IBS (Irritable Bowel Syndrome)

Irritable bowel syndrome is the most common gastrointestinal diagnosis in the world, and the framing has changed substantially. It was once described as functional, implying nothing was wrong. It is now classified as a disorder of gut-brain interaction, with identifiable abnormalities in visceral sensitivity, motility, immune activation and microbial composition. Diagnosis is positive, not a diagnosis of exclusion. The Rome IV criteria require recurrent abdominal pain at least one day per week over three months, associated with two or more of: defaecation, a change in stool frequency, or a change in stool form. Subtypes are defined by predominant stool pattern — IBS-D (diarrhoea), IBS-C (constipation), IBS-M (mixed) and IBS-U (unclassified) — and subtype drives treatment choice. Limited testing is still required. Coeliac serology should be checked in everyone, along with a full blood count, CRP and faecal calprotectin to exclude inflammatory bowel disease. In diarrhoea-predominant cases, bile acid malabsorption is a frequently missed cause affecting perhaps a quarter and treatable with a bile acid sequestrant. Alarm features — bleeding, weight loss, onset after 50, family history of bowel cancer or IBD, nocturnal symptoms — require investigation. Visceral hypersensitivity is the central mechanism: people with IBS perceive normal degrees of gut distension as painful, demonstrated repeatedly with balloon distension studies. This explains why the same volume of gas that goes unnoticed in one person causes significant pain in another, and why treatments targeting perception — hypnotherapy, certain antidepressants — work as well as they do. The evidence base for treatment is better than its reputation suggests. A supervised low-FODMAP diet improves symptoms in around 70%; gut-directed hypnotherapy achieves comparable response rates; enteric-coated peppermint oil has consistent trial support for pain.

• •Recurrent abdominal pain related to defaecation
• •Bloating and visible abdominal distension that worsens across the day
• •Diarrhoea, constipation or alternation between them
• •Urgency, particularly in the morning or after eating
• •Sense of incomplete evacuation
• •Mucus in the stool
• •Symptoms that improve after passing a stool
• •Fatigue and poor sleep, both commonly associated

• •Visceral hypersensitivity — heightened perception of normal gut signals
• •Altered gut motility
• •Post-infectious onset after gastroenteritis, accounting for around 10% of cases
• •Altered gut microbiota composition
• •Low-grade mucosal immune activation and mast cell involvement
• •Disrupted gut-brain axis signalling
• •Psychological stress, anxiety and a history of adverse life events
• •Food intolerances, particularly to fermentable carbohydrates
• •Genetic predisposition in a minority

IBS is a heterogeneous condition with several mechanisms that vary in importance between patients, which is why no single treatment works for everyone. Visceral hypersensitivity is the most consistently demonstrated abnormality. Rectal balloon distension studies show that people with IBS report pain at significantly lower volumes than controls, and functional imaging shows amplified processing of gut signals in pain-related brain regions. This is a real, measurable difference in signal processing rather than an imagined symptom. Post-infectious IBS provides the clearest causal model. Around 10% of patients develop symptoms after an episode of bacterial gastroenteritis, with risk related to the severity and duration of the initial infection. Persistent low-grade mucosal inflammation and altered enteroendocrine cell populations follow, sometimes for years. Fermentable carbohydrates act as a trigger rather than a cause. FODMAPs are poorly absorbed, osmotically active, and rapidly fermented, producing gas and luminal distension. In someone with normal visceral sensitivity this is unnoticeable; in someone with hypersensitivity it produces pain. This is why FODMAP restriction reduces symptoms without addressing the underlying sensitivity — and why the reintroduction phase matters, since permanent restriction harms the microbiome without treating anything. The gut-brain axis operates bidirectionally. Stress alters motility, permeability and pain perception through the HPA axis and autonomic pathways, and gut signals in turn influence mood — which is why psychological therapies produce genuine gastrointestinal improvement rather than merely helping people cope.