Xiang Liu1, Kendra Vehik2, Yangxin Huang3, Helena Elding Larsson4, Jorma Toppari5,6, Anette G Ziegler7,8,9, Jin-Xiong She10, Marian Rewers11, William A Hagopian12, Beena Akolkar13, Jeffrey P Krischer2. 1. Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL xiang.liu@epi.usf.edu. 2. Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL. 3. Department of Epidemiology and Biostatistics, College of Public Health, University of South Florida, Tampa, FL. 4. Department of Clinical Sciences, Lund University/Clinical Research Center, Skane University, Malmö, Sweden. 5. Department of Pediatrics, Turku University Hospital, Turku, Finland. 6. Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland. 7. Institute of Diabetes Research, Helmholtz Zentrum München (German Research Center for Environmental Health), Munich-Neuherberg, Germany. 8. Forschergruppe Diabetes, Klinikum rechts der Isar, Technical University Munich, Munich, Germany. 9. Forschergruppe Diabetes e.V., Helmholtz Zentrum München (German Research Center for Environmental Health), Munich-Neuherberg, Germany. 10. Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA. 11. Barbara Davis Center for Childhood Diabetes, University of Colorado, Aurora, CO. 12. Pacific Northwest Research Institute, Seattle, WA. 13. National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Abstract
OBJECTIVE: This study investigates two-phase growth patterns in early life and their association with development of islet autoimmunity (IA) and type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: The Environmental Determinants of Diabetes in the Young (TEDDY) study followed 7,522 genetically high-risk children in Sweden, Finland, Germany, and the U.S. from birth for a median of 9.0 years (interquartile range 5.7-10.6) with available growth data. Of these, 761 (10.1%) children developed IA and 290 (3.9%) children were diagnosed with T1D. Bayesian two-phase piecewise linear mixed models with a random change point were used to estimate children's individual growth trajectories. Cox proportional hazards models were used to assess the effects of associated growth parameters on the risks of IA and progression to T1D. RESULTS: A higher rate of weight gain in infancy was associated with increased IA risk (hazard ratio [HR] 1.09 [95% CI 1.02, 1.17] per 1 kg/year). A height growth pattern with a lower rate in infancy (HR 0.79 [95% CI 0.70, 0.90] per 1 cm/year), higher rate in early childhood (HR 1.48 [95% CI 1.22, 1.79] per 1 cm/year), and younger age at the phase transition (HR 0.76 [95% CI 0.58, 0.99] per 1 month) was associated with increased risk of progression from IA to T1D. A higher rate of weight gain in early childhood was associated with increased risk of progression from IA to T1D (HR 2.57 [95% CI 1.34, 4.91] per 1 kg/year) in children with first-appearing GAD autoantibody only. CONCLUSIONS: Growth patterns in early life better clarify how specific growth phases are associated with the development of T1D.
OBJECTIVE: This study investigates two-phase growth patterns in early life and their association with development of islet autoimmunity (IA) and type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: The Environmental Determinants of Diabetes in the Young (TEDDY) study followed 7,522 genetically high-risk children in Sweden, Finland, Germany, and the U.S. from birth for a median of 9.0 years (interquartile range 5.7-10.6) with available growth data. Of these, 761 (10.1%) children developed IA and 290 (3.9%) children were diagnosed with T1D. Bayesian two-phase piecewise linear mixed models with a random change point were used to estimate children's individual growth trajectories. Cox proportional hazards models were used to assess the effects of associated growth parameters on the risks of IA and progression to T1D. RESULTS: A higher rate of weight gain in infancy was associated with increased IA risk (hazard ratio [HR] 1.09 [95% CI 1.02, 1.17] per 1 kg/year). A height growth pattern with a lower rate in infancy (HR 0.79 [95% CI 0.70, 0.90] per 1 cm/year), higher rate in early childhood (HR 1.48 [95% CI 1.22, 1.79] per 1 cm/year), and younger age at the phase transition (HR 0.76 [95% CI 0.58, 0.99] per 1 month) was associated with increased risk of progression from IA to T1D. A higher rate of weight gain in early childhood was associated with increased risk of progression from IA to T1D (HR 2.57 [95% CI 1.34, 4.91] per 1 kg/year) in children with first-appearing GAD autoantibody only. CONCLUSIONS: Growth patterns in early life better clarify how specific growth phases are associated with the development of T1D.
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