11.1 : Irritable Bowel Syndrome I: Introduction

Irritable Bowel Syndrome (IBS) is characterized by functional disturbances in the gastrointestinal system, presenting a cluster of symptoms without evident structural or biochemical abnormalities. It primarily affects the large intestine and may cause abdominal pain, bloating, excessive gas, diarrhea, constipation, or both.

IBS is a chronic condition that can persist over a long period or recur frequently.

The pathogenesis of IBS involves a complex interplay of the following factors:

Altered Gut Motility:

1. Gastrointestinal Muscle Dysfunction: Abnormal contractions of the gastrointestinal tract muscles can disrupt the coordinated movement of food through the digestive system. This dysregulation may result in rapid transit times, leading to diarrhea, or sluggish movements, causing constipation.
2. Enteric Nervous System Involvement: The enteric nervous system regulates gut motility. Dysfunction in this system can contribute to irregular muscle contractions, exacerbating IBS symptoms.

Visceral Hypersensitivity:

1. Nociceptive Receptor Activation: Sensory receptors in the gut wall, known as nociceptive receptors, become more sensitive in individuals with IBS. This heightened sensitivity can cause normal or mildly uncomfortable stimuli to be perceived as painful, contributing to abdominal pain and discomfort.
2. Central Sensitization: Chronic activation of nociceptive pathways can lead to central sensitization, where the brain becomes more responsive to visceral stimuli. This amplification of signals may further intensify the perception of pain.

Neurotransmitter Imbalances:

1. Serotonin Dysregulation: Serotonin, a neurotransmitter found in the gut, is crucial for regulating bowel function. Imbalances in serotonin levels or receptor sensitivity can disrupt the intricate balance of gut-brain communication, influencing mood and gastrointestinal function. Other neurotransmitters, such as gamma-aminobutyric acid and dopamine, also play critical roles in the interaction between the nervous system and the gut in individuals with IBS.

Gut Microbiota:

1. Microbial Diversity: Changes in the diversity and composition of the gut microbiota can impact gut health. Dysbiosis, an imbalance in the microbiota, may affect food processing, produce gas, and contribute to inflammation, all of which can exacerbate IBS symptoms.
2. Microbial Metabolites: Metabolites produced by microbes, such as short-chain fatty acids, can influence gut motility and immune responses. Alterations in these metabolites may contribute to the pathogenesis of IBS.

Other Factors:

1. Genetic Factors: While the exact genetic components of IBS are not fully understood, there is evidence of a genetic predisposition, suggesting that specific individuals may be more susceptible to developing IBS based on their genetic makeup.
2. Inflammatory Processes: Low-grade inflammation within the intestines can contribute to the manifestation of IBS symptoms. Various factors, including infections or immune system dysregulation, may trigger this inflammation.
3. Food Intolerance: Certain food triggers, such as specific carbohydrates and FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), can induce symptoms in susceptible individuals by influencing gut fermentation and gas production.
4. Stress and the Gut-Brain Axis: Stress and emotional factors can impact the gut-brain axis bidirectionally. Stress can exacerbate IBS symptoms; conversely, gastrointestinal symptoms can induce stress, creating a feedback loop.