Identifying early risk factors for the development of social anxiety symptoms has important translational implications. Accurately identifying which children are at the highest risk is of critical importance, especially if we can identify risk early in development. We examined continued risk for social anxiety symptoms at the transition to adolescence in a community sample of children (n = 112) that had been observed for high fearfulness at age 2 and tracked for social anxiety symptoms from preschool through age 6. In our previous studies, we found that a pattern of dysregulated fear (DF), characterized by high fear in low threat contexts, predicted social anxiety symptoms at ages 3, 4, 5, and 6 years across two samples. In the current study, we re-evaluated these children at 11–13 years of age by using parent and child reports of social anxiety symptoms, parental monitoring, and peer relationship quality. The scores for DF uniquely predicted adolescents’ social anxiety symptoms beyond the prediction that was made by more proximal measures of behavioral (e.g., kindergarten social withdrawal) and concurrent environmental risk factors (e.g., parental monitoring, peer relationships). Implications for early detection, prevention, and intervention are discussed.

Despite considerable efforts to understand the processes that underlie the development of externalizing behavior problems, it is still unclear why externalizing problems remain chronically high for some children, emerge early and cease by late childhood for others, and arise in adolescence in some cases. The purpose of this study was to examine how a wide range of child and family risk factors are linked to trajectories of externalizing behavior and how these relationships vary from infancy to middle adolescence. We used data from the community-based Norwegian Tracking Opportunities and Problems (TOPP) study sample (n = 921). A Cholesky factorization model was specified to separate stable and emerging risk doses across four developmental periods (infancy, early and middle childhood, and middle adolescence). Children in the High Stable class were characterized by substantially elevated risk levels in multiple domains throughout the study period. Children in the High Childhood Limited class had very high levels of temperamental emotionality, internalizing symptoms, and maternal mental distress, suggesting a substantial intrinsic emotional basis for their externalizing problems. Intrinsic factors seemed less salient for the Adolescent Onset class. These findings emphasize the need for a dynamic perspective on risk factors and support the importance of prevention and intervention efforts across multiple domains from early childhood and throughout adolescence.

The current study aimed to understand the mediating and/or moderating role of prenatal hypothalamic–pituitary–adrenal (HPA) axis function in the association between maternal adverse childhood experiences (ACEs) and child internalizing and externalizing behavior problems at age 4. The influence of timing and child sex were also explored. Participants were 248 mother–child dyads enrolled in a prospective longitudinal cohort study (the Alberta Pregnancy Outcomes and Nutrition Study). Maternal ACEs were retrospectively assessed while maternal self-reported depression and diurnal salivary cortisol were assessed prospectively at 6–26 weeks gestation (T1) and 27–37 weeks gestation (T2). Maternal report of child internalizing and externalizing problems was assessed at 4 years (T3). Results revealed that there was a negative indirect association between maternal ACEs and child internalizing behavior via a higher maternal cortisol awakening response (CAR). Maternal diurnal cortisol slope moderated the association between maternal ACEs and child behavior problems. Some of these effects were dependent on child sex, such that higher ACEs and a flatter diurnal slope at T1 was associated with more internalizing behavior in female children and more externalizing behavior in male children. There were timing effects such that the mediating and moderating effects were strongest at T1.

Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.

The current study used daily assessments of sleep to examine stability and change in sleep chronotype in adolescents and their parents. The study assessed adolescent sleep chronotype according to age, gender, and parent chronotype, and evaluated its associations with emotional and behavioral problems in youth. Participants included of 417 Mexican American adolescents (Mage = 16.0 years, Range = 13.9–20.0) and 403 caregivers, who reported bed and wake times daily for 2 consecutive weeks at two time points spaced 1 year apart. In addition, adolescents completed established self-report questionnaires of emotional and behavioral problems. Chronotype was computed as the midsleep point from bed to wake time on free days, correcting for sleep debt accumulated across scheduled days. Multilevel modeling showed a curvilinear association between adolescent age and chronotype, with a peak eveningness observed between ages 16 to 17. Adolescent and parent chronotypes were contemporaneously correlated, but each was only moderately stable over the 1-year period. Later adolescent chronotype was contemporaneously associated with more substance use in all adolescents. Individual development and the family context shape sleep chronotype in adolescents and parents. Sleep chronotype is implicated in adolescent behavioral health.

Although children with incarcerated parents exhibit more behavior problems, health concerns, and academic difficulties than their peers, few interventions or resources are available to support affected children. This randomized, controlled, multisite efficacy trial evaluated Sesame Street’s "Little Children, Big Challenges: Incarceration" initiative with children aged 3 to 8 years with a jailed father. Seventy-one diverse children and their caregivers were randomized to an educational outreach group (n = 32) or wait list control group (n = 39). Researchers observed children during jail visits and interviewed caregivers by phone 2 and 4 weeks later. The effects of the intervention on children’s behavior and emotions occurring during a jail visit depended on what children had been told about the father’s incarceration. Children who were told honest, developmentally appropriate explanations showed less negative affect at entry, an increase in negative affect when the intervention was administered, and a decrease in negative affect during the visit. Intervention group children who were told distortions, nothing, or explanations that were not developmentally appropriate showed more negative affect initially, and their negative affect remained relatively stable during their time in the jail. In addition, children who were told the simple, honest truth about the parent’s incarceration (a recommendation in the educational materials) exhibited more positive affect during the visit, with a medium effect size. Caregivers in the educational outreach group reported more positive change in how they talked to children about the incarceration over time compared to the control group.

Twenty-six percent of children experience a traumatic event by the age of 4. Negative events during childhood have deleterious correlates later in life, including antisocial behavior. However, the mechanisms that play into this relation are unclear. We explored deficits in neurocognitive functioning, specifically problems in passive avoidance, a construct with elements of inhibitory control and learning as a potential acquired mediator for the pathway between cumulative early childhood adversity from birth to age 7 and later antisocial behavior through age 18, using prospective longitudinal data from 585 participants. Path analyses showed that cumulative early childhood adversity predicted impaired passive avoidance during adolescence and increased antisocial behavior during late adolescence. Furthermore, poor neurocognition, namely, passive avoidance, predicted later antisocial behavior and significantly mediated the relation between cumulative early childhood adversity and later antisocial behavior. This research has implications for understanding the development of later antisocial behavior and points to a potential target for neurocognitive intervention within the pathway from cumulative early childhood adversity to later antisocial behavior.

This study used a person-centered approach to identify subgroups of adolescents who are at risk for depression and suicidal ideation. Latent class analysis was first applied to 1,290 adolescents from a Canadian cohort study in order to identify latent vulnerability subtypes based on 18 psychosocial vulnerability factors. Logistic regression analyses were conducted to study the associations between class membership and depressive symptoms and suicidal ideation 2 years later. The moderating role of sex in the associations between latent classes and depressive symptoms was explored. Five latent classes were identified: Low Vulnerability (42%), Substance Use Only (13%), Moderate Vulnerability (28%), Conduct Problems (8%) and High Vulnerability (9%). Compared with the Low Vulnerability class, the probabilities of presenting depressive symptoms were higher for the Substance Use Only class, OR = 1.93, 95% CI [1.21, 3.06], the Moderate Vulnerability class, OR = 2.96, 95% CI [2.09, 4.20], the Conduct Problems class, OR = 3.03, 95% CI [1.84, 4.98], and the High Vulnerability class, OR = 5.4, 95% CI [3.42, 8.53]. Furthermore, interaction effects with sex were identified in relation to depressive symptoms only. The probability of presenting suicidal ideation was higher only for the High Vulnerability class, OR = 4.51, 95% CI [2.41, 8.43]. This study highlights the importance of a person-centered perspective that considers both vulnerability subtypes and sex because these associations are complex rather than linear or additive.

Social anhedonia is well established as a transdiagnostic factor, but little is known about its development. This study examined whether temperament and parenting in early childhood predict social anhedonia in early adolescence. We also explored whether the relationships between early predictors and social anhedonia are moderated by a child's sex. A community sample of children participated in laboratory observations of temperament and parenting practices at age 3 (n = 275). The participants returned at age 12 and completed the Anticipatory and Consummatory Interpersonal Pleasure Scale–Child Version (ACIPS-C). Our results indicated that, at age 3, lower observed sociability predicted higher levels of social anhedonia at age 12. These associations were moderated by child sex, such that males with diminished sociability reported greater social anhedonia. These findings indicate that predictors of early adolescent social anhedonia are evident as early as 3 years of age. However, these effects were evident only for males, suggesting that the pathways to social anhedonia in early adolescence differ as a function of sex.