HPA-SAM co-activation among racially diverse, economically disadvantaged early adolescents: Secondary analysis with a preliminary test of a multisystem, person-centered approach.

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.

Targeting the Proximal Mechanisms of Stress Adaptation in Early Adolescence to Prevent Mental Health Problems in Youth in Poverty.

OBJECTIVE: This study used a randomized clinical trial design to evaluate the success with which The Building a Strong Identity and Coping Skills intervention (BaSICS) engaged the proximal mechanisms of poverty-related stress's impact on the psychosocial functioning and mental health of young adolescents living in high poverty contexts. METHOD: 129 youth from very low-income families were randomized to receive the 32-hour group-based intervention or no-treatment control - 16 of these families withdrew before the intervention groups began. The remaining 113 youth aged 11-12 (53% assigned to intervention; 54% female; 40% Hispanic, 63% Black, 20% White) participated in the study, which included four assessment waves: pretest, posttest, 6-month follow-up and 12-month follow-up assessments. Primary control, secondary control, and disengagement coping were assessed via a combination of parent and youth reports as well as via interviews and questionnaires. Hypothalamic-pituitary-adrenal axis (HPA) reactivity was assessed via salivary cortisol responses occurring during a lab-based stress induction (Trier Social Stress Test). RESULTS: Multilevel regression models with repeated measures nested within subjects revealed that in comparison to controls, intervention youth had sustained significant increases in their knowledge about primary control coping (e.g., problem solving, emotion modulation), knowledge and utilization of secondary control (e.g., cognitive restructuring) coping, as well as decreased reliance on disengagement coping. These were accompanied by decreased cortisol reactivity in intervention versus control youth. CONCLUSIONS: These findings support that BaSICS engages several proximal mechanisms of poverty-related stress' impact on early adolescent mental health - coping skills and HPA reactivity - during the neurodevelopmentally plastic pubertal period.

Family environmental antecedents of pubertal timing in girls and boys: A review and open questions.

Across nonhuman species, pubertal timing is affected by the social environment, with consequences for reproductive success and behavior. In human beings, variations in pubertal timing have not been systematically examined in relation to social environmental antecedents, although their psychological consequences are well documented. This paper focuses on links in human beings between pubertal timing and the childhood social environment, with several sections: A review of studies relating pubertal timing to the family context, a key aspect of the social environment; challenges in studying the issue; and opportunities for future work that takes advantage of and creates links with evidence in other species. The review shows that pubertal timing in girls is accelerated by adversity in aspects of the early family social context, with effects small in size; data in boys are not sufficient to enable conclusions. Inferences from existing studies are limited by variations in conceptualizations and measurement of relevant aspects of puberty and of the family social environment, and by methodological issues (e.g., reliance on existing data, use of retrospective reports, nonrandom missing data). Open questions remain about the nature, mechanisms, and specificity of the links between early family social environment and pubertal timing (e.g., form of associations, consideration of absence of positive experiences, role of timing of exposure). Animal studies provide a useful guide for addressing these questions, by delineating potential hormonal mechanisms that underlie links among social context, pubertal timing, and behavior, and encouraging attention to aspects of the social environment outside the family, especially peers.

Family Experiences and Parent Personality as Antecedents of Pubertal Timing in Girls and Boys.

Pubertal timing may be influenced by typical variations in early family environmental events, but questions remain concerning the roles of specific parenting factors, developmental age of exposure to events, moderation by child temperament, and comparability of effects for girls and boys. This study focused on these questions utilizing longitudinal data from 733 same-sex twins (45% girls) in the U.S.; family context was measured at ages 1-3, 4-5, and 6-7 years and pubertal status was assessed annually via self-report at ages 9-15, enabling estimates of pubertal timing. Home environment at ages 4-5 years predicted pubertal timing better than home environment at other ages for both girls and boys, but parent personality was more predictive than home experiences (e.g., divorce, parental harshness, family conflict). Thus, effects of family environment must be considered within the context of parent characteristics, encouraging caution in implicating early environmental experiences as direct influences on early pubertal timing.

Sympathetic nervous system dominance during stress recovery mediates associations between stress sensitivity and social anxiety symptoms in female adolescents.

Social anxiety disorder (SAD) is commonly diagnosed during adolescence and is associated with psychological stress reactivity and heightened physiological arousal. No study, however, has systematically examined which aspects of autonomic nervous system function mediate likely links between stress sensitivity and social anxiety symptoms in adolescents. Here, we assessed 163 adolescents (90 females; 12.29 ± 1.39 years) with respect to life stress and social anxiety symptoms, and measured respiratory sinus arrhythmia (RSA) and skin conductance levels (SCL) during a psychosocial stress paradigm. We operationalized stress sensitivity as the residual variance in subjective stress severity after accounting for objective severity and changes in autonomic regulation using standardized change scores in RSA and SCL. In females only, stress sensitivity and social anxiety symptoms were significantly correlated with each other (p < .001) and with autonomic regulation during both reactivity and recovery (all ps < 0.04). Further, sympathetic nervous system dominance during recovery specifically mediated associations between stress sensitivity and social anxiety symptoms (B = 1.06, 95% CI: 0.02-2.64). In contrast, in males, stress sensitivity, autonomic regulation during reactivity or recovery, and social anxiety symptoms were not significantly associated (all ps > 0.1). We interpret these results in the context of psychobiological models of SAD and discuss implications for interventions targeting autonomic processes.