Search the Community

Showing results for tags 'celiac disease'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Celiac Disease: Diagnosis, Recovery, Related Disorders & Research
    • Gluten-Free and Celiac Disease Calendar of Events
    • Celiac Disease - Pre-Diagnosis, Testing & Symptoms
    • Celiac Disease - Post Diagnosis, Recovery/Treatment(s)
    • Celiac Disease - Related Disorders & Research
    • Dermatitis Herpetiformis
    • Gluten Intolerance and Behavior
  • Celiac Disease Support & Help
    • Celiac Disease - Coping With
    • Celiac Disease - Parents of Kids or Babies With Celiac Disease
    • Gab/Chat Room - To Discuss Anything BUT Celiac Disease / Gluten-Free Diet
    • Celiac Disease - Doctors
    • Celiac Disease - Teenagers & Young Adults Only
    • Celiac Disease - Pregnancy
    • Celiac Disease - Friends and Loved Ones of Celiacs
    • Celiac Meeting Room
    • Celiac Disease - Sleep
    • Celiac Disease - Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes - Baking & Cooking Tips
    • Gluten-Free Restaurants
    • Gluten-Free Ingredients & Food Labeling Issues
    • Celiac Disease - Publications & Publicity
    • Gluten-Free Travel
    • Gluten-Free Diet & Weight Issues
    • Gluten-Free International Room (Outside USA)
    • Gluten-Free Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Other Food Intolerance and Leaky Gut Issues
    • Super Sensitive Celiacs & Gluten Sensitive
    • 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 Reviews
  • Gluten-Free Recipes
    • 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 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
  • 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 1,156 results

  1. Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia. So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9). With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection. Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal. There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments. My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question. Sources: 1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44. 2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15. 3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454. 4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23. 5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26. 6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11. 7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454. 8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48 9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4. 10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/ 13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29. 14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.
  2. Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things. To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat. They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD. The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. Source: Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023
  3. Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs). The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan. To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses. This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups. Source: Alimentary Pharmacology & Therapeutics
  4. WHAT IS CELIAC DISEASE? Celiac disease is an autoimmune condition that affects around 1.4% of the population (91.2 million people worldwide, and 3.9 million in the U.S.A.). People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems. Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases. Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. CLASSIC CELIAC DISEASE SYMPTOMS Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others. LESS OBVIOUS SYMPTOMS Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important. NO SYMPTOMS Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. CELIAC DISEASE VS. GLUTEN INTOLERANCE Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS) Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there. There are four main differences between celiac disease and non-celiac gluten sensitivity: No Hereditary Link in NCGS Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)? IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS. To add more confusion, many cases of IBS are, in fact, celiac disease in disguise. That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. Crohn’s Disease and celiac disease share many common symptoms, though causes are different. In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis. Crohn’s treatment consists of changes to diet and possible surgery. Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection. Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS Diagnosis of celiac disease can be difficult. Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult. Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis. TESTING There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis. Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products. BIOPSY Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide. WHY A GLUTEN-FREE DIET? Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years. For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease. WHAT ABOUT ENZYMES, VACCINES, ETC.? There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease. There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes. Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement. ASSOCIATED DISEASES The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions: Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include: Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers: Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES: Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology 2018;16:823–836 Celiac Disease Center, Columbia University Gluten Intolerance Group National Institutes of Health U.S. National Library of Medicine Mayo Clinic University of Chicago Celiac Disease Center
  5. Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination. A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain. For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage. The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development. Source: Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.
  6. Celiac.com 06/11/2018 - Untreated celiac disease causes damage to the small intestine, which can interfere with proper nutrient absorption. Most patients can recover proper nutritional absorption via vitamins and mineral therapy, according to the CDF. Avoiding gluten is key. However, many people with celiac disease may not know that their pharmacist might just be one of their best allies in the fight to avoid gluten. Currently, there are no rules that require drug manufacturers to disclose the source of medication ingredients. Consumers can contact the manufacturer directly with questions, and some drug companies strive for clear, helpful answers, but getting correct information can be challenging. Many times though, an answer won't address possible cross contamination during the manufacturing process. This is where pharmacists can be a strong ally for patients with celiac disease. Here are a few way that pharmacists can help people with celiac disease to avoid hidden gluten in their prescriptions and over-the-counter drugs. The first thing pharmacists can do is to check ingredients on prescription medications these patients are taking. They can also share related information to help educate patients, and to improve their choices, and speak with drug manufacturers on patients’ behalf. In addition to assisting with prescription medicines, pharmacists can offer recommendations on vitamins and supplements. As with prescription drugs, both doctors and patients should do their best to review the ingredients used to manufacture vitamins and supplements, and to share this information with celiac patients. So, if you have celiac disease, definitely consider enlisting your pharmacist in an effort to get complete drug and supplement information. This simple tactic can help you to remain gluten-free during your course of drug treatment, however long that may last? Do you have a story about gluten in prescription drugs or supplements? Do you use your pharmacist to help you better understand your gluten-free drug and supplement options? Share your story with us. Source: medscape.com
  7. Celiac.com 05/28/2018 - Myasthenia gravis is a medical condition caused by a disturbance in the communication between nerves and muscles. Symptoms include weakness of arm or leg muscles, double vision, drooping eyelids, and difficulties with speech, chewing, swallowing and breathing. There is no cure for myasthenia gravis, but treatment can help symptoms to improve. Some case reports have indicated a connection between celiac disease and myasthenia gravis (MG). A team of researchers recently set out to determine if those reports are accurate, and, if so, what the connection might be between celiac disease and risk for myasthenia gravis. The research team included Sujata P. Thawani, Thomas H. Brannagan, Benjamin Lebwohl, Peter H. R. Green, and Jonas F. Ludvigsson. They are variously affiliated with the Department of Neurology, New York University School of Medicine, New York, NY USA; the Peripheral Neuropathy Center, Neurological Institute, Columbia University, College of Physicians and Surgeons, New York, NY USA; the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY USA; the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden; the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; and with the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK. The team found 29,086 people who had celiac disease in Sweden between 1969 to 2008. The team then compared these individuals with 144,480 matched control subjects. They used Cox regression to estimate hazard ratios (HRs) for future MG, as identified through ICD codes. Their study period covered 326,376 person-years of follow-up in celiac patients. Over that period, they found 7 cases of MG, for a total of 21 cases per million person-years. In the control group, the team found 22 cases of MG over 1,642,273 years of follow-up, for a total of 14 cases per million person-years, which yielded an HR of 1.48 (95% CI = 0.64–3.41). The HRs did not change when stratifying for age, sex or calendar period. HRs were highest in the first year after follow-up, though insignificant. Individuals with celiac disease showed no increased MG risk for more than 5 years after celiac diagnosis (HR = 0.70; 95% CI = 0.16–3.09). Fortunately, this study showed no increased risk for myasthenia gravis in celiac disease patients. Source: BMC Neurol. 2018; 18: 28.Published online 2018 Mar 12. doi:  10.1186/s12883-018-1035-2
  8. Celiac.com 05/17/2018 - Celiac disease is not one of the most deadly diseases out there, but it can put you through a lot of misery. Also known as coeliac, celiac disease is an inherited immune disorder. What happens is that your body’s immune system overreacts to gluten and damages the small intestine. People who suffer from the disease cannot digest gluten, a protein found in grain such as rye, barley, and wheat. While it may not sound like a severe complication at first, coeliac can be unpleasant to deal with. What’s worse is it would lower your body’s capacity to absorb minerals and vitamins. Naturally, the condition would cause nutritional deficiencies. The key problem that diagnosing celiac is difficult and takes take longer than usual. Surprisingly, the condition has over 200 identified symptoms. More than three million people suffer from the coeliac disease in the United States alone. Even though diagnosis is complicated, there are symptoms that can help you identify the condition during the early stages to minimize the damage. Here is how you can recognize the main symptoms of celiac disease: Diarrhea In various studies conducted over years, the most prominent symptom of celiac disease is chronic diarrhea. People suffering from the condition would experience loose watery stools that can last for up to four weeks after they stop taking gluten. Diarrhea can also be a symptom of food poisoning and other conditions, which is why it makes it difficult to diagnose coeliac. In certain cases, celiac disease can take up to four years to establish a sound diagnosis. Vomiting Another prominent symptom is vomiting. When accompanied by diarrhea, vomiting can be a painful experience that would leave you exhausted. It also results in malnutrition and the patient experiences weight loss (not in a good way though). If you experience uncontrolled vomiting, report the matter to a physician to manage the condition. Bloating Since coeliac disease damages the small intestine, bloating is another common system. This is due to inflammation of the digestive tract. In a study with more than a 1,000 participants, almost 73% of the people reported bloating after ingesting gluten. Bloating can be managed by eliminating gluten from the diet which is why a gluten-free diet is necessary for people suffering from celiac disease. Fatigue Constant feeling of tiredness and low energy levels is another common symptom associated with celiac disease. If you experience a lack of energy after in taking gluten, then you need to consult a physician to diagnose the condition. Now fatigue can also result from inefficient thyroid function, infections, and depression (a symptom of the coeliac disease). However, almost 51% of celiac patients suffer from fatigue in a study. Itchy Rash Now the chances of getting a rash after eating gluten are slim, but the symptom has been associated with celiac disease in the past. The condition can cause dermatitis herpetiformis, which causes a blistering skin rash that occurs around the buttocks, knees, and elbows. A study found out that almost 17% of patients suffering from celiac disease might develop dermatitis herpetiformis due to lack of right treatment. Make sure you schedule an online appointment with your dermatologist or visit the nearest healthcare facility to prevent worsening of symptoms. Even with such common symptoms, diagnosing the condition is imperative for a quick recovery and to mitigate the long-term risks associated with celiac disease. Sources: ncbi.nlm.nih.gov Celiac.com ncbi.nlm.nih.gov mendfamily.com
  9. Celiac.com 06/04/2018 - Rates of contamination in commercial food advertised as gluten-free are improving, but nearly one in ten still show unacceptable levels of gluten. As part of a government mandated food sampling program, the city of Melbourne, Australia recently conducted a survey of 127 food businesses advertising gluten-free options. For the tests, government officers conduct unannounced site visits and take a sample of at least one food item declared to be gluten-free. Ridascreen Gliadin R5 ELISA analysis showed that 14 of 158 samples (9%) contained detectable gluten in excess of the official Food Standards Australia New Zealand (FSANZ) definition of gluten-free. Nine of the 14 samples (6% overall) registered gluten above 20 parts per million, which exceeds the official threshold for foods labeled gluten-free in Europe and the United States. At one business, food labeled gluten-free registered above 80 ppm, even though they were asked directly for a gluten-free sample. These findings confirm the lack of understanding reported by many people with celiac disease. The good news is that rates of gluten non-compliance has improved over earlier audits, from 20% of samples in 2014 to 15% of samples in 2015. The survey team notes that one-third of the businesses in this study had previously been audited) and education seems to be paying off. In one burger chain alone, four of five venues which were non-compliant in 2014, were fully compliant in 2015 and 2016. The survey results showed that businesses that provided gluten-free training for staff showed 75% better odds of compliance. The overall good news here is that gluten-free compliance in commercial food businesses has improved steadily since the first surveys in 2014. One in ten odds of getting gluten contamination from food labeled gluten-free is still to high, but even though there is room for improvement more and more businesses are providing gluten-free training for their staff, and those that do are reaping benefits. Look for this trend to continue as more businesses offer training, gluten-free and celiac disease awareness increases, and more consumers demand safe gluten-free foods. Read more at: The Medical Journal of Australia
  10. Celiac.com 06/01/2018 - Sharon Stone is gluten-free and glamorous. Even at 59, the veteran screen star manages to look great and keep landing new work. Stone is in the news recently, promoting her work in two new projects. Stone currently stars in Steven Soderbergh’s innovative murder mystery “Mosaic,” which began as an app and evolved into a full-blown HBO mini-series. She also stars in the romantic comedy “All I Wish,” which premiered at the end of March. A recent article in the New York Times details Stone’s picks for makeup, hair and beauty products, along with some tips on diet and fitness. Among her diet tips, the seasoned star shares the fact that she has celiac disease, so she eats gluten-free. She also avoids processed food, caffeine, and rarely drinks soda or alcohol. For more on Sharon Stone, including her beauty and health routines, check out other recent articles.
  11. Celiac.com 06/22/2017 - Once upon a time, bananas were thought by many doctors to possess tremendous healing properties. Bananas were used to help diabetics to use weight. Doctors told mothers to feed bananas to their infants starting at 4 weeks. And for a long time, the diet seemed to help people "recover" from celiac disease. Invented by Dr. Sidney Haas in 1924, the high-calorie, banana-based diet excluded starches, but included bananas, milk, cottage cheese, meat and vegetables. The diet was so effective in celiac disease patients that it was adopted by numerous doctors, and endorsed in the 1930s by the University of Maryland, according to pediatric gastroenterologist Alessio Fasano, chair of pediatrics at Harvard Medical School and a specialist in celiac disease. The general public picked up the trend, and embraced bananas as one of the great health foods. But, whatever the medical and public perception about bananas may have been, Dr. Haas was wrong about the curative powers of bananas, and that seemingly honest mistake had long-term consequences for numerous patients with celiac disease. That's because the bananas did not cure the condition, as was commonly thought. The bodies of the patients involved did not become tolerant to wheat. So, when they reintroduced wheat into their diets, as many did, assuming they were cured, they suffered physical consequences. One such patient was Lindy Redmond, whose celiac disease was “cured” with the banana diet as a child. "All my life I have told doctors I had celiac as a child," says Lindy Redmond, "and that I grew out of it. And all my life I have eaten wheat." Thinking she was cured, but suffering years of symptoms, Redmond, at 66 years old, finally underwent a gluten-antibody test and and received an intestinal biopsy. "My intestine was very damaged," she reports. "My doctor said she didn't know if it would ever recover." It was then that Redmond wondered about the possible connection between lifelong, untreated celiac disease and her two miscarriages, frequent bouts of colds and bronchitis, and interminable constipation. Now 74 and off gluten, Redmond says the colds and constipation are gone. It wasn't until 1952 that Dutch pediatrician, Willem Karel Dicke, and his colleagues identified gluten as the trigger for celiac disease, and the gluten-free diet was born. But Haas railed against the gluten-free diet and went on promoting his banana-based cure, claiming that only the banana diet could achieve "a cure which is permanent." The European medical community quickly adopted Dicke's gluten-free diet treatment, but in the United States, at least partly due to these erroneous medical beliefs, celiac disease remained under-diagnosed, and many patients suffered needlessly. Reda more at NPR.org
  12. Celiac.com 05/31/2018 - Explaining the genetics of many diseases is challenging because most genetic associations occur in regulatory regions that just aren’t very well understood and documented. In an effort to provide better genetic information about certain regulatory regions, a team of researchers recently used new computational methods to demonstrate that transcription factors (TFs) occupy multiple loci associated with individual complex genetic disorders. Their work has important implications for celiac disease, and numerous other medical disorders. The research team included John B. Harley, Xiaoting Chen, Mario Pujato, Daniel Miller, Avery Maddox, Carmy Forney, Albert F. Magnusen, Arthur Lynch, Kashish Chetal, Masashi Yukawa, Artem Barski, Nathan Salomonis, Kenneth M. Kaufman, Leah C. Kottyan and Matthew T. Weirauch. They are variously affiliated with the Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Developmental Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; US the Department of Veterans Affairs Medical Center, Cincinnati, OH, USA; the Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Allergy & Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; and the Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA. The group conducted an assessment of 213 phenotypes and 1,544 TF binding datasets that identified 2,264 relationships between hundreds of TFs and 94 phenotypes, including androgen receptor in prostate cancer and GATA3 in breast cancer. In one interesting finding, the team noted that the gene loci for systemic lupus erythematosus risk are occupied by the Epstein–Barr virus EBNA2 protein, along with many co-clustering human TFs, which suggests gene–environment interaction. Similar EBNA2-anchored connections are seen in multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease. Allele-dependent DNA binding and downstream effects on gene expression support genetic mechanisms dependent on EBNA2. These results indicate that such mechanisms are operating across risk loci within disease phenotypes, which offers a new hypothesis for the origins of numerous diseases, including celiac disease. Such complex gene–environment interactions may help explain the origins of numerous autoimmune diseases. Specifically, Epstein–Barr virus (EBV) infection is associated with the autoimmune mechanisms and epidemiology of systemic lupus erythematosus (SLE), increasing SLE risk by as much as 50-fold in children. Despite strong associations between EBV and multiple autoimmune diseases, the underlying molecular mechanics are not understood. That said, genome-wide association studies (GWAS) have identified more than 50 possible European-ancestry SLE susceptibility loci, offering strong support for germline DNA polymorphisms altering SLE risk. The team’s analyses found strong connections with an EBV gene product (EBNA2), offering a potential origin of gene–environment interaction, along with a set of human transcription factors and cofactors (TFs), in SLE and six other auto-immune diseases. The team presents allele- and EBV-dependent TF binding interactions and gene expressions that nominate cell types, molecular agents and environmental factors to disease mechanisms for more than 85 diseases and physiological phenotypes. The team’s analysis suggest that numerous causal autoimmune combinations may act through allele-dependent binding of these proteins, altering downstream gene expression. These results offer promise for the development of future therapies for manipulating the action of these proteins in individuals harboring risk alleles at EBNA2-bound loci. The team’s current current data point to particular TFs and cell types for 94 phenotypes, offering ways to verify, via experiment and exploration, the potential molecular and cellular origins of disease risk, potentially including celiac disease. As new genetic association and TF binding data are collected, approaches such as this will undoubtedly identify additional disease mechanisms. As researchers gain an understanding of the genetics behind the origins of numerous diseases, look for them to make progress on new methods of testing, diagnosis and treatment of many of these conditions. Source: NATURE GENETICS | VOL 50 | MAY 2018 | 699–707
  13. Celiac.com 04/29/2010 - May is designated as National Celiac Awareness Month. As such, I thought it would be a great opportunity to explore the history of celiac disease. Most people think of celiac disease as a modern day ailment, which predominantly affects those of European descent and in Westernized societies. However in my research, I found that the best place to start when referencing the history of celiac disease, is actually the beginning of humans. In the beginning of humans, known as the Neolithic Period, humans were hunters and gatherers and primarily survived on fruits, nuts, and meat when available. During the Neolithic Period, humans evolved and began cultivating plants which quickly led to the agricultural revolution. With the agricultural revolution came a myriad of food antigens, such as dairy, eggs and processed grains. It was during this time that celiac disease was born. Some 8,000 years after making its debut, celiac was identified and named by a Greek physician known as Aretaeus of Cappadocia. In the first century A.D., Aretaeus documented information about, “The Coeliac Affection.” He named celiac disease, “koiliakos” derived from the Greek word for “abdomen”. In his descriptions of celiac Aretaeus stated, “If the stomach be irretentive of food and if it pass through undigested and crude, and nothing ascends into the body, we call such persons coeliacs”. While a name had been given to the disease, people with celiac still had no idea how to heal from the condition, and were still vastly unaware of the cause for their ailments. It wasn't until the early 19th Century that Dr. Mathew Baillie published his observations on celiac disease which he sited as, 'chronic diarrheal disorder causing malnutrition and characterized by a gas-distended abdomen'. In his observations, Dr. Baillie documented that some of his patients appeared to benefit from eating only rice. However important Dr. Baillie's findings were, they still went largely unnoticed by the medical community until 75 years later when an English doctor known as Dr. Samuel Gee, came into the scene. In 1888 Dr. Gee was working for the Great Ormond Street Hospital for Children in the United Kingdom when he demonstrated a set of clinical trials performed on children and adults with celiac disease. Dr. Gee was quoted as saying, “To regulate the food is the main part of treatment. The allowance of farinaceous foods must be small, but if the patient can be cured at all, it must be by means of diet.” As an example he sited a very sick child that was fed the best Dutch mussels every day during mussel season. The child thrived during mussel season, but as soon as the season was over, the child regressed and died before the next mussel season. In the 1920's, Sidney Hass presented the “Banana diet”. Sydney successfully treated 8 out of 10 children suffering with celiac disease using the banana diet. He claimed to have cured the 8 children that were on the banana diet, but the other 2 children not on the banana diet, died. The banana diet included the elimination of all bread, crackers, potatoes and cereals and for several decades, the banana diet was the only cure for celiac disease. Another important marker in the history of celiac disease were the findings by Dutch pediatrician, Dr. Willem Karel Dicke. In 1953 Dr. Dicke wrote his doctoral thesis for the University of Utrecht based on his observations that the ingestion of wheat proteins specifically, and not carbohydrates in general, were the cause of celiac disease. He was able to exemplify his findings based on bread shortages in the Netherlands during World War II. During the bread shortages, he found that the health of children with celiac improved tremendously. However, when the allied planes began dropping bread to the Netherlands, the same children quickly deteriorated. In the 1960's, it became evident that the best method for testing for celiac disease was to perform a biopsy. However, doctors were urged not to diagnose people as having celiac disease until it was proven that gluten was the cause for the damage. To determine if a patient had celiac disease, a biopsy would be performed to evaluate the damage done to the intestines. The patient would then be put on a gluten-free diet. Another biopsy would then be preformed to determine improvement in the intestines. After improvement the patient would be put back on a gluten diet, and another (3rd) biopsy would be preformed to determine reoccurring damages to the intestine, and thus the presence of celiac disease. This method was used for over 20 years as the best method for testing for celiac disease. Then in the 1980's studies by Dr. Stefano Guandalini, showed that the presence of celiac could be found in 95% of celiac cases by performing a single biopsy. In 1990 these findings helped create the new guidelines for celiac testing which were approved by ESPGHAN (European Society for Pediatric Gastroenterology). Also during this time, professionals starting recognizing celiac as an autoimmune disease and also began recognizing the correlation between gluten sensitivity and other autoimmune diseases. Here we are now in the year 2010; thirty years after the medical profession has successfully established the causes, tests and treatments for celiac disease, and thousands of years since celiac first made it's debut. Yet, as far as early diagnosis is concerned, we are still living in the dark ages. In this day and age, knowing what we know about celiac disease, childhood screening for celiac should already be mandatory. It's almost as if, when doctors were told in the 1960's to hold off on celiac diagnosis until they knew undoubtably that gluten was the cause for damage to intestines, they were never told, 'okay, now it's safe to diagnose for celiac'. Unfortunately, many (if not most) doctors still don't know how to appropriately diagnose patients for celiac disease, and therefor they continue to 'hold off' making celiac diagnoses, or misdiagnose regularly. Enforcing mandatory celiac screening in school age children has potential to eliminate the unnecessary suffering of millions of children and adults worldwide. My dearest hope is that we all get to see mandatory celiac testing in this lifetime. If you would like more information on “Celiac Awareness Month,” please check out the links below. The following links are trusted sites that also provide suggestions on how you can get involved and contribute to celiac awareness in your community. Celiac Disease Foundation Celiac Sprue Association Celiac Disease Timeline: Agricultural Revolution - celiac disease is born 1st Century A.D.- Aretaeus named celiac, “ koiliakos” 1st Century A. D.- Aretaeus documented“The Coeliac Affection.” 19th Century- Dr. Mathew Baillie published his observations on celiac 1888- Dr. Gee established the correlation between celiac and diet 1920's - Sydney Hass successfully treated celiac patients with “the banana diet” 1953 - Dr. Willem Karel Dicke confirmed wheat protein to be the cause for celiac disease 1960's - Biopsy established as the most accurate test for celiac 1980's - Dr. Stefano Guandalini established a single biopsy test for celiac 1990 - ESPGHAN established new guidelines for celiac biopsy testing Sources: Impact America's Silent Epidemic
  14. Celiac.com 08/21/2015 - Here's every celiac disease treatment currently in development in a single list: ALV003, by Alvine Pharmaceuticals, is a combination of two enzymes that break down gluten before it can provoke an immune reaction. The drug is a powder to be dissolved in water and taken before meals. ALV003 most recently passed a phase 2 clinical trial, results of which appeared in the June 2014 issue of Gastroenterology. Post-trial biopsies showed that ALV003 prevented intestinal damage in 34 volunteers with celiac disease who ate 2 grams of gluten each day for six weeks and also took the drug. Phase 2b, a 12-week trial, is now underway. AN-PEP, by DSM Food Specialties, is another enzyme that degrades gluten. AN-PEP is believed to work best when taken while gluten is still in the stomach. Results from a small 2013 study showing AN-PEP to be safe, appeared in the World Journal of Gastroenterology. For the study, 16 people ate 7 grams of gluten every day for two weeks and half of them also ate AN-PEP, and half took a placebo. However, the placebo group did not get sick enough during the course of the study to show that the enzyme had any effect, so further study is under way. ActoBiotics by ActoGenX uses Lactococcus lactis as an expression system to locally secrete bio-therapeutics such as cytokines, antibodies, hormones, etc. Early pre-clinical work with a genetically altered L. lactis secreting a peptide derived from gliadin demonstrated an in vivo suppression of gluten sensitization. Specifically, Huigbregtse et al. engineered L. lactis to secrete a deamidated DQ8 gliadin epitope (LL-eDQ8d) and studied the induction of Ag-specific tolerance in NOD ABo DQ8 transgenic mice [34]. Although apparently not part of the ActoGenX development program, recent work by Galipeau et al. also deserves mention in this context. The group treated gluten-sensitive mice with elafin, a serine protease inhibitor, delivered by the L. lactis vector, and found normalization of inflammation, improved permeability, and maintained ZO-1 expression. There is speculation that this is due to reduced deamidation of gliadin peptide. AVX176 by Avaxia Biologics, is an investigational oral antibody drug patented to provide "Antibody Therapy for Treatment of Diseases Associated with Gluten Intolerance." The patent, which expires on May 27 2029, provides broad coverage for treating celiac disease using orally administered antibodies produced by Avaxia's proprietary platform technology. BL-7010, by BioLineRx, is a novel co-polymer for the treatment of celiac disease, which significantly reduces the immune response triggered by gluten. This drug has been shown in mice to reduce the immune system response that leads to intestinal damage and villous atrophy in celiac disease. BL-7010 actually binds to the gluten protein, reducing the protein's toxicity.The drug, with the gluten molecule attached, then passes harmlessly through the digestive system to be expelled as stool. BL-7010 has undergone safety testing in humans and was found to be well tolerated. According to BioLineRx, testing will begin in mid-2015 to see if the drug works as expected to diminish gluten's effects on the body. However, BL-7010 is designed to protect only against gluten cross-contamination; it won't allow people with celiac disease to eat large amounts of gluten. CCR9, by Chemocentryx, is a drug called vercirnon, which is also known as Traficet-EN, or CCX282B), and was originally intended for patients with moderate-to-severe Crohn's disease. CCR9 has completed one Phase 2 trial in 67 patients with celiac disease. However, despite the completion of the trial several years ago, no results relating to celiac disease have been made public or published. Egg Yolk Enzyme. Little is known about efforts to develop a celiac treatment that uses egg yolk to coat gluten and allow it to pass through the body undetected, thus preventing an adverse gluten reaction in sensitive individuals. Like most other drugs being developed, this treatment would work to prevent reactions to small amounts of gluten, rather than as a cure. Larazotide Acetate by Alba Therapeutics. How it works: Larazotide acetate blocks a protein that carries pieces of gluten across the gut, where immune cells can see them. Fasano and his colleagues found that this carrier protein, called zonulin, is overproduced by celiac patients after they eat gluten. Results of the most recent phase 2 trial of larazotide acetate, published in February 2015 in Gastroenterology. The volunteers who took the drug experienced fewer days with disease symptoms during the 12 week-long study. Nexvax2, by ImmusanT, works much like an allergy shot. Nexvax2 exposes the immune system to gluten in a controlled way so that immune cells that are usually activated get turned off or eliminated. So far, Nexvax2 has completed a phase 1 trial showing it to be safe. More research is being done to test whether it is effective. Designed to work as a vaccine, Nexvax2 combines three proprietary peptides that elicit an immune response in celiac disease patients who carry the immune recognition gene HLA-DQ2. Similar to allergy shots, the vaccine is designed to reprogram gluten-specific T cells triggered by the patient's immune response to the protein. ZED1227 by Dr. Falk Pharma and Zedira recently announced the start of phase I clinical trials for the drug candidate ZED1227, a direct acting inhibitor of tissue transglutaminase. The small molecule targets the dysregulated transglutaminase within the small intestine in order to dampen the immune response to gluten which drives the disease process. Stay tuned for updates and progress reports as these drugs work their way through their various trial phases. Finally, share your thoughts on all these celiac drugs in the development pipeline. Are you excited, wary, both? Let us know by commenting below. Source: Gastroenterology Report
  15. Celiac.com 05/30/2018 - One of the key aspects of non-celiac gluten sensitivity (NCGS) is that patients are diagnosed partly by the absence of celiac disease. That is, patients with NCGS, whatever their symptoms, do not have celiac disease. But could those patients still have some kind of gut damage, or permeability issues? Do people with non-celiac gluten sensitivity have distinct duodenal histological features? Researchers are seeking a better understanding of this still undefined condition. Some researchers have suggested that histology may play a key role in NCGS, but there is still no consensus. A recent review by Bardella et al. revealed that histology is not always reported in NCGS studies, and exclusion of celiac disease is generally done by showing negative serology and/or genetic typing. In June 2015, researchers published what is now called the Salerno Experts’ criteria, which proposes a double (or single)-blind, placebo-controlled, (DBPC), crossover gluten challenge as the gold standard to NCGS diagnosis In order to investigate histological findings of people with suspicion of NCGS, we retrospectively evaluated duodenal biopsies of a cohort of patients undergoing clinical diagnostic algorithm for NCGS as proposed by the Salerno consensus. The research team included B Zanini, V Villanacci, M Marullo, M Cadei, F Lanzarotto, A Bozzola, and C Ricci. They are variously affiliated with the Gastroenterology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123, Brescia, Italy; and with the Institute of Pathology Spedali Civili, Piazzale Spedali Civili 1, 25123, Brescia, Italy. Their team’s main goal was to underline that the peculiar IEL distribution and the increased eosinophil count may represent a valid warning that help to identify patients with NCGS, given the absence of serological markers for NCGS. The team also performed a CD3 immunohistochemical evaluation of T lymphocytes confirming that the IEL numbers were normal, but their distribution is peculiar, as noted by the clusters of T lymphocytes in the superficial epithelium and linear disposition of T lymphocytes in the deeper part of the mucosa above the muscularis mucosae. They also note that their failure to fully match study subjects with placebo challenge is a limitation of this study, but stress the current uncertainty of the actual clinical diagnostic algorithm as supported by recent reviews of the literature. The team’s observations led them to note that histology may play a similar role in NCGS diagnosis as it does in celiac diagnosis. Researchers do know that, unlike with celiac disease, there is an absence of damage or change to intestinal mucosa in patients with NCGS, especially an absence of villous atrophy. In addition, the morphological exclusion of celiac disease is a crucial assessment, because some patients classified as NCGS show increased duodenal IEL count (> 25 IELs/100 enterocytes), corresponding to Marsh I, or grade A lesions of celiac histological classification. To properly diagnose NCGS, the team says it’s very important to confirm these features, to rule out any type of organic malabsorption diseases, and to definitively rule out celiac disease, via a negative celiac disease serology. Taken as a whole, the team’s results provide evidence that both intraepithelial lymphocytes and eosinophils play a role in the physiopathology behind NCGS. They are calling for more studies to confirm their findings and to determine whether the results they observed were specific to NCGS. Source: Virchows Arch. 2018 Apr 4. doi: 10.1007/s00428-018-2346-9
  16. Celiac.com 05/25/2018 - People with celiac disease need to follow a lifelong gluten-free diet. However, once their guts have healed, they can still be sensitive to gluten. Sometimes even more sensitive than they were before they went gluten-free. Accidental ingestion of gluten can trigger symptoms in celiac patients, such as pain in the gut and diarrhea, and can also cause intestinal damage. A new drug being developed by a company called Amgen eases the effects of people with celiac disease on a gluten-free diet. Researchers working on the drug have announced that their proof-of-concept study shows AMG 714, an anti-IL-15 monoclonal antibody, potentially protects celiac patients from inadvertent gluten exposure by blocking interleukin 15, an important mediator of celiac disease, and leads to fewer symptoms following gluten exposure. The drug is intended for people with celiac disease who are following a gluten-free diet, and is designed to protect against modest gluten contamination, not to permit consumption of large amounts of gluten, like bread or pasta. AMG 714 is not designed for celiac patients to eat gluten at will, but for small, incidental contamination. Francisco Leon, MD, PhD, study director and consultant for Amgen, says that their team is looking at AMG 714 “for its potential to protect against modest contamination, not deliberately eating large amounts of gluten, like bread or pasta.” Amgen hopes that AMG 714 will help celiac patients on a gluten-free diet to experience fewer or less sever gluten-triggered events. Findings of the team’s first phase 2 study of a biologic immune modulator in celiac disease will be presented at the upcoming Digestive Disease Week 2018. Read more at ScienceDaily.com
  17. Celiac.com 05/29/2017 - Currently, a gluten-free diet is the only way to manage celiac disease. Can a celiac vaccine change that? One company thinks so. ImmusanT corporation has developed a therapeutic vaccine, Nexvax2, that is specifically designed to treat celiac disease. The vaccine is an adjuvant-free mix of three peptides that include immunodominant epitopes for gluten-specific CD4-positive T cells. The vaccine is designed to neutralize gluten-specific CD4-positive T cells to further antigenic stimulation. As part of their efforts to evaluate the vaccine, a team of researchers recently set out to investigate the efficacy of epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease. Specifically, they assessed the safety and pharmacodynamics of the Nexvax2 vaccine in patients with celiac disease on a gluten-free diet. An article detailing the findings of their most recent effort, titled Epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease: two randomized, double-blind, placebo-controlled phase 1 studies, appeared in the Lancet. The research team included Gautam Goel, PhD, Tim King, MBBChir, A James Daveson, MBBS, Jane M Andrews, MBBS, Janakan Krishnarajah, MBBS, Richard Krause, MD, Gregor J E Brown, MBBS, Ronald Fogel, MDCM, Charles F Barish, MD, Roger Epstein, MD, Timothy P Kinney, MD, Philip B Miner Jr, MD, Jason A Tye-Din, MBBS, Adam Girardin, BS, Juha Taavela, MD, Alina Popp, MD, John Sidney, BS, Prof Markku Mäki, MD, Kaela E Goldstein, BS, Patrick H Griffin, MD, Suyue Wang, PhD, John L Dzuris, PhD, Leslie J Williams, MBA, Prof Alessandro Sette, DrBiolSc, Prof Ramnik J Xavier, MD, Prof Ludvig M Sollid, MD, Prof Bana Jabri, MD, and Dr Robert P Anderson, MBChB. To assess the safety and pharmacodynamics of the vaccine in patients with celiac disease on a gluten-free diet, ImmusanT recently conducted two randomized, double-blind, placebo-controlled, phase 1 studies at 12 community sites in Australia, New Zealand, and the USA, in HLA-DQ2·5-positive patients aged 18–70 years who had celiac disease and were following a gluten-free diet. The goal of the study was to document the number and percentage of adverse events in the treatment period in an intention-to-treat analysis. The study enrolled a total of 108 participants from Nov 28, 2012, to Aug 14, 2014, in the three-dose study, and from Aug 3, 2012, to Sept 10, 2013, in the 16-dose study. Overall, 62 (57%) of 108 participants were randomly assigned after oral gluten challenge and 20 (71%) of 28 participants were randomly assigned after endoscopy. None of the study participants, investigators, or staff knew which patients received a given treatment; these details were known only by the study’s lead pharmacist. In the three-dose study, participants received either Nexvax2 60 μg, 90 μg, or 150 μg weekly, or placebo over 15 days; in a fourth biopsy cohort, patients received either Nexvax2 at the maximum tolerated dose (MTD) or a placebo. In the 16-dose study, participants received Nexvax2 150 μg or 300 μg or placebo twice weekly over 53 days; in a third biopsy cohort, patients also received either Nexvax2 at the MTD or a placebo. In both studies, about 5% of the participants reported were vomiting, nausea, and headache. Among participants given the MTD, four of eight subjects in the third cohort experienced adverse gastrointestinal treatment-emergent events; zero of three participants had adverse events in the biopsy cohort in the three-dose study, while five events occurred in five (63%) of eight participants in the first cohort, and three events in two (29%) of seven participants in the biopsy cohort of the 16-dose study. Those who received the vaccine at the MTD on either schedule showed no significant difference between average villous height to crypt depth ratio in distal duodenal biopsies, as compared with those who received placebo. In the 4-week post-treatment period, ascending dose cohorts underwent a further double-blind crossover, placebo-controlled oral gluten challenge, which had a fixed sequence. Meanwhile, biopsy cohorts received a gastroscopy with duodenal biopsies and quantitative histology within 2 weeks without oral gluten challenge. Of the participants who completed the post-treatment oral gluten challenge per protocol, interferon γ release assay to Nexvax2 peptides was negative in two (22%) of nine placebo-treated participants in the three-dose study. Compared with two (33%) of six who received Nexvax2 60 μg, five (63%) of eight who received Nexvax2 90 μg, and six (100%) of six who received Nexvax2 150 μg (p=0·007); in the 16-dose study, none (0%) of five placebo-treated participants had a negative assay versus six (75%) of eight who received Nexvax2 150 μg (p=0·021). The MTD of Nexvax2 was 150 μg for twice weekly intradermal administration over 8 weeks, which modified immune responsiveness to Nexvax2 peptides with no adverse impact on duodenal histology. Patients who received the intradermal administration of the vaccine reported gastrointestinal symptoms were not subtantially different to those seen with oral gluten challenge. While the commercial release of a viable vaccine is likely still some time away, early-phase trials have shown promise. Based on these results, ImmusanT will continue clinical development of this potentially therapeutic vaccine for celiac disease. Both trials were completed and closed before data analysis. Trials were registered with the Australian New Zealand Clinical Trials Registry, numbers ACTRN12612000355875 and ACTRN12613001331729. Source: The Lancet Affiliations: The researchers are variously affiliated with the Division of Gastroenterology and Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA, the Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, USA; the Department of Gastroenterology, Auckland City Hospital, Auckland, New Zealand; the School of Medicine, University of Queensland, Brisbane, QLD, Australia; the Department of Gastroenterology & Hepatology, Royal Adelaide Hospital, Adelaide, SA, Australia; the Linear Clinical Research, Nedlands, WA, Australia; the Department of Gastroenterology, Alfred Hospital, Prahran, VIC, Australia; the Clinical Research Institute of Michigan, Chesterfield, MI, USA; the University of North Carolina School of Medicine, Chapel Hill, NC, USA; Wake Gastroenterology and Wake Research Associates, Raleigh, NC, USA; Atlantic Digestive Specialists, Portsmouth, NH, USA; Ridgeview Medical Center, Waconia, MN, USA; Oklahoma Foundation for Digestive Research, Oklahoma City, OK, USA; ClinSearch, Chattanooga, TN, USA; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Murdoch Children's Research Institute and Department of Gastroenterology, Royal Melbourne Hospital, Parkville, VIC, Australia; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Alfred Rusescu Institute for Mother and Child Care and Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Centre for Immune Regulation, KG Jebsen celiac Disease Research Centre, and Department of Immunology, University of Oslo, Oslo, Norway; the Oslo University Hospital-Rikshospitalet, Oslo, Norway; Department of Pediatrics, Department of Medicine, University of Chicago, Chicago, IL, USA; and ImmusanT in Cambridge, MA, USA.
  18. I need to make a post because I am starting to really trust my gut. (*IT is a SUPER LONG POST). I am very curious if anyone else in this world has experienced or is experiencing something similar to this. I don't know where to go where anyone will believe me. I have had 3 separate passing out/ still conscious incidents where I end up having muscle convulsions. The first one happened New Year's Day 2017, I wasn't eating gluten free at this time. I keep being told I am negative for celiac disease. I was drinking and eating a s$#& ton of gluten. I went to the bathroom and my heart was beating too fast. I felt like I was dizzy, lightheaded, and I was going to faint. I eventually had convulsions on the toilet. Then they stopped I was able to wash my hands then go to the couch. My head dropped losing muscle tone in my body and falling to the floor. On the floor I had were 20-30 different muscle contractions/convulsions. I kept crying and I couldn't talk when they were happening. Eventually, they stopped. April 2017 I had another one in the waiting area of a new GI doctors waiting area. I had just started a high blood pressure medication. I went to pee before my appointment. I sat down. I started sweating on my palms, getting really hot, my heart palpitating, and I got really dizzy again. I told the nurse I am going to faint. My head dropped, and lose muscle tone before convulsing. Of course, my blood pressure dropped too low but was also not gluten free at this point. I was 100% alert and hearing everyone freaking out. I want everyone to understand from August 2017 until end-January 2018 I was on a gluten-free diet. The reason I got off of it at the end of January was for a food sensitivity/allergy test in February. My GI doctor said celiac disease was negative (again) but it seemed that a gluten-free diet would be best. The third time was February 18, 2018. I was at a wedding. I was drinking (and when I was on a gluten-free diet, of course, I made sure what I was eating, and drinking was gluten-free). I am drinking, and I have no care if it's made with gluten. I was eating food too. I sat down for the dinner and the hot sweaty feeling happened, my heart is racing, I feel sick. I feel worried. I know I am going to faint. In the women's bathroom, on this fancy couch with my fiancé. She and I are sitting there and my head drops… I lose all muscle tone. And I have multiple muscle convulsions on the ground… until the ambulance came. I have been to two neurologists who refuse to believe me that the ONE thing these 3 incidents have in common is the fact I was not eating gluten-free. They said to stop drinking.. but I was in Mexico for 1-week January 6th to 13th. Drinking every day and eating gluten-free with no incident like this. They refuse to take a head scan or believe this can be caused by gluten. The people who see it believe they are seizures, but I am 100% alert. It cannot be a seizure. Doctors think it can be trauma, anxiety, convulsion disorder or some other mental illness. I need to know I am not crazy and I know I am not. I believe it is gluten related. My body is telling me it is. Also, I have passed out other times in my life without convulsions that I alreadys related to some kind of food but I didn't know which kind. Thank you for reading.
  19. Celiac.com 05/24/2018 - England is facing some hard questions about gluten-free food prescriptions for people with celiac disease. Under England’s National Health Plan, people with celiac disease are eligible for gluten-free foods as part of their medical treatment. The latest research shows that prescription practice for gluten-free foods varies widely, and often seems independent of medical factors. This news has put those prescribing practices under scrutiny. "Gluten free prescribing is clearly in a state of flux at the moment, with an apparent rapid reduction in prescribing nationally," say the researchers. Their data analysis revealed that after a steady increase in prescriptions between 1998 and 2010, the prescription rate for gluten free foods has both fallen, and become more variable, in recent years. Not only is there tremendous variation in gluten free prescribing, say the researchers, “this variation appears to exist largely without good reason…” Worse still, the research showed that those living in the most deprived areas of the country are the least likely to be prescribed gluten-free products, possibly due to a lower rate of celiac diagnosis in disadvantaged groups, say the researchers. But following a public consultation, the government decided earlier this year to restrict the range of gluten free products rather than banning them outright. As research data pile up and gluten-free food becomes cheaper and more ubiquitous, look for more changes to England’s gluten-free prescription program to follow. Read more about this research in the online journal BMJ Open.
  20. Celiac.com 05/22/2018 - Proteins are the building blocks of life. If scientists can figure out how to create and grow new proteins, they can create new treatments and cures to a multitude of medical, biological and even environmental conditions. For a couple of decades now, scientists have been searching for a biological Rosetta stone that would allow them to engineer proteins with precision, but the problem has remained dauntingly complex. Researchers had a pretty good understanding of the very simple way that the linear chemical code carried by strands of DNA translates into strings of amino acids in proteins. But, one of the main problems in protein engineering has to do with the way proteins fold into their various three-dimensional structures. Until recently, no one has been able to decipher the rules that will predict how proteins fold into those three-dimensional structures. So even if researchers were somehow able to design a protein with the right shape for a given job, they wouldn’t know how to go about making it from protein’s building blocks, the amino acids. But now, scientists like William DeGrado, a chemist at the University of California, San Francisco, and David Baker, director for the Institute for Protein Design at the University of Washington, say that designing proteins will become at least as important as manipulating DNA has been in the past couple of decades. After making slow, but incremental progress over the years, scientists have improved their ability to decipher the complex language of protein shapes. Among other things, they’ve gained a better understanding of how then the laws of physics cause the proteins to snap into folded origami-like structures based on the ways amino acids are attracted or repelled by others many places down the chain. It is this new ability to decipher the complex language of protein shapes that has fueled their progress. UCSF’s DeGrado is using these new breakthroughs to search for new medicines that will be more stable, both on the shelf and in the body. He is also looking for new ways to treat Alzheimer’s disease and similar neurological conditions, which result when brain proteins fold incorrectly and create toxic deposits. Meanwhile, Baker’s is working on a single vaccine that would protect against all strains of the influenza virus, along with a method for breaking down the gluten proteins in wheat, which could help to generate new treatments for people with celiac disease. With new computing power, look for progress on the understanding, design, and construction of brain proteins. As understanding, design and construction improve, look for brain proteins to play a major role in disease research and treatment. This is all great news for people looking to improve our understanding and treatment of celiac disease. Source: Bloomberg.com
  21. Celiac.com 05/12/2018 - Dear researchers/scientists at NIDDK: RE: Misinformation on your website? I am encouraged that you have information about celiac disease on your website (Provider Points: Testing for Celiac Disease). My wife has had celiac disease (CD) for more than 35 years and we always welcome more public/professional exposure for this perplexing condition. I'm a gluten-sensitive-patient advocate and concerned that your information does not appear to be supportable by laboratory science. (Yes, I saw the references and the reviewers—very prestigious literature and referees for your document.) Let's review the information from an accountant's perspective. Before we get into the details of your site, I must mention that I was a medical laboratory technologist in California for 15 years and am quite familiar with the issues that you discuss related to laboratory testing. I was actually working in the lab years ago when the PSA (prostate-specific antigen) was proclaimed the ultimate test for prostate cancer. Now the U.S. Preventive Services Task Force (USPSTF) recommends against PSA screening. Because of this reversal of support for the PSA and other similar tests that were first introduced with blazing reviews throughout the years, I take a skeptic's view whenever I see amazing claims about lab tests. I have read much of the CD research literature and have not changed my cynical ways after reviewing the astounding claims for the blood tests and the biopsy in preparation for writing my book, Celiac Disease & Gluten Sensitivity: A Troubled Past but a Promising Future. Before we put the accountant to work, I want to point out that you have taken the safe road when stating that, "For accurate diagnostic test results, patients must be on a gluten-containing diet." One reason you made that statement is because the news sources certainly give us the impression that an expanding portion of the population is attempting the gluten-free diet (GFD) first, before any testing. Many patients would therefore need to return to a gluten-containing diet. Most major celiac organizations designate a certain number of weeks or months for a person to be on this diet in order to get the accurate results to which you refer. I assume you are aware that no one really knows exactly how long patients must consume gluten to ensure high rates of accuracy for the blood tests. You will find a variety of time spans on the various university and public advocacy websites. Since yours is a Provider Points site, it would seem prudent for you to explain to the providers that the exact length of time is unknown—therefore the doctor would need to take his/her best guess because each person is unique. It's worth noting that currently most doctors know little or nothing about CD and its myriad ramifications. This is my first point. Before we stick that needle in the patient's arm, we may already be in error by specifying a certain time span for the gluten-containing diet and therefore introducing inaccurate results for those patients who did not perform within the limitations. And neither you nor the providers know how large, or small, that number may be. Now the accountant can clock in. You seem to favor the tTG test as the best. You say that it has a sensitivity of more than 90% (very few false negatives) and a specificity of more than 95% (very few false positives). As you know, those are remarkably good numbers for any lab test (not to mention the EMA, which Dr. Green says is approaching 100% accuracy). Let's break those figures down. You assert that 2–3% of celiac patients have selective IgA deficiency. Are those people included in the 90/95? I assume they are, since we can't know who these patients are until they're tested. If they are included, then those 90/95 numbers are even more amazing, because we now have a small (but significant) percentage of cases who will immediately show up as false negatives. Let's move to the other group that you've stated might not be accurate because the "tTG and EMA tests may yield false negative results"—young tykes. Again, every individual is unique, and to assume that your 18-month cutoff age will work for every child is pushing the limits. I noticed you also did not include the elderly here, although the two clusters have similar problems—immune systems that are immature (kids) or faulty (seniors). So both ends of the age continuum may show false negative results for the tTG. In fact, it wouldn't be a scientific stretch to expand this idea further, because we know there are millions worldwide within these age specifications that are immunocompromised due to undernutrition. When you add the age factor plus the nutrition factor together in one patient, he/she is even more unlikely to be able to produce a robust autoantibody response, and therefore would show up as a false negative. I'm not sure the accountant can keep track of these numbers—they keep adding up and making those 90/95 values seem like a dream. I've already introduced the undernutrition topic, so let's throw in a few million people who are undernourished, and therefore may be immunocompromised but are not at the extremes of the age spectrum. Let's now go beyond the undernutrition group and identify more of the immunocompromised. That list is quite long, but here are just a few examples of patient conditions/illnesses: HIV/AIDS, alcoholism, diabetes, corticosteroid use, and immunosuppressant use. There are two recent developments that help answer a question that may be rolling around in the back of your mind, "How many more hours do I need to pay this accountant before she's finished calculating the total number of patients who may show false negative results on the CD blood tests?" The answer is, "You're going to need to her full time." First, new research on patients' responses to vaccines (International Journal of Obesity, "Obesity Affects Influenza Vaccine Response", October, 2011) suggests that obesity may impede a person's immune system such that they may not be able to produce sufficient antibodies as would normally be expected: another subset of the population who may show false negatives when tested for CD. This is preliminary research which will be further explored because the finding is critical to the vaccine industry. If true, can you imagine the number of people added to the accountant's ledger in the U.S. alone? Second, on page 27 of a monograph titled, 21st Century Medicine: A New Model for Medical Education and Practice, by David Jones, MD, Laurie Hofmann, MPH, and Sheila Quinn, the researchers describe the affect that various influences may have on gene expression. "The evidence clearly reveals that each patient is a unique individual—one whose gene expression patterns are constantly in flux and whose complex and ever-changing response to treatment, environment, and lifestyle will challenge physicians to listen differently, see differently, and respond differently than taught by the linear model of acute care." That statement allows us to question the accepted position of the CD community which clings to the principle that once the celiac genes are turned on, they stay on forever—theoretically at the same level of expression—such that once a patient becomes sensitive to gluten, that patient is forever relegated to a gluten–free diet. The authors' statement adds support to the controversial concept of "transient celiac disease," which suggests that a person may have a full blown case of symptomatic CD with all the tests showing positive, and then at some time later in life, the gene expression modulates and the person either becomes less sensitive to gluten or even may return to a totally normal diet without any untoward consequences. The patients' blood tests and biopsies would also potentially resort to normal. If you decide to read my book, you will observe that we already have documented cases of blood tests that reverted back to normal in people who had been officially diagnosed with CD but continued on a normal diet (fluctuating antibody levels). I think you get the picture. All of the aforementioned patients may show up as false negatives; I suspect the accountant can give you a strong estimate as to how accurate the 90/95 numbers are. Since you have only briefly discussed the biopsy on these web pages, I won't critique it, beyond stating that using that test as the "gold standard" also pushes the limits of credibility. If you would like to read my ebook it's on Amazon.com. It clearly identifies the shortcomings of the testing suggested for CD using accepted research and common laboratory knowledge. I am, as you are, a gluten-sensitive-patient advocate, but misinformation can be just as bad as no information. I'd love to have a professional conversation with you about the issues I have raised. Thank you for your time, Gordon Heinrichs, DC P.S. I am retired from seeing patients and write about gluten-health issues as a hobby and passion.
  22. Celiac.com 02/08/2017 - "What if the kid you bullied at school, grew up, and turned out to be the only surgeon who could save your life?" --Lynette Mather If you ask any high school senior what in their life has changed the most since kindergarten, statistics show that many would answer moving from one school to another. However, the more drastic of changes are seen such as illnesses diagnosed during these critical school ages. In 2009 I was diagnosed with celiac disease, and that diagnosis has impacted my life in both positive and negative ways for my past, present, and future time at Indiana Area High School and beyond. Personally I have had to deal with bullying because of my disabilities. Bullying by definition is the use of force or coercion to abuse or intimidate others. I along with 20% of my peers nationwide in grades 9-12 (The Youth Risk Behavior Surveillance System) experience bullying in many different forms. Bullying can be teasing, hitting, leaving someone out, whispering behind backs, online harassment, shoving, remarks about race, sexuality, and disabilities. Before my diagnosis I was considered "normal" but as a result of my illness and "strange" dietary needs therefore I have been bullied. However, looking back on my experience I am happy to have dealt with the resistance because it has made me a better, more confident individual. I, like three million fellow Americans nationwide (National Celiac Disease), must deal with the stress of having celiac disease. I was diagnosed in 2009 after having lost my eyesight to a migraine. Celiac Disease is an often under-diagnosed autoimmune disease wherein the person cannot eat wheat, rye, barley, or oats, otherwise known as gluten, because their antibodies will attack their own system leading to other serious health issues such as cancer. Celiac Disease is spread through genes; my entire family, including my father, mother, and sister, has this disease. However, even with the growing awareness of celiac disease, there is also a growing skepticism. "Critics" of my disease claim that the gluten free diet is a fad. Many celebrities have tried to lose weight and failed to stay on this difficult diet. Restaurant chains are coming out with new gluten free menus every day to raise prices and profits, though they refuse to educate their servers about what someone with a gluten "allergy" cannot eat. While some people are sympathetic and know the outstanding facts about celiac disease, most of the population stays in the dark about this ailment. This causes frustration for people with celiac disease, like me, to have to deal with the resulting brick wall of resistance. In my small community it is very rare for someone to have such a disease that the public knows little about. This can cause doubt and disbelief, especially at a high school where everyone is just trying to "fit in". When I was diagnosed in 2009, I had just started ninth grade and I had also started playing two high school sports, softball and tennis. For the softball team it was a well-known fact that after every away game the softball boosters would buy each girl a twelve inch sub from a local deli to eat on the way home. Whenever my parents and I contacted the booster president to explain the situation with my disability and that I simply would like to have a salad, we were met with backlash. I did not understand at the time why a parent would refuse to supply another child with food after a physical activity when everyone else was getting a meal. This quickly made me an outcast on the softball team as the "strange girl with the made up disease", causing me to feel stressed and awful about myself over something that I could not control. I would have loved to have been able to "fit in" and eat the subs like my teammates rather than being different, especially after growing up able to eat gluten! It was a hard transition to make. I went from being able to eat the subs, donuts, pizza, and any other fast-food product to a strict dietary regime. After my long process through the education system, I finally got the meal I had a right to have. Unfortunately, the boosters' actions, forced us to go through the school system to "prove" I had a legitimate excuse not to eat the subs. I was distanced from other members of the team and, in subsequent years, had to deal with backlash from my teammates. They do not understand that it is not a personal choice to avoid gluten. I have a disability. I simply cannot eat it. Instead, they go back to the first year when I was eating the same foods they ate, and I get blamed for wanting to be "special" and get the more expensive food. I know that I am not alone in my struggle and that people with celiac disease around the world deal with what I deal with everyday - just like others who are bullied for being different. The after effects from my being bullied have shown themselves even in everyday situations. I have learned a great deal about myself and respect for other individuals' differences. I believe that if I had not been bullied I would not have the self-confidence, integrity, sense of right and wrong, or leadership skills that I have now. It has allowed me to go above and beyond in tough situations, knowing that I can overcome them. I know that even though the times are tough with my disability, and that while others may never understand mine, I can certainly understand and respect theirs. I respect and do not judge others simply based on what they can or cannot eat. I also know that just because someone does not "look" ill on the outside does not mean they are not dealing with something awful on the inside. This allows me to make friends easily and to understand others more effectively. Being bullied has also allowed me to learn new leadership skills that I use in my volunteer work. I am confident in myself that I can go forward into the world of higher education and succeed because of the values I now hold dear. The most drastic change I have encountered in my high school career is the diagnosis of celiac disease in 2009. This diagnosis has impacted my life in both positive and negative ways, in the past, present, and future at Indiana Area High School and beyond. I have had to deal with bullying because of my disabilities. Bullying, by definition. is the use of force or coercion to abuse or intimidate others. I along with 20% of my peers nationwide in grades 9-12 (The Youth Risk Behavior Surveillance System) experience bullying in many different forms. After dealing with the effects of my being bullied, I know that it has made me a better person. I can travel the world and make lasting relationships based on acknowledging and respecting differences in every person I encounter.
  23. Celiac.com 05/16/2018 - Galectins are a family of animal lectins marked by their affinity for N-acetyllactosamine-enriched glycoconjugates. Galectins control several immune cell processes and influence both innate and adaptive immune responses. A team of researchers recently set out to assess the role of galectins, particularly galectin-1 (Gal-1), in the treatment of celiac disease. The research team included Victoria Sundblad, Amado A. Quintar, Luciano G. Morosi, Sonia I. Niveloni, Ana Cabanne, Edgardo Smecuol, Eduardo Mauriño, Karina V. Mariño, Julio C. Bai, Cristina A. Maldonado, and Gabriel A. Rabinovich. The researchers examined the role of galectins in intestinal inflammation, particularly in Crohn’s disease, ulcerative colitis, and celiac disease patients, as well as in murine models resembling these inflammatory conditions. Maintaining the fine balance between host immunity and tolerance promotes gut homeostasis, and helps to prevent inflammation. To gain insight into the role of Gal-1 in celiac patients, the team demonstrated an increase in Gal-1 expression following a gluten-free diet along with an increase in the frequency of Foxp3+ cells. The resolution of the inflammatory response may promote the recovery process, leading to a reversal of gut damage and a regeneration of villi. Among other things, the team’s findings support the use of Gal-1 agonists to treat severe mucosal inflammation. In addition, Gal-1 may serve as a potential biomarker to follow the progression of celiac disease treatment. Gut inflammation may be governed by a coordinated network of galectins and their glycosylated ligands, triggering either anti-inflammatory or pro-inflammatory responses. That network may influence the interplay between intestinal epithelial cells and the highly specialized gut immune system in physiologic and pathologic settings. The team’s results demonstrate that the anti-inflammatory and tolerogenic response associated with gluten-free diet in celiac patients is matched by a substantial up-regulation of Gal-1. This suggests a major role of this lectin in favoring resolution of inflammation and restoration of mucosal homeostasis. This data highlights the regulated expression of galectin-1 (Gal-1), a proto-type member of the galectin family, during intestinal inflammation in untreated and treated celiac patients. Further study of this area could lead to better understanding of the mechanisms behind celiac disease, and potentially to a treatment of the disease. Source: Front. Immunol., 01 March 2018. The researchers in this study are variously affiliated with the Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina; the Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba, Argentina; the Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Sección Intestino Delgado, Departamento de Medicina, Hospital de Gastroenterología Dr. C. Bonorino Udaondo, Buenos Aires, Argentina; the Unidad de Patología, Hospital de Gastroenterología, Bonorino Udaondo, Buenos Aires, Argentina; the Instituto de Investigaciones, Universidad del Salvador, Buenos Aires, Argentina; and the Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.
  24. The following detailed explanation of serological tests for celiac disease was written by Tom Ryan, Technical Service Specialist, INOVA Diagnostics, Inc. There has been a lot of discussion about serological testing for celiac disease recently, specifically regarding tTG (tissue Transglutaminase) testing. I will try to answer some of the many questions that have appeared on this list about all of the tests. First, and this applies to any of the blood tests, you must currently be on a gluten containing diet for the tests to be accurate. Antibodies are produced by the immune system in response to substances that the body perceives as threatening. The immune response that your body produces is its response to being exposed to gluten in the diet and its subsequent effect on the intestinal mucosa. If there is no gluten in the diet, then there is no response that we can measure. A brief change in diet will not have a noticeable effect. If you have been gluten free for a week or so, it will not make any great difference. The response might be marginally less but the difference is insignificant because the body has not had time to respond to the change. Conversely, if you have been gluten free for a protracted period of time and decide to be tested, a brief challenge of a couple of weeks is not enough to elicit a response and get an accurate test. There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus. Talk with your Doctor. My personal feeling is that the minimum is 2 slices of bread per day for 6 weeks to get an accurate test but I would not try to second-guess the Doctor. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc. What are all of these? Some contributors to the list make reference to the IgA or IgG test or to the ELISA test. These labels are incomplete for our purposes and could be referring to any number of different tests. We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal sera in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies. Anti-Gliadin Antibodies: Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results. A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for Enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower. Endomysial Antibodies: IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge. The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies. Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently, (1998) the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out. In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with: An initial positive gut biopsy; 6 months on a gluten free diet; A second, negative gut biopsy; A gluten challenge for 6 months and; A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure. Through the auspices of the Celiac Disease Foundation and others, a professional symposium and workshop was organized earlier this year in Marina Del Rey, California with participants from Europe as well as the U.S. to establish standards for reporting test results. This should improve testing and diagnosis even more. At the conclusion of this conference a Celiac Disease Standardization Committee was formed to investigate and make recommendations on a standardized method of reporting results.
  25. Celiac.com 05/14/2018 - An imbalance or defect in gut bacteria function may be a major cause of hair loss and pattern baldness. Pattern baldness (alopecia areata) affects approximately 1.7 per cent of the population and we still don’t know precisely what causes it. In addition to promoting a healthy digestive tract, our gut bacteria play an important function in our overall health. Recent experiments with antibiotics and bacteria-free mice reveal how a single a single gut bacteria, Lactobacillus murinus, could cause pattern baldness by triggering deficiencies in biotin. Biotin, vitamin B7, is a crucial vitamin. Biotin deficiency can lead to skin disease and hair loss. Some bacteria in our gut produces biotin, while other bacteria breaks down and consumes biotin. Biotin deficiency is most often seen in patients with serious conditions, such as celiac disease, but it can also be common among pregnant women. Previous research has shown that bacteria-free mice that lack biotin in their diet, develop mild hair loss (alopecia). Could an imbalance or defect in gut bacteria function be a major cause of hair loss and pattern baldness? To determine if the underlying cause of hairless might be an imbalance of our gut bacteria, a team of Japanese scientists conducted experiments with antibiotics and bacteria-free mice to see if variations gut bacteria might cause pattern baldness by influencing biotin levels. The team first fed laboratory mice a diet with and without biotin, but saw no impact on hair loss. They then repeated the experiment, but this time they also gave the mice a long course of antibiotics to destroy the balance of bacteria in their gut. The laboratory mice on a biotin-free diet coupled with antibiotics saw an increase in a particular gut bacteria that corresponded to patten hair loss, as was previously shown in bacteria-free mice. By studying what had happened in the gut bacteria of these mice, the scientists discovered that a particular type of lactic acid bacteria, Lactobacillus murinus, had expanded after the antibiotic treatment. When the team fed bacteria-free mice with Lactobacillus murinus, they saw that the hair loss became even worse and the mice became almost entirely bald. Further tests followed, in which regular mice and bacteria-free mice received a regular diet with normal levels of biotin, but added Lactobacillus murinus. These mice showed no hair loss at all. Direct injections of biotin also stopped hair loss; although the team did concede that skin bacteria could also play a role. The discovery that gut bacteria and diet to influence hair loss creates new avenues for treating baldness and hair loss simply by adjusting gut microbiota. It’s possible that probiotic dietary supplements can be used to influence gut bacteria, and prevent the biotin-eating bacteria now known to cause hair loss. Stay tuned for news on the role of gut bacteria in hair loss, and on any new treatment approaches to hair loss and alopecia that may result. Their results appear in the scientific journal Cell Reports.