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

on behalf of the JPB Research Network on Toxic Stress

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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. [Figure not available: see fulltext.].

Original languageEnglish (US)
Pages (from-to)564-574
Number of pages11
JournalPediatric Research
Issue number2
StatePublished - Aug 2023

Bibliographical note

Funding Information:
We thank the patients, families, providers, medical staff, and affiliated pediatric clinics of the Health’s Early Roots & Origins (HERO) project. We thank the JPB Research Network on Toxic Stress, active members of the Pediatric Innovation Cluster, and Community Leadership Council, who have worked in partnership with the scientific leadership members making substantial contributions to the content of this paper with data collection and helpful comments on early drafts over a 8-year period. These contributors include Javier Aceves (University of New Mexico Albuquerque, NM), Byron Amos (Capacity Builders, Inc., Atlanta City Council District 3 Member, Atlanta, GA), Louis Appel (People’s Community Clinic, Austin, TX), Rahil Briggs (Albert Einstein College of Medicine, Bronx, NY), Kathleen Conroy (Boston Children’s Hospital Harvard Medical School, Boston, MA), Cerella Craig (Yale University School of Medicine, New Haven, CT), Kate Cuno (Montefiore Medical Center, Bronx, NY), Sara del Campo de Gonzalez (Children’s Hospital of San Antonio, San Antonio, TX), Harwood Egan (Revere HealthCare Center, Revere, MA), Michelle Foley (Center for the Developing Child), Miguelina German (Montefiore Medical Center, Bronx, NY), Dan Hall (Revere HealthCare Center), Joan Jeung (University of California, San Francisco, CA), Alise Morrissey (Children’s Home Society of Washington), Celina Fuentes Nance (People’s Community Clinic, Austin, TX), Sally Pfitzer (Center on the Developing Child at Harvard University, Cambridge, MA), Nora Razón (San Mateo Small Business Development Center, San Mateo, CA), Suzanne Roberts (Keck School of Medicine University of South California Division of General Pediatrics Children’s Hospital Los Angeles, Los Angeles, CA), Michael F. Troy (Children’s Hospital of Minnesota, Saint Paul, MN), Michael Yogman (CHA Cambridge Pediatrics, Cambridge, MA), and Wayne Ysaguirre (The CAYL Institute, Roxbury, MA).

Funding Information:
This research was supported by The JPB Foundation through a grant to the JPB Research Network on Toxic Stress: A Project of the Center on the Developing Child at Harvard University, with additional support from a Postdoctoral Fellowship from the McGill-Douglas Max Planck Institute of Psychiatry International Collaborative Initiative in Adversity and Mental Health, an international partnership funded by the Healthy Brains for Healthy Lives initiative (to E.J.d.M.F.).

Publisher Copyright:
© 2022, The Author(s).


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