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Found 11 results

  1. Celiac.com 10/28/2016 - Researchers still don't know why some people develop celiac disease or gluten intolerance, but a number of studies have focused on factors including breast-feeding, dietary habits, the timing of the introduction of gluten and geographical origin. Sweden is a high-risk country for the development of celiac disease in early life, with rates in some areas approaching 2%, nearly double that of most population baseline levels. Carin Andrén Aronsson is a dietician and doctoral student at Sweden's Lund University. Her research, ahead of her public thesis defense, indicates that the amount of gluten matter more than breast-feeding or the timing of introduction of gluten as a trigger for celiac disease. This is one of the findings from several extensive studies of children with an increased genetic risk of celiac disease conducted by researchers at Lund University in Sweden. "Our findings indicate that the amount of gluten triggers the disease," says Aronsson. Her research team has also observed that the dietary habits among the children they studied vary from one country to another, and that "there are reasons to analyze the significance of this variation more closely," she added. All the research in Aronsson's thesis is based on small children born with an increased genetic risk of celiac disease. Some of her most important conclusions are: Swedish children who reported consuming more than 5 grams of gluten per day up to the age of two years had twice the risk of developing celiac disease compared to children who consumed a smaller amount, while children with celiac disease reported eating more gluten druing that period. The risk of developing the autoimmunity which gives rise to celiac disease was highest in Sweden compared to Finland, Germany and USA, which were also studied. There was no apparent connection between the duration of the period of breast-feeding and the risk of developing celiac disease. Further study could help explain why Swedish children develop celiac disease earlier than children in other countries. Source: Lund University
  2. 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
  3. Celiac.com 12/08/2015 - Is the rate of food sensitivity and allergy growing? Or are we just more concerned about it because children experience anaphylactic crisis, sometimes even dying from exposure to peanuts, strawberries, and all the other foods that most of us think of as harmless? Even if the rates are growing, what is the cause? And should we, in the gluten sensitive community, be concerned about developing such allergies? After all, celiac patients were often told that there was no greater risk of developing IgE food allergies among those with celiac disease than is experienced by the general population (1, 2). I was certainly told this, on more than one occasion, by apparently well qualified medical practitioners. Yet, more recent research is showing that those with any autoimmune disease, including celiac disease, have a much greater risk of developing such allergies (3). Unfortunately, we still have more questions than answers. Nonetheless, the issue really does warrant exploration, especially among those who are gluten sensitive. Further, since the numbers of those with non-celiac gluten sensitivity remain controversial, we can also look at the issue from another perspective. For instance, a study of childhood IgE allergy frequency, at a center in Texas devoted to treating allergies and similar ailments, the investigators looked at antibody reactions to cow's milk, eggs, fish, peanuts, sesame, shellfish, soy, tree nuts, and wheat. They reported that the rate of all of these allergies combined had almost tripled (from 3% to 8%) in only five years (4). That is a startling rate of increase. If this finding can be applied more broadly, it should be alarming. However, another research group at Cornell University in Ithaca, New York, reported that childhood emergency department visits for food allergy reactions remained stable over a nine year period, while adult visits for food allergy reactions declined over this same time period (5). The central thrust of their report appears to be that we have an improving understanding of how to manage our own and our children's allergic reactions, so emergency room visits are becoming, relatively less frequent. This may simply signal that allergies are becoming so common that, as a culture, we are becoming better versed in how to avoid or manage mild allergic manifestations. Yet another group of investigators in Australia state that there has been a "dramatic rise in the prevalence of IgE-mediated food allergy over recent decades, particularly among infants and young children " (6). They go on to suggest that this increase may be due to "the composition, richness and balance of the microbiota that colonize the human gut during early infancy" (6). They further assert that IgE food allergies are connected to an impaired barrier function of epithelial cells that line the intestinal wall, in combination with immune dysregulation (6). Still others assert that the increase in allergies may be tied to climate change via several factors including "variability of aeroallergens, food allergens and insect-based allergic venoms" (7). Martin Blazer, M.D., in his book titled Missing Microbes argues that overuse of antibiotics may be at the root of both the increase in food allergies, as well as the increasing prevalence of celiac disease, through disrupting the gut microbiome and selection for antibiotic-resistant strains of microbes (8). Some or all of the foregoing theories may well have a legitimate influence on our growing rates of allergies. As I see it, however, the various theories postulated to explain these increasing rates have left out one powerful dietary trend that has also accompanied these increases in IgE food allergy prevalence. For instance, compromised intestinal barrier function is a well documented feature of gluten grain consumption, although it is greatest in the context of celiac disease. The increased release of zonulin, triggered by eating gluten grains, may also be a critical factor in the development and persistence of the disease process, especially in cases of celiac disease, type 1 diabetes, rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, systemic lupus erythematosus, and about one quarter of cases of multiple sclerosis (9, 10). In the gut, gluten triggers increased release of zonulin, which weakens the junction between the epithelial cells that form the intestinal walls, and usually provide a protective barrier where these cells connect (11). The "gap" between these cells, caused by increased zonulin release, allows undigested proteins and peptides to bypass the cells that usually transport digested particles from the intestine to the bloodstream. Partly digested proteins, small peptides, also move through these epithelial cells, following the same path that fully digested food particles follow. However, according to Dr. Fasano, those are usually so degraded that they don't trigger antibody production (9). Thus, the leaky gut that has long been associated with celiac disease, and is often seen as a characteristic of, but not restricted to this ailment, is a critical stage in the development of this illness. This leakiness is, as most readers will know, reversed by a gluten-free diet. We are now seeing, in the peer reviewed medical literature, a wide range of ailments being identified as manifestations of undigested food proteins being "leaked" into the circulatory system. Further, there is a dose-dependent relationship between increasing gut permeability and increased gluten consumption, both in celiac disease and in other forms of autoimmunity (12). If this dose-dependent relationship also applies to many of those with other sensitivities, at admittedly lower levels of permeability (13), and if that is the dynamic that underlies much of the increasing trend of IgE food allergies, we should be seeing the rates of these allergies continue to rise in the general population. And, if we continue with our gluten gluttony, who can say how many ailments are associated with gluten consumption and increased zonulin release? It is also possible, perhaps even probable, that some of us experience increased zonulin release into the bloodstream, rather than into the intestinal lumen. If so, those peoples' epithelial linings of lungs, nasal passages, and blood brain barriers, may be more compromised than those individuals who primarily experience a leaky gut. By weakening these other barriers, they may invite other ailments that are less obviously triggered by gluten and other food proteins. Dr. Alessio Fasano has stated that new understandings of zonulin's role in autoimmunity, inflammation, and some cancers, "suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by reestablishing [sic] the intestinal barrier function" (9). An animal study showed that AT1001, an experimental drug that blocks the action of zonulin, protected against autoimmune attack on pancreatic islet cells (9) which produce insulin. A human study of twenty-one subjects, reported similar findings (14). While it is true that intestinal infections have also been shown to induce zonulin release in the gut, the issue of microbes may not be as large a factor as it at first appears. When bacteria colonize our intestines, there are three possible outcomes: First, the infection may run rampant and kill us, thus solving the problem in a most undesirable manner. Second, and much more likely, we may take antibiotics and deplete or eliminate these infectious agents in our intestines. Third, and most likely, a combination of our immune systems, other microbes resident in our gut, antibiotics, and other, possibly unknown factors, may quickly or slowly bring the infectious agent under control. By reducing its numbers sufficiently that it won't pose a serious threat to our well being, and the harmful impact of these microbes has been muted. The second and third possibilities will be both the most common and most desirable. Also, as soon as the microbe in question is under control, zonulin release should be diminished to a point where it is either a minor factor in triggering continued zonulin release or, because it has been eradicated, the microbe will become irrelevant to zonulin release. On the other hand, for as long as we consume gluten, zonulin continues to be released, thus disrupting tight junctions in the intestinal, pulmonary, sinus, and other mucosal membranes, permitting allergens to reach our circulatory systems, ultimately giving rise to the growing prevalence of dangerous allergies that may sometimes manifest in anaphylactic reactions. The most important issue here seems to be the impact of gluten consumption on zonulin release, along with its impact on several protective barriers in the body, weakening them at the previously tight junctions between their cells. These include the blood brain barrier, which usually protects the brain from impurities and antibodies in the blood. It also includes the mucosa that line the lungs and nasal passages that protect us from airborne toxins and microbes. When that barrier is compromised, small particles from the air that we breathe will reach our circulation and trigger immune reactions...also known as allergies. Perhaps the most important barrier is in the digestive tract. It is made up of several variants of mucosa that protect the tissues of the gastrointestinal tract from toxins and the unwanted particles in our foods and beverages (well, most of them anyway). This, it seems to me, is the crux of our growing crisis with environmental allergies and the elevated zonulin levels that sometimes accompany them. And we can't even begin to combat this dynamic without first understanding it better. In the meantime, adding AT1001 to gluten-containing flours might be useful. Conversely, the media voices that are selling the idea that a gluten-free diet is an expensive fad might soon see research that reveals the gluten-free diet as an excellent prophylactic against developing IgE allergies, a variety of cancers, autoimmunity, some psychiatric illnesses, and many neurological diseases. In the interim, we can only use our own best judgement and decide for ourselves. Would the dietary products of gluten grains really be that great a loss to the palate? Is it a reasonable trade-off to risk falling prey to all of the potential consequences that come to us through elevated release of zonulin? More compellingly, perhaps, Professor Loren Cordain's assertion that humans have not had enough time to become fully adapted to eating cereal grains, especially as a dominant portion of our diet (15), appears to gain considerable support from the discovery and characterization of zonulin. Further, although some European, Asian, and northern African genes may have had as much as 15,000 years to adapt to this food source, most of the world's inhabitants have had a much shorter time to adapt. These are periods that are most appropriately measured in centuries and decades. The assumption that gluten grains can be safely consumed by all humans, because we have been eating them for "thousands of years" is unlikely to be true for most of the world's current population, and may represent a Eurocentric perspective. Sources: Csorba S, Jezerniczky J, Ilyés I, Nagy B, Dvorácsek E, Szabó B. Immunoglobulin E in the sera of infants and children. Acta Paediatr Acad Sci Hung. 1976;17(3):207-14. Greco L, De Seta L, D'Adamo G, Baldassarre C, Mayer M, Siani P, Lojodice D. Atopy and coeliac disease: bias or true relation? Acta Paediatr Scand. 1990 Jun-Jul;79(6-7):670-4. Fraser K, Robertson L. Chronic urticaria and autoimmunity. Skin Therapy Lett. 2013 Nov-Dec;18(7):5-9. Amin AJ, Davis CM. Changes in prevalence and characteristics of IgE-mediated food allergies in children referred to a tertiary care center in 2003 and 2008. Allergy Asthma Proc. 2012 Jan-Feb;33(1):95-101. Clark S, Espinola JA, Rudders SA, Banerji A, Camargo CA. Favorable trends in the frequency of U.S. emergency department visits for food allergy, 2001-2009. Allergy Asthma Proc. 2013 Sep-Oct;34(5):439-45. Molloy J, Allen K, Collier F, Tang ML, Ward AC, Vuillermin P. The potential link between gut microbiota and IgE-mediated food allergy in early life. Int J Environ Res Public Health. 2013 Dec 16;10(12):7235-56. Bielory L(1), Lyons K, Goldberg R. Climate change and allergic disease. Curr Allergy Asthma Rep. 2012 Dec;12(6):485-94. Blazer M. Missing Microbes. Harper Collins, Toronto, Canada, 2014. Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011 Jan;91(1):151-75. Yacyshyn B, Meddings J, Sadowski D, Bowen-Yacyshyn MB. Multiple sclerosis patients have peripheral blood CD45RO+ B cells and increased intestinal permeability. Dig Dis Sci. 1996 Dec;41(12):2493-8. Tripathi A, Lammers KM, Goldblum S, Shea-Donohue T, Netzel-Arnett S, Buzza MS, Antalis TM, Vogel SN, Zhao A, Yang S, Arrietta MC, Meddings JB, Fasano A. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16799-804. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8. Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A,Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006 Apr;41(4):408-19. Paterson BM, Lammers KM, Arrieta MC, Fasano A, Meddings JB. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT-1001 in coeliac disease subjects: a proof of concept study. Aliment Pharmacol Ther. 2007 Sep 1;26(5):757-66. Cordain L. Cereal Grains: Humanity's Double-Edged Sword. in Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73
  4. Celiac.com 05/21/2015 - Some studies have indicated higher rates of reflux in patients with celiac disease, but there hasn't really been any clear data on the risk for celiac disease in patients presenting with reflux. A team of researchers recently set out to determine rates of celiac disease in patients with GORD, and to better understand the nature of reflux symptoms in newly diagnosed celiac disease patients. The research team included P.D. Mooney, K.E. Evans, M. Kurien, A.D. Hopper, and D.S. Sanders. They are affiliated with the Regional GI and Liver Unit, Royal Hallamshire Hospital, Sheffield, South Yorks, UK. The team divided the patients into groups as follows: Group A included 3368 patients who had undergone routine duodenal biopsy, and prospectively recruited between 2004 and 2014. Researchers compared these results with those of a screening control group. Group B included 32 patients with newly diagnosed celiac disease who had undergone esophageal manometry and 24-h pH studies, prospectively recruited. The results showed the following: Of the 3368 patients in Group A who received routine duodenal biopsy, 850 (25.2%) presented with GORD. Rates of celiac disease among GORD patients was just 1.3% (0.7-2.4%), about the same as in the general population (P=0.53). Routine duodenal biopsy at endoscopy showed that reflux was negatively associated with celiac disease, with an adjusted odds ratio of 0.12 (0.07-0.23), P<0.0001. In group B, about one third of patients complained of reflux. Manometry showed that just under 10% had a hypotensive lower esophageal sphincter, and 40.6% had esophageal motor abnormalities, with 25% showing significant hypocontraction. Also, pH study did show that one in three did in fact suffer reflux episodes. The main takeaway from this study is that GORD patients have undiagnosed celiac disease at about the same rate as the general population, and so routine duodenal biopsy cannot be recommended for patients with GORD. Interestingly, pH/manometry studies showed a fairly high percentage of newly diagnosed celiac patients with reflux and/or esophageal dysmotility; which might explain the high prevalence of reflux symptoms in celiac disease. Source: Eur J Gastroenterol Hepatol. 2015 Jun;27(6):692-7. doi: 10.1097/MEG.0000000000000359.
  5. Celiac.com 07/22/2013 - Celiac disease is known to be caused by a combination of genetic and environmental factors. The genetic markers are fairly well established by now, but the environmental factors that are associated with celiac disease are still pretty foggy. A recent study suggests that antibiotic use might be one such factor. In a population-based case-control study analyzing Swedish population data, antibiotic use was compared against diagnosis of celiac disease. 2,933 people with celiac disease diagnoses were linked to the Swedish Prescribed Drug Register, in order to provide a history of antibiotic use. 2,118 people with inflammation (early celiac disease) and 620 people with normal mucosa but positive celiac disease blood test results were also compared. The control group consisted of 28,262 individuals matched for age and sex from the general population. The results of the study significantly suggest that antibiotic use is associated with celiac disease, at an odds ratio of 1.4 (1.27-1.53 confidence interval). Early celiac disease was also connected, with an odds ratio of 1.90 (1.72-2.10 confidence ratio), as well as positive celiac disease blood tests, at 1.58 odds ratio (1.30-1.92 confidence interval). Even when antibiotic use in the last year was ruled out, the results were very similar at 1.30 odds ratio (1.08-1.56 confidence interval). When ruling out patients with additional diseases, which could potentially be factors, the results were also very similar at 1.30 odds ratio (1.16-1.46 confidence interval). What does all that mean? A 1.4 odds ratio basically means that people who had a history of antibiotic use were 1.4 times as likely as those who had not taken antibiotics to develop celiac disease. The fact that inflammation associated with early celiac disease was also highly connected suggests that antibiotics' role in disrupting the biology of the GI tract could in some way cause celiac disease. There is still some question of causality, but it would seem that antibiotics could very likely be a culprit in the development of celiac disease, and should be avoided when possible. Source: http://www.biomedcentral.com/1471-230X/13/109/abstract
  6. Celiac.com 02/04/2015 - For kids with a predisposition to celiac disease, does the age at which they first eat gluten have any connection with their risk for celiac disease? A team of researchers wanted to figure out whether the age at which a child first eats gluten carried any associated with risk for celiac disease, for genetically predisposed children. The Environmental Determinants of Diabetes in the Young (TEDDY) is a prospective birth cohort study. The research team included Carin Andrén Aronsson, MSca, Hye-Seung Lee, PhD, Edwin Liu, MD, PhD, Ulla Uusitalo, PhD, Sandra Hummel, PhD, Jimin Yang, PhD, RD, Michael Hummel, MD, PhD, Marian Rewers, MD, PhD, Jin-Xiong She, PhD, Olli Simell, MD, PhD, Jorma Toppari, MD, PhD, Anette-G. Ziegler, MD, PhD, Jeffrey Krischer, PhD, Suvi M. Virtanen, MD, PhD, Jill M. Norris, MPH, PhD, and Daniel Agardh, MD, PhD, for the The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group. They are variously affiliated with the Department of Clinical Sciences, Lund University, Malmö, Sweden; the Pediatrics Epidemiology Center at the Department of Pediatrics of the Morsani College of Medicine at University of South Florida in Tampa, Florida; the Digestive Health Institute at the University of Colorado, Children’s Hospital Colorado in Denver; the Barbara Davis Center for Childhood Diabetes at the University of Colorado in Aurora, Colorado; the Department of Epidemiology, Colorado School of Public Health, University of Colorado at Denver in Aurora, Colorado; the Institute of Diabetes Research, Helmholtz Zentrum München, and Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes e.V., Neuherberg, Germany; The Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia; Department of Pediatrics, Turku University Hospital, Turku, Finland; the Department of Physiology and Pediatrics, University of Turku, Turku, Finland; the National Institutes for Health and Welfare, Nutrition Unit, Helsinki, Finland; the School of Health Sciences, University of Tampere, Tampere, Finland; and the Research Center for Child Health at Tampere University and University Hospital and the Science Center of Pirkanmaa Hospital District, Tampere, Finland. For their study, the team followed up on 6,436 newborn infants who had been screened for high-risk HLA-genotypes for celiac disease in Finland, Germany, Sweden, and the United States. At clinical visits every third month, the team collected information about infant feeding. The first outcome was persistent positive for tissue transglutaminase autoantibodies (tTGA), the marker for celiac disease. The second outcome was celiac disease, defined as either a diagnosis based on intestinal biopsy results, or as persistently high levels of tTGA. The team found that Swedish children consumed their first gluten at an earlier age, 21.7 weeks on average, compared with 26.1 weeks for children from Finland, and just over 30 weeks for kids from Germany, and the United States (P < .0001). Over about a follow-up period ranging from 1.7–8.8 years, but averaging about five years, the team found that 773 (12%) children developed tTGA and 307 (5%) developed celiac disease. Compared with US children, Swedish children saw an increased risk for tTGA, with a hazard ratio of 1.74 [95% CI: 1.47–2.06]) and celiac disease, with a hazard ratio of 1.76 [95% CI: 1.34–2.24]), respectively (P < .0001). Gluten introduction before kids turn 17 weeks or after 26 weeks was not associated with increased risk for tTGA or celiac disease, adjusted for country, HLA, gender, and family history of celiac disease, neither in the overall analysis nor on a country-level comparison. TEDDY, is one of several recent studies that confirm that the age at first gluten introduction was not an independent risk factor for developing celiac disease. Source: Pediatrics; January 19, 2015. doi: 10.1542/peds.2014-1787
  7. Celiac.com 06/15/2010 - A clinical team conducted a functional analysis of celiac risk loci, and found that SH2B3 offers protection against bacterial infection. The team included Alexandra Zhernakova, Clara C. Elbers, Bart Ferwerda, Jihane Romanos, Gosia Trynka, Patrick C. Dubois, Carolien G.F. de Kovel, Lude Franke, Marije Oosting, Donatella Barisani, Maria Teresa Bardella, the Finnish Celiac Disease Study Group, Leo A.B. Joosten, Paivi Saavalainen, David A. van Heel, Carlo Catassi, Mihai G. Netea, and Cisca Wijmenga. Celiac disease has a fairly high morbidity, yet it is prevalent in Western populations at rates of of 1%–2%. So far, scientists don't understand why the celiac disease phenotype is so common despite its obvious negative impact on human health. This is especially true when one considers that doctors only developed a gluten-free diet to treat celiac disease in the 1950's. The research team scientists hypothesize that the high prevalence of celiac disease might suggest that the process of natural selection favors genes that trigger celiac disease, and thus, that the gene may convey some evolutionary advantage to those who inherit them. The study group included 8,154 controls from four European populations, and 195 individuals from a North African population. By examining haplotype lengths using the integrated haplotype score (iHS) method, the team looked at selection signatures for ten confirmed celiac-associated loci in several genome-wide data sets. They found consistent indications of positive selection for celiac-associated derived alleles in three loci: IL12A, IL18RAP, and SH2B3. For the SH2B3 risk allele, they also found a variation in allele frequency distribution (Fst) between HapMapphase II populations. Functional investigation of the effect of the SH2B3 genotype in response to lipopolysaccharide and muramyl dipeptide showed that carriers of the SH2B3 rs3184504*A risk allele provided more robust triggering of the NOD2 recognition pathway. This suggests that SH2B3 plays a role in protection against bacteria infection, and it provides a possible explanation for the selective sweep on SH2B3, which occurred sometime between 1,200 and 1,700 years ago. Source: AJHG - 2010, 04 May. doi:10.1016/j.ajhg.2010.05.004
  8. Celiac.com 08/30/2011 - In a first of its kind study, a team of researchers is attempting a global estimate of the burden of celiac disease in childhood, and to to determine what role childhood celiac disease might play in global mortality due to diarrhea. The research team included Peter Byass, Kathleen Kahn, and Anneli Ivarsson. They are affiliated with the Umeå Centre for Global Health Research, Department of Public Health and Clinical Medicine at Umeå University in Umeå, Sweden, and with the MRC/Wits Rural Public Health and Health Transitions Research Unit (Agincourt), School of Public Health, Faculty of Health Sciences at University of the Witwatersrand in Johannesburg, South Africa. In the last several decades, celiac disease has become an an increasingly recognized public health problem. More recently, celiac disease has emerged as a global earth issue, in spite scant globally representative epidemiological data. Because children with celiac disease often have chronic diarrhea and malnutrition, a proper diagnosis is often missed, especially in poorer settings, where water-borne infectious diarrheas are common, and many children fail to thrive. To make their assessment, the two used available data to build a basic model of childhood celiac disease, incorporating estimates of population prevalence, probability of non-diagnosis, and likelihood of mortality among undiagnosed children of all countries from 1970 to 2010. In their paper, the two state the assumptions underlying their model, and make the model available as a supplementary file. Based on their model, in 2010 there were around 2.2 million children under 5 years of age living with celiac disease, while each year, there would be about 42,000 deaths related to celiac disease in these children. That would mean that, in 2008, deaths related to celiac disease likely totaled about 4% of all childhood diarrhea deaths worldwide. Even if celiac disease accounts for only a small proportion of global diarrhea deaths, these deaths are preventable, but not by normal diarrhea treatment, which can often involve gluten-based food supplements. They also note that, as other causes of diarrhea mortality decline, celiac disease will become a proportionately greater problem unless clinicians begin to try gluten-free diets for children with chronic diarrhea and malnutrition. Source: PLoS One. 2011; 6(7): e22774. doi: 10.1371/journal.pone.0022774
  9. Celiac.com 06/01/2010 - A clinical research team recently examined the increased expression of hypoxia inducible factor 1alpha in celiac disease. The team included A. Vannay, E. Sziksz, A. Prókai, G. Veres, K. Molnár, D. Nagy Szakál, A. Onódy, I. R. Korponay-Szabó, A. Szabó, T. Tulassay, A. Arató, and B. Szebeni. They are affiliated with the First Department of Pediatrics at Semmelweis University, and with the Department of Gastroenterology-Nephrology of Heim Pal Children's Hospital, both in Budapest, Hungary. They are also involved with the Research Group for Pediatrics and Nephrology, a joint project between the two institutions. The team set out to follow-up on the hypothesis that hypoxia inducible factor (HIF) 1 signaling may play a key role in maintaining the barrier function of the intestinal epithelium in cases of inflammatory bowel disease (IBD). In their 2008 article, "The human side of hypoxia-inducible factor," which appeared in the British Journal of Haematology, Smith, Robbins and Ratcliffe define Hypoxia-inducible factors (HIFs) as transcription factors that respond to changes in available oxygen in the cellular environment, specifically, to decreases in oxygen, or hypoxia. The team wanted to characterize the variation of HIF-1alpha and related genes in celiac disease, where the importance of the barrier function is well understood. To accomplish their goal, they gathered duodenal biopsy specimens from 16 children with untreated celiac disease, 9 children with treated celiac disease, and 10 control subjects. They assessed HIF-1alpha, trefoil factor 1 (TFF1), ecto-5-prime nucleotidase (CD73) and multi-drug resistance gene 1 (MDR1) mRNA and HIF-1alpha protein expression by real-time PCR and Western blot, respectively. They assessed localization of HIF-1alpha by immunofluorescent staining. The team observed increased HIF-1alpha and TFF1 mRNA and HIF-1alpha protein expression in the duodenal mucosa of children with untreated celiac disease compared to either the control subjects, or those with treated celiac disease (p<0.05). Children with untreated celiac disease showed HIF-1alpha staining in cytoplasmic and nuclear region of the villous enterocytes. Children with treated celiac disease showed increased mRNA expression of CD73 and MDR1 versus control subjects (p<0.01 and 0.05, respectively). The results of increased mucosal HIF-1alpha expression in children with celiac disease suggests influences from this signaling pathway in the pathological mechanisms of celiac disease. Source: Pediatr Res. 2010 May 5. PMID: 20453713
  10. Celiac.com 05/19/2010 - Enteropathy-associated T cell lymphoma is a serious complication of celiac disease, and a major cause of mortality in untreated celiac disease. One possible trigger for Enteropathy-associated T cell lymphoma development is chronic exposure of intraepithelial lymphocytes (IELs) to strong anti-apoptotic signals, that is, signals that interfere in the normal mortality of the IEL cells. These signals are triggered by IL-15, a cytokine that is over-expressed in the enterocytes of people with celiac disease. However, researchers have not yet fully mapped the signaling pathway by which IL-15 transmits these anti-apoptotic signals. Researchers consider type II refractory celiac disease (RCDII) to be a middle step between celiac disease and enteropathy-associated T cell lymphoma. Eliminating abnormal IELs at the RCDII stage would likely block EATL development. So far, though, scientists have not found successful immunosuppressive and/or chemotherapeutic approaches able to accomplish this, and RCDII outcomes remain very poor. A team of researchers recently set out to map the IL-15–driven survival pathway in human IELs, and to determine whether IL-15 triggered pathway in human intraepithelial lymphocytes represents a possible new target in type II refractory celiac disease and enteropathy-associated T cell lymphoma. The research team was made up of Georgia Malamut, Raja El Machhour, Nicolas Montcuquet, Séverine Martin-Lannerée, Isabelle Dusanter-Fourt, Virginie Verkarre, Jean-Jacques Mention, Gabriel Rahmi, Hiroshi Kiyono, Eric A. Butz, Nicole Brousse, Christophe Cellier, Nadine Cerf-Bensussan, and Bertrand Meresse. The are variously affiliated with INSERM U989, the Université Paris Descartes, Faculté de Médecine René Descartes, the Department of Gastroenterology, AP-HP, Hôpital Européen Georges Pompidou, the Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), INSERM U1016, the Department of Pathology, AP-HP, of the Hôpital Necker-Enfants Malades in Paris, with the Division of Mucosal Immunology, Department of Microbiology and Immunology at the Institute of Medical Science at the University of Tokyo in Japan, and the Inflammation Department of AMGEN Inc., in Seattle, Washington, USA. Their current findings reveal that the survival signals IL-15 directs to freshly isolated human IELs, and to human IEL cell lines derived from celiac disease patients with type II refractory celiac disease, depend on anti-apoptotic factors Bcl-2 and/or Bcl-xL. The signals require IL-15Rβ, Jak3, and STAT5 for proper function, but functioned independently of PI3K, ERK, and STAT3. In support of these findings, the team recorded elevated levels of Bcl-xL, phospho-Jak3, and phospho-STAT5 in IELs from patients with active celiac disease and RCDII. Moreover, by incubating patient duodenal biopsies with a fully humanized human IL-15–specific Ab, the team effectively blocked Jak3 and STAT5 phosphorylation. Also, treatment with IL-15–specific Ab caused IEL cell mortality, and wiped out the massive IEL build-up in mice over-expressing human IL-15 in their gut epithelium. The study marks the first successful mapping of the IL-15–driven survival pathway in human IELs, and demonstrates that IL-15 and its downstream effectors are meaningful therapeutic targets in RCDII. These findings will likely help to pave the way for the development of successful immunosuppressive and/or chemotherapeutic treatments that destroy abnormal IELs at the RCDII stage and help to block EATL development, improving outcomes for RCDII patients. Source: Journal of Clinical Investigation doi:10.1172/JCI41344
  11. Celiac.com 06/26/2007 - The results of a study recently published in the online science journal Nature Genetics have revealed a previously unknown genetic risk factor for celiac disease. An international team of researchers set out to study the genetic causes of intestinal inflammatory disorders. When the study began, it was well known that individuals with celiac disease have specific tissue types that identify wheat proteins. Why healthy individuals with the same tissue type failed to develop celiac symptoms or celiac disease remained unknown, and was a key question the team set out to answer. The team was led David van Heel, Professor of Gastrointestinal Genetics at Queen Mary, University of London. The Human Genome Project and the Hap Map Project played key support roles in the study. The results show that a protective DNA sequence in a specific gene segment, generally found in healthy individuals are missing in people with celiac disease. The research team evaluated genome data of 778 individuals with celiac disease and 1,422 controls non-celiacs within the British, Irish and Dutch populations. Key DNA Sequence Missing in Celiacs Researchers discovered that, compared to people with celiac disease, healthy people more commonly have a DNA sequence in the interleukin-2 and interleukin-21 gene region that protects against celiac disease. Interleukin-2 and interleukin-21 are cytokine proteins that are secreted by white blood cells, and which control inflammation. In people with celiac disease, the protective DNA sequence most likely leads to lesser amounts of these cytokines being produced, which weakens the defense against intestinal inflammation. Breakthrough in Better Understanding Risk Factors for Development of Celiac Disease About 1 in 133 people develop the disease, but, so far, predicting those at risk to develop the disease has been haphazard at best. Present methods of genetic testing can only narrow down the search to about 30% of the general population. These results give doctors a means to discover what further genetic risk factors leave people vulnerable to developing celiac disease. Queen Mary, University of London Press Release - Public release date: 10-Jun-2007 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
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