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I just got home from my monthly CSA support group meeting and it was reported there that Pepsi and Coke and other cola products, while technically gluten free actually test at 18ppm because of the carmel coloring. I understand that anything under 20 ppm can be considered gluten free but a lot of us react to that level. I am curious to any information or experiences you may have on this.
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We got some "gluten free" English muffins from trader Joe's and they made me quite sick from gluten. The latest post about trader Joe's bread being questionable was from 2018. They're new locally and I was hoping their gluten-free processes had improved in the years since I last lived near one, but I'm paying a heavy toll for that hope. Whatever their practices and contamination levels this is what I would call severe exposure, certainly gluten, and worse cross contamination than I've experienced in years. Hopefully someone else will skip trying trader Joe's brand "gluten free", I'm certainly not risking any of their bread.
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Celiac.com 07/29/2015 - Numerous studies have shown that a high percentage of patients with irritable bowel syndrome (IBS) are also sensitive to gluten. A team of researchers recently set out to evaluate the effect of a gluten-free diet on gastrointestinal symptoms in patients with IBS. The research team included B. Shahbazkhani, A. Sadeghi, R. Malekzadeh, F. Khatavi, M. Etemadi, E. Kalantri, M. Rostami-Nejad, and K. Rostami. They are variously affiliated with the Gastroenterology Unit of Imam Khomeini Hospital at the Tehran University of Medical Sciences, Tehran, Iran, the Digestive Disease Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Shariati Hospital, Tehran, Iran, the Sasan Alborz Biomedical Research Center, Masoud Gastroenterology and Hepatology Clinic, Tehran, Iran, the Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran, the Gholhak Medical Laboratory, Tehran, Iran, the Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran, and with the Department of Gastroenterology, Alexandra Hospital, Worcestershire, UK. For their double-blind randomized, placebo-controlled trial, the team enrolled 148 IBS patients who fulfilled Rome III criteria between 2011 and 2013. Unfortunately, only 72 out of the 148 remained on a gluten-free diet for the six weeks needed to complete the study. The team recorded clinical symptoms biweekly using a standard visual analogue scale (VAS). In the second stage after six weeks, patients whose symptoms improved to an acceptable level were randomly divided into two groups; The first group of 35 patients received packages containing powdered gluten, while 37 patients received a gluten-free placebo powder. Nearly 84% of the gluten-free placebo group showed a significant improvement in symptoms compared to just under 26% for the gluten consuming group (p < 0.001). This study confirms that a large number of patients diagnosed with irritable bowel syndrome are sensitive to gluten. The team suggests that the term of IBS might be misleading and may change or delay an "effective and well-targeted treatment strategy in gluten sensitive patients." Source: Nutrients. 2015 Jun 5;7(6):4542-54. doi: 10.3390/nu7064542.
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Hello! I have been searching extensively for a topic similar to this and I haven't been able to find anything - sorry if this has already been addressed. I had a blood test for lots of different things a few months back and it transpired I had shown up as having Coeliac disease. The doctor suggested I go on a gluten-free diet (what a turd) before getting my appointment for a gastroscopy to 'rigorously confirm' my diagnosis. Went on the gluten-free diet - felt amazing. Two months after this I had my appointment date for the gastroscopy and started my 6 week Gluten Challenge. First three weeks were okay - minor tummy discomfort, lots of tiredness but generally fine. Last three weeks weren't great. I had my gastroscopy on Thursday 5th July - it was awful but quick. I had no sedation and went home the same day with some discomfort but nothing unbearable. Since then, however, things haven't been fantastic. For the last few days I've adopted a low FODMAP diet (as well as back to Gluten-Free) to try to ease my problems which has helped, but it seems like on the two occasions this weeks I've eaten/tried kidney beans/haricot beans/chickpeas/lentils I have THE WORST STOMACH EVER. What is going on?! I'm Vegan and I gotta say this stuff makes (and made) up quick a large chunk of my diet. Has anybody else had any extra sensitivities after their Gluten Challenge/Gastroscopy? I'm taking charcoal tablets, drinking peppermint tea.. All that jazz. I was so looking forward to going back to normal and it's just not happening. Would love to know if I'm not alone with these issues! Yours fed-upedly, Beth
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The Problem with Oats in the Gluten Sensitive Diet
Dr. Ron Hoggan, Ed.D. posted an article in Winter 2004 Issue
This article originally appeared in the Winter 2004 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 09/19/2014 - Experts have decreed that pure oats are safe for people with celiac disease(1,2,3). The definition of this disease is based on a very specific type of injury to the intestinal wall that heals following the removal of gluten from the diet. This intestinal damage, called villous atrophy, is caused by the interaction between the immune system and certain proteins found in wheat, rye, and barley. Identical proteins are not found in oats (although there is also some variation between the protein groups found in wheat, rye, and barley). Further, many newly diagnosed celiac patients have been shown to recover from their celiac symptoms while eating significant quantities of oats and their intestinal biopsies do not show signs of villous atrophy1 (Admittedly, the quantity of oats consumed by these study subjects does not rival the grain protein consumption in a regular, gluten-laden diet, but the quantity is significant). Therefore, this food is considered safe for celiac consumption. Given these facts, it is not surprising that many gastroenterologists are now recommending that their patients eat oats. Some claim that patients are more likely to follow a gluten-free diet if that diet allows oats. Others point to the definition of celiac disease, which clearly requires gluten-induced villous atrophy. Still others insist that since we now know which proteins cause the villous atrophy, oats must be safe for celiac patients to consume. There are several problems with these perspectives, beginning with the assumption that patients will be more compliant with the diet if it includes oats. I have explored the medical literature and have been unable to find a single study that investigates dietary compliance as a function of including oats in the gluten-free diet. I’d be happy to hear about such a study. But until the question is investigated, the assumption is just one more opinion afloat in a sea of unfounded beliefs about grains and diet. Many celiac patients experience an addictive element in gluten. I have long suspected that is the result of morphine-like, opioid peptides found in the digests of gluten(4-8). Are some peptides from oats capable of producing these opioids? Has anyone investigated that issue? Again, I can find no evidence that this issue has been studied. Reliance on the biopsy to reveal problems with oat consumption is another relevant problem. As many of us can attest, and the medical literature reports, gluten challenges that intentionally involve ingestion of relatively large quantities of gluten often fail to reveal villous atrophy for weeks, months, and sometimes, years(9). Many celiac patients will also agree that despite our best efforts at compliance, gluten sometimes manages to sneak into our diets, particularly in the early months of following the diet. Yet a second biopsy usually shows dramatic healing of the intestinal wall, despite these dietary errors. Clearly, the intestinal biopsy is a fairly crude tool for measuring intestinal health. Its use in exonerating oats thus becomes suspect. An even more troubling element of this issue is that there are gastroenterologists who are recommending that their patients consume breakfast cereals that contain malt flavoring, because patients consuming such small quantities of malt do not show villous atrophy(10). Also troubling is the fact that many of the studies that support the safety of oats have not employed the Marsh system for identifying intestinal injury, a refinement that significantly increases the sensitivity of the intestinal biopsy. The greatest weakness of the pro-oats position is the underlying assumption that we fully understand celiac disease and gluten sensitivity. This is simply not the case. The research shows that some celiacs do develop symptoms when consuming oats. While most newly diagnosed celiacs experience reduced symptoms and improved health, this may simply be the result of consuming less grain-derived protein. Researchers have long known that even partial compliance with the gluten-free diet produces health improvements in celiac patients(11). The definition of celiac disease that requires villous atrophy followed the discovery of the beneficial impact of the gluten-free diet by more than 20 years (If in doubt about this point, please refer to the English translation of Dr. Dicke’s Ph.D. thesis at http://www.dangerousgrains.com). Our current understanding of the disease began with the observed benefits of the gluten-free diet. Intestinal biopsies were a much later development. A similar debate arose regarding the inclusion of wheat starch. It was long held to be a safe nutrient in the gluten-free diet in many European countries. In fact, the studies that showed a reduced risk of cancer and a variety of celiac-associated conditions were often conducted among patient groups living where wheat starch was deemed acceptable(12, 13). Yet when wheat starch consumption was studied in Canada, against a back-drop of zero tolerance, most of the subjects developed signs and symptoms of celiac disease(14). Many celiacs and gluten-sensitive individuals know that their symptoms do not fit with the conventional view of celiac disease. Some of us believe that there is a continuum of severity. Others believe that there are many sub-types of celiac disease. Still others believe, me included, that it really doesn’t matter whether a person has intestinal damage. The important, defining characteristic should be whether a person is mounting an immune response against the proteins in the most common substance in our food supply. Whatever our beliefs we turn to the experts when faced with health concerns and crises. However, those answers often rely on the medical definition of celiac disease, where villous atrophy heals in response to a gluten-free diet. In cases where the biopsy was improperly taken, or too few samples were taken, or patchy intestinal lesions were missed, or other forms of gluten-induced ailments are causing symptoms, we may not get answers that aid our health. Many individuals who are gluten sensitive will be, under such circumstances, dismissed with a diagnosis of IBS. Given the facts, we have several hurdles to overcome before we can, in my opinion, render an informed judgment about the safety of oats. We need a much better understanding of gluten-induced disease in all of its manifestations. We also need a definition of celiac disease that is more useful to the patient who is experiencing symptoms of gluten sensitivity/celiac disease. As part of this, we also need a test that is more accurate, and can identify celiac disease after beginning the diet––a challenge that many of us face. Until we have overcome these hurdles, any pronouncement regarding the safety of oats is premature. Further research is, in my opinion, the greatest need of the celiac community. We need to know more, not just about celiac disease, but about the whole range of nutritional and pathological impacts of eating grains. In my own quest, I have learned from the experiences of other celiac patients. Each new facet of my own experience has been illuminated by someone else’s story. I have come to understand ADHD as a frequent companion of celiac disease. Learning disabilities are also common among celiacs. Behavioral disturbances are the norm, and speech problems are common. My understanding continues to grow as I hear from others who struggle with gluten sensitivity. Despite its usefulness, this patient-to-patient network of information sharing is not enough. We need well designed, well executed research. We need a better understanding of our disease and how to protect future generations from the current, inaccurate assumptions about grains. The oats question is only one facet of a much larger need for more information and better testing methods. Sources: Storsrud S, Olsson M, Arvidsson Lenner R, Nilsson LA, Nilsson O, Kilander A. Adult coeliac patients do tolerate large amounts of oats. Eur J Clin Nutr. 2003 Jan;57(1):163-9. Kilmartin C, Lynch S, Abuzakouk M, Wieser H, Feighery C. Avenin fails to induce a Th1 response in coeliac tissue following in vitro culture. Gut. 2003 Jan;52(1):47-52. Janatuinen EK, Kemppainen TA, Julkunen RJ, Kosma VM, Maki M, Heikkinen M, Uusitupa MI. No harm from five year ingestion of oats in coeliac disease. Gut. 2002 Mar;50(3):332-5. Teschemacher H. Opioid receptor ligands derived from food proteins. Curr Pharm Des. 2003;9(16):1331-44. Review. Yoshikawa M, Takahashi M, Yang S. Delta opioid peptides derived from plant proteins. Curr Pharm Des. 2003;9(16):1325-30. Review. Horvath K, Graf L, Walcz E, Bodanszky H, Schuler D. Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Lancet. 1985 Jul 27;2(8448):184-5. Zioudrou C, Streaty RA, Klee WA. Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7):2446-9. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. Fukudome S, Yoshikawa M. Opioid peptides derived from wheat gluten: their isolation and characterization. FEBS Lett. 1992 Jan 13;296(1):107-11. Kuitunen P, Savilahti E, Verkasalo M. Late mucosal relapse in a boy with coeliac disease and cow's milk allergy. Acta Paediatr Scand. 1986 Mar;75(2):340-2. Holmes, et. al. "Malignancy in coeliac disease - effect of a gluten free diet" Gut 1989; 30: 333-338 Holmes GK. Coeliac disease and malignancy.Dig Liver Dis. 2002 Mar;34(3):229-37 Collin P, Pukkala E, Reunala T. Malignancy and survival in dermatitis herpetiformis: a comparison with coeliac disease. Gut. 1996 Apr;38(4):528-30. Chartrand LJ, Russo PA, Duhaime AG, Seidman EG. Wheat starch intolerance in patients with celiac disease. J Am Diet Assoc. 1997 Jun;97(6):612-8. -
Neurology 2001;56:385-388. Celiac.com 02/15/2001 - According to a new study published in the February issue of Neurology, severe, chronic migraine headaches can be triggered in gluten-sensitive individuals who do not exclude gluten from their diets. The study examined ten patients who had a long history of chronic headaches that had recently worsened, or were resistant to treatment. Some patients had additional symptoms such as lack of balance. Dr. Marios Hadjivassiliou, from the Royal Hallamshire Hospital in Sheffield, UK, and colleagues tested each patient and found that all were sensitive to gluten. . The patients were tested and each was found to be gluten-sensitive. Additionally, MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Results: Nine out of 10 patients went on a gluten-free diet, and seven of them stopped having headaches completely. The patients heightened immune responses, which are triggered by the ingestion of gluten, could be one of the factors causing the headaches. The other two patients who were on a gluten-free diet experienced significant relief, but not complete relief. Conclusion: According to Dr. Hadjivassiliou, removal of the trigger factor by the introduction of a gluten-free diet may be a promising therapeutic intervention for patients with chronic headaches. Further studies are needed to confirm Dr. Hadjivassilious preliminary findings.
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This article originally appeared in the Autumn 2010 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 12/06/2010 - The hazards to health created by celiac disease and gluten sensitivity are well understood. From nutritional deficiencies to osteoporosis, from depression to autoimmune disease, and from psoriasis to thyroid disease, there are few areas of the human body that gluten doesn’t touch in a negative way. There is so much emphasis on our inadequate abilities to diagnose gluten intolerance, that when we do finally make the diagnosis I believe we are guilty of another problem—lack of adequate education to those affected patients. Just last month a research study was released by the American Journal of Gastroenterology, 2010 Jun; 105(6):1412-20. The article was entitled “Mucosal recovery and mortality in adults with celiac disease after treatment with a gluten-free diet”. The research team hailed from the Division of Gastroenterology and Hepatology at Mayo Clinic College of Medicine. They stated that while a positive clinical response is typically observed in most adults with celiac disease after treatment with a gluten-free diet, the rate of small intestine recovery is less certain. Their aims were to estimate the rate of intestinal recovery after a gluten free diet in a cohort [a group of people with statistical similarities] of adults with celiac disease, and to assess the clinical implications of persistent intestinal damage after a gluten-free diet. Of 381 adults with biopsy-proven celiac disease, 241 had both a diagnostic and follow-up biopsy. Among these 241, the confirmed mucosal recovery at 2 years following diagnosis was 34% and at 5 years was 66%. Most patients (82%) had some positive clinical response to the gluten-free diet, but it did not prove a reliable marker of intestinal recovery. Poor compliance to the gluten-free diet, severe celiac disease as defined by diarrhea and weight loss, and total villous atrophy at diagnosis were strongly associated with persistent intestinal damage. There was a trend toward an association between mucosal recovery and a reduced rate of all-causes of death, adjusted for gender and age. The conclusions were that intestinal recovery was absent in a substantial portion of adults with celiac disease despite treatment with a gluten-free diet, and that there was an association between confirmed intestinal recovery (vs. persistent damage) and reduced mortality independent of age and gender. So what can we learn from this? Eating gluten-free when you are sensitive will cause you to feel better. Going on a gluten-free diet is not enough to ensure that your intestines will heal. Failing to heal your intestines puts you at increased risk for disease and death. Successfully healing your intestines reduces your incidence of death from disease. While you likely knew the first point, 2, 3, and 4 are perhaps less well known. Where I see that we are failing the gluten intolerant population is in the narrow focus of eliminating gluten as the only needed treatment. What the above research proves is that, unfortunately, for over 30% of those diagnosed simply eliminating gluten is insufficient to ensure intestinal healing. If patients were educated that healing their intestine would make the difference between contracting disease or not and extending their life expectancy or not, I think they’d be more interested in ensuring that it occurs. I am not a researcher but my clinic sees hundreds of patients who align with the results of this study completely. Patients come to see us who have been told that they shouldn’t consume gluten and for the most part they follow that recommendation. They know that they feel better when they are gluten-free so that is an impetus to not cheat. When they do cheat they know that they’ll “pay” for it but they still do so fairly regularly. Why do they cheat? Because they believe that the diarrhea, headache, bloating, etc is temporary and that when it goes away they are “fine” again. Their thought process is not unreasonable, it’s just wrong! If each patient was educated that cheating created intestinal destruction that in turn put them on a fast track towards disease and early death, I believe that cheating would take on a whole new perspective. Patients need this education and they need it often. Our book “The Gluten Effect” was written with this intention—our patients actually requested it. They asked for a written reminder of why they should maintain their gluten-free lifestyle. Later I began taping Youtube videos because other patients preferred a reminder in a video form. I’m trying to say this in a few different ways because it is terribly upsetting to meet patients, as I so often do, who have been diagnosed celiac or gluten sensitive and do not follow their diet solely due to ignorance. After almost 25 years of clinical experience I also know that some people “hear what they want to hear” and doctors with the best of intentions cannot get through to everyone. But I strongly believe that we could be doing a much better job at enlightenment. Further, we also need to educate patients about the secondary effects associated with gluten. When the immune system of the intestine is suppressed, as is the case in the presence of gluten pathology, inhospitable and pathogenic organisms can gain entry into the intestine and remain there. These organisms may be in the form of bacteria, parasites, amoebas or worms and if they are not identified and eradicated, complete healing of the intestines is all but impossible. The good bacteria that are housed in the gut, known as the microbiome or probiotics, make up much of the intestinal immune system. In gluten intolerant patients this important population of organisms is often insufficient due to the onslaught from gluten and pathogenic organisms. If the population of these probiotics is not restored to a healthy, robust balance, any attempt to achieve a healthy intestine will be unsuccessful. Lastly, it is an interesting catch-22 that in order to digest our food we need enzymes and enzymes are made from the nutrients we digest. This circular pattern is dramatically interrupted in the gluten intolerant patient. Celiacs in particular suffer from very poor absorption. It shouldn’t then come as a surprise that augmenting with proper enzymes may be critical for “priming the pump” until proper digestion of nutrients is restored. Unfortunately I find that few, if any, of these points are made clear to patients who are gluten intolerant. Most believe they are doing all they need to do simply by maintaining a mostly gluten-free diet. Nothing could be further from the truth. To review we need to do the following: Maintain a “perfect” avoidance of gluten Test for the presence of pathogenic organisms Test for any imbalance of the probiotic organisms Evaluate the need for enzymes Evaluate for the presence of any other food sensitivities, e.g. dairy Educate the patient until they have a full understanding of the above Test to ensure that the intestine is healed
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Celiac.com 06/25/2003 - Below is an abstract of yet another study that supports the use of human anti-tTG type IgA serological tests to accurately diagnose celiac disease: Alimentary Pharmacology & Therapeutics Volume 17 Issue 11 Page 1415 - June 2003 Antibodies to human recombinant tissue transglutaminase may detect coeliac disease patients undiagnosed by endomysial antibodies N. Tesei*, E. Sugai*, H. Vázquez*, E. Smecuol*, S. Niveloni*, R. Mazure*, M. L. Moreno*, J. C. Gomez, E. Mauriño* & J. C. Bai* Background: The screening and diagnosis of coeliac disease have been simplified by the advent of new serological tools. Aim: To assess the clinical utility of a newly developed kit for antibodies to human recombinant tissue transglutaminase (hu-anti-tTG) in a large population of patients undergoing intestinal biopsy for suspected intestinal disorders. Methods: We evaluated 426 serum samples from consecutive adult patients (250 from untreated coeliac disease patients and 176 from individuals in whom a diagnosis of coeliac disease had been excluded), obtained at the time of intestinal biopsy. Samples were tested for immunoglobulin A (IgA) hu-anti-tTG by enzyme-linked immunoabsorbent assay, IgA endomysial antibodies (EmA) by indirect immunofluorescence and IgA and IgG antigliadin antibodies by enzyme-linked immunoabsorbent assay. A sub-group of samples was also assessed for a guinea-pig-based anti-tissue transglutaminase. Results: According to the cut-off for hu-anti-tTG, the sensitivity, specificity and positive and negative predictive values were 91%, 96%, 97% and 87%, respectively. Simultaneous determination of EmA showed values of 86%, 100%, 100% and 83% for the same parameters. Although 19 coeliac disease patients (7.6%) were negative for EmA and hu-anti-tTG, both tests rendered superior statistical values to antigliadin antibody tests. At diagnosis, IgA deficiency was detected in 11 patients, but both assays were able to detect samples with mild to moderate deficiency. The comparison of hu-anti-tTG with EmA showed excellent concordance between the tests ( statistic, 0.85). Discordance was observed in 20 samples from coeliac disease patients (8%) and in nine samples from controls (5%). Fifteen samples had an EmA-negative but hu-anti-tTG-positive serology, and five showed the converse pattern. Comparison of human recombinant and guinea-pig tests showed concordant results in 96% of cases. Conclusions: The quantitative determination of hu-anti-tTG type IgA using a commercial enzyme-linked immunoabsorbent assay kit was highly sensitive and specific for the detection of coeliac disease. Our results in a large population of patients with a clinical condition suggestive of the disorder demonstrated that the test can be used to detect a substantial number of patients otherwise unrecognized by IgA EmA.
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