Irritable Bowel Syndrome

❍ At a glance

• IBS is a clinical diagnosis using Rome IV criteria: recurrent abdominal pain at least one day per week for three months, associated with a change in bowel frequency or form, and pain linked to defaecation.¹ No test diagnoses it - investigation is to exclude mimics (coeliac, IBD, thyroid disease).
• Red flags requiring investigation before attributing to IBS: rectal bleeding, unexplained weight loss, symptoms consistently waking from sleep, family history of bowel cancer or IBD, and new onset after age 50.
• CBT and gut-directed hypnotherapy have strong evidence and are considered first-line options in NICE guidelines⁷ - offer these actively, not as a last resort. Low FODMAP diet has the strongest dietary evidence; works best with FODMAP-trained dietitian guidance.
• Low-dose tricyclics (amitriptyline) are used for visceral hypersensitivity and slow gut transit (IBS-D) - not primarily for mood. Antispasmodics for cramping. Osmotic laxatives for IBS-C.

❍ Patient information

This section is written in patient-friendly language and can be used as a basis for consultation or directed reading.

Irritable bowel syndrome is one of the most common conditions a GP sees - and one of the most misunderstood. It is not dangerous, and it does not lead to bowel cancer. But it can be genuinely disruptive to daily life.

What is IBS? IBS is a functional gut disorder. The bowel looks completely normal on any scan or scope, but does not work the way it should - contractions are poorly regulated, and the gut becomes more sensitive to sensations that most people would not notice. IBS is split into IBS with predominant constipation (IBS-C), IBS with predominant diarrhoea (IBS-D), and mixed IBS (IBS-M). Subtype matters because it shapes treatment.

Why does it happen? IBS is best understood as the result of several overlapping problems: disruption of the gut-brain axis (the two-way signalling between the gut's own nervous system and the brain), visceral hypersensitivity (lower pain thresholds in the gut, measurable but not visible on imaging), altered gut motility (faster in IBS-D, slower in IBS-C), and sometimes post-infectious triggers (roughly 10% of people develop IBS after gastroenteritis⁴). Stress, anxiety, and mood do not cause IBS in the way that a germ causes an infection - but they amplify symptoms considerably through this gut-brain connection.

What helps? IBS is manageable for most people, usually requiring a combination of approaches. Diet: low FODMAP (temporary restriction of fermentable carbohydrates) has the strongest evidence⁵ - works best with a dietitian, as it is easy to do incorrectly. Soluble fibre (oats, linseeds, psyllium) tends to help; insoluble fibre (wheat bran) can worsen symptoms. Lifestyle: regular physical activity⁶ and good sleep are core - not optional extras. Psychological therapies: gut-directed CBT and hypnotherapy are first-line in NICE guidelines⁷ and work by retraining gut-brain pathways. Medications: antispasmodics for cramping; low-dose tricyclics (amitriptyline) for visceral hypersensitivity and IBS-D; osmotic laxatives for IBS-C; loperamide for urgency and diarrhoea.

Long-term prognosis: IBS is chronic but variable - symptoms wax and wane, flare-ups are common, and a meaningful proportion of people improve significantly over years, particularly with dietary and psychological engagement. It does not progress to IBD or bowel cancer and does not shorten life expectancy.

On the gut-brain connection: when a GP mentions that stress plays a role, some patients hear "you are making it up." That is not what is being said. The gut produces roughly 95% of the body's serotonin. The vagus nerve carries far more information upward from gut to brain than downward. Treating the nervous system is treating the gut. The two are not separate.