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Celiac.com 03/11/2019 - Many researchers believe that intestinal microbiota play a key role in the development of celiac disease. Since gut microbiota are strongly influenced by systemic antibiotics, especially in early life, the role of antibiotics in the development of celiac disease comes into question. Do antibiotics in infancy influence celiac disease rates later on? The team’s observational nationwide register-based cohort study included all children born in Denmark from 1995 through 2012, and Norway from 2004 through 2012. They followed the children born in Denmark until May 8, 2015 and the children born in Norway until December 31, 2013. In all, they gathered medical data on more than 1.7 million children, including 3,346 with a diagnosis of celiac disease. Any patient who received a dispensed systemic antibiotic in the first year of life was defined as having been exposed to systemic antibiotics. In both the Danish and in the Norwegian groups, infants exposed to systemic antibiotics in the first year of life had higher rates of celiac disease than those with no exposure. The team found that the relationship between an increasing number of dispensed antibiotics and the risk of celiac disease was dose-dependent. That is, more antibiotics correlated to higher celiac rates of celiac disease, and vice versa. The data did not single out any one antibiotic, or narrow the age window within the first year of life. Rates were similar for infants who had been hospitalized versus those who had not. This study was both large and comprehensive. The findings provide more evidence that childhood exposure to systemic antibiotics in the first year of life may be a risk factor for later celiac disease. Read more at Gastroenterology The research team included Stine Dydensborg Sander, MD, PhD, Anne-Marie Nybo Andersen, MD, PhD, Joseph A. Murray, MD, Øystein Karlstad, MSci, PhD, Steffen Husby, MD, DMSci, and Ketil Størdal, MD, PhD. They are variously affiliated with the Hans Christian Andersen Children’s Hospital, Odense University Hospital, Denmark, the Department of Clinical Research, University of Southern Denmark, Denmark, the Department of Public Health, University of Copenhagen, Denmark, the Division of Gastroenterology and Hepatology, Mayo Clinic, USA, the Department of Non-Communicable Diseases, Norwegian Institute of Public Health, Norway, and the Department of Pediatrics, Ostfold Hospital Trust, Norway.
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Celiac.com 08/13/2018 - It’s not uncommon for people to have psychiatric reactions to stressful life events, and these reactions may trigger some immune dysfunction. Researchers don’t yet know whether such reactions increase overall risk of autoimmune disease. Are psychiatric reactions induced by trauma or other life stressors associated with subsequent risk of autoimmune disease? Are stress-related disorders significantly associated with risk of subsequent autoimmune disease? A team of researchers recently set out to determine whether there is an association between stress-related disorders and subsequent autoimmune disease. The research team included Huan Song, MD, PhD; Fang Fang, MD, PhD; Gunnar Tomasson, MD, PhD; Filip K. Arnberg, PhD; David Mataix-Cols, PhD; Lorena Fernández de la Cruz, PhD; Catarina Almqvist, MD, PhD; Katja Fall, MD, PhD; Unnur A. Valdimarsdóttir, PhD. They are variously affiliated with the Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Department of Epidemiology and Biostatistics, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Rheumatology, University Hospital, Reykjavík, Iceland; the Centre for Rheumatology Research, University Hospital, Reykjavík, Iceland; the National Centre for Disaster Psychiatry, Department of Neuroscience, Psychiatry, Uppsala University, Uppsala, Sweden; the Stress Research Institute, Stockholm University, Stockholm, Sweden; the Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; the Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; the Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden; the Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. The team conducted a Swedish register-based retrospective cohort study that included 106, 464 patients with stress-related disorders, 1,064 ,640 matched unexposed individuals, and 126 ,652 full siblings to determine whether a clinical diagnosis of stress-related disorders was significantly associated with an increased risk of autoimmune disease. The team identified stress-related disorder and autoimmune diseases using the National Patient Register. They used Cox model to estimate hazard ratios (HRs) with 95% CIs of 41 autoimmune diseases beyond 1 year after the diagnosis of stress-related disorders, controlling for multiple risk factors. The data showed that being diagnosed with a stress-related disorder, such as post-traumatic stress disorder, acute stress reaction, adjustment disorder, and other stress reactions, was significantly associated with an increased risk of autoimmune disease, compared with matched unexposed individuals. The team is calling for further studies to better understand the associations and the underlying factors. Source: JAMA. 2018;319(23):2388-2400. doi:10.1001/jama.2018.7028
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Celiac.com 07/18/2018 - Despite many studies on immune development in children, there still isn’t much good data on how a mother’s diet during pregnancy and infancy influences a child’s immune development. A team of researchers recently set out to assess whether changes in maternal or infant diet might influence the risk of allergies or autoimmune disease. The team included Vanessa Garcia-Larsen, Despo Ierodiakonou, Katharine Jarrold, Sergio Cunha, Jennifer Chivinge, Zoe Robinson, Natalie Geoghegan, Alisha Ruparelia, Pooja Devani, Marialena Trivella, Jo Leonardi-Bee, and Robert J. Boyle. They are variously associated with the Department of Undiagnosed Celiac Disease More Common in Women and Girls International Health, Johns Hopkins School of Public Health, Baltimore, Maryland, United States of America; the Respiratory Epidemiology, Occupational Medicine and Public Health, National Heart and Lung Institute, Imperial College London, London, United Kingdom; the Section of Paediatrics, Department of Medicine, Imperial College London, London, United Kingdom; the Centre for Statistics in Medicine, University of Oxford, Oxford, United Kingdom; the Division of Epidemiology and Public Health, University of Nottingham, Nottingham, United Kingdom; the Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, United Kingdom; and Stanford University in the USA. Team members searched MEDLINE, Excerpta Medica dataBASE (EMBASE), Web of Science, Central Register of Controlled Trials (CENTRAL), and Literatura Latino Americana em Ciências da Saúde (LILACS) for observational studies conducted between January 1946 and July 2013, and interventional studies conducted through December 2017, that evaluated the relationship between diet during pregnancy, lactation, or the first year of life, and future risk of allergic or autoimmune disease. They then selected studies, extracted data, and assessed bias risk. They evaluated data using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). They found 260 original studies, covering 964,143 participants, of milk feeding, including 1 intervention trial of breastfeeding promotion, and 173 original studies, covering 542,672 participants, of other maternal or infant dietary exposures, including 80 trials of 26 maternal, 32 infant, or 22 combined interventions. They found a high bias risk in nearly half of the more than 250 milk feeding studies and in about one-quarter of studies of other dietary exposures. Evidence from 19 intervention trials suggests that oral supplementation with probiotics during late pregnancy and lactation may reduce risk of eczema. 44 cases per 1,000; 95% CI 20–64), and 6 trials, suggest that fish oil supplementation during pregnancy and lactation may reduce risk of allergic sensitization to egg. GRADE certainty of these findings was moderate. The team found less evidence, and low GRADE certainty, for claims that breastfeeding reduces eczema risk during infancy, that longer exclusive breastfeeding is associated with reduced type 1 diabetes mellitus, and that probiotics reduce risk of infants developing allergies to cow’s milk. They found no evidence that dietary exposure to other factors, including prebiotic supplements, maternal allergenic food avoidance, and vitamin, mineral, fruit, and vegetable intake, influence risk of allergic or autoimmune disease. Overall, the team’s findings support a connection between the mother’s diet and risk of immune-mediated diseases in the child. Maternal probiotic and fish oil supplementation may reduce risk of eczema and allergic sensitization to food, respectively. Stay tuned for more on diet during pregnancy and its role in celiac disease. Source: PLoS Med. 2018 Feb; 15(2): e1002507. doi: 10.1371/journal.pmed.1002507
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Celiac.com 02/28/2018 - In an effort to discover more genes that trigger type 1 diabetes, a team of researchers recently conducted a large, prospective study of children at risk for type 1 diabetes. The end goal is to reveal more targets for treating or even preventing the disease. The research team included A Sharma, X Liu, D Hadley, W Hagopian, WM Chen, S Onengut-Gumuscu, C Törn, AK Steck, BI Frohnert, M Rewers, AG Ziegler, Å Lernmark, J Toppari, JP Krischer, B Akolkar, SS Rich, JX She; and TEDDY Study Group. The team identified six new chromosomal regions in young people who have already developed type 1 diabetes, or who have started making antibodies against their insulin-producing cells, often a step toward full-blown diabetes that requires lifelong insulin therapy. Their analysis of 5,806 individuals, which is published in the Journal of Autoimmunity, also confirms three regions already associated with one of those related conditions. The team observed two top autoantibodies. The first, called IAA, acts directly against insulin. The second, called GADA, acts against the enzyme glutamate decarboxylase, which regulates the insulin-producing beta cells in the pancreas. According to Dr. She, about 90 percent of patients with type 1 diabetes start with one of the autoantibodies, and many patients eventually end up with both. The second autoantibody may surface in a few days or even years later. They began this study with 176,586 SNPs, or single nucleotide polymorphisms. Nucleotides are basic building blocks of our genetic information. According to Sharma, the SNPs evaluated by TEDDY scientists were already linked with other autoimmune conditions like rheumatoid arthritis or celiac disease, but not type 1 diabetes. The researchers figured out which of these SNPs are different in TEDDY participants with type 1 diabetes versus those with Islet cell autoantibodies versus those with neither. Previous research has shown that the genes associated with IA and actual type 1 diabetes can differ. Dr. She says that even though clinicians regard Islet cell autoantibodies (IA) as a red flag for type 1 diabetes, not every child with IA goes on to develop diabetes, though multiple autoantibodies definitely increase that risk. The team notes that it is possible that the genes that promote IA development may differ from those that lead to full-blown disease progression. She says that this is the first study of gene identification for any disease to use this sort of longitudinal information. She add that this and other studies by the TEDDY research group help to clarify the search for important non-HLA genes by adding the "time to disease" perspective. Source: J Autoimmun. 2018 Jan 5. pii: S0896-8411(17)30739-4. doi: 10.1016/j.jaut.2017.12.008. The researchers are variously affiliated with the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Division of Biostatistics and Data Science, Department of Population Health Sciences, Medical College of Georgia, Augusta University, Augusta, GA, US; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA; the Division of Population Health Sciences and Education, St George's University of London, London, United Kingdom; the Pacific Northwest Research Institute, Seattle, WA, USA; the Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA; the Department of Clinical Sciences, Lund University/CRC, Malmö, Sweden; the Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, Aurora, CO, USA; the Institute of Diabetes Research, Helmholtz Zentrum München, Munich-Neuherberg, Germany; Klinikum rechts der Isar, Technische Universität München, Munich-Neuherberg, Germany; Forschergruppe Diabetes e.V., Munich-Neuherberg, Germany; the Department of Pediatrics, Turku University Hospital, Turku, Finland; the National Institutes of Diabetes and Digestive and Kidney Disorders, National Institutes of Health, Bethesda, MD, USA; and the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
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Celiac.com 01/29/2018 - Researchers suspect that certain environmental factors, including infectious agents, might play a role in making celiac disease more prevalent and more widespread. Researchers in the USA and Sweden studying regional variation in the frequency of celiac disease have found similarities in the geographic distribution of Lyme disease, an emerging multisystemic infection caused by Borrelia burgdorferi spirochete, which invites questions about a possible connection with celiac disease. One research team recently set out to determine if infection with Borrelia contributes to an increased risk of celiac disease. The research team included Armin Alaedini, Benjamin Lebwohl, Gary P. Wormser, Peter H. Green, and Jonas F. Ludvigsson. They are variously affiliated with the Department of Medicine, Columbia University Medical Center, New York, NY USA; the Celiac Disease Center, Columbia University Medical Center, New York, NY USA; the Institute of Human Nutrition, Columbia University Medical Center, New York, NY USA; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla, NY USA; the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; and with the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK. Using biopsy reports, the team identified 15,769 individuals with celiac disease. By linking to the nationwide Patient Register, they were able to compare the rate of earlier occurrence of Lyme disease in the patients with celiac disease to that in 78,331 matched controls. To further assess the temporal relationship between Borrelia infection and celiac disease, they also examined the risk of subsequent Lyme disease in patients with a diagnosis of celiac disease. The team found that twenty-five patients with celiac disease had a prior diagnosis of Lyme disease (0.16%), whereas 79 had a subsequent diagnosis of Lyme disease (0.5%). This showed a modest association between Lyme disease and celiac disease was seen both before and after celiac diagnosis, with celiac risk being highest in the first year of follow-up. So, only a small portion of the celiac disease patients had a prior diagnosis for Lyme disease. The research team asserts that the supposed association between Lyme disease and celiac disease, both before and after the diagnosis of celiac disease, is likely driven by surveillance bias, at least in part. These data show that patients with Borrelia infection do not face a substantially higher risk for developing celiac disease. Source: BMC Med. 2017; 15: 169. doi: 10.1186/s12916-017-0926-1. PMCID: PMC5599869
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Celiac.com 01/17/2018 - People with celiac disease face a higher risk of infections like tuberculosis, influenza, and pneumococcal pneumonia, but researchers don't know how this might apply to risk of Clostridium difficile infection in those patients. A team of researchers recently set out to identify celiac disease patients using biopsy data from all pathology departments in Sweden over the 39-year period covering July 1969 through February 2008. They compared the risk of Clostridium difficile infection, based on stratified Cox proportional hazards models, among patients with celiac disease versus a control group of patients without celiac disease--matched by age, sex, and calendar period. The research team included Benjamin Lebwohl MD, MS, Yael R Nobel MD, Peter H R Green MD, Martin J Blaser MD, and Jonas F Ludvigsson MD, PhD. They are variously affiliated with the Department of Medicine, Celiac Disease Center, Columbia University Medical Center, New York, New York, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA; the New York University Langone Medical Center, New York, New York, USA; the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and with the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden. In all, they isolated 28,339 celiac patients, along with 141,588 control subjects. None of the celiac patients or control subjects had any history of Clostridium difficile infection. Celiac patients showed a Clostridium difficile infection rate of 56 cases per 100,000 person-years, compared with a rate of 26 cases per 100,000 person-years among control subjects, yielding an overall hazard ratio (HR) of 2.01. Compared with control subjects, celiac patients in their first 12 months after diagnosis showed the highest risk. However, the risk remained high up to 5 years after celiac diagnosis. The researchers found antibiotic data for 251 of the 493 patients with Clostridium difficile infection; they found no significant differences in previous antibiotic use between patients with celiac disease and control subjects. This large population-based cohort study showed that celiac patients had substantially higher rates of Clostridium difficile infection than did control subjects. The results of this study match prior studies that confirm higher infection rates in celiac patients, and indicate that celiac patients may suffer from altered gut immunity and/or microbial composition. Source: The American Journal of Gastroenterology (2017) 112, 1878–1884 (2017). doi:10.1038/ajg.2017.400
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Celiac.com 12/12/2017 - Does a gluten-free diet have any effect on cardiovascular risk in people with celiac disease? Does it effect people without celiac disease? So far, both questions have remained unanswered. Recently, a team of researchers set out to conduct a systematic review to shed some light on the matter. The team was led by Michael D.E. Potter, MBBS (Hons), from the University of New Castle, Australia. The team focused their review on the "potential of the gluten-free diet to affect modifiable cardiovascular risk factors including weight, blood pressure, cholesterol and blood sugars," and to do this they searched for "studies which measured these risk factors in individuals before and after the institution of a gluten-free diet." In all, Potter and colleagues reviewed 27 studies that evaluated the effect of a gluten-free diet, as followed for a minimum of 6 months, on cardiovascular risk factors such as BMI, waist circumference, blood pressure, fasting glycemia, hemoglobin A1c and serum lipids. Despite their efforts, they found no clear evidence that a gluten-free diet increases cardiovascular risk in celiac patients. They found no evidence that it increases heart disease risk in people without celiac disease. They really found nothing much at all. While the results varied across studies, and researchers did see changes in some cardiovascular risk factors, they say the data do not support a gluten-free diet for cardiovascular health in individuals without celiac disease. True, perhaps. But it's also true that the data neither support nor condemn a gluten-free diet in people without celiac disease. Unless and until researchers get some solid data from large groups and can make accurate, informative comparisons between those groups, it seems foolish for them to advocate or discourage a gluten-free diet in people without celiac disease. Source: Healio.com
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Celiac.com 10/05/2017 - Recent data show that more adults with celiac disease may face a higher risk for cardiovascular disease compared with the general population. A team of researchers recently set out to investigate the association of with cardiovascular disease risk factors at late adolescence in a cross-sectional population-based study. The research team included Assa A, Frenkel-Nir Y, Tzur D, Katz LH, and Shamir R. They are variously affiliated with the Institute of Gastroenterology, Nutrition and Liver Disease, Schneider Children's Medical Center, Petah-Tikva; the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, and with the Medical Corps of the Israeli Defense Force. The study group included 2,001,353 Jewish Israeli adolescents who underwent general health examinations from 1988 to 2015. The average participant age was 17.1 years of age. Additional participant information included demographic measures, blood pressure, resting heart rate, and risk factors associated with cardiovascular disease. The team identified a total of 10,566 cases of celiac disease. They conducted multivariate analysis that showed average diastolic blood pressure to be significantly lower in celiac patients; 72.0±8.7 in celiac men vs 70.4 ±â€Š8.5 in non-celiac men; and 70.0 ±â€Š8.3 in celiac women vs 69.0 ±â€Š8.2 in non-celiac women. There were no differences in systolic blood pressure, while resting heart rate was slightly higher in celiac patients, with an absolute difference of 0.4 beats per minute. The team saw no increase in blood pressure, or in rates of overweight and obesity among celiac patients. Patients with celiac disease far more likely to have non-insulin-dependent diabetes mellitus, hypercoagulability, and hyperlipidemia, than were non-celiacs. By age 17, people with celiac disease have a higher prevalence of risk factors for cardiovascular disease compared with the general population. There is, however, neither increase in blood pressure nor increase in overweight and obesity rates. Source: J Pediatr Gastroenterol Nutr. 2017 Aug;65(2):190-194. doi: 10.1097/MPG.0000000000001487.
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Celiac.com 09/18/2017 - Many researchers feel that the rising number of celiac disease cases supports the idea that common infections prior to the onset of autoimmune diseases could play a role in triggering the immune response. Do more respiratory infections in childhood mean a greater likelihood of celiac disease later in life? To answer that question, a team of researchers recently set out to explore the relationship between early clinical events and the development of celiac disease in genetically predisposed infants. The research team included Renata Auricchio, Donatella Cielo, Renato de Falco, Martina Galatola, Valentina Bruno, Basilio Malamisura, Maria Giovanna Limongelli, Riccardo Troncone, Luigi Greco. They are variously affiliated with the Department of Translational Medical Science, and the European Laboratory for the Investigation of Food Induced Diseases, University of Naples Federico II, Naples, Italy; the Department of Pediatrics, University Hospital of Salerno, Salerno, Italy; and Azienda Ospedaliera Gaetano Rummo Via dell'Angelo, Benevento, Italy. The team studied 373 newborns from families with at least 1 relative with celiac disease. They tested participants for human leukocyte antigen DQ2- or DQ8- and followed-up positive infants with clinical and serological assessments. They used cross tabulation and odds ratios to explore the risk associated with single variables, and logistic regression analysis was performed to determine the variables that contributed to the risk of developing celiac disease. They also used stepwise discriminant analysis to determine which variables could distinguish case patients from controls before diagnosis. The overall rate of celiac disease in this group was 6% at 3 years and 13.5% at 5 years of age, while a total of 34 children, developed celiac disease before the sixth year of life, a rate of 14%. According to analysis of adverse events, people with celiac disease shoed a higher frequency of respiratory tract infections in their first 24 months of life. In a stepwise discriminant analysis, which included sex and human leukocyte antigen risk class, only respiratory infections in the second and first years of life significantly contributed to discrimination of case patients versus controls. The team's analysis showed that the frequency of respiratory infections in the first 2 years of life can be used to identify children who later developed celiac disease. Kids with more infections were much more likely to develop celiac disease later on. Clinicians may use this information during diagnosis to help zero in on patients likely to have celiac disease. Source: Pediatrics, September 2017
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Celiac.com 07/21/2017 - In previous studies, a team of scientists led by Professor Anette-Gabriele Ziegler had already shown an association between infections in early childhood and the development of type 1 diabetes. In that study, the researchers saw the highest risk for type 1 diabetes in children who experienced repeated respiratory infections in the first six months of life. Recently, Zeigler and another team of colleagues from the Institute for Diabetes Research at Helmholtz Zentrum München, a partner in the German Center for Diabetes Research (DZD), set out to determine whether infections during infancy are associated with increased risk for celiac disease later on. Their current study shows that the risk of developing celiac disease is particularly high when gastrointestinal tract infections occur during the first year of life. To a lesser extent, an increased disease risk was also seen in connection with early respiratory tract infections. The risk seems to be particularly high for people who experience repeated gastrointestinal infections in the first year of life. Whether the connections with early infections and later celiac risk are causal or are based on changes in the microbiome or specific immune responses is not clear from the data, said first author Dr. Andreas Beyerlein. "However," Beyerlein added, "it seems that the increased risk of celiac disease is associated with a permanent inflammation of the gastrointestinal tract in early childhood and is not caused by a specific viral or bacterial pathogen." The team reached their conclusion after analyzing fully anonymized data provided by the Bavarian Association of Statutory Health Insurance Physicians (Kassenärztliche Vereinigung Bayern) of 295,420 children who were born between 2005 and 2007. Medically attended infections from birth until a median age of 8.5 years were considered in the analysis. A total of 853 children developed gluten intolerance, equivalent to 0.3 percent. Their results appear in the American Journal of Epidemiology. Source: Helmholtz Zentrum München - German Research Center for Environmental Health
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Is a Gluten-free Diet Bad for Your Heart?
Jefferson Adams posted an article in Heart Failure and Celiac Disease
Celiac.com 05/08/2017 - Do non-celiacs who eat a gluten-free diet face a greater risk of developing coronary heart disease? To shed some light on this question, a team of researchers recently set out to assess levels of long-term term gluten consumption in connection with the development of coronary heart disease. The research team included Benjamin Lebwohl, Yin Cao, instructor, Geng Zong, Frank B Hu, Peter H R Green, Alfred I Neugut, Eric B Rimm, Laura Sampson, Lauren W Dougherty, Edward Giovannucci, Walter C Willett, Qi Sun, and Andrew T Chan. They are variously affiliated with the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA; the Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA; the Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA; and the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. For their prospective cohort study, the team looked at 64,714 women in the Nurses’ Health Study and 45,303 men in the Health Professionals Follow-up Study. None of the subjects had any history of coronary heart disease, and all completed a 131 item semiquantitative food frequency questionnaire in 1986 that was updated every four years through 2010. The researchers estimated gluten consumption based on the results of the food frequency questionnaires. Their study looked for patients who developed coronary heart disease, specifically fatal or non-fatal myocardial infarction. The team’s study data covered 26 years of follow-up, totaling 2,273,931 person years, 2431 women and 4098 men developed coronary heart disease. Participants in the lowest fifth of gluten intake had 352 incidences of coronary heart disease per 100,000 person years, while those in the highest fifth had a rate of 277 events per 100,000 person years. This equates to 75 fewer cases of coronary heart disease per 100,000 person years. After adjusting for known risk factors, the researchers noted that patients in the highest fifth of estimated gluten intake had a multivariable hazard ratio for coronary heart disease of 0.95 (95% confidence interval 0.88 to 1.02; P for trend=0.29). After further adjusting for intake of whole grains, and leaving the remaining variance of gluten corresponding to refined grains, the multivariate hazard ratio was 1.00 (0.92 to 1.09; P for trend=0.77). In contrast, after additional adjustment for intake of refined grains (leaving the variance of gluten intake correlating with whole grain intake), estimated gluten consumption was associated with a lower risk of coronary heart disease (multivariate hazard ratio 0.85, 0.77 to 0.93; P for trend=0.002). Long term dietary intake of gluten was not associated with risk of coronary heart disease. However, the researchers do stress the importance of dietary whole grains, and that their absence may increase the risk of cardiovascular disease. Because of this, the team discourages people without celiac disease, or some other medical reason, from adopting a gluten-free diet. Source: BMJ 2017;357:j1892 (Published 02 May 2017)- 6 comments
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Celiac.com 04/18/2017 - Even though gluten-free diets are more popular than ever, researchers still don't have much good data on gluten intake and long-term health. A team of researchers recently set out to assess three large cohort studies, the Nurses' Health Study (NHS, n=69,276), the NHSII (n=88,610), and the Health Professionals Follow-Up Study (HPFS, n=41,908), and to estimate gluten intake using a validated food-frequency questionnaire collected every 2-4 years. The research team included Geng Zong, of the Harvard T.H. Chan School of Public Health, Boston, MA; Benjamin Lebwohl, Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY; Frank Hu, Laura Sampson, Lauren Dougherty, Walter Willett, Andrew Chan, and Qi Sun, of the Harvard T.H. Chan School of Public Health in Boston, MA. The team defined incidental Type 2 diabetes as physician diagnosed diabetes, and confirmed with supplementary information. Their results showed that average gluten intake, give or take standard deviation, was 5.83±2.23, 6.77±2.50, and 7.06±2.76 grams/day in NHS, NHSII, and HPFS, respectively. That gluten intake cam, mainly from carbohydrate sources, especially refined grains, starch, and cereal fiber (Spearman correlation coefficients > 0.6). The team confirmed 15,947 Type 2 diabetes cases over 4.24 million years of follow-up time. In all three groups, the team observed an inverse connection between gluten consumption and Type 2 diabetes risk. The multivariate adjustment (table), and hazard ratio (HR, 95% confidence intervals [95%CI]) comparing extreme quintiles were 0.80 (0.76, 0.84; P<0.001). The connection dissipated slightly after adjusting for cereal fiber (HR [95%CI]= 0.87 [0.81, 0.93]), but not for other carbohydrate components. For study participants under 65 years of age, and without major chronic diseases, changes in gluten intake were not associated with weight gain in multivariate adjusted model. Overall, the 4-year weight change (95%CI) was 0.08 (-0.06, 0.22; P=0.25) in NHS, -0.05 (-0.18, 0.08; P=0.43) in NHSII, and 0.36 (-0.24, 0.96; P=0.24) HPFS for each 5 grams increase in gluten intake. These findings suggest that gluten intake likely doesn't cause or promote Type 2 diabetes or excess weight gain. Reducing dietary gluten is unlikely to help prevent Type 2 diabetes, and may actually reduce consumption of cereal fiber or whole grains that help to lower overall diabetes risk. Source: AHA EPI
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Celiac.com 04/13/2017 - A team of researchers recently set out to determine whether hospital admission for autoimmune disease is associated with an elevated risk of future admission for dementia. The research team included Clare J Wotton, and Michael J Goldacre, both affiliated with the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford, Oxford, UK. The pair set up their retrospective, record-linkage cohort study using national hospital care and mortality administrative data from 1999–2012. From that patient data, they assembled a study group of people admitted to hospital with a range of autoimmune diseases, along with a control group, and followed forward in time to see if how many patients eventually developed dementia. Data revealed a total of 1,833,827 people admitted to hospital with an autoimmune disease. The number of patients for each autoimmune disease group ranged from 1,019 patients in the Goodpasture's syndrome group, to 316,043 people in the rheumatoid arthritis group. The researchers found that the rate ratio for dementia after admission for an autoimmune disease, compared with the control cohort, was 1.20 (95% CI 1.19 to 1.21). For patients whose dementia type was specified, the rate ratio ranged from 1.04 to 1.08 for Alzheimer's disease, and 1.26 to 1.31 for vascular dementia. Of the 25 autoimmune diseases studied, 18 showed significant positive associations with dementia, 14 of which were statistically significant. Significant associations include Addison's disease (1.48, 1.34 to 1.64), multiple sclerosis (1.97, 1.88 to 2.07), psoriasis (1.29, 1.25 to 1.34) and systemic lupus erythematosus (1.46, 1.32 to 1.61). The connections with vascular dementia may be one aspect of a wider connection between autoimmune diseases and vascular damage. Though findings were significant, effect sizes were small. Researchers advise clinicians to note the possibility of dementia in patients with autoimmune disease. The researchers are calling for further studies to assess their findings and to explore possible ways to reduce any increased risk. Source: BMJ
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