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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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    SHOULD HLA COME FIRST IN CELIAC DISEASE SCREENING FOR ARTHRITIS PATIENTS?


    Jefferson Adams

    Celiac.com 03/16/2017 - When screening arthritis patients for celiac disease, should HLA be done before serology? During the past decades, an accumulating evidence shows a dramatic rise in the frequency of autoimmune diseases, including rheumatoid arthritis and gastrointestinal conditions, such as celiac disease.


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    HLA genes have been shown to be strongly associated with numerous autoimmune diseases, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and celiac disease. A team of researchers recently set out to assess the performance of celiac disease associated serology in face of a rheumatologic patient, when gluten enteropaty is suspected.

    The research team included Hakim Rahmoune, Nada Boutrid, Mounira Amrane, and Belkacem Bioud. They are variously affiliated with the Pediatrics Department and the Biochemistry Department of Setif University Hospital at Setif-1 University in Algeria.

    The main question they sought to answer was: Should HLA be done prior to the serology? Could unnecessary serial serological celiac disease screening in such rheumatology patient be avoided by performing an HLA typing, as a long-life marker of genetically celiac disease-susceptible patients?

    Serogenetic screening without the requirement for follow-up small bowel biopsies provides a flexible, cost-effective methodology that could be widely applied to obtain accurate estimates of the prevalence of celiac disease in large group studies.

    Source:


    Image Caption: Photo: CC--Keoni Cabral
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    Guest Audrey VanWyk

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    I lived 67 years with so many issues including severe arthritis, gut, migraine, neurophy, depression, acne, leg pain and other issues. I went to specialists at university teaching hospitals and after everything was eliminated, I asked if it could be gluten related. No, you didn't test for celiac. Three sisters and we all have issues and my younger sister determined it was gluten and I went gluten-free. I did DNA research. Yes HLA DQA1. No doctor asks for that info perhaps because they don't know. Rhumatoligist for scleroderma acknowledged confirmation of gluten intolerance. My 21 year old grandson confirmed autoimmune diseases. Why isn't DNA used as a tool? Years of illness untreated means years of lost quality of life.

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    admin
    Arthritis may be an allergic response to materials in the food supply. Diet revision may be helpful in reducing the activity of inflammatory arthritis and in some instances may halt the progression of the disease. There are many patterns of arthritis. A group of related joint and connective disorders have been called rheumatic diseases. All these diseases are immune-mediated, and all are expressions of inflammation in connective tissues. Inflammation damages joints and surrounding tissues resulting in loss of function and deformities. Variations in the patterns of these diseases reflect the many possibilities for immune damage to disturb and distort structure and function. Severity ranges from mildly painful, chronic activity to drastic, disabling disease. Rheumatoid arthritis, often severe and disabling, is the dominant rheumatic disease that can attack all joints in the body.
    Rheumatoid arthritis is often considered to be an autoimmune disease. Our idea is that no disease is just internally generated and must involve outside contributions. Arthritis is often associated with inflammatory bowel disease. The mechanisms of food allergy link abnormal Gastrointestinal Tract (GIT) function with immune attacks on connective tissue. In all arthritic patients, normal GIT function should be rigorously sought by adaptive dietary adjustments.
    Simple allergic arthritis is a definite entity that is often not recognized as a food allergy. Typically, a dramatic, acute, and painful swelling develops in one or more joints asymmetrically. Eating a food, either an unusual food eaten for the first time or sometimes a regular food eaten in excess usually brings on the joint inflammation. This presentation is similar to and often confused with gout. Any food can cause allergic arthritis. Staple foods such as milk, eggs, and wheat (rye, oats, barley), coffee, beef, pork, and food additives are the most common food triggers. Carinini and Brostroff reviewed the concepts of and evidence for food-induced arthritis. They stated:


    Despite an increasing interest in food allergy and the conviction of innumerable patients with joint disease that certain foods exacerbate their symptoms, relatively little scientific attention has been paid to this relationship. Abnormalities of the gastrointestinal tract are commonly found in rheumatic disease...Support for an intestinal origin of antigens comes from studies of patients whose joint symptoms have improved on the avoidance of certain foods antigens, and become worse on consuming them. These have included patients with both intermittent symptoms, palindromic rheumatism and more chronic disease.
    In another study, 33 of 45 patients with rheumatoid arthritis improved significantly on a hypoallergenic diet. The authors concluded: Increasing numbers of scientific studies suggest that dietary manipulation may help at least some rheumatoid patients and perhaps the greatest need now is for more careful and well-designed research so that preconceptions may be put aside and role of diet, as a specific or even a nonspecific adjunctive therapy, may be determined.
    Unfortunately, dairy products, wheat and its close relatives, oats, barley, and rye, have proved to be a major problem in the diets of our patients. There are many possible reasons for cereal grains to become pathogenic. Hypersensitivity mechanisms triggered by grain proteins, collectively called Gluten, are the likely cause of the illnesses related to intake of cereal grains. Gluten is a mixture of individual proteins classified in two groups, the Prolamines and the Glutelins. The prolamine fraction of gluten concerns us the most when grain intolerance is suspected. The prolamine, Gliadin, seems to be a problem in celiac disease; gliadin antibodies are commonly found in the immune complexes associated with this disease. Recently marketed grains, spelt and kamut, are wheat variants (despite claims to the contrary) and are likely to cause problems similar to other wheat varieties.
    A wheat gluten mechanism has been studied in rheumatoid arthritis patients. The clinical observation is that wheat ingestion is followed within hours by increased joint swelling and pain. Little and his colleagues studied the mechanism, as it developed sequentially following gluten ingestion. Dr. Parke and colleagues concurred with this explanation of the gut-arthritis link in their report of three patients with celiac disease and rheumatoid arthritis. The mechanism involves several stages:
    GIT must be permeable to antigenic proteins or peptide fragments, derived from digested gluten. The food antigens appear in the blood stream and are bound by a specific antibody (probably of IgA or IgG, not IgE class), forming an antigen-antibody complex, a circulating immune complex (CIC). The antigen-antibody complex then activates the rest of the immune response, beginning with the release of mediators - serotonin is released from the blood platelets. Serotonin release causes symptoms as it circulates in the blood stream and enhances the deposition of CICs in joint tissues. Once in the joint, the immune complexes activate complement, which in turn damages cells and activates inflammation. More inflammation results in more pain, swelling, stiffness, and loss of mobility.
    Arthritis is usually treated with salicylates or related anti-inflammatory drugs generally referred to as NSAIDs. These drugs alleviate the terrible pain of active arthritis but do not favorably affect the outcome of the disease. All anti-arthritic medication can produce asthma or chronic rhinitis and a variety of allergic skin rashes. Gastrointestinal surface irritation, bleeding, and ulceration are routine problems of anti-arthritic medication.
    The first attack of joint swelling and pain should be treated as an urgent problem to be solved. Inflammation may damage joints. Often NSAIDs and physiotherapy are the only treatments prescribed and inflammation is given every opportunity to ravage tissues. We have seen countless patients, just treated with NSAIDs, who progressed rapidly to a severe disabling disease, often with poor pain control. In unlucky patients, severe deformities of joints accumulate in the first few months of a severe attack. There is a trend to recommend more aggressive treatments, using drugs that impair the immune response. The best drug is prednisone, but it is seldom used because it has long-term side effects which scare both physicians and patients. Prednisone is often a magic drug that relieves terrible pain and suffering often in the first 48 hours of therapy. Beyond prednisone, there is a grab bag of immune suppressant drugs to treat arthritis-chloroquine, penicillamine, gold and methotrexate have emerged as the favored drug therapies. All these drugs have impressive side effects and great potential for toxicity.
    Our preference is to try to stop the inflammatory activity as soon as possible with diet revision. All inflammation is likened to a fire. You get out the fire-extinguishers and go to work. No matter what pattern the immune attack assumes, our standard defense can be tried first. The Core Program method of diet revision is used. Food is replaced with an elemental nutrient formula, ENFood, for a clearing period of 10 to 20 days. Prednisone and/or NSAIDs are drug options during the clearing period and then the dosage is reduced after pain and swelling have subsided. Improvement is followed by slow food reintroduction (see Core Program). Each returning food is carefully screened for arthritis- triggering effects. You hope that food allergy caused the problem and that food control can be successful controlling the disease in the long- term. Nothing is lost by taking this approach and complete control of the disease can sometimes be obtained. If strict food control proves to be inadequate, then other drug treatments can be instituted.
    End Notes/Sources:
    Carinini C, Brostroff J. Gut and joint disease. Annals of Allergy 1985;55:624-625. Darlington et al. Lancet Feb 1 1986;236-238. Keiffer M et al. Wheat gliadin fractions and other cereal antigens reactive with antibodies in the sera of of celiac patients. Clin Exp Immunol 1982;50:651-60. Little C, Stewart AG, Fennesy MR. Platelet serotonin release in rheumatoid arthritis: a study in food intolerant patients. Lancet 1983;297-9. Parke AI et al. Celiac disease and rheumatoid arthritis. Annals of Rheum Dis 1984;43:378-380. Voorneveld CR, Rubin LA Disease-modifying antirheumatic drugs: early use is better. Medicine North Amer. Oct 1991 3177-3184.

    Jefferson Adams
    Celiac.com 06/08/2007 - In the first study, doctors Ibrahim S. Alghafeer, and Leonard H. Sigal conducted a routine gastroenterology follow-up of 200 adult celiac patients. Arthritis was present in 52 of 200 patients, or 26%. The arthritis was peripheral in 19 patients, Axial in 15 patients, and an overlap of the two in 18 patients. The doctors found that joint disease was much less common in those patients who were following a gluten-free diet (1).
    A related study by Usai, et al found that 63% of patients with celiac disease show axial joint inflammation (2).
    In that study, doctors conducted bone scintigraphy using 99m Tc methylene diphosphonate. 14 of these patients (65%) signs compatible with sacroiliitis. 11 of the 14 suffered from low back pain. In five of the 11 patients with low back pain, scintigraphy was negative. Sacroiliac radiographs were conducted on 4 of those 5 patients, and all of them were shown to have bilateral sacroiliitis. One patient had rheumatoid arthritis, but all patients in the studied showed negative HLA-B27 results.
    Rheumatoid Symptoms Less Common in Celiacs on Gluten-free Diet
    In patients with gluten enteropathy, symptoms of arthritis and other rheumatic complaints are common, and the associated clinical abnormalities routinely show improvement on a gluten-free diet. (3,4,5)
    In 9 of 74 patients with spondyloarthropathies, results show increased level of antigliadin antibodies, with 1 patient showing elevated antiendomysium antibodies and biopsy proven celiac disease (6). These results show that antiendomysial antibody testing is recommended as a screening tool in patients with suspected gluten enteropathy. Another study found that 3.3% of sprue patients had Sjogrens syndrome (7).
    55 celiac patients who were tested for serial bone density showed osteoporosis in 50% of men and 47% of women. These findings confirm that celiac disease was an independent risk factor for osteoporosis (8).
    Bulletin on the Rheumatic Diseases, Volume 51, Number 2.
    Usai P. Adult celiac disease is frequently associated with sacroiliitis. Dig Dis Sci 1995;40:1906-8 Lubrano E, Ciacci C, Ames PR, et al. The arthritis of celiac disease: prevalence and pattern in 200 adult patients. Br J Rheumatol 1996;35:1314-8. Usai P. Adult celiac disease is frequently associated with sacroiliitis. Dig Dis Sci 1995;40:1906-8. Bagnato gluten-free, Quattrocchi E, Gulli S, et al. Unusual polyarthritis as a unique clinical manifestation of celiac disease. Rheumatol Int 2000;20:29-30. Borg AA, Dawes PT, Swan CH, Hothersall TE. Persistent monoarthritis and occult celiac disease. Postgrad Med J 1994;70:51-3. Collin P, Korpela M, Hallstrom O, et al. Rheumatic complaints as a presenting symptom in patients with celiac disease. Scan J Rheumatol 1992;21:20-3. Kallilorm R, Uibo O, Uibo R. Clin Rheumatol 2000;19:118-22. health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.

    Jefferson Adams
    Celiac.com 04/08/2013 - Numerous studies have shown a connection between celiac disease and various types of arthritis.
    A team of researchers recently set out to investigate the occurrence of lower limb enthesopathy in celiac disease patients without clinical signs of articular involvement. Entheses are the places where collagen fibers of a tendon, ligament or muscle are mineralized and connected into bone tissue. Entheseal abnormalities are abnormalities of these areas, and are often associated with arthritis.
    The team wanted to use ultrasound to investigate the presence of entheseal abnormalities in patients with celiac disease without clinical signs of articular involvement, and then compare the results with healthy control subjects.
    The research team included M. Atteno, L. Costa, R. Tortora, A. Cozzolino , A. Del Puente, F. Caso, P. Sfriso, R. Scarpa, and C. Ciacci. They are affiliated with the Rheumatology Research Unit in the Department of Clinical and Experimental Medicine of the Gastroenterology Research Unit in the Department of Clinical and Experimental Medicine at University Federico II of Naples, Naples, the Gastroenterology Unit at Santo Ottone Hospital in Ariano Irpino, Avellino, the Rheumatology Research Unit of the Department of Clinical and Experimental Medicine at the University of Padova in Padova, and the Department of Medicine and Surgery, Gastroenterology, at the University of Salerno in Salerno, Italy.
    For their study, the team looked at sixty patients with asymptomatic celiac disease who attended the gastroenterology outpatient clinic of the University Federico II of Naples. They then compared the celiac patients with sixty healthy control subjects matched for age and sex. Both groups of patients received clinical and ultrasound examination.
    The results showed that 24 of the sixty celiac disease patients (40%) showed at least one entheseal abnormality, compared with just six of the sixty (10%) healthy control subjects (P < 0.01).
    Interestingly, the celiac disease patients more commonly showed abnormalities of the patella (distal and proximal), while nearly all abnormalities in the healthy controls were found in the Achilles tendon.
    The results of this study demonstrate the ability of ultrasound to detect signs of subclinical entheseal abnormalities, and reveal higher rates of subclinical entheseal abnormalities in people with asymptomatic celiac disease.
    Source:
    Rheumatology (Oxford). 2013 Jan 7.

    Jefferson Adams
    Celiac.com 07/09/2015 - Children presenting for rheumatology evaluation have undiagnosed celiac disease at double the rates of the general population, says the latest study.
    However, current clinical guidelines do not consider patients with rheumatic conditions to be at high risk for celiac disease despite numerous reported associations between the two in adults and children.
    A team of researchers set out to assess the prevalence of celiac disease among kids receiving a rheumatology evaluation. The research team included Yekaterina Sherman, BA, Rose Karanicolas, MD, Brittany DiMarco, BA, Nancy Pan, MD, Alexa B. Adams, MD, Laura V. Barinstein, MD, L. Nandini Moorthy, MD, and Thomas J. A. Lehman, MD. They are variously affiliated with the Division of Pediatric Rheumatology, Hospital for Special Surgery, New York, New York; the Division of Rheumatology, Mount Sinai Medical Center, New York, New York; and the Division of Pediatric Rheumatology, Robert Wood Johnson Medical School in New Brunswick, New Jersey.
    The team conducted celiac disease screenings on a total of 2,125 patients presenting for initial evaluation by the Division of Pediatric Rheumatology at the Hospital for Special Surgery between June 2006 and December 201, as a part of the standard initial serologic evaluation. The team then reviewed the charts at the end of this period. From this information, the team diagnosed celiac disease in a total of 36 patients (30 girls, 6 boys, mean age 9.4 ± 4.3 years, range 2–16 years), after serologic testing and evaluation by pediatric gastroenterology.
    Eight additional patients with known celiac disease diagnoses presented during this time period. The total prevalence of celiac disease over this 6.5-year period was 2.0%. The most commonly reported complaints among patients diagnosed with celiac disease were myalgias, arthralgias, and skin rash.
    Less frequently, patients reported gastrointestinal complaints including abdominal pain, nausea, and diarrhea.
    All patients reported improvement or complete resolution of their musculoskeletal symptoms after beginning a gluten-free diet.
    In this study, the team found 36 new cases of celiac disease among children presenting for rheumatology evaluation, for an overall prevalence rate of 2.0%.
    The majority of patients who ultimately received a diagnosis of celiac disease presented with extra-intestinal manifestations.
    These results underscore the importance of celiac disease screening in children receiving a rheumatology evaluation.
    Source:
    http://pediatrics.aappublications.org/content/early/2015/06/09/peds.2014-2379.abstract

  • 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