Linking specific biological signatures to different childhood adversities: findings from the HERO project.


Journal

Pediatric research
ISSN: 1530-0447
Titre abrégé: Pediatr Res
Pays: United States
ID NLM: 0100714

Informations de publication

Date de publication:
08 2023
Historique:
received: 29 04 2022
accepted: 02 11 2022
revised: 23 09 2022
medline: 31 7 2023
pubmed: 18 1 2023
entrez: 17 1 2023
Statut: ppublish

Résumé

Although investigations have begun to differentiate biological and neurobiological responses to a variety of adversities, studies considering both endocrine and immune function in the same datasets are limited. Associations between proximal (family functioning, caregiver depression, and anxiety) and distal (SES-D; socioeconomic disadvantage) early-life adversities with salivary inflammatory biomarkers (IL-1β, IL-6, IL-8, and TNF-α) and hair HPA markers (cortisol, cortisone, and dehydroepiandrosterone) were examined in two samples of young U.S. children (N = 142; N = 145). Children exposed to higher SES-D had higher levels of TNF-α (B = 0.13, p = 0.011), IL-1β (B = 0.10, p = 0.033), and DHEA (B = 0.16, p = 0.011). Higher family dysfunction was associated with higher cortisol (B = 0.08, p = 0.033) and cortisone (B = 0.05, p = 0.003). An interaction between SES-D and family dysfunction was observed for cortisol levels (p = 0.020) whereby children exposed to lower/average levels of SES-D exhibited a positive association between family dysfunction and cortisol levels, whereas children exposed to high levels of SES-D did not. These findings were partially replicated in the second sample. Our results indicate that these biological response systems may react differently to different forms of early-life adversity. Different forms of early-life adversity have varied stress signatures, and investigations of early-life adversities with inflammation and HPA markers are lacking. Children with higher socioeconomic disadvantage had higher TNF-α, IL-1β, and DHEA. Higher family dysfunction was associated with higher hair cortisol and cortisone levels, and the association between family dysfunction and cortisol was moderated by socioeconomic disadvantage. Biological response systems (immune and endocrine) were differentially associated with distinct forms of early-life adversities.

Sections du résumé

BACKGROUND
Although investigations have begun to differentiate biological and neurobiological responses to a variety of adversities, studies considering both endocrine and immune function in the same datasets are limited.
METHODS
Associations between proximal (family functioning, caregiver depression, and anxiety) and distal (SES-D; socioeconomic disadvantage) early-life adversities with salivary inflammatory biomarkers (IL-1β, IL-6, IL-8, and TNF-α) and hair HPA markers (cortisol, cortisone, and dehydroepiandrosterone) were examined in two samples of young U.S. children (N = 142; N = 145).
RESULTS
Children exposed to higher SES-D had higher levels of TNF-α (B = 0.13, p = 0.011), IL-1β (B = 0.10, p = 0.033), and DHEA (B = 0.16, p = 0.011). Higher family dysfunction was associated with higher cortisol (B = 0.08, p = 0.033) and cortisone (B = 0.05, p = 0.003). An interaction between SES-D and family dysfunction was observed for cortisol levels (p = 0.020) whereby children exposed to lower/average levels of SES-D exhibited a positive association between family dysfunction and cortisol levels, whereas children exposed to high levels of SES-D did not. These findings were partially replicated in the second sample.
CONCLUSIONS
Our results indicate that these biological response systems may react differently to different forms of early-life adversity.
IMPACT
Different forms of early-life adversity have varied stress signatures, and investigations of early-life adversities with inflammation and HPA markers are lacking. Children with higher socioeconomic disadvantage had higher TNF-α, IL-1β, and DHEA. Higher family dysfunction was associated with higher hair cortisol and cortisone levels, and the association between family dysfunction and cortisol was moderated by socioeconomic disadvantage. Biological response systems (immune and endocrine) were differentially associated with distinct forms of early-life adversities.

Identifiants

pubmed: 36650307
doi: 10.1038/s41390-022-02415-y
pii: 10.1038/s41390-022-02415-y
pmc: PMC10382309
doi:

Substances chimiques

Hydrocortisone WI4X0X7BPJ
Cortisone V27W9254FZ
Tumor Necrosis Factor-alpha 0
Dehydroepiandrosterone 459AG36T1B

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

564-574

Informations de copyright

© 2022. The Author(s).

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Auteurs

Euclides José de Mendonça Filho (EJ)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada.
Department of Psychiatry, McGill University, Montreal, QC, Canada.

Irina Pokhvisneva (I)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada.

Christina Maria Maalouf (CM)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada.

Carine Parent (C)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada.

Shanna B Mliner (SB)

Institute of Child Development, University of Minnesota, Minneapolis, MN, USA.

Natalie Slopen (N)

Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

David R Williams (DR)

Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

Nicole R Bush (NR)

Department of Psychiatry and Behavioral Sciences, Weill Institute for Neurosciences, San Francisco, CA, USA.
Division of Developmental Medicine, Department of Pediatrics, University of California, San Francisco, San Francisco, CA, USA.

William Thomas Boyce (WT)

Division of Developmental Medicine, Department of Pediatrics, University of California, San Francisco, San Francisco, CA, USA.

Pat Levitt (P)

Department of Pediatrics and Program in Developmental Neuroscience and Developmental Neurogenetics, The Saban Research Institute, Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Charles A Nelson (CA)

Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Harvard Graduate School of Education, Cambridge, MA, USA.

Megan R Gunnar (MR)

Institute of Child Development, University of Minnesota, Minneapolis, MN, USA.

Michael J Meaney (MJ)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada.
Department of Psychiatry, McGill University, Montreal, QC, Canada.
Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research (A*STAR), Brenner Centre for Molecular Medicine, Singapore, Republic of Singapore.

Jack P Shonkoff (JP)

Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Harvard Graduate School of Education, Cambridge, MA, USA.
Center on the Developing Child, Harvard University, Cambridge, MA, USA.

Patricia Pelufo Silveira (PP)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada. patricia.silveira@mcgill.ca.
Department of Psychiatry, McGill University, Montreal, QC, Canada. patricia.silveira@mcgill.ca.

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Classifications MeSH