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Physiological attunement in mother–infant dyads at clinical high risk: The influence of maternal depression and positive parenting

Published online by Cambridge University Press:  19 September 2017

Cassandra L. Hendrix*
Affiliation:
Emory University
Zachary N. Stowe
Affiliation:
University of Wisconsin
D. Jeffrey Newport
Affiliation:
University of Miami Miller School of Medicine
Patricia A. Brennan
Affiliation:
Emory University
*
Address correspondence and reprint requests to: Cassandra L. Hendrix, 36 Eagle Row, Emory University, Atlanta, GA 30322; E-mail: clhendr@emory.edu.

Abstract

A growing number of research studies have examined the intradyadic coregulation (or attunement) of hypothalamus–pituitary–adrenal axis functioning in mothers and their children. However, it is unclear how early this coregulation may be present in dyads at clinical high risk and whether certain factors, such as maternal depression or positive parenting, are associated with the strength of this coregulation. The present study examined cortisol attunement within mother–infant dyads in a high-risk sample of 233 mothers who received treatment for psychiatric illness during pregnancy and whose infants were 6 months old at the study visit. Results showed that maternal and infant cortisol covaried across four time points that included a stressor paradigm and a mother–infant interaction task. Greater maternal positive affect, but not depression, predicted stronger cortisol attunement. In addition, infants’ cortisol level following separation from the mother predicted mothers’ cortisol level at the next time point. Mothers’ cortisol level following the separation and the laboratory stress paradigm predicted infants’ cortisol levels at each successive time point, over and above infants’ own cortisol at the previous time point. These findings suggest that maternal and infant cortisol levels influence one another in a bidirectional fashion that may be temporally and context dependent.

Type
Regular Articles
Copyright
Copyright © Cambridge University Press 2017 

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Footnotes

This research was supported by a NARSAD Young Investigator Grant (to P.A.B.) as well as NIH Grants MD009746, MH088609, MH58922, and MH68036. The first author is supported by the National Science Foundation Graduate Research Fellowship Program under Grant DGE-1444932. Dr. Brennan and Ms. Hendrix declare no conflicts of interest. Dr. Stowe has received research support from the National Institutes of Health, GlaxoSmithKline, Pfizer, and Wyeth; served on speakers or advisory boards for Pfizer, Eli Lilly, Wyeth, Bristol-Myers Squibb, and GlaxoSmithKline; and received honoraria from Eli Lilly, GlaxoSmithKline, Pfizer, and Wyeth. Dr. Newport has received research support from Eli Lilly, GlaxoSmithKline, Janssen, the National Institutes of Health, NARSAD, Takeda Pharmaceuticals, and Wyeth; served on speakers or advisory boards for AstraZeneca, Eli Lilly, GlaxoSmithKline, Pfizer, and Wyeth; and received honoraria from AstraZeneca, Eli Lilly, GlaxoSmithKline, Pfizer, and Wyeth.

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