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DNC News DNC News: Celiac Disease, Gluten Ataxia and Candidiasis Subject: Celiac disease, triggered by gluten proteins from wheat in susceptible people, can damage the central nervous system. The cell walls of Candida, the yeast responsible for oral thrush, vaginal infections and intestinal Candidiasis, contain the same protein sequence as wheat gluten and may trigger or stimulate Celiac Disease. Our understanding of celiac disease has come a long way in the last few years. Several recent studies have linked celiac disease to central nervous system damage which may cause sporadic ataxia. Other studies have identified the particular protein sequence in gluten which causes celiac disease. Other researchers have identified a similar protein in candida yeast and suggest that it may also trigger the same disease. These studies suggest that the typical digestive symptoms we associate with celiac disease are present less than 20% of the time. Having "normal" digestion no longer rules out the disease. This is a complicated business but I think rather than gloss over it many people deserve and need the details. So please bear with me and skip over the parts that get to thick. First a bit of background: Celiac disease is also called coeliac disease or celiac sprue. The Merck Manual defines it as a "chronic intestinal malabsorption disorder caused by intolerance to gluten." [1] The villi of the small intestine atrophy and nutrients are poorly absorbed resulting in steatorrhea (frequent greasy stools) and malnutrition. Sufferers usually get better when gluten containing cereal grains are removed from the diet. Although the syndrome was described earlier, [2] it wasn't until 1950 that the link between dietary cereals and the disease was figured out. [3] During the Second World War when the Germans occupied Holland , children with celiac sprue improved dramatically only to get sick again disease again at the end of the war. During the war, wheat and rye were in short supply in Holland . The researcher who noticed this was able to show that it was the gluten protein in grains which triggered the disease. [4] Celiac is a genetic disorder and the incidence varies among different populations. Ireland and people of Irish descent have the highest incidence, about 1 person in 300. In Europe and the United States the incidence is much lower, reported at about 1 in 2,500 or less. The longer a population has eaten wheat the lower the incidence. Europeans have cultivated wheat for almost 9,000 years while the Irish have grown it for only about 3,000 years. I suppose we could rename the disease Celtic Sprue rather than celiac sprue. When tested 90% of people with celiac disease are positive for the HLA-B8 antigen in their blood. The classic problems associated with celiac disease are those of malabsorption and nutritional deficiency. Children with the disease fail to thrive; they are deficient in all of the fat soluble vitamins (A, E, K, and D) and many of the minerals, especially calcium and magnesium. While children are prone to osteomalacia, adults usually develop osteoporosis. This has been the description of celiac disease that medical text books have talked about for decades. Now for what's new. For the last ten years we have known that celiac disease is associated with hypothyroid disease, specifically Hashimoto's Disease. About 10- 14% of celiac patients are hypothyroid. Celiac patients are about ten times as likely to have thyroid nodules. [5,6,7] Is it the same genetic predisposition making people overly prone to develop autoimmune diseases that causes both conditions? Or is it the chronic bowel inflammation that stimulates these autoimmune reactions? At this point it isn't clear. Celiac is clearly an autoimmune disease. The gliaden portion of the gluten protein contains a sequence of amino acids that trigger the immune reaction. When they bind on to the intestinal mucosa they act as an antigen and summon killer lymphocytes to attack. The immune system also develops an immune reaction to the muscle lining of the intestine, the endomysium and the enzyme transglutaminase. [8] People with celiac disease make antibodies which attack both the endomysium and the enzyme transglutaminase. Once this autoimmune process has been triggered, damage occurs in other parts of the body and not just the intestine. Neurological damage occurs with celiac disease. Early on this was thought to be due to nutrient deficiencies caused by malabsorption. Current research shows that the problem is more complex. Celiac disease stimulates the production of antibodies which attack areas besides the intestine including the central nervous system. About 40% of patients who suffer from idiopathic sporadic ataxia have celiac disease which damages their central nervous systems. [9,10,11] The neurological symptoms of celiac disease mimic the symptoms of multiple sclerosis to the degree that celiac must always be ruled out when diagnosing this disease. [12] The neurological conditions caused by celiac disease are now called gluten ataxia and cause damage to the cerebellum, the posterior columns of the spinal cord, and the peripheral nerves. [13] The studies on gluten ataxia have revealed a significant statistic. In patients who had clearly measurable antibodies that are diagnostic of celiac disease and were suffering from gluten ataxia, only 13% had any gastrointestinal complaints. In other words, the hallmark symptoms of poor digestion we associate with celiac disease and use to diagnose the condition may be absent in 87% of patients with gluten related problems! [14] This suggests that celiac may be way under diagnosed. Now we come to what to me is the most interesting of the recent research regarding celiac. It seems fitting that the research again comes from Holland , where celiac disease was first linked to diet. Dr. Nieuwenhuizen, from the research group TNO Nutrition and Food Research, published a paper in the June, 2003, Lancet. He links celiac disease with Candida albicans. Dr. Nieuwenhuizen, knowing the actual sequence of proteins which trigger celiac disease from the published work of other scientists, had searched the databases available to him through TNO to see if the same sequence existed in other places. It turns out the identical sequence of proteins occur in the cell walls of Candida albicans. [15] These Candida gluten-like proteins turn out to be the yeast's "hypha-specific surface protein" nicknamed Hwp1. This is the yeast's version of Velcro and allows it to attach and hang onto the endomysium in the wall of the intestine. It is also targeted by transglutaminase, the enzyme which acts on the gluten protein and serves as a target for immune antibodies. Candida species which don't have this Hwp1 protein can't attach themselves to the digestive tract. [16] If Candida can trigger the same chemical and immunological reactions as wheat gluten do we can imagine a number of interesting implications. First, in people with celiac disease, symptoms usually get better rapidly when they eliminate gluten from their diet. This isn't always the case. Even without gluten some people continue to have symptoms. They may have intestinal Candidiasis. The Candida in their gut may be acting like gluten and continues triggering symptoms. Second, an acute Candida infection may trigger the onset of celiac disease. Even if the Candida is treated and eliminated, the person could be left with a permanent sensitivity to wheat gluten. Candida infections occur frequently with antibiotic usage. In people genetically susceptible to celiac, extra caution should be exercised when using antibiotics to prevent Candida overgrowth. Third, if wheat can cause neurological damage as in gluten ataxia, it is reasonable to assume that Candida could also do so by the same process. Reports of Candida infections causing neurological symptoms are not uncommon; now we have a possible explanation. Fourth, if only a small portion of the people with gluten ataxia have gastrointestinal symptoms despite their severe damage elsewhere in their bodies, it is reasonable to assume that Candida could stimulate significant problems while producing slight or no digestive symptoms. So what does all this mean? Here's my bottom line: Celiac disease may be grossly under diagnosed. It should be ruled out in any chronic digestive condition even if the symptoms don't fit the classic picture. Celiac disease should also be ruled out in osteoporosis and in neurological problems, especially MS. Celiac disease should also be ruled out in Hashimoto's Disease and other thyroid abnormalities. Whenever Celiac disease is diagnosed, Candida infections should be tested for and treated aggressively. People of Irish descent are far more likely to get celiac disease than others and should be extra cautious to avoid Candida infections and treat them aggressively if they occur. References: 1. Merck Manual, Seventeenth Edition 2. Thaysen T, Non-Tropical Sprue. Copenhqagen, Levin and Munsgaard. 1932. 3. Dicke, W. Coeliac Disease: Investigation of harmful effects of certain types of cereal on patients with celiac disease. Doctoral Thesis, University of Utrecht . Netherlands , 1950. 4. Van de Kramer, Weijers, Dicke. Coeliac Disease. IV. An investigation into the injurious constituents of wheat in connection with their action on pateinets with celiac disease. Acta Paediat. 42.223, 1953 5. Counsell et al. Coeliac disease and autoimmune thyroid disease. Gut 1994;35: 844-846 6. Collin et al. Autoimmune thyroid disorders and coeliac disease. European Journal of Endocrinology 1994;130:137-140 7. Freeman H. Deliac associated autoimmune thyroid disease: A study of 16 patients with overt hypothyroidism. 1995; July/Aug: 9(5): 242-246 8. Nat Med. 1997 Jul;3(7):797- Identification of tissue transglutaminase as the autoantigen of celiac disease. Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken EO, Schuppan D. 9. Brain. 2001 May;124(Pt 5):1013-9. Sporadic cerebellar ataxia associated with gluten sensitivity. Burk K, Bosch S, Muller CA, Melms A, Zuhlke C, Stern M, Besenthal I, Skalej M, Ruck P, Ferber S, Klockgether T, Dichgans J 10. Neurology. 2002 Apr 23;58(8):1221-6The humoral response in the pathogenesis of gluten ataxia. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. 11. J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1221-4 Dietary treatment of gluten ataxia. Hadjivassiliou M, Davies-Jones GA, Sanders DS, Grunewald RA. 12. Neurol Sci. 2001 Nov;22 Suppl 2:S117-22 Neurological manifestations of gastrointestinal disorders, with particular reference to the differential diagnosis of multiple sclerosis. Ghezzi A, Zaffaroni M. 13. Lancet. 1998 Nov 14;352(9140):1582-5 Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Davies-Jones GA, Gibson A, Jarratt JA, Kandler RH, Lobo A, Powell T, Smith CM. 14. J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1221-4 Dietary treatment of gluten ataxia. Hadjivassiliou M, Davies-Jones GA, Sanders DS, Grunewald RA. 15. Lancet. 2003 Jun 21;361(9375):2152-4. Is Candida albicans a trigger in the onset of coeliac disease? Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ. 16. Science. 1999 Mar 5;283(5407):1535-8. Adhesive and mammalian transglutaminase substrate properties of Candida albicans Hwp1. Staab JF, Bradway SD, Fidel PL, Sundstrom P. ............................................................ |
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