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Found 26 results

  1. Celiac.com 10/08/2018 - A new population based study reveals that celiac disease is associated with a wide range of medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism, according to a database study of more than 35 million people. Moreover, people with autism have celiac disease at rates almost 20 times higher than in those without autism, reported lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland. That raises the question of whether people with autism should be screened for celiac disease, and whether they might benefit form a gluten-free diet. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," Dr. Karb told the World Congress of Gastroenterology last year. It is known that there are unusual symptoms of celiac disease, which include anything outside the classic symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Karb and his fellow researchers used the Explorys database to pull health record data from 26 major integrated healthcare systems in the United States. Their search covered the period from 2012 to 2017. Of 35,854,260 people in the database, they found 83,090 with diagnosed celiac disease. Overall, the age-adjusted prevalence of celiac disease in that group was 0.22%, which is much lower than the 1% to 2% range previously estimated. Those numbers are not unusual, said Dr. Karb says that the researchers “don't think there are fewer people with celiac disease, just that it may be under-diagnosed.” The rates are, he says, “what you might expect when you screen asymptomatic people." Overall, the team found a significant connection between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. Moreover, celiac disease is associated with every autoimmune disease the team looked at, except for primary biliary cholangitis, Dr Karb says. This is some pretty startling study data. We knew that celiac disease was linked to other autoimmune conditions, and there has been some surprising data about gluten-free diets helping patients with autism, but these numbers are enlightening. It seems that people with autism should definitely be screened for celiac disease, and placed a gluten-free diet, if tests confirm celiac disease. Stay tuned for more information on this important celiac disease topic. Source: World Congress of Gastroenterology 2017
  2. 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.
  3. Dr. Ron Hoggan, Ed.D.

    It's Not Just Me

    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
  4. 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.
  5. 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
  6. Celiac.com 01/11/2017 - Researchers know that canonical Wnt/β-catenin signaling controls the homeostasis of intestinal epithelium by regulating the balance between intestinal stem cell regeneration and differentiation, but they really don't know much at all about the non-genetic mechanics of the process. One research team recently set out to test a hypothesis that the epigenetic regulator, Polycomb Repressive Complex-2 (PRC2), plays a role in Wnt-mediated epithelial homeostasis on the crypt-villus axis, and that defects in the process are implicated both in celiac disease and intestinal cancers. The research team included Mikko Oittinen, Alina Popp, Kalle Kurppa, Katri Lindfors, Markku Mäki, Minna U. Kaikkonen, and Keijo Viiri. They are variously associated with the Tampere Centre for Child Health Research, University of Tampere, Department of Pediatrics and Tampere University Hospital, Tampere, Finland, with the Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, and with the University of Medicine and Pharmacy “Carol Davila” at the Department of Pediatrics and Institute for Mother and Child Care in Bucharest, Romania. Their study showed that PRC2 establishes repressive crypt and villus specific trimethylation of histone H3 lysine 27 (H3K27me3) signature on genes responsible for nutrient transport and cell killing in crypts and, proliferation and differentiation in mature villi, suggesting that PRC2 facilitates the Wnt-governed intestinal homeostasis. When celiac patients regularly consume gluten, PRC2 goes out-of-bounds active, and its target genes in the intestinal epithelium are negatively impacted. Colorectal adenomas, and carcinomas, also differentially express a significant set of effective intestinal PRC2 targets. This indicates that PRC2 initiates and maintains polar crypt and villus specific H3K27me3 signatures. Because H3K27me3 is a mark enriched in developmentally important genes, identified intestinal PRC2 targets are possibe imperative drivers for enterocyte differentiation and intestinal stem cell maintenance downstream to Wnt-signaling. This research also clarifies the mechanics driving crypt hyperplasia in celiac disease, and suggests that PRC2-dependent fostering of epithelial stemness is a common aspect of intestinal diseases marked by epithelial hyperplasia or neoplasia. Lastly, the team's research shows that in the gut, PRC2 represses genes having both pro-stemness and pro-differentiation functions, a fact that should be weighed when designing non-genetic therapies including PRC2 as a drug target. Source: Stem Cells 2016
  7. 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.
  8. Celiac.com 05/16/2016 - A number of epidemiological and clinical studies suggest a connection between inflammation and Alzheimer disease, their relationship is not well understood and may have implications for treatment and prevention strategies. A research team recently set out to figure out if a subset of genes involved with increased risk of inflammation are also associated with increased risk for Alzheimer disease. The research team included JS Yokoyama, Y Wang, AJ Schork, WK Thompson, CM Karch, C Cruchaga, LK McEvoy, A Witoelar, CH Chen, D Holland, JB Brewer, A Franke, WP Dillon, DM Wilson, P Mukherjee, CP Hess, Z Miller, LW Bonham, J Shen, GD Rabinovici, HJ Rosen, BL Miller, BT Hyman, GD Schellenberg, TH Karlsen, OA Andreassen, AM Dale, RS Desikan; and the Alzheimer’s Disease Neuroimaging Initiative. They are variously affiliated with the Departments of Neurosciences, Cognitive Sciences, Psychiatry, and Radiology at the University of California, San Diego, La Jolla, the Departments of Neurology, Radiology and Biomedical Imaging at the University of California, San Francisco, the Department of Psychiatry, Washington University, St Louis, Missouri, the Division of Mental Health and Addiction, Oslo University Hospital, the Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, the Division of Gastroenterology, and the Norwegian PSC Research Center and KG Jebsen Inflammation Research Centre, Research Institute of Internal Medicine, Division of Cancer Medicine, Surgery and Transplantation at Oslo University Hospital Rikshospitalet, Oslo, Norway, the Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany, the Department of Neurology, Massachusetts General Hospital, Boston, and the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine, Philadelphia. Using data from numerous genome-wide association studies from several clinical research centers, the team conducted a genetic epidemiology study in July 2015, in which they systematically investigated genetic overlap between Alzheimer disease (International Genomics of Alzheimer's Project stage 1) and Crohn's disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis. The team assessed P values and odds ratios from genome-wide association studies of more than 100, 000 individuals from previous comparisons of patients vs respective control groups. They used consensus criteria to confirm diagnosis for each disorder previously made in the parent study. The main outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging Initiative); and gene expression in Alzheimer disease vs control brains (Gene Expression Omnibus data). These findings confirm genetic overlap between Alzheimer disease and immune-mediated diseases, and suggest that immune system processes influence Alzheimer disease pathogenesis and progression. For more detail, and exact data results, see JAMA Neurol. 2016 Apr 18. doi: 10.1001/jamaneurol.2016.0150.
  9. Celiac.com 01/26/2012 - A Canadian woman is fighting a battle with the government of British Columbia to protect the services that allow her 18-year old daughter to live at home in Quesnel, B.C., with 24-hour care — much of it provided by Shelley McGarry herself. The woman's daughter, Chelsea McGarry already has a long list of challenges — Down syndrome, autism, early onset Alzheimer's disease, diabetes, and celiac disease, among other conditions. The problem is that Chelsea turns 19 in December, at which point her responsibility for her care transfers from Ministry of Children and Family to Community Living B.C., the government agency that provides services to adults with developmental disabilities. Shelley McGarry says she's been battling for months with Community Living B.C. According to McGarry, Community Living B.C. has refused to approve the a plan for Chelsea. Moreover, the agency has threatened to reduce the minimal care Chelsea now receives, McGarry says. "It just turns my stomach to think of taking this public," she said. "But I don't know where else or what else to do." Independent provincial politician Bob Simpson and B.C. Representative for Children and Youth Mary Ellen Turpel-Lafond both say Chelsea's case is a classic example of Community Living B.C.'s failure to work with families and find solutions. Instead, they say, the agency is worsening the McGarrys' situation. "This is a young woman whose life is in crisis," said Turpel-Lafond, who has been pushing Chelsea's cause since her family since Ausgust 2011, when they asked him to advocate on her behalf. Turpel-Lafond says that Community Living B.C.'s efforts have been lacking so far. "I've written, I've met with the head of CLBC, I've done just about everything I can," she says. "I've said to them very clearly, 'This is a case that needs a review by you, she added'" Simpson represents Chelsea and her family in the provincial legislature. He says that the family has followed all of the government's rules. Shelley McGarry has thoroughly documented Chelsea's fragile medical conditions. She developed a plan with the local non-profit society, also known as a micro-board. McGarry arranged for Chelsea to receive home care for about $340,000 a year. That amount is far less than the CLBC's plan to put Chelsea in a care home capable of managing her complex needs. Simpson called the plan that the McGarry's have offered the CLBC a 'very reasonable and appropriate plan.' However reasonable that plan may be, the CLBC has refused to approve it. Worse still, their proposed alternatives would either be unsafe, or cost up to three times what it would to keep Chelsea at home, Simpson said. Simpson says that he suspects the CLBC is punishing Shelley McGarry for her vocal and tireless advocacy on Chelsea's behalf. Simpson adds that he also suspects that officials, as he says they have done in other recent cases, have lost sight of Chelsea as a person. Both Social Development Minister Stephanie Cadieux and Community Living B.C. have declined to comment on specific cases. However, Cadieux said in an interview that she is aware of the file, and that she has appointed a new client support team, which she hopes can resolve the matter. "I agree that it needs attention," Cadieux said, adding that the new team includes a number of "high-ranking officials" from the Ministry of Social Development, and the Ministry of Children and Family Development. Source: http://www.canada.com/Disabled+woman+faces+battle+government+care/5593715/story.html
  10. 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.
  11. 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
  12. 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
  13. Celiac.com 11/28/2014 - According to a new study, obesity plays a major part in triggering and prolonging autoimmune diseases, such as celiac disease, Crohn's disease and multiple sclerosis. The study appeared recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer. According to the research, obesity erodes the body's ability to protect itself, triggering a pro-inflammatory environment that promotes the development of autoimmune diseases, hastens their progression, and impairs their treatment. For some time now, says Professor Shoenfeld, researchers have been aware of the “negative impact of contributing disease factors, such as infections, smoking, pesticide exposure, lack of vitamins, and the like. But in last five years, a new factor has emerged that cannot be ignored: obesity.” According to the World Health Organization, about one-third of the global population is overweight or obese, nearly a dozen autoimmune diseases are now associated with excess weight, which now impact nearly 5-20% of the global population. That is why, according to Shownfeld, it is “critical to investigate obesity's involvement in the pathology of such diseases." The main culprit is not fat itself, but adipokines, compounds secreted by fat tissue, which impact numerous physiological functions, including the immune response. In tandem with their own study, Shoenfeld and his colleagues reviewed 329 studies from across the globe that focused on the connections between obesity, adipokines, and immune-related conditions like rheumatoid arthritis, multiple sclerosis, type-1 diabetes, psoriasis, inflammatory bowel disease, psoriatic arthritis, and Hashimoto thyroiditis. "According to our study and the clinical and experimental data reviewed, the involvement of adipokines in the pathogenesis of these autoimmune diseases is clear," says Shoenfeld. "We were able to detail the metabolic and immunological activities of the main adipokines featured in the development and prognosis of several immune-related conditions." One of the team’s more interesting findings was that obesity also promotes vitamin D deficiency, which, “once corrected, alleviated paralysis and kidney deterioration associated with the disorder… [and] improved the prognosis and survival of the mice.” Source: Science Daily, November 10, 2014
  14. Celiac.com 11/21/2014 - When most people think of celiac disease, they think about gastrointestinal symptoms. However, researchers have documented a number of other medical conditions that are associated with celiac disease, and which improve when patients follow a strict gluten-free diet. The recent case of a 75-year old man who experienced a dramatic recovery from Parkinson's disease after eliminating all forms of gluten from his diet for three months, has researchers thinking about the possibility that gluten sensitivity may be related to Parkinson's disease. In fact, there is some evidence that patients with epilepsy and other conditions may benefit from ketogenic low carb and gluten-free diets. The ketogenic diet is a high-fat, low-carbohydrate, and adequate protein diet developed 90 years ago at the Mayo Clinic. The high fat content creates ketosis, which appears to prevent seizures. In addition to the ketogenic diet, there are several other high-fat, low-carbohydrate diets for seizure control: low-glycemic-index, medium-chain triglyceride, and modified Atkins diets. All require medical supervision and vitamin and mineral supplements. In another example of food serving as medicine, high fat low carb ketogenic diets increasingly are being used to control seizures in epilepsy patients. As reported in Medscape, ketogenic diets made a significant difference for many patients with epilepsy who cannot control their seizures with medication. In one study, more than 20 percent of the patients used the traditional ketogenic diet, while the rest used a modified Atkins diet that included medium-chain triglyceride supplements. These patients saw dramatic improvements. In addition to reducing the number and severity of seizures, 65 percent of patients felt "more alert or brighter," while 35 percent had "more energy." Many of the patients also had shorter seizures when they occurred. Sources: Epilepsy Behav. 2014;37C:59-70. doi: 10.1016/j.yebeh.2014.05.031 J Neurol. 2014 Feb;261(2):443-5. doi: 10.1007/s00415-014-7245-7
  15. 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.
  16. Celiac.com 06/17/2013 - To investigate the prevalence of human leukocyte antigen (HLA) DQ2/8 alleles in Southern Italians with liver and gastrointestinal (GI) diseases outside of celiac disease, a team of researchers recently looked at human leukocyte antigen DQ2/8 prevalence in non-celiac patients with gastrointestinal diseases. The research team included Daniel DiGiacomo, Antonella Santonicola, Fabiana Zingone, Edoardo Troncone, Maria Cristina Caria, Patrizia Borgheresi, Gianpaolo Parrilli, and Carolina Ciacci. They are variously affiliated with the Gastrointestinal Unit of University Federico â…¡ in Naples, Italy, the Department of Medicine, Celiac Disease Center of Columbia University in New York, in the United States, The Celiac Center of Loreto Crispi Hospital in Naples, Italy, the Celiac Center, Gastrointestinal Unit in San Giovanni di Dio e Ruggi d’Aragona Hospital at the University of Salerno, and the Department of Medicine and Surgery, Campus di Baronissi at the University of Salerno Medical School in Baronissi, Italy. The team assessed HLA DQ2/8 status in 443 patients from three ambulatory gastroenterology clinics in Southern Italy. The clinics were located at the University of Federico â…¡ and Loreto Crispi Hospital in Naples, and Ruggi D’Aragona Hospital in Salerno. The team grouped patients according disease status for pre-post transplant liver disease, esophageal/gastric organic and functional diseases, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), along with DQ2/8 alleles, which correspond to a celiac disease genetic risk scale. They then compared allele frequencies in the test subjects with healthy Italian control subjects. Out of 443 subjects, the team found that 196 subjects (44.2%), tested positive for DQ2/8. The average age of DQ2/8 positive subjects was 56 years, and 42.6% were female. Overall, the team found that 86/188 (45.7%) patients with liver disease were HLA DQ2/8 positive, 39/73 (53.4%) with functional upper GI diseases and 19/41 (46.3%) with organic upper GI diseases were positive. Moreover, 38/105 (36.2%) patients with IBS and 14/36 (38.9%) with IBD were HLA DQ2/8 positive (P = 0.21). Additionally, people with functional upper GI diseases disorders had rates of DQ2/8 positivity that were nearly double those of healthy control subjects. Those with liver disease had rates of DQ2/8 positivity that were 1.3 percent higher than controls, though this rate is not statistically significant. People with IBS and IBD had a lower rates of DQ2/8 positivity compared to healthy controls. Compared to general population estimates, the percentage of individuals who were HLA DQ2/8 positive is higher in those with liver/upper functional GI disease and lower in IBS/IBD. Source: World J Gastroenterol 2013 April 28; 19(16): 2507-2513. ISSN 1007-9327 (print) ISSN 2219-2840 (online). doi:10.3748/wjg.v19.i16.2507
  17. 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.”
  18. Celiac.com 03/01/2010 - Common autoimmune disorders often coexist in the same subjects, and to cluster in families. A research team recently set out to quantify the risk of diagnosis of coexisting autoimmune diseases in more than 3000 index cases with clinically proven Graves' disease or Hashimoto's thyroiditis. The research team included Kristien Boelaert, PhD, Paul R. Newbya, Matthew J. Simmonds, PhD, Roger L. Holder, Jacqueline D. Carr-Smith, Joanne M. Heward, PhD, Nilusha Manjia, Amit Allahabadia, MD, Mary Armitage, DM, Krishna V. Chatterjee, PhD, John H. Lazarus, MD, Simon H. Pearce, PhD, Bijay Vaidya, PhD, Stephen C. Gough, PhD, and Jayne A. Franklyn, PhD. To establish the prevalence of coexisting autoimmune disorders, the team conducted a cross-sectional multi-center study of 3286 Caucasian subjects from UK hospital thyroid clinics. 2791 of those had Graves' disease, 495 had Hashimoto's thyroiditis. The team used a comprehensive questionnaire to obtain complete personal and parental history for each subject, including information on common autoimmune disorders, and parental history of hyperthyroidism or hypothyroidism. The frequency of other autoimmune disorders was 9.67% for patients with Graves' disease and 14.3% for those with Hashimoto's thyroiditis index cases (P=.005). Rheumatoid arthritis was the most common coexisting autoimmune disorder, striking 3.15% of patients with Graves' disease, and 4.24% of Hashimoto's thyroiditis cases. However, both conditions carried substantially higher relative risks for nearly all other autoimmune diseases (>10 for pernicious anemia, systemic lupus erythematosus, Addison's disease, celiac disease, and vitiligo). Cases of Graves' disease showed relative “clustering” among index subjects with parental hyperthyroidism, while cases of Hashimoto's thyroiditis showed relative “clustering” among index subjects with parental hypothyroidism. Relative risks for most other coexisting autoimmune disorders were markedly increased among parents of index cases. This study is one of the largest so far to quantify the risk of diagnosis of coexisting autoimmune diseases among more than 3000 index cases with clinically proven Graves' disease or Hashimoto's thyroiditis. These results emphasize the the importance of screening for other autoimmune diagnoses when patients with autoimmune thyroid disease show new or nonspecific symptoms. Source: Am. J. Med. Volume 123, Issue 2, Pages 183.e1-183.e9 (February 2010)
  19. Celiac.com 08/30/2012 - Rates of autoimmune disease are on the rise, and not just in the United States, with diseases like type 1 diabetes, celiac disease and lupus being diagnosed in increasingly higher numbers. Rates of type 1 diabetes, for example, rose 23%, from 2001 to 2009, according to the American Diabetes Association, with a similar increase reported in Finland. Researchers for the Center for Disease Control have no good explanation for the surge, which is not due simply to better diagnosis. Epidemiologists in Norway have been arguing that the rising rates are are the result of a genuine "biological change of the disease," not the result of better diagnostics. They are concerned about higher rates of autoimmunity in urban areas compared to their rural counterparts. Swedish and German researchers concur that enhanced diagnostics alone cannot explain the current rise in MS. Meanwhile, celiac disease also seems to be on the rise in the United States, with recent population-based data suggest a sharp increase in rates over the last several decades. As science has helped eliminate worms from our bodies, once a common intestinal parasite, the incidence of inflammatory bowel disease (IBD) has gone from 1 in 10,000 people to one in 200. Deaths and complications from lupus are also on the rise. According to a new study published in the journal Arthritis & Rheumatism, there was a significant increase in end-stage renal disease in young people over the period from 1995 to 2006. Of those with the condition, half were African American. In fact, blacks suffer end-stage renal disease at rates six to seven times greater than whites. Dr. Frederick Miller of the National Institute of Environmental Health Sciences agrees with Ladd. He also believes that the surge in autoimmune disease diagnosis likely has an environmental component. So, what does all this mean? At the moment, there is no clear answer. Numerous researchers are busy studying the more than 80 different types of autoimmune disease, and struggling to find causes and develop treatments. According to Dr. Miller, research offers the best way to fight rising rates of autoimmune disease, by helping to understand the genetic and environmental risk factors. This will help doctors spot those at risk for developing any given disease after certain environmental exposures, and perhaps to minimize those exposures and prevent the disease from developing in the first place. In the mean time, people with celiac disease and other autoimmune conditions can only continue their own treatments, and perhaps find some small solace in knowing that they are not alone, and that science is working to provide answers. Source: American Autoimmune Related Diseases Association (AARDA)
  20. Among celiacs and their relatives, there appears to be a higher incidence of other disorders related to the immune system. A partial listing of these includes insulin dependent diabetes mellitus (type I), Graves disease, Addisons disease, scleroderma, chronic active hepatitis, myasthenia gravis, systemic lupus erythematosus, and Sjogrens syndrome. In addition, a gluten-free diet appears to have helped some individuals with autism, chronic fatigue syndrome (myalgic encephalomyelitis or ME, PVS, post viral fatigue syndrome or PVFS), attention deficit disorder (ADD), and ADHD; though it is by no means a cure for any of these. For more information on this topic visit the Related Disorders page.
  21. Celiac.com 06/08/2012 - In a new study, researchers at Brigham and Women's Hospital (BWH) addressed whether the genetic risk of the most common medical conditions, including celiac disease, stems from many rare mutations that each confer a high degree of risk in various people, or from common differences throughout the genome that modestly influence risk. They used data and new analysis tools to assess new methods to better understand gene mutations for celiac and three other diseases, rheumatoid arthritis, coronary artery disease and myocardial infarction (heart attack); and type 2 diabetes. The researchers developed a new statistical method that used what is called "polygenic risk score analysis," to estimate the heritable genetic markers of these diseases that is explained by common differences across the genome. The method makes use of data from earlier genome-wide association studies, or GWAS, an approach used to scan DNA samples for common genetic markers seen throughout the population—called SNPs (single nucleotide polymorphisms). For rheumatoid arthritis, the team used computer simulations to show that the underlying genetic risk is largely due to many common alleles rather than rare mutations. They observed similar results for celiac disease (43 percent), myocardial infarction (48 percent) and type 2 diabetes (49 percent). "What is remarkable," says senior author Robert Plenge, MD, PhD, BWH director of Genetics and Genomics in the Division of Rheumatology, Immunology and Allergy, "is that our statistical model was broadly applicable to several common diseases, not just rheumatoid arthritis...Our study provides a clear strategy for discovering additional risk alleles for these and likely many other common diseases." According to the researchers, these methods can be applied to other genome-wide datasets (e.g., GWAS or whole genome sequencing) to estimate the degree to which there is a genetic component. Source: Nature Genetics 44, 483–489 (2012) doi:10.1038/ng.2232
  22. Celiac.com 12/29/2011 - About one in 100 people in America has celiac disease, while about one in four of those will develop dermatitis herpetiformis Duhring, which occurs when celiac disease manifests cutaneously, in the skin. Dermatitis herpetiformis Duhring is uncommon in children, with only 5% of cases appearing in children younger than 7 years. Most often, it presents in people over forty. Making a proper clinical diagnosis of dermatitis herpetiformis Duhring, also known as Duhring’s disease, is challenging, and often requires the help of skin biopsy and direct immunofluorescence. To do this, clinicians should look for antibodies against gliadin, endomysium, and transglutaminase, said Dr. Magdalene A. Dohil, of the University of California, San Diego, at a seminar sponsored by Skin Disease Education Foundation (SDEF). The fact that manifestations of celiac disease in the mucous and skin may point to Duhring's disease was one of the more important aspects of Dr. Dohil's discussion, for people with celiac disease, and those treating them. Dr. Dohil noted that, at some point during the course of their disease, more than seven in ten people (74%) with celiac disease will have some type of skin manifestation. Most often, this skin manifestation occurs in the form of xerosis, which often triggers pruritus. Mucosal manifestations occur in 27% of patients, especially in patients with longer history of celiac disease. Dr. Dohil pointed out numerous diseases, disorders, syndromes, and structural epithelial defects with clear connections between skin and gut. For example, 60%-82% people with asymptomatic inflammatory bowel disease present with mucocutaneous findings that include skin tags, fistulas, fissures, or abscesses in the perianal and genital areas. In 25%-30% of cases, these will precede GI complaints. Dr. Dohil said. Overall, 6%-20% of all patients with inflammatory bowel disease develop oral lesions, but up to 80% of pediatric cases with Crohn’s disease and 41% with ulcerative colitis develop such lesions. Source: http://www.skinandallergynews.com/news/medical-dermatology/single-article/diseases-of-the-gut-may-present-cutaneously/57197f4ef7.html
  23. Scand J Gastroenterol. 2005 Apr;40(4):437-43. Celiac.com 07/28/2005 - In an effort to determine whether gluten exposure in those with celiac disease can cause additional autoimmune diseases, Finnish researchers evaluated the frequency of autoimmune disorders in 703 adults and children with celiac disease, and compared them with 299 controls (normal duodenal histology). For each person in the study the researchers assessed the effect of age at the end of follow-up, age at diagnosis; actual gluten exposure time; and the gender and diagnostic delay time. They then determined autoimmune disease incidence figures that were expressed as a dependent variable via logistic regression analysis (per 10,000 person-years). The researchers found that the celiac disease group had a significantly higher prevalence of additional autoimmune diseases that was not affected by exposure to gluten. Additional Comments on this Study by Roy Jamron: Autoimmune disease has a high prevalence in celiacs. The following study concludes that the duration of gluten exposure in celiacs is not a significant factor in the risk of developing autoimmune disease. One diagnosed late in life with celiac disease does not appear to be at greater risk for developing autoimmune disease. This seems counter-intuitive, but there may be a good explanation for this result. Studies in the UK and Italy have demonstrated that the prevalence of celiac disease in young children is essentially the same as in adults, meaning celiac disease begins in infancy. Infancy is the critical time period for the development of the immune system. Gluten exposure and the onset of celiac disease symptoms early in life, therefore, have a much greater and more important impact on the immune system and its development than exposure to gluten later in life. Malabsorption during infancy and early childhood can also adversely affect the crucial function of the thymus, T cell production, and T cell repertoire. So the stage is set early in life rather than later for increased risk of autoimmune disease. The timing of gluten exposure in life seems to be more critical to autoimmune disease risk rather than the overall lifetime duration of gluten exposure. It is, therefore, extremely important to diagnose celiac disease and initiate a gluten-free diet as soon as possible during infancy and young childhood to lower the risk of autoimmune disease later in life.
  24. Celiac.com 07/16/2010 - Advances in genetic science are allowing researchers to look more deeply into the genetic causes of auto-immune diseases, including celiac disease. One recent study showed that a particular variation, called the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in European Caucasian populations. At the conclusion of that study, though, there was still no comparable study of shared autoimmunity with CD226 in non-European populations. An international research team set out to investigate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations. The team included Amit K. Maiti, Xana Kim-Howard, Swapan K. Nath, Celi Sun, and Parvathi Viswanathan; Laura Guillén and Alejandra C. Cherñavsky; Xiaoxia Qian and Nan Shen; Adriana Rojas-Villarraga and Juan-Manuel Anaya; Carlos Cañas, Gabriel J. Tobón; and Koichi Matsuda They are affiliated variously with the Genetic Epidemiology Unit of the Arthritis and Immunology Research Program at the Oklahoma Medical Research Foundation in Oklahoma City, OK, USA, the Immunogenetic Laboratory of the Hospital de Clínicas José de San Martín at the Universidad de Buenos Aires in Buenos Aires, Argentina, the Shanghai Institute of Rheumatology at Renji Hospital, JiaoTong University School of Medicine in Shanghai, P.R. China, the Centre for Autoimmune Diseases Research (CREA) at the Universidad del Rosario-Corporación para Investigaciones Biológicas in Bogota, Colombia, the Rheumatology Unit of the Fundación Valle del Lili in Cali, Colombia and the Laboratory of Molecular Medicine at the Human Genome Centre of the Institute of Medical Science at the University of Tokyo, Japan. To evaluate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations, the team compared case–control association between rs763361 and celiac disease (CED) samples from Argentina; SLE, RA, type-1 diabetes (T1D) and primary SS (pSS) from Colombia; and SLE samples from China and Japan. They then genotyped rs763361 and used 2-test to evaluate its genetic association with multiple auto-immune disorders. For each association, the team calculated odds ratio (OR) and 95% CI. Their results show clearly that rs763361 shares a significant association with celiac disease in Argentina (P = 0.0009, OR = 1.60). They also noted indications of possible association with Chinese SLE (P = 0.01, OR = 1.19), RA (P = 0.047, OR = 1.25), SLE (P = 0.0899, OR = 1.24) and pSS (P = 0.09, OR = 1.33) in Colombians. The team then conducted meta-analyses for SLE, using their three populations, and T1D, using their population together with three published populations. Those analyses showed a significant association with rs763361, P = 0.009 (OR = 1.16) and P = 1.1.46 x 10–9 (OR = 1.14), respectively. The team's results show clearly that the coding variation rs763361 in the CD226 gene is associated with multiple auto-immune disorders in non-European populations. Taken together, these studies show that the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in both European Caucasian and non-European populations. Source: Rheumatology 2010 49(7):1239-1244; doi:10.1093/rheumatology/kep470
  25. Celiac.com 02/26/2010 - Data increasingly supports an association between rs6822844 at the IL2-IL21 region and multiple autoimmune diseases in individuals of European descent. A number of autoimmune diseases share susceptibility genes, pointing to similar molecular mechanisms. A team of researchers recently set out to assess evidence for a general susceptibility locus by looking for association between rs6822844 at the Il2-Il21 region and numerous autoimmune diseases. The research team included Amit K. Maiti, Xana Kim-Howard, Parvathi Viswanathan, Laura Guillén, Adriana Rojas-Villarraga, Harshal Deshmukh, Haner Direskeneli, Güher Saruhan-Direskeneli, Carlos Cañas, Gabriel J. Tobön, Amr H. Sawalha, Alejandra C. Cherñavsky, Juan-Manuel Anaya, and Swapan K. Nath Their joint effort was underwritten by grants from the National Institutes of Health (NIH - Grant Number: 5R01-AI-063622, P20-RR-020143), Colciencias (Grant Number: 2213-04-16484), Rosario University School of Medicine, and the Colombian Association of Rheumatology. The goal of the study was to replicate the association between rs6822844 and 6 different immune-mediated diseases in non-European populations, and to conduct disease-specific and overall meta-analyses using data from previously published studies. The team evaluated case-control associations between rs6822844 and celiac disease in subjects from Argentina; rheumatoid arthritis, type 1 diabetes mellitus, primary Sjögren's syndrome, and systemic lupus erythematosus in subjects from Colombia; and Behçet's disease in subjects from Turkey. They compared allele and gene distribution between cases and controls. They conducted meta-analyses using data from the present study and previous studies. The team found significant associations of rs6822844 with systemic lupus erythematosus (P = 0.008), type 1 diabetes mellitus (P = 0.014), rheumatoid arthritis (P = 0.019), and primary Sjögren's syndrome (P = 0.033) but not with Behçet's disease (P = 0.34) or celiac disease (P = 0.98). Cases and controls from Argentina and Colombia showed little evidence of population differentiation (FST = 0.01), which suggests that association was not influenced by population substructure. Disease-specific meta-analysis shows strong association for rheumatoid arthritis (Pmeta = 3.61 × 10-6), inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) (Pmeta = 3.48 × 10-12), type 1 diabetes mellitus (Pmeta = 5.33 × 10-5), and celiac disease (Pmeta = 5.30 × 10-3). Total meta-analysis across all autoimmune diseases supports association with rs6822844 (23 data sets; Pmeta = 2.61 × 10-25, odds ratio 0.73, with 95% confidence interval 0.69-0.78). The team concludes that an association exists between rs6822844 and multiple autoimmune diseases in non-European populations. Meta-analysis provides strong confirmation for strong association across multiple autoimmune diseases in populations of both European and non-European ancestry. Arthritis & Rheumatism; Volume 62 Issue 2, Pages 323 - 329 http://www3.interscience.wiley.com/journal/123266977/abstract?CRETRY=1&SRETRY=0
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