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Biological aging in childhood and adolescence following experiences of threat and deprivation: a systematic review and meta-analysis
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Abstract
= -0.43), but deprivation and SES were unrelated to accelerated development. Systematic review revealed associations between ELA and accelerated cortical thinning, with threat-related ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks. There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
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“This indicates that adversity during childhood may accelerate cellular aging and increase susceptibility to a broad spectrum of illnesses at a younger age (Belsky et al., 2017; Colich et al., 2020; Mian et al., 2022).”
From Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project (2026) · cites this paper as Colich et al., 2020
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“To date, few studies of cellular aging have focused on severe forms of childhood adversity, such as psychosocial deprivation in institutional care (Colich et al., 2020)”
From Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project (2026) · cites this paper as Colich et al., 2020
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Metadata
- Authors
- Colich, N. L., Rosen, M. L., Williams, E. S., & McLaughlin, K. A.
- Affiliations
- University of Washington (US)
- Harvard University (US)
- Stanford University (US)
- Corresponding author
- Colich, Natalie L.
- Venue
- Psychological Bulletin
- Published
- 2020-09
- Volume
- 146
- Issue
- 9
- Pages
- 721-764
- ISSN
- 0033-2909 (ISSN-L)
- 1939-1455
- PMC
- PMC7484378
- OpenAlex
- W3047379485
- Cited by
- 433
- References
- 315
- Citations by year
- 2026: 67 · 2025: 66 · 2024: 65 · 2023: 84 · 2022: 83 · 2021: 49 · 2020: 15
- FWCI
- 4.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Psychological Bulletin (publishedVersion, other-oa)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Smith ScholarWorks (Smith College) (submittedVersion)
- OSF Preprints (OSF Preprints) (submittedVersion)
- Funders
- National Institutes of Health (F32-MH114317, F32-HD089514; K99-HD099203, R01-MH103291; R01-MH106482; R56-MH119194; R37-MH119194)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- biological aging, childhood adversity, deprivation, socioeconomic status, accelerated development, cortical thinning, ventromedial prefrontal cortex, default mode network, health disparities, early intervention
- MeSH terms
- Adverse Childhood Experiences, Food Insecurity, Adolescent, Aging, Brain, Child, Child Abuse, Humans, Psychosocial Deprivation, Puberty, Social Class, Violence, Biomarkers, Cellular Senescence, DNA Methylation, Aging, Premature
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