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Irritable Bowel Syndrome

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The pathophysiology of irritable bowel syndrome involves several interconnected mechanisms.

Altered gastrointestinal motility varies by IBS subtype. In IBS with diarrhea, rapid colonic transit results in loose stools, while IBS with constipation features delayed transit, causing straining and hard stools. IBS with mixed alternates between diarrhea and constipation, leading to urgency, bloating, and a feeling of incomplete evacuation.

Dysregulation of the gut-brain axis, the two-way communication system linking the brain and digestive tract through neural, hormonal, and immune pathways, contributes to the disease.

Dysbiosis, or an imbalance in gut microbiota, develops when harmful bacteria outnumber beneficial ones, triggering immune pathways, increasing gas production, and disrupting bowel rhythms.

Visceral hypersensitivity in IBS causes exaggerated responses to normal gut stimuli due to abnormal sensory processing in the peripheral and central nervous systems.

Increased intestinal permeability allows bacteria and toxins to cross the gut barrier, triggering inflammation.

Overview

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Definition

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by recurrent combinations of abdominal pain, bloating, diarrhea, or constipation.

Pathophysiology of irritable bowel syndrome

Its pathophysiology is multifactorial, involving disturbances in motility, sensory processing, microbial balance, barrier integrity, and gut–brain communication. These mechanisms interact to produce symptoms that vary across IBS subtypes.

Altered Motility Patterns

Disordered gastrointestinal motility is a defining feature of IBS. In IBS with diarrhea (IBS-D), accelerated colonic transit leads to loose or frequent stools, often accompanied by urgency. In IBS with constipation (IBS-C), delayed transit results in infrequent bowel movements, straining, and passage of hard stools. IBS with mixed bowel habits (IBS-M) alternates between these two patterns, contributing to bloating, abdominal discomfort, and a persistent sensation of incomplete evacuation.

Gut–Brain Axis Dysregulation

The gut–brain axis, which integrates neural, hormonal, and immune signaling between the central nervous system and gastrointestinal tract, is disrupted in IBS. Stress, emotional states, and altered autonomic regulation can amplify gastrointestinal symptoms by modulating motility, pain perception, and immune responses.

Microbiome Imbalance and Immune Activation

Dysbiosis—an imbalance in gut microbial composition—has been implicated in IBS. Shifts toward pro-inflammatory or gas-producing bacteria may stimulate immune pathways, increase fermentation, and alter bowel patterns. These microbial changes can further disturb motility and contribute to symptom exacerbation.

Visceral Hypersensitivity and Barrier Dysfunction

Visceral hypersensitivity is another key feature, in which normal intestinal stimuli produce exaggerated pain or discomfort because of enhanced sensory signaling in both peripheral nerves and central processing pathways. Increased intestinal permeability, sometimes referred to as a “leaky gut,” allows luminal bacteria and metabolites to cross the epithelial barrier. This promotes low-grade inflammation, which can reinforce hypersensitivity and alter motility.

Collectively, these interconnected mechanisms contribute to the heterogeneous clinical presentation of IBS.

Transcript

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Irritable Bowel Syndrome

Altered Motility Patterns

Visceral Hypersensitivity

Microbiome Imbalance

Intestinal Permeability

Gastrointestinal Motility

Barrier Dysfunction

Immune Activation