TY - JOUR
T1 - HPA–SAM co-activation among racially diverse, economically disadvantaged early adolescents
T2 - Secondary analysis with a preliminary test of a multisystem, person-centered approach
AU - Pham, Holly T.
AU - Bendezú, Jason José
AU - Wadsworth, Martha E.
N1 - Publisher Copyright:
© 2023
PY - 2023/4
Y1 - 2023/4
N2 - Investigating the co-activation of hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenomedullary (SAM) responses to acute stress can provide insight into how risk might become biologically embedded during early adolescence and improve understanding of what distinguishes physiological dysregulation from normative/expected physiological responses to stress. Evidence has thus far been mixed as to whether symmetric or asymmetric co-activation patterns are associated with higher exposure to chronic stress and poorer mental health outcomes during adolescence. This study expands on a prior multisystem, person-centered analysis of lower-risk, racially homogenous youth by focusing on HPA–SAM co-activation patterns in a higher-risk, racially diverse sample of early adolescents from low-income families (N = 119, Mage=11.79 years, 55.5% female, 52.7% mono-racial Black). The present study was conducted by performing secondary analysis of data from the baseline assessment of an intervention efficacy trial. Participants and caregivers completed questionnaires; youth also completed the Trier Social Stress Test-Modified (TSST–M) and provided six saliva samples. Multitrajectory modeling (MTM) of salivary cortisol and alpha-amylase levels identified four HPA–SAM co-activation profiles. In accordance with the asymmetric-risk model, youth exhibiting Low HPA–High SAM (n = 46) and High HPA–Low SAM (n = 28) profiles experienced more stressful life events, posttraumatic stress, and emotional and behavioral problems relative to Low HPA–Low SAM (n = 30) and High HPA–High SAM (n = 15) youth. Findings highlight potential differences in biological embedding of risk during early adolescence based on individuals’ exposure to chronic stress and illustrate the utility of multisystem and person-centered approaches in understanding how risk might get “underneath the skin” across systems.
AB - Investigating the co-activation of hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenomedullary (SAM) responses to acute stress can provide insight into how risk might become biologically embedded during early adolescence and improve understanding of what distinguishes physiological dysregulation from normative/expected physiological responses to stress. Evidence has thus far been mixed as to whether symmetric or asymmetric co-activation patterns are associated with higher exposure to chronic stress and poorer mental health outcomes during adolescence. This study expands on a prior multisystem, person-centered analysis of lower-risk, racially homogenous youth by focusing on HPA–SAM co-activation patterns in a higher-risk, racially diverse sample of early adolescents from low-income families (N = 119, Mage=11.79 years, 55.5% female, 52.7% mono-racial Black). The present study was conducted by performing secondary analysis of data from the baseline assessment of an intervention efficacy trial. Participants and caregivers completed questionnaires; youth also completed the Trier Social Stress Test-Modified (TSST–M) and provided six saliva samples. Multitrajectory modeling (MTM) of salivary cortisol and alpha-amylase levels identified four HPA–SAM co-activation profiles. In accordance with the asymmetric-risk model, youth exhibiting Low HPA–High SAM (n = 46) and High HPA–Low SAM (n = 28) profiles experienced more stressful life events, posttraumatic stress, and emotional and behavioral problems relative to Low HPA–Low SAM (n = 30) and High HPA–High SAM (n = 15) youth. Findings highlight potential differences in biological embedding of risk during early adolescence based on individuals’ exposure to chronic stress and illustrate the utility of multisystem and person-centered approaches in understanding how risk might get “underneath the skin” across systems.
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U2 - 10.1016/j.biopsycho.2023.108546
DO - 10.1016/j.biopsycho.2023.108546
M3 - Article
C2 - 36990378
AN - SCOPUS:85151293694
SN - 0301-0511
VL - 179
JO - Biological Psychology
JF - Biological Psychology
M1 - 108546
ER -