At the United European Gastroenterology Week 2015 in Barcelona, Spain, Dr. Giovanni Barbara from the University of Bologna reported exciting new findings concerning so-called non-celiac gluten-sensitivity, NCGS, and irritable bowel syndrome, IBS.
They studied the blood levels of zonulin protein in each of these conditions and in celiac disease. Readers of the Wheat Belly books may recall that Dr. Alessio Fasano and his team, while working at the University of Maryland, deciphered the complex pathway by which the gliadin protein of wheat, rye, and barley triggers release of zonulin protein into the blood. Zonulin also plays a crucial role in modulating intestinal permeability and initiating autoimmune conditions such as rheumatoid arthritis, type 1 diabetes, and multiple sclerosis, and may also play a role in triggering asthma. Higher levels of zonulin protein in the bloodstream suggest increased levels of abnormal intestinal permeability and greater potential for an autoimmune condition. It also suggests that the gliadin protein of grains underlies this effect, since so few other factors increase zonulin levels.
By measuring the blood levels of the zonulin protein as a marker for the degree of intestinal permeability, Barbara and his team found that the highest zonulin levels were found in the people with celiac disease (0.033 ng/mg), levels in people with NCGS (0.030 ng/mg) were only slightly less, and lower in IBS (0.012 ng/mg). The mean level in healthy volunteers with none of these conditions was 0.007 ng/mg. It means that the level of abnormal intestinal permeability triggered by the gliadin protein is nearly identical in people with celiac disease and NCGS. It also means that people with IBS do not just have a “functional” disorder, i.e., a condition with symptoms but no identifable abnormality, but do indeed have some degree of abnormal intestinal permeability over and above that of people without IBS.
Oddly, though not surprisingly, Dr. Barbara stated: “Hopefully, our work will lead to new diagnostic and therapeutic strategies for patients with these and possibly other autoimmune conditions.” In other words, measuring zonulin levels in other conditions may turn up abnormal levels of intestinal permeability in those conditions, as well, and that opportunities may open for new drug development.
If you ask me, if the whole mess was started by ingesting the gliadin protein of wheat, rye, and barley, well, why not just stop eating wheat, rye, and barley?
By the way, the above graphic is an illustration showing the structure of the gliadin protein and what Dr. Fasano calls “gliadin motifs” that are responsible for its varied and destructive effects: Mapping of α-gliadin motifs exerting cytotoxic activity (red), immunomodulatory activity (light green), zonulin release and gut-permeating activity (blue), and CXCR3-IL-8 release in CD patients (dark green). It’s a darned nasty protein with a host of health-damaging effects not restricted to celiac disease, but a protein we are told to eat more of every meal, every day.