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Found 43 results

  1. Celiac.com 10/06/2018 - In a recent discussion of Dangerous Grains, we (Mike and Ron) began to speculate about future prospects for those who are gluten sensitive. We talked about future directions for research into how gluten impacts on human health, the growing focus on celiac disease excluding gluten sensitivity, and whether grain consumption is a factor in health problems among those who are not gluten sensitive (according to currently available testing). This inevitably led to debate about whether gluten grains are harmful to all humans. In the context of this discussion, we agreed to write this article inviting further discussion of this matter and offering some suggestions to researchers and contributors to gluten-related research. These include several of our personal concerns and a number of questions that remain unanswered. Where is the research taking us? Perhaps the most important lesson that current research teaches is that a great deal more research is needed if we are to fully understand this ubiquitous hazard to human physical and mental health. There are several emerging trends in the research literature that warrant our attention and further investigation. For instance, celiac disease research has been conducted on the margins for so long that the recent, very rapid expansion of this field may have helped foster neglect of related and equally important research into non-celiac gluten sensitivity. Previous issues of the Scott-Free Newsletter have contained articles outlining the importance of extensive and appropriate testing (and subsequent dietary compliance) for those who have non-celiac gluten sensitivity as identified by a variety of tests including IgG ELISA testing for common food allergies. Further, our growing reliance upon endomysium or tissue transglutaminase antibody testing alone risks overlooking a significant portion of the population with celiac disease. Several reports indicate that in cases where serology testing is negative but symptoms and signs suggest celiac disease, a series of jejunal biopsies should also be taken and assessed by a pathologist who is familiar with celiac disease and uses the Marsh system for evaluating intestinal biopsies. Research into the oats question reveals that known toxic proteins in celiac disease are absent from oats. Yet one small study showed that a significant percentage of celiac patients will develop intestinal lesions characteristic of celiac disease from eating pure oats in the context of an otherwise gluten-free diet. This suggests that we have not yet identified all of the toxic proteins in gluten grains. Some current research is also aimed at developing similar grains without the toxic proteins found in regular gluten grains. The problems associated with oats research have a clear bearing on this issue as well. If celiac patients are developing intestinal lesions from pure oats, which have repeatedly been shown to lack the known toxic proteins, then we do not yet know all the harmful proteins. Thus, genetic development of “safe” wheat is not yet possible. Still, this research may help in the identification of additional toxic proteins. Current research has also led to a growing awareness, among the medical community and the general public, of the connections between gluten consumption and type I diabetes, epilepsy, thyroid disease, osteoporosis and a host of previously unsuspected autoimmune ailments. This is raising many questions about the potential value of a gluten-free diet as part of the treatment protocol for many of these ailments. Current research into zonulin may be one of the most exciting areas of investigation. The work of Dr. Fasano and many others in this important area may well lead to a better understanding of the impact of gluten on schizophrenia, attention deficit disorder, autism, bi-polar disorder, and a variety of ailments that have shown improvement on a gluten-free, dairy-free diet. Where would we like to see the research go? Gluten research is largely overlooked by many of today’s scientists. Despite the growing body of research that discredits gluten grains as healthy foods, the widespread, erroneous assumption of their nutritional value continues to foster gluten consumption. There is a pressing need to dispel the myths that protectively shroud this issue. Our first priority is to see a clear delineation of the gluten-derived proteins and peptides that are currently known to threaten human health. The next logical step would be to initiate an extensive investigation of the various other gluten proteins and peptides in order to identify all of the harmful substances in gluten. The relevance of gluten research reaches far beyond the concerns of academia and the individuals diagnosed with gluten sensitivity or celiac disease. We now know that many health problems could be wholly or partly the result of gluten, making this field worthy of investigation as well. The driving force for people to pursue research of these topics might well be found in a broader awareness of the preliminary findings that connect this wide variety of health conditions to gluten consumption. Further research into this field would reveal many aspects of our current lifestyle. For instance, why are we facing such a widespread variety and increasing rates of psychoses? And how does gluten relate to the multitude of diseases, seldom seen until the advent of agriculture? Gathering more information about gluten and its effect on both gluten sensitive and non-gluten sensitive individuals may provide a greater understanding of modern illnesses. For instance, Dr. Hadjivassiliou’s extensive investigations of neurological diseases of unknown origin, in association with gluten sensitivity, reveal several important research concerns which include: Does current testing identify all important immune reactions to gluten? What other, as yet unidentified proteins are toxic to celiac patients? How often is gluten sensitivity/celiac disease considered in the context of these related ailments? What portion of the population is at risk of developing gluten sensitivity? What portion of the population is at risk of developing celiac disease? What other problems may be associated with gluten consumption? What is the cost-benefit of our escalating consumption of gluten? What vested interests are inhibiting the widespread recognition of health hazards associated with gluten consumption? Concurrent with this research, we would like to see investment in the development of safe, healthy, alternative food sources. Realistically, everyone would probably be better off on a diet of fruits, vegetables, and various meats. But is this possible for the world’s overwhelming and growing population? The necessary resources, including the cost to the consumer, would be prohibitive by current standards and methods of food production. New, more efficient food sources must be found, developed, and widely adopted. These foods must be a better fit with our evolutionary adaptations. This search will require considerable investment and social resolve. What questions should have priority? The question on peoples’ minds is how the research will directly affect them. This means that the research will have to explain the relevance of gluten proteins to such diseases as cancer, autoimmune disorders, obesity and food addiction. Each of these food-related topics is a common concern, widely discussed, and a key topic for gluten-related research. The many applications of food addiction research will attract widespread attention and discussion. The current spotlight on dieting in the popular press reflects a great deal of personal concern, among the general public, regarding this topic. Cancer and autoimmunity have been examined in great detail and a universal cure is still a distant dream. Yet the high rate of gluten sensitivity among these patients suggests a pressing need for research. Such investigations could provide a monumental step toward finding the causes and the explanations for these widespread, devastating health problems. Since these topics have yet to be explored, mainly due to limited research funding, a shift in research focus may yield the solutions to many of these conditions that plague our society. An important hurdle to overcome There is a dichotomy between governmental dietary recommendations that encourage gluten grain consumption and the growing body of research that discredits grains as a healthy food for a significant portion of the population. Unfortunately this is an area where progress is necessary for gluten research to really thrive. Since grain production, processing, and consumption constitute huge portions of various state economies, it is in the best interests of governing bodies to keep grains on everyone’s plate for many years to come. It will require a truly overwhelming body of knowledge, based on solid research proving the hazards of grains to topple the current, flawed structure of governmental dietary recommendations. Conclusion Without this vast array of research, leading to widespread recognition of the hazards of gluten, we can expect little social change. Thus, future prospects for gluten sensitive individuals may be somewhat dim. Increasing population densities may lead to escalating competition for finite food resources. Cheap and available foods derived from gluten grains will become increasingly attractive. Future generations of our families (remember that gluten sensitivity and celiac disease have a large genetic component) will be at risk. The best answer, as we see it, is to fund research aimed at the questions posed here, as well as those that arise out of these investigations. We have offered several directions that we consider important. Whether or not you agree with our priorities, we hope you agree that we need further research into the human health hazards posed by gluten grain consumption. This article was co-written by Mike Pearson.
  2. celieacresearch

    Celiac Research

    Do you or someone you know have Celiac Disease? Do you or someone you know have a Gluten Intolerance or Sensitivity? We Want to Hear Your Story! We are two cultural anthropology students from Linfield College conducting research on Celiac disease and how it affects the lives of those who have it. Cultural anthropologists aim to learn about human lives within their society and how different variables affect them. Celiac disease is one of those variables. Your story is what we’re looking for and everyone has something to tell. If you are interested in participating, email Rose or Carmen at celiacresearch24@gmail.com or reply to this post for more details or to set up an interview time and date.
  3. Forum Members, This is a follow up question to a link posted in this thread I have read the Patient Celiac site before but she noted the possible use of Losartan (Potassium) contributing to Villi Blunting? This concerns me because I am now taking Losartan for blood pressure. Can any one describe their experience with Losartan and/or provide the link that states Losartan's could be a contributing factor in Villi Blunting. The Patient Celiac did not site her source and I couldn't find it. Any help as to the source would be helpful because I would like to read it for myself. Also what other blood pressure medicine's do others on this forum take instead of Losartan. My BP seems to be under control now that I have been taking Folic Acid but don't won't to stop cold turkey until I have another BP medicine I can take in it's place that won't contribute to possible Villi Blunting. I recently had to "catch up" on Vitamin D for my prediabetes so I know absorption is still a problem and thought it was curious because years ago after my celiac diagnosis I had caught up on Vitamin D once before so I was surprised to find I was again low in it again. The Losartan and Villi blunting (if indeed they are linked) could explain why I am still low (again) in Vitamin D. I knew NSAIDS could cause and why I don't take them generally unless I am in unbearable pain but wasn't aware common BP medicines other than Benicar (olmesartan) could cause similar villi blunting. Here is the link on the NSAIDs study. http://www.thedailybeast.com/research-shows-link-between-nsaid-use-and-gut-disease but the cureceliac.org site does not mention Losartan as other causes of Villi Blunting. http://www.cureceliacdisease.org/faq/what-else-can-cause-damage-to-the-small-intestine-other-than-celiac-disease/ So does any body know if Losartan has also been linked to Villi blunting. If it has I need to get off of it for good and find another BP medicine without this severe side effect. Thanks in Advance. posterboy,
  4. Celiac.com 12/12/2017 - Does a gluten-free diet have any effect on cardiovascular risk in people with celiac disease? Does it effect people without celiac disease? So far, both questions have remained unanswered. Recently, a team of researchers set out to conduct a systematic review to shed some light on the matter. The team was led by Michael D.E. Potter, MBBS (Hons), from the University of New Castle, Australia. The team focused their review on the "potential of the gluten-free diet to affect modifiable cardiovascular risk factors including weight, blood pressure, cholesterol and blood sugars," and to do this they searched for "studies which measured these risk factors in individuals before and after the institution of a gluten-free diet." In all, Potter and colleagues reviewed 27 studies that evaluated the effect of a gluten-free diet, as followed for a minimum of 6 months, on cardiovascular risk factors such as BMI, waist circumference, blood pressure, fasting glycemia, hemoglobin A1c and serum lipids. Despite their efforts, they found no clear evidence that a gluten-free diet increases cardiovascular risk in celiac patients. They found no evidence that it increases heart disease risk in people without celiac disease. They really found nothing much at all. While the results varied across studies, and researchers did see changes in some cardiovascular risk factors, they say the data do not support a gluten-free diet for cardiovascular health in individuals without celiac disease. True, perhaps. But it's also true that the data neither support nor condemn a gluten-free diet in people without celiac disease. Unless and until researchers get some solid data from large groups and can make accurate, informative comparisons between those groups, it seems foolish for them to advocate or discourage a gluten-free diet in people without celiac disease. Source: Healio.com
  5. Celiac.com 09/20/2017 - A half-time report on what we've learned about each other so far in the Relational Aspects of Food Sensitivities research. The study is geared toward gaining perspective on the perceived impact one adult's food restrictions cause in a household when cohabitating with other adults. It may ultimately yield strategies to address the social and emotional impact of living with food sensitivities. It aims to provide coping strategies, solidarity and empowerment to our community. If you haven't had a chance to take the survey, unfortunately it's not too late. If you have, thank you! More about the survey will appear in the next issue and the four lucky $25 Amazon gift card winners will be announced next month as well. Here's what we've learned so far: Ninety-six percent (96%) of those who took the survey have a diagnosis that leads them to be on a gluten-free diet. Fifty-one percent (51%) have been diagnosed for 8+ years; 28% have been diagnosed between 4-7 years, 13% between 1-3 years, 5% between 7 months and 1 year, and 3% between 0-6 months. Most began eating a gluten-free diet immediately after being diagnosed. Fifty-two percent feel that the way they were diagnosed affects how seriously the other adult(s) living in the household take their dietary requirements and 23% report that the way they were diagnosed doesn't affect the behavior of the other residential adults at all. When it comes to how diagnosed, 73% were diagnosed by an MD; 12% by themselves; 5% by a Practitioner, 5% by "Other;" 3% by a Naturopath and 2% by a Nutritionist. Forty-six percent (46%) report that they check in with a medical or health professional to monitor their health/diet once a year, and 21% get checkups several times a year. Most of us get our medical, health and dietary information we implement into our lifestyle from online sources (39%), books/magazines (21%) and from the MD (17%). The other 23% who took the survey get information from TV/Media, friends, and other sources. Because of the high-quality content available on websites such as Celiac.com, 87% report they are definitely not confused as to which foods are considered to be gluten-free. Sixty-percent (62%) of the respondents' report that other adults in the household are definitely not confused as to which foods are considered to be gluten-free. Ninety-two percent (92%) of us are not confused about what constitutes a "healthy diet." Thirty-eight percent (38%) feel they eat a healthy diet all the time, 48% eat a healthy diet most of the time, 11% eat a healthy diet sometimes, and 3% never eat a healthy diet. Our diet includes gluten-free grains 83% of the time, while 17% of us are grain-free. Adult cohabitants 'almost always' follow the same dietary requirements as we do in 56% of the households, 'sometimes' in 32% and 'rarely' in 12% of the households. Fifty-seven percent (57%) of us report that we eat different foods than the other adults living in the household 'sometimes,' while 22% of us do that 'rarely' and 21% almost always eat different foods. Adults with food sensitivities in 19% of the households enjoy meals prepared by another adult most of the time, 'sometimes' in 46% and never in 36% of the homes. Sixty-seven percent (67%) of those who eat meals prepared by another adult in their household trust that the meals are safe for them to eat. Fifty-one percent (51%) of those who took the survey report that someone else in the household prepares meals for them one to five times a week while 45% report they make all of their meals themselves. Most of us (95%) never cheat on the gluten-free diet. Demographics of the Respondents Eighty-five percent (85%) of the respondents are female and 15% are male. Ninety-two (92%) are white, most (65%) live with one other adult. Thirty-four point sixty two percent (34%) have a Bachelor's degree and 23% have a Masters degree. Household income was between $75-149K for 33% of the respondents. In-Depth Interview – Phase II For those of you who answered, "yes" to the Phase II interview (the longer-term portion of the research) and haven't heard from me yet, please be patient. I'm working with some time constraints now that fall quarter classes have begun and will be contacting some of you in the coming months to schedule a time to talk.
  6. I recently read a on a Celiac research site, that when a non Celiac gluten sensitive person is blood tested for evidence of an autoimmune disease, they will never test positive for that disease and therefore continue to go without a correct diagonises. I am looking for a copy of that research document because I have to change my rheumatologist because he retired and I have met others who continue to live without the correct diagnoses all because we are gluten sensitive! He headed the Rhumatology department of a large teaching hospital and knew just by looking at me that I have Scleroderma and Raynaud's. I went on to be seen for Sjogren's by a cornea specialist and there was a great debate as to whether I qualified because of my ANA test. (I have the most severe dry eye with cornea damage, dry mouth and dry vagina and the DNA that indicates I could be a candidate for Sjogren's.). This would be an important find for the community of us that continue on our search for health. I am 100% gluten free for 5 years; research gluten and its impact on our life; coach people that have gluten issues on how to build their life without gluten and embrace a new way to live; my 21 year old grandson is gluten sensitive and has several autoimmune diseases and my sisters and cousins have both also.
  7. 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/
  8. Celiac.com 11/21/2016 - This article is the result of an email exchange between Scott Adams and Dr. Sachin Rustgi, which took place between January and March, 2014. Scott Adams: For many years researchers have known that a non-genetically modified, celiac safe wheat does, in fact, exist. Please see: Is Triticum Monococcum (Einkorn) a Safe Wheat for those with Celiac Disease? Baking Quality Wheat Ancestors May be Safe for Those with Celiac Disease I believe that what you are actually doing, which is supported by an approximately $900K corporate grant (if I recall correctly), is to create a GMO version that you can patent in order to make money selling the seeds. This may not be necessary, as what you seek already exists naturally, and I did explain this to your cooperator years ago. Sachin Rustgi: We are aware of these publications mentioned in your post. It is unfortunate that some of these research papers make broad claims not fully supported by the data presented in these reports. This practice is damaging to society in these two ways: i) These publications mislead the public, which gives rise to misconceptions or myths, making it difficult for the general public to accept other innovative ideas. ii) It could even negatively impact public health if the results were blindly accepted and changes were made in routine eating practices without having careful scientific scrutiny of the findings. The popular press and media is partly responsible, because without assessing the credibility of results, they pick broad claims from these publications and serve them to the public in language laden with emotional impact, which the public receives and bases their opinion on. This is also true for the general claims made in the publications cited earlier. Different celiac patients are sensitive to different ‘gluten' proteins (prolamins). If one feeds peripheral blood cells sampled from a patient or a small group of patients (from a specific geographical location) with gluten proteins derived from a wheat genotype, it is expected either to see a reaction (monitored by the production of interferon gamma) or no apparent effect. But in the latter case it does not mean that the wheat genotype is non-toxic to all celiac patients. Because the sample is not a good representative of the genetic variability for disease susceptibility available in the global population, and is likely representing the prevalent disease predisposition allele present in a population inhabiting a particular geographical area or a common disease predisposition allele existing in a larger population (like the one that interacts with the immunogenic 33-mer peptide derived from alpha 2 gliadin). Thus, these T-cell based assays using cell-lines restricted to specific gliadin epitopes are not sufficient to claim general low-toxicity of wheat lines for all celiac patients. I also recommend that readers consult the following publications: Kasarda DD (2007) Letter to the editor: Triticum moncoccum and celiac disease. Scandinavian Journal of Gastroenterology 42(9):1141-1142; Vaccino P, et al. (2009) A catalogue of Triticum monococcum genes encoding toxic and immunogenic peptides for celiac disease patients. Mol Genet Genomics 281(3):289–300. The results of screening hexaploid wheat material under the Celiac Disease Consortium (CDC) funded projects in the Netherlands resulted in a number of publications (Molberg et al. 2005; van Herpen et al. 2006; van den Broeck et al. 2009; van den Broeck et al. 2010). But the authors of these publications never claimed that the material can be used generally. Rather, they suggested these lines to have ‘low-toxicity', as they are devoid of specific epitopes or gluten proteins. Thus, they are good for consumption by a group of celiac patients who share a specific susceptibility allele. We have summarized this material and associated limitations in our publication under two headings, "Wheat Genotypes Naturally Deficient in Immunogenic Gluten Peptides" and "Discussion" [consult Wen et al. 2012 Proc Natl Acad Sci U S A 109(50):20543-20548 for details]. In addition, there is a misconception that with breeding for improved yield, protein content and quality has enhanced the toxicity of the wheat lines, which has resulted in higher incidence of disease over the last couple of decades. Although careful analysis of the facts suggests that nothing has changed over time other than eating habits, procedures of disease diagnosis (became more sophisticated) and public awareness grew, which might have resulted in this increase in the estimated number of celiac patients [also consult Kasarda (2013) J Agric Food Chem 61:1155-1159; Brouns et al. (2013) J Cereal Sci 58:209-215]. However, it is possible to identify low toxicity wheat lines showing reduced accumulation of certain prolamins or immunogenic epitopes, but these lines are not good for general use by celiac patients making labeling of these lines a nightmare, because with the present technology it almost impossible to make recommendations to the patients that they are sensitive only to a specific gluten protein and thus can consume a particular wheat variety. Thus, this trait is an obvious candidate for genetic engineering. Two major achievements in this direction are: i) Gil-Humanes J, Pistón F, Tollefsen S, Sollid LM, Barro F (2010) Effective shutdown in the expression of celiac disease-related wheat gliadin T-cell epitopes by RNA interference. Proc Natl Acad Sci USA 107(39):17023–17028. ii) Wen et al. (2012) Structural genes of wheat and barley 5-methylcytosine DNA glycosylases and their potential applications for human health. Proc Natl Acad Sci U S A 109(50):20543-20548. Collectively, as different celiac patients have sensitivities for different gliadins and glutenins, it is almost impossible to breed wheat lines safe for all celiac patients using conventional breeding approaches. A second issue is the identification of a product's suitability for a group of celiac patients and its labeling, which would be a great logistic challenge. After careful scrutiny of the literature and that the Codex Alimentarius Commission declared that all wheat, barley and rye species including spelt (Triticum spelta L.), khorasan or kamut (T. polonicum L.), durum, einkorn (T. monococcum), triticale, tritordium and their hybrids are immunogenic, and should be avoided by celiac patients (also consult http://wheat.pw.usda.gov/ggpages/topics/celiac.html) add to that challenge. Moreover, some individuals are now known to be sensitive to oat gluten proteins (however, all oat varieties are not toxic, e.g., PrOatina™), and in rare cases, some are even sensitive to maize gluten proteins. According to the latest (August 2, 2013) FDA recommendations any product having Another issue that I want to raise is genetic modification. Why can't we look at transgenics more objectively without having negative feelings toward the technology before we start? Of course, researchers should first look for a solution in nature, and that's what we did, but there is no perfect solution available in nature. Although, the approaches we undertook are inspired by nature, the only way to deliver them is through biotechnology. This approach is where we are silencing the transcriptional regulator of all immunogenic prolamins. It was inspired by a mutation in a regulatory gene in barley. But, this mutation is ‘leaky'. That means it is not completely devoid of immunogenic prolamins. Similarly, the approach to express gluten-detoxifying enzymes in wheat grains was inspired by a barley enzyme that expresses during grain germination and degrades gluten proteins, along with a similar enzyme (but with complementary function) from the black mold Aspergillus, which naturally grows on bread slices. Another example is enzymes secreted by Lactobacillus species, a cocktail of acidifying and proteolytic lactic acid bacteria traditionally used for long-time fermentation by sourdough. These natural enzymes are capable of detoxifying gluten but express at a wrong time or a wrong location or are industrially inapplicable. We have no intention to patent the technology or the product. We will license the varieties to the Washington Grain Commission, which is a general trend at Washington State University. Scott Adams: From my perspective, your endeavor faces two big problems: What you end up with will be a genetically modified form of wheat, which is not allowed in Europe and other places (the list seems to be growing here); What you end up with will still be called wheat, and according to current laws in the USA, cannot be labeled "gluten-free." This is a huge issue that would also be true for einkorn. It would likely be a much easier process to further test einkorn's safety in celiac patients than to create a new genetic variant (that would really be similar to einkorn...right?), then have to go through the same process of testing. Sachin Rustgi: I agree with you on the first point, but as I mentioned previously, this debate about the so-called ‘GMOs' will settle down with time, which has happened in the past with several other technologies. For instance, people initially learned to make genetic crossbreeds in the 18th century, but the general acceptance of this technology as a breeding tool had to wait until the rediscovery of the Mendel's laws in 1900. Embracing this technology resulted in the production of hybrid maize that significantly boosted its yield. The second example is the reluctance to use induced mutagenesis in plant breeding, which is now well accepted and used as a standard procedure to increase genetic variability. The major advantage of shifting to this technology was the production of semi-dwarf rice and wheat cultivars that resulted in the ‘green revolution'. Similarly, the general public will accept the transgenic approach, as there is no other way to meet the growing demand for quality food. I foresee the outcome as an ‘evergreen revolution'. Moreover, if you look in depth at the outcome of using any of the above mentioned procedures, it is always a genetically modified organism, but it is up to us where we would like to draw a line. We are not in favor of releasing ‘reduced or low-toxicity' wheat lines because, as I mentioned earlier, sensitive to, at present. there is no way of telling patients which gluten protein(s) they are sensitive to. In addition, the wheat varieties are not marketed on the basis of their protein composition (however, it is possible to determine the protein profile of a wheat variety). Thus, our ultimate goal is to develop ‘celiac-safe' wheat genotypes completely devoid of immunogenic prolamins or expressing large quantities of gluten detoxifying enzymes. In the former case, the gluten-level of the wheat line is expected to be lower than or equal to the FAO recommended limit of 20 ppm, allowing its labeling as a ‘gluten-free' commodity. In the latter case, the genotype will contain the dietary enzyme supplement within its grains, and hence, will be labeled differently, and will serve as a natural dietary therapy for celiac patients. (These grains or derived flours can be blended into normal flour to bake different products). Two research groups, one in the US and the other in The Netherlands, are producing large quantities of these therapeutic enzymes in bacteria, and their utility as a dietary therapy for celiac patients is currently under advanced clinical trials. In this situation it will be the consumer's decision whether to get enzymes derived from a bacterium to be use as a food supplement or from wheat bread. These enzymes will not only be advantageous for celiac patients but will also prove beneficial to healthy individuals as these enzymes dramatically improve gluten digestibility and bioavailability. Healthy individuals, like celiac patients, cannot fully digest gluten proteins, but unlike celiacs, their intestines are impermeable to the undigested/partially digested gluten proteins, thus they are capable of flushing it out of their systems before it can induce an immune response. (Healthy individuals also do not carry disease predisposition alleles.) This indicates that even in healthy individuals the bioavailability of gluten proteins is low, which can be improved by feeding on these enzyme-fortified grains. It will also reduce how much must be eaten to get a similar amount of nutrition. As I mentioned previously, Triticum monococcum (popularly known as einkorn), is good for consumption by one group of patients, but the major difficulty is determining who can have it without causing damage to their intestines. Thus, we are continuously working toward obtaining wheat genotypes that will be safe for all celiac patients, not just for a sub-group of celiac patients. This will avoid problems with labeling and diagnosis. Scott Adams: If possible, I also just want to clarify my point #2, and get your reply to it. I believe that you said anything testing below 20ppm can be labeled "gluten-free" in the USA, but the new regulations are a bit more complicated (http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm363069.htm): An ingredient that is any type of wheat, rye, barley, or crossbreeds of these grains; An ingredient derived from these grains and that has not been processed to remove gluten; An ingredient derived from these grains and that has been processed to remove gluten, if it results in the food containing 20 or more parts per million (ppm) gluten. I guess you could argue that the genetic modification process has removed the gluten, but this would be a legal argument that certainly isn't obvious in the new laws. For example, it is my understanding that beers which contain barley and have used an enzyme to render them gluten-free cannot, at present, be labeled "gluten-free" under the new law, even though they test below 20 ppm. Sachin Rustgi: I agree with you on the issue of labeling under the new regulations, but as you said it could be argued that these new wheat strains (devoid of immunogenic prolamins) should not be counted with the immunogenic wheat varieties, and should be classified as a new market class of wheat. The additional support for this argument comes from the preliminary feeding trials performed on transgenic gluten sensitive mice, and advanced trials performed under the NIH guidelines on existing gluten sensitive monkeys, and on interested celiac patients. Hopefully, the argument, supported by strong evidence, will foster reconsideration of the present labeling regulations. Scott Adams: What are the chances that cross-pollination of your celiac-safe variety of wheat by normal unsafe wheat will occur, and cause a percentage of the celiac-safe crop to become unsafe? Sachin Rustgi: Wheat is a strictly self-pollinated plant with a natural out-crossing rate of less than 4% in cultivated varieties (in exceptional cases up to 6.05% of out-crossing was reported). Out-crossing occurs mainly in the late emerging wheat spikes, which contribute very little to the total seed count of a plant. Moreover, wheat pollens are relatively heavier in comparison with the other grass pollens, thus could travel to a maximum of 1 m distance from the pollen source, and under optimal field conditions (20C and 60% relative humidity) can survive up to one half hour after release from anthers. Thus, if the APHIS (Animal and Plant Health Inspection Service) recommendations about isolation distances are followed a contamination of ‘celiac-safe' wheat with the ‘immunogenic' wheat can easily be avoided. In addition, a positive correlation between the rate of out-crossing in wheat and the length of flowering period was documented. Thus, the celiac-safe wheat genotypes can be selected for early and synchronously flowering phenotype to further reduce the rate of out-crossing.
  9. Celiac.com 05/20/2016 - The Celiac Disease Foundation (CDF) has received an award from the Patient-Centered Outcomes Research Institute (PCORI). The PCORI Eugene Washington Engagement Award will help the CDF to create a national network of advocates trained in patient-centered outcomes research (PCOR), known as the Patient Engagement Celiac Disease Network (PECDN). The project is aimed at patients and caregivers who may be eager to participate in research, but who may feel unprepared to work with researchers, as researcher expectations and terminology can be confusing. Through this network, CDF will train patients and caregivers to become more involved in research in ways that will impact the treatment of their disease. The first training program for patients and caregivers will be offered at Celiac Disease Foundation's National Conference April 30, 2016. Read more at: Bezinga.com
  10. Celiac.com 01/10/2007 – Celiac disease researchers in Italy and at the Center For Celiac Research in Baltimore, Maryland have conducted a multi center, double-blind, placebo-controlled, randomized trial involving 49 adult individuals who have biopsy-proven celiac disease, and who have been on a gluten-free diet that contains less than 5mg of gluten per day for a minimum of two years. The aim of this study was to determine whether there is a safe threshold for prolonged, daily exposure to minute amounts of gluten. Subjects in the study were divided into 3 groups which were given daily capsules that contained 0mg, 5mg or 50mg of gluten. They were given biopsies and serological screening before and after a gluten challenge. One patient who was given 10mg of gluten daily did experience a clinical relapse, but at the end of the study no significant differences in the IEL count were found between the 3 groups, which lead the researchers to conclude that "(t)he ingestion of contaminating gluten should be kept lower than 50 mg/d in the treatment of celiac disease." This study is in line with past gluten threshold studies, and to help you put the amounts of gluten used in the study into perspective, and to demonstrate why the 20 ppm for naturally gluten-free products used in the Codex Alimentarius gluten-free standards is considered to be a safe threshold for those with celiac disease, the following discussion will attempt to quantify just how much gluten it takes to make 50mg. The amount of gluten contained in your average 30g slice of wheat bread is around 4.8 grams, or 4,800 milligrams (amount of gluten in wheat bread is normally 10% by weight). If you divide 4,800 by 50 it equals 96, so if divide an ordinary slice of bread into 96 pieces, that is roughly how much daily gluten, according to this study, appears to be safe for those with celiac disease. Here is a formula that can be used to determine the number of milligrams of gluten in foods based on the parts per million (ppm) of gluten in the product. The formula is: Products ppm times the number of grams of food divided by 1,000 which equals the number of milligrams. The Codex Alimentarius specifies that naturally gluten-free products contain less than 20ppm, and products that are rendered gluten-free such as Codex quality wheat starch contain less than 200ppm. Using this formula we can determine how many slices of 20ppm and 200ppm gluten-free bread a person with celiac disease would have to eat to consume 50mg of gluten. Here is the math: 20ppm x 30g/1,000 = 0.6 mg. So each slice of 20ppm gluten bread contains 0.6mg of gluten. To get 50mg of gluten per day while eating this type of bread you would have to consume 83.33 slices of it! 200ppm x 30g/1,000 = 6 mg. So each slice of 200ppm gluten bread contains 6mg of gluten. To get 50mg of gluten per day while eating this type of bread you would have to consume 8.33 slices of it. The goal of this study (and this article) is not to encourage people with celiac disease to eat gluten. The reality is that cross-contamination of supposedly gluten-free products is very common, and many of us who are on gluten-free diets still unknowingly ingest tiny amounts of gluten on a daily basis. Studies like this can help provide some sense of perspective with regard to how concerned one should be about minute gluten ingestion, and hopefully this article will help you to understand exactly what the 50mg threshold found in the study means. An article called Gluten-phobia in the Winter 2007 issue of Scott-Free Newsletter further addresses what can happen when someone takes their fear of gluten too far and lets it disrupt their life in ways that are so psychologically unhealthy that the negative effects to the author and those around her may actually rival those of the disease itself. Here are some links to additional information on this topic: FDAs Responses to Public Comments on the Draft Report Approaches to Establish Thresholds for Major Food Allergens and for Gluten in Food Detection of Cereal Proteins and DNA Using MS, ELISA, and PCR Comments by Susan Phillips Clavarino: I read with interest your remarks about the Catassi/Fasano study. As an active member of the AIC (Association of Italian Celiacs), sponsors of the study, and as the person responsible for revising the language of the text for publication…the study does raise some serious queries about background gluten contamination and its impact on the celiac intestine. When the authors remark that the IELs do not show a difference among the three groups of celiacs on long term gluten free diet (though not compared to the non celiac disease controls), they point out that the villous height/crypt depth ratio is a more valid and more sensitive marker of gluten trace contamination in celiacs on long-term dietary treatment. They also remark that "Despite the restricted criteria adopted in this study, the baseline duodenal biopsy results showed evidence of histologic damage (decreased median Vh/celiac disease count and increased median IEL count in adult celiac disease patients receiving long-term dietary treatment. Furthermore, 4 of 49 subjects had to be excluded from the protocol because severe enteropathy (obscuring the possible effects of the micro challenge) was detected at the baseline evaluation. These results confirm that an abnormal small bowel morphology persists in a significant proportion of celiac disease patients treated with a gluten-free diet, despite full resolution of their symptoms..."(due to)"... the ongoing ingestion of gluten, either deliberate or inadvertent, causing persistent inflammation in the small-intestinal mucosa..." etc. As all medically diagnosed Italian celiacs receive a free monthly allowance of naturally (i.e. no wheat starch) gluten free products containing less than 20 ppm from the Italian government health service, and as all the volunteers for the study considered themselves to be healthy (otherwise they would certainly not have volunteered), the finding that 4 out of 49 had to be excluded for severe enteropathy and that histologic damage persists in a significant proportion of adult celiac disease patients on long-term gluten-free diet, besides the other findings of the study (i.e. that 50 mg of gluten per day for only 3 months of trial results in measurable intestinal damage, while there was significant improvement in the placebo group during the strictly monitored trial) is not reassuring. In the light of the Catalan study on the amount of gluten-free dietary foods actually consumed by celiacs in Europe - together with the constant risk of involuntary background contamination and the varying degrees of individual sensitivity - the absolute maximum threshold of ppm in gluten-free products must be kept below 20 ppm. This is a very far cry from the current wording of the Codex Alimentarius which is based on the old standard of the nitrogen content in food. I hope that these words may help to clarify the importance of the work done by Profs. Catassi and Fasano, the Association of Italian Celiacs, the study by the Catalan research group (previously cited on your website), and the need for further research and information as to the impact of micro-traces of gluten on celiac disease and its complications so as to ensure that celiacs may make fully informed decisions about their dietary choices.
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    Please join Beyond Celiac for our webinar: When Your Body Turns on Itself: Understanding Autoimmune Disease, on Thursday, April 28, 2016 at 2:00 p.m. EDT For information: http://www.beyondceliac.org/community/Free-Webinars/Upcoming-Webinars/110/ and to register for the webinar: https://attendee.gotowebinar.com/register/4022227213364925441. The presentation will be lead by celiac disease experts: Robert Anderson, BMedSc, MB, ChB, PhD, FRACP and noted author and New York Times columnist Moises Velasquez-Manoff, MA and Stephen Roberts a member of the Beyond Celiac Patient and Family Advisory Council. Learn more about autoimmune diseases, including risk factors, signs and symptoms and why their prevalence is on the rise during the webinar. Discuss what is happening in the body and more common conditions, and complications if left untreated. Beyond Celiac April 2016 Webinar .docx
  12. Celiac.com 12/22/2015 - Kansas wheat farmers are funding genetic research to figure out exactly why some people struggle to digest wheat, and to try to produce an wheat-friendly alternative. The Kansas Wheat Commission has put $200,000 toward the first two years of the project, which intends to identify anything in wheat DNA that can trigger an auto-immune reaction in people with celiac disease. Ultimately, the project seeks to promote the development new wheat varieties that might be tolerated by celiac sufferers, and meet other gluten-free needs. This, at a time when the market for gluten-free goods has skyrocketed, driven partly by non-celiac sufferers who see such products as a healthier alternative, and is now worth nearly a billion dollars a year in just the US alone. People with celiac disease need to eat a gluten-free diet, avoiding anything containing wheat, rye, or barley. So far, researchers have identified about 20 protein fragments in wheat that trigger celiac reactions, but no one has identified all of them, or bred a variety of wheat that is safe for celiac sufferers to eat. Kansas researchers are hoping to be the first to establish a full screening of celiac-promoting proteins in wheat, then to develop a gluten-free wheat using traditional breeding methods. "If you know you are producing a crop that is not tolerated well by people, then it's the right thing to do," said the project's lead researcher, Chris Miller, senior director of research for Engrain, a Kansas company that makes products to enhance the nutrition and appearance of products made by the milling and cereal industry. Their plan however, has some skeptics. After reviewing the Kansas plan online, expert celiac researcher, Armin Alaedini, assistant professor of medical sciences at Columbia University and a researcher at the New York-based school's Celiac Disease Centre, said the plan may be "too simplistic," and ultimately fail to isolate all the toxic protein sequences that can trigger a celiac reaction. Alaedini added that the project may result in a less toxic wheat product that isn't completely safe for all celiac disease patients, and may be no better in terms of nutritional value or baking properties and taste than current gluten-free alternatives. So, what do you think about gluten-free wheat for celiac sufferers? Would you try it? Trust it? Source: au.finance.yahoo.com
  13. Medication….. What a dreaded word, surrounded by stigmas and scapegoats. I have been on over 35 prescription medications since I was 13. I am now 19, almost 20, and the list seems to just keep growing. Between My eczema, DH, allergies, and now my un-responsive celiac, I have been a mess of a teenager; but seemed to have grown quickly into an adult. A lot parents are quick to take their children to the doctor, pop pills in their mouth, rub creams on their asses, and expect a result; but that is not how it works. Both my mother and I learned the hard way that standing up agents your doctor is the best way to get the results you want. Now I’m not saying to march into your doctor’s office cussing and making a seen (though I have done that once….. or twice), but to ask the question you want to know. Too many people walk out of their doctor’s office not understanding a world that was said. Not understanding what they are taking or the side effects, and unable to do any research themselves on the effects this might have. So where is my rant taking this conversation? Well, sometimes it’s ok to tell your doctor no; maybe suggest your own solution. Numerous times I have walked into my doctor’s office with a better solution than the doctor had. It’s hard to imagine sometimes, but some doctors think they know EVERYTHING about you, about your body, and how to heal you. You know your body better than anyone else. Fight for that right. I had a very bad reaction to prednisone about 3 years ago, and my doctor at the time told me that I was lying because he had never heard of these side effects. He said that it must have been cause by something else. Really? Yes, because peeing my paints in my seat, at school is totally something a teenager goes through. It must be “just a phase”. The bull s$#& that patients have to go through when they don’t have the right doctor is just plain painful. As a patient, don’t expect your doctor to know and do everything they can to help you. Do your research! I could never emphasize that enough. Don’t become the stigma of medication, the “pill popper” that solves all of their problems through every single medication they are prescribed. Become your own person, and do not let your medication define who you are.
  14. Celiac.com 05/04/2015 - Kansas farmers grow a lot of wheat. People with celiac disease avoid wheat like the plague. Not only are people with celiac disease avoiding wheat, but the vast majority of people who avoid wheat now do so for non-medical reasons. With celiac disease rates on the rise, and millions of non-celiacs now avoiding gluten for non-medical reasons, the gluten-free food industry is worth nearly a billion dollars a year in the U.S. alone. This reality has wheat farmers and researchers scrambling to develop wheat strains and products that are safe for consumption by people who follow gluten-free diets. If the The Kansas Wheat Commission has its way, people with and without celiac disease will eat gluten-free wheat in the future. The Commission is providing $200,000 in seed money to support a project intended to identify every component in wheat’s genetic sequence that might trigger adverse reactions in people with celiac disease. The project is being led by researcher Chris Miller, senior director of research for Engrain, a Kansas company that makes products to enhance the nutrition and appearance of products made by the milling and cereal industry. Understanding the causes of celiac disease and gluten intolerance is the goal of numerous researchers worldwide. Some researchers focus on human diagnosis and treatment, while others work on better understanding the 20 or so wheat protein fragments currently known to cause celiac reactions. But no research team has identified every component in wheat that contributes to adverse reactions in people with celiac disease. No researcher or team has yet bred a variety of wheat that is safe for celiac sufferers to eat. Miller says his team hopes to be "one of the first to establish this comprehensive screening of reactive proteins in wheat." The research began in July at the Wheat Innovation Center in Manhattan, Kansas, and remains in its early stages, with researchers extracting proteins from various varieties of wheat in the Kansas wheat repository that dates back to the 1900s in hopes of finding a variety that might already be low in reactivity for celiac sufferers. Later on, the team intends to combine the proteins with anti-gluten antibodies produced by the human immune system to test for immune reactions. Eventually, researchers hope to develop a gluten-free wheat using traditional breeding methods. What do you think? Will they succeed? Would you eat products made from gluten-free wheat? Read more at AP.
  15. Celiac.com 11/13/2014 - An anonymous donor has made a $2 million dollar contribution to the National Foundation for Celiac Awareness (NFCA). The donation is the largest in the organization's history, and will support the NFCA’s mission is to raise celiac disease awareness, promote research and testing testing, and improve the quality of life for celiacs eating a gluten-free diet. Since 2003, the NFCA has worked to promote celiac disease research and awareness. The grant will help to ensure support for the NFCA as it looks to increase research and awareness into the future. Stay tuned for updates on how the NFCA supplements or expands its ongoing efforts on behalf of people with celiac disease and gluten intolerance.
  16. The following was written by one of the CEDAR staff, Stephanie Tudor - TudorS@jove.uchsc.edu. Anyone with further questions should contact her directly. If you live in Denver and are biopsy-confirmed, they would love to hear from you. The Celiac Disease Autoimmunity Research (CEDAR) project is affiliated with the Department of Preventive Medicine and Biometrics in the School of Medicine of the University of Colorado, Health Sciences Center. It is a project supported by a grant from the National Institutes of Health (NIH), and will collect data for a total of five years. The principal investigator is Marian J. Rewers, MD, MPH, Ph.D. Other co-investigators include: Jill Norris, Ph.D.; George Eisenbarth, MD, Ph.D.; Ronald J. Sokol, MD; and Edward Hoffenberg, MD. The goals of this study are primarily to investigate the genetic and environmental causes of celiac disease, through the determination of the prevalence of anti-endomysial antibodies (EMA) in children considered to be at risk based on their family history (first degree relative) of either diabetes mellitus (Type I) or celiac disease or based on their HLA genotype (DR3) that is suspected to put them at an increased risk. The study is anticipating an enrollment of approximately 3,000 eligible children under the age of ten years. Most of the children reside in the Denver metro area, and a large proportion (approximately 40%) of the children involved with this research are concurrently enrolled in the Diabetes Autoimmunity Study in the Young (DAISY), which is run by the same principal investigator. The DAISY project is evaluating the presence of autoimmunity in relation to a pre-diabetic (insulin dependent diabetes mellitus) condition. The enrolled subjects are screened initially between the ages of two and five years of age with a serum sample tested using an IgA-based anti-endomysial antibody assay. The serum samples are also screened for IgA levels in order to rule out the potential for false negative results in IgA deficient children. For the subjects who are tested at a positive titration, follow-up includes a clinic evaluation and small bowel biopsy at the Pediatric Gastroenterology Department at the Childrens Hospital of Denver, Colorado. If a diagnosis of celiac is made, the subject is referred for nutritional counseling and follow-up serum testing is done six months after the diagnosis to confirm effective treatment. Dietary factors are also collected upon enrollment of the subjects, reflecting dietary changes that are made between the ages of one and two years of age, as the introduction of gluten into the diet usually occurs in this time frame. Information on family history of other autoimmune conditions is also collected. Subjects who test negative for the presence of anti-endomysial antibodies will be re-screened two years after their initial testing, to verify their immune status with respect to the anti-endomysial antibodies. By the end of the study period, we hope to have data that more accurately defines the prevalence of celiac disease in a United States population. The children recruited based on their HLA type are from a general population screening, and their data should be able to provide more accurate statistics on prevalence, and perhaps incidence, as some of these children have been followed since birth. We also hope to have identify associations with potential environmental exposures which may increase susceptibility to celiac disease.
  17. March 2000 Volume 6 Number 3 pp 337 - 342 Robert P. Anderson, Pilar Degano, Andrew J. Godkin, Derek P. Jewell & Adrian V.S. Hill Celiac.com 06/25/2001 - Researchers from the Institute of Molecular Medicine and the Nuffield Department of Gastroenterology at Oxford University lead by Dr Robert Anderson have published a study regarding the toxic fraction of gluten, and the specific immune response to this fraction. To date scientists basic understanding of the mechanism that causes celiac disease has been linked to a broad immune response to a variety of gluten peptides, but researchers lacked specifics about both processes. This general understanding has now become very specific based on this new research. By subjecting 12 people with celiac disease to a gluten challenge and monitoring 51 fragments of the A-gliadin gluten protein in their bodies, researchers have determined the specific celiac disease antigen responsible for damage caused by the disorder, and the specific immune response that is caused by the antigen. The results of the study indicate that initial immune reaction to gluten was caused by only two adjacent fragments of the protein, which actually represented a single A-gliadin sequence. The immune response to this single fragment was identical in 11 out of 12 test subjects with celiac disease, and the immune response was not seen in the control subjects who did not have celiac disease. Researchers in Norway have also replicated these results. These findings may lead to better diagnostic tests and treatment for celiac disease, including the possibility of a vaccine or a genetically-modified version of wheat that excludes the harmful A-gliadin sequence, thus making it harmless to celiacs. Dr. Robert Anderson believes that a vaccine for celiac disease would likely involve using the toxic peptide itself, or a variation of it, to desensitize a person with the disease to the A-gliadin sequence. Further research in the area is now underway by the team.
  18. 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.
  19. Celiac.com 07/25/2012 - While a great deal of progress has been made with gluten-free food over the last ten years, many celiacs still feel that they are 'missing out' on gluten-containing foods. Fadi Aramouni, professor of food science at Kansas State University is working to change this through extensive research and testing on sorghum, as well as other wheat alternatives. Sorghum is an appealing alternative to wheat because it is already widely produced in the United States (it is primarily used as feed). The problem is that sorghum is different from wheat, and requires different processing methods to yield food products that are comparable to their wheat counterparts. Aramouni and his team of students and researchers began their search for a non-gluten wheat substitute by carefully inspecting the six varieties of sorghum that are grown in Kansas. Qualities such as grain hardness, dough quality, stretching and rolling qualities, protein, carbohydrates and fiber content as well as taste and look of the finished product were all considered. According to Aramouni, this stage of their research yielded an important discovery: the milling stage dramatically alters the properties of sorghum flour. Different particle sizes yield different results, so the consistency and taste of sorghum-based foods can be modulated before they are even prepared or cooked. In addition to the taste and consistency, Aramouni's team also found that particle size alters sorghum's glycemic index, so it is possible that a very specific milling practice could make products healthier, perhaps even compared to other gluten-free wheat alternatives like corn and rice. Along with the grain science and industry department at Kansas State University and the U.S. Department of Agriculture laboratory in Manhattan, Kansas, Aramouni and his team have developed a variety of sorghum-based tortillas, waffle ice cream cones, breads and Belgian waffles. Time and many taste tests will tell whether Aramouni's research will pay off in the form of more appetizing gluten-free products, but at the very least he and his team are helping us understand that is not just about what grains you use, but how they are processed. Source: http://www.newswise.com/articles/research-with-gluten-alternatives-shows-promise-for-kansas-sorghum-farmers-and-consumers
  20. Celiac.com 02/15/2012 - At the American College of Gastroenterology (ACG) 2011 Annual Scientific Meeting held in Washington, DC, Caris Diagnostics, a leader in anatomic pathology services, presented 15 abstracts highlighting new findings that reflect and expand Caris' commitment to gastrointestinal disease research. Highlights from the presentation include two studies, in particular. The first study, "High Prevalence of Celiac Disease in Women With Young Onset Collagenous Colitis," found that young women with collagenous colitis are eight times more likely than the general population to have celiac disease. That study was authored by Ahmed Bedeir, MD, Bhaskar Ganguly, and Mukunda Ray, MD, PhD. As Dr. Bedeir's finding is gleaned from the largest series of young patients with collagenous colitis ever reported, the study team recommends that women age 40 or younger who have a diagnosis of collagenous colitis also undergo an EGD with duodenal biopsies to exclude concurrent celiac disease. The second study, "Seasonal Patterns in Eosinophilic Esophagitis: An Analysis by Month of Diagnosis and Month of Birth," showed that, contrary to previous suggestions derived from smaller series, there was no evidence of monthly or seasonal variation even within known regions with diverse climates among our 10,000 patients with eosinophilic esophagitis. That study was authored by Jennifer M. Hurrell, DO, Amnon Sonnenberg, MD, and Robert M. Genta, MD, FACG. Regarding Caris' commitment to gastrointestinal disease research, Richard H. Lash, MD, Chief Medical Officer for Caris says that the "establishment of the Caris Research Institute as a structure for promoting and carrying out research has again generated a strong presence at the annual ACG meeting in Washington, D.C," adding that Caris remains "committed to leveraging our tremendous database and academic talent to answer important questions in the field of gastroenterology and are honored to have the opportunity to present our findings at ACG 2011." Source: http://www.carislifesciences.com/news/caris-diagnostics-presents-research-at-2011-annual-meeting-of-the-american-college-of-gastroenterology/
  21. Celiac.com 11/22/2010 - A $45 million donation to University of Maryland Center for Celiac Research will be used to create a first-of-its-kind institute to find new treatments, and perhaps a cure, for celiac disease. The donation comes at the behest of the family of a grateful patient from Indiana, Shelia Cafferty. The institute made possible by the donation could eventually employ up to 200 doctors and researchers who will not only study celiac disease, but use it as a model to better understand other associated autoimmune disorders, including diabetes, rheumatoid arthritis and multiple sclerosis. Dr. Alessio Fasano, Director of the Center for Celiac Research announced the donation at a press conference at West Baltimore's University of Maryland BioPark. Speaking about the donation, Fasano told interviewers that raising "enough money is always a problem" for celiac research, and that what has been needed "for a major breakthrough is thinking out of the box, and this will allow us to do just that." In some ways, Cafferty's nutritional health battle is similar to that fought by many people with celiac disease and gluten-intolerance. She suffered nine years of debilitating gastrointestinal symptoms and rashes before she began to suspect wheat a few years ago. Cafferty, a nurse, put herself on a gluten-free diet, which provided relief, but not all of the answers. She continued to visit doctors looking for answers. About a year ago, Cafferty's determined husband tracked down Dr. Fasano, who was able to diagnose her gluten sensitivity. Fasano's diagnosis provided tremendous relief for the Caffertys, and left them with a resolve to help save others from going through similar suffering. "There are a lot of people like me, not getting answers," she said by phone from Indiana. She was unable to make the announcement with her husband Ken. "When you don't feel good, it impacts your activity and your daily living." As a result of their gratitude and resolve, Sue Cafferty and her husband Ken gave $5 million to Fasano's center and arranged for the donation of another $40 million from a foundation with which they are affiliated, but which declined to be named. Ken Cafferty said he and his wife want their money to raise the public's and doctors' awareness, as well as to fund research into treatments and a cure for celiac disease and other autoimmune disorders. "It's heartbreaking to see someone you love suffer," he said. During the press conference, Dr. Jay Perman, president of the University of Maryland, Baltimore, said he expected the celiac center to collaborate with numerous researchers across, and that research done "using the Cafferty's funds will...enable research to result in real solutions for patients and their families."
  22. Celiac.com 05/02/2011 - David van Heel, gastrointestinal genetics professor at Barts and The London School of Medicine and Dentistry, has shown the world the progress that's possible by researching celiac disease after he headed a group of researchers from around the world who studied the genetic maps of more than 9,400 celiacs. Van Heel's research will surely be followed by other studies, which may possible lead to improved ways of diagnosing and treating the autoimmune disease. As an author, researcher, and gluten-free advocate, I have been raising awareness for celiac disease because I know that with increased awareness will come more research, better diagnoses, and better treatment. Illustrating this point is the fact that van Heel's studies on the genetic links to celiac disease are leading to more research which may lead to new and more effective ways to treat the disease, a prospect which should please celiacs around the globe. Celiac disease is caused by an autoimmune reaction to gluten, a protein found in wheat, rye, and barley, affecting approximately 1% of the population and 300 million Americans. The disease attacks the villi, the finger-shaped structures that line the small intestine, leading to stomach troubles and malabsorption of nutrients. When left untreated, celiac disease can cause severe health conditions and complications such as anemia, osteoporosis, miscarriage, and even cancer. "Substantial" evidence has been found by British researchers that the genes which are connected with celiac disease are also linked to other autoimmune disease such as rheumatoid arthritis. Thus scientists are able to understand how the genetic risk factors for the disease operate by changing the number of immune system genes that cells make. Additionally, it's now understood that there are "hundreds" of genetic risk factors, which means that scientists should be able to "have a good guess at nearly half of the genetic risk at present," van Heel wrote in the Nature Genetics journal, which published his study. How come only 3% of celiac Americans have been properly diagnosed? Chances are, they or their doctors haven't even heard of the disease. Research on celiac disease in the U.S. depends completely on the generosity of benefactors for its funding. There would be no way to continue this research and the efforts to raise awareness without these charitable donations. Out of the estimated fifty autoimmune diseases that have been discovered by doctors, celiac disease is the only one for which research isn't supported by the U.S. government. After years of running around in circles with clueless doctors in a quest to find the cause of my painful symptoms, I finally researched my symptoms on my own. Luckily, as a result of my own findings, I've been properly diagnosed, but managing the gluten-free diet is still a challenge. A pill that could offset genetic factors is appealing to many celiacs like myself. Although the treatment for celiac disease is simple, it calls for a lot of work and can be disheartening at times, requiring a total lifestyle change and a lot of time on home-cooking. With this research into genetic links to celiac disease, we have more studies to look forward to, increased awareness, and possibly other treatment options. In the meantime, it's best to keep doing our parts to raise awareness and funds for research.
  23. This article originally appeared in the Summer 2002 edition of Celiac.coms Scott-Free newsletter. On June 2, 2002, hundreds of researchers traveled from all over the world to Paris, France, in order to hear the latest scientific reports on celiac disease research and to present results from their own investigations. Over the course of three days, scientists presented dozens of reports, and displayed over a hundred posters covering all aspects of celiac disease, from laboratory research on the microbiologic aspects of the disease, to quality of life issues in patients who are on the gluten-free diet. There were so many exciting reports presented at the conference, and the following describes the research findings from these new reports concerning the screening and clinical presentation of celiac disease, osteoporosis and osteopathy and neurological conditions. SCREENING ISSUES IN CELIAC DISEASE In order to understand how best to screen populations for celiac disease, it is important to know how celiac disease affects a portion of the population, and how it compares to similar populations in other countries. Mayo Clinic Retrospective Study Dr. Joseph Murray from the Mayo Clinic conducted a retrospective study on the population of people living in Olmsted County, Minnesota. This county has kept medical records on all of its residents for over 100 years. Dr. Murray looked at the medical records to determine which residents were diagnosed with celiac disease from 1950 to 2001. He found 82 cases of celiac disease, with 58 in females and 24 in males. The average age of diagnosis was 45. Pediatric diagnoses of celiac disease during this time period were extremely rare. Dr. Murray found that while the diagnosis rate of dermatitis herpetiformis (DH) remained constant over the 51 year period, the diagnosis rate of celiac disease increased from 0.8 to 9.4 per 100,000 people. He also noted that over time, adults with celiac disease were less likely to present diarrhea and weight loss as symptoms. Encouragingly, he determined that the average life expectancy for a diagnosed celiac in this community was no less than that of the normal population, despite the fact that celiac disease was often diagnosed later in life. What does this mean? The celiac disease diagnosis rate in this county is much lower than the actual incidence rates that have been reported in other studies; however, that rate has greatly increased over the past 51 years. It is also noteworthy that so few children were diagnosed with celiac disease. The analysis highlights interesting and useful information about the presentation of celiac disease in adults, and about the potential life expectancy for people with celiac disease who are diagnosed later in life. United States and Europe Compared Dr. Carlo Catassi of Ancona, Italy is currently a visiting researcher at the University of Maryland Celiac Research Center. He presented an analysis of the similarities and differences between the clinical presentations of celiac disease in the United States and Europe. Dr. Catassi established that the prevalence of celiac disease in the U.S. and Europe are the same and range between 0.5 to 1.0 percent of the general population. The prevalence in at-risk populations is much higher, ranging between 5 and 10 percent, and the prevalence in people with Type 1 Diabetes is approximately 5 percent in both the U.S. and Europe. He found that the typical (symptomatic) cases of celiac disease were less common in the U.S., and that the latent (asymptomatic) cases were much more common. Dr. Catassi stated that these differences could be due to genetic factors (for example, there are more Asians in the United States than in Europe), but are more likely due to environmental factors. He noted that infants born in the U.S. are often breastfed longer than their European counterparts. There is also a lower gluten intake in the first months of life for infants in the U.S. The timing of the introduction of cereals could help explain why many American children have somewhat milder symptoms and a more unusual presentation of the disease. What does this mean? Dr. Catassis analysis underscores the need to better educate physicians in the U.S. so that they learn to see typically atypical signs of celiac disease in children and adults. He also reinforced the importance of breastfeeding as a protective factor for children with a genetic predisposition to celiac disease, which could also improve the outlook for European children in the future. United States Prevalence Research Dr. Alessio Fasano presented a poster which outlined his recent findings that are a follow-up to his now famous 1996 blood screening study. The original study found that 1 in 250 Americans had celiac disease. It was performed using anti-gliadin antibodies (AGA), and when a blood sample tested AGA positive it was confirmed using anti-endomysial (EMA) antibody testing. Now that human tissue transglutaminase (tTG) testing is available, Dr. Fasano and his colleagues wanted to see if the results of their original study would be different using the tTG test. He and his colleagues tested the negative samples in the original study, and found 10 more positives using the tTG test. Two of these samples were confirmed positive when checked using the AGA antibody test. Dr. Fasano concluded that the original (1996) prevalence estimate of 1 in 250 understated the true prevalence rate, which could actually be greater than 1 in 200 Americans. Dr. Michelle Pietzak, a pediatric gastroenterologist at the University of California at Los Angeles, also presented a poster which described the prevalence of celiac disease in Southern California. In a study of 1,094 participants, Dr. Pietzak found that 8% of Hispanics tested positive for celiac disease. The most common symptoms presented by subjects in her study included abdominal pain, diarrhea, constipation, joint pain and chronic fatigue. What does this mean? It is important to understand that the foundation of all U.S. prevalence research on celiac disease began with the blood donor study performed by Dr. Fasano in 1996. His newly revised findings, which have been supported by at least one other major study, show that the prevalence of celiac disease in the U.S. population is much higher than originally believed, and that it could be greater than 1 in 200 people. Additionally, the California study is one of the first to establish a celiac disease prevalence figure for the Hispanic population in the U.S., and if the 8 percent figure is supported by further research it would indicate that celiac disease significantly affects Hispanic Americans. OSTEOPOROSIS AND OSTEOPATHY Dr. Julio Bai of Argentina presented important information on a condition that affects many people with celiac disease, and one that is often overlooked by physicians—osteoporosis or osteopathy (its milder form). Both children and adults with celiac disease can have low bone mineral density, and its method of treatment can have important consequences. Dr. Bai treats adults with bone loss, and has studied the nature of fractures and bone health in adults with celiac disease. In a case-control study of 78 celiac disease patients, Dr. Bai found that symptomatic patients were more likely to experience bone fractures than the normal population. Interestingly, he also found that patients with latent (asymptomatic) celiac disease had lower fracture rates than those with symptoms, and that the rate was equal to that of the normal population. None of the patients, however, experienced a fracture of the more serious type—in the hip, spine or shoulder, and the fractures tended to occur in their arms, legs, hands and feet. The doctor also discussed preliminary evidence which showed that most women with osteopathy and celiac disease who go on a gluten free diet will experience an improvement in bone density, while many men do not. There was, however, no difference found between the fracture rates of men and women. Dr. Bai also found that nutritional and metabolic deficiencies in patients with celiac disease and osteopathy might also contribute to fractures by weakening the muscles that surround essential bones. He added that immunological factors could also enhance or inhibit bone rebuilding, and that there is a bone-specific tissue transglutaminase (tTG) that plays a role in this process. What does this mean? It was certainly good news to hear that most people with low bone density due to celiac disease can reverse the damaging process, and if celiac-related fractures do occur they tend to be of the less serious type. Additionally, it was interesting to learn just how important a role muscle health plays in preventing celiac-related fractures. Osteopathy in Children Dr. Mora, an Italian researcher, presented data on osteopathy in children with celiac disease. His results indicate that a gluten-free diet can improve bone mass, and the effect is maintained even after 10 years. He also added that a gluten-free diet improved the overall bone metabolism of the children, and that the diet alone could cure their osteopathy. Osteopenia and Osteoporosis: Conditions Related to Celiac Disease In a chart prepared by Dr. David Sanders of the United Kingdom, data on 674 patients, 243 with osteoporosis and 431 with osteopenia, were presented. He found 10 cases of celiac disease among a mostly female population that had an average age of 53. In all ten cases, patients either had a history of iron-deficient anemia or gastrointestinal symptoms. He concluded that all patients with osteopenia or osteoporosis and a history of anemia or gastrointestinal symptoms should be screened for celiac disease. What does this mean? Dr. Sanders has identified a subset of people with osteoporosis and osteopenia that should be screened for celiac disease—those who have been anemic or have gastrointestinal symptoms. This helps physicians know when to refer patients for celiac disease screening. NEUROLOGICAL SYMPTOMS Dr. Marios Hadjivassiliou of the United Kingdom presented data on neurological symptoms and gluten sensitivity. In an eight-year study, Dr. Hadjivassiliou screened people who had neurological symptoms of unknown origin using the anti-gliadin antibody (AGA) test. He found that 57 percent of these patients had antibodies present in their blood, compared to 12 percent of healthy controls or 5 percent of patients with a neurological condition of known origin. From this group, he studied 158 patients with gluten sensitivity and neurological conditions of unknown origin (only 33 percent of these patients had any gastrointestinal symptoms). The most common neurological conditions in this group were ataxia, peripheral neuropathies, myopathy, and encephalopathy (very severe headache). Less common were stiff person syndrome, myelopathy and neuromyotonia. He noted that ataxia is not a result of vitamin deficiencies, but is instead an immune-mediated condition. Patients with ataxia have unique antibodies that are not found in patients with celiac disease. Dr. Hadjivassiliou felt that up to 30 percent of idiopathic neuropathies could be gluten-related, and that there is preliminary evidence which indicates that a gluten-free diet is helpful in cases of neuropathy and ataxia. What does this mean? It is interesting to note that Dr. Hadjivassiliou has studied gluten sensitivity and not celiac disease. The test used in this study is not specific enough to identify people who were likely to have celiac disease. However, his finding that the gluten-free diet may be helpful in people with certain types of neuropathy and ataxia opens the door for further research on these conditions in people with celiac disease.
  24. The Wm. K. Warren Medical Research Center for Celiac Disease at the University of California, San Diego is pleased to announce that the recipient of the 2011 William K. Warren, Jr. Prize for Excellence in Celiac Disease Research is Frits Koning, Ph.D. Professor Koning has been head of the Immunochemistry Section in the Department of Immunohematology and Blood Transfusion of the Leiden University Medical Centre (LUMC), the Netherlands, since 1993. He is the chairman of the scientific advisory board of the LUMC and the CEO of the Dutch Celiac Disease Consortium (CDC), funded through a 11.7 million euro grant from the Dutch Government for the period 2004 - 2012. In the CDC, immunologists, geneticists, food specialists and medical doctors collaborate with industrial partners to develop practical solutions to improve the quality of life of patients with celiac disease. Frits Koning received his Ph.D. from the University of Leiden and continued with postdoctoral studies at the NIH, Bethesda, USA where he identified γδ T cell receptors expressed by dendritic epidermal T cells. Back in Leiden he set up his own group within the LUMC and continued his research on the characterization and functionality of γδ T cell receptors in humans. Simultaneously he started to investigate the molecular basis for autoimmune diseases by determining the peptide-binding motifs specific for disease associated HLA-molecules. This work led to the identification of a peptide binding motif specific for HLA-DQ2 and subsequent work identified gluten peptides that could bind to the celiac disease associated HLA-DQ molecules and the realization that many of such peptides require modification by the enzyme tissue transglutaminase to facilitate high affinity binding to either HLA-DQ2 or HLA-DQ8 and the initiation of gluten-specific T cell responses. This provided a molecular explanation for the association between these HLA-DQ molecules and the development of celiac disease. Based on these results studies have been carried out to determine how gluten proteins can be detoxified and thus made suitable for consumption by celiac disease patients. Presented annually by The William K. Warren Foundation, the $25,000 William K. Warren, Jr. Prize is awarded internationally to an individual or group who has made a significant contribution to the field of celiac disease research through basic, translational, or clinical research. Professor Koning will be presented with the award on Friday, June 3 at the University of California, San Diego, at which time he will present the 2011 Warren Prize Lecture, “Celiac Disease: How Complicated Can It Get?” Details can be found on the Center website, at http://celiaccenter.ucsd.edu.
  25. The following report comes to us from The Sprue-Nik Press, which is published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan (Volume 7, Number 6, September 1998). The degree of mucosal damage varies from one celiac patient to another. Also, the amount of the small intestine that is affected also varies, with the damage usually progressing from the beginning of the small intestine and then moving downward toward the end of the small intestine. This may explain the variable symptoms in different patients. For example, when a significant portion of the small intestine is involved, diarrhea, malabsorption, and weight loss result. When damage is isolated to only the top portion of the small intestine, the only affect may be iron deficiency. (Incidentally, when iron deficiency is not corrected by iron supplements, it is highly likely that celiac disease is the cause of the deficiency.) Gluten in a celiacs diet causes the immune system to produce gliadin antibodies in the intestine. Some of these leak into the bloodstream where they can be detected in blood tests. These blood tests are useful for screening for celiac disease, though a small intestinal biopsy remains the gold standard for diagnosing celiac disease (celiac disease). There are few diseases for which diet and nutritional issues are more important than for celiac disease. At this time, the only known treatment of celiac disease is the removal of wheat, barley, rye, and oats from the celiacs diet. On the surface this sounds simple, but complete removal of dietary gluten can be very difficult. Gluten-containing grains are ubiquitous in the Western diet. Also, grain-derived food additives such as partially hydrolyzed vegetable protein [and modified food starch] are widely used in processed foods and oral medications. Content labels are often vague or incomplete regarding these additives. What further complicates matters is a lack of significant experience on the part of physicians and dietitians in the dietary treatment of celiac disease. This is mainly because there are so few celiac patients for anyone practitioner. Therefore the best sources of dietary information for a new patient are other knowledgeable, more experienced celiacs. It is very important that the diet be followed with full and strict compliance. Celiacs, especially if theyve had active celiac disease for a longtime, are at higher than normal risk for GI malignancies.(Fortunately, compliance to a good gluten-free diet returns the risk of malignancy and life expectancy to that of the general population.)Another complication of long-term untreated celiac disease is bone loss, which maybe irreversible in older patients. When a large portion of the small intestine is affected by active celiac disease, the result can be a generalized malabsorption problem, resulting in deficiencies of water- and fat-soluble vitamins and minerals. Folic acid deficiency is particularly common in celiac disease because, like iron, it is absorbed in the upper small intestine [where the highest concentration of celiac-related damage generally occurs]. Folic acid is necessary for DNA replication, which occurs in cell turnover. So a deficiency of folic acid can impair the regenerative ability of the small intestine. Vitamin B12, also essential to DNA synthesis, is not malabsorbed as commonly as folic acid. Magnesium and calcium deficiency are also common in active celiac disease, because of decreased intestinal absorption AND because these minerals tend to bind with malabsorbed fat which passes through the system. It is particularly important for doctors to assess the magnesium status of celiacs, because without correction of a magnesium deficiency, low levels of calcium and potassium in the blood cannot usually be corrected with supplements. In severe cases, magnesium supplementation should be done intravenously because of the tendency of oral magnesium to cause diarrhea. Supplemental calcium generally should be provided to celiacs, possibly with vitamin D, to help restore tissue and bone calcium levels to normal. The exact dose of calcium is not known. Dr. Fine usually recommends 1500-2000 mg of elemental calcium per day, divided into two doses, for several years and sometimes indefinitely. [4], [5], [6] Zinc is another mineral that often becomes depleted in patients with chronic malabsorption. Zinc supplementation (usually the RDA via multi-vitamin and mineral supplements) helps avoid skin rashes and restores normal taste. Up to 20% of celiacs will continue to experience loose or watery stools even after going on a gluten-free diet. Sometimes this is due to inadvertent gluten in the diet, but a recent study at Dr. Fines medical center showed that in these cases other diseases epidemiologically associated with celiac disease are present.[7] These include microscopic colitis, exocrine pancreatic insufficiency, lactose intolerance, selective IgA deficiency, hypo- or hyperthyroidism, and Type I diabetes mellitus. When diarrhea continues after beginning a gluten-free diet, a search for these associated diseases or others should be undertaken and treated if found. The use of cortico steroids has been advocated in celiacs when the response to the gluten-free diet is sluggish or absent. This is necessary more often in older than in younger patients. However, pancreatic enzyme supplements (prescribed by a doctor) may be needed to help digestion and resolve ongoing malabsorption in some patients. The endomysial antibody blood test is highly accurate and specific for detecting celiac disease. However, the current method of detecting these antibodies involves an operator looking through a microscope and observing the antibody binding on monkey esophagus or human umbilical cord tissue substrates. The correct interpretation of results is highly dependent on the skill and experience of the technician interpreting the fluorescence pattern through the microscope. Moreover, determination of the amount of antibody present relies upon repeat examinations following dilutions of the blood serum, with the last positive test being reported as a titer. A new discovery was reported by a research group in Germany.[8] The antigen substrate of the endomysial antibodies has been identified. This allows the development of a new test that can detect and measure serum endomysial antibodies in one, chemically-based test run [thus greatly reducing the potential for human error and significantly reducing the time needed for each test--ed.] These new tests should be available for clinical use shortly. In a recent study, Dr. Fine found that the frequency of positive stool blood tests was greater in patients with total villous atrophy relative to partial villous atrophy, and all tests were negative in treated patients without villous atrophy.[9] This suggests that fecal occult blood may be a non-invasive and inexpensive method of following the response of the damaged intestine to treatment. Also, it should be noted that the high frequency of positive tests due to villous atrophy will decrease the accuracy of the tests when used for cancer screening in this same patient population (which is how these tests are normally used by health care providers). There have been two recent reports touting the lack of deleterious effects when 50 grams of oats per day are added to the diet of celiac patients. Although this finding is exciting for celiacs, both studies possess certain limitations. In the first study, published by a Finnish group, the exclusion criteria for symptoms and histopathology were somewhat strict, so that patients with more mild forms of celiac disease seemingly were selected for study. And though no damage to duodenal histology occurred after one year of oats consumption, no physiologic or immunologic parameters of disease activity were measured. Furthermore, several patients in the treatment group dropped out of the study for reasons not mentioned in the article.[10] The second and more recent study involved only 10 patients, studied for twelve weeks. The favorable results of this study must be interpreted with caution because of the small sample size and short study period.[11] Even the one-year treatment period in the Finnish study may be too short to observe a harmful effect, as it is known that small intestinal damage sometimes will not occur for several years following there introduction of gluten to a treated celiac. At the worst, an increase in the incidence of malignancy may result from chronic ingestion of oats, an effect that could take decades to manifest. Therefore, this issue will require further study before oats can be recommended for the celiac diet. 3. From the September 1998 newsletter of the Houston Celiac-Sprue Support Group, a chapter of CSA/USA, Inc. 4. Ciacci C, Maurelli L, et el, Effects of dietary treatment on bone mineral density in adults with celiac disease; factors predicting response, Am J Gastroenterol, 1997; 92 (6): 992-996. 5. Mautalen C, Gonzalez D, et al, Effect of treatment on bone mass, mineral metabolism, and body composition in untreated celiac patients, Am J Gastroenterol, 1997; 2 (2):313-318. 6. Corazza gluten-free, Di Sario A, et al, Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease, Bone, 1996; 18 (6):525-530. 7. Fine, KD, Meyer RL, Lee EL, The prevalence and causes of chronic diarrhea in patients with celiac sprue treated with a gluten-free diet, Gastroenterol, 1997; 112 (6):1830-1838. 8. Dieterich W, Ehnis T, et al, Identification of tissue transglutaminase as the autoantigen of celiac disease, Nat Med, 1997; 3 (7):797-801. 9. Fine KD, The prevalence of occult gastrointestinal bleeding in celiac sprue, N Engl J Med, 1996; 334 (18):1163-1167. 10. Janatuinen EK, Pikkarainen PH, et al, A comparison of diets with and without oats in adults with celiac disease, N Engl J Med, 1995; 333 (16):1033-1037. 11. Srinivasan U, Leonard N, et al, Absence of oats toxicity in adult coeliac disease, BMJ, 1996; 313 (7068):1300-1301.
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