Here is a small compilation about intestinal permeability (IP). In fact I will knock you down with this study right at the beginning. It seems that viruses like HIV (so maybe XMRV too) induce IP and antiviral therapy cures it: PMID: 18936106 CONCLUSIONS: Suppressive HAART abrogates HIV-induced intestinal barrier defect and villous atrophy. The HIV-induced barrier defect is due to altered tight junction protein composition and elevated epithelial apoptoses. Mucosal cytokines are mediators of the HIV-induced mucosal barrier defect and villous atrophy. The following study is from 1994. Can you imagine that? These scientists are probably 20 years ahead of their colleagues. If you tell a doctor about leaky gut he will likely think that you are mental case. The doctors today know nothing. They don't know anything about reactivating viral infections nor do they know anything about leaky gut and the consequences for so many diseases. Neonatal babies (up to the fourth week of life) seem to have an increased intestinal permeability because the digestive tract still has to develop. These scientists took a look at it and come to the conclusion: Evidence exists that the increased uptake of intact food proteins in early infancy could play a role in the development of various clinical disorders, including food allergy, coeliac disease and pancreatic insufficiency, but this uptake might also be important for the normal development of oral tolerance. IP plays a role in milk allergy. Intestinal permeability is thought to play a role in the pathophysiology of cow's milk allergy. Furthermore, it is a common diseasein early infancy, often the first presentationo f the atopic syndrome. In the first study,(chapter3 .2) we showedt hat intestinal permeability as measuredb y the SAT, increasesd uring cow's milk challengei n infants with clinically positive cow's milk challengesc omparedt o children with clinically negativec ow's milk challenge Then they found out that IP is increased in celiac patients AND to some lower degree in many relatives. After that they looked at pancreatic insufficiency and found out the following: We measured intestinal permeability in rystic fibrosis- and nonrystic fibrosis patients with pancreatic insufficienry and found that intestinal permeability was increased in both groups. In rystic fibrosis patients, we found that intestinal permeability did not changeb y increasingp ancreatice nzFmes upplementationb y 30-50o/ofo r 2 weeks, nor by decreasing the osmolarity of the test solution of the SAT by 75o/oW. e conclude that an increased intestinal permeability in cystic fibrosisis probably a consequence of pancreatic insufficienry, and is not related to the dose of pancreatic enzyme supplementation nor the osmolarity of the test solution. The increase is due to an increased permeability for lactulose which might point towards a defect in the tight junctions of the villi and/or the crypts. http://dissertations.ub.rug.nl/FILE.../r.m.van.elburg/The_Sugar_Absorption_Test.PDF Another study: http://www.springerlink.com/content/e463k422t2116154/ A defective skin barrier and increased intestinal permeability appear to facilitate allergen sensitization. A new study that links intestinal permeability to atopic disease. The researchers concluded: "Atopic patients had increased intestinal permeability and density of IgE-bearing cells compared with non-atopic patients, but gastrointestinal symptoms did not differ between groups." http://www.pharmacynews.eu/hospital...dical-department-target-serine-endopeptidases Next, viral connections: PMID: 20386714 Collectively, our data shows that mucosal epithelial cells respond directly to envelope glycoprotein of HIV-1 by upregulating inflammatory cytokines that lead to impairment of barrier functions. The increased permeability could be responsible for small but significant crossing of mucosal epithelium by virus and bacteria present in the lumen of mucosa. This mechanism could be particularly relevant to mucosal transmission of HIV-1 as well as immune activation seen in HIV-1 infected individuals. PMID: 19372990 In addition HIV infection of humans and SIV-infection of rhesus macaques are characterized by enteropathy and increased intestinal permeability. Some not so good news: PMID: 19732776 CONCLUSIONS: HIV PIs induce ER stress and activate the unfolded protein response in intestinal epithelial cells, thus resulting in disruption of the epithelial barrier integrity. Is this a direct connection to HHV-6/7? PMID: 17570213 LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for herpes virus entry on T cells) is a tumor necrosis factor core family member that regulates T-cell activation and causes experimental inflammatory bowel disease. ... T cell-derived LIGHT activates intestinal epithelial LT beta R to disrupt barrier function. This requires MLCK activation and caveolar endocytosis. These data suggest a novel role for LIGHT in disease pathogenesis and suggest that inhibition of MLCK-dependent caveolar endocytosis may represent an approach to restoring barrier function in inflammatory bowel disease. Thank you for reading this.