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Found 12 results

  1. This article appeared in the Autumn 2006 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 12/11/2006 - Yes, thats what I think. Gluten-sensitivity is a disease of your brain and nerves. The gluten puzzle I have come to this conclusion after studying the effects of gluten on my patients for over a decade. I am a pediatric gastroenterologist and allergist. I run a busy clinic for children and their parents. I have been increasingly concerned by the large numbers of my patients who are affected by gluten. I was perplexed by their wide-ranging symptoms. The puzzle was to explain how gluten could cause so much ill health to so many people in so many different ways, including celiac disease. Faulty brain control Eureka! The solution came when deep in discussion with my friend and colleague, Ron Harper, Professor of Neurobiology, UCLA. We were both struggling with the concept of multiple symptoms that needed to be explained. The answer appeared absurdly simple: disturbed "brain control". It suddenly seemed obvious—gluten could disturb the neural pathways of the body. Gluten was gradually damaging the brain and the nerves of susceptible people. It was the brain that was the common pathway for the manifestations of all of the gluten symptoms. So I set out to research what the world medical literature had to say. Is gluten a neurotoxin? I felt excited. I reviewed my patients in this new light—I began looking for a brain-grain connection. I began to see gluten as a neurotoxin—this could provide a universal model of gluten-sensitivity. This toxicity might act through inflammatory mechanisms or cross-reactivity with neurons. I began accumulating the evidence for my proposal that gluten-sensitivity is a brain and nerve disease. "Full Of It!" The concept of "Full of it" developed from the stories from my patients. I wrote my hypothesis down in a book now called Full of it! It refers to our diets being full of gluten; to the world being full of gluten-sensitive people; to the medical practitioners who are so skeptical of adverse reactions to gluten; to the enthusiasm of people who are feeling vibrant again on a gluten-free diet; and to those who are brimming with hope that the problem of gluten has now been recognized. Food allergy skeptics As a junior doctor I decided to formally research the food allergy phenomenon. I was awarded a research post and carried out the first comprehensive food allergy studies in New Zealand. I triumphantly demonstrated that food allergy was both a real entity and that it was common. But, to my disappointment, my colleagues were reluctant to believe me or my data. They professed a "disbelief" in food allergy. This surprised me as I had the research data. My next step was to conduct four more years of investigation of food allergy in Australia (at the Royal Childrens Hospital, Melbourne). This was a bigger and more elaborate study. My Doctoral Thesis (1982) based on this work is called: Food hypersensitivity in children: diagnostic approaches to milk and egg hypersensitivity. Since then I have continued my investigations into food allergy—but still today (25 years later) medical skepticism abounds. This "disbelief" is held despite the vast body of research describing food allergy. There seems to be an underlying unwillingness for doctors to consider food allergy as a possibility. Unfortunately, this also applies to gluten reactions. The shocking truth The shocking truth about gluten is that gluten foods are causing tremendous damage—but currently this is going mostly unrecognized. Unfortunately, gluten grains have become our staple diet. The quantity of gluten in our food supply has been steadily increasing. Yet worse, official Health Policies endorse gluten grains as the foundation of our food pyramid. Medics turn a blind eye Gluten is sapping the energy and wellbeing of countless millions. To date, the medical profession has turned a blind eye to glutens wider problems whilst focusing all of their attention on the narrow problem of celiac disease. A typical story I received emails like this every day: "Dr Ford, I have emailed you a number of times regarding our two children. I thought I should let you know that since going gluten free for the last three months, at last our son and daughter have put on some weight. If I had kept them on a normal gluten diet (which they recommended at the hospital) we would be still be having the headaches and sore tummies as well as the bad moods which our son would have. People just thought he was a naughty child, but now he is so different - we can talk to him without getting into any fights. I congratulate you for all your efforts on bringing gluten intolerance to the media and medical profession. More children and their families may find long awaited help. We have had to put up with this for seven years! At long last there is light at the end of the tunnel. Kind regards, Sue and Garry." Can gluten damage your brain? I believe that gluten was actually causing these two children to be sick. That is the explanation for their "naughty" behavior, their moods and their headaches. I postulate that gluten can damage your brain. I have come to this conclusion by the abundant circumstantial evidence from my observations of my patients who are gluten-sensitive. I have pondered the next questions: "Why do they have such an array of symptoms from gluten?" "Why do they recover so quickly when gluten is removed?" And "Why do they deteriorate so rapidly when only tiny amounts of gluten are eaten?" The concept of a brain/nerve disease can explain everything. The brain/nerve hypothesis "The symptoms from gluten occur through its action on the nervous system". I propose that gluten-sensitivity is a brain condition. Each and every organ in your body has some form of brain/nerve control. I propose that gluten can injure the delicate nervous networks that control your guts functions. A malfunction will subsequently lead to all of the gut symptoms that have so well been described. In addition, gluten can also directly affect brain function, which leads to the primary neurological symptoms that are so commonly seen with gluten-sensitivity. What is new? There are a number of new ideas that I put forward. These are based on circumstantial evidence. They produce a unifying theory of the symptoms that are attributed to gluten toxicity. A brain disease I consider that gluten-sensitivity is mostly a neurological problem. A major contribution to this debate is the realization that the brain has a central role in the expression of the symptoms that have, until now, been attributed to the local toxicity of gluten in the gut. A nerve disease I propose that gluten-sensitivity is a nerve disease. There is a gigantic network of nerves that controls every function that your gut is programmed to do. There are as many nerve cells in your gut as there are in your head! (about 25 billion nerve cells). I call it your tummy brain (or gut brain). Your tummy brain can be directly damaged by gluten reactions. This is the cause of so many sore tummies and bowel troubles. A wide spectrum of neurological manifestations For decades, there have been reports of unexplained brain and nerve symptoms which are associated with celiac disease. Although these associations have been described, there has been no universal mechanism proposed. However, if gluten is seen as a neurotoxin, then the explanation has been found. A very common disease Reactions to gluten have recently been documented to be extremely common. About one-in-ten people (as ascertained by blood donor studies) have high levels of gluten antibodies in their blood. My clinical studies have arrived at this same high number of gluten-sensitive people. Others have data to show that it is even more prevalent. Am I full if it? You might ask, "Is he full of it?" Yes, I am full of excitement and hope for the future. So many people can now be helped, if only this information can be widely distributed. I am full of ideas and full of enthusiasm. I hope that you are full of hope for your healthy and vibrant future. Tariq's story: "Dear Rodney, Thank you for your care and support of my family in regard to our allergies, gluten sensitivity and celiac disease that exists within that framework. My son Tariq, who is nearly 12 years old, has been a patient of yours over a number of years for his multiple food allergies. Tariq also suffers from dyslexia. Over the last several years Tariq has been becoming increasingly tired, lacking in energy and motivation, struggling with school work and constantly scratching due to his eczema and rashes covering all of his body. During this time, even though he has attended soccer training up to four times a week he somehow gained a lot of weight. Tariq was constantly grumpy and had low mood levels. Two months ago you diagnosed Tariq with gluten-sensitivity (his tTG 4; IgG-gliadin 86; IgA-gliadin 9). Tariq was extremely reluctant to go on a gluten free diet. But as the rest of the family had gone gluten-free—so he was forced also to become gluten-free. The changes that a gluten-free diet has evoked in Tariq have been astounding. His energy levels have increased, his skin has vastly improved, he has lost a lot of his excess weight (even though his appetite has increased) and he has shown improvement in his dyslexia. Tariq is not as grumpy as he was and his mood levels have improved. Tariq is now vigilant about gluten and can see the differences it has made to his life and the quality of it. Also, the other soccer parents have noticed a vast improvement in Tariqs energy levels and speed. His teacher has also noticed a big difference. Thanks again. Regards, Rosemary" Are you affected? The shocking truth is that gluten can damage your brain and that so many people are being encouraged to eat gluten-foods that might be steadily eroding their health and energy. If you have any lingering doubt about your own health, then I suggest that you check out the possibility of gluten-sensitivity. If you have any comments or questions we would love to hear from you. Dr Rodney Ford is a Pediatric Gastroenterologist, Allergist and Nutrition Consultant. He has been Associate Professor of Pediatrics at the Christchurch School of Medicine, University of Otago. He runs a busy Childrens Gastroenterology and Allergy Clinic in Christchurch, New Zealand. He has written over a hundred scientific papers including book chapters and books. www.doctorgluten.com This includes a series of five books on gluten: why it can make you ill and how to go gluten-free. Are You Gluten-Sensitive? Your Questions Answered Going Gluten-Free: How to Get Started The Gluten-Free lunch book The book for the Sick, Tired and Grumpy (Gluten-Free kids) Full of it! The shocking truth about gluten (The brain-grain connection - ISBN 978-0-473-10407-8)
  2. Celiac.com 02/19/2018 - It's very important that people with celiac disease maintain a gluten-free diet. Still, there has been some data to suggest that some people with celiac disease may be "hyper vigilant" in their approach to a gluten-free diet, and that such extreme vigilance can cause them stress and reduce their overall quality of life. Can a more relaxed approach improve quality of life for some people with the disease? A team of researchers recently set out to determine whether "extreme vigilance" to a strict gluten-free diet may increase symptoms such as anxiety and fatigue, and therefore, lower quality of life (QOL). The research team included Randi L. Wolf, Benjamin Lebwohl, Anne R. Lee, Patricia Zybert, Norelle R. Reilly, Jennifer Cadenhead, Chelsea Amengual, and Peter H. R. Green. They are variously affiliated with the Department of Health and Behavior Studies, Program in Nutrition, Teachers College Columbia University New York USA, the Department of Medicine, Celiac Disease Center Columbia University Medical Center, Harkness Pavilion New York, USA. The team assessed the influence of QOL with energy levels and adherence to, and knowledge about, a gluten-free diet. For their cross-sectional prospective study, the team looked at 80 teenagers and adults, all with biopsy-confirmed celiac disease, living in a major metropolitan area. They assessed QOL using celiac disease-specific metrics. The team based dietary vigilance on 24-hour recalls and an interview. They based knowledge on a food label quiz. They used open-ended questions to describe facilitators and barriers to following a gluten-free diet. Overall, extremely vigilant adults had greater knowledge, but significantly lower QOL scores than their more relaxed counterparts. Both teens and adults who reported lower energy levels had much lower overall QOL scores than those with higher energy levels. To maintain a strict gluten-free diet, hyper-vigilant celiacs were more likely to avoid eating out, to cook at home, and to use internet sites and apps. For hyper vigilant eaters, eating out was especially challenging. Being hyper-vigilant about maintaining a strict gluten-free diet can cause stress and adverse effects in both teens and adults with celiac disease. Doctors may want to look toward balancing advocacy of a gluten-free diet with promoting social and emotional well-being for celiac patients. In some cases, allowing a more relaxed approach may increase well-being and, thus, make dietary adherence easier. Obviously, people would need to tailor any relaxation in their gluten-free vigilance to make sure they weren't suffering preventable symptoms or doing themselves any harm. Source: Dig Dis Sci (2018)
  3. Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease. Professor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms. To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2. "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them. So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses. Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease. "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated." At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed. This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future. Source: Med.uio.no
  4. Celiac.com 07/01/2016 - Between five to ten percent of Germans may suffer from wheat intolerance. These people suffer immune reactions when they eat wheat and other cereals such as spelt, rye, and barley. They suffer symptoms including diarrhea, fatigue, psychological disorders, and worsening of chronic inflammatory diseases. They may have celiac disease, wheat allergy, and non-celiac-non allergy wheat sensitivity (NCWS). Now doctors and biomedical and agricultural researchers at Johannes Gutenberg University Mainz (JGU) and the University of Hohenheim have joined forces to study these disorders, especially NCWS. They are gearing their research towards the breeding of new types of wheat that lack these disease causing properties, while maintaining favorable characteristics, such as good baking properties and palatability. The researchers have three main aims. Firstly, they want to find out how the content of wheat proteins called alpha-amylase-trypsin inhibitors (ATI's) has naturally evolved in the various wheat varieties. For this purpose, they are looking at whether there are differences in ATI content in older and newer varieties, the extent to which this is genetically determined in each variety, and whether environmental influences play a role. They also hope to establish exactly how many proteins belong to the family of ATIs in the wheat varieties examined and which of these proteins mainly cause the immune response. The harvested samples are thus being analyzed for ATI content by genetic and proteome methods, while human cell lines are being used to evaluate their immune system-activating effects in the laboratory. Lastly, the scientists hope to be able to establish how far ATI content affects baking properties and palatability, evaluating the wheat variants on the basis of standard quality criteria. Finally, and outside of the current proposal, "we plan several proof-of-concept clinical studies with patients that suffer from defined chronic diseases to assess how far a significant reduction of ATIs in the diet, for example by approximately 90 percent, may improve their condition," said Schuppan. The goal over the medium term is to use the findings to breed new varieties of wheat that sensitive population groups will better tolerate. "We thus need to get the balance correct and create wheat varieties with a low ATI content that still have good baking properties and palatability," concluded Longin. Source: eurekalert.org.
  5. Celiac.com 08/18/2009 - Many of you know that DQ8 is one of the two major genes which may lead to celiac disease. You may also know that celiac disease is often associated with various other autoimmune diseases. What you may not know is that DQ8 may be the direct cause of these other autoimmune diseases, for these autoimmune diseases are found in increased incidence not just in celiac disease, but also with DQ8 itself. What follows is a list I have compiled showing the various diseases that are found in increased frequency among people who have the DQ8 gene (DQB1*0302). I will show the reference number next to each, and the corresponding references will appear below: Celiac disease (1) Scleroderma (2) Rheumatoid arthritis (1) Autoimmune thyroiditis (3) Pemphigus (4) Lupus (6) Pemphigoid (5) Focal myositis (7) Multiple sclerosis (8) Myasthenia gravis (1) Insulin dependant latent autoimmune diabetes of adults and adult Type 1 diabetes (9) Type 1 juvenile diabetes (1) Sjogren’s syndrome (10) Addisons’s disease (11) Complex regional pain syndrome with dystonia (12) Latex allergy (13) This list is not intended to be exhaustive. It is a starter list. Hopefully more research will be done on these, including carefully controlled research as to whether gluten plays any role in triggering these other autoimmune diseases even in the absence of gluten blood antibodies or positive duodenal biopsies. I, for one have DQ8 and numerous of these autoimmune diseases, even though my gluten blood antibodies and duodenal biopsies are negative. We who have this gene need to know for certain #1 whether a gluten free diet will help prevent the triggering of these other various autoimmune diseases, and #2 whether a gluten-free diet will help mitigate autoimmune symptoms that have already developed. I feel no better on the gluten-free diet than before I started it a year and a half ago. However, if I had not been on the diet, perhaps I would be feeling even worse now. Only controlled research will give us the answer.References: http://en.wikipedia.org/wiki/HLA-DQ8 Autoantibodies to fibrillarin in systemic sclerosis (scleroderma). An immunogenetic, serologic, and clinical analysis. Frank C. Arnett, MD, John D. Reveille, MDet al. See abstract at http://www3.interscience.wiley.com/journal/112212324/abstract. A strong association between thyrotropin receptor-blocking antibody- positive atrophic autoimmune thyroiditis and HLA-DR8 and HLA-DQB1*0302 in Koreans. Cho, JH Chung, YK Shong, YB Chang, H Han, JB Lee, HK Lee and CS Koh. See abstract at http://jcem.endojournals.org/cgi/content/abstract/77/3/611. Association between HLA-DRB1, DQB1 genes and pemphigus vulgaris in Chinese HansBy Zhou SH, Lin L, Jin PY, Ye SZ. See abstract at: http://www.ncbi.nlm.nih.gov/pubmed/12579512. Polymorphisms of HLA-DR and -DQ Genes in Japanese Patients with Bullous Pemphigoid. By Okazaki A, Miyagawa S, et al. See abstract at: http://sciencelinks.jp/j-east/article/200017/000020001700A0339663.php. HLA-DRB1*03 and DQB1*0302 associations in a subset of patients severely affected with systemic lupus erythematosus from western India. By U Shankarkumar, K Ghosh, S S Badakere, D Mohanty. See abstract at: http://ard.bmj.com/cgi/content/extract/62/1/92. HLA typing in focal myositis. By Kenji Sekiguchi, Fumio Kanda, Kenichi Oishi, Hirotoshi Hamaguchi, Kenichiro Nakazawa, Nobuya Maeda, Hiroyuki Ishihara and Kazuo Chihara. See abstract at: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T06-4DB5B4F-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=975695599&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=36883393fca9b990607eeb0d38116c5a. HLA-DRB1*1501, -DQB1*0301, -DQB1*0302, -DQB1*0602, and -DQB1*0603 alleles are associated with more severe disease outcome on MRI in patients with multiple sclerosis. By Zivadinov Robert; Uxa Laura et al. See abstract at: http://www.biomedexperts.com/Abstract.bme/17531857/HLA-DRB1_1501_-DQB1_0301_-DQB1_0302_-DQB1_0602_and_-DQB1_0603_alleles_are_associated_with_more_severe_disease_outcome. Similar Genetic Features and Different Islet Cell Autoantibody Pattern of Latent Autoimmune Diabetes in Adults (LADA) Compared With Adult-Onset Type 1 Diabetes With Rapid ProgressionBy Nóra Hosszúfalusi, MD, PHD, Ágnes Vatay, MD1, et al. See abstract at http://care.diabetesjournals.org/content/26/2/452.full. Specific amino acid residues in the second hypervariable region of HLA- DQA1 and DQB1 chain genes promote the Ro (SS-A)/La (SS- autoantibody responses. ByJD Reveille, MJ Macleod, K Whittington and FC Arnett. See abstract at http://www.jimmunol.org/cgi/content/abstract/146/11/3871. Analysis of extended human leukocyte antigen haplotype association with Addison’s disease in three populations. ByGombos, Hermann, et al. See study at: http://www.eje-online.org/cgi/reprint/157/6/757.pdf. HLA-B62 and HLA-DQ8 are associated with Complex Regional Pain Syndrome with fixed dystonia. By Rooij, Gosso, et al. See study at: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0K-4WH0JWP-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=c869b6d3a38081820fad17c162b510ba. HLA-DQ8 and the HLA-DQ8-DR4 haplotype are positively associated with the hevein-specific IgE immune response in health care workers with latex allergy. By Rihs Hans-Peter; Chen Zhiping; Ruëff Franziska; et al. See abstract at: http://www.biomedexperts.com/Abstract.bme/12209103/HLA-DQ8_and_the_HLA-DQ8-DR4_haplotype_are_positively_associated_with_the_hevein-specific_IgE_immune_response_in_health_c
  6. maddierozell

    Suspected Celiac In Toddler

    I have a 19 month old son that I am suspecting may have Celiac. He is very small. He is 19lbs and only 27" tall. He has been sick since the day he was born. He is constantly constipated and vomits almost daily. He also has chronic respiratory infections. As of about 4 months ago, I started seeing these small liquid filled sacs in his stools. They are comparatively about the size of a grain of rice. The will pop if you squeeze them and a clearish yellow liquid will come out. I have had him tested for parasites and it came back negative. My son has always had issues with constipation and gas. His stomach stays big and swollen. We have an appointment at Texas Children's with a GI next month, I am just trying to narrow down things I can bring up to the doctor. When looking at the symptoms of Celiac's everything seemed to click. Right down to his asthma and size issues. When I asked his pediatrician about the sacs in his stool he was at a loss and could not even begin to make a guess. I myself also have had a diagnosis of IBS with bad episodes of constipation and diarrhea. Celiac is the first thing in my mind and I am kind of just wondering if these things sound like this may be the answer to our problems? Any help would be extremely helpful and appreciated.
  7. Celiac.com 05/29/2014 - Many people with celiac disease report symptoms of depression, which usually subside upon treatment with a gluten-free diet. But a new study out of Australia suggests that gluten can cause depression in people with non-celiac gluten-sensitivity. Current evidence shows that many patients with self-reported non-celiac gluten sensitivity (NCGS) continue to have gastrointestinal symptoms on a gluten-free diet, but say that avoiding gluten makes them feel ‘better'. So, why do people with non-celiac gluten sensitivity seem to feel better on a gluten-free diet, even if they still have gastrointestinal symptoms? A team of researchers wanted to know if this might be due to gluten’s effects on the mental state of those with NCGS, and not necessarily because of gastrointestinal symptoms. The research team included S. L. Peters, J. R. Biesiekierski, G. W. Yelland, J. G. Muir, and P. R. Gibson. They are affiliated with the Department of Gastroenterology, Central Clinical School of Monash University at The Alfred Hospital in Melbourne, the Department of Gastroenterology at the Eastern Health Clinical School of Monash University in Box Hill, and the School of Health Sciences at RMIT University in Bundoora, Victoria, Australia. For their double-blind cross-over study, they looked at 17 women and five men, aged 24–62 years. All participants suffered from irritable bowel syndrome, but not from celiac disease, and their symptoms were controlled on a gluten-free diet. The team gave the participants one of three random dietary challenges over 3 days, followed by a minimum 3-day washout before moving to the next diet. All participants got all three diets over the course of the study. For each phase, the team supplemented the challenge gluten-free food with gluten, (16 g/day), whey (16 g/day) or nothing at all (placebo). The team assessed mental state as determined by the Spielberger State Trait Personality Inventory (STPI), cortisol secretion and gastrointestinal symptoms. They found that gluten ingestion was associated with higher overall STPI state depression scores compared to placebo [M = 2.03, 95% CI (0.55–3.51), P = 0.010], but not whey [M = 1.48, 95% CI (−0.14 to 3.10), P = 0.07]. They found no differences for other STPI state indices or for any STPI trait measures, and they saw no difference in cortisol secretion between challenges. Gastrointestinal symptoms were similar for each dietary challenge. Short-term exposure to gluten specifically induced current feelings of depression with no effect on other indices or on emotional disposition. Moreover, the team saw no gluten-specific trigger of gastrointestinal symptoms. Such findings might explain why patients with non-coeliac gluten sensitivity feel better on a gluten-free diet despite the continuation of gastrointestinal symptoms. Source: Aliment Pharmacol Ther. 2014;39(10):1104-1112.
  8. Celiac.com 09/09/2013 - Many people with celiac disease show slightly elevated liver enzymes, though these enzyme levels usually return to normal after gluten-free diet. A team of researchers recently set out to investigate the cause and prevalence of altered liver function tests in celiac patients, basally and after 1 year of gluten-free diet. The research team included Giovanni Casella, Elisabetta Antonelli, Camillo Di Bella, Vincenzo Villanacci, Lucia Fanini, Vittorio Baldini, and Gabrio Bassotti. They are affiliated with the Medical Department, and the Clinical Pathology Department of Desio Hospital in Monza and Brianza, Italy, the Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology Section at the University of Perugia in Perugia, Italy, and with the Department of Laboratory Diagnostics, Pathology Section, Brescia, Italy. The team gathered data from 245 untreated celiac disease patients, 196 women and 49 men, ranging in age from 15 to 80 years. They then analyzed the data, and assessed the results of liver function tests performed before and after diet, as well as associated liver pathologies. They found that 43 (17.5%) of the 245 patients, showed elevated levels of one or both aminotransferases; In 41 patients (95%) the elevation was mild, meaning that it was less than five times the upper reference limit. The remaining two patients (5%) showed marked elevation, meaning levels more than ten times the upper reference limit. After patients eliminated gluten for one year, aminotransferase levels normalized in all but four patients, who had HCV infection or primary biliary cirrhosis. Celiac patients who show hypertransaminaseaemia at diagnosis, and who do not show normalization of liver enzymes after 12 months of gluten-free diet, likely suffer from coexisting liver disease. In such cases, the research team recommends further assessment to assess the possible coexisting liver disease. Spotting and treating coexisting liver disease in celiac patients is important for improving liver function and preventing possible complications. Source: Liver International. 2013;33(7):1128-1131.
  9. Celiac.com 03/18/2009 - A recent study used lactulose hydrogen-breath assays to show that small intestine bacterial overgrowth (SIBO) is likely a routine cause of non-responsive celiac disease. A team of researchers from the Mayo Clinic College of Medicine recently set out to assess the rates and significance of SIBO in celiac disease based on the results of quantitative culture of intestinal aspirate. The team was made up of Alberto Rubio-Tapia, M.D., Susan H. Barton, M.D., Joseph A. Murray, M.D., of the Mayo’s Division of Gastroenterology and Hepatology, and Jon E. Rosenblatt, M.D., of the Mayo’s department of Laboratory Medicine and Pathology. Their efforts were supported by the American College of Gastroenterology (ACG) International Training Grant 2006 (ART) and the NIH grants DK-57892 and DK-070031 (JAM). Currently, the rate of SIBO in celiac disease diagnosed by quantitative culture of intestinal aspirate is not known. The team set out to assess the rate and determine the significance of SIBO in celiac disease based on the results of quantitative culture of intestinal aspirate. The team set out to examine the causes of non-responsive celiac disease by looking at people with celiac disease in whom culture of intestinal aspirate was assessed for the presence of both aerobic and anaerobic bacteria. They defined bacterial overgrowth as culture >105 colony forming units/mL. In all, they evaluated 149 people with biopsy-confirmed celiac disease. They took intestinal aspirate samples from 79 (53%) patients with non-responsive celiac disease, 47 (32%) as initial work-up for mal-absorption, and in 23 (15%) with asymptomatic treated celiac disease. The team diagnosed 14 cases of SIBO (9.3%), nine cases of non-responsive celiac disease (11%), five cases at initial work-up for mal-absorption (11%), and 0 cases in asymptomatic treated celiac disease. Patients with a positive culture showed signs of worse mal-absorption. 67% of patients with both non-responsive celiac disease and bacterial overgrowth showed a coexistent disorder. The results showed that nearly 1 in 10 celiac patients had SIBO as diagnosed by quantitative culture of intestinal aspirate (9.3%). This figure included both patients with symptomatic treated or untreated celiac disease. This shows that SIBO may exist along with other maladies associated with non-responsive celiac disease. Journal of Clinical Gastroenterology: Volume 43(2)February 2009pp 157-161
  10. Am J Gastroenterol. 2002 Aug;97(8):2016-21 Celiac.com 01/29/2004 - According to researchers at the Mayo Clinic in Rochester Minnesota, the main causes of non-responsive celiac disease are: "1) gluten contamination is the leading reason for non-responsive celiac disease; 2) of non-responsive celiac disease cases, 18% are due to Refractory Sprue; and 3) alternative diseases or those coexistent with celiac disease and gluten contamination should be ruled out before a diagnosis of Refractory Sprue is made." The researchers define Refractory Sprue as "failure of a strict gluten-free diet to restore normal intestinal architecture and function in patients who have celiac-like enteropathy," and conducted a study to determine possible causes, including how many people actually have Refractory Sprue compared with how many are diagnosed with it. The researchers examined the medical records of 55 patients who were, between 1997 and 2001, presumed to have non-responsive celiac disease, six of which were later found not to have celiac disease. Of the 49 remaining patients 25 were identified as having gluten contamination in their diet. The researchers add: "Additional diagnoses accounting for persistent symptoms included: pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, T-cell lymphoma, pancreatic cancer, fructose intolerance, protein losing enteropathy, cavitating lymphadenopathy syndrome, and tropical sprue." I think that it is clear that if you have celiac disease and continue to have symptoms your first step should be to look closely at your diet for any possible gluten contamination. Your next step should be eliminating other common food intolerance items such as cows milk, soy, eggs or corn. -Scott Adams
  11. Arch Intern Med. 2003;163:1566-1572. Ulrike Peters, PhD, MPH; Johan Askling, MD; Gloria Gridley, MS; Anders Ekbom, MD, PhD; Martha Linet, MD Celiac.com 07/30/2003 - The following abstract paints a fairly bleak picture for those of us with celiac disease; however, after taking a closer look at it I believe that it has some serious limitations that should not be overlooked, and have likely produced skewed or irrelevant results. For example, the study does not indicate whether or not the patients in it followed a strict gluten-free diet. Other studies have shown that the mortality risk for celiacs decreases to that of the normal population when a gluten-free diet is followed for at least five years, and that it is also affected by how soon the diagnosis is made and how soon treatment begins. It is well known that not following a gluten-free diet will increase a celiacs risk of death by many causes to many times that of the normal population, which is precisely why it is so important to include such information in studies of this type. In my opinion doing a study like this and not including such data is like doing a study on diabetes where perhaps half or more people in the study do not take insulin but ought to, and then publishing the ultra-high mortality rate that would be its outcome: "Conclusion: Diabetics have a 20-fold mortality rate over the normal population." The conclusion would clearly not be true for those who took their insulin. Additionally the time period that is covered by this study, 1964-1993, could be considered the dark ages of celiac disease, even in Europe (we actually may be just entering the Renaissance age for celiac disease here in the USA, but this could be argued!). Many doctors during this time did not stress enough to their patients the importance of following a strict gluten-free diet, just as many still do not even do this day. My doctor didnt. He just diagnosed me and said I shouldnt eat gluten (as opposed to telling me that it could kill me if I kept eating it), and he didnt even explain to me HOW to avoid it! Is it possible that some of the folks in this study, diagnosed as far back as 1964, might have had similar experiences with their doctors? I would be willing to bet that at least 50% of the people in this study (if not more) were not following a strict gluten-free diet, or were not following the diet at all. If this is true, it is kind of like studying a group of diabetics whose only treatment was to be told by their doctors that they should avoid sugar, which seems absurd if you think about it. Last, the study has considerable bias in that it recruited only hospitalized celiacs, presumably because they were already significantly ill, and those who never made it into a hospital were excluded. It reports findings of auto-immune diseases and small bowel/lymphomaexcesses--these are already well known--but what other researchers may disagree with is the scale of the excess--SMR is always a very crude method ofexpressing this in such studies. - Scott Adams (special thanks to Dr. Geoff Helliwell for his comments on this study) Abstract: "Background: Patients with celiac disease have an increased risk of death from gastrointestinal malignancies and lymphomas, but little is known about mortality from other causes and few studies have assessed long-term outcomes." "Methods: Nationwide data on 10,032 Swedish patients hospitalized from January 1, 1964, through December 31, 1993, with celiac disease and surviving at least 12 months were linked with the national mortality register. Mortality risks were computed as standardized mortality ratios (SMRs), comparing mortality rates of patients with celiac disease with rates in the general Swedish population." "Results: A total of 828 patients with celiac disease died during the follow-up period (1965-1994). For all causes of death combined, mortality risks were significantly elevated: 2.0-fold (95% confidence interval [CI], 1.8-2.1) among all patients with celiac disease and 1.4-fold (95% CI, 1.2-1.6) among patients with celiac disease with no other discharge diagnoses at initial hospitalization. The overall SMR did not differ by sex or calendar year of initial hospitalization, whereas mortality risk in patients hospitalized with celiac disease before the age of 2 years was significantly lower by 60% (95% CI, 0.2-0.8) compared with the same age group of the general population. Mortality risks were elevated for a wide array of diseases, including non-Hodgkin lymphoma (SMR, 11.4), cancer of the small intestine (SMR, 17.3), autoimmune diseases (including rheumatoid arthritis [sMR, 7.3] and diffuse diseases of connective tissue [sMR, 17.0]), allergic disorders (such as asthma [sMR, 2.8]), inflammatory bowel diseases (including ulcerative colitis and Crohns disease [sMR, 70.9]), diabetes mellitus (SMR, 3.0), disorders of immune deficiency (SMR, 20.9), tuberculosis (SMR, 5.9), pneumonia (SMR, 2.9), and nephritis (SMR, 5.4)." "Conclusion: The elevated mortality risk for all causes of death combined reflected, for the most part, disorders characterized by immune dysfunction."
  12. The following is a list of causes of flattened villi which was published in a book titled Coeliac Disease by W. T. Cooke and G. K. Holmes, published by Churchill Livingstone, Medical Division of Longman Group Limited (1984). Celiacs on a gluten-free diet (for a prolonged period) who continue to have flatten villi may be want to look for other causes to their problem. Keep in mind that some of the items listed rarely cause flatened villi, and are usually found in conjunction with Celiac Disease or immuno-deficiencies. Coeliac Disease Cows Milk Protein Intolerance Soy Protein Intolerance Refractory Sprue Collagenous Sprue Immunodefiency Synodromes Mediterranean Lymphoma Intestinal Ulceration Gastroenteritis Intractable Diarrhoea of Infancy Protein Calorie Malnutrition Kwashiorkor Tropical Sprue Parasitic Disease: Giardiasis Strongyloidiasis Coccidiosis Intestinal Capillariasis Hookworm Disease Eosinophilic Gastroenteritis Contaminated Bowel Syndrome Drug and Radiation Damage
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