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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    DOES A LONG NONCODING RNA INFLUENCE SUSCEPTIBILITY TO CELIAC DISEASE?


    Jefferson Adams

    Celiac.com 04/11/2016 - Growing evidence suggests that long noncoding RNAs (lncRNAs) play an important role in gene expression, especially that which influences inflammation. For example, researchers recently found that one lncRNA, lnc13, suppresses inflammatory gene expression in macrophages by interacting with proteins that regulate chromatin accessibility.


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    Image: CC--AndreaLaurelReduced levels of lnc13 in intestinal tissue from individuals with celiac disease suggests that lnc13 might also play a role in the development of immune-mediated diseases. In a recent issue of Science, a research team reports on the identification and characterization of a lncRNA, lnc13, that harbors a celiac disease–associated haplotype block and represses expression of certain inflammatory genes under homeostatic conditions.

    The research team included Ainara Castellanos-Rubio, Nora Fernandez-Jimenez, Radomir Kratchmarov, Xiaobing Luo, Govind Bhagat, Peter H. R. Green, Robert Schneider, Megerditch Kiledjian, Jose Ramon Bilbao, and Sankar Ghosh. They are variously affiliated with the Department of Microbiology and Immunology, the Department of Pathology and Cell Biology, and the Center for Celiac Disease, Department of Medicine at Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA; the Department of Genetics, Physical Anthropology, and Animal Physiology, University of the Basque Country (UPV-EHU), at BioCruces Research Institute in Leioa, Basque Country, Spain; the Alexandria Center for Life Sciences, New York University School of Medicine, New York, NY, USA; and with the Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.

    Their article describes how Lnc13 regulates gene expression by binding to hnRNPD, a member of a family of ubiquitously expressed heterogeneous nuclear ribonucleoproteins (hnRNPs). Upon stimulation, lnc13 levels decrease, thereby allowing increased expression of the repressed genes.

    The fact that Lnc13 levels are substantially decreased in small intestinal biopsy samples from patients with celiac disease suggests that down-regulation of lnc13 may contribute to the inflammation associated with celiac disease.

    Furthermore, the lnc13 disease-associated variant binds hnRNPD less efficiently than its wild-type counterpart, thus helping to explain how these single-nucleotide polymorphisms contribute to celiac disease.

    This discovery could lead to future treatment methods for celiac disease.

    Source:


    Image Caption: Image: CC--AndreaLaurel
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  • Related Articles

    Dr. Scot Lewey

    This article appeared in the Summer 2006 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 08/31/2006 - All of us have patterns of proteins on the surface of our white blood cells. These proteins are known as human leukocyte antigens (HLA), one of which is DQ. Celiac disease and non-celiac gluten sensitivity (NCGS), and several autoimmune conditions occur more frequently with certain HLA DQ types. DQ gene testing is performed by analyzing cells from a blood sample or from a Q-tip swab of the mouth. HLA types have a naming system that can be confusing even to scientists and physicians but here is my explanation of the testing, the results, and what they may mean to you and your family.
    Each of us has two copies of HLA DQ. Because there are 9 serotypes of DQ we are all DQx/DQx where x is a number between 1 & 9. For example, I am DQ2/DQ7. I received the DQ2 from one of my parents and the DQ7 from the other. Because we get one DQ type from each of our parents and give one to each of our children it is easy to to see how the DQ genes pass through a family. This is important because two DQ types, DQ2 and DQ8, are estimated to be present in over 98% of all people who have celiac disease, the most severe form of gluten sensitivity.
    Rarely, true celiac disease or dermatitis herpetiformis, the skin disease equivalent of celiac, have been reported to occur in people who do not have DQ2 and/or DQ8. However, according to unpublished data from Dr. Ken Fine of Enterolab, the other six types, except DQ4, are associated with risk for elevated stool antibodies to gliadin, the toxic fraction of gluten, and/or tissue transglutaminase (tTG) an enzyme. Both of these antibodies are usually elevated in the blood of individuals with celiac disease though they may be normal in the blood of individuals who are gluten sensitive and have a normal small intestine biopsy but respond favorably to a gluten-free diet.
    Fine has publicly reported that elevated stool antibodies to gliadin and/or tTG have been detected in all of the untreated celiacs tested in his lab and 60% of non-celiacs who have symptoms consistent with gluten sensitivity but in none of the controls tested including cow manure. Follow up surveys of those individuals with elevated stool antibodies who initiated a gluten-free diet compared with those with elevated antibodies who did not reportedly showed significantly improved quality of life and improved symptoms in the gluten-free group.
    He also reported DQ2 and DQ8 positive individuals have had, as a rule, the highest elevations of stool gliadin antibody followed by those who are DQ7 positive. Only those who are doubly positive for DQ4 have not been found to have significantly elevated antibodies to indicated gluten sensitivity. This is consistent with the differences in prevalence rates of celiac disease seen in various parts of the world since DQ4 is not generally found in Caucasians of Northern European ancestry where celiac incidence is highest but in those from Asia or Southern Africa where there is a very low incidence of celiac disease and gluten intolerance.
    DQ2 & DQ8, the two major types present in 90-99% of people who have celiac disease, are present in approximately 35-45% of people in the U.S., especially those of Caucasian race of Northern European ancestry, with highest risk of celiac disease but the prevalence in U.S. of celiac disease is 1%. Though a prevalence of 1 in 100 is very common and much higher than had been believed for years, only a fraction of the genetically at risk are confirmed to have celiac disease by abnormal blood tests and small intestine biopsies. However, the number of people who report a positive response to gluten-free diet is much higher.
    The stool antibody tests results would support this and the concept of a spectrum of gluten sensitivity that is much broader and in need of better diagnostic definitions. I am an example of someone who is DQ2/DQ7 who has normal blood tests for celiac disease but abnormal stool antibody tests and symptoms that responded to gluten-free diet. The strict criteria for diagnosing celiac disease, which is abnormal blood tests and a characteristic small intestine biopsy showing classic damage from gluten, is much narrower than what is being seen clinically.
    It is becoming obvious to many of us who have personal and professional medical experience with gluten intolerance and celiac disease that the problem of gluten sensitivity is much greater and extends beyond the high risk celiac genes DQ2 and DQ8. Traditionally it is reported and believed by many that if you are DQ2 and DQ8 negative you are unlikely to have celiac disease or ever develop it, though this cannot be said with 100% certainty especially since there are documented cases of celiac disease and the skin equivalent of celiac disease, known as dermatitis herpetiformis (DH) in individuals who are DQ2 and DQ8 negative.
    Therefore, knowing your DQ specific serotype pattern may be helpful for several reasons. For example, if you have more than one copy of DQ2 or DQ8, you carry two of the major genes. For example, if you are DQ2/DQ2, DQ2/DQ8, or DQ8/DQ8, a term Scott Adams of www.celiac.com has dubbed a "super celiac" you may be at much higher risk for celiac disease and have more severe gluten sensitivity. Certainly if you are DQ2 and/or DQ8 positive you are at increased risk for celiac disease. After a single copy of DQ2 or DQ8, it appears that DQ7/DQ7 might be next highest risk. Dr. Fine has also noted some other associations of the DQ patterns with microscopic or collagenous colitis, neurologic manifestations of gluten sensitivity and dermatitis herpetiformis, which has been one of the gluten sensitive conditions noted to be, at times, occurring in DQ2, DQ8 negative individuals.
    Why some people get celiac Disease or become gluten sensitive is not well understood but certain factors are believed to include onset of puberty, pregnancy, stress, trauma or injury, surgery, viral or bacterial infections including those of the gut, medication induced gut injury or toxicity e.g. non-steroidal anti-inflammatory medications such as aspirin, ibuprofen, etc., immune suppression or autoimmune diseases especially since several of those factors are associated with onset or unmasking of gluten sensitivity in someone who is at risk or not manifesting any recognizable symptoms. There is also well known group of individuals who are termed "latent" celiacs. They are at high risk because they have close relatives who have celiac disease with whom they share one or more of the celiac genes DQ2 and/or DQ8 though they usually have few or no symptoms but sometimes have abnormal blood tests and/or biopsies indicating possible or definite celiac disease. Others have negative blood tests and normal biopsies but symptoms that respond to a gluten-free diet.
    The severity of the sensitivity to gluten appears to be related to the DQ type, family history (highest risk is in the non affected identical twin of a celiac), pre-existing intestinal injury, degree of exposure to gluten (how frequent and large a gluten load an individual is exposed to), and immune status. Once initiated, gluten sensitivity tends to be life long. True celiac disease requires life-long complete gluten avoidance to reduce the increased risk of serious complications of undiagnosed and untreated celiac such as severe malabsorption, cancers, especially of the GI tract and lymphoma, other autoimmune diseases and premature death due to these complications.
    Again, DQ testing can be done with cells from blood or by a swab of the inside of the mouth but not all labs test for or report the full DQ typing but only the presence or absence of DQ2 and DQ8. The lab that performs DQ testing is usually determined by an individual insurance company on the basis of contracts with specific commercial labs. However, if your insurance contracts with Quest Labs or the Laboratory at Bonfils (Denver, CO) full DQ can be done if ordered and authorized by the insurance company.
    For those willing to pay out of pocket, Bonfils performs full DQ testing for Enterolab (www.enterolab.com) on a sample obtained by a Q tip swab of the mouth. Since it is painless and non-invasive it is well tolerated especially by young children. Also because the testing can be ordered without a physician and the sample obtained in their home using a kit obtained from Enterolab it is convenient. The kit is returned by overnight delivery by to Enterolab who forwards the test onto Bonfils. The cost is $149 for the genetic testing alone and has to be paid for in advance by credit card or money order and is generally not reimbursed by insurance.
    Enterolab also provides the stool testing for gliadin and tissue transglutaminase antibodies to determine if gluten sensitivity is evident. The gliadin antibody alone is $99 or the full panel includes genetic typing, stool testing for gluten and cows milk protein antibodies, and a test for evidence of malabsorption is $349.
    Again, the advantages of full DQ testing is determining if someone has more than one copy of DQ2 or DQ8 or carry both and therefore have a higher risk for celiac disease or more severe gluten intolerance. If you are DQ2 or DQ8 negative then your risk of celiac disease is low, though not non-existent. If you are not DQ4/DQ4 then you do have risk for gluten sensitivity. If you determine all DQ types within enough family members you can piece together a very accurate history of the origin of celiac and gluten sensitivity within a family and make some very accurate predictions of risk to other family members.
    Though the lay public and many clinicians are finding the genetic tests helpful, many, including most physicians, do not understand the genetics of gluten sensitivity. We are awaiting Dr. Fines published data on the significance of stool antibody tests and their association to the other DQ types as his lab is the only lab offering the stool antibody tests in the U.S. Other celiac researchers in U.S. have failed to reproduce his assay but scattered reports in the literature are appearing including a recent article in the British Medical Journal indicating stool antibody testing is feasible, non-invasive, and using their protocol, highly specific but not sensitive for celiac disease in children. (Editors note: When present, these antibodies indicate celiac disease. However, they are not present in many cases of celiac disease.)
    In the meantime, many patients are faced with the uncertainty and added cost of full DQ testing and stool testing due to the failure of traditional blood tests, small bowel biopsies, and the presence or absence of DQ2 and DQ8 to diagnose or exclude gluten sensitivity. Physicians unfamiliar with this testing are increasingly presented with the results and confused or skeptical pending published reports. The medical community continues to lack a consensus regarding the definitions of non-celiac gluten sensitivity and what tests justify recommendations for gluten-free diet. It is clear that gluten sensitivity, by any criteria, is much more common than ever thought and a hidden epidemic exists.
    Dr. Scot Lewey is a physician who is specialty trained and board certified in the field of gastroenterology (diseases of the digestive system) who practices his specialty in Colorado. He is the physician advisor to the local celiac Sprue support group and is a published author and researcher who is developing a web based educational program for people suffering from food intolerances, www.thefooddoc.com
    Article Source: EzineArticles.com

    Jefferson Adams
    Celiac.com 06/20/2014 - Celiac disease is a T cell–mediated disease triggered by the protein in wheat gluten. More than 9 out of 10 of people with celiac disease carry human leukocyte antigen (HLA)-DQ2 locus.
    A team of researchers recently set out to determine if T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease.
    The researchers included Jan Petersen, Veronica Montserrat, Jorge R Mujico, Khai Lee Loh, Dennis X Beringer, Menno van Lummel, Allan Thompson, M Luisa Mearin, Joachim Schweizer, Yvonne Kooy-Winkelaar, Jeroen van Bergen, Jan W Drijfhout, Wan-Ting Kan, Nicole L La Gruta, Robert P Anderson, Hugh H Reid, Frits Koning, and Jamie Ross.
    They are variously affiliated with the Department of Biochemistry and Molecular Biology at the School of Biomedical Sciences, and the Australian Research Council Centre of Excellence in Advanced Molecular Imaging at Monash University in Clayton, Victoria, Australia, the Department of Pediatrics, and the Department of Immunohematology and Blood Transfusion at Leiden University Medical Center in Leiden, The Netherlands, the Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, at the University of Melbourne in Parkville, Victoria, Australia, ImmusanT, Inc., in Cambridge, Massachusetts, USA, and the Institute of Infection and Immunity at Cardiff University School of Medicine in Heath Park, Cardiff, UK.
    The team first determined T-cell receptor (TCR) usage and fine specificity of patient-derived T-cell clones specific for two epitopes from wheat gliadin, DQ2.5-glia-α1a and DQ2.5-glia-α2.
    They also determined the ternary structures of four distinct biased TCRs specific for those epitopes. They were able to establish a basis for the biased TCR usage through mutagenesis and affinity measurements, together with the fact that all three TCRs specific for DQ2.5-glia-α2 docked centrally above HLA-DQ2. They found that a non–germline–encoded arginine residue within the CDR3β loop served as key of this common docking footprint.
    Although the TCRs specific for DQ2.5-glia-α1a and DQ2.5-glia-α2 docked similarly, their interactions with the respective gliadin determinants differed markedly, thereby providing a basis for epitope specificity.
    This is the first time a research team has determined that T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease. Further study is needed to better understand the nature of their relationship.
    Source:
    NATURE STRUCTURAL & MOLECULAR BIOLOGY

    Jefferson Adams
    Celiac.com 09/16/2015 - Autoimmune disease, such as type 1 diabetes, Crohn's disease, and juvenile idiopathic arthritis, affect about 7 to 10 percent of the population in the Western Hemisphere.
    Using genome-wide association studies (GWASs), researchers have identified hundreds of susceptibility genes, including shared associations across clinically distinct autoimmune diseases.
    A team of researchers recently conducted an inverse χ2 meta-analysis across ten pediatric-age-of-onset autoimmune diseases (pAIDs) in a case-control study including more than 6,035 cases and 10,718 shared population-based controls.
    The research team included Yun R Li, Jin Li, Sihai D Zhao, Jonathan P Bradfield, Frank D Mentch, S Melkorka Maggadottir, Cuiping Hou, Debra J Abrams, Diana Chang, Feng Gao, Yiran Guo, Zhi Wei, John J Connolly, Christopher J Cardinale, Marina Bakay, Joseph T Glessner, Dong Li, Charlly Kao, Kelly A Thomas, Haijun Qiu, Rosetta M Chiavacci, Cecilia E Kim, Fengxiang Wang, James Snyder, and Marylyn D Richie.
    The are variously affiliated with The Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; Medical Scientist Training Program, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA; the Department of Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.; the Division of Allergy and Immunology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.; the Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, USA; the Program in Computational Biology and Medicine, Cornell University, Ithaca, New York, USA, and the Department of Computer Science, New Jersey Institute of Technology, Newark, New Jersey, USA.
    For their study, the team identified 27 genome-wide significant loci associated with one or more pAIDs, mapping to in silico–replicated autoimmune-associated genes (including IL2RA) and new candidate loci with established immunoregulatory functions such as ADGRL2, TENM3, ANKRD30A, ADCY7 and CD40LG.
    The team functionally enriched the pAID-associated single-nucleotide polymorphisms (SNPs) for deoxyribonuclease (DNase)-hypersensitivity sites, expression quantitative trait loci (eQTLs), microRNA (miRNA)-binding sites and coding variants.
    They also identified biologically correlated, pAID-associated candidate gene sets on the basis of immune cell expression profiling and found evidence of genetic sharing.
    Network and protein-interaction analyses demonstrated converging roles for the signaling pathways of type 1, 2 and 17 helper T cells (TH1, TH2 and TH17), JAK-STAT, interferon and interleukin in multiple autoimmune diseases.

    Source:
    Nature Medicine 21, 1018–1027 (2015) doi:10.1038/nm.3933

    Jefferson Adams
    Celiac.com 03/02/2016 - A team of researchers recently completed the first extensive study comparing gene expression in children and adults with celiac disease, and found some key differences between the two groups.
    The research team included V. Pascual, L. M. Medrano , N. López-Palacios, A. Bodas, B. Dema, M. Fernández-Arquero, B. González-Pérez, I. Salazar, and C. Núñez. They are variously affiliated with Servicio de Pediatría, Servicio de Aparato Digestivo, and Servicio de Inmunología Clínica at the Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain, and with the Departamento de Producción Animal, Facultad de Veterinaria, and the Departamento de Estadística e Investigación Operativa I, Facultad de Matemáticas, Universidad Complutense de Madrid in Madrid, Spain.
    For their study, the team collected 19 duodenal biopsies of children and adults with celiac disease and compared the expression of 38 selected genes between each other, and in 13 non-celiac disease control subjects matched by age.
    The team used a Baysian methodology to analyze the differences of gene expression between groups. They found that, compared to controls, children and adults with celiac disease all had seven genes with a similarly altered expression. These were C2orf74, CCR6, FASLG, JAK2, IL23A, TAGAP and UBE2L3.
    The team found differences in 13 genes, six of which were altered only in adults (IL1RL1, celiac disease28, STAT3, TMEM187, VAMP3 and ZFP36L1) and two only in children (TNFSF18 and ICOSLG); while four genes show a significantly higher alteration in adults (CCR4, IL6, IL18RAP and PLEK) and one in children (C1orf106).
    Between the two groups, the team found significant differences in the expression level of several genes, most notably the higher alteration seen in adults.
    The team is calling for further research to assess possible genetic influences behind the changes, along with the specific physical consequences of the reported differences.
    Source:
    PLOS.ORG. Published: February 9, 2016. DOI: 10.1371/journal.pone.0146276

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/20/2018 - A digital media company and a label data company are teaming up to help major manufacturers target, reach and convert their desired shoppers based on dietary needs, such as gluten-free diet. The deal could bring synergy in emerging markets such as the gluten-free and allergen-free markets, which represent major growth sectors in the global food industry. 
    Under the deal, personalized digital media company Catalina will be joining forces with Label Insight. Catalina uses consumer purchases data to target shoppers on a personal base, while Label Insight works with major companies like Kellogg, Betty Crocker, and Pepsi to provide insight on food label data to government, retailers, manufacturers and app developers.
    "Brands with very specific product benefits, gluten-free for example, require precise targeting to efficiently reach and convert their desired shoppers,” says Todd Morris, President of Catalina's Go-to-Market organization, adding that “Catalina offers the only purchase-based targeting solution with this capability.” 
    Label Insight’s clients include food and beverage giants such as Unilever, Ben & Jerry's, Lipton and Hellman’s. Label Insight technology has helped the Food and Drug Administration (FDA) build the sector’s very first scientifically accurate database of food ingredients, health attributes and claims.
    Morris says the joint partnership will allow Catalina to “enhance our dataset and further increase our ability to target shoppers who are currently buying - or have shown intent to buy - in these emerging categories,” including gluten-free, allergen-free, and other free-from foods.
    The deal will likely make for easier, more precise targeting of goods to consumers, and thus provide benefits for manufacturers and retailers looking to better serve their retail food customers, especially in specialty areas like gluten-free and allergen-free foods.
    Source:
    fdfworld.com

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
     
    The research team included Åsa Torinsson Naluai, Ladan Saadat Vafa, Audur H. Gudjonsdottir, Henrik Arnell, Lars Browaldh, and Daniel Agardh. They are variously affiliated with the Institute of Biomedicine, Department of Microbiology & Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institute, Stockholm, Sweden; the Department of Clinical Science and Education, Karolinska Institute, Sodersjukhuset, Stockholm, Sweden; the Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden; the Diabetes & Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; and with the Nathan S Kline Institute in the U.S.A.
    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
    Compared with the control group, seven out of twenty-three children with celiac disease showed elevated levels of the the following amino acids: tryptophan; taurine; glutamic acid; proline; ornithine; alanine; and methionine.
    The significance of the individual amino acids do not survive multiple correction, however, multivariate analyses of the amino acid profile showed significantly altered amino acid levels in children with celiac disease overall and after correction for age, sex and experimental effects.
    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.
    Source:
    cnbc.com

    admin
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1% of the population. 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:
    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

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com