• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    71,819
    Total Members
    3,093
    Most Online
    Debbie1234
    Newest Member
    Debbie1234
    Joined
  • Announcements

    • admin

      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
  • 0

    SCIENTISTS FINALLY KNOW WHAT CAUSES CELIAC DISEASE!


    Jefferson Adams

    Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Photo: CC--Ryan HydeProfessor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms.

    To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2.

    "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them.

    So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses.

    Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease.

    "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated."

    At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed.

    This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future.

    Source:


    Image Caption: Champagne toast! Photo: CC--Ryan Hyde
    0


    User Feedback

    Recommended Comments

    Guest Ed Arnold

    Posted

    Gluten destroyed my health. I don't have HLA-DQ2 or HLA-DQ8. So for many of us with a gluten problem, this explanation is not helpful.

    Share this comment


    Link to comment
    Share on other sites
    Gluten destroyed my health. I don't have HLA-DQ2 or HLA-DQ8. So for many of us with a gluten problem, this explanation is not helpful.

    If you don't have either genetic marker you don't have celiac disease...which is what this article is about.

    Share this comment


    Link to comment
    Share on other sites

    There is a small percentage of those with celiac disease who have neither DQ2 nor 8. Search for HLA negative celiac disease to find the articles.

    Share this comment


    Link to comment
    Share on other sites
    If you don't have either genetic marker you don't have celiac disease...which is what this article is about.

    Those are only the 'known' markers so far. Science does not yet know it all.

     

    This may help some people and may not help others. It may also help some people that are not listed because testing abilities are still so underdeveloped. Time will tell.

     

    They may also just be trying to come up with another big sell item for big pharma that turns out to be more toxic than just avoiding gluten altogether... as with so many current meds on the market.

     

    Share this comment


    Link to comment
    Share on other sites
    Guest Mary Thorpe

    Posted

    Guess I'll have to read the article. I don't see anything new reported in this article.

    Share this comment


    Link to comment
    Share on other sites
    Guest Christy

    Posted

    There have been people who tested positive for celiac through endoscopy and biopsy (gold standard test) and tested negative for both HAD-DQ2 and 8. The University of Chicago Celiac Disease Center talked about this a couple of years ago. They are aware that there are other causes that have not yet been identified.

    Share this comment


    Link to comment
    Share on other sites
    Gluten destroyed my health. I don't have HLA-DQ2 or HLA-DQ8. So for many of us with a gluten problem, this explanation is not helpful.

    This website is called celiac.com - why comment if you are not celiac?

     

    ..and it is very good news they have identified the cause. Another step forward.

    Share this comment


    Link to comment
    Share on other sites
    Guest William

    Posted

    This is old news. It has been known for some time that HLA DQ2/DQ8 are the precursors for the disease. So, what's new?

    Share this comment


    Link to comment
    Share on other sites
    There is a small percentage of those with celiac disease who have neither DQ2 nor 8. Search for HLA negative celiac disease to find the articles.

    From questdiagnostics.com: "Negative results for both HLA-DQ2 and HLA-DQ8 virtually exclude the diagnosis of celiac disease..." I am aware of research that shows that it is still a very slight possibility (Karell K, Louka AS, Moodie SJ, et al. HLA types in celiac disease patients not carrying the DQA1*05–DQB1*02 (DQ2) heterodimer: results from the European Genetics Cluster on Celiac Disease. Hum Immunol. 2003;64:469-477.) but this research is focused on what triggers celiac disease in the vast majority of cases.

    Share this comment


    Link to comment
    Share on other sites
    Guest BareFood George

    Posted

    "...Professor Sollid and his group are investigating how antibodies against transglutaminase are formed..." Hello , overdose maybe of gluten from fortified pastries and thousands of high - gluten products that made the body to handle them as toxic substance!

    Share this comment


    Link to comment
    Share on other sites
    Guest Darlene S C

    Posted

    Not exactly the whole story - why they keep missing this is beyond me

    Celiac disease existed way back when - yes , but it was extremely rare ( One in 4000)

    Reason it was linked to wheat in the late 1940s and then to gluten in the 1950s was because Norman Borlaug bioengineered modern wheat (a Tribred- 3 different plants ) right after World War II . His new wheat was pest & disease-resistant shorter stock larger bud higher-yield per acre. The seed started being used soon after that, & in increasing numbers of cases for celiac started popping up in the 1950s. The Side effect of Borlaug's new modern wheat was the gluten was different - more gluten in the grain perhaps ? - but was different than the gluten in the heirloom wheats.

    Share this comment


    Link to comment
    Share on other sites
    Not exactly the whole story - why they keep missing this is beyond me

    Celiac disease existed way back when - yes , but it was extremely rare ( One in 4000)

    Reason it was linked to wheat in the late 1940s and then to gluten in the 1950s was because Norman Borlaug bioengineered modern wheat (a Tribred- 3 different plants ) right after World War II . His new wheat was pest & disease-resistant shorter stock larger bud higher-yield per acre. The seed started being used soon after that, & in increasing numbers of cases for celiac started popping up in the 1950s. The Side effect of Borlaug's new modern wheat was the gluten was different - more gluten in the grain perhaps ? - but was different than the gluten in the heirloom wheats.

    This is a common myth that I've seen repeated in several forms, but it has no scientific validity.

    Share this comment


    Link to comment
    Share on other sites
    Guest Sandra

    Posted

    This is a common myth that I've seen repeated in several forms, but it has no scientific validity.

    I believe genetically engineered products have changed us and there is no scientific evidence because it hasn't been long enough to study or no one really is studying it!

    Share this comment


    Link to comment
    Share on other sites
    Guest Jefferson

    Posted

    Guess I'll have to read the article. I don't see anything new reported in this article.

    What't new is the fact that scientists have finally connected the dots between the DQ2/DQ8 markers and the actual mechanics of gut damage from celiac disease. That's huge, and potentially of great benefit to researchers looking for treatments and cures, and thus, to people with celiac disease.

    Share this comment


    Link to comment
    Share on other sites
    Guest Jefferson

    Posted

    I believe genetically engineered products have changed us and there is no scientific evidence because it hasn't been long enough to study or no one really is studying it!

    So your belief is based on nothing but your imagination?

    Share this comment


    Link to comment
    Share on other sites

    Certainly not helpful in the long run for people suffering from this terrible disease right now. Cancer isn't curable but there are meds to help people. Why is it taking so long to find or release drugs for trial more widely in the states than is or should be done. A diet is not the answer.

    Share this comment


    Link to comment
    Share on other sites
    There is a small percentage of those with celiac disease who have neither DQ2 nor 8. Search for HLA negative celiac disease to find the articles.

    I have heard this I thought from Dr. Fasano but I am not sure it was from him.

    At any rate, there is a very valid issue with feeling excluded, which is to say, if you have celiac, you have what 99% of other people do not have. If you do not have either HLA-DQ2 or HLA-DQ8 AND are celiac, you are even MORE of an "odd bird." The idea that physicians are able to find this out on their own initiative also is a lot like in my long experience thinking that pigs can fly. So I agree with Anne here.

    Share this comment


    Link to comment
    Share on other sites
    Guest Michael

    Posted

    It is supremely ignorant to call our genes "defective HLAs". These genes are much older than the defective practice of eating grains or hybridizing wild grasses to create the first form of wheat. Certain gliadin peptides are not digestible by any human's enzymes and some cause temporary intestinal permeability in all, according to Alessio Fasano's research.

     

    Despite the addiction to gluteomorphins and the worship of wheat and the resulting irritation and madness fueling endless war in the Mideast by all 3 religions originating there, where the creation of wheat occurred, and the knowledge that high antibodies to gliadin in a pregnant mother results in higher probability for schizophrenia in adulthood for her child, as well as depression and the likelihood that this young adult will be put on an SSRI drug and become a mass shooter, the brainwashing, ignorance proliferated by medical school deans refusing to teach the dangers of gluten to central nervous systems, and the fact that the majority of Caucasians have an HLA gene that predisposes them to have an autoimmune attack if their brain induced by gluten they have the audacity to call wheat, barley and rye "safe food" and declare us defective. This is a genocidal mindset by Nazi inspired capitalists.

    Share this comment


    Link to comment
    Share on other sites
    Guest Lauren

    Posted

    So your belief is based on nothing but your imagination?

    Is it possible to do scientific studies without imagination? Someone's imagination worked with observation and decided to set up a study. Is there really anything other than imagination driving us? Is a skewed scientific study better than the imagination exercised by everyone every day to create the environment we live in? Look at us today, avoiding fat because the sugar industry wanted to distract us from the harm of sugar. You can't metabolize many nutrients without fat. Does the science presented make it true that avoiding valuable nutrients to keep the sugar industry happy will make us healthy? Sometimes common sense applied to imagination or common sense applied to science is all we've got to go on. My father decided that the battle over whether to cut fat or not didn't matter, he was going with fat. He existed because his ancestors ate fat so it made sense to his imagination. The scientific evidence has come around to proving him right.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoticons maximum are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Popular Contributors

  • Ads by Google:

  • Who's Online   7 Members, 1 Anonymous, 334 Guests (See full list)

  • Related Articles

    admin

    Nature Immunology 2, 353 - 360 (April 2001)
    Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation.
    The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process.

    admin

    Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H
    Natural killer cell activity in coeliac disease: effect of in vitro treatment on effector lymphocytes and/or target lymphoblastoid, myeloid and epithelial cell lines with gliadin
    Folia Microbiol, 1995 (Praha) 40; 6: 615-620.
    In this study researchers tested the levels of natural killer cell activation in normal people and compared the results with treated celiacs, and found no significant difference. However, after exposing the celiacs blood to gliadin for thirty minutes the researchers found a reduced activation of natural killer cells, which is the bodys first line of defense against malignancy. These results provide further support to the theory that gluten is a carcinogen to celiacs.

    admin
    Author: Auricchio S; De Ritis G; De Vincenzi M; Silano V.
    Source: J Pediatr Gastroenterol Nutr, 1985 Dec, 4:6, 923-30.
    This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The peptidase deficiency, primary immune defect, and gluten-lectin theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten-lectin theory is the one best able to explain celiac disease. It also explains some secondary intolerance that may occur in temporarily predisposed individuals as a consequence to viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects that are administered very high amounts of gluten.

    admin

    Oberhuber G, Schwarzenhofer M, Vogelsang H
    Dig Dis 1999 Nov- Dec;16(6):341-4
    Department of Clinical Pathology, University of Vienna, Vienna, Austria. The in vitro challenge of duodenal mucosa with gliadin is a useful model to reproduce the immunological features of celiac disease (celiac disease) and allows the study of early pathogenetic events in this disease. With this model it was shown that antigens such as ICAM-1 and HLA-DR are upregulated as early as 1-2 h after gliadin challenge in patients with celiac disease. After 24 h the lamina propria contained CD4+ T cells expressing the IL-2 receptor alpha-chain, which is a sign of activation. Intraepithelial lymphocytes increased in number and showed proliferative activity. After in vitro stimulation with gliadin, endomysial antibodies were found in the supernatant of the cultured mucosa from patients with celiac disease following a gluten-free diet. This supported the notion that endomysial antibodies are at least in part produced locally. The model was also successfully used to identify toxic constituents of gliadin. Presently, organ culture is not commonly used for diagnostic purposes.

  • 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