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Found 1,242 results

  1. Celiac.com 10/16/2018 - Apparently, local St. Louis radio station Z1077 hosts a show called “Dirty Little Secret.” Recently, a woman caller to the show drew ire from listeners after she claimed that she worked at a local bakery, and that she routinely lied to customers about the gluten-free status of baked goods. The woman said she often told customers that there was no gluten in baked goods that were not gluten-free, according to local tv station KTVI. Apparently the woman thought this was funny. However, for people who cannot eat gluten because they have celiac disease, telling people that food is gluten-free when it is not is about as funny as telling a diabetic that food is sugar-free when it is not. Now, of course, eating gluten is not as immediately dangerous for most celiacs as sugar is for diabetics, but the basic analogy holds. That’s because many people with celiac disease suffer horrible symptoms when they accidentally eat gluten, including extreme intestinal pain, bloating, diarrhea, and other problems. Some people experience more extreme reactions that leave them in emergency rooms. As part of a story on the “joke” segment, KTVI interviewed celiac sufferer Dana Smith, who found the punchline to be less than funny. “It’s absolutely dangerous, somebody could get very sick,” said Smith. KTVI also interviewed at least one doctor, Dr. Reuben Aymerich of SSM St. Clare Hospital, who pointed out that, while celiac disease is “not like diabetes where you can reduce the amount of sugar intake and make up for it later, it’s thought you need to be 100 percent compliant if you can.” For her part, Smith sought to use the incident as a teaching moment. She alerted the folks at Z1077 and tried to point out how serious being gluten-free is for many people. Mary Michaels, owner of Gluten Free at Last Bakery in Maryville, Illinois, says it’s time people became more respectful. “I wouldn’t make fun of you if you had diabetes or a heart condition it’s kind of like that,” Michals said. We will likely never know if the radio station caller was telling the truth, or just putting listeners on. The Z1077 morning team did post a follow-up comment, which stated that they take celiac disease seriously, and that they did not intend to offend anyone. One host said his mom has celiac disease. It’s good to see a positive response from the radio station. Their prank was short-sighted, and the caller deserved to be called out on her poor behavior. Hopefully, they have learned their lesson and will avoid such foolishness in the future. Let us know your thoughts below.
  2. Celiac.com 10/22/2018 - A team of researchers recently set out to determine if there is any association between prenatal gluten exposure and offspring risk of type 1 diabetes in humans. The research team first designed a national prospective cohort study using the national health information registries in Denmark. They looked at data on pregnant Danish women enrolled into the Danish National Birth Cohort, between January 1996 and October 2002, and assessed maternal gluten intake, based on maternal consumption of gluten containing foods, as reported in a 360 item food frequency questionnaire at week 25 of pregnancy. The team gathered information on type 1 diabetes occurrence in the participants’ children, from 1 January 1996 to 31 May 2016 by linking to the Danish Registry of Childhood and Adolescent Diabetes. Overall, their study included data on 101,042 pregnancies in 91,745 women, of whom 70,188 filled out the food frequency questionnaire. Once they corrected the figures to account for multiple pregnancies, pregnancies ending in abortions, stillbirths, lack of information regarding the pregnancy, and pregnancies with implausibly high or low energy intake, they included 67,565 pregnancies and 63,529 women. Gluten intake averaged 13.0 grams per day, ranging from under 7 grams per day to more than 20 grams per day. There were 247 children with type 1 diabetes among the group, for an incidence rate of 0.37%, with an average follow-up of 15.6 years. 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. These numbers indicate that high gluten intake by mothers during pregnancy may increase the risk of their children developing type 1 diabetes. However, the team is calling for further study to confirm the findings, preferably in an intervention setting. Read more in BMJ 2018;362:k3547. doi: https://doi.org/10.1136/bmj.k3547 The research team included Julie C Antvorskov, assistant professor, Thorhallur I Halldorsson, professor in food science and nutrition, Knud Josefsen, senior researcher, Jannet Svensson, associate professor5, Charlotta Granström, statistician, Bart O Roep, professor, Trine H Olesen, research assistant, Laufey Hrolfsdottir, director, Karsten Buschard, professor, and Sjudur F Olsen, adjunct professor of nutrition. They are variously affiliated with the Bartholin Institute, Rigshospitalet in Copenhagen, Denmark; the Centre for Foetal Programming, Department of Epidemiology Research, Statens Serum Institute, Copenhagen, Denmark; the Unit for Nutrition Research, Landspitali University Hospital, Reykjavik, Iceland; the Faculty of Food Science and Nutrition, University of Iceland, Reykjavik, Iceland; the Copenhagen Diabetes Research Center (CPH-DIRECT), Department of Children and Adolescents, Copenhagen University Hospital Herlev, Herlev, Denmark; the Department of Diabetes Immunology, Diabetes and Metabolism Research Institute at the Beckman Diabetes Research Institute, City of Hope, Duarte, CA, USA; the Departments of Immunohematology and Blood Transfusion, Leiden University Medical Centre, Leiden, Netherlands; the Department of Education, Science, and Quality, Akureyri Hospital, Akureyri, Iceland; and the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  3. Celiac.com 07/13/2018 - I went to a friend’s home for dinner. A few days before, she called and asked me what I could eat. I asked her what she was planning to make, and she said she was grilling meats with side dishes. I said, “Great. Please just grill a piece of chicken for me with salt and pepper, and I’ll be happy to bring a side.” She said, “No need to bring a side. I’ve got this.” When I arrived, she greeted me and said, “I spent all day cooking tonight’s dinner so you can eat it. Hey would you just check this salad dressing to see if it is OK for you?” I looked at the ingredients and it contained gluten and dairy, both of which I cannot eat. Then I glanced around the kitchen and saw evidence of wheat cross-contamination, including buns being toasted on the grill, and gluten-containing barbeque sauce spilling on the grill where my “clean” chicken was cooking. She had other guests to tend to, and I couldn’t offer instruction or read the ingredients of everything she used in the meal. At social gatherings, I’ve been challenged too by those who ask if I am really “allergic,” or just eating gluten free as a “fad.” I’ve been told many times by hosts and hostesses that, “a little won’t hurt you,” or “everything in moderation,” or “if it is made with loving hands, it is good for you to eat.” Of course, all of this is bunk for those with food allergies or celiac disease. A little bit may kill us, and whether made with loving hands or not, it will certainly make us sick. Those of us with food allergies and/or celiac disease walk a tightrope with friends and relatives. The old rules of etiquette just don’t work anymore. We don’t want to insult anybody, we don’t want to be isolated, and we also don’t want to risk our health by eating foods that may contain ingredients we cannot tolerate. So what do we do? Etiquette books advise us to eat what is put in front of us when we are guests in someone’s home. They caution us at all costs not to insult our hostess. Rather, we are instructed to compliment the hostess on her good cooking, flavor combinations, and food choices. But when foods are prepared in a cross-contaminated environment with ingredients we are allergic to, we cannot follow the old social constructs that do not serve us. We need to work together to rewrite the rules, so that we can be included in social gatherings without fear of cross-contamination, and without offending anyone. Let’s figure out how to surmount these social situations together. Each edition of this column will present a scenario, and together, we’ll determine appropriate, polite, and most importantly, safe ways to navigate this tricky gluten-free/food allergies lifestyle in a graceful way. If someone disagrees with our new behavior patterns, we can refer them to this column and say, “Here are the new rules for those of us with food allergies or celiac disease.” When we are guests in someone’s home, we can give them links to this column so they understand the plight we are faced with, bite after bite. Perhaps this will help those of us living with us to understand, be more compassionate, and accepting of our adaptations to keep ourselves safe. This column will present a scenario such as the one above, and ask that you comment on how you would navigate it. Let’s talk about it. Let’s share ideas. Using the example above, here’s the scenario for this issue: What would you do? Your kind-hearted friend invites you to dinner and insists on cooking for you. You arrive and the first thing she says is, “I’ve spent all day making this for you. Oh, I bought this salad dressing for you, but you might want to read the ingredients first.” You do, and it contains malt vinegar. You look around the kitchen and notice evidence of cross-contamination in the rest of the meal. What do you do? Please comment below and feel free to share the tricky scenarios that you’ve encountered too. Let’s discuss how to surmount these social situations. What would you do?
  4. Celiac.com 10/19/2018 - Work to develop a vaccine for celiac disease could soon lead to a vaccine for diabetes. After successful phase 1 studies of Nexvax2, their peptide-based therapeutic vaccine for celiac disease, ImmusanT has seen a significant investment from venture philanthropy organization JDRF T1D. ImmusanT's peptide therapy program for celiac disease may provide lessons for a similar therapeutic treatment for Type 1 diabetes. The investment will support ImmusanT as it attempts to develop a vaccine to prevent Type 1 diabetes, based on the early success of its peptide immunotherapy program for celiac disease, the two entities announced in a press release. ImmusanT’s celiac peptide therapy program works by identifying antigens that trigger an inflammatory responses in people with autoimmune diseases. Once identified, the peptide therapy is used to neutralize the autoimmune response. This celiac disease program goes back to 1998, when Anderson first began his efforts to find and identify the peptides. The findings were published in 2010, and the company was founded shortly afterward by Leslie Williams, BS, RN, MBA, director, president and CEO of ImmusanT. From there, ImmusanT conducted five phase 1 trials for its celiac therapy. Those trials have proven very promising, and the latest investment into a similar drug for diabetes is proof of that promise. In the case of celiac disease, the drug works by “targeting T cells in patients. Those T cells that are engaged as peptides are distributed throughout the body after the injection, and we see evidence that the T cells are being activated about 2 hours later,” Robert Anderson, BMedSc, MB, ChB, PhD, FRACP, chief scientific officer for ImmusanT, told Endocrine Today. “We found that if we gradually increase the dose in patients building up to a maintenance dose level, they become non-reactive to those peptides.” With much of the early research targeted towards demonstrating the drug’s safety, and getting the right dose and dose regimen, the development of a version targeted at diabetes, says Anderson, “should be more streamlined due to the lessons learned during the celiac disease program. That’s partly because the team knows “a lot more going into Type 1 diabetes about how peptide therapy works and how to optimize it than we did when we started celiac disease, where it was a blank slate.” This is really exciting news. A vaccine for celiac disease is exciting, to be sure, but a viable vaccine for diabetes would be a major development in disease prevention. Stay tuned for more news as the story develops. Read more at Healio.com
  5. Celiac.com 10/10/2018 - The Technical University in Vienna has announced a new remedy for celiac disease symptoms that they say can “alleviate or even completely eliminate the symptoms of celiac disease.” It should be available commercially in only a few years. Because most current efforts to treat celiac disease affect the immune system, possible side effects must therefore be fully assessed. This means years of study, and a long approval process. However, the TU Wien research team worked in collaboration with the industrial partner Sciotech Diagnostic Technologies GmbH to create a different approach. Their team based its approach for a celiac disease treatment on using only the part of the antibody that binds to gluten, which allowed them to create a product that works extremely well, but does not rely on triggering an immune response. Instead of a drug that works on the immune system, TU Wien created a simple medical product that directly attacks the gluten molecules to render them harmless. This makes the approval process much simpler, meaning that the product should be available in ordinary pharmacies as early as 2021. According to Professor Oliver Spadiut, head of the Integrated Bioprocess Development Research Group at TU Wien, “bodies produce antibodies that fit intruding antigens precisely, like a key to a lock. This immune response makes these antigens harmless.” He goes on to say that “If a new antibody fragment is found and produced that docks to and blocks the invading gluten molecule without triggering the immune system, the symptoms of celiac disease can be suppressed." The goal of their research project was to produce a complex of two such antibody fragments that envelop the gluten molecule at a molecular level, so that it can no longer have any further effects in the intestines. The result is a groundbreaking treatment for celiac disease and gluten intolerance. The process is complicated, and requires the team to re-program certain bacteria so that they produce exactly the desired antibody fragment. The full process took a while to iron out, but, says Spadiut, it “can be easily reproduced, can be scaled up to industrial application and delivers a very good yield of the desired product." This is very exciting news. Aside from efforts toward an outright vaccine, this is the first news of a potential treatment that can negate the effects of gluten without affecting the immune system itself. If all goes well, Spadiut says, the product “will be available in ordinary pharmacies in a few years.” Stay tuned for news about ongoing developments of this interesting treatment for celiac disease. Read: Additional scientific information Source: TUWien.ac.at
  6. Celiac.com 10/03/2018 - Gluten-related disorders include the full spectrum of adverse clinical symptoms and conditions triggered by eating gluten. A team of researchers recently set out to review the available medical literature concerning MDs and gluten sensitivity with and without enteropathy. The research team included A Vinagre-Aragón, P Zis, RA Grunewald, and M Hadjivassiliou, with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, South Yorkshire, UK. Celiac disease or gluten sensitive enteropathy is the most common manifestation, but clinicians have reported a number of extra-intestinal manifestations, which may occur without enteropathy. Gluten sensitivity is another term that has been used to include all gluten-related disorders, including those where blood tests show antibodies to gluten in the absence of any enteropathy. Gluten ataxia is the most common extra-intestinal neurological manifestation, and has been well documented. Clinicians have reported movement disorders related to gluten sensitivity. To assess the current medical literature on movement disorders and gluten sensitivity, both with and without enteropathy, the team conducted a systematic search on the PubMed database, and included 48 articles that met the inclusion criteria into the present review. This review demonstrates that the range of gluten related movement disorders goes beyond gluten ataxia, and shows that the majority of patients with gluten-related disorders benefit from a gluten-free diet. Read the full review at: Nutrients. 2018 Aug 8;10(8). pii: E1034. doi: 10.3390/nu10081034.
  7. Celiac.com 09/20/2018 - Some people with celiac disease experience extreme symptoms when they eat gluten. These folks adopt various strategies for navigating the world. One of those strategies involves getting a gluten-sniffing service dog. We’ve done a few stories on gluten-sniffing dogs over the years. Dogs like Zeus and Hawkeye are famous for helping their owners sniff out gluten before they can eat it. Can Gluten-Sniffing Dogs Help People with Celiac Disease? The stories are always popular. People love the stories, and people love the dogs. After all, pretty much anyone with celiac disease who has ever read about gluten-sniffing dogs would love to have one. Who could say no to a warm, fuzzy dog that can take a sniff of your food and signal you when it contains gluten? The stories almost always generate plenty of feedback and more than a few questions. To answer some of those questions, we’ve decided to do an article that provides some facts about gluten-sniffing dogs. Here are a few factors to keep in mind about gluten-sniffing service dogs: Gluten-free Dog Status: One thing to remember is that proper gluten-sniffing dogs are professionally trained service animals, much like seeing-eye dogs or hearing-ear dogs. As professional service animals, the dogs must be trained and certified as service animals. The dogs may then accompany their master pretty much anywhere they go, and are available to assess all food and snacks. Gluten-free Dog Training: Proper training takes time, which equals money. Professional trainers might only train one or two dogs, and the training can take about a year. There are very few trainers for gluten-sniffing dogs, and there are also currently no official guidelines or certification. Gluten-free Dog Cost: In our recent story on the gluten-sniffing black Lab, Hawkeye, we noted that the dog cost $16,000, not including food, and vet bills. Gluten-free Dog Reliability: Nimasensor.com notes that “[g]luten-sniffing dogs may detect gluten in amounts as small as .0025 parts per million with 95 percent to 98 percent accuracy.” The Mercola.com website says that Willow, a gluten-sniffing German shorthaired pointer in Michigan, can detect gluten with 95 percent to 98 percent accuracy. Read more on gluten-sniffing dogs: Gluten-Sniffing Dogs Are Game Changers for People With Celiac Disease Gluten-sniffing dogs help people with celiac disease What to Know About Gluten-Sniffing Dogs Gluten-Sniffing Assistance Dog Helps Celiac Sufferer Lead Normal Life
  8. I've become very sick after eating a homemade soup which contained organic carrots, organic broccoli, organic white potatoes, Harvestland organic chicken and no dry seasonings (bland). My usual symptoms kicked in immediately such as severe stomach pain, hot flashes, chills, diarrhea, nausea, brain fog, muscle, and joint pain, etc., I was diagnosed with celiac disease earlier this year and I've spent lots of money on food, but to no avail. The elimination diet causes a complexity of issues for me—money wasted, further damage my gut and delayed healing. Even healthy foods pose a problem for me and my "tolerable" list of foods are minimal. My symptoms are either a delayed response or immediate, depending on the food. I often ask, "How can a healthy food cause this much discomfort?" I have good days and bad days and symptoms waxes and wanes. I joked with someone that I'm to the point of resorting to eating cardboard. Anyone have advice for me, I'd truly appreciate it.
  9. Celiac.com 01/11/2006 - For many years, biopsy of the small bowel demonstrating villous atrophy has been fundamental to the diagnosis of celiac disease. Older celiacs will remember, fondly or otherwise, the Crosby suction biopsy device which was swallowed attached to a long tube and made its way down to the small bowel where, position confirmed by x-rays, it guillotined a small portion of tissue. The procedure was tedious and technical failures common—only identified when the device was hauled up after several hours. Later it became clear that biopsies from the duodenum obtained during endoscopy were just as good, and the biopsy process became a five minute job with no need for X-rays. Nevertheless, many celiacs are reluctant to undergo biopsy and its necessity is increasingly questioned, particularly now that blood tests for celiac-related antibodies are highly sensitive and specific. There are a number of reasons why, in my own practice, biopsies continue to be helpful in celiacs diagnosed in adulthood. Biopsies are necessary when blood tests are negative. While endomysial (EmA) and tissue transglutaminase (TTGA) antibodies are detectable in most cases where villous atrophy is present, 5-10% of patients lack these antibodies1. In this situation, where the story is suggestive of celiac, perhaps with a family history or strongly suggestive symptoms, biopsy is the only way to make the diagnosis. Increasingly, physicians recognize that many patients with gluten sensitivity do not have villous atrophy (Grade III of the Marsh classification) of "classic" celiac disease, but have milder abnormalities such as crypt hyperplasia (Marsh II) or an excess of the inflammatory cells called lymphocytes (Marsh I). Patients in these categories are less likely to have positive serology2. Biopsies are necessary where false positive blood tests may occur. TTGA, particularly where levels are low, may be associated with diseases other than celiac: ulcerative colitis, Crohns disease, arthritis and liver diseases without any evidence of celiac disease have been linked3. Newer TTGA tests have steadily improved in this regard but I still would be reluctant to diagnose celiac on a TTGA test alone. "False positive" EmA is a different issue which I will return to. Biopsies give a baseline for comparison. Suppose a patient starts a gluten-free diet without biopsy—we dont know whether she or he had Marsh I, II or III or even normal histology. A year later, same patient develops new symptoms of diarrhea, weight loss, whatever. Well get a duodenal biopsy as part of the workup, but its going to be difficult to interpret without knowing what things were like before going gluten-free. Specifically, a baseline to look back at tells us whether the small bowel is better, worse or no different, and helps us decide whether we need to focus on celiac disease as the most likely cause of new problems or explore other possibilities involving the rest of the gut. The biggest diagnostic disaster of all, of course, is the gluten-free diet started without any sort of baseline investigation including antibodies, raising the specter of the infamous gluten challenge if a definitive diagnosis is needed. Biopsies provide a "gold standard" assessment of the state of the bowel. There has been much excitement recently about capsule endoscopy, a wireless device the size of a large pill (not to be confused with the Crosby capsule!) which makes its own way down the small bowel taking pictures as it goes. Characteristic abnormalities can be seen in celiac disease, raising the possibility that this device might be useful in diagnosis. If experience with conventional endoscopes is any guide, however, these abnormalities are missing in a sizeable minority of celiacs particularly with mild disease4 (Capsule endoscopy in its present state of development can not take biopsies). Certainly the capsule allows assessment of the bowel beyond the reach of conventional "anaconda-style" endoscopes, but I am not convinced at present that it can replace biopsy. A follow-up biopsy gives an indicator of progress. I offer my patients a repeat biopsy after two years gluten-free and perhaps surprisingly most take up the offer and are keen to hear how things have improved. Ive increased the biopsy interval from one to two years because only 40% of people had complete recovery after 12 months gluten-free5. EmA and TTGA disappearance is only a marker of how successful gluten exclusion has been and is not a reliable indicator of bowel recovery. Does persisting villous atrophy matter if the patient is doing well on a gluten-free diet? Intuitively, one might like to keep a closer eye on the patient with persistently flat biopsies, who could be at greater risk of complications in the future6. The endoscopy not only allows examination and biopsy of the duodenum but also a look at the esophagus and stomach. Sad fact of the ageing process is that you start to collect diseases like trading cards, and just because youre celiac doesnt mean you cant have something else. Its important to have a good look for bleeding lesions in the upper gut even if the blood work for a seventy year old with anemia says celiac (and check out the colon too, but thats a topic for another day). On the other hand, we recognize that biopsies are not always the final arbiter in diagnosis. While the jury is still out on what a TTGA positive, biopsy negative result means with regard to gluten sensitivity, there is plenty of evidence that a positive EmA generally does mean that biopsy abnormalities will follow: My own follow-up of EmA positive, biopsy negative patients indicates that they will develop abnormal histology if not treated7. So it makes sense to start EmA positive people on gluten-free without waiting for significant bowel damage—and as already stated, even a normal baseline biopsy will provide a reference for any problems that might arise in the future. Sometimes I meet a patient with bad gut symptoms but completely normal blood work up and biopsies and when all else fails I will run a trial of gluten-free. It often works, particularly if there is a family history of celiac. But then again, if it doesnt, we have a baseline normal biopsy to say there is no need to persevere. I guess in the future diagnosis of gluten sensitivity will rely on totting up various factors, none individually essential: blood tests, biopsies, family history, genetic testing for the HLA celiac genes. Some researchers are making a case for dropping the biopsy requirement if the antibody blood work checks out in children8, for whom (and for the parents) endoscopy and biopsy is a major issue. In adults however it is quick, straightforward and safe and will remain a key part of my celiac workup. William Dickey is a gastroenterologist at Altnagelvin Hospital, Londonderry, Northern Ireland, with over 400 celiac patients attending his clinics. His interest in celiac disease goes back some fourteen years and he has published extensively on the subject. He is an associate member of Coeliac UKs Medical Advisory Council. References: Dickey W, McMillan SA, Hughes DF. Sensitivity of serum tissue transglutaminase antibodies for endomysial antibody positive and negative coeliac disease. Scand J Gastroenterol 2001; 36: 511-4. Wahab PJ, Crusius JBA, Meijer JWR, Mulder CJJ. Gluten challenge in borderline gluten-sensitive enteropathy. Am J Gastroenterol 2001; 96: 1464-69. Di Tola M, Sabbatella L, Anania MC, Viscido A, Caprilli R, Pica R, Paoluzi P, Picarelli A. Anti-tissue transglutaminase antibodies in inflammatory bowel disease: new evidence. Clin Chem Lab Med. 2004;42(10):1092-7. Oxentenko AS, Grisolano SW, Murray JA, Burgart LJ, Dierkhising RA, Alexander JA. The insensitivity of endoscopic markers in celiac disease. Am J Gastroenterol. 2002 Apr;97(4):933-8. Dickey W, Hughes DF, McMillan SA. Disappearance of endomysial antibodies in treated celiac disease does not indicate histological recovery. Am J Gastroenterol 2000; 95: 712-4. Meijer JWR, Wahab PJ, Mulder CJJ. Histologic follow-up of people with celiac disease on a gluten-free diet: slow and incomplete recovery. Am J Clin Pathol 118(3):459-63, 2002 Sep. Dickey W, Hughes DF, McMillan SA. Patients with serum IgA endomysial antibodies and intact duodenal villi: clinical characteristics and management options. Scand J Gastroenterol 2005: in press Barker CC, Mitton C, Jevon G, Mock T.Can tissue transglutaminase antibody titers replace small-bowel biopsy to diagnose celiac disease in select pediatric populations? Pediatrics. 2005 May;115(5):1341-6
  10. Celiac.com 10/05/2018 - This short quiz includes basic celiac facts, recent celiac and gluten-free news and other information that appeared in the last few months on Celiac.com. The answers are in the section below the quiz, so don't peek! True or False? A tainted gluten-free meal nearly killed an Australian woman. Bifidobacterium infantis NLS super strain reduces a-Defensin-5 expression in celiac disease patients. Vitamin A and D deficiency common in kids with newly diagnosed celiac disease. New UK fund promotes celiac research and gluten-free food improvement. Easy to spot tooth wear and enamel defects point to celiac disease. Undiagnosed celiac disease more common in women and girls. Research indicates 1.4% of humans have celiac disease. A new urine test can spot gluten in the blood of people with celiac disease. Women's diet during pregnancy has little impact on celiac disease risk in their infants. Gluten-Free condoms are available for people concerned about topical exposure to gluten. A Phoenix realtor recently advertised a house as 'gluten-free.’ Current screening methods miss significant cases of celiac disease. A new vaccine makes it safe for people with celiac disease to safely consume gluten. A long-distance conversation with a guru can help treat your celiac disease. Food made with gluten-free ingredients is safe for people with celiac disease. Celiac disease is a food allergy. Celiac disease rarely affects people of non-European ancestry. Celiac disease is a children’s condition. Celiac disease can be painful, but isn't life-threatening. A little gluten is okay for people with celiac disease and gluten-intolerance to eat. ANSWERS Here are the answers for our short quiz above on basic celiac facts, recent celiac news and other information. True or False? A tainted gluten-free meal nearly killed an Australian woman. TRUE Bifidobacterium infantis NLS super strain reduces a-Defensin-5 expression in celiac disease patients. TRUE Vitamin A and D deficiency common in kids with newly diagnosed celiac disease. TRUE New UK fund promotes celiac research and gluten-free food improvement. TRUE Easy to spot tooth wear and enamel defects point to celiac disease. TRUE Undiagnosed celiac disease more common in women and girls. TRUE Research indicates 1.4% of humans have celiac disease. TRUE A new urine test can spot gluten in the blood of people with celiac disease. TRUE Does Diet During Pregnancy Have Any Impact on Celiac Disease Risk in Infants? TRUE Gluten-Free condoms are available for people concerned about topical exposure to gluten. TRUE A Phoenix realtor recently advertised a house as 'gluten-free.’ TRUE. Phoenix realtor Mike D’Elena recently advertised a house as 'gluten-free’. Current screening methods miss significant cases of celiac disease. TRUE A new vaccine makes it safe for people with celiac disease to safely consume gluten. FALSE. While several such vaccines are under development, with some even undergoing clinical and human trials, no such drug has been proven to work and approved by the FDA. Hopefully the clinical tests will work and this will one day be an alternative for some people. A long-distance conversation with a guru can help treat your celiac disease. FALSE Food made with gluten-free ingredients is safe for people with celiac disease. FALSE. Just because food is made with gluten-free ingredients does not necessarily make it safe for people with celiac disease. Case in point, Domino’s Pizza recently introduced gluten-free pizza crusts. However, these pizzas are prepared in the same areas and ovens as Domino’s regular pizzas, and may be contaminated with gluten from wheat flour. These pizzas are not considered safe for people with celiac disease. There are many similar cases in the restaurant world. Contamination is a serious issue for some celiacs, so buyers be aware and be wary. Celiac disease is a food allergy. FALSE. Celiac disease is not a food allergy or an intolerance, it is an autoimmune disease. People with celiac disease suffer damage to the lining of the small intestine when they eat wheat, rye or barley. They also face higher risks for many other auto-immune conditions. Celiac disease rarely affects people of non-European ancestry. FALSE. Celiac disease is more common in people of northern European ancestry, but it affects all ethnic groups and is found in southern Asia, the Middle East, North Africa and South America. Celiac disease is a children’s condition. FALSE. Celiac disease can develop at any age. In fact, celiac disease is most commonly diagnosed in people aged 40-60 years old. Celiac disease can be painful, but isn't life-threatening. FALSE. It’s true that classic celiac disease symptoms, like stomach pain, bone pain, fatigue, headaches, skin rash, and digestive issues, won’t kill patients outright. However, undiagnosed or untreated, celiac disease can trigger other autoimmune disorders, and leave patients at much greater risk of developing certain types of deadly cancer. A little gluten is okay for people with celiac disease and gluten-intolerance to eat. FALSE. Gluten levels above 20 parts per million can cause adverse immune reactions and chronic damage in people with celiac disease. Read more about celiac disease, gluten, gluten-free and gluten intolerance facts at Celiac.com.
  11. Celiac.com 03/27/2017 - A number of researchers are looking to provide alternative or adjunct treatments to the gluten-free diet in celiac disease. Meanwhile, a number of companies are currently developing a wide variety of such options, ranging from various kinds of enzyme therapies, to treatments that eliminate celiac disease reactions, even to vaccines to inoculate celiac sufferers against their condition, perhaps allowing for full recovery and a return to non-gluten-free eating habits, as desired. At least, that's one dream. More likely will be the development of enzymes or other treatments that offer celiacs varying degrees of protection from gluten ingestion. Most likely, such treatments would be designed to augment an existing gluten-free diet, and to provide protection against moderate gluten-contamination when eating out. One particular enzyme that shows strong potential in breaking down toxic peptides in A-gliadin, the main culprit in celiac reactions, is caricain. A recent paper discusses the scientific principles behind the use of caricain for enzyme therapy. The paper is based on a recent study, in which a team of researchers set out to review the structures of the toxic peptides in A-gliadin for key sequences of amino acids or motifs related to toxicity, especially with respect to digestive difficulties, or immunogenicity. The research team included Hugh J. Cornell and Teodor Stelmasiak. They are affiliated with the RMIT University, School of Applied Sciences, Melbourne, Australia, and with Glutagen Pty Ltd, Maribyrnong, Victoria, Australia. For their study, they first evaluated structures of synthetic A-gliadin peptides shown to be toxic in the fetal chick assay, both before and after digestion with duodenal mucosa from patients in long remission. They also measured synthetic peptides corresponding to the undigested residues, and compared the key amino acid sequences, to see if they might be related to direct toxicity and immunogenicity of the peptides. They found that the smallest toxic peptides from celiac mucosal digestion were octa-peptides, which they found in greater amounts than similar products from normal digestion. One of those peptides corresponded to residues 12-19 of A-gliadin and contained the key motifs PSQQ and QQQP of De Ritis et al., while the other corresponded to residues 72-79, and contained the key motif PYPQ (extending to PYPQPQ). These key motifs have been noted by other workers, especially those investigating immunological activity over the past two decades. They are present in undigested residues from celiac mucosal digestion These motifs, along with the greater prevalence of these residues, as compared with residues from normal digestion, supports the basic notions underpinning enzyme therapy for celiac disease. This study also supports the basic scientific merits of research and development of the enzyme caricain to break down gliadin peptides with two different types of toxicity, and thus to potentially benefit people with celiac disease. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 113-120. doi: 10.12691/ijcd-4-4-2 Previous study: NCBI
  12. Celiac.com 09/28/2018 - MIT researchers have found that intestinal stem cells removed from mice after fasting for 24 hours and grown in culture have twice the regenerative capacity of stem cells grown in culture from non-fasting mice. The study provides evidence that fasting induces a metabolic switch in the intestinal stem cells, switching from utilizing carbohydrates to burning fat. Switching these cells to fatty acid oxidation enhances their function significantly. The study also found that the beneficial effects of fasting can be reproduced by treating mice with a molecule that mimics the effects. Stem cell regeneration is dramatically improved by fasting in both young and older mice. Intestinal stem cells in humans lose their ability to regenerate as humans age, making it more difficult for older people to recover from gastrointestinal disease and disorders. Fasting and/or the use of drugs to mimic the regenerative effects of fasting on intestinal stem cells may, therefore, be useful to improve recovery from intestinal injury in older patients if the mice study findings are shown applicable to humans. This study brings to mind past research on the protein R-spondin1 which showed great potential in completely regenerating and restoring the intestinal lining. R-spondin1 was being developed as a drug by Nuvelo, Inc. of San Carlos, CA designated as NU206 in 2005. Despite early successful human safety clinical trials in 2008, research was shelved and the promising drug has continued to sit idle on the shelf for years. The patent for NU206 is now owned by ARCA Biopharma http://arcabio.com/ of Westminster, CO after a merger with Nuvelo, Inc. in 2009. Fasting to regenerate the intestinal lining is free and requires no FDA approvals (though physician supervision may be advised.) Fasting may provide other potential health benefits. A Yale study found that during dieting or fasting the compound beta-hydroxybutyrate is produced which inhibits the inflammatory response in several disorders including autoimmune diseases, type 2 diabetes, Alzheimer's disease, atherosclerosis, and autoinflammatory disorders. Fasting can also affect the activation of T cells. T cells are leukocytes, white blood cells. T cells are activated by antigens from pathogens presented to T cell receptors which initiates an immune response against the pathogens. In autoimmune disease, antigen presented to T cell receptors initiates an immune response which results in damage to the body itself. A Luxembourg Institute of Health study found that glutathione, important for metabolic waste disposal and detoxification, also acts as a switch which stimulates T cell energy metabolism while keeping T cells clear of metabolic wastes. Without glutathione, T cells remain inactive and sit in a hibernation state. T cell inactivity is undesirable for fighting off an infection, but, otherwise, keeping T cells inactive may ward off harmful effects of autoimmune disease. Fasting lowers the body's glutathione level as the body constantly consumes glutathione. In one 7-day fasting study involving healthy humans, a progressive decline in total glutathione concentration in leukocytes was found during seven days of starvation due to a decrease in free glutathione content. This study provides proof that fasting lowers glutathione levels in T cells. Hence, based on the Luxembourg study, fasting can reduce or stop the activity of T cells. Thus, fasting can be used to relieve the symptoms of autoimmune disease resulting from a T cell immune response, providing that the subject is otherwise infection free and has no condition requiring an active T cell response. Finally, as shown in a University of Southern California study, multiple fasting cycles lasting 2 to 4 days over a period of 6 months in both mice and humans work to rid the body of older and damaged white blood cells and trigger white blood stem cells to self-regenerate and fully repopulate the immune system with new white blood cells. Besides having applications to recovery from immune system damage caused by cancer chemotherapy toxicity, these immune system rejuvenation effects from fasting may have potential benefit applicable to treatment of autoimmune disorders. Sources: Fasting boosts stem cells' regenerative capacity. A drug treatment that mimics fasting can also provide the same benefit, study finds. Anne Trafton - MIT News Office May 3, 2018 http://news.mit.edu/2018/fasting-boosts-stem-cells-regenerative-capacity-0503 Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging. Mihaylova MM, Cheng CW, Cao AQ, Tripathi S, Mana MD, Bauer-Rowe KE, Abu-Remaileh M, Clavain L, Erdemir A, Lewis CA, Freinkman E, Dickey AS, La Spada AR, Huang Y, Bell GW, Deshpande V, Carmeliet P, Katajisto P, Sabatini DM, Yilmaz ÖH. Cell Stem Cell. 2018 May 3;22(5):769-778.e4. doi: 10.1016/j.stem.2018.04.001. https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(18)30163-2 Mitogenic influence of human R-spondin1 on the intestinal epithelium. Kim KA, Kakitani M, Zhao J, Oshima T, Tang T, Binnerts M, Liu Y, Boyle B, Park E, Emtage P, Funk WD, Tomizuka K. Science. 2005 Aug 19;309(5738):1256-9. https://www.ncbi.nlm.nih.gov/pubmed/16109882 Nuvelo, Inc. Announces Positive Results from Phase 1 Clinical Trial of NU206 in Healthy Volunteers. Published: Dec 10, 2008 https://www.biospace.com/article/releases/nuvelo-inc-announces-positive-results-from-phase-1-clinical-trial-of-nu206-in-healthy-volunteers-/?keywords=nu206 Anti-inflammatory mechanism of dieting and fasting revealed. By Karen N. Peart February 16, 2015 https://news.yale.edu/2015/02/16/anti-inflammatory-mechanism-dieting-and-fasting-revealed Master detox molecule boosts immune defenses. Scientists discover an unknown immune mechanism. April 18, 2017 https://www.sciencedaily.com/releases/2017/04/170418120923.htm Glutathione Primes T Cell Metabolism for Inflammation. Mak TW, Grusdat M, Duncan GS, Dostert C, Nonnenmacher Y, Cox M, Binsfeld C, Hao Z, Brüstle A, Itsumi M, Jager C, Chen Y, Pinkenburg O, Camara B, Ollert M, Bindslev-Jensen C, Vasiliou V, Gorrini C, Lang PA, Lohoff M, Harris IS, Hiller K, Brenner D. Immunity. 2017 Apr 18;46(4):675-689. doi: 10.1016/j.immuni.2017.03.019. https://www.cell.com/immunity/fulltext/S1074-7613(17)30129-2 The effect of fasting on leukocyte and plasma glutathione and sulfur amino acid concentrations. Martensson J. Metabolism. 1986 Feb;35(2):118-21. https://www.ncbi.nlm.nih.gov/pubmed/3945186 Fasting triggers stem cell regeneration of damaged, old immune system BY Suzanne Wu - USC News June 5, 2014 https://news.usc.edu/63669/fasting-triggers-stem-cell-regeneration-of-damaged-old-immune-system/ Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression Chia-Wei Cheng, Gregor B. Adams, Laura Perin, Min Wei, Xiaoying Zhou, Ben S. Lam, Stefano Da Sacco, Mario Mirisola, David I. Quinn, Tanya B. Dorff, John J. Kopchick, Valter D. Longo Cell Stem Cell. 2014 Jun 5; 14(6): 810-823. https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(14)00151-9 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4102383/
  13. Celiac.com 09/25/2018 - In a patent application that could have a huge impact on the gluten-free industry, General Mills, Inc. has described its method and system for removing foreign, gluten-containing grains to establish gluten-free oats. Current FDA guidelines require all products labeled gluten-free to have a maximum gluten content of 20 parts per million (ppm). Published August 23rd, patent application No. US 20180236453 A1 details a method for producing oat grains with gluten levels below 20 ppm and, more preferably, below 10 ppm. Natural oats generally do not contain gluten, but after harvest, transport and storage, large batches of raw oats may contain small amounts of gluten-containing grains, such as wheat, barley, rye and triticale. These can sometimes occur at levels exceeding 20 ppm. The General Mills patent application describes a method of arranging mechanical oat sorting operations in series, or in both series and parallel operations. The multi-step process best includes width grading, multiple length grading steps, along with a potential de-bearding step. The resulting oats will be gluten-free to under 20 ppm, and possibly to under 10 ppm, and are suitable for the production of gluten-free oat food products, including cereals and granolas. To receive a patent, General Mills will have to prove that their process does what they say it does. A successful patent for General Mills could have a huge effect on the gluten-free oat foods industry. For one, it may allow General Mills to become a major supplier of gluten-free oats for other manufacturers. The benefits of larger scale, more economical gluten-free oat production could include more, and more readily available, gluten-free oat products, along with lower prices for both manufacturers and consumers. Stay tuned for more developments on this and related stories. Read more at Justicia.com
  14. Celiac.com 10/01/2018 - A team of researchers recently set out to establish the rates of epilepsy in patients with celiac disease or gluten sensitivity and vice versa and to characterize aspects of the epileptic syndromes presented by these patients. The research team included Thomas Julian, Marios Hadjivassiliou, and Panagiotis Zis. They are variously affiliated with the Sheffield Institute for Translational Neuroscience University of Sheffield in Sheffield, UK; and the Academic Department of Neurosciences Sheffield Teaching Hospitals NHS Trust Sheffield, UK. The team conducted a systematic computer-based literature search on the PubMed database, and gathered information on rates, demographics and epilepsy phenomenology. Patients with celiac disease are nearly twice as likely to have epilepsy as the general population. Celiac disease is twice as common in epilepsy patients as in the general population. Researchers still need to do more studies to assess rates of gluten sensitivity in epilepsy patients. The data indicate that the prevalence of celiac disease or gluten sensitivity is higher for certain epilepsy scenarios, including childhood partial epilepsy with occipital paroxysms, adult patients with fixation off sensitivity (FOS) and those with temporal lobe epilepsy (TLE) with hippocampal sclerosis. Epilepsy in the context of gluten-related disorders is a syndrome of celiac disease, epilepsy and cerebral calcification (CEC syndrome), which is frequently described in the literature. The good news is that gluten-free diet helps to control epilepsy in 53% of cases, either reducing seizure frequency, enabling reduced doses or even termination of anti-epileptic drugs. Patients with epilepsy of unknown cause should receive blood tests for markers of gluten sensitivity, and may benefit from a gluten-free diet. Read more at: Springer.com
  15. Celiac.com 09/27/2018 - Microscopic colitis is a frequent culprit in cases of chronic watery diarrhea among elderly patients. Although patients with microscopic colitis seem to have higher rates of celiac disease, researchers haven’t done much research on the relationship between dietary gluten consumption, and risk of microscopic colitis in people who do not have celiac disease. A team of researchers recently prepared a prospective study of US women without celiac disease. The research team included Po-Hong Liu MD, MPH; Benjamin Lebwohl MD, MS; Kristin E. Burke MD; Kerry L. Ivey PhD; Ashwin N. Ananthakrishnan MBBS, MPH; Paul Lochhead MBChB, PhD; Ola Olen MD, PhD; Jonas F. Ludvigsson MD, PhD; James M. Richter MD; Andrew T. Chan MD, MPH; & Hamed Khalili MD, MPH. The research team studied 160,744 US women without celiac disease who were enrolled in the Nurses’ Health Study (NHS) and the NHSII. They then estimated dietary gluten intake using validated food frequency questionnaires at four year intervals. They confirmed cases of microscopic colitis through a review of medical records. The team used Cox proportional hazard modeling to estimate the multivariable-adjusted hazard ratio (HR) and 95% confidence interval (CI). The researchers found 219 cases of microscopic colitis over more than 20 years of follow-up covering 3,716,718 person-years, for a crude incidence rate of 5.9 cases per 100,000 person-years, in NHS and NHSII. Most significantly, they found that dietary gluten intake did not influence the risk of developing microscopic colitis. Compared to individuals in the lowest quintile of energy-adjusted gluten intake, the adjusted HR of microscopic colitis was 1.18 for the middle quintile and 1.03 for the highest quintile. Even adjusting the figures to account for primary gluten sources, including refined and whole grains, made no substantial difference in the effect estimates. Further, there was no difference in association rates according to lymphocytic or collagenous subtypes; nor were the rates changed by age, smoking status, or body mass index. The good news from this study is that gluten intake plays no role in promoting microscopic colitis in adult women without celiac disease. Read more at: The American Journal of Gastroenterology (2018)
  16. Celiac.com 09/26/2018 - Non-celiac gluten sensitivity (NCGS) is a clinical syndrome marked by both intestinal and extra-intestinal symptoms that respond to the elimination of gluten-containing food and the adoption of a gluten-free diet. A team of researchers recently set out to review the diagnostic challenges surrounding non-celiac gluten sensitivity, and to summarize recent advances in research and provide a brief overview of the history of the condition for the benefit of professionals working in gastroenterology. The research team included Giovanni Casella, Vincenzo Villanacci, Camillo Di Bella, Gabrio Bassotti, Justine Bold, and Kamran Rostami. They are variously affiliated with General Practioner National Health Italy; the Institute of Pathology Spedali Civili Brescia Italy; the Pathology Department, Carate Brianza Hospital, ASST-Vimercate (Monza Brianza), Italy; the Gastroenterology and Hepatology Section of the Department of Medicine at the University of Perugia School of Medicine in Perugia, Italy; the Department of Gastroenterology Milton Keynes University Hospital, Milton Keynes, UK; and with Allied Health and Social Sciences, University of Worcester, UK. The researchers searched academic databases such as PubMed and Google Scholar using key words like ”non-celiac gluten sensitivity,” “gluten related disorders,” and the studies outlined in reference page were selected and analyzed. Clinical opinion generally holds that NCGS is best diagnosed by ruling out celiac disease and wheat allergy. Currently there is no blood test that can pinpoint NCGS. The underlying causes of symptoms in NCGS patients is poorly understood. However, there have been a few recent insights. Professional estimates of NCGS rates currently vary between 0.6 and 6%. Gastrointestinal symptoms of NCGS overlap slightly with those of irritable bowel syndrome. Researchers are currently investigating the histologic characteristics of NCGS, which range from normal histology to slightly elevated rates of T lymphocytes in the superficial epithelium of villi. Positive response to gluten free diet for up to 6 weeks, followed by a recurrence of symptoms after a gluten challenge, is still the best confirmation of NCGS. The Salerno expert criteria may help to accurately diagnose NCGS, especially in research settings, but isn’t particularly useful for diagnosis in clinical practice. Source: Gastroenterol Hepatol Bed Bench 2018;11(3):197-202).
  17. Celiac.com 12/03/2014 - It is important for pregnant women seeking medical consultation to get good, evidence-based information. This is especially true for pregnant women with celiac disease, who might wonder whether they face an increased risk of adverse birth outcomes and pregnancy complications as a result of their disease. So, does celiac disease increase a woman’s risk for pregnancy complications and adverse birth outcomes? Until now, there hasn’t been much good, solid data to give women a clear answer. With that in mind, a research team in England recently conducted a population-based study on pregnancy outcomes and adverse birth conditions in women with celiac disease. The research team included Alyshah Abdul Sultan PhD, Laila J Tata PhD, Kate M. Fleming PhD, Colin J. Crooks PhD, Jonas F. Ludvigsson PhD, Nafeesa N. Dhalwani PhD, Lu Ban PhD, and Joe West PhD. They are variously affiliated with the Division of Epidemiology and Public Health, City Hospital Campus at the University of Nottingham, Nottingham, UK; the Department of Medical Epidemiology and Biostatistics at the Karolinska Institute in Stockholm, Sweden; and with the Department of Paediatrics at Örebro University Hospital in Örebro, Sweden. The team used linked primary care data from the Clinical Practice Research Datalink and secondary care Hospital Episode Statistics data to assess all singleton pregnancies between 1997 and 2012. They used logistic/multinomial regression to compare pregnancies of women with and without celiac disease for risks of pregnancy complications (antepartum and postpartum hemorrhage, pre-eclampsia, and mode of delivery), and for adverse birth outcomes (preterm birth, stillbirth, and low birth weight). They stratified risk levels based on whether women were diagnosed or undiagnosed before delivery. They found 363,930 pregnancies resulting in a live birth or stillbirth, 892 (0.25%) of which were among women with celiac disease. Women with diagnosed celiac disease showed no increased risk of pregnancy complications or adverse birth outcomes compared with women without celiac disease. However, pregnant women with diagnosed celiac disease did show a higher risk of postpartum hemorrhage and assisted delivery, with an adjusted odds ratio (aOR) of 1.34. Importantly, the team found no increased risk of any pregnancy complication among those with undiagnosed celiac disease. In all, they found just a 1% absolute excess risk of preterm birth and low birth weight among mothers with undiagnosed celiac disease, which corresponds to aOR=1.24 (95% confidence interval (CI)=0.82–1.87) and aOR=1.36 (95% CI=0.83–2.24), respectively. Overall, the results of this study offer some good news to pregnant women with celiac disease. Whether diagnosed or undiagnosed during pregnancy, celiac disease is not associated with a significantly higher risk of pregnancy complications and adverse birth outcomes. Source: Am J Gastroenterol. 2014;109:1653-1661.
  18. Celiac.com 09/24/2018 - A team of researchers recently set out to investigate the degradation of gluten in rye sourdough products by means of a proline-specific peptidase. The research team included Theresa Walter, Herbert Wieser, and Peter Koehler, with the Deutsche Forschungsanstalt für Lebensmittelchemie, Leibniz Institut in Freising, Germany. Their team monitored gluten content of rye sourdough during fermentation using competitive ELISA based on the R5 antibody. The team noted a decrease in gluten over time, but found that even prolonged fermentation did not bring gluten levels below 20 ppm requirement for gluten-free foods. Interestingly, they did find that Aspergillus niger prolyl endopeptidase (AN-PEP) extensively degraded gluten concentrations of up to 80,000 mg/kg in rye flour, rye sourdough, and sourdough starter under specific temperatures and pH values. Nor did the enzyme inactivate the microorganisms in the sourdough starter. Gluten-free rye flour alone or in combination with sourdough starter was used to produce gluten-free bread, which the team then assessed for its sensory characteristics. Whereas gluten-free sourdough bread lacked any of the favorable qualities of conventional rye bread, the replacement of sourdough by egg proteins yielded gluten-free bread comparable to the conventional rye, and with better qualities than bread made with naturally gluten-free ingredients. This study demonstrates the feasibility of using ANPEP treatment to produce high-quality gluten-free sourdough bread from originally gluten-containing cereals, such as rye. Rye products rendered gluten-free in this manner have the potential to increase the choice of high-quality foods for celiac patients. Source: European Food Research and TechnologyMarch 2015, Volume 240, Issue 3, pp 517–524
  19. Hi my daughter has celiac disease and we are vegetarians. While looking for different kinds of flours to make flat breads , I came across corn flour in bulk barn . I had been looking for that for a long time. But all the tag / board said was “ made without wheat ingredients” . Does that translate to - safe for celiacs ? Who can I contact to get this clarified thanks in advance
  20. Celiac.com 09/14/2018 - If it is really true that nobody really wants to see a grown man cry, then certainly nobody would have wanted to hang around me near the onset of a long illness whose mystery would take 14 years to solve. It began subtly and mildly in 1989, my 43rd year. I had just finished a long and exhausting malpractice suit on behalf of my daughter, an attractive, genetically-normal child who had contracted quadriplegic cerebral palsy in a completely avoidable incident of post-natal asphyxia which had radically changed the nature of life for my spouse and I. By the time 1989 rolled around, I was thoroughly exhausted and carrying a toxic load of anger directed at an incompetent member of the medical profession who had never learned the importance of state-of-the-art skills in a profession that literally has the power of life, death, and disability. From late 1989 on through 1990, I experienced strange episodes of profound sadness, usually of one to two hours duration, that became increasingly disruptive to my ability to handle a job and child-care duties. Initially, these episodes seemed to come from nowhere. Later on, I found that playing certain pieces of music of which I was fond, would send me into such intense sobbing that I would be forced to pull over if this occurred while driving. By the time 1991 rolled around, something was to be added to these periodic bouts of intense sadness. Early in that year, my daughter became very ill, keeping both my spouse and I awake at night for weeks on end. By the time the problem was diagnosed to be a dental infection and dental surgery was done, I had begun to have a sensation of “hollowness”, as though I really weren’t part of this world, most of the time. In late summer of that year, a series of events in which my subconscious had informed me that a friend had a serious illness, sent me into a final “dive”: I simply stopped sleeping more than about two hours per night. When I first stopped sleeping, I soon noticed that even low-level use of alcoholic beverages would further interrupt sleep and throw me into a state in which I couldn’t think of anything but how terrible I felt. This state of pronounced alcohol intolerance would continue for 14 years. The final blow came in November 1991, when I went into a completely disabling panic/anxiety attack that sent me to bed, cowering. I had no alternative but to seek treatment from the psychiatric profession. Unfortunately, the first two psychiatrists prescribed drugs which either had no effects, or had effects that seemed worse than the problem they were supposed to solve. The third psychiatrist, whom I stuck with for about six months, came up with a treatment plan that was partially effective (but certainly not restorative). I stayed with this psychiatrist until it became clear that his treatment was equivalent to Jefferson Airplane singing “one pill makes you larger, and one pill makes you small”. I was being jacked up every morning by a toxic, activating SSRI anti-depressant so I could semi-function, and then dropped by benzodiazepenes every night into a non-restorative twilight sleep state. In retrospect, the most amazing thing about these first three psychiatrists was that not one of them ordered any tests of my endocrine function. Treatment consisted solely of a series of benzodiazepenes, anti-depressants, mood stabilizers, and anti-psychotics, administered in a trial-and-error fashion that yanked my psyche and body chemistry around like a manic pit bull on a two-foot leash. Throughout the latter part of 1992, I transitioned to care with my primary-care physician, mostly because I trusted him more than any of the psychiatrists I had seen up to that time. He was able to stabilize me with one of the old tri-cyclic anti-depressants, doxepin, along with low doses of valium. Although doxepin packs a big morning hangover for many who use it, and has very strong anti-cholinergic effects, its ability to put me out at night helped me function satisfactorily for much of the 1990s, even at doses as low as 10mg, once daily in the evening. In 1993 I consulted a highly-recommended psychiatrist, who was the first psychiatrist who actually looked at my thyroid function. When my TSH was measured at 3.5, without also checking my FT3 and FT4, that doctor concluded that thyroid was not my problem. Of course, standards of thyroid diagnosis and treatment have changed radically in the 12 years since. Under the new AACE guidelines, a TSH of 3.5 would now be suspect, because studies of patients with TSH over 3.0 have shown that most progress to hypothyroidism (i.e., TSH greater than 5.5). The new AACE guidelines would mean that further testing and evaluation should be done. Until the fall of 1997, I continued treatment with doxepin and intermittent valium, adding the practice of meditation to help calm myself. At that time, I came back to my primary-care physician with the symptom of profound exhaustion on top of the symptoms of insomnia, anxiety, and depression I had suffered for years. Fortunately, my GP was suspicious of thyroid function, and found that my TSH was floating above 8. Since this was well above the old/traditional limit of 5.5, he was ready to start treatment, with (as would be expected of most GPs) T4-only replacement. I began taking thyroxine (T4) shortly thereafter with high hopes. Initially, the treatment was successful: getting the added thyroxine into my system caused an immediate improvement in quality of sleep. However, the use of T4 did not turn out to be an unqualified success. After use of T4 for about a month, it was apparent that use of thyroxine alone did not produce a full recovery—I still suffered from anxiety, which the medication seemed to be increasing. In the meantime, hair loss became an issue. Several years earlier, I had noticed that running my fingers through my hair would produce an unpleasant sensation, almost as though the hair roots were tender. By the time of my 50th birthday, in 1996, I had noticed that my pillow was virtually coated with hair by the time I would remove it for washing. Unfortunately, nobody, including my GP, reminded me that hair loss is a prime symptom of hypothyroidism; and, like most males, I was ready to assume it was plain old male pattern baldness. By the time I was treated correctly and the hair loss stopped, I had pronounced thinning on the crown which was too advanced to be reversed in response to the treatment of the thyroid problem. In about 1998, I began experimentation with amino acids which was to last for almost seven years. I found that use of tryptopan, 5-HTP, and GABA could reduce (but not correct) the worst of my symptoms. In retrospect, though, use of amino acids is a poor substitute for a well-functioning thyroid, as well as being expensive and inconvenient. By the summer of 1999, I had reached a paradoxical situation. Experimentation had shown that my body needed on the order of 100 micrograms of thyroxine (T4) to keep my TSH down to a reasonable level; yet taking that much T4 was causing intense anxiety, requiring me to use strong sleeping medications. By late summer 1999, I had noticed another distressing symptom—my acute sense of hearing was being increasingly impacted by tinnitus. Evidently, the root cause that drove me into hypothyroidism, could also impact hearing. It was soon after a household move in the spring of 2000, that I had a partially-disabling attack of severe epicondylitis (more commonly known as tennis elbow). It was obvious that my body was no longer able to handle the short-term stresses of the hard physical work required by a move. This obvious physical symptom, accompanied by increasing periodontal issues and continuing mental issues, prompted me to seek other treatment. In September 2000, I began seeing a prominent “metabolic” doctor (M.D.) who is well known for his treatment of the metabolic disorders of diabetics. This doctor has written a number of books related to dietary changes and supplements needed to stave off metabolic degeneration as one ages. I was switched to Armour thyroid, and began treatment with other hormones (primarily hydrocortisone in low doses to supplement adrenal function, and pregnenolone). I took an enormous range of nutritional supplements recommended by this doctor, and also made radical changes in diet, which I maintained for nearly two years. Unfortunately, nothing seemed to really work—I did not obtain substantial relief of my symptoms. A thyroid test in Sep 2001 still showed unsatisfactory results—my TSH was 4.7, and my FT3 was below the bottom of the normal range. By the spring of 2002, I had decided I would have to take my care elsewhere if there were to be progress. After doing a brief telephone consult with a naturopath outside my home state, I began seeing a naturopath in my home town for whom I had obtained very positive recommendations via a web search. By March 2002, the naturopath had informed me that testing showed my hypothyroidism was due to anti-thyroid antibodies, i.e., my body was attacking its own thyroid gland. This condition is officially known as Hashimoto’s Autoimmune Thyroiditis (HAIT—as I now know, HAIT is the leading cause of hypothyroidism). I found this discovery quite amazing; how come the three endocrinologists I had seen between 1998 and 2002, had not given me this information? I was started on Thyrolar (synthetic combination T3/T4) by the naturopath, because she said that my body’s ability to make T3 may have been compromised by HAIT. Soon after beginning to see the naturopath, I learned that Dr. Stephen Langer of Berkeley, CA might have additional information on the problem I had been having with thyroid hormone causing anxiety in a hypothyroid patient. I had searched for information about this syndrome in a number of places but found nothing; for instance, the well-known book “Thyroid Solution”, by Ridha Arem M.D., contains no information on the condition. So, I consulted with Dr. Langer and learned that a small percentage of people with Hashimoto’s are exquisitely sensitive to even low doses of Thyrolar. In fact, the condition is rare enough that virtually no GPs, and only a few endocrinologists, know of its existence. Apparently, it does not have an official name attached to it. I decided to refer to it as “HAIT anxiety syndrome”, although there are a few doctors who prefer to refer to any neurological symptoms accompanying HAIT as “Hashimoto’s Encephalopathy”. I began to feel a little better between March 2002 and June 2003. I’m not sure why the message about gluten grains had not penetrated before, but by June 2003, the naturopath reminded me again that she had seen a positive result to a test for antibodies to gliadin (one of the two major proteins in gluten grains) in 2002, and that I really should consider removing gluten grains from my diet. This recommendation was based on three factors: I had antibodies to the protein gliadin found in wheat and other gluten grains such as rye and barley; I had anti-thyroid antibodies which were over the threshold that defines HAIT; Medicine really is an experimental science, and this experiment, in spite of its inconvenience, appeared to be worth a try. In a numbers sense, the response of my anti-thyroid antibodies to the removal of gluten grains from my diet was slow, but gratifying. My thyroperox test started off at 25, dropped to 19 within 6 months, 7 within 10 months, and became zero in less than 2 years. I eventually concluded that the removal of gluten grains from my diet was not all that difficult, partly because I wasn’t a celiac who had to worry about that last 1%. I also concluded that removal of gluten would have a positive health effect in terms of the reduced glycemic index of the foods I consumed. My symptomatic improvement thereafter was not immediate. It soon became obvious that T3/T4 treatment is not an exact science, and the proportion of T3 to T4 needs to be closer to the human body’s need, not the pig’s need (Both Armour and Thyrolar have the T3/T4 ratio of one part T3 for every four parts T4, typical of the pig’s biochemistry). For instance, in late 2003, my TSH had dropped very low, i.e. I had become clinically hyperthyroid due to excess T3 as revealed by a free T3 test. I have since gone through a couple more of these “yo-yo” episodes while being treated, which is a not uncommon event—thyroid treatment is as much art as science. Cost of treatment also became a problem. By June 2004, I began seeing a highly-recommended Physician’s Assistant (P.A.), who was known locally to be very good at thyroid treatment, and whose clinic would accept my health insurance. I continued to see the naturopath, although at less frequent intervals, since my insurance (like most) would pay nothing for naturopathy. The P.A. and the naturopath did not completely agree on treatment methods, particularly the use of adrenal supplements (hydrocortisone and DHEA in low/biologic doses) along with thyroid supplements; but they were both in agreement that I should continue to pursue combination T3/T4 therapy. So, I blended recommendations from the two for awhile, transitioning to T3 and T4 in separate tablets of Cytomel and Synthroid, so the percentage of T3 could be altered. I gradually transitioned off adrenal supplements during 2005, and very gradually increased my T3/T4 supplementation over the course of the year. Finally, by September 2005, I began to realize that I truly had recovered my health—I had episodes of feeling really good again! Still, my sleep was not perfect—I had discovered what Ridha Arem M.D. has documented in the book Thyroid Solution: a return to the euthyroid state may not immediately eliminate all symptoms. After going to a small dose of the atypical anti-depressant mirtazapine, I finally could feel, every day, like I had in my 30s. Unfortunately, it had taken an agonizing 14 years to get there. Today, I religiously take my 10 micrograms T3, and 75 micrograms T4, split into two doses each day. I also religiously avoid all traces of gluten grains in my diet because I now understand that the gluey, hard-to-digest proteins in them are a substance which can cause major metabolic disruption. Like the co-author of the book “Dangerous Grains”, Ron Hoggan, with whom I have corresponded, I have come to realize that our society’s over-use of a potentially toxic substance isn’t just dangerous to the 1 in 133 people who have full-blown celiac disease—it can cause a very poor quality of life for the approximately 1 in 5 who have gluten intolerance. I have also come to the realization that, to those few who are unlucky enough to encounter the HAIT Anxiety Syndrome, you may require combination T3/T4 therapy to feel better; and, you may never feel as well as you did when you were young, unless you find a way to stop your immune system from waging war on your thyroid. Most of all, 14 years after it started, I feel as though a significant part of my life has been taken from me. I was unable get joy or pleasure from life, I was unable to work effectively, and I was unable to be the kind of parent I could have been between my 45th and 59th years of life. I never imagine that I would be looking forward to the relatively advanced age of 60. However, given that I now feel better than I did at anytime between the ages of 43 and 59, 60 looks like a good place to be. Summary: In retrospect, the most important things I ended up learning from 14 years of very unpleasant experience are: If you have psychiatric symptoms, e.g., depression, anxiety, panic disorder, etc., make sure your endocrine system is evaluated, with thyroid testing as the cornerstone. Beware of doctors who offer an antidepressant first thing, without endocrine evaluation. The emotional/psychiatric effects of hypothyroidism are just as important, and just as damaging, as the physical ones. Unfortunately, many MD’s focus on the physical. If you want to get well, you have to apply all your skills and intelligence to investigating your problem, which most MD’s may not understand. You may also have to turn to “alternative” practitioners. If your TSH is above 3.0, or maybe even 2.5, and your doctor will not do more comprehensive testing (e.g. FT3/FT4), and/or try a test run of thyroid supplementation, find another doctor. If your doctor diagnoses you as hypothyroid, demand that a test for anti-thyroid antibodies be done. If you have any antibodies, even if they are under the threshold where HAIT is considered to start, get testing for allergy to foods, and testing for allergy to common environmental toxins if food testing reveals nothing. You may find, as did I, that you won’t feel as well as possible until you free your body from antibodies.
  21. Celiac.com 09/17/2018 - Her name is Hawkeye, she’s a black lab, and her mission is to detect gluten for a young man named Toby, who gets terribly sick if he eats food that contains gluten. Hawkeye is up to 98% accurate at detecting gluten with just a few sniffs. Hawkeye was also expensive, costing a princely $16,000, not including food, and vet bills. That may sound expensive, but, says Toby’s mom, Amy "when you think about it trainers are often training only one to two dogs at a time and our trainer, she only trained one dog at a time and it took a year.” In Toby’s case, the community rallied to raise the money to buy Hawkeye, who is a registered service dog, and so can accompany Toby nearly everywhere. Everyone loves Hawkeye and her role in Toby’s life. Amy calls Hawkeye a “life-giver, and says that Amy continued “she's breathed life and confidence into Toby that we haven't seen in a really long time." She adds that the family has “really seen just growth and development in him because he's not getting sick as often and he's now able to learn more. So he can now say his alphabet, learn his numbers and colors, things that just a year ago he wasn't doing." Gluten-sniffing dogs are rare, but their numbers are growing. The Mercola.com website says that Willow, a gluten-sniffing German shorthaired pointer in Michigan, can detect gluten with 95 percent to 98 percent accuracy. The website Nimasensor.com notes that “[g]luten-sniffing dogs may detect gluten in amounts as small as .0025 parts per million with 95 percent to 98 percent accuracy.” Love the idea of a gluten sniffing dog, but maybe daunted by the price, logistics or commitment? There are portable gluten sensors currently on the market, with greater accuracy than Hawkeye, for a few hundred dollars. Disclosure: Nima Labs is a paid advertiser for Celiac.com
  22. Celiac.com 09/03/2018 - Can an office-based point of care test (POCT) improve celiac disease detection and diagnosis? A team of researchers recently set out to measure the diagnostic performance of an IgA/IgG-deamidated gliadin peptide (DGP)-based POCT for celiac disease detection, patient acceptability, and inter-observer variability of the POCT results. The research team included Michelle S. Lau MBChB, Peter D. Mooney MD, William L. White MBChB, Michael A. Rees BMedSci, Simon H. Wong MBChB, Marios Hadjivassiliou FRCP, Peter H. R. Green MD, Benjamin Lebwohl MD & David S. Sanders FRCP. They are variously affiliated with the Academic Department of Gastroenterology, the Academic Department of Neurosciences and University of Sheffield, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield, UK, and with the Celiac Disease Centre at Columbia University Medical Centre in New York, NY, USA. Beginning in 2013, and running through 2017, the team recruited patients who had been referred for secondary care with gastrointestinal symptoms, anemia and/or weight loss (group 1), along with a group of patients with self-reported gluten sensitivity, but unknown celiac disease status (group 2). Every patient in the study received a POCT, tests for IgA-tissue transglutaminase (IgA-TTG), IgA-endomysial antibodies (IgA-EMA), total IgA levels, and a duodenal biopsy. A total of 500 patients completed acceptability questionnaires, and the team compared inter-observer variability of the POCT results among five clinical staff for 400 cases. Group 1 included 1,000 patients. The team saw forty-one patients (4.1%) diagnosed with celiac disease. The sensitivities of the POCT, IgA-TTG, and IgA-EMA were 82.9, 78.1, and 70.7%; the specificities were 85.4, 96.3, and 99.8%. Group 2 included 61 patients. The POCT showed 100% sensitivity, but negative predictive value in detecting celiac disease in group 2. A majority of patients preferred the POCT to a blood draw (90.4% to 2.8%). A Fleiss Kappa coefficient of 0.895 reflected good inter-observer agreement on the POCT results. The POCT had comparable sensitivity to a blood test, and accurately spotted all celiac disease cases in a gluten sensitive group. But, because its low specificity may could cause further unnecessary tests, it’s not good enough to take the place of blood testing. It turns out that spotting celiac disease is only part of the battle. Making sure to rule out people who don’t have celiac disease is equally important. That’s why it’s important that any diagnostic test be both sensitive, to spot celiac disease, and specific, to rule out celiac disease in those who don’t have it. Until we get a PCOT with high enough sensitivity and specificity to make accurate celiac diagnosis and accurate elimination of those without celiac disease, the current blood testing regime will continue. Read more at: The American Journal of Gastroenterology; volume 113, pages1238–1246 (2018)
  23. Celiac.com 10/30/2013 - Rates of celiac disease and the use of drugs to inhibit the secretion of stomach acid have both increased in recent decades. A research team recently set out to explore the association between anti-secretory medication exposure and subsequent development of celiac disease. The research team included Benjamin Lebwohl, Stuart J. Spechler, Timothy C. Wang, Peter H.R. Green, and Jonas F. Ludvigsson. They are affiliated with the Celiac Disease Center at the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, NY. For their population-based case control study, the research team looked at data for celiac disease patients diagnosed at any of the pathology departments in Sweden from July 2005 through February 2008. They matched each patient by age and gender with up to 5 control subjects. They found prior prescriptions for proton pump inhibitors and histamine-2 receptor antagonists in all subjects. Using conditional logistic regression to measure the association between these prescriptions and the subsequent diagnosis of celiac disease, they also found that patients with proton pump inhibitor prescriptions were much more likely to have celiac disease (OR 4.79; 95% CI 4.17–5.51). Patients prescribed both proton pump inhibitors and histamine-2 receptor antagonists had an even higher risk for celiac disease (OR 5.96; 95% CI 3.58–9.91) than those who received proton pump inhibitors alone (OR 4.91; 95% CI 4.26–5.66) or histamine-2 receptor antagonists alone (OR 4.16; 95% CI 2.89–5.99). The data clearly show that patients who use anti-secretory medications are at much greater risk for developing celiac disease following the use of these medicines. The fact that this connection persisted even after the team excluded prescriptions for anti-secretory medicines in the year preceding the celiac disease diagnosis suggests a causal relationship. Source: Digestive and Liver Disease
  24. Celiac.com 09/11/2018 - Gluten sensitivity is the most common sign of celiac disease. Clinical celiac diagnosis usually involves a positive blood test followed by biopsy confirmation of a typical enteropathy. The body’s immune response to celiac disease involves both adaptive and innate immunity, and is marked by anti-gliadin (AGA) and anti-transglutaminase 2 antibodies (tTGA), lymphocytic infiltration in the intestinal epithelial membrane, and expression of multiple cytokines. Researchers know that long pentraxin 3 (PTX3), an acute-phase inflammatory molecule, plays an important role in innate immunity. A pair of researchers recently set out to assess the relationship between Pentraxin 3 and biopsy status in celiac patients. Roberto Assandri and Alessandro Montanelli of the Department of Clinical Pathology, Clinical Chemistry Laboratory ASST Ospedale Maggiore di Crema, Italy, and the Clinical Chemistry Laboratory, Spedali Civili di Brescia, Italy, set out to explore a possible relationship between PTX3 and celiac disease. They used Marsh Histological grade following Marsh criteria classification to dividing 108 celiac disease patients into three groups: Group 1: Marsh 0, patients with a known history of celiac disease under gluten free diet, complete remission; Group 2: Marsh 1 and Marsh 2; Group 3: Marsh 3. As a control group, they used 30 healthy age-matched individuals with no known history of celiac disease or gastrointestinal symptoms. They used sandwich ELISA on an automated platform to measure PTX3 serum levels. They found that PTX3 serum levels were substantially higher in group 3 and group 2 compared with the healthy control group. They found no statistically significant differences between group 1 and the healthy control group. They noted a strong linear correlation between PTX3 serum levels and AGA levels in group 2, and group 3, but no such correlations between PTX3 serum levels and tTGA levels. Blood tests showed that PTX3 correlated with major gastrointestinal damage in celiac patients. PTX3 is a part of the innate immune system’s humoral branch. Data from this study show that PTX3 serum levels are high in active disease patients with pathological levels of AGA. They also show that patients with normal AGA IgA levels had PTX3 serum levels compared to healthy control subjects. The team proposes that PTX3 can modulate the innate response to gliadin in celiac disease, and may also regulate the adaptive immune response. Read more at: Gastroenterology and Hepatology
  25. Celiac.com 09/05/2018 - About one out of every twenty celiac patients fails to respond to a gluten-free diet, and goes on to develop refractory celiac disease (RCD). RCD is a serious condition marked by appearance of intraepithelial T lymphocytes. Depending on the phenotype of the lymphocytes, people develop either RCD I or RCD II. Patients with RCD type II (RCDII) show clonal expansions of intraepithelial T lymphocytes, and face an especially poor prognosis. Just over half of these patients will die within five years of onset due to aggressive enteropathy-associated T-cell lymphoma. At this time, researchers don’t know whether genetic variations might play a role in the severe progression from celiac disease to RCDII. A team of researchers recently set out to try to get some answers. The team began by conducting the first genome-wide association study to identify the causal genes for RCDII, along with the molecular pathways at play in cases of RCDII. For their genome-wide association study, the team used 38 Dutch patients with RCDII, and replicated the 15 independent top-associated single nucleotide polymorphism (SNP) variants (P<5×10) in 56 independent French and Dutch patients with RCDII. The team found that, after replication, SNP rs2041570 on chromosome 7 was significantly associated with progression to RCDII (P=2.37×10, odds ratio=2.36), but not to celiac disease susceptibility. They also found that SNP rs2041570 risk allele A was associated with lower levels of FAM188B expression in blood and small intestinal biopsies. Stratifying RCDII biopsies by rs2041570 genotype revealed differential expression of innate immune and antibacterial genes that are expressed in Paneth cells. The team’s efforts resulted in the identification of a new SNP associated with the severe progression of celiac disease to RCDII. Their data suggest that genetic susceptibility to celiac disease might be unrelated to celiac progression to RCDII, and suggests that Paneth cells might play a role in RCDII progression. Source: Eur J Gastroenterol Hepatol. 2018 Aug;30(8):828-837. The research team included B Hrdlickova, CJ Mulder, G Malamut, B Meresse, M Platteel, Y Kamatani, I Ricaño-Ponce, RLJ van Wanrooij, MM Zorro, M Jan Bonder, J Gutierrez-Achury, C Cellier, A Zhernakova, P Nijeboer, P Galan, S Withoff, M Lathrop, G Bouma, RJ Xavier, B Jabri, NC Bensussan, C Wijmenga, and V Kumar. They are variously affiliated with the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Department of Gastroenterology, VUMC, Amsterdam, The Netherlands, INSERM U1163, Imagine Institute and Paris Descartes University, the Department of Gastroeneterology, Georges Pompidou European Hospital, the Paris 13 University Sorbonne Paris Cité, UREN, Inserm (U557), Inra (U1125), Cnam, Bobigny, France, the scientific director of McGill University and Génome Québec Innovation Centre, Montréal, Québec, Canada, the Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, the Department of Medicine, University of Chicago, Chicago, Illinois, USA., and the K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Norway.
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