Improved characterization of quantitative traits and dimensionally distributed complex behaviors during toddlerhood may improve early identification of autism spectrum disorder and related neurodevelopmental disorders. Parents of 205 community-ascertained toddlers (age: mean = 20.2, SD = 2.6 months) completed the Repetitive Behavior Scales for Early Childhood (RBS-EC) and the Video-Referenced Rating of Reciprocal Social Behavior (vrRSB), with longitudinal follow-up of behavioral assessments and/or another round of parent-report questionnaires. Criterion validity was examined both concurrently and longitudinally using the Infant Toddler Social Emotional Assessment (ITSEA) as a criterion anchor. Reciprocal social behavior as measured by the vrRSB was significantly associated with social competence as measured by the ITSEA, longitudinally and concurrently. Reciprocal social behavior was not associated with the externalizing subscale on the ITSEA, providing evidence of discriminant validity. Higher-order repetitive behaviors (restricted interests; rituals and routines) as measured by RBS-EC subscales were associated with the dysregulation and internalizing subscales of the ITSEA, longitudinally and concurrently. All RBS-EC subscales (excepting repetitive motor) were associated concurrently and longitudinally with the dysregulation subscale of the ITSEA. We report evidence of criterion-oriented and discriminant validity for the constructs/domains captured by the RBS-EC and vrRSB. These instruments may be particularly useful in characterizing dimensional variability across the typical-to-atypical continuum.

This study used repeated measures data to identify developmental profiles of elevated risk for ADHD (i.e., six or more inattentive and/or hyperactive-impulsive symptoms), with an interest in the age at which ADHD risk first emerged. Risk factors that were measured across the first 3 years of life were used to predict profile membership. Participants included 1,173 children who were drawn from the Family Life Project, an ongoing longitudinal study of children's development in low-income, nonmetropolitan communities. Four heuristic profiles of ADHD risk were identified. Approximately two thirds of children never exhibited elevated risk for ADHD. The remaining children were characterized by early childhood onset and persistent risk (5%), early childhood limited risk (10%), and middle childhood onset risk (19%). Pregnancy and delivery complications and harsh-intrusive caregiving behaviors operated as general risk for all ADHD profiles. Parental history of ADHD was uniquely predictive of early onset and persistent ADHD risk, and low primary caregiver education was uniquely predictive of early childhood limited ADHD risk. Results are discussed with respect to how changes to the age of onset criterion for ADHD in DSM5 may affect etiological research and the need for developmental models of ADHD that inform ADHD symptom persistence and desistance.

There has been a longstanding debate about the link between callous-unemotional traits and fearlessness. However, biological evidence for a relationship in adolescents is lacking. Using two adolescent samples, we measured emotional reactivity and cardiac measures of sympathetic (pre-ejection period) and parasympathetic (respiratory sinus arrhythmia) reactivity during 3D TV and virtual reality fear induction. Study 1 included 62 community adolescents from a stratified sample. Study 2 included 60 adolescents from Emotional and Behavioral Difficulties schools. Results were consistent across both studies. Adolescents with high callous-unemotional traits showed coactivation of the sympathetic and parasympathetic nervous system. Consistent with these results, youths with callous-unemotional traits self-reported that they felt more in control after the fear induction. Thus, in both samples, youth with callous-unemotional traits displayed a physiological and emotional profile suggesting they maintained control during fear induction. Therefore, it is proposed here that a shift in thinking of youth with callous-unemotional traits as fearless to youth with callous-unemotional traits are better able to manage fearful situations, may be more appropriate.

Exposure to adverse events is prevalent among youths and robustly associated with risk for depression, particularly during adolescence. The Dimensional Model of Adversity and Psychopathology (DMAP) distinguishes between adverse events that expose youths to deprivation versus threat, positing unique mechanisms of risk (cognitive functioning deficits for deprivation, and altered fear and emotion learning for threat) that may require different approaches to intervention. We examined whether deprivation and threat were distinctly associated with behavioral measures of cognitive processes and autonomic nervous system function in relation to depression symptom severity in a community sample of early adolescents (n = 117; mean age 12.73 years; 54.7% male). Consistent with DMAP, associations between threat and depression symptoms, and between economic deprivation and depression symptoms, were distinctly moderated by physiological and cognitive functions, respectively, at baseline but not follow-up. Under conditions of greater cognitive inhibition, less exposure to deprivation was associated with lower symptom severity. Under conditions of blunted resting-state autonomic response (electrodermal activity and respiratory sinus arrhythmia), greater exposure to threat was associated with higher symptom severity. Our findings support the view that understanding risk for youth depression requires parsing adversity: examining distinct roles played by deprivation and threat, and the associated cognitive and biological processes.

Among children exposed to elevated maternal depression symptoms (MDS), recent studies have demonstrated reduced internalizing and externalizing problems for those who have attended formal childcare (i.e., center-based, family-based childcare). However, these studies did not consider whether childcare attendance is associated with benefits for the child only or also with reduced MDS. Using a four-wave longitudinal cross-lagged model, we evaluated whether formal childcare attendance was associated with MDS or child behavior problems and whether it moderated longitudinal associations between MDS and child behavior problems and between child behavior problems and MDS. The sample was drawn from a population-based cohort study and consisted of 908 biologically related mother–child dyads, followed from 5 months to 5 years. Attending formal childcare was not associated with MDS or child behavior problems but moderated the association between MDS at 3.5 years and child internalizing and externalizing problems at 5 years as well as between girls’ externalizing problems at 3.5 years and MDS at 5 years. No other moderation of formal childcare was found. Findings suggest that attending formal childcare reduces the risks of behavior problems in the context of MDS but also the risk of MDS in the context of girls’ externalizing problems.

Hypertensive disorders of pregnancy (HDP) may increase the risk of offspring depression in childhood. Low birth weight is also associated with increased risk of mental health problems, including depression. This study sought to investigate (a) whether there is an association between HDP and the risk of depression in childhood and (b) whether low birth weight mediates this association. The current study is based on the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective, population-based study that has followed a cohort of offspring since their mothers were pregnant (n = 6,739). Depression at the age of 7 years was diagnosed using parent reports via the Development and Well-Being Assessment (DAWBA). Log-binomial regression and mediation analyses were used. Children exposed to HDP were 2.3 times more likely to have a depression diagnosis compared with nonexposed children, adjusted Risk Ratio [RR], 2.31; 95% CI, [1.20, 4.47]. Low birth weight was a weak mediator of this association. Results were adjusted for confounding variables including antenatal depression and anxiety during pregnancy.This study suggests that fetal exposure to maternal hypertensive disorders of pregnancy increased the risk of childhood depression. The study adds to the evidence suggesting that the uterine environment is a critical determinant of neurodevelopmental and psychiatric outcomes.

Early life adversity (ELA) has been associated with inflammation and immunosenescence, as well as hyporeactivity of the HPA axis. Because the immune system and the HPA axis are tightly intertwined around the glucocorticoid receptor (GR), we examined peripheral GR functionality in the EpiPath cohort among participants who either had been exposed to ELA (separation from parents and/or institutionalization followed by adoption; n = 40) or had been reared by their biological parents (n = 72).

Expression of the strict GR target genes FKBP5 and GILZ as well as total and 1F and 1H GR transcripts were similar between groups. Furthermore, there were no differences in GR sensitivity, examined by the effects of dexamethasone on IL6 production in LPS-stimulated whole blood. Although we did not find differences in methylation at the GR 1F exon or promoter region, we identified a region of the GR 1H promoter (CpG 1-9) that showed lower methylation levels in ELA.

Our results suggest that peripheral GR signaling was unperturbed in our cohort and the observed immune phenotype does not appear to be secondary to an altered GR response to the perturbed HPA axis and glucocorticoid (GC) profile, although we are limited in our measures of GR activity and time points.

Research suggests that childhood adversity (CA) is associated with a wide range of repercussions, including an increased likelihood of interpersonal stress generation. This may be particularly true following interpersonal childhood adversity (ICA) and for youth with high hypothalamic-pituitary-adrenal (HPA) axis-related genetic risk. In the current study, we applied a multilocus genetic profile score (MGPS) approach to measuring HPA axis-related genetic variation and examined its interaction with ICA to predict interpersonal stress generation in a sample of adolescents aged 14–17 (N = 241, Caucasian subsample n = 192). MGPSs were computed using 10 single nucleotide polymorphisms from HPA axis-related genes (CRHR1, NRC31, NRC32, and FKBP5). ICA significantly predicted greater adolescent interpersonal dependent stress. Additionally, MGPS predicted a stronger association between ICA and interpersonal dependent (but not independent or noninterpersonal dependent) stress. No gene–environment interaction (G×E) effects were found for noninterpersonal CA and MGPS in predicting adolescent interpersonal dependent stress. Effects remained after controlling for current depressive symptoms and following stratification by race. Findings extend existing G×E research on stress generation to HPA axis-related genetic variation and demonstrate effects specific to the interpersonal domain.

Children reared in orphanages typically experience the lack of stable, reliable caregivers and are at increased risk for deficits in regulatory abilities including difficulties in inhibitory control, attention, and emotion regulation. Although adoption results in a radical shift in caregiving quality, there remains variation in postadoption parenting, yet little research has examined postadoption parenting that may promote recovery in children experiencing early life adversity in the form of institutional care. Participants included 93 postinstitutionalized children adopted between 15 and 36 months of age and 52 nonadopted same-aged peers. Parenting was assessed four times during the first 2 years postadoption (at 2, 8, 16, and 24 months postadoption) and children's regulation was assessed at age 5 (M age = 61.68 months) and during kindergarten (M age = 71.55 months). Multiple parenting dimensions including sensitivity/responsiveness, structure/limit setting, and consistency in routines were examined. Both parental sensitivity and structure moderated the effect of preadoption adversity on children's emotion regulation while greater consistency was associated with better inhibitory control and fewer attention problems. Results support the notion that postadoption parenting during toddlerhood and the early preschool years promotes better regulation skills following early adversity.

Early behaviors that differentiate later biomarkers for psychopathology can guide preventive efforts while also facilitating pathophysiological research. We tested whether error-related negativity (ERN) moderates the link between early behavior and later psychopathology in two early childhood phenotypes: behavioral inhibition and irritability. From ages 2 to 7 years, children (n = 291) were assessed longitudinally for behavioral inhibition (BI) and irritability. Behavioral inhibition was assessed via maternal report and behavioral responses to novelty. Childhood irritability was assessed using the Child Behavior Checklist. At age 12, an electroencephalogram (EEG) was recorded while children performed a flanker task to measure ERN, a neural indicator of error monitoring. Clinical assessments of anxiety and irritability were conducted using questionnaires (i.e., Screen for Child Anxiety Related Disorders and Affective Reactivity Index) and clinical interviews. Error monitoring interacted with early BI and early irritability to predict later psychopathology. Among children with high BI, an enhanced ERN predicted greater social anxiety at age 12. In contrast, children with high childhood irritability and blunted ERN predicted greater irritability at age 12. This converges with previous work and provides novel insight into the specificity of pathways associated with psychopathology.

This study examined whether the interaction between parenting and inhibitory control predicts hyperactivity-impulsivity and inattention in 195 children. Observation data of positive parenting were collected at 4 years, and mother reports of coercive parenting at 5 years, inhibitory control at 6 years, and hyperactivity-impulsivity/inattention at 7 years were obtained. The common and unique variance of hyperactivity-impulsivity and inattention symptoms were examined as outcomes using a bifactor model. Results indicated that positive parenting practices predicted lower levels of hyperactivity-impulsivity/inattention behaviors at age 7 only when children's inhibitory control was high. These results support the vantage sensitivity model, which posits that some individuals show an increased sensitivity to positive experiences exclusively, and support the appropriateness of a targeted prevention approach in early childhood.

While child self-regulation is shaped by the environment (e.g., the parents’ caregiving behaviors), children also play an active role in influencing the care they receive, indicating that children's individual differences should be integrated in models relating early care to children's development. We assessed 409 children's observed temperamental behavioral inhibition (BI), effortful control (EC), and the primary caregiver's parenting at child ages 3 and 5. Parents reported on child behavior problems at child ages 3, 5, and 8. Mediation analyses were conducted to examine relations between child temperament and parenting in predicting child problems. BI at age 3 was positively associated with structured parenting at age 5, which was negatively related to child internalizing and attention-academic problems at age 8. In contrast, parenting at child age 3 did not predict child BI or EC at age 5, nor did age 3 EC predict parenting at age 5. Findings indicate that child behavior may shape the development of caregiving and, in turn, long-term child adjustment, suggesting that studies of caregiving and child outcomes should consider the role of child temperament toward developing more informative models of child–environment interplay.

Adverse effects of early exposure to parental mood disturbance on child adjustment have been documented for both mothers and fathers, but are rarely examined in tandem. Other under-researched questions include effects of changes over time in parental well-being, similarities and contrasts between effects of parental mood disturbance on children's internalizing versus externalizing problems, and potential mediating effects of couple relationship quality. The current study involved 438 couples who reported symptoms of depression and anxiety at each of four time points (i.e., last trimester of pregnancy and 4, 14, and 24 months postbirth). Mothers and fathers also rated their couple relationship quality and their child's socioemotional adjustment at 14 months, as well as internalizing and externalizing problems at 24 months. Latent growth models indicated direct effects of (a) maternal prenatal well-being on externalizing problems at 24 months, and (b) paternal prenatal well-being on socioemotional problems at 14 months. Internalizing symptoms at 24 months showed only indirect associations with parental well-being, with couple relationship quality playing a mediating role. Our findings highlight the importance of prenatal exposure to parental mood disturbance and demonstrate that, even in a low-risk sample, poor couple relationship quality explains the intergenerational stability of internalizing problems.

Child maltreatment is a robust risk factor for suicidal ideation and behaviors during adolescence. Elevations in internalizing and externalizing symptomology have been identified as two distinct developmental pathways linking child maltreatment and adolescent risk for suicide. However, recent research suggests that the co-occurrence of internalizing and externalizing symptomology may form a distinct etiological pathway for adolescent risk behaviors. Using the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN) sample (N = 1,314), the present study employed a person-centered approach to identify patterns of concurrent change in internalizing and externalizing psychopathology over five time points from early childhood to adolescence in relation to previous experiences of child maltreatment and subsequent suicidal ideation and behaviors. Results indicated four distinct bivariate externalizing and internalizing growth trajectories. Group membership in a heightened comorbid internalizing and externalizing symptom trajectory mediated the association between childhood abuse and adolescent suicidal ideation and suicidal behaviors. These findings suggest that the concurrent development of externalizing and internalizing symptoms in childhood and adolescence may constitute a unique developmental trajectory that confers risk for suicide-related outcomes.

Individual differences in social-emotional functioning emerge early and have long-term implications for developmental adaptation and competency. Research is needed that specifies multiple early risk factors and outcomes simultaneously to demonstrate specificity. Using multigroup longitudinal path analysis in a sample of typically developing children (N = 541), we examined child temperament dimensions (surgency, negative affectivity, and regulation/effortful control) and maternal anxiety in infancy and age 2 as predictors of child externalizing, internalizing, dysregulation, and competence behaviors at age 3. Four primary patterns emerged. First, there was stability in temperament dimensions and maternal anxiety from infancy to age 3. Second, negative affectivity was implicated in internalizing problems and surgency in externalizing problems. Third, effortful control at age 2 was a potent mediator of maternal anxiety in infancy on age 3 outcomes. Fourth, there was suggestive evidence for transactional effects between maternal anxiety and child effortful control. Most pathways operated similarly for boys and girls, with some differences, particularly for surgency. These findings expand our understanding of the roles of specific temperamental domains and postnatal maternal anxiety in a range of social-emotional outcomes in the preschool period, and have implications for efforts to enhance the development of young children's social-emotional functioning and reduce risk for later psychopathology.

Depression is associated with a multiplicity of adverse outcomes in adolescence, including peer victimization and low self-esteem. Depressive symptoms, peer victimization, and self-esteem are linked in cross-sectional studies, but no longitudinal study has been conducted assessing their developmental pathways in one integrated model across adolescence. We explored their temporal sequencing in a normative sample of 612 Canadian adolescents (54% girls) assessed annually over 5 years (Grade 7 to Grade 11). Potential confounders such as biological sex, ethnicity/race, and parent income and education were statistically controlled. We found evidence for the vulnerability model (self-esteem predicting depression) and the symptoms-driven model (depression predicting peer victimization). Our findings also supported the integration of these pathways into a self-perception driven model characterized by the indirect effect of self-esteem on later peer victimization via depressive symptoms. Specifically, poor self-esteem initiated a developmental cascade that led to poor mood and poor peer relations. These results highlight the importance of helping youth form a healthy identity that promotes positive mental health and peer relations, and the need to intervene with depressed, victimized, and at-risk adolescents to instill positive self-regard. Our results also emphasize the central role that self-perceptions play in the onset and maintenance of poor outcomes.

Cognitive strategies that adolescents use to cope with negative emotions might show distinct profiles of cognitive emotion regulation strategies, which could be differentially associated with depressive symptoms. In total, 411 Dutch adolescents who had experienced at least one stressful life event that required some coping strategy participated in this study, including 334 nonclinical and 77 clinically depressed adolescents (12–21 years). A person-centered approach with Latent Profile Analysis was used to identify underlying profiles of cognitive emotion regulation based on the adolescents’ reports of their use of cognitive emotion regulation strategies when they were confronted with stressful life events. Nine different strategies, five adaptive and four maladaptive, were used as indicators. Four profiles with distinct features were found in the nonclinical sample, as well as in the combined sample of nonclinical and clinically depressed adolescents: Low Regulators, High Regulators, Maladaptive Regulators, and Adaptive Regulators. In both samples, the High Regulators profile was most commonly used, followed by the Adaptive, Maladaptive, and Low Regulators profile. Maladaptive Regulators endorsed higher levels of depressive symptoms relative to Low, High, and Adaptive Regulators. The findings underscore the utility of using a person-centered approach in order to identify patterns of cognitive emotion regulation deficits in psychopathology.

Sleep disturbance is a symptom of and a well-known risk factor for depression. Further, atypical functioning of the HPA axis has been linked to the pathogenesis of depression. The purpose of this study was to examine the role of adolescent HPA axis functioning in the link between adolescent sleep problems and later depressive symptoms. Methods: A sample of 157 17–18 year old adolescents (61.8% female) completed the Pittsburgh Sleep Quality Inventory (PSQI) and provided salivary cortisol samples throughout the day for three consecutive days. Two years later, adolescents reported their depressive symptoms via the Center for Epidemiological Studies Depression Scale (CES-D). Results: Individuals (age 17–18) with greater sleep disturbance reported greater depressive symptoms two years later (age 19–20). This association occurred through the indirect effect of sleep disturbance on the cortisol awakening response (CAR) (indirect effect = 0.14, 95%CI [.02 -.39]). Conclusions: One pathway through which sleep problems may lead to depressive symptoms is by up-regulating components of the body’s physiological stress response system that can be measured through the cortisol awakening response. Behavioral interventions that target sleep disturbance in adolescents may mitigate this neurobiological pathway to depression during this high-risk developmental phase.

Impaired cognitive functioning constitutes an important symptom of major depressive disorder (MDD), potentially associated with elevated cortisol levels. Adverse childhood experiences (ACE) enhance the risk for MDD and can contribute to disturbances in the stress systems, including cortisol and cognitive functions. In healthy participants, cortisol administration as well as acute stress can affect cognitive performance. In the current study, we tested cognitive performance in MDD patients with (N = 32) and without (N = 52) ACE and healthy participants with (N = 22) and without (N = 37) ACE after psychosocial stress induction (Trier Social Stress Test, TSST) and a control condition (Placebo-TSST). MDD predicted lower performance in verbal learning and both selective and sustained attention, while ACE predicted lower performance in psychomotoric speed and working memory. There were no interaction effects of MDD and ACE. After stress, MDD patients were more likely to show lower performance in working memory as well as in selective and sustained attention compared with participants without MDD. Individuals with ACE were more likely to show lower performance in verbal memory after stress compared with individuals without ACE. Our results indicate negative effects of MDD and ACE on distinct cognitive domains. Furthermore, MDD and/or ACE seem to enhance susceptibility for stress-related cognitive impairments.

This is the first review to rigorously examine the mediating role of cognitive factors in the relationship between childhood trauma and subsequent adult psychopathology, and highlight areas for future research. A database search (Child Development & Adolescent Studies, ERIC, Global Health, PsycARTICLES, and PsycINFO) was conducted to identify empirical studies on cognitive factors, explaining the relationship between different types of adverse childhood experiences and adult psychopathology across clinical and nonclinical populations. A narrative synthesis and appraisal of the methodological quality of the studies was conducted. Ninety-eight mediation studies were identified, comprising 4,137 clinical and 28,228 nonclinical participants. Despite great variation in methodological quality of the studies, our narrative synthesis suggests that cognitive factors mediate the relationship between early trauma and later psychopathology. This finding is consistent across different measures of traumatic experiences, psychopathology, and cognitive mediators. Cognitive mediators represent potentially valuable intervention targets for (non)clinical patients who have experienced childhood adversity. Future studies are needed to (a) establish longitudinal causal connections, and (b) assess the effect of interventions that specifically target cognitive change in patients with different levels and types of pathology.