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3. The influence of pubertal development on autoantibody appearance and progression to type 1 diabetes in the TEDDY study

Author

Warncke, Katharina, primary, Tamura, Roy, additional, Schatz, Desmond A, additional, Veijola, Riitta, additional, Steck, Andrea K, additional, Akolkar, Beena, additional, Hagopian, William, additional, Krischer, Jeffrey P, additional, Lernmark, Åke, additional, Rewers, Marian J, additional, Toppari, Jorma, additional, McIndoe, Richard, additional, Ziegler, Anette-G, additional, Vehik, Kendra, additional, Haller, Michael J, additional, and Elding Larsson, Helena, additional

Published
2024
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8. A combined risk score enhances prediction of type 1 diabetes among susceptible children

Author

Ferrat, Lauric A., Vehik, Kendra, Sharp, Seth A., Lernmark, Åke, Rewers, Marian J., She, Jin-Xiong, and Ziegler, Anette-G.

Subjects
Type 1 diabetes -- Diagnosis -- Risk factors, Genetic susceptibility -- Identification and classification -- Health aspects -- Measurement, Islet cell stimulating antibodies -- Health aspects -- Measurement, Biological sciences, Health
Abstract

Type 1 diabetes (T1D)--an autoimmune disease that destroys the pancreatic islets, resulting in insulin deficiency--often begins early in life when islet autoantibody appearance signals high risk.sup.1. However, clinical diabetes can follow in weeks or only after decades, and is very difficult to predict. Ketoacidosis at onset remains common.sup.2,3 and is most severe in the very young.sup.4,5, in whom it can be life threatening and difficult to treat.sup.6-9. Autoantibody surveillance programs effectively prevent most ketoacidosis.sup.10-12 but require frequent evaluations whose expense limits public health adoption.sup.13. Prevention therapies applied before onset, when greater islet mass remains, have rarely been feasible.sup.14 because individuals at greatest risk of impending T1D are difficult to identify. To remedy this, we sought accurate, cost-effective estimation of future T1D risk by developing a combined risk score incorporating both fixed and variable factors (genetic, clinical and immunological) in 7,798 high-risk children followed closely from birth for 9.3 years. Compared with autoantibodies alone, the combined model dramatically improves T1D prediction at [greater than or equal to]2 years of age over horizons up to 8 years of age (area under the receiver operating characteristic curve [greater than or equal to] 0.9), doubles the estimated efficiency of population-based newborn screening to prevent ketoacidosis, and enables individualized risk estimates for better prevention trial selection. In a study of children with high genetic risk aged 2 years or older, a risk score integrating pancreatic islet autoantibodies, genetic factors and family history is highly predictive of type 1 diabetes in the subsequent 8 years., Author(s): Lauric A. Ferrat [sup.1] , Kendra Vehik [sup.2] , Seth A. Sharp [sup.1] , Åke Lernmark [sup.3] , Marian J. Rewers [sup.4] , Jin-Xiong She [sup.5] , Anette-G. Ziegler [...]

Published
2020
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9. Prospective virome analyses in young children at increased genetic risk for type 1 diabetes

Author

Vehik, Kendra, Lynch, Kristian F., Wong, Matthew C., Tian, Xiangjun, Ross, Matthew C., Gibbs, Richard A., and Ajami, Nadim J.

Subjects
Children -- Diseases, Type 1 diabetes -- Risk factors -- Genetic aspects, Viruses -- Health aspects, Biological sciences, Health
Abstract

Viruses are implicated in autoimmune destruction of pancreatic islet [beta] cells, which results in insulin deficiency and type 1 diabetes (T1D).sup.1-4. Certain enteroviruses can infect [beta] cells in vitro.sup.5, have been detected in the pancreatic islets of patients with T1D.sup.6 and have shown an association with T1D in meta-analyses.sup.4. However, establishing consistency in findings across studies has proven difficult. Obstacles to convincingly linking RNA viruses to islet autoimmunity may be attributed to rapid viral mutation rates, the cyclical periodicity of viruses.sup.7 and the selection of variants with altered pathogenicity and ability to spread in populations. [beta] cells strongly express cell-surface coxsackie and adenovirus receptor (CXADR) genes, which can facilitate enterovirus infection.sup.8. Studies of human pancreata and cultured islets have shown significant variation in enteroviral virulence to [beta] cells between serotypes and within the same serotype.sup.9,10. In this large-scale study of known eukaryotic DNA and RNA viruses in stools from children, we evaluated fecally shed viruses in relation to islet autoimmunity and T1D. This study showed that prolonged enterovirus B rather than independent, short-duration enterovirus B infections may be involved in the development of islet autoimmunity, but not T1D, in some young children. Furthermore, we found that fewer early-life human mastadenovirus C infections, as well as CXADR rs6517774, independently correlated with islet autoimmunity. Analysis of known viruses in stool samples from young children with high genetic risk for type 1 diabetes shows that sustained enterovirus B (EV-B) infections, rather than independent, short-duration EV-B infections, might be involved in the development of islet autoimmunity, but not type 1 diabetes., Author(s): Kendra Vehik [sup.1] , Kristian F. Lynch [sup.1] , Matthew C. Wong [sup.2] , Xiangjun Tian [sup.2] , Matthew C. Ross [sup.2] , Richard A. Gibbs [sup.3] , Nadim [...]

Published
2019
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10. Diabetes Study of Children of Diverse Ethnicity and Race: Study design.

Author

Redondo, Maria J., Harrall, Kylie K., Glueck, Deborah H., Tosur, Mustafa, Uysal, Serife, Muir, Andrew, Atkinson, Elizabeth G., Shapiro, Melanie R., Yu, Liping, Winter, William E., Weedon, Michael, Brusko, Todd M., Oram, Richard, Vehik, Kendra, Hagopian, William, Atkinson, Mark A., and Dabelea, Dana

Subjects
DIABETES in children, GENETIC risk score, RACE, TYPE 1 diabetes, EXPERIMENTAL design, TYPE 2 diabetes
Abstract

Aims: Determining diabetes type in children has become increasingly difficult due to an overlap in typical characteristics between type 1 diabetes (T1D) and type 2 diabetes (T2D). The Diabetes Study in Children of Diverse Ethnicity and Race (DISCOVER) programme is a National Institutes of Health (NIH)‐supported multicenter, prospective, observational study that enrols children and adolescents with non‐secondary diabetes. The primary aim of the study was to develop improved models to differentiate between T1D and T2D in diverse youth. Materials and Methods: The proposed models will evaluate the utility of three existing T1D genetic risk scores in combination with data on islet autoantibodies and other parameters typically available at the time of diabetes onset. Low non‐fasting serum C‐peptide (<0.6 nmol/L) between 3 and 10 years after diabetes diagnosis will be considered a biomarker for T1D as it reflects the loss of insulin secretion ability. Participating centres are enrolling youth (<19 years old) either with established diabetes (duration 3–10 years) for a cross‐sectional evaluation or with recent onset diabetes (duration 3 weeks–15 months) for the longitudinal observation with annual visits for 3 years. Cross‐sectional data will be used to develop models. Longitudinal data will be used to externally validate the best‐fitting model. Results: The results are expected to improve the ability to classify diabetes type in a large and growing subset of children who have an unclear form of diabetes at diagnosis. Conclusions: Accurate and timely classification of diabetes type will help establish the correct clinical management early in the course of the disease. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Gastrointestinal infections modulate the risk for insulin autoantibodies as the first-appearing autoantibody in the TEDDY Study

Author

Lönnrot, Maria, primary, F. Lynch, Kristian, primary, Rewers, Marian, primary, Lernmark, Åke, primary, Vehik, Kendra, primary, Akolkar, Beena, primary, Hagopian, William, primary, Krischer, Jeffrey, primary, A. McIndoe, Rickhard, primary, Toppari, Jorma, primary, Ziegler, Anette G., primary, Petrosino, Joseph F., primary, Lloyd, Richard, primary, and Hyöty, Heikki, primary

Published
2023
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12. HLA genotype and probiotics modify the association between timing of solid food introduction and islet autoimmunity in the TEDDY Study

Author

Hagopian, William, primary, Uusitalo, Ulla, primary, Mramba, Lazarus K., primary, Aronsson, Carin Andrén, primary, Vehik, Kendra, primary, Yang, Jimin, primary, Hummel, Sandra, primary, Lernmark, Åke, primary, Rewers, Marian, primary, McIndoe, Richard, primary, Toppari, Jorma, primary, Ziegler, Anette G., primary, Akolkar, Beena, primary, Krischer, Jeffrey P., primary, Virtanen, Suvi M., primary, and Norris, Jill M., primary

Published
2023
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14. The human gut microbiome in early-onset type 1 diabetes from the TEDDY study

Author

Vatanen, Tommi, Franzosa, Eric A., Schwager, Randall, Tripathi, Surya, Arthur, Timothy D., Vehik, Kendra, Lernmark, Åke, Hagopian, William A., Rewers, Marian J., She, Jin-Xiong, Toppari, Jorma, Ziegler, Anette-G., Akolkar, Beena, Krischer, Jeffrey P., Stewart, Christopher J., Ajami, Nadim J., Petrosino, Joseph F., Gevers, Dirk, Lähdesmäki, Harri, Vlamakis, Hera, Huttenhower, Curtis, and Xavier, Ramnik J.

Published
2018
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15. Temporal development of the gut microbiome in early childhood from the TEDDY study

Author

Stewart, Christopher J., Ajami, Nadim J., O’Brien, Jacqueline L., Hutchinson, Diane S., Smith, Daniel P., Wong, Matthew C., Ross, Matthew C., Lloyd, Richard E., Doddapaneni, HarshaVardhan, Metcalf, Ginger A., Muzny, Donna, Gibbs, Richard A., Vatanen, Tommi, Huttenhower, Curtis, Xavier, Ramnik J., Rewers, Marian, Hagopian, William, Toppari, Jorma, Ziegler, Anette-G., She, Jin-Xiong, Akolkar, Beena, Lernmark, Ake, Hyoty, Heikki, Vehik, Kendra, Krischer, Jeffrey P., and Petrosino, Joseph F.

Published
2018
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17. Gastrointestinal Infections Modulate the Risk for Insulin Autoantibodies as the First-Appearing Autoantibody in the TEDDY Study.

Author

Lönnrot, Maria, Lynch, Kristian F., Rewers, Marian, Lernmark, Åke, Vehik, Kendra, Akolkar, Beena, Hagopian, William, Krischer, Jeffrey, McIndoe, Rickhard A., Toppari, Jorma, Ziegler, Anette-G., Petrosino, Joseph F., Lloyd, Richard, Hyöty, Heikki, TEDDY Study Group, Bautista, Kimberly, Baxter, Judith, Felipe-Morales, Daniel, Frohnert, Brigitte I., and Stahl, Marisa

Abstract

OBJECTIVE: To investigate gastrointestinal infection episodes (GIEs) in relation to the appearance of islet autoantibodies in The Environmental Determinants of Diabetes in the Young (TEDDY) cohort. RESEARCH DESIGN AND METHODS: GIEs on risk of autoantibodies against either insulin (IAA) or GAD (GADA) as the first-appearing autoantibody were assessed in a 10-year follow-up of 7,867 children. Stool virome was characterized in a nested case-control study. RESULTS: GIE reports (odds ratio [OR] 2.17 [95% CI 1.39–3.39]) as well as Norwalk viruses found in stool (OR 5.69 [1.36–23.7]) at <1 year of age were associated with an increased IAA risk at 2–4 years of age. GIEs reported at age 1 to <2 years correlated with a lower risk of IAA up to 10 years of age (OR 0.48 [0.35–0.68]). GIE reports at any other age were associated with an increase in IAA risk (OR 2.04 for IAA when GIE was observed 12–23 months prior [1.41–2.96]). Impacts on GADA risk were limited to GIEs <6 months prior to autoantibody development in children <4 years of age (OR 2.16 [1.54–3.02]). CONCLUSIONS: Bidirectional associations were observed. GIEs were associated with increased IAA risk when reported before 1 year of age or 12–23 months prior to IAA. Norwalk virus was identified as one possible candidate factor. GIEs reported during the 2nd year of life were associated with a decreased IAA risk. [ABSTRACT FROM AUTHOR]

Published
2023
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18. HLA Genotype and Probiotics Modify the Association Between Timing of Solid Food Introduction and Islet Autoimmunity in the TEDDY Study.

Author

Uusitalo, Ulla, Mramba, Lazarus K., Aronsson, Carin Andrén, Vehik, Kendra, Yang, Jimin, Hummel, Sandra, Lernmark, Åke, Rewers, Marian, Hagopian, William, McIndoe, Richard, Toppari, Jorma, Ziegler, Anette-G., Akolkar, Beena, Krischer, Jeffrey P., Virtanen, Suvi M., and Norris, Jill M.

Subjects
BABY foods, PROPORTIONAL hazards models, TYPE 1 diabetes, GENOTYPES, PROBIOTICS, AUTOIMMUNITY, JUNK food
Abstract

OBJECTIVE: To study the interaction among HLA genotype, early probiotic exposure, and timing of complementary foods in relation to risk of islet autoimmunity (IA). RESEARCH DESIGN AND METHODS: The Environmental Determinants of Diabetes in the Young (TEDDY) study prospectively follows 8,676 children with increased genetic risk of type 1 diabetes. We used a Cox proportional hazards regression model adjusting for potential confounders to study early feeding and the risk of IA in a sample of 7,770 children. RESULTS: Any solid food introduced early (<6 months) was associated with increased risk of IA if the child had the HLA DR3/4 genotype and no probiotic exposure during the 1st year of life. Rice introduced at 4–5.9 months compared with later in the U.S. was associated with an increased risk of IA. CONCLUSIONS: Timing of solid food introduction, including rice, may be associated with IA in children with the HLA DR3/4 genotype not exposed to probiotics. The microbiome composition under these exposure combinations requires further study. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Joint modeling of longitudinal autoantibody patterns and progression to type 1 diabetes: results from the TEDDY study

Author

Köhler, Meike, Beyerlein, Andreas, Vehik, Kendra, Greven, Sonja, Umlauf, Nikolaus, Lernmark, Åke, Hagopian, William A., Rewers, Marian, She, Jin-Xiong, Toppari, Jorma, Akolkar, Beena, Krischer, Jeffrey P., Bonifacio, Ezio, Ziegler, Anette-G., Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Driscoll, Kimberly, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Ahonen, Suvi, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Karlsson, Leena, Kähönen, Miia, Knip, Mikael, Kovanen, Lea, Koreasalo, Mirva, Kurppa, Kalle, Latva-aho, Tiina, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Niinistö, Sari, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Riikonen, Mika, Rouhiainen, Jenni, Romo, Minna, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Leppänen, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lindfors, Katri, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Young, Gabriela, Anderson, Stephen W., Jacobsen, Laura, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Janz, Nicole, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Scholz, Marlon, Stock, Joanna, Warncke, Katharina, Wendel, Lorena, Winkler, Christiane, Lernmark, Åke, Agardh, Daniel, Aronsson, Carin Andrén, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Hyberg, Susanne, Johansen, Fredrik, Jonsdottir, Berglind, Larsson, Helena Elding, Lindström, Marielle, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Ottosson, Karin, Rahmati, Kobra, Ramelius, Anita, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Carson, Josephine, Dalzell, Maria, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Avendano, Maryouri, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, PerezLaras, Francisco, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, Meulemans, Steven, Parikh, Hemang, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, McLeod, Wendy, Akolkar, Beena, Yu, Liping, Miao, Dongmei, Bingley, Polly, Williams, Alistair, Chandler, Kyla, Rokni, Saba, Williams, Claire, Wyatt, Rebecca, George, Gifty, Grace, Sian, Erlich, Henry, Mack, Steven J., Ke, Sandra, Mulholland, Niveen, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, Triplett, Eric, TEDDY study group, Ancillary Studies, Diet, Genetics, Human Subjects/Publicity/Publications, Immune Markers, Infectious Agents, Laboratory Implementation, Maternal Studies, Psychosocial, Quality Assurance, Steering, Study Coordinators, Celiac Disease, Clinical Implementation, and Quality Assurance Subcommittee on Data Quality

Published
2017
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20. Dietary Intake and Body Mass Index Influence the Risk of Islet Autoimmunity in Genetically At-Risk Children: A Mediation Analysis Using the TEDDY Cohort

Author

Andrén Aronsson, Carin, primary, Tamura, Roy, additional, Vehik, Kendra, additional, Uusitalo, Ulla, additional, Yang, Jimin, additional, Haller, Michael J., additional, Toppari, Jorma, additional, Hagopian, William, additional, McIndoe, Richard A., additional, Rewers, Marian J., additional, Ziegler, Anette-G., additional, Akolkar, Beena, additional, Krischer, Jeffrey P., additional, Norris, Jill M., additional, Virtanen, Suvi M., additional, and Elding Larsson, Helena, additional

Published
2023
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21. Effects of Gluten Intake on Risk of Celiac Disease: A Case-Control Study on a Swedish Birth Cohort

Author

Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Foghis, Gabriela, Anderson, Stephen W., Robinson, Richard, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Stock, Joanna, Strauss, Elisabeth, Warncke, Katharina, Winkler, Christiane, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Kähönen, Miia, Knip, Mikael, Koivu, Annika, Koreasalo, Mirva, Kurppa, Kalle, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Romo, Minna, Simell, Satu, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Särmä, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lernmark, Åke, Agardh, Daniel, Aronsson, Carin Andrén, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Harmby, Cecilia, Hyberg, Susanne, Johansen, Fredrik, Jonasdottir, Berglind, Larsson, Helena Elding, Forss, Sigrid Lenrick, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Rahmati, Kobra, Ramelius, Anita, Rosenquist, Anna, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Trulsson, Erika, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Ayres, Stephen, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Scott, Elizabeth, Stabbert, Joshua, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, Laras, Francisco Perez, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, McLeod, Wendy, Meulemans, Steven, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, Akolkar, Beena, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, Triplett, Eric, Andrén Aronsson, Carin, and Norris, Jill M.

Published
2016
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23. Rising Hemoglobin A1c in the Non-Diabetic Range Predicts Progression of Type 1 Diabetes As Well As Oral Glucose Tolerance Tests

Author

Vehik, Kendra, primary, Boulware, David, primary, Killian, Michael, primary, Rewers, Marian, primary, McIndoe, Richard, primary, Toppari, Jorma, primary, Lernmark, Ake, primary, Akolkar, Beena, primary, Ziegler, Anette-Gabriele, primary, Rodriguez, Henry, primary, Schatz, Desmond A, primary, P. Krischer, Jeffrey, primary, Hagopian, William A., primary, Group, TrialNet Study, primary, and Group, TEDDY Study, primary

Published
2022
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24. Integration of Infant Metabolite, Genetic, and Islet Autoimmunity Signatures to Predict Type 1 Diabetes by Age 6 Years

Author

Webb-Robertson, Bobbie-Jo M, primary, Nakayasu, Ernesto S, additional, Frohnert, Brigitte I, additional, Bramer, Lisa M, additional, Akers, Sarah M, additional, Norris, Jill M, additional, Vehik, Kendra, additional, Ziegler, Anette-G, additional, Metz, Thomas O, additional, Rich, Stephen S, additional, and Rewers, Marian J, additional

Published
2022
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28. Heterogeneity of DKA Incidence and Age-Specific Clinical Characteristics in Children Diagnosed With Type 1 Diabetes in the TEDDY Study

Author

Jacobsen, Laura M., primary, Vehik, Kendra, primary, Veijola, Riitta, primary, Warncke, Katharina, primary, Toppari, Jorma, primary, Steck, Andrea K., primary, Gesualdo, Patricia, primary, Akolkar, Beena, primary, Lundgren, Markus, primary, Hagopian, William A., primary, She, Jin-Xiong, primary, Rewers, Marian, primary, Ziegler, Anette G., primary, Krischer, Jeffrey P., primary, Larsson, Helena Elding, primary, Haller, Michael J., primary, and Group, the TEDDY Study, primary

Published
2022
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30. Rising Hemoglobin A1c in the Nondiabetic Range Predicts Progression of Type 1 Diabetes As Well As Oral Glucose Tolerance Tests.

Author

Vehik, Kendra, Boulware, David, Killian, Michael, Rewers, Marian, McIndoe, Richard, Toppari, Jorma, Lernmark, Åke, Akolkar, Beena, Ziegler, Anette-G., Rodriguez, Henry, Schatz, Desmond A., Krischer, Jeffrey P., Hagopian, William, The TEDDY Study Group Colorado Clinical Center, Barbour, Aaron, Bautista, Kimberly, Baxter, Judith, Felipe-Morales, Daniel, Frohnert, Brigitte I., and Stahl, Marisa

Subjects
*BLOOD sugar analysis, *AUTOANTIBODIES, *RESEARCH, *RESEARCH methodology, *TYPE 1 diabetes, *EVALUATION research, *COMPARATIVE studies, *GLUCOSE tolerance tests, *LONGITUDINAL method
Abstract

Objective: Biomarkers predicting risk of type 1 diabetes (stage 3) among children with islet autoantibodies are greatly needed to prevent diabetic ketoacidosis and facilitate prevention therapies.Research Design and Methods: Children in the prospective The Environmental Determinants of Diabetes in the Young (TEDDY) study (n = 707) with confirmed diabetes-associated autoantibodies (GAD antibody, IA-2A, and/or insulin autoantibody) and two or more HbA1c measurements were followed to diabetes or median age 11.1 years. Once confirmed autoantibody positive, HbA1c was measured quarterly. Cox models and receiver operative characteristic curve analyses revealed the prognostic utility for risk of stage 3 on a relative HbA1c increase from the baseline visit or an oral glucose tolerance test (OGTT) 2-h plasma glucose (2-hPG). This HbA1c approach was then validated in the Type 1 Diabetes TrialNet Pathway to Prevention Study (TrialNet) (n = 1,190).Results: A 10% relative HbA1c increase from baseline best marked the increased risk of stage 3 in TEDDY (74% sensitive; 88% specific). Significant predictors of risk for HbA1c change were age and HbA1c at the baseline test, genetic sex, maximum number of autoantibodies, and maximum rate of HbA1c increase by time of change. The multivariable model featuring a HbA1c ≥10% increase and these additional factors revealed increased risk of stage 3 in TEDDY (hazard ratio [HR] 12.74, 95% CI 8.7-18.6, P < 0.0001) and TrialNet (HR 5.09, 95% CI 3.3-7.9, P < 0.0001). Furthermore, the composite model using HbA1c ≥10% increase performed similarly to an OGTT 2-hPG composite model (TEDDY area under the curve [AUC] 0.88 and 0.85, respectively) and to the HbA1c model in TrialNet (AUC 0.82).Conclusions: An increase of ≥10% in HbA1c from baseline is as informative as OGTT 2-hPG in predicting risk of stage 3 in youth with genetic risk and diabetes-associated autoantibodies. [ABSTRACT FROM AUTHOR]

Published
2022
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34. Associations of breastfeeding with childhood autoimmunity, allergies, and overweight: The Environmental Determinants of Diabetes in the Young (TEDDY) study

Author

Hummel, Sandra, primary, Weiß, Andreas, additional, Bonifacio, Ezio, additional, Agardh, Daniel, additional, Akolkar, Beena, additional, Aronsson, Carin A, additional, Hagopian, William A, additional, Koletzko, Sibylle, additional, Krischer, Jeffrey P, additional, Lernmark, Åke, additional, Lynch, Kristian, additional, Norris, Jill M, additional, Rewers, Marian J, additional, She, Jin-Xiong, additional, Toppari, Jorma, additional, Uusitalo, Ulla, additional, Vehik, Kendra, additional, Virtanen, Suvi M, additional, Beyerlein, Andreas, additional, and Ziegler, Anette-G, additional

Published
2021
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35. Genetic scores to stratify risk of developing multiple islet autoantibodies and type 1 diabetes: A prospective study in children

Author

Bonifacio, Ezio, Beyerlein, Andreas, Hippich, Markus, Winkler, Christiane, Vehik, Kendra, Weedon, Michael N., Laimighofer, Michael, Hattersley, Andrew T., Krumsiek, Jan, Frohnert, Brigitte I., Steck, Andrea K., Hagopian, William A., Krischer, Jeffrey P., Lernmark, Åke, Rewers, Marian J., She, Jin-Xiong, Toppari, Jorma, Akolkar, Beena, Oram, Richard A., Rich, Stephen S., and Ziegler, Anette-G.

Subjects
Pancreatic beta cells -- Genetic aspects -- Health aspects, Genotypes -- Identification and classification, Autoantibodies -- Genetic aspects -- Health aspects, Type 1 diabetes -- Genetic aspects -- Risk factors, Biological sciences
Abstract

Background Around 0.3% of newborns will develop autoimmunity to pancreatic beta cells in childhood and subsequently develop type 1 diabetes before adulthood. Primary prevention of type 1 diabetes will require early intervention in genetically at-risk infants. The objective of this study was to determine to what extent genetic scores (two previous genetic scores and a merged genetic score) can improve the prediction of type 1 diabetes. Methods and findings The Environmental Determinants of Diabetes in the Young (TEDDY) study followed genetically at-risk children at 3- to 6-monthly intervals from birth for the development of islet autoantibodies and type 1 diabetes. Infants were enrolled between 1 September 2004 and 28 February 2010 and monitored until 31 May 2016. The risk (positive predictive value) for developing multiple islet autoantibodies (pre-symptomatic type 1 diabetes) and type 1 diabetes was determined in 4,543 children who had no first-degree relatives with type 1 diabetes and either a heterozygous HLA DR3 and DR4-DQ8 risk genotype or a homozygous DR4-DQ8 genotype, and in 3,498 of these children in whom genetic scores were calculated from 41 single nucleotide polymorphisms. In the children with the HLA risk genotypes, risk for developing multiple islet autoantibodies was 5.8% (95% CI 5.0%-6.6%) by age 6 years, and risk for diabetes by age 10 years was 3.7% (95% CI 3.0%-4.4%). Risk for developing multiple islet autoantibodies was 11.0% (95% CI 8.7%-13.3%) in children with a merged genetic score of >14.4 (upper quartile; n = 907) compared to 4.1% (95% CI 3.3%-4.9%, P 14.4 compared with 2.7% (95% CI 1.9%-3.6%) in children with a score of [less than or equal to]14.4 (P 14.4. Scores were higher in European versus US children (P = 0.003). In children with a merged score of >14.4, risk for multiple islet autoantibodies was similar and consistently >10% in Europe and in the US; risk was greater in males than in females (P = 0.01). Limitations of the study include that the genetic scores were originally developed from case-control studies of clinical diabetes in individuals of mainly European decent. It is, therefore, possible that it may not be suitable to all populations. Conclusions A type 1 diabetes genetic score identified infants without family history of type 1 diabetes who had a greater than 10% risk for pre-symptomatic type 1 diabetes, and a nearly 2-fold higher risk than children identified by high-risk HLA genotypes alone. This finding extends the possibilities for enrolling children into type 1 diabetes primary prevention trials., Author(s): Ezio Bonifacio 1, Andreas Beyerlein 2,3,4, Markus Hippich 2,3,4, Christiane Winkler 2,3,4, Kendra Vehik 5, Michael N. Weedon 6, Michael Laimighofer 7, Andrew T. Hattersley 6, Jan Krumsiek 7, [...]

Published
2018
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37. Early Childhood Gut Microbiomes Show Strong Geographic Differences Among Subjects at High Risk for Type 1 Diabetes

Author

Kemppainen, Kaisa M., Ardissone, Alexandria N., Davis-Richardson, Austin G., Fagen, Jennie R., Gano, Kelsey A., León-Novelo, Luis G., Vehik, Kendra, Casella, George, Simell, Olli, Ziegler, Anette G., Rewers, Marian J., Lernmark, Åke, Hagopian, William, She, Jin-Xiong, Krischer, Jeffrey P., Akolkar, Beena, Schatz, Desmond A., Atkinson, Mark A., and Triplett, Eric W.

Published
2015
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38. Effects of Gluten Intake on Risk of Celiac Disease: A Case-Control Study on a Swedish Birth Cohort

Author

Aronsson, Carin Andrén, Lee, Hye-Seung, Koletzko, Sibylle, Uusitalo, Ulla, Yang, Jimin, Virtanen, Suvi M., Liu, Edwin, Lernmark, Åke, Norris, Jill M., Agardh, Daniel, Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Foghis, Gabriela, Anderson, Stephen W., Robinson, Richard, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Stock, Joanna, Strauss, Elisabeth, Warncke, Katharina, Winkler, Christiane, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Kähönen, Miia, Knip, Mikael, Koivu, Annika, Koreasalo, Mirva, Kurppa, Kalle, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Romo, Minna, Simell, Satu, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Särmä, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lernmark, Åke, Agardh, Daniel, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Harmby, Cecilia, Hyberg, Susanne, Johansen, Fredrik, Jonasdottir, Berglind, Larsson, Helena Elding, Forss, Sigrid Lenrick, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Rahmati, Kobra, Ramelius, Anita, Rosenquist, Anna, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Trulsson, Erika, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Ayres, Stephen, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Scott, Elizabeth, Stabbert, Joshua, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, Laras, Francisco Perez, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, McLeod, Wendy, Meulemans, Steven, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, Akolkar, Beena, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, and Triplett, Eric

Published
2016
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40. An Age-Related Exponential Decline in the Risk of Multiple Islet Autoantibody Seroconversion During Childhood

Author

Bonifacio, Ezio, primary, Weiß, Andreas, primary, Winkler, Christiane, primary, Hippich, Markus, primary, Rewers, Marian J., primary, Toppari, Jorma, primary, Lernmark, Åke, primary, She, Jin-Xiong, primary, Hagopian, William A., primary, Krischer, Jeffrey P., primary, Vehik, Kendra, primary, Schatz, Desmond A., primary, Akolkar, Beena, primary, Ziegler, Anette-Gabriele, primary, and Group, the TEDDY Study, primary

Published
2021
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43. Heterogeneity of DKA Incidence and Age-Specific Clinical Characteristics in Children Diagnosed With Type 1 Diabetes in the TEDDY Study.

Author

Jacobsen, Laura M., Vehik, Kendra, Veijola, Riitta, Warncke, Katharina, Toppari, Jorma, Steck, Andrea K., Gesualdo, Patricia, Akolkar, Beena, Lundgren, Markus, Hagopian, William A., She, Jin-Xiong, Rewers, Marian, Ziegler, Anette-G., Krischer, Jeffrey P., Larsson, Helena Elding, Haller, Michael J., Barbour, Aaron, Bautista, Kimberly, Baxter, Judith, and Felipe-Morales, Daniel

Subjects
*TYPE 1 diabetes, *TYPE 2 diabetes, *GLUCOSE tolerance tests, *DIABETIC acidosis, *HETEROGENEITY, *AGE groups, *RESEARCH, *AGE distribution, *DISEASE incidence, *EVALUATION research, *INSULIN, *COMPARATIVE studies, *RESEARCH funding, *DISEASE complications
Abstract

Objective: The Environmental Determinants of Diabetes in the Young (TEDDY) study is uniquely capable of investigating age-specific differences associated with type 1 diabetes. Because age is a primary driver of heterogeneity in type 1 diabetes, we sought to characterize by age metabolic derangements prior to diagnosis and clinical features associated with diabetic ketoacidosis (DKA).Research Design and Methods: The 379 TEDDY children who developed type 1 diabetes were grouped by age at onset (0-4, 5-9, and 10-14 years; n = 142, 151, and 86, respectively) with comparisons of autoantibody profiles, HLAs, family history of diabetes, presence of DKA, symptomatology at onset, and adherence to TEDDY protocol. Time-varying analysis compared those with oral glucose tolerance test data with TEDDY children who did not progress to diabetes.Results: Increasing fasting glucose (hazard ratio [HR] 1.09 [95% CI 1.04-1.14]; P = 0.0003), stimulated glucose (HR 1.50 [1.42-1.59]; P < 0.0001), fasting insulin (HR 0.89 [0.83-0.95]; P = 0.0009), and glucose-to-insulin ratio (HR 1.29 [1.16-1.43]; P < 0.0001) were associated with risk of progression to type 1 diabetes. Younger children had fewer autoantibodies with more symptoms at diagnosis. Twenty-three children (6.1%) had DKA at onset, only 1 (0.97%) of 103 with and 22 (8.0%) of 276 children without a first-degree relative (FDR) with type 1 diabetes (P = 0.008). Children with DKA were more likely to be nonadherent to study protocol (P = 0.047), with longer duration between their last TEDDY evaluation and diagnosis (median 10.2 vs. 2.0 months without DKA; P < 0.001).Conclusions: DKA at onset in TEDDY is uncommon, especially for FDRs. For those without familial risk, metabolic monitoring continues to provide a primary benefit of reduced DKA but requires regular follow-up. Clinical and laboratory features vary by age at onset, adding to the heterogeneity of type 1 diabetes. [ABSTRACT FROM AUTHOR]

Published
2022
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