The role of adolescent lifestyle habits in biological aging: A prospective twin study
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Curated by eLife
eLife assessment
This paper provides evidence that an unhealthy lifestyle during adolescence accelerates epigenetic age in adulthood, and that these associations are largely explained by the effect of shared genetic influences. The main strengths of this valuable paper are the relatively large sample size, longitudinal assessment of lifestyle factors, and sophisticated statistical analyses. The paper is methodologically compelling and will be of interest for a broad audience, including individuals working on methylation, epidemiology, and/or ageing.
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Abstract
Adolescence is a stage of fast growth and development. Exposures during puberty can have long-term effects on health in later life. This study aims to investigate the role of adolescent lifestyle in biological aging.
Methods:
The study participants originated from the longitudinal FinnTwin12 study (n = 5114). Adolescent lifestyle-related factors, including body mass index (BMI), leisure-time physical activity, smoking, and alcohol use, were based on self-reports and measured at ages 12, 14, and 17 years. For a subsample, blood-based DNA methylation (DNAm) was used to assess biological aging with six epigenetic aging measures in young adulthood (21–25 years, n = 824). A latent class analysis was conducted to identify patterns of lifestyle behaviors in adolescence, and differences between the subgroups in later biological aging were studied. Genetic and environmental influences on biological aging shared with lifestyle behavior patterns were estimated using quantitative genetic modeling.
Results:
We identified five subgroups of participants with different adolescent lifestyle behavior patterns. When DNAm GrimAge, DunedinPoAm, and DunedinPACE estimators were used, the class with the unhealthiest lifestyle and the class of participants with high BMI were biologically older than the classes with healthier lifestyle habits. The differences in lifestyle-related factors were maintained into young adulthood. Most of the variation in biological aging shared with adolescent lifestyle was explained by common genetic factors.
Conclusions:
These findings suggest that an unhealthy lifestyle during pubertal years is associated with accelerated biological aging in young adulthood. Genetic pleiotropy may largely explain the observed associations.
Funding:
This work was supported by the Academy of Finland (213506, 265240, 263278, 312073 to J.K., 297908 to M.O. and 341750, 346509 to E.S.), EC FP5 GenomEUtwin (J.K.), National Institutes of Health/National Heart, Lung, and Blood Institute (grant HL104125), EC MC ITN Project EPITRAIN (J.K. and M.O.), the University of Helsinki Research Funds (M.O.), Sigrid Juselius Foundation (J.K. and M.O.), Yrjö Jahnsson Foundation (6868), Juho Vainio Foundation (E.S.) and Päivikki and Sakari Sohlberg foundation (E.S.).
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eLife assessment
This paper provides evidence that an unhealthy lifestyle during adolescence accelerates epigenetic age in adulthood, and that these associations are largely explained by the effect of shared genetic influences. The main strengths of this valuable paper are the relatively large sample size, longitudinal assessment of lifestyle factors, and sophisticated statistical analyses. The paper is methodologically compelling and will be of interest for a broad audience, including individuals working on methylation, epidemiology, and/or ageing.
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Reviewer #1 (Public Review):
Previous studies have linked several lifestyle-related factors, such as body mass index and smoking, alcohol use with accelerated biological aging measured using epigenetic clocks, however, most of them focused on single lifestyle factors based on cross-sectional data from older adults. The current study has a couple of major strengths: it has a decent sample size, lifestyle was measured longitudinally during puberty and adolescence, it looked at the effect of multiple lifestyle measures collectively, it looked at multiple epigenetic clocks, and due to the data from twins, it could examine the contribution of genetic and environmental influences to the outcomes. I have a couple of comments that are mainly aimed at improving the clarity of the methods (e.g. how was multiple testing correction done, how did …
Reviewer #1 (Public Review):
Previous studies have linked several lifestyle-related factors, such as body mass index and smoking, alcohol use with accelerated biological aging measured using epigenetic clocks, however, most of them focused on single lifestyle factors based on cross-sectional data from older adults. The current study has a couple of major strengths: it has a decent sample size, lifestyle was measured longitudinally during puberty and adolescence, it looked at the effect of multiple lifestyle measures collectively, it looked at multiple epigenetic clocks, and due to the data from twins, it could examine the contribution of genetic and environmental influences to the outcomes. I have a couple of comments that are mainly aimed at improving the clarity of the methods (e.g. how was multiple testing correction done, how did the association model account for the clustering of twin data, how many samples were measured on 450k vs EPIC and were raw or pre-QC'd data supplied to the online epigenetic age calculator), and interpretation of findings (why were 2 measures of Dunedin PACE of aging used, how much are results driven by BMI versus the other lifestyle factors, and the discussion on shared genetic influences should be more nuanced; it includes both pleiotropic effects and causal effects among lifestyle and biological ageing).
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