Early Adversity Imprints Multisystem Biological Aging: A Longitudinal Study of Adversity Dimensions and Aging Phenotypes Across Adolescence.

Chase Antonacci, Eugenia Giampetruzzi, Jessica L Buthmann, Sarah Rocha, Xinyan Tao, Ian H Gotlib

Abstract read

In one paragraph

Article in Biological psychiatry global open science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Chase AntonacciDepartment of Psychology, Stanford University, Stanford, California.

Eugenia GiampetruzziDepartment of Psychology, Stanford University, Stanford, California.

Jessica L ButhmannDepartment of Psychology, Stanford University, Stanford, California.

Sarah RochaDepartment of Psychology, Stanford University, Stanford, California.

Xinyan TaoDepartment of Psychology, Stanford University, Stanford, California.

Ian H GotlibDepartment of Psychology, Stanford University, Stanford, California.

Funding

Psychobiological Mechanisms Underlying the Association Between Early Life Stress and Depression Across AdolescenceR37MH101495 · NIMH · STANFORD UNIVERSITY · PI IAN H GOTLIB · 2018 to 2026

$6.6M

NIMH NIH HHS R37 MH101495

6 · The paper itself

Abstract

Background: Early-life stress (ELS) is associated with accelerated biological aging; however, it is unclear whether dimensions of adversity such as threat and deprivation produce distinct multisystem aging phenotypes. Here we characterize, for the first time, the multivariate copatterning of stress dimensions and aging biomarkers and examine whether such phenotypes predict psychopathology 6 years later. Methods: In a longitudinal sample ( Results: CCA identified 2 significant CVs at baseline. CV1 linked deprivation-related stress (low parental support/neighborhood disadvantage) to a cellular-metabolic aging profile (higher BMI, older brain age, and lower mtDNA) ( Conclusions: ELS is biologically embedded along adversity type-specific pathways detectable by late childhood, supporting a developmental imprinting model. A threat-related multisystem aging phenotype conferred transdiagnostic psychiatric risk in late adolescence, pointing to pre-adolescent development as an important window for prevention.

Indexed as

AdolescenceBiological agingDevelopmental imprintingDevelopmental timingEarly-life adversityPubertal development

Identifiers

PMID42602875

DOI10.1016/j.bpsgos.2026.100782

PMCPMC13475218

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