“Leaky Gut,” clinically referred to as increased intestinal permeability, describes a physiological state where the tight junctions between the epithelial cells lining the small intestine become compromised, allowing undigested food particles, toxins, and microbes to pass into the systemic circulation. This breach of the mucosal barrier can trigger a chronic, low-grade inflammatory response throughout the body, potentially contributing to systemic dysfunction, including autoimmune reactions and the disruption of the delicate endocrine balance.
Origin
While long discussed in functional medicine, the scientific understanding of increased intestinal permeability gained rigorous validation through the discovery of zonulin, a protein that modulates the tight junctions. The term “leaky gut” is a descriptive, colloquial term for this underlying pathological process. Its clinical relevance has grown as research connects gut barrier integrity to systemic inflammation and the regulation of the neuroendocrine-immune axis.
Mechanism
The mechanism involves the breakdown of the protective barrier due to factors such as chronic stress, dietary components like gluten or high-fructose corn syrup, and dysbiosis, an imbalance in the gut microbiome. The compromised tight junctions allow the translocation of lipopolysaccharides (LPS) and other antigens, activating the immune system and leading to the release of pro-inflammatory cytokines. This systemic inflammation can then interfere with hormonal signaling, such as thyroid function and insulin sensitivity, disrupting metabolic homeostasis.
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