Zonulin levels are increased in celiac disease. However, chronic gluten (gliadin) exposure also affects zonulin in non-celiac intestine. The result is an increased gut permeability (or leaky gut). Just published in Gut is an article reporting abnormal claudin proteins result in patchy loss of barrier function or tight junctions (leaky gut) in active Crohn’s disease. Drago et al published a report in the Scandinavian Journal of Gastroenterology in April 2006 that transient zonulin release could be triggered by exposure to gliadin even in normal intestine. An increase in intestinal permeability was noted in normal intestine though it was not as pronounced as in celiac disease patients. Intestinal tissue from celiac patients, even those in remission, exposed to gliadin demonstated a sustained increase in zonulin release resulting in significant and sustained increased intestinal permeability. Zonulin affects expression of the proteins claudin and occludin that constitute the cytoskeleton between intestinal epithelial cells that maintain the tight junctions or zonula occludens. There is increasing scientific research indicating that an altered intestinal barrier with increased intestinal permeability is important in the development of celiac disease, inflammatory bowel disease, and possibly even irritable bowel syndrome.
Research is also revealing that altered gut permeability or leaky gut may be present in “normal” people and/or when the intestinal biopsy appears normal. Gluten can trigger this in the intestine of normal people and early celiac disease. When altered gut microflora or dysbiosis (bacteria and/or yeast) in a genetically predisposed person during altered immune states such as during pregnancy, post-pregnancy, surgery, puberty or periods of severe stress, may activate latent celiac disease or trigger inflammatory bowel disease. In some new onset or more severe IBS may develop, especially after a bowel infection such as viral gastroenteritis or dysentery.
Altered gut flora from antibiotics, including those in provided to animals from which we get meat, milk or eggs are also likely contributing as well as our cleaner environment. This effect is becoming known as the hygiene effect that is theorized as possible cause for increasing incidence of Crohn's disease and autoimmune disorders occurring in well developed countries. Co-existing gut injury from non-steroidal anti-inflammatory drugs (NSAID) like ibuprofen, motrin, or advil also appears to be a risk factor. The use of acid blockers, recently reported to increase the risk of osteoporosis, may also adversely impair breakdown of food proteins and predispose to abnormal gut bacterial or yeast levels increasing the risk of gut injury resulting in the leaky gut. For regular updates from this blog subscribe. Forward this blog to friends and family via e-mail by clicking on the letter icon below.
References:
Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Drago, S et al. Scand J Gastroenterol. 2006; 41(4): 408-419
Inflammatory bowel disease: Is it really just another break in the wall? Weber, CR and Turner, JR. Gut 2007; 56(1): 6-8
Changes in expression and distribution of claudin 2,5, and 8 lead to discontinuous tight junctions and barrier dysfunction in active Crohn’s disease. Zeissig S. et al. Gut 2007; 56(1): 61-72
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