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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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    WHAT IS CORN GLUTEN, AND IS IT SAFE FOR MY PET?


    Jefferson Adams


    • No, Corn Gluten Won't Hurt Your Pets, Your Livestock, or You


    Celiac.com 12/08/2017 - A quick glance at many pet and livestock food labels will show that they contain corn gluten feed (CGF) and corn gluten meal (CGM).


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    But don't worry. Unlike wheat, barley and rye, corn is naturally gluten-free, as are corn gluten feed and corn gluten meal, says Randy Wiedmeier, livestock specialist with University of Missouri Extension.

    Addressing concerns from people with celiac disease and/or gluten-intolerance over the presence of corn gluten in their livestock feed, Wiedmeier stressed that "Corn gluten meal is a byproduct of processing corn. There is no true gluten in corn, but simply corn proteins."

    He stated that he had no idea who came up with the terms corn gluten feed and corn gluten meal, but that they are "obviously misnomers." He added his assurances that it is "perfectly safe to consume meat, milk or eggs produced by farm animals consuming corn gluten feed or corn gluten meal."

    Even if corn gluten contained actual wheat gluten, it would not be a problem, as anything eaten and digested by an animal is absorbed into the animal's body, and "reassembled by the animal's metabolism into proteins specific to that animal, not back into gluten that would show up in the animal products," said Wiedmeier.

    So, if you have celiac disease or gluten intolerance, you don't have to worry if you see corn gluten listed as an ingredient in your favorite pet food or livestock feed. It is corn-based and gluten-free, and is unlikely to harm you or your pet.

    Additional information can be found online at missouri.edu.

    Source:


    Image Caption: Corn gluten is gluten-free, not a danger to pets, livestock or people. Photo: CC--USDA
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    admin
    Preface: The following information was supplied originally in 1991 in the form of a letter to Phyllis Brogden, Chairperson of the Greater Philadelphia Celiac Sprue Support Group, by Donald D. Kasarda, who was a Research Chemist with the US Department of Agriculture at that time. Copies were sent to four other major celiac patient groups in the US. Dr. Kasarda retired from the USDA in 1999, but updated the information in February of 2000. Dr. Kasarda wishes to add the following disclaimer to the information: These are my opinions based on quite a few years of research in the area of proteins as they relate to celiac disease. They do not necessarily represent those of the Agricultural Research Service, U. S. Department of Agriculture. If you have any questions or comments regarding the piece, you can address them to Don at: kasarda@pw.usda.gov
    The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are those from wheat, rye, and barley (and the man-made wheat-rye cross called triticale). Although oats had generally been considered harmful until 1996, several high quality studies published since then indicate that oats are not harmful either in celiac disease or dermatitis herpetiformis. Some physicians choose not to accept these findings or else point out that there is some potential problem of contamination of oats by wheat. The contamination question has not yet been adequately researched, but may be overemphasized. The three harmful species are members of the grass family and are quite closely related to one another according to various schemes of plant classification (taxonomy). However, not all members of the grass family damage the intestines of celiac patients. Rice and corn, for example, are apparently harmless.
    Many other grains have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oats, rice, and corn in relation to celiac disease. In fact, only wheat and oats have been extensively studied in controlled experiments with the most up-to-date methods. If we accept corn and rice as safe, however, and this seems reasonable to me, then members of the grass family that are more closely related to these species (on the basis of taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Jobs tears, which appear to be reasonably closely related to corn. In some cases, there are protein studies in support of this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide a better answer. However, such studies are not likely to be carried out in the next few years because of high costs and the difficulty of obtaining patient participation (such studies would likely involve intestinal biopsy). In lieu of feeding studies, further studies of protein (and DNA) would provide the next best way to evaluate my suggestion that millet, sorghum, teff, ragi, and Jobs tears are not likely to be toxic in celiac disease, although even such studies are hampered at present by a lack of knowledge of which sequences in the wheat gluten proteins are harmful. There is evidence that a few sequences are harmful, but not all possibilities have yet been tested.
    The scientific name for bread wheat is Triticum aestivum var. aestivum--the first part of the name defines the genus (Triticum) and the second part, the species (aestivum). Species falling in the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins of these species include the various types characteristic of the gluten proteins found in bread wheats (including the alpha-gliadins) that cause damage to the small intestine in celiac disease. Durum wheats (Triticum turgidum var. durum) used for pasta are also harmful to celiac patients. Some Triticum species of current concern include Triticum aestivum var. spelta (common names include spelt or spelta), Triticum turgidum var. polonicum (common names include Polish wheat, and, recently, Kamut), and Triticum monococcum var. monococcum (common names include einkorn and small spelt). I recommend that celiac patients avoid grain from these species. Also, given their very close relationship to bread and durum wheats, I think it is unlikely that these grains would be safe for those with classical allergic responses to wheat.
    Rye (Secale cereale) and barley (Hordeum vulgare) are toxic in celiac disease even though these two species are less closely related to bread wheat than spelta and Kamut. They belong to different genera, Secale and Hordeum, respectively, and lack alpha-gliadins, which may be an especially toxic fraction.
    There have been anecdotal reports suggesting a lack of toxicity in celiac disease for spelta and Kamut, along with anecdotal reports of the opposite, at least in the case of spelt-celiac patients who have been harmed by eating it. Controlled tests would be necessary to draw a firm conclusion, although they hardly seem necessary insofar as spelt and Kamut should be considered forms of wheat.
    The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of reasonably rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are diagnosed in this way without rigorous testing may not actually have celiac disease. Claims that particular foods cause this latter group no problems in relation to their celiac disease could cause confusion.
    Furthermore, celiac patients who report no problems in the short run with spelt or Kamut might experience relapse later. There is now adequate evidence that when celiac patients on a gluten-free diet (that is, a diet free of any proteins or peptides from wheat, rye, and barley) have wheat reintroduced to their diets, times-to-relapse vary enormously among individuals, ranging from hours to months, or even years. And this is for wheat, presumably the most toxic of all cereal grains to celiac patients.
    Additionally, the relapse may not be accompanied by obvious symptoms, but be recognized only by physicians through observation of characteristic changes in the small intestinal tissues obtained by biopsy. The reasons for the enormous variability of response times are not known. It may be speculated that the variability has something to do with the degree of recovery of the lining of the small intestine on a gluten-free diet, the degree of stress that the patient had been experiencing (including infections), and individual genetic differences.
    As I have indicated, all known grain species that cause problems for celiac patients are members of the grass family. In plant taxonomy, the grass family belongs to the Plant Kingdom Subclass known as monocotyledonous plants (monocots). The only other grouping at the Subclass level is that of dicotyledonous plants (dicots). Some other species about which celiac patients have questions actually are dicots, which places them in very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. The seed of the last plant listed, rape, is not eaten, but an oil is pressed from the seeds that is commonly used in cooking. This oil is being marketed as canola oil. Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that these dicots will contain the same type of protein sequence found in wheat proteins that causes problems for celiac patients. Of course, some quirk of evolution could have given rise in these dicots to proteins with the toxic amino acid sequence found in wheat proteins. But if such concerns were carried to a logical conclusion, celiac patients would have to exclude all plant foods from their diets. For example, buckwheat and rhubarb belong to the same plant family (Polygonaceae). If buckwheat were suspect for celiac patients, should not rhubarb, its close relation, be suspect as well?
    It may be in order to caution celiac patients that they may have undesirable reactions to any of these foods--reactions that are not related to celiac disease. Allergic reactions may occur to almost any protein, including proteins found in rice, but there is a great deal of individual variation in allergic reactions. Also, buckwheat, for example, has been claimed to contain a photosensitizing agent that will cause some people who have just eaten it to develop a skin rash when they are exposed to sunlight. Quinoa and amaranth may have high oxalate contents-approaching those of spinach and these oxalate levels may cause problems for some people. Such reactions should be looked for, but for most people, buckwheat, quinoa, or amaranth eaten in moderation apparently do not cause problems. (Buckwheat is sometimes found in mixture with wheat, which of course would cause a problem for celiac patients.) It seems no more necessary for all people with celiac disease to exclude buckwheat from their diets because some celiac patients react to it than it would be for all celiac patients to exclude milk from their diets because some celiac patients have a problem with milk.
    In conclusion, scientific knowledge of celiac disease, including knowledge of the proteins that cause the problem, and the grains that contain these proteins, is in a continuing state of development. There is much that remains to be done. Nevertheless, steady progress has been made over the years. As far as I know, the following statements are a valid description of the state of our knowledge:
    Spelt or spelta and Kamut are wheats. They have proteins toxic to celiac patients and should be avoided just as bread wheat, durum wheat, rye, barley, and triticale should be avoided. Rice and corn (maize) are not toxic to celiac patients. Certain cereal grains, such as various millets, sorghum, teff, ragi, and Jobs tears are close enough in their genetic relationship to corn to make it likely that these grains are safe for celiac patients to eat. However, significant scientific studies have not been carried out for these latter grains. There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat. These include buckwheat, quinoa, amaranth, and rapeseed oil (canola). Some celiac patients might suffer allergies or other adverse reactions to these grains or foodstuffs made from them, but there is currently no scientific basis for saying that these allergies or adverse reactions have anything to do with celiac disease. A celiac patient may have an allergy to milk, but that does not mean that all celiac patients will have an adverse reaction to milk. Again, however, scientific studies are absent or minimal for these dicots. A list of my publications with pertinence to celiac disease follows. Cross-references to the literature for most of the points discussed above can be found in these publications.
    Kasarda, D. D., and DOvidio, R. 1999. Amino acid sequence of an alpha-gliadin gene from spelt wheat (Spelta) includes sequences active in celiac disease. Cereal Chem. 76:548-551. Kasarda, D. D. 1997. Celiac Disease. In Syllabus of the North American Society for Pediatric Gastroenterology & Nutrition, 4th Annual Postgraduate Course, Toronto, Ontario, Canada, pp. 13-21. Kasarda, D. D. 1997. Gluten and gliadin: precipitating factors in coeliac disease. In Coeliac Disease: Proceedings of the 7th International Symposium on Coeliac Disease (September 5-7, 1996), edited by M. Mäkki, P. Collin, and J. K. Visakorpi, Coeliac Disease Study Group, Institute of Medical Technology, University of Tampere,Tampere, Finland, pp. 195-212. Srinivasan, U., Leonard, N., Jones, E., Kasarda, D. D., Weir, D. G., OFarrelly, C., and Feighery, C. 1996. Absence of oats toxicity in coeliac disease. British Medical Journal 313:1300-1301. Tatham, A. S., Fido, R. J., Moore, C. M., Kasarda, D. D., Kuzmicky, D. D., Keen, J. N., and Shewry, P. R. Characterization of the major prolamins of tef (Eragrostis tef) and finger millet (Eleusine coracana). J. Cereal Sci. 24:65-71. 1996. Kasarda, D. D. 1994. Defining cereals toxicity in coeliac disease. In Gastrointestinal Immunology and Gluten-Sensitive Disease, edited by C. Feighery, and F. OFarrelly, Oak Tree Press, Dublin, pp. 203-220. Shewry, P. R., Tatham, A. S., and Kasarda, D. D. 1992. Cereal proteins and coeliac disease. In Coeliac Disease, edited by M. N. Marsh, Blackwell Scientific Publications, Oxford, U. K., pp. 305-348. De Ritis, G., Auricchio, S., Jones, H. W., Lew, E. J.-L., Bernardin, J. E. and Kasarda, D. D. 1988. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease. Gastroenterology 94:41-49. Kagnoff, M. F., Patterson, Y. J., Kumar, P. J., Kasarda, D. D., Carbone, F. R., Unsworth, D. J. and Austin, R. K. 1987. Evidence for the role of a human intestinal adenovirus in the pathogenesis of celiac disease. Gut 28:995-1001. Levenson, S. D., Austin, R. K., Dietler, M. D., Kasarda, D. D. and Kagnoff, M. F. 1985. Specificity of antigliadin antibody in celiac disease. Gastroenterology 89: 1-5. Kagnoff, M. F., Austin, R. K., Hubert, J. J., Bernardin, J. E. and Kasarda, D. D. 1984. Possible role for a human adenovirus in the pathogenesis of celiac disease. J. Exp. Med. 160: 1544-1557. Grains in Relation to Celiac (Coeliac) Disease by Donald D. Kasarda.
    An annotated copy: http://wheat.pw.usda.gov/topics/

    admin

    The term gluten in reference to the cohesive, elastic protein mass remaining after starch is washed from a dough goes back to Beccari in 1745. Strictly speaking, gluten is found only in wheat because it is difficult to wash a cohesive protein mass even from rye, the closest relative to wheat, let alone from barley or oats or anything else. Unfortunately, a misuse of the term by the corn industry has become common in recent years. It has become fairly common to call corn storage proteins corn gluten. Personally, I think there is no justification for such usage. Corn may contain prolamins, as does wheat, but not gluten.
    When it comes to celiac disease, a similar corruption of the term has become very common. There are certain related proteins in wheat, rye, and barley that give rise to particular peptides during digestion that are capable of triggering the responses typical of celiac disease. Only in the case of wheat can these be strictly considered to be derived from the gluten proteins. But for lack of a suitable term, patients and their physicians began speaking of gluten-free or gluten-containing foods. People ask me, How much gluten is there in quinoa? I have to translate this into, Are there any harmful peptide sequences in the proteins of quinoa? There is nothing in quinoa that is like gluten prepared from a wheat flour dough, which has an unusual, perhaps unique, viscoelastic character.
    In any case, as far as we know, corn does not seem to cause harm to celiac patients. Corn has not been studied in the extensive way that wheat has in relation to celiac disease, but for 40+ years patients and their physicians have seemed to agree that corn is OK. The sequences in the corn zein (prolamin) fraction are suspicious, but they do differ in an apparently crucial way from the protein sequences of the wheat gliadin (prolamin) fraction. There have been no modern biopsy-based studies of the effects of purified corn proteins on the celiac intestine as there have been for wheat, but the mass of evidence still seems to point in the direction of corn being safe for celiac patients.

    Jefferson Adams
    Celiac.com 12/03/2010 - An interesting finding regarding corn from a research team based in Sweden that studied the effects of both gluten and corn on patients with celiac disease.
    The research team included G. Kristjánsson, M. Högman, P. Venge, R. and Hällgren, who are affiliated variously with the Department of Gastroenterology, the Department of Medical Cell Biology, Section of Integrative Physiology, the Laboratory for Inflammation Research, and the Department of Rheumatology at Uppsala University Hospital in Uppsala, Sweden.
    Specifically, the team sought to better understand the facets of nitric oxide (NO) production induced by rectal gluten challenge and the relationship between nitric oxide production and mucosal granulocyte activation.
    The team measured the release of rectal nitric oxide in 13 patients with celiac disease and in 18 control subjects. The team measured levels both before and after rectal wheat gluten challenge.
    To collect the gas, the team used a rectal balloon and a newly developed instrument, which allows simultaneous measurements of concentrations of granulocyte mediators in the rectal mucosa. This new technique is called the “mucosal patch technique”.
    The technique allowed the team to measure myeloperoxidase (MPO), eosinophil cationic protein (ECP), and histamine.
    They found that concentrations of rectal nitric oxide increased in ALL celiac patients after wheat gluten challenge, peaking at 15 hours (average concentrations of 9464 (SEM 2393) parts per billion (ppb), with a range of 250–24982 ppb.
    The maximum MPO and ECP increase occurred five hours after challenge. At the fifteen hour mark, the team observed a correlation between mucosal MPO and nitric oxide production.
    They then compared their results against measurements taken after corn gluten challenge. Six of the celiac patients showed an increase in nitric oxide production 15 hours after rectal corn gluten challenge, though much smaller than after gluten challenge. The control group showed no increases after either challenge.
    The main findings showed that mucosal activation of neutrophils and eosinophils precedes pronounced enhancement of mucosal nitric oxide production after rectal wheat gluten challenge in patients with celiac disease.
    The researchers also found that some patients with celiac disease show signs of an inflammatory reaction after rectal corn gluten challenge, shown by increased nitric oxide production and activation of granulocyte markers.
    The fact that nearly half of the celiac patients in this small sample showed increases in nitric oxide production after a corn challenge is definitely interesting, and calls out for further study.
    Source:

    Gut 2005;54:769-774. doi:10.1136/gut.2004.057174 Update by Elaine E. Thompson, Ph.D. submitted 12/03/2010:
    In this study the researchers discovered that the cornmeal they tested was contaminated with wheat. Please revise this blog entry to reflect the flaw in the study."The manufacturer claimed that their corn product was free from wheat or other cereals. We tested the product at the Swedish National Food Administration (Livsmedelsverket) and it was found to be contaminated with 82 μg/g (ppm), which is less than the usual allowed amount in a gluten free diet (<200 ppm) according to the Codex Alimentarius Standard for gluten free foods, and far less than what has been found to be a safe amount of gluten contamination when correlated with histology in oral challenge studies. It cannot be excluded that the small amounts of gluten present in the corn preparation induced an inflammatory reaction as the mucosal patch technique is very sensitive. "


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    Source:
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    Jefferson Adams
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    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.
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    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.
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    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