The functioning of the hypothalamic–pituitary–adrenal (HPA) axis is implicated in the etiology and maintenance of depressive and posttraumatic stress disorder (PTSD) symptoms. However, different maltreatment experiences as well as the increased sensitivity of the HPA axis during puberty may alter associations between the HPA axis and mental health. To address these gaps, the current study examined the potential bidirectional associations between cortisol reactivity to a stressor, PTSD symptoms, and depressive symptoms among early adolescents across two time points, 1 year apart (n = 454; Mage = 10.98 at Time 1 and Mage = 12.11 at Time 2). Multiple-group path models tested the pathways between cortiol reactivity and mental health prior to and during puberty, for different types of maltreatment . Overall, the results showed that associations between cortisol output and symptoms of PTSD and depression were driven by those in the midst of puberty. Specifically, higher cortisol output at Time 1 was linked with higher levels of subsequent PTSD and depressive symptoms for neglected youth who had reached puberty. However, depressive symptoms predicted subsequent lower cortisol output for the physical abuse and emotional abuse groups. These findings demonstrate longitudinal links between cortisol, depressive symptoms, and PTSD symptoms among youth with different types of maltreatment histories and highlight the need to consider the reorganization of the stress system during puberty in order to advance our understanding of the HPA axis and mental health.

The Young Adolescent Project (YAP) is an ongoing longitudinal study investigating the effects of abuse and neglect on adolescent development. It is a multidisciplinary study guided by a developmental, ecological perspective, and designed to consider the physical, social, and psychological effects of childhood maltreatment through the transition from childhood to adolescence. Four waves of data collection have been completed, ranging from early (Mean age = 10.95) to late adolescence (Mean age = 18.24). Members of the maltreated group (n = 303) were selected from new cases that had been opened by the Department of Child and Family Services, whereas the comparison group (n = 151) were not involved with child welfare but lived in the same neighborhoods as the maltreated group. The study assessed a wide variety of domains including physical development (e.g., height, weight, body mass, pubertal development); physiological reactivity (e.g., cortisol); cognitive abilities; mental health (e.g., symptoms of depression, anxiety, trauma, and aggression); risk behavior (e.g., sexual activity, delinquency, or substance use); social development (e.g., self-esteem, competence, and social support); family environment; and exposure to community violence. Overall, our findings demonstrated the pervasive and persistent adverse effects of child maltreatment both within and across domains, but they also identified maltreated youth with positive functioning. Our hope is that this work will help move us toward identifying targets for intervention to cultivate resilience and positive adaptation after early maltreatment experiences.

The aims were to identify the correspondence between simultaneous, longitudinal changes in cortisol reactivity and diurnal testosterone and to test the hypothesis that cortisol reactivity and diurnal testosterone interact so as to influence antisocial behavior. Participants were 135 children and young adolescents assessed at 6-month intervals over 1 year. Upon enrollment girls were age 8, 10, or 12 years (N = 69, M = 10.06 years) and boys were age 9, 11, or 13 years (N = 66, M = 10.94 years). Assessments included Tanner staging by a nurse, cortisol reactivity (Trier Social Stress Test for Children), diurnal testosterone, and interviews and questionnaires. Growth models showed that cortisol reactivity and diurnal testosterone basal levels (intercept) and rate of change (slopes) were not related, suggesting different mechanisms of growth. Longitudinal regression analyses assessed cortisol reactivity and diurnal testosterone longitudinally. The interactions of cortisol reactivity and diurnal testosterone showed that when diurnal testosterone was low, boys with low cortisol reactivity were reported to have more behavior problems (i.e., oppositional defiant disorder symptoms and attention problems) than when testosterone was high. In addition, when diurnal testosterone was high, boys with high or moderate cortisol reactivity were significantly higher on total antisocial behavior, attention behavior problems, and oppositional defiant disorder symptoms than when testosterone was low or moderate. The results were similar but less frequent for girls. These findings advance the science of young adolescence by showing the interaction between preexisting sensitivity to stressors and the normative testosterone changes of puberty and antisocial behavior.

Throughout the life span, exposure to chronic stress such as child maltreatment is thought to contribute to future dysfunction of the stress response system (SRS) through the process of adaptive calibration. Dysfunction of the SRS is associated with numerous health and behavior problems, so it is important to understand under what conditions and what time frame adaptive calibration occurs. The present study tested for adaptive calibration of the SRS in a sample of maltreated (n = 303) and nonmaltreated (n = 151) youth during the important developmental period of adolescence. Data were used from Waves 2, 3, and 4 of a larger study of the consequences of maltreatment on health and well-being. At each time point, participants underwent the Trier Social Stress Test for Children and provided a baseline and four poststressor saliva samples to measure cortisol reactivity. Adaptive calibration was tested by performing a latent profile analysis using the five samples of salivary cortisol provided at each time point, and testing whether maltreatment status predicted the likelihood of profile membership at Time 2, Time 3, and Time 4. Three cortisol profiles emerged from the data at each time point (blunted, moderate, and elevated), and results indicated that maltreated youth were more likely than nonmaltreated youth to present with the blunted cortisol profile compared to the moderate and elevated profiles at Time 2 and Time 3, even after controlling for recent exposure to violence and trauma. At Time 4, there was no longer a difference in profile membership between maltreated and nonmaltreated youth, suggesting adaptive calibration may be a lengthy process requiring a period of years to become evident. Overall, the findings provide support for adaptive calibration and offer insight into the conditions under which adaptive calibration occurs.

The purpose of this report is to provide evidence of an association between within-person variability in diurnal testosterone over 1 year, lifetime exposure to violence, and the manifestation of antisocial behavior in 135 pubertal-aged adolescents across 1 year. Adolescents' sex and lifetime history of violence exposure moderated the association between within-person variability in diurnal testosterone and antisocial behavior. Furthermore, sex-stratified analyses revealed that lifetime history of exposure to violence moderated the association between within-person variability in diurnal testosterone and antisocial behavior in females only. This report is unique in that it illuminates sex differences in within-person associations among exposure to violence, individual variability in diurnal testosterone, and antisocial behavior.

Accelerated pubertal development has been linked to adverse early environments and may heighten subsequent mental and physical health risks. Hypothalamic–pituitary–adrenal axis functioning has been posited as a mechanism whereby stress may affect pubertal development, but the literature lacks prospective tests of this mechanism. The current study assessed 277 youth (M = 10.84 years, SD = 1.14), 138 boys and 139 girls, who reported on their pubertal development and underwent the Trier Social Stress Test for Children at baseline and returned to the laboratory approximately 1 year later (M = 1.12 years, range = 0.59–1.98 years). For girls, lower cortisol area under the curve (with respect to ground) at Time 1 predicted more advanced pubertal development at Time 2, controlling for Time 1 pubertal development. This association persisted after additional covariates including age, body mass index, race, and maltreatment history were introduced, and was driven by adrenal rather than gonadal development. Cortisol was not linked to boys' subsequent pubertal development, and no interaction by gender or by maltreatment appeared. These results suggest that attenuated cortisol, reported in other studies of children exposed to early adversity, may contribute to accelerated pubertal tempo in girls.

Prenatal cocaine exposure may affect developing stress response systems in youth, potentially creating risk for substance use in adolescence. Further, pathways from prenatal risk to future substance use may differ for girls versus boys. The present longitudinal study examined multiple biobehavioral measures, including heart rate, blood pressure, emotion, and salivary cortisol and salivary alpha amylase (sAA), in response to a stressor in 193 low-income 14- to 17-year-olds, half of whom were prenatally cocaine exposed (PCE). Youth's lifetime substance use was assessed with self-report, interview, and urine toxicology/breathalyzer at Time 1 and at Time 2 (6–12 months later). PCE × Gender interactions were found predicting anxiety, anger, and sadness responses to the stressor, with PCE girls showing heightened responses as compared to PCE boys on these indicators. Stress Response × Gender interactions were found predicting Time 2 substance use in youth (controlling for Time 1 use) for sAA and sadness; for girls, heightened sadness responses predicted substance use, but for boys, dampened sAA responses predicted substance use. Findings suggest distinct biobehavioral stress response risk profiles for boys and girls, with heightened arousal for girls and blunted arousal for boys associated with prenatal risk and future substance use outcomes.

The study examined the interaction between early maturational timing (measured by premature adrenarche [PA]) and executive functioning and cortisol reactivity on symptoms of psychopathology. The study included 76 girls aged 6 through 8 years (mean = 7.50, SD = 0.85) with PA (n = 40) and on-time adrenarche (n = 36). Girls completed a battery of psychological and neuropsychological tests and blood sampling for cortisol. Parents completed the Child Behavior Checklist. The results demonstrated that girls with PA with lower levels of executive functioning had higher externalizing and anxious symptoms compared to other girls. In addition, girls with PA who demonstrated increases in serum cortisol had higher externalizing symptoms than those with stable patterns. Finally, girls with PA who demonstrated decreases in cortisol reported higher depressive symptoms. The findings from this study provide important information concerning the impact of cognitive functioning and stress reactivity on adjustment to early maturation in girls with PA. The results of this research may inform screening and intervention efforts for girls who may be at greatest risk for emotional and behavioral problems as a result of early maturation.

Inconsistencies exist in literature examining hypothalamic–pituitary–adrenal (HPA) axis activity in children and adults who have experienced childhood abuse. Hence, the extent and manner to which childhood abuse may disrupt HPA axis development is largely unknown. To address these inconsistencies, the developmental course of nonstress cortisol in a long-term longitudinal study was assessed at six time points from childhood through adolescence and into young adulthood to determine whether childhood abuse results in disrupted cortisol activity. Nonstress, morning cortisol was measured in 84 females with confirmed familial sexual abuse and 89 nonabused, comparison females. Although dynamically controlling for co-occurring depression and anxiety, hierarchical linear modeling (HLM) showed that relative to comparison females, the linear trend for abused females was significantly less steep when cortisol was examined across development from age 6 to age 30, t (1, 180) = −2.55, p < .01, indicating attenuation in cortisol activity starting in adolescence with significantly lower levels of cortisol by early adulthood, F (1, 162) = 4.78, p < .01. As a more direct test of the attenuation hypothesis, supplemental HLM analyses of data arrayed by time since the disclosure of abuse indicated that cortisol activity was initially significantly higher, t (1, 425) = 2.18, p < .05, and slopes were significantly less steep t (1, 205) = −2.66, p < .01, for abused females. These findings demonstrate how the experience of childhood abuse might disrupt the neurobiology of stress, providing some support for the attenuation hypothesis that victims of abuse may experience cortisol hyposecretion subsequent to a period of heightened secretion.

An understanding of the interactions among developmental psychobiological and psychological and contextual aspects of conduct disorder has the potential for contributing new insights on the etiology and stability of conduct problems. The purpose here is to present theoretical and methodological issues germane to integrating a psychophysiological theory of conduct disorder with psychological developmental perspectives. These issues are theoretical concerns germane to a developmental perspective on conduct disorder, stability and change in conduct disorder, and bidirectionality in biological and psychological influences on conduct disorder.