Rationale for Investigating Stool Metabolites and Microbiota in Women With Fecal Incontinence

Abstract

Childbirth and its associated neuromuscular injury to the anal sphincter muscles have traditionally been considered as a common cause of fecal incontinence (FI) in women.1 However, the onset of FI is usually after age 50 which is remote from delivery.2 Recent large epidemiologic studies report that bowel symptoms related to gut motility and sensation, such as diarrhea and fecal urgency, are significant contributing factors that are more important than obstetric factors in the pathogenesis of FI.1–3 In these studies examining the association of multiple demographic, obstetric, and gastrointestinal risk factors for FI, the number of fecal urgency episodes per month and diarrhea emerged as risk factors that were most closely associated with FI.1–3 Therefore, investigating mechanisms that worsen fecal urgency and diarrhea could advance our understanding of factors that modulate the severity of FI and its response to treatment. Stool metabolites, produced by the interaction of gut microbiota with the host, can modulate neuro-hormonal mechanisms implicated in gut motility and gut sensation. Several studies show that stool metabolites enhance contractile responses of intestinal smooth muscle and neuronal excitability of the enteric nervous system resulting in symptoms such as diarrhea, fecal urgency, and sense of incomplete emptying that are common in women with FI.4–5 Given that stool metabolites and microbiota are potentially modifiable, understanding the role of these factors in the pathogenesis of FI could provide a paradigm change to its management.