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Found 25 results

  1. Celiac.com 04/18/2019 - Cases of type 1 diabetes have been on the rise in western countries, which suggests an environmental role in the development of the disease. Still, after decades of study, researchers have yet to nail down the factors driving the increase, and so they have no clear way to prevent new cases. A potential association that deserves closer scrutiny is one of environmental causes as a driver of diabetes, including dietary factors, such as gluten. At the moment, there is a great deal of focus on maternal and childhood dietary factors. To remedy the current impasse, researchers Maija E Miettinen and Suvi M Virtanen of the National Institute for Health and Welfare in Helsinki, Finland, cite the need for comprehensive prospective studies with carefully collected data to define and confirm associations. Only with such data can effective solutions be devised and tested. In a linked article, also in the BMJ, Antvorskov and colleagues investigated the association between maternal gluten intake during pregnancy and risk of type 1 diabetes in offspring. The authors analyzed data from the large Danish National Birth Cohort, covering about a third of all pregnancies in Denmark during the recruitment period of 1996-2002, in which more than 70,000 pregnant women reported their diet with a food frequency questionnaire. That analysis revealed that risk of type 1 diabetes in offspring increased proportionally with maternal gluten intake during pregnancy per 10 grams per day increase of gluten. Compared to women with the lowest gluten intake of under 7 grams per day, those with the highest gluten intake, who consumed 20 or more grams a day, had double the risk for type 1 diabetes development in their children. Basically, higher gluten intake during pregnancy meant higher diabetes risk for the children. However, that’s one study with good data. The authors stress the urgency to understand what is driving alarmingly fast-rising diabetes rates. People’s health, well-being, and lives are at stake. For that, further study is needed, and soon. Read more at BMJ 2018; 362
  2. Celiac.com 03/25/2019 - Some researchers have suspected that myelin proteins may be involved in multiple sclerosis (MS). A recent report in Science and Translational Medicine, suggests that additional non-myelin-related protein may also play a role. Researchers examined protein samples from the brains of 31 people who had died from suspected or confirmed MS. They found that T cells from 12 people reacted to the enzyme guanosine diphosphate-L-fucose synthase, or GDP-L-fucose-synthase. The enzyme usually helps to process sugars that are crucial to cell function and communication, including the function and communication of neurons. Researcher Dr Roland Martin, from the University Hospital of Zurich, Switzerland, has helped to figure out which myelin proteins and peptides come under attack in MS, and which cells and immune molecules do the attacking. Paper coauthor Mireia Sospedra, of University Hospital of Zurich, suggests that “other auto-antigens might be involved in initiating the disease." She believes that the attack on this newly identified auto-antigen triggers tissue damage that exposes other myelin proteins that are likely targets for attack. Sospedra suspects that some variations in myelin protein structure might be susceptible to immune attack, and that genetic variation in immune cells might influence the body’s response to a given infection. She suggests that the offending antigens may differ between individuals, as the structure of our molecular machinery is genetically determined. Northwestern University immunology professor Stephen Miller, who did not work on this research, but has worked with Dr. Martin in the past, suggests that there’s likely not just “one particular virus or bacteria or environmental factor that triggers MS in every patient. There are probably many things that can trigger an autoimmune reaction against a particular infection," he says. "But the more antigens we identify that can contribute to the disease, the better." Researchers have pointed out that numerous autoimmune diseases seem to cluster in certain gene sequences. Multiple gene areas seem to correlate with numerous autoimmune conditions. Prior comprehensive genetic association studies have found 90 genetic areas associated with T1DM, celiac disease, multiple sclerosis, and/or rheumatoid arthritis. Celiac disease and MS sufferers share some things in common, including a tendency to develop rosacea. Rosacea is a common inflammatory skin condition that shares the same genetic risk location as autoimmune diseases such as type 1 diabetes mellitus (T1DM) and celiac disease. The connections between multiple sclerosis and celiac disease is a common topic of discussions on many forums. Read more at: medscape.com
  3. Celiac.com 12/23/2009 - One of the main and largely unrecognized health problems facing the Western world and people on diets of highly refined, processed and starchy foods, which are often low in or devoid of dietary fiber, is that of constipation. This is a particular issue with Celiacs where the gluten-free flours they use are largely starch based and often low in protein and dietary fiber. Unfortunately, we live in a world where it is often considered normal and acceptable to empty the bowels perhaps 2 -3 times a week, rather than the more desirable 2 – 3 times per day. What are the difficulties in this you may ask? Firstly the lymphatic system drains through the bowels and if the bowels are clogged and constipated the lymph system, which is a major part of the human body’s excretory system, does not function properly. This means that instead of continuously draining, as it should, the lymph system becomes a long term storage system for the body’s waste matter when confronted with a constipated digestive system, which provides a home and breeding ground for bacteria and perhaps becoming a precursor for infection and many chronic health problems including cancer. Constipation also leads to dry and hard stools which are difficult to pass and may contribute to the development of hemorrhoids or “piles”, as they are commonly known, and possibly longer term issues leading to colon and rectal cancers. Constipation also leads to greatly increased and undesirable residence time for waste matter in the body which solidifies and putrifies in the process possibly contributing to various forms of gastric and bowel cancer. Other parts of the body’s excretory systems including the sinuses; the lungs and the skin, the body’s largest excretory organ, can also become overloaded if the bowels and lymph system are not functioning correctly. Sinus overload can be reflected in having heavy mucus discharge via a cold or the flu, glandular fever and in nasal, eye and ear infections, from infected, stored mucus. Lung overload may be reflected by mucus discharges associated with a cold or influenza, pleurisy, pneumonia and various other forms of mucus containing fluid which may also become infected by hostile germs and bacteria. Skin overload can be reflected in rashes, eczema, psoriasis, measles, hives, shingles, chicken pox and the like: all symptoms of an acidic body condition and an overloaded elimination or excretory system. If the body cannot dispose of its waste matter by other means, it often resorts to throwing the waste matter out through the skin. Chronic fatigue syndrome is possibly another manifestation of this same issue. Sadly, the vast majority of the human race, end their lives with all of their excretory organs, lungs and blood circulatory systems overloaded with stored waste matter with significantly shortened life expectancy and diminished quality of life as a result. None of the latter problems have anything to do with or need to be part of the aging process. For example, I have a very spry, mentally alert 90 year old father, A blood group type, who still works on a daily basis, drives a car, is totally medication free, has no prostrate, heart or cancer problems and has a good head of hair; clear skin, eyes, arteries and lungs. He should be the model of normality. Sadly, he is not typical. How and why? A fairly spartan diet based mainly upon fruit and vegetables with very sparing consumption of meat, dairy products, fried foods, salt, sugar, animal fats, cakes, lollies, convenience foods and alcohol. He has never smoked. He drinks mainly water and fresh juice with fresh citrus juice first thing every morning. He eats slowly and chews his food thoroughly. He never overeats. He remains curious, physically active and engaged with the world. My paternal grandmother, Daisy, was still walking around without the aid of a stick at age 106 – 107 with all her faculties and complaining about all the other “old chooks” in the nursing home on their walking frames etc: many of them 40 years her junior. Adequate sleep and minimizing stress is also critical to maintaining good health. Most of the chronic health problems facing our community are mainly unnecessary consequences of over indulgence and the accumulations of a lifetime’s bad habits and, in most instances, with a little care these habits are largely avoidable. Fevers and colds are natural processes. They are part of the body’s armoury of natural defense mechanisms for dealing with a cleansing crisis. All too often these and other natural processes are medically suppressed rather than being allowed to run their natural course. They are one of the body’s ways of saying it is overloaded with waste matter and that it needs a chance to deal with this problem. Antibiotics, taken orally, also tend to indiscriminately kill both good and bad gut bacteria often inadvertently disrupting the long term performance of the digestive system to the long term detriment of the patient’s health especially when no restorative probiotics are prescribed as part of the process: which is mainly the case. How do we avoid these problems? By a host of small, simple and easily implemented strategies over a lifetime: by a little self discipline and the formulation of good eating and nutritional habits which enable our bodies to function effectively, naturally, healthily and sustainably for a lifetime, as they are intended to. Ill health is not our natural state but one we impose upon ourselves, or otherwise, through our dietary and lifestyle choices, both individually and collectively.
  4. Celiac.com 04/10/2017 - Fibromyalgia syndrome is a debilitating condition of unknown cause, and only treatment approaches at present offer only limited relief from symptoms. Some fibromyalgia sufferers seem to benefit from a gluten-free diet, but there's not a great amount of data on the benefits of a gluten-free diet in fibromyalgia sufferers who do not have celiac disease. A team of researchers recently set out to describe 20 selected patients with fibromyalgia, but without celiac disease, whose symptoms improved when they followed a gluten-free diet. The research team included Carlos Isasi, Isabel Colmenero, Fernando Casco, Eva Tejerina, Natalia Fernandez, José I. Serrano-Vela, Maria J. Castro, and Luis F. Villa. They are variously associated with the Department of Rheumatology, Hospital Puerta de Hierro, Majadahonda Madrid, Spain; the Department of Pathology, Hospital Infantil Niño Jesús, Madrid, Spain; the Department of Pathology, Hospital Puerta de Hierro, Majadahonda Madrid, Spain; the Department of Gastroenterology, Hospital Puerta de Hierro, Majadahonda Madrid, Spain; the Celiac and Gluten Sensitive patients Association of Madrid, Madrid, Spain; and with the Department of Immunology, Hospital Doce de Octubre, Madrid, Spain. What researchers now call non-celiac gluten-sensitivity is a daily common, yet treatable condition, with a range of symptoms that dovetail with many symptoms of fibromyalgia, including chronic musculoskeletal pain, asthenia, and irritable bowel syndrome. All patients underwent anti-transglutaminase assay, duodenal biopsy, and HLA typing. To rule out celiac disease in their test subjects, the research team used negative anti-transglutaminase assay results, together with the absence of villous atrophy in the duodenal biopsy. All patients showed signs of intraepithelial lymphocytosis with no villous atrophy. The doctors defined a positive clinical response as the achievement of at least one of the following: remission of fibromyalgia-associated pain, return to work, return to normal life, or the discontinuation of opioids. Doctors followed on the patients from 5 to 31 months, with a follow-up period of 16 months, on average. The level of widespread chronic pain improved dramatically for all patients; for 15 patients, chronic widespread pain was no longer present, indicating remission of FM. Fifteen patients returned to work or normal life. In three patients who had been previously treated in pain units with opioids, these drugs were discontinued. Fatigue, gastrointestinal symptoms, migraine, and depression also improved together with pain. Patients #2 and #3, both with oral aphthae, went into complete remission for psoriatic arthritis and undifferentiated spondyloarthritis. These results strengthen the idea that non-celiac gluten sensitivity may play a key role in the development of fibromyalgia syndrome. Source: Rheumatol Int. 2014; 34(11): 1607–1612. Published online 2014 Apr 12. doi: 10.1007/s00296-014-2990-6
  5. Celiac.com 04/17/2017 - A team of researchers recently set out to test this hypothesis and to gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens. To do so, they developed a viral infection model that makes use of two reovirus strains that infect the intestine, but which differ in their immunopathological outcomes. The research team included Romain Bouziat, Reinhard Hinterleitner, Judy J. Brown, Jennifer E. Stencel-Baerenwald, Mine Ikizler, Toufic Mayassi, Marlies Meisel, Sangman M. Kim, Valentina Discepolo, Andrea J. Pruijssers, Jordan D. Ernest, Jason A. Iskarpatyoti, Léa M. M. Costes, Ian Lawrence, Brad A. Palanski, Mukund Varma, Matthew A. Zurenski, Solomiia Khomandiak, Nicole McAllister, Pavithra Aravamudhan, Karl W. Boehme, Fengling Hu, Janneke N. Samsom, Hans-Christian Reinecker, Sonia S. Kupfer, Stefano Guandalini, Carol E. Semrad, Valérie Abadie, Chaitan Khosla, Luis B. Barreiro, Ramnik J. Xavier, Aylwin Ng, Terence S. Dermody, and Bana Jabri. Reoviruses usually infect humans and mice without overt physical symptoms. Prior research by Bouziat et al., has shown that immune responses to two gut-infecting reoviruses take different paths in mice, as noted in the Perspective by Verdu and Caminero. Both reoviruses triggered protective immune responses. However, when one of the reoviruses occurred in the presence of a dietary antigen, such as gluten or ovalbumin, tolerance to the dietary antigen disappeared. This was because this strain blocked the formation of tolerogenic T cells. Instead, it promoted T helper 1 immunity to the dietary antigen through interferon regulatory factor 1 signaling. Moreover, celiac disease patients also showed elevated levels of antibodies against reovirus. Reovirus is an avirulent pathogen that elicits protective immunity, but these researcher have shown that it can also cause a disruption of intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion, and promoting TH1 immunity to dietary antigen. TH1 immunity to dietary antigen depended on interferon regulatory factor 1, and was unconnected to suppression of pTreg conversion, which was mediated by type-1 interferon. This study provides important scientific support for the idea that this seemingly mild reovirus plays a major role in the development of celiac disease. Clearly further study is needed to determine the exact nature of the role of reovirus in celiac disease, and to determine if these connections might prompt any changes in celiac diagnosis and treatment. Source: Science 07 Apr 2017: Vol. 36, Issue 6333, pp. 44-50. DOI: 10.1126/science.aah5298 The researchers are variously affiliated with the Department of Medicine, the Department of Pathology, and the Committee on Immunology at the University of Chicago in Chicago, IL, USA; the Department of Pathology, Microbiology, and Immunology, the Department of Pediatrics, and the Elizabeth B. Lamb Center for Pediatric Research at Vanderbilt University Medical Center in Nashville, TN, USA; the Department of Translational Medical Sciences, Section of Pediatrics, University of Naples Federico II, and CeInGe–Biotecnologie Avanzate, Naples, Italy; the Laboratory of Pediatrics, Division of Gastroenterology and Nutrition, Erasmus University Medical Center Rotterdam-Sophia Children’s Hospital, Rotterdam, Netherlands; the Department of Chemistry, Stanford University, Stanford, CA, USA; the Division of Gastroenterology, Department of Medicine, Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Broad Institute of MIT and Harvard University, Cambridge, MA, USA; the University of Chicago Celiac Disease Center at the University of Chicago, Chicago, IL, USA; the Section of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Chicago, Chicago, IL, USA; the Department of Microbiology, Infectiology, and Immunology, University of Montreal, and the Centre Hospitalier Universitaire (CHU) Sainte-Justine Research Center, Montreal, Quebec, Canada; the Department of Chemical Engineering, Stanford University, Stanford, CA, USA; the Stanford ChEM-H, Stanford University, Stanford, California, USA; the Department of Genetics, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada; the Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; and the Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
  6. I recently tested positive for Yersinia Enterocolitica. My doctor mentioned there is a correlation between this and the onset of autoimmune diseases. Has anyone had this? And if so, how did you treat?
  7. Celiac.com 01/02/2017 - New research shows that a group of proteins in wheat, called ATIs, may be responsible for activating inflammation in such disorders as celiac disease, multiple sclerosis, asthma, and rheumatoid arthritis. Scientists also believe that the proteins may promote the development of non-celiac gluten sensitivity. The findings were presented at UEG Week 2016 in Vienna in Vienna, Austria, a meeting organized by United European Gastroenterology for specialists to communicate the latest research in digestive and liver diseases. One group of proteins found in wheat - amylase-trypsin inhibitors (ATIs) - has been shown to trigger an immune response in the gut that can spread to other tissues in the body. ATIs are plant-derived proteins that inhibit enzymes of common parasites - such as mealworms and mealybugs - in wheat. Interestingly, ATIs also have an important role in metabolic processes that occur during seed development. The finding that ATIs may promote inflammation in the and beyond the gut, is a major step forward in understanding the mechanics of celiac disease and/or gluten-intolerance. Stay tuned for more news on this and other breaking stories in celiac disease research. Read more at MedicalNewsToday.com.
  8. Celiac.com 08/24/2016 - Although serological tests are useful for identifying celiac disease, it is well known that a small minority of celiacs are seronegative, and show no blood markers for celiac disease. A team of researchers wanted to define the prevalence and features of seronegative compared to seropositive celiac disease, and to establish whether celiac disease is a common cause of seronegative villous atrophy. The research team included U Volta, G Caio, E Boschetti, F Giancola, KJ Rhoden, E Ruggeri, P Paterini, and R De Giorgio. They are all affiliated with the Department of Medical and Surgical Sciences, University of Bologna, St. Orsola-Malpighi Hospital, Italy. They looked at clinical, histological and laboratory findings from 810 celiac disease diagnoses, and retrospectively characterized seronegative patients. Of the original 810 patients, they found fourteen patients who fulfilled diagnostic criteria for seronegative celiac disease, which were antibody negativity, villous atrophy, HLA-DQ2/-DQ8 positivity and clinical/histological improvement after gluten free diet. Their review showed that, compared to seropositive patients, seronegative celiac patients showed a significantly higher median age at diagnosis and a higher prevalence of classical phenotype, such as malabsorption, along with autoimmune disorders and severe villous atrophy. The most common diagnosis in the 31 cases with seronegative flat mucosa was celiac disease at 45%, along with Giardiasis at 20%, common variable immunodeficiency at 16%, and autoimmune enteropathy at 10%. Although rare, seronegative celiac disease is the most common cause of seronegative villous atrophy with a high median age at diagnosis; a close association with malabsorption and flat mucosa; and a high prevalence of autoimmune disorders. Physicians treating seronegative villous atrophy should consider seronegative celiac disease as a possibility. Source: Dig Liver Dis. 2016 Jun 11. pii: S1590-8658(16)30460-1. doi: 10.1016/j.dld.2016.05.024.
  9. Years before I developed full gluten intolerance (probably celiac) while I could enjoy many wheat products, I would get odd, unpleasant reactions to Ritz crackers and Cheerios. I did not think much of it and generally just avoided those products. I periodically retried them thinking it was a temporary problem with the product. I subsequently developed the same problem with any wheat and gluten product. Has anyone else noticed a similar prodrome to any food products?
  10. The average gluten-containing diet contains roughly 10-40 grams of gluten per day. This figure is based on the amounts of gluten in your average slice of whole wheat bread, which contains around 4.8 grams of gluten (10% gluten by weight), and the amount of gluten in a serving of pasta, which is roughly 6.4 grams of gluten (11% gluten by weight). The smallest amount of gluten which has been shown by a biopsy to cause damage to a celiac is 0.1 gram per day (Catassi et al.). This is approximately the amount of gluten contained in 1/48th of a slice of bread! The biopsies in this study showed an increase in intraepithelial lymphocyte count, one of the earliest signs of damage. The challenge was on 10 patients (children) for 28 days each. Four of the patients showed an increase in IgA antigliadin antibodies. The intestinal permeability test remained normal.
  11. 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.
  12. Celiac.com 01/18/2016 - How come only 2% to 5% of genetically susceptible individuals develop celiac disease? Researchers attempting to answer that question have turned their focus to environmental factors, including gut microorganisms, that may contribute to the development of celiac disease. In a recent study, published in The American Journal of Pathology, researchers using a humanized mouse model of gluten sensitivity found that the gut microbiome can play an important role in the body's response to gluten. Their data show that the rise in overall celiac disease rates over the last 50 years may be driven, at least partly, by variations in gut microbiota. If this proves to be true, then doctors may be able to craft "specific microbiota-based therapies" that "aid in the prevention or treatment of celiac disease in subjects with moderate genetic risk," says lead investigator Elena F. Verdu, MD, PhD, Associate Professor, Division of Gastroenterology, Department of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON (Canada). For their study, the team used mice that express the human DQ8 gene, which makes them genetically susceptible to inflammatory responses to gluten, researchers compared immune responses and pathology in the guts of mice that differed in their gut microorganisms. The three groups included germ-free mice, clean–specific-pathogen-free (SPF) mice with microbiota free of opportunistic pathogens and Proteobacteria, and conventional SPF mice that were colonized with a mixture of microorganisms including opportunistic pathogens and Proteobacteria. For example, the microbial profile of conventional SPF mice included Staphylococcus, Streptococcus, and Helicobacter, while the clean SPF had none. Researchers already know that growth and activation of intraepithelial lymphocytes (IELs) is an early sign of celiac disease. This research team saw that gluten treatment led to increased IEL counts in germ-free mice, but not in clean SPF mice. The gluten-induced IEL response in germ-free mice was accompanied by increased cell death in the cells lining the gastrointestinal tract (enterocytes), as well as anatomical changes in the villi lining the small intestine. The germ-free mice also developed antibodies to a component of gluten, known as gliadin, and displayed pro-inflammatory gliadin-specific T-cell responses. A non-gluten protein, zein, did not affect IEL counts, indicating that the response was gluten specific. Meanwhile, the mice colonized with limited opportunistic bacteria (clean SPF), did not develop gluten-induced pathology, compared to germ-free mice or conventional SPF mice with a more diverse microbiota. Interestingly, this protection was suppressed when clean SPF mice were supplemented with an enteroadherent E. coli isolated from a patient with celiac disease. These results are preliminary, and other researchers stress that the specific role of Proteobacteria in celiac disease should not be over interpreted. In an accompanying Commentary, Robin G. Lorenz, MD, PhD, of the Department of Pathology at the University of Alabama at Birmingham, writes that these findings "implicate opportunistic pathogens belonging to the Proteobacteria phylum in celiac disease; however, this does not indicate that Proteobacteria cause celiac disease." Instead, Dr. Lorenz suggests, there may be numerous possible avenues by which Proteobacteria enhance the exposure and immune response to gluten or gliadin. So, the takeaway here is that, while these early results are highly interesting and certainly merit follow-up, it's way too early to say that certain types of gut bacteria may be driving celiac disease, and any types of bacterial treatments that might prevent celiac disease from developing are just the stuff of imagination. Still, this is an important discovery that might pave the way for exactly such types of therapy in the future, so stay tuned. Source: The American Journal of Pathology
  13. Celiac.com 10/02/2014 - Most people have heard about kidney stones, or gall stones, due to calcium build up. Others may know that calcium deposits can affect the heart, and even the brain. However, until now, it was not known that, in certain cases, celiac disease can trigger calcification in the brain. Doctors examining a 24-year-old Brazilian man with a history of recurrent headaches revealed a rare condition known as the CEC syndrome, a combination of celiac disease, epilepsy, and cerebral calcification, commonly referred to as ‘brain stones.’ The man had been treated for migraine headaches over a period of 10 years, with little response. Standard blood tests showed a mildly decreased folate level (2.2 ng per milliliter [5.0 nmol per liter]; compared to a reference range of 3.1 to 17.5 ng per milliliter [7.0 to 39.0 nmol per liter]). A computed tomographic scan of his brain showed bilateral occipital calcification, or ‘brain stones.’ Laboratory testing showed normal cerebrospinal fluid and elevated levels of serum IgA antitransglutaminase antibodies (45 U per milliliter). The man received an endoscopy, and his jejunal-biopsy specimen showed crypt hyperplasia, villous atrophy of the jejunal mucosa, and an increased number of intraepithelial lymphocytes; all classic indications of celiac disease. Doctors started treatment with a gluten-free diet, folic acid supplementation, and carbamazepine, and the patient's symptoms disappeared and his condition improved. In this case, there was no indication that the man suffered from epilepsy. The likely culprit is folate malabsorption, because cerebral calcification has been seen in other conditions related to folate deficiency, such as treatment with methotrexate, congenital folate malabsorption, and the Sturge–Weber syndrome. So, physicians treating celiac patients with low folate levels may want to keep an eye out for any indications of cerebral calcification, and to make sure that patients receive appropriate supplemental folate. Source: New England Journal of Medicine
  14. Br J Haematol 2000;111:898-901. Celiac.com 02/15/2001 - As reported in the December issue of the British Journal of Haematology, Dr. D. J. Unsworth of Southmead Hospital in Bristol, UK, and colleagues examined 483 blood samples that were found to be anemic (hemoglobin Results: The researchers found that by screening anemic adults for celiac disease they ended up with a detection rate of 6%, compared with 0% detection of celiac disease using EDTA blood samples from 250 non-anemic blood donors. Conclusion: Celiac disease in menstruating women is under-investigated as a potential cause of iron-deficiency anemia. Celiac disease serology is easy, cheap and reliable, and the researchers recommend that all cases of anemia with an uncertain cause, including when the only cause is though to be menstruation, be tested for celiac disease-associated autoantibodies.
  15. When I was 8 years old, I attended a summer camp. My friend and I were in charge of running the spongy-floaty thing that is labeled LIFEGUARD that they always sit with. Anyways, I had the strap around my and my best friend was holding onto the spongy-floaty part. We were running and she ran faster than me. We got to concrete steps and I slowed down, but she kept on barreling down the stairs. I lost my footing and was dragged down the stairs. The top of the back of my head landed on the corner of each concrete step. We never went to the doctor because I have a high pain tolerance and wasn't telling them just how badly it hurt. We iced it, etc etc etc. About a month, not even, after that, the symptoms of my Celiac's disease started up. I have a friend who had an appendicitis and after her surgery, she was diagnosed with Celiac's because of the change in her system from the surgery. I was wondering if something similar happened with me. Did the eleven blows to my head initiate my Celiac's disease?
  16. This article originally appeared in the Spring 2011 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 06/22/2011 - Gluten intolerance among people who do not have celiac disease seems to be an increasing reality, yet scientists have not been able to find any evidence explaining it. A team of researchers in Australia noted that the question of whether gluten can contribute to gastrointestinal symptoms and/ or induce injury to the proximal small intestine had never been directly assessed. So, they set out to assess it. Their results are published in the January 11, 2011 issue of The American Journal of Gastroenterology. They conclude that “non-celiac gluten intolerance” may in fact exist, although they were unable to discern the potential mechanism. Their study population consisted of patients with irritable bowel syndrome (IBS) whose symptoms were alleviated by the elimination of gluten from their diet and who definitely did not have celiac disease, as determined by the absence of the HLA-DQ2 or HLA-DQ8 haplotypes. If patients did express these haplotypes, celiac disease was excluded by a normal duodenal biopsy while they were on a gluten containing diet. Unfortunately the authors could only find 34 patients who met these criteria, but they maintain that they could still infer a statistically robust result from their data. Participants had to have been on a gluten free diet for at least six weeks at the beginning of the study. At that point, they were given a study muffin and two slices of study bread to eat every day for six weeks. These goods were baked from gluten free mixes in a gluten free facility, but half of them had gluten added. Importantly, it was only gluten, not wheat; the carbohydrates found in wheat, which are known to elicit GI symptoms, were not included. The study was randomized, double-blind, and placebo controlled, so neither the researchers nor the participants knew who was eating the gluten. After only one week, 68% of the patients eating gluten reported more severe pain, bloating, and tiredness, and less satisfaction with their stool consistency, than the cohort who got the gluten free study muffins and bread. This remained the case over the course of the six week study; six patients eating gluten even had to withdraw from the study after the first week because their symptoms got too bad. There did not seem to be much difference between the two groups in what the authors deemed the “less relevant” symptom of nausea. Interestingly, the symptom most exacerbated by gluten was tiredness. Since tiredness is a common symptom of IBS, its induction by gluten may shed some light into a mechanism of action. Neither treatment group showed any changes from baseline in assayed biomarkers. These included celiac antibodies; fecal lactoferrin, which increases during intestinal inflammation; C-reactive protein, a sensitive marker for the systemic circulation of cytokines; and intestinal permeability. The authors suggest that perhaps their assays were not sensitive enough to detect subtle molecular changes. About half of the study participants were positive for the HLA-DQ2/8 haplotype, but there were no differences between those who were and those who were negative, either in gluten’s effect on their symptoms or in their biomarkers. This study is significant as the first demonstration that gluten may trigger gut symptoms in people who don’t have celiac disease. Subsequent work should elucidate how exactly it does so, but in the meantime, these findings have valuable clinical implications – perhaps more people with GI symptoms will be put on a gluten free diet. Source: Am. J Gastroenterol advance online publication 11 January 2011; doi:10.1038/ajg.2010.487
  17. Brain. 2003 Mar;126(Pt 3):685-91. Celiac.com 08/11/2005 – Researchers in the United Kingdom screened 224 patients with various forms of ataxia (59 with familial, 132 sporadic idiopathic, and 33 with clinically probable cerebellar variant of multiple system atrophy MSA-C) for the presence of antigliadin antibodies and found that 24% of the ataxia patients were sensitive to gluten, and 72% of them had the HLA DQ2 genetic marker. Their results were compared with those of 1,200 healthy controls. Among the familial ataxia group 8 or 59 (14%), 54 of 132 (41%) of the sporadic idiopathic group, 5 of 33 (15%) in the MSA-C group, and 149 of the 1,200 (1.24%) controls, screened positive for antigliadin antibodies. The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant. Gastrointestinal symptoms were present in only 13% of the ataxia patients. MRI testing found atrophy of the cerebellum in 79% and white matter hyperintensities in 19% of the ataxia patients, and 45% of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. The researchers conclude that gluten ataxia is the single most common cause of sporadic idiopathic ataxia, and antigliadin antibody testing is should be done immediately on everyone with symptoms of sporadic ataxia.
  18. Celiac.com 04/07/2009 - Idiopathic portal hypertension is a malady ofunknown cause, typically manifesting portal hypertension, splenomegalyand anemia secondary to hypersplenism. Recently, a team ofIranian researchers encountered the case of a a 54-year-old maleadmitted for evaluation of malaise, weight loss, abdominal swelling andedema of the lower limbs. The reporting team was made up ofdoctors Farhad Zamani, Afsaneh Amiri, Ramin Shakeri, Ali Zare, andMehdi Mohamadnejad, of the Department of Pathology, and theGastrointestinal and Liver Disease Research Center of FirouzgarHospital at the University of Medical Sciences in Tehran, and theDigestive Disease Research Center of Shariati Hospital at TehranUniversity of Medical Sciences. The patient's clinicalevaluation showed pancytopenia, large ascites, splenomegaly andesophageal anomalies associated with portal hypertension. Bloodtests and small intestinal biopsy showed the presence of celiacdisease. Patient's symptoms improved with a gluten-free diet, butimprovement was further impaired by ulcerative jejunoileitis, andintestinal T-cell lymphoma. From these results, the researchersconclude that celiac disease, by means of a heightened immune responsein the splenoportal axis, can lead to the development of idiopathicportal hypertension in susceptible affected patients. J Med Case Reports. 2009; 3: 68.
  19. This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter. Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not. If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease. Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5] Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory. Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies. Sources: [1] Immunol Lett. 2008 May 22. Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity. D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M. http://dx.doi.org/10.1016/j.imlet.2008.04.006 [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008. Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10 [3] Vitamin D Preserves the Intestinal Mucosal Barrier Roy S. Jamron https://www.celiac.com/articles/21476/ [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13. Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis. Zipitis CS, Akobeng AK. http://adc.bmj.com/cgi/content/full/93/6/512 [5] Diabetologia. 2008 Jun 12. [Epub ahead of print] The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Mohr SB, Garland CF, Gorham ED, Garland FC. http://www.springerlink.com/content/32jx3635884xt112/ [6] Am J Gastroenterol. 2004 May;99(5):905-6. A role for bacteria in celiac disease? Sollid LM, Gray GM. http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x [7] Am J Gastroenterol. 2004 May;99(5):894-904. Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease. Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML. http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease? Roy S. Jamron https://www.celiac.com/articles/779/
  20. Celiac.com 05/31/2006 - I previously discussed how liver abnormalities are highly prevalent in celiac disease. Why damage to the liver occurs is unknown, and gluten toxicity and increased intestinal permeability have been proposed as factors. The following free full text article appearing in the current issue of Gastroenterology may shed light on why liver damage occurs in celiacs. Toll-like receptors (TLRs) reside on the surface of many cells which participate in the immune system. TLRs sense molecules present in pathogens but not the host, and when the immune system senses these molecules, chemicals are released which set off inflammatory and anti-pathogen responses. One class of molecules recognized by TLRs and common to most pathogenic bacteria is lipopolysaccharides (LPS). Gluten increases intestinal permeability in celiacs. The disruption of the intestinal barrier permits endotoxins, such as LPS, from gut bacteria to reach the portal vein of the liver triggering a TLR response from immune cells in the liver. Proinflammatory mediators are released cascading into the release of more chemicals leading to inflammation and liver damage. This may be the cause of liver damage in celiacs. Gluten itself could also trigger a liver immune response. Kupffer cells in the liver are capable of antigen presentation to T cells, along with liver dendritic cells, and could initiate a T cell response to gluten within the liver. The following article is somewhat technical, but discusses the role of various liver cells involved in the immune process and how intestinal permeability and TLRs contribute to liver injury. The article is a good read and provides valuable information about the liver I have not seen elsewhere. Gastroenterology Volume 130, Issue 6, Pages 1886-1900 (May 2006) Toll-Like Receptor Signaling in the Liver Robert F. Schwabe, Ekihiro Seki, David A. Brenner Free Full Text: http://www.gastrojournal.org/article/PIIS0016508506000655/fulltext
  21. Gastroenterology 2002;122:881-888. Celiac.com 05/02/2002 - In the April issue of Gastroenterology Dr. Pekka Collin of the University of Tampere, Finland, and colleagues describe four patients with severe liver disease who were also found to have celiac disease. One of the patients had congenital liver fibrosis, one had massive hepatic steatosis, and two had progressive hepatitis without apparent origin. Three of the four were considered for liver transplantation. In each case a gluten-free diet reversed heptic dysfunction. The reasearchers then studied the prevalence of celiac disease in 185 adults who had already undergone liver transplantation. Eight of them (4.3%) tested positive for celiac disease, and it had already been detected in six of the eight prior to transplantation. Only one the the diagnosed patients followed a strict gluten-free diet. Of these eight patients, three had primary biliary cirrhosis, one had autoimmune hepatitis, one had primary sclerosing cholangitis, and one had congenital liver fibrosis. Additionally, one of the patients had autoimmune hepatitis and one had secondary sclerosing cholangitis. The researchers also noted that not all of patients with both liver and celiac disease showed symptoms of celiac disease, which suggests that the liver disease may not be caused by malabsorption. Dr. Collin suggests that it could be a "gluten-dependent immunologically induced extraintestinal manifestation of celiac disease." The researchers conclude that some cases of serious liver disease may result from unrecognized celiac disease, and patients with severe liver disease should also be evaluated for celiac disease. Further, dietary treatment in patients with both celiac and liver diseases may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.
  22. Celiac.com 09/30/2002 - As reported in the September 27, 2002 issue of Science, Dr. Chaitan Khosla, professor of chemistry and chemical engineering at Stanford University, and colleagues have identified the specific protein fragment that causes intestinal damage when people with celiac disease eat grains such as wheat, rye, and barley. Graduate student Lu Shan from the Stanford team was able to identify the specific protein fragment in gluten that triggers the damaging attack by T-cells in individuals with the disease. The key fragment is made up of 33 amino acids that are normally broken down in the digestive systems of healthy individuals, but not in those with celiac disease. In addition to this discovery, the Stanford team is also beginning their search for a celiac disease cure. To that end they have developed an enzyme treatment that renders the newly discovered harmful amino acid sequence in gluten harmless in the guts of test animals, and hope that it will do the same in humans. Several more years of research must be done in order to determine if it will be effective in humans. Dr. Khosla warns against undue optimism regarding the preliminary results of their new enzyme therapy, and stresses that it is too early to raise the hopes of those with celiac disease. To fund the teams future research efforts Dr. Khosla and colleagues have established the Celiac Sprue Research Foundation, whose goal is finding a cure for the disease. The foundation must raise two million dollars by 2003 in order to begin serious scientific research to that end. Anyone interested in making a tax deductible contribution should go to their Web site: www.celiacsprue.org. I personally believe that the work of the Celiac Sprue Research Foundation represents our best shot at a cure for celiac disease. - Scott Adams, Celiac.com. Medline Abstract: Intestinal Digestive Resistance of Immunodominant Gliadin Peptides. Am J Physiol Gastrointest Liver Physiol 2002 Oct;283(4):G996-G1003 Hausch F, Shan L, Santiago NA, Gray GM, Khosla C. Department of Chemical Engineering, Stanford University, Stanford, California 94305-5025. Two recently identified immunodominant epitopes from alpha-gliadin account for most of the stimulatory activity of dietary gluten on intestinal and peripheral T lymphocytes in patients with celiac sprue. The proteolytic kinetics of peptides containing these epitopes were analyzed in vitro using soluble proteases from bovine and porcine pancreas and brush-border membrane vesicles from adult rat intestine. We showed that these proline-glutamine-rich epitopes are exceptionally resistant to enzymatic processing. Moreover, as estimated from the residual peptide structure and confirmed by exogeneous peptidase supplementation, dipeptidyl peptidase IV and dipeptidyl carboxypeptidase I were identified as the rate-limiting enzymes in the digestive breakdown of these peptides. A similar conclusion also emerged from analogous studies with brush-border membrane from a human intestinal biopsy. Supplementation of rat brush-border membrane with trace quantities of a bacterial prolyl endopeptidase led to the rapid destruction of the immunodominant epitopes in these peptides. These results suggest a possible enzyme therapy strategy for celiac sprue, for which the only current therapeutic option is strict exclusion of gluten-containing food. PMID: 12223360
  23. Gut 2002;50:624-628 Celiac.com 05/02/2002 – Results of the first large population-based twin study of celiac disease were recently published in the April edition of the journal Gut. The study was conducted by Professor L Greco and colleagues at the Università di Napoli Federico II, Dipartimento di Pediatria. The study compared identical twins (genetically identical) to fraternal twins (genetically not identical) who share only the same number of genes as non-twin siblings. This methodology allowed the researchers to determine what role a shared environment plays in the onset of celiac disease in comparison to a genetic role. The researchers matched the Italian Twin Registry with the membership lists of a patient support group for celiacs. Forty seven twin pairs were found and screened for antiendomysial (EMA) and antihuman-tissue transglutaminase (anti-tTG) antibodies. Identical twins were verified using DNA fingerprinting and fraternal twins were typed for HLA class II DRB1 and DQB1 molecules. Their results indicate that 38% of the combined twin pairs showed signs of celiac disease, which breaks down to 75% of the identical twin pairs and 11% of the non-identical twin pairs. Additionally, females who had a twin with celiac disease were 30% more likely to develop it themselves, in comparison to an unaffected male twin. Further, the results of the study indicate that environmental factors have little or no effect on the acquisition of celiac disease, and that there is substantial evidence of a very strong genetic component that is only partially related to the HLA region. The researchers suggest that several genes work collectively to cause celiac disease, and a single missing or altered gene is probably not its cause.
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