About a week ago, some of the research into zonulin came into my field of view . I hadn’t been keeping up on celiac research, so the five-year-old news that they’d discovered a protein that regulates intestinal permeability  had quite escaped me.
In short, high levels of zonulin make the intestine more permeable, allowing stuff that shouldn’t get into the body to get there. The study points out that there are high levels of zonulin in people with four autoimmune diseases: celiac disease, multiple sclerosis, rheumatoid arthritis, and insulin-dependent diabetes. (One side effect of this research is that celiac seems to have been promoted to a genuine autoimmune disease rather than a quasi-autoimmune disease, but I digress.)
It’s also possible that said stuff is mis-recognized by the immune system and triggers the auto-immune diseases in the first place, rather than just making them worse. Which, of course, leads to the question about how the zonulin levels got elevated so that the entire mess occurred in the first place.
I tried to read some recent papers on zonulin (having Medline access), but unfortunately immunology papers are simply beyond my ken for the most part — they’re not really written in English.
I was pondering what the role of zonulin was — clearly, the most obvious advantage to being able to change intestinal permeability is avoidance of starvation. At some short-term (and possibly critical) gain, one may cause long-term effects. No great shocker there.
So, my brain then went on to the issue of dieting (being obese and all). It’s fairly well-known that excess dieting may make it much more difficult to lose weight. So what if that’s one of the things that triggers high zonulin levels? I always felt like shit when I dieted, what if that’s literally true?
Let’s look for a minute into some of the known epidemiology of multiple sclerosis. Two to three times as many women as men get MS . While not mentioned on said page, a fairly common trigger for women is pregnancy, though that’s certainly not the only trigger. Worldwide, one is far more likely to contract MS if one is raised further from the equator, which generally correlates to colder states. In colder climates, the body’s composition changes somewhat between summer and winter — which may trigger some kind of “starvation” signal, especially in women. My armchair hypothesis is that this is related to the increased zonulin levels found in MS patients.
On a different tack, one of the other things that occurred to me: what if some of the increases in obesity of Americans were coming from dietary changes that increased zonulin levels?
So, what does the recent research mean? They’ve found something that can inhibit excess intestinal permeability by finding a zonulin inhibitor. This is HUGE. Even if it doesn’t fully prevent the damage of the four aforementioned autoimmune diseases, consider the possibilities in obesity control: no longer will people feel compelled to remove part of the intestine to control digestion in obese patients.
I suspect that the number of obese patients who have genuine metabolic disorders, if one considers intestinal permeability a metabolic disorder (which it should be), is much higher than previously suspected. This research opens the door to an answer.
To me, anything that could help reduce the effects of several autoimmune diseases and obesity, well, that sounds like the kind of Grand Unified Theory that could win a Nobel prize.