Intestinal permeability
Evidence of impaired intestinal permeability: Leaky Gut Syndrome
If intestinal colonisation is abnormal, the intestinal flora is only able to fulfil its physiological tasks to a limited extent. The resulting disorder of the microbial barrier ultimately results in pathomechanisms that lead to latent inflammatory changes of the mucosa with subsequent permeability disorders. This makes it easier for pathogenic bacteria, viruses, fungi or parasites to gain access to mucosal receptors in the context of microecological disorders, and to multiply more quickly and therefore trigger infections more easily. Depending on the germ species, the microbial metabolism ultimately produces either substrates that are useful for the intestinal environment or that damage the system in many ways. A loosening of the “tight junctions” of the intestinal epithelium results in an increased permeability of the mucosa, also known as Leaky Gut. Many molecules can therefore enter the bloodstream from the gastrointestinal area and trigger various reactions.
Enterotoxins are of particular importance. This molecule, also known as lipopolysaccharide (LPS), originates from the surface of gram-negative bacteria and serves as an inflammatory marker. If the blood is chronically overloaded with LPS, this can lead to silent inflammation and, due to the constant inflammatory situation, may promote other diseases, such as metabolic syndrome, obesity, type 2 diabetes or arteriosclerosis. The LPS concentration in the blood can be determined directly by laboratory diagnostics. The protein zonulin binds to specific receptors in the intestinal wall epithelial cells and therefore activates a cascade of biochemical events that induce the opening of tight junctions and increase the permeability of the intestinal epithelial cells. Patients with active coeliac disease show elevated concentrations of zonulin and zonulin antibodies. Many coeliac patients also suffer from other autoimmune diseases, such as insulin-dependent diabetes, multiple sclerosis and rheumatoid arthritis. Increased zonulin levels are believed to be a decisive factor.