Linking specific biological signatures to different childhood adversities: findings from the HERO project.
Autor: | 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., Pokhvisneva I; Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada., Maalouf CM; Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada., Parent C; Ludmer Centre for Neuroinformatics and Mental Health, Douglas Hospital Research Center, Montreal, QC, Canada., Mliner SB; Institute of Child Development, University of Minnesota, Minneapolis, MN, USA., Slopen N; Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA., Williams DR; Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA., 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., Boyce WT; Division of Developmental Medicine, Department of Pediatrics, University of California, San Francisco, San Francisco, CA, USA., 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., Nelson CA; Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.; Harvard Graduate School of Education, Cambridge, MA, USA., Gunnar MR; Institute of Child Development, University of Minnesota, Minneapolis, MN, USA., 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., 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., 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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Jazyk: | angličtina |
Zdroj: | Pediatric research [Pediatr Res] 2023 Aug; Vol. 94 (2), pp. 564-574. Date of Electronic Publication: 2023 Jan 17. |
DOI: | 10.1038/s41390-022-02415-y |
Abstrakt: | 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. (© 2022. The Author(s).) |
Databáze: | MEDLINE |
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