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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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    SO YOU THINK YOU KNOW ALL ABOUT GLUTEN?


    Dr. Tom O'Bryan


    • Journal of Gluten Sensitivity Winter 2016 Issue - Originally published January 5, 2016


    Celiac.com 04/18/2016 - In the last 3 years, there has been an evolving spectrum around celiac disease and gluten sensitivity. The acceptance of Non-Celiac Gluten Sensitivity (NCGS) in the medical community as a distinct clinical entity has gone from that of being an orphaned child crying in the world for recognition, to an accepted, unique component of the triad of gluten-related disorders.(i) Differentiating among gluten-related disorders, guides clinicians in making an accurate diagnosis and recommending specific dietary, nutritional and other medical advice; however, clinical and laboratory diagnosis is complex and evolving.(ii)


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    Gluten sensitivity is a state of heightened immunological responsiveness to ingested gluten in genetically susceptible people. It represents a spectrum of diverse manifestations, of which, the gluten sensitive enteropathy known as celiac disease is one of many. Adverse reactions to the toxic family of gluten proteins found in wheat, barley, rye, and their derivatives may trigger a heterogeneous set of conditions, including wheat allergy (IgE), NCGS, and celiac disease, that, combined, affect between 10–35% of the population.(iv,v,vi,vii)

    TRUE or FALSE
    1. Even in the presence of negative small bowel biopsy, positive Endomysial antibody (EMA) IgA predicts development of celiac disease.

    2. The prevalence of celiac disease varies by race/ethnicity, with a marked predominance among non-Hispanic whites.

    3. With more sophisticated diagnostic markers now available, the majority of celiac disease cases are being recognized.

    4. Complete histological normalization of the small-intestinal mucosa occurs in the majority of adult patients after commencing a gluten-free diet.

    5. An American College of Gastroenterology Task force recommends that patients presenting with diarrhea-predominant IBS type symptoms should be serologically tested for celiac disease.

    6. What percent of individuals with NCGS suspect they may have a problem with wheat?
    A. 32%
    B. 76%
    C. 50%
    D. 12%

    7. Of the following three scenarios, which is the most dangerous for increased mortality in celiac disease?
    A. Total villous atrophy
    B. Positive celiac serology with negative villous atrophy
    C. Increased intraepithelial lymphocytes (IEL) with negative serology and negative villous atrophy

    8. In differentiating wheat sensitivity from IBS, which one of the following features is significantly more frequent in wheat sensitive patients compared to IBS patients?
    A. Anemia
    B. Self-reported fructose intolerance
    C. Weight gain
    D. Self-reported lactose intolerance

    9. Compared to patients with celiac disease, what are the characteristic features, other than self-reported wheat intolerance, of patients with wheat sensitivity?
    A. Anemia and family history of celiac disease
    B. Weight loss and increased IEL count
    C. Coexistent atopy and food allergy in infancy
    D. Increased serum C reactive protein and erythrocyte sedimentation rate

    Current therapeutic protocols for celiac disease, NCGS and wheat allergy include dietary counseling from a trained professional, nutritional therapy addressing biomarkers of malabsorption and creating a more balanced intestinal environment.(ix) Currently, there are no approved pharmaceutical treatments for this silent epidemic, however a number of Phase 3 trials are underway. Promising gluten-based research is currently being done including wheat alternatives and wheat selection, enzymatic alteration of wheat, oral enzyme supplements and polymeric binders as exciting new therapies for treatment of celiac disease.

    There appears to be at least two distinct groups of NCGS individuals. There are those who are sensitive to wheat and those who have multiple food sensitivities. Furthermore, the multiple food sensitivity group had a higher prevalence of coexisting atopy or food allergy in infancy.(xi) It is critically important to identify whether a NCGS individual has multiple food sensitivities or exclusively has NCGS.(xii) This suggests the world of NCGS is greater than just one mechanism and invites the clinician to explore its pathophysiology.

    ANSWERS
    1. True
    2. True
    3. False
    4. False
    5. True
    6. C
    7. C
    8. A
    9. C

    Request the complete article, complete answers and references by sending a request to info@theDr.com.

    References
    (i) Ludvigsson JF, Leffler DA, Bai JC, Biagi F, et.al., The Oslo definitions for coeliac disease and related terms, Gut. 2013 Jan;62(1):43-52
    (ii) O'Bryan T, Ford R, Kupper C, Celiac Disease and Non-Celiac Gluten Sensitivity-An Evolving Spectrum, in Advancing Medicine with Diet and Nutrients, Johns Hopkins, CRC Press, December 2012
    (iii) Carroccio A, Mansueto P, Iacono G, Soresi M, et.al., Non-celiac wheat sensitivity diagnosed by double-blind placebo-controlled challenge: exploring a new clinical entity, Am J Gastroenterol. 2012 Dec;107(12):1898-1906
    (iv) Catassi, C. and Fasano, A. 2008. Celiac disease. Curr Opin Gastroenterol 24: 687-91.
    (v) Anderson, L.A., McMillan, S.A., Watson, R.G., et al. 2007. Malignancy and mortality in a population based cohort of patients with coeliac disease or 'gluten sensitivity'. World J Gastroenterol 13: 146-51.
    (vi) Ferguson, A., Gillett, H., Humphreys, K., and Kingstone, K. 1998. Heterogeneity of celiac disease: clinical, pathological, immunological, and genetic. Intestinal Plasticity in Health and Disease. 859: 112-20.
    (vii) Constantin, C., Huber, W.D., Granditsch, G., Weghofer, M. and Valenta, R. 2005. Different profiles of wheat antigens are recognised by patient suffering from coeliac disease and IgE–mediated food allergy. Int Arch Allergy Immunol 138:257-66.
    (viii) Vermeersch P, Geboes K, Mariën G, Hoffman I, Hiele M, Bossuyt X. Diagnostic performance of IgG anti-deamidated gliadin peptide antibody assays is comparable to IgA anti-tTG in celiac disease. Clin Chim Acta. 2010 Jul 4;411(13-14):931-935.
    (ix) Ibid, reference 2
    (x) Stoven S, Murray JA, Marietta E., Celiac disease: advances in treatment via gluten modification, Clin Gastroenterol Hepatol. 2012 Aug;10(8):859-62
    (xi) ibid reference 3
    (xii) Bondsa, R., Midoro-Horiutib, T. and Goldblum, R. 2008. A structural basis for food allergy: the role of cross-reactivity. Current Opinion in Allergy and Clinical Immunology 8: 82-86.
    (xiii) Kurppa K, Ashorn M, Iltanen S et al. Celiac disease without villous atrophy in children: a prospective study. J Pediatr 2010;157:373–380
    (xiv) Kurppa K, Collin P, Viljamaa M et al. Diagnosing mild enteropathy celiac disease: a randomized, controlled clinical study. Gastroenterology 2009;136:816–823
    (xv) Mayo Clinic, news release, July 31, 2012
    (xvi) Rubio-Tapia A, Ludvigsson JF, Brantner TL, Murray JA, Everhart JE., The prevalence of celiac disease in the United States. Am J Gastroenterol. 2012 Oct;107(10):1538-44
    (xvii) Tuire I, Marja-Leena L, Teea S, Katri H, et.al. Persistent duodenal intraepithelial lymphocytosis despite a long-term strict gluten-free diet in celiac disease, Am J Gastroenterol. 2012 Oct;107(10):1563-9
    (xviii) Sanders DS, Aziz I. Editorial: non-celiac wheat sensitivity: separating the wheat from the chat! Am J Gastroenterol. 2012 Dec;107(12):1908-12
    (xix) Ludvigsson JF, Montgomery SM, Ekbom A, Brandt L, Granath F., Small-intestinal histopathology and mortality risk in celiac disease, JAMA. 2009 Sep 16;302(11):1171-8
    (xx) Carroccio A, Mansueto P, Iacono G, Soresi M, et.al., Non-celiac wheat sensitivity diagnosed by double-blind placebo-controlled challenge: exploring a new clinical entity, Am J Gastroenterol. 2012 Dec;107(12):1898-906


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    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