Previously Institutionalized Youths’ Cortisol Reactivity to Stress across the Pubertal Period: Associations with Psychopathology and Behavioral Functioning

• In Event: Pubertal Recalibration in PI Youth: Associations with Physiology, Mental Health, Behavior, and Inflammation

Abstract

Early institutional care, which lacks consistent and responsive caregiving, is a chronic stressor for infants. It results in hypocortisolism, presumably an adaptation following frequent elevations in cortisol (Koss et al., 2016; McLaughlin et al., 2015), which is subsequently associated with poorer behavioral outcomes and mental health (Hawk & McCall, 2010). Recently, work from our lab showed that puberty may be a period of recalibration for PI youth, such that cortisol reactivity increases to levels that are similar to non-adopted (NA) peers. Importantly, however, the implications of pubertal recalibration of the HPA axis for psychosocial and behavioral functioning have yet to be examined.
Thus, we investigated whether changes in cortisol reactivity to a social evaluative stressor during the peripubertal period would be significantly associated with changes in youth’s internalizing and externalizing symptoms, as well as their observed behavioral anxiety during the stressor. Because of the novelty of this question, we did not have specific hypotheses about the direction of these associations.

This hypothesis was examined using a short-term accelerated longitudinal study of 132 youth who experienced institutional care in infancy/toddlerhood before being adopted into well-resourced families in a Midwestern region of the United States. PI youth had spent at least 50% of their pre-adoptive life in an institution and were adopted before 60 months of age. At each of three annual sessions, cortisol reactivity was assessed via the Trier Social Stress Test for Children (TSST-C). Child internalizing and externalizing symptoms were assessed via child- and parent-report of the MacArthur Health and Behavior Questionnaire (HBQ), and youth’s observed anxiety was behaviorally coded during the TSST-C.

Hypotheses were investigated using cross-lagged panel models with latent intercepts (Berry & Willoughby, 2017; Curran et al., 2014). Models were fit separately for internalizing symptoms, externalizing symptoms, and observed behavior. However, internalizing symptoms were controlled for in the externalizing model and vice versa.
Results suggest that increasing cortisol reactivity was associated with increasing, not decreasing, self-reported internalizing symptoms. Conversely, increasing internalizing symptoms were associated with increasing cortisol reactivity. There were no associations between cortisol reactivity and externalizing symptoms for PI youth. Finally, similar to the internalizing findings, greater cortisol reactivity significantly predicted increases in observed anxious behavior during the TSST-C over time. Interestingly, however, greater cortisol reactivity negatively predicted concurrent anxious behavior. Thus, increased cortisol may serve as a biological resource for PI youth to handle the challenge in the moment but also have negative consequences over time.

Overall, findings indicate that, while PI youth’s cortisol reactivity becomes more similar to that of NA youth during puberty, this does not necessarily indicate an improvement behavioral functioning or mental health, and may in fact play a role in increasing anxiety and depressive symptoms.

Authors

• Nicole Perry, University of Texas at Austin
  Presenting Author

• Carrie E DePasquale, Pennsylvania State University, University Park
  Non-Presenting Author

• Bonny Donzella, University of Minnesota - Twin Cities
  Non-Presenting Author

• Megan R. Gunnar, University of Minnesota - Twin Cities
  Non-Presenting Author