Irritable bowel syndrome (IBS) is a disorder of gut-brain interaction — characterised by recurrent abdominal pain related to defaecation or associated with a change in stool frequency or form, in the absence of structural disease. It affects approximately 4-10% of adults worldwide and is the most common diagnosis in gastroenterology practice. Subtypes: IBS-C (constipation-predominant); IBS-D (diarrhoea-predominant); IBS-M (mixed); IBS-U (unclassified). IBS is a real, physical condition with identifiable mechanisms — visceral hypersensitivity, altered motility, mucosal immune activation, altered microbiota and altered central pain processing. It is emphatically not "all in the mind," and framing it that way to patients is both inaccurate and clinically counterproductive.

How is IBS diagnosed?

IBS is a POSITIVE diagnosis based on the Rome IV criteria — not a diagnosis of exclusion. In a patient meeting Rome IV criteria without alarm features, limited testing is sufficient: full blood count; CRP; coeliac serology (tissue transglutaminase IgA plus total IgA); faecal calprotectin (to exclude IBD). Colonoscopy is NOT routinely required. Alarm features that DO require further investigation: age >50 at symptom onset; rectal bleeding; unintentional weight loss; nocturnal symptoms waking the patient; iron deficiency anaemia; family history of colorectal cancer, IBD or coeliac disease; palpable abdominal or rectal mass; recent change in bowel habit in an older patient. Also consider bile acid diarrhoea (SeHCAT) in IBS-D, particularly post-cholecystectomy.

Does the low FODMAP diet work?

Yes — approximately 50-70% of patients respond, making it one of the most effective IBS interventions. But it must be delivered correctly, in three phases, ideally by a trained dietitian: (1) Restriction: strict low FODMAP for 4-6 weeks ONLY, to establish whether the patient responds. (2) Reintroduction: systematic, structured challenge of each FODMAP subgroup to identify which specific ones trigger symptoms and at what threshold. (3) Personalisation: a long-term, least-restrictive diet including all tolerated foods. The common failure mode is patients remaining on strict phase 1 indefinitely — this reduces dietary diversity, significantly depletes beneficial bifidobacteria, risks nutritional inadequacy, and can precipitate or worsen disordered eating. If a patient does not respond within 4-6 weeks, the diet should be stopped, not intensified.

Why has my doctor prescribed an antidepressant for IBS?

Low-dose tricyclic antidepressants (typically amitriptyline 10-30mg at night) are prescribed for IBS as gut-brain neuromodulators — not as antidepressants. At these doses (far below the 75-150mg+ used for depression), they act on visceral pain pathways: modulating pain signalling between the gut and brain, reducing visceral hypersensitivity, and slowing gut transit (which is why they suit IBS-D particularly). The ATLANTIS trial (Lancet 2023) confirmed amitriptyline as an effective second-line treatment for IBS in primary care. This does not mean the doctor thinks the symptoms are imaginary or psychological — the same class of drug is used at low dose for neuropathic pain, migraine prophylaxis and fibromyalgia for the same pain-modulating reason. If this is not explained, patients frequently stop the medication or lose confidence in their clinician.

IBS is a chronic, relapsing-remitting condition rather than one with a single cure — but it is highly treatable, and the majority of patients achieve good symptom control with a structured, multimodal approach. Prognosis is better than commonly assumed: post-infectious IBS resolves in approximately 50% of patients within 5-8 years; many others achieve long periods of remission. Key principles for good outcomes: a confident positive diagnosis (uncertainty perpetuates symptoms and anxiety); a clear physiological explanation of the gut-brain mechanism; identification and treatment of overlooked contributors (bile acid diarrhoea, coeliac disease, lactose intolerance, pelvic floor dyssynergia in IBS-C); a stepped approach combining diet, pharmacotherapy and psychological therapy; and continuity with one clinician rather than repeated re-investigation by different teams.

How does GMJ News cover IBS?

GMJ News covers Rome IV positive diagnostic criteria, faecal calprotectin as the IBD discriminator, the three-phase low FODMAP protocol and the harm of indefinite restriction, gut-brain neuromodulators (ATLANTIS trial), psychological therapies (hypnotherapy, ACTIB internet CBT), subtype-directed pharmacotherapy, bile acid diarrhoea as a missed diagnosis in 25-30% of IBS-D, the soluble vs insoluble fibre distinction, post-infectious IBS, and visceral hypersensitivity mechanisms. Directly relevant to PHIG's gastroenterology and primary care programme.

Home › Topics › Irritable Bowel Syndrome

Irritable Bowel Syndrome

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Irritable bowel syndrome (IBS) — a disorder of gut-brain interaction characterised by recurrent abdominal pain associated with defaecation or a change in stool form or frequency — affects approximately 4-10% of the global population and is the single most common diagnosis in gastroenterology practice, yet remains widely dismissed as a diagnosis of exclusion despite having clear positive diagnostic criteria (Rome IV) that permit confident diagnosis without extensive investigation in patients without alarm features (WHO). The evidence base has matured substantially: the low FODMAP diet produces symptom improvement in approximately 50-70% of patients when delivered by a trained dietitian in three structured phases (restriction, reintroduction, personalisation), and gut-brain neuromodulators (low-dose tricyclic antidepressants) and psychological therapies (gut-directed hypnotherapy, CBT) have Grade A evidence — making IBS one of the most treatable conditions in gastroenterology when managed systematically.

Key messages

Rome IV — a positive diagnosis, not a diagnosis of exclusion

Rome IV criteria: recurrent abdominal pain on average ≥1 day per week in the last 3 months, associated with ≥2 of: related to defaecation; associated with a change in stool frequency; associated with a change in stool form. Onset ≥6 months before diagnosis. This is a POSITIVE diagnostic framework — in a patient meeting Rome IV criteria without alarm features, IBS can be diagnosed confidently after limited testing (FBC, CRP, coeliac serology, faecal calprotectin) without colonoscopy. Treating IBS as a diagnosis of exclusion generates unnecessary investigation, cost, radiation exposure and patient anxiety.

Faecal calprotectin — the key discriminator from IBD

Faecal calprotectin: a neutrophil-derived protein measured in stool, reflecting intestinal mucosal inflammation. Calprotectin <50 μg/g: IBD very unlikely (negative predictive value >95%) — supports IBS. Calprotectin >150-250 μg/g: investigate for IBD with colonoscopy. Intermediate (50-150): repeat, or consider colonoscopy based on clinical picture. NICE recommends faecal calprotectin to distinguish IBS from IBD in adults under 45 with lower GI symptoms — avoiding large numbers of unnecessary colonoscopies. Note: calprotectin is elevated by NSAIDs, PPIs, infection and colorectal cancer — it is a marker of inflammation, not specific to IBD.

Low FODMAP diet — 50-70% response, but must be delivered in three phases

The low FODMAP diet (Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols) restricts short-chain carbohydrates that are poorly absorbed, osmotically active and rapidly fermented — producing gas, distension and pain in visceral-hypersensitive patients. Response: approximately 50-70% in RCTs. Critical: it must be delivered in THREE phases by a trained dietitian — (1) Restriction (4-6 weeks only); (2) Systematic reintroduction (identify individual triggers); (3) Personalisation (long-term least-restrictive diet). Indefinite strict restriction is harmful: it reduces dietary diversity, depletes beneficial bifidobacteria and risks nutritional inadequacy and disordered eating.

Gut-brain neuromodulators — Grade A evidence, low dose, explained properly

Low-dose tricyclic antidepressants (amitriptyline 10-30mg nocte; nortriptyline) have Grade A evidence for global IBS symptoms and pain — the ATLANTIS trial (Lancet 2023) confirmed amitriptyline as an effective second-line treatment in primary care. Mechanism at this dose: peripheral and central visceral pain modulation, not antidepressant effect. Also slows gut transit — preferable in IBS-D. SSRIs: modest evidence; accelerate transit — better in IBS-C. Essential: explain that these are prescribed as gut-brain neuromodulators at doses far below antidepressant doses, otherwise patients interpret the prescription as "the doctor thinks it is in my head" and adherence collapses.

Psychological therapies — as effective as any drug

Gut-directed hypnotherapy: 6-12 sessions; response rates approximately 70% in specialist centres; effects durable over years. Cognitive behavioural therapy (CBT), including internet-delivered CBT (the ACTIB trial, Gut 2019, showed significant benefit at 12 months): effective for symptom severity and impact. These are not "for patients whose symptoms are psychological" — they work by modulating the gut-brain axis and visceral hypersensitivity, and should be offered as mainstream treatments alongside dietary and pharmacological options rather than as a last resort.

Subtype-directed pharmacotherapy

IBS-D (diarrhoea-predominant): loperamide (symptom control, no effect on pain); rifaximin (non-absorbable antibiotic — TARGET trials; approximately 40% response, repeatable); eluxadoline (mixed opioid receptor agonist/antagonist — avoid in patients without a gallbladder or with pancreatitis history); ondansetron; bile acid sequestrants (colestyramine — for bile acid diarrhoea, which is present in approximately 25-30% of patients labelled IBS-D and is frequently missed — SeHCAT testing). IBS-C (constipation-predominant): soluble fibre (ispaghula, NOT insoluble bran which worsens IBS); macrogol; linaclotide (guanylate cyclase-C agonist); lubiprostone; prucalopride. Antispasmodics (mebeverine, hyoscine, peppermint oil) for pain and bloating in all subtypes.

Key statistics

4-10%

global adult prevalence of IBS (Rome IV criteria)

Lancet Gastro/Rome Foundation

<50 μg/g

faecal calprotectin makes IBD very unlikely (NPV >95%) — supports IBS diagnosis

NICE/BSG

50-70%

symptom response to a dietitian-delivered low FODMAP diet

Gut/BDA

ATLANTIS 2023

low-dose amitriptyline confirmed effective second-line for IBS in primary care (Lancet)

Lancet 2023

~70%

response rate to gut-directed hypnotherapy in specialist centres

Gut/BSG

25-30%

of patients labelled IBS-D actually have bile acid diarrhoea — frequently missed

BSG/SeHCAT

IBS treatments — approximate response rates (BSG/ACG guidelines)

Source: BSG 2021/ACG 2021. Dietary, psychological and neuromodulator therapies all have Grade A or B evidence.

Glossary of key terms

Rome IV criteria and IBS subtypes
Rome FoundationRome IV (2016) diagnostic criteria for IBS: recurrent abdominal PAIN (note: Rome IV removed "discomfort") on average at least 1 day per week in the last 3 months, associated with two or more of: (1) related to defaecation; (2) associated with a change in stool frequency; (3) associated with a change in stool form (appearance). Criteria fulfilled for the last 3 months with symptom onset at least 6 months before diagnosis. Subtypes by predominant stool form on abnormal-stool days (Bristol Stool Form Scale): IBS-C (constipation — >25% type 1-2, <25% type 6-7); IBS-D (diarrhoea — >25% type 6-7, <25% type 1-2); IBS-M (mixed — both >25%); IBS-U (unclassified).

FODMAPs — the biochemistry
Nutrition/GIFODMAPs are short-chain carbohydrates that are poorly absorbed in the small intestine, osmotically active (drawing water into the lumen) and rapidly fermented by colonic bacteria (producing hydrogen, methane and CO2). Categories: Oligosaccharides — fructans (wheat, rye, onion, garlic) and galacto-oligosaccharides (legumes, pulses); Disaccharides — lactose (milk, soft cheese, yoghurt); Monosaccharides — excess fructose (honey, apple, mango, high-fructose corn syrup); Polyols — sorbitol, mannitol, xylitol, maltitol (stone fruits, mushrooms, sugar-free gum and confectionery). In patients with visceral hypersensitivity, the resulting luminal distension produces disproportionate pain and bloating. Developed at Monash University; Monash maintains the definitive FODMAP food database and app.

Bile acid diarrhoea
GI/DiagnosticsBile acid diarrhoea (BAD) — excess bile acids reaching the colon, stimulating secretion and motility — is present in approximately 25-30% of patients diagnosed with IBS-D and is very frequently missed. Types: Type 1 (ileal disease/resection — Crohn's, ileal resection); Type 2 (primary/idiopathic — the type mislabelled as IBS-D); Type 3 (secondary — post-cholecystectomy, coeliac disease, chronic pancreatitis, small bowel bacterial overgrowth). Diagnosis: SeHCAT scan (75-selenium homocholic acid taurine retention at 7 days: <15% = BAD; <5% = severe) — the gold standard but limited availability; serum 7α-hydroxy-4-cholesten-3-one (C4) or FGF19 as alternatives. Treatment: bile acid sequestrants — colestyramine, colesevelam (better tolerated), colestipol. Response is often dramatic — making this a high-yield diagnosis to actively seek in any patient with IBS-D, particularly post-cholecystectomy.

Visceral hypersensitivity and the gut-brain axis
NeurogastroenterologyThe central pathophysiological mechanism in IBS: an amplified perception of normal or mildly abnormal gut stimuli. Components: peripheral sensitisation (mucosal immune activation, mast cell mediators, increased permeability, post-infectious changes); spinal sensitisation; altered central processing (imaging shows altered activity in the anterior cingulate cortex, insula and prefrontal cortex in response to rectal distension); descending pain modulation impairment; and bidirectional signalling via the vagus, HPA axis and microbiota-derived metabolites. This framework explains why treatments as diverse as diet (reducing the peripheral stimulus), neuromodulators (altering signal transmission) and hypnotherapy (altering central processing) all work — they intervene at different points on the same axis.

Post-infectious IBS
Epidemiology/GIApproximately 10% of patients develop IBS after an episode of acute infectious gastroenteritis — post-infectious IBS (PI-IBS). Risk factors: severity and duration of the initial illness; bacterial (Campylobacter, Salmonella, Shigella, E. coli) more than viral; female sex; psychological distress at the time of infection; antibiotic use during the infection. Mechanism: persistent low-grade mucosal immune activation, increased enterochromaffin cells and serotonin signalling, altered permeability and microbiota. Prognosis: better than non-PI-IBS — approximately 50% resolve within 5-8 years. Recognition matters because it gives the patient a clear, non-stigmatising explanation of a physical trigger for their symptoms.

Fibre in IBS — the soluble/insoluble distinction
Nutrition/GIA frequent and harmful clinical error is advising "more fibre" generically. Soluble fibre (ispaghula/psyllium, oats, ispaghula husk): forms a gel, improves stool consistency in both directions, improves global IBS symptoms — Grade B evidence; recommended. Insoluble fibre (wheat bran, insoluble cereal fibre): increases luminal distension and gas production — WORSENS pain and bloating in IBS; multiple studies show deterioration. BSG and ACG guidelines both specifically recommend soluble fibre and specifically advise AGAINST insoluble bran in IBS. Start ispaghula at a low dose and titrate slowly with adequate fluid, as rapid introduction causes transient bloating and leads patients to abandon an effective treatment.