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Celiac.com 08/01/2016 - Symptoms and damage in celiac disease is caused by partially-degraded gluten peptides from wheat, barley and rye. Susceptibility genes are necessary to trigger celiac disease, but they can't do it alone. Some researchers suspect that these susceptibility genes might get help from conditions resulting from unfavorable changes in the microbiota. To better understand the whole picture, a team of researchers recently set out to examine gluten metabolism by opportunistic pathogens and commensal duodenal bacteria, and to characterize the ability of the resulting peptides to activate gluten-specific T-cells from celiac patients. The research team included A Caminero, HJ Galipeau, JL McCarville, CW Johnston, S Bernier, AK Russell, J Jury, AR Herran, J Casqueiro, JA Tye-Din, MG Surette, NA Magarvey, D Schuppan, and EF Verdu. They are variously affiliated with the Farncombe Family Digestive Health Research Institute, and the Department of Biochemistry & Biomedical Sciences, M. G. DeGroote Institute for Infectious Disease Research at McMaster University, Hamilton, Ontario, Canada; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, Australia; the Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia; Área de Microbiología, Facultad de Biología y Ciencias Ambientales, Universidad de León, León, 24071 Spain; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, 3052 Australia; the Department of Gastroenterology, The Royal Melbourne Hospital, Grattan St., Parkville, Victoria, 3050 Australia, and the Institute for Translational Immunology and Research Center for Immunotherapy, University Medical Center, Johannes Gutenberg University, Mainz, Germany. For their study, the team colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of celiac patients or healthy controls, selected by their in vitro gluten-degrading capacity. They then measured gliadin levels and proteolytic action in intestinal contents after gluten feeding. Using peripheral blood mononuclear cells from celiac patients after receiving a 3-day gluten challenge, the research team characterized by LC-MS/MS the eptides produced by bacteria used in mouse colonizations from the immunogenic 33-mer gluten peptide. They found that the bacterial colonizations created clear gluten degradation patterns in the small intestine of the mice. Pseudomonas aeruginosa (Psa), an opportunistic pathogen from celiac patients, exhibited elastase activity and produced peptides that better translocated the mouse intestinal barrier. Psa-modified gluten peptides activated gluten-specific T-cells from celiac patients. In contrast, Lactobacillus spp. from the duodenum of non-celiac controls degraded gluten peptides produced by human and Psa proteases, reducing their immunogenicity. From these data, the research team concludes that small intestinal bacteria show clear gluten metabolic patterns in vivo, increasing or reducing gluten peptide immunogenicity. This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie any connection between celiac disease and microbial imbalance or maladaptation in the digestive tract. Source: Gastroenterology. 2016 Jun 30. pii: S0016-5085(16)34713-8. doi: 10.1053/j.gastro.2016.06.041.

Celiac.com 05/30/2016 - People with HLA genes have the highest risk factor for developing autoimmune disorders. The vast majority of people with celiac disease carry the HLA DQA1*05 and DQB1*02 alleles, both of which encode the DQ2.5 molecule. A research team recently set out to examine the implications for anti-gluten T cell response of the preferential expression of HLA-DQ2.5 genes associated with celiac disease with respect to non-predisposing HLA genes. The research team included L Pisapia, A Camarca, S Picascia, V Bassi, P Barba, G Del Pozzo, and C Gianfrani. They are variously affiliated with the Institute of Protein Biochemistry-CNR, the Institute of Genetics and Biophysics-CNR in Naples, Italy, and the Institute of Food Sciences-CNR in Avellino, Italy. In order to activate pathogenic CD4+ T lymphocytes, that is, to trigger active celiac disease, it is necessary for the body to form complexes between DQ2.5 and gluten peptides on antigen-presenting cells (APCs). It is widely accepted by clinicians that the DQ2.5 genes establish the different intensities of anti-gluten immunity, depending on whether they are in a heterozygous or a homozygous configuration, that is, whether both genes are activated, or only one gene is activated. The research team's recent study shows that, in celiac patients, HLA DQA1*05 and DQB1*02 gene expression is much higher than expression of non-celiac-associated genes. This, in turn, impacts protein levels and causes a comparable cell surface exposure of DQ2.5 heterodimers between DQ2.5 homozygous and heterozygous celiac patients. As a consequence, the magnitude of the anti-gluten CD4+ T cell response is strictly dependent on the antigen dose, and not on the DQ2.5 gene configuration of APCs. These findings are important, because they support the idea that the expression of DQ2.5 genes is an important risk factor in celiac disease. The preferential expression of DQ2.5 alleles observed in this study offers a new explanation of why these genes are so frequently associated with celiac disease and with other autoimmune disorders. Source: J Autoimmun. 2016 Apr 12. pii: S0896-8411(16)30029-4. doi: 10.1016/j.jaut.2016.03.016.

Celiac.com 10/31/2014 - The relationship between the risk of celiac disease and both the age at which gluten is introduced to a child’s diet and a child’s early dietary pattern is unclear. A team of researchers set out to examine how the introduction of dietary gluten and HLA status impact the risk of celiac disease in children. The research team included Elena Lionetti, M.D., Stefania Castellaneta, M.D., Ruggiero Francavilla, M.D., Ph.D., Alfredo Pulvirenti, Ph.D., Elio Tonutti, M.D., Sergio Amarri, M.D., Maria Barbato, M.D., Cristiana Barbera, M.D., Graziano Barera, M.D., Antonella Bellantoni, M.D., Emanuela Castellano, M.D., Graziella Guariso, M.D., Maria Giovanna Limongelli, M.D., Salvatore Pellegrino, M.D., Carlo Polloni, M.D., Claudio Ughi, M.D., Giovanna Zuin, M.D., Alessio Fasano, M.D., and Carlo Catassi, M.D., M.P.H. They are variously affiliated with the Departments of Pediatrics (E.L.) and Clinical and Molecular Biomedicine (A.P.), University of Catania, the Department of Pediatrics, San Paolo Hospital (S.C.), and the Department of Developmental Biomedicine, University of Bari (R.F.), Bari, the Department of Immunopathology and Allergology, Udine Hospital, Udine (E.T.), the Department of Pediatrics, Azienda Ospedaliera IRCCS Santa Maria Nuova Hospital, Reggio Emilia (S.A.), the Department of Pediatrics, Sapienza University of Rome, Rome (M.B.), the Department of Pediatrics, University of Turin, Turin (C.B.), the Department of Pediatrics, San Raffaele Hospital (G.B.), and the Department of Pediatrics, Vittore Buzzi Children’s Hospital, Milan (G.Z.), the Department of Pediatrics, Bianchi Melacrino Morelli Hospital, Reggio Calabria (A.B.), Pediatric Gastroenterology Unit, Giannina Gaslini Institute, Genoa (E.C.), the Department of Pediatrics, University of Padua, Padua (G.G.), the Department of Pediatrics, Federico II University of Naples, Naples (M.G.L.), Pediatric Gastroenterology and Cystic Fibrosis Unit, University Hospital Gaetano Martino, Messina (S.P.), the Department of Pediatrics, Rovereto Hospital, Rovereto (Trento) (C.P.), the Department of Pediatrics, University of Pisa, Pisa (C.U.), and the Department of Pediatrics, Marche Polytechnic University, Ancona (C.C.) — all in Italy; and the Division of Pediatric Gastroenterology and Nutrition and Center for Celiac Research, MassGeneral Hospital for Children (A.F.), and the Celiac Program, Harvard Medical School (A.F., C.C.) — both in Boston. For their study, the team randomly divided 832 newborns who had first-degree relatives with celiac disease into groups that received their first dietary gluten at 6 months (group A) or 12 months (group . The team determined HLA genotype at 15 months of age, and conducted serologic screening for celiac disease at 15, 24, and 36 months, and again at 5, 8, and 10 years. Patients with positive serologic findings received intestinal biopsies. The primary focus was on rates of celiac disease autoimmunity and of overt celiac disease among the children at 5 years of age. A total of 707 children completed the 36 month trial. Of those, 553 had a standard-risk or high-risk HLA genotype and completed the study. At 2 years of age, substantially higher percentages of children in group A than in group B had celiac disease autoimmunity (16% vs. 7%, P=0.002) and overt celiac disease (12% vs. 5%, P=0.01). At 5 years of age, there were no longer significant differences between the groups in terms of autoimmunity (21% in group A and 20% in group B, P=0.59) or overt disease (16% and 16%, P=0.78 by the log-rank test). At 10 years, the risk of celiac disease autoimmunity was far higher among children with high-risk HLA than among those with standard-risk HLA (38% vs. 19%, P=0.001), as was the risk of overt celiac disease (26% vs. 16%, P=0.05). Other variables, including breast-feeding, were not associated with the development of celiac disease. So, the short take away here is that, according to this study, neither delayed introduction of gluten nor breast-feeding had any effect on celiac disease rates among at-risk infants. However, children who experienced later introduction of gluten showed a delay in the onset of disease. Lastly, the important predictor of disease was having a high-risk HLA genotype. Source: N Engl J Med 2014; 371:1295-1303October 2, 2014. DOI: 10.1056/NEJMoa1400697

Celiac.com 01/11/2012 - In an effort to understand how delayed celiac disease diagnosis became the norm for most patients over the last few decades, a research team conducted a study to assess the issue. Their study also looked at how delayed diagnosis affects health-related quality of life (HRQoL) for those with celiac disease, and considered differences with respect to sex and age. For the study, the team collaborated with the Swedish Society for Coeliacs to send a questionnaire to 1,560 randomly-chosen members, divided equally by age and sex. A total of 1,031 members (66%) responded. The team first measured HRQoL using the EQ-5D descriptive system, then translated the results to quality-adjusted life year (QALY) scores. The team then compared the results against the results from a survey of the general population. There was some good news and some bad news. The good news is that, while the average QALY score during the year before treatment was 0.66, it improved after diagnosis and treatment to 0.86, which is better than that the score of 0.79 for the general population. The bad news is that they found the average person with celiac disease faced a delay in diagnosis of 9.7 years from the first symptoms, and 5.8 years from the first doctor visit. The team concede that the delay has been reduced over time for some age groups, but contend that it still remains unacceptably long for large numbers of people. Untreated celiac disease results in poor HRQoL, which improves or exceeds that of the general population if diagnosed and treated. Reducing the delay in diagnosing celiac disease will go a long way toward reducing the burden of celiac disease. To do so, they say it is necessary to raise awareness of celiac disease as a common health problem, and to intensify diagnosis practices. This may, the note, make mass-screening for celiac disease an desirable option in the future. Authors: Fredrik Norstrom, Lars Lindholm, Olof Sandstrom, Katrina Nordyke, Anneli Ivarsson Source: BMC Gastroenterology 2011, 11:118. doi:10.1186/1471-230X-11-118

Celiac.com 01/06/2003 - Evolution is an interactive process. Those of us who learn quickly and well are more likely to survive, thrive, and reproduce. Learning capacities then, are factors in the survival of our genes. Research is now revealing that cereal grains, along with other allergenic and highly glycemic foods, pose a serious threat to our sustained ability to learn. These foods have been shown to interfere at almost any stage of the learning process, impeding our attempts to focus our attention, observe, ponder, remember, understand, and apply that understanding. Grains can alter learning capacities in four specific ways: as sequelae of untreated celiac disease; through an immune sensitivity to gluten; through dietary displacement of other nutrients and; through the impact of grain on blood sugar/insulin levels. There are many reports of learning problems in association with untreated celiac disease. A majority of children with celiac disease display the signs and symptoms of attention deficit disorder (ADD/ADHD)1, 2 a range of learning difficulties3 and developmental delays4-6. Many of the same problems are found more frequently among those with gluten sensitivity7 a condition signaled by immune reactions against this most common element of the modern diet. Grain consumption can also cause specific nutrient deficiencies that are known to play an important role in learning. Grains can also cause problems with blood sugar/insulin levels resulting in reduced capacities for learning. Further, foods derived from grain are an important element in the current epidemic of hypoglycemia, obesity, and Type 2 diabetes8-10. Our growing understanding of the biological impact of cereal grain consumption must move educators to challenge current dietary trends. Part of our improved understanding comes from new testing protocols which are revealing that celiac sprue afflicts close to 1% of the general population, making it the most common life-long ailment among humans, with frequencies ranging from 0.5% to more than 5% of some populations11, 12. It is widespread and appears to occur more frequently among populations that have experienced relatively shorter periods of exposure to these grains13. The importance of this newly recognized high frequency of celiac disease becomes obvious when we examine the impact it has on learning and behavior. Research has identified ADHD in 66-70% of children with untreated celiac disease, which resolves on a gluten-free diet, and returns with a gluten challenge1, 2. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD13-15. Other reports have connected untreated celiac disease with similarly abnormal blood flow patterns in the brain16. One might be able to dismiss such reports if viewed in isolation, but the increased rates of learning disabilities among celiac patients3, and the increased rates of celiac disease among those with learning disabilities leave little to the imagination17. Further, there is one report of gluten-induced aphasia (a condition characterized by the loss of speech ability) that resolved after diagnosis and institution of a gluten-free diet18. Still other investigations suggest a causal link between the partial digests of gluten (opioid peptides) and a variety of problems with learning, attention, and development. Gluten sensitivity, afflicting close to 15% of the general population19, 20 is an immune reaction to one or more proteins in found in grains. When a persons immune system has developed antibodies against any of these proteins, undigested and partly digested food particles have been allowed entry into the bloodstream21. The leakage of food proteins through the intestinal wall signals a failure of the protective, mucosal lining of the gastrointestinal tract, as is consistently found in untreated celiac disease. Many of the same health and learning problems that are found in celiac disease are significantly overrepresented among those with gluten sensitivity for the very good reason that many of the same proteins are being leaked into the blood of those with gluten sensitivity. Our cultural obeisance to grains is at odds with the remains of ancient humans. Archaeologists have long recognized that grains are a starvation food—one for which we are not well suited. Grains result in consistent signs of disease and malnourishment in every locale and epoch associated with human adoption of grain cultivation. Grains are a poverty food. As we increase our grain consumption, we cause deficiencies in other nutrients by overwhelming the absorptive and transport mechanisms at work in our intestines. For instance, diets dominated by grains have been shown to induce iron deficiency22—a condition that is widely recognized as causing learning disabilities23-29. This should not be surprising since iron is the carrier used to distribute oxygen throughout our bodies, including various regions of our brains. There is little room to dispute the hazards to learning posed by reductions in oxygen supply to the brain. Iron deficiency reduces available oxygen in the brain, revealing yet another dimension of gluten grains as mediators of learning difficulties. There is more. The impact of grain consumption on our blood sugar levels is yet another facet of its contribution to learning problems. We evolved as hunter-gatherers, eating meats, and complex carbohydrates in the form of fruits, vegetables, and seeds. Refined sugars were a rare treat wrested from bees with some difficulty. At best, it was a rare treat for our pre-historic ancestors. Today, with unprecedented agricultural/industrial production of refined sugars along with cultivation and milling of grain flours, these products have become very cheap and available, particularly over the last fifty years. During that time, we have added enormous quantities of grain-derived starches to the overwhelming quantities of sugar we consume. The result of this escalating dietary trend may be observed in the current epidemic rates of Type 2 diabetes, hypoglycemia, obesity, and cardiovascular disease. In the classroom, we see these trends manifest in students mood swings, behavioral disorders (fluctuating between extreme lethargy and hyperactivity), chronic depression, forgetfulness, and muddled thinking—all of which reflects the inordinate, counter-evolutionary burden placed on many homeostatic systems of the body, particularly those related to blood sugar regulation. The pancreas has many functions. One important activity of the pancreas is to stabilize blood sugar levels. When blood sugar is not well regulated, learning is impaired30. The pancreas secretes carefully monitored quantities of glucagon and insulin. The pancreas responds to the presence of proteins, sugar, and starch in the digestive tract by producing insulin. It produces glucagon in response to fats. The balanced presence of both of these hormones in the bloodstream is critical to learning because they regulate the transport of nutrients into cells. Too little or too much insulin can cause blood sugar levels go out of control inducing a wide range of symptoms. Today, when the insulin/glucagon balance goes awry, it is frequently due to insulin overproduction due to a diet dominated by sugars and starches. This overproduction is caused by chronic consumption of highly glycemic foods. The resulting elevated levels of insulin cause rapid movement of nutrients into cells, either for storage as fat, or to be burned as energy, causing increased activity levels, "hot spells", sweating, increased heart rate, etc. This energized stage requires a constant supply of sugars and starches to be maintained. Otherwise, it is soon followed by bouts of lethargy, light-headedness, tremors, and weakness, which are all signs of hypoglycemia or very low blood sugar levels. Despite having stored much of the blood sugars as fats, there is insufficient glucagon to facilitate its use for energy. As this condition progresses, and as blood sugar levels plummet, periods of irrational anger and/or confusion often result. These moods often result from adrenaline secreted to avoid a loss of consciousness due to low blood sugar levels. The next step in the progression, in the absence of appropriate nutritional intervention, is lapsing into a coma. In the short term, the answer to these fluctuations is more frequent consumption of sugars/starches. However, the long term result of such an approach is either a state of insulin resistance, where more and more insulin is required to do the same task, or a state of pancreatic insufficiency, where the pancreas is simply unable to keep pace with the demand for insulin. In either case, once this stage is reached, the individual may be diagnosed with type 2 diabetes. This disease has so increased among North Americans, particularly among children, that an autoimmune form of diabetes, previously called juvenile onset, had to be renamed to "Type 1 diabetes". By now, it will not surprise the reader to learn that Type 1 diabetes has also been shown to be significantly associated with gluten. Research reveals that there is considerable overlap between celiac disease and Type 1 diabetes. About 8% of celiacs also have Type 1 diabetes31-33, and 5-11% of Type 1 diabetics have celiac disease34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten39-42. The growing reaction against gluten and other allergenic foods should not be confused with the several dietary fads of the 20th Century. The vegetarian perspective ignores the vitamin deficiencies that result from a strict vegetarian diet. The low-fat craze is another fad that has mesmerized the industrialized world for the last 30-40 years. Fortunately, this perspective has recently come under scrutiny. Despite having served as the driving force behind most physicians dietary recommendations during the last several decades, the low fat dictum is overwhelmingly being discredited by research reported in peer reviewed publications. Recognition and avoidance of allergenic and highly glycemic foods is a whole new trend that is based on scientific research and evidence. It reflects an improved understanding of the function of the gastrointestinal tract, the endocrine system, particularly the pancreas, and the immune system. Past dietary fads are consistently deficient in important nutrients that are necessary to our good health and survival. Further, they frequently contain substances that are harmful to us, such as the phytates that are abundantly present in whole grain foods, and interfere with absorption of many minerals. It is increasingly clear that grains, especially those that contain gluten, are contraindicated for human learning. The evidence is overwhelming. The mandate of eating to learn is learning to eat as our ancestors did. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be Open Original Shared Link. References: Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2),130-134. Paul, K., Todt, J., Eysold, R. (1985) [EEG Research Findings in Children with Celiac Disease According to Dietary Variations]. Zeitschrift der Klinische Medizin. 40, 707-709. Grech, P.L., Richards, J., McLaren, S., Winkelman, J.H. (2000) Psychological sequelae and quality of life in celiac disease. Journal of Pediatric Gastroenterology and Nutrition 31(3): S4 Reichelt, K., Sagedal, E., Landmark, J., Sangvic, B., Eggen, O., Helge, S. (1990a). The Effect of Gluten-Free Diet on Urinary peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4), 169-181. Reichelt, K., Ekrem, J., Scott, H. (1990b). Gluten, Milk Proteins and Autism: DIETARY INTERVENTION EFFECTS ON BEHAVIOR AND PEPTIDE SECRETION. Journal of Applied Nutrition. 42(1), 1-11. Reichelt, K., Knivsberg, A., Lind, G., Nodland, M. (1991). Probable etiology and Possible Treatment of Childhood Autism. Brain Dysfunction. 4, 308-319. Hoggan, R. (1997a). Absolutisms Hidden Message for Medical Scientism. Interchange. 28(2/3), 183-189. Caterson ID, Gill TP. Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab. 2002 Dec;16(4):595-610. Hennessy AR, Walker JD.Silent hypoglycaemia at the diabetic clinic. Diabet Med. 2002 Mar;19(3):261. Kue Young T, Chateau D, Zhang M. Factor analysis of ethnic variation in the multiple metabolic (insulin resistance) syndrome in three Canadian populations.Am J Human Biol. 2002 Sep-Oct;14(5):649-58. Wahab PJ, Meijer JW, Dumitra D, Goerres MS, Mulder CJ. Coeliac disease: more than villous atrophy.Rom J Gastroenterol. 2002 Jun;11(2):121-7. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. Why is coeliac disease endemic in the people of the Sahara?Lancet. 1999 Aug 21;354(9179):647-8. Langleben DD, Acton PD, Austin G, Elman I, Krikorian G, Monterosso JR, Portnoy O, Ridlehuber HW, Strauss HW. Effects of Methylphenidate Discontinuation on Cerebral Blood Flow in Prepubescent Boys with Attention Deficit Hyperactivity Disorder.J Nucl Med. 2002 Dec;43(12):1624-1629. 2: Kim BN, Lee JS, Shin MS, Cho SC, Lee DS. Regional cerebral perfusion abnormalities in attention deficit/hyperactivity disorder Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci. 2002 Oct;252(5):219-25. Lou, H., Henriksen, L., Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology. 825-829. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Knivsberg AM. Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia.Pediatr Rehabil. 1997 Jan-Mar;1(1):25-33. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia.N Engl J Med. 1988 Oct 27;319(17):1139-48. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002 Apr 23;58(8):1221-6. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness.J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Review. Husby, V., Jensenius, C., Svehag, S.(1985). Passage of Undegraded DietaryAntigen into the Blood of Healthy Adults. Scandinavian Journal of Immunology. 22, 83-92. Ma A, Chen X, Zheng M, Wang Y, Xu R, Li J. Iron status and dietary intake of Chinese pregnant women with anemia in the third trimester. Asia Pac J Clin Nutr. 2002;11(3):171-5. Kapil U, Bhavna A. Adverse effects of poor micronutrient status during childhood and adolescence. Nutr Rev. 2002 May;60(5 Pt 2):S84-90. Review. Youdim MB, Yehuda S. The neurochemical basis of cognitive deficits induced by brain iron deficiency: involvement of dopamine-opiate system. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):491-500. Otero GA, Aguirre DM, Porcayo R, Fernandez T. Psychological and electroencephalographic study in school children with iron deficiency. Int J Neurosci. 1999 Aug;99(1-4):113-21. Guesry P. The role of nutrition in brain development. Prev Med. 1998 Mar-Apr;27(2):189-94. Review. Bruner AB, Joffe A, Duggan AK, Casella JF, Brandt J. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet. 1996 Oct 12;348(9033):992-6. Soewondo S. The effect of iron deficiency and mental stimulation on Indonesian childrens cognitive performance and development. Kobe J Med Sci. 1995 Apr;41(1-2):1-17. McCarthy AM, Lindgren S, Mengeling MA, Tsalikian E, Engvall JC. Effects of diabetes on learning in children. Pediatrics. 2002 Jan;109(1):E9. Bertini M, Sbarbati A, Valletta E, Pinelli L, Tato L. Incomplete gastric metaplasia in children with insulin-dependent diabetes mellitus and celiac disease. An ultrastructural study.BMC Clin Pathol. 2001;1(1):2. Schuppan D, Hahn EG. Celiac disease and its link to type 1 diabetes mellitus.J Pediatr Endocrinol Metab. 2001;14 Suppl 1:597-605. Holmes GK. Coeliac disease and Type 1 diabetes mellitus - the case for screening.Diabet Med. 2001 Mar;18(3):169-77. x Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E. Coeliac disease in children and adolescents with type 1 diabetes: a study of growth, glycaemic control, and experiences of families.Acta Paediatr. 2002;91(3):297-302. Spiekerkoetter U, Seissler J, Wendel U. General Screening for Celiac Disease is Advisable in Children with Type 1 Diabetes.Horm Metab Res. 2002 Apr;34(4):192-5. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori G, Meschi F, Bianchi C, Chiumello G. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study.Pediatrics. 2002 May;109(5):833-8. Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, Hegedu LS, Jacobsen BB, Husby S. High prevalence of coeliac disease in Danish children with type I diabetes mellitus.Acta Paediatr. 2001 Nov;90(11):1238-43. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt DT, Werlin SL. The prevalence and clinical characteristics of celiac disease in juvenile diabetes in Wisconsin.J Pediatr Gastroenterol Nutr. 2001 Oct;33(4):462-5. MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. A type 1 diabetes-related protein from wheat (triticum aestivum): cDNA clone of a wheat storage globulin, Glb1, linked to islet damage.J Biol Chem. 2002 Oct 29. Scott FW, Rowsell P, Wang GS, Burghardt K, Kolb H, Flohe S. 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Celiac.com 01/04/2010 - The practice of using antibody testing to diagnose celiac disease has led to an explosion in the number of cases detected among children, coupled with a rise in median age at diagnosis, a new study suggests. European studies have shown that celiac disease is a multi-system disorder, affecting 0.3% to 1.0% of all children. A team of researchers recently set out to examine the impact of serological testing on childhood celiac disease in North America The research team consisted of Kelly E. McGowan, BHSc, Derek A. Castiglione and J. Decker Butzner, MD with the Department of Pediatrics, University of Calgary, Calgary, Canada. Serological testing makes it easier to spot children with atypical or extra-intestinal symptoms or with conditions associated with celiac disease. Serological testing has resulted in a huge increase in celiac disease cases; it has tripled incidence levels, quadrupled diagnosis age, and brought about a greater understanding of the wide variety of presentations of celiac disease in North America. Younger children are more likely to develop classic celiac disease, whereas older children seem more likely to show atypical presentations. The goal of the study was to determine the effects of immunoglobulin A endomysial antibody testing on the incidence and clinical presentation of childhood celiac disease. Researchers compared the incidence and clinical presentation of celiac disease in two groups of patients. Both groups were under a pretesting group of patients under 18 years of age in 1990–1996 and compared with a testing group of patients under 18 years of age in 2000–2006. Average age at diagnosis was 2 years (95% confidence interval: 2–4 years) in the pretest group (N = 36), compared with 9 years (95% confidence interval: 8–10 years) in the test group (N = 199; P < .001); female/male ratios (1.6:1) were similar (P = .982). Incidence of celiac disease increased from 2.0 cases per 100,000 children in the pretest group to 7.3 cases per 100,000 children in the test group (P = .0256). Frequency of classic celiac disease decreased from 67% in the pretest group to 19% (test group; P < .001), but the incidence of classic celiac disease did not change (0.8 vs 1.6 cases per 100000; P = .154). In the test group, researchers uncovered 13 previously unnoticed clinical presentations in 98 children, including 35 with family history, 18 with abdominal pain, and 14 with type 1 diabetes mellitus. The frequency of Marsh IIIc lesions decreased from 64% in the pretest group to 44% in the test group (P = .0403). In the test group, classic celiac disease was most common, making up 67% of cases in young children under 3 years, whereas atypical gastrointestinal and silent presentations were more common in older children. Overall, the contribution of serological testing to the diagnosis of celiac disease has been enormous. Antibody testing for celiac disease has tripled the incidence of celiac disease and quadrupled the average age at diagnosis, thus offering millions of children a higher quality of health. Source: Pediatrics, December 2009.