Relationships between adverse childhood experiences, oxidative stress, and development of mental disorders: A systematic review of animal and human studies.

Gespeichert in:
Bibliographische Detailangaben
Titel: Relationships between adverse childhood experiences, oxidative stress, and development of mental disorders: A systematic review of animal and human studies.
Autoren: Stocker A; CERPOP, Inserm, UPS, University of Toulouse, 37, allées Jules Guesde, Toulouse Cedex 9 31062, France; Department of Child and Adolescent Psychiatry, Toulouse University Hospital, CHU de Toulouse, Place du Dr Baylac, TSA 40031, Toulouse Cedex 9 31059, France. Electronic address: stocker.a@chu-toulouse.fr., Giangreco B; Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Route de Cery 11bis, 1008 Prilly, Switzerland. Electronic address: basilio.giangreco@unil.ch., Revet A; CERPOP, Inserm, UPS, University of Toulouse, 37, allées Jules Guesde, Toulouse Cedex 9 31062, France; Department of Child and Adolescent Psychiatry, Toulouse University Hospital, CHU de Toulouse, Place du Dr Baylac, TSA 40031, Toulouse Cedex 9 31059, France. Electronic address: revet.a@chu-toulouse.fr., Alameda L; Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, National Psychosis Unit, South London and Maudsley NHS Foundation Trust, Institute of Psychiatry, Psychology & Neuroscience (IoPPN), IoPPN, 16 De Crespigny Park, London SE5 8AB, United Kingdom; Service of General Psychiatry, Treatment and Early Intervention in Psychosis Program, Lausanne University Hospital (CHUV), Lausanne University Hospital, Rue de Bugnon 21, Lausanne. Vaud CH-1011, Switzerland; Department of Psychiatry, Instituto de Investigación Sanitaria de Sevilla, IBiS, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Avda. Doctor Fedriani, S/N, Sevilla 41009, Spain. Electronic address: luis.alameda@kcl.ac.uk., Bui E; University of Caen Normandy & Caen University Hospital, avenue de la Cote de Nacre, Caen 14000, France. Electronic address: bui-th@chu-caen.fr., Bürgin D; Child and Adolescent Psychiatric Research Department, University Psychiatric Clinics Basel (UPK), University of Basel, Universitäre Psychiatrische Kliniken Universität Basel, Wilhelm Klein-Strasse 27, Basel 4002, Switzerland; Jacobs Center for Productive Youth Development, University of Zurich, Andreasstrasse 15, Zurich CH-8050, Switzerland. Electronic address: david.buergin@jacobscenter.uzh.ch., Clemens V; Department for Child and Adolescent Psychiatry/Psychotherapy, University of Ulm, Ulm, Steinhövelstraße 5, Ulm 89075, Germany; German Center for Mental Health (DZPG), Partner Site Ulm, Mannheim 68159, Germany. Electronic address: Vera.Clemens@uniklinik-ulm.de., Cortese S; Developmental EPI (Evidence Synthesis, Prediction, Implementation) Lab, Centre for Innovation in Mental Health, School of Psychology, Faculty of Environmental and Life Sciences, University of Southampton, University Road, Southampton SO17 1BJ, United Kingdom; Clinical and Experimental Sciences (CNS and Psychiatry), Faculty of Medicine, University of Southampton, University Road, Southampton SO17 1BJ, United Kingdom; Hampshire and Isle of Wight Healthcare National Health Service Foundation Trust, Southampton, Sterne 7, Tatchbury Mount, Calmore SO40 2RZ, United Kingdom; Hassenfeld Children's Hospital at New York University Langone, New York University Child Study Center, 430 East 34th Street, New York, NY 10016, United States; DiMePRe-J-Department of Precision and Regenerative Medicine-Jonic Area, University of Bari 'Aldo Moro', Piazza Umberto, Bari 70121, Italy. Electronic address: Samuele.Cortese@soton.ac.uk., Schechter DS; Division of Child and Adolescent Psychiatry, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Avenue d'Echallens 9, 1004 Lausanne, Switzerland. Electronic address: Daniel.Schechter@chuv.ch., Schmid M; Child and Adolescent Psychiatric Research Department, University Psychiatric Clinics Basel (UPK), University of Basel, Universitäre Psychiatrische Kliniken Universität Basel, Wilhelm Klein-Strasse 27, Basel 4002, Switzerland. Electronic address: Marc.Schmid@upk.ch., Steullet P; Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Route de Cery 11bis, 1008 Prilly, Switzerland. Electronic address: Pascal.Steullet@chuv.ch., Dwir D; Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Route de Cery 11bis, 1008 Prilly, Switzerland. Electronic address: Daniella.dwir@chuv.ch., Klauser P; Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Route de Cery 11bis, 1008 Prilly, Switzerland; Division of Child and Adolescent Psychiatry, Department of Psychiatry, Lausanne University Hospital and University of Lausanne, Avenue d'Echallens 9, 1004 Lausanne, Switzerland. Electronic address: Paul.klauser@unil.ch.
Quelle: Neuroscience and biobehavioral reviews [Neurosci Biobehav Rev] 2025 Dec; Vol. 179, pp. 106393. Date of Electronic Publication: 2025 Oct 14.
Publikationsart: Systematic Review; Journal Article; Review
Sprache: English
Info zur Zeitschrift: Publisher: Pergamon Press Country of Publication: United States NLM ID: 7806090 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7528 (Electronic) Linking ISSN: 01497634 NLM ISO Abbreviation: Neurosci Biobehav Rev Subsets: MEDLINE
Imprint Name(s): Publication: New York Ny : Pergamon Press
Original Publication: Fayetteville, N. Y., ANKHO International Inc.
MeSH-Schlagworte: Oxidative Stress*/physiology , Adverse Childhood Experiences* , Mental Disorders*/metabolism , Mental Disorders*/etiology , Mental Disorders*/physiopathology , Stress, Psychological*/metabolism, Humans ; Animals
Abstract: Competing Interests: Declaration of Competing Interest SC, NIHR Research Professor (NIHR303122) is funded by the NIHR for this research project. The views expressed in this publication are those of the author(s) and not necessarily those of the NIHR, NHS or the UK Department of Health and Social Care. SC is also supported by NIHR grants NIHR203684, NIHR203035, NIHR130077, NIHR128472, RP-PG-0618–20003 and by grant 101095568-HORIZONHLTH- 2022-DISEASE-07–03 from the European Research Executive Agency. Prof. SC has declared reimbursement for travel and accommodation expenses from the Association for Child and Adolescent Central Health (ACAMH) in relation to lectures delivered for ACAMH, the Canadian AADHD Alliance Resource, the British Association of Psychopharmacology, Healthcare Convention and CCM Group team for educational activity on ADHD, and has received honoraria from Medice. DD is funded by a fellowship from the Adrian and Simone Frutiger Foundation.
Adverse childhood experiences (ACE) are common risk factors for many psychiatric disorders. Their underlying biological mechanisms may involve oxidative stress (OS), which has deleterious effects on cells through its own actions and through its interactions with inflammation and the stress axes, particularly in the brain. In order to assess the role of OS in the association between ACE and psychopathology, we performed a systematic review of animal and human research (PROSPERO CRD42023378418 and CRD42022378376), funded by the Swiss National Science Foundation (grant number 204033). PubMed, Web of Science, PsycInfo, Scopus and Embase were searched from inception until 31 October 2024. We included 130 studies involving animal models exposed to stressor-paradigms recognized as ACE analogs before they reached adulthood, or human participants with a history of ACE and assessment of psychopathology, and reporting outcomes on OS-related markers. Animal studies overall show increased OS and psychopathology after stress, thus supporting the hypothesis that OS mediates the relationship between ACE and psychopathology. Human studies are heterogeneous and less conclusive. Although the association between ACE exposure and OS, in animals and humans, was likely affected by the nature, the timing, and the intensity of the exposure, these parameters were only evaluated in a small fraction of studies. Similarly, though some studies hinted at sex differences in the OS response to ACE in animals, the majority of studies did not address this issue. Further research, using longitudinal designs and more thorough examination of ACE history in participants, is therefore needed.
(Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Contributed Indexing: Keywords: Adverse childhood experiences; Animal research; Antioxidants; Child abuse; Child neglect; Childhood trauma; Oxidative stress
Entry Date(s): Date Created: 20251016 Date Completed: 20251114 Latest Revision: 20251114
Update Code: 20251115
DOI: 10.1016/j.neubiorev.2025.106393
PMID: 41101714
Datenbank: MEDLINE
Beschreibung
Abstract:Competing Interests: Declaration of Competing Interest SC, NIHR Research Professor (NIHR303122) is funded by the NIHR for this research project. The views expressed in this publication are those of the author(s) and not necessarily those of the NIHR, NHS or the UK Department of Health and Social Care. SC is also supported by NIHR grants NIHR203684, NIHR203035, NIHR130077, NIHR128472, RP-PG-0618–20003 and by grant 101095568-HORIZONHLTH- 2022-DISEASE-07–03 from the European Research Executive Agency. Prof. SC has declared reimbursement for travel and accommodation expenses from the Association for Child and Adolescent Central Health (ACAMH) in relation to lectures delivered for ACAMH, the Canadian AADHD Alliance Resource, the British Association of Psychopharmacology, Healthcare Convention and CCM Group team for educational activity on ADHD, and has received honoraria from Medice. DD is funded by a fellowship from the Adrian and Simone Frutiger Foundation.<br />Adverse childhood experiences (ACE) are common risk factors for many psychiatric disorders. Their underlying biological mechanisms may involve oxidative stress (OS), which has deleterious effects on cells through its own actions and through its interactions with inflammation and the stress axes, particularly in the brain. In order to assess the role of OS in the association between ACE and psychopathology, we performed a systematic review of animal and human research (PROSPERO CRD42023378418 and CRD42022378376), funded by the Swiss National Science Foundation (grant number 204033). PubMed, Web of Science, PsycInfo, Scopus and Embase were searched from inception until 31 October 2024. We included 130 studies involving animal models exposed to stressor-paradigms recognized as ACE analogs before they reached adulthood, or human participants with a history of ACE and assessment of psychopathology, and reporting outcomes on OS-related markers. Animal studies overall show increased OS and psychopathology after stress, thus supporting the hypothesis that OS mediates the relationship between ACE and psychopathology. Human studies are heterogeneous and less conclusive. Although the association between ACE exposure and OS, in animals and humans, was likely affected by the nature, the timing, and the intensity of the exposure, these parameters were only evaluated in a small fraction of studies. Similarly, though some studies hinted at sex differences in the OS response to ACE in animals, the majority of studies did not address this issue. Further research, using longitudinal designs and more thorough examination of ACE history in participants, is therefore needed.<br /> (Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.)
ISSN:1873-7528
DOI:10.1016/j.neubiorev.2025.106393