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Found 1,259 results

  1. Celiac.com 09/01/2017 - A recent story by Buzzfeed does little to answer the question of whether Cheerios and other General Mills cereals are actually gluten-free and safe for people with celiac disease. There are a number of folks in the gluten-free community who complain that General Mills is making people sick by selling Cheerios that they know to be contaminated with gluten due to a faulty sorting process. Because General Mills uses a flawed sorting process, the story goes, their boxes of Cheerios are subject to gluten "hot spots," which is making some gluten-sensitive folks sick, thus the complaints. They point to regular complaints logged by the FDA to argue that Cheerios are clearly not gluten-free, and thus not safe for people with celiac disease. Comment sections on articles covering this topic show that plenty of people claim that Cheerios makes them sick, and triggers gluten-related symptoms. But, one useful measure of the basic scope of an issue is numbers. What kind of numbers are we talking about? How many complaints? How many boxes of Cheerios? It's important to realize that General Mills produces huge numbers of Cheerios each week. How many exactly? Well, according to their website, General Mills ships 500,000 cases of Cheerios each week. At about 12 boxes per case, that's about 6 million boxes each week, or 24 million boxes each month. We know that the FDA received a number of consumer complaints in 2015, when a mix-up at a Cheerios plant in California led to mass gluten contamination, and eventually to a full recall of 1.8 million boxes by General Mills. During that three month period, after the gluten contamination but prior to the recall, when many consumers were eating Cheerios made with wheat flour, the FDA says it received 136 complaints about adverse reactions to the product. So, during the 90 days when we know there was gluten contamination in nearly 2 million boxes of Cheerios, when people were definitely having gluten reactions, the FDA got 136 complaints. During that time General Mills shipped about 72 million boxes, and later recalled nearly 2 million of those due to gluten contamination. That's a complaint rate of about one complaint per 529,411 total boxes, and about one complaint for every 5,000 people with celiac disease; if each person with celiac ate 1 box, and the complaints came only from people with celiac disease. (Obviously this is simplified assumption for discussion purposes). Let's imagine another 2 million gluten-contaminated boxes got to consumers. Again, imagine that 1% of those buyers were celiac, so that 20,000 boxes of the 2 million went to celiacs—one box each. 146 complaints for 20,000 boxes is about 1 complaint per 140 boxes, give or take, for each person with celiac disease. That seems like a substantial complaint rate. So, how does that rate compare to the current rate, after the recall? Since the beginning of 2016, the FDA has received 46 reports of people with celiac disease or sensitivity to gluten or wheat linking their illness to General Mills cereals, including Cheerios and Lucky Charms. Let's forget about Lucky Charms for a minute, let's focus on Cheerios. During the 18 months from January 2016 to July 2017, General Mills has shipped something like 450 million boxes. That's about one complaint for every 10 million boxes of Cheerios, or about one complaint for every 100,000 people with celiac disease. And those numbers don't include Lucky Charms, which account for some portion of the 46 complaints since early 2016. If General Mills is having an issue with sorting oats, then why have complaint ratios gone down so sharply? Also, General Mills uses its optically sorted gluten-free oats for other products. The FDA is certainly taking all of this into account. When they get complaints, they look at large amounts of data to help them put things into perspective. Has the FDA seen corresponding numbers of complaints for different General Mills products made from the same oat sorting process? It doesn't seem so. Celiac.com has covered the gluten-free Cheerios story from the beginning, and will continue to do so. We stand on the side of science, and accurate information. Beyond the obvious gluten-contamination that led to the recall, we have been skeptical of claims that General Mills' sorting process is flawed, and that their products, including Cheerios are routinely contaminated with gluten. If this were true, we think the numbers would be very different, and that the pattern of official complaints would reflect that reality. We also feel that General Mills would be facing down lawsuits from hungry trial lawyers looking to put a big trophy on the wall. We have simply not seen any good evidence that supports claims that Cheerios and other General Mills products are contaminated with gluten "hotspots" that cause reactions in people with celiac disease. We have also not seen evidence that rules out adverse oat reactions as the cause of many of these claims. If someone out there has different numbers, or better information, we are all ears. However, until we see convincing evidence to the contrary, Celiac.com regards Cheerios and other General Mills products as safe for people with celiac disease and gluten-sensitivity. We do offer the caveat that people should trust their own judgement and avoid any food they think makes them sick. Stay tuned for more on this and other stories on gluten-free cereals and other products. Read more at BuzzFeed.com and GeneralMills.com.
  2. Celiac.com 11/27/2017 - For centuries, physicians have used cannabis to treat numerous disorders. Modern research shows that various cannabis compounds can alleviate symptoms from numerous conditions, including neurological disorders, cancer, rheumatism, epilepsy, sexual disorders, pain, among others. Many people with celiac disease suffer from neuropathy, which causes nerve pain, among other symptoms. Neuropathy can be difficult to treat. Nerve pain is a debilitating symptom that can significantly impair a patient's quality of life. Could a new cannabis patch change that? Some researchers think so. One California-based company, Cannabis Science, is developing an innovative new medicinal patch specifically designed to treat nerve pain. In addition to celiac related neuropathy, the patch could be helpful in treating nerve pain from many illnesses including fibromyalgia, diabetes, and multiple sclerosis. The National Institute of Health estimates that over 5 million Americans suffer from fibromyalgia, which has no known cure, and is difficult to treat. With diabetes on the rise in the U.S., diabetic nerve pain is also on the rise. When placed on the patient's skin, the patch developed by Cannabis Science delivers a measured dose of high potency cannabidiol (CBD) extract. CBD is the second major cannabinoid in marijuana after THC, but CBD has no psychoactive effects, so it won't get people high. When the patch is applied, the CBD is first absorbed into the blood, then moves to the central nervous system, where it delivers pain relief. Numerous studies have documented CBD's “anti-inflammatory and pain-relieving properties. More recent studies have shown that CBD provides relief from many kinds of pain. In addition to nerve pain, CBD has been shown to relieve inflammatory pain. Some studies have shown CBD to be more effective than current medication in treating inflammatory pain, such as pain from arthritis. As researchers home in on the pain-relieving properties of cannabis, look for more treatments to be developed, including treatments that may helpful for peopl with celiac disease. Read more: cannatech.news
  3. Celiac.com 11/22/2017 - A team of physicians recently reported on the case of a 3-year-old Albanian girl who presented at their clinic with carpal spasms and hand paresthesia. The physicians include Atifete Ramosaj-Morina; A. Keka-Sylaj; V. Hasbahta; A. Baloku-Zejnullahu; M. Azemi; and R. Zunec. A physical exam showed the girl to be in good physical condition, with a body weight of 10.5 kg (10 percentile). She was suffering from carpal spasms and paresthesias of her extremities. Positive Chvostek and Trousseau signs indicated neuromuscular irritability. Blood tests showed severe hypocalcemia with a total serum calcium of 1.2 mmol/L (normal range 2.12 to 2.55 mmol/L), ionized calcium of 0.87 (normal range 1.11 to 1.30 mmol/L), and 24-hour urine calcium excretion of 9.16 mmol (normal range female The team screened the girl for celiac disease with antigliadin immunoglobulin A, anti-tissue transglutaminase, and anti-endomysial immunoglobulin A antibodies. All tests were positive. The girl underwent a duodenal biopsy, which showed lymphocyte infiltration, crypt hyperplasia, and villous atrophy compatible with celiac disease grade IIIb according to the Marsh classification. Following her celiac diagnosis, the team conducted human leukocyte antigen typing, which provided a definite diagnosis of celiac disease. She was started on a gluten-free diet. Apparently, the girl did not follow a gluten-free diet, which caused a recurrence of carpal spasms. At 7 years of age, the girl showed signs of delayed psychophysical development. Although hypocalcemia is not uncommon in people with celiac disease, it is rare for hypocalcemic carpal spasm to be the first manifestation of the disease. Because of this, the doctors urge other physicians to consider the possibility of celiac disease in patients with repeated carpal spasms that seem to resist easy treatment. They indicate that celiac disease should be considered even in the absence of gastrointestinal symptoms, since hypocalcemia and carpal spasm may appear as the first symptoms of celiac disease, even in young children. Source: J Med Case Reports. 2017;11(252)
  4. Celiac.com 11/20/2017 - People who do not have celiac disease, but who have celiac-like symptoms that improve on a gluten-free diet are prime candidates for a condition called non-celiac gluten sensitivity (NCGS). Researchers don't know much about the condition. There are no biomarkers, so they can't just do a blood test. People with this condition often experience celiac-like symptoms. Many of people with non-celiac gluten sensitivity see their symptoms improve on a gluten-free diet. However, these people may also have puzzling sensitivities to other foods that just don't seem to add up. Interestingly, foods with gluten often contain fructans, a type of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). Fructan is one such compound. Could fructan be the culprit? A team of researchers recently set out to investigate the effect of gluten and fructans separately in individuals with self-reported gluten sensitivity. The research team includes Gry I. Skodje, Vikas K. Sarna, Ingunn H. Minelle, Kjersti L. Rolfsen, Jane G. Muir, Peter R. Gibson, Marit B. Veierød, Christine Henriksen, Knut E.A. Lundin. They are variously affiliated with the Division of Cancer Medicine, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway; the K. G. Jebsen Celiac Disease Research Centre, University of Oslo, Norway; the Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway; the Department of Gastroenterology, Monash University and Alfred Hospital, Melbourne, Victoria, Australia; the Department of Immunology and Transfusion Medicine, Oslo University Hospital, 0424 Oslo, Norway; and the Centre for Immune Regulation, University of Oslo, 0424 Oslo, Norway. For their double-blind crossover challenge, the team enrolled 59 individuals without celiac disease, but who followed a self-driven gluten-free diet. The team conducted the study at Oslo University Hospital in Norway from October 2014 through May 2016. The team randomly assigned study subjects to groups. For 7 days, each group ate muesli bars containing either 5.7 grams of gluten, 2.1 grams fructans, or a placebo. Subjects then underwent a washout period that lasted until the symptoms caused by the previous challenge were resolved. Washout period was a minimum of 7 days. After the washout period, participants crossed over into a different group, until they completed all 3 challenges. To measure symptoms, the team used the gastrointestinal symptom rating scale irritable bowel syndrome (GSRS-IBS) version. They used a linear mixed model for analysis. In this study of individuals with self-reported non-celiac gluten sensitivity, researchers found that fructans induced symptoms of irritable bowel syndrome, as measured by the gastrointestinal symptom rating scale. Clinicaltrials.gov no: NCT02464150 See the article below for more information, including study results. Source: Gastrojournal.org DOI: http://dx.doi.org/10.1053/j.gastro.2017.10.040
  5. Celiac.com 11/16/2017 - If people with celiac disease hope to avoid complications, then it's important for their gut mucosa to heal. However, besides biopsy, there is currently no good way for doctors to assess that a patient has healed enough to experience full remission. A team of researchers recently set out to assess the role of a point-of-care test (POCT) based on IgA/IgG-deamidated gliadin peptide, in detecting persistent villous atrophy in celiac disease. The research team included Michelle S Lau, Peter D Mooney, William L White, Michael A Rees, Simon H Wong, Matthew Kurien, Nick Trott, Daniel A Leffler, Marios Hadjivassiliou and David S Sanders. They are affiliated with the Academic Department of Gastroenterology at Royal Hallamshire Hospital, Sheffield Teaching Hospitals, in Sheffield, UK, and with the Celiac Center and Division of Gastroenterology at Beth Israel Deaconess Medical Center in Boston, Massachusetts, USA. The research team recruited celiac disease patients undergoing endoscopy for the assessment of histological remission. All patients had IgA-endomysial (EMA) antibodies, IgA-tissue transglutaminase (TTG) antibodies, received a POCT, and completed a validated dietary questionnaire. All patients received a gastroscopy, with four biopsies taken from the second part of the duodenum and one from the duodenal bulb. The research team then compared the diagnostic performance of the surrogate markers against duodenal histology as the reference standard. From 2013 to 2017, the team evaluated a total of 217 celiac disease patients. 70% of patients were female, ranging in age from 16–83 years, with an average age of 53 years. Patients had been on a gluten-free diet for an average of 6 years when recruited. Eighty-five (39.2%) patients had persistent villous atrophy. The sensitivities of the POCT, TTG, EMA, and the adherence score in detecting villous atrophy were 67.1%, 44.7%, 37.7%, and 24.7% respectively (P=0.0005). The combination of the POCT and adherence score only marginally increased the sensitivity to 70.6% (59.7–80.0%). The POCT showed a higher sensitivity than the other markers in predicting villous atrophy. A POCT may help doctors get a quick, accurate assessment of mucosal healing levels during simple follow-up office visits. Source: The American Journal of Gastroenterology , (10 October 2017). doi:10.1038/ajg.2017.357
  6. Celiac.com 11/09/2016 - Although exocrine pancreatic insufficiency (EPI) has been reported in a number of patients with celiac disease (celiac disease), it is not clear if this is primarily a functional or a structural defect. We studied pancreatic structural abnormalities by endoscopic ultrasound (EUS) in adult celiac disease patients with EPI. A team of researchers recently set out to prospectively assess pancreatic exocrine function in recently diagnosed celiac patients. The research team included Surinder S. Rana, Arvind Dambalkar, Puneet Chhabra, Ravi Sharma, Vishal Sharma, Satyavati Rana, Deepak K. Bhasin and Ritambhra Nada. They are variously affiliated with the Department of Gastroenterology, and the Department of Histopathology at the Post Graduate Institute of Medical Education and Research (PGIMER) in Chandigarh, India. For their study, the team measured fecal elastase to prospectively assess pancreatic exocrine function in 36 recently diagnosed celiac patients. They relied on EPI by EUS and elastography to assess pancreatic structural changes in celiac patients. The team then reassessed exocrine functions in these patients after 3 months of gluten-free diet. Of the 36 celiac patients the team studied, 30 patients had anemia, 21 had diarrhea, and 7 had hypothyroidism. Ten patients had EPI with mean elastase levels of 141.6 μg/g of stool, only one of whom had a history of recurrent acute pancreatitis, while the other 9 patients had no history of either acute or chronic pancreatitis. Of these 10 patients, 8 (80%) had diarrhea, 8 (80%) anemia, and 2 (20%) had hypothyroidism. The team performed EUS in 8 patients. Five showed normal pancreas, 3 showed hyperechoic strands, and 2 patients showed hyperechoic foci without shadowing. None showed lobularity or parenchymal calcification. All patients, except the patient with recurrent pancreatitis, showed normal strain ratio. In 6 of the remaining 7 patients, follow-up fecal elastase fell within normal range. EPI, as measured by fecal elastase levels in adult celiac patients, possibly does not relate to structural alterations in the pancreatic parenchyma, and may be reversible by following a gluten-free diet. Source: Ann Gastroenterol. 2016 Jul-Sep;29(3):363-6. doi: 10.20524/aog.2016.0042. Epub 2016 May 11.
  7. Celiac.com 11/07/2017 - Researchers still don't have much good data on the consequences of antibiotic use in early life and how that relates to the risk of certain autoimmune diseases. A team of researchers recently set out to test the association between early-life antibiotic use and islet or celiac disease autoimmunity in genetically at-risk children prospectively followed up for type 1 diabetes (T1D) or celiac disease. Their study is part of a larger study called The Environmental Determinants of Diabetes in the Young, or TEDDY, for short. The reasearch team enrolled HLA-genotyped newborns from Finland, Germany, Sweden, and the United States between November 20, 2004, and July 8, 2010, and analyzed data from November 20, 2004, to August 31, 2014. They also enrolled individuals from the general population, and those having a first-degree relative with T1D, with any 1 of 9 HLA genotypes associated with a risk for T1D. The team charted parental reports of the most common antibiotics, such as cephalosporins, penicillins, and macrolides, used between age 3 months and age 4 years. Islet autoimmunity and celiac disease autoimmunity were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 consecutive clinic visits at least 3 months apart. The team used Cox proportional hazards regression models to assess the relationship between antibiotic use in early life before seroconversion and the development of autoimmunity, and to calculate hazard ratios and 95% CIs. The team conducted tests for islet and tissue transglutaminase autoantibodies on 8,495 children (49.0% female), and 6,558 children (48.7% female) who were enrolled in the TEDDY study, and they found that antibiotic exposure and frequency of use in early life or before seroconversion did not influence the risk of developing islet autoimmunity or celiac disease autoimmunity. Additionally, cumulative use of any antibiotic during the first 4 years of life was not tied to the appearance of any autoantibody (hazard ratio , 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or the transglutaminase autoantibody (HR, 1.00; 95% CI, 0.98-1.02). Using any of the most common antibiotics during the first 4 years of life, in any geographic region, did not influence the later development of autoimmunity for T1D or celiac disease. Based on these results, the team concluded that doctors recommending antibiotics for young children at risk for T1D or celiac disease need not be concerned that the use will lead to islet or tissue transglutaminase autoimmunity. Source: JAMA Pediatr. Published online October 9, 2017. doi:10.1001/jamapediatrics.2017.2905 The research team included Kaisa M. Kemppainen, PhD; Kendra Vehik, PhD; Kristian F. Lynch, PhD; Helena Elding Larsson, MD, PhD; Ronald J. Canepa, BSc; Ville Simell, MSc; Sibylle Koletzko, MD, PhD; Edwin Liu, MD; Olli G. Simell, MD, PhD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD, PhD; Marian J. Rewers, MD, PhD; Åke Lernmark, PhD; William A. Hagopian, MD, PhD; Jin-Xiong She, PhD; Beena Akolkar, PhD; Desmond A. Schatz, MD; Mark A. Atkinson, PhD; Martin J. Blaser, MD; Jeffrey P. Krischer, PhD; Heikki Hyöty, MD, PhD; Daniel Agardh, MD, PhD; and Eric W. Triplett, PhD; for The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group. They are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa; the Department of Clinical Sciences, Lund University Clinical Research Center, Skåne University Hospital, Malmö, Sweden; the MediCity Laboratory, University of Turku, Turku, Finland; the Division of Paediatric Gastroenterology and Hepatology, Dr von Hauner Children's Hospital, Ludwig Maximilian University, München, Germany; the Digestive Health Institute, Children's Hospital Colorado, Anschutz Medical Campus, University of Colorado Denver, Aurora; the Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland; the Department of Pediatrics, University of Turku, Turku University Hospital, Turku, Finland; the Department of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland Institute of Diabetes Research, Helmholtz Zentrum München, München, Germany; the Klinikum Rechts der Isar, Technische Universität München, München, Germany; the Forschergruppe Diabetes e.V., Neuherberg, Germany; the Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora; the Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville; the Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville; the Department of Medicine and Microbiology, New York School of Medicine, New York; the Department of Virology, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland; and with Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
  8. Celiac.com 06/23/2017 - Dr. Alessio Fasano from the University of Maryland's Celiac Research Center published a paper in Clinical and Developmental Immunology last month. It focused on a new drug developed by Dr. Fasano that has shown promising results in both animal and human trials. But is this the 'magic pill' that will cure celiac disease and gluten sensitivity? Let's take a look. The new drug, formerly called AT1001 but now renamed Larazotide Acetate, is a zonulin inhibitor. For those who have never heard the word 'zonulin', you might think it's a term from a science fiction movie. But zonulin is the protein that causes the 'gates' or openings between the cells making up the lining of the small intestine to open and close. These openings are called tight junctions and when zonulin gets excessive, a leaky gut ensues. Dr. Fasano has made great inroads to prove that a leaky gut is a problem that must be handled with gluten intolerance. The leaky gut perpetuates gluten's negative impact on other parts of the body. It can also initiate autoimmune disease. One key point to keep in mind is that 'leaky gut' occurs because molecules can pass between cells when they shouldn't. In addition, molecules can pass through cells which they also shouldn't. Unfortunately this new drug only impacts the former, not the latter. So, the drug Larazotide Acetate is a zonulin inhibitor. Now that we've reviewed what zonulin does as regards opening the gates, the purpose of inhibiting its action should make sense. How well does it work? In the recent human trials that were double-blind, randomized placebo-controlled (the best type of study, but I would expect no less from the stellar Dr. Fasano), a gluten exposure created a 70% increase in intestinal permeability (leaky gut) in 57% of the placebo group but only 28.6% of the patients receiving the drug (4 out of 14 patients) experienced such increased permeability. Further, gastrointestinal symptoms were significantly more frequent among patients of the placebo group as compared to the group that received the Larazotide. A pro-inflammatory substance known as interferon gamma was also evaluated. This is manufactured by the body when a specific foreign/toxic agent is recognized by the body's immune system. As expected, levels of interferon gamma increased in 4 out of 7 of the placebo patients (57%) but only 4 out of 14 larazotide patients (28.6%) saw any increase. The good news is that this drug seems well tolerated and it does reduce the leaky gut response that gluten ingestion normally creates. Further, it also reduces the percentage, by about half, of the production of interferon gamma. These are all excellent results. But, and it's unfortunately a very big 'but', we have a very long way to go before such a drug would be useful for your typical celiac or gluten sensitive patient. Will Dr. Fasano and his team be able to tweak this drug such that it functions at a higher level of efficacy? I certainly hope so, but let's analyze exactly what this drug does in its present state: The drug still resulted in almost 30% of the patients experiencing a 70% increase in permeability (leaky gut) – Not good. A highly pro-inflammatory (this means that it creates degenerative disease) substance known as interferon gamma was also produced in nearly 30% of the drug-consuming patients tested – Not good. Leakiness, or the passage of negative substances through cells is not affected by this drug – Not good. Of course on the plus side, over 70% of those tested DID have a very good result with apparently no untoward side effects – Very good. At what point is the efficacy high enough that you'd be willing to subject yourself to a possible reaction? Do realize that any gluten ingested increases your chance of disease, chief amongst them cancer and autoimmune disease. Is there a level of function of the drug that you would chance taking it? Is it 90%, 99%? Does any drug ever get that good? Well, as a big fan of Dr. Fasano's, I would say that if anyone can do it, he and his team can. But at the same time, I cannot help but think of all the other drugs I have encountered. As 'wonderful' as they sometimes seem initially, they almost always fall from grace when some horrible side effect is realized. Would I guinea pig my own health that I've fought so hard to regain? Would I recommend taking such a chance to my children just so that they could consume some white flour product? I don't think so. How about you? What do you think? If the drug were available right now at its efficacy of 71%, would you take it and hope you weren't in the 29% for whom it didn't work? I'd love to hear your thoughts. If you are wondering if you're gluten intolerant or know that you are but still aren't enjoying good health, consider calling us for a free health analysis: 408-733-0400. We are here to help! Our destination clinic sees patients from across the country and internationally so you do not need to live locally to receive assistance. To your good health! Reference: Alessio Fasano, Clinical and Developmental Immunology, Published online 2012 October 10. "Novel Therapeutic/Integrative Approaches for Celiac Disease and Dermatitis Herpetiformis."
  9. Celiac.com 07/19/2016 - The world's first vaccine aimed at curing celiac disease is slated to begin full trials later this year, and residents of the Australian state of Victoria will be among the first humans to give it a try against celiac disease. The vaccine, called Nexvax2, was developed by Australian scientist Dr Bob Anderson, and is aimed at giving celiac patients a chance to overcome their immune reaction to the gluten found in products containing wheat, rye and barley. Nexvax2 aims to de-sensitise patients to three peptides contained in gluten that trigger a damaging reaction in their immune system. Previous trials on 150 patients from Melbourne, Perth, Adelaide, Brisbane and Auckland were aimed at finding a safe dosage rather than assessing its ability to beat celiac disease. Results from those favorable earlier trials were released in May, and Dr Anderson says that the larger phase II study, also being undertaken in the US and Europe, will assess how well the vaccine works against celiac disease. Dr Anderson first identified the peptides triggering coeliac disease and began developing the vaccine while working at Melbourne's Walter and Eliza Hall Institute, before travelling to Boston for six weeks as part of a sister city arrangement through the City of Melbourne, where he made contact with ImmusanT to further the discovery. This is certainly exciting news for people with celiac disease, many of whom may benefit from such treatment. Stay tuned for news on the progress of these trials. Source: dailysecrets.press
  10. Celiac.com 11/02/2017 - What is the link between the autoimmune diseases Sjögren's syndrome and celiac disease? In a study, 14.7% of Sjögren's syndrome patients were found to have celiac disease and 11.8% of non-celiac Sjögren's syndrome patients were found to have inflamed mucosa in the small intestine. With this knowledge, people who suffer from Sjögren's syndrome may be able to find relief for their symptoms with the gluten-free diet. Four million Americans are suffering from a disease they don't even know they have and their doctors don't even know to test for. Sound familiar? If you're familiar with my work as a gluten-free advocate, you have probably guessed that what I'm describing is celiac disease, an autoimmune reaction triggered by gluten, a protein component in wheat, barley, and rye. If that was your guess, you would actually be wrong: there is another underdiagnosed and common autoimmune disease that we and our doctors need to be aware of—Sjögren's syndrome, which affects the exocrine, or moisture-producing, glands. Unlike celiac disease, Sjögren's syndrome doesn't have a standardized effective treatment, but fortunately, research is demonstrating a link between these two autoimmune diseases, bringing good news for Sjögren's patients who may see relief of their symptoms by eliminating gluten from their diet. Chances are, many haven't heard of Sjögren's syndrome. This relatively unknown and underdiagnosed disease is an autoimmune disease in which the immune system attacks the tear and saliva glands of the body, reducing their production and resulting in dry mouth and eyes and other symptoms. Complications of Sjögren's include tooth decay, corneal ulcers, and non-Hodgkin's lymphoma. In women, vaginal dryness can also be a symptom. According to the UK's National Health Service, 9 out of 10 people who suffer from this condition are women, and the average age onset is between the ages of 40 and 60 years old. In a study by the Institute of Medical Technology, University of Tampere, Finland, 34 Sjögren's syndrome patients and a control group of 28 people were given a small bowel biopsy; five (14.7%) of the Sjögren's patients tested positive for celiac disease and four (11.8%) of the non-celiac patients were found to have inflammation in the mucous membrane of the small intestine. According to the study's conclusions, "The findings show a close association between Sjögren's syndrome and celiac disease." Currently, there are two classifications of Sjögren's syndrome as either primary, meaning that it has developed on its own, or secondary, which means that it has developed as the result of another autoimmune disease, such as rheumatoid arthritis or lupus. There is no "cure" for Sjögren's; researchers have identified a combination of factors—environmental, genetic, and hormonal, according to the National Health Service. There are a variety of treatments which can vary in effectiveness, including saliva-stimulating medication and eye drops. The good news is that Sjögren's patients who are found to be celiac may see the relief of their symptoms through a gluten-free diet, currently the effective and only treatment used for celiac disease. Just as with celiac disease, Sjögren's syndrome is under diagnosed relative to its frequency. As a diagnosed celiac American, I consider myself very lucky that I've been correctly diagnosed with celiac disease. With the help of advocate groups all over the country, gluten-free awareness and celiac diagnosis is on the rise. By spreading the word about the association between Sjögren's syndrome and celiac disease, we can help those with Sjögren's achieve better health and quality of life. Resources: National Health Service (UK): Sjögren's syndrome http://www.nhs.uk/conditions/Sjogrens-syndrome/Pages/Introduction.aspx National Institutes of Health: Celiac disease and markers of celiac disease latency in patients with primary Sjögren's syndrome http://www.ncbi.nlm.nih.gov/pubmed/10201480 Nutritional Healing: Articles. Sjögren's World: Links http://www.sjogrensworld.org/links.htm
  11. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. Gall bladder disease or malfunction is often associated with celiac disease. It can cause pain in the upper right quadrant of the abdomen, just at the lowest rib on the right side. In one study of 1300 celiacs in Canada, 9% indicated that gall stones were the earliest presentation, sometimes followed by many years prior to correct diagnosis of their celiac disease. In another report, Dr. Kozlowska indicated that 13 of the 41 newly diagnosed celiacs she investigated were suffering from atresia, a condition which is a partial or complete blockage of the bile duct. CCK (cholecystokinin) is the hormone responsible for gall bladder contraction. The bulk of this hormone is produced in the duodenum. Active celiac disease would be likely, then, to cause a reduction or a cessation of duodenal production of CCK. A radiologist in Hungary is currently researching this problem. In private correspondence, one gastroenterologist reports having found (accidentally) a gallstone in a 12 year old girl who had active celiac disease. The 30% incidence of atresia among celiac children, as reported by Dr. Kozlowska, would suggest an even higher number among adults with active celiac disease. Given the low level of clinical suspicion for celiac disease in North America, it would not be at all surprising if a large portion of patients with gall bladder disease were suffering from occult celiac disease. Future research may reveal that gall stones and atresia are only symptoms of celiac disease. I did a Medline search on cck and celiac disease. I got 65 hits. Researchers repeatedly identified a connection between celiac disease and gall bladder malfunction with such comments as: Thus the already impaired fat absorption in celiac sprue is magnified by the lack of bile delivery.....; and We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease. and Cholecystokinin (cck) release and gall bladder emptying in response to a fatty meal are completely abolished in celiac disease. and the abnormally decreased gallbladder contraction in celiac patients is the result of endogenous cck secretion and not a lack of end-organ responsiveness to cck. There just isnt much ambiguity there. If youve got celiac disease, you have gall bladder malfunction, of the sort that may well develop into atresia and gallstones. Upon receiving a diagnosis of gall bladder disease, whether gall stones or atresia, one might be wise to request a blood test for celiac disease. The anti-endomysial antibody test is currently the most reliable and available test. Now, given the low level of clinical suspicion for celiac disease, I anticipate the suggestion that absent gall bladder emptying, atresia, and gall stones might occur in the absence of celiac disease. I did another Medline search, and I cant find a single study that has tested atresia patients or gallstone patients for celiac disease. My answer to the suggestion that gall bladder disease may occur in the absence of celiac disease is that there is no evidence to support such a contention. Considerable evidence exists, however, which points to celiac disease as a likely cause of gall bladder malfunction, atresia, or stones. As for childhood gallstones, there appears to be only one answer.... it is associated with celiac disease. A view that incorporates the association of gall bladder disease, and celiac disease, but does not preclude the above, has been expressed by Dr. Joseph Murray, of the University of Iowa, who is a gastroenterologist specializing in treating celiac disease. He believes there are several triggers that can activate Celiac disease in genetically susceptible people. One of them is: Surgery, particularly GI (gall bladder, etc.) In any case, the connection between celiac disease and gall bladder disease is well known.
  12. Celiac.com 10/20/2017 - Are doctors even getting close to diagnosing the actual number of cases of celiac disease? Or are they missing the vast majority? Researchers have said for some time that there are far more people with celiac disease than are being diagnosed, and that the vast majority of cases go undiagnosed. So, just how far are we from the actual number? Well, if a new study by Canadian nutrition researchers is any indication, doctors are very far from diagnosing most cases. The team studied the blood work of nearly 3,000 people, and their conclusions are stunning. They say that ninety percent of celiac cases go undiagnosed. How could this be? One reason is that even classic celiac disease symptom, such as abdominal pain, bloating, gas, diarrhea, anemia and weight loss can mimic other conditions. Less classic symptoms such as fatigue, low vitamin C, D and calcium levels can be misleading. Ahmed El-Sohemy, a professor of nutritional science at the University of Toronto, wanted to see whether celiac disease results in subpar nutrition because of poorer absorption of vitamins and minerals. But to find out, he needed Canadian data on the frequency of undiagnosed celiac disease. To that end, El-Sohemy and his colleagues checked blood samples from more than 2,800 individuals in Toronto. One group had an average age of 23, and the other 45. Among their findings is likely ~1%, with 87% of cases being undiagnosed. These findings suggest the need for better screening in high genetic risk groups. Source: BMJOPEN.com
  13. Celiac.com 10/26/2017 - Making an accurate count of intraepithelial lymphocytes (IEL) is important to making an accurate diagnosis of celiac disease, but so far, researchers have not been able to establish a definitive 'normal' IEL range. In a recent multi-center study, a team of researchers set out to do just that. The research team included Kamran Rostami, Michael N Marsh, Matt W Johnson, Hamid Mohaghegh, Calvin Heal, Geoffrey Holmes, Arzu Ensari, David Aldulaimi, Brigitte Bancel, Gabrio Bassotti, Adrian Bateman, Gabriel Becheanu, Anna Bozzola, Antonio Carroccio, Carlo Catassi, Carolina Ciacci, Alexandra Ciobanu, Mihai Danciu, Mohammad H Derakhshan, Luca Elli, Stefano Ferrero, Michelangelo Fiorentino, Marilena Fiorino, Azita Ganji, Kamran Ghaffarzadehgan, James J Going, Sauid Ishaq, Alessandra Mandolesi, Sherly Mathews, Roxana Maxim, Chris J Mulde, Andra Neefjes-Borst, Marie Robert, Ilaria Russo, Mohammad Rostami-Nejad, Angelo Sidoni, Masoud Sotoudeh, Vincenzo Villanacci, Umberto Volta, Mohammad R Zali, Amitabh Srivastava. They are variously affiliated with the twenty-eight institutions listed below. The study was designed at the International Meeting on Digestive Pathology, Bucharest 2015. Investigators from 19 centers in eight countries on three continents, recruited 198 patients with Marsh III histology, and another 203 control subjects. They used a single agreed upon protocol to count IEL/100 enterocytes in well-oriented duodenal biopsies. They also collected demographic and serological data. The research team used receiver operating characteristic (ROC) curve analysis to determine the optimal cut-off between normal and celiac disease (Marsh III lesion) duodenal mucosa, based on IEL counts on >400 mucosal biopsy specimens. The average ages of celiac and control groups were 45.5 and 38.3 years, respectively. They found that mean IEL count was 54±18/100 enterocytes in celiac disease and 13±8 in normal controls (p=0.0001). ROC analysis indicated an optimal cut-off point of 25 IEL/100 enterocytes, with 99% sensitivity, 92% specificity and 99.5% area under the curve. Other cut-offs between 20 and 40 IEL were less discriminatory. Additionally, there was a sufficiently high number of biopsies to explore IEL counts across the sub-classification of the Marsh III lesion. Their ROC curve analyses show that a cut-off of 25 IEL/100 enterocytes for Marsh III lesions provides the best way to distinguish between normal control and celiac disease biopsies. They saw no differences in IEL counts between Marsh III a, b and c lesions. There was an indication of a continuously graded dose–response by IEL to environmental gluten antigenic influence. Source: GUT Affiliations: The team members for this study are affiliated with the Department of Gastroenterology and Pathology, Milton Keynes University Hospital, Milton Keynes, UK; the Department of Gastroenterology, Luton and Dunstable University Hospital, Luton, UK; the Wolfson College, University of Oxford, Oxford, UK; the Gastroenterology and Liver Diseases Research Centre, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, The Islamic Republic of Iran; the Centre for Biostatistics, Faculty of Biology, Academic Health Science Centre, University of Manchester, Manchester, UK; the Department of Gastroenterology, Royal Derby Hospital, Derby, UK; the Department of Pathology, Ankara University Medical School, Ankara, Turkey; the Department of Gastroenterology, Warwick Hospital, Warwick, UK; the Service de Pathologie, Centre de Biologie et Pathologie Groupe Hospitalier du Nord, Hospices Civils de Lyon, Lyon, France; University of Perugia Medical School, Perugia, Italy; the Department of Cellular Pathology, University Hospital Southampton NHS Foundation Trust, Southampton, UK; Department of Pathology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; Institute of Pathology Spedali Civili, Brescia, Italy; Internal Medicine and Pathology Unit, University of Palermo, Giovanni Paolo II Hospital, Sciacca, Italy; Department of Pediatrics and Surgical Pathology, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine and Surgery, Scuola Medica Salernitana, University of Salerno, Salerno, Italy; Departments of Gastroenterology and Pathology, Grigore T. Popa University of Medicine and Pharmacy, Iasi, Romania; College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK; Digestive Disease Research Center, Tehran University Medical Science, Tehran, Iran; Center for Prevention and Diagnosis of Coeliac Disease and Pathology Unit, Fondazione IRCCS Ca' granda Ospedale Maggiore Policlinico, Milano, Italy; Department of Medical and Surgical Sciences, University of Bologna and Diagnostic and Experimental, University of Bologna, Bologna, Italy; Gastroenterology and Hepatology, Faculty of Medicine, Mashhad University 0f Medical Sciences, Mashhad, Iran; Pathology department, Razavi hospital, Mashhad, Iran; Department of Pathology, Southern General Hospital, Lanarkshire, UK; Department of Hepatogastroenterology and Pathology, Free University Medical Centre, Amsterdam, The Netherlands; Department of Pathology and Medicine, Yale University School of Medicine, New Haven, USA; Digestive Disease Research Center, Tehran University Medical Science, Tehran, Iran; Department of Pathology, Brigham & Women's Hospital, Boston, USA.
  14. Celiac.com 10/18/2017 - Celiac disease is a chronic inflammatory disease of the small intestine mucosa due to permanent intolerance to dietary gluten. A team of researchers recently set out to clarify the role of small intestinal epithelial cells in the immunopathology of celiac disease, especially the influence of celiac disease-associated bacteria. The research team included G Pietz, R De, M Hedberg, V Sjöberg, O Sandström, O Hernell, S Hammarström, and ML Hammarström. They are variously affiliated with the Department of Clinical Microbiology, Immunology, and the Department of Clinical Sciences and Pediatrics at Umeå University, in Umeå, Sweden. The team collected duodenal biopsies from children with active celiac disease, treated celiac disease, and a group of clinical control subjects. They then purified intestinal epithelial cells, and analyzed them for gene expression changes at the mRNA and protein levels. To assess how interferon-γ, interleukin-17A, celiac disease-associated bacteria and gluten influence intestinal epithelial cells, they used two in vitro models for human intestinal epithelium, small intestinal enteroids and polarized tight monolayers. In patients with active celiac disease, intestinal epithelial cells significantly upregulated more than 25 defense-related genes, including IRF1, SPINK4, ITLN1, OAS2, CIITA, HLA-DMB, HLA-DOB, PSMB9, TAP1, BTN3A1, and CX3CL1. Of these genes, 70 percent were upregulated by interferon-γ via the IRF1 pathway. Notably, IRF1 was also upregulated by bacteria associated with celiac disease. Intestinal epithelial cells also expressed the NLRP6/8 inflammasome yielding CASP1 and biologically active interleukin-18, which induces interferon-γ in intraepithelial lymphocytes. Over-expression of IRF1 appears to be a key factor in the epithelial reaction in celiac disease. This may be inherent, but may also be due to presence of undesirable microbes that trigger or influence IRF1. From this study, the researchers conclude that activation of IRF1 and IRF1-regulated genes together, both directly and via the interleukin-18 dependent inflammasome, would greatly increase the severity of the inflammatory response, and trigger the pathological gut response that is common in active celiac disease. Could this provide a key to unlocking the mysteries of celiac disease and its associated symptoms? Source: PLoS One. 2017 Sep 21;12(9):e0185025. doi: 10.1371/journal.pone.0185025.
  15. Celiac.com 10/13/2017 - Tissue transglutaminase (tTG) immunoglobulin A (IgA) testing is a sensitive adjunct to the diagnosis of coeliac disease. The threshold for positivity was developed for diagnosis, with negative results reported as below the reference value (<4 U/mL). A team of researchers recently set out to investigate if an undetectable tissue transglutaminase IgA antibodies (tTG IgA<1.2 U/mL) is more predictive of healing compared to patients with negative but detectable serology (1.2-3.9 U/mL). The research team included H. Fang, K. S. King, J. J. Larson, M. R. Snyder, T. T. Wu, M. J. Gandhi, and J. A. Murray. They are variously affiliated with the Department of Medicine, the Division of Gastroenterology and Hepatology, the Division of Anatomic Pathology, the Division of Clinical Biochemistry and Immunology, the Division of Biomedical Statistics and Informatics, and the Division of Transfusion Medicine at the Mayo Clinic, Rochester, MN, USA. The research team conducted a retrospective study of 402 treated coeliac disease patients seen at the Mayo Clinic with negative tTG IgA values drawn within 1 month of duodenal biopsy between January 2009 and December 2015. The team used Corazza-Villanacci scores to assess mucosal healing, and logistic regression to assess the relationship of clinical variables with a normal biopsy. They also noted the presence of gastrointestinal symptoms. Their results showed that patients with undetectable test levels more frequently had normal duodenal histology, as compared with patients with detectable tTG IgA levels. Asymptomatic patients more often showed normal duodenal histology as compared to symptomatic patients. Patients with undetectable blood levels, and who followed a gluten-free diet for ≥2 years were more likely to have no villous atrophy, as compared to patients with detectable blood levels. Follow-up biopsies revealed that people recovering from celiac disease with negative tTG IgA serology showed that undetectable test levels are associated with normal histology. Source: AP&T
  16. Celiac.com 10/11/2017 - A Merrill Lynch broker in Denver has sued the firm in federal court, claiming that its systemic "sabotage" of his relationship with clients during and following two medical leaves have cost him hundreds of thousands of dollars. In a case filed this summer in federal court in Colorado, Kirk Kringel, a broker with Merrill since 2010, alleges that the company violated his rights under the Family Medical Leave Act by retaliating against him for taking the two medical leaves, including one that was related to celiac disease. A seasoned broker, Mr. Kringel worked previously with Morgan Stanley and Dean Witter for nearly 15 years before joining Merrill Lynch. According to the complaint, colleagues and managers at Merrill "systematically interfered with and sabotaged Kringel's relationships with his clients by failing to service some of his clients, permanently re-assigning some of his clients to other financial advisors, and providing misinformation to his clients that undermined his relationships." Kringel claims that the sabotage cost him annual income in excess of $250,000, and that the actions were taken deliberately as retaliation for Kringel's three-month leave in 2015 and an unpaid medical leave that he began in February 2017. Kringel alleges in the suit that the losses to his accounts were engineered by a former business partner and colleague who moved with him to Merrill, and is claiming that the alleged violation of federal FMLA law justifies a courtroom trial. If successful, he will avoid arbitration, which would be the standard course for such complaints. Merrill Lynch spokesman Bill Halldin disputed the allegations on behalf of the company, but offered no comment on whether it will seek to have the complaint moved to arbitration. Neither Kringel, nor his lawyers at the firm of Moye, White offered further comment. Stay tuned for more on Mr. Kringel's efforts, and on legal issues regarding celiac disease and employment, disability, and the like. Read more at Advisorhub.com
  17. The term gluten in reference to the cohesive, elastic protein mass remaining after starch is washed from a dough goes back to Beccari in 1745. Strictly speaking, gluten is found only in wheat because it is difficult to wash a cohesive protein mass even from rye, the closest relative to wheat, let alone from barley or oats or anything else. Unfortunately, a misuse of the term by the corn industry has become common in recent years. It has become fairly common to call corn storage proteins corn gluten. Personally, I think there is no justification for such usage. Corn may contain prolamins, as does wheat, but not gluten. When it comes to celiac disease, a similar corruption of the term has become very common. There are certain related proteins in wheat, rye, and barley that give rise to particular peptides during digestion that are capable of triggering the responses typical of celiac disease. Only in the case of wheat can these be strictly considered to be derived from the gluten proteins. But for lack of a suitable term, patients and their physicians began speaking of gluten-free or gluten-containing foods. People ask me, How much gluten is there in quinoa? I have to translate this into, Are there any harmful peptide sequences in the proteins of quinoa? There is nothing in quinoa that is like gluten prepared from a wheat flour dough, which has an unusual, perhaps unique, viscoelastic character. In any case, as far as we know, corn does not seem to cause harm to celiac patients. Corn has not been studied in the extensive way that wheat has in relation to celiac disease, but for 40+ years patients and their physicians have seemed to agree that corn is OK. The sequences in the corn zein (prolamin) fraction are suspicious, but they do differ in an apparently crucial way from the protein sequences of the wheat gliadin (prolamin) fraction. There have been no modern biopsy-based studies of the effects of purified corn proteins on the celiac intestine as there have been for wheat, but the mass of evidence still seems to point in the direction of corn being safe for celiac patients.
  18. Celiac.com 10/05/2017 - Recent data show that more adults with celiac disease may face a higher risk for cardiovascular disease compared with the general population. A team of researchers recently set out to investigate the association of with cardiovascular disease risk factors at late adolescence in a cross-sectional population-based study. The research team included Assa A, Frenkel-Nir Y, Tzur D, Katz LH, and Shamir R. They are variously affiliated with the Institute of Gastroenterology, Nutrition and Liver Disease, Schneider Children's Medical Center, Petah-Tikva; the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, and with the Medical Corps of the Israeli Defense Force. The study group included 2,001,353 Jewish Israeli adolescents who underwent general health examinations from 1988 to 2015. The average participant age was 17.1 years of age. Additional participant information included demographic measures, blood pressure, resting heart rate, and risk factors associated with cardiovascular disease. The team identified a total of 10,566 cases of celiac disease. They conducted multivariate analysis that showed average diastolic blood pressure to be significantly lower in celiac patients; 72.0±8.7 in celiac men vs 70.4 ±â€Š8.5 in non-celiac men; and 70.0 ±â€Š8.3 in celiac women vs 69.0 ±â€Š8.2 in non-celiac women. There were no differences in systolic blood pressure, while resting heart rate was slightly higher in celiac patients, with an absolute difference of 0.4 beats per minute. The team saw no increase in blood pressure, or in rates of overweight and obesity among celiac patients. Patients with celiac disease far more likely to have non-insulin-dependent diabetes mellitus, hypercoagulability, and hyperlipidemia, than were non-celiacs. By age 17, people with celiac disease have a higher prevalence of risk factors for cardiovascular disease compared with the general population. There is, however, neither increase in blood pressure nor increase in overweight and obesity rates. Source: J Pediatr Gastroenterol Nutr. 2017 Aug;65(2):190-194. doi: 10.1097/MPG.0000000000001487.
  19. Celiac.com 05/01/2014 - While estimates indicate that about 1% of the world's population is affected by celiac disease, it is thought to be uncommon in both India and Asia. However, very little study has been done on celiac disease in Asian nations. A team of researchers recently set out to estimate rates of celiac disease in the Indian population. The research team included G.K. Makharia, A.K. Verma, R. Amarchand, S. Bhatnagar, P. Das, A. Goswami, V. Bhatia, V. Ahuja, S. Datta Gupta, and K. Anand. They are affiliated with the Department of Gastroenterology and Human Nutrition at the All India Institute of Medical Sciences in New Delhi, India. For their cross sectional study, the team estimated rates of celiac disease in urban and rural populations in the National Capital Region in Delhi, India. For their estimate, they made door-to-door visits with a structured questionnaire, collecting socio-demographic data, and screening for features of celiac disease, namely chronic or recurrent diarrhea and, anemia. In children, they included short stature, and failure to thrive/gain weight. All respondents who screened positive for any of the above factors, and 10% of screen negative individuals received blood tests for the anti-tissue transglutaminase antibody. Those with positive blood tests were invited to undergo further evaluation including endoscopic biopsy. Diagnosis for celiac disease was made on the basis of a positive blood test, the presence of villous atrophy and/or response to gluten free diet. Overall, the team had 10,488 participants, just over 50% of which were male. A total of 5622 participants (53.6%) showed positive first screens. Of those, 2167 (38.5%) received blood test. The team also blood tested an additional 712 (14%) negative first screens. The team found a total celiac disease blood screen rate of 1.44%, with 95% confidence interval [CI] 1.22 1.69, and a total celiac disease rate of 1.04%, with 95% CI 0.85 1.25. The prevalence of celiac disease in this north Indian community is slightly over one percent, which is about the same as many western nations, and higher than generally recognized in India. Source: J Gastroenterol Hepatol. 2011 May;26(5):894-900. doi: 10.1111/j.1440-1746.2010.06606.x.
  20. Celiac.com 10/02/2017 - For anyone following the efforts by ImmusanT to develop a vaccine for celiac disease, the company's recent presentations at the 2017 International Celiac Disease Symposium (ICDS) in New Delhi, India, were welcome news. Nexvax2® is a therapeutic vaccine intended to protect against the effects of gluten exposure while maintaining a gluten-free diet in HLA-DQ2.5+ patients with celiac disease. The company announced at ICDS 2017 that it has presented data showing the immunologic basis for the early clinical effects of gluten in celiac disease. Presented in two poster presentations and an oral presentation, the company says its data show that "early cytokine changes in blood following gluten ingestion could provide the basis for a new diagnostic for celiac disease in patients on a gluten free diet with an uncertain diagnosis," said Robert Anderson, MBChB, Ph.D., Chief Scientific Officer of ImmusanT. The company says its results are "significant" because celiac disease sufferers often adopt a gluten-free diet prior to being diagnosed by a doctor. This can cause problems and lead to unreliable or misleading results with current diagnostic tests. ImmusanT says that their data demonstrate that early changes in circulating cytokines after a single gluten exposure may offer a clinical way to assess celiac disease activity. The company says that the data, along with the potential to differentiate between celiac disease and non-celiac gluten sensitivity (NCGS) by assessing IL-2 levels, support the science behind targeted immunotherapies such as Nexvax2®. Read more at BusinessWire.com
  21. Celiac.com 08/28/2008 - Gluten intolerance can affect all the mucous membranes of the body in sensitive individuals, including the bladder lining. I was diagnosed in 1996 with an incurable, progressive, painful disease called interstitial cystitis. The symptoms mimic those of a bad bladder infection, although most lab tests are negative for bacteria, and antibiotics generally do not help. I knew as a nurse how the bladder functions, and that it needs to have an intact lining to tolerate holding all the toxic wastes of the body prior to elimination. It made sense to me to try a dietary approach, and I had good luck immediately by excluding from my diet known bladder irritants like tomatoes, caffeine, chocolate, citrus, and alcohol, even though most doctors at the time gave diet little credit for a reduction in symptoms. Nevertheless, the disease did progress over time, and I eventually needed to take pain medications, anti-spasmodics, and other medications to enable me to function. Every urine test showed that I had significant amounts of blood in my urine. No one ever tested me for food allergies, gluten intolerance, or considered any other possible cause. No one suggested that my symptoms were part of a systemic dysfunction in my body. I had a painful disease, and they would give me as much pain medicine as I wanted, but there was no cure. I was no longer getting enough sleep to enable me to function well as a nurse. I made the choice to stop working for a few years to concentrate on rebuilding my health. I was in constant pain. It was about this time that I began turning to alternative practitioners for help, and started experimenting with my diet, as well as having food allergy and sensitivity testing done. I had some success eliminating the swelling in my pelvic area using castor oil packs, enough so that when I had increased swelling from eating a particular food, I could tell the difference. Careful observation showed me what did and did not negatively affect my bladder. Eliminating gluten resolved a long-standing rash on my legs, called dermatitis herpetiformis, and after about two years and a lot of alternative bodywork, my bladder began to significantly recover. It was the first area to show symptoms, and the last to recover. Now, twelve years after my interstitial cystitis diagnosis, my urologist readily agrees that gluten negatively affects the bladder in some portion of her patients, and that eliminating gluten leads to a reduction in symptoms. All of my urine tests are perfectly normal and I sleep at night. Still, there are almost no published journal articles linking gluten intolerance and the bladder. I am trying to get the word out there, specifically, the idea that we do not have to live with constant pain, and that what we eat can affect our health. My future goals include beginning an informal clinical trial in the form of a support group for patients willing to try a gluten-free diet as a treatment for chronic bladder symptoms. If anyone is interested in the link between bladder symptoms and gluten sensitivity, I have pages of anecdotes gathered from many people who have experienced healing on a gluten-free diet. The Connection Between Bladder Symptoms And Gluten Sensitivity - A Collection Of Personal Experiences* *Names have been changed to initials to protect individualsprivacy.The author has the originalweb-posts or other identifying information. A summary of web posts from icpuzzle@yahoogroups.com and intersitialcystitischronicpain@yahoogroups.com and personal communications revealing strong evidence of a connection between bladder symptoms and gluten sensitivity. This article is an adjunct/follow-up to the above article on gluten sensitivity and bladder disease. …”The main help came from W.’ssuggestion to try to eliminate wheat-barley-rye (gluten).The Elmiron was getting close it it’s maxwithout constantly abusing the situation with gluten…about three months ago Istarted eliminating gluten-carrying grains, “wallah” absolutely the mostsignificant change started happening about 3 or 4 days from the last day ofgluten. How much better am I now sincethen – about 500% better (close to where I was when I first noticed the IC,even though I didn’t know what was happening – close to TWENTY YEARS AGO). I am still of the opinion that some kind ofcritters have and maybe still play a part of this. I have taken every kind of antibiotic, with alittle success now and then, but not enough to kill it.” “It took about 3 months to seemild improvement, about a year to see moderate improvement, and about 2 yearsto feel much better. I am not 100percent symptom free, but most of the time I am a very manageable level ofsymptoms, and when I flare (from diet or sex) it is very short lived.I am down to one Elmiron a day (from theoriginal dose of 3) and I also do a gluten and sugar free version of the ICdiet, which I also think has helped me a lot.” “I have had IC for 30 yearspretty severely. It was only this pastyears that I got tested …and found out I had a severe wheat-gluten allergy tothe point that I cannot ingest one bite of anything with wheat or gluten…theysaid my whole digestive tract was inflamed…Over the years I knew I was wheat,dairy, and sugar intolerant but these (latest) tests are more specific and letyou know the levels. I feel muchstronger and have many days when I am symptom free. I finally feel different.” “I have started cutting wheat andgluten out of my diet, its been about 2 weeks now. I, like M., have IBS. I am feeling better every day.I am following a diet very similar toyours.Thank you for posting it again!” “I have had IC for over adecade. I have been on a gluten freediet for over 6 years and that has been the only thing that has given me anyrelief from the IC. I no longer take anymeds at all – haven’t even been to a doctor for the IC in several years.Glad to hear someone else is seeing thebenefits of the gluten-free diet for IC and getting the word out. I would definitely suggest anyone with ICgive it a try. It definitely gave me mylife back." “Where have you been for the lasttwenty plus years?You may have saved mylife.I have described these symptomsfor years to doctors and never got an answer that sounded even close to whatwas happening. Just “try these antibiotics”once in a while at the beginning (there was minimal change), but more and morethe antibiotics got more and more expensive with less and less effect if any atall, it even included the kill-all antibiotic – kills everything except me…Went to nerve doctor ($2,500 plus, pelvic x-rays (2 or 3 types).One of the urologists… never said anythingbut “prostatitis” over and over again. My head now also has a nearperfectly clear thinking ability, before it was always a bit cloudy even thoughI may not have been totally aware of it.The feel of carrying extra weight is now almost gone. The gluten issue may not be theonly issue I have – prostatitis is likely to be part of the pain problem, butthere is no question that the gluten issue has been a very, very large part andis now subsiding.” “I was tested for glutenintolerance but it came out negative but while I awaited results I went gluten free and I felt so goodI never went back. I have had a lot ofimprovement going gluten and sugar free as well.I can find rice pasta, lasagna etc.easily. It’s amazing how you don’t haveto try hard to substitute (for) it.” “I have gone from having to gowith urgency every 5 to 10 minutes and being in constant pain (especially atnight) to having almost no symptoms. I am not “cured”. I am still working on healing. I occasionally have a mild flare. Gradually I am able to add foods back into mydiet – a very different diet than before. Whole foods, more veggies, only whole grains (no wheat), no sugar, and anoverall more alkaline diet….There is help. There is hope.” “I am just into the first severalchapters of the book (Solving the IC Puzzle, by Amrit Willis, R.N.), but wantedto stop and ask if there were any people who were celiac or gluten intolerant thatalso suffer from IC. In my celiacsgroup, there are quite a few that have celiacs that (also) have IC.Autoimmune – allergy – poor lifestyle choices– toxic body – all related. So, I amwondering if there are others in this IC group that are glutenintolerant/celiacs or who have suffered from, have, or have healed fromautoimmune diseases…” “I have celiac disease also. I was diagnosed via a blood test about 4months before the IC thing came to a head. I disregarded the doctor’s warning to stay away from gluten/wheat.I went to a gastroenterologist because I feltlike I was having a stomach flu every 2 weeks. So I saw this guy and he gave me the blood test results (which Iignored) until finally, I felt so bad I decided to whit the gluten/wheat.I had a friend who has celiac really severelyand she told me that I might as well cancel my hydrodistention to test for ICbecause eliminating wheat/gluten might clear everything up for me. Unfortunately, I had thehydrodistention which made me much worse, IC-wise….Sorry for the long-windedanswer.I finally stopped taking theElmiron…So far so good.I really don’texpect to have a problem. It was justhard letting go. I don’t know which came first(the celiac or the IC).Looking back,every time I drank beer I always felt bloated right away. Classic example, on our way to skiing, wewould stop for two beers. Relievingmyself before getting back in the car, I would be dying for the bathroom beforewe reached our destination, 45 minutes later. I though this was normal.Isuppose it was the celiac and IC kicking in. Too bad it would take 10 years and 3 pregnancies later to diagnose it…” “I have been diagnosed withgluten sensitivity and am gluten-free. Since I was already eating very little in the way of grains at mynutritionist’s urging, I don’t find the diet that difficult to follow.I try to be very careful.” “I agree with these 2 types ofpastas. I also find that when I eatwheat (which is an allergy I have) that my bladder gets irritated…” “…So, W. your IC is totally goneright now – especially after cutting out gluten? I have known for years and years that I wasgluten sensitive as whenever I wouldn’t eat gluten or wheat, if I just atevegetables and protein my stomach would be soooo quiet.Hindsight is 20/20 – just wish I would havegiven up gluten years ago and maybe this wouldn’t have happened. I am checking into pelvic floortherapy and will have that done along with many other things – I am soterrified of this getting worse, absolutely scared to death. Thanks for your words ofencouragement and comfort.” (Personal Communication)“Suddenly some of the mysteriesof what's been called my "wheat intolerance"or "allergy" were resolved. In particular, I no longer thinkI'm crazy for suspecting a link between my 2.5-year-long urinary tract infection and the onset of my moreobviously wheat-related symptoms. Thanks so much for getting theword out, and sharing your experience!” (Personal Communication) “I about fell off my chair when Iread about your bladder stuff. I've seen 3 specialists (including adigestive doc and a urologist!!), a regular PCP, and a naturopath, andnone of them were willing to consider a link between wheat issues and my poorbladder's troubles. It was like the world lifted offmy shoulders - I'm not crazy! And my body is not the wreck I thought itwas at the ripe old age of 31!Seems funny to be exultant aboutprobably having celiac disease, but that's whatI've been since.”
  22. Celiac.com 09/29/2017 - What is it about the Internet that seems to bring out the worst in some people? In this case, internet trolls making nasty comments about reality star and popular UK country singer Megan McKenna. The body-shaming began almost immediately after McKenna posted two photos of herself on Instagram this summer. According to BuzzFeed, comments calling her things like "boney" and a "skinny rat," flooded in. McKenna recently explained that, at the time the photos were taken, she was in the hospital dealing with the the effects of a medical condition. McKenna has been open about having celiac disease, even speaking about her digestive struggles on Celebrity Big Brother. "Everyone knows I'm a celiac, and I've just been diagnosed with Irritable Bowel Syndrome," she told The Sun. Before filming her new show, There's Something About Megan McKenna, she was "in and out of the hospital and no one knew what was wrong with me, so yes I was thin as I was unwell," she said. As is often the case, the nastiness of the commenters was simply out of touch with the reality that McKenna was struggling with an illness, and thus likely did not need to be told how horrible and thin she looked. McKenna is likely having the last laugh in all of this. Now that she has a diagnosis, and can get treatment, her symptoms should improve, and her health should improve with it. In the meantime, she is currently outselling Taylor Swift on iTunes. Read more at: refinery29.com.
  23. Celiac.com 09/27/2017 - Patients who have clinical, genetic and histological signs of celiac disease, but no serological markers, present a challenge when it comes to making a diagnosis. If the patient doesn't have elevated antibodies, what signs do doctors look for? What's the best way to evaluate the patient's natural history and response to a gluten-free diet? A team of researchers recently set out to outline a specific profile, and to evaluate the natural history and response to a gluten-free diet of patients with seronegative celiac disease. The research team included Maria Pina Dore; Giovanni Mario Pes; Ivana Dettori; Vincenzo Villanacci; Alessandra Manca and Giuseppe Realdi. They are variously affiliated with the Internal Medicine Section, Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy, with the Baylor College of Medicine, Michael E. DeBakey VAMC, Houston, TX, USA, the Pathology Section, Department of Molecular and Translational Medicine, Spedali Civili and University of Brescia, Brescia, Italy, and with the Pathology Section, Department of Clinical and Experimental Medicine, University of Sassari in Sassari, Italy. Patients with duodenal mucosa damage Marsh I, II and III stages, HLA DQ2/DQ8 haplotype and clinical features suggestive of celiac disease, but with negative celiac serology, were defined as seronegative celiac patients. The team excluded other common causes of duodenal mucosa damage. They the compared HLA–DR and DQ genotype/haplotype between all Marsh stages of patients with seronegative and seropositive celiac disease. They then assessed clinical features, lab tests and histological findings after a gluten-free diet and a gluten re-challenge. The group provided the team with a long follow-up period to gather data. The researchers enrolled a total of 48 patients who fulfilled diagnostic criteria over a 4-year period. Patients with seronegative and seropositive celiac disease showed similar clinical phenotype and HLA−DR and DQ frequencies. However, Marsh I stage was seen in 42% of seronegative patients (42% vs 22%; p<0.05). After a 1-year gluten-free diet trial, clinical symptoms, histological features and laboratory testing improved in 40 patients and worsened in those who underwent a 6-months gluten challenge. Five patients with seronegative celiac disease (25%) experienced the occurrence of autoimmune diseases during an average follow-up of about 11 years. Patients with seronegative celiac disease did not show any specific profile, but they did see benefits from a gluten-free diet similar to seropositive patients. In the absence of more sensitive serological markers, diagnosing seronegative celiac disease remains an often confusing and challenging process of excluding various other possibilities. Source: BMJ Open Gastro. 2017;4(1):e000159
  24. Celiac.com 11/30/2016 - Trials using hookworm as a possible treatment for celiac disease are already underway in Australia, but they latest hookworm news indicates that they might also be useful for treating asthma. The New World hookworm, aka necator americanus, is long and slender as an angel hair noodle. Adults are large enough to be seen with the naked eye. Seen up close, they look more like the sand worms in the movie Dune than anything people are used to seeing here on earth. Researchers are reporting that a protein produced by hookworms reduces the symptoms of asthma in mice, and could one day be used to treat asthma in humans, says the journal Science Translational Medicine. These parasites are some of the most maligned creatures in the animal kingdom. They chew into the human intestinal wall and suck blood to survive, but they just might be the key to making millions of people healthier. Says Severine Navarro, the paper's lead author and a senior research fellow at James Cook University in Australia, data from immunological studies shows that populations with no parasites also have "the highest incidence of autoimmune diseases and allergies." The data in this study arose from an effort by Navarro and her fellow researchers to look for a connection between success of de-worming programs around the world and the rise of immune system problems like asthma and celiac disease. Among other things, when hookworms infect humans, they secrete chemicals that turn off the immune alarm bells and repair the tissue around it. The worms limit blood consumption to a few drops a day and keeps its own numbers in check by plants offspring in the host's poop to ensure an orderly exit from the body. Navarro and her team wonder if the hookworm's stealthy adaptations also benefit their host by controlling in adverse immune reactions. The team's initial small study of one dozen trial participants showed that the hookworm did improve their tolerance of gluten. Since infecting large numbers of patients directly with hookworm might lead to other issues, the team isolated the active ingredient in hookworm spit - a compound called AIP-2 - and injected it into asthmatic mice on a daily basis for five days. Results showed a sharp decline in asthma symptoms, and reduced inflammation in airways. These benefits persisted for 10 weeks after the mice stopped getting the treatment. The researchers also noticed that AIP-2 seemed to have a calming effect on the body's dendritic cells - a part of the immune system responsible for processing threats. According to Navarro, the drug works by "basically rewiring the cells in that tissue into promoting very efficient regulatory T cells." This suggests that AIP-2 might also help humans, since dendritic cells have the same function in us that they do in mice. Navarro said the team's next step is a phase one clinical trial, which would test the effectiveness of an AIP-2 pill. Successful phase one trials will lead the way toward a safe drug that could help tens of millions of asthma sufferers. As seen in earlier studies using hookworm, the compound might be useful in treating autoimmune disorders, like celiac disease, inflammatory bowel disease and multiple sclerosis. Read more on hookworms and celiac disease. Source: ChicagoTribune.com.
  25. Celiac.com 09/21/2017 - Current guidelines by the British Society of Gastroenterology recommend that doctors take at least four duodenal biopsy specimens at the time of upper gastrointestinal (UGI) endoscopy when looking for celiac disease. The practice has been shown to increase celiac diagnoses, and to reduced missed diagnoses. The Society recently sought to assess compliance with their own guidelines within their institution. They then sought to apply measures to improve their compliance rate, and to assess the resulting impact on our diagnostic rate for celiac disease. The research team included Nilofer Husnoo; Wafaa Ahmed; and Muhammad Hanif Shiwani. They are variously affiliated with the Urology Department, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK, the Gastroenterology Department, Maidstone and Tunbridge Wells NHS Trust, Tunbridge Wells, UK, and the General Surgery Department, Barnsley General Hospital NHS Foundation Trust, Barnsley, UK. The team performed a retrospective audit of electronic records for patients with no prior celiac diagnosis, who underwent UGI endoscopy with duodenal biopsies between August 2014 and May 2015. They then used the information to raise awareness among endoscopy users at the Society, and conducted a follow-up audit between February and May 2016. They found and registered a total of 924 eligible patients for the first part of the study, and 278 for the second part. The proportion of patients who had ≥4 biopsy specimens submitted increased from 21.9% to 60.8% (p<0.001). The study by the BSG suggests that taking less than four duodenal biopsy specimens can result in missed celiac diagnoses. However, a few simple steps can help doctors avoid such missed diagnoses. Since atypical symptoms are more common in patients these days, and since the lifetime risk of malignancy, especially intestinal lymphoma and other gastrointestinal cancers, is higher in celiac patients, it's important that doctors conduct a thorough investigation when they suspect celiac disease to avoid missing the diagnosis. For the BSG, that means taking 4 or more biopsy samples. Source: BMJ Open Gastro. 2017;4(1):e000140
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