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  • Jefferson Adams
    Jefferson Adams

    Study Connects Antibiotics in First Year of Life with Celiac Disease

      A team of researchers recently set out to explore the association between exposure to a systemic antibiotic in the first year of life and risk of diagnosed celiac disease.

    Caption: Image: CC--oliver.dodd

    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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    Guest Evidence Based Science FTW

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    Or it could mean that infants who are predisposed to celiac disease are also predisposed to other ailments for which antibiotics are prescribed.

    Correlation does not equal causation!

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    For me it was 3 weeks of daily penicillin shots at 21 months of age.  Then off and on through life until 18 months of daily tetracycline plus mega shots of penicillin following an accident. Shortly after that I developed not only celiac, but was diagnosed with multiple food and chemical allergies/sensitivities.  I know now that I was undiagnosed through childhood because of the symptoms I remember having: cramps, alternating constipation/diarrhea, mouth sores, mood swings, fussy eating, unexplainable low grade fevers associated with fatigue, and later in my early 20's - unexplainable, transient, periodic pain during intercourse.  I hope they find a way to treat the underlying problems, i.e. gut biota? instead of throwing enzymes and pharmaceuticals at the symptoms. 

     

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    On ‎3‎/‎15‎/‎2019 at 5:58 PM, Guest Evidence Based Science FTW said:

    Or it could mean that infants who are predisposed to celiac disease are also predisposed to other ailments for which antibiotics are prescribed.

    Correlation does not equal causation!

    This was an excellent well worded reply. I was thinking the same thing but didn't know how to properly articulate my thoughts. My children both started on antibiotics at 6 weeks of age and both continued being heavily dosed with antibiotics through out age 2 due to constant double ear infections. One child has celiac and the other thankfully does not. 

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Jefferson Adams
    Celiac.com 11/28/2012 - A team of researchers recently set out to determine whether childhood antianaerobic antibiotic exposure is associated with the development of inflammatory bowel disease (IBD). Their findings show that children who are treated with antianaerobic antibiotics face a significantly higher risk of developing IBD.
    The team included Matthew P. Kronman, MD, MSCE, Theoklis E. Zaoutis, MD, MSCE, Kevin Haynes, PharmD, MSCE, Rui Feng, PhD, and Susan E. Coffin, MD, MPH.They are affiliated variously with the Division of Infectious Diseases, Seattle Children’s Hospital at the University of Washington in Seattle, Washington, the Division of Infectious Diseases at The Children’s Hospital of Philadelphia, and the Department of Biostatistics and Epidemiology, the Center for Clinical Epidemiology and Biostatistics at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, Pennsylvania. The team's findings appear in the 24 September issue of Pediatrics.
    To get a better picture regarding use of antibiotics on children and a possible connection to IBD, the team conducted a retrospective cohort study using data from 464 UK ambulatory practices in The Health Improvement Network.
    The study looked at all children in the network with 2 or more years of follow-up from 1994 to 2009. The team screened and excluded anyone with previous IBD. They then cataloged all antibiotic prescriptions used by all children in the study. Finally, they tracked the children's data from practice enrollment and IBD development, practice de-registration, 19 years of age, or death.
    Their defined study parameters included the following antianaerobic antibiotics: penicillin, amoxicillin, ampicillin, penicillin/β-lactamase inhibitor combinations, tetracyclines, clindamycin, metronidazole, cefoxitin, carbapenems, and oral vancomycin.
    Their study looked at 1,072,426 children for a total of 6.6 million person-years of follow-up. Of those children, 748 developed IBD. Children treated with antianaerobic antibiotics had nearly 1.52 cases of IBD per ten-thousand person years, while those who were not given antibiotics saw just 0.83 cases per ten-thousand person-years; for an 84% relative risk differential.
    Antibiotic exposure throughout childhood was associated with the development of IBD, but this relationship decreased with increasing age at exposure. That is, the longer doctors waited to give children antibiotics, the more the risk of iBD went down.
    Children treated with antibiotics before 1 year of age showed an adjusted hazard ratio of 5.51 (95% confidence interval [CI]: 1.66–18.28), while that decreased to 2.62 (95% CI: 1.61–4.25) for children first treated at 5 years old, and to 1.57 (95% CI: 1.35–1.84) for those first treated at 15 years of age. Overall, each course of antibiotics increased the IBD hazard by 6% (4%–8%).
    The study showed that children who received two or more antibiotic courses were more highly likely to develop IBD than those who received 1 to 2 courses, with adjusted hazard ratios of 4.77 (95% CI: 2.13–10.68) versus 3.33 (95% CI: 1.69–6.58).
    So, based on this study, treating children with antianaerobic antibiotics puts them at risk for developing IBD. It will be interesting to see how the medical community responds to this study, and whether there is greater effort made to avoid giving these powerful antibiotics to children.
    What do you think? Do you have IBD? Did you receive these antibiotics as a kid? Let us know your thoughts by commenting below.
    Source:
    Pediatrics; 24 September 2012

    Gryphon Myers
    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

    Jefferson Adams
    Celiac.com 08/27/2014 - Can antibiotic exposure in pregnancy increase the risk of celiac disease in children? Some researchers suspect that infant microbiota play a pathogenic role in celiac disease. The idea that antibiotic treatment in pregnancy could significantly impact the infant microbiota, and thus influence the development of celiac disease, has led many to ponder the possible connection.
    To get a clearer picture, a research team recently set out to study the effects on offspring of antibiotic exposure in pregnancy.
    The team included Karl Mårild, Johnny Ludvigsson, Yolanda Sanz, and Jonas F. Ludvigsson. They are variously affiliated with the Deptartment of Medical Epidemiology and Biostatistics, Karolinska Institutet in Stockholm, the Astrid Lindgren Children's Hospital at Karolinska University Hospital in Solna, Sweden, the Division of Paediatrics in the Department of Clinical and Experimental Medicine at Linköping University, Östergötland County Council in Linköping, Sweden, the Department of Paediatrics of Örebro University Hospital in Örebro, Sweden, and the Microbial Ecology and Nutrition Research Group at the Institute of Agrochemistry and Food Technology of the National Research Council (IATA-CSIC) in Valencia, Spain.
    The team started by reviewing existing data on antibiotic exposure in pregnancy in 8,729 children recorded in the All Babies in Southeast Sweden (ABIS) cohort study. Through December 2006, 46 of the 8,729 had developed celiac disease. The team then used Cox regression to estimate celiac disease hazard ratios (HRs) in children whose mothers received antibiotics during pregnancy. The ratios were adjusted based on parent-reported diary data on breastfeeding, age at gluten introduction, and the number of infections in the child's first year of life.
    Of the 1,836 children exposed to antibiotics during pregnancy, 12 (0.7%) children developed celiac disease as compared with 34/6893 (0.5%) unexposed children (HR = 1.33; 95% CI = 0.69–2.56).
    Risk estimates remained unchanged after adjustment for breastfeeding, age at gluten introduction and infection load in the child's first year of life (HR = 1.28; 95% CI = 0.66–2.48).
    When all the data were factored, the team found no statistically significant connection between antibiotic exposure during pregnancy and celiac disease in offspring. The team suggests that this data may present an accurate picture, or it may be that they simply lack the statistical power to make a clear connection.
    Further studies are likely needed before researchers can confidently conclude that there is no connection between antibiotic exposure in pregnancy and celiac disease in offspring.
    Source:
     BMC Gastroenterol. 2014;14(75)

    Jefferson Adams
    Celiac.com 11/07/2017 - Researchers still don't have much good data on the consequences of antibiotic use in early life and how that relates to the risk of certain autoimmune diseases.
    A team of researchers recently set out to test the association between early-life antibiotic use and islet or celiac disease autoimmunity in genetically at-risk children prospectively followed up for type 1 diabetes (T1D) or celiac disease. Their study is part of a larger study called The Environmental Determinants of Diabetes in the Young, or TEDDY, for short.
    The reasearch team enrolled HLA-genotyped newborns from Finland, Germany, Sweden, and the United States between November 20, 2004, and July 8, 2010, and analyzed data from November 20, 2004, to August 31, 2014.
    They also enrolled individuals from the general population, and those having a first-degree relative with T1D, with any 1 of 9 HLA genotypes associated with a risk for T1D. The team charted parental reports of the most common antibiotics, such as cephalosporins, penicillins, and macrolides, used between age 3 months and age 4 years.
    Islet autoimmunity and celiac disease autoimmunity were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 consecutive clinic visits at least 3 months apart. The team used Cox proportional hazards regression models to assess the relationship between antibiotic use in early life before seroconversion and the development of autoimmunity, and to calculate hazard ratios and 95% CIs.
    The team conducted tests for islet and tissue transglutaminase autoantibodies on 8,495 children (49.0% female), and 6,558 children (48.7% female) who were enrolled in the TEDDY study, and they found that antibiotic exposure and frequency of use in early life or before seroconversion did not influence the risk of developing islet autoimmunity or celiac disease autoimmunity.
    Additionally, cumulative use of any antibiotic during the first 4 years of life was not tied to the appearance of any autoantibody (hazard ratio
    , 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or the transglutaminase autoantibody (HR, 1.00; 95% CI, 0.98-1.02). Using any of the most common antibiotics during the first 4 years of life, in any geographic region, did not influence the later development of autoimmunity for T1D or celiac disease.
    Based on these results, the team concluded that doctors recommending antibiotics for young children at risk for T1D or celiac disease need not be concerned that the use will lead to islet or tissue transglutaminase autoimmunity.
    Source:
    JAMA Pediatr. Published online October 9, 2017. doi:10.1001/jamapediatrics.2017.2905  
    The research team included Kaisa M. Kemppainen, PhD; Kendra Vehik, PhD; Kristian F. Lynch, PhD; Helena Elding Larsson, MD, PhD; Ronald J. Canepa, BSc; Ville Simell, MSc; Sibylle Koletzko, MD, PhD; Edwin Liu, MD; Olli G. Simell, MD, PhD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD, PhD; Marian J. Rewers, MD, PhD; Åke Lernmark, PhD; William A. Hagopian, MD, PhD; Jin-Xiong She, PhD; Beena Akolkar, PhD; Desmond A. Schatz, MD; Mark A. Atkinson, PhD; Martin J. Blaser, MD; Jeffrey P. Krischer, PhD; Heikki Hyöty, MD, PhD; Daniel Agardh, MD, PhD; and Eric W. Triplett, PhD; for The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group.
    They are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa; the Department of Clinical Sciences, Lund University Clinical Research Center, Skåne University Hospital, Malmö, Sweden; the MediCity Laboratory, University of Turku, Turku, Finland; the Division of Paediatric Gastroenterology and Hepatology, Dr von Hauner Children's Hospital, Ludwig Maximilian University, München, Germany; the Digestive Health Institute, Children's Hospital Colorado, Anschutz Medical Campus, University of Colorado Denver, Aurora; the Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland; the Department of Pediatrics, University of Turku, Turku University Hospital, Turku, Finland; the Department of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland Institute of Diabetes Research, Helmholtz Zentrum München, München, Germany; the Klinikum Rechts der Isar, Technische Universität München, München, Germany; the Forschergruppe Diabetes e.V., Neuherberg, Germany; the Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora; the Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville; the Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville; the Department of Medicine and Microbiology, New York School of Medicine, New York; the Department of Virology, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland; and with Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.

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    Doritos does make a few gluten-free versions.     
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