Adverse childhood experiences and depressive symptoms in later life: Longitudinal mediation effects of inflammation.

Adverse childhood experiences C-reactive protein Depressive symptoms Longitudinal mediation Older adults

Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
11 2020
Historique:
received: 10 06 2020
revised: 17 07 2020
accepted: 29 07 2020
pubmed: 7 8 2020
medline: 28 4 2021
entrez: 7 8 2020
Statut: ppublish

Résumé

Adverse childhood experiences (ACEs) have been associated with both inflammation and depression. However, few studies have examined the role of inflammation as a possible biological mechanism underlying the association of ACEs with depression in later life using longitudinal data. This study investigated the longitudinal mediation effects of inflammation in the relationship between ACEs and depressive symptoms in older adults. We utilised data from the English Longitudinal Study of Ageing (N = 4382). ACEs (i.e. threat, family dysfunction, low parental bonding, loss experiences) were assessed retrospectively at wave 3 (2006/07). C-reactive protein (CRP), an inflammatory marker, was measured at waves 2 (2004/05), 4 (2008/09), and 6 (2012/13). Depressive symptoms were ascertained from wave 6 to 8 (2016/17). The mediation analysis was conducted using parallel process latent growth curve modelling. Greater ACEs cumulative exposure was associated with higher CRP and depressive symptoms at baseline (β ACEs were related to higher depressive symptoms partly via elevated CRP levels. Inflammation might be one of the psychobiological mechanisms underlying the link between ACEs and depression. Psychosocial and behavioural interventions to prevent and reduce the negative impact of ACEs might help to lower the risk of inflammation and depression in the population.

Sections du résumé

BACKGROUND
Adverse childhood experiences (ACEs) have been associated with both inflammation and depression. However, few studies have examined the role of inflammation as a possible biological mechanism underlying the association of ACEs with depression in later life using longitudinal data. This study investigated the longitudinal mediation effects of inflammation in the relationship between ACEs and depressive symptoms in older adults.
METHODS
We utilised data from the English Longitudinal Study of Ageing (N = 4382). ACEs (i.e. threat, family dysfunction, low parental bonding, loss experiences) were assessed retrospectively at wave 3 (2006/07). C-reactive protein (CRP), an inflammatory marker, was measured at waves 2 (2004/05), 4 (2008/09), and 6 (2012/13). Depressive symptoms were ascertained from wave 6 to 8 (2016/17). The mediation analysis was conducted using parallel process latent growth curve modelling.
RESULTS
Greater ACEs cumulative exposure was associated with higher CRP and depressive symptoms at baseline (β
CONCLUSION
ACEs were related to higher depressive symptoms partly via elevated CRP levels. Inflammation might be one of the psychobiological mechanisms underlying the link between ACEs and depression. Psychosocial and behavioural interventions to prevent and reduce the negative impact of ACEs might help to lower the risk of inflammation and depression in the population.

Identifiants

pubmed: 32755647
pii: S0889-1591(20)31310-6
doi: 10.1016/j.bbi.2020.07.045
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

97-107

Subventions

Organisme : NIA NIH HHS
ID : R01 AG017644
Pays : United States
Organisme : Biotechnology and Biological Sciences Research Council
Pays : United Kingdom

Informations de copyright

Copyright © 2020. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Eleonora Iob (E)

Department of Behavioural Science and Health, University College London, UK. Electronic address: eleonora.iob.17@ucl.ac.uk.

Rebecca Lacey (R)

Department of Epidemiology and Public Health, University College London, UK.

Andrew Steptoe (A)

Department of Behavioural Science and Health, University College London, UK.

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