The current study advances past research by studying the impact of juvenile justice decision making with a geographically and ethnically diverse sample (N = 1,216) of adolescent boys (ages 13–17 years) for the 5 years following their first arrest. Importantly, all youth in the study were arrested for an eligible offense of moderate severity (e.g., assault, theft) to evaluate whether the initial decision to formally (i.e., sentenced before a judge) or informally (i.e., diverted to community service) process the youth led to differences in outcomes. The current study also advanced past research by using a statistical approach that controlled for a host of potential preexisting vulnerabilities that could influence both the processing decision and the youth's outcomes. Our findings indicated that youth who were formally processed during adolescence were more likely to be re-arrested, more likely to be incarcerated, engaged in more violence, reported a greater affiliation with delinquent peers, reported lower school enrollment, were less likely to graduate high school within 5 years, reported less ability to suppress aggression, and had lower perceptions of opportunities than informally processed youth. Importantly, these findings were not moderated by the age of the youth at his first arrest or his race and ethnicity. These results have important implications for juvenile justice policy by indicating that formally processing youth not only is costly, but it can reduce public safety and reduce the adolescent's later potential contributions to society.

Adolescent aggression was explored in relation to neighborhood and genetic characteristics. Child saturation (the proportion of the population consisting of children under the age of 15), ethnic heterogeneity, poverty, and urbanicity of neighborhoods were examined in relation to adolescent aggression in 12,098 adolescents followed longitudinally for 1 year. Longitudinal analyses indicated that child saturation was positively associated with increases in aggression, with this finding emerging among those living in the same neighborhood at both testing times and those who moved between testing times. In a subsample of males for whom genetic data were available, the relation of child saturation to adolescent aggression was moderated by the monoamine oxidase A (MAOA) gene. The regression of aggression on child saturation was steeper for those with the low activity version of the MAOA allele than among those with the high activity version of the allele. The implications of the results for an understanding of the origins and ontogeny of aggression and personality disorders are discussed.

This study was designed to investigate a genetic moderation effect of dopamine receptor 4 gene (DRD4) alleles that have seven or more repeats (long alleles) on an intervention to deter drug use among rural African American adolescents in high-risk families. Adolescents (N = 291, M age = 17) were assigned randomly to the Adults in the Making (AIM) program or to a control condition and were followed for 27.5 months. Adolescents provided data on drug use and vulnerability cognitions three times after pretest. Pretest assessments of caregiver depressive symptoms, disruption in the home, and support toward the adolescent were used to construct a family risk index. Adolescents living in high-risk families who carried at least one DRD4 long allele and were assigned to the control condition evinced greater escalations in drug use than did (a) adolescents who lived in high-risk families, carried the DRD4 long allele, and were assigned to AIM, or (b) adolescents assigned to either condition who carried no DRD4 long alleles. AIM-induced reductions in vulnerability cognitions were responsible for the Family Risk × AIM × DRD4 status drug use prevention effects. These findings support differential susceptibility predictions and imply that prevention effects on genetically susceptible individuals may be underestimated.

Experiencing maltreatment during childhood can have long-lasting consequences for both mental and physical health. Immune cell telomere length (TL) shortening might be one link between child maltreatment (CM) experiences and adverse health outcomes later in life. While the stress hormone cortisol has been associated with TL attrition, the attachment-related hormone oxytocin may promote resilience. In 15 mothers with and 15 age- and body mass index-matched mothers without CM, we assessed TL in peripheral blood mononuclear cells and selected immune cell subsets (monocytes, naive, and memory cytotoxic T cells) by quantitative fluorescence in situ hybridization, as well as peripheral cortisol and oxytocin levels. Memory cytotoxic T cells showed significantly shorter TL in association with CM, whereas TL in monocytes and naive cytotoxic T cells did not significantly differ between the two groups. Across both groups, cortisol was negatively associated with TL, while oxytocin was positively associated with TL in memory cytotoxic T cells. These results indicate that long-lived memory cytotoxic T cells are most affected by the increased biological stress state associated with CM. Keeping in mind the correlational and preliminary nature of the results, the data suggest that cortisol may have a damaging and oxytocin a protective function on TL.

Power dynamics in the marital dyad and systemic elements of whole-family functioning (cohesion, subsystem boundary formations) were examined in relation to each other and also in relation to child adjustment in a multiethnic sample of families. Support was found for a mediational model, such that family functioning was found to mediate the relationship between marital power dynamics and children's internalizing and externalizing behavior. Some support also was found for ethnicity as a moderator of the association between systemic family processes and children's adjustment. Disturbances in family cohesion and subsystem boundaries were more strongly related to internalizing symptomatology for children in European American families compared to children in Hispanic American families.This research was funded by National Institute of Mental Health Grant R03 MH54631. We thank Jean–Philippe Laurenceau for his feedback on drafts of this manuscript and for statistical consultation. We also are very grateful to the participating families for the generous donation of their time and effort.

Background: Negative body image predicts many adverse outcomes. The current study prospectively examined patterns of body esteem development in early adolescence and identified predictors of developmental subtypes. Methods: 328 girls and 429 boys reported annually across a 4-year period (Mage at baseline = 11.14, SD = 0.35) on body esteem, appearance ideal internalization, perceived sociocultural pressures, appearance comparisons, appearance-related teasing, self-esteem, positive and negative affect, and dietary restraint. We performed latent class growth analyses to identify the most common trajectories of body esteem development and examine risk and protective factors for body image development. Results: Three developmental subgroups were identified: (a) high body esteem (39.1%); (b) moderate body esteem (46.1%); and (c) low body esteem (14.8%). Body esteem was stable within the low trajectory and there were minor fluctuations in the high and moderate trajectories. Greater appearance-related teasing, lower self-esteem, less positive affect, and higher dietary restraint predicted the low trajectory, whereas higher self-esteem and lower dietary restraint best predicted the high trajectory. Conclusions: Low body esteem appears to be largely stable from age 11 years. Prevention programming may be enhanced by incorporating components to address transdiagnostic resilience factors such as self-esteem and positive affect.

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

Abnormalities in attention have long been viewed as one of the fundamental underlying cognitive deficits in schizophrenia, likely contributing both to formation of some types of symptoms and particularly to the substantial work and social impairments that often accompany schizophrenia. Yet, the precise nature of the attentional deficits in schizophrenia remains poorly understood. Translating advances in cognitive psychology to clinical research brings paradigms with greater analytic power to the study of attention in schizophrenia. In particular, these paradigms should shed light on whether the attentional dysfunction in schizophrenia is best conceptualized as arising from limitations in amount or allocation of processing capacity or from more specific structural bottlenecks that do not allow certain processes to be carried out in two tasks simultaneously. Certain types of dual-task paradigms are particularly well suited to make distinctive predictions, particularly those involving a psychological refractory period paradigm. The background and design of a series of ongoing studies of prodromal, first-episode, and chronic schizophrenia patients are described that are addressing the developmental course of attentional dysfunction in this disorder. These refined paradigms should substantially increase our understanding of the specific forms of attentional impairment characterizing schizophrenia and their connections to symptom development and functional outcome.

Self-inflicted injury (SII) in adolescence is a serious public health concern that portends prospective vulnerability to internalizing and externalizing psychopathology, borderline personality development, suicide attempts, and suicide. To date, however, our understanding of neurobiological vulnerabilities to SII is limited. Behaviorally, affect dysregulation is common among those who self-injure. This suggests ineffective cortical modulation of emotion, as observed among adults with borderline personality disorder. In borderline samples, structural and functional abnormalities are observed in several frontal regions that subserve emotion regulation (e.g., anterior cingulate, insula, dorsolateral prefrontal cortex). However, no volumetric analyses of cortical brain regions have been conducted among self-injuring adolescents. We used voxel-based morphometry to compare cortical gray matter volumes between self-injuring adolescent girls, ages 13–19 years (n = 20), and controls (n = 20). Whole-brain analyses revealed reduced gray matter volumes among self-injurers in the insular cortex bilaterally, and in the right inferior frontal gyrus, an adjacent neural structure also implicated in emotion and self-regulation. Insular and inferior frontal gyrus gray matter volumes correlated inversely with self-reported emotion dysregulation, over-and-above effects of psychopathology. Findings are consistent with an emotion dysregulation construal of SII, and indicate structural abnormalities in some but not all cortical brain regions implicated in borderline personality disorder among adults.

Few studies have investigated developmental strengths and weaknesses within the cognitive profile of children and adolescents with fragile X syndrome (FXS), a single-gene cause of inherited intellectual impairment. With a prospective longitudinal design and using normalized raw scores (Z scores) to circumvent floor effects, we measured cognitive functioning of 184 children and adolescents with FXS (ages 6 to 16) using the Wechsler Scale of Intelligence for Children on one to three occasions for each participant. Participants with FXS received lower raw scores relative to the Wechsler Scale of Intelligence for Children normative sample across the developmental period. Verbal comprehension, perceptual organization, and processing speed Z scores were marked by a widening gap from the normative sample, while freedom from distractibility Z scores showed a narrowing gap. Key findings include a relative strength for verbal skills in comparison with visuospatial–constructive skills arising in adolescence and a discrepancy between working memory (weakness) and processing speed (strength) in childhood that diminishes in adolescence. Results suggest that the cognitive profile associated with FXS develops dynamically from childhood to adolescence. Findings are discussed within the context of aberrant brain morphology in childhood and maturation in adolescence. We argue that assessing disorder-specific cognitive developmental profiles will benefit future disorder-specific treatment research.

Using a population-based birth cohort in upstate New York (2008–2010), we examined the determinants of brain-derived neurotrophic factor (BDNF) measured in newborn dried blood spots (n = 2,637). We also examined the association between neonatal BDNF and children's development. The cohort was initially designed to examine the influence of infertility treatment on child development but found no impact. Mothers rated children's development in five domains repeatedly through age 3 years. Socioeconomic and maternal lifestyle determinants of BDNF were examined using multivariable linear regression models. Generalized linear mixed models estimated odds ratios for neonatal BDNF in relation to failing a developmental domain. Smoking and drinking in pregnancy, nulliparity, non-White ethnicity/race, and prepregnancy obesity were associated with lower neonatal BDNF. Neonatal BDNF was not associated with failure for developmental domains; however, there was an interaction between BDNF and preterm birth. In preterm infants, a higher BDNF was associated with lower odds of failing any developmental domains, after adjusting for confounders and infertility treatment. This result was particularly significant for failure in communication. Our findings suggest that BDNF levels in neonates may be impacted by maternal lifestyle characteristics. More specifically, lower neonatal BDNF might be an early marker of aberrant neurodevelopment in preterm infants.

Experiencing poverty increases vulnerability for dysregulated hypothalamic–pituitary–adrenal (HPA) axis functioning and compromises long-term health. Positive parenting buffers children from HPA axis reactivity, yet this has primarily been documented among families not experiencing poverty. We tested the theorized power of positive parenting in 124 parent–child dyads recruited from Early Head Start (Mage = 25.21 months) by examining child cortisol trajectories using five samples collected across a standardized stress paradigm. Piecewise latent growth models revealed that positive parenting buffered children's stress responses when controlling for time of day, last stress task completed, and demographics. Positive parenting also interacted with income such that positive parenting was especially protective for cortisol reactivity in families experiencing greater poverty. Findings suggest that positive parenting behaviors are important for protecting children in families experiencing low income from heightened or prolonged physiologic stress reactivity to an acute stressor.

Vibrant expression of emotion is the principal means infants and young children use to elicit appropriate and timely caregiving, stimulation, and support. This study examined the depression–inhibition hypothesis: that declines in mothers' support as their depressive symptoms increase inhibit children's emotional communication. Ninety-four mothers and their 14- to 27-month-olds interacted in a university playroom. Based on microanalytic coding of discrete facial displays, results supported three components of the hypothesis. (a) As mothers' depressive symptoms increased, children displayed less facial emotion (more flat affect, less joy, less sadness, less negative). (b) Mothers' low emotional and behavioral support predicted children's low facial communication and mediated relations between mothers' depressive symptoms and children's infrequent emotion. (c) Children who were passive with mothers behaviorally expressed emotion infrequently. Children's passivity mediated relations between mothers' depressive symptoms and children's infrequent emotion displays. Contrary to modeling and contagion theories, mothers' facial displays did not mediate relations between their depressive symptoms and children's facial displays. Nor were the outcomes children experienced regulating their facial displays. Rather, findings suggest that, even when depressive symptoms are modest, young children inhibit emotion as mothers' depressive symptoms increase to withdraw from unresponsive mothers, which may adversely affect children's subsequent relationships and competencies.

Qualitative methods are well suited to advance the understanding of the role of social context in the development of maladaptation and psychopathology. However, they have not been widely used by developmental psychopathologists, despite being utilized in related fields, particularly in the sociological study of crime and delinquency. This article assesses the potential for the increased use of qualitative methods in developmental psychopathology and addresses the challenges involved in integrating them with quantitative research strategies. The interplay of qualitative and quantitative methods in the study of juvenile delinquency is reviewed for relevant lessons about both the utility and the difficulties of integrating the two types of methods. The problem of assessing continuities and discontinuities over the life course in patterns of antisocial behavior is discussed as an example of the challenge of integrating methodological paradigms. Schools of thought about qualitative methods and their relationship to quantitative research paradigms are identified and compared. Examples are discussed of narrative life history interviewing and qualitative observational techniques and of recent research endeavors integrating these qualitative techniques with quantitative data analyses.

This study investigates suicide risk in late childhood and early adolescence in relation to a family-centered intervention, the Family Check-Up, for problem behavior delivered in early childhood. At age 2, 731 low-income families receiving nutritional services from Women, Infants, and Children programs were randomized to the Family Check-Up intervention or to a control group. Trend-level main effects were observed on endorsement of suicide risk by parents or teachers from ages 7.5 to 14, with higher rates of suicide risk endorsement in youth in the control versus intervention condition. A significant indirect effect of intervention was also observed, with treatment-related improvements in inhibitory control across childhood predicting reductions in suicide-related risk both at age 10.5, assessed via diagnostic interviews with parents and youth, and at age 14, assessed via parent and teacher reports. Results add to the emerging body of work demonstrating long-term reductions in suicide risk related to family-focused preventive interventions, and highlight improvements in youth self-regulatory skills as an important mechanism of such reductions in risk.

Identifying developmental endophenotypes on the pathway between genetics and behavior is critical to uncovering the mechanisms underlying neurodevelopmental conditions. In this proof-of-principle study, we explored whether early disruptions in visual attention are a unique or shared candidate endophenotype of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). We calculated the duration of the longest look (i.e., peak look) to faces in an array-based eye-tracking task for 335 14-month-old infants with and without first-degree relatives with ASD and/or ADHD. We leveraged parent-report and genotype data available for a proportion of these infants to evaluate the relation of looking behavior to familial (n = 285) and genetic liability (using polygenic scores, n = 185) as well as ASD and ADHD-relevant temperament traits at 2 years of age (shyness and inhibitory control, respectively, n = 272) and ASD and ADHD clinical traits at 6 years of age (n = 94).

Results showed that longer peak looks at the face were associated with elevated polygenic scores for ADHD (β = 0.078, p = .023), but not ASD (β = 0.002, p = .944), and with elevated ADHD traits in mid-childhood (F(1,88) = 6.401, p = .013, $\eta _p^2$=0.068; ASD: F (1,88) = 3.218, p = .076), but not in toddlerhood (ps > 0.2). This pattern of results did not emerge when considering mean peak look duration across face and nonface stimuli. Thus, alterations in attention to faces during spontaneous visual exploration may be more consistent with a developmental endophenotype of ADHD than ASD. Our work shows that dissecting paths to neurodevelopmental conditions requires longitudinal data incorporating polygenic contribution, early neurocognitive function, and clinical phenotypic variation.

This paper examined whether childhood maltreatment increases the risk of living in neighborhoods with less desirable characteristics (i.e., more disorder and disadvantage, less social cohesion, social control and advantage, and fewer resources) in middle adulthood and whether these neighborhood characteristics influence subsequent illicit drug use. Using a prospective cohort design study, court documented cases of childhood abuse and neglect and matched controls (n = 833) were first interviewed as young adults (mean age = 29 years) from 1989 to 1995 and again in middle adulthood from 2000 to 2002 (mean age = 40 years) and 2003 to 2005 (mean age = 41 years). In middle adulthood, individuals with histories of childhood abuse and neglect were more likely to live in neighborhoods with more disorder and disadvantage and less social cohesion and advantage compared to controls and to engage in illicit drug use during the past year. Path analyses showed an indirect effect on illicit drug use via neighborhood disorder among maltreated children, even after accounting for drug abuse symptoms in young adulthood, although this was sex specific and race specific, affecting women and Whites. Overall, child abuse and neglect places children on a negative trajectory that dynamically influences negative outcomes at multiple levels into middle adulthood.

Little is known about the role of stress reactivity in the emergence of psychopathology across early childhood. In this longitudinal study, we tested the hypothesis that child cortisol reactivity at age 3 moderates associations between early parenting and children's internalizing and externalizing symptoms from age 3 to age 6. One hundred and sixty children were assessed at age 3, and 135 children were reassessed at age 6. At age 3, we exposed children to stress-inducing laboratory tasks, during which we obtained four salivary cortisol samples, and parental hostility was assessed using an observational parent–child interaction task. At ages 3 and 6, child psychiatric symptoms were assessed using a clinical interview with parents. The results indicated that the combination of high child cortisol reactivity and high observed parental hostility at age 3 was associated with greater concurrent externalizing symptoms at age 3 and predicted increases in internalizing and externalizing symptoms from age 3 to age 6. Findings highlight that increased stress reactivity, within the context of hostile parenting, plays a role in the emergence of psychopathology from preschool to school entry.

Racial/ethnic minorities are more vulnerable to mental and physical health problems, but we know little about the psychobiological underpinnings of these disparities. In this study, we examined racial/ethnic differences in cortisol diurnal patterns and affect as initial steps toward elucidating long-term health disparities. A racially/ethnically diverse (39.5% White, 60.5% minority) sample of 370 adolescents (57.3% female) between the ages of 11.9 and 18 years (M = 14.65 years, SD = 1.39) participated in this study. These adolescents provided 16 cortisol samples (4 samples per day across 4 days), allowing the computation of diurnal cortisol slopes, the cortisol awakening response, and diurnal cortisol output (area under the curve), as well as daily diary ratings of high-arousal and low-arousal positive and negative affect. Consistent with prior research, we found that racial/ethnic minorities (particularly African American and Latino youth) exhibited flatter diurnal cortisol slopes compared to White youth, F (1, 344.7) = 5.26, p = .02, effect size g = 0.25. Furthermore, African American and Asian American youth reported lower levels of positive affect (both high arousal and low arousal) compared to White youth. Racial/ethnic differences in affect did not explain differences in cortisol patterns, suggesting a need to refine our models of relations between affect and hypothalamic–pituitary–adrenocortical activity. We conclude by proposing that a deeper understanding of cultural development may help elucidate the complex associations between affect and hypothalamic–pituitary–adrenocortical functioning and how they explain racial/ethnic differences in both affect and stress biology.