Examining Health Behaviors as Mechanisms Linking Earlier Pubertal Timing with Accelerated Epigenetic Aging in Late Adolescence.
Epigenetic Aging
Health Behaviors
Longitudinal
Mediation
Pubertal Timing
Journal
Journal of youth and adolescence
ISSN: 1573-6601
Titre abrégé: J Youth Adolesc
Pays: United States
ID NLM: 0333507
Informations de publication
Date de publication:
03 Oct 2024
03 Oct 2024
Historique:
received:
10
07
2024
accepted:
24
09
2024
medline:
3
10
2024
pubmed:
3
10
2024
entrez:
3
10
2024
Statut:
aheadofprint
Résumé
Earlier pubertal timing is associated with accelerated epigenetic aging, but the underlying mechanisms are not well understood. This three-wave longitudinal study examined negative health behaviors, specifically substance use, short sleep duration, and poor diet quality in middle adolescence, as mediators of links between earlier phenotypic and perceived pubertal timing measured in early adolescence and epigenetic aging on three epigenetic clocks in late adolescence (GrimAge, DunedinPACE, and PhenoAge). Phenotypic pubertal timing measured physical pubertal maturation relative to chronological age, whereas perceived pubertal timing was based on adolescents' subjective interpretation of their pubertal timing relative to their peers. Participants included 1213 youth (51% female, 49% male; 62% Black, 34% White) who participated during early adolescence (mean age = 13.10 years), middle adolescence (mean age = 16.1 years) and late adolescence (mean age = 19.7 years). Results from a mediation model revealed a mediation effect of earlier phenotypic pubertal timing on accelerated GrimAge in late adolescence through higher substance use during middle adolescence. There was also a direct effect of earlier phenotypic pubertal timing on accelerated DunedinPACE in males. Sleep duration and diet quality did not emerge as mediators but shorter sleep duration predicted accelerated GrimAge in females. These findings suggest that higher substance use presents a mechanism through which earlier maturing youth experience faster epigenetic aging that puts them at risk for poorer health across the lifespan.
Identifiants
pubmed: 39361160
doi: 10.1007/s10964-024-02096-2
pii: 10.1007/s10964-024-02096-2
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : Foundation for the National Institutes of Health
ID : R01MH098348
Organisme : CDC HHS
ID : CCU409679
Pays : United States
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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