Early pubertal timing is associated with adverse health in adulthood. These effects may be mediated by DNA methylation changes associated with accelerated cellular aging and mortality risk, but few studies tested associations between pubertal timing and epigenetic markers in adulthood. Additionally, pubertal timing effects often vary by sex and are understudied in diverse youth. Thus, this longitudinal study examined links between pubertal timing and later epigenetic aging and mortality risk together with sex differences in predominantly Black youth. Participants included 350 individuals (58% female, 42% male; 80% Black, 19% non-Hispanic White). Perceived pubertal timing relative to peers and self-reported phenotypic pubertal timing based on age-adjusted Tanner scores were assessed during early adolescence ( = 13) whereas epigenetic aging (GrimAge, DunedinPace of Aging Calculated from the Epigenome, and PhenoAge) and mortality risk were measured during young adulthood ( = 27). After adjusting for covariates (smoking, body mass index, family income, early-life stress, race/ethnicity, sex, parenthood), early pubertal timing (both perceived and phenotypic) predicted higher epigenetic mortality risk, and early phenotypic pubertal timing predicted accelerated DunedinPace of Aging Calculated from the Epigenome. Both perceived and phenotypic early pubertal timing were correlated with accelerated GrimAge. Off-time phenotypic pubertal timing (i.e., early and late) was associated with accelerated PhenoAge in males only whereas perceived off-time pubertal timing was unexpectedly linked with lower PhenoAge acceleration. These findings extend prior research by linking two dimensions of early pubertal timing with epigenetic mortality risk and accelerated aging in racially diverse young adults and showing nonlinear effects on PhenoAge acceleration that differ across pubertal timing measures and show some sex differences. (PsycInfo Database Record (c) 2025 APA, all rights reserved).
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http://dx.doi.org/10.1037/dev0001903 | DOI Listing |
Dev Psychol
January 2025
Department of Psychology, University of Alabama at Birmingham.
Early pubertal timing is associated with adverse health in adulthood. These effects may be mediated by DNA methylation changes associated with accelerated cellular aging and mortality risk, but few studies tested associations between pubertal timing and epigenetic markers in adulthood. Additionally, pubertal timing effects often vary by sex and are understudied in diverse youth.
View Article and Find Full Text PDFAnn Epidemiol
January 2025
Center for Clinical Research and Prevention, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark.
Purpose: Whether breast density mediates associations between early life body size and pubertal timing with postmenopausal breast cancer is underexplored.
Methods: We studied 33,939 Danish women attending the Capital Mammography Screening Program at ages 50-69 years. Early life anthropometry and pubertal timing information came from the Copenhagen School Health Records Register.
Child Dev
January 2025
Department of Psychology and Center for Brain Science, Harvard University, Cambridge, Massachusetts, USA.
Using data from the Human Connectome Project in Development (N = 1304; ages 5-21 years; 50% male; 59% White, 17% Hispanic, 13% Black, 9% Asian), multiple measures (self-report, salivary hormones) and research designs (longitudinal, cross-sectional) were used to characterize age-related changes and sex differences in pubertal development. Both sexes exhibit a sigmoid trajectory of pubertal development; females show earlier pubertal timing and increased tempo ~9-13 years, while males show greater tempo ~14-18 years. All hormones increased with age, with sex differences in testosterone and DHEA levels and in testosterone rates of change.
View Article and Find Full Text PDFmedRxiv
December 2024
Division of Endocrinology, Department of Pediatrics, Boston Children's Hospital.
Background: In women, both earlier and later age at menarche (AAM) are associated with increased risk of coronary artery disease (CAD). This study sought to determine if the relationship of AAM with CAD and CAD risk factors differs for different underlying sources of variation in AAM - specifically, variation attributable to common genetic variants as represented by a polygenic score (PGS) vs. variation in AAM adjusted for the PGS.
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