Parental support is a powerful regulator of stress and fear responses for infants and children, but recent evidence suggests it may be an ineffective stress buffer for adolescents. The mechanisms underlying this developmental shift are not well-understood. The goal of the present study was to examine the independent and joint contributions of pubertal status and chronological age in explaining this shift. A sample of 75 typically developing youth (M age = 12.95 years, SD= 0.70, range = 11.7-14.6 years; 37 females) was recruited to complete a modified Trier Social Stress Test (TSST-M) in the laboratory. Participants were recruited in such a way as to disentangle pubertal stage and chronological age by phone screening for markers of pubertal stage and then recruiting roughly equal numbers of younger and older, pre/early and mid/late pubertal youth who were then randomly assigned within groups to condition. The TSST-M was used as the stressor and youth prepared either with their parent or stranger (parent condition: N= 39). Pubertal stage was confirmed by the Petersen Pubertal Development Scale at the time of testing and treated, along with chronological age, as a continuous variable in the analyses. The results revealed an interaction of pubertal stage and support condition for cortisol reactivity to the TSST-M such that preparing for the speech with the parent became a less potent buffer of the HPA axis as pubertal stage increased. Age did not interact with condition in predicting cortisol reactivity. In contrast, the parent's presence during speech preparation decreased in its effectiveness to hasten recovery of the HPA axis as children got older, but pubertal stage was not predictive of recovery rate. These patterns were specific to cortisol and were not observed with salivary alpha-amylase levels or subjective stress ratings for the task. These analyses suggest that the switch away from using parents as social buffers may be the result of neurobiological mechanisms associated with puberty.
Bibliographical noteFunding Information:
The authors were supported by the following grants: T32MH015755 from NIMH to J.R. Doom, NSF Graduate Research Fellowship to A.A. VanZomeren-Dohm, and F32HD078048 from NICHD to C.E. Hostinar. This research was supported by funds from the Canadian Institute for Advanced Research Experience-based Brain and Biological Development Program and NICHD HD075349 . The authors would like to thank Bonny Donzella, Amanda Burkholder, Zamzam Ahmed, Hannah Meyers, and Michelle Brown for their assistance with the study.
© 2015 Elsevier Ltd.
- HPA axis
- Social buffering