As challenges to child well-being through economic disadvantage, family disruption, and migration or displacement escalate world wide, the need for cross-culturally robust understanding of childhood adversity proportionately increases. Toward this end, developmental risk was assessed in four contrasting groups of 107 Nepali children ages 10–14 years that represent distinctive, common conditions in which contemporary children grow up. Relative cumulative burden (allostatic load) indexed by multiple dimensions of physical and psychosocial stress was ascertained among homeless street boys and three family-based groups, from poor urban squatter settlements, urban middle class, and a remote rural village. Biomarkers of stress and vulnerability to stress included growth status, salivary cortisol, antibodies to Epstein–Barr virus, acute phase inflammatory responses (alpha1-antichymotrypsin), and cardiovascular fitness and reactivity (flex heart rate and pressor response). Individual biomarkers of risk and allostatic load differed markedly among groups, were highest in villagers, and varied by components of allostatic load. Such data suggest a need for critical appraisal of homelessness and migration as a risk factor to youth, given prevailing local conditions such as rural poverty, and represents the only multidimensional study of childhood allostatic load and developmental risk in non-Western settings.

Children with severe antisocial behavior have an increased risk of showing violently aggressive and other forms of problem behavior in adolescence and adulthood. It is well established that both biological and social factors are involved in the development of antisocial behavior. The primary aim of this paper is to discuss the evidence that specific neurobiological systems are involved in the etiology of childhood-onset antisocial behavior. These factors are responsible for the severity of the behavioral problems observed in antisocial children, but they also play a role in their persistence, because they influence children's interactions with their environment. We will discuss the possible causes of disruptions in neurobiological systems in childhood antisocial behavior and point out the implications of these findings for theory and clinical practice. We will argue that familial factors (e.g., genetic influences, early childhood adversity) are linked to negative behavioral outcomes (e.g., antisocial behavior problems) through the mediating and transactional interplay with neurobiological deficits. An investigation of neurobiological functioning in antisocial children might not only indicate which children are most likely to persist in engaging in severe antisocial behavior, but also guide the development of new interventions.

This study builds upon prior findings of elevated substance use among suburban high school students, examining the ramifications of different parenting dimensions on substance use and related behaviors. The sample consisted of 258 11th graders in an affluent suburban community. Parenting predictors considered included those well-studied previously such as monitoring and closeness, as well as two newer dimensions: perceived containment (stringency of anticipated reactions in reaction to negative behaviors) and perceived commitment (e.g., helping the child despite other commitments). Outcomes included self-reported substance use, delinquency, and rule breaking, as well as teacher-rated inattentiveness and school grades. Findings showed elevated substance use among these 17-year-olds compared with national norms, especially among girls. Of the parent predictors, significant unique links with multiple outcomes were found for parents' knowledge of their children's activities and perceived parental containment (stringent repercussions) in reaction to the children's substance use. Notably, students reported that their parents were much more tolerant of their substance use than of other problem behaviors such as rudeness to adults and minor acts of delinquency. Results are discussed along with the implications for practice and research.

Despite the assumed prevalence of risk-taking behavior in adolescence, the laboratory evidence of risk taking remains scarce, and the individual variation poorly understood. Drawing from neuroscience studies, we tested whether risk and reward orientation are influenced by the perspective that adolescents take when making risky decisions. Perspective taking was manipulated by cuing participants prior to each choice whether the decision was made for “self,” or from the perspective of an “other” (the experimenter in Experiment 1; a hypothetical peer in Experiment 2). In Experiment 1, we show a developmental decrease in risk-taking behavior across different stages of adolescence. In addition, all age groups made fewer risky choices for the experimenter, but the difference between self and other was larger in early adolescence. In Experiment 2, we show that high sensation-seeking (SS) adolescents make more risky choices than low SS adolescents, but both groups make a similar differentiation for other individuals (low risk-taking or high risk-taking peers). Together, the results show that younger adolescents and high SS adolescents make more risky choices for themselves, but can appreciate that others may make fewer risky choices. The developmental change toward more rational decisions versus emotional, impulsive decisions may reflect, in part, more efficient integration of others’ perspectives into one's decision making. These developmental results are discussed regarding brain systems important for risk taking and perspective taking.

The present study evaluated the independent and cumulative effects of recent life stress, previous trauma, and recent trauma exposure on salivary cortisol levels among school-aged children. Sixty-eight children (mean age = 10.7 years) reported their exposure to life stressors and traumatic events in the 12 months preceding the study. Children and their caregivers reported frequency of exposure to trauma earlier in life. Exposure to life stress within the past 12 months was related to higher afternoon cortisol levels. Exposure to high levels of recent trauma in combination with frequent exposure to trauma earlier in life was related to both lower morning cortisol levels and higher afternoon cortisol levels. Results suggest that frequency, duration, and severity of exposure to stress and trauma played key roles in the prediction of basal cortisol levels in a community sample of urban youth.

Disturbances in the detection of, response to, and interpretation of emotion are common in many forms of psychopathology. The amygdala, striatum, and structures within the prefrontal cortex are highly involved in mediating these stages of emotion processing, and evidence indicates that these regions show structural and functional alterations in different types of psychopathology, including anxiety, depression, and autism spectrum disorders. However, we do not know how genes and the environment interact to alter development of these brain regions in ways that give rise to emotion-related psychopathology. This review discusses the current understanding of brain regions that are involved in emotional functioning, how they develop, and how they are altered in three forms of psychopathology: anxiety, depression, and autism spectrum disorders. Following this, a framework is described that may facilitate the integration of investigations of genetic variation and brain function with symptom and diagnostic measures. The framework involves three components: (a) a greater emphasis on simultaneously analyzing multiple levels (genes, brain function, behavior, symptoms, and diagnoses); (b) further integration of developmental considerations, including timing of environmental events, adaptations (or maladaptations), and disorder-related trajectories that guide some children toward atypical experiences; and (c) greater cross-talk between animal and human investigations to take advantage of biological measures that cannot be acquired in humans.

Altered functioning of the hypothalamic–pituitary–adrenal (HPA) axis is a robust correlate of major depression in adults, and to a lesser extent, in adolescents. Premorbid differences in HPA axis function have been found to prospectively predict the onset of adolescent depression. To what extent might our knowledge of HPA axis function in adolescents with, or at risk for, depression, help guide efforts to prevent depression in this age group? We review evidence regarding the role of the HPA axis in the development of adolescent depression, and examine whether and which HPA axis measures might be useful in guiding prevention efforts as (a) as a criterion by which to select youth at risk for depression, (b) as a predictor of which youth will be most responsive to prevention efforts, and (c) as an indicator of whether prevention/intervention efforts are working. We conclude that our current understanding of the HPA axis, and its measurement, in adolescent depression are not sufficiently precise to be of immediate practical use in improving prevention efforts. Incorporating HPA axis measures into prevention studies, however, would be immensely useful in clarifying the role of the HPA axis in adolescent depression, such that future prevention efforts might more confidently rely on HPA axis information.

Because marijuana use often precedes the use of other psychoactive substances, it has been characterized as a gateway to these other substances. The present study used data from both monozygotic (MZ) and dizygotic (DZ) twin pairs drawn from the National Longitudinal Study of Adolescent Youth (Add Health) to examine the “gateway effect” role of earlier marijuana on later hard drug use. Difference score analyses reveal that within-pair differences in earlier marijuana use, controlling for differences in earlier hard drug use, and peer marijuana use predicted later within-pair hard drug use differences for DZ twin pairs. In contrast, earlier differences in marijuana use among MZ twin pairs did not predict later hard drug use differences. Rather than supporting the interpretation that earlier marijuana use “triggers” later hard drug use, these results suggest that the longitudinal pattern of drug use that has been interpreted as the “gateway effect” might be better conceptualized as a genetically influenced developmental trajectory.

Foster children exhibit high rates of atypical neuroendocrine functioning compared to children in the general population. In particular, alterations in the daytime diurnal activity of the hypothalamic–pituitary–adrenal (HPA) axis have been observed in foster children, often characterized by blunted salivary cortisol levels (i.e., low morning levels that remain low throughout the day). There is emerging evidence that therapeutic interventions for foster children can affect this pattern of HPA axis activity, but the specific intervention components responsible for change have not been fully explicated. Within a randomized trial to evaluate a therapeutic intervention for foster preschoolers (n = 57 intervention condition; n = 60 comparison condition; n = 60 community comparison condition), the present study examined whether diurnal cortisol activity was associated with caregiver self-reported stress in response to child problem behavior. Results showed immediate reductions in caregiver stress that were sustained through 12 months postbaseline in the intervention condition. In contrast, caregivers in the regular foster care condition showed higher rates of stress across time and increased stress sensitivity to child problem behaviors. In addition, among caregivers in regular foster care, higher self-reported stress was associated with lower morning cortisol levels and more blunted diurnal cortisol activity. These results provide evidence that interventions can simultaneously impact caregiver stress and buffer children from the negative impacts of caregiver stress on HPA axis regulation.

Functional imaging studies have reported with remarkable consistency hyperactivity in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and caudate nucleus of patients with obsessive–compulsive disorder (OCD). These findings have often been interpreted as evidence that abnormalities in cortico–basal ganglia–thalamo–cortical loops involving the OFC and ACC are causally related to OCD. This interpretation remains controversial, however, because such hyperactivity may represent either a cause or a consequence of the symptoms. This article analyzes the evidence for a causal role of these loops in producing OCD in children and adults. The article first reviews the strong evidence for anatomical abnormalities in these loops in patients with OCD. These findings are not sufficient to establish causality, however, because anatomical alterations may themselves be a consequence rather than a cause of the symptoms. The article then reviews three lines of evidence that, despite their own limitations, permit stronger causal inferences: the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD. Converging evidence from these various lines of research supports a causal role for the cortico–basal ganglia–thalamo–cortical loops that involve the OFC and ACC in the pathogenesis of OCD in children and adults.

Low socioeconomic status (SES) background has been identified as a risk for several mental disorders. However evidence regarding SES and the developmental course of personality disorder (PD) has not been addressed. Nor is it clear whether an SES relationship to PD symptom course may be attributable to known associated risks. Further, specificity of such relationships to a particular PD diagnostic pattern independent of comorbidity with other PD or with depression has not been investigated. Data are from a general population studied longitudinally between ages 10 and 36 in four assessment waves. Effects of SES-associated risks on the level of symptoms of schizotypal and borderline disorders are estimated and compared to effects on depressive symptoms. Low family SES had robust modest independent effects on both PDs over the entire age span despite substantial cumulative effects of trauma history, stressful recent life events, IQ, poor parenting, and comorbid symptoms. SES effects on depressive symptoms were generally absent, but a small “protective” effect of low SES appeared when comorbidity with PD symptoms was taken into account. Cumulatively, these risks account for developmental failures of substantial magnitude and consequence, marking the importance of understanding the remaining mechanisms of SES effects and programmatic implications for minimizing associated risk.

Qualitative studies suggest that children react to parental imprisonment by developing internalizing as well as externalizing behaviors. However, no previous study has examined the effects of parental imprisonment on children's internalizing problems using standardized instruments, appropriate comparison groups, and long-term follow-up. Using prospective longitudinal data from the Cambridge Study in Delinquent Development, we compared boys separated because of parental imprisonment during their first 10 years of life with four control groups: boys who did not experience separation, boys separated because of hospitalization or death, boys separated for other reasons (usually parental disharmony), and boys whose parents were only imprisoned before the boys' births. Individual, parenting, and family risk factors for internalizing problems were measured when boys were ages 8–11 years. Separation because of parental imprisonment predicted boys' internalizing problems from age 14 to 48, even after controlling for childhood risk factors including parental criminality. Separation because of parental imprisonment also predicted the co-occurrence of internalizing and antisocial problems. These results suggest that parental imprisonment might cause long-lasting internalizing and antisocial problems for children.

Data from a community-based sample of 1,126 10th- and 11th-grade adolescents were analyzed using a model-based cluster analysis approach to empirically identify heterogeneous adolescent subpopulations from the person-oriented and pattern-oriented perspectives. The model-based cluster analysis is a new clustering procedure to investigate population heterogeneity utilizing finite mixture multivariate normal densities and accordingly to classify subpopulations using more rigorous statistical procedures for the comparison of alternative models. Four cluster groups were identified and labeled multiproblem high-risk, smoking high-risk, normative, and low-risk groups. The multiproblem high risk exhibited a constellation of high levels of problem behaviors, including delinquent and sexual behaviors, multiple illicit substance use, and depressive symptoms at age 16. They had risky temperamental attributes and lower academic functioning and educational expectations at age 15.5 and, subsequently, at age 24 completed fewer years of education, and reported lower levels of physical health and higher levels of continued involvement in substance use and abuse. The smoking high-risk group was also found to be at risk for poorer functioning in young adulthood, compared to the low-risk group. The normative and the low risk groups were, by and large, similar in their adolescent and young adult functioning. The continuity and comorbidity path from middle adolescence to young adulthood may be aided and abetted by chronic as well as episodic substance use by adolescents.

The amygdala has received great interest as a possible neurophysiological substrate of bipolar disorder (BD). This review summarizes information about the structure and function of the amygdala with attention to its role in experienced emotion and mood. We review the evidence for amygdala pathology in psychiatric conditions and discuss the role of the amygdala in BD during development. There appear to be consistent findings in the neuroimaging literature that suggest an etiological model for BD that involves abnormalities in the structure and function of the amygdala, but also depends on the failure of prefrontal cortical regions to modulate amygdala activity. In addition, evidence is accumulating to suggest that this model has flexible outcomes, depending on factors intrinsic and extrinsic to BD, and may follow several possible paths across the course of maturational development.

In conjunction with prospective ratings of child maltreatment (i.e., sexual abuse, physical abuse, and physical neglect) and measures of dissociation and somatization, this study examined prospective pathways between child maltreatment and nonsuicidal, direct self-injurious behavior (SIB; e.g., cutting, burning, self-hitting). Ongoing participants in the Minnesota Longitudinal Study of Parents and Children (N = 164; 83 males, 81 females) completed a semistructured interview about SIB when they were 26 years old. SIB emerged as a heterogeneous and prominent phenomenon in this low-income, mixed-gender, community sample. Child sexual abuse predicted recurrent injuring (i.e., three or more events; n = 13), whereas child physical abuse appeared more salient for intermittent injuring (i.e., one to two events; n = 13). Moreover, these relations appeared largely independent of risk factors that have been associated with child maltreatment and/or SIB, including child cognitive ability, socioeconomic status, maternal life stress, familial disruption, and childhood exposure to partner violence. Dissociation and somatization were related to SIB and, to a lesser degree, child maltreatment. However, only dissociation emerged as a significant mediator of the observed relation between child sexual abuse and recurrent SIB. The findings are discussed within a developmental psychopathology framework in which SIB is viewed as a compensatory regulatory strategy in posttraumatic adaptation.

Schizophrenia has been thought of as a disorder of reduced functional and structural connectivity. Recent advances in neuroimaging techniques such as functional magnetic resonance imaging, structural magnetic resonance imaging, diffusion tensor imaging, and small animal imaging have advanced our ability to investigate this hypothesis. Moreover, the power of longitudinal designs possible with these noninvasive techniques enable the study of not just how connectivity is disrupted in schizophrenia, but when this disruption emerges during development. This article reviews genetic and neurodevelopmental influences on structural and functional connectivity in human populations with or at risk for schizophrenia and in animal models of the disorder. We conclude that the weight of evidence across these diverse lines of inquiry points to a developmental disruption of neural connectivity in schizophrenia and that this disrupted connectivity likely involves susceptibility genes that affect processes involved in establishing intra- and interregional connectivity.

This article reports on the childhood origins and adult outcomes of female versus male antisocial behavior trajectories in the Dunedin longitudinal study. Four antisocial behavior trajectory groups were identified among females and males using general growth mixture modeling and included life-course persistent (LCP), adolescent-onset, childhood-limited, and low trajectory groups. During childhood, both LCP females and males were characterized by social, familial and neurodevelopmental risk factors, whereas those on the adolescent-onset pathway were not. At age 32, women and men on the LCP pathway were engaging in serious violence and experiencing significant mental health, physical health, and economic problems. Females and males on the adolescent-onset pathway were also experiencing difficulties at age 32, although to a lesser extent. Although more males than females followed the LCP trajectory, findings support similarities across gender with respect to developmental trajectories of antisocial behavior and their associated childhood origins and adult consequences. Implications for theory, research, and practice are discussed.

This paper examines the relationship between self-esteem in adolescence and later mental health, substance use, and life and relationship outcomes in adulthood. The investigation analyzed data from a birth cohort of approximately 1,000 New Zealand young adults studied to the age of 25. Lower levels of self-esteem at age 15 were associated with greater risks of mental health problems, substance dependence, and lower levels of life and relationship satisfaction at ages 18, 21, and 25. Adjustment for potentially confounding factors reduced the strength of these associations to either moderate or statistically nonsignificant levels. It was concluded that the effects of self-esteem during adolescence on later developmental outcomes were weak, and largely explained by the psychosocial context within which self-esteem develops.

Borderline personality disorder (BPD) is a paradigmatic disorder of adult attachment, with high rates of antecedent childhood maltreatment. The neurocognitive correlates of both attachment disturbance and maltreatment are both presently unknown in BPD. This study evaluated whether dimensional adult attachment disturbance in BPD is related to specific neurocognitive deficits, and whether childhood maltreatment is related to these dysfunctions. An outpatient BPD group (n = 43) performed nearly 1 SD below a control group (n = 26) on short-term recall, executive, and intelligence functions. These deficits were not affected by emotionally charged stimuli. In the BPD group, impaired recall was related to attachment–anxiety, whereas executive dysfunction was related to attachment–avoidance. Abuse history was correlated significantly with executive dysfunction and at a trend level with impaired recall. Neurocognitive deficits and abuse history exhibited both independent and interactive effects on adult attachment disturbance. These results suggest that (a) BPD patients' reactivity in attachment relationships is related to temporal–limbic dysfunction, irrespective of the emotional content of stimuli, (b) BPD patients' avoidance within attachment relationships may be a relational strategy to compensate for the emotional consequences of frontal-executive dysregulation, and (c) childhood abuse may contribute to these neurocognitive deficits but may also exert effects on adult attachment disturbance that is both independent and interacting with neurocognitive dysfunction.

Extraordinary progress in functional brain imaging, primarily advances in functional magnetic resonance imaging, now allows scientists to understand the neural systems serving reading and how these systems differ in dyslexic readers. Scientists now speak of the neural signature of dyslexia, a singular achievement that for the first time has made what was previously a hidden disability, now visible. Paralleling this achievement in understanding the neurobiology of dyslexia, progress in the identification and treatment of dyslexia now offers the hope of identifying children at risk for dyslexia at a very young age and providing evidence-based, effective interventions. Despite these advances, for many dyslexic readers, becoming a skilled, automatic reader remains elusive, in great part because though children with dyslexia can be taught to decode words, teaching children to read fluently and automatically represents the next frontier in research on dyslexia. We suggest that to break through this “fluency” barrier, investigators will need to reexamine the more than 20-year-old central dogma in reading research: the generation of the phonological code from print is modular, that is, automatic and not attention demanding, and not requiring any other cognitive process. Recent findings now present a competing view: other cognitive processes are involved in reading, particularly attentional mechanisms, and that disruption of these attentional mechanisms play a causal role in reading difficulties. Recognition of the role of attentional mechanisms in reading now offer potentially new strategies for interventions in dyslexia. In particular, the use of pharmacotherapeutic agents affecting attentional mechanisms not only may provide a window into the neurochemical mechanisms underlying dyslexia but also may offer a potential adjunct treatment for teaching dyslexic readers to read fluently and automatically. Preliminary studies suggest that agents traditionally used to treat disorders of attention, particularly attention-deficit/hyperactivity disorder, may prove to be an effective adjunct to improving reading in dyslexic students.