Irritable bowel syndrome (IBS) is the most frequently diagnosed gastrointestinal disorder that affects up to 10% of people worldwide and can seriously impact the quality of life. It is characterized by recurring abdominal pain linked to changes in bowel habits.
There is no single cause of IBS, which includes altered gut-brain communication, unbalanced gut microbiota, and a lower threshold for pain in the internal organs (i.e., visceral hypersensitivity). Emerging evidence highlights that intestinal immune activation may explain abdominal pain, bloating, diarrhea, or constipation in a subgroup of patients.
The majority of people with IBS report food-related symptoms, many of whom use exclusion diets for symptom relief. Multiple mechanisms involve food-related symptoms, including immune-mediated and non-immune-mediated reactions, such as gut distension due to undigested carbohydrates attracting water and electrolytes into the small bowel, fermentation-derived gas that lead to colon distention, chemical reactions, and fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) driving mast cell activation via lipopolysaccharide, a key component of some gut bacteria’s outer membrane, which in turn leads to colonic barrier loss.
While the low FODMAP diet is the most researched diet for IBS, there is no one-size-fits-all diet for IBS, and non-dietary strategies should also be considered on an individualized basis.
April is IBS Awareness Month, an opportunity to raise awareness of this common, misunderstood, vexing condition.
We invite everyone to join our awareness campaign by sharing the infographic below on the role of immune activation in IBS and available science-backed dietary interventions for symptom management.
References:
- Singh P, Grabauskas G, Zhou SY, et al. High FODMAP diet causes barrier loss via lipopolysaccharide-mediated mast cell activation. JCI Insight. 2021; 6(22):e146529. doi: 10.1172/jci.insight.146529.
- Ford AC, Staudacher HM, Talley NJ. Postprandial symptoms in disorders of gut-brain interaction and their potential as a treatment target. Gut. 2024; 73(7):1199-1211. doi: 10.1136/gutjnl-2023-331833.