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Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning

Published online by Cambridge University Press:  03 March 2020

Ethan S. Young Open the ORCID record for Ethan S. Young [Opens in a new window] ,
Jenalee R. Doom Open the ORCID record for Jenalee R. Doom [Opens in a new window] ,
Allison K. Farrell ,
Elizabeth A. Carlson ,
Michelle M. Englund ,
Gregory E. Miller ,
Megan R. Gunnar ,
Glenn I. Roisman  and
Jeffry A. Simpson
Ethan S. Young*
Affiliation:
Department of Psychology, University of Minnesota, Minneapolis, MN, USA
Jenalee R. Doom
Affiliation:
Department of Psychology, University of Denver, Denver, CO, USA
Allison K. Farrell
Affiliation:
Department of Psychology, Miami University, Oxford, OH, USA
Elizabeth A. Carlson
Affiliation:
Institute of Child Development, University of Minnesota, Minneapolis, MN, USA
Michelle M. Englund
Affiliation:
Institute of Child Development, University of Minnesota, Minneapolis, MN, USA
Gregory E. Miller
Affiliation:
Department of Psychology and Institute for Policy Research, Northwestern University, Evanston, IL, USA
Megan R. Gunnar
Affiliation:
Institute of Child Development, University of Minnesota, Minneapolis, MN, USA
Glenn I. Roisman
Affiliation:
Institute of Child Development, University of Minnesota, Minneapolis, MN, USA
Jeffry A. Simpson
Affiliation:
Department of Psychology, University of Minnesota, Minneapolis, MN, USA
*
Author for Correspondence: Ethan S. Young, Department of Psychology, University of Minnesota, 75 E. River Road, Minneapolis, MN, 55455; [email protected]
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Abstract

Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.

Keywords

cortisol reactivitycumulative stressdevelopmentlife stressTrier Social Stress Test
Type
Regular Articles
Information
Development and Psychopathology , Volume 33 , Issue 1 , February 2021 , pp. 301 - 312
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Copyright
Copyright © Cambridge University Press 2020

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