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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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    CAN AUTOIMMUNE DISEASE SYMPTOMS VARY DEPENDING ON THE TIME OF DAY?


    Jefferson Adams


    • Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease. Does this tell us something about new about autoimmune diseases?


    Celiac.com 01/03/2018 - A recent study indicates that symptoms for some autoimmune disease can vary depending on the time of day.


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    A substance called transcription factor BMAL1 plays a crucial role in the human molecular clock, regulating biological pathways that drive 24 hour circadian rhythms in behavior and physiology. The molecular clock has a major influence on innate immune function, and disturbances in circadian rhythms are associated with increases in multiple sclerosis (MS), for example.

    But, researchers just don't have much good information on the factors that influence this association. A team of researchers recently set out to better understand the factors that influence this association. The research team included Caroline E. Sutton, Conor M. Finlay, Mathilde Raverdeau, James O. Early, Joseph DeCourcey, Zbigniew Zaslona, Luke A. J. O'Neill, Kingston H. G. Mills, and Annie M. Curtis.

    They are variously affiliated with the Immune Regulation Research Group, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; the Inflammatory Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; and with the Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland (RCSI), Dublin, Ireland.

    In a recent study, the research team found that BMAL1 and time-of-day regulate the accumulation and activation of various immune cells in a CNS autoimmune disease model, experimental autoimmune encephalomyelitis (EAE).

    In myeloid cells, BMAL1 maintains anti-inflammatory responses and reduces T cell polarization. Loss of myeloid BMAL1 or midday immunizations to induce EAE create an inflammatory environment in the CNS through expansion and infiltration of IL-1β-secreting CD11b+Ly6Chi monocytes, resulting in increased pathogenic IL-17+/IFN-γ+ T cells.

    These findings show the important role played by the molecular clock in processing innate and adaptive immune crosstalk under autoimmune conditions.

    Understanding the exact ways in which the human molecular clock influences innate immune function, and by extension, autoimmune diseases, will help doctors to better understand these disease, and to develop better approaches to treatment, among other things.

    Source:


    Image Caption: Photo: CC--David Dennis
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  • Related Articles

    Jefferson Adams
    Celiac.com 02/20/2013 - Scientific evidence indicates that the risk of developing celiac disease cannot be explained solely by genetic factors. There is some evidence to support the idea that the season in which a child is born can influence the risk for developing celiac disease. It is known that babies born in summer months are likely to be weaned and introduced to gluten during winter, when viral infections are more frequent.
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    To better answer the question, a research team recently set out to conduct a more thorough study of the relationship between birth month and celiac disease.
    The research team included B. Lebwohl, P.H. Green, J.A. Murray, and J.F. Ludvigsson. The study was conducted through the Department of Paediatrics at Örebro University Hospital in Örebro, Sweden.
    To conduct the study, the team used biopsy reports from all 28 Swedish pathology departments to identify individuals with celiac disease, which they defined as small intestinal villous atrophy (n=29 096).
    Using the government agency Statistics Sweden the team identified 144,522 control subjects, who they matched for gender, age, calendar year and county.
    The team then used conditional logistic regression to examined the association between summer birth (March-August) and later celiac disease diagnosis (outcome measure).
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    So, being born in the summer is associated with a slightly higher risk of later celiac disease (OR 1.06; 95% CI 1.03 to 1.08; p).
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    In this study, the data show that people born during the summer months had a slightly higher risk of developing celiac disease, but that excess risk was small, and general infectious disease exposure early in life were not likely to increase that risk.
    Source:
    Arch Dis Child. 2013 Jan;98(1):48-51. doi: 10.1136/archdischild-2012-302360.

    Jefferson Adams
    Celiac.com 07/28/2016 - Celiac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals. Researchers know that innate immunity plays a role in triggering celiac disease, but they don't understand the connection very well at all.
    Although previous in vitro work suggests that gliadin peptide p31-43 acts as an innate immune trigger, the underlying pathways are unclear and have not been explored in vivo.
    The research team included RE Araya, MF Gomez Castro, P Carasi, JL McCarville, J Jury, AM Mowat, EF Verdu, and FG Chirdo. They are variously affiliated with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Catedra de Microbiología, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; the Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom; and with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina.
    Their team observed that introduction of p31-43 into the gut of normal mice causes structural changes in the small intestinal mucosa consistent with those seen in celiac disease, including increased cell death and expression of inflammatory mediators. The effects of p31-43 were dependent on MyD88 and type I IFNs, but not Toll-like receptor 4 (TLR4), and were enhanced by co-administration of the TLR3 agonist polyinosinic:polycytidylic acid.
    Together, these results indicate that gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, such as IFN-dependent inflammation.
    These findings also suggest a common mechanism for the potential interaction between dietary gluten and viral infections in the pathogenesis of celiac disease, meaning that certain viral infections may pave the way for celiac disease to develop.
    Source:
    Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.

    Jefferson Adams
    Celiac.com 04/11/2017 - A new study shows that people living in the southern United States have less celiac disease than their Northern counterparts, regardless of race or ethnicity, socioeconomic status, or body mass index.
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    Source:
    Gastroenterology

    Jefferson Adams
    Celiac.com 01/01/2018 - A team of researchers recently set out to conduct a genome-wide association study (GWAS) of general cognitive ability ("g"), further enhanced by combining results with a large-scale GWAS of educational attainment.
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    Their study provided a large-scale GWAS of cognitive performance, combined with GWAS of educational attainment; 70 independent genomic loci associated with individual differences in cognition. The study found that implicated genes suggest potential treatment targets for cognitive enhancement. The team also observed genetic overlap between cognitive ability and multiple health-related phenotypes.
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    Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.11.028 
    The research team members are variously associated with the following:
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Peters VA Medical Center, Bronx, NY, USA Department of Neurology, Bryan Alzheimer's Disease Research Center and Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA Department of Psychiatry and Behavioral Sciences, Division of Medical Psychology, Duke University Medical Center, Durham, NC, USA Laboratory of NeuroGenetics, Department of Psychology & Neuroscience, Duke University, Durham, NC, USA Human Longevity Inc., Durham, NC, USA Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA Department of Psychology, Yale University, New Haven, CT, USA Department of Psychology, Stanford University, Palo Alto, CA, USA Clinical and Translational Neuroscience Branch, Intramural Research Program, National Institute of Mental Health, National Institute of Health, Bethesda, MD, USA Lieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA Neuroimaging, Cognition & Genomics (NICOG) Centre, School of Psychology and Discipline of Biochemistry, National University of Ireland, Galway, Ireland Neuropsychiatric Genetics Research Group, Department of Psychiatry and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK Department of Psychology, University of Edinburgh, Edinburgh, UK Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK Division of Brain Sciences, Department of Medicine, Imperial College, London, UK Centre for Epidemiology, Division of Population Health, Health Services Research & Primary Care, The University of Manchester, Manchester, UK Centre for Integrated Genomic Medical Research, Institute of Population Health, University of Manchester, Manchester, UK Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, UK Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway Department of Medical Genetics, Oslo University Hospital, University of Bergen, Oslo, Norway NORMENT, K.G. Jebsen Centre for Psychosis Research, University of Bergen, Bergen, Norway Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway Department of Psychology, University of Edinburgh, Edinburgh, UK Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK Department of Medical Genetics, University of Helsinki and University Central Hospital, Helsinki, Finland Department of General Practice, University of Helsinki and Helsinki University Hospital, Helsinki, Finland National Institute for Health and Welfare, Helsinki, Finland Folkhälsan Research Center, Helsinki, Finland Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland Department of Psychiatry, Martin Luther University of Halle-Wittenberg, Halle, Germany Department of Psychology, University of Crete, Crete, Greece Department of Psychiatry, National and Kapodistrian University of Athens Medical School, Eginition Hospital, Athens, Greece University Mental Health Research Institute, Athens, Greece Neurobiology Research Institute, Theodor-Theohari Cozzika Foundation, Athens, Greece Department of Psychiatry and Behavioral Sciences, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA 23andMe, Inc., Mountain View, CA, USA

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    Connie Sarros
    Celiac.com 04/21/2018 - Dear Friends and Readers,
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    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
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    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