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Elevated infant cortisol is necessary but not sufficient for transmission of environmental risk to infant social development: Cross-species evidence of mother–infant physiological social transmission

Published online by Cambridge University Press:  11 January 2021

Rosemarie E. Perry*
Affiliation:
Department of Applied Psychology, New York University, New York, NY, USA
Stephen H. Braren
Affiliation:
Department of Applied Psychology, New York University, New York, NY, USA
Maya Opendak
Affiliation:
Emotional Brain Institute, Nathan Kline Institute & Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, NY, USA
Annie Brandes-Aitken
Affiliation:
Department of Applied Psychology, New York University, New York, NY, USA
Divija Chopra
Affiliation:
Department of Applied Psychology, New York University, New York, NY, USA
Joyce Woo
Affiliation:
Emotional Brain Institute, Nathan Kline Institute & Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, NY, USA
Regina Sullivan
Affiliation:
Emotional Brain Institute, Nathan Kline Institute & Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, NY, USA
Clancy Blair
Affiliation:
Department of Applied Psychology, New York University, New York, NY, USA Department of Population Health, New York University School of Medicine, New York, NY, USA
*
Author for Correspondence: Rosemarie E. Perry, RP: New York University, Department of Applied Psychology, 627 Broadway, Room 810, New York, NY 10012; E-mail: rosemarie.perry@nyu.edu.

Abstract

Environmental adversity increases child susceptibility to disrupted developmental outcomes, but the mechanisms by which adversity can shape development remain unclear. A translational cross-species approach was used to examine stress-mediated pathways by which poverty-related adversity can influence infant social development. Findings from a longitudinal sample of low-income mother–infant dyads indicated that infant cortisol (CORT) on its own did not mediate relations between early-life scarcity-adversity exposure and later infant behavior in a mother-child interaction task. However, maternal CORT through infant CORT served as a mediating pathway, even when controlling for parenting behavior. Findings using a rodent “scarcity-adversity” model indicated that pharmacologically blocking pup corticosterone (CORT, rodent equivalent to cortisol) in the presence of a stressed mother causally prevented social transmission of scarcity-adversity effects on pup social behavior. Furthermore, pharmacologically increasing pup CORT without the mother present was not sufficient to disrupt pup social behavior. Integration of our cross-species results suggests that elevated infant CORT may be necessary, but without elevated caregiver CORT, may not be sufficient in mediating the effects of environmental adversity on development. These findings underscore the importance of considering infant stress physiology in relation to the broader social context, including caregiver stress physiology, in research and interventional efforts.

Type
Special Section 2: Early Adversity and Development: Contributions from the Field
Copyright
Copyright © The Author(s), 2020. Published by Cambridge University Press

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Footnotes

*

Authors contributed equally as first authors to this manuscript

Authors contributed equally as last authors to this manuscript

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