Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis.
Level 1 - systematic review of randomized trials
Systematic review and meta-analysis of observational studies (graded by design analogy)
PubMed 32744840 · doi:10.1037/bul0000270
What was done
Meta-analysis of 54 studies (n = 116,010) testing associations of early life adversity (ELA) with pubertal timing and cellular aging (telomere length and DNA methylation age), alongside a systematic review of 25 studies (n = 3,253) examining neural markers (cortical thickness and amygdala-prefrontal cortex functional connectivity), stratified by adversity type (threat vs. deprivation and low socioeconomic status [SES]).
What was found
Overall ELA was associated with accelerated pubertal timing (d = -0.10) and cellular aging (d = -0.21). Moderator analyses showed: - Threat-related ELA was associated with accelerated pubertal development (d = -0.26) and cellular aging (d = -0.43). - Deprivation and low SES were unrelated to accelerated pubertal or cellular development. - ELA was associated with accelerated cortical thinning, with threat linked to ventromedial prefrontal cortex thinning, and deprivation/SES linked to frontoparietal, default, and visual networks. - No consistent association was found between ELA and amygdala-prefrontal cortex connectivity.
Why it matters
It demonstrates specificity in biological aging pathways, indicating that threat exposures drive cellular and pubertal acceleration whereas deprivation impacts distinct neural networks rather than systemic biological aging.
Limits
Primary studies are observational, precluding direct causal conclusions. Neural markers were systematically reviewed rather than meta-analyzed quantitatively, and exact confidence intervals or heterogeneity metrics are not reported in the abstract.
Cited by
- supports Traumatic experiences, especially during youth and early childhood, leave an imprint associated with shorter telomeres.