This study evaluated the efficacy of a family-centered preventive intervention, the Family Check-Up (FCU), delivered as an online, eHealth model to middle school families. To increase accessibility of family-centered prevention in schools, we adapted the evidence-based FCU to an online format, with the goal of providing a model of service delivery that is feasible, given limited staffing and resources in many schools. Building on prior research, we randomly assigned participants to waitlist control (n = 105), FCU Online as a web-based intervention (n = 109), and FCU Online with coaching support (n = 108). We tested the effects of the intervention on multiple outcomes, including parental self-efficacy, child self-regulation, and child behavior, in this registered clinical trial (NCT03060291). Families engaged in the intervention at a high rate (72% completed the FCU assessment) and completed 3-month posttest assessments with good retention (94% retained). Random assignment to the FCU Online with coaching support was associated with reduced emotional problems for children (p = .003, d = −0.32) and improved parental confidence and self-efficacy (p = .018, d = 0.25) when compared with waitlist controls. Risk moderated effects: at-risk youth showed stronger effects than did those with minimal risk. The results have implications for online delivery of family-centered interventions in schools.

Child maltreatment represents a pervasive societal problem. Exposure to maltreatment is predictive of maladjustment across development with enduring negative effects found in adulthood. Compelling evidence suggests that some parents with a history of child abuse and neglect are at elevated risk for the maltreatment of their own children. However, a dearth of research currently exists on mediated mechanisms that may underlie this continuity. Ecological and transactional theories of child maltreatment propose that child maltreatment is multiply determined by various risk factors that exist across different ecological systems. Intimate partner violence (IPV) often co-occurs with child maltreatment and may represent a pathway through which risk for child abuse and neglect is transmitted across generations within a family. Informed by theories on the intergenerational transmission of child maltreatment and utilizing a community-based, cross-sectional sample of 245 racially and ethnically diverse, low-income mothers and daughters, the objective of this study was to investigate IPV as a propagating process through which risk of child abuse and neglect is conferred from parent to child. We found evidence suggesting that mothers’ history of maltreatment is associated with both their IPV involvement and their adolescent daughters’ maltreatment victimization (with exposure to IPV as a maltreatment subtype excluded for clarity). Maternal IPV also partially accounted for the continuity of maltreatment victimization from mother to adolescent. A secondary analysis that included the adolescent's own engagement in dating violence provided compelling but preliminary evidence of the emergence of a similar pattern of relational violence, whereby adolescent girls with maltreatment histories were likewise involved in abusive intimate relationships. Future directions and clinical implications of these findings are discussed.

The observations of family members as well as the results of past research suggest that a variety of developmental pathways can precede the onset of schizophrenia in early adulthood. In this article, we describe recent findings from our research on the childhood precursors of schizophrenia. Taken together, the results indicate that childhood behavioral, emotional, and motoric dysfunction occur at a higher rate in preschizophrenia subjects when compared to control subjects. Further, there are developmental changes as well as significant variability among schizophrenia patients in the nature and severity of childhood impairment. Drawing on the prevailing diathesis-stress model, we explore the moderating role that stress exposure and reactivity may play in the expression of the organic diathesis for schizophrenia. Specifically, we consider the role of the biological stress response in the production of developmental changes and individual differences in the pathways to schizophrenia. Given extant models of dopamine involvement in the neuropathology of schizophrenia, stress-induced Cortisol release may alter the expression of subcortical abnormalities in dopamine neurotransmission. Thus, we present a neural mechanism for the hypothesized behavioral sensitivity to stress exposure in schizophrenia, and explore the capacity of the model to account for the changing behavioral manifestations of vulnerability.

Reflective thinking occurs when information stored in long-term memory (LTM) is not sufficient to allow one to respond “automatically” to an object or event. Instead, stored information must be entered into working memory and a novel response or solution produced. In this article I argue that mental imagery plays a central role in this process, and that over the course of normal cognitive development the process of reflective thinking “programs” LTM so that an increasingly large number of tasks can be performed without reflective thinking. Normal cognitive development thus results in a decreasing reliance on imagery. However, if highly emotional images are formed, additional retrieval cues can be entered into LTM, making such images more likely to occur in the future. Such images induce arousal, similar to that induced by the actual event. This line of thinking leads to a novel perspective on the neurocognitive deficits that underlie the development of posttraumatic stress disorder, and may also help to explain some symptoms seen in hyperactivity, impulsiveness, and difficulties in self-control.The work summarized in this paper was supported in part by NSF ROLE Grant REC-0106760 and NIH Grant 5 R01 MH60734. Portions of this article were adapted from a draft of Kosslyn (2005). I thank the Editors and Robin Rosenberg for helpful comments on earlier drafts.

This article represents an effort to extend our understanding of paranoia or suspicion and its development by integrating findings across clinical, developmental, and neuroscience literatures. We first define “paranoia” or paranoid thought and examine its prevalence across typically and atypically developing individuals and theoretical perspectives regarding its development and maintenance. We then briefly summarize current ideas regarding the neural correlates of adaptive, appropriately trusting interpersonal perception, social cognition, and behavior across development. Our focus shifts subsequently to examining in normative and atypical developmental contexts the neural correlates of several component cognitive processes thought to contribute to paranoid thinking: (a) attention bias for threat, (b) jumping to conclusions biases, and (c) hostile intent attribution biases. Where possible, we also present data regarding independent links between these cognitive processes and aggressive behavior. By examining data regarding the behavioral and neural correlates of varied cognitive processes that are likely components of a paranoid thinking style, we hope to advance both theoretical and empirical research in this domain.

Genetic moderation of the effects of child maltreatment on depression and internalizing symptoms was investigated in a sample of low-income maltreated and nonmaltreated African American children (N = 1,096). Lifetime child maltreatment experiences were independently coded from Child Protective Services records and maternal report. Child depression and internalizing problems were assessed in the context of a summer research camp by self-report on the Children's Depression Inventory and adult counselor report on the Teacher Report Form. DNA was obtained from buccal cell or saliva samples and genotyped for polymorphisms of the following genes: serotonin transporter linked polymorphic region (5-HTTLPR), brain-derived neurotrophic factor (BDNF), norepinephrine transporter, and corticotropin releasing hormone receptor 1. Analyses of covariance with age and gender as covariates were conducted, with maltreatment status and respective polymorphism as main effects and their Gene × Environment (G × E) interactions. Maltreatment consistently was associated with higher Children's Depression Inventory and Teacher Report Form symptoms. The results for child self-report symptoms indicated a G × E interaction for BDNF and maltreatment. In addition, BDNF and triallelic 5-HTTLPR interacted with child maltreatment in a G × G × E interaction. Analyses for counselor report of child anxiety/depression symptoms on the Teacher Report Form indicated moderation of child maltreatment effects by triallelic 5-HTTLPR. These effects were elaborated based on variation in developmental timing of maltreatment experiences. Norepinephrine transporter was found to further moderate the G × E interaction of 5-HTTLPR and maltreatment status, revealing a G × G × E interaction. This G × G × E was extended by consideration of variation in maltreatment subtype experiences. Finally, G × G × E effects were observed for the co-action of BDNF and the corticotropin releasing hormone receptor 1 haplotype. The findings illustrate the variable influence of specific genotypes in G × E interactions based on variation in maltreatment experiences and the importance of a multigenic approach for understanding influences on depression and internalizing symptoms among African American children.

The current study assessed whether the proportion of childhood (age 0–9 years) in poverty altered the developmental trajectories (ages 9–24) of multimethodological indicators of psychological well-being. In addition, we tested whether exposure to cumulative risk over time mediated the association between poverty exposure and psychological well-being. Measures of psychological well-being included internalizing and externalizing symptoms, a behavioral index of learned helplessness (task persistence), and chronic physiological stress (allostatic load). Exposure to poverty during childhood predicted the trajectory of each development outcome: individuals with more poverty exposure during childhood showed (a) relatively high levels of internalizing symptoms that diminished more slowly with maturation, (b) relatively high levels of externalizing symptoms that increased faster over time, (c) less task persistence indicative of greater learned helplessness, and (d) higher levels of chronic physiological stress which increased faster over time relative to persons with less childhood poverty exposure. Trajectories of cumulative risk exposure from physical and psychosocial surroundings from 9–24 years accounted for the association between childhood poverty and the growth curves of internalizing and externalizing symptoms but not for learned helplessness or chronic physiological stress. Additional sensitivity analyses indicate that early childhood disadvantage is particularly problematic for each outcome, except for internalizing symptoms which seem sensitive to the combination of early and lifetime poverty exposure. We also explored whether domains of cumulative risk as well as two alternatives, maternal sensitivity or family cohesion, functioned as mediators. Little evidence emerged for any of these alternative mediating constructs.

Childhood adversity is associated with poor mental and physical health outcomes across the life span. Alterations in the hypothalamic–pituitary–adrenal axis are considered a key mechanism underlying these associations, although findings have been mixed. These inconsistencies suggest that other aspects of stress processing may underlie variations in this these associations, and that differences in adversity type, sex, and age may be relevant. The current study investigated the relationship between childhood adversity, stress perception, and morning cortisol, and examined whether differences in adversity type (generalized vs. threat and deprivation), sex, and age had distinct effects on these associations. Salivary cortisol samples, daily hassle stress ratings, and retrospective measures of childhood adversity were collected from a large sample of youth at risk for serious mental illness including psychoses (n = 605, mean age = 19.3). Results indicated that childhood adversity was associated with increased stress perception, which subsequently predicted higher morning cortisol levels; however, these associations were specific to threat exposures in females. These findings highlight the role of stress perception in stress vulnerability following childhood adversity and highlight potential sex differences in the impact of threat exposures.

Acute reactivity of the stress hormone cortisol is reflective of early adversity and stress exposure, with some studies finding that the impact of adversity on the stress response differs by race. The objectives of the current study were to characterize cortisol reactivity to two dyadically based stress paradigms across the first year of life, to examine cortisol reactivity within Black and White infants, and to assess the impact of correlates of racial inequity including socioeconomic status, experiences of discrimination, and urban life stressors, as well as the buffering by racial socialization on cortisol patterns. Salivary cortisol reactivity was assessed at 4 months of age during the Still Face paradigm (N = 207) and at 12 months of age across the Strange Situation procedure (N = 129). Infants demonstrated the steepest recovery after the Still Face paradigm and steepest reactivity to the Strange Situation procedure. Race differences in cortisol were not present at 4 months but emerged at 12 months of age, with Black infants having higher cortisol. Experiences of discrimination contributed to cortisol differences within Black infants, suggesting that racial discrimination is already “under the skin” by 1 year of age. These findings suggest that race-related differences in hypothalamic–pituitary–adrenal reactivity are present in infancy, and that the first year of life is a crucial time period during which interventions and prevention efforts for maternal–infant dyads are most likely able to shape hypothalamic–pituitary–adrenal reactivity thereby mitigating health disparities early across the life course.

Identifying Research Domain Criteria (RDoC) constructs in early childhood is essential for understanding etiological pathways of psychopathology. Our central goal was to identify early emotion knowledge and self-regulation difficulties across different RDoC domains and examine how they relate to typical versus atypical symptom trajectories between ages 3 and 10. Particularly, we assessed potential contributions of children's gender, executive control, delay of gratification, and regulation of frustration, emotion recognition, and emotion understanding at age 3 to co-occurring patterns of internalizing and externalizing across development. A total of 238 3-year-old boys and girls were assessed using behavioral tasks and parent reports and reassessed at ages 5 and 10 years. Results indicated that very few children developed “pure” internalizing or externalizing symptoms relative to various levels of co-occurring symptoms across development. Four classes of co-occurring internalizing and externalizing problems were identified: low, low-moderate, rising, and severe-decreasing trajectories. Three-year-old children with poor executive control but high emotion understanding were far more likely to show severe-decreasing than low/low-moderate class co-occurring internalizing and externalizing symptom patterns. Child gender and poor executive control differentiated children in rising versus low trajectories. Implications for early intervention targeting self-regulation of executive control are discussed.

Difficulties in regulating affect are core characteristics of a wide range of mental health conditions and are associated with deficits in cognitive control, particularly in affective contexts, affective control. The current study explored how affective control relates to mental health over the course of adolescence. We developed an Affective Control Task, which was administered to young adolescents (11–14 years; n = 29); mid-adolescents (15–18 years; n = 31), and adults (22–30 years; n = 31). The task required individuals to sort cards according to continuously changing rules: color, number, or item type. There was a neutral condition in which items were shapes, and an affective condition, in which items were emotional facial expressions. Better affective control was associated with fewer mental health difficulties (p < .001, R2 = .15). Affective control partially accounted for the association between age group and mental health problems, z = 2.61, p = .009, Akaike information criterion = 484, with the association being strongest in young adolescents, r (27) = −.44, p = .018. Affective control further accounted for variance in the association between self-reported (but not experimental) emotion regulation and mental health (z = −3.44, p < .001, Akaike information criterion = 440). Poor affective control, especially in young adolescents, is associated with more mental health problems and higher levels of emotion regulation difficulties. Improving affective control therefore may constitute a promising target for prevention.

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 known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene–environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene–environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.

Construct validity of the newly developed Preschool Assessment of Attachment (PAA) was examined in a sample of depressed and nondepressed mothers and their preschoolers, focusing on attachment related differences in children's general caregiving environments, maternal psychosocial functioning, and child behavior during interactions with mother. Mothers of secure children were more emotionally and verbally responsive to their children than were mothers of insecure children, and secure children were emotionally more positive to their mothers than were insecure children. Mothers of secure children also reported higher levels of social supports than did mothers of insecure children. Finally, dyads with children who lacked unitary, coherent attachment strategies (i.e., anxious depressed, defended/coercive, and insecure other) showed the worst functioning in all domains relative to all other attachment groups. Similar but slightly less robust findings were obtained with socioeconomic variables statistically controlled. These results lend support to the PAA as a valid system for the conceptualization and measurement of quality of attachment among preschoolers. Future research applications with the PAA are discussed.

This study examined links between the unresolved loss of a significant person and current functioning in marital and parenting relationships. Participants were 80 women who had experienced loss, their husbands, and their preschool children. Unresolved loss was assessed using the Adult Attachment Interview, and individual, marital, and parenting adaptation was assessed through videotaped observations and women's self-reports. As predicted, women with unresolved loss displayed less positive emotion and more anxiety and anger with both their husbands and children, compared to women who were not unresolved. They also displayed less authoritative and more authoritarian parenting styles with their children. Yet unresolved women did not report more individual or relationship difficulties, suggesting that direct observations are needed to assess the implications of unresolved loss for family functioning.

Psychoanalysis ushered in this century. Will its influence on developmental psychopathology end in the next? The paper explores some critical obstacles in the way of psychodynamic research, including the fragmentation of psychoanalytic theory, the relative independence of theory from its clinical and empirical base, the predominance of inductive scientific logic, the polymorphous use of terms, the privacy of clinical data, the dominance of the reconstructionist stance, and the isolation of psychoanalysis from psychology and neurobiology. Notwithstanding these limitations, core psychoanalytic precepts are not only consistent with some of the most important advances of the last decade but may also be helpful in elaborating these new discoveries in the next century. Psychoanalysis is centered on the notion that complex, conflicting, unconscious representations of mental states constitute a key facet of normal and abnormal development. This notion retains its power, and deserves a prominent position among the major frames of reference to guide developmental science in the next century.

Risky decision making, a hallmark phenotype of substance use disorders (SUD), is thought to be associated with deficient feedback processing. Whether these aberrations are present prior to SUD onset or reflect merely a consequence of chronic substance use on the brain remains unclear. The present study investigated whether blunted feedback processing during risky decision making reflects a biological predisposition to SUD. We assessed event-related potentials elicited by positive and negative feedback during performance of a modified version of the Balloon Analogue Risk Task (BART) among high-risk adolescents with a parental history of SUD (HR; n = 61) and normal-risk controls (NR; n = 91). HR males made significantly more risky and faster decisions during the BART than did NR controls. Moreover, HR adolescents showed significantly reduced P300 amplitudes in response to both positive and negative feedback as compared to NR controls. These differences were not secondary to prolonged substance use exposure. Results are discussed in terms of feedback-specific processes. Reduced P300 amplitudes in the BART may reflect poor processing of feedback at the level of overall salience, which may keep people from effectively predicting the probability of future gains and losses. Though conclusions are tentative, blunted feedback processing during risky decision making may represent a promising endophenotypic vulnerability marker for SUD.

The current study explored longitudinal associations between interparental aggression, the development of child attention skills, and early childhood behavior problems in a diverse sample of 636 families living in predominately low-income, nonmetropolitan communities. The results of latent-variable, cross-lagged longitudinal models revealed that maternal-reported interparental aggression in infancy predicted reduced observed attention skills in toddlerhood; no association was observed, however, between attention in infancy and interparental aggression during the toddler years. Further, reduced toddler attention and high interparental aggression were both associated with increased risk for attention-deficit/hyperactivity disorder symptoms and conduct problems at 3 years of age. Processes largely operated in similar ways regardless of child gender or low-income status, although a few differences were observed. Overall, the results suggest that interparental aggression undermines attention development, putting children's early behavioral adjustment at risk.

Prospective longitudinal studies of idiopathic autism spectrum disorder (ASD) have provided insights into early symptoms and predictors of ASD during infancy, well before ASD can be diagnosed at age 2–3 years. However, research on the emergence of ASD in disorders with a known genetic etiology, contextualized in a developmental framework, is currently lacking. Using a biobehavioral multimethod approach, we (a) determined the rate of ASD in N = 51 preschoolers with fragile X syndrome (FXS) using a clinical best estimate (CBE) procedure with differential diagnoses of comorbid psychiatric disorders and (b) investigated trajectories of ASD symptoms and physiological arousal across infancy as predictors of ASD in preschoolers with FXS. ASD was not diagnosed if intellectual ability or psychiatric disorders better accounted for the symptoms. Our results determined that 60.7% of preschoolers with FXS met the Diagnostic and Statistical Manual of Mental Disorders (fifth edition) (DSM-5) criteria for ASD using the CBE procedure. In addition, 92% of these preschoolers presented with developmental delay and 45.4% also met criteria for psychiatric disorders, either anxiety, ADHD, or both. ASD diagnoses in preschoolers with FXS were predicted by elevated scores on traditional ASD screeners in addition to elevated autonomic arousal and avoidant eye contact from infancy.

Gene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene–environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.