Irritable Bowel Syndrome

2026 UPDATE
Rome V is now available and updates IBS diagnostic criteria: recurrent abdominal pain or discomfort, on average ≥3 days/month during the previous 3 months, with symptom onset ≥6 months before diagnosis, plus ≥2 of: relationship to defecation, change in stool frequency, or change in stool form. The 2021 ACG/BSG guidance and 2022 AGA pharmacologic guidelines remain important treatment references, while the 2025 AGA quality indicators provide a current quality-of-care framework.

Key point

Take-home message

Diagnosis

IBS is a positive clinical diagnosis; not a diagnosis of exclusion.

Rome V

Recurrent abdominal pain/discomfort ≥3 days/month + ≥2 stool/defecation associations; onset ≥6 months for standardized criteria.

Alarm features

Bleeding/anemia, weight loss, fever, nocturnal symptoms, later-onset/change, relevant family history or abnormal examination.

IBS-D work-up

Celiac serology; fecal calprotectin when IBD is a concern.

IBS-C

Soluble fibre is central; linaclotide has the strongest AGA recommendation among listed agents.

IBS-D treatment

Rifaximin for global symptoms; loperamide mainly controls diarrhea.

Diet

Short structured low-FODMAP trial → reintroduction → personalization.

Brain–gut therapy

Gut-directed CBT/hypnotherapy are evidence-based options.

Pain

Avoid chronic opioids; consider TCAs and selected antispasmodic/peppermint approaches.

Probiotics

Evidence is inconsistent and strain-specific; no routine blanket prescribing.

Criterion

Rome IV

Rome V

Change in Rome V

Core symptom

Recurrent abdominal pain, on average ≥1 day/week in the last 3 months.

Recurrent abdominal pain OR discomfort, on average ≥3 days/month in the last 3 months.

Lower symptom-frequency threshold; “discomfort” is accepted alongside pain.

Symptom onset

Symptom onset at least 6 months before diagnosis.

Symptom onset at least 6 months before diagnosis.

Defecation relationship

Associated with ≥2 of the listed features, including relation to defecation.

Associated with ≥2 of the listed features, including relation to defecation.

Stool frequency

Associated with a change in stool frequency.

Associated with a change in stool frequency.

Stool form/appearance

Associated with a change in stool form (appearance).

Associated with a change in stool form or appearance.

Subtype

Predominant stool pattern

Practical interpretation

IBS-C

Constipation

Hard/lumpy stools predominate; pain remains a defining feature.

IBS-D

Diarrhea

Loose/watery stools predominate; evaluate for celiac disease and intestinal inflammation when appropriate.

IBS-M

Mixed

Both hard/lumpy and loose/watery stools are prominent at different times.

IBS-U

Unclassified

IBS criteria met but stool pattern does not fit C, D or M.

Risk factor / association

Previous acute gastroenteritis: post-infectious IBS may follow bacterial, viral or protozoal infection.

Female sex and younger age

Psychological comorbidity, chronic stress and adverse life experiences

Repeated antibiotic exposure may alter intestinal microbial communities and metabolite profiles.

Dietary triggers, especially poorly absorbed fermentable carbohydrates, may precipitate bloating, pain and altered bowel habits.

Overlap with other DGBIs, including functional dyspepsia and centrally mediated abdominal pain disorders.

Mechanism

Pathophysiology / clinical relevance

Altered gastrointestinal motility

• IBS-C may show slower colonic transit, impaired propulsive activity and altered rectal sensation. • IBS-D may show accelerated transit, exaggerated post-prandial colonic activity and increased rectal sensitivity. • The gastrocolic response can be exaggerated in some patients, particularly after meals.

Visceral hypersensitivity

Enhanced perception of physiologic intestinal distension is a major contributor to abdominal pain and bloating. Mediaters include serotonin, neurokinins, calcitonin gene-related peptide and other signaling molecules. Pain severity therefore does not necessarily correlate with the amount of luminal gas or stool.

Brain–gut axis and central processing

Stress can modify motility and visceral perception, while persistent gastrointestinal symptoms can increase anxiety and hypervigilance. This is a physiologic mechanism, not imaginary or “only psychological.”

Serotonergic signaling

Enterochromaffin cells release serotonin, which influences intestinal secretion, motility and sensory signaling. Altered serotonin availability and reuptake have been implicated in IBS and provide a mechanistic rationale for 5-HT3 antagonists in IBS-D and 5-HT4 agonism in selected constipation syndromes.

Mucosal immune activation and low-grade inflammation

Some patients demonstrate subtle mucosal immune activation, altered epithelial barrier function and changes in immune–neural signaling. This does not mean that IBS is equivalent to inflammatory bowel disease; objective inflammatory markers are generally absent in uncomplicated IBS.

Microbiome and post-infectious mechanisms

Post-infectious changes may persist after an episode of gastroenteritis. Altered microbial composition and microbial metabolites may influence gas production, bile acid handling, mucosal signaling and intestinal motility. Findings across studies are heterogeneous; therefore, routine microbiome testing is not currently recommended for clinical diagnosis.

Food intolerance and FODMAPs

Fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) are incompletely absorbed and can increase luminal water and fermentation.  A low-FODMAP intervention should be time-limited and followed by systematic reintroduction and personalization rather than indefinite broad restriction.

Core symptom

Recurrent abdominal pain or discomfort, commonly lower abdominal or diffuse.

Pain related to defecation and/or associated with a change in stool frequency or form.

Constipation, diarrhea or alternating stool pattern.

Bloating is common and may be prominent even when objective abdominal distension is limited.

Associated feature

Urgency, straining, sensation of incomplete evacuation or altered stool consistency.

Mucus may occur without implying inflammatory bowel disease.

Dyspeptic symptoms and gastroesophageal reflux symptoms may coexist.

Sleep disturbance, fatigue, anxiety, mood symptoms and other chronic pain syndromes may coexist and should be assessed when clinically relevant.

Type

Description

Clinical use

1–2

Hard/lumpy stools

Supports constipation-predominant pattern.

3–4

Formed stools

Generally normal consistency.

5

Soft blobs

May occur with rapid transit or low fibre intake.

6–7

Mushy to watery stools

Supports diarrhea-predominant pattern.

Bristol stool form is useful for documenting the phenotype and monitoring treatment response. In mixed disease, ask the patient to record stool form over time rather than assigning the subtype from a single bowel movement.

Alarm feature

Gastrointestinal bleeding, melena or unexplained iron-deficiency anemia.

Unintentional or progressive weight loss.

Fever or systemic inflammatory features.

Persistent nocturnal diarrhea or symptoms that repeatedly wake the patient.

New or rapidly changing symptoms, particularly later in life.

Family history suggesting colorectal cancer, inflammatory bowel disease or celiac disease.

Abdominal mass, organomegaly, marked focal tenderness or other abnormal examination findings.

Persistent vomiting, progressive dysphagia or other upper-GI alarm symptoms.

History point

Characterize pain: site, duration, relationship to meals and defecation, severity, nocturnal occurrence and functional impact.

Document stool frequency and stool form using the Bristol scale.

Ask about urgency, straining, incomplete evacuation and fecal incontinence.

Screen for bleeding, fever, weight loss, anemia symptoms and nocturnal symptoms.

Review medication and supplement exposure, including metformin, magnesium, laxatives, antibiotics, opioids and drugs associated with diarrhea or constipation.

Ask about prior gastroenteritis, travel, food triggers and dietary restriction.

Assess psychosocial context, sleep, anxiety/depression and other chronic pain conditions when relevant.

Review family history of colorectal cancer, IBD and celiac disease.

Examination point

General examination: nutritional status, pallor, fever, weight and evidence of systemic disease.

Abdominal examination: distension, focal tenderness, mass, organomegaly and bowel sounds.

Perianal examination when symptoms or history suggest anorectal disease.

Digital rectal examination in selected patients with difficult evacuation, obstructive defecation or suspected pelvic floor dysfunction.

Clinical phenotype

Test

Why?

Routine?

IBS-D / IBS-M

Celiac serology

Exclude celiac disease, especially with diarrhea-predominant symptoms.

Yes, targeted

IBS-D

Fecal calprotectin ± CRP

Screen for intestinal inflammation/IBD when appropriate.

Recommended

Typical IBS, no red flags

CBC / basic tests as indicated

Assess anemia/systemic disease when suggested by history.

Selective

Typical IBS, no red flags

Colonoscopy

Not a diagnostic test for uncomplicated IBS.

No, unless CRC screening/alarm indication

Persistent watery diarrhea

Bile-acid diarrhea evaluation

Consider when symptoms suggest bile-acid malabsorption.

Selective

Suspected malabsorption

Directed stool/serologic testing

Investigate celiac, pancreatic or other malabsorptive disorders.

Selective

Differential diagnosis

Celiac disease.

Inflammatory bowel disease.

Colorectal neoplasia, particularly with alarm features or age-appropriate screening indications.

Microscopic colitis in chronic watery diarrhea.

Bile-acid diarrhea.

Lactose or fructose intolerance and other carbohydrate malabsorption.

Medication-induced diarrhea or constipation.

Chronic infection in selected epidemiologic settings.

Endocrine/metabolic disorders, especially thyroid disease when clinically suspected.

Pelvic floor dysfunction or defecatory disorder in refractory constipation.

First-consultation point

Explain that IBS is a real disorder of gut–brain interaction with identifiable biological mechanisms.

Provide a positive diagnosis when criteria are met rather than framing the condition as “nothing found.”

Identify the patient’s most troublesome symptom and agree on a small number of measurable treatment goals.

Set expectations: improvement is often incremental and may require sequential trials rather than a single curative drug.

Lifestyle measure

Regular meals and avoidance of very large meals.

Adequate fluid intake.

Regular physical activity.

Adequate sleep and attention to sleep–symptom relationships.

Avoid unnecessary elimination diets; dietary restriction should be structured and reversible.

Therapy

Key point

PEG

May not adequately improve abdominal pain/global IBS symptoms alone.

Linaclotide

Improves constipation and abdominal symptoms; diarrhea is the main adverse effect.

Plecanatide

GC-C agonist; diarrhea can occur.

Lubiprostone

Nausea may occur; take with food/water.

Tenapanor

Diarrhea is the major adverse effect.

Therapy

Important caution

Loperamide

Improves stool frequency/urgency more than global IBS symptoms.

Rifaximin

Courses may be repeated for recurrence according to guideline/label.

Eluxadoline

Avoid in patients without a gallbladder, with pancreatitis history, biliary obstruction/Sphincter of Oddi disease, severe hepatic disease or significant alcohol exposure.

Alosetron

Risk of ischemic colitis and severe constipation; use only within appropriate prescribing restrictions.

TCA

Anticholinergic effects can worsen constipation.

Management point

Peppermint oil may provide short-term global symptom benefit.

Antispasmodics can be considered for episodic cramping; anticholinergic adverse effects should be considered.

Low-dose tricyclic antidepressants are useful neuromodulators for global IBS symptoms and pain, with careful dose selection according to stool phenotype.

Avoid centrally acting opioids for chronic IBS pain because of poor long-term benefit and risk of opioid-related bowel dysfunction and hyperalgesia.

Behavioral therapy point

Cognitive behavioral therapy, gut-directed hypnotherapy and related brain–gut behavioral approaches can improve global IBS symptoms and coping.

Particularly useful when symptoms are persistent, stress-responsive, associated with hypervigilance or accompanied by anxiety/depression.

Probiotic/microbiome point

Routine use of probiotics is difficult to recommend because benefits are strain-, dose- and outcome-dependent and results are inconsistent.

If a patient wishes to try a probiotic, use a defined product for a time-limited trial and stop it if there is no meaningful improvement.

Routine commercial microbiome profiling is not currently a standard diagnostic test for IBS.

Situation

Practical approach

Post-infectious IBS

Consider when symptoms begin after acute gastroenteritis and persist after infection resolves; management is generally phenotype-directed.

IBS-like symptoms in IBD

Confirm objective inflammatory control before labeling symptoms IBS-like; consider psyllium when safe, short structured low-FODMAP, targeted symptom therapy and brain–gut behavioral therapy.

IBS-like symptoms in celiac disease

Confirm adherence and mucosal response; assess inadvertent gluten exposure and consider lactose intolerance, microscopic colitis, bile-acid diarrhea or superimposed DGBI.

Avoid

Do not repeatedly tell a patient that IBS is a diagnosis of exclusion.

Do not order routine colonoscopy solely because IBS is suspected in a patient without alarm features or a separate screening indication.

Do not prescribe antibiotics empirically for nonspecific IBS symptoms without a guideline-supported indication.

Do not recommend an indefinite highly restrictive low-FODMAP diet.

Do not rely on probiotics as a universal therapy.

Do not use opioids as chronic therapy for IBS-related abdominal pain.

Do not escalate laxatives indefinitely when symptoms suggest a defecatory disorder.

Do not interpret bloating alone as evidence of small intestinal bacterial overgrowth.

Step

Action

1

Confirm recurrent abdominal pain/discomfort with compatible bowel-habit relationship and establish likely IBS phenotype.

2

Screen systematically for alarm features and medication/dietary causes.

3

Perform focused examination.

4

For IBS-D/IBS-M, obtain celiac serology; use fecal calprotectin when IBS-D is being differentiated from IBD.

5

Avoid routine colonoscopy/imaging when there is no alarm feature and no independent screening/diagnostic indication.

6

Start education + soluble fibre/dietary intervention + lifestyle measures.

7

Choose one dominant therapeutic target: constipation, diarrhea, pain/bloating, or global symptoms.

8

If inadequate response, reassess diagnosis, adherence, phenotype, comorbid DGBIs and psychosocial contributors before adding multiple medications.

9

Escalate to evidence-based prescription therapy and/or brain–gut behavioral therapy.

10

Review response using patient-important outcomes: pain, stool pattern, bloating, daily function and quality of life.