Genetic variation in the oxytocin receptor gene (OXTR) is associated with several psychiatric conditions characterized by deficits in executive functioning (EF). A specific OXTR variant, rs2254298, has previously been associated with brain functioning in regions implicated in EF. Moreover, birth weight variation across the entire range is associated with individual differences in cortical structure and function that underlie EF. This is the first study to examine the main and interactive effect between rs2254298 and birth weight on EF in children. The sample consisted of 310 children from an ongoing longitudinal study. EF was measured at age 4.5 using observational tasks indexing working memory, cognitive flexibility, and inhibitory control. A family-based design that controlled for population admixture, stratification, and nongenomic confounds was employed. A significant genetic association between rs2254298 and EF was observed, with more copies of the major allele (G) associated with higher EF. There was also a significant interaction between rs2254298 and birth weight, such that more copies of the major allele in combination with higher birth weight predicted better EF. Findings suggest that OXTR may be associated with discrete neurocognitive abilities in childhood, and these effects may be modulated by intrauterine conditions related to fetal growth and development.

Existing research has suggested children of caregivers with histories of exposure to trauma are at heightened risk for victimization, but few studies have explored potential mechanisms that explain this intergenerational transmission of risk. With data from peri-urban households in Lima, Peru (N = 402), this study analyzes parenting behaviors in the relation between caregivers’ trauma history and child victimization for children aged 4–17. Results indicated caregivers’ trauma history and negative parenting behaviors related to child victimization, and negative parenting behaviors mediated this relation. Positive parenting behaviors did not have significant direct effects and were not mediators of risk transmission. Parenting behaviors did not moderate the relation between caregiver and child victimization, suggesting parenting behaviors may not buffer or exacerbate intergenerational transmission. Post-hoc analyses revealed family type (e.g., single, cohabitating/married) exerted significant direct and moderating effects on child risk, interacting with positive parenting. Families with married/cohabitating caregivers reported overall lower levels of child victimization; however, the relation between positive parenting and victimization was slightly stronger for children in single-parent families. Results highlight potential pathways of the intergenerational cycle of victimization and suggest high-risk families in Peru may benefit from parenting supports, especially pertaining to remediation of negative parenting behaviors.

American Indians and Alaska Natives suffer from disproportionately high rates of chronic mental and physical health conditions. These health inequities are linked to colonization and its downstream consequences. Most of the American Indian and Alaska Native health inequities research uses a deficit framework, failing to acknowledge the resilience of American Indian and Alaska Native people despite challenging historical and current contexts. This scoping review is based on a conceptual model which acknowledges the context of colonization and its consequences (psychological and health risk factors). However, rather than focusing on health risk, we focus on protective factors across three identified domains (social, psychological, and cultural/spiritual), and summarize documented relationships between these resilience factors and health outcomes. Based on the scoping review of the literature, we note gaps in extant knowledge and recommend future directions. The findings summarized here can be used to inform and shape future interventions which aim to optimize health and well-being in American Indian and Alaska Native peoples.

In this study, we sought to combine two lines of research to better understand risk for the intergenerational transmission of depression. The first focuses on the role of maternal criticism as a potential mechanism of risk for depression in youth while the second builds from interpersonal and stress generation models regarding the potential impact of youth depression on future escalations in maternal criticism. Specifically, we examined the role of maternal criticism within a transactional mediation model using data from a multi-wave study. Participants were 251 mother–offspring pairs consisting of mothers with (n = 129) and without (n = 122) a history of major depressive disorder (MDD) during their child’s lifetime who completed assessments every 6 months for 2 years. We found support for the hypothesized transactional mediational model in which maternal expressed emotion-criticism (EE-Crit) mediated the link between maternal history of MDD and residual change in youth’s depressive symptoms over the previous 6 months and, reciprocally, youth depressive symptoms mediated the relation between maternal MDD history and residual change in EE-Crit 6 months later. These results indicate that maternal criticism and offspring depressive symptoms may contribute to a vicious cycle of depression risk, which should be considered for interventions targeted toward youth at risk of developing MDD.

Parenting and child impulsivity are consistent predictors of children’s externalizing symptoms; however, the role of the range of parenting (i.e., variation in parenting across contexts), and its interactions with child impulsivity, are poorly understood. We examined whether characteristic parenting practices and parenting range predicted the course of externalizing symptoms in 409 children (Mage = 3.43 years at baseline, 208 girls) across ages 3, 5, 8, and 11. We assessed parent positive affectivity (PPA), hostility, and parenting structure at child age 3 using three behavioral tasks that varied in context, examining range by modeling a latent difference score for each parenting dimension. Greater PPA range, mean structure, and parenting structure range all predicted fewer symptoms at age 3 for children with higher impulsivity. Lower mean hostility predicted fewer symptoms at age 3 for children with lower impulsivity. Greater PPA, and smaller PPA range, predicted a decrease in symptoms for children higher in impulsivity. Lower hostility range predicted a decrease in symptoms for children with lower impulsivity but predicted maintaining symptoms for children with higher impulsivity. Results demonstrate the differential roles average parenting practices and parenting range play in the development of child externalizing psychopathology, especially in the context of child impulsivity.

The relationship between attachment and posttraumatic stress symptoms (PTSS) has been researched extensively within adult samples, with findings consistently demonstrating a relationship between insecure attachment and increased PTSS, and between secure attachment and decreased PTSS. To a lesser extent, such relationships have also been explored within child and adolescent samples. The evidence to date is equivocal and there have been no attempts to synthesize studies. This meta-analysis aimed to provide a quantitative synthesis of studies reporting a relationship between attachment orientation (on both developmental and social psychological measures) and PTSS within children and adolescents. A random effects model was used to pool 30 studies (N = 10,431) reporting exposure to a range of traumatic events including maltreatment and war trauma. Results demonstrate a negative correlation between secure attachment and PTSS (r = −.16) and a positive correlation between insecure attachment (r = .20), avoidant attachment (r = .20), anxious attachment (r = .32), and disorganized attachment (r = .17) and PTSS. These findings indicate a small but significant relationship between attachment and PTSS in children and adolescents. Exposure to maltreatment did not moderate the relationship between secure attachment and PTSS, though strengthened the relationship between insecure attachment and PTSS.

Refugee children are often exposed to substantial trauma, placing them at increased risk for mental illness. However, this risk can be mitigated by a capacity for resilience, conferred from multiple ecological systems (e.g., family, community), including at an individual biological level. We examined the ability of hair cortisol concentrations and polygenic scores for mental health to predict risk and resilience in a sample of Syrian refugee children (n = 1359). Children were categorized as either at-risk or resilient depending on clinical thresholds for posttraumatic stress disorder, depression, and externalizing behavior problems. Logistic regression was used to examine main and interacting effects while controlling for covariates. Elevated hair cortisol concentrations were significantly associated with reduced resilience (odds ratio (OR)=0.58, 95%CI [0.40, 0.83]) while controlling for levels of war exposure. Polygenic scores for depression, self-harm, and neuroticism were not found to have any significant main effects. However, a significant interaction emerged between hair cortisol and polygenic scores for depression (OR=0.04, 95%CI [0.003 0.47]), suggesting that children predisposed to depression were more at risk for mental health problems when hair cortisol concentrations were high. Our results suggest that biomarkers (separately and in combination) might support early identification of refugee children at risk for mental health problems.

How we are influenced by our environment is a fundamental question in developmental science. Theories and empirical research have claimed that some individuals are susceptible to environmental influences and others are much less susceptible. The present study addressed four questions: (1) Is environmental susceptibility a continuous or categorical construct? (2) Is environmental susceptibility unidimensional (i.e., domain general) or multidimensional (i.e., domain specific)? (3) Are there genetic contributions to individual differences in environmental susceptibility? (4) What are the temperamental characteristics of different environmental susceptibility patterns? We used child- and mother-report data from a sample of 11-year-old twins (N = 1,507) and applied a novel data-driven approach to assess an environmental susceptibility space, based on simultaneous associations between multiple environmental exposures (18 measures relating to parenting, parent, peer, and twin relationships) and developmental outcomes (10 measures relating to empathy, prosocial behavior, aggression, and self-esteem). The results suggest that the environmental susceptibility space we assessed is better conceptualized as continuous and multidimensional. Different children showed susceptibility to different contexts and variation in domain-general versus domain-specific patterns. A comparison of distances between monozygotic and dizygotic twins within the space demonstrated genetic contributions. Finally, susceptibility patterns could not be differentiated based on a specific temperament trait, but rather related to temperament profiles.

Unraveling the neurobiological foundations of childhood maltreatment is important due to the persistent associations with adverse mental health outcomes. However, the mechanisms through which abuse and neglect disturb resting-state network connectivity remain elusive. Moreover, it remains unclear if positive parenting can mitigate the negative impact of childhood maltreatment on network connectivity. We analyzed a cohort of 194 adolescents and young adults (aged 14–25, 47.42% female) from the Neuroscience in Psychiatry Network (NSPN) to investigate the impact of childhood abuse and neglect on resting-state network connectivity. Specifically, we examined the SAN, DMN, FPN, DAN, and VAN over time. We also explored the moderating role of positive parenting. The results showed that childhood abuse was linked to stronger connectivity within the SAN and VAN, as well as between the DMN-DAN, DMN-VAN, DMN-SAN, SAN-DAN, FPN-DAN, SAN-VAN, and VAN-DAN networks about 18 months later. Positive parenting during childhood buffered the negative impact of childhood abuse on network connectivity. To our knowledge, this is the first study to demonstrate the protective effect of positive parenting on network connectivity following childhood abuse. These findings not only highlight the importance of positive parenting but also lead to a better understanding of the neurobiology and resilience mechanisms of childhood maltreatment.

The current study evaluated risk factors in adolescence on problem drinking and emotional distress in late adolescence and emerging adulthood, and meeting criteria for diagnosed disorders in adulthood. The study included 501 parents and their adolescent who participated from middle adolescence to adulthood. Risk factors in middle adolescence (age 18) included parent alcohol use, adolescent alcohol use, and parent and adolescent emotional distress. In late adolescence (age 18), binge drinking and emotional distress were assessed, and in emerging adulthood (age 25), alcohol problems and emotional distress were examined. Meeting criteria for substance use, behavioral, affective, or anxiety disorders were examined between the ages of 26 and 31. Results showed parent alcohol use predicted substance use disorder through late adolescent binge drinking and emerging adulthood alcohol problems. Behavioral disorders were indirectly predicted by adolescent and emerging adult emotional distress. Affective disorders were indirectly predicted by parent emotional distress through adolescent emotional distress. Finally, anxiety disorders were predicted by parent alcohol use via adolescent drinking; parent emotional distress via adolescent emotional distress, and through adolescent alcohol use and emotional distress. Results provided support for the intergenerational transmission of problem drinking and emotional distress on meeting criteria for diagnosed psychiatric disorders in adulthood.

In explaining the “parenting – callous-unemotional traits – antisocial behavior” axis, recent theoretical advances postulate a critical role for affiliative reward. Existing empirical studies focus on early childhood and the appetitive phase of the reward process (i.e. affiliation-seeking behavior) rather than the consummatory phase (i.e. affective rewards). This study focuses on experienced affiliative reward (i.e. companionship, intimacy, affection, and worth) in relation to parents and best friends in early adolescence. The Alabama Parenting Questionnaire, Network of Relationships Inventory, Inventory of Callous and Unemotional Traits, and Youth Self Report were completed by 1132 12-year-olds and analyzed via structural equation models. In this cross-sectional sample, parent-related affiliative reward mediated the path from perceived parenting practices to callousness and further to aggression and rule-breaking. Parent-related affiliative reward was also related to uncaring traits and further to aggression and rule-breaking. In contrast, friend-related affiliative reward was not a mediator in this theoretical causal chain and largely not related to perceived parenting practices or CU traits. Low parent-related experienced affiliative reward is a mechanism through which corporal punishment, poor monitoring, and low involvement translate into callousness, and therefore to aggression and rule-breaking. Friend-related affiliative reward does not yet play a role in early adolescence.

Greater childhood adversity predicts a higher likelihood of later self-injurious thoughts and behaviors (SITB). There is little research focused on whether the timing of childhood adversity predicts SITB. The current research examined whether the timing of childhood adversity predicted parent- and youth-reported SITB at age 12 and 16 years in the Longitudinal Studies of Child Abuse and Neglect (LONGSCAN) cohort (n = 970). We found that greater adversity at age 11–12 years consistently predicted SITB at age 12 years, while greater adversity at age 13–14 years consistently predicted SITB at age 16 years. These findings suggest there may be sensitive periods during which adversity may be more likely to lead to adolescent SITB, which can inform prevention and treatment.

Youth with different developmental disorders might experience challenges when dealing with facial emotion recognition (FER). By comparing FER and related emotional and cognitive factors across developmental disorders, researchers can gain a better understanding of challenges and strengths associated with each condition. The aim of the present study was to investigate how social anxiety and executive functioning might underlie FER in youth with and without autism spectrum disorders (ASD) and specific learning disorders (SLD). The study involved 263 children and adolescents between 8 and 16 years old divided into three groups matched for age, sex, and IQ: 60 (52 M) with ASD without intellectual disability, 63 (44 M) with SLD, and 140 (105 M) non-diagnosed. Participants completed an FER test, three executive functions’ tasks (inhibition, updating, and set-shifting), and parents filled in a questionnaire reporting their children’s social anxiety. Our results suggest that better FER was consistent with higher social anxiety and better updating skills in ASD, while with lower social anxiety in SLD. Clinical practice should focus on coping strategies in autistic youth who could feel anxiety when facing social cues, and on self-efficacy and social worries in SLD. Executive functioning should also be addressed to support social learning in autism.

Mid-adolescence is a critical time for the development of stress-related disorders and it is associated with significant social vulnerability. However, little is known about normative neural processes accompanying psychosocial stress at this time. Previous research found that emotion regulation strategies critically influence the relationship between stress and the development of psychiatric symptoms during adolescence. Using functional magnetic resonance imaging (fMRI), we examined neural responses to acute stress and analyzed whether the tendency to use adaptive or maladaptive emotion regulation strategies is related to neural and autonomic stress responses. Results show large linear activation increases from low to medium to high stress levels mainly in medial prefrontal, insulae and temporal areas. Caudate and subgenual anterior cingulate cortex, neural areas related to reward and affective valuations, showed linearly decreasing activation. In line with our hypothesis, the current adolescent neural stress profile resembled social rejection and was characterized by pronounced activation in insula, angular and temporal cortices. Moreover, results point to an intriguing role of the anterior temporal gyrus. Stress-related activity in the anterior temporal gyrus was positively related to maladaptive regulation strategies and stress-induced autonomic activity. Maladaptive coping might increase the social threat and reappraisal load of a stressor, relating to higher stress sensitivity of anterior temporal cortices.

Children with callous–unemotional (CU) traits are at risk for severe conduct problems. While CU traits are moderately heritable, parenting also predicts risk. However, few studies have investigated whether parenting factors (e.g., acceptance, conflict, parental psychopathology) moderate the etiology of CU traits, while accounting for gene–environment correlations. To address this knowledge gap, we used data from 772 twin pairs from the Adolescent Brain and Cognitive Development Study to test bivariate models that explored overlapping etiological influences on CU traits and child reports of their parenting environment. We also used gene-by-environment interaction models to test whether parenting moderated genetic versus environmental influences. There were no overlapping etiological influences on CU traits and parental acceptance, but modest genetic and non-shared environmental overlap between CU traits and family conflict. Parental acceptance and psychopathology moderated non-shared environmental influences, with stronger non-shared environmental influences on CU traits among children who experienced lower parental acceptance and greater parental psychopathology. Family conflict only moderated environmental influences when models did not covary for conduct problems. Parental acceptance and parental psychopathology may be specific environmental protective and risk factors for CU traits, whereas family conflict may represent a general environmental risk factor for both CU traits and conduct problems.

Although child maltreatment is associated with short- and long-term maladaptive outcomes, some children are still able to display resilience. Currently, there is a limited understanding of how children’s resilience changes over time after experiencing maltreatment, especially for young children. Therefore, the current study used a longitudinal, multidimensional approach to examine trajectories of resilience among very young children involved in child protective services and determine whether placement setting and caregiving behaviors are associated with resilience trajectories. This study used data from National Survey of Child and Adolescent Well-Being I and conducted repeated measures latent class analysis, focusing on children under 2 years old at baseline (n = 1,699). Results suggested that there were three trajectories of resilience: increasing resilience, decreasing resilience, and stable, low resilience. Caregiver cognitive stimulation was related to increasing trajectories of resilience compared to both decreasing and stable, low resilience. These findings illustrate the importance of caregiving behaviors for promoting resilience among a particularly vulnerable population.

Aggressive reactions to peer victimization may be tempered by hormone levels. Grounded on the dualhormone hypothesis (DHH), which proposes that testosterone (T) is associated with aggressive behavior only when cortisol (C) is low, this study assessed whether the combination of T and C moderated adolescents’ aggressive responses to peer victimization. The study involved 577 adolescents (50.4% girls, aged 12–17 years), who completed measures of online and offline victimization and perpetration of aggressive behavior in three waves over the course of one year. Moreover, they provided salivary samples to measure T and C levels. Multilevel analyses showed a three-way interaction between T, C, and victimization levels for both online and offline aggressive behaviors. In both cases, the adolescents with high T and high C or low T and low C responded with more aggressive behaviors when victimized or provoked by peers. The T/C ratio was only associated with aggressive behavior in the girls’ sample. The results are opposite to those predicted by the DHH, but they are consistent with the findings of other studies that examined aggressive behaviors as reactions to provocations. These results suggest that some combinations of T and C predict higher aggressive reactions to peer victimization.

Perinatal and later postnatal adversities have been shown to adversely affect socioeconomic trajectories, while enhanced early cognitive abilities improve them. However, little is known about the combined influence of these exposures on social mobility. In this study, we examined if childhood IQ moderated the association between four different types of postnatal adversity (childhood socioeconomic disadvantage, childhood sexual abuse, lifetime psychiatric disorder, and trait neuroticism) and annual earnings at 30–35 years of age in a sample of 88 extremely low birth weight survivors. Our results suggested that higher childhood IQ was associated with greater personal income at age 30–35. Extremely low birth weight survivors who did not face psychological adversities and who had higher childhood IQ reported higher income in adulthood. However, those who faced psychological adversity and had higher childhood IQ generally reported lower income in adulthood. Our findings suggest that cognitive reserve may not protect preterm survivors against the complex web of risk factors affecting their later socioeconomic attainment.