Irritable Bowel Syndrome — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Irritable bowel syndrome (IBS) is a chronic functional disorder of the gut-brain axis, characterised by recurrent abdominal pain associated with a change in bowel habits, without demonstrable structural or biochemical abnormality. It is the most common gastrointestinal disorder worldwide, affecting 10-15% of adults — over 500 million people — and is twice as prevalent in women. IBS is not life-threatening but causes significant morbidity and impairs quality of life, with many patients experiencing worse quality of life scores than those with organic GI conditions. It is classified into subtypes by predominant bowel habit: IBS with constipation (IBS-C), IBS with diarrhoea (IBS-D), IBS with mixed bowel habits (IBS-M), and IBS unclassified (IBS-U). The condition involves abnormal gut-brain interactions, visceral hypersensitivity (lower pain threshold in the colon), altered gut motility, gut microbiome dysbiosis, and psychological comorbidities — not simply 'in the mind' but a genuine disorder of gut physiology and neural signalling.

The aetiology of IBS is multifactorial and not fully elucidated. Key mechanisms: gut-brain axis dysregulation — abnormal bidirectional signalling between enteric and central nervous systems mediated by serotonin (90% of body's serotonin is in the GI tract), GABA, and substance P; visceral hypersensitivity — colonic afferent neurons have a lower activation threshold, causing pain at normal gut distension pressures; altered gut motility — accelerated (IBS-D) or slowed (IBS-C) intestinal transit; gut microbiome dysbiosis — altered composition and reduced diversity; post-infectious IBS (PI-IBS) — develops in 10-25% of patients after acute gastroenteritis (Campylobacter, Salmonella, Shigella — release cytokines and alter mucosal permeability); food sensitivities — FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) cause osmotic fluid retention and gas fermentation in susceptible patients; low-grade mucosal inflammation and increased intestinal permeability. Psychological risk factors: depression, anxiety, and trauma (childhood adversity, sexual abuse) are strongly associated — the gut-brain axis transmits stress signals bidirectionally. Risk factors: female sex, age 18-40, anxiety and depression, antibiotic use (alters microbiome), acute enteric infection, and dietary triggers.

IBS is diagnosed clinically using Rome IV criteria (2016): recurrent abdominal pain for at least 1 day per week in the last 3 months (with onset at least 6 months prior), associated with 2 or more of: related to defecation; associated with change in stool frequency; associated with change in stool form/appearance. Subtypes defined by Bristol Stool Chart: IBS-D (predominant loose/watery stools — types 6-7); IBS-C (predominant hard/lumpy stools — types 1-2); IBS-M (both). Bloating and abdominal distension — extremely common; particularly severe in the evening. Excessive flatulence. Mucus in stools — common, not blood. Symptoms typically worsen with stress, anxiety, menstruation, and specific foods (wheat, dairy, onions, garlic, pulses). Symptoms that improve with defecation are characteristic. Complete resolution of symptoms for periods is common — variable day-to-day severity. IBS does NOT cause: rectal bleeding, systemic symptoms (fever, weight loss), symptoms waking from sleep, or family history of IBD or bowel cancer — these are red flags requiring investigation.

IBS is a positive clinical diagnosis based on Rome IV criteria in patients without red flags — not a diagnosis of exclusion requiring exhaustive testing. NICE recommends a specific diagnostic approach. Required blood tests: FBC (anaemia), CRP and ESR (inflammatory bowel disease), coeliac antibodies (tTG-IgA — coeliac disease in 1-2% of 'IBS'), thyroid function. Calprotectin (stool marker): faecal calprotectin below 50 mcg/g suggests IBS rather than IBD (negative predictive value 89-96%); elevated calprotectin warrants colonoscopy referral. Stool culture only if acute onset diarrhoea after travel or suspected infection. Red flags requiring further investigation (colonoscopy referral): rectal bleeding; weight loss; nocturnal symptoms; onset above age 60; family history of colorectal cancer or IBD; rising CRP/calprotectin. Colonoscopy is NOT routinely required to diagnose IBS in younger patients without red flags. IBS-D should prompt assessment for SIBO (small intestinal bacterial overgrowth) with glucose hydrogen breath test or empirical rifaximin in selected cases. Anorectal physiology/biofeedback assessment for refractory constipation.

IBS management is stepped and personalised, addressing diet, gut-directed pharmacotherapy, and psychological treatment. Dietary interventions: low-FODMAP diet (King's College London protocol — 3 stages: elimination of all high-FODMAP foods for 4-8 weeks; reintroduction phase; personalisation) — reduces symptoms in 50-80% of patients; requires RD dietitian guidance. Soluble fibre (psyllium/ispaghula husk) for IBS-C and global symptoms; avoid insoluble fibre (bran) which worsens bloating. Peppermint oil capsules (Colpermin, IBgard): antispasmodic effect on colonic smooth muscle; effective for abdominal pain and bloating; number needed to treat approximately 5. Antispasmodics: mebeverine hydrochloride 135 mg TDS (smooth muscle relaxant); hyoscine butylbromide 20 mg as required; alverine citrate with simethicone (Spasmonal). For IBS-C: osmotic laxatives (polyethylene glycol/Movicol); linaclotide 290 mcg before breakfast (guanylate cyclase C agonist — reduces visceral hypersensitivity and accelerates transit — NICE recommended); prucalopride (5-HT4 agonist) for severe IBS-C. For IBS-D: loperamide (first-line antidiarrhoeal); rifaximin 550 mg TDS for 14 days (non-absorbable antibiotic — targets gut microbiome and SIBO — FDA approved for IBS-D, not NICE); alosetron (5-HT3 antagonist — US only, restricted use). Antidepressants: tricyclic antidepressants (amitriptyline 10-30 mg nocte) — first-line for pain-predominant IBS (analgesic properties at sub-antidepressant doses — NICE/BNF recommended); SSRIs (sertraline, citalopram) for IBS-D if depression/anxiety co-exists. Psychological therapies: CBT, gut-directed hypnotherapy (proven to reduce IBS symptom severity score by 50%+ in randomised trials), mindfulness-based CBT — NICE-recommended for inadequate response to 12 months of pharmacotherapy.

IBS does not cause structural damage or increase colorectal cancer risk, but it carries significant health and psychosocial consequences. Anxiety and depression are the most common comorbidities, affecting 50-90% of patients with moderate-to-severe IBS — the gut-brain axis creates a bidirectional cycle where psychological distress and gut symptoms each worsen the other. Chronic pain sensitisation (central sensitisation) develops in longstanding IBS, causing hypersensitivity to both visceral and somatic pain stimuli. Sleep disorders (insomnia, non-restorative sleep) affect approximately 50% of IBS patients and independently worsen symptom severity. Significant occupational and social impairment: IBS causes substantial absenteeism, reduced productivity, and social withdrawal from fear of symptoms in public. Fibromyalgia, chronic fatigue syndrome, interstitial cystitis, and temporomandibular disorder cluster with IBS through shared central sensitisation mechanisms. Misdiagnosis risk: IBS symptoms overlap with IBD, coeliac disease, and colorectal cancer — a missed serious diagnosis is possible when red flags are not appropriately investigated. Opioid-induced constipation or narcotic bowel syndrome develops from inappropriate opioid prescribing for IBS abdominal pain — an iatrogenic complication that is difficult to reverse.

Regular meals at consistent times (avoid skipping); adequate dietary fibre from soluble sources (oats, linseeds, psyllium); adequate hydration (1.5-2L fluid daily). Exercise: aerobic exercise significantly reduces constipation and improves IBS symptoms overall (evidence from multiple RCTs — 30 minutes, 5x weekly). Stress management is critical — the gut-brain axis means psychological stress directly triggers IBS flares; yoga, mindfulness, and relaxation techniques reduce flare frequency. Probiotic supplements: Lactobacillus and Bifidobacterium strains (e.g., VSL#3, Symprove, Alflorex) reduce global IBS symptom scores by 20-25% in meta-analyses — NICE recommends trying a single strain probiotic for at least 4 weeks. Avoid antibiotic overuse (disrupts gut microbiome). Keep a food and symptom diary to identify personal dietary triggers — common triggers include: alcohol, caffeine, spicy food, carbonated drinks, fatty foods, and high-FODMAP foods (wheat, milk, onions, garlic, apples, stone fruits).

Seek urgent GP assessment (within days) or attend A&E for: rectal bleeding (blood in stools is NOT a feature of IBS); unexplained weight loss alongside bowel symptoms; onset of symptoms above age 60 (higher risk of colorectal cancer); severe abdominal pain not relieved by defecation; any new bowel symptoms in someone with a family history of bowel cancer or IBD. See your GP for: new onset IBS symptoms not previously investigated (require blood tests and faecal calprotectin at minimum); symptoms significantly worsening or changing character; nocturnal diarrhoea or pain that wakes you from sleep (not a feature of IBS). The following symptoms are NOT typical of IBS and require investigation: fever, joint swelling, skin rashes alongside GI symptoms (consider IBD); pale fatty stools (consider malabsorption); persistent vomiting.