IBS — irritable bowel syndrome

Definition and scope

Irritable Bowel Syndrome (IBS) is the most prevalent condition within the category of Disorders of Gut-Brain Interaction (DGBI). The prevalence varies considerably depending on criteria and study methodology; Rome V-specific population figures are still under development. A clear predominance among women and younger adults is nonetheless consistently observed.^[5],[1]

Rome V continues the positive, symptom-based diagnostic approach and updates, among other things, the symptom definition and frequency threshold compared with previous Rome criteria.^[2],[1]

Rome V — diagnostic criteria Established consensus

IBS may be consistent with recurrent, non-continuous abdominal pain or discomfort occurring on average at least 3 days per month over the last 3 months, associated with at least 2 of the following:^[1]

1. Related to defecation — the pain/discomfort changes (better or worse) in connection with a bowel movement.
2. Associated with a change in stool frequency — more or less often than usual.
3. Associated with a change in stool form — harder, looser or more watery consistency.

The criteria must have been met over the last 3 months, and symptom onset must have occurred at least 6 months before assessment. The criteria must always be interpreted in clinical context.^[1],[2]

Subtypes (Bristol Stool Form Scale)

Subtyping requires documentation that > 25% of abnormal stools are Bristol type 1–2 and/or type 6–7. A single, arbitrarily chosen Bristol type cannot on its own establish a subtype.^[4],[1] Laxatives, loperamide and other bowel-modulating medication affect classification and must be taken into account.

IBS subtype cannot be reliably assessed from insufficient information. A stool diary (e.g. 14 days) may be necessary.

Pathophysiology: a heterogeneous gut-brain disorder Debated

IBS is heterogeneous. Different combinations of visceral hypersensitivity, altered motility, central pain processing, psychosocial factors, immune activation, diet and the microbiome may play a role in different patients — there is no single mechanism that applies to everyone.^[2],[5]

• Visceral hypersensitivity — in some patients, nerves in the gut wall are hyper-reactive, so normal processes (gas bubbles, postprandial distension) are experienced as pain.
• Gut-brain axis dysregulation — in some patients, two-way communication between the CNS and gut is disrupted, which may involve the HPA axis and altered motility.
• Possible low-grade mucosal inflammation — in certain subgroups, particularly post-infectious IBS, an increased occurrence of mast cells close to gut nerve endings has been described.
• Altered intestinal permeability — described in some studies as a possible finding in subgroups. The concept of "leaky gut" is debated and should not be regarded as an established causal mechanism.
• Dysbiosis — changes in the gut microbiome have been observed in some IBS patients, but it is not established whether this is a cause, contributing factor or consequence.

Schematic overview

Symptomatology and clinical manifestations

• IBS-C: hard, lumpy stools, incomplete evacuation, distension, postprandial pain relieved by defecation.
• IBS-D: loose/watery stools, urgency, postprandial urge, cramps that improve after a bowel movement.
• IBS-M: alternating between hard constipation and loose diarrhoea, often in shifting periods.
• Common features: bloating, distension, mucus in stool (not blood), worsening with stress and, in some, with certain foods.

Diagnostic workflow

Rome V cautions against unnecessary, invasive investigations (e.g. routine colonoscopy without indication), which may increase medicalisation and anxiety. Red flags increase the need for individual assessment of organic disease. The choice of blood tests, imaging or endoscopy depends on symptoms, age, screening history, family history and overall clinical judgement.^[1],[3]

Red flags

The following symptoms should prompt individual consideration of further investigation, e.g. colonoscopy for lower GI symptoms or gastroscopy for upper GI symptoms:

• Symptom onset after the age of 50 without prior screening.
• Unexplained weight loss or fever.
• Visible blood in stool (haematochezia) or unexplained iron-deficiency anaemia.
• Nocturnal diarrhoea (wakes the patient).
• Family history of colorectal cancer, coeliac disease or IBD.

Targeted laboratory tests

Coeliac serology, faecal calprotectin and CRP are targeted tests — not mandatory for everyone — that are particularly relevant with diarrhoea-predominant symptoms or other clinical suspicion of organic disease.^[3],[12]

• Faecal calprotectin — a low value makes active inflammatory bowel disease less likely, but cannot alone rule out all forms of IBD. The result must be interpreted relative to pre-test probability, symptoms and other findings.^[12]
• Coeliac serology — anti-tissue transglutaminase (tTG) IgA + total IgA.
• CRP and haemoglobin — relevant when systemic inflammation or anaemia is suspected.

SIBO breath test Debated is not a routine part of IBS assessment. It may be considered in selected symptomatic patients with relevant risk factors or specific clinical suspicion. Bloating alone cannot distinguish SIBO from IBS or other conditions.^[5]

Studies have reported higher breath-test positivity in some IBS populations, but estimates vary considerably depending on patient selection, substrate and diagnostic criteria. A positive breath test does not by itself demonstrate that SIBO is the cause of the IBS symptoms.

Differential diagnoses in selected patients

In selected patients — for example with lack of improvement, atypical features or particular risk factors — the following differential diagnoses should briefly be considered before symptoms are attributed to IBS alone:

• Bile acid diarrhoea — can resemble IBS-D but results from disrupted bile acid absorption.
• Microscopic colitis — particularly relevant with chronic watery diarrhoea in older patients; requires colonoscopy with biopsies.
• Medication side effects — several drugs can cause IBS-like symptoms and should be reviewed in the history.
• Defecation or pelvic floor dysfunction — can produce symptoms resembling IBS-C and requires a different work-up and treatment.

Treatment options — tailored by subtype

Treatment is tailored to the dominant subtype (IBS-C vs. IBS-D) and symptom severity, and should always be based on an individual medical assessment. The core pillars (diet, fibre, psychological intervention) are relevant across several subtypes.^[3],[5]

Diet and non-pharmacological measures

• Soluble fibre (psyllium): documented effect on bowel regulation and discomfort in many patients. Insoluble fibre (wheat bran) may worsen pain and bloating in some.^[7]
• Low-FODMAP diet Conditional recommendation — a time-limited, structured elimination diet may be considered in selected patients (see section below).^[6]
• Psychological intervention: gut-directed hypnotherapy and cognitive behavioural therapy (CBT) have shown effect in some patients, particularly with moderate to severe symptoms.^[11]

IBS-C (constipation)

• Osmotic laxatives (macrogol/PEG) are a documented treatment for constipation, but have not been shown to improve global IBS symptoms or pain.
• Linaclotide Conditional recommendation may be an option for IBS-C following individual medical assessment.^[8]

Neuromodulators

• Tricyclic antidepressants (TCAs) may be used at low dose as a neuromodulator in pain-predominant IBS, following individual medical assessment. Specific doses are not set generically but individually.^[11]
• SSRIs/SNRIs may be considered in selected patients, particularly with coexisting anxiety, depression or other relevant comorbidity. The effect on global IBS symptoms varies.^[11]

Possible accompanying symptoms and comorbidities

IBS is associated with several other conditions and symptoms outside the gastrointestinal tract. The associations are reported in studies, but a causal relationship has not been established in every case.^[5],[2]

• Fatigue and sleep disturbance: commonly reported in IBS patients, often linked to disrupted sleep.
• Headache and migraine: increased reported occurrence compared with the background population. A possible shared mechanism via CGRP signalling has not been conclusively established and should be considered a hypothesis.
• Fibromyalgia and chronic musculoskeletal pain: frequent comorbidity, where central sensitisation has been proposed as a shared factor.
• Urological and gynaecological symptoms: overactive bladder, interstitial cystitis/painful bladder syndrome, dyspareunia and worsening around menstruation are reported in some patients.
• Psychiatric comorbidity: anxiety, depression and somatisation occur more frequently in IBS patients — the association likely runs in both directions.
• Temporomandibular dysfunction (TMD) and atypical chest pain without a cardiac explanation are reported as comorbidities, without a shared causal mechanism being conclusively established.
• Skin symptoms: some studies report increased occurrence of atopic eczema, urticaria and rosacea in IBS patients. A possible microbiome-immune-related link is a hypothesis under investigation, not an established causal mechanism.

Identifying accompanying symptoms can influence the overall assessment: for example, neuromodulators may be relevant where there is overlap with fibromyalgia or depression, and gut-directed hypnotherapy/CBT can address both GI and psychological symptoms. Any multidisciplinary approach should always be arranged individually.^[3],[11]

The low-FODMAP diet in practice Conditional recommendation

The low-FODMAP diet is one of the best-studied dietary interventions for IBS. The evidence is moderate and varies depending on which symptom is measured; the effect is not the same in every patient. FODMAP stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols — short-chain carbohydrates that osmotically draw fluid into the small intestine and are rapidly fermented in the colon, producing gas.^[6]

The three phases

Low-FODMAP is not a strict, permanent exclusion of all high-FODMAP foods, but a time-limited, structured reduction phase followed by systematic reintroduction and individualisation — ideally guided by a dietitian with relevant experience.

1. Phase 1 – Structured reduction (4–6 weeks): time-limited reduction of high-FODMAP foods. Effect is assessed after 6 weeks at the latest — lack of response means the diet should be discontinued (not continued).
2. Phase 2 – Reintroduction (6–8 weeks): systematic testing of one FODMAP group at a time in individually adapted doses, with washout between groups. Specific amounts and test foods vary between protocols. The aim is to identify individual triggers and tolerance thresholds — not to remain on the reduction phase.
3. Phase 3 – Personalisation (ongoing): a liberalised diet where only the identified triggers are restricted. The goal is the most varied diet that keeps symptoms controlled — to preserve microbiome diversity and nutritional status.

Practical advice and pitfalls

• Dietitian support recommended: self-managed low-FODMAP is often overly restrictive and carries a risk of insufficient fibre, calcium and iron intake.
• Portion size matters: many foods are lower in FODMAPs in smaller portions and higher in larger ones. The amounts given are illustrative examples — actual FODMAP content depends on product, ripeness and preparation, and is not calibrated against a specific database. Amounts and test foods in reintroduction schedules vary between protocols and should always be adapted individually.
• Particular caution and nutritional assessment: with an active eating disorder, underweight (BMI < 18.5) or an already highly restrictive diet, low-FODMAP should only be started after a specific nutritional assessment and with close follow-up — it is not necessarily excluded, but requires particular caution. Other first-line options (psyllium, neuromodulator, hypnotherapy) should often be considered in these cases.
• Reintroduction is central: a prolonged, unnecessarily restrictive diet can affect nutritional intake and the microbiome. The elimination phase should therefore not continue longer than necessary.

Prognosis

IBS is often a chronic, intermittent condition with spontaneous remissions and flares (often triggered by life stress or infections). It is important for patients to know that IBS does not increase the risk of colorectal cancer, IBD or other malignancies, and does not shorten life expectancy.^[5],[1]

Quality of life often depends on whether the vicious cycle between gut discomfort and psychological strain can be broken — potentially via a multidisciplinary approach (diet, possibly medication and psychological support). This should always be arranged individually in consultation with the treating doctor.^[2],[3]

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