Jump to content
Frequently Asked Questions About Celiac Disease Read more... ×
  • Sign Up

Search the Community

Showing results for tags 'trigger'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Diagnosis & Recovery, Related Disorders & Research
    • Calendar of Events
    • Celiac Disease Pre-Diagnosis, Testing & Symptoms
    • Post Diagnosis, Recovery & Treatment of Celiac Disease
    • Related Disorders & Celiac Research
    • Dermatitis Herpetiformis
    • Gluten Sensitivity and Behavior
  • Support & Help
    • Coping with Celiac Disease
    • Parents' Corner
    • Gab/Chat Room
    • Doctors Treating Celiac Disease
    • Teenagers & Young Adults Only
    • Pregnancy
    • Friends and Loved Ones of Celiacs
    • Meeting Room
    • Celiac Disease & Sleep
    • Celiac Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes & Cooking Tips
    • Gluten-Free Restaurants
    • Ingredients & Food Labeling Issues
    • Publications & Publicity
    • Traveling with Celiac Disease
    • Weight Issues & Celiac Disease
    • International Room (Outside USA)
    • Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Food Intolerance & Leaky Gut
    • Super Sensitive People
    • Alternative Diets
  • Forum Technical Assistance
    • Board/Forum Technical Help
  • DFW/Central Texas Celiacs's Events
  • DFW/Central Texas Celiacs's Groups/Organizations in the DFW area

Blogs

There are no results to display.

There are no results to display.

Categories

  • Celiac.com Sponsors
  • Celiac Disease
  • Safe Gluten-Free Food List / Unsafe Foods & Ingredients
  • Gluten-Free Food & Product Reviews
  • Gluten-Free Recipes
    • American & International Foods
    • Gluten-Free Recipes: Biscuits, Rolls & Buns
    • Gluten-Free Recipes: Noodles & Dumplings
    • Gluten-Free Dessert Recipes: Pastries, Cakes, Cookies, etc.
    • Gluten-Free Bread Recipes
    • Gluten-Free Flour Mixes
    • Gluten-Free Kids Recipes
    • Gluten-Free Recipes: Snacks & Appetizers
    • Gluten-Free Muffin Recipes
    • Gluten-Free Pancake Recipes
    • Gluten-Free Pizza Recipes
    • Gluten-Free Recipes: Soups, Sauces, Dressings & Chowders
    • Gluten-Free Recipes: Cooking Tips
    • Gluten-Free Scone Recipes
    • Gluten-Free Waffle Recipes
  • Celiac Disease Diagnosis, Testing & Treatment
  • Miscellaneous Information on Celiac Disease
    • Additional Celiac Disease Concerns
    • Celiac Disease Research Projects, Fundraising, Epidemiology, Etc.
    • Conferences, Publicity, Pregnancy, Church, Bread Machines, Distillation & Beer
    • Gluten-Free Diet, Celiac Disease & Codex Alimentarius Wheat Starch
    • Gluten-Free Food Ingredient Labeling Regulations
    • Celiac.com Podcast Edition
  • Celiac Disease & Gluten Intolerance Research
  • Celiac Disease & Related Diseases and Disorders
    • Lists of Diseases and Disorders Associated with Celiac Disease
    • Addison's Disease and Celiac Disease
    • Anemia and Celiac Disease
    • Anorexia Nervosa, Bulimia and Celiac Disease
    • Arthritis and Celiac Disease
    • Asthma and Celiac Disease
    • Ataxia, Nerve Disease, Neuropathy, Brain Damage and Celiac Disease
    • Attention Deficit Disorder and Celiac Disease
    • Autism and Celiac Disease
    • Bacterial Overgrowth and Celiac Disease
    • Cancer, Lymphoma and Celiac Disease
    • Candida Albicans and Celiac Disease
    • Canker Sores (Aphthous Stomatitis) & Celiac Disease
    • Casein / Cows Milk Intolerance and Celiac Disease
    • Chronic Fatigue Syndrome and Celiac Disease
    • Cognitive Impairment and Celiac Disease
    • Crohn's Disease and Celiac Disease
    • Depression and Celiac Disease
    • Dermatitis Herpetiformis: Skin Condition Associated with Celiac Disease
    • Diabetes and Celiac Disease
    • Down Syndrome and Celiac Disease
    • Dyspepsia, Acid Reflux and Celiac Disease
    • Epilepsy and Celiac Disease
    • Eye Problems, Cataract and Celiac Disease
    • Fertility, Pregnancy, Miscarriage and Celiac Disease
    • Fibromyalgia and Celiac Disease
    • Flatulence (Gas) and Celiac Disease
    • Gall Bladder Disease and Celiac Disease
    • Gastrointestinal Bleeding and Celiac Disease
    • Geographic Tongue (Glossitis) and Celiac Disease
    • Growth Hormone Deficiency and Celiac Disease
    • Heart Failure and Celiac Disease
    • Infertility, Impotency and Celiac Disease
    • Inflammatory Bowel Disease and Celiac Disease
    • Intestinal Permeability and Celiac Disease
    • Irritable Bowel Syndrome and Celiac Disease
    • Kidney Disease and Celiac Disease
    • Liver Disease and Celiac Disease
    • Lupus and Celiac Disease
    • Malnutrition, Body Mass Index and Celiac Disease
    • Migraine Headaches and Celiac Disease
    • Multiple Sclerosis and Celiac Disease
    • Myasthenia Gravis Celiac Disease
    • Obesity, Overweight & Celiac Disease
    • Osteoporosis, Osteomalacia, Bone Density and Celiac Disease
    • Psoriasis and Celiac Disease
    • Refractory Celiac Disease & Collagenous Sprue
    • Sarcoidosis and Celiac Disease
    • Scleroderma and Celiac Disease
    • Schizophrenia / Mental Problems and Celiac Disease
    • Sepsis and Celiac Disease
    • Sjogrens Syndrome and Celiac Disease
    • Skin Problems and Celiac Disease
    • Sleep Disorders and Celiac Disease
    • Thrombocytopenic Purpura and Celiac Disease
    • Thyroid & Pancreatic Disorders and Celiac Disease
    • Tuberculosis and Celiac Disease
  • The Origins of Celiac Disease
  • Gluten-Free Grains and Flours
  • Oats and Celiac Disease: Are They Gluten-Free?
  • Frequently Asked Questions
  • Journal of Gluten Sensitivity
    • Journal of Gluten Sensitivity Autumn 2018 Issue
    • Journal of Gluten Sensitivity Summer 2018 Issue
    • Journal of Gluten Sensitivity Spring 2018 Issue
    • Journal of Gluten Sensitivity Winter 2018 Issue
    • Journal of Gluten Sensitivity Autumn 2017 Issue
    • Journal of Gluten Sensitivity Summer 2017 Issue
    • Journal of Gluten Sensitivity Spring 2017 Issue
    • Journal of Gluten Sensitivity Winter 2017 Issue
    • Journal of Gluten Sensitivity Autumn 2016 Issue
    • Journal of Gluten Sensitivity Summer 2016 Issue
    • Journal of Gluten Sensitivity Spring 2016 Issue
    • Journal of Gluten Sensitivity Winter 2016 Issue
    • Journal of Gluten Sensitivity Autumn 2015 Issue
    • Journal of Gluten Sensitivity Summer 2015 Issue
    • Journal of Gluten Sensitivity Spring 2015 Issue
    • Journal of Gluten Sensitivity Winter 2015 Issue
    • Journal of Gluten Sensitivity Autumn 2014 Issue
    • Journal of Gluten Sensitivity Summer 2014 Issue
    • Journal of Gluten Sensitivity Spring 2014 Issue
    • Journal of Gluten Sensitivity Winter 2014 Issue
    • Journal of Gluten Sensitivity Autumn 2013 Issue
    • Journal of Gluten Sensitivity Summer 2013 Issue
    • Journal of Gluten Sensitivity Spring 2013 Issue
    • Journal of Gluten Sensitivity Winter 2013 Issue
    • Journal of Gluten Sensitivity Autumn 2012 Issue
    • Journal of Gluten Sensitivity Summer 2012 Issue
    • Journal of Gluten Sensitivity Spring 2012 Issue
    • Journal of Gluten Sensitivity Winter 2012 Issue
    • Journal of Gluten Sensitivity Autumn 2011 Issue
    • Journal of Gluten Sensitivity Summer 2011 Issue
    • Journal of Gluten Sensitivity Spring 2006 Issue
    • Journal of Gluten Sensitivity Summer 2005 Issue
  • Celiac Disease Support Groups
    • United States of America: Celiac Disease Support Groups and Organizations
    • Outside the USA: Celiac Disease Support Groups and Contacts
  • Celiac Disease Doctor Listing
  • Kids and Celiac Disease
  • Gluten-Free Travel
  • Gluten-Free Cooking
  • Gluten-Free
  • Allergy vs. Intolerance
  • Tax Deductions for Gluten-Free Food
  • Gluten-Free Newsletters & Magazines
  • Gluten-Free & Celiac Disease Links
  • History of Celiac.com
    • History of Celiac.com Updates Through October 2007
    • Your E-mail in Support of Celiac.com 1996 to 2006

Find results in...

Find results that contain...


Date Created

  • Start

    End


Last Updated

  • Start

    End


Filter by number of...

Joined

  • Start

    End


Group


AIM


MSN


Website URL


ICQ


Yahoo


Jabber


Skype


Interests


Location

Found 24 results

  1. Celiac.com 01/10/2019 - Microbial transglutaminase is an enzyme that is commonly used by food manufacturers to improve product quality and increase shelf life. Transglutaminase is commonly used in the meat industry to add value to meat by allowing smaller pieces of meat, fish, or meat product to be glued together. The result is a large chunk of virtually intact piece of meat or fish that looks like a single chunk. Transglutaminase is rarely labeled and usually invisible to consumers. According to the food website, Delishably, “"Meat glue" is industry standard, and chances are if you eat meat, or even tofu, you're consuming this binding agent on a monthly, if not weekly, basis.” Because it is functionally similar to the tTg, microbial transglutaminase acts like glue, binding gliadin peptides together to form neo-complexes that trigger an immune response, and may also trigger a pathogenic response in people with celiac disease. Even when it lacks sequence identity, microbial transglutaminase functionally mimics endogenous tissue transglutaminase, which researchers understand to be an autoantigen of celiac disease and a key actor in genesis and progression of celiac disease. A team of researchers recently set out to review the effects of microbial transglutaminase in children with celiac disease. Researchers Matthias Torsten and Lerner Aaron are affiliated with AESKU, KIPP Institute, Wendelsheim, Germany, and the Rappaport School of Medicine at the Technion-Israel Institute of Technology in Haifa, Israel. In their review, they report on the enzyme’s characteristics, exogenous intestinal sources, its ability to cross-link to gluten or gliadin, and to thus turn seemingly harmless proteins into disease triggering ones. Their report relays several observations about the immunogenicity of microbial transglutaminase cross-linked complexes in celiac patients, as well as summarizing their pathogenicity, and highlighting possible risks for the gluten dependent conditions. Their stated hope is to promote additional research into the mechanics and disease-triggering channels underlying the gliadin cross linked enzyme and its promotion of celiac disease. The team anticipates that corroboration of their observations could reveal a new environmental trigger for the initiation of celiac disease. They are calling for further study, particularly of the physical mechanics of the process. The team’s research could lead to new understandings of the genesis of celiac disease in certain patients. Such a development would be very helpful to celiac disease research and understanding, in general, and could lead to new diagnosis and treatment options in the future. Sources: Front. Pediatr., 11 December 2018 | https://doi.org/10.3389/fped.2018.00389 Sciencedirect.com
  2. Celiac.com 02/29/2016 - Previous studies have shown that oat proteins trigger an adverse anti-33-mer monoclonal antibody reaction that is proportional to the immune responses in terms of T-cell proliferation. Although there has been some research regarding the impact of these varieties on the adaptive response, researchers still don't know very much about the role of the dendritic cells. A research team recently set out to characterize different oat fractions and to study their effect on dendritic cells from celiac patients. The research team included Isabel Comino, David Bernardo, Emmanuelle Bancel, María de Lourdes Moreno, Borja Sánchez, Francisco Barro, Tanja Šuligoj, Paul J. Ciclitira, Ángel Cebolla, Stella C. Knight, Gérard Branlard and Carolina Sousa. They are variously affiliated with the Departamento de Microbiología y Parasitología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain; the Gastroenterology Unit, Antigen Presentation Research Group, Imperial College London & St Mark′s Hospital, Harrow, United Kingdom; the Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa (IIS-IP), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain; the INRA UMR-1095, Clermont-Ferrand, France; the Nutrition and Bromatology Group, Department of Analytical and Food Chemistry, Food Science and Technology Faculty, University of Vigo-Ourense Campus, Ourense, Spain; the Instituto de Agricultura Sostenible (CSIC), Córdoba, Spain; the Division of Diabetes and Nutritional Sciences, King's College London, Gastroenterology, The Rayne Institute, St Thomas' Hospital, London, United Kingdom; and the Biomedal S.L., Sevilla, Spain. The team first isolated protein fragments from oat grains and then analyzed them using SDS–PAGE. They then characterized several proteins in the prolamin fraction using immunological and proteomic tools, as well as Nano-LC-MS/MS. These proteins were very similar to α- and γ-gliadin, and showed reactive sequences to anti-33-mer antibody, indicating their potential for causing adverse immune reactions. Furthermore, the team found that some of the newly identified oat peptides triggered a range of immune responses on circulating dendritic cells from celiac patients, as compared with healthy controls. This is the first study to show that newly identified oat peptides can trigger a range of stimulatory responses on circulating dendritic cells from celiac patients, which highlights the potential of these oat peptides to trigger adverse immune responses in people with celiac disease. Source: Food & Nutrition Research eISSN 1654-661X
  3. Celiac.com 08/22/2014 - It is often hard to tell if isolated case reports have anything to contribute to the larger understanding of celiac disease. However, some case reports are enough in themselves to cause reflection, whatever their contribution to the larger scientific understanding may be. For most people with celiac disease, symptoms disappear and healing begins with the adoption of a gluten-free diet. For one 9-year-old girl, however, the battle to beat her symptoms and feel better did not end with a gluten-free diet. The girl had initially complained of non-specific abdominal discomfort, and showed positive blood tests for celiac disease. Duodenal biopsies revealed Marsh 3B histopathology. So, she definitely had celiac disease with corresponding symptoms. Despite following a strict gluten-free diet, the girl continued to have symptoms and show positive blood tests for active disease. Gluten is a common additive in plastics. After some detective work, the team discovered that the child was being exposed to gluten from her orthodontic retainer that contained a plasticized methacrylate polymer. She discontinued its use and her symptoms disappeared and her celiac blood tests returned to normal. This case illustrates that, even for patients on the strictest gluten-free diet, exposure to non-dietary sources of gluten, such as those used to make plastics, dental equipment, and cosmetics, can trigger or exacerbate celiac disease symptoms. This case also emphasizes the importance of ferreting out and removing all possible sources of gluten, including non-dietary, when managing celiac disease. Source: Clin Pediatr (Phila). 2013 Nov;52(11):1034-7. doi: 10.1177/0009922813506254.
  4. Celiac.com 11/04/2016 - Patients in the earliest stages of celiac disease have TG2-autoantibodies present in serum and small-intestinal mucosa. Many suffer abdominal symptoms long before the development of villus atrophy. The classic small-bowel mucosal damage that marks celiac disease develops over time and in stages; from normal villi to inflammation and finally to villus atrophy with crypt hyperplasia. Previously, researchers have shown that intraperitoneal injections of sera from celiac patients or of purified immunoglobulin fraction into mice trigger a condition mimics early-stage celiac disease. Those same researchers recently set out to show whether re-combinantly produced, patient-derived TG2-targeted autoantibodies are alone sufficient to trigger such condition in immune-compromised mice. The research team included Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors. They are various affiliated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences, the Department of Internal Medicine, with BioMediTech at Tampere University Hospital and School of Medicine at the University of Tampere in Tampere, Finland, with the Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, and Department of Bacteriology and Immunology at the University of Helsinki in Helsinki, Finland, with the Central Animal Laboratory at the University of Turku in Turku, Finland, with the Comparative Medicine Karolinska Institutet in Stockholm, Sweden, with the Department of Life Sciences at the University of Trieste in Trieste, Italy, and with the Celiac Disease Center, Medical and Health Science Center, Heim Pál Children’s Hospital and Department of Pediatrics at the University of Debrecen in Debrecen, Hungary. Interestingly, mice injected with celiac patient TG2-antibodies showed changes to small-intestinal mucosa, increased lamina propria cellular infiltration and disease-specific autoantibodies in the small bowel, but did not show any clinical signs of celiac disease. Thus, celiac patient-derived TG2-specific autoantibodies seem to be enough to trigger small-bowel mucosal changes in mice, but probably not enough to trigger clinical features on their own. Triggering clinical celiac features likely requires other factors, such as other antibody populations implicated in celiac disease. Source: Amino Acids, pp 1–12. DOI: 10.1007/s00726-016-2306-0
  5. Celiac.com 07/27/2016 - Celiac disease is an immune-based disorder triggered by an adverse immune reaction to gluten proteins in genetically susceptible people. A new study shows that certain viral diseases may increase celiac risk, and confirms a link between intestinal viral infections and celiac disease. Reinhard Hinterleitner earned his PhD from the Medical University of Innsbruck in molecular cell biology and oncology at the group of Gottfried Baier at the Department of Medical Genetics, Molecular and Clinical Pharmacology. He is currently doing postdoctoral research at the University of Chicago as part of an Erwin Schrödinger Fellowship. Dr. Hinterleitner looked at blood samples and 150 small-intestine biopsies from celiac patients and compared them with those of a healthy control group. He found that intestinal viruses can trigger a sort of long-term false alarm in celiac patients by upsetting the small intestine and transforming regulatory T lymphocytes into pro-inflammatory T lymphocytes. "The dendritic cells are also alerted by the infection. If gluten...is consumed at the same time as a viral infection occurs, the already alerted dendritic cells also present gluten antigens to the T lymphocytes," said Dr. Hinterleitner. This can result in the transmission of incorrect information, and can trigger an inflammatory response in T lymphocytes that attacks both the virus and the gluten. They have seen as much in genetically engineered celiac mouse models, wherein a reoviral infection of the small intestine of mice triggers clinical symptoms similar to those experienced by celiac patients who consume gluten. This might also explain why infants who have already had a rotavirus infection are more likely to develop celiac disease. Because if an infant is suffering from a viral infection at the same time, the first intake of gluten, which is supposed to establish oral tolerance to gluten, might in fact have the opposite effect. If this is true, early vaccination against intestinal viruses such as rota- and reovirus in early childhood might reduce the incidence of celiac disease. They estimate that introducing gluten at the same time as intestinal virus infection results in a long-term loss of oral tolerance to gluten in the 20 percent of the population with the genetic predisposition for celiac disease, especially in patients who respond more strongly to virus infections. Source: SCILOG
  6. Lancet. 2003 Jun 21;361(9375):2152-4. Celiac.com 08/25/2003 – This interesting study compares a specific amino acid sequence found in Candida cell wall protein to a the gliadin amino acid sequence that triggers the immune response in celiac disease. The researchers found that the sequences are "identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes," and propose that Candida is the trigger for the onset of celiac disease. Below is the abstract for this study. Is Candida albicans a trigger in the onset of coeliac disease? Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ. Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains amino acid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.
  7. Celiac.com 07/09/2014 - Does the blood pressure medication Benicar (Olmesartan medoxomil) trigger celiac-like gut symptoms? The law firm Levin, Papantonio has filed a lawsuit claiming just that, on behalf of a Texas man who allegedly developed a rare gastrointestinal condition known as sprue-like enteropathy while taking Benicar. According to the complaint, Benicar caused the plaintiff to suffer severe gastrointestinal symptoms, including chronic diarrhea, weight loss, malnutrition, and dehydration. These symptoms are commonly associated with a rare sprue-like enteropathy. The lawsuit comes as Benicar faces scrutiny following a Mayo Clinic study linking the popular drug to rare sprue-like enteropathy in users. The connection between Benicar and the sprue-like enteropathy symptoms was first noted by Mayo Clinic gastroenterologist, Dr. Joseph Murray, after he observed two patients taking Benicar experience relief from symptoms thought to be associated with Celiac disease. Upon discontinuing the use of Benicar, the gastrointestinal symptoms vanished. Dr. Murray then conducted a three-year study of 22 people who experienced celiac-like symptoms while taking Benicar. He found that 14 of those patients had symptoms so severe that hospitalization was required. Moreover, none of the 22 original patients responded to a gluten-free diet, and none showed any detectable levels of tissue transglutaminase in the blood, which would point to celiac disease. After discontinuing the Benicar treatments, the intestinal symptoms disappeared in each of the 22 patients, and they all regained lost weight. In 2013, in keeping with Dr. Murray’s findings, the U.S. Food and Drug Administration changed Benicar’s label to include a warning that the drug may trigger sprue-like enteropathy and symptoms similar to celiac disease. If you think you may have suffered adverse effects from Benicar, check with your doctor, and possibly with a lawyer. Sources: Mayo Clinic: Study on Benicar and sprue-like enteropathy FDA Safety Communication Concerning Label Change on Benicar, 2013. digitaljournal.com.
  8. Celiac.com 11/11/2014 - There have been claims that certain strains of wheat, especially ancient strains, such as einkorn, do not trigger adverse reactions in people with celiac disease, or that they trigger less severe reactions. Until now, researchers haven't been able to say for certain that celiac disease patients react adversely to all varieties of wheat, or whether there may be differences in reactions to certain strains. A research team recently evaluated the safety of ancient strains of wheat in celiac disease. The researchers included Tanja Šuligojemailemail, Armando Gregorinidemail, Mariastella Colombaeemail, H. Julia Elliscemail, and Paul J. Ciclitirac To get a better idea of the nature of celiac factions to wheat, the team studied seven Triticum accessions showing different origin (ancient/modern) and ploidy (di-, tetra- hexaploid). In all, they tested ancient Triticum monococcum precoce (AA genome) and Triticum speltoides (BB genome), accessions of Triticum turgidum durum (AABB genome) including two ancient (Graziella Ra and Kamut) and two modern (Senatore Cappelli and Svevo) durum strains of wheat and Triticum aestivum compactum (AABBDD genome). They evaluated small intestinal gluten-specific T-cell lines generated from 13 celiac patients with wheat accessions by proliferation assays. They found that all strains of wheat they tested triggered a range of adverse responses, independent of ploidy or ancient/modern origin. Based on these results, they suggest that all strains of wheat, even ancient strains previously suggested to be low or devoid of celiac toxicity, should be tested for immunogenicity using gluten-specific T-cell lines from multiple celiac patients rather than gluten-specific clones to assess their potential toxicity. They also emphasize the need for celiac patients to follow a strict gluten-free diet, including avoidance of ancient strains of wheat. Source: Clin Nutr. 2013 Dec;32(6):1043-9. doi: 10.1016/j.clnu.2013.02.003
  9. Celiac.com 09/16/2009 - People with certain genetic markers may be more likely to develop adverse gut-reactions, which may help trigger the development of other immune problems, such as Type 1 diabetes, according to Dr. Fraser Scott, a member of the research team and a senior scientist at the Ottawa Hospital Research Institute. In a recent study of 42 Ottawa-area young adults with Type 1 diabetes researchers analyzed white blood cells, looking for a response to partially-digested wheat proteins. They found that people with certain genes are more likely to develop an over-reaction to wheat in the gut. Type 1 diabetes occurs when the immune system attacks the pancreas, the organ that regulates blood sugar. No such response was seen in another 22 diabetics in the study, nor in a separate control group of non-diabetics. The gastrointestinal tract is home to the largest variety of immune cells in the human body. In healthy people, the presence of food molecules in the gut does not spark an immune response against food molecules, Scott said. However, if the normal process breaks down, the gut can become inflamed or damaged. Celiac disease is one example of such a breakdown. Folks with Type 1 diabetes suffer higher rates of celiac disease than non-diabetics. One hypothesis for this is that certain immune cells may be stimulated by food triggers and migrate to the pancreas, where they damage insulin-producing cells, Scott said. The human gut is one of the main places where the human body interacts with its environment, including food, chemicals, bacteria and toxins. “It important to understand the role the gastrointestinal tract plays in this disease and other autoimmune diseases,” says Scott. “There are probably a large number of people who have diabetes risk genes, but only a small proportion of them develop Type 1 diabetes. These people have difficulty handling what is present in the environment.” Previous research has shown a gluten-free diet to reduce rates of diabetes in animal models. However, that does not mean that parents who want to keep their children from developing diabetes should adopt a gluten-free diet, says Scott. The genetic risk for diabetes is very complex, he adds. First, it's not easy to know for certain who will contract diabetes; 9 out of 10 people who develop Type 1 diabetes don’t have a relative with Type 1, Scott said. In the mean time, the Ottawa study touches on a very important part of the diabetes mystery. A number of scientists have suspected a link between diet, the gut and Type 1 diabetes for about 20 years now, Scott said. This is one of the first studies to affirm this connection in human cells. For Scott, the fact that 22 diabetics in the Ottawa study did not show a reaction to wheat protein means only that the condition is far more complicated than clinicians can conceive at present. In theory, there are myriad ways in which people may come to develop diabetes, and, says Scott, each may have developed by a separate route. Source: Ottawa Hospital Research Institute
  10. Hi! I'm totally new here, in fact, I haven't even been diagnosed with having Celiac... yet. I went to the doctors and got a blood test yesterday, I think she ordered tests for my thyroid, something else, and Celiac. My history could possibly explain everything... I hope nobody minds reading a wall of text! I could just really use some advice and guidance because I feel pretty hopeless about my situation right now. So lets just start from the beginning. As a child I was always extremely healthy. Sometimes I would even fake sick so I could stay home from school because all my friends got to miss a day or two for being sick. The first real health issue I had was when I found out that I was severely allergic to tree nuts at age 11 (and more recently I've been diagnosed with a peanut allergy as well). Other than that my health was superb. I had always had keratosis pilaris on my arms.. and on my face when I was younger if that means anything.. At the end of freshman year of high school in 2011 my life was completely turned upside down. I contracted Mono during spring sports tryouts from sipping out of the wrong water bottle. It really hit me hard.. I probably had it for a month before I even got diagnosed.. I only went to the doctor once I collapsed. I was very very sick, sleeping nearly 24/7 and barely able to eat for probably three months. Though, it took me over a year and a half to actually make a recovery from all of it. During that time I had severe severe migraines on a daily basis, I would ALWAYS get sick, constantly, and I was also diagnosed with chronic fatigue syndrome during that time and had to go through physical therapy for it. After a lot of work and patience I regained a reasonable amount of health, but I was never what I was before having mono. All of this time I had been out of school, trying to struggle through on online high school but sometimes I was even too sick to do that. When I would get sick I would feel sick to my stomach, get headaches, and just feel like I was in a fog, unable to think about anything let alone school. In the fall of 2012 I decided that I wanted to go back to high school. I made it through the first three weeks.. getting sick just about every week.. until I finally contracted viral meningitis and after that whole ordeal we just decided to pull me out of school all together and home school me. The migraines that has subsided started up again after having had viral meningitis. They were brutal, at one point I had one that lasted 11 days and I was hospitalized multiple times. I was put on Topamax after that whole ordeal AND had regular acupuncture. My migraines started to subside.. which made me feel better and in turn.. eat even healthier. I've always been a vegetarian first of all... I ate better than most people bit not clean. Since I was feeling well I started eating clean, which also meant that I was eating a lot less bread, in addition I exercised daily. I was feeling great, no migraines, only the occasional stomach pains, no migraines. I was even able to stop taking the Topamax and my migraines stayed away. So I've been pretty healthy up until this winter. Around christmas season I started to slack with how healthy I was eating and I haven't really gone back. I've been eating more bread and cheese than I normally would. Before I was eating a lot of veggies, quinoa, brown rice, beans, etc. I began having those sick days where my stomach would just hurt, I would be in a fog, and all I would want to do is lie around. It all really went downhill four weeks ago when I injured my knee while skiing. As a homeschooler I have the freedom to be extremely athletic and would ski 3 to 5 times a week for 10 hour days sometimes. It was a freak accident that put me on crutches. I tore my lateral meniscus and I have a micro fracture on my tibial plateau if that's even relevant. Since I was sitting around and sort of bummed out I ate a lot more breaded products as opposed to healthy things. A few days after the injury I got a strange "virus" where my stomach started to gurgle a lot and I was burping like every 30 or even 15 seconds. I assumed it was a virus because it came on in a fairly short period of time.. but it hasn't gone away. It got a little better at one point but now it's gotten worse. I've also been getting migraines again, I've been in a brain fog, I've felt incredibly tired, and I just haven't been doing well.. and it's certainly not due to my knee.. which is doing a little better.. no crutches anymore. The keratosis has spread down to my forearms. I've been getting hives on occasion in random places for random reasons. I've been extremely bloated and uncomfortable.. but I've always bloated a lot after eating very little. The burping and stomach/intestine pain is ridiculous, I literally cannot stop burping. It's SORT of voluntary because I have to let the air out.. It's air.. or gas.. but it isn't acid.. at least not very much. Each morning I was getting up, eating some sort of bread product for breakfast in conjunction with some fruit or something.. then an hour later I would be knocked flat with a wave of tiredness and a brain fog and I would have to go back to bed. I went to the doctor's yesterday and she felt my stomach.. there's nothing wrong with my gal bladder or anything. She took blood for thyroid, something else, and Celiac disease. She said that it would take 4 to 7 days for the results to show but she actually just called saying that the results were in.. but my mom didn't pick up the phone. She also scheduled me for a lactose breath test for next week. Just some other things about me... I'm 17 years old, 5'2" and 105lbs. I've always been thin and small. I'm shorter than both my parents, though they're both pretty short to begin with. I won't be getting any taller. I haven't been diagnosed with endometriosis but I'm pretty sure that I have it... my periods are awful and have always been extremely heavy and painful. Today was the worst I've ever had it, I literally screamed in pain for two hours.. and I wasn't being dramatic. I heard endometriosis is sometimes associated with Celiac. My hair has also been falling out A LOT lately. I've had extremely thick hair my whole life.. and it has thinned out considerably in the past few months. It isn't one spot.. it's just all over. In addition to all of this I have about a zillion food allergies and I carry an epipen. I'm allergic to all nuts, oats, peaches, celery.. and probably other things that I haven't been tested for yet. It wouldn't be surprising to find that I have a problem with gluten too... and probably dairy in addition to that. Nobody in my family has been diagnosed with Celiac (except for maybe one or two of my first cousins who have a lot of health issues but I don't know).. there are some family members that I suspect could possibly have it.. but there are no confirmed cases. I almost want to be diagnosed with this.. not that it would make my life any easier.. it would actually suck a lot.. but it would at least be the answer to why I've been feeling this way for SO long. Two days ago I stopped eating gluten and less dairy... I've improved a little bit.. I've had ups and downs and I'm still burping and my stomach still hurts from everything that it has been through but it isn't as bad as it was the other day. I apologize for the whole novel.. I would really appreciate it if I could get some answers. I'm just so frustrated and just want an answer.. Judging by what I've read.. this seems like this could be what has been causing all my ailments for the past couple years. Does this sound like Celiac or a gluten intolerance? Even though my doctor said that we wouldn't have the results for 4 to 7 days (she didn't say which test) and she just called in with them a second ago (a little over 24 hours after having my blood drawn)?
  11. Celiac.com 11/04/2013 - The mechanisms of cerebellar degeneration associated to prolonged and excessive alcohol intake remain unclear. Additional or even alternative causes of cerebellar degeneration are often overlooked in suspected cases of alcohol-related ataxia. A team of researchers recently set out to investigate the prevalence of gluten-related serological markers in patients with alcohol-related ataxia, and to compare the pattern of brain involvement on magnetic resonance imaging between patients with alcohol and gluten ataxias. The research team included Stuart Currie, Nigel Hoggard, Matthew J. R. Clark, David S. Sanders, Iain D. Wilkinson, Paul D. Griffiths, and Marios Hadjivassiliou. They are variously affiliated with the Academic Unit of Radiology at the University of Sheffield, and with the Department of Gastroenterology, and the Department of Neurology of Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, United Kingdom. For their study, the team used a retrospective review of patients attending an outside clinic to identify patients diagnosed with alcohol and gluten ataxias. The team recorded HLA genotype and serological markers of gluten-related disorders. They also conducted cerebellar volumetry, MR spectroscopy and voxel-based morphometric analyses on the patients and compared the results to matched control data. Results from 904 registered patients showed 104 patients with alcohol ataxia, and 159 patients with gluten ataxia. The data also showed that 61% of the patients with alcohol ataxia, and 70% of the patients with gluten ataxia had HLA DQ2/DQ8 genotype compared to just 30% of people with healthy local blood donors. Interestingly, 44% of patients with alcohol ataxia showed antigliadin antibodies compared to 12% in the healthy local population and 10% in patients with genetically confirmed ataxias. None of the patients with alcohol ataxia and antigliadin antibodies had celiac disease, while 40% in patients with gluten ataxia had celiac disease. Patients with alcohol ataxia who had antigliadin antibodies showed patterns of structural brain abnormality that were different from gluten ataxia, but were the same as those common in alcohol ataxia. The results show that alcohol related cerebellar degeneration can trigger gluten sensitivity in certain genetically susceptible individuals. Such sensitivity might be caused directly by the cerebellar impact of alcohol, but factors other than duration and amount of exposure to alcohol may also be responsible for the resulting sensitivity to gluten. Further study is needed to nail down the exact mechanisms at work here, but this is certainly an interesting study. Source: Currie S, Hoggard N, Clark MJR, Sanders DS, Wilkinson ID, et al. (2013) Alcohol Induces Sensitization to Gluten in Genetically Susceptible Individuals: A Case Control Study. PLoS ONE 8(10): e77638. doi:10.1371/journal.pone.0077638
  12. Celiac.com 10/07/2013 - People with non-celiac gluten-sensitivity often report gut and non-gut symptoms shortly after eating gluten; symptoms disappear on gluten-free diets, although these patients have no serologic markers of celiac disease, and no intestinal damage. However, there is no evidence to suggest any changes to blood or mucosa in those individuals. To better understand non-celiac gluten sensitivity, a research team recently assessed immunologic responses of duodenal mucosa samples and peripheral blood basophils, isolated from NCGS patients, after exposure to gliadin. The research team included Cristina Bucci, Fabiana Zingone, Ilaria Russo, Ivonne Morra, Raffaella Tortora, Norberto Pogna, Giulia Scalia, Paola Iovino, and Carolina Ciacci. They are affiliated with CEINGE in Naples, Italy; the Consiglio per la Ricerca e la Sperimentazione in Agricoltura in Rome, Italy; the Gastrointestinal Unit of the Department of Medicine and Surgery at the University of Salerno in Salerno, Italy; and with the Gastrointestinal Unit at the Department of Clinical and Experimental Medicine of Federico II University of Naples. Between January 2010 and July 2011, the research team gathered mucosa samples from 34 celiac disease patients who followed gluten-free diets for at least 6 months, 35 patients with untreated celiac disease, 16 patients with non-celiac gluten sensitivity (NCGS) and 34 healthy control subjects. The team diagnosed non-celiac gluten sensitivity based on patient symptoms and current diagnositic guidelines. For each of the 119 patients, the team conducted a complete clinical evaluation to exclude celiac disease while on a gluten-containing diet, a skin prick test to exclude wheat allergy, and upper endoscopy at 2 tertiary medical centers in Italy. After incubating each biopsy sample with gliadin, the team measured inflammatory markers, including anti-phosphotyrosine-monoclonal antibody (PY99), HLA-DR, intercellular cell adhesion molecule-1 (ICAM-1), CD3, CD25 and CD69. After incubation with gliadin, mucosa samples from the 69 patients with celiac disease showed increased immunofluorescence intensity for early and delayed markers of inflammation. They also found low levels of some of these markers in three patients with non-celiac gluten sensitivity and three controls. The team found normal mucosal architecture in 56.3% of patients with non-celiac gluten sensitivity. The remaining seven patients showed increased intraepithelial infiltration, but without eosinophils. They found no villous atrophy in patients with non-celiac gluten sensitivity, and no significant increases in the levels of CD63 and CD203c. The team did find that one patient each in the NCGS and control groups, whose results indicated only weak PY99 and ICAM-1 positivity, also had Helicobacter pylori infection. Unlike mucosa from patients with celiac disease, once incubated with gliadin, mucosa from patients with NCGS does not express markers of inflammation, nor does the gliadin activate their basophils. The in vitro gliadin challenge therefore should not be used to diagnose NCGS. This study does suggest that wheat components, other than proteins, might be associated with GI symptoms in patients with IBS, and should be assessed for a possible role in the pathogenesis of NCGS. Source: Clinical Gastroenterology and Hepatology. Volume 11, Issue 10 , Pages 1294-1299.e1, October 2013
  13. Celiac.com 09/12/2013 - There is evidence that certain types of gut trauma can trigger celiac disease, but almost nothing is know about whether traumatic brain injury might trigger a neurological form of celiac disease in some individuals. TG6 is a brain expressed form of transglutaminase that seems to be connected to neurological expressions of celiac disease. Researchers Jonas F Ludvigsson and Marios Hadjivassiliou wanted to test the hypothesis that earlier brain injury due to head trauma may be more common in patients with celiac disease, potentially through trauma-induced TG6 leading to interaction with TG2. Ludvigsson and Hadjivassiliou are variously affiliated with the Department of Pediatrics at Örebro University Hospital in Örebro, Sweden, the Clinical Epidemiology Unit, Department of Medicine at Karolinska Institutet in Stockholm, Sweden, the Division of Gastroenterology and Hepatology at the Mayo Clinic College of Medicine in Rochester, USA, and with the Department of Neurology at Royal Hallamshire Hospital in Sheffield, UK. For their study, they used biopsy reports from all 28 pathology departments in Sweden to identify 29,096 individuals with celiac disease, which they defined as the presence of villous atrophy. They then assessed the risk of earlier head trauma in celiac disease patients compared to the risk in 144,522 controls matched for age, sex, county and calendar year. They used logistic regression to calculate odds ratios (ORs). They found that a record of earlier head trauma in 981 (3.4%) patients with celiac disease, and in 4,449 (3.1%) control subjects. People who had suffered from head trauma showed a 1.10-fold increased risk of future celiac disease (95% CI = 1.02-1.17); independent of sex or age at celiac disease. The highest risk of future celiac disease was seen during the first year after trauma. There was no connection between severity of trauma and risk of developing celiac disease. These results show a very small excess risk for future celiac disease in individuals with an earlier head trauma. Source: BMC Neurology 2013, 13:105. doi:10.1186/1471-2377-13-105
  14. Celiac.com 08/26/2013 - Celiac disease and its cutaneous manifestation, dermatitis herpetiformis are both disease marked by sensitivity to gluten. Metabolic bone disease is common among in people with celiac disease, but there isn't much data on rates of bone density in patients with dermatitis herpetiformis. A team of researchers recently set out to determine if dermatitis herpetiformis triggers bone loss, as does celiac disease. The research team included K. Lorinczy, M. Juhász, A. Csontos, B. Fekete, O. Terjék, P.L. Lakatos, P. Miheller, D. Kocsis, S. Kárpáti, Tulassay Z, Zágoni T. For their study, the team wanted to compare bone mineral density (BMD) of celiac and dermatitis herpetiformis patients. The study group included 34 celiac patients, 53 with dermatitis herpetiformis and 42 healthy controls. Average age for celiac patients was 38.0 +/- 12.1 years, for dermatitis herpetiformis it was 32.18 +/- 14.95 years, while it was 35.33 +/- 10.41 years for healthy control subjects. The team used dual-energy X-ray absorptiometry to measure bone mineral density of the lumbar spine, the left femoral neck and radius. They defined low bone density, osteopenia and osteoporosis as a body mass density (BMD) T-score between 0 and -1, between -1 and -2.5, and under -2.5, respectively. They found decreased BMD in the lumbar region, consisting of dominantly trabecular compartment, in 26 patients (49%) with dermatitis herpetiformis, 21 patients with celiac disease (62%), and in 12 of the healthy control subjects (29%). They also measured lower BMD at the lumbar region in dermatitis herpetiformis and celiac patients, compared to healthy subjects (0.993 +/- 0.136 g/cm2 and 0.880 +/- 0.155 g/cm2 vs. 1.056 +/- 0.126 g/cm2; p < 0.01). They found no difference in density of bones consisting of dominantly cortical compartment (femoral neck) between dermatitis herpetiformis patients and healthy control subjects. The results show that a low bone mass is also common in patients with dermatitis herpetiformis. Bone mineral content in these patients is significantly lower in those parts of the skeleton which contain more trabecular bone, and less reduced in areas with more cortical bone. Source: Rev Esp Enferm Dig. 2013 Apr;105(4):187-193.
  15. Celiac.com 10/28/2010 - A team of researchers recently found that gluten sensitivity can play a role in triggering a certain type of neurologic dysfunction, called sensory ganglionopathy, and that the condition may respond to a strict gluten-free diet. The team conducted a retrospective observational case study on 409 patients with different types of peripheral neuropathies, including seventeen patients with sensory ganglionopathy and gluten sensitivity. The research team was made up of M. Hadjivassiliou, MD, D.G. Rao, MD, S.B. Wharton, PhD, D.S. Sanders, MD, R.A. Grünewald, DPhil, and A.G.B. Davies-Jones, MD. They are affiliated variously with the Departments of Neurology, Neurophysiology, Neuropathology, and Gastroenterology at Royal Hallamshire Hospital in Sheffield, UK. Neurological issues are common in people with celiac disease and gluten-sensitivity. On eof the most common neurological issues in these people is called peripheral neuropathy. The most common type of neuropathy seen in people with gluten sensitivity is sensorimotor axonal. The team reviewed data on 409 patients with different types of peripheral neuropathies. All of these patients had been followed for a number of years in dedicated gluten sensitivity/neurology and neuropathy clinics. Fifty-three of these patients (13%) showed clinical and neurophysiologic evidence of sensory ganglionopathy. Seventeen of these fifty-three patients (32%) showed positive blood screens for gluten sensitivity. The median age of those with gluten sensitivity was 67 years, with symptom onset starting at 58 years on average. Seven of those with positive blood screen evidence gluten sensitivity showed enteropathy upon biopsy. Fifteen patients went on a gluten-free diet, resulting in stabilization of the neuropathy in eleven of the fifteen. The remaining four patients did not follow the gluten-free diet and their conditions worsened, as did the two patients who declined dietary treatment. Autopsy tissue from three patients showed inflammation in the dorsal root ganglia with degeneration of the posterior columns of the spinal cord. These results led the team to conclude that sensory ganglionopathy can result from gluten sensitivity and may respond positively to a strict gluten-free diet. Source: Neurology 2010;75:1003–1008
  16. Celiac.com 12/03/2010 - An interesting finding regarding corn from a research team based in Sweden that studied the effects of both gluten and corn on patients with celiac disease. The research team included G. Kristjánsson, M. Högman, P. Venge, R. and Hällgren, who are affiliated variously with the Department of Gastroenterology, the Department of Medical Cell Biology, Section of Integrative Physiology, the Laboratory for Inflammation Research, and the Department of Rheumatology at Uppsala University Hospital in Uppsala, Sweden. Specifically, the team sought to better understand the facets of nitric oxide (NO) production induced by rectal gluten challenge and the relationship between nitric oxide production and mucosal granulocyte activation. The team measured the release of rectal nitric oxide in 13 patients with celiac disease and in 18 control subjects. The team measured levels both before and after rectal wheat gluten challenge. To collect the gas, the team used a rectal balloon and a newly developed instrument, which allows simultaneous measurements of concentrations of granulocyte mediators in the rectal mucosa. This new technique is called the “mucosal patch technique”. The technique allowed the team to measure myeloperoxidase (MPO), eosinophil cationic protein (ECP), and histamine. They found that concentrations of rectal nitric oxide increased in ALL celiac patients after wheat gluten challenge, peaking at 15 hours (average concentrations of 9464 (SEM 2393) parts per billion (ppb), with a range of 250–24982 ppb. The maximum MPO and ECP increase occurred five hours after challenge. At the fifteen hour mark, the team observed a correlation between mucosal MPO and nitric oxide production. They then compared their results against measurements taken after corn gluten challenge. Six of the celiac patients showed an increase in nitric oxide production 15 hours after rectal corn gluten challenge, though much smaller than after gluten challenge. The control group showed no increases after either challenge. The main findings showed that mucosal activation of neutrophils and eosinophils precedes pronounced enhancement of mucosal nitric oxide production after rectal wheat gluten challenge in patients with celiac disease. The researchers also found that some patients with celiac disease show signs of an inflammatory reaction after rectal corn gluten challenge, shown by increased nitric oxide production and activation of granulocyte markers. The fact that nearly half of the celiac patients in this small sample showed increases in nitric oxide production after a corn challenge is definitely interesting, and calls out for further study. Source: Gut 2005;54:769-774. doi:10.1136/gut.2004.057174 Update by Elaine E. Thompson, Ph.D. submitted 12/03/2010: In this study the researchers discovered that the cornmeal they tested was contaminated with wheat. Please revise this blog entry to reflect the flaw in the study."The manufacturer claimed that their corn product was free from wheat or other cereals. We tested the product at the Swedish National Food Administration (Livsmedelsverket) and it was found to be contaminated with 82 μg/g (ppm), which is less than the usual allowed amount in a gluten free diet (<200 ppm) according to the Codex Alimentarius Standard for gluten free foods, and far less than what has been found to be a safe amount of gluten contamination when correlated with histology in oral challenge studies. It cannot be excluded that the small amounts of gluten present in the corn preparation induced an inflammatory reaction as the mucosal patch technique is very sensitive. "
  17. Celiac disease is known to be triggered, at least in part, by environmental factors. These factors can even affect one identical twin and not the other and seem to have their greatest impact during infancy when gluten is first introduced to the diet. Gut flora makeup and vitamin D levels are 2 factors which differ in infants and could affect the development of the immune system in ways leading to celiac disease. Recent research has shown that gut Bifidobacterium levels are lower in both treated and untreated celiac disease patients. Bifidobacterium species have properties which are beneficial to the immune system such as increasing IL-10 secretion and decreasing intestinal permeability. But other microbiota species may also have important effects and benefits to the developing immune system. Scientists are only beginning to scratch the surface both in cataloging the microbiota species found in the gut and understanding how environmental factors, such as antibiotics, affect their makeup and, in turn, how the makeup of gut microbiota affects human health. A new article on Medscape.com discusses the current state of this research and is excellent reading: Gut Reaction: Environmental Effects on the Human Microbiota Melissa Lee Phillips Published on Medscape.com: 07/15/2009 http://www.medscape.com/viewarticle/705512_print It may be years before research fully understands how gut microbiota and vitamin D deficiency may be involved in triggering celiac disease. Both vitamin D and probiotic supplements (such as Bifidobacterium infantis) are cheap, readily available, and generally safe. There is much current research showing how important vitamin D is for overall health. Your infant's health is a matter of immediate concern and cannot wait 5 or 10 years for research to confirm whether such supplements can help prevent celiac disease. It would seem prudent to make use of these supplements now in both mother and infant during pregnancy, while breast-feeding, and prior to introducing gluten to your baby. Consult with your physician about how much is the right dose.
  18. Celiac.com 07/23/2010 - In a breakthrough that may pave the way for the development of the first drug treatments for celiac disease, researchers claim to have identified the molecular triggers for the chronic, painful gut disorder. Since people with celiac disease must remain gluten-free for life, and since many foods are contaminated with gluten, many people with celiac disease are at risk of developing intestinal damage and other associated problems over time, says Robert Anderson, senior author of the study, and head of the celiac disease research laboratory at the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia. In Anderson's view, developing a drug that would control the immune response to gluten "would be a much more efficient way of dealing with celiac disease." However, he adds, a lack of understanding about how gluten triggers the immune system response in celiacs has prevented researchers from pursuing such therapies. Gluten is actually made-up of numerous different protein strands, and, until now, no one has teased out just which protein strands are inducing the immune response seen in celiac disease. To design drugs that will effectively treat celiac disease, scientists must first understand exactly which of the gluten molecules are triggering the immune response. For their study, Anderson and his associates analyzed immune responses in blood samples from more than 200 celiac disease patients who had eaten meals containing gluten. The team then performed thousands of gluten challenges on the samples using isolated fragments of gluten protein. Interestingly, of the thousands of gluten fragments they tested, only three of them triggered an immune reaction. That only three of the thousands of protein fragments in gluten provokes an immune response suggests that "a very precise trigger is driving the immune response" in celiac disease, Anderson said. "The problem is not so much gluten, it's really these three peptides." The authors also noted that most of the immune response to gluten appears tied to a single type of immune system cell, called the T cell. Their results appear in the July 21 issue of Science Translational Medicine. According to Dr. Alessio Fasano of the University of Maryland School of Medicine in Baltimore, even with strong evidence against the three peptides in question, there may be more to the story. It's possible that the study missed other offending protein fragments, and that there are more players in the adverse immune response in people with celiac disease. Interestingly, sequences from ω-gliadin (wheat) and C-hordein (barley), rather than α-gliadin, proved to be the immunodominant trigger, regardless of the grain consumed. But before folks with celiac disease get too worked up about a possible cure, they need to remember that, because the study looked at patients with a particular genetic susceptibility to the disease, the findings do not apply to all people with celiac disease. Although most people with celiac disease share this genetic background, others do not. That means the findings won't apply to everyone with the disease. Anderson and his colleagues are currently working to identify which gluten proteins induce the immune response in the other celiac patients. The limited diversity of pathogenic T cells in celiac disease indicates that researchers should be able to develop peptide-based treatments for both celiac disease and likely for other HLA-restricted immune diseases. Phase I clinical trials of a drug based on the three isolated fragments of gluten protein are currently underway in Australia. Researchers hope the drug will successfully desensitize celiac patients by introducing small amounts of the offending proteins under controlled conditions. They expect results within the next couple of months. The current study received funding from Nexpep, the Australian National Health and Medical Research Council, Coeliac UK, the Coeliac Research Fund, and others. Source: Sci Transl Med 21 July 2010: Vol. 2, Issue 41, p. 41ra51
  19. Celiac.com 05/12/2010 - Diarrhea, weight loss and malabsorption represent the major clinical presentation of celiac disease, but the exact mechanisms of these symptoms are not fully understood. A team of researchers recently set out to determine whether celiac disease impairs the function of solute transporters and aquaporins. The research team included U. Laforenza, E. Miceli, G. Gastaldi, M. F. Scaffino, U. Ventura, J. M. Fontana, M. N. Orsenigo, and G. R. Corazza. The team looked for possible alteration in the expression and localization of water channels, known as aquaporins, and certain solute transporters in duodenal mucosa of celiac disease patients. To do this, the team evaluated duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls. The team used semi-quantitative RT-PCR and real time RT-PCR to determine the expression of some aquaporins and transporters mRNA in the duodenal biopsies. They relied on immunohistochemistry to evaluate the localization of aquaporin 3, 7 and 10, and of Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger. They found that the duodenal biopsies of healthy controls, treated celiac patients and disease controls expressed aquaporin 3, 7, 10, 11, Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger, cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter mRNAs. Transcript expression was largely absent in the duodenal biopsies of untreated celiac disease patients, except for cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter. Immunohistochemistry of healthy control subjects showed a labeling in the apical membrane of surface epithelial cells of duodenum. Immunolabeling was heavily reduced or absent in untreated celiac patients, but normal patients who had followed a gluten free diet for at least 1 year. The results of the study show that people with celiac disease have defects in their primary pathways for water and solute absorption that may play a role in the onset of malabsorption symptoms. Source: Biol Cell. 2010 Apr 26.
  20. Celiac.com 03/22/2010 - The main cause for gluten intolerance continues to puzzle scientists, but pathogenesis theories include both genetic susceptibility and environmental triggers, like a virus or infection. For the first time, scientists working with the Academy of Finland’s Research Program on Nutrition, Food, and Health have found genes in the body that are associated both with the immune system and with the body's ability to properly digest gluten in the intestinal tract. Gluten intolerance arises from an autoimmune reaction in the small intestine to the gluten protein found in wheat, barley and rye. Academy Research Fellow Paivi Saavalainen, a veteran researcher in hereditary risk factors for gluten intolerance, says that "some of the genes we have identified are linked with human immune defense against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance.” Data shows that rates of celiac disease in America have increased more than 400% since World War II. Meanwhile, a Finnish scientist internationally known for his gluten research says that the number of people in Finland who suffer from gluten intolerance has doubled over the last two decades. Since the early 1980s, the percentage of Finns with gluten intolerance has risen from about 1 percent of adults to about 2 percent, according to Professor Markku Mäki, head of a research project in the Academy of Finland's Research Program on Nutrition, Food and Health. "We've already seen a similar trend emerge earlier on where allergies and certain autoimmune disorders are concerned. Screening has shown that gluten intolerance occurs in 1.5 per cent of Finnish children and 2.7 per cent of the elderly. The higher figure for older people is explained by the fact that the condition becomes more frequent with age," says Mäki. For the immune study, when researchers scanned the genetic maps of more than 9400 celiac patients, they found areas of immune system disturbance. Their evidence also indicated that genes connected with the inability to digest gluten were also connected with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis. Saavalainen and his team have succeeded in localizing risk genes in both individual patients and entire families, which adds weight to the notion that gluten intolerance is inherited. The researchers are hoping to use the genetic information to craft better screening tests for gluten intolerance, as up to 75% of people with gluten intolerance remain undiagnosed due to mild or atypical symptoms, and many with condition may unwittingly suffer damage to their intestinal villi. Professor Maki points out that many present first with iron deficient, or folic acid deficient, anemia. Source: Academy of Finland
  21. Nature Immunology 2, 353 - 360 (April 2001) Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation. The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process.
  22. Am J Gastroenterol. 2004 May;99(5):894-904 Celiac.com 06/08/2004 – To determine what triggers celiac disease, researchers recently used an electron microscope to look at the jejunal biopsies of several groups of children: A group with untreated celiac disease, one with treated celiac disease, another with challenged celiac disease, and a healthy control group. The researchers discovered rod-shaped bacteria attached to the small intestinal epithelium in both the treated and untreated celiac-disease groups, but not in the healthy control group. The researchers conclude: "Unique carbohydrate structures of the glycocalyx/mucous layer are likely discriminating features of celiac disease patients. These glycosylation differences could facilitate bacterial adhesion. Ectopic production of MUC2, HD-5, and lysozyme in active celiac disease is compatible with goblet and Paneth cell metaplasia induced by high interferon-gamma production by intraepithelial lymphocytes." The idea that bacteria may be involved in the pathogenesis of celiac disease is a hypothesis that was also proposed by Roy S. Jamron in an article that originally appeared in the Spring 2004 edition of Celiac.coms Scott-Free Newsletter, which is further supported by this research.
  23. Celiac.com 03/16/2004 - According to Dr. Erika Jensen-Jarolim, professor of medicine and immunology at the University of Vienna, there may be a connection between the development of food allergies and the use of antacids. Dr. Jensen-Jarolim presented her teams preliminary findings at the World Allergy Congress on September 10, 2003. Individuals who take medications that reduce or neutralize the acidity in the stomach may be at a higher risk of developing food allergies, possibly caused by normally harmless food proteins passing in tact through the digestive system. Normally acid and pepsin break down food proteins before they pass into the digestive tract, and if Dr. Jensen-Jarolim is correct, interrupting this process could cause serious, lifelong consequences. Dozens of over the counter and prescription medications suppress acid production or neutralize it. The Austrian research team conducted experiments on mice which were fed hazelnut proteins and other allergens. The normal group of mice did not develop allergies to these foods, while mice that were given the ulcer drugs omeprazole (Prilosec) or ranitidine (Zantac) with the foods they ate did develop allergies to those foods. The animal results were further backed by data on 153 human patients who are taking part in a Hungarian acid-suppression therapy study. One interesting finding in their study was that mice only developed food allergies in response to novel foods that were introduced, not to their regular daily diets. Since an estimated ten percent of the population is taking acid-suppression/neutralization medications, Dr. Jensen-Jarolim recommends that these people should not try eating any novel foods during their treatment.
  24. Gastroenterology. 2003 Aug;125(2):337-344. Celiac.com 08/07/2003 - This studys aim was to determine the feasibility of altering gluten proteins to make them harmless to those with celiac disease. Unfortunately the altered protein still produced a toxic T-cell reaction in almost half of the patients studied. Here is the abstract: Intestinal T-cell responses to high-molecular-weight glutenins in celiac disease. Molberg O, Solheim Flaete N, Jensen T, Lundin KE, Arentz-Hansen H, Anderson OD, Kjersti Uhlen A, Sollid LM. BACKGROUND & AIMS: The chronic, small intestinal inflammation that defines celiac disease is initiated by a HLA-DQ2 restricted T-cell response to ingested gluten peptides after their in vivo examination by tissue transglutaminase (TG2). To date, celiac disease can only be treated by a lifelong abstinence from foods that contain wheat, rye, or barley; better therapeutic options are hence needed. An attractive target would be to identify nontoxic wheat cultivars or components thereof with intact baking qualities. Because these qualities are mainly determined by the high molecular weight (HMW) glutenin proteins of gluten, it is critical to know if these proteins are toxic or, more specifically, if they will trigger the activation of T cells in the celiac lesion. METHODS: Different, highly purified HMW glutenins were isolated from wheat cultivars or expressed as recombinant proteins. The proteins were first tested for recognition by a large panel of gluten-specific T-cell lines established from celiac lesions and then applied during ex vivo challenges of celiac biopsies to allow for a direct identification of HMW specific T cells. RESULTS: Intestinal T-cell responses to TG2-deamidated HMW glutenins but not the corresponding native proteins were detectable in 9 of the 22 adult and childhood celiac disease patients tested. CONCLUSIONS: T cells within celiac lesions frequently recognize deamidated HMW glutenin proteins. This finding questions the possibility of implementing these proteins in novel food items destined to be nontoxic for celiac disease patients.
×