University of Oulu

Zhiguo Li and others, Childhood Height Growth Rate Association With the Risk of Islet Autoimmunity and Development of Type 1 Diabetes, The Journal of Clinical Endocrinology & Metabolism, Volume 107, Issue 6, June 2022, Pages 1520–1528,

Childhood height growth rate association with the risk of islet autoimmunity and development of type 1 diabetes

Saved in:
Author: Li, Zhiguo1; Veijola, Riitta2; Koski, Eileen1;
Organizations: 1Center for Computational Health, IBM T.J. Watson Research Center, Yorktown Heights, 10598 NY, and Cambridge, 02142 MA, USA
2Department of Pediatrics, PEDEGO Research Unit, University of Oulu, 90014 Oulu, and Oulu University Hospital, 90029 Oulu, Finland
3JDRF, New York, 10281 NY, USA
4Barbara Davis Center for Diabetes, University of Colorado, Denver, 80440 CO, USA
5Department of Virology, Faculty of Medicine and Health Technology, Tampere University, and Fimlab Laboratories, Pirkanmaa Hospital District, 33520 Tampere, Finland
6Institute of Diabetes Research, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Munich-Neuherberg, Germany
7Forschergruppe Diabetes e.V. at Helmholtz Zentrum, München, German Research Center for Environmental Health, 85764 Munich-Neuherberg, Germany
8Forschergruppe Diabetes, Technical University Munich, at Klinikum rechts der Isar, 80934 Munich, Germany
9Pacific Northwest Research Institute, Seattle, 98122 WA, USA
10Department of Clinical Sciences, Lund University Diabetes Center, 21428 Malmö, Sweden
11Department of Pediatrics, Kristianstad Hospital, 29133 Kristianstad, Sweden
12Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, and Centre for Population Health Research, University of Turku, and Department of Pediatrics, Turku University Hospital, 20520 Turku, Finland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 8.4 MB)
Persistent link:
Language: English
Published: Endocrine society, 2022
Publish Date: 2023-06-16


Context: Rapid growth has been suggested to promote islet autoimmunity and progression to type 1 diabetes (T1D). Childhood growth has not been analyzed separately from the infant growth period in most previous studies, but it may have distinct features due to differences between the stages of development.

Objective: We aimed to analyze the association of childhood growth with development of islet autoimmunity and progression to T1D diagnosis in children 1 to 8 years of age.

Methods: Longitudinal data of childhood growth and development of islet autoimmunity and T1D were analyzed in a prospective cohort study including 10 145 children from Finland, Germany, Sweden, and the United States, 1-8 years of age with at least 3 height and weight measurements and at least 1 measurement of islet autoantibodies. The primary outcome was the appearance of islet autoimmunity and progression from islet autoimmunity to T1D.

Results: Rapid increase in height (cm/year) was associated with increased risk of seroconversion to glutamic acid decarboxylase autoantibody, insulin autoantibody, or insulinoma-like antigen-2 autoantibody (hazard ratio [HR] = 1.26 [95% CI = 1.05, 1.51] for 1-3 years of age and HR = 1.48 [95% CI = 1.28, 1.73] for <3 years of age). Furthermore, height rate was positively associated with development of T1D (HR = 1.80 [95% CI = 1.15, 2.81]) in the analyses from seroconversion with insulin autoantibody to diabetes

Conclusion: Rapid height growth rate in childhood is associated with increased risk of islet autoimmunity and progression to T1D. Further work is needed to investigate the biological mechanism that may explain this association.

see all

Series: Journal of clinical endocrinology & metabolism
ISSN: 0021-972X
ISSN-E: 1945-7197
ISSN-L: 0021-972X
Volume: 107
Issue: 6
Pages: 1520 - 1528
DOI: 10.1210/clinem/dgac121
Type of Publication: A1 Journal article – refereed
Field of Science: 3123 Gynaecology and paediatrics
3121 General medicine, internal medicine and other clinical medicine
Funding: This work was supported by funding from JDRF (IBM: 1-RSC-2017-368-I-X, 1-IND-2019-717-I-X), (DAISY: 1-SRA2019-722-I-X, 1-RSC-2017-517-I-X, 5-ECR-2017-388- A-N), (DiPiS: 1-SRA-2019-720-I-X, 1-RSC-2017-526-I-X), (DIPP: 1-RSC-2018-555-I-X), (DEW-IT: 1-SRA-2019-719- I-X, 1-RSC-2017-516-I-X) as well as National Institutes of Health (NIH) (DAISY: DK032493, DK032083, DK104351; DiPiS: DK26190 and the Center for Disease Control (CDC) (DEW-IT: UR6/CCU017247). The DIPP study was funded by JDRF (grants 1-SRA-2016- 342-M-R, 1-SRA-2019-732-M-B); European Union (grant BMH4-CT98-3314); Novo Nordisk Foundation; Academy of Finland (Decision No 292538 and Centre of Excellence in Molecular Systems Immunology and Physiology Research 2012-2017, Decision No. 250114); Special Research Funds for University Hospitals in Finland; Diabetes Research Foundation, Finland; and Sigrid Juselius Foundation, Finland. The BABYDIAB study was funded by the German Federal Ministry of Education and Research to the German Center for Diabetes Research. The DiPiS study was funded by Swedish Research Council (grant no. 14064), Swedish Childhood Diabetes Foundation, Swedish Diabetes Association, Nordisk Insulin Fund, SUS funds, Lion Club International, district 101-S, The Royal Physiographic Society, Skåne County Council Foundation for Research and Development, and LUDC-IRC/EXODIAB funding from the Swedish foundation for strategic research (Dnr IRC15-0067) and Swedish Research Council (Dnr 2009-1039). Additional funding for DEW-IT was provided by the Hussman Foundation and by the Washington State Life Science Discovery Fund.
Dataset Reference: The data that support the findings of this study are not publicly available because they were used under license for the current study only. Data are, however, available upon reasonable request with permission from the originating sites, whose representatives are William Hagopian (DEW-IT), Markus Lundgren (DiPiS), Marian Rewers (DAISY), Riitta Veijola (DIPP), and Anette Ziegler (BABYDIAB). Zhiguo Li is responsible for the accuracy of the data analysis. The resources used included open-source software; however, the specific code is subject to proprietary constraints but can be made available upon reasonable request to the corresponding author.
Copyright information: © The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.