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Associations between developmental trajectories of peer victimization, hair cortisol, and depressive symptoms: a longitudinal study
Author(s) -
OuelletMorin Isabelle,
Cantave Christina,
Paquin Stéphane,
Geoffroy MarieClaude,
Brendgen Mara,
Vitaro Frank,
Tremblay Richard,
Boivin Michel,
Lupien Sonia,
Côté Sylvana
Publication year - 2021
Publication title -
journal of child psychology and psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.652
H-Index - 211
eISSN - 1469-7610
pISSN - 0021-9630
DOI - 10.1111/jcpp.13228
Subject(s) - peer victimization , psychology , longitudinal study , hypothalamic–pituitary–adrenal axis , clinical psychology , depressive symptoms , association (psychology) , poison control , developmental psychology , injury prevention , young adult , psychiatry , medicine , anxiety , hormone , environmental health , pathology , psychotherapist
Background Peer victimization has been associated with long‐lasting risks for mental health. Prior research suggests that stress‐related systems underlying adaptation to changing environments may be at play. To date, inconsistent findings have been reported for the hypothalamic–pituitary–adrenal (HPA) axis, and its end product cortisol. This study tested whether peer victimization was associated with hair cortisol concentrations (HCC), and whether this association varied according to sex, timing, and changes in exposure. We also examined whether peer victimization differentially predicted depressive symptoms according to HCC. Methods The sample comprised 556 adolescents (42.0%; 231 males) who provided hair for cortisol measurement at 17 years of age. Peer victimization was reported at seven occasions between the ages of 6 and 15 years. Results Peer victimization was nonlinearly associated with HCC for boys only, whereas changes in peer victimization were related to HCC for boys and girls. Peer victimization predicted more depressive symptoms for all participants, except those with lower HCC. Conclusions Our findings provide further support for persistent dysregulation of the HPA axis following exposure to chronic adversity, of which the expression may change according to sex and the severity of victimization.