Gerontology Research Center (GEREC), Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland.
Methodology Center for Human Sciences, University of Jyväskylä, Jyväskylä, Finland.
Elife. 2022 Nov 8;11:e80729. doi: 10.7554/eLife.80729.
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.
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.
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.
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.
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.).
青春期是一个快速生长和发育的阶段。青春期的暴露可能会对以后的生活健康产生长期影响。本研究旨在探讨青少年生活方式在生物衰老中的作用。
研究参与者来自纵向 FinnTwin12 研究(n=5114)。青少年生活方式相关因素,包括体重指数(BMI)、休闲时间体力活动、吸烟和饮酒,基于自我报告,并在 12、14 和 17 岁时测量。对于亚样本,使用基于血液的 DNA 甲基化(DNAm)在年轻成人期(21-25 岁,n=824)评估六个表观遗传衰老测量值来评估生物衰老。使用定量遗传建模估计遗传和环境对与生活方式行为模式共享的生物衰老的影响。
我们确定了具有不同青少年生活方式行为模式的五个亚组参与者。当使用 GrimAge、DunedinPoAm 和 DunedinPACE 估算值时,最不健康生活方式的类和 BMI 较高的参与者类比具有更健康生活习惯的类更显生物老化。与生活方式相关的因素差异一直持续到成年早期。与青少年生活方式共享的生物衰老的大部分变异可以用共同的遗传因素来解释。
这些发现表明,青春期不健康的生活方式与成年早期的生物衰老加速有关。遗传多效性可能在很大程度上解释了观察到的关联。
这项工作得到了芬兰科学院(213506、265240、263278、312073 给 J.K.,297908 给 M.O.和 341750、346509 给 E.S.)、欧盟 FP5 GenomEUtwin(J.K.)、美国国立卫生研究院/国立心肺血液研究所(HL104125 号资助)、欧盟 MC ITN 项目 EPITRAIN(J.K.和 M.O.)、赫尔辛基大学研究基金(M.O.)、西格里德·朱厄尔森基金会(J.K.和 M.O.)、耶尔约·扬松基金会(6868 号)、尤霍·瓦宁基金会(E.S.)和 Päivikki 和 Sakari Sohlberg 基金会(E.S.)的资助。