Child-to-adult body size change and risk of type 2 diabetes and cardiovascular disease

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Abstract

Aims/hypothesis
Childhood overweight increases the risk of type 2 diabetes and cardiovascular disease in adulthood. However, the impact of childhood leanness on adult obesity and disease risk has been overlooked. We examined the independent and combined influences of child and adult body size on the risk of type 2 diabetes and cardiovascular disease.

Methods
Data from the UK Biobank on 364,695 individuals of European ancestry and free of type 2 diabetes and cardiovascular disease were divided into nine categories based on their self-reported body size at age 10 and measured BMI in adulthood. After a median follow-up of 12.8 years, 33,460 individuals had developed type 2 diabetes and/or cardiovascular disease. We used Cox regression models to assess the associations of body size categories with disease incidence.

Results
Individuals with low body size in childhood and high body size in adulthood had the highest risk of type 2 diabetes (HR 4.73; 95% CI 4.50, 4.99), compared to those with average body size in both childhood and adulthood. This was significantly higher than the risk in those with high body size in both childhood and adulthood (HR 4.05; 95% CI 3.84, 4.26). By contrast, cardiovascular disease risk was determined by adult body size, irrespective of childhood body size.

Conclusions/interpretation
Low body size in childhood exacerbates the risk of type 2 diabetes associated with adult obesity but not the risk of cardiovascular disease. Thus, promoting healthy weight management from childhood to adulthood, among lean children, is crucial.
OriginalsprogEngelsk
TidsskriftDiabetologia
Vol/bind67
Sider (fra-til)864–873
Antal sider10
ISSN0012-186X
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
Open access funding provided by Royal Library, Copenhagen University Library. Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research centre at the University of Copenhagen partially funded by an unrestricted donation from the Novo Nordisk Foundation (NNF18CC0034900). GDC was supported by a grant from the Danish Diabetes Academy that is funded by the Novo Nordisk Foundation (NNF17SA0031406), and from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No. 846502. TOK was supported by the grants NNF17OC0026848, NNF21SA0072102 and NNF22OC0074128 from the Novo Nordisk Foundation. RJFL was supported by the grants NNF20OC0059313 from the Novo Nordisk Foundation.

Publisher Copyright:
© 2023, The Author(s).

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