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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.
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Celiac.com 09/19/2017 - Hookworms. Intestinal parasites. They sound gross. The thought of having one's gut infected with a parasitic worm generally makes people's skin crawl. Indeed, intestinal worms, like hookworm, have a bad reputation among health experts, and have been the subject of fierce public health campaigns seeking their eradication. However, researchers have also documented the gut healing abilities of parasites like hookworm. In fact, part of how hookworms seem to work in nature is to promote an optimal gut environment in which they can thrive. In nature, the guts of people infected with hookworm are generally healthy. Could hookworms and other intestinal parasites prove key to treating and possibly eliminating diseases like celiac, and asthma? A number of clinicians and researchers feel that if they can just get the right strain of hookworm, at the right levels, they can basically eradicate celiac disease, and possibly asthma and other inflammatory diseases. When hookworms are introduced into the gut of people with celiac disease in the right amount, and kept at therapeutic levels, patients see their celiac symptoms disappear and their guts return to a healthy, normal condition. In fact, hookworms do not reproduce once inside the human gut, so if doctors put , say, 10 hookworms into a gut to treat celiac disease, there will be 10 there later, not more. In nature, the way humans build up dangerous levels of hookworm is via unsanitary environmental conditions and repeated exposure to more hookworms. Done clinically, the hookworm would present little or no danger to the human who was hosting it. While still very much in the experimental phase, researchers hope to investigate a number of strains to determine the best therapeutic levels for such disease treatments. For that, they will need FDA approval. Remember, the fecal transplant was first described in the 1950s, but took decades to catch on as a conventional treatment for gut disorders, such as c-dif bacteria, partly because it was seen as crude and somehow objectionable. But it proved to work. Really well. So much so that it's now a fairly conventional treatment. Could the hookworm follow a similar path from crude and weird to cool and effective? Could hookworms be used to cure celiac disease? Only close study will tell us for sure, and that's why the move to get FDA approval is an important one. For that, special strains of hookworm must be approved. "One of the big roadblocks is having the parasites that the FDA will allow you to infect people with," says John Hawdon, vice president of the American Society of Parasitologists and a researcher at the George Washington University. He and his colleagues are applying for permission to grow hookworm larvae to standards fit for testing in humans, which is not currently permitted in the United States. Hawdon says he anticipates a lengthy application process. Stay tuned for news on efforts to develop hookworm as a potential cure to celiac disease, asthma, and more. Sources: popsci.com iflscience.com
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Celiac.com 10/12/2015 - There's been a good deal of attention devoted to gluten sensitivity in people without celiac disease, but researchers still don't know much about potential risks associated with the condition. A research team recently looked at the prevalence of autoimmune diseases among patients with non-celiac wheat sensitivity (NCWS), and investigated whether they carry antinuclear antibodies (ANA). The research team included A. Carroccio, A. D'Alcamo, F. Cavataio, M. Soresi, A. Seidita, C. Sciumè, G. Geraci, G. Iacono, and P. Mansueto. They are variously affiliated with the DiBiMIS University of Palermo, Palermo, Italy; the department of Internal Medicine at Giovanni Paolo II Hospital in Sciacca, Italy; the DiBiMIS University of Palermo, in Palermo, Italy; the department of Pediatric Gastroenterology in ARNAS Di Cristina Hospital, Palermo, Italy; and the Surgery Department at the University of Palermo in Palermo, Italy. The research team conducted a retrospective study of 131 patients diagnosed with NCWS, 121 of whom were female. The average patient age was 29.1 years, and the study was conducted at 2 hospitals in Italy from January 2001 through June 2011. The team also collected data from 151 patients with celiac disease or irritable bowel syndrome, who served as control subjects. They reviewed patient medical records to identify those with autoimmune diseases. They then conducted a prospective study of 42 patients, 38 of whom were female, with an average age of 34 years, who had been diagnosed with NCWS from July 2011 through March 2014 at 3 hospitals in Italy. For the prospective study, one hundred age- and sex-matched subjects with celiac disease or IBS served as control subjects. The team collected serum samples from all subjects and measured ANA levels using immunofluorescence analysis. Participants completed a questionnaire and the team reviewed patient medical records to identify those with autoimmune diseases. In the retrospective analysis, about 30% of patients with either NCWS or celiac disease developed autoimmune diseases; mainly Hashimoto's thyroiditis, of which there were 29 cases. Compare this with about 4% of IBS who developed an autoimmune disease (P < .001). In the prospective study, 24% of patients with NCWS, 20% of patients with celiac disease, and 2% of patients with IBS developed autoimmune diseases (P < .001). In the retrospective study, serum samples tested positive for ANA in 46% of subjects with NCWS (median titer, 1:80), 24% of subjects with celiac disease (P < .001), and just 2% of subjects IBS (P < .001). In the prospective study, serum samples were positive for ANA in 28% of subjects with NCWS, 7.5% of subjects with celiac disease (P = .02), and 6% of subjects with IBS (P = .005 vs patients with NCWS). From these results, they conclude that positive ANA results are associated with the presence of the HLA DQ2/DQ8 haplotypes (P < .001). Source: Gastroenterology. 2015 Sep;149(3):596-603.e1. doi: 10.1053/j.gastro.2015.05.040.
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Celiac.com 08/01/2017 - Although autoimmune disorders are not widely associated with Parkinson disease, there is increasing evidence for a link between immunity and neurodegenerative disorders. Indeed, both innate and adaptive immunity have been implicated in neurodegenerative disorders. A team of researchers recently set out to examine the connection between immunity and neurodegenerative disorders. The research team included Nikolaus R. McFarland, MD, PhD; Karen N. McFarland, PhD; and Todd E. Golde, MD, PhD. They are variously associated with the Center for Movement Disorders and Neurorestoration, Department of Neurology, College of Medicine, University of Florida, Gainesville, the Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, the McKnight Brain Institute, University of Florida, Gainesville, and the Department of Neuroscience, College of Medicine, University of Florida, Gainesville. One of the more interesting examples the researchers examined is TREM2, a member of the immunoglobulin receptor superfamily that expresses itself in microglia and tissue macrophages, and which has gene variants associated increased Alzheimer ’s risk. They also took a look at other TREM2 variants that are linked to the development of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, a dementia associated with bone cystic lesions. Another example with less clear biological significance is the reproducible genetic association between a single-nucleotide polymorphism (SNP) in the locus and type 1 diabetes. We are at the very beginning of a research effort to better understand the connection between immunity and neurodegenerative disorders. It may take a while, but the results of these efforts will likely help researchers design better diagnostic and treatment regimes. Source: JAMA Neurol. Published online June 5, 2017. doi:10.1001/jamaneurol.2017.0843
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Celiac.com 04/13/2017 - A team of researchers recently set out to determine whether hospital admission for autoimmune disease is associated with an elevated risk of future admission for dementia. The research team included Clare J Wotton, and Michael J Goldacre, both affiliated with the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford, Oxford, UK. The pair set up their retrospective, record-linkage cohort study using national hospital care and mortality administrative data from 1999–2012. From that patient data, they assembled a study group of people admitted to hospital with a range of autoimmune diseases, along with a control group, and followed forward in time to see if how many patients eventually developed dementia. Data revealed a total of 1,833,827 people admitted to hospital with an autoimmune disease. The number of patients for each autoimmune disease group ranged from 1,019 patients in the Goodpasture's syndrome group, to 316,043 people in the rheumatoid arthritis group. The researchers found that the rate ratio for dementia after admission for an autoimmune disease, compared with the control cohort, was 1.20 (95% CI 1.19 to 1.21). For patients whose dementia type was specified, the rate ratio ranged from 1.04 to 1.08 for Alzheimer's disease, and 1.26 to 1.31 for vascular dementia. Of the 25 autoimmune diseases studied, 18 showed significant positive associations with dementia, 14 of which were statistically significant. Significant associations include Addison's disease (1.48, 1.34 to 1.64), multiple sclerosis (1.97, 1.88 to 2.07), psoriasis (1.29, 1.25 to 1.34) and systemic lupus erythematosus (1.46, 1.32 to 1.61). The connections with vascular dementia may be one aspect of a wider connection between autoimmune diseases and vascular damage. Though findings were significant, effect sizes were small. Researchers advise clinicians to note the possibility of dementia in patients with autoimmune disease. The researchers are calling for further studies to assess their findings and to explore possible ways to reduce any increased risk. Source: BMJ
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Celiac.com 03/16/2017 - When screening arthritis patients for celiac disease, should HLA be done before serology? During the past decades, an accumulating evidence shows a dramatic rise in the frequency of autoimmune diseases, including rheumatoid arthritis and gastrointestinal conditions, such as celiac disease. HLA genes have been shown to be strongly associated with numerous autoimmune diseases, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and celiac disease. A team of researchers recently set out to assess the performance of celiac disease associated serology in face of a rheumatologic patient, when gluten enteropaty is suspected. The research team included Hakim Rahmoune, Nada Boutrid, Mounira Amrane, and Belkacem Bioud. They are variously affiliated with the Pediatrics Department and the Biochemistry Department of Setif University Hospital at Setif-1 University in Algeria. The main question they sought to answer was: Should HLA be done prior to the serology? Could unnecessary serial serological celiac disease screening in such rheumatology patient be avoided by performing an HLA typing, as a long-life marker of genetically celiac disease-susceptible patients? Serogenetic screening without the requirement for follow-up small bowel biopsies provides a flexible, cost-effective methodology that could be widely applied to obtain accurate estimates of the prevalence of celiac disease in large group studies. Source: International Journal of Celiac Disease, 2017, Vol. 5, No. 1, xx. DOI:10.12691/ijceliac disease-5-1-2
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Want to Help Catalog, Track Autoimmune Diseases?
Jefferson Adams posted an article in Additional Concerns
Celiac.com 03/18/2017 - Do you have an autoimmune disease? Does someone you know? Did you know that the numbers regarding autoimmune rates are all over the place, and that incomplete or wrong information can result in delayed or missed diagnoses? Want to help researchers create a database that will help them understand exactly how many people are living with autoimmune conditions? Then behold the latest project from ARI, a 501c(3) nonprofit, with a mission "to create a hub for research, statistics, and patient data on all autoimmune illnesses." The project seeks to provide data that will help researchers nail down some basic answers about the numbers of people who live with one or more autoimmune conditions. The ARI website says that the company "operate a national database for patients who suffer from any autoimmune disease." ARI's mission is to "reduce the time of diagnosis, support research, compute prevalence statistics, and establish autoimmune disease as a major class of disease so that it receives the awareness of the public, the attention of healthcare providers, and the appropriate funding needed to improve upon existing treatment protocols and disease management strategies." This is one reason why Aaron Abend, the founder and president of ARI, decided to create the Autoimmune Registry after his mother was misdiagnosed for 10 years because, based on incorrect statistical data, "doctors thought Sjogren's syndrome was a rare disease with only 37,000 cases in the U.S." Today, researchers agree there are probably 3 million cases in the U.S., so not so rare at all. Researchers currently estimate that anywhere from 9 million to 50 million people in the United States have an autoimmune disease. That's quite a wide range. Pinpointing the actual prevalence is part of what ARI will try to do. So, they are reaching out directly to patients to information about diseases like rheumatoid arthritis (RA), lupus, psoriasis, diabetes, Crohn's, celiac disease, Sjogren's syndrome, multiple sclerosis (MS), and many others fall under the autoimmune umbrella. The registry is easy to join. It is free to sign up and consists of a simple survey that people with autoimmune diseases answer. The information that people provide to ARI remains secure. The data may be used to compile statistics and qualify them for research opportunities, but no identifying information will be shared without permission. The hope is that the registry can help researchers connect with people and the data. You can view the registry here.-
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Celiac.com 02/14/2017 - In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases (1). Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race" (2). A year later, medical doctor and professor of Anthropology, S. Boyd Eaton and colleagues suggested a mismatch between the human genome and our current agricultural diet/lifestyle (3). And more than a decade prior to that, gastroenterologist, Walter L. Voegtlin, M.D., self published a book apparently asserting, based on his treatments and observations of patients, that dietary avoidance of cereal grains and sugars, offset by increased consumption of meats and animal fats, is an effective treatment regimen for a variety of intestinal ailments including Crohn's disease, colitis, irritable bowel syndrome, and indigestion (4). Each of these perspectives was informed by a different but solidly scientific approach to human health. The academic field of each of these authors varied from Exercise Physiology to Physiology, to Gastroenterology, to Anthropology. Yet each of these specialist researchers arrived at the very similar conclusion that cereal grains are not healthful foods for humans. Their strident declarations to that effect leave little room for doubt. Dr. Cordain acknowledges that the roots of some of his thinking lie with Dr. Eaton and his colleagues. Nonetheless, there is a convergence here, of ideas and insights drawn from separate bodies of data and investigative approaches. While there is some overlap between these scientific disciplines, they all lead to a clear indictment of cereal grains as little more than a starvation food for humans. These scientists point to myriad signs of illness that arise more commonly when populations make the transition to eating diets dominated by grains, especially when the grains are refined and when they are combined with sugar. One critic of this paradigm is the evolutionary biologist, Dr. Marlene Zuk of the University of California at Riverside. According to Alison George at New Scientist, Zuk asserts that the 10,000 years that humans have been cultivating and consuming cereal grains is an adequate time period for humans to evolve an adaptation to these foods (5). But surely this is a Eurocentric view. Simply because some Europeans have been cultivating and consuming cereal grains for ten or more thousands of years does not mean that the entire world's population, or even all Europeans, would or could have adapted to consuming these foods. Let's look back to see what we currently know about our human roots and how those early humans spread all over the world. A group thought to number about 200 humans left Africa sometime between 85,000 and 70,000 years ago, during a glacial maximum that lowered worldwide sea levels by about 300 feet below current levels. The enormous glaciers of the time so depleted the oceanic barriers we see today, that these bodies of water were made navigable even with very primitive flotation devices. The progeny of this relatively small group of early modern people multiplied and went on to parent almost all of today's non-African people of the world with some 1% to 4% of today's human, non-African genes having been derived from the Neanderthal branch of the hominid tree (6). This predominantly early modern human group's progeny would quickly find its way to Australia, the South Pacific, across Asia, to China, east to the Americas and west across India, finally arriving in Europe, where they would supplant the long-time Neanderthal residents who had survived some of Europe's harsh and inhospitable glaciations but apparently could not survive having our forebears as neighbors. While specific paths and dates for exiting Africa, and worldwide patterns and timing of human distribution remain controversial, most experts now accept that indigenous Australians had arrived there at least 60,000 years ago (6). A similarly recent finding places people in the Americas by at least 55,000 years ago, long prior to the date at which the Bering Land Bridge was thought to be available for human movement from Siberia into the Americas (8). This newer, admittedly controversial date raises the likely possibility that people arrived in the Americas, from Asia, by boats or rafts on which they followed the shoreline east to what is now Alaska, then south of the glaciated wastelands of much of what is now Canada. (Or perhaps they arrived by some other means that we have not yet imagined.) But only a small portion of these early Americans would eat wheat, rye, oats, or barley before the last 200 years or so, especially those living on the Great American Plains, or in the frigid north, the dense jungles or places that were otherwise isolated from the encroaching wave of "immigrants" from Europe and beyond. And none of those aboriginal peoples of the Americas were eating these grains prior to 1492. The epidemics of autoimmunity and obesity that may be seen among indigenous Americans are clear reflections of their recent shift to the gastronomic wonders of foods derived from these European grains. Further, even among Europeans, grain cultivation and consumption had not uniformly spread across most of Europe until, at most, less than half of the 10,000 years that Zuk says would be sufficient for human adaptation. In Britain, for instance, grain farming was only getting under way about 4,000 years ago, and availability of grains varied according to local geographies and economies. Also, in parts of Scandanavia, wheat bread was a rare treat until after World War II. Some Europeans are thought to have been cultivating grains for even longer than the 10,000 years ago suggested by Cordain, but the evidence is contradictory and accompanied by a range of expert opinions. Further, the health consequences of this nutritional path are consistently seen in the skeletal remains of those early farmers, many of which can now be seen reflected among indigenous peoples of the Americas, as they assimilate our grain and sugar dominated diet. Adaptation to eating grains is not a gentle, joyful process. Early farmers may have produced many more children than their hunting and gathering neighbors, but their lives were shorter, their bodies were less robust, with substantial reductions in stature, and they experienced widespread infectious diseases and ailments driven by nutritional deficiencies. By the time grains became a cash crop for many European farmers, cereals were disproportionately consumed by affluent urbanites. Those who were large consumers of cereal grains did not include all Europeans, even where yields were prodigious. In more remote, northerly, or mountainous areas, cereal grains, or foods made from them, were likely a rare treat rather than a daily staple. Jared Diamond points out, that in addition to "..... malnutrition, starvation, and epidemic diseases, farming helped bring another curse upon humanity: deep class divisions." He goes on to argue that only with farming and the storage and accumulation of food can Kings "and other social parasites grow fat on food seized from others". He also presents evidence that farming led to inequality between men and women. Conversely, contemporary hunter-gatherers have repeatedly been shown to be quite egalitarian, both regarding gender and political leadership (9). Roger Lewin is another critic of the health impact of European grain cultivation on humans. He points out that even in the very heart of the Fertile Crescent, where agriculture got its start, there was not a uniform adoption of farming. One agricultural center at Abu Hureyra, experienced two cycles of abandonment, one at 8,100 B.C.E., lasting about 500 years, and another at 5,000 B.C.E. These periods when agriculture at this locale was abandoned are "thought to be related to climatic change that became less and less conducive to agriculture" (10). Lewin also harkens to Mark Nathan Cohen's collation of "physical anthropological data that appear to show increasingly poor nutritional status coincident with the beginnings of agriculture.... " (10) suggesting, again, that grains were a starvation food. Eaton et al also approach grain cultivation from an anthropological perspective, suggesting that increased dietary protein and fats from animal/meat sources likely gave rise to increased stature of earlier humans, along with providing the necessary fatty acids for building larger brains, and allowing smaller gut sizes over the past 2.5 million years. It seems reasonable to assume that if it took our pre-historic ancestors that long to adapt to eating meats and animal fats, the very irregular adaptation period of between less than one hundred years and about 10,000 years that various world populations have been cultivating and consuming wheat, rye, barley and oats would be insufficient to allow full adaptation to eating these immune sensitizing cereal grains. Dr. Zuk's perspective might be tempered a bit if she considers that Europeans and their descendants do not comprise the entirety of the world's populations. There are several Asian populations that are not insignificant when compared with European populations and their progeny, including the residents of China, India, Pakistan, and South-East Asia. Even among those of us who appear quite European, there may be a mixture of genes derived from peoples of any of the other five populated continents. The approximately 10,000 year maximum period since humans began to cultivate cereal grains would have little adaptive impact on populations that have only been exposed to these grains for a period of somewhere between four or five centuries and seven or eight decades, as is the case among the indigenous people of the Americas, Australia, New Zealand, and much of Asia (6). Even if all humans had been cultivating and consuming cereal grains for the 10,000 years since this practice was first begun in the Middle East, the high frequency of intestinal, autoimmune, and other diseases that can be mitigated by a gluten free diet, even among descendants of Europeans, leaves little room to doubt that Dr. Zuk's projected adaptation simply has not occurred. The current prevalence of celiac disease and non-celiac gluten sensitivity identifies, at a bare minimum, between 7% and 12% of the American population that has not adapted to cereal grain consumption. While a few research projects suggest that molecular mimicry and the opioids from cereal grains contribute to autoimmunity, obesity, type 2 diabetes and cardio-vascular disease, current research does not provide any clear sense of how many cases or to what degree these health conditions are driven by gluten consumption. We know that foods derived from cereal grains are often laced with refined sugar, but the insulin stimulating properties of gluten alone are such that their role in these conditions cannot, reasonably, be denied. I feel vindicated by these many experts who decry the folly in humanity's embrace of the European grains. I wonder how long it will take for this information to filter into, and be acknowledged by, those who claim that science has led them to advocate cereal grain consumption for everyone without celiac disease and, more recently, non celiac gluten sensitivity? Sources: Cordain, Loren. Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 http://thepaleodiet.com/wp-content/uploads/2012/08/Cerealgrainhumanitydoublesword.pdf Jared Diamond, "The Worst Mistake in the History of the Human Race," Discover Magazine, May 1987, pp. 64-66. http://www.ditext.com/diamond/mistake.html Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Voegtlin, Walter L. (1975). The stone age diet: Based on in-depth studies of human ecology and the diet of man. Vantage Press. ISBN 0-533-01314-3 George, A. " The Paleo Diet Is a Paleo Fantasy" New Scientist. April 7, 2013. http://www.slate.com/articles/health_and_science/new_scientist/2013/04/marlene_zuk_s_paleofantasy_book_diets_and_exercise_based_on_ancient_humans.single.html Oppenheimer, Stephen. The Real Eve: Modern Man's Journey Out of Africa. Basic Books, NY, NY. 2004 Fagan, Brian. Cro-Magnon: How the Ice Age Gave Birth to the First Modern Humans. Bloomsbury Press, New York. 2011 http://www.utep.edu/leb/Pleistnm/sites/pendejocave.htm Brody, Hugh. The Other Side of Eden: Hunters, Farmers and the Shaping of the World. Douglas 7 McIntyre Ltd., Vancouver, B.C., Canada. 2000 Lewin, Roger. A Revolution of Ideas in Agricultural Origins. Science. vol 240, May 20, 1988
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Celiac.com 02/13/2017 - Researchers have noted a strong clinical association between autoimmune thyroid disease and adult celiac disease. In part, at least, this appears to be related to common genetically-based determinants as well as a common embryonic origin since the fetal thyroid is derived from the pharyngeal gut. Dr. Hugh J Freeman of the Department of Medicine, Gastroenterology, at the University of British Columbia in Vancouver, BC, Canada recently set out to review evidence from earlier prevalence studies and recent population-based studies. Specific phenotypic features have been described if both disorders are defined, including dermatitis herpetiformis, and a greater risk for a malignant complication, including lymphoma, especially if celiac disease is initially diagnosed at a late age. Some phenotypic characteristics of autoimmune thyroid disease, such as orbitopathy, may be an important clue to occult celiac disease. Similarly, patients requiring a high thyroxine dose to treat their autoimmune thyroid disease may reflect another aspect of undetected celiac disease. In some studies, the relationship has also been extended to other phenotypic features, such as dermatitis herpetiformis, and a greater risk of malignant complication, especially if celiac disease is detected in late or elderly age groups. In addition, some phenotypic characteristics of thyroid disease, such as orbitopathy and a high dose requirement for replacement may be added clinical clues to occult or undetected celiac disease. Dr. Freeman recommends that doctors consider serological screening for adult celiac disease in patients with autoimmune thyroid disease. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 121-123. doi: 10.12691/ijcd-4-4-6
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Celiac.com 01/31/2017 - In my practice, I have had the pleasure and honor of helping hundreds of people reverse their diabetes and put their autoimmune diseases into remission. One of the many things that we test for is gluten reactivity. The research, much of which has been cited in our book on gluten, Lose the Gluten, Lose your Gut. Ditch the Grain, Save your Brain, clearly demonstrates the connection between gluten reactivity and most autoimmune diseases, including but not limited to: Hashimoto's thyroiditis, rheumatoid arthritis and psoriasis. I intentionally didn't mention celiac disease, because, although it is very well established and accepted that gluten triggers celiac disease, what most don't realize is that those with celiac disease represent only a small percentage of people with autoimmunity that are impacted by gluten reactivity. What's alarming and disappointing to me is how many doctors 'pooh pooh' the concept of gluten reactivity, especially among their chronically ill patients. Because of this disconnect, patients continue to suffer needlessly with chronic diseases that, with the removal of gluten from the diet, would in many cases, clear up or go into remission. Hundreds of my patients tell me that when they told their health practitioner they had eliminated gluten from their diet, the health care worker didn't believe gluten would make a difference, or that since they didn't have celiac disease, eliminating gluten wouldn't help them. All this was said in the face of autoimmune diseases going into remission, or diabetes reversing right before their eyes, following the elimination of gluten from their diet. The issue is that many health care practitioners are just not keeping current with the research. As such, they are inadvertently preventing their patients from truly getting healthy. The additional travesty with this is that so many people look to their health care practitioners as 'experts'. When these providers, who are not 'experts' in a particular subject, (in fact, many are completely ignorant of how dietary changes and supplement therapy can help people thrive) advise a patient against something that the research shows would likely help them, it becomes an issue of negligence and, quite frankly, laziness. One patient in particular comes to mind when I think of this disconnect. I had the pleasure of working with a retired nurse who, in her seventies, had come to me with several medical issues. For purposes of this article, I will refer to her as Mary. Mary suffered with hypothyroidism, which we quickly discovered through additional testing, was caused by an autoimmune disease called Hashimoto's thyroiditis. Interestingly, it is estimated that roughly 90% of the 26 million people in the U.S. that have hypothyroidism actually have Hashimoto's. This is an autoimmune disease in which your immune system attacks and destroys the thyroid gland. The research, and our clinical experience, has demonstrated that gluten will cause your immune system to flare-up and attack the thyroid. In addition to Hashimoto's, Mary also suffered with cardiac arrhythmia and she had a history of blood clots and strokes. She also had a long-standing issue with another autoimmune disease, called pleva, whereby her skin would rash up, itch and scab. Mary was very overweight, and exhausted all of the time. Mary had a full functional work-up in our office and she was confirmed, with testing, to be very gluten-reactive. After working with her for several months, with one very important instruction to go completely gluten-free, she easily lost over 40 lbs (with no additional exercise), her energy increased to the point where she stated she hadn't felt that good in decades, and her arrhythmia and pleva cleared up completely. Her cardiologist was ecstatic and her general practitioner told her to keep up whatever she was doing because she was so healthy now. I hadn't seen Mary for almost 6 months when she emailed me one day to update me on something that had happened with her. She went to a food class taught by a vegan. At the class the guests were told very directly that eating gluten-free was a 'billion dollar hoax' and that eating gluten-free could be dangerous and bad for your health. Mary, even after all of her success, in part from going gluten-free, was suddenly doubtful of her diet. She tested it, and for 3 days brought back gluten-containing foods. She told me she reacted very badly and felt horrible. For Mary, the point was driven home that gluten-reactivity was a very real issue regarding her health. The difference in how she felt was like night and day. Lucky for her, she observed this first hand and immediately went back on her gluten-free diet before her skin disease and arrhythmia flared-up. Whether one is a doctor, a nutritionist, or a regular Joe, making statements about any subject without having researched that subject in earnest, is unethical, and may even be harmful. We have done the research and have seen first-hand, with thousands of patients reversing everything from psoriasis to diabetes, that eating gluten-free, while very 'trendy' right now, is a trend that is solidly backed up by the evidence.
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Celiac.com 02/06/2017 - People with celiac disease have higher rates of autoimmune thyroiditis, and vice versa. Both of these common autoimmune diseases share multiple aspects lodging at the two ends of the gut-thyroid axis where the cross-talks' pathways are still unrivaled. A team of researchers recently set out to better understand the parameters for effectively screening patients with either disease for the presence of the other. The research team included Aaron Lerner, and Torsten Matthias of the Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel, and with AESKU.KIPP Institute, Wendelsheim, Germany. Many clinicians recommend screening patients with thyroid autoimmunity for celiac disease associated antibodies. However, the wisdom of routinely screening of celiac patients for anti-thyroid antibodies is less certain. Despite the fact that the latter screening fulfills most of the criteria for screening a disease, the timing and cost-effectiveness remains undetermined. For now, in face of celiac disease, the researchers are recommending that clinicians and practitioners keep in mind the higher rates of autoimmune thyroid disease in the interests of making timely and accurate diagnosis. Read their full report. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 124-126. doi: 10.12691/ijcd-4-4-10
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Celiac.com 10/13/2016 - Researchers don't currently know much about rates of celiac disease autoimmunity or tissue transglutaminase autoantibodies (TGA) in patients with type 1 diabetes (T1D) and autoimmune thyroid disease (AITD) in the Chinese population. A team of researchers recently set out to assess rate of celiac disease autoimmunity amongst patients with T1D and AITD in the Chinese population. The research team included Zhiyuan Zhao, Jing Zou, Lingling Zhao, Yan Cheng, Hanqing Cai, Mo Li, Edwin Liu, Liping Yu, and Yu Liu. The study included 178 patients with type 1 diabetes, along with 119 with AITD where 36 had both T1D and AITD, classified as autoimmune polyglandular syndrome type 3 variant (APS3v). The study also included 145 patients with type 2 diabetes (T2D), 97 patients with non-autoimmune thyroid disease (NAITD), and 102 healthy control subjects. The team used radioimmunoassay to measure serum islet autoantibodies, thyroid autoantibodies and TGA. They found TGA positivity in 22% of patients with either type 1 diabetes or AITD, much higher than the 3.4% seen in T2D patients (p< 0.0001) the 3.1% seen in NAITD patients (P < 0.0001) or the 1% seen in healthy controls (1%; p<0.0001). Thirty-six percent of patients with APS3v who had both T1D and AITD positive for TGA, significantly higher than patients with T1D alone (p = 0.040) or with AITD alone (p = 0.017). At diagnosis, T1D and AITD showed overlap frequencies of 20% and 30%, respectively. Chinese population with existing T1D and/or AITD shows high rates of TGA positivity, which are even higher in people with both diseases. The study team recommends routine TGA screening in patients with T1D or AITD will help to identify celiac disease autoimmunity early on, and will yield better clinical patient care. Source: Plos.org
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Celiac.com 08/29/2016 - In 2005 the National Institute of Health indicated more than 23 million Americans suffered from autoimmune disease. Today the projection is 30 million who experience extreme fatigue, muscle and joint pain, muscle weakness, sleeplessness, weight loss or gain, and memory problems as symptoms of autoimmune disorders. Celiac disease has gotten the most attention in antibody research, but the current data on cross-reactivity of antibodies is allowing a better understanding of gluten sensitivity. Antigen reactivity to alpha-gliadin can trigger immune attacks on many individuals beyond those with positive DQ 2, DQ 8 and TTG test results. Gluten ataxia has been identified not only in people with celiac disease, but also in autism, lupus and multiple sclerosis. The lack of muscle control for movement, speech, eye coordination and swallowing can now be assessed in most autoimmune disorders. Gliadin reacts with foods and human tissue antigens causing symptoms beyond the gastro-intestinal tract. A low inflammatory diet customized to each person through testing for cross-reactivity or elimination diet protocols is needed to restore a state of health and well-being (for a copy of Low Inflammatory Diet & Elimination Diets check the author's website at the end of this article). According to Aristo Vojdani, PhD, professor of neuroimmunology at Carrick Institute and Chief Science Advisor for Cyrex Labs, about 50 percent gluten-sensitive individuals are also sensitive to dairy proteins (cow's milk, casein, whey) and sensitivity to oats depends on the variety of the grain and not just contamination from the milling process. In the author's personal experience, a gluten-free diet has many limitations. The reactivity between alpha gliadin and corn, millet, oats, rice and dairy has been denounced as invalid by gastroenterologists and celiac disease researchers. While at a medical school in Missouri, biopsies did not show improvement in villous atropy until all alpha gliadin sources and corn, millet, rice and oats were removed from the diet. Intestinal permeability or leaky gut allows antigens into the blood stream including food proteins, pathogens, and toxic chemicals which can cause inflammation. Continuous antigen exposure to tissues and organs is a factor in developing autoimmune disorders. Symptoms develop silently in the gut, joints and endocrine glands for several years. Tissue destruction with T and B lymphocyte reactions are a warning that autoimmune issues are developing during the next 5 to 10 year period until immunosuppressive drugs like corticosteroids are needed. To reduce the triggers to autoimmune diseases early, nutrition and lifestyle habits need adjusting. A Gluten-free Diet may seem easier today than 10 years ago, but current regulations in many countries allow up to 20 ppm gluten to be labeled "gluten-free". Many gliadin and cross -reactive proteins are most likely still available to create inflammatory symptoms. Assessing Viral Activity is key to managing autoimmune disease symptoms. Viral panels for EBV, Lyme, Bartonella, Mycoplasma, Chlamydia, CMV are available. Nutrition management of viral load is critical for the person with celiac disease and other autoimmune diseases. Reducing Toxic Chemicals is just as important as omitting gluten. Plastics like bisphenol A, heavy metals, pesticide residues, solvents all create inflammation. Water filtration devices that remove fluoride, heavy metals and pathogens plus stainless steel water bottles could reduce the body burden of chemicals that influence digestive function, joint movement, and immune well-being.
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Celiac.com 06/20/2016 - Are there genetic correlations between PTSD and mental disorders or immune-related disorders? What role does genetics play in PTSD, if any? A team of researchers recently set out to discover genetic loci associated with the lifetime risk for PTSD in 2 groups from the Army Study to Assess Risk and Resilience in Service members (Army STARRS). The research team included Murray B. Stein, MD, MPH, Chia-Yen Chen, ScD; Robert J. Ursano, MD; Tianxi Cai, ScD; Joel Gelernter, MD; Steven G. Heeringa, PhD; Sonia Jain, PhD; Kevin P. Jensen, PhD; Adam X. Maihofer, MS; Colter Mitchell, PhD; Caroline M. Nievergelt, PhD; Matthew K. Nock, PhD; Benjamin M. Neale, PhD; Renato Polimanti, PhD; Stephan Ripke, MD5; Xiaoying Sun, MS; Michael L. Thomas, PhD; Qian Wang, PhD; Erin B. Ware, PhD; Susan Borja, PhD; Ronald C. Kessler, PhD; Jordan W. Smoller, MD, ScD; for the Army Study to Assess Risk and Resilience in Service-members (STARRS). They are variously affiliated with the Department of Psychiatry, and the Department of Family Medicine and Public Health, UCSD, La Jolla, the Psychiatry Service of the Veterans Affairs San Diego Healthcare System, San Diego, California, the Department of Psychiatry at Massachusetts General Hospital and Harvard Medical School, Boston, the Stanley Center for Psychiatric Research, Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, the Department of Psychiatry, Uniformed Services University of the Health Sciences in Bethesda, Maryland, the Harvard T. H. Chan School of Public Health, Boston, Massachusetts, the Department of Psychiatry, Genetics, and Neurobiology at Yale University in New Haven, Connecticut, the Institute for Social Research, University of Michigan, Ann Arbor, the Department of Psychology, Harvard University, Cambridge, Massachusetts, the Department of Computational Biology and Bioinformatics, Graduate School of Arts and Sciences at Yale University, New Haven, Connecticut, the National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, and with the Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts The study looked at subjects from two coordinated genome-wide association studies of mental health in the US military. The first study, the New Soldier Study (NSS), included 3,167 unique patients with PTSD and 4,607 trauma-exposed control subjects. The NSS data were collected from February 1, 2011, to November 30, 2012. The second study, the Pre/Post Deployment Study (PPDS), included 947 unique patients with PTSD and 4,969 trauma-exposed control subjects. The PDDS data were collected from January 9 to April 30, 2012. The primary analysis compared lifetime DSM-IV PTSD cases with trauma-exposed controls without lifetime PTSD. Data were analyzed from March 18 to December 27, 2015. The team used logistic regression models to conduct association analyses for PTSD among European, African, and Latino Americans by study, followed by meta-analysis. They also estimated heritability, genetic correlation and pleiotropy with other psychiatric and immune-related disorders. The NSS population of 7,774 patients was just over 80% male, and about 21 years old, while the PPDS population of 5,916 patients was 94.4% male, and about 26.5 years old. A genome-wide significant locus was found in ANKRD55 on chromosome 5 (rs159572; odds ratio [OR], 1.62; 95% CI, 1.37-1.92; P = 2.34 × 10−8) and persisted after adjustment for cumulative trauma exposure (adjusted OR, 1.64; 95% CI, 1.39-1.95; P = 1.18 × 10−8) in the African American samples from the NSS. They also found a genome-wide significant locus in or near ZNF626 on chromosome 19 (rs11085374; OR, 0.77; 95% CI, 0.70-0.85; P = 4.59 × 10−8) in the European American samples from the NSS. They did not find any similar results for either single-nucleotide polymorphism in the corresponding ancestry group from the PPDS sample, in other ancestral groups, or in transancestral meta-analyses. Overall, they saw no significant evidence for single-nucleotide polymorphism–based heritability, and they found no significant genetic correlations between PTSD and 6 mental disorders or 9 immune-related disorders. They did find significant evidence of a single-gene linking PTSD and rheumatoid arthritis and, to a lesser extent, psoriasis. Beyond that, they didn't find not much to support any connection to specific gene locations. The researchers are calling for additional studies "to replicate the genome-wide significant association with ANKRD55—associated in prior research with several autoimmune and inflammatory disorders—and to clarify the nature of the genetic overlap observed between PTSD and rheumatoid arthritis and psoriasis." Source: JAMA Psychiatry. Published online May 11, 2016. doi:10.1001/jamapsychiatry.2016.0350
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Do Autoimmune Diseases Cause Some Epilepsy?
Jefferson Adams posted an article in Epilepsy and Celiac Disease
Celiac.com 06/11/2014 - A new study provides strong evidence for an autoimmune cause for a significant number of epilepsy cases, and that screening autoimmune patients for epilepsy and vice versa may be helpful in making more complete diagnosis. The team used insurance claims data from more than 2.5 million members of a national health insurance provider to examine the relationship between epilepsy and 12 autoimmune diseases: type 1 diabetes mellitus, psoriasis, rheumatoid arthritis, Graves' disease, Hashimoto's thyroiditis, Crohn's disease, ulcerative colitis, systemic lupus erythematosus, antiphospholipid syndrome, Sjögren syndrome, myasthenia gravis, and celiac disease. Patients with an autoimmune disease faced a nearly four-fold higher risk for epilepsy (odds ratio [OR], 3.8; 95% confidence interval [CI], 3.6 - 4.0; P < .001). The elevated risk was consistently observed across all 12 autoimmune diseases, and was especially high in children (OR, 5.2; 95% CI, 4.1 - 6.5; P < .001). The data showed that 17.5% of patients with epilepsy also had an autoimmune disease. In about 70% of epilepsy patients, the autoimmune diagnosis came first. Seizures tended to occur within the first 1 to 2 years after diagnosis of an autoimmune disease. The results of the study prompted lead investigator Kenneth Mandl, MD, MPH, from Intelligent Health Laboratory, Harvard Medical School and Boston Children's Hospital, Boston, Massachusetts, to remark that health professionals “need to expand our thinking when it comes to clinical management of these conditions.” The research team further added that the “potential role of autoimmunity must be given due consideration in refractory epilepsy” so that they do not overlook treatable causes for epilepsy Source: JAMA Neurology, March 31, 2014.- 1 comment
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Celiac.com 01/19/2016 - Cases of autoimmune diseases are on the rise, and mirror the expansion of industrial food processing and increased use of food additives. The intestinal epithelial barrier, with its intercellular tight junction, controls the balance between tolerance and immunity to non-self-antigens. Recently, a team of researchers set out to assess the role of tight junction dysfunction in the pathogenesis of autoimmune disease. Researchers Aaron Lerner and Torsten Matthias are associated with the Pediatric Gastroenterology and Nutrition Unit, Carmel Medical Center, B, Rappaport School of Medicine, Technion-Israel Institute of Technology, Michal in Haifa, Israel, and the Aesku Kipp Institute in Wendelsheim, Germany. Numerous common industrial food additives increase tight junction leakage. These include glucose, salt, emulsifiers, organic solvents, gluten, microbial transglutaminase, and nanoparticles, widely and increasingly used in industrial food production. According to manufacturers, these additives improve food quality. However, all of the aforementioned additives increase intestinal permeability by breaching the integrity of tight junction paracellular transfer. So why is this a problem? Well, it turns out that tight junction dysfunction is common in multiple autoimmune diseases, and the central part played by the tight junction in autoimmune diseases development is widely described. The researchers hypothesize that commonly used industrial food additives undermine human epithelial barrier function, which increases intestinal permeability through the opened tight junction, resulting in entry of foreign immunogenic antigens and activation of the autoimmune cascade, and the development of autoimmune conditions, such as celiac disease. The team is calling for additional research on the connections between food additives exposure, intestinal permeability, and autoimmunity interplay to expand our knowledge of the common mechanisms associated with autoimmune progression. Source: tx.technion.ac.il
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Celiac.com 09/16/2015 - Autoimmune disease, such as type 1 diabetes, Crohn's disease, and juvenile idiopathic arthritis, affect about 7 to 10 percent of the population in the Western Hemisphere. Using genome-wide association studies (GWASs), researchers have identified hundreds of susceptibility genes, including shared associations across clinically distinct autoimmune diseases. A team of researchers recently conducted an inverse χ2 meta-analysis across ten pediatric-age-of-onset autoimmune diseases (pAIDs) in a case-control study including more than 6,035 cases and 10,718 shared population-based controls. The research team included Yun R Li, Jin Li, Sihai D Zhao, Jonathan P Bradfield, Frank D Mentch, S Melkorka Maggadottir, Cuiping Hou, Debra J Abrams, Diana Chang, Feng Gao, Yiran Guo, Zhi Wei, John J Connolly, Christopher J Cardinale, Marina Bakay, Joseph T Glessner, Dong Li, Charlly Kao, Kelly A Thomas, Haijun Qiu, Rosetta M Chiavacci, Cecilia E Kim, Fengxiang Wang, James Snyder, and Marylyn D Richie. The are variously affiliated with The Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; Medical Scientist Training Program, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA; the Department of Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.; the Division of Allergy and Immunology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.; the Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, USA; the Program in Computational Biology and Medicine, Cornell University, Ithaca, New York, USA, and the Department of Computer Science, New Jersey Institute of Technology, Newark, New Jersey, USA. For their study, the team identified 27 genome-wide significant loci associated with one or more pAIDs, mapping to in silico–replicated autoimmune-associated genes (including IL2RA) and new candidate loci with established immunoregulatory functions such as ADGRL2, TENM3, ANKRD30A, ADCY7 and CD40LG. The team functionally enriched the pAID-associated single-nucleotide polymorphisms (SNPs) for deoxyribonuclease (DNase)-hypersensitivity sites, expression quantitative trait loci (eQTLs), microRNA (miRNA)-binding sites and coding variants. They also identified biologically correlated, pAID-associated candidate gene sets on the basis of immune cell expression profiling and found evidence of genetic sharing. Network and protein-interaction analyses demonstrated converging roles for the signaling pathways of type 1, 2 and 17 helper T cells (TH1, TH2 and TH17), JAK-STAT, interferon and interleukin in multiple autoimmune diseases. Source: Nature Medicine 21, 1018–1027 (2015) doi:10.1038/nm.3933
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Celiac.com 07/27/2015 - First-degree relatives of individuals with celiac disease are at increased risk for this disorder, but little is known about their risk for other autoimmune diseases. A research team recently set out to assess the risk of non-celiac autoimmune disease in first-degree relatives and spouses of people with celiac disease. The research team included Louise Emilsson, Cisca Wijmenga, Joseph A. Murray, and Jonas F. Ludvigsson. They are variously affiliated with the Primary Care Research Unit, Vårdcentralen Värmlands Nysäter, Värmland County, Sweden, the Department of Health Management and Health Economy, Institute of Health and Society, University of Oslo, Oslo, Norway, the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, the Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden. The team found individuals with celiac disease by searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden. The team found 29,096 patients with celiac disease based on biopsy reports of villous atrophy of Marsh grade 3 or higher and matched individuals with celiac disease with up to 5 of 144,522 non-celiac control patients based on sex, age, county, and calendar year. Through Swedish health care registries, the team identified all first-degree relatives (fathers, mothers, siblings, and offspring) and spouses of 84,648 individuals with celiac disease, and 430,942 control subjects. The team used Cox regression analysis to calculate hazard ratios (HRs) for non-celiac autoimmune disease, such as Crohn’s disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis, within these groups. Cox analysis showed that during the follow-up period averaging just under 11 years, nearly 3333, or 4%, of the first-degree relatives of patients with celiac disease, and 12,860 relatives of controls (3.0%), had an autoimmune disease other than celiac disease. First-degree relatives of people with celiac disease had an increased risk of non-celiac autoimmune disease, compared with controls (HR, 1.28; 95% confidence interval, 1.23–1.33), as did spouses (HR, 1.20; 95% confidence interval, 1.06–1.35). Risk estimates for non-celiac autoimmune disease did not differ between first-degree relatives and spouses of individuals with celiac disease (interaction test: P = .11). Hazard Ratios for non-celiac autoimmune disease were highest in the first 2 years of follow-up evaluation. First-degree relatives and spouses of individuals with celiac disease have a significantly higher risk of non-celiac autoimmune disease. In addition to genetic factors, environmental factors and better awareness, testing and diagnosis might influence rates of autoimmune disorders in first-degree relatives of individuals with celiac disease. Source: Clinical Gastroenterology and Hepatology. DOI: http://dx.doi.org/10.1016/j.cgh.2015.01.026
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Celiac.com 02/02/2012 - A team of researchers recently conducted a prospective controlled study on a gluten-free diet and autoimmune thyroiditis in patients with celiac disease. The research team included S. Metso, H. Hyytiä-Ilmonen, K. Kaukinen, H. Huhtala, P. Jaatinen, J. Salmi, J. Taurio, and P. Collin. They are affiliated with the Department of Internal Medicine at Tampere University Hospital in Tampere, Finland. Prior to the study, there had been contradictory data regarding the ways in which early diagnosis and a gluten-free diet might slow the progression of associated autoimmune diseases in celiac disease. The research team investigated the course of autoimmune thyroid diseases in newly diagnosed celiac disease patients, both before and after gluten-free dietary treatment. For their study, the team examined twenty-seven adults with newly diagnosed celiac disease, both at the time of diagnosis and after one year on gluten-free diet. They also recorded and examined previously diagnosed and subclinical autoimmune thyroid diseases. The team used ultrasound to measure thyroid gland volume and echo-genicity. They also measured autoantibodies against celiac disease and thyroiditis, and conducted thyroid function tests. As a control group, they enrolled twenty-seven non-celiac subjects, all of whom followed a normal, gluten-containing diet. The data showed that, upon diagnosis, ten of 27 celiac disease patients had either manifest (n = 7) or subclinical (n = 3) thyroid diseases. Only three of 27 control subjects (10/27 vs. 3/27, p = 0.055) had thyroid disease. After treatment with a gluten-free diet, thyroid volume continued to decrease significantly in the patients with celiac disease compared with the control subjects, indicating the progression of thyroid gland atrophy regardless of the gluten-free diet. Overall, celiac patients faced a higher risk of thyroid autoimmune disorders than non-celiac control subjects. Moreover, a gluten-free diet did not seem to stop or reverse the progression of autoimmune disease after one year. Source: Scand J Gastroenterol. 2012 Jan;47(1):43-8. Epub 2011 Nov 30.
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Celiac.com 03/25/2015 - In what may prove to be a remarkable step in understanding human diseases, a team of scientists affiliated with Northeastern University has found a way to connect diseases based on their shared molecular interactions. A paper by the Northeastern team appears in the journal Science. The paper details their creation of a mathematical tool to analyze the map of the molecular interactions within cells, called the human interactome, and the discovery that over-lapping disease modules, or "neighborhoods" of disease-associated proteins, can give rise to some very unexpected relationships between diseases. Increasing amounts of research, says Albert-László Barabási, are making it very clear that "human diseases can be interpreted only in the context of the intricate molecular network between the cell’s components." Barabási is Robert Gray Dodge Professor of Network Science and University Distinguished Professor and director of Northeastern’s Center for Complex Network Research. The Northeastern researchers are based in the Center for Complex Network Research. The team comprises Barabási, Menche, postdoctoral researcher Maskim Kitsak, research assistant professor Amitabh Sharma, and graduate physics student Susan Dina Ghiassian, PhD’15. For their study, the Northeastern team analyzed 299 diseases that had at least 20 associated genes. They found that 226 of the diseases had their own specific "neighborhood" within the interactome. They noticed that diseases within the same neighborhood had more in common in terms of molecular functions or symptoms, while diseases that were far away from each other within the interactome had very little in common in terms of molecular functions or symptoms. Among their findings, they noted that asthma, and celiac disease are localized in overlapping neighborhoods, which suggests shared molecular roots, even though they have very different pathobiologies. This is the first study to show that the available network maps offer enough coverage and accuracy to provide valuable information about the molecular origins of disease-disease relationships, says Jörg Menche, a postodoctoral researcher and one of the authors on the paper. This is a very interesting and potentially promising discovery that may pave the way for a much deeper understanding of relationships between celiac and numerous other diseases. Stay tuned for more news. Source: Northeasternnews.edu
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Celiac.com 06/28/2010 - 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, an exciting prospect for celiacs who may want to enjoy some gluten now and then. Celiac disease is an autoimmune disease, the source of this being gluten, a protein found in wheat, rye, and barley, affecting about 1% of the population and 300 million Americans. The disease attacks the villi,the finger-like structure which line the small intestine, leading to stomach troubles and malabsorption of nutrients. Left untreated, it can cause severe health conditions and complications such as anemia, osteoporosis, miscarriage, and even cancer. David van Heel, a gastrointestinal genetics professor at Barts and The London School of Medicine and Dentistry, headed a group of researchers from around the world who studied the genetic maps of more than 9,400 celiacs. British researchers have found what they term “substantial” evidence that the genes which are connected with celiac disease are also linked to other autoimmune disease such as rheumatoid arthritis. As a result, 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. Furthermore, it is 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 in his published study. Why is that only 3% of celiac Americans have been properly diagnosed? It’s likely that 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. Without charitable donations, there would be no way to continue this research and the efforts to raise awareness. Out of the estimated fifty autoimmune diseases that have been discovered by doctors, it is the only one for which research isn’t supported by the U.S. government. I spent years running in circles with doctors who had no clue as to the cause of my painful symptoms, which finally drove me to research my symptoms on my own. I’m grateful lto have been properly diagnosed, but managing the gluten-free diet can be a challenge. The prospect of a pill to offset genetic factors will appeal 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 home cooking. With this genetic research in the area of celiac disease, we can look forward to more research, more awareness, and perhaps another treatment option. Meanwhile, it’s best to keep doing our parts to raise awareness and funds for research. Source: Reuters
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Celiac.com 07/08/2009 - Kids whose moms have autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and celiac disease face a risk of autism that is up to three times higher than that of the general population, according to a new study. Although earlier studies have documented a connection between autism and a maternal history of type 1 diabetes and rheumatoid arthritis, this is the first study to document a link between autism and celiac disease, according to the study's authors. A team of researchers led by Dr. William W. Eaton, chairman of the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University recently set out to review data related to autoimmune deficiency and autism. Eaton's team collected data on 3,325 Danish children diagnosed with autism spectrum disorder, including 1,089 diagnosed with infantile autism. All of the children were born between 1993 and 2004, and their data was part of the Danish National Psychiatric Registry. Data on family members with autoimmune diseases came from the Danish National Hospital Register. The data showed that children whose mothers had autoimmune disease faced a higher risk of developing autism spectrum disorder than children of mothers who did not have these conditions. Moreover, children with a family history of type 1 diabetes faced an increased risk of infantile autism. Overall, the increased risk of autism in people with autoimmune diseases is not huge, Eaton said. "The increased risk for type 1 diabetes is a little less than two times, for rheumatoid arthritis it's about 1.5 times and for celiac disease it's more than three times," Eaton said. "That's enough to impress an epidemiologist, but not enough to make anybody in the general population start changing their behavior." Eaton added that this finding "reinforces the suggestion that autoimmune processes are connected somehow with the cause of autism and autism spectrum disorder, and...may point a flashlight to areas of the genome that connect to autism." The finding itself has no clinical significance, says Eaton, but could guide future efforts by researchers to determine the cause or causes of autism. One reason autoimmune diseases might have a role in autism lies in genetic history, Eaton said. Children who were underweight or premature at birth face a higher risk for autism, and both of these obstetric problems are associated with celiac disease, he added. There may be a significant overlap "in the genetics of some of the autoimmune diseases and autism," he said. "Autism is strongly inherited, but we don't have the faintest idea where...this finding is on the pathway of finding the cause of autism." Various environmental triggers may also affect the fetus, he said. Lead researcher, Dr. Hjordis O. Atladottir, from the Institute of Public Health at the University of Aarhus in Denmark calls the findings important because they support the theory that autism is somehow tied to problems with the immune system. PEDIATRICS
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Celiac.com 07/03/2013 - Researchers have completed a genetic study of six autoimmune diseases, including diabetes, the largest such study of human disease genetics to date. The study will help scientists in their efforts to uncover the causes of these diseases, which include autoimmune thyroid disease, celiac disease, Crohn’s disease, psoriasis, multiple sclerosis and type 1 diabetes. While currently unknown, the underlying causes of these conditions are believed to involve a complex combination of genetic and environmental factors. In each of the six diseases, the identified genetic variants explained only a proportion of the heritability. Under one of the current major genetic disease hypotheses, the so called ‘rare-variant synthetic genome-wide association hypothesis,’ a small number of rare variants in risk genes are likely the major cause of the heritability of these conditions. In their study, the research team used high-throughput sequencing techniques, in an effort to identify new genetic variants, including rare and potentially high risk variants, in 25 previously identified risk genes taken from a sample of nearly 42,000 patients. Their data suggest that the genetic risk of these diseases more likely results from a complex interaction of hundreds of variants, each small on its own, but which, taken together impact the development of these six diseases. They estimate that rare variants in these risk genes make up only about three per cent of the heritability of these conditions that can be explained by common variants. The results, says lead study author David van Heel, suggest that "risk for these autoimmune diseases is not due to a few high-risk genetic variations." Rather, risk is likely due to a "random selection from many common genetic variants which each have a weak effect.” This could mean that it will never be possible to accurately predict a person's risk of developing any of these six autoimmune diseases, simply because there are too many variables. “However, the results do provide important information about the biological basis of these conditions and the pathways involved, which could lead to the identification new drug targets,” said van Heel. Source: Nature Genetics 42, 295–302 (2010). doi:10.1038/ng.543; and Firstpost.com.
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Celiac.com 06/19/2013 - Currently, immunosuppressant drugs are the only real treatment option for most autoimmune disorders, such as celiac disease and Type 1 diabetes. However, researchers are busily exploring the possibilities offered therapeutic vaccines, known as antigen-specific immunotherapy. ImmusanT is one company working to develop a vaccine that will allow patients with celiac disease to safely eat gluten (the antigen). That vaccine is presently undergoing clinical trials. ImmusanT and its research partners are looking to build on their expertise in celiac disease to improve their understanding of antigen-specific immunotherapy for other autoimmune diseases. In Current Opinion in Immunology, researchers Bob Anderson and Bana Jabri describe how identification of pathogenic T cell epitopes (segment of the antigen) and recent initiatives to optimize immune monitoring have helped drive rational vaccine design in human autoimmune diseases. Celiac disease has provided researchers with the first opportunity to design and test epitope-specific immunotherapy with a thorough understanding of disease-causing T cell epitopes. This approach offers "truly customized immunotherapy for patients with celiac disease according to their genetics and the molecular specificity of their immune response to gluten," said Bob Anderson, PhD, MBChB, Chief Scientific Officer of ImmusanT. Because celiac disease shares key features, such as susceptibility genes, presence of autoantibodies and destruction of specific cells, with other autoimmune disorders, like Type 1 diabetes and rheumatoid arthritis, it provides a model for understanding and exploring the triggers and drivers of autoimmunity, in general, write Drs. Bana Jabri and Ludvig Sollid in the Perspectives section in Nature Reviews Immunology. By factoring in the association with the major histocompatibility complex (MHC), post-translation modifications, the antigen and the tissue, researchers can design methods that help to the spot potential drivers of autoimmune disease. Because peptide-specific therapy specifically targets the immune cells that drive the disease process, "it offers the potential to prevent and cure disease, without inducing general immunosuppression," said Bana Jabri, MD, PhD, Director, University of Chicago Celiac Center; Professor, Department of Medicine, Pathology and Pediatrics, University of Chicago; and Senior Scientific Advisor to ImmusanT. Ludvig M. Sollid, MD, PhD, is Director, Centre for Immune Regulation; Professor of Medicine, Department of Immunology, University of Oslo; Consultant, Oslo University Hospital-Rikshospitalet; and member of ImmusanT's Scientific Advisory Board. Dr. Jabri is Co-Chair of the 15(th) International Celiac Disease Symposium to be hosted by the University of Chicago Celiac Disease Center, September 22-25, 2013. The event will draw the world's top scientists and physicians to discuss the most recent scientific advances in managing and treating celiac disease and gluten-related disorders.
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American Journal of Psychiatry 163:521-528, March 2006 Celiac.com 03/14/2006 – Danish researchers have found yet another link between celiac disease and schizophrenia. In a large epidemiologic study the researchers looked at 7,704 Danish people who were diagnosed with schizophrenia between 1981 and 1998, including their parents, and matched them to comparison control subjects. The data linkage required that the autoimmune disease be diagnosed before the diagnosis of schizophrenia. The researchers found that patients with a history of an autoimmune disease had a 45% increased risk for schizophrenia, and nine autoimmune disorders were indicators of a higher prevalence for schizophrenia when compared to the controls. The researchers conclude: “Schizophrenia is associated with a larger range of autoimmune diseases than heretofore suspected. Future research on co-morbidity has the potential to advance understanding of pathogenesis of both psychiatric and autoimmune disorders.”
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