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Adolescent risk for self-injurious thoughts and behaviors (STBs) involves disturbance across multiple systems (e.g., affective valence, arousal regulatory, cognitive and social processes). However, research integrating information across these systems is lacking. Utilizing a multiple-levels-of-analysis approach, this person-centered study identified psychobiological stress response profiles and linked them to cognitive processes, interpersonal behaviors, and STBs. At baseline, adolescent girls (N = 241, Mage = 14.68 years, Range = 12-17) at risk for STBs completed the Trier Social Stress Test (TSST), questionnaires, and STB interviews. Positive affect (PA), negative affect (NA), and salivary cortisol (SC) were assessed before and after the TSST. STBs were assessed again during 3, 6, and 9 month follow-up interviews. Multitrajectory modeling of girls' PA, NA, and SC revealed four profiles, which were compared on cognitive and behavioral correlates as well as STB outcomes. Relative to normative, girls in the affective distress, hyperresponsive, and hyporesponsive subgroups were more likely to report negative cognitive style (all three groups) and excessive reassurance seeking (hyporesponsive only) at baseline, as well as nonsuicidal self-injury (all three groups) and suicidal ideation and attempt (hyporesponsive only) at follow-up. Girls' close friendship characteristics moderated several profile-STB links. A synthesis of the findings is presented alongside implications for person-centered tailoring of intervention efforts.

Prior research has struggled to differentiate cortisol stress response patterns reflective of well-regulated versus dysregulated hypothalamic-pituitary-adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPA-inflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure may aid such distinction. Adolescent girls (N = 157, Mage  = 14.72 years, SD = 1.38) at risk for psychopathology completed assessments of salivary cortisol and pro-inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-1β, and interleukin-6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents' cortisol and cytokine levels revealed three profiles: low cortisol response-stably low cytokine (n = 75), high cortisol response-stably moderate cytokine (n = 47), and low cortisol response-stably high cytokine (n = 35). Relative to low cortisol response-stably low cytokine, adolescents exhibiting the high cortisol response-stably moderate cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from low cortisol response-stably low cytokine, adolescents exhibiting the low cortisol response-stably high cytokine profile were more pubertally advanced, but also more likely to have experienced chronic peer strain (self-report) and relational peer victimization (close friend-report). These findings thus illustrate the potential value of taking a multisystem approach to studying adolescent stress responsivity and underscore the importance of considering developmental and social factors when interpreting cortisol stress response patterns. Ultimately, such work may help inform developmental models of neuroendocrine dysregulation and related risk for psychopathology.

Dysregulation of biological stress response, as measured by cortisol output, has been a primary candidate mechanism for how social experiences become biologically embedded. Cortisol is the primary output of the hypothalamic pituitary adrenal (HPA) axis. Cortisol levels vary systematically across the day and change in response to both sudden, acute stress experiences as well as prolonged exposure to environmental stress. Using data from 8- to 15-year-old twins in the Texas Twin Project, we investigate the extent to which genetic influences are shared across different measures of cortisol output: chronic cortisol accumulations in hair (n = 1,104), diurnal variation in salivary output (n = 488), and salivary response to a standardized, acute in-laboratory stressor (n = 537). Multivariate twin models indicate that genetic factors regulating cortisol response to the in-laboratory stressor are separable from those regulating baseline cortisol levels, naturally occurring diurnal variation in cortisol, and hair cortisol levels. These findings illustrate that novel environments can reveal unique genetic variation, reordering people in terms of their observed phenotype rather than only magnifying or mitigating preexisting differences.

IntroductionFor adolescent girls, close friendships may facilitate stress management and mitigate risk for internalizing psychopathology. However, little is known about how friendship processes may buffer (or potentially exacerbate) acute psychobiological responses to interpersonal stressors in ways that affect risk.MethodsIn a sample of 220 girls (ages 12-17 years) with a history of internalizing symptoms, this study investigated friendship dynamics following the Trier Social Stress Test (TSST) to evaluate associations between post-stressor friendship behaviors (expressions of vulnerability by the stressed teen; support offered by their close friend) and hypothalamic-pituitary-adrenal (HPA) axis stress responses.ResultsMultilevel regression modeling revealed that girls who displayed more pronounced cortisol reactivity expressed greater vulnerability to, and received greater support from, their close friend. Expressed vulnerability was associated with more efficient cortisol recovery. Close friend support was not significantly associated with cortisol recovery, nor did it influence the connection between expressed vulnerability and cortisol recovery.ConclusionsFindings suggest that HPA reactivity may prompt expressions of vulnerability to girls' close friends, and in this context, promote more efficient HPA recovery. Findings highlight the role friendship dynamics may play in HPA-related risk for internalizing symptoms and point to expressed vulnerability in adolescent girls' close friendships as a potential consideration for interpersonally-centered therapeutic approaches.

Physical health in childhood is crucial for neurobiological as well as overall development, and can shape long-term outcomes into adulthood. The landmark, longitudinal Adolescent Brain Cognitive Development StudySM (ABCD study®), was designed to investigate brain development and health in almost 12,000 youth who were recruited when they were 9-10 years old and will be followed through adolescence and early adulthood. The overall goal of this paper is to provide descriptive analyses of physical health measures in the ABCD study at baseline, including but not limited to sleep, physical activity and sports involvement, and body mass index. Further this summary will describe how physical health measures collected from the ABCD cohort compare with current normative data and clinical guidelines. We propose this data set has the potential to facilitate clinical recommendations and inform national standards of physical health in this age group. This manuscript will also provide important information for ABCD users and help guide analyses investigating physical health including new avenues for health disparity research as it pertains to adolescent and young adult development.

Symptoms of anxiety and depression are commonly comorbid and partially share a genetic etiology. Mean levels of anxiety and depression increase over the transition to adolescence, particularly in girls, suggesting a possible role of pubertal development in the activation of underlying genetic risks. The current study examined how genetic and environmental influences on anxiety and depression differed by chronological age and pubertal status. We analyzed composite scores from child self-reports and parent informant-reports of internalizing symptomology in a racially and socioeconomically diverse sample of 1,913 individual twins from 1,006 pairs (ages 8--20 years) from the Texas Twin Project. Biometric models tested age and pubertal status as moderators of genetic and environmental influences shared between and specific to anxiety and depression to determine whether etiology of internalizing symptomology differs across development as a function of age or puberty. Genetic influences did not increase as a function of age or puberty, but instead shared environmental effects decreased with age. In an exploratory model that considered the moderators simultaneously, developmental differences in etiology were reflected in genetic and environmental effects unique to depression. Results suggest that genetic variance in internalizing problems is relatively constant during adolescence, with environmental influences more varied across development.

Adolescence is a peak period for risk‐taking, but research has largely overlooked positive manifestations of adolescent risk‐taking due to ambiguity regarding operationalization and measurement of positive risk‐taking. We address this limitation using a mixed‐methods approach. We elicited free responses from contemporary college students (N = 74, Mage = 20.1 years) describing a time they took a risk. Qualitative analysis informed the construction of a self‐report positive risk‐taking scale, which was administered to a population‐based sample of adolescents (N = 1,249, Mage = 16 years) for quantitative validation and examination of associations with normative and impulsive personality. Sensation seeking predicted negative and positive risk‐taking, whereas extraversion and openness were predominantly related to positive risk‐taking. Results provide promising evidence for a valid measure of adolescents' engagement in positive risks. [ABSTRACT FROM AUTHOR]

Prior research has struggled to differentiate cortisol stress response patterns reflective of well-regulated versus dysregulated hypothalamic–pituitary–adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPA– inflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure may aid such distinction. Adolescent girls (N = 157, Mage = 14.72 years, SD = 1.38) at risk for psychopathology completed assessments of salivary cortisol and pro-inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-1β, and interleukin-6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents’ cortisol and cytokine levels revealed three profiles: low cortisol response–stably low cytokine (n = 75), high cortisol response–stably moderate cytokine (n = 47), and low cortisol response–stably high cytokine (n = 35). Relative to low cortisol response–stably low cytokine, adolescents exhibiting the high cortisol response–stably moderate cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from low cortisol response–stably low cytokine, adolescents exhibiting the low cortisol response–stably high cytokine profile were more pubertally advanced, but also more likely to have experienced chronic peer strain (self-report) and relational peer victimization (close friend-report). These findings thus illustrate the potential value of taking a multisystem approach to studying adolescent stress responsivity and underscore the importance of considering developmental and social factors when interpreting cortisol stress response patterns. Ultimately, such work may help inform developmental models of neuroendocrine dysregulation and related risk for psychopathology. [ABSTRACT FROM AUTHOR]