Actually a mixture of several harmless proteins from cereal grains, this so-called adhesive protein is fought by the celiac patient’s body as an invader. Vanishingly small amounts of around 20 to 50 milligrams of gluten are enough to cause severe diarrhea or abdominal pain. By comparison, this amount is a component of 0.3 to 0.8 grams of commercial bread.
Currently help comes only from strict abstension from rye and wheat, spelt and barley. As alternatives there are amaranth, buckwheat, millet, potatoes, corn or rice on the menu which – especially when baking – are no guarantee of culinary highlights. Opinions differ on the question of oats. Several studies from Scandinavian countries confirm a good tolerance, with one catch: the indicated products used were purified by food technology and were proven to be particularly low in allergy potential. In Germany, these are not currently available.
Celiac disease cannot always be recognised at first glance and relieved by dietary measures. Instances of milder forms hide behind vague symptoms such as diarrhea during stressful situations or discomfort. However, a depression or severe sleep disturbance may be due to the underlying disease. With children, pediatricians observe difficult-to-interpret developmental disorders. Given the vague symptoms, the Gastronenterologist Prof. Dr. Andreas Stallmach from the University Hospital of Jena characterised celiac disease as the chameleon of the gastro-intestinal diseases. Sometimes overlooked as a possibility for many years, many patients have, until that diagnosis, a real medical odyssey behind them. And the number of people affected is increasing rapidly. This was the conclusion reached through analyses by specialists from the U.S. Mayo Clinic patient data. Their results from screening studies: Almost every 100th U.S. patient is troubled by this particular food intolerance, the trend is rising. For Germany, individuals sufferers are specified as being 1 in 500. Manifest symptoms however appear only with a fraction of them.
One ailment appears rarely by itself
Researchers from the University of Oslo got onto the track that leads to finding the triggers of Celiac disease: A mutated gene leads to changes in the immune system. T-cells then form atypical surface structures, which has consequences: gluten is bound by these immune cells more strongly than is needed, categorised as hazardous, and finally attacked. Via the body’s own enzyme tissue transglutaminase, harmless grain proteins transform into biological super weapons. Through several steps, metabolites then activate the body’s own messengers. The result: damage to the mucosal layer and inflammation of the small intestine. In the blood, the presence of the respective antibodies can then be demonstrated by a method that has recently been developed as a quick-test for home use.
Another piece of the puzzle: celiac sufferers often suffer from type I diabetes, which it turns out is no mere coincidence. The explanation has now been found by an international consortium in the form of risk genes which are associated with both diseases. All in all, Swedish researchers identified a four-fold higher mortality risk. They evaluated data from 20,000 patients with various forms of highly-pronounced celiac disease. The mortality rate was increased in severe forms by 39 percent and in latent forms by 35 percent. In addition to cardiovascular risks, the authors cite, above all else, small bowel lymphoma (known as Non-Hodgkin’s lymphoma) as the reason. Exact mechanisms are not yet deciphered, but again researchers believe that the autoimmune disease provides a decisive contribution.
Small children – big concerns
If mothers, after weaning, begin with a normal, gluten-containing diet, the young celiac patients are tormented with massive bloating, diarrhea and nausea. In order to provide better recommendations, researchers throughout Europe brought the “PreventCD” study into being. This studied in children with an increased hereditary risk the extent to which the effects of the diet has at a young age in the manifestation of the disease. From this pediatricians could, in the best of scenarios, derive new dietary guidelines. A starting point: For the prevention of celiac disease, the immune system of the offspring should learn, through using smaller amounts of gluten, how to sensibly deal with this protein. Information from Sweden already presents positive experiences. During the nursing phase, targeted “vaccination” with small doses of gluten could prevent that the afforementioned symptoms develop. “The introduction of gluten-containing foods, as long as breastfeading is still being given, seems to reduce the risk for celiac disease and type 1 diabetes,” said Dr. Anke Weissenborn of the Federal Institute for Risk Assessment in Berlin.
A cauldron of minestrone
At the molecular level, there is concealed in gluten a wealth of components. Biologists have now been able to identify the genuinely dangerous components: gliadins in wheat, avenins in oats, secalinine in rye, hordeins in barley. Australian and British researchers have even gone a step further. In a longitudinal study, they established a method in order to record approximately 2,700 protein fragments. Then human volunteers were “in for it“: they had to eat gluten-containing foods for several days. Doctors then detected in the blood about 90 protein fragments that cause an immune reaction. All fragments were able to be categorised into essentially three major subunits which are recognized by T-helper cells. With this knowledge, targeted immunotherapy against the celiac disease trigger could be realised.
There is much to do
A research paper recently caused a sensation. American researchers had managed to demonstrate increased levels of the inflammatory factor interleukin-15 in tissue samples from patients. And mice which, on the basis of a targeted generated genetic defect, were particularly prone to celiac disease, showed with an artificial transfer of the neurotransmitter the corresponding symptoms. By contrast, symptoms of the disease improved in the animal subjects after the nasty immune molecule was blocked. But that isn’t quite the end. Retinoic acid, a metabolite of vitamin A, activates this inflammatory process. Already earlier, fellow researchers working in systemic acne therapy with structurally-similar compounds described cases of chronic inflammatory bowel disease. As the next step, researchers are looking for strategies to control the processes. In this case, drugs that work on autoimmune diseases with similar mechanisms are the center of attention.
A completely different strategy involves plans to treat grain products through food technology processes. Enzymatically-chopped gluten can simply do no harm. Transgenic crops of kinds of cereals that synthesise no allergenic adhesive components are also conceivable. And transglutaminase in the gut presents a further target structure for treatment. Its suppression could prevent the activation of gluten.