In my almost 10 years of being gluten free I have made countlessly attempts to attest to the actual east of a GF lifestyle. Although, I believe it is fairly simple, most people tend not to get past the no bread for their sandwiches part. Their blank expression screams "you lost me at no bread." The other expression I get is as if they are giving me the 5 year olds response in the heads "LALALALALA I'm not listening!" Fortunately adults have learned that the act of actually covering their ears whilst someone speaks is inappropriate. Nevertheless, I can see the desire to resort to this when I explain how gluten affects the system.
You can cover your eyes if this starts to have the previously explained effect on you.
Here it is...
Gluten is a molecule contained in wheat, rye, barley and through cross-contamination on oats. The offending protein in gluten is called gliadin. This gliadin is further dissected into several areas that all have very separate effect on the gastrointestinal tract depending on genetic expression.
What does that mean for you? This stupid little molecule can exacerbate any inflammatory condition in the body. This is a non-discriminatory statement. Meaning you do not have to have celiac or gluten sensitivity to be affected by gluten. Gliadin, the offending protein in gluten, causes an initial insult at the intracellular tight junctions located on the luminal side of the intestine. These tight junctions are responsible for maintaining the integrity of the intestinal wall and keeping out macromolecules. Gliadin binds with CXCR3, a chemokine receptor responsible for leukocyte recruitment and eventually involvement of T-helper cells. Lammers and colleagues (2008) reported a higher concentration of CXCR3 in the gut epithelium of those with celiac disease as compared to those without.
CXCR3 recruits myD88, an adaptor protein, allowing the release of zonulin to the apical side of the epithelium (Lammers et al. 2008, Clemente et al. 2003). Zonulin, in celiac, is responsible for the changes in cellular structure and arrangement of the cytoskeleton which allows for increased gut permeability. Interestingly, in non-celiac intestinal epithelium, zonulin strengthens the tight junctions (Drago et al. 2006). While both celiac and non-celiac tissue reacted to gliadin, only the celiac epithelial membrane up-regulated the production of the mRNA for CXCR3 gene expression at a 9.6 fold increase. When gliadin was removed, the expression of the CXCR3 in the tissues of celiac patients decreased to what was seen in those without celiac disease (Lammers et al. 2008). It is important to note that CXCR3 is expressed in several other cells including natural killer cells, and CD3+/CD8+ T cells which could account for the instigation of the innate immune response associated with celiac disease. In addition, toll like receptors, which are also responsible for innate immune response, have been reported to be increased in the duodenum of children with celiac as compared to healthy controls (Szebeni et al. 2007).
Tight junctions in the epithelial wall are critical for maintaining the integrity of the gut. The increased permeability seen in celiac disease appears to be associated with the onset of other autoimmune disorders (Drago et al. 2006, Sapone et al. 2006, and Watts et al. 2005). Although, I would not be surprised if it was a bit more chicken and egg-ish.
If you are suffering from any autoimmune disorder gluten is probably one of the most detrimental pieces of the puzzle. Stop eating gluten and you can begin to heal depending on the amount of damage done.
If you do not have an autoimmune disorder gluten is your russian roulette for one.
Gluten causes intestinal permeability changes in celiacs and non-celiacs alike.