Celiac disease and gluten allergy symptoms are life-changing, no doubt about it. The standard western diet is filled to bursting with foods containing gluten, making adhering to a gluten-free diet both challenging and limiting, especially for children. Those who have recently been diagnosed often ask themselves “Why me?” – a question to which, until recently, doctors and researchers had no good answer.

A new study, published in September 2009, may go some way towards answering that question, however, and hopefully towards meaningful research into a cure, or at least an effective treatment. For several years, scientists have suspected the existence of an unidentified protein which they called “zonulin”. Zonulin, they hypothesized, caused people with celiac disease, gluten allergies, and other food allergies to have larger-than normal holes or gaps in their intestinal lining.

Now, everyone has holes in their intestinal lining, of course; that’s how digested food gets into the bloodstream, so it can nourish the rest of the body. In healthy people, though, the holes are so minuscule that only highly digested, physically tiny molecules can get through. The body – more specifically, the immune system – recognize these tiny molecules as “food”, and let them pass through the body freely. In a normal gut, big, complicated molecules like, oh, gluten, for instance, either get chopped into tiny pieces (by chemicals called enzymes) and pass through the intestinal wall harmlessly to be used as nourishment, or they stay safely inside the intestine and get passed out the other end with anything else which wasn’t fully digested.

Scientists thought that people with allergies and celiac disease might produce too much of this hypothetical protein called zonulin. The zonulin would weaken their intestinal walls, causing the gaps between cells in the intestinal lining to be too big. Now, when a good sized molecule like gluten travels down the digestive tract, instead of passing harmlessly by, it can be absorbed through the intestinal wall and end up in a part of the body where it’s not supposed to be. The immune system doesn’t like it when large, unfamiliar proteins are floating around where they aren’t supposed to be– after all, they could be viruses or bacteria or heaven-knows-what. So the immune system does its job: it attacks them, and swarms to the site of the “infection”.

Mind you, when you’ve accidentally scraped your elbow on a filthy piece of metal, this is exactly what you want– thousands of angry immune cells swarming the site, causing inflammation and attacking anything that moves until all the intruders are dead. When the source of the “infection” is your own intestinal wall, though… yeah. Not so much. All of the sudden the body is attacking itself, and that’s celiac disease.

Well, now the mysterious zonulin has been positively identified. A group led by Dr. Alessio Fasano, M.D. has discovered then zonulin is actually a protein called haptoglobin 2 precursor. All humans, and many other animals as well, have haptoglobin, which is part of the normal and natural process of inflammation. Haptoglobin 2 is a mutation which is thought to have occurred in humans about 2 million years ago, and is now present in about 80% of the population. In itself, it’s not a problem. Where the problem comes in, according to researchers, is with the haptoglobin 2 precursor– the molecule that the body originally produces, which becomes haptoglobin 2 after an additional chemical reaction. Haptoglobin 1 precursor (the old, un-mutated variety) doesn’t do anything… except become haptoglobin 1. Haptoglobin 2 precursor does do something else, unfortunately; it makes the gaps in membranes like the intestinal lining bigger.

For this reason, overproduction of haptoglobin 2 precursor is now thought to be the root cause of not only celiac disease, but several other autoimmune diseases such as diabetes and multiple sclerosis. This is exciting, because it gives scientists something concrete on which to focus when it comes to searching for a cure, or a treatment– until you know exactly what is causing the disease, it’s difficult to know exactly what to treat. Now, perhaps, instead of just removing and avoiding the triggering factor (gluten, in the case of celiac disease), progress can be made in correcting the underlying problem, allowing celiac sufferers to lead a more normal and healthy life.