Adolescent weight gain trajectories and their associations with biological aging: a genetically informed study
Authors' conclusion
Our findings indicate that high BMI in adolescence may accelerate biological aging, especially in individuals with a genetic predisposition to high BMI.
Study context
- Population
- Participants of the Young Finns Study, ages 3–18 at baseline, followed from 1980 to 2018–2020; biological aging measured at three follow-ups (ages 15–56)2,045 with DNA methylation
- Participants
- 3,596 participants
- Exposure
- Genetic liability to body mass index (BMI) (BMI-PRS) and adolescent BMI trajectories vs biological aging
- Outcome
- Biological aging estimated by DNA methylation epigenetic clocks DunedinPACE (years/calendar year) and PC-GrimAge (years)
- Follow-up
- Three follow-ups (ages 15-56)
Methodological detailsgenetically informed, latent growth curve modelling, path analysis, individual-level Mendelian randomisation
- Genetically informed
- Latent growth curve modelling
- Path analysis
- Individual-level Mendelian randomisation
Main finding
As reported in the abstract
Biological aging
Mendelian randomisation (MR) causal estimate, DunedinPACE in 2011
0.020
95% CI 0.008, 0.031
MR causal estimate, DunedinPACE in 2018
0.019
95% CI 0.003, 0.035
Observational data: associations, not effects.
Original publication
Adolescent weight gain trajectories and their associations with biological aging: a genetically informed study. Int J Obes (Lond). Published 12 August 2026. doi:10. 1038/ s41366-026-02194-0
Composed by AI from the published abstract and checked against it. How Briefs are made →