University of Oulu

Peltonen, E.J., Veijola, R., Ilonen, J. et al. What is the role of puberty in the development of islet autoimmunity and progression to type 1 diabetes?. Eur J Epidemiol 38, 689–697 (2023).

What is the role of puberty in the development of islet autoimmunity and progression to type 1 diabetes?

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Author: Peltonen, Essi J.1; Veijola, Riitta2,3; Ilonen, Jorma4;
Organizations: 1Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland
2Department of Pediatrics, Research Unit of Clinical Medicine, Medical Research Center, University of Oulu, Oulu, Finland
3Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland
4Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, Turku, Finland
5Pediatric Research Center, New Children’s Hospital, Helsinki University Hospital, Helsinki, Finland
6Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland
7Center for Child Health Research, Tampere University and Tampere University Hospital, Tampere, Finland
8Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
9Department of Pediatrics, Turku University Hospital, Turku, Finland
10Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland
11Centre for Population Health Research, University of Turku and Turku University Hospital, Turku, Finland
12Tays Research, Development and Innovation Center, Tampere University Hospital, Tampere, Finland
13Health and Well-Being Promotion Unit, Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland
14Faculty of Information Technology and Communication Sciences, Tampere University, Tampere, Finland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 0.8 MB)
Persistent link:
Language: English
Published: Springer Nature, 2023
Publish Date: 2023-09-25


In many populations, the peak period of incidence of type 1 diabetes (T1D) has been observed to be around 10–14 years of age, coinciding with puberty, but direct evidence of the role of puberty in the development of T1D is limited. We therefore aimed to investigate whether puberty and the timing of its onset are associated with the development of islet autoimmunity (IA) and subsequent progression to T1D. A Finnish population-based cohort of children with HLA-DQB1-conferred susceptibility to T1D was followed from 7 years of age until 15 years of age or until a diagnosis of T1D (n = 6920). T1D-associated autoantibodies and growth were measured at 3- to 12-month intervals, and pubertal onset timing was assessed based on growth. The analyses used a three-state survival model. IA was defined as being either positive for islet cell antibodies plus at least one biochemical autoantibody (ICA + 1) or as being repeatedly positive for at least one biochemical autoantibody (BC1). Depending on the IA definition, either 303 (4.4%, ICA + 1) or 435 (6.3%, BC1) children tested positive for IA by the age of 7 years, and 211 (3.2%, ICA + 1)) or 198 (5.3%, BC1) developed IA during follow-up. A total of 172 (2.5%) individuals developed T1D during follow-up, of whom 169 were positive for IA prior to the clinical diagnosis. Puberty was associated with an increase in the risk of progression to T1D, but only from ICA + 1-defined IA (hazard ratio 1.57; 95% confidence interval 1.14, 2.16), and the timing of pubertal onset did not affect the association. No association between puberty and the risk of IA was detected. In conclusion, puberty may affect the risk of progression but is not a risk factor for IA.

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Series: European journal of epidemiology
ISSN: 0393-2990
ISSN-E: 1573-7284
ISSN-L: 0393-2990
Volume: 38
Issue: 6
Pages: 689 - 697
DOI: 10.1007/s10654-023-01002-7
Type of Publication: A1 Journal article – refereed
Field of Science: 3121 General medicine, internal medicine and other clinical medicine
3123 Gynaecology and paediatrics
Funding: Open access funding provided by Tampere University including Tampere University Hospital, Tampere University of Applied Sciences (TUNI). The study was supported by the Academy of Finland (grants 63672, 68292, 79685, 79686, 80846, 114666, 126813, 129492, 139391, 201988, 210632, 276475, 307996, 308065, 308066, and Center of Excellence in Molecular Systems Immunology and Physiology Research 2012–2017, Decision No. 250114), URL:; European Foundation for the Study of Diabetes (EFSD) award supported by EFSD/JDRF/Lilly, URL:; the Finnish Diabetes Association, URL:; the Finnish Diabetes Research Foundation, URL:; the Juho Vainio Foundation, URL:; the JDRF International (grants 4-1998-274, 4-1999-731, 4-2001-435, 1-SRA-2016-342-M-R, 1-SRA-2019-732-M-B, and 3-SRA-2020-955-S-B), URL:; the Competitive State Research Financing of the Expert Responsibility area of Tampere University Hospital (grants 9E082, 9F089, 9G087, 9H092, 9J147, 9K149, 9L042, 9L117, 9M114, 9N086, 9P057, 9R055, 9S074, 9U065, and 9V072); Oulu University Hospital Research Funds; Turku University Hospital (state research funding VTR); the European Comission (grant BMH4-CT98-3314), URL:; the Novo Nordisk Foundation, URL:; Special Research Funds for University Hospitals in Finland; the Sigrid Jusélius Foundation, URL:; and author E.J.P. has received research support from the Alfred Kordelin Foundation (200356), URL: The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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