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Found 10 results

  1. Celiac.com 01/11/2016 - Is celiac disease a disability under the federal Americans with Disabilities Act? The Department of Justice says not necessarily. On the heels of a federal lawsuit that claiming that restaurants are violating federal disability laws by charging more for gluten-free food than for non-gluten-free counter parts, a Department of Justice spokesperson has stated that a 2012 civil rights settlement on behalf of Lesley University students with celiac disease does not make the condition a disability in all cases. DOJ public affairs specialist, Patrick Rodenbush, said settlement at Leslie University did not set a legal precedent, because the "…settlement enforces the rights of students whose food allergies were disabilities, [but] it doesn't necessarily make celiac disease a disability in all cases." This is relevant to a case in California, where federal judge recently denied a motion to dismiss a class action lawsuit alleging P.F. Chang's violates the Americans with Disabilities Act because it charges more for gluten-free items. In the P.F. Chang's case, Judge Ronald Whyte denied P.F. Chang's motion to dismiss because, he wrote, that, although the court had not found specific information proving that celiac disease constituted a disability under the ADA, the "plaintiff has pled sufficient facts to support her claim that she has a disability that impacts a major life activity." Whyte noted "on a more complete factual record, the court might reach a different conclusion." He also stated that it may be difficult, or impossible for Phillips to prove her claims. "The ultimate question is whether P.F. Chang's, in providing gluten-free meals, is providing different products or whether the price differential with regular meals is a pretext for discrimination against those with celiac disease," Whyte wrote. At stake is whether or not food vendors, such as P.F. Chang's can charge higher prices for gluten-free foods than they do for non-gluten-free items. The results of this case are being watched closely by celiacs and by restaurant companies, because a ruling that establishes that people with celiac disease are covered under the federal Americans with Disabilities Act could conceivably have a serious impact on how the restaurant industry approaches gluten-free food. Stay tuned for new developments. Source: legalnewsline.com
  2. Celiac.com 06/09/2017 - More and more people are avoiding gluten these days, even folks who do not have a medical reason to do so. Perhaps looking to take advantage of the popularity of gluten-free dieting, or perhaps hoping their targets are easily fooled, one cheeky police department in California is offer to run a gluten check on people's meth. The Newark Police Department posted the offer on their Facebook page. The offer reads: "Is your meth laced with deadly gluten? Not sure? Bring your meth down…and we will test it for you for free!" Of course, however bad may be, and meth is plenty bad, it likely contains no gluten. Also, gluten aside, anyone who takes the police up on the offer will likely be arrested, which seems to be the point. The post appeared on Thursday, and by Saturday, had been shared over 80,000 times, and received more than 14,000 'likes.' According to the National Institute on Drug Abuse, over 12.3 million Americans age 12 and older have tried meth at least once. So far, no word from the Newark PD about whether their plan has actually found any gluten in meth, or led to any arrests. Read more at HuffingtonPost.uk.
  3. 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/
  4. Celiac.com 12/26/2012 - The Justice Department today announced an agreement with Lesley University in Cambridge, Mass., to ensure that students with celiac disease and other food allergies can fully and equally enjoy the university’s meal plan and food services in compliance with the Americans with Disabilities Act (ADA). Food allergies may constitute a disability under the ADA. Individuals with food allergies may have an autoimmune response to certain foods, the symptoms of which may include difficulty swallowing and breathing, asthma and anaphylaxis. For example, celiac disease, which is triggered by consumption of the protein gluten (found in foods such as wheat, barley and rye), can cause permanent damage to the surface of the small intestines and an inability to absorb certain nutrients, leading to vitamin deficiencies that deny vital nourishment to the brain, nervous system, bones, liver and other organs. Celiac disease affects about 1 in 133 Americans. “By implementing this agreement, Lesley University will ensure students with celiac disease and other food allergies can obtain safe and nutritional food options,” said Thomas E. Perez, Assistant Attorney General for the Civil Rights Division. “The agreement ensures that Lesley’s meal program is attentive to the schedules and demands of college students with food allergies, an issue colleges and universities across the country need to consider.” Under the settlement, Lesley University agrees to amend its policies and practices to: Continually provide ready-made hot and cold gluten- and allergen-free food options in its dining hall food lines; Develop individualized meal plans for students with food allergies, and allow those students to pre-order allergen free meals, that can be made available at the university’s dining halls in Cambridge and Boston; Provide a dedicated space in its main dining hall to store and prepare gluten-free and allergen-free foods and to avoid cross-contamination; Enable students to request food made without allergens, and ensure that a supply of allergen-free food is available; Work to retain vendors that accept students’ prepaid meal cards that offer food without allergens; Display notices concerning food allergies and identify foods containing specific allergens; Train food service and University staff about food allergy related issues; Pay $50,000 in compensatory damages to previously identified students who have celiac disease or other food allergies. The settlement agreement was reached under the ADA, which prohibits discrimination against individuals with disabilities by public accommodations, including colleges and universities, in their full and equal enjoyment of goods, services, and facilities. More information about the Civil Rights Division and the laws it enforces is available at www.justice.gov/crt . More information about the settlement with Lesley University can be found at www.ada.gov or by calling the toll-free ADA Information Line at 800-514-0301 or 800-514-0383 (TTY).
  5. 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.
  6. We have recently reported on Lancet (1) a consistent cohort of patients affected by drug-resistant epilepsy with cerebral calcifications, half of which were cured by a gluten-free diet. All had an atrophic jejunal mucosa, which recovered on a gluten free diet. Gluten intolerance is now a recognized cause of brain calcifications and epilepsy, of dementia, of psychiatric disturbances: many researchers believe that, in genetically predisposed subjects, gluten is not healthy for the brain function (2). This is just too much. Having had over 25 years of variegated experience with gluten intolerance I find hard to imagine that the single most common food intolerance to the single most diffuse staple food in our environment might provoke such a complexity of severe adverse immune-mediated reactions in any part of the human body and function. The list is endless, but malignancies, adverse pregnancy outcome and impaired brain function are indeed complications above the tolerable threshold of this food intolerance. On the other end today we know very well that the majority (as many as 9 to 1) of gluten intolerant subjects, identified by familial or population screening, do not manifest any complaint, although they do have a flat intestinal mucosa (3). In conclusion a sizable proportion of our population (from 0.3 to 1%) is gluten intolerant and reacts with a wide spectrum of symptoms from no apparent reaction to severe life-threatening diseases. This intolerance is strongly linked to specific genetic markers which have indeed required thousands years to develop and be selected: the 'population genetic' time is of this dimension, while the changes in the environment and in the food we eat, require centuries or less. Where did they come from? Hunters, Fishers and Gatherers Human beings have been on Earth for over 3 millions year, but Homo Sapiens Sapiens, our nearest parent, is only 100,000 years old. For ninety thousand years he conducted a nomadic life getting food by hunting, fishing and collecting fruits, seeds, herbs and vegetables from nature. Only quite recently (about 10.000 years ago) did some nomadic tribes start to have stable settlements because they developed the ability to gather enough food to be stored. The cultivation of wild seeds begun. Ten thousand years ago the last glaciation came to an end: a Neo-thermal period ensued which marked the passage from the Paleolithic to the Neolithic age. Ices melted gradually from the equator to the poles over several thousands years when new fertile and humid lands were uncovered in South East Asia all of Europe was still covered with ice and Northern Countries had to wait up to 4000 years more to get out from a frozen environment. The Great Revolution: The First Farmers The discovery in the Neolithic age of ways to produce and store food has been the greatest revolution mankind ever experienced. Passage from collection to production originates the first system in which human labor is transferred onto activities which produced income for long periods of time. The principle of property was consolidated and fortifications to protect the land and food stores were developed. Archeological findings suggest that this revolution was not initiated by the man hunter and warrior, but by the intelligent observations made by the woman. The woman carried the daily burden of collecting seeds, herbs, roots and tubers. Most probably she used a stick to excavate roots and tubers: during this activity she observed the fall of grain seeds on the ground and their penetration into the soil with rain. She may have been surprised to find new plants in the places which she herself dug with a stick, and made the final connection between fallen seeds and new 'cultivated' plants. She was, for thousands years, the sole leader of the farming practices and provided a more and more consistent integration to the scanty products of the man hunter (6). To our actual knowledge, the origin of farming practices should be located in the 'Fertile Crescent': the wide belt of South East Asia which includes Southern Turkey, Palestine, Lebanon and North Iraq. In the highlands of this area abundant rainfall was caused by the neo-thermal switch. In all of this area existed, and still exists, a wide variety of wild cereals, sometimes in natural extended fields, induced by the rainfalls. Triticum Dicoccoides (wheat) and Hordeum Spontaneum (barley) were common and routinely collected by the local dwellers. The wild cereals had very few seeds (2-4) which fell easily on the ground on maturation. The people from the Uadi el-Natuf Tell of South East Asia (7800 B.C.) provided the first traces of the gradual shift from hunters to grain cultivators. Their economy was based on the hunt of the gazelle, but their diet also included collected grain seeds. These gradually came to form a substantial proportion of their energy input, as cultivation practices ensued. There were no grinding stones or mills and it was most probable that gathering prevailed on cultivation. But during the Proto-Neolithic superior a cuneiform mortar appeared. 1000-2000 years later (5000 B.C.) wild animals, more rare due to incoming drought, formed only 5% of the daily diet, while cereals and farmed animals become a sizable part of it (4). Stable settlements were founded: the village of Catal-Huyuk in Southern Turkey had a population of 5000 inhabitants 9000 years B.C. In that area a collection of sickles was found with inserted oxidian blades, smoothed by the routine contact with the siliceous stalk of cereals. The sickles indicate that it was possible to collect seeds not only by picking on the ground, but also by cutting stems of plants which were capable of retaining the seed in an ear (5). 'Mesopotamic' populations, originated in the first farmers, developed a great civilization with large cities and powerful armies to defend their land property and food stores. In Egypt a civilization based on farming practices developed in the 5th millennium: they became specialists in the cultivation of wheat, barley (to produce beer) and flax. The Expansion Of The Farmers While in South East Asia the progressive drought made hunting difficult and encouraged farming, in Europe the Paleolithic culture of hunters and gatherers persisted for 5000 years more, gradually transforming into the Mesolithic age. In the 'Fertile Crescent' the availability of food stores and the gradual development of animal farming stimulated an unprecedented demographic explosion. The nuclear family had had a small dimension for hundreds thousands of years: the birth rate had been limited by nomadic life. In transmigrations the mother had been able to carry one infant, while the others had been obliged to walk and move on their own. Small babies in between had less chances of surviving. Thus mankind remained of approximately the same size during entire ages. Farmers, on the contrary, were settlers, possessed food stores and most probably took advantages in the farming practices of more hands in the family. In this manner the family size exploded and, as a result, a progressive continuous need to gain more lands ensued. The farmer's expansion lasted from 9000 B.C. up to the 4000 B.C. when they reached Ireland, Denmark and Sweden covering most cultivable lands in Europe. The expansions followed the waterways of Mediterranean and of Danube across the time of Egyptians, Phoenicians, Greeks and Romans (7). The farmers' expansion was not limited to the diffusion of the agricultural practices, but was a 'demic' expansion: that is a substantial replacement of the local dwellers, the Mesolithic populations of Europe, by the Neolithic from South East Asia. More than 2/3 of our actual genetic inheritance originated in this new population, while the native genetic background has been progressively lost or confined to isolated geographical areas. The genetic replacement of the native European population is marked by the B8 specificity of the HLA system. Cavalli Sforza and coworkers showed that the migration of farmers is paralleled by the diffusion of B8. The frequency of B8 is inversely proportional to the time length of wheat cultivation. In practice B8 appears to be less frequent in populations which have lived on wheat for a longer time, as it is caused by a negative genetic selection in wheat cultivators (7). We are aware that in Ireland, where the wheat cultivation came only 3000 years B.C., a very high frequency of gluten intolerance has been reported. The Evolution Of Cereals The early wild cereals, of the Triticum (wheat) and Hordeum (barley) species were genetically diploid and carried few seeds, which usually fell on the ground at maturation, making any harvest very difficult. A chromosomes in single couples (diploidicity) allowed for a wide genetic and phenotypic heterogeneity with remarkable variations in the content of protein and starches. Poliploid plants occasionally originated in nature, but they had few chances to survive, without artificial (cultivation) practices and were usually lost (8). The beginning of farming, with the use of irrigation, allowed the survival, and the expansion, of poliploid grains. But the new poliploid grains had substantially reduced genetic variations (since each gene is represented in several copies) and more frequently autoimpollinate themselves, causing remarkable increase of the genetic uniformity. The first stable formation of poliploid grains is dated around 6000 years B.C.: the genetic uniformity caused a considerable rise in stability and yield, convincing the early farmer to induce a progressive and rapid replacement of the wild species. Genetic variability of grains was essential in order to adapt the plant to the very different environmental conditions of different areas, but the yield was generally low (9). Triticum Turgide Dicoccoides was crossed with Triticum Fanschii to originate the Triticum Aestivum, which is the progenitor of all our actual wheat. The Aestivum is an esaploid wheat with 42 chromosomes, versus the 14 of the T. Monococcum. Such powerful grain replaced all existing varieties to the point where genetic variability nowadays is lost: over the world we have 20,000 cultivated species of the same unique T. Aestivum wheat. The Triticum Turgidum Dicoccoides, progenitor of the actual 'durum' wheat with which pasta is made, had just few seeds encapsulated into a pointed and twilled kernel: at maturation the seeds fell on the soil and penetrated into it with rain, eased by the arrow-shaped structure of the kernel. Ten thousand years ago it was difficult to pick them up: hence the attempt, made by the Neolithics, to select varieties which could retain the seed longer, in order to allow for an harvest. Genetic variability was already substantially reduced in Roman times: 'farrum', i.e. spelt, (T. Dicoccoides) and 'Siligo' (T. Vulgaris) were the common grains. Siligo was used for bread making and contained a certain amount of gluten, while spelt, used mainly for soups, was poorer in gluten content (10). But cultivation of wheat and barley was not started or diffused in the whole world: only a small geographic area (South East Asia) developed gluten-containing cereals. In Asia rice was the cultivated species, while in America maize prevailed and in Africa sorghum and millet. All these plants were present in nature and were gradually cultivated in the places of origin (7). In our part of the world grains had for centuries been selected in order to improve their homogeneity and productivity, but soon (Roman times or before?) another desirable quality was preferred: the ability to stick, to glue up a dough to improve bread making. Early bread making activities pushed towards grains that contained greater amounts of a structural protein which greatly facilitated the bread making: the gluten. Gluten was not chosen because of its, at the time unknown, nutritional value (which is not absolutely special, since it is a protein with relatively low nutritional value), but for its commercial qualities. Rice, maize, sorghum, millet do not contain gluten: no leavened bread was prepared with them: the majority of mankind never lived on bread, as we do know it. Over the last 200 years of our modern age active genetic selection, and actual genetic manipulation, have changed the aspect of the original Triticacee enormously: from few grains and little gluten to great wheat harvests very enriched in gluten (50% of the protein content), well adapted to cultivation practices and ready to be handled by monstrous machinery. The Rise Of The Intolerance To Gluten Did everybody adapt to such profound changes in the basic nutrition over such a short period of time? South Eastern populations, presumably well adapted to the new foods, grossly replaced the existing Mesolithic European dwellers who still lived on hunting and gathering. But a proportion of the local populations (or, rather, of their inheritance ) persisted beside the invaders. The feeding changes were not well tolerated by everybody. The best similar example is lactose intolerance: populations that have more recently adapted to milk consumption, still lack the genetic ability to digest lactose over the infancy period. Environment has changed centuries before any change in the inheritance may have been possible. Similarly a considerable proportion of the hunters and gatherers of the pre-Neolithic ages have not fully adapted to the great feed changes induced by the cultivation of wheat. These people could not recognize gluten as a 'tolerable' protein available for digestion and absorption: they may have not have any problem or complaint for centuries, since the content of gluten in the grains was very low, but when 'industrial' quantities of gluten were induced by selection of wheat in order to improve bread making, they were exposed to unbearable quantities of an 'intolerable' protein or peptide. This population, genetically identifiable today by their specific HLA pattern, did not recognized, through their HLA system, the gluten peptide as a tolerable item, but, because of the similarity of some sequences of gliadin peptides with several pathogenic viruses, they generate a complex defense mechanism (an immune response) which does not eventually find the pathogen to destroy, and most probably activate an auto-immune response which ultimately is the origin of the damage to their intestine and other organs. These fierce descendants of hunters and fishers, exposed to this subtle enemy, could not develop the defense of tolerance and, in the attempt to fight the unknown, they ultimately develop a disease due to excess defense. For centuries they underwent a negative selective pressure, with less chances to survive, and then to be manifest (11). In the last millennium gluten-intolerant children mostly had a harsh time behind them: after weaning, malabsorption and malnutrition were the underlying causes of poor defense to infections during infancy and early childhood. Acute infectious diarrhea was the main killer of infants up to 50 years ago in Europe and up to 15 babies every thousand died for this condition. In the suburbs of Naples, only 25 years ago, infectious diarrhea was the main killer (25% on an infant mortality rate of 100 per thousands live births) (12). The vast majority of gluten intolerance occurred among these poor infants. In my own clinical experience 25 years ago I observed several fatal gastrointestinal infections in babies with the 'celiac crisis', which has now disappeared from our wards. Few chances to survive, few intolerant children that reached the reproductive age, and become capable of transmitting the intolerance, few adult cases. Then gluten intolerance may have become extinct, as was in fact the case with several other pathogenic conditions? Not at all. The intolerance most probably had some selective advantage which counterbalanced the gluten intolerance: it is possible to suggest that it was their very effective HLA Class II system that gave them a selective advantage against infections, which compensated the disadvantage due to gluten intolerance. When, in the last 50 years, infantile infections greatly diminished, the descendants of the hunters and gatherers with very active immune-defense, 'over reacted' more frequently to the gluten than to their ordinary enemy. Hence the rise of the cohort that now appears to manifest, in different manners, a gluten intolerance. However, not all populations of the world were ever exposed to such a nasty protein: the vast majority of mankind, after the development of agriculture, lived on maize, rice, sorghum and millet, tubers: all gluten free. All of them did not underwent the selective pressure of gluten intolerance and they may in fact have been the reservoir of wild genes. Finally, breast feeding most probably played a major role in preserving some children from the fatal infection of infancy (13). The capacities of breast milk to protect against viral and bacterial attack, the protection given by maternal antibodies and the delaying effect on the manifestation of symptoms of gluten intolerance (in the predisposed subjects) may all have protected the hunters and gatherers, who in this manner avoided to develop fatal symptoms and managed to survive and transmit their genes to our population. Hints On The Epidemiology Of Gluten Intolerance The epidemiology of gluten intolerance, as we know it today, is the complex result of the apparition of the population of hunters and gatherers in our modern world. As the cohort of those born before the World War II had few chances to survive infancy, we nowadays have few adult cases and few long term complications. Where the intolerance is still manifested mainly in the classical way (infants and small children, malabsorption, diarrhea, often switched on by an infection) we do not frequent encounter 'atypical' presentations and adult cases or long term complications. In this case the epidemiological calculations on observed cases made by gastroenterologist may be in great contrast with those made by pediatricians. On the contrary the rarity of 'classical' cases, which has been used as the proof of the 'disappearance' of gluten intolerance, is counterbalanced by the presence of atypical and late diagnosis, where actively searched for. Finally nutritional attitudes have played a major role with regard to the chances for hunters to manifest themselves in different age groups: the example of Sweden as compared to the nearest Denmark or Finland is paradigmatic (14). As shown by Maki et al, the ability to identify atypical cases may completely change the observed epidemiological pattern in a given region. Hence the reason for the 'iceberg': most cases still to be discovered (15). Similarly, population-based screening programs uncover more 'silent' than overt cases (3). Nevertheless, the 'cohort effect', regional differences and so on, have up to now failed to overcome the limits of numbers: when local incidence rates are compared with other regions' rates, the 95% Confidence Intervals of the rates are very often so wide to contain the all lot of observed rates. No clear-cut statistical difference has really been shown in the incidence of gluten intolerance in Europe (16). Wherever extensive studies on symptomatic cases have been run an incidence of 1 case per each 1000 live births has been reached, but very often the incidence has been much lower: up to 1 cases every 250 live births. Population screening studies invariably come to an incidence rate of 1 every 250. This is very close to the rate predicted by age-adjusted incidence density studies (17). Recent reports indicate an incidence close to 1 case per every 100 live births, but this finding needs confirmation. Gluten Sensitive Versus Gluten Intolerant But the epidemiology of gluten intolerance, which entails the tracing of a group of our ancestors, may completely change once we consider the increasing knowledge about the 'gluten-sensitive' individuals. 6 to 10% of first degree relatives of known cases themselves are gluten intolerant and have a flat intestinal mucosa (these are silent cases), but up to 30% of sibs of cases, when challenged with a dose of gluten (or its digest) activates a specific mucosal immune-response (with increase in intraepithelial infiltration and activation of T-Cells), without having any sign of mucosal damage (potential cases?) (18). We may, in the near future, have a substantial group of individuals who do not activate, in presence of gluten, a 'pathogenic' immune response (auto-immunity), but who recognize gluten as a 'suspect' protein in the same way as their peers really intolerant. Finally gluten intolerance is indeed linked to a specific genetic predisposition: most probably at least two genetic loci are involved in running the risk of intolerance. How many possess these specific genetic risk at a 'carrier' state? Certainly more than 5% of the actual population. In conclusion we have a wide population of 'gluten-reactants' in Europe (EC): at least 1 million cases of total intolerance to gluten - an estimated similar amount of 'gluten sensitive' people - 10-15 times more 'carriers' of the risk of becoming gluten intolerant. So we have found our ancestral hunters and gatherers: they are a substantial proportion of our actual community and do deserve a 'gluten-free' alternative not only as a therapeutic mean, but as an option of our daily life. References Gobbi G, Bouquet F, Greco L, Lambertini A, Tassinari CA, Ventura A, Zaniboni MG: "Coeliac Disease, epilepsy and cerebral calcifications" Lancet, 340, Nx 8817, 439-443, 1992 Epilepsy and other neurological disorders in Coeliac Disease. Republic of S. Marino Meeting, April 10-12 1995, G. Gobbi edt., Raven Press, in preparation. Catassi C, Ratsch IM, Fabiani E, Rossini M, Bordicchia F, Candela F, Coppa GV, Giorgi PL: Coeliac Disease in the year 2000: exploring the iceberg. Lancet, 1994, 343: 200-203. Furon R. Manuel de Prehistorie Generale., 1958, Payor, Paris. Cambel H, Braidwood RJ. An old farmer's village in Turkey. Le Scienze, 1970, 22: 96-103. Heichelheim F. An Ancient Economic History. A.W. Sijthoff edt., Leiden, 1970. Cavalli-Sforza L. Chi Siamo (Who are we). 1993 Mondadori, Milano. Raven PH, Evert RF, Eichorn S Biology of plants. 4th ed. Worth Publ. Inc, New York, 1986. Feldman M, Sears ER The wild gene resources of wheat. Scientific American, 1981: 98-109. Lucio Giunio Moderato Columella " Libri rei rusticae" Anni 60-65 dopo Cristo. Ed. Einaudi,1977. Simoons FJ: Coeliac Disease as a Geographic Problem. Food, Nutrition and Evolution, 1982, 179-199. Greco,L.: " Malnutrizione di classe a Napoli" Inchiesta, 24, 53-63, 1976. Greco,L., Mayer,M., Grimaldi,M., Follo,D., De Ritis,G., Auricchio,S.: "The effect of Early Feeding on the onset of Sympthoms in Coeliac Disease" J.Pediat. Gastroenterology Nutrition, 4:52-55, 1985. Maki M, Holm K, Ascher H, Greco L.: Factors affecting clinical presentation of coeliac disease: role of type and amount of gluten containing cereals in the diet. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 76-83. Maki M, Kallonen K, Landeaho ML, Visakorpi JK.:Changing pattern of childhood coeliac disease in Finland. Acta Paediatr Scand 1988; 77:408-412. Greco L, Maki M, Di Donato F, Visakorpi JK. Epidemiology of Coeliac Disease in Europe and the Mediterranean area. A summary report on the Multicentric study by the European Society of Paediatric Gastroenterology and Nutrition. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 14-24. Magazzu, Bottaro G, Cataldo F, Iacono G, Di Donato F, Patane R, Cavataio F, Maltese I, Romano C, Arco A, Totolo N, Bragion E, Traverso G, and Greco L: "Increasing Incidence of childhood celiac disease in Sicily: results of a multicentric study" Acta Paediatr, 83:1065-1069, 1994. Troncone R, Greco L, Mayer M, Mazzarella G, Maiuri L, Congia M, Frau F, De Virgiliis S, Auricchio S.: "In half of Siblings of Coeliac Children rectal gluten challenge reveals gluten sensitivity not restricted to coeliac HLA.
  7. The following was written by Donald D. Kasarda who is a research chemist in the Crop Improvement and Utilization Research Unit of the United States Department of Agriculture. If you have any questions or comments regarding the piece, you can address them to Don at: kasarda@pw.usda.gov. Most sprouted wheat still has gluten or gluten peptides remaining. Although the sprouting begins enzymatic action that starts to break down the gluten (a storage protein for the plant) into peptides and even amino acids. Generally this is not a complete process for sprouts used in foods so some active peptides (active in celiac disease) remain.
  8. Celiac.com - 07/24/2001 Study: Holmes, Prior, Lane, et. al. Malignancy in Coeliac Disease - Effect of a Gluten-Free Diet Gut 1989; 30: 333-338 Comments Regarding the Study to the List (January 8, 1997): I would like to suggest that you check out some of the information on malignancy and celiac disease, especially lymphoma. One of the studies established three categories: One for those who adhere to the diet strictly; one for those who follow the diet, but not very strictly; and one for those who do not follow the diet. The first group, after 5 years, shows a significant reduction in risk. In fact, it is quite close to the risk experienced by members of the general population. The second group does experience some reduction in risk, but it remains closer to the rate of malignancy in untreated celiac disease. The third group has a very high risk of malignancy. Response by Donald D. Kasarda (January 9, 1997 - Donald D. Kasarda is a research chemist in the Crop Improvement and Utilization Research Unit of the United States Department of Agriculture): I point out that the people in the first group, which supposedly was adhering to a strict gluten-free diet, were likely to have been including foods made with wheat starch in their diet because that was, and is, common in England where the study was carried out. I have asked several celiac researchers in England if I am correct in this assumption. They agreed that I am. Therefore these people in the strictly gluten-free group were likely to be eating a small amount of gluten each day. The amount is unknown because we dont know the amount of gluten in the starch (this varies according to the manufacturer and possibly according to lot) nor which subjects ingested how much starch. The apparent small increase in cancer risk for the first group was not statistically significant for those who had been on the diet more than 5 years. In the group with a normal diet, the relative risk of lymphoma was increased 78 fold, but it should be pointed out that the incidence of lymphoma of the gastrointestinal tract in the normal population is rather low. For the 210 patients in the study, the cancer morbidity was expected to be 0.21. For the 46 patients in the normal diet group, 7 cases of lymphoma were observed. For the 108 patients on the strict gluten-free diet, 3 cases of lymphoma were observed. The statistical significance of the numbers is weak because of the relatively small numbers of patients involved. These are extremely valuable and well-done studies. No criticism is intended. To arrange a study with larger numbers will be extremely difficult although a group in Leiden (The Netherlands) is trying to arrange such a study. I have no quarrel with those who wish to play it safe, but I dont think we can say for sure that small amounts of gluten in the range of a milligram to a few milligrams per day are harmful on the basis of any scientific study of which I am aware. They may be, or they may not be. I offer these comments only with the intent of providing as much information to celiac patients as possible so that they can make informed decisions. If anything I have said is incorrect, I hope someone will point out my errors on the net. Don Kasarda, Albany, CA FYI: According to the calculations made with Don Kasarda in Nov 1995, 0.1 grams = 100 milligrams is about one-50th of a slice. Therefore, 10 milligrams is about one-500th of a slice of bread.
  9. 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, please address them to Don at: kasarda@pw.usda.gov The work from Prof. Auricchios laboratory (Troncone et al.) in Naples is certainly of interest and I shall look forward to seeing the details, but I will just point out for the sake of balance that studies with patients who ingest, or have instilled into their intestines, the substance to be tested represent the gold standard and in vitro testing (that is, in glass, or in the test-tube), while valuable, does not carry as much weight. The results from the Finnish group and from Dr. Feigherys group (not yet published), Dublin, Ireland, are very impressive. The results based on in vitro testing would have to be truly exceptional to undermine the excellent work that has been done on the safety of oats. So, we shall have to wait and see, but I doubt there is reason to be overly concerned just yet.
  10. 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, please address them to Don at: kasarda@pw.usda.gov I have not seen the NEJM article from the Finnish group although I had heard second hand about a meeting presentation of the work. I have no reason to doubt the results. I am co-author of a paper from an independent study carried out by the laboratory of Dr. Conleth Feighery, Trinity College, Dublin, Ireland, and this study (paper submitted) also supports the lack of toxicity for a PURE oats sample. I will remind people that it is EASY for oats to be contaminated with wheat both in the field and in processing. I have no reason to think that oats must be limited to small amounts, but, of course, it isnt good to focus ones diet too much on a single food, so moderation of the normal sort is probably good. There are bound to be some people who are sensitive to oats, possibly through an allergic reaction to one component or another (just as there are people allergic to rice), but this sensitivity, on the basis of current results, seems unlikely to be celiac disease in its strict sense. The term gluten in celiac disease is not used in a proper sense (in that sense it is present only in wheat), but rather as a shorthand term for peptides derived from prolamins (proteins) that include the harmful amino acid sequences found in wheat. These peptides set off (in an unknown way) a series of reactions that ultimately may lead to flattening of the mucosa, malabsorption, and possibly other effects as well. Wheat, rye, and barley have prolamins that contain the toxic sequence(s). The finding that oats is (are?) not toxic indicates that the key sequences are NOT found in the avenins, the prolamins of oats. Comparison of the amino acid sequences of avenins and gliadins yields clues to possibly important differences and I am pursuing the significance of these differences. I am currently trying to find sources of pure, uncontaminated oats, and will post them here as soon as they are available. -Scott The oats used in the Irish study (see Doctor #2 below) came from a company called Peter Kölln in Germany. The oats from this company were tested and found to be safe. Their address is: Peter Kölln Postfach 609 D-25306 Elmshorn Germany
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