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      Frequently Asked Questions About Celiac Disease   04/24/2018

      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 is Celiac Disease and the Gluten-Free Diet? 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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    Interpretation of Celiac Disease Blood Test Results


    Scott Adams

    The following detailed explanation of serological tests for celiac disease was written by Tom Ryan, Technical Service Specialist, INOVA Diagnostics, Inc.


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    There has been a lot of discussion about serological testing for celiac disease recently, specifically regarding tTG (tissue Transglutaminase) testing. I will try to answer some of the many questions that have appeared on this list about all of the tests. First, and this applies to any of the blood tests, you must currently be on a gluten containing diet for the tests to be accurate. Antibodies are produced by the immune system in response to substances that the body perceives as threatening. The immune response that your body produces is its response to being exposed to gluten in the diet and its subsequent effect on the intestinal mucosa. If there is no gluten in the diet, then there is no response that we can measure. A brief change in diet will not have a noticeable effect. If you have been gluten free for a week or so, it will not make any great difference. The response might be marginally less but the difference is insignificant because the body has not had time to respond to the change. Conversely, if you have been gluten free for a protracted period of time and decide to be tested, a brief challenge of a couple of weeks is not enough to elicit a response and get an accurate test.

    There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus. Talk with your Doctor. My personal feeling is that the minimum is 2 slices of bread per day for 6 weeks to get an accurate test but I would not try to second-guess the Doctor. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc. What are all of these? Some contributors to the list make reference to the IgA or IgG test or to the ELISA test. These labels are incomplete for our purposes and could be referring to any number of different tests.

    We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal sera in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies.

    Anti-Gliadin Antibodies:

    Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results.

    A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for Enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower.

    Endomysial Antibodies:

    IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge.

    The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies.

    Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently, (1998) the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out.

    In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with:

    • An initial positive gut biopsy;
    • 6 months on a gluten free diet;
    • A second, negative gut biopsy;
    • A gluten challenge for 6 months and;
    • A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure.

    Through the auspices of the Celiac Disease Foundation and others, a professional symposium and workshop was organized earlier this year in Marina Del Rey, California with participants from Europe as well as the U.S. to establish standards for reporting test results. This should improve testing and diagnosis even more. At the conclusion of this conference a Celiac Disease Standardization Committee was formed to investigate and make recommendations on a standardized method of reporting results.

    Edited by admin


    Image Caption: Images: CC--Scott Robinson
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    Finally an explanation! I was low on my IgA but high positive on IgG and so sick and my doc said, 'at some point in the past, gluten made you very sick, but you're fine now.'.. He was totally ignoring my symptoms! That was two years ago and he still doesn't believe I have it, even though since then he diagnosed me with osteopenia.. I've been off gluten for about 3 months now, and my chronic migraines and stomach problems are gone! my doc still doesn't believe I have it, but IBS instead! give me a break! And these are Seattle gastroenterologists!

    Me too! In Australia - "dying" for a proper diagnosis.

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    Oh wow. I hadn't had gluten for months when I had the blood test, and my doctor wouldn't do an endoscopy. He also wouldn't show me the results. Just said, "I told you that you didn't have it."

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    Guest Pouya K

    Posted

    Interesting article. One note: the definitions of sensitivity and specificity are not correct: in this context, sensitivity is the fraction of people with celiac that would have a positive test result. Likewise, specificity is the fraction of people without celiac that would have a negative test result. The terms you describe are positive and negative predictive value, which are usually harder to measure because they depend on the fraction of a population that is being treated. The difference between these can be quite large: if you assume 1% of a population has a disease a specificity of 97% means that most people (>74%) that test positive actually don't have the disease. Which is presumably why additional confirmation tests are necessary. For more information, see the Wikipedia article for sensitivity and specificity.

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    In the hopes this will help someone, I'm posting my before and after Celiac panel test results.

     

    On 4/10/09 (diagnosed)

    Deamidated Gliad IgAH 127

    Deaminated Gliad IgGH 104

    Tranglut IgA 43

     

    On 6/12/09 (gluten free diet)

    127 -> 58 (goal under 10)

    104-> 48 (goal under 10)

    43 -> 10 (goal under 3)

     

    So after being on gluten free diet from 4/10/09-6/12/09, 8 weeks, already seeing dramatic reductions in antibody levels. Not done yet, but are headed in the right direction. I didn't see this kind of information posted anywhere, so hoping this information is helpful.

    I was diagnosed yesterday. She said something about my results being 57.6 and they are suppose to be under 15. I have no idea what this means but she has told me absolutely no gluten.

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    Scott Adams

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    Dr. Rodney Ford M.D.
    This article appeared in the Summer 2007 edition of Celiac.com's Scott-Free Newsletter.
    This question, “how early can you diagnose celiac disease?” is a major concern for both parents and paediatricians.  This is because, like many diseases, celiac disease comes on slowly.  This means that it can take a long time to make the diagnosis.
    Celiac disease can develop slowly?
    Yes, celiac disease can develop very slowly.  The symptoms can be subtle.  It is a progressive disease.  When you are first born, you cannot have celiac disease as you have never been exposed to gluten.  However, if you have the right genetic make up (that is you have the celiac gene) and the right environmental circumstances (eating gluten and getting gut inflammation), then celiac disease can develop.
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    Celiac disease is a condition that is recognised when you get damage to your small bowel tissue.  This damage is triggered by gluten.
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    Early antibody changes – IgG-gliadin
    Importantly, long before the tissue becomes obviously damaged by gluten, your body can begin to react to the gluten in your diet.
    An early sign of a gluten immune reaction is that your body produces antibodies to the gluten in your diet.  This can be seen in a blood test that looks for an antibody called the IgG-gliadin antibody (also known as anti-gliadin-antibody).  Also the IgA-gliadin antibody can develop at this time.
    Even in these early stages of gluten reactions (before the development of any gut damage of celiac disease), you or your child can be feeling unwell.  Many of the symptoms of celiac disease can be recognized in these early stages.  This is before the tissue damage can be seen by the histologist.
    The blood test to look for tissue damage is called the tissue transglutaminase antibody (abbreviated as tTG).
    Early bowel damage cannot be seen
    The next thing to happen is that the tissue in the small bowel gets slightly injured but not enough to be identified by the histologist.  However, such damage can be shown by an electron microscope.  This early damage can also be detected by the presence of the tTG antibody.
    Usually, when the tTG blood test goes up, then this is an indication to do the endoscopy and look for any tissue damage.  However, early in the progression of celiac disease, this damage may not show up by conventional methods.  This means that the small bowel biopsy and the histology results are good for confirming celiac disease, but they cannot rule it out.
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    Jefferson Adams
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    Alimentary Pharmacology & Therapeutics. 2009;30(3):236-244.


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    Vomiting
    Another prominent symptom is vomiting.  
    When accompanied by diarrhea, vomiting can be a painful experience that would leave you exhausted. It also results in malnutrition and the patient experiences weight loss (not in a good way though). If you experience uncontrolled vomiting, report the matter to a physician to manage the condition.
    Bloating
    Since coeliac disease damages the small intestine, bloating is another common system. This is due to inflammation of the digestive tract. In a study with more than a 1,000 participants, almost 73% of the people reported bloating after ingesting gluten. 
    Bloating can be managed by eliminating gluten from the diet which is why a gluten-free diet is necessary for people suffering from celiac disease.
    Fatigue
    Constant feeling of tiredness and low energy levels is another common symptom associated with celiac disease. If you experience a lack of energy after in taking gluten, then you need to consult a physician to diagnose the condition. Now fatigue can also result from inefficient thyroid function, infections, and depression (a symptom of the coeliac disease). However, almost 51% of celiac patients suffer from fatigue in a study.
    Itchy Rash
    Now the chances of getting a rash after eating gluten are slim, but the symptom has been associated with celiac disease in the past. The condition can cause dermatitis herpetiformis, which causes a blistering skin rash that occurs around the buttocks, knees, and elbows. 
    A study found out that almost 17% of patients suffering from celiac disease might develop dermatitis herpetiformis due to lack of right treatment. Make sure you schedule an online appointment with your dermatologist or visit the nearest healthcare facility to prevent worsening of symptoms.
    Even with such common symptoms, diagnosing the condition is imperative for a quick recovery and to mitigate the long-term risks associated with celiac disease. 
    Sources:
    ncbi.nlm.nih.gov  Celiac.com ncbi.nlm.nih.gov  mendfamily.com

    Jefferson Adams
    Celiac.com 05/16/2018 - Galectins are a family of animal lectins marked by their affinity for N-acetyllactosamine-enriched glycoconjugates. Galectins control several immune cell processes and influence both innate and adaptive immune responses. A team of researchers recently set out to assess the role of galectins, particularly galectin-1 (Gal-1), in the treatment of celiac disease.
    The research team included Victoria Sundblad, Amado A. Quintar, Luciano G. Morosi, Sonia I. Niveloni, Ana Cabanne, Edgardo Smecuol, Eduardo Mauriño, Karina V. Mariño, Julio C. Bai, Cristina A. Maldonado, and Gabriel A. Rabinovich.
    The researchers examined the role of galectins in intestinal inflammation, particularly in Crohn’s disease, ulcerative colitis, and celiac disease patients, as well as in murine models resembling these inflammatory conditions. 
    Maintaining the fine balance between host immunity and tolerance promotes gut homeostasis, and helps to prevent inflammation. To gain insight into the role of Gal-1 in celiac patients, the team demonstrated an increase in Gal-1 expression following a gluten-free diet along with an increase in the frequency of Foxp3+ cells. 
    The resolution of the inflammatory response may promote the recovery process, leading to a reversal of gut damage and a regeneration of villi. Among other things, the team’s findings support the use of Gal-1 agonists to treat severe mucosal inflammation. In addition, Gal-1 may serve as a potential biomarker to follow the progression of celiac disease treatment.
    Gut inflammation may be governed by a coordinated network of galectins and their glycosylated ligands, triggering either anti-inflammatory or pro-inflammatory responses. That network may influence the interplay between intestinal epithelial cells and the highly specialized gut immune system in physiologic and pathologic settings.
    The team’s results demonstrate that the anti-inflammatory and tolerogenic response associated with gluten-free diet in celiac patients is matched by a substantial up-regulation of Gal-1. This suggests a major role of this lectin in favoring resolution of inflammation and restoration of mucosal homeostasis. 
    This data highlights the regulated expression of galectin-1 (Gal-1), a proto-type member of the galectin family, during intestinal inflammation in untreated and treated celiac patients. Further study of this area could lead to better understanding of the mechanisms behind celiac disease, and potentially to a treatment of the disease.
    Source:
    Front. Immunol., 01 March 2018.  
    The researchers in this study are variously affiliated with the Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina; the Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba, Argentina; the Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Sección Intestino Delgado, Departamento de Medicina, Hospital de Gastroenterología Dr. C. Bonorino Udaondo, Buenos Aires, Argentina; the Unidad de Patología, Hospital de Gastroenterología, Bonorino Udaondo, Buenos Aires, Argentina; the Instituto de Investigaciones, Universidad del Salvador, Buenos Aires, Argentina; and the Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.

    Jefferson Adams
    Celiac.com 05/15/2018 - There is a good amount of anecdotal evidence that people with non-celiac gluten sensitivity can tolerate sourdough bread, but there is no good science to support such claims. To determine if sourdough bread help conquer wheat sensitivity, the Alberta Wheat Commission (AWC) is funding a team of researchers to see if the sourdough fermentation process can reduce or eliminate wheat components that trigger wheat sensitivity.
    The project will study the way the sourdough bread fermentation process breaks down proteins and carbohydrates in wheat flour.
    Chair of the AWC Research Committee, Terry Young, said new research suggests that wheat protein may not be the cause of gluten sensitivity in people without celiac disease. Longer fermentation, aka sourdough fermentation, is more common in Europe. Young says that reports indicate that “incidents of non-celiac sensitivity…are actually lower in Europe." He adds the current research will focus on the fermentation, but the future may include the development of wheat varieties for gluten sensitive individuals.
    The research will be led by food microbiologist at the University of Alberta, Dr. Michael Gänzle, who said the use of sourdough bread in industrial baking reduces ingredient costs and can improve the quality of bread as well.
    Dr. Gänzle wants to assess anecdotal claims that people with non-celiac wheat or gluten intolerance can tolerate sourdough bread. His team wants to “determine whether fermentation reduces or eliminates individual wheat components that are known or suspected to cause adverse effects.”
    The team readily admits that their project will not create products that are safe for people with celiac disease. They may, however, create products that are useful for people without celiac disease, but who are gluten sensitivity.
    The AWC is collaboratively funding the project with the Saskatchewan Wheat Development Commission, and the Minnesota Wheat Research Promotion Council, which will contribute $57,250, and $20,000, respectively. The research team will issue a report of its findings after the project is completed in 2021.
    Studies like this are important to shed light on the differences between celiac and non-celiac gluten sensitivity. Stay tuned for more developments in this exciting area of research.
    Source:
    highriveronline.com