-only definitions can misclassify patients and disregard physiologic subgroups[105,107].

There are several objective tests used for the diagnosis of constipation, such as radiopaque marker or scintigraphic colonic transit, anorectal manometry, balloon-expulsion test, and defecography. These tests help to delineate between NTC, STC, and evacuation disorders (pelvic floor dysfunction). In practice, however, trials often enroll patients based only on symptoms. Reviews emphasize that detailed tests are usually reserved for refractory cases[15,108]. Because physiological testing is unevenly applied and not standardized across studies, physiologic subtypes are under-recognized in trials and heterogeneity persists[15,109,110].

Clinical trials in constipation use a wide array of outcome measures. One systematic review of adult STC trials found 59 different outcome types[111]. Pediatric trials are equally variable: A Rome Foundation committee highlighted that outcome definitions in children’s trials are heterogeneous and suggested that endpoints should be tailored to developmental age[112].

Inconsistency also extends to endpoint type-for instance, some drug trials define success as “≥ 3 complete spontaneous bowel movements per week,” whereas others use composite or global improvement criteria. Notably, placebo response rates vary dramatically depending on endpoint choice[113]. Together, these findings underscore that inconsistent endpoints across studies preclude the easy comparison or pooling of results[111,113].

Many constipation trials are relatively brief, which may be insufficient for a chronic condition. Adult RCTs often last only 4-12 weeks, and pediatric studies similarly have short treatment periods. Consensus guidelines have begun to address this. For example, pediatric experts recommend a minimum 8-week treatment period to assess efficacy in the pediatric population[113]. However, even these durations are modest given that 40%-50% of children with constipation remain symptomatic 5-10 years later[112]. Long-term follow-up is often not done, so data on sustained benefits or relapse rates are lacking. In practice, this means that evidence on the durability of treatments (both pharmacological and nonpharmacological) is scant. In summary, short trial durations and the lack of long-term follow-up limit understanding of how treatment effects endure over time[112,113].

The majority of constipation research is focused on the Western populations. Epidemiological data show that prevalence and symptom profiles can differ by region-for example, stool frequency and consistency norms in Eastern patients do not perfectly match Western patterns[114]. Similarly, placebo response patterns in drug trials have differed by region (e.g., Europe vs Asia)[113]. Cultural factors, diet, and healthcare practices all vary, yet many international trials still enroll mainly North American or European patients. This underrepresentation means findings may not apply to other ethnic or cultural groups. For instance, Asian studies report lower constipation prevalence (11%) than Western reports (15%-17%)[114]. In summary, non-Western populations have been relatively ignored in trials, even though geographic and lifestyle differences play a significant role in constipation and its treatment[104,114].

A notable methodological gap is the lack of a combined assessment of patients’ symptoms with objective physiological tests. The Rome criteria emphasize symptoms, but many patients undergo tests like colonic transit studies or anorectal manometry only if first-line therapy fails.

The optimal diagnosis integrates clinical symptoms and various tests, and objective findings. In practice, however, trials usually focus on symptomatology and patient-reported outcomes, without correlating these with changes in transit time or motility.

A few studies hint at the utility of such correlation: For example, data show that the Bristol Stool Scale and stool frequency do predict delayed transit in constipated patients[114]. But comprehensive approaches are rare. This disconnect may obscure subtypes (normal vs slow transit vs pelvic floor dysfunction) and limit personalization of therapy.

In short, there is a pressing need to link physiological testing with symptomatology in both trials and practice, in order to optimize treatment for such patients[114].

FUTURE DIRECTIONS IN CONSTIPATION RESEARCH

The future of constipation management should shift towards precision medicine, where treatment is tailored to an individual’s physiological subtype, microbial profile, genetics, and symptoms.

Therapeutic approaches

Recent studies highlight the limitations of one-size-fits-all therapeutic approaches, noting that pharmacologic response varies widely across constipation subtypes[115]. Studies concerning colonic transit profiles, anorectal manometry patterns, and neurogastroenterology biomarkers argue that distinct pathophysiologic clusters can be identified, enabling subtype-specific therapies[116].

There are a number of drug options for FC, but their efficacy is unknown, and comparative studies between these medications and traditional approaches such as a high-fiber diet and laxatives is required. Constipation sufferers also frequently complain of developing tolerance to various medications, this should be further investigated[117].

Digital health and remote monitoring

Digital health tools, such as smartphone symptom trackers, wearable motility sensors, and remote monitoring platforms, are being evaluated in the management of constipation.

Stool diaries and sensor-based colonic motility trackers are expected to provide more accurate information regarding bowel patterns than traditional recall-based methods. Telemedicine has also expanded access to behavioral therapies such as biofeedback, with early trials demonstrating comparable efficacy between tele-biofeedback and in-person programs for defecatory disorders[118]. Integration of digital platforms into research can help overcome existing methodological challenges, particularly inconsistent endpoints and short follow-up durations[119].

Microbiome and metabolomics

The gut microbiome and metabolomics is emerging as a focus in constipation research. Multiple studies report distinct microbes in STC vs FC, with reductions in short-chain fatty acid-producing bacteria being highly prevalent[120]. Emerging advances in artificial intelligence (AI) offer avenues to refine phenotyping and personalize management strategies. At this time, AI can be used as a platform to integrate datasets like metabolomics, dietary patterns, and symptom clusters to delineate constipation subtypes. Although these approaches are largely investigational, they represent a potential framework for the personalized treatment of constipation.

Metabolomic analyses show that altered bile acid metabolites and fermentation profiles influence colonic motility[121]. Early interventional trials using targeted probiotics or prebiotic–fiber combinations demonstrate improvements[122].

Standardization of diagnostic and outcome frameworks

One of the most pressing needs in constipation research is the harmonization of diagnostic and outcome frameworks. New international working groups have proposed standardized outcome sets incorporating stool form (BSFS), spontaneous bowel movement frequency, straining metrics, satisfaction scores, and durability endpoints[111]. Standardization is essential to reduce diagnostic heterogeneity, improve clinical trials, and strengthen the evidence base for emerging pharmacologic and nonpharmacologic therapies.

CONCLUSION

Constipation is a highly prevalent condition with a broad clinical spectrum, shaped by diverse pathophysiological mechanisms and a growing array of therapeutic options. Its impact on daily functioning and quality of life is substantial, and yet, meaningful progress continues to be limited by persistent gaps in diagnostic standardization, outcome reporting, and long-term follow-up in research.

Modern management integrates multimodal assessment, combining transit studies, structural evaluation, and targeted neuromuscular retraining, such as biofeedback, to more accurately define and treat constipation subtypes. The mainstays of treatment have not changed; only newer modalities have been added.

Despite advancements, methodological inconsistencies remain a major barrier. Some hurdles before we can aim for precise treatment are the current research’s focus on single population subsets, non-uniform study endpoints, and the lack of studies on non-Western and pediatric populations. These gaps complicate evidence synthesis and limit the development of universally applicable treatment algorithms.