Antibiotics (Basel, Switzerland)Aug 27, 2026

Antibiotic Use May Increase the Risk of Irritable Bowel Syndrome

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Aug 28, 2026

Abstract

A consistent, dose-dependent relationship exists between cumulative antibiotic courses and an elevated risk of developing irritable bowel syndrome (IBS).

Antibiotic-induced microbial depletion may act as a predisposing factor for incident IBS.
The review highlights that broad-spectrum antibiotics are particularly associated with increased IBS risk, independent of previous acute gut infections.
Systemic antibiotics could lead to lasting changes in gut bacteria diversity, known as dysbiosis.
Dysbiosis may trigger a cascade of effects, including damage to the gut lining, chronic low-level inflammation, and changes in bile acid processing.
These disruptions might contribute to increased sensitivity in the gut and irregular bowel movements through the gut-brain connection.
Antibiotic exposure is suggested as a significant, modifiable risk factor for IBS, highlighting the need for careful antibiotic use.

Simplified

The intricate interplay between the gut microbiome and the enteric nervous system remains a paramount focus in understanding the multifactorial pathogenesis of disorders of gut-brain interaction (DGBI), most notably irritable bowel syndrome (IBS). While the clinical entity of post-infectious IBS is well-established, the independent, long-term pathophysiological impact of iatrogenic antibiotic exposure is garnering critical attention within neurogastroenterology. This narrative review provides a comprehensive synthesis of current epidemiological and mechanistic evidence positioning antibiotic-induced microbial depletion as a potential predisposing factor for incident IBS. By evaluating recent literature, we highlight epidemiological trends demonstrating a consistent, dose-dependent relationship between cumulative antibiotic courses, particularly broad-spectrum agents, and an elevated risk of developing IBS, independent of prior acute enteric infections. Furthermore, we explore the mechanistic underpinnings of this association, focusing on how systemic antibiotics induce persistent, detrimental alterations in commensal diversity. This resulting dysbiosis initiates a proposed cascade of downstream consequences, including compromised epithelial barrier integrity, persistent low-grade mucosal inflammation, and altered bile acid metabolism. These localized disruptions serve as established triggers for visceral hypersensitivity and dysregulated gastrointestinal motility communicated via the gut-brain axis. Ultimately, this review underscores that antibiotic exposure may act as a significant, modifiable risk factor for IBS pathogenesis. Recognizing this substantial iatrogenic risk reinforces an urgent clinical imperative for stringent antimicrobial stewardship and emphasizes the necessity for future research directed toward prophylactic, microbiome-sparing strategies to mitigate the escalating global burden of DGBIs.