Leaky Gut Syndrome: Myths and Management

Abstract

Leaky gut syndrome is a condition widely popularized in the lay literature, although it is not currently accepted as a formal medical diagnosis. Multiple gastrointestinal symptoms are ascribed to leaky gut syndrome, including diarrhea, bloating, distension, abdominal pain, and dyspeptic symptoms of early satiety, nausea, and postprandial fullness. The etiology and pathophysiology of leaky gut syndrome are multifactorial; a preceding gastrointestinal infection, inflammatory bowel disease, and certain medications may be relevant factors in some patients. The diagnosis of leaky gut syndrome is problematic. Although patients are frequently informed that the diagnosis can be readily made using results from blood work or stool studies, no validated test currently exists to make this diagnosis. Patients report a variety of myths about the etiology, diagnosis, and treatment of leaky gut syndrome, which can cause alarm and can frequently lead to expensive, unnecessary tests and unproven, sometimes dangerous treatments. This article reviews some of the most common myths about leaky gut syndrome and provides data from the scientific literature to correct these statements. Management strategies, based on data, are provided when available.

Keywords: Bloating; confocal laser endomicroscopy; glutamine; intestinal permeability; leaky gut syndrome; tight junctions.

Figure 1.

Normal gut barrier and disrupted barrier. The intestinal epithelial cells comprise the most important part of the intestinal barrier (A). Above this lies a layer of mucus; plasma cells may secrete IgA into the mucosal layer. Bacteria, viruses, and medications need to penetrate the mucus layer and the epithelial cell barrier to obtain access to the submucosal layer, where the intestinal immune system resides. Small particles normally cannot penetrate the tight junctions. However, after an insult to the epithelial cell barrier (eg, inflammation, ischemia, medications), tight junctions may open, allowing penetration of small particles with access to the submucosal region (B). The adherens junction and desmosomes help to stabilize cell-cell adhesion and interaction with the cytoskeleton. AMPs, antimicrobial peptides; IgA, immunoglobulin A; MLCK, myosin light chain kinase; SCFAs, short-chain fatty acids; ZO1, zonula occludens-1.

Figure 2.

Representative confocal laser endomicroscopy image of the ileum. The intestinal lumen and epithelial lining are labeled. The red arrow indicates a break in the epithelial wall with hyperdense areas along the epithelial lining representing increased fluorescein uptake; leakage of fluorescein into the intestinal lumen is also noted by the red arrow.