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Celiac.com 06/20/2016 - One evening in October 1999, while in my academic office at Baylor University Medical Center, Dallas, my professional and personal life changed in an instant. I had recently had the idea of testing stool for gluten sensitivity to possibly prove that patients with microscopic colitis, whom displayed an epidemiologic, pathologic, and genetic overlap with celiac disease but who rarely had positive blood tests against gluten (because they rarely had the small bowel villous atrophy of celiac disease; they had colitis which is inflammation in the colon). I had remembered that previous researchers in Scotland invasively placing tubes into certain patients without villous atrophy had been able to find antibodies to gluten deep inside the small intestine when they were absent from the blood. They called these patients latent celiacs. However, they never reported results of testing stool, which would have been a lot easier to collect because it did not require the multiple hours and patient invasion of placing tubes deep inside the intestine. That October afternoon I received the first set of results from my laboratory of a newly improved method we had developed for testing stool for the presence of antigliadin IgA, the main antibody against wheat gluten. It was about 7:00PM, it was dark outside, and late enough in the office for everyone to have gone home, allowing me a quiet setting to review these results. What I saw that night seemed like a window into the future and a medical-scientific Pandora's box, all at the same time. Not only did I see that about 75% of the microscopic colitis patients had a positive fecal antigliadin test but 25% of asymptomatic volunteers did also. I quickly did the math, and realized that celiac disease at a prevalence of even 1% would pale in comparison to these statistics, revealing that hundreds of thousands of people in the US and the world may be gluten sensitive without having celiac disease. I knew that I had just been given information that no one else in the world knew, and that it would likely have major public health implications resulting from a new dietary-induced disease paradigm. That the main staple food of Western civilization may be causing large percentages of the population to have symptoms and syndromes, not only colitis, but perhaps also irritable bowel syndrome, autoimmune syndromes, short stature in children, multiple allergies and chemical sensitivities, and even idiopathic psycho-neurologic syndromes like depression, Parkinson's Disease or Lou Gehrig's disease. Not to mention what it might mean for me as the holder of this information. Then it happened—the most significant moment of my life up to that point—it felt like someone had tapped me on my left shoulder. Though I knew I was alone in the office, I turned to the left and looked upward for some reason for what or whom might have tapped me on my shoulder. And though, while I saw no one there, I immediately knew there was a presence with me at that moment, a spiritual or angelic presence. And then I heard these words in my head "You have to leave this place". And within minutes, the decision came to me that I indeed did have to leave my academic post of 15 years to bring the results of this new fecal testing method to the public: to the 25% of otherwise asymptomatic people reacting to dietary gluten with the same immunologic reaction measured in celiac disease, antigliadin antibody, as well as to the 75% of patients with microscopic colitis and perhaps other GI ailments and syndromes who, with a gluten-free diet, might heal their chronic refractory inflammatory bowel conditions. This was a bold line of thinking for me, as I had been on a professional trajectory toward the normal milestones of a successful young academic medicine career, becoming head of a sub-specialty medical department (for me, Gastroenterology), the prospects for which had just begun to surface in my life. Yet, I had just been called it seemed, by an encounter with a supernatural force, to an assignment of sorts with a mission to fulfill. And so, the idea of creating a specialty intestinal laboratory to make this new line of testing available to those in need of its benefits was born, EnteroLab.com (entero means intestine in Greek and in medical terminology). A "dot com" I thought? Yes, this form of testing should originate "in the comfort of your own home". Why make people with GI problems fly on an airplane half way across the country merely to give stool specimens for lab analysis (the practice of my Dallas hospital for decades up until that time). If I could create a mechanism whereby only the specimens but not the person could do the flying, then we could deliver results and follow-up dietary recommendations electronically, and the healing would begin shortly thereafter with dietary elimination of the causative antigenic foods. And if the client desired, they could have a paid phone consult with me or my nurse and still not have to spend the time, money, and difficulty flying to Dallas. And I have to admit, in 2000 it was kind of exciting to be the first doctor in the world to turn his entire medical career over to the internet, as well as to have created the first clinical laboratory serving people directly without the need of a prescription or previous doctor's visit, both incredibly bold and revolutionary ideas at the time (and perhaps still). I had learned from similar major paradigm shifts in my field of gastroenterology (specifically, in 1983 when doctors in Australia found in their research that ulcers might be caused by bacteria, but whom were laughed at and ignored for about 15 years, yet later in 2005 received a Nobel prize) that it would likely take 15-20 years before anyone in the medical field would believe my new research findings relating to non-celiac gluten sensitivity and its simple diagnosis with fecal testing. This, even though I was regarded even at my young age as an expert in the field, with a significant track record for developing unique and successful ideas for diagnosis and treatment of GI diseases (see my CV at www.intestinalhealth.org/CV), and having been trained by one of the most successful and respected gastroenterologists of all time, Dr. John Fordtran. While my medical peers might not believe my results for some time, people suffering the symptoms would not care whether or not it was too soon for a scientific paradigm to shift, because they would want to try a gluten-free diet to get better. And try, they did. Following positive stool test results from EnteroLab, they got better in droves going gluten-free, and in most cases with complete healing of long-standing symptoms and syndromes. And eventually I predicted, with such remarkable improvements that had never been possible before, their health practitioners (at least the honest, inquisitive, and non-egotistical ones) would ask them what had brought on such improvement. Eventually these practitioners would begin sending other patients for the same testing that had opened the door to the dietary miracle the gluten-free diet posed for those previously tested. Beyond the consequences of having to leave my academic positions and stature behind, I had to withstand some public and more often professional criticism for undertaking a bold and somewhat maverick professional move without the permission of my peers in doing so. This does not always go over smoothly in scientific and medical professional circles. Despite having been a highly respected young published researcher at that time (40 publications by the time I was in my mid-30's), my submissions both to professional GI society meetings and GI journals (journals that I had served as a reviewer for years) were rejecting my research submissions relating to this new paradigm of non-celiac gluten sensitivity. And it seemed, the rejections were not for objective reasons, but more subjective and for principle. Other researchers in this specific field and other fields have had to endure similar treatment. Sadly, submissions to these journals addressing paradigm-shifting topics are not always reviewed in unbiased, objective ways if they deal with a subject or contain conclusions that go against what the reviewers inherently believe to be true at that time (the "I'll see it when I believe it" scenario rather than "I'll believe it when I see it"). And yet, despite submissions of excellently performed and written studies that were rejected for these reasons by a system that seemed unready for this new paradigm, the most common public and professional criticisms of my methods primarily centered around my "lack of publication". This seemed circular and nonsensical to me. After all, had Michael Dell ever published his methods of making computers delivered in a revolutionary way (mail order) to its customers? These computers worked and served its customers well without a published method? Why is lack of publication of a medical technologic method equated with lack of Truth or efficacy? My response was and still is to remain true to my own data and experience, and my desire to serve and help people, and to not proceed according to the needs and critical dictates of others having no experience with my techniques. And so, 15 years later, as EnteroLab approaches our millionth patient tested, and with the current number of referring health practitioners in excess of 1,500, EnteroLab.com stands as a successful purveyor of medical Truth and public service. I ask people "How could hundreds of thousands of people be satisfactorily served over 15 years if what we are doing was not worthy and True?"; at some point, a person's or business' track record has got to stand for something positive and meaningful. And it seems my estimate of the time it would take for other researchers or mainstream practitioners to begin getting on board with the new paradigm was correct. Non-celiac gluten sensitivity has recently been further researched and substantiated to exist, just as I reported in public and professional lectures as early as 1999 (but published by others as early as 1980). And it has only been in the last 2 years or so that I have seen the question being raised at national and international GI meetings by "celiac researchers", but at least they are now doing so. Yet, the public has been the patron of the paradigm all along. In the last 4-5 years gluten-free food companies have carried the ball farther down the field than ever before. Yet interestingly, this focus on the food has mistakenly led people to regard this serious clinical syndrome as "a diet" not a disorder. And as we all know, "diets" come and go for people, even week to week. This is not healthful for any diet, but especially not for a gluten-free diet where the immune system can be hyperstimulated by repeatedly withdrawing and reintroducing such an immunogenic food. And yet, whether or not people choose to test for the syndrome with our stool test (the only test available to sensitively detect non-celiac gluten sensitivity), if they decide to go gluten-free, that must be a lifelong dietary decision. Otherwise, the test should be employed to help determine how serious the circumstances might be, and to further reinforce the clinical need of its permanency. Because after all, 25% of people, even when asymptomatic, have detectable immune reactions to gluten, and in many of these, damage to the intestine can be detected as well (measurable by EnteroLab from a fecal fat test from the same stool specimen). We have stood firm on the Truth of our research and clinical results, patiently waiting these 15 years for the public and professional paradigm-thinking to catch up. And catch up it has. Everyone today has at least heard about gluten, and people are not called crazy because going gluten-free makes them better physically, mentally and/or emotionally. But our work is not done. There are many millions more children and adults suffering not only from gluten sensitivity, but from other food sensitivities as well, and other diet-related maladies (obesity, endocrine problems including diabetes, eating disorders, food addictions, etc.). I am appreciative of the support and respect given to me and EnteroLab by Celiac.com and its founder, Scott Adams, who also knew early on there was something real about gluten sensitivity. His 14 year old "Journal of Gluten Sensitivity" is evidence of that. And so now, we are proud to partner with Celiac.com by allowing them to be the first company outside our own to offer our proprietary EnteroLab tests for sale, having created some special gluten-oriented testing panels for them. And as we go into the next decades of service, I leave you with a hint of the next, new paradigm… which is really the old paradigm. Gluten sensitivity is not limited to wheat, barley, and rye, but often includes oats as well (not just because of wheat contamination of the oats). This was the clinical standard from its beginning by the founder of the gluten-free diet, Dr. Willem Dicke, but that got changed in the last 10-15 years by substandard research methods based only on celiac disease as the end point and bias toward wanting to find such a result (all studies contain bias by the researchers, it's the nature of the mind influencing reality). So for the first time anywhere, we are using a diagnostic test for non-celiac oat sensitivity, and showing that about 50% of people reacting to wheat, barley, and rye, also react to oats with a similar immunologic reaction detectable in stool. But more on this as the information and paradigm-acceptance develops. Hopefully, this one won't take another 15 years to be accepted. We at EnteroLab and my non-profit public educational institute, The Intestinal Health Institute (www.IntestinalHealth.org), have been greatly honored to serve all our patrons to date, and we look forward to meeting and serving more of you in the future. For more information on testing at EnteroLab.com, please call 972-686-6869 or go to www.EnteroLab.com. Thank you for reading this historic account.
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Celiac.com 03/30/2016 - New guidelines reverse previous recommendations on infant gluten introduction to prevent celiac disease. What's going on? New evidence shows that the age of introduction of gluten into the infant diet, or the practice of introducing gluten during breast-feeding, does not reduce the risk of celiac disease in infants at risk. Two earlier studies did claim to show that the time of introduction to gluten had an impact on later development of celiac disease. Based on those studies, in 2008, ESPGHAN issued a recommendation to introduce gluten into the infant diet between 4 months and 7 months, and to introduce gluten while the infant is still being breastfed. But since then, two randomized controlled trials have shown that the age at gluten introduction does not affect overall rates, nor does it affect the incidence or the prevalence of celiac disease during childhood. The latest findings show that "primary prevention of celiac disease through nutritional interventions is not possible at the present time," says Professor Szajewska of The Medical University of Warsaw, the lead author of the new guidelines. These new guidelines say that parents may introduce gluten into their infant's diet anytime between four to twelve months of age, and that the introduction does not need to be made via breastfeeding. It remains true that, according to study data, earlier gluten introduction does cause the celiac disease to present at an earlier age. However, current evidence indicates that neither breastfeeding, nor breastfeeding during gluten introduction can reduce the risk of celiac disease. The new evidence shows no difference in celiac disease risk when gluten is introduced while the infant is still breast-feeding, compared to after weaning. Because breastfeeding has many other health benefits, doctors recommend it for all infants, regardless of celiac disease risk. The updated recommendations are based on studies of infants with known risk genes for celiac disease. However, because parents don't often know this at the time solid foods are introduced, the recommendations apply to all infants. Source: Wolters Kluwer Health, January 19, 2016
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Celiac.com 02/15/2013 - If you think the FDA has dropped the ball on gluten-free food labeling, you are not alone. In 2004, the Food Allergen Labeling and Consumer Protection Act (FALCP) gave the FDA four years to create and implement final rules for gluten-free food labeling. The FALCP requires manufacturers to identify these allergens by their common names (i.e. wheat, milk, or soy) on labels so that consumers can easily identify them. In 2007, the FDA followed FALCP's mandate by issuing a proposed rule "Food Labeling: Gluten-Free Labeling of Foods." The proposed rule states that a food is gluten-free if the food does not contain any of the following: an ingredient that is any type of wheat, rye, barley, or crossbreeds of these grains; an ingredient derived from these grains and that has not been processed to remove gluten; an ingredient derived from these grains and that has been processed to remove gluten, if it results in the food containing 20 or more parts per million (ppm) gluten; or 20 ppm or more gluten. -- "Food Labeling; Gluten-Free Labeling of Foods," 72 Fed. Reg. 2795 (proposed January 23, 2007) (to be codified at 21 CFR Part 101). The FDA's proposed rule was based on the fact that currently-adopted analytical methods can reliably detect gluten at or above 20 parts per million in most foods. Also, under that rule, food manufacturers looking to market products as 'gluten-free' would voluntarily test those products prior to labeling. However, the FDA allowed the comment period for the proposed rule to pass with no action, and issued no final rule for gluten-free labeling. In 2011, the FDA announced a second comment period for their proposed rule, but that comment period also closed with the FDA taking no action. A full year and a half later, on Dec. 14, 2012, the FDA issued a new proposed rule titled "Request for Comments and Information on Initiating a Risk Assessment for Establishing Food Allergen Thresholds; Establishment of a Docket." They opened comment period on this proposed rule until Feb. 12, 2013, and scheduled an advisory committee meeting of the FDA for March 7, 2013 from 8 a.m. to 5 p.m. It has been eight years, since FALCP mandated the FDA to devise standards for gluten-free labeling, and five years since the legal deadline for final gluten-free rule, and the FDA has yet to accurately define the term "major food allergen," establish safe gluten thresholds for food products, and meet its statutory mandate to create and implement final rules for gluten-free food labeling. Until the FDA formally adopts a final rule for gluten-free labeling, there is no legal definition for what makes food "gluten-free" in the United States, and people with celiac disease will no clear assurance that when a product claims to be gluten-free, it is safe to consume. Please go to the Federal Register and comment on the FDA's latest ofrmulation of their rule (Docket No. FDA-2012-N-0711) regarding gluten-food.
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Celiac.com 10/26/2010 - A recent study shows that, since 1974, the rate of celiac disease has doubled every fifteen years, and that celiac rates increase as people grow older, with many developing the disease in their 50s or 60s. The Center for Celiac Research led the study, which looked at 3,511 volunteers who submitted blood samples in 1974 and 1989, along with updates every two to three years until 2007. Because researchers in the study surveyed the same people over time, says Mayo Clinic gastroenterologist Dr. Joseph Murray, the study adds weight to the concept that celiac disease can emerge at any age. The study results also echo those of a 2008 Finnish study that found that elderly people had rates of celiac disease nearly two and a half times higher than the general population. The fact that celiac disease seems to be increasing among older age groups is significant because, if someone can be gluten-tolerant for 40 or 50 years before developing celiac disease, environmental factors may outweigh genetic causes for the disease, says Alessio Fasano, director of the Center for Celiac Research. Fasano says that other unknown environmental changes and changes in "the composition of bacteria in our guts" may be causing gluten autoimmunity to present itself later in life. Although researchers have identified specific genetic markers for the development of celiac disease, the exact way in which people lose tolerance to gluten remains unknown. However, it's important to understand that even people who have the genetic markers in question are not fated to develop an autoimmune disease, says Fasano. That's because recent study shows "that environmental factors cause an individual's immune system to lose tolerance to gluten, given the fact that genetics was not a factor in our study since we followed the same individuals over time," he says. If environmental factors do play a role in celiac disease, then it will be interesting to see if certain areas and regions have high celiac rates that are not due to genetic factors. More importantly, the research team notes that by identifying the environmental factors behind celiac disease, researchers may lead to better treatment and possible prevention of celiac disease and other autoimmune disorders, including type 1 diabetes, rheumatoid arthritis and multiple sclerosis. SOURCE: Annals of Medicine: October 2010, Vol. 42, No. 7 , Pages 530-538 doi:10.3109/07853890.2010.514285
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Celiac.com 12/15/2010 - A small study in Swedish children has found no association between early childhood psychological stress and later development of celiac disease. Previous studies have shown links between psychological stress and a number immunological diseases, such as inflammatory bowel disease. A team of researchers sought to look more closely at the connection between psychological stress in families and biopsy-proven celiac disease in children. The team included Karl Mårild, Anneli Sepa Frostell, and Jonas F. Ludvigsson. Their measure of psychological stress included factors such as serious life events, parenting stress, and parental worries. Using a questionnaire data from the ABIS study (All Babies In southeast Sweden), the team collected data on 11,000 children at one-year, and on 8,800 at two-years old. They confirmed celiac disease though observing of villous atrophy in small intestinal biopsy, and confirmed the diagnosis through patient chart data. Their data showed that no association between future celiac disease and a serious life event in the family in the child's first 1 or 2.5 years after childbirth (Odds Ratio (OR) = 0.45; 95% Confidence Interval (CI) = 0.01–2.65; P = 0.72; and OR = 1.21; 95% CI = 0.43–3.05; P = 0.64, respectively). They also found no association between celiac disease and parenting stress at age 1 year and at 2.5 years (OR = 0.40; 95% CI = 0.01–2.38; P = 0.73 and OR = 0.74; 95% CI = 0.01–4.56; P = 1.00, respectively). No children exposed to parental worries at 2.5 years were diagnosed with celiac disease before end of follow-up, compared to 25 diagnosed out of 8082 children not exposed to parental worry (OR = 0.00; 95% CI = 0.00–2.34; P = 0.64). Nor was there any associations between the combined measures of stress and celiac disease. This particular study found no association between celiac disease in Swedish children and psychological stress early in life. However, a wider and more statistically robust study is needed to entirely rule out any possible associations between early psychological stresses in children and later development of celiac disease. Source: BMC Gastroenterology. 2010;10(106)
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