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Found 1,856 results

  1. Celiac.com 12/06/2018 - The growing popularity of gluten-free foods has led to numerous new products for consumers, but it has also led to some problems. One recent study showed that up to one-third of foods sold as gluten-free contain gluten above 20ppm allowed by federal law. Other studies have shown that restaurant food labeled as “gluten-free” is often contaminated with gluten. The problem of gluten in commercial food labeled gluten-free is not isolated to the United States. Recent studies abroad show that the problem exists in nearly every gluten-free market in every country. In Australia, for example, researchers from the Walter and Eliza Hall Institute in Melbourne found detectable gluten in almost 3% of 256 commonly purchased “gluten-free” manufactured foods, a study published in the Medical Journal of Australia on Monday says. Furthermore, the study shows that nearly 10% of restaurant dishes sold as "gluten-free" contain unacceptable levels of gluten. Now, the Australians have a stricter standard than nearly anyone else, so look for them to be on top of potential problems with gluten contamination in gluten-free products. The study did not name the food manufacturers responsible for the contaminated products, but did note that better, more frequent gluten testing by manufacturers would make gluten-free foods safer for people with celiac disease. In a related study, the same researchers found in May that nearly one in ten samples of “gluten-free” dishes from restaurants within the City of Melbourne contained gluten levels in excess of the official Food Standards Australia New Zealand definition of gluten-free. “It’s troubling to think that these foods could be hindering the careful efforts of patients trying their best to avoid gluten,” an author of the study, Dr Jason Tye-Din, said. A spokeswoman from Coeliac Australia said the organization was taking the findings seriously. “The research team that conducted this study has liaised with the food companies and is following up the positive samples with further retesting to ensure the issue is resolved,” she said. In addition to urging consumers to be diligent in reading labels, and to report any suspect products, “Coeliac Australia advises all people with coeliac disease to have regular medical check-ups as they do have a serious autoimmune condition and medical assessment is important to determine that their gluten-free diet is going well and no complications are developing.” Read more at: TheGuardian.com
  2. Celiac.com 12/04/2018 - In a major development in wheat genetics, the International Wheat Genome Sequencing Consortium (IWGSC) recently presented the first high-quality fully annotated reference genome sequence of the bread wheat variety Chinese Spring. The IWGSC Reference Sequence (RefSeqv1.0), catalogues the location and structure of more than 107,000 genes, and 4 million markers, across all 21 chromosomes of the wheat variety - some associated with important agricultural features. According to the authors, the sequence can be used for both genetic research projects and CRISPR- based genome modification. The results of a later study appear in Science. In that study, researchers used the new reference genome to perform a genome-wide analysis of the expression of homoelogs, genetic copies that are similar, but have different origins. Mapping these genetic features will improve scientists’ understanding of the basic structures of polyploid wheat. By combining gene expression datasets with the IWGSC RefSeqv1 wheat genome sequence, the researchers demonstrated the balance of gene expression among homeologs across the various tissues, developmental stages and cultivars of wheat. The team identified tissue-specific biases in gene expression and co-expression networks during development and exposure to stress, and their work offers a way to target key genes responsible for valuable agricultural traits in wheat. In a third study that also made use of the new IWGSC reference sequence, researchers closely examined the proteins contributing to various wheat-immune diseases and allergies, such as celiac disease, baker's asthma and wheat-dependent exercise-induced anaphylaxis (WDEIA). Certain proteins in wheat can trigger serious allergic reactions in sensitive individuals. Celiac disease, for example, is triggered by prolamin proteins gliadin and glutenin in wheat. Moreover, respiratory or skin exposure to other types of proteins have also been implicated in adverse immune responses. However, because of the complexity of the wheat genome, and the paucity of comprehensive genome information, a detailed description of these proteins has remained out of reach until now. A research team led by Angela Juhász used the IWGSC RefSeqv1.0 wheat genome to search for the genes that encode known allergy-inducing wheat proteins and mapped each across the entire sequence. The team’s analysis revealed previously unknown genes potentially related to immune-responsive proteins. Their results show that the genes associated with celiac and WDEIA are found in wheat’s starchy endosperm, the main ingredient in baking flour. Also, several lipid transfer proteins and alpha-amylase trypsin inhibitor gene families play a role in baker's asthma. Interestingly, the study showed that temperature stress during flowering can boost wheat’s natural levels of prominent celiac and WDEIA proteins. The researchers' detailed analysis offers important insights into the role of environment and growing conditions on the levels of proteins problematic for human consumers, they say. Their work will also inform production of low allergy wheat varieties, among others useful to the food industry. The many discoveries and breakthroughs in genetic analysis and engineering promise a very bright future when it comes to understanding and treating celiac disease, and numerous other anti-inflammatory diseases. Stay tuned as more developments unfold. Read more at Eurekalert.org
  3. Celiac.com 12/10/2018 - More and more people are eating gluten-free for non-medical reasons. These days, people with celiac disease make up a small percentage of overall gluten-free food sales. However, the effects of eliminating or reducing wheat, barley and rye ingredients from the diets of in healthy adults have not been well studied. A team of researchers recently set out to assess the effects of a gluten-free diet in healthy adults. To make their assessment, the researchers conducted a randomized, controlled, cross-over trial of 60 middle-aged Danish adults with no known diseases. The trial included two 8-week assessments comparing a low-gluten diet of 2 grams of gluten per day, and a high-gluten diet of 18 grams of gluten per day, separated by a washout period of at least six weeks with habitual diet including 12 grams of gluten per day. Compared with a high-gluten diet, the data show that a low-gluten diet triggers slight changes in the intestinal microbiome, increases food and drink intake and postprandial hydrogen exhalation, and reduces self-reported bloating. The team’s data indicate that results of a low-gluten diet in non-celiac adults are likely triggered by qualitative changes in dietary fiber. Studies like this are important for understanding the effects of a gluten-free diet in both celiacs and non-celiacs alike. Better understanding of a gluten-free diet will help doctors, celiac patients, and healthy individuals to make better, more informed dietary decisions. Source: Nature Communications; volume 9, Article number: 4630 (2018) The research team included Lea B. S. Hansen, Henrik M. Roager, Nadja B. Søndertoft, Rikke J. Gøbel, Mette Kristensen, Mireia Vallès-Colomer, Sara Vieira-Silva, Sabine Ibrügger, Mads V. Lind, Rasmus B. Mærkedahl, Martin I. Bahl, Mia L. Madsen, Jesper Havelund, Gwen Falony, Inge Tetens, Trine Nielsen, Kristine H. Allin, Henrik L. Frandsen, Bolette Hartmann, Jens Juul Holst, Morten H. Sparholt, Jesper Holck, Andreas Blennow, Janne Marie Moll, Anne S. Meyer, Camilla Hoppe, Jørgen H. Poulsen, Vera Carvalho, Domenico Sagnelli, Marlene D. Dalgaard, Anders F. Christensen, Magnus Christian Lydolph, Alastair B. Ross, Silas Villas-Bôas, Susanne Brix, Thomas Sicheritz-Pontén, Karsten Buschard, Allan Linneberg, Jüri J. Rumessen, Claus T. Ekstrøm, Christian Ritz, Karsten Kristiansen, H. Bjørn Nielsen, Henrik Vestergaard, Nils J. Færgeman, Jeroen Raes, Hanne Frøkiær, Torben Hansen, Lotte Lauritzen, Ramneek Gupta, Tine Rask Licht and Oluf Pedersen. They are variously affiliated with the National Food Institute; the Department of Biotechnology and Biomedicine, Technical University of Denmark; the Department of Bio and Health Informatics; the Department of Chemical and Biochemical Engineering at the Technical University of Denmark in Lyngby, Denmark; the Department of Plant and Environmental Sciences; the Department of Nutrition, Exercise and Sports; the Department of Nutrition, Exercise and Sports; and the Department of Veterinary Disease Biology, Faculty of Science, University of Copenhagen in Frederiksberg, Denmark; the Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark; the Department of Clinical Biochemistry, Copenhagen University Hospital Hvidovre in Hvidovre, Denmark; the Department of Radiology, Bispebjerg Hospital in Copenhagen, Denmark; the Department of Autoimmunology & Biomarkers, Statens Serum Institut in Copenhagen, Denmark; the Department of Biology and Biological Engineering, Chalmers University of Technology in Gothenburg, Sweden; the School of Biological Sciences, The University of Auckland in Auckland, New Zealand; the Bartholin Institute, Rigshospitalet in Copenhagen, Denmark; the Research Centre for Prevention and Health, The Capital Region of Denmark in Frederiksberg, Denmark; the Research Unit and Department of Gastroenterology, Herlev and Gentofte Hospital, the Capital Region of Denmark in Herlev, Denmark; with Clinical-Microbiomics A/S in Copenhagen, Denmark; the Department of Microbiology and Immunology, KU Leuven–University of Leuven, Rega Institute; and VIB, Center for Microbiology in Leuven, Belgium; with Biostatistics, Department of Public Health, University of Copenhagen in Copenhagen, Denmark; the Laboratory of Genomics and Molecular Biomedicine, Department of Biology; the Novo Nordisk Foundation Center for Basic Metabolic Research; the Department of Radiology, Bispebjerg Hospital, Copenhagen, Denmark; and the Department of Biomedical Sciences; and the department of Biostatistics at the Department of Public Health at the University of Copenhagen, Copenhagen, Denmark.
  4. Celiac.com 12/05/2018 - Everyone with celiac disease has their war stories. Stories of uncomfortable of painful symptoms. Stories of tough, slow diagnosis. Of accidental gluten ingestion. Picture the worst case of celiac disease you can imagine with bad symptoms and a seemingly endless quest for a diagnosis. Now imagine you’re ten years old and that worst case is you. That’s the story of 10-year-old Lillian Bordoni, whose positive attitude is helping her to recover from the worst case of Celiac Disease that Children’s Hospital Colorado has ever seen, and inspiring even the doctors she credits with saving her life. Bordoni’s book, “Cecilia the Celiac Superhero,” tells the story of her long and complicated fight with celiac disease, and she prevailed via a diagnosis, a gluten-free diet, and eventually, a change of location. She hopes to someday share her story with others. It’s a story that starts when Lillian was around four years old and living with her family in Kansas. Lillian suffered from what were, in retrospect classic symptoms of celiac disease. However, a diagnosis remained elusive. The family saw numerous doctors until they found a doctor who tested her for celiac disease and made a formal diagnosis. Even after the whole family cut out gluten, Lillian will still unable to keep food down, and lacked the energy to play outdoors. Eventually, the Bordonis traveled to the celiac clinic at Children’s Hospital Colorado, where Dr. Edward Hoffenberg helped them to figure out that Lillian’s problems were being aggravated by the fact that the family lived “in the heart of wheat country,” said Lillian’s mom, Miriah Bordoni. “There was wheat farming all around us. There were four of the largest grain elevators within blocks of our house that were processing wheat 365 days a year.” Breathing gluten every day was not an option, so the family moved to Colorado. Ever since then, Lillian has been healthy. Her experience has inspired her to write a book about her challenges with celiac disease. Of her book, Lillian says “It’s about Cecilia which is this girl here, and she has to beat gluten and cross contamination, which I had to beat too, but I turned it into like a superhero story so that it would be fun and interesting for all kids.” Lillian is in the beginning stages of having her book published. Once that happens, Children’s Hospital Colorado will distribute copies to all newly diagnosed celiac patients. Read more.
  5. Celiac.com 11/19/2018 - People with celiac disease cannot reliably determine whether they ate gluten or not based on symptoms, however severe those symptoms may be, according to research presented by Amanda K. Cartee, MD, of the Mayo Clinic, and her colleagues, at the American College of Gastroenterology Annual Meeting in Philadelphia. Because there is presently no FDA-approved test to confirm gluten exposure, celiac patients commonly rely on the presence or absence of gastrointestinal or other symptoms as an indicator of gluten exposure. But how reliable is that method? Not very reliable at all, says Dr. Cartee. Now, the study was small, but it was also rigorous. Dr. Cartee and her associates developed a double-blind, placebo-controlled gluten challenge to identify the rapid onset of symptoms after gluten ingestion, and to figure out if celiac patients could really tell whether they had been exposed to gluten. Researchers recruited 14 patients with celiac disease and 14 healthy controls for the trial. They then randomly assigned each patient to receive either a 6 g gluten suspension or placebo. Each patient completed a 100 mm visual analog questionnaire to assess their symptoms at baseline, every 30 minutes to 60 minutes for 6 hours and then daily for 3 days. The researchers also asked patients at each time point if they believed they received gluten. During the study, only two of the seven celiac patients who received gluten were able to correctly identify the gluten suspension. Cartee said it took a full day for one patient to come to that conclusion, while another gave varied responses sporadically throughout the study. Nausea and abdominal pain were the most common symptoms for celiac patients. Interestingly, there was no statistical difference in symptoms in the gluten celiac disease group compared with the placebo celiac disease group. That is, celiac disease patients receiving the placebo reported symptoms that the same rate as those who received actual gluten. So, not only could the celiac patients not tell when they got gluten, they also couldn’t tell when they got a placebo. Dr. Cartee said because physical symptoms are subjective and non-specific, they are largely unreliable for self-diagnosing gluten exposure. Dr. Cartee is calling for the development of a better, more objective way to identify gluten-related symptoms, especially in celiac patients with ongoing gastrointestinal symptoms. Do you have celiac disease? Would you welcome an easy reliable way to determine gluten exposure? How would you find it helpful? Source: Healio
  6. Celiac.com 12/07/2018 - What do hypertension, obesity, smoking and celiac disease have in common? They’re all important risk factors for coronary heart disease (CHD), a disease that kills more than a half a million people annually in the U.S. alone.(1) Based on emerging research, celiac disease may be a major contributor to heart disease in the Western world –making celiac disease an even greater public health threat than is currently understood. CHD and Celiac Disease: A Brief History The connection between CHD and celiac disease has a 35-year history. It began with a 1976 study conducted by Southampton University Hospital researchers, who found that there was an “… apparent protective effect of coeliac disease on CHD risk which “…might result from malabsorption of dietary lipids.”(2) However, this study had a number of significant flaws including a small sample size of only seventy seven. The most significant confounder in this study was the mortality rate of young subjects, which precluded them from the privilege of living long enough to develop CHD. Additionally, our understanding of CHD has undergone a paradigm shift since the low-fat 1970’s. CHD is not the result of excess dietary fat consumption, but instead is a manifestation of prolonged inflammation.(3) Based on this study and two others published around the same time period which found no link between CHD and celiac disease, researchers largely stopped investigating the heart health of people with celiac disease. The assumption was that celiac disease provided protection or, at the very least, was benign in terms of CHD risk. Then came a paper published in the July 2003 Archives of Internal Medicine which reported that celiac disease patients had a sixty percent increased risk of CHD death.(4) More recently, in a January 2011 Circulation paper, Swedish researchers published eye-catching results from an investigation of more than 15,000 individuals with celiac disease.(5) The key finding from this research was an approximately twenty percent increased risk of CHD death in people with celiac disease. While this research remains in its infancy, the biological connections between celiac disease and CHD are crystal clear, bolstering the epidemiological findings that people with celiac disease are at heightened CHD risk. CHD Today Before delving into the physiological link between CHD and celiac disease, it’s crucial to understand the pathogenesis of atherosclerosis, or narrowing of the heart’s arteries. Atherosclerosis begins with an injury to the endothelial lining of the coronary artery. A hyperactive response by immune cells, particularly macrophages and inflammatory cytokines, causes macrophage cells to become lodged inside the injured endothelium. Through a complex cascade of cell signaling, “trapped” macrophages transform into what are known as foam cells. These foam cells take in circulating blood lipids, especially low density lipoproteins (LDL). Over time this LDL/foam cell mishmash transforms into the arterial plaque most people are familiar with.(6) Inflammation fuels atherosclerosis from start to finish –from the initial injury to the development and accumulation of plaque. The Inflammation Connection Unfortunately, inflammation is something that people with celiac disease have more than enough of. Serum C-reactive protein (CRP) is a commonly used parameter for celiac disease diagnoses –suggesting that nearly all uncontrolled celiac disease patients have elevated inflammation levels.(7) CRP also happens to be a more sensitive indicator of impending heart disease risk than serum cholesterol. Cleveland Clinic cardiologist Eric Topol claims that “…in the past, people talked about their cholesterol levels. In the next decade everyone will need to know their C-reactive protein level (a marker of inflammation).”(8) Other inflammatory mediators –such as IL-6 and TNF-a—are also present in greater amounts in celiac disease patients compared to the general population. In addition to the inflammatory response to ingested gluten, a March 2009 genetic analysis found that individuals with celiac disease were more likely to have polymorphisms that promote inflammatory cytokine production. (9) Other Links in the Chain And, there’s more to this celiac disease/CHD story than inflammation. People with celiac disease tend to have comorbidities that compound celiac disease’s damage to the cardiovascular system. Fat Malabsorption Dietary fats are a heart-health double edged sword. Excessive intake of trans fats are strongly linked to dyslipidemia and heart disease. However, a recent American Journal of Clinical Nutrition meta-analysis which included over 340,000 research subjects in its analysis found no connection between saturated fat and heart disease. (10) Monounsaturated and polyunsaturated fats are protective against atherosclerosis. Omega-3 fats appear to confer a particularly strong cardiovascular disease prevention benefit.(11) Adequate intake and absorption of fats is crucial for CHD prevention. Indeed, a low-fat dietary pattern was shown to increase heart disease risk in a large-scale randomized control trial involving more than 48,000 subjects.(12) Absorption of dietary fats is severely impacted by celiac disease due to villous atrophy, pancreatic insufficiency and dysbiosis. Lewis et al found that untreated celiac disease patients had approximately twenty one percent lower serum cholesterol levels compared to the general population, suggesting severe fat malabsorption.(13) Based on this research and others it’s conceivable that many celiac disease patients don’t absorb the dietary fats required to combat heart disease. Vitamin Malabsorption Suboptimal nutrient absorption is a near-universal issue in celiac disease patients – even for individuals consuming a gluten free diet. Fat soluble vitamin absorption is particularly affected by celiac disease.(14) Poor absorption of fat soluble vitamins E and D has been tied to increased heart disease risk in several studies. (15) Homocysteine Homocysteine is an amino acid that becomes elevated in cases of vitamin B6, folic acid or vitamin B12 deficiency. Poor B-complex vitamin absorption is common in both newly diagnosed celiac disease and in celiac disease patients following a gluten free diet.(16) An October 2002 Meta-analysis found that homocysteine levels twenty five percent above normal levels boosted heart attack risk by eleven percent.(17) Due to its strong correlation with heart disease, the American Heart Association suggests that individuals with malabsorption symptoms, including celiac disease, should be screened for homocysteine.(17) Simone Saibeni, MD and her University of Milan colleagues justified this recommendation by finding that celiac disease patients were 3.5 times more likely to have elevated hyperhomocysteinemia than the general population.(16) Type 1 Diabetes (DM1) Approximately five percent of people with celiac disease also suffer from DM1.(18) Hyperglycemia promotes inflammation, endothelium stiffness and arterial plaque formation. Rheumatism Symptoms of rheumatism, especially Sjogrens syndrome and unexplained joint pain, are common symptoms of undiagnosed celiac disease. Lubrano et al found that twenty five percent of individuals with celiac disease also have arthritis.(19) A 2008 population study discovered that people with rheumatoid arthritis have double the heart attack and stroke risk of the general population.(20) Whole Grain Intake Whole grain intake is strongly associated with a decreased risk of CHD.(21). Avoidance of fortified whole grains by people with celiac disease may impact dietary intake of B-vitamins, dietary fiber and antioxidants. How People With Celiac Disease Can Fight CHD Preventing CHD in the celiac disease population isn’t dramatically different from what’s typically recommended to the general population. Maintaining a healthy body weight, eating adequate amounts of dietary fiber, staying physically active, avoiding trans fats and consuming monounsaturated fats regularly are the keys to cardiovascular health whether or not one has been diagnosed with celiac disease. However, there are a few important heart health caveats that those with celiac disease should keep in mind. Gluten-Free Diet The importance of a 100 percent gluten free diet for CHD risk reduction and overall health cannot be emphasized enough. Not only is it the most effective treatment for celiac disease, but it is also critical for limiting the inflammatory response that promotes atherosclerosis.(22,23) Additionally, a strict gluten free diet allows the intestine to heal and recover, boosting absorption of nutrients necessary for cardiovascular health. Multivitamin Supplementation Multivitamin/Multimineral supplementation is standard treatment for celiac disease today.(24) Supplementation helps partly compensate for malabsorption and suboptimal intake of vitamins and minerals. A multivitamin supplement for CHD prevention should include at least 100 percent of the RDA for folic acid, vitamin B12, vitamin B6, and fat-soluble vitamins D and E. Dietary Fats “Fat is the most commonly and severely affected nutrient in celiac disease,” reports Jay W. Marks, M.D., of Baylor University College of Medicine.(25) Individuals with celiac should aim to consume at least twenty five percent of their calories in the form of dietary fat. Healthy monounsatured and polyunsatured fat sources such as extra virgin olive oil, nuts, legumes, fatty fish, and seeds should form the foundation of a heart healthy celiac disease diet. Pancreatic enzymes may be used to aid lipid absorption and reduce gastrointestinal symptoms like diarrhea and bloating. Omega-3 Fats Omega-3 fats reduce inflammation, increase HDL cholesterol and make cardiovascular arteries resistant to injury. Zhang et al discovered that habitual fish consumption was associated with a forty percent reduction in CHD mortality in healthy populations.(26) Omega-3 fatty acids may have additional benefits for celiac disease patients, especially acceleration of intestinal healing. Celiac disease patients should consume fatty fish like mackerel and salmon at least twice weekly. Conclusion Celiac disease needn’t be an automatic CHD death sentence. Although the connection between heart disease and celiac disease is very real, lifestyle changes can dramatically reduce the chances that someone with celiac disease will develop CHD. Simply eating a gluten-free diet, supplementing with vitamins, minerals and pancreatic enzymes and consuming omega-3 fats –four measures that those with celiac disease should be doing anyway – will shield the cardiovascular system from much of the celiac disease-derived damage that can lead to CHD. In fact, this new link can ultimately become a net positive for many celiac disease patients as it can motivate them to become more proactive and aggressive in their self-care. References: 1. Centers for Disease Control and Prevention; Heart Disease Facts; Available at: https://www.cdc.gov/heartdisease/facts.htm. Accessed April 18th 2011. 2. Whorwell PJ, Foster KJ, Alderson MR, Wright R. Death From Ischaemic Heart-Disease and Malignancy in Adult Patients With Celiac Disease. Lancet 1976;113-114. 3. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease, application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation [serial online].2003;107:499-511 4. Peters U, Askling J, Gridley G, et al. Causes of death in patients with celiac disease in a population-based Swedish cohort. Arch Intern Med. 2003;163:1566–1572. 5. Ludvigsson JF, James S, Askling J, Stenestrand U, Ingelsson E. Nationwide cohort study of risk of ischemic heart disease in patients with celiac disease. Circulation. 2011 Feb 8;123(5):483-90 6. Gotta A, Farmer F. Atherosclerosis: Pathogenesis, Morphology, and Risk Factors. Cardiovascular Medicine. 3rd Edition, Springer, London, pp. 1593-1613. 7. Lahat N, Shapiro S, Karban A, et al. Cytokine profile in coeliac disease. Scand J Immunol 1999;49:441–446 8. Role of inflammation-Growing proof inflammation is a major risk factor for heart disease. Available at: http://www.clevelandclinic.org/heartcenter/pub/news/hot/inflammation8_02.asp?firstCat=1&secondCat=429&thirdCat=524. Updated 8/02. Accessed April 18th 2011. 9. Dema B, Martínez A, Fernández-Arquero M, The IL6-174G/C polymorphism is associated with celiac disease susceptibility in girls. Hum Immunol 2009;70:191-4 10. Siri-Tarino SW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr [serial online]. 2010;91:535-546. 11. Perez-Jimenez F, Lopez-Miranda J, Mata P. Protective effect of dietary monounsaturated fat on arteriosclerosis: beyond cholesterol. Atherosclerosis 2002;163:385–98 12. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006; 295:655-66 13. Lewis NR, Sanders DS, Logan RF, Fleming KM, Hubbard RB, West J. Cholesterol profile in people with newly diagnosed coeliac disease: a comparison with the general population and changes following treatment. Br J Nutr. 2009 Aug;102(4):509-13 14. Hallert C, Grant C, Grehn S, Granno C, Hulten S, Midhagen G, Strom M, Svensson H, Valdimarsson T. Evidence of poor vitamin status in coeliac patients on a gluten-free diet for 10 years. Aliment Pharmacol Ther. 2002;16:1333–1339 15. Sesso HD et al.Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians’ Health Study II randomized controlled trial. JAMA. 2008 Nov 12;300(18):2123-33 16. Saibeni S, Lecchi A, Meucci G, et al. Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis: role of B12, folate, and genetics. Clin Gastroenterol Hepatol 2005;3:574e80 17. Malinow MR, Bostom AG, Krauss RM. Homocyst(e)ine, diet, and cardiovascular diseases: a statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation. 1999;99:178–182 18. Ludvigsson JF, Olsson T, Ekbom A, Montgomery SM. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Aliment Pharmacol Ther 2007; 25:1317 19. Lubrano E, Ciacci C, Ames PR, et al. The arthritis of celiac disease: prevalence and pattern in 200 adult patients. Br J Rheumatol 1996;35:1314-8 20. Dhawan SS, Quyyumi AA. Rheumatoid arthritis and cardiovascular disease. Curr Atheroscler Rep. 2008;10:128-133 21. Jensen MK, Koh-Banerjee P, Hu FB, et al. Intakes of whole grains, bran, and germ and the risk of coronary heart disease in men. Am J Clin Nutr. 2004;80(6):1492-1499 22. Meresse B, Cerf-Bensussan N. Celiac disease: from oral tolerance to intestinal inflammation, autoimmunity and lymphomagenesis. Mucosal Immunol. 2009;2:8e23 23. Popa C, Netea MG, van Riel PL, van der Meer JW, Stalenhoef AF. The role of TNF-a in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk. J Lipid Res. 2007;48:751–62 24. See J, Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutr Clin Pract. 2006;21(1):1-15. 25. Marks, J. “Celiac Disease (Gluten Enteropathy)”Available at: https://www.medicinenet.com/celiac_disease_gluten_enteropathy/article.htm. Accessed April 29th 2011. 26. Zhang J, Sasaki S, Amano K, et al. Fish consumption and mortality from all causes, ischemic heart disease, and stroke: an ecological study. Prev Med. 1999; 28: 520–529.
  7. How long did it take you to get your blood test results? How were you notified of the results (letter, phone call etc.)?
  8. Celiac.com 11/26/2018 - Many people with celiac disease suffer from headaches. A team of researchers recently set out to more thoroughly explore the relationship between celiac disease and headaches. The research team included Panagiotis Zis, Thomas Julian, and Marios Hadjivassiliou. They are variously affiliated with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield S10 2JF, UK, and the Medical School of the University of Sheffield in Sheffield, UK. The team's goal was to establish the relationship between headaches and celiac disease, and vice versa, to explore the role of a gluten-free diet, and to describe the imaging findings in celiac patients affected by headaches. For their systematic review and meta-analysis, the team reviewed 40 articles published in the the PubMed database between 1987 and 2017. They included information regarding study type, population size, the age group included, prevalence of celiac disease among those with headache and vice versa, imaging results, the nature of headache, and response to gluten-free diet. They found that the average pooled rate of headaches in celiac patients was 26% (95% CI 19.5–33.9%) in adult populations and 18.3% (95% CI 10.4–30.2%) in pediatric populations. The headaches usually resemble migraines. Children with headaches of unknown origin, have celiac disease rates of 2.4% (95% CI 1.5–3.7%). There is presently no good data for adult populations. In such cases, brain imaging can be normal, but can also reveal cerebral calcifications with CT, white matter abnormalities with MRI, and deranged regional cerebral blood flow with SPECT. The good news is that a gluten-free diet seems to be an effective treatment. Up to 75% of celiac patients saw their headaches resolve when they followed a gluten-free diet. Celiac patients have high rates of idiopathic headache (that is, headaches of unknown cause), and patients with such headaches have higher rates of celiac disease. Therefore, patients with headache of unknown origin should be screened for celiac disease, since they may gain symptom relief from a gluten-free diet. Source: Nutrients 2018, 10(10), 1445; doi:10.3390/nu10101445
  9. Open Letter to the many GI sufferers etc Part 1’ Like IBS, UC and other GI diseases like Infant Heartburn (GERD) that grows into (in time) to IBS, UC, Chron’s and NCGS as a teenager or Celiac disease in time as an adult— Look Beyond these symptom’s to the parent disease –- Pellagra. *** a couple of notes to begin with. You can see I meant this to be one post -- but as usual it got too long to read at one seating. 2) because I might be having a medical procedure soon (I am posting part 1) in case I don't get to part 2 until latter. ****This is only my experience (and my research) that has lead me to my conclusions. They are NOT endorsed by celiac.com nor should this blog post be considered and endorsement of these ideas by celiac.com. Thank you in advance for letting me share my opinions and conclusions. (God being my help) may this posterboy blog post benefit those who take the time to read them/it. What follows is something that has been on my heart to share for a while. It is my story only. . . yours may be different but I have found if it helps you . . . it will help others too! And as they say "Without Further Ado" Here are my thoughts about my original celiac diagnosis and what/why I think was also low in stomach acid but a proper diagnosis was not made because not enough/proper test's were done to rule it out as an official "differential diagnosis". If it is happening to me. . . it is happening to others! Below begins the body of blog post of "An Open Letter Part 1 to Fellow GI Sufferers" Because as I am fond of saying “To Educate is to (Truly) Free” God being my help 2 Timothy 2: 7 as always“Consider what I say; and the Lord give thee understanding in all things” this included and all the knowledge I have absorbed in 10 years of researching this topic for myself (God being my help) how I discovered this forgotten medical fact after 4 years of research (see below) and have been helping people for over 6 years (those who will listen) and who better to learn from than someone who has done it himself and not only for himself but 100’s of his friend too! See this celiac.com article where much of this information is summarized in something called a white paper about the “When Myth becomes Medical Fact People suffer unnecessarily; The Case of Mistaken Identity: How Pellagra now thought to be rare became known as Celiac Disease — A White Paper linked at the end of the article. Referenced here if you have not had a chance to read the article since it was featured on celiac.com https://www.celiac.com/articles/24658/1/A-Differential-Diagnosis-How-Pellagra-Can-be-Confused-with-Celiac-Disease/Page1.html “A white paper is an authoritative report or guide that informs readers concisely about a complex issue and presents the issuing body’s philosophy on the matter. It is meant to help readers understand a (complex) issue, solve a problem, or make a decision.” By reading this blog post I hope to convenience you that your experience can be the same as mine. A differential diagnosis is one of the best standard of medicine rarely practiced today and how specialists decide between competing diseases like UC or Chron’s or IBS or Celiac Disease and if I am right Co-Morbid Pellagra now forgotten for 75+ years since the “War on Pellagra” is now over according to medical professionals’ but sadly the battle rages on for at least for the 60 Million American’s alone who get (Infant) Heartburn once a month not counting the heartburn that grows up to be IBS, UC, Chron’s or Celiac disease. See link below from Creighton University that mention’s this medical fact. Pellagra is not a disease of TODAY. Celiac is the disease of Choice today! But in 58% of those diagnosed with Celiac TODAY 58% are Co-Morbid with Pellagra as I was and most ALL my friends because they ALL get better when they take the Niacinamide. I now it works. I have seen it work for too many people. And I believe it can/could work for you too! See end of this blog posts and my doctor does too. He now uses this method in his practice with great success! And it can work for you too! (I believe) Lord willing if you do as I suggest and take Niacinamide 2or 3/day for 6 months (see below). I now describe myself as the Celiac and Pellgara Posterboy as a “Former Celiac Sufferer” who blogs about digestive disorders that Co-Morbid Pellagra causes often presenting as other GI diseases like IBS, UC, Chons, NCGS and GERD” Note **** This IS NOT medical advice only my personal experience of how through deep research (and the Grace of God) after 4 years of study I found what the doctors have always known but overlook in treating the many symptoms of Celiac Disease. The true cause as recorded in medical textbooks the world over the cause of 90+ percent of Digestive disorders (I believe) is because of one Vitamin Deficiency/Dependency. This blog post and (Posterboy blog) is about that ONE nutrient/vitamin/mineral that is lacking and the causative agent for most Digestive Disorder(s) presenting as the Iceberg Disease(s) of Gluten Insensitivity aka Celiac Disease in its most advanced stage (with enough time). And I hope at least ONE other Celiac besides me will believe also and be helped from this post. As proven/researched by Prousky almost 17 years ago that low Niacin levels lead too low stomach acid. It is time this information was known by a wider audience – the Celiac audience. http://www.yourhealthbase.com/database/niacin-treats-digestive-problems.htm see also by posterboy blog about this topic. It is a devastating delay. 2 Timothy 2:7 “Consider what I say; and the Lord give thee understanding in all things” this included. When Celiac Disease points it head (rears it head) out of the water 20+ symptoms (known as associated diseases) have already presented themselves in various malady’s. When only 3 (the 3 Ds) symptoms where need 75 years ago to diagnose the condition once considered cured but is rampant in today’s society because we are more STRESSED than ever. Digestive disorders, dermatitis syndromes, and dementia disorders – known then as Pellagra 75+ years ago but now is known mostly as various GI diseases depending on how long or low you are in Pellagra Preventive Factor as it was called in the day. Here is the best research article I have ever read on the topic. https://www.hindawi.com/journals/cggr/2012/302875/ They called it “Lessons from Pellagra” but the problem is we haven’t learned them. What does this look like in human beings? If one is critically low in Niacin the 3 D’s of Pellagra (Dementias, Dermatitis’s, and Digestive Issues) show up. (see hindawi link about for the exhaustive complete diagnostic picture of all the ways Pellagra might present itself. It is very exhaustive and informative) We will not count the 4th D of death if you are reading this blog. Explained here well http://blogs.creighton.edu/heaney/2013/11/18/pellagra-and-the-four-ds/ To quote Dr. Heaney a Past Professor of Medicine at Creighton University “2014 marks the 100th anniversary of the war on Pellagra, a war that lasted nearly 25 of those years before victory could finally be declared. You have not heard of the war on Pellagra? The celebration is not on your calendar? You’re not alone.” I have been in remission now for 5+ years after suffering 30+ years. Remission is possible! From Pellagra! Epigenetics has been discovered as the cause for Pellagra being diagnosed as Non-Celiac Gluten Sensitivity (NCGS) or Celiac disease when Heartburn/Gerd then IBS etc. and NCGS in time grows up to become your Celiac Diagnosis. Learn how Lifestyle (STRESS) is a risk factor for Celiac Disease. see this article entitled ‘Lifestyle is a Risk Factor for Celiac Disease”. https://www.sciencedaily.com/releases/2015/11/151102100302.htm Quoting an article that appears on Celiac.com http://www.celiac.com/articles/24166/1/Could-Changing-Gut-Bacteria-Prevent-Celiac-Disease/Page1.html “According to Dr. Decker Butzner, a Calgary-based pediatric gastroenterologist, there are another triggering factor which we’ve never understood…[t]here is an environmental trigger.“ i,e. STRESS Have you been stressed of late? Stress is said to kill you well it also maims you. NCGS is that maiming of people who have eaten wheat without resetting their stress clock. Find out how you can reset your stress clock (my words). Also see this very well article on pregnancy. https://www.verywell.com/can-pregnancy-trigger-celiac-disease-562302 where they say quoting First Comes Baby, Then Comes Symptoms "Most women are diagnosed with celiac disease after at least one pregnancy — in fact, a comprehensive Italian study published in 2010 on the reproductive effects of celiac found that 85.7% of women received their celiac diagnosis following their first pregnancy." WE also know stress is a trigger for Celiac disease. https://www.celiac.com/articles/23506/1/Stress-Common-Before-Celiac-Diagnosis/Page1.html Join his friends who no longer suffer from heartburn, gas, constipation, diarrhea, IBS , UC, Chron’s and Ulcer’s etc. of NCGS/GERD. You too can be in remission in as little as six months if you follow this ground breaking discovery hidden in medical text books now brought to light about how to manage digestive stress from Pellagra. When he (God being his help) rediscovered Pellagra as a disease of TODAY now often Diagnosed as Celiac disease instead of one conquered 75+ years ago as the doctors teach. A brief history: over 4+ years ago after being able to eat gluten again after being Gluten Free for 4 years and suffering 30+ years before I received a diagnosis as Celiac disease I begun to realize I had low stomach acid instead. So now I speak about it freely and blog about it regularly with only modest success and why I participate on celiac.com to Educate those still suffering unnecessarily to help explain how Pellagra is often confused for many GI issues up to and including Celiac Disease in time – usually 10 years or more. *** This is not medical advice and should not be considered such. Results may vary. Always consult your doctor before making any changes to your diet or your prescribed medical regimen. After 4 years of research and 5+ years of GI symptom remission I am convinced more than ever that 90+ percent of the most common GERD/Gluten issues are related to sub-clinical presentation of Pellagra unrecognized in a clinical setting. So much so that I tell those who will listen. As I am fond of saying Learn from my mistakes. Honey is like knowledge sticky and sweet when good news comes. “This posterboy blog is just that storehouse of knowledge learned from life experiences. The blog’s author has been stung so you don’t have to be. No man is so dumb as the man who won’t learn from other people’s mistakes. Take as much honey (knowledge) as you can from my mistakes so bad health will not sting your quality of life. Feel free to ladle and dollop your life with the sweet stickiness of the truth found here. For honey like truth stick to you once in contact and you can’t just wash it away.” This posterboy blog is about my struggle to reach people yet only about 10 percent believe and are helped when they read these things though 95+ percent are helped when they treat their Pellagra symptoms with Niacinamide taking it 3 times/daily for 4 to 6 months. Education (this blog) is about raising the conversion rate so people don’t have to suffer any longer. I will go on telling those who will listen. How can they hear if no one tells’ them? Romans 10:14 (I speak as a man) Tell others about this blog post if you decide to try Niacinamide for yourself and see If it helps you. It will help others/them too most likely! At least it helps most of my friends that will/have believe/believed and tried it for themselves. Take the Niacinamide and get/be better in 6 months (begin BURPING) (w/o bloating I might add) for the first time in years IF EVER from Pellagra undiagnosed. No one seems to believe (or at least not many) becoming deficient in (a) vitamin or vitamin(s)/minerals will/can make us sick. What a novel concept. You would not think I would need to write a blog post to tell people that! Maybe it is not true in your case. But you won’t know if you don’t try it. All I know it has been true in my life! and Hundreds’ and hundreds’ of my friends. Thanks bee to God who helped me to see these things. 2 Corinthians (KJV) 1:3,4 3) “Blessed be God, even the Father of our Lord Jesus Christ, the Father of mercies, and the God of all comfort; 4) who comforteth us in all our tribulation, that we may be able to comfort them which are in any trouble, by the comfort wherewith we ourselves are comforted of God.” Tell someone (share) is all I ask tell others is all I ask –when you are BURPING for the first time in years or (EVER) – tell a friend about this blog post “is all I ask” but don’t let the chain break with you. There a lot of fellow sufferers’ who still need help. I always say the number one mistake people make with Niacinamide is not taking it long enough (3 to 6 months 3/day in divided doses) but now I am going to amend that. The number one mistake people make with GI problems is the mistake of not taking the Vitamin in the first place. The 2nd biggest mistake is they don’t take it long enough! If you want to try and educate your doctor/friends and think he/she/they will listen tell them how Niacinamide helped you or some fellow who says it helped him but I was too scared to try it. Maybe they will listen to your better than they will/do me. *** This is not medical advice and should not be considered such. Results may vary. Always consult your doctor before making any changes to your medical regimen. But mine has taken Niacinamide and his digestive/GI problems are in remission. And his difficult to help/treat patients who don’t respond to “popular” medicine’s like Linzess etc. are better for IBS-C. And have stopped the medicine because their symptoms are in remission. He has even given Niacinamide to his sister to help her Chrons symptoms’ though research bears this out people don’t (Heck doctors don’t even) well understand the connection. See this article entitled “Pellagra as the presenting manifestation of Crohn's disease.” https://www.ncbi.nlm.nih.gov/pubmed/7060914 (***Note: this is an update. I saw my doctor recently and he admitted as such. But I could see it in his eyes (and hear it in his voice) because it did not fit his paradigm (world view of Vitamins/medicine) he spoke only of her Chron’s being in remission. It never occurs too him that her co-morbid Pellagra is better and it (Pellagra) could be being misdiagnosed as Chron’s instead (and won’t/wouldn’t) even if I brought him the research.) But Vitamin(s)/Minerals especially Niacinamide and Magnesium don’t get the attention they deserve because Vitamins’ don’t have a USP today in this genetic age we now live in. They (drugs) are popular because they have drug companies who have the money to advertise them. I do not. I do not have a Unique Selling Position (USP). Nor do Vitamins these days! And I say too you too. Put your Pellagra symptoms into remission too! (Your Celiac diagnosis can remain your primary disease diagnosis) as the doctor's wonder why your (Pellagra misdiagnosed) symptom's are in remission. No body profits if you get better in 6 months or a year and you no longer need the Vitamin! We don’t’ get sick from being low in “a Medicine” to quote the frustrated pharmacist but a Vitamin. I usually end up giving Niacinamide away and often they (friends) give it back instead much like a Johnny Appleseed character. Such is the fear of Vitamins these days. See also the posterboy blog post on celiac.com why this is so. . . entitled it is time for a Vitamin Reformation; Why all the hate for Vitamin’s these days. 2 Timothy 2:7 “Consider what I say; and the Lord give thee understanding in all things” this included. I am just trying to help those who still haven’t heard yet Pellagra is being diagnosed as Celiac disease today and your Pellagra undiagnosed/mistakeningly diagnosed as Celiac can be in remission from a Vitamin deficiency. If we follow most normal paths’ for adoption it will take another 20 years (a generation) for the medical community to accept Pellagra as the proper diagnosis. ****Note: I am only reporting what medical journals have concluded. It is just not well understood today one disease is being diagnosed as the other because it can take a generation for this knowledge to filter down to the clinical level. How do we know this??? Or can we? The International Journal of Celiac disease notes this association/connection. http://pubs.sciepub.com/ijcd/3/1/6/ Not only did/does the Journal of Celiac cite common symptom’s 58 percent of the time in Celiac and Pellagra but they also cite that Pellagra has been described in a Celiac Disease diagnosis. Now if the symptoms’ are similar it is easy to confuse one disease for the other and if not well understood they might be considered “exceptional” or, i.e., not well understood and discounted as the cause. I would argue that it should be the other way around if the majority (58 Percent) of the time Pellagra symptoms are described in a Celiac diagnosis it stands to reason that medical science is identifying the wrong disease. The math doesn’t add up. 58% is the Majority (primary/parent) disease and as such should be treated first. Pellagra has 3 faces that often confuse doctors today but 75 years ago they were able to diagnose this disease with only 3 symptoms the D’s of Pellagra. Dementia’s, Digestive Disorder and Dermatitis issues. Are You starting to see a pattern here? If it starts with a D then Pellagra a Niacinamide deficiency is involved. Quoting the Celiac Posterboy “These D’s a Celiac patient encounters are not the sign of several different diseases but one parent disease Pellagra with many children.” I could go on and on and on . .. but there is no need for that. I need to stop for now. Either you will believe and be helped or go on suffering needlessly if indeed Pellagra is the parent disease and GERD, IBS, UC, Chrons, NCGS and Celiac disease it‘s unruly children. 2 Corinthians (KJV) 1:3,4 3) “Blessed be God, even the Father of our Lord Jesus Christ, the Father of mercies, and the God of all comfort; 4) who comforteth us in all our tribulation, that we may be able to comfort them which are in any trouble, by the comfort wherewith we ourselves are comforted of God.” ****Again this is not medical advice but it is too easy, simple and cheap not to try and see if it works for you . . . I have found it works for others. Remember Occams’ Razor. . . The Simple answer is a Vitamin. But convincing people of that fact has not been simple or easy. I can’t convince you either way. You will have to decide for yourself . . . I only know it help’s those (of my friends) who have tried it for themselves. Praise bee to God and I want other’s still suffering from Pellagra disease if the research is to be believed being diagnosed as Celiac disease to be the next to be helped Praise bee to God! But I know now you will have to discover it for yourself. I stand as your witness. I tried! Posterboy by the Grace of God, 2 Timothy 2:7 As always, “Consider what I say; and the Lord give thee understanding in all things” this included. **** I will update this blog post in a month to 6 weeks with Part 2 about how you can test these things for yourself (if I am not recovering (God forbid) from a medical procedure) depending on how and if my CT scan shows any blockage that might require a stent to be implanted like my brother had to have done. . . Otherwise I wish you all who read this posterboy blog post God speed! And good GI health soon! Praise bee to God if you are encouraged enough from this post to try the Niacinamide 3/day for 6 months for yourself.
  10. Celiac.com 12/03/2018 - Biomarkers in blood samples are not effective indicators for diagnosis or monitoring of celiac disease. A team of researchers recently set out to assess biomarkers of celiac disease derived from neoepitopes of deamidated gliadin peptides (DGP) and tTG fragments, and to assess their usefulness in identifying patients with celiac disease with mucosal healing. The research team included RS Choung, SK Rostamkolaei, JM Ju, EV Marietta, CT Van Dyke, JJ Rajasekaran, V Jayaraman, T Wang, K Bei, KE Rajasekaran, K Krishna, HK Krishnamurthy, and JA Murray. They are variously affiliated with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA; Vibrant Sciences LLC, San Carlos, CA, USA; and with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA. The team began by analyzing serum samples from 90 patients with biopsy-proven celiac disease, along with 79 healthy control subjects for immune reactivity against the tTG-DGP complex. They used a fluorescent peptide microarray platform to estimate the antibody binding intensity of each synthesized tTG-DGP epitope. They validated results in 82 patients with newly diagnosed celiac disease, and in 217 control subjects. They assessed the ability of the peptide panel to spot patients with mucosal healing based on histologic results and using serum samples from 85 patients with treated and healed celiac disease; 81 patients with treated but unhealed celiac disease who showed villous atrophy despite adhering to a gluten-free diet; 82 patients with untreated celiac disease; 27 disease control subjects who showed villous atrophy without celiac disease; and 217 healthy control subjects. To assess their data, they relied on principal component analysis followed by machine learning and support vector machine modeling. In all, the team found 172 immunogenic epitopes of the tTG-DGP complex. Compared with control subjects, celiac patients showed substantially higher immune reactivity against these epitopes. In the test group, neoepitopes derived from the tTG-DGP complex identified people with celiac disease with a remarkable 99% sensitivity and 100% specificity. Blood samples from untreated celiac patients showed the greatest average antibody-binding intensity against the tTG-DGP complex. Blood from patients with treated but unhealed CeD mucosa (15.1 ± 7.5) showed significantly higher average antibody-binding intensity than blood from patients with treated and healed CeD mucosa (5.5±3.4) (P<.001). The test spotted celiac patients with healing mucosa with 84% sensitivity and 95% specificity. The research team discovered immunogenic epitopes of the tTG-DGP complex, and found that a test that measures immune response to epitopes accurately identified both celiac patients and patients with mucosal healing. From this study, the team concludes that the biomarker method for celiac testing could be useful in both the detection and monitoring of celiac disease. Read more at: Gastroenterology.
  11. Celiac.com 11/15/2018 - Gluten-free products, marketed as such, were largely unknown 20 years ago, but the gluten-free industry is set to reach an estimated $2.34 billion in sales by 2019. That’s more than double figures for 2014. The growth has been exponential. What sets gluten-free foods apart from other culinary trends or diet fads is that they address a legitimate health concern that affects millions of people around the world. With the massive influx of gluten-free products, and the expansion of “gluten-free” restaurant options, it’s easy to forget that gluten exists in some obvious and not so obvious places that people with celiac disease need to avoid. Here are 15 foods or food ingredients that many people wrongly assume are gluten-free: Beer Light or dark, lager, IPA or Stout, traditional beer is brewed with barley, and is not gluten-free. However, a number of major and micro breweries create tasty gluten-free alternatives. There are a number of tasty, award winning beers that are brewed from gluten-free ingredients and are fully gluten-free. There are also gluten-reduced beers. These beers are brewed like traditional beers and EU regulations allow for gluten-removed beer to be labeled as gluten-free. Plenty of people with celiac disease do fine drinking these beers, but many do not. Know your beer, know your body, and drink accordingly. Read more at Celiac.com's Oktoberfest Beer Guide! Gluten-free vs. Gluten-removed Beers. Barbecue Sauce Many barbecue sauces use artificial colors, flavorings or thickeners that may contain gluten, so it’s important to check labels, and even contact a manufacturer if you're not sure about something. Couscous, Tabbouleh and Falafel Couscous and bulgar are wheat and are used in many different Middle-eastern foods, and some people do not realize that they contain gluten. Bulgar or couscous are also used to make another popular Middle-eastern dish called tabbouleh (salad). Couscous or wheat flour are sometimes used to make falafel, so be sure to ask about the ingredients before eating. Candy Always be careful about candy. Many candies are safe and gluten-free, but many candies are not. Sometimes trusted products can change. Read labels, check websites, contact manufacturers as needed, and be careful! If you’re not sure, Celiac.com’s Annual Safe Gluten-Free Halloween Candy List is a good place to start. Cookie Dough This might seem obvious, but cookie dough, unless specifically gluten-free, almost always contains standard wheat flour and is not gluten-free. Dried Spices Some manufacturers actually use flour to keep their spices from clumping. Pay special attention to spice blends and mixes, including curry powders, which may contain wheat. Gravies, Soups, Sauces and Mixes—Packaged, Canned, or Jarred If you’ve ever made gravy from scratch, you might recall that it involves making a roux, a paste of butter and flour which thickens the gravy and gives it a nice sheen. Well, roux is also used as a thickening agent in many packaged, canned or jarred gravies, soups, sauces and mixes. Even some fresh soups may contain wheat or flour. Gazpacho, for example, can be made gluten-free, but most recipes call for a piece of bread soaked in sherry vinegar and blended into the soup. When it comes to gluten in soup, eater beware! Hot Dogs & Sausages The bun is an obvious source of gluten, but the dog itself can contain traces of wheat as well in the form of both filler and binder. So check labels, know the ingredients, and double-check when it comes to hot dogs and sausages. Ice Cream Although many ice creams are gluten-free, some may contain wheat in the form of added ingredients, like cookie dough, toppings or candy pieces. Double-check the ingredients to be safe. Packaged Deli Meats, Marinated or Pre-Seasoned Meats & Vegetable Proteins Packaged, marinated meat, fish, chicken, or other meats may contain gluten as a binder or hidden ingredient. Some vegetable-based proteins like Seitan contain gluten. Also, many deli meats claim to be gluten-free, but the same companies have released specific lines of gluten-free meats, raising the question of why they needed a separate product in the first place. Deli meats are controlled by the U.S. Department of Agriculture, not the Food and Drug Administration, which currently uses a different gluten-free standard. Prescription Drugs, Vitamins and Supplements Even though they are not technically foods, and they are meant to keep you healthy, prescription drugs, vitamins and supplements may contain gluten as binders, typically in the form of wheat starch. Ask you pharmacist for guidance, read labels closely, and make phone calls to companies or visit their Web sites to be sure. Salad Dressings Many salad dressings have updated their recipes to exclude any wheat or barley-derived additives, but some still contain gluten, especially the powdered mix kind. Soy Sauce Most soy sauces contain wheat and should be avoided. Be sure to find a gluten-free soy sauce. Sushi Although raw fish by itself is gluten-free, there are many ingredients in sushi rolls and other items that contain soy sauce and other sources of gluten. The seaweed wrappers in sushi may contain soy sauce, and the wasabi or fake crab may contain gluten. Teriyaki sauce is another source of gluten because it is made with soy sauce. See our How to Safely Order Sushi article for more info. Teriyaki Sauce Teriyaki is nearly always made with made with soy sauce, and most commercial brands contain wheat, so be careful. Read more on: Celiac.com UNSAFE Food List Celiac.com SAFE Food List Celiac.com's SAFE and UNSAFE Halloween Candy List
  12. Celiac.com 11/28/2018 - Patients with gluten ataxia without enteropathy have lower levels of antigliadin antibodies (AGA) compared to patients with celiac disease. Magnetic Resonance Spectroscopy (NAA/Cr area ratio) of the cerebellum improves in patients with gluten ataxia following a strict gluten-free diet, and is associated with an improvement in symptoms. A team of researchers recently set out to present their experience of the effect of a gluten-free diet in patients with ataxia and low levels of AGA antibodies measured by a commercial assay. The research team included Marios Hadjivassiliou, Richard A Grünewald, David S Sanders, Panagiotis Zis, Iain Croall, Priya D Shanmugarajah, Ptolemaios G Sarrigiannis, Nick Trott, Graeme Wild, and Nigel Hoggard. They are variously affiliated with the Academic Departments of Neurosciences and Neuroradiology; the Departments of Gastroenterology, the Departments of Dietetics; the Departments of Immunology, Sheffield Teaching Hospitals NHS Trust, in Sheffield, UK. The team conducted MR spectroscopy on 21 consecutive patients with ataxia and serum AGA levels below the positive cut-off for celiac disease, but above a re-defined cut-off in the context of gluten ataxia, at baseline and after a gluten-free diet. Of the 21 included patients with gluten ataxia, the team found that ten were on a strict gluten-free diet with elimination of AGA, 5 were on a gluten-free diet, but continued to have AGA, while 6 patients did not follow a gluten-free diet. The NAA/Cr area ratio from the cerebellar vermis increased in all patients on a strict gluten-free diet, increased in only 1 out of 5 patients on a gluten-free diet with persisting circulating AGA, and decreased in all patients who did not follow a gluten-free diet. From these results, the team concludes that patients with ataxia and low levels of AGA benefit from a strict gluten-free diet. The results suggest an urgent need to redefine the serological cut-off for circulating AGA in the diagnosis of gluten ataxia. Read more in Nutrients 2018, 10(10), 1444; doi:10.3390/nu10101444
  13. Hello, This is my first time posting to this board. My daughters were both recently diagnosed with celiac. We are getting used to it. It's so much easier to control on the home front, trickier when we travel. We suspect we've gluttoned our youngest, who seems to have it much more severely, via cross contact a few times. Dish towels, sponges, cutting boards etc. while visiting family. They go to extraordinary lengths to accommodate us food wise, it's the environmental piece that feels insurmountable right now. What are your best travel tips when visiting family or going on vacation when you want to cook in a kitchen? We love to cook, food is a big deal to us. Do you bring your own items? If so, what do you bring? WOuld love to hear how other approach this. Thanks!
  14. Celiac.com 11/23/2018 - The complex factors that lead to the development of celiac disease in a given individual are the subject of much research. The immune system, genetics and the environment (meaning factors in an individual’s life that would influence the development of disease) all play an important part in this process. Current research on celiac disease focuses on the immune system; scientists are working to understand the exact chain of events that occur in the gut when gluten is introduced for the first time. Understanding these events could yield insight into treatments for celiac disease that interrupt this process. Celiac disease is the only autoimmune disorder where the trigger is known: gluten. Researchers use celiac disease as a model for studying the pathogenesis of other autoimmune diseases. Other researchers are examining the role of environmental factors and the added risk they bring to an individual who already is at risk for celiac disease. These factors include the influence of breastfeeding, the timing of the introduction of cereals, intestinal infection as a precursor to celiac disease, cultural factors, geography, and more. Genetic research has determined that there are two genetic haplotypes that are necessary for the development of celiac disease; an affected individual need only to have one of these genetic haplotypes to be at risk. These factors are HLA DQ2 and HLA DQ8. HLA stands for Human Leukocyte Antigen. Antigens are substances that produce an immune response—we have many antigens in our bodies that are supposed to do that. HLA are molecules that present on the surface of cells to help the immune system to distinguish antigens that are supposed to be in the body, versus antigens that aren’t. While other genes may play a role in the process, we can conclude with virtual certainty that an individual who tests negative for DQ2 or DQ8 will not develop celiac disease. We also know that 30% of the US population has the genetic makeup for celiac disease. While it is encouraging to see a surge of interest in celiac disease research, people with celiac disease have to make choices every day that affect their health, and knowing a bit more about the immune system may make this process easier. Myths about what it means to have an autoimmune disorder are common. Knowledge about this area can help one sort out the myths and find the facts about what it means to have celiac disease. What Does the Immune System Do? The immune system provides the human body with several levels of defense from foreign invaders like bacteria and viruses. The first layer of protection is our skin. If an invader finds its way into the body, however, the second level of defense mobilizes to destroy the invader before it can replicate. Some types of invaders already replicate and invade surrounding cells before the immune system can destroy them—and there is a sophisticated type of immune response to eliminate these types of invaders. The most important decision that the immune system makes when it encounters an “invader” is to determine whether or not it is “self” (is it supposed to be in the human body?) or “non-self” (is this a virus or bacteria that will cause illness?). HLA helps the immune system by tagging cells as “self” or “non-self” to allow the immune system to attack the true invaders. In the case of celiac disease, HLA tags the antigen presenting cell as non-self, when it should be tagged as self. The human body as a house Think of the human body as a house. The exterior of the house (the roof, the brick, the door, and the windows) is like the skin of a human body, protecting everything inside. The house has an alarm system, to detect invaders. The alarm system is the body’s immune system. There is a cat inside the house, sleeping on the couch. How is the immune system supposed to work? If a burglar (who is not supposed to be in the house) comes to the side window and tries to break in, there may be a broken window, but the alarm sounds and the burglar runs away. Everything inside the house is safe. How does the immune system work when someone has celiac disease? The cat wakes up from its nap and gets a drink of water. The alarm goes off, when it’s not supposed to. The cat sets off the alarm every time it moves, but other than this, the alarm works perfectly, keeping out all of the true invaders. In other words, the immune system of an individual with celiac disease is healthy and normal in every respect, save one. The presence of gluten, and only gluten, causes a malfunction of the immune system. In our example, the cat represents gluten—it is supposed to be in the house, yet every time it moves the alarm goes off. This means that removing gluten from the diet of a person with celiac disease returns their immune system to a normal and healthy state, equal to that of someone who does not have celiac disease. Many people with celiac disease feel that they are immune compromised, which is not the case. If the house in our example represented someone with an immune compromised condition, the alarm would rarely if ever go off (invaders could enter the body without any resistance). For this reason, flu shots for people with celiac disease do not represent a concern (unless you are allergic to eggs) and people with celiac disease should receive the shot with the general population, and not the special populations who are immune compromised (the elderly, children, etc.). When should gluten be introduced to a child at risk for celiac disease? When a person with celiac disease has a baby, there is a great deal of concern regarding the child’s potential for developing celiac disease—this is understandable. One of the most troubling questions facing parents is when to introduce gluten to their child. It is a common recommendation to delay the introduction of gluten until one year of age. Unfortunately, this recommendation is based on wheat allergy, and not autoimmunity. Fortunately, recent research published in the Journal of the American Medical Association has affirmed earlier research from Finland on this subject as well as what has been a common practice throughout Europe. A protective window Researchers at the University of Colorado recently announced the results of a 10 year study on the introduction of cereals in children at risk for celiac disease. Their study demonstrated that infants who received cereals containing gluten between four to six months of age were not as likely to develop celiac disease by the age of five as were children who received gluten containing cereals at younger and older ages. The infants who received cereals between one and three months of age were five times as likely to develop celiac disease, and children who received cereals after six months of age had an elevated risk for developing celiac disease, but not to the extent of the youngest age group. Is it a gluten response? Many parents are concerned about whether or not their child will have an autoimmune response to gluten when introduced to cereals. It may help to know that it typically takes six to nine months for a child to mount an autoimmune response to gluten—if celiac disease is to occur early in their life. Therefore, a response (such as diarrhea or vomiting) shortly after cereals are introduced or eaten is usually not related to celiac disease. What about breast milk? A mother with celiac disease needs to remain on the gluten-free diet throughout pregnancy and breast-feeding. However, it is a common misconception that breast-feeding moms who are not celiac should go on a gluten-free diet while nursing. Microscopic amounts of gluten are carried in breast milk, but it is not enough to harm a child. In fact, research from Finland shows that breast milk has a protective effect in the gut when gluten is introduced to a child. This research recommends that when introducing gluten between four and six months of age, breast feeding should continue during this time to confer an added immune benefit. Understanding a bit more about the immune system may be helpful as you make decisions about your health, and the health of your family. It can be reassuring to know that the immune system of a person with celiac disease on the gluten-free diet is as healthy as an average person without celiac disease.
  15. Celiac.com 11/05/2018 - ImmusanT, Inc. is a clinical stage company looking to deliver innovative peptide-based immunomodulatory vaccine therapies to patients with autoimmune diseases, initiated enrollment in Australia and New Zealand for its celiac disease vaccine. Along with Nexvax2, ImmusanT is working to develop vaccines for other HLA-associated autoimmune diseases, including type 1 diabetes. The Phase 2 trials will assess the safety, tolerability and efficacy of its celiac vaccine, Nexvax2, on celiac patients who carry the immune recognition genes for HLA-DQ2.5. Carriers of HLA-DQ2.5 account for approximately 90% of people with disease, and Nexvax2 is designed to protect these patients from the effects of gluten exposure. Nexvax2 is currently the only disease-modifying therapeutic candidate in clinical development for patients with celiac disease. Injections of Nexvax2 are designed to reprogram T cells that trigger an inflammatory response to gluten, thereby suppressing inflammation in patients with celiac disease. Phase 1 studies showed Nexvax2 to be safe and well-tolerated at even its highest dose levels. In Phase 2 clinical trials, ImmusanT hopes to confirm clinical efficacy of Nexvax2 administered by injection into the skin for treatment of celiac disease. The study plan consists of an initial screening period of 6 weeks, an approximately 16 week treatment period, and a 4 week post-treatment observational follow-up. The trials will be conducted at sites in Melbourne, Perth, Adelaide and Brisbane, in addition to sites in New Zealand. For the U.S. study researchers will enroll approximately 150 patients across the U.S., Australia and New Zealand. Phase 2 is a randomized, double-blind, placebo-controlled clinical study of Nexvax2 in adults with confirmed celiac disease who have followed a gluten-free diet for at least a year prior to screening. “This trial is important in establishing clinical proof-of-concept for a treatment that would provide benefit beyond that of the gluten-free diet,” and will “test if Nexvax2 can specifically target the immune response to gluten in people with celiac disease and modify associated symptoms,” said Jason Tye-Din, MBBS, Ph.D., principal investigator at the Royal Melbourne Hospital and head of celiac research at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia. For more information about RESET CeD, including inclusion and exclusion criteria, please visit www.clinicaltrials.gov (Identifier: NCT03644069).
  16. Celiac.com 10/30/2018 - Products with “gluten-free” were unknown just 20 years ago. Now, driven by new labeling standards and demand that far exceeds those on medical diets, the market for gluten-free foods is expected to hit $2.34 billion in sales by 2019. That’s more than double the 2014 level. How has the influx of new gluten-free products in the last few years changed the experience of people with celiac disease? A team of researchers recently set out to investigate how the recent proliferation of the gluten‐free industry has affected individuals living with celiac disease, with a primary focus on their social lives and relationships. The research team included J. A. King, G. G. Kaplan, and J. Godley. They are variously affiliated with the Department of Sociology, Faculty of Arts, University of Calgary, Calgary, Alberta, Canada, and the O’Brien Institute for Public Health, University of Calgary, Calgary, Alberta, Canada. The team employed interpretive phenomenology for study design and analysis. Team members held semi‐structured interviews with 17 adults with clinically diagnosed celiac disease in Calgary, Alberta. They recorded the interviews and transcribed them for analysis. These 17 Canadians living with celiac disease reported that they perceive the growth of the gluten‐free industry as a "double‐edged sword." Although they are grateful for more readily available, more palatable gluten‐free options, they are increasingly faced with misunderstandings about the severity of celiac disease as a perceived result of many non-celiac disease individuals subscribing to the gluten‐free diet. Participants also felt they may be perceived or even perceived themselves differently, such as "high maintenance," etc. To help mitigate these social ramifications of following the gluten‐free diet, participants utilized various strategies. According to the study’s authors, simply telling celiac patients to adopt a gluten‐free diet ignores the regular challenges faced by those patients. The authors of the report are calling for doctors to consider the indirect burdens for celiac patients who must adopt a gluten-free diet when making their recommendations. But how? The report says nothing about what exactly doctors are supposed consider, or what they should tell patients about the challenges of a gluten-free diet. People with celiac disease probably do need more information up front as they begin to follow a gluten-free diet, but clearly far more input and study are needed. This study tells us that seventeen people in Alberta, Canada say that being gluten-free by medical necessity is both easier and more challenging than it was in the past. That it was both more manageable, but also more stressful, because gluten-free fad dieters are confusing everything. What are we to make of this? Talking informally with 17 celiac patients and writing up the results may not rise to the level of a solid study, and their input doesn’t really tell us much about how to improve their situation. Also, blaming the popularity of the gluten-free diet as a cause of confusion or stress in people with celiac disease could be an overreaction. Remember, ten or twenty years ago when most people had nearly zero awareness of celiac disease or the gluten-free diet? That included doctors who were trying to diagnose it. To have these inconvenient misunderstandings, people must first have some idea that celiac disease exists, and that a gluten-free diet is part of it. Is it possible that, as annoying as such misunderstandings may be, they represent progress, however incremental? Perhaps the annoyances are real, perhaps they are perceived. Perhaps they are a reflection of slowly rising awareness levels. But the study doesn’t tell us any of these important details. Again, there’s little question that people with celiac disease need more information up front as they begin to follow a gluten-free diet, but clearly more input and study is needed so that we can come up with an accurate picture of the challenges and provide the best ways to meet them. What’s your experience of the rapidly changing gluten-free landscape? Read more at: JOURNAL OF HUMAN NUTRITION & DIETETICS. First published: 02 October 2018 https://doi.org/10.1111/jhn.12597
  17. Celiac.com 11/07/2018 - A team of researchers recently set out to explore the relationship between dermatitis herpetiformis, as a common extraintestinal manifestation of celiac disease, and a gluten-free diet as a path to overall dermatitis herpetiformis improvement. The research team included Timo Reunala, Teea T. Salmi, Kaisa Hervonen, Katri Kaukinen and Pekka Collin. They are variously affiliated with the Celiac Disease Research Center, Faculty of Medicine and Life Sciences at the University of Tampere, the Department of Dermatology, Tampere University Hospital, the Department of Internal Medicine, Tampere University Hospital, and with the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital in Tampere, Finland. Dermatitis herpetiformis is a condition marked by itchy papules and vesicles on the elbows, knees, and buttocks. Dermatitis herpetiformis is a common in people with celiac disease. People who have just dermatitis herpetiformis alone rarely have obvious gastrointestinal symptoms. Dermatitis herpetiformis is easily diagnosed by immunofluorescence biopsy showing pathognomonic granular immunoglobulin A (IgA) deposits in the papillary dermis. One theory currently in play is that dermatitis herpetiformis is triggered by celiac disease in the gut and eventually develops into an immune complex deposition of high avidity IgA epidermal transglutaminase (TG3) antibodies, together with the TG3 enzyme, in the papillary dermis. The age at which people are diagnosed with dermatitis herpetiformis has risen steeply in recent decades to the current average of 40–50 years. The researchers found that the ratio of dermatitis herpetiformis to celiac disease is 1:8 in Finland and the United Kingdom (U.K.). Additionally, the incident rates of dermatitis herpetiformis are currently 2.7 per 100,000 in Finland and 0.8 per 100,000 in the U.K., is decreasing, whereas incidents of celiac disease are on the rise. One positive finding is that Dermatitis herpetiformis patients who are on a gluten-free diet face an excellent long-term outlook, with an even lower mortality rate than the general population. Read more in: Nutrients 2018, 10(5), 602; doi:10.3390/nu10050602
  18. Celiac.com 11/13/2018 - Ubiquitin is highly conserved across eukaryotes and is essential for normal eukaryotic cell function. The bacterium Bacteroides fragilis is part of the standard human gut microbiome, and the only bacterium known to encode a homologue of eukaryotic ubiquitin. The B. fragilis gene sequence points to a previous horizontal gene transfer from a eukaryotic source. The sequence encodes a protein (BfUbb) with 63% identity to human ubiquitin, which is exported from the bacterial cell. Is molecular mimicry of human ubiquitin by gut microbe linked to autoimmune diseases like celiac disease? A team of researchers recently set out to determine if there was antigenic cross‐reactivity between B. fragilis ubiquitin and human ubiquitin and also to determine if humans produced antibodies to BfUbb. The research team included L. Stewart, J. D. M. Edgar, G. Blakely and S. Patrick. They are variously affiliated with the School of Biological Sciences, University of Edinburgh, Edinburgh, UK; the School School of Biological Sciences, Queen’s University Belfast, Belfast, UK; the Regional Immunology Laboratory, Belfast Health and Social Care Trust, Belfast, UK; and the Wellcome‐Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast, UK. Molecular model comparisons of BfUbb and human ubiquitin predicted likely structural similarity with 99.8% confidence. The team used linear epitope mapping to identify cross-reacting epitopes in BfUbb and human ubiquitin. Also, at least one epitope of BfUbb does not cross‐react with human ubiquitin. The team used enzyme‐linked immunosorbent assay to compare the reaction of human serum to BfUbb and human ubiquitin from 474 subjects among four groups: (1) newly autoantibody‐positive patients, (2) allergen‐specific immunoglobulin (Ig)E‐negative patients, (3) ulcerative colitis patients and (4) healthy volunteers. The team’s data show that the exposure to BfUbb into the human immune system triggers the creation of IgG antibodies. Patients referred for first‐time autoimmune disease testing are more likely to have a high levels of antibodies to BfUbb than are healthy volunteer subjects. From this, the team concludes that molecular mimicry of human ubiquitin by BfUbb could be a trigger for autoimmune disease. Finding and understanding potential triggers for autoimmune conditions helps to take us one step further to understanding and potentially curing celiac disease. Stay tuned for further developments in their arena. First published: 04 August 2018 https://onlinelibrary.wiley.com/doi/full/10.1111/cei.13195
  19. Celiac.com 11/12/2018 - Here’s an uplifting celiac story. Now, this happened a while back, but it's all just coming to light in the way that so many warm and fuzzy family stories do. It starts like this: Once upon a time, a simple check for celiac disease opened the door to parenthood for couple. Just over ten years ago, AnnMarie Bradley from Celbridge, Co Kildare, thought she’d never become a mother. After two devastating miscarriages over a decade, Bradley, who is 47 years old, and her husband Christopher (48) were at wit’s end. "I was just heartbroken,” said Ms Bradley. Then, a simple visit to her doctor changed everything. A blood test indicated she might have celiac disease, which further evaluation confirmed. She began a gluten-free diet, and less than a year later, Bradley was pregnant with her son, Cameron. “Being a mother had been everything I'd wanted," she said. Cameron is nearly 16 now, and has an 11-year old sister, Emily. And they all lived happily and gluten-free ever after. In the UK, the Coeliac Society advises women struggling to conceive to consider celiac testing. Read more at: Independent.ie
  20. The following was written by Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease: In response to your questions about DH, The following represents my views about this curious and very itchy condition. In general DH is a severely itchy skin condition that often starts abruptly, affecting the elbows knees buttocks and scalp and the back. It usually starts as little bumps that can become tiny blisters and then are usually scratched off. It can occur in one spot only but usually occurs in many different areas. The condition is related to the deposit under the skin of IgA deposits. These occur in response to the ingestion of gluten in the diet. However, once deposited there, they are only slowly cleared by the body even when the individual is gluten free. While most individuals with DH do not have obvious GI symptoms almost all have some damage in their intestine. They the potential for all of the nutritional complications of celiac disease. The diagnosis is made by taking a skin biopsy and performing immunoflorescence studies on it (a specialized type of stain in major laboratories) The test is usually reliable but it takes a significant dedication to detect early cases where there is a short history of rash rather than years or months of rash. It is unusual to develop DH after the start of a GFD for celiac disease. About 5 % of celiac disease patients will develop DH usually in the first 6-12 months. This probably reflects the long lasting nature of the deposits under the skin. Treatment for DH is twofold. (1) Remove the cause: gluten. (2) Suppress the skin response with drugs such as Dapsone or some other sulphones. The latter is the most common treatment used as it is rapidly relieves the itch. However there are some side effects associated with these medications and they need to be taken under medical monitoring with blood tests to detect side effects. It is my practice that DH should be treated with a gluten-free diet for life and use of drugs to get immediate relief in the short term. It is usually possible to get patient off the Dapsone after several months of a strict gluten-free diet. The most common complication of DH is scarring which usually fades with time. Occasionally there can be secondary infection from scratching. There is probably a slightly increased chance of malignancy in those with DH who are not on a gluten-free diet. Several physical triggers are known to set off an attack of DH, especially exposure to iodides and bromides which are contained in household cleaners. A very good reference for DH is available from the GIG in Washington.
  21. The following detailed explanation of serological tests for celiac disease was written by Tom Ryan, Technical Service Specialist, INOVA Diagnostics, Inc. There has been a lot of discussion about serological testing for celiac disease recently, specifically regarding tTG (tissue Transglutaminase) testing. I will try to answer some of the many questions that have appeared on this list about all of the tests. First, and this applies to any of the blood tests, you must currently be on a gluten containing diet for the tests to be accurate. Antibodies are produced by the immune system in response to substances that the body perceives as threatening. The immune response that your body produces is its response to being exposed to gluten in the diet and its subsequent effect on the intestinal mucosa. If there is no gluten in the diet, then there is no response that we can measure. A brief change in diet will not have a noticeable effect. If you have been gluten free for a week or so, it will not make any great difference. The response might be marginally less but the difference is insignificant because the body has not had time to respond to the change. Conversely, if you have been gluten free for a protracted period of time and decide to be tested, a brief challenge of a couple of weeks is not enough to elicit a response and get an accurate test. There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus. Talk with your Doctor. My personal feeling is that the minimum is 2 slices of bread per day for 6 weeks to get an accurate test but I would not try to second-guess the Doctor. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc. What are all of these? Some contributors to the list make reference to the IgA or IgG test or to the ELISA test. These labels are incomplete for our purposes and could be referring to any number of different tests. We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal sera in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies. Anti-Gliadin Antibodies: Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results. A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for Enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower. Endomysial Antibodies: IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge. The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies. Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently, (1998) the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out. In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with: An initial positive gut biopsy; 6 months on a gluten free diet; A second, negative gut biopsy; A gluten challenge for 6 months and; A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure. Through the auspices of the Celiac Disease Foundation and others, a professional symposium and workshop was organized earlier this year in Marina Del Rey, California with participants from Europe as well as the U.S. to establish standards for reporting test results. This should improve testing and diagnosis even more. At the conclusion of this conference a Celiac Disease Standardization Committee was formed to investigate and make recommendations on a standardized method of reporting results.
  22. WHAT IS CELIAC DISEASE? Celiac disease is an autoimmune condition that affects around 1.4% of the population (91.2 million people worldwide, and 3.9 million in the U.S.A.). People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems. Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases. Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. CLASSIC CELIAC DISEASE SYMPTOMS Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others. LESS OBVIOUS SYMPTOMS Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important. NO SYMPTOMS Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. CELIAC DISEASE VS. GLUTEN INTOLERANCE Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS) Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there. There are four main differences between celiac disease and non-celiac gluten sensitivity: No Hereditary Link in NCGS Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)? IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS. To add more confusion, many cases of IBS are, in fact, celiac disease in disguise. That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. Crohn’s Disease and celiac disease share many common symptoms, though causes are different. In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis. Crohn’s treatment consists of changes to diet and possible surgery. Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection. Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS Diagnosis of celiac disease can be difficult. Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult. Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis. TESTING There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis. Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products. BIOPSY Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide. WHY A GLUTEN-FREE DIET? Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years. For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease. WHAT ABOUT ENZYMES, VACCINES, ETC.? There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease. There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes. Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement. ASSOCIATED DISEASES The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions: Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include: Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers: Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES: Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology 2018;16:823–836 Celiac Disease Center, Columbia University Gluten Intolerance Group National Institutes of Health U.S. National Library of Medicine Mayo Clinic University of Chicago Celiac Disease Center
  23. Celiac.com 10/08/2018 - A new population based study reveals that celiac disease is associated with a wide range of medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism, according to a database study of more than 35 million people. Moreover, people with autism have celiac disease at rates almost 20 times higher than in those without autism, reported lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland. That raises the question of whether people with autism should be screened for celiac disease, and whether they might benefit form a gluten-free diet. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," Dr. Karb told the World Congress of Gastroenterology last year. It is known that there are unusual symptoms of celiac disease, which include anything outside the classic symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Karb and his fellow researchers used the Explorys database to pull health record data from 26 major integrated healthcare systems in the United States. Their search covered the period from 2012 to 2017. Of 35,854,260 people in the database, they found 83,090 with diagnosed celiac disease. Overall, the age-adjusted prevalence of celiac disease in that group was 0.22%, which is much lower than the 1% to 2% range previously estimated. Those numbers are not unusual, said Dr. Karb says that the researchers “don't think there are fewer people with celiac disease, just that it may be under-diagnosed.” The rates are, he says, “what you might expect when you screen asymptomatic people." Overall, the team found a significant connection between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. Moreover, celiac disease is associated with every autoimmune disease the team looked at, except for primary biliary cholangitis, Dr Karb says. This is some pretty startling study data. We knew that celiac disease was linked to other autoimmune conditions, and there has been some surprising data about gluten-free diets helping patients with autism, but these numbers are enlightening. It seems that people with autism should definitely be screened for celiac disease, and placed a gluten-free diet, if tests confirm celiac disease. Stay tuned for more information on this important celiac disease topic. Source: World Congress of Gastroenterology 2017
  24. Celiac.com 11/06/2018 - Autoimmune pancreatitis is a rare disorder whose association with celiac disease (celiac disease) has never been investigated, although celiac patients show high rates of both endocrine and exocrine pancreatic affections. To address this lack of information, a team of researchers recently set out to evaluate the frequency of celiac disease in patients with autoimmune pancreatitis and in further medical pancreatic disorders. The research team included G De Marchi, G Zanoni, MC Conti Bellocchi, E Betti, M Brentegani, P Capelli, V Zuliani, L Frulloni, C Klersy, and R Ciccocioppo. They are variously affiliated with the Department of Medicine, the Department of Pathology and Diagnostics, the Gastroenterology Unit, the Immunology Unit, and the Pathology Unit of the Department of Pathology and Diagnostics; and the Gastroenterology Unit of the Department of Medicine, AOUI Policlinico G.B. Rossi, University of Verona in Verona, Italy; the Clinica Medica I, Department of Internal Medicine, IRCCS Policlinico San Matteo Foundation in Pavia, Italy; and the Clinical Epidemiology & Biometry Unit, IRCCS Fondazione Policlinico San Matteo; Pavia, Italy. They screened for celiac disease by looking for tissue transglutaminase (tTG) autoantibodies in the blood of patients retrospectively enrolled and divided in four groups: autoimmune pancreatitis, chronic pancreatitis, chronic asymptomatic pancreatic hyperenzymemia (CAPH), and control subjects with functional dyspepsia. In patients with borderline or positive anti-tTG values, the team also looked at anti-endomysium autoantibodies. They offered duodenal biopsy to all patients with positive results. They found just one patient out of 72 (1.4%) with autoimmune pancreatitis who had already been diagnosed with celiac and was following a gluten-free diet, while one case out of 71 (1.4%) with chronic pancreatitis and one out of 92 (1.1%) controls were found to have celiac disease. They found no celiac disease in the CAPH group. By contrast, a high prevalence of cases with ulcerative colitis was found in the AIP group (13.8%). Despite an alleged connection between celiac disease and several autoimmune disorders, the data in this study do not support celiac screening for autoimmune pancreatitis patients. Celiac screening may be useful in other pancreatic disorders, but further study is needed to make a determination. Source: Nutrients. 2018 Aug 24;10(9). pii: E1157. doi: 10.3390/nu10091157.
  25. 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.
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