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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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    HOW COMMON IS CELIAC DISEASE


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    On Thursday, 16 November 1995 14:46:57 -0500, The SPRUENIK AFD had:

    Dr. Alexander: In reviewing the syllabus for the Baltimore conference, there are some points that I wonder about. The syllabus suggests the frequency of celiac disease (celiac disease) may be 1 in 250 people. Perhaps it is in Ireland and certain other locations where there is a homogenous population this may be true. But could it really be 1 in 250 people in Italy, which is practically synonymous with pasta? You would expect there to be an epidemic of complications. Perhaps the definition of celiac disease used in these studies is less stringent than it is here. If the studies are based on symptoms or positive blood tests, they could be including a lot of false positives in their statistics. Or perhaps the studies are based on relatives of celiacs, in which case you would pick up a higher percentage of celiacs than you would from the general population.


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    admin

    Scand J Gastroenterol. 2005 Apr;40(4):437-43. Celiac.com 07/28/2005 - In an effort to determine whether gluten exposure in those with celiac disease can cause additional autoimmune diseases, Finnish researchers evaluated the frequency of autoimmune disorders in 703 adults and children with celiac disease, and compared them with 299 controls (normal duodenal histology). For each person in the study the researchers assessed the effect of age at the end of follow-up, age at diagnosis; actual gluten exposure time; and the gender and diagnostic delay time. They then determined autoimmune disease incidence figures that were expressed as a dependent variable via logistic regression analysis (per 10,000 person-years).
    The researchers found that the celiac disease group had a significantly higher prevalence of additional autoimmune diseases that was not affected by exposure to gluten.
    Additional Comments on this Study by Roy Jamron:
    Autoimmune disease has a high prevalence in celiacs. The following study concludes that the duration of gluten exposure in celiacs is not a significant factor in the risk of developing autoimmune disease. One diagnosed late in life with celiac disease does not appear to be at greater risk for developing autoimmune disease. This seems counter-intuitive, but there may be a good explanation for this result.
    Studies in the UK and Italy have demonstrated that the prevalence of celiac disease in young children is essentially the same as in adults, meaning celiac disease begins in infancy. Infancy is the critical time period for the development of the immune system. Gluten exposure and the onset of celiac disease symptoms early in life, therefore, have a much greater and more important impact on the immune system and its development than exposure to gluten later in life. Malabsorption during infancy and early childhood can also adversely affect the crucial function of the thymus, T cell production, and T cell repertoire. So the stage is set early in life rather than later for increased risk of autoimmune disease. The timing of gluten exposure in life seems to be more critical to autoimmune disease risk rather than the overall lifetime duration of gluten exposure. It is, therefore, extremely important to diagnose celiac disease and initiate a gluten-free diet as soon as possible during infancy and young childhood to lower the risk of autoimmune disease later in life.

    Jefferson Adams
    Celiac.com 07/09/2009 - Rates of celiac disease are four times higher today than they were just fifty years ago, according to the results of a new study by scientists at the Mayo clinic. In addition, the study showed that people with undiagnosed celiac disease died at rates four times higher than non-celiacs over the 45 year follow-up period.
    Celiac disease is an immune system reaction to gluten in the diet which, left untreated, celiac disease causes damage to the lining of the digestive tract and leaves sufferers at risk for various cancers and other associated conditions. When people with celiac disease eat wheat, barley or rye, a protein called gluten triggers an immune system attack, which damages the villi in the small intestine.Villi are finger-like folds in the intestine that increase surface area for nutrient absorption.
    Celiac disease symptoms may include diarrhea, abdominal discomfort, weight loss, anemia, unexplained infertility, loss of teeth or even premature or severe osteoporosis, among others.
    Joseph Murray, M.D., the Mayo Clinic gastroenterologist who led the study says celiac disease "now affects about one in a hundred people. We also have shown that undiagnosed or 'silent' celiac disease may have a significant impact on survival. The increasing prevalence, combined with the mortality impact, suggests celiac disease could be a significant public health issue."
    So, celiac disease is striking a higher than ever portion of the population, yet doctors don't yet fully understand the reasons for this reality.
    A team of Mayo Clinic scientists team performed celiac disease antibody tests on blood samples gathered at Wyoming's Warren Air Force Base (AFB) between 1948 and 1954. They then compared those blood test results with results from two recently collected groups from Olmsted County, Minn. Tests for the first group were matched by age to those from the Warren AFB group at the time of the blood draw, while the second group was matched by birth years.
    Researchers found that young people today are 4.5 times more likely to have celiac disease than young people were in the 1950s, while those whose birth years matched the Warren AFB participants were four times more likely to have celiac disease.
    Celiac disease was once thought to be rare, and many physicians still regard it as so, but, according to Dr. Murray, that is no longer the case.
    "Celiac disease is unusual, but it's no longer rare," he says.
    Dr. Murray adds: "Something has changed in our environment to make it much more common. Until recently, the standard approach to finding celiac disease has been to wait for people to complain of symptoms and to come to the doctor for investigation. This study suggests that we may need to consider looking for celiac disease in the general population, more like we do in testing for cholesterol or blood pressure."
    For Dr. Murray, the findings underscore the importance of raising awareness of celiac disease, both among physicians and patients. He adds that some studies "have suggested that for every person who has been diagnosed with celiac disease, there are likely 30 who have it, but are not diagnosed. And given the nearly quadrupled mortality risk for silent celiac disease we have shown in our study, getting more patients and health professionals to consider the possibility of celiac disease is important."
    One interesting point not touched on in the study is the increase in the gluten content of commercial varieties of wheat now being grown compared to gluten levels of 50 years ago. Additionally, people are eating more wheat and gluten than ever before.
    (http://www.mayoclinic.org/bio/13032852.html)
    Gastroenterology, July 2009;137(1)pp 373-374


    Jefferson Adams
    A team of researchers recently to examine the design of new high affinity peptide ligands for HLA-DQ2 using a positional scanning peptide library.
    The research team included U. Jüse, Y. van de Wal, F. Koning, L. M. Sollid, B. Fleckenstein with the Centre for Immune Regulation, Institute of Immunology, Oslo University Hospital-Rikshospitalet, Oslo, Norway.
    HLA-DQ2 (DQA1*0501/DQB1*0201) is associated with several immune disorders including celiac disease, which results from an inappropriate T-cell response to gluten.
    Researchers hope that interference with peptide presentation by HLA-DQ2, perhaps through the use of of peptide blockers, might lead to new treatment strategy for such HLA associated disorders. For such strategies to work, it will be necessary to identify ligands that bind much better to HLA-DQ2 than the disease related epitopes.
    The team used a positional scanning nonapeptide library to determine the optimal amino acids for each position of the HLA-DQ2 binding frame. By combining the optimal residues in each position, the team was able to design high affinity binders to HLA-DQ2.
    Interestingly, the decapeptide with highest affinity was composed of the most favorable residues in each position. This sequence bound 50-fold better than the immunodominant gluten epitope DQ2-alpha-I-gliadin what makes it an interesting lead compound for the development of blockers.
    The correlation between measured and predicted affinities was poorer for some natural HLA-DQ2 ligands, but notably these peptides did not have optimal amino acids at all positions.
    The team's method offers a straightforward approach for developing high affinity binders to HLA class II molecules.
    Source: Hum Immunol. 2010 Jan 24.


    Diana Gitig Ph.D.
    This article originally appeared in the Spring 2011 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 06/22/2011 - Gluten intolerance among people who do not have celiac disease seems to be an increasing reality, yet scientists have not been able to find any evidence explaining it. A team of researchers in Australia noted that the question of whether gluten can contribute to gastrointestinal symptoms and/ or induce injury to the proximal small intestine had never been directly assessed. So, they set out to assess it. Their results are published in the January 11, 2011 issue of The American Journal of Gastroenterology. They conclude that “non-celiac gluten intolerance” may in fact exist, although they were unable to discern the potential mechanism.
    Their study population consisted of patients with irritable bowel syndrome (IBS) whose symptoms were alleviated by the elimination of gluten from their diet and who definitely did not have celiac disease, as determined by the absence of the HLA-DQ2 or HLA-DQ8 haplotypes. If patients did express these haplotypes, celiac disease was excluded by a normal duodenal biopsy while they were on a gluten containing diet. Unfortunately the authors could only find 34 patients who met these criteria, but they maintain that they could still infer a statistically robust result from their data. Participants had to have been on a gluten free diet for at least six weeks at the beginning of the study. At that point, they were given a study muffin and two slices of study bread to eat every day for six weeks. These goods were baked from gluten free mixes in a gluten free facility, but half of them had gluten added. Importantly, it was only gluten, not wheat; the carbohydrates found in wheat, which are known to elicit GI symptoms, were not included. The study was randomized, double-blind, and placebo controlled, so neither the researchers nor the participants knew who was eating the gluten.
    After only one week, 68% of the patients eating gluten reported more severe pain, bloating, and tiredness, and less satisfaction with their stool consistency, than the cohort who got the gluten free study muffins and bread. This remained the case over the course of the six week study; six patients eating gluten even had to withdraw from the study after the first week because their symptoms got too bad. There did not seem to be much difference between the two groups in what the authors deemed the “less relevant” symptom of nausea. Interestingly, the symptom most exacerbated by gluten was tiredness. Since tiredness is a common symptom of IBS, its induction by gluten may shed some light into a mechanism of action.
    Neither treatment group showed any changes from baseline in assayed biomarkers. These included celiac antibodies; fecal lactoferrin, which increases during intestinal inflammation; C-reactive protein, a sensitive marker for the systemic circulation of cytokines; and intestinal permeability. The authors suggest that perhaps their assays were not sensitive enough to detect subtle molecular changes. About half of the study participants were positive for the HLA-DQ2/8 haplotype, but there were no differences between those who were and those who were negative, either in gluten’s effect on their symptoms or in their biomarkers.
    This study is significant as the first demonstration that gluten may trigger gut symptoms in people who don’t have celiac disease. Subsequent work should elucidate how exactly it does so, but in the meantime, these findings have valuable clinical implications – perhaps more people with GI symptoms will be put on a gluten free diet.
    Source:

    Am. J Gastroenterol advance online publication 11 January 2011; doi:10.1038/ajg.2010.487

  • Recent Articles

    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

    Jefferson Adams
    Celiac.com 04/16/2018 - A team of researchers recently set out to investigate whether alterations in the developing intestinal microbiota and immune markers precede celiac disease onset in infants with family risk for the disease.
    The research team included Marta Olivares, Alan W. Walker, Amalia Capilla, Alfonso Benítez-Páez, Francesc Palau, Julian Parkhill, Gemma Castillejo, and Yolanda Sanz. They are variously affiliated with the Microbial Ecology, Nutrition and Health Research Unit, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), C/Catedrático Agustín Escardin, Paterna, Valencia, Spain; the Gut Health Group, The Rowett Institute, University of Aberdeen, Aberdeen, UK; the Genetics and Molecular Medicine Unit, Institute of Biomedicine of Valencia, National Research Council (IBV-CSIC), Valencia, Spain; the Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire UK; the Hospital Universitari de Sant Joan de Reus, IISPV, URV, Tarragona, Spain; the Center for regenerative medicine, Boston university school of medicine, Boston, USA; and the Institut de Recerca Sant Joan de Déu and CIBERER, Hospital Sant Joan de Déu, Barcelona, Spain
    The team conducted a nested case-control study out as part of a larger prospective cohort study, which included healthy full-term newborns (> 200) with at least one first relative with biopsy-verified celiac disease. The present study includes 10 cases of celiac disease, along with 10 best-matched controls who did not develop the disease after 5-year follow-up.
    The team profiled fecal microbiota, as assessed by high-throughput 16S rRNA gene amplicon sequencing, along with immune parameters, at 4 and 6 months of age and related to celiac disease onset. The microbiota of infants who remained healthy showed an increase in bacterial diversity over time, especially by increases in microbiota from the Firmicutes families, those who with no increase in bacterial diversity developed celiac disease.
    Infants who subsequently developed celiac disease showed a significant reduction in sIgA levels over time, while those who remained healthy showed increases in TNF-α correlated to Bifidobacterium spp.
    Healthy children in the control group showed a greater relative abundance of Bifidobacterium longum, while children who developed celiac disease showed increased levels of Bifidobacterium breve and Enterococcus spp.
    The data from this study suggest that early changes in gut microbiota in infants with celiac disease risk could influence immune development, and thus increase risk levels for celiac disease. The team is calling for larger studies to confirm their hypothesis.
    Source:
    Microbiome. 2018; 6: 36. Published online 2018 Feb 20. doi: 10.1186/s40168-018-0415-6