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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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    GLUTEN-FREE GRAINS IN RELATION TO CELIAC DISEASE - BY DONALD D. KASARDA, FORMER RESEARCH CHEMIST FOR THE UNITED STATES DEPARTMENT OF AGRICULTURE


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    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


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    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/



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    Guest f.brock

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    I wanted information about amaranth - this article was the first I found to put the scientific knowledge in a clear, concise way, so I could make up my own mind - thank you!

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    I was looking for information on Quinoa, because I had assumed there was no way I could eat it. Now, I'm willing to give it a try! I printed a copy of this so I can take it to the grocery store. You feel so restricted when you have Celiac and I feel like a wide window was just opened to me - exciting!

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    Guest Amanda CCC

    Posted

    This article was clear. I enjoyed reading it and understood the material. However, this information appears to be only hope for those who don't have a known allergy to corn. Most of the distant grains are closely related to corn. I think that corn allergies should be mentioned as a caution.

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    Guest Bernice Dalby

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    You have covered many grains that have had me wondereing what they are and if they are safe. I thank you.

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    Thank you for this information. I had made the same conclusions about the grass family. However, I did not know that canola oil was actually rapeseed oil and had been concerned about canola's origins.

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    It should be noted that canola is a cultivar of rapeseed, and is said to be much less toxic than traditional rapeseed. So, there is a difference, apparently. Also, 80% of the canola acres are said to be genetically modified.

     

    So in essence, canola may be considered rapeseed (by some), but rapeseed is not necessarily canola.

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    My infant son was diagnosed with celiac and I am still nursing him, so by default my diet became gluten free. I had been trying to find good information on all things related to gluten and gluten free diets, this article and entire site has been a God send!! Thank you so much!!

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    Enjoyed reading about all the grains... I had just read the ingredient Buckwheat on a product and wondered if I should eat it. Decided not too, Can't wait until tomorrow to eat it! Thanks for one more product to eat. Also didn't know about Canola oil. Again interesting.

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    Guest Stuart Sherring

    Posted

    This article is extremely helpful as I am looking to broaden the scope slightly of my excellent Bircher recipes. Many thanks.

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    Guest B Bond

    Posted

    Clear excellent advice. Someone who has 2 daughters who may both have this disease thanks you.

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    Guest Pamela

    Posted

    I was diagnosed with celiac disease. I was born with it and doctors did not discover the problem until I was 2 years. I was born in 1987 and one of the first out of 100 to be diagnosed with this rare disease that is now becoming more common.

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    Guest Julia

    Posted

    I have been experiencing intestinal problems for years and will be tested for celiac disease in August. I have been researching and reading to alter my diet which will most likely remain altered regardless of the diagnosis because my stomach has felt better on the altered diet. This information has been more helpful than most that I have read. Thank you.

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    Guest Marcela Rose

    Posted

    I was looking for information on Quinoa, because I had assumed there was no way I could eat it. Now, I'm willing to give it a try! I printed a copy of this so I can take it to the grocery store. You feel so restricted when you have Celiac and I feel like a wide window was just opened to me - exciting!

    Quinoa is a fantastic grain and we love it. There is so much you can do with it!! Its fast replacing my love of rice.

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    Guest Resentful in Cali

    Posted

    I have been suffering for the past 2 weeks with a bad rash on my arms and legs every time I eat. I remember when I was little I had many allergies and had an allergy test done on my back when I was younger and I was allergic to practically everything. I was talking to someone and all the symptoms have been pointing to me being gluten intolerant. All my symptoms such as dry, itchy scalp in which for years I was told by my doctor that I was utilizing the wrong type of shampoo, but my research on this disease indicate otherwise. I have seriously started altering my diet, but I am not too thrilled since I am a true foodie! This sucks...resentful in Cali!

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    Guest Sugarland Girl

    Posted

    It's my understanding that quinoa has a molecule that mimics gluten so eat at your own risk. I react to quinoa by feeling tired, the same as when I eat corn. I have to be grain free. Bummer.

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    It's my understanding that quinoa has a molecule that mimics gluten so eat at your own risk. I react to quinoa by feeling tired, the same as when I eat corn. I have to be grain free. Bummer.

    Quinoa is gluten-free, and it is a myth that there is anything in it that mimics gluten.

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    Guest P Miller

    Posted

    This article is written using old, outdated reference sources. Corn and oats BOTH can and do illicit a response in some celiacs. I can cite several newer reference sources (pubmed) that debunk the theory that corn and oats are safe for all celiacs. I tried to provide proof links but they weren't allowed.

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    Guest aileen

    Posted

    I wanted information about amaranth - this article was the first I found to put the scientific knowledge in a clear, concise way, so I could make up my own mind - thank you!

    AMARANTH ALLERGY! I do not have celiac but an intolerance to wheat. My stomach bloats and I have IBS symptoms. Maybe I have IBS as I have many of those symptoms. However a shocking surprise was an allergy to amaranth. I try different foods to substitute wheat and after having vomiting reactions to prepared food I eventually narrowed it down to the amaranth I was adding. The re-action comes about 2-3 hours after eating amaranth - numb dry mouth followed by upper stomach discomfort and eventually vomiting. Very uncomfortable for quite a few hours. I do not have this re-action to buckwheat or quinoa so if anyone can explain I would be grateful. Thanks.

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    Guest Rebecca

    Posted

    It should be noted that canola is a cultivar of rapeseed, and is said to be much less toxic than traditional rapeseed. So, there is a difference, apparently. Also, 80% of the canola acres are said to be genetically modified.

     

    So in essence, canola may be considered rapeseed (by some), but rapeseed is not necessarily canola.

    Understand that canola is the genetic modification of industrial rapeseed oil into a palatable oil for human consumption. So yes, 100% of canola is genetically mutated rapeseed. There was no such thing as canola in nature before this human manipulation to create it. The industry does not want it considered to be a GMO because that berates its credibility.

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    admin
    The following was written by Donald D. Kasarda who is a research chemist in the Crop Improvement and Utilization Research Unit of the United States 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 connection with wheat (and rye and barley) wasnt recognized until the 1950s - (a)nd it wasnt until the 1960s that intestinal biopsies began to become commonly used in the diagnosis of celiac disease. With regard to the harmfulness of barley malt, the situation is complicated. I will give you my best shot with the qualification that the ideal experiments have not been done and a definitive statement is not possible at this time.
    Because barley malt is made from barley grain that has been germinated it is reasonably certain to be less toxic than barley itself. The hordein proteins and starch in the endosperm of barley grains, like the equivalent gluten proteins and starch in wheat, are there for storage purposes. In a sense, they provide food for the new plant upon germination. In order to use the hordein proteins, the grain releases and generates enzymes upon germination that break down the storage proteins into their constituent amino acids. The problem is that the process is not complete during a short germination, so some peptides (short pieces of the proteins) remain intact in malted barley. There is experimental evidence for this. The resulting mix of peptides is highly complex.
    We know from work described in the scientific literature that relatively small polypeptide chains can still retain activity in celiac disease and we know something about a few sequences that seem to be harmful. But we probably dont know all the sequences that are harmful and we havent put our fingers on the common theme that gives rise to the activity in celiac disease. So the question arises as to whether or not the remaining sequences in malted barley are harmful.
    The possibilities that come to my mind are:
    There are sufficient remaining harmful peptides (with sizes including approximately 12 or more amino acid residues) to give a significant activity in celiac disease to barley malt (remember though that barley malt is usually a minor component of most foods in which it is used and processing might decrease the amount of harmful peptides in a malt product); There are traces of these peptides, but they are sufficiently minimal so as to cause no discernible harm; or The key harmful amino acid sequences are completely destroyed by the enzymes during germination (I can speculate that there might be an important enzyme, very active, in germination that clips a key bond in active sequences, thus reducing the concentration of those active sequences to almost nil while still allowing non-harmful peptides to exist; no evidence exists for this speculation, but it could be used as a working hypothesis for experimentation). There is no completely solid evidence for or against there being a threshold of gluten consumption below which no harm, or at least no lasting harm, occurs and above which definite harm occurs (but see my previous post to the list on starch/malt question). This is a difficult area to study where zero consumption is being approached and the arguments that come up are at least similar to those that have arisen in regard to the question of whether or not there is a minimal level of radiation exposure below which no harm is caused, but above which there is harm that increases with dosage. Accordingly, celiac patients must choose arbitrarily the path they feel comfortable with.
    Here are some references that deal with the question of peptide toxicity. It is not a simple situation:
    Shewry, P. R., Tatham, A. S., Kasarda, D. D. Cereal proteins and coeliac disease. In Coeliac Disease, Ed. M. N. Marsh. Blackwell Scientific, London 1992;pp. 305-348. Kasarda, D. D. Toxic cereal grains in coeliac disease. In: Gastrointestinal Immunology and Gluten Sensitive Disease: Proc. 6th International Symp. On Coeliac Disease, C. Feighery and C. OFarrelly, eds., Oak Tree Press, Dublin 1994;pp. 203-220. Wieser, H., Belitz, H.-D., Idar, D., Ashkenazi, A. Coeliac activity of the gliadin peptides CT-1 and CT-2. Zeitschrift fur Lebensmittel-Untersuchung und-Forschung 1986;182:115-117. De Ritis, G., Auricchio, S., Jones, H. W., Lew, E. J.-L., Bernardin, J. E., Kasarda, D. D. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease Gastroenterology 1988;94:41-49. Fluge, 0, K. Sletten, G. Fluge, Aksnes, L., S. Elsayed. In vitro toxicity of purified gluten peptides tested by organ culture. Journal of Pediatric Gastroenterology and Nutrition 1994;18:186-192. Sturgess, R., Day, P., Ellis, H. J., Lundin, K. A., Gjertsen, H. A, Kontakou, M., Ciclitira, P. J. Wheat peptide challenge in coeliac disease. Lancet 1994;343:758-761. Marsh, M. N., Morgan, S., Ensari, A., Wardle, T., Lobley, R., Mills, C., Auricchio, S. In vivo activity of peptides 31-43, 44-55, 56-68 of a-gliadin in gluten sensitive enteropathy (GSE). Supplement to Gastroenterology 1995;108:A871.

    admin

    The following was written by Donald D. Kasarda who is a research chemist in the Crop Improvement and Utilization Research Unit of the United States Department of Agriculture. If you have any questions or comments regarding the piece, you can address them to Don at: kasarda@pw.usda.gov.
    Most sprouted wheat still has gluten or gluten peptides remaining. Although the sprouting begins enzymatic action that starts to break down the gluten (a storage protein for the plant) into peptides and even amino acids. Generally this is not a complete process for sprouts used in foods so some active peptides (active in celiac disease) remain.

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    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