Irritable bowel syndrome

• Irritable bowel syndrome (IBS) is a chronic, relapsing disorder of gut-brain interaction: recurrent abdominal pain with a change in stool form or frequency, without any structural or biochemical explanation that accounts for the symptoms.
• It affects roughly one person in ten worldwide and is more common in younger women; anxiety, depression, somatic symptoms and fibromyalgia travel with it.
• There is no test that diagnoses IBS. The diagnosis is positive and symptom-based on the Rome IV criteria, after ruling out alarm features and doing only limited tests.
• Management begins with a confident diagnosis, explanation and reassurance, then lifestyle and diet (soluble fibre such as psyllium, a short, dietitian-supervised low-FODMAP trial, exercise) before drug therapy aimed at the predominant symptom.
• IBS is not progressive and does not increase mortality, but it reduces quality of life, and poor diagnostic certainty keeps patients cycling through repeated investigations.

By the end of this page you should be able to:

1. State the Rome IV criteria and the Bristol-based IBS subtypes, and apply them to a short clinical vignette.
2. Explain the gut-brain, motility, sensory and microbial mechanisms that produce IBS symptoms and link them to the dominant symptom.
3. Recognise alarm features, list the limited investigations recommended, and judge when a colonoscopy is needed.
4. Construct a stepwise management plan for IBS-C and IBS-D, with non-drug measures first and drugs matched to the predominant symptom.
5. Outline the evidence and the guideline positions behind positive diagnosis, fibre, antispasmodics and peppermint oil.
6. Counsel a patient about prognosis, comorbidity screening and low-resource practice.

IBS is the most common functional bowel disorder seen in gastroenterology clinics and one of the commonest reasons for a primary care visit. It is defined by symptoms, not by any structural lesion, and for most patients it is a benign but burdensome condition that fluctuates over years. The challenge for a clinician is therefore twofold: to make the diagnosis positively and cheaply, without over-investigating, and to treat the patient's actual predominant symptom rather than a label. That is the arc of this page.

The Rome Foundation is an international panel of experts in functional gastrointestinal disorders that writes symptom-based definitions. The current definition is Rome IV (2016). Irritable bowel syndrome is diagnosed when all of the following are present ^[1]:

Two of the three last features are needed in addition to the pain frequency, giving the familiar "pain plus two of three". A practical reading of the criteria is that abdominal pain is the essential symptom: if there is no abdominal pain, the diagnosis of IBS is untenable. Abdominal pain relieved by defecation but without a change in stool frequency or form points to other functional bowel disorders, not to IBS.

The time rule matters. Symptoms should have been present during the last 3 months and to have started at least 6 months before diagnosis. The reason for the 6-month rule is to let any organic disease declare itself; a new change in bowel habit in an older adult is a different clinical problem, and it is not IBS by default.

Stool form is recorded with the Bristol stool form scale, a seven-point picture scale from separate hard lumps (type 1) to watery stool (type 7), developed as a rough surrogate for colonic transit. Types 1 and 2 correspond to constipation, types 6 and 7 to diarrhoea, and types 3 and 4 to normal stools. A 14-day bowel diary improves the accuracy of subtyping ^[1].

IBS is split by the predominant bowel habit on days with abnormal movements ^[2]:

Subtyping is not academic: drug therapy and dietary advice differ between IBS-C and IBS-D, and the mixed group is the hardest to treat.

IBS is common but its exact prevalence depends on the criteria used and the country studied. Worldwide prevalence is reported as 11.2 percent ^[2], and most population surveys that use Rome criteria find a band between 10 and 15 percent ^[3]. Incidence is estimated at 1.35 to 1.5 percent per year in adults ^[2].

• Sex. Women are affected more often than men in most surveys ^[3], and the condition is more often reported in women of reproductive age.
• Age. Onset is usually in adolescence or young adulthood; new-onset symptoms after the age of 50 are unusual and should raise the question of organic disease.
• Comorbidity. Anxiety, depression and other somatic symptom disorders are strongly over-represented ^[3]. Fibromyalgia, chronic fatigue syndrome, chronic pelvic pain, temporomandibular joint disorder and other functional gastrointestinal disorders cluster with IBS ^[3]. These comorbidities matter for management, not just for labelling: psychological treatment helps the gut symptoms too.
• Regional differences. Post-infectious IBS is reported after bacterial dysentery at rates around 10 percent ^[2], and its burden is higher where enteric infections are common. Reported IBS prevalence is lower in some East Asian populations, but underdiagnosis and cultural differences probably contribute.

There is no single cause. IBS is best understood as the clinical expression of a set of interacting susceptibilities.

• Prior infection. Post-infectious IBS develops after an episode of gastroenteritis. It occurs in approximately 10 percent of patients after infectious enteritis, and the risk is six- to seven-fold higher in people with a prior infection than in those without ^[2]. Risk factors for the post-infectious form include young age, female sex, prolonged or severe initial illness, and pre-existing anxiety or depression.
• Psychological and stress factors. Stress is a major trigger. Depressive and anxiety disorders can precede and also follow the onset of IBS gut symptoms, which is evidence for a truly bidirectional gut-brain axis rather than for a purely psychiatric disorder ^[3]. Childhood adverse experiences, including physical, emotional and sexual abuse, are also linked to later IBS.
• Gut microbiota changes. Dysbiosis, reduced microbial diversity and shifts in specific taxa are described in many IBS patients, but no single microbial signature is diagnostic.
• Food and diet. Many patients report that specific foods trigger symptoms, particularly fermentable carbohydrates and sometimes gluten, even in the absence of coeliac disease.
• Genetics. Twin data show a modest heritable component, with concordance 17.2 percent in monozygotic twins versus 8.4 percent in dizygotic twins ^[2].
• Other factors. Antibiotic use and other adverse life events can precipitate symptoms, and a family history of IBS is common.

IBS is a disorder of gut-brain interaction in which several mechanisms overlap and patients differ in which ones dominate. The principal ones are:

1. Gut-brain axis dysregulation. Bidirectional signalling between the gut (enteric nervous system, microbiota, immune and endocrine cells) and the central nervous system is disturbed. Serotonin (5-hydroxytryptamine) and corticotropin-releasing hormone are key transmitters, and both act in the gut and the brain ^[2].
2. Visceral hypersensitivity. The gut wall becomes sensitive to distension so that a normal stimulus such as gas or a normal stool volume is felt as pain. Prevalence in surveys ranges widely, from 33 to 90 percent, and it is more common in IBS-D ^[3]. This is the mechanism most patients mean when they say the pain "comes out of nowhere".
3. Altered motility. Transit can be fast (diarrhoea), slow (constipation) or disorganised, and it is modulated by serotonin: higher levels are described in IBS-D and lower levels in IBS-C ^[3].
4. Low-grade inflammation and immune activation. Some patients have increased mucosal immune cells and raised pro-inflammatory cytokines (interleukin-6, tumour necrosis factor-alpha, interleukin-1 beta) with increased intestinal permeability, sometimes triggered by a prior infection, sometimes by dysbiosis ^{[3] [2]}.
5. Post-infectious IBS. A subset begins after an episode of gastroenteritis, with mucosal low-grade inflammation and altered permeability persisting after the infection clears.
6. Bile acid malabsorption. In some patients with IBS-D, excess bile acids reach the colon because of impaired reabsorption in the terminal ileum or increased hepatic synthesis. This activates TGR5 (a bile acid receptor) and drives colonic hypermotility, and it is the reason that bile acid sequestrants can relieve diarrhoea-predominant symptoms ^[4]. In patients with bile acid diarrhoea, colonic mucosal FXR (farnesoid X receptor) expression and serum FGF19 are abnormal ^[4].
7. Microbiome dysbiosis. IBS patients often show dysbiosis (reduced diversity, altered phyla, and in IBS-D reduced Faecalibacterium and Bifidobacteria) compared with healthy subjects ^[3]. Whether the dysbiosis is cause, effect or amplifier is still unsettled.

No single mechanism is present in every patient. The same symptom (abdominal pain with loose stools) can arise from visceral hypersensitivity in one patient, bile acid malabsorption in another and post-infectious inflammation in a third, which is why a stepwise approach beats a single "IBS drug".

In the patient's own words, the history usually contains some combination of:

• Recurrent lower abdominal pain or cramping, often in the left lower quadrant, relieved by passing stool or passing wind, or worsening before a bowel movement and easing afterwards.
• Altered bowel habit: constipation, diarrhoea, or alternating. Stools may be urgent, accompanied by tenesmus and a sensation of incomplete evacuation.
• Abdominal bloating and visible distension, often worse as the day goes on and after meals.
• Mucus in the stool, flatulence, nausea and dyspeptic symptoms.
• Extraintestinal symptoms: fatigue, poor sleep, migraine, backache, joint pain, and low mood.

The abdominal pain must be there for the diagnosis to be considered. Pain that wakes the patient from sleep, pain that is steadily progressive, or pain that localises to the right upper quadrant or epigastrium points away from IBS and needs investigation.

Physical examination is usually normal, and that normal examination is itself reassuring. Look specifically for:

• General appearance: pallor, weight loss, fever.
• Abdomen: distension, tenderness, any mass, organomegaly, ascites.
• Perianal and rectal examination: in constipated patients this can identify pelvic floor dyssynergia and faecal loading, which changes management.
• Signs of anaemia or thyroid disease where relevant.

If the patient has pain with deep pressure but not with light touch, and if routine tests are normal, a functional disorder is the likely explanation.

Two specific traps are worth stating. Lactose and fructose intolerance can mimic IBS diarrhoea exactly, and trying one months-long exclusion diet after another without supervision leads to malnutrition; a time-limited, structured trial is better. And a normal colonoscopy does not rule out microscopic colitis, which is invisible without biopsies.

The guiding principle is to do the least that is safe. Routine panels of tests are discouraged: they do not find alternative diagnoses in patients who meet Rome IV criteria with a normal examination and no alarm features, and they undermine the patient's confidence in the diagnosis ^[1].

Recommended basic testing ^{[1] [2]}:

• Complete blood count to exclude iron-deficiency anaemia.
• C-reactive protein (and/or erythrocyte sedimentation rate). A C-reactive protein of 0.5 mg/dL or less essentially excludes inflammatory bowel disease in a patient with diarrhoea, giving a likelihood of 1 percent or less ^[2].
• Coeliac serology (tissue transglutaminase antibody with immunoglobulin A), ideally while the patient eats gluten.
• Faecal calprotectin, particularly in IBS-D or mixed IBS, to distinguish IBS from inflammatory bowel disease: under 50 mg/g is usually considered normal, and over 100 mg/g suggests intestinal inflammation. The best-supported single cut-off is under 50 mg/g, which gives the highest sensitivity and specificity, and a value of 40 micrograms per gram or less makes inflammatory bowel disease unlikely, with a probability of less than 1 percent ^[2]. (Calprotectin rises with proton pump inhibitors, non-steroidal anti-inflammatory drugs, infection, obesity, older age and malignancy, so it is not specific.)
• Thyroid-stimulating hormone where clinically indicated.

Colonoscopy is indicated, not routine ^[2]: in patients with alarm features; in those aged 50 years or more with new-onset symptoms or a change in bowel habit, as part of colorectal cancer screening; in patients who do not respond to standard treatment; and in patients who have not had appropriate screening. In patients under 50 without alarm features, routine colonoscopy has a low yield and is discouraged. If chronic diarrhoea is being investigated, take biopsies from several colonic segments to exclude microscopic colitis. In one prospective study, colonoscopy did not change the diagnosis of IBS in 98.1 percent of patients ^[1].

Alarm features (red flags) are the reason to investigate further, including with colonoscopy ^{[1] [2]}:

• Onset of symptoms after the age of 50.
• Unintentional weight loss.
• Rectal bleeding or melaena.
• Nocturnal symptoms (waking from sleep to defecate).
• Family history of colorectal cancer, inflammatory bowel disease or coeliac disease.
• Iron-deficiency anaemia.
• A palpable abdominal mass or lymphadenopathy; fever.
• Recent antibiotic use (post-infectious causes).
• A personal history suggesting another disease (for example inflammatory bowel disease or endometriosis).

If any of these are present, investigate for organic disease first. If none are present and the patient meets Rome IV criteria, the diagnosis is IBS and reassurance and treatment should follow.

For most patients the diagnosis is complete at this point: positive Rome IV criteria plus a normal examination and limited normal tests, with no alarm features. Two points of debate are worth knowing for examinations ^{[1] [2]}:

• Positive diagnosis versus diagnosis of exclusion. Traditionally, many clinicians have treated IBS as a diagnosis of exclusion and ordered broad testing. The modern view, supported by a randomised trial and by cost data, is that a positive diagnostic approach (meeting Rome criteria, no alarm features, limited targeted testing) is as safe and considerably cheaper, with roughly 40 percent lower overall healthcare costs, and allows earlier treatment ^[2]. Most community providers still believe IBS is a diagnosis of exclusion, which is part of why patients stay over-investigated.
• Clinics should stop looking for a "gold standard" test. None exists. The Rome criteria are imperfect but are the best available and they are good enough for clinical use.

Before drugs or diets, the most important step is to make a confident diagnosis and explain it ^[1]. Many patients fear cancer or inflammatory bowel disease; time spent letting the patient tell the story, reviewing previous tests so that nothing is repeated, and stating plainly "you have IBS, and this is why" is therapeutic. Diagnostic certainty in language reduces further testing and repeated consultations ^[1]. Education is then matched to the subtype, because the predominant symptom determines therapy.

These come first ^[2]:

• Explain and reassure. IBS is not progressive, not infectious, not cancer and not usually dangerous. Symptoms fluctuate and can be improved even when not eliminated.
• Dietary fibre: ispaghula (psyllium) rather than wheat bran. Soluble fibre in the form of ispaghula improves symptoms compared with placebo; a meta-analysis found a number needed to treat (NNT) of about 6 for ispaghula, whereas wheat bran (an insoluble fibre) is no better than placebo and may worsen bloating. NICE and British Society of Gastroenterology guidance recommend soluble fibre such as ispaghula when fibre supplementation is needed and discourage insoluble fibre ^[5].
• Low-FODMAP diet, supervised by a dietitian. This eliminates and then reintroduces fermentable oligo-, di- and mono-saccharides and polyols. It improves global symptoms, bloating and bowel habits and it has three phases: elimination, reintroduction and long-term personalisation. Because most studies involved dietitians and restrictive diets carry a risk of malnutrition, a dietitian's supervision is strongly encouraged; if none is available, high-quality teaching materials should be used ^[2]. A low-FODMAP trial is not a permanent diet: the aim is to identify the patient's personal triggers and keep the diet as liberal as possible.
• Exercise. Appropriate, gentle exercise such as walking, yoga and cycling improves overall symptoms. Hard, strenuous exercise is not recommended on the evidence available ^[2].
• Trigger reduction in general. Avoid large meals, excess alcohol and caffeine if they reproduce symptoms; eat at regular times. Identify personal food triggers with a short, structured diary rather than an open-ended restriction. Address sleep and stress.
• Sleep and stress management. Anxiety and stress worsen gut motility and sensation; behavioural activation, stress reduction and treatment of comorbid anxiety or depression help the gut.

Drug choices below follow the ACG 2021 clinical guideline ^[6] and the AGA 2022 pharmacologic guidelines for IBS with diarrhoea ^[7] and for IBS with constipation ^[8], together with the open-access consensus papers and reviews cited in the references.

Match the drug to the symptom and start low ^{[2] [7]}:

• Loperamide can improve stool frequency and consistency in IBS-D; titrate the dose and duration carefully because it can cause severe constipation, abdominal pain, bloating and nausea ^[2].
• Rifaximin, a non-absorbable antibiotic, improves global symptoms and stool consistency in IBS-D and is licensed for IBS-D in the United States; roughly 40 percent of patients achieve symptom relief. Retreatment is useful for recurrent symptoms after an initial response. It is unavailable for this indication in many countries ^[4].
• Eluxadoline, a mixed mu- and kappa-opioid agonist and delta-antagonist, is an option for IBS-D; contraindications include a gall bladder removed, sphincter of Oddi problems, heavy alcohol use, and pancreatitis risk, and it is used with caution.
• Alosetron, a 5-HT3 receptor antagonist, is approved in the United States and is recommended as a second-line agent for women with severe IBS-D symptoms; it can cause severe constipation and ischaemic colitis, so it is reserved for patients who have not responded to other therapies ^[2].
• Bile acid sequestrants (for example cholestyramine or colesevelam) help when bile acid diarrhoea is suspected or proven.
• Peppermint oil is an effective antispasmodic for pain and cramping; a meta-analysis of randomised trials found a NNT of 2.5 for persisting symptoms, and it is available over the counter ^[5].
• Antispasmodics are discussed below for pain.

• Polyethylene glycol (PEG) laxatives improve stool frequency and consistency in IBS-C, though their effect on abdominal pain is uncertain; lactulose is best avoided because its fermentation worsens bloating ^[2].
• Linaclotide and plecanatide, guanylate cyclase-C agonists, improve bowel movements, abdominal pain and bloating in IBS-C; diarrhoea is the usual side effect. They are not available in many markets ^[2].
• Lubiprostone, a chloride channel activator, improves abdominal pain and bloating in IBS-C. It should be taken with meals to reduce nausea, its most common side effect ^[2].
• Tegaserod, a 5-HT4 agonist, is approved in the United States for adult women under 65 years of age with IBS-C who have not responded to the usual laxatives; it is not available in most Asian countries ^[2].
• Prucalopride can be considered when constipation is refractory to simple laxatives; there are no randomised trials specifically in IBS-C ^[2].
• Antispasmodics have a poorer evidence base in constipation and should be used with care.

• Antispasmodics as a class reduce symptoms; antispasmodics (including alverine derivatives, mebeverine, and pinaverium where available) are a rational early choice for cramping. The strongest evidence in meta-analyses is for hyoscine (NNT about 3.5) and pinaverium (NNT about 3); otilonium and cimetropium were also effective, while trimebutine was not ^[5]. Antispasmodics also produce predictable side effects of dry mouth, dizziness and blurred vision, with a number needed to harm of about 17.5 ^[5]. Hyoscine is often used as first-line antispasmodic therapy ^[5].
• Peppermint oil is a good alternative or addition to antispasmodics ^[5].
• Tricyclic antidepressants (for example amitriptyline) in low doses modulate visceral pain perception and slow colonic transit, so they are particularly useful for predominant abdominal pain and for IBS-D because their main side effect is constipation ^[2]. In studies, antispasmodics and these agents are both more effective than placebo.
• Selective serotonin reuptake inhibitors (SSRIs) are less well supported. They may help when mood disorder is present or other measures have failed, and because they can cause diarrhoea they are generally preferred in IBS-C ^[2].

Gut-directed hypnotherapy and cognitive behavioural therapy are the two best-evidenced psychological treatments for IBS. They are appropriate for patients with moderate to severe or refractory symptoms, for those in whom conventional drug treatment has failed, or whose symptoms have persisted beyond 12 months, and for those with prominent anxiety or depression ^[2]. Multidisciplinary management (dietitian, psychologist, physiotherapist for pelvic floor dysfunction) is the standard for refractory disease ^[2].

Review the patient after starting or changing treatment. Adjust the dose, reassess the subtype (it can change), and re-check for new alarm features. Refer early to a multidisciplinary IBS service when symptoms remain moderate to severe after the standard steps, or when refractory disease is suspected.

IBS itself does not cause structural damage to the bowel and does not progress to cancer or inflammatory bowel disease. The complications are of quality of life, missed work, unnecessary surgery (a real risk when the diagnosis is uncertain) and unnecessary repeated investigations. Pelvic floor dyssynergia causing constipation and, rarely, faecal incontinence with chronic diarrhoea are practical complications to look for.

IBS is a chronic, relapsing and remitting condition ^[5]. Many patients improve with accurate diagnosis and reassurance alone, and treatment helps most of the rest, but symptoms often persist or recur over years. Symptom subtypes can change. Prognosis is best when psychological comorbidity is identified and treated alongside the bowel symptoms. The greatest disutility comes from diagnostic uncertainty, so the greatest single intervention is often a confident diagnosis plus explanation.

• Pregnancy and breastfeeding. First-line non-drug measures remain the foundation. Many drugs used for IBS are avoided in pregnancy; loperamide is used only if clearly needed, stimulant and osmotic laxatives and dietary advice are preferred, and any drug decision should be made with the obstetric clinician.
• Children and adolescents. Although symptoms often begin in adolescence, formal diagnosis and drug therapy in children use paediatric criteria and paediatric dosing; reassure families and involve paediatric gastroenterology.
• Older adults. New symptoms after age 50 are not IBS until proved otherwise; comorbidities and polypharmacy dominate management.

• Diagnosis is clinical and essentially free. Rome IV criteria, a careful history and a physical examination; a blood count, C-reactive protein and coeliac serology are the highest-value tests. Faecal calprotectin is useful when inflammatory bowel disease is a real alternative, but it depends on laboratory availability. A 14-day stool diary costs nothing and fixes the subtype.
• Avoid colonoscopy for typical symptoms. In younger patients without alarm features, colonoscopy rarely changes the diagnosis and uses scarce resources that are better spent on alarm cases and cancer screening for those aged 50 or more ^[2].
• Use cheap, available drugs. Soluble fibre (ispaghula), peppermint oil, generic antispasmodics such as hyoscine and, where licensed, generic low-dose tricyclic antidepressants deliver most of the benefit. Gut-directed hypnotherapy and cognitive behavioural therapy require training but can be delivered by primary care clinicians with modest training and are highly cost-effective.
• Treat malnutrition. In settings where parasitic and infectious diarrhoea are common, exclude infection (stool microscopy if possible) and treat malnutrition before finalising the diagnosis of IBS.
• Refer according to alarm features, not according to symptom label. A red flag in a low-resource clinic is the same red flag anywhere.

• IBS is a common, chronic gut-brain interaction disorder with no structural lesion; it does not progress to cancer.
• Rome IV: recurrent abdominal pain at least 1 day per week for the last 3 months, plus at least 2 of (linked to defecation; altered stool frequency; altered stool form), with onset at least 6 months earlier.
• Subtypes (IBS-C, IBS-D, IBS-M, IBS-U) are based on the Bristol stool form scale, using a 25 percent threshold.
• Women and younger people are affected most; anxiety, depression and fibromyalgia are common comorbidities.
• Alarm features (age over 50 at onset, weight loss, bleeding, nocturnal symptoms, anaemia, family history, abnormal examination) redirect investigation.
• Testing should be limited: complete blood count, C-reactive protein, coeliac serology, faecal calprotectin in diarrhoea-predominant disease; colonoscopy for alarm features or age 50 or more.
• Modern practice favours a positive diagnosis (Rome criteria, no alarm features, limited testing) over diagnosis by exclusion, with around 40 percent lower costs in supportive data.
• Management is stepwise and symptom-directed: explanation and reassurance, ispaghula (not wheat bran), a dietitian-supervised low-FODMAP trial, exercise; then loperamide, rifaximin, eluxadoline, alosetron for women with severe disease; PEG, linaclotide, plecanatide, tegaserod or lubiprostone for IBS-C; pain control with antispasmodics, peppermint oil and low-dose tricyclic antidepressants; cognitive behavioural therapy and gut-directed hypnotherapy for refractory disease.
• NNTs of about 6 for soluble (ispaghula) fibre, 5 for antispasmodics and 2.5 for peppermint oil are the best-supported single numbers in the literature.
• Gut-directed psychological therapy belongs in the core pathway for moderate to severe or refractory IBS.

Coeliac disease, inflammatory bowel disease, microscopic colitis, lactose intolerance, bile acid diarrhoea, colorectal cancer, chronic pelvic pain, anxiety and depression, fibromyalgia.