Utilizing a large (N = 739), ancestrally homogenous sample, the current study aimed to better understand biological risk processes involved in the development of depressive symptoms in maltreated, African American children age 8-12 years. Maltreatment was independently coded from Child Protective Services records and maternal report. Self-reported depressive symptoms were attained in the context of a week-long, summer research camp. DNA was acquired from buccal cell or saliva samples and genotyped for nine polymorphisms in four hypothalamic-pituitary-adrenal (HPA)-axis-related genes: FKBP5, NR3C1, NR3C2, and CRHR1. Salivary cortisol samples were collected each morning (9 a.m.) and late afternoon (4 p.m.) throughout the week to assess HPA functioning. Results revealed that experiences of maltreatment beginning prior to age 5 were most predictive of depressive symptoms, whereas maltreatment onset after age 5 was most predictive of HPA axis dysregulation (blunted daytime cortisol patterns). Multigenic risk did not relate to HPA functioning, nor did it moderate the relationship between maltreatment and HPA activity. There was no mediation of the relationship between maltreatment and depressive symptoms by HPA dysfunction. Results are interpreted through a developmental psychopathology lens, emphasizing the principle of equifinality while carefully appraising racial differences. Implications for future research, particularly the need for longitudinal studies, and important methodological considerations are discussed.

Megan Gunnar's pubertal stress recalibration hypothesis was supported in a recent study of previously institutionalized (PI) youth such that increases in pubertal stage were associated with increases in cortisol stress reactivity. This work provides evidence that puberty may open up a window of recalibration for PI youth, resulting in a shift from a blunted to a more typical cortisol stress response. Using the same sample (N = 132), the current study aimed to elucidate whether increases in cortisol are associated with increases in adaptive functioning or whether they further underlie potential links to developmental psychopathology. Specifically, we examined the bidirectional associations between cortisol stress reactivity and both internalizing and externalizing symptoms across three timepoints during the pubertal period. Youth reported on their own internalizing symptoms and parents reported on youths’ externalizing symptoms. Cortisol reactivity was assessed during the Trier social stress test. Analyses revealed no associations between cortisol reactivity and externalizing symptoms across puberty for PI youth. However, longitudinal bidirectional associations did emerge for internalizing symptoms such that increases in cortisol reactivity predicted increases in internalizing symptoms and increases in internalizing symptoms predicted increases in cortisol reactivity. Findings suggest that recalibrating to more normative levels of cortisol reactivity may not always be associated with adaptive outcomes for PI youth.

Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21–27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (β = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (β = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (β = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood.

The hypothalamic–pituitary–adrenal (HPA) axis is sensitive to early life stress, with enduring consequences for biological stress vulnerability and health (Gunnar & Talge, 2008). Low socioeconomic status (SES) is associated with dysregulation of the stress hormone cortisol in early childhood. However, a mechanistic understanding of this association is lacking. Multidimensional assessment of both SES and cortisol is needed to characterize the intricate relations between SES and cortisol function in early childhood. We assessed parent-reported family income, parent education, occupational prestige, neighborhood risk, food insecurity, and household chaos for 12-month-old infants (N = 90) and 3.5-year-old children (N = 91). Hair cortisol concentration (HCC) was obtained from parent and child, indexing chronic biological stress, and diurnal salivary cortisol was measured in the children. Controlling for parent HCC, parent education uniquely predicted infant and child HCC and, in addition, neighborhood risk uniquely predicted infant HCC. Household chaos predicted bedtime salivary cortisol concentration (SCC) for both infants and children, and infant daily cortisol output. Food insecurity was associated with flattened cortisol slope in 3.5-year-old children. Parental sensitivity did not mediate relations between SES and cortisol. Results highlight the utility of SES measures that index unpredictable and unsafe contexts, such as neighborhood risk, food insecurity, and household chaos.

There is emerging evidence that the development of problematic aggression in childhood may be associated with specific physiological stress response patterns, with both biological overactivation and underactivation implicated. This study tested associations between sex-specific patterns of stress responses across the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis and peer nominations of aggression among 271 kindergarten children (Mean age = 5.32 years; 52% Female; 44% White). Upon entry to kindergarten, children participated in a multidomain standardized stress paradigm. Changes in pre-ejection period (PEP) and salivary cortisol were assessed. On a separate day, children provided peer ratings of physical and relational aggression in a standardized interview. As expected, there was a significant three-way interaction between PEP, cortisol reactivity, and sex, but only for physical aggression. Among boys, cortisol reactivity was positively associated with physical aggression only for those with higher SNS reactivity. Findings suggest that for boys, asymmetrical and symmetrical HPA/SNS reactivity may be associated with lower and higher risk for peer-directed physical aggression, respectively. Understanding the complex associations between multisystem physiology, child sex and peer-directed aggression in early childhood may offer insight into individual differences underlying the emergence of behavioral dysregulation in early peer contexts.

To be ready to learn, children need to be focused, engaged, and able to bounce back from setbacks. However, many children come to school with heightened or diminished physiological arousal due to exposure to poverty-related risks. While stress physiology plays a role in explaining how adversity relates to processes that support students’ cognitive development, there is a lack of studies of physiological stress response in educational settings. This review integrates relevant studies and offers future directions for research on the role of stress physiology in the school adaptation of elementary school students, focusing on these important questions: (a) What are the links between physiological stress response and learning-related skills and behaviors, and do they vary as a function of proximal and distal experiences outside of school? (b) How are school experiences associated with students’ physiological stress response and related cognitive and behavioral adaptations? (c) How can we leverage measures of students’ physiological stress response in evaluations of school-based interventions to better support the school success of every student? We hope to stimulate a new wave of research that will advance the science of developmental stress physiology, as well as improve the application of these findings in educational policy and practice.

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.

Understanding individual differences in neural responses to stressful environments is an important avenue of research throughout development. These differences may be especially critical during adolescence, which is characterized by opportunities for healthy development and increased susceptibility to the development of psychopathology. While the neural correlates of the psychosocial stress response have been investigated in adults, these links have not been explored during development. Using a new task, the Minnesota Imaging Stress Test in Children (MISTiC), differences in activation are found in fusiform gyrus, superior frontal gyrus, insula, and anterior cingulate cortex when comparing a stressful math task to a nonstressful math task. The MISTiC task successfully elicits cortisol responses in a similar proportion of adolescents as in behavioral studies while collecting brain imaging data. Cortisol responders and nonresponders did not differ in their perceived stress level or behavioral performance during the task despite differences in neuroendocrine function. Future research will be able to leverage the MISTiC task for many purposes, including probing associations between individual differences in stress responses with environmental conditions, personality differences, and the development of psychopathology.

Few conditions epitomize severe and chronic stress to a greater extent than child maltreatment, which can derail development across multiple domains of functioning and throughout the life course. Furthermore, child maltreatment tends to co-occur with other adversities, such as poverty. Many individuals grow up under the stressful conditions of these adversities and exhibit developmental competence. The current study prospectively charted the developmental progression of economically disadvantaged maltreated and nonmaltreated children from childhood to emerging adulthood, and examined patterns of competence across multiple developmental domains of functioning central to the period of emerging adulthood. The study investigated childhood precursors to these patterns of adaptation and maladaptation, as well as the physiological cost of these patterns of adaptation (i.e., C-reactive protein; CRP). Latent class analysis revealed four distinct classes of functioning: multifaceted competence across domains (Multifaceted Competence); (multifaceted maladaptation across domains (Multi-Problem); (c) and two classes with mixed patterns of competence and maladaptation (Externalizing Problems and Work/School Impairment). Maltreated individuals were less likely than nonmaltreated individuals to demonstrate patterns of multifaceted competence and more likely to demonstrate aggregate maladaptation across domains. Additionally, Black men who demonstrated a pattern of multifaceted psychosocial competence also evidenced higher levels of low-grade inflammation (indexed by CRP), suggesting physiological distress was associated with adaptation in the context of stress among these individuals. Findings demonstrate the heterogenous patterns of functioning and diverse developmental outcomes that follow early adversity.