This is Part-Two of a series of short articles trying to explain my reactions to wheat, which I deeply love, and help others to: 1) better understand people like me, 2) understand what is going on with their bodies, 3) understand what on earth is going on with our food and bodies and how to change it back.
As you can learn from Part One of this wheat sensitivity series, the usual blood tests my GP prescribed did not suggest I have celiac disease. I had not undergone biopsy, but the praxis here in Sweden is to avoid performing a biopsy in the absence of a positive screening test. So let’s assume that I do not have celiac disease.
Does this mean I am not truly sensitive to gluten? I always (errouneusly) thought that celiac disease had a strong genetic component so, I thought, if I am negative at the screening tests at any given moment, this may mean that I will never be celiac (excluding obviously the possibility of measurement error, to simplify).
Wrong. Celiac disease is not you, it is something that happens to you, and it can actually happen at any time. The genetic aspect of it is well known. Nearly every person who ends up developing celiac disease (about 95% of them) presents with one or both of two genetic variations of the HLA genenes, namely, they have the DQ2 and/or DQ8 haplotype. However, as I now realize, these are merely susceptibility genes.
Celiac disease patients share their disease’s susceptibility genes with a large part of the overall population. More precisely, an impressive 30-40% (on average) of us has the genes that predispose to celiac disease. So why is it often said that celiac disease is genetically determined -making it sound as if most of us are safely not at risk?
It is true that most of those carrying the susceptibility forms of these genes may never develop celiac disease, but to figure out a priori who is who is not as straight forward as I thought. It is nonetheless interesting to notice that, when tested, the majority of non celiac gluten sensitive subjects observed in a recent study had the DQ2 and/or DQ8 genetic variations (preliminary results from Barbara et al presented at the last United European Gastroenterology Week).
According to Fasano‘s group, people with the DQ2 and/or the DQ8 haplotype may produce too much of a protein which causes the “opening” of the gut walls. This protein has been called zonulin and is an analogue of a toxin that is involved in something as scary as… cholera.
Normally, zonulin is an inflammatory protein that helps regulate leakiness in the gut by opening and closing the spaces between cells in the lining of the digestive tract. Zonulin is triggered by harmful bacteria and offers important protection to the body: as nicely put in a previous article on the topic “…if you accidentally eat a food contaminated with salmonella, you rely on zonulin to help trigger diarrhea and flush out the bugs.” That surely is something useful. But it seems that in certain cases zonulin goes bizarre.
Interestingly, besides bacteria in the small intestine (where bacteria should not go), another compound that triggers zonulin is… gluten.
This happens to all of us, Fasano observes. Only, in an healthy gut, the “doors” momentaneusly opened by gluten close again right away and nothing really happens. In celiac disease insetad, these doors opened by gluten stay opened way too long and gluten, as well as other compounds, passes the barrier with the negative consequences we all know (severe gut leakage and tissue alterations).
In people with gluten sensitivity, we probably would observe something in between. The doors would be opened long enough for the immune system to recognize gluten and generate an inflammatory response, but not long enough to have a real leakage of the gut and cause a more permanent damage.
Well, this all makes lots of sense to me. And would explain why I do show clear reactions to gluten itself, not only to wheat in general. Try giving me a seitan* based dish and you will see me cramping (or more likely quickly disappearing) soon after the meal.
*seitan, for the non vegan-savvy, is food made out of gluten -which resembles meat and is indeed protein rich.
To further support the reality of gluten sensitivity in the absence of (yet) overt celiac disease, another recent study (Nutrients 2015 Mar; 7: 1565–1576) compared people with: active celiac disease, celiac disease in remission (due to the exclusion of gluten from the diet), no celiac disease but self-reported gluten sensitivity, and no celiac disease plus no self-reported gluten sensitivity.
OK then: the researchers compared the groups in terms of permeability of the intestine tissue to gliadin (the “bad” part of gluten). With permeability it is meant how much intestinal tissue “opens up” (when it shouldn’t) as a reaction to the ingestion of the gliadin component of wheat gluten, in this case.
Guess which groups were most similar to one another?
Not surprisingly, the non celiac gluten sensitive had the worst permeability scores after the active celiac disease group. The celiac disease group in remission scored lower than the non celiac gluten sensitive group, and their results resembled instead those of people with no celiac disease and no gluten sensitivity. This also confirms that increased permeability occurs in everyone after exposure to gliadin.
OK. So if gluten increases gut permeability in all of us, and in people with gluten sensitivity in particular, it is likely that my gut is truly not that happy when I eat gluten. And this means that while others (and the younger version of me) can tolerate some degree of gut walls stress when ingesting gluten, I can’t any longer. And maybe, if I keep eating gluten, especially if I belong to that large 30-40% of the population with celiac disease susceptibility genes, I may one day develop the full disease. However, I still have hope. Indeed, all this still does not explain:
a) why do I react (differently, but still) also to some foods that do not contain gluten?
b) how come do I have fewer reactions to some wheat varieties rather than to others?
c) finally, if it is true that we have carried these genetic variations since forever, why did not we experience before pandemic adverse reactions to the “stuff of life”, “our daily bread”, “what is accompanied by food” – i.e. the bread of our companatico?
Part Three is on its way. I hope you found here something new and interesting to chew on and please don’t miss the next post, where I will discuss FODMAPs and fructans, my way. And please, join the discussion by leaving a comment and… keep breading –solutions are at hand