Several studies have suggested that the neuropeptide oxytocin may enhance aspects of social communication in autism. Little is known, however, about its effects on nonsocial manifestations, such as restricted interests and repetitive behaviors. In the empathizing–systemizing theory of autism, social deficits are described along the continuum of empathizing ability, whereas nonsocial aspects are characterized in terms of an increased preference for patterned or rule-based systems, called systemizing. We therefore developed an automated eye-tracking task to test whether children and adolescents with autism spectrum disorder (ASD) compared to matched controls display a visual preference for more highly organized and structured (systemized) real-life images. Then, as part of a randomized, double-blind, placebo-controlled crossover study, we examined the effect of intranasal oxytocin on systemizing preferences in 16 male children with ASD, compared with 16 matched controls. Participants viewed 14 slides, each containing four related pictures (e.g., of people, animals, scenes, or objects) that differed primarily on the degree of systemizing. Visual systemizing preference was defined in terms of the fixation time and count for each image. Unlike control subjects who showed no gaze preference, individuals with ASD preferred to fixate on more highly systemized pictures. Intranasal oxytocin eliminated this preference in ASD participants, who now showed a similar response to control subjects on placebo. In contrast, control participants increased their visual preference for more systemized images after receiving oxytocin versus placebo. These results suggest that, in addition to its effects on social communication, oxytocin may play a role in some of the nonsocial manifestations of autism.

Maternal trauma is a complex risk factor that has been linked to adverse child outcomes, yet the mechanisms underlying this association are not well understood. This study, which included adoptive and biological families, examined the heritable and environmental mechanisms by which maternal trauma and associated depressive symptoms are linked to child internalizing and externalizing behaviors. Path analyses were used to analyze data from 541 adoptive mother–adopted child (AM–AC) dyads and 126 biological mother–biological child (BM–BC) dyads; the two family types were linked through the same biological mother. Rearing mother's trauma was associated with child internalizing and externalizing behaviors in AM–AC and BM–BC dyads, and this association was mediated by rearing mothers’ depressive symptoms, with the exception of biological child externalizing behavior, for which biological mother trauma had a direct influence only. Significant associations between maternal trauma and child behavior in dyads that share only environment (i.e., AM–AC dyads) suggest an environmental mechanism of influence for maternal trauma. Significant associations were also observed between maternal depressive symptoms and child internalizing and externalizing behavior in dyads that were only genetically related, with no shared environment (i.e., BM–AC dyads), suggesting a heritable pathway of influence via maternal depressive symptoms.

Harsh and restrictive parenting are well-established contributors to the development of oppositional defiant disorder (ODD) among children. However, few studies have explored whether interpersonal relationships that develop outside the family environment attenuate the risk for ODD that is associated with harsh parenting. The current study tested multireporter measures of teacher–child closeness and peer acceptance as moderators of the association between harsh parenting and children's ODD as children's social worlds widen during the kindergarten year (N = 338 children, 48% girls, M age = 5.32 years). Harsh parenting interacted with peer nominations of peer acceptance and children's report of teacher–child closeness to predict children's ODD symptoms in the spring, adjusting for fall symptoms. Children exposed to harsh parenting exhibited greater symptom increases when they were less liked/accepted playmates and in the context of lower teacher–child closeness. However, harsh parenting was not associated with symptom change among children with higher levels of peer-nominated acceptance and those who reported closer relationships with teachers. There were no significant interactions using teacher's report of peer acceptance or teacher's report of teacher–child closeness. Findings highlight positive peer and teacher relationships as promising targets of intervention among children exposed to harsh parenting and support the importance of assessing multiple perspectives of children's social functioning.

Pubertal timing matters for psychological development. Early maturation in girls is linked to risk for depression and externalizing problems in adolescence and possibly adulthood, and early and late maturation in boys are linked to depression. It is unclear whether pubertal timing uniquely predicts problems; it might instead mediate the continuity of behavior problems from childhood to adolescence or create psychological risk specifically in youth with existing problems, thus moderating the link. We investigated these issues in 534 girls and 550 boys, measuring pubertal timing by a logistic model fit to annual self-report measures of development and, in girls, age at menarche. Prepuberty internalizing and externalizing behavior problems were reported by parents. Adolescent behavior problems were reported by parents and youth. As expected, behavior problems were moderately stable. Pubertal timing was not predicted by childhood problems, so it did not mediate the continuity of behavior problems from childhood to adolescence. Pubertal timing did not moderate links between early and later problems for girls. For boys, early maturation accentuated the link between childhood problems and adolescent substance use. Overall, the replicated links between puberty and behavior problems appear to reflect the unique effects of puberty and child behavior problems on the development of adolescent behavior problems.

This study examined the mediating role of maternal unsupportive parenting in explaining associations between family instability and children's externalizing symptoms during the transition to formal schooling in early childhood. Participants included 243 preschool children (M age = 4.60 years) and their parents. Findings from cross-lagged autoregressive models conducted with multimethod (survey and observations), multi-informant (parent, teacher, and observer), longitudinal (three annual waves of data collection) data indicated that experiences with heightened family instability predicted decreases in supportive parenting, which in turn predicted increases in children's externalizing symptoms. Analyses also revealed a bidirectional association between parenting and family instability over time, such that higher levels of instability predicted decreases in supportive parenting, which in turn predicted increases in family instability.

Attention control plays an important role in the development of internalizing symptoms in children. We explored the degree to which infants' genetic and environmentally based risk moderated the link between attention control and internalizing problems during toddlerhood. These associations were examined within a prospective adoption design, enabling the disentanglement of genetic and environmental risk for internalizing problems. Attention control in adopted infants was observed during periods of distress at age 9 months. Birth parents' anxiety symptoms were used as an index of genetic risk, while adoptive parents' anxiety symptoms were used as an index of environmental risk. Adoptive mothers and fathers reported on children's internalizing problems when children were 18 and 27 months old. Greater attention control in infancy appeared to mitigate genetically based risk for internalizing problems during toddlerhood when children were raised by adoptive parents who were low in anxiety. Findings suggest that for genetically susceptible children who are raised in low-risk environments, attention control may provide a protective factor against developing internalizing problems across early life.

Institutional caregiving is associated with significant deviations from species-expected caregiving, altering the normative sequence of attachment formation and placing children at risk for long-term emotional difficulties. However, little is known about factors that can promote resilience following early institutional caregiving. In the current study, we investigated how adaptations in affective processing (i.e., positive valence bias) and family-level protective factors (i.e., secure parent–child relationships) moderate risk for internalizing symptoms in previously institutionalized (PI) youth. Children and adolescents with and without a history of institutional care performed a laboratory-based affective processing task and self-reported measures of parent–child relationship security. PI youth were more likely than comparison youth to show positive valence biases when interpreting ambiguous facial expressions. Both positive valence bias and parent–child relationship security moderated the association between institutional care and parent-reported internalizing symptoms, such that greater positive valence bias and more secure parent–child relationships predicted fewer symptoms in PI youth. However, when both factors were tested concurrently, parent–child relationship security more strongly moderated the link between PI status and internalizing symptoms. These findings suggest that both individual-level adaptations in affective processing and family-level factors of secure parent–child relationships may ameliorate risk for internalizing psychopathology following early institutional caregiving.

Although there is some evidence to suggest that depressive symptoms show age-related changes, it remains uncertain as to whether there are also developmental variations in the etiology of depression. In this article, we present findings from a population-based study of twins aged 8 to 16 years with the aim of examining the genetic etiology of depressive symptoms and the effects of age. The results suggest that environmental factors influence the transmission of depressive symptoms in childhood. However depressive symptoms in adolescence appear to be highly heritable. The etiology of depressive symptoms was further explored using factor-derived scores that again suggested the importance of genetic factors in adolescence. However there was some suggestion that genetic influences may contribute to certain types of symptoms (self-deprecation/self-esteem) even in childhood.

A comparison of offspring of parents with bipolar disorder (OBD) and offspring of parents with no mental disorder (ONMD) showed that parents' neuroticism was associated with internalizing and externalizing problems among their children. The present study examined whether parents' neuroticism predicted poor interpersonal functioning among offspring 10 years later and whether the problems observed in middle childhood mediated the association between parents' neuroticism and offspring functioning. When offspring were in middle childhood, parents completed the revised NEO Personality Inventory and rated the child's behavior on the Child Behavior Checklist. Ten years later, 65 OBD and 59 ONMD completed interviews assessing mental disorders and interpersonal and noninterpersonal functioning. High neuroticism and low agreeableness in parents predicted poor interpersonal functioning in their offspring in late adolescence–early adulthood. The offspring's externalizing and internalizing problems in middle childhood partially mediated the association between parents' personality and offspring interpersonal functioning. Moreover, the association between parents' neuroticism and offspring internalizing problems was stronger among the OBD than the ONMD. Overall, the results suggested an intergenerational transmission of risk whereby high neuroticism and low agreeableness in parents were associated with behavioral problems among offspring in middle childhood that, in turn, predicted poor interpersonal functioning 10 years later.

This study examined the role of maternal psychopathology and maternal warmth as mediators of the association between prenatal cocaine and other substance exposure and toddler behavior problems. It was also hypothesized that infant cortisol reactivity and environmental risk may moderate these associations. Participants were 220 caregiver–infant dyads (119 cocaine exposed, 101 not cocaine exposed; 49% boys). Mother–infant dyads were recruited at delivery with assessments at 4–8 weeks and 7, 13, and 18 months of child ages. Results yielded no direct associations between prenatal cocaine/other substance exposure and toddler behavior problems, but significant indirect associations between prenatal cigarette/alcohol exposure and toddler behavior problems at 18 months. With regard to moderation, results indicated an indirect association between prenatal cocaine exposure and toddler behavior problems via lower maternal warmth for children with higher, but not lower, cortisol reactivity at 7 months. Results suggest potential pathways to toddler behavior problems among children at high biological risk.

Effortful control is thought to foster adaptive action in defensive contexts and may thereby protect individuals against anxious inhibition and focus on their own distress. We examined if effortful control predicted adolescents' perceived arousal, unpleasantness, and control as well as autonomic (heart rate [HR]) and hypothalamic–pituitary–adrenal axis (cortisol) responses during social stress. The data came from a focus sample of the Tracking Adolescents' Individual Lives Survey, a prospective population study of Dutch adolescents (N = 715, 50.9% girls; mean age = 16.11, SD = 0.59), who participated in a laboratory session including a social stress task (public speaking and mental arithmetic). Perceived and physiological stress measures were assessed before, during, and after the social stress task. Effortful control was measured using various questionnaires and informants, as well as by means of a reaction time (RT) task assessing response inhibition. Overall, adolescents with high questionnaire-based effortful control tended to feel more relaxed, pleasant, and in control during the laboratory session than adolescents with lower levels of control and had stronger HR responses to the stress test. Adolescent girls with high inhibitory control as measured by the RT task also had strong HR responses, but inhibitory control was associated with high rather than low perceived arousal. Our results suggest that both questionnaire and RT measures of effortful control predict strong HR responses to challenging situations, but associational patterns diverge with regard to perceived stress measures.

Adolescence is a period of social, physical, and neurobiological transitions that may leave individuals more vulnerable to the development of internalizing and externalizing symptomatology. Extant research demonstrates that executive functioning (EF) is associated with psychopathology outcomes in adolescence; however, it has yet to be examined how EF and psychopathology develop transactionally over time. Data were collected from 167 adolescents (47% female, 13–14 years old at Time 1) and their primary caregiver over 4 years. At each time point, adolescents completed three behavioral tasks that capture the underlying dimensions of EF, and both adolescents and their primary caregiver completed measures of adolescent psychopathology. Latent growth curve modeling was used to test the associations between initial levels and trajectories of EF and psychopathology. Results indicated that higher initial levels of internalizing and externalizing symptomatology were associated with lower EF at Time 4 (controlling for Time 1 EF). Initial levels of EF did not predict changes in internalizing and externalizing symptomatology. These findings suggest that early psychopathology may be a risk factor for maladaptive EF development in adolescence.

McGee and Wolfe (1991) have taken on an important and very challenging topic, the meaning of psychological maltreatment and its significance for child development. They start from the definitions offered by several students of this phenomenon (Garbarino, Guttmann, & Seeley, 1986), and proceed to a formulation that they believe advances the cause of research.

Information-processing biases may contribute to the intergenerational transmission of depression. There is growing evidence that children of depressed mothers exhibit attentional biases for sad faces. However, findings are mixed as to whether this bias reflects preferential attention toward, versus attentional avoidance of, sad faces, suggesting the presence of unmeasured moderators. To address these mixed findings, we focused on the potential moderating role of genes associated with hypothalamic–pituitary–adrenal axis reactivity. Participants included children (8–14 years old) of mothers with (n = 81) and without (n = 81) a history of depression. Eye movements were recorded while children passively viewed arrays of angry, happy, sad, and neutral faces. DNA was obtained from buccal cells. Children of depressed mothers exhibited more sustained attention to sad faces than did children of nondepressed mothers. However, it is important that this relation was moderated by children's genotype. Specifically, children of depressed mothers who carried reactive genotypes across the corticotropin-releasing hormone type 1 receptor (CHRH1) TAT haplotype and FK506 binding protein 5 (FKBP5) rs1360780 (but not the solute carrier family C6 member 4 [SLC6A4] of the serotonin transporter linked polymorphic region [5-HTTLPR]) exhibited less sustained attention to sad faces and more sustained attention to happy faces. These findings highlight the role played by specific genetic influences and suggest that previous mixed findings may have been due to genetic heterogeneity across the samples.

Perturbations to the gut microbiome are implicated in altered neurodevelopmental trajectories that may shape life span risk for emotion dysregulation and affective disorders. However, the sensitive periods during which the microbiome may influence neurodevelopment remain understudied. We investigated relationships between gut microbiome composition across infancy and temperament at 12 months of age. In 67 infants, we examined if gut microbiome composition assessed at 1–3 weeks, 2, 6, and 12 months of age was associated with temperament at age 12 months. Stool samples were sequenced using the 16S Illumina MiSeq platform. Temperament was assessed using the Infant Behavior Questionnaire-Revised (IBQ-R). Beta diversity at age 1–3 weeks was associated with surgency/extraversion at age 12 months. Bifidobacterium and Lachnospiraceae abundance at 1–3 weeks of age was positively associated with surgency/extraversion at age 12 months. Klebsiella abundance at 1–3 weeks was negatively associated with surgency/extraversion at 12 months. Concurrent composition was associated with negative affectivity at 12 months, including a positive association with Ruminococcus-1 and a negative association with Lactobacillus. Our findings support a relationship between gut microbiome composition and infant temperament. While exploratory due to the small sample size, these results point to early and late infancy as sensitive periods during which the gut microbiome may exert effects on neurodevelopment.

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.

Anabolic–androgenic steroids (AASs) are synthetic hormones used by individuals who want to look better or perform better in athletics and at the gym. Their use raises an interesting paradox in which drug use is associated with a number of health benefits, but also the possibility of negative health consequences. Existing models of AAS addiction follow the traditional framework of drug abuse and dependence, which suggest that harmful use occurs as a result of the drug's ability to hijack the motivation–reward system. However, AASs, unlike typical drugs of abuse, are not used for acute intoxication effects or euphoria. Rather, AASs are used to affect the body through changes to the musculoskeletal system and the hypothalamic–pituitary–gonadal axis as opposed to stimulating the reward system. We offer an allostatic model of AAS addiction to resolve this inconsistency between traditional drug addiction and AAS addiction. This allostatic framework provides a way to (a) incorporate exercise into AAS misuse, (b) identify where AAS use transitions from recreational use into a drug problem, and (c) describe individual differences in vulnerability or resilience to AASs. Implications for this model of AAS addiction 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.

The aim of the study was to examine possible influences on individual differences in adolescence in response to early institutional care in infancy not involving either generalized privation or subnutrition. Fifty-two adopted adolescents aged 13 years who received institutional care in infancy at the Metera Babies Centre and 36 adolescents of the same age who were raised in their biological families participated in the study. Adolescents' attachment relationships, cognition, behavioral adjustment and use of psychological services were assessed. Marked heterogeneity in outcomes was found. No predictive effects were found for preinstitutional features or for adoptive circumstances. By contrast a large effect was found for institutional care extending beyond the age of 2 years and for quality of institutional care as experienced at an individual level. There was a close association between prolonged institutional care and disorganized attachment while in the institution, but the main institutional effect derived from the length of time in the institution.