The ability to regulate stress is a critical developmental milestone of early childhood that involves a set of interconnected behavioral and physiological processes and is influenced by genetic and environmental stimuli. Prenatal exposure to traumatic stress and trauma, including intimate partner violence (IPV), increases risk for offspring biobehavioral regulation problems during childhood and adolescence. Although individual differences in susceptibility to prenatal stress have been largely unexplored, a handful of studies suggest children with specific genetic characteristics are most vulnerable to prenatal stress. We evaluated the brain-derived neurotrophic factor Val66Met gene (BDNF) as a moderator of the effect of prenatal IPV exposure on infant temperamental and cortisol regulation in response to a psychosocial challenge. Ninety-nine mother–infant dyads recruited from the community were assessed when infants (51% female) were 11 to 14 months. Maternal reports of IPV during pregnancy and infant temperament were obtained, and infant saliva was collected for genotyping and to assess cortisol reactivity (before and after the Strange Situation Task). Significant genetic moderation effects were found. Among infants with the BDNF Met allele, prenatal IPV predicted worse temperamental regulation and mobilization of the cortisol response, while controlling for infant postnatal exposure to IPV, other maternal traumatic experiences, and infant sex. However, prenatal IPV exposure was not associated with temperamental or cortisol outcomes among infant carriers of the Val/Val genotype. Findings are discussed in relation to prenatal programming and biological susceptibility to stress.

The objective of the current study was to apply the novel technique of time-varying effect modeling to examine age-varying associations between specific coping strategies and depressive symptoms across adolescence and emerging adulthood (ages 14–24). The participants were drawn from a community sample and followed across 4 years of high school and once 5 years postgraduation (N = 1,251, 53% female, 58% non-Hispanic White). Coping and depressive symptom questionnaires were administered across all data collection time points. Time-varying effect modeling used all available data (N = 5,651 measurement occasions) and adjusted for gender. Venting emotions and denial were associated with more depressive symptoms at a similar magnitude across adolescence and emerging adulthood. A positive association between problem solving oriented strategies (planning, active coping) and depressive symptoms was not observed until age 17.5, after which the magnitude of the association strengthened. More frequent instrumental and emotional support seeking were linked to fewer depressive symptoms between ages 18.8 and 23.6. More frequent use of humor was associated with greater depressive symptoms from ages 14.0 to 14.6, but with fewer depressive symptoms from ages 16.8 to 18.8. The findings illuminate when and how associations between specific coping strategies and depressive symptoms may emerge and change across developmental age, generating both theoretical and clinical implications.

Violence exposure during childhood is common and associated with poor cognitive and academic functioning. However, little is known about how violence exposure influences cognitive processes that might contribute to these disparities, such as working memory, or their neural underpinnings, particularly for cognitive processes that occur in emotionally salient contexts. We address this gap in a sample of 54 participants aged 8 to 19 years (50% female), half with exposure to interpersonal violence. Participants completed a delayed match to sample task for emotional faces while undergoing functional magnetic resonance imaging scanning. Violence-exposed youth performed worse than controls on happy and neutral, but not angry, trials. In whole-brain analysis, violence-exposed youth had reduced activation in the left middle frontal gyrus and right intraparietal sulcus during encoding and the left superior temporal sulcus and temporal–parietal junction during retrieval compared to control youth. Reduced activation in the left middle frontal gyrus during encoding and the left superior temporal sulcus during retrieval mediated the association between violence exposure and task performance. Violence exposure influences the frontoparietal network that supports working memory as well as regions involved in facial processing during working memory for emotional stimuli. Reduced neural recruitment in these regions may explain atypical patterns of cognitive processing seen among violence-exposed youth, particularly within emotional contexts.

Substantial evidence links socioeconomic status to internalizing and externalizing behavior problems. However, it is unclear how these two categories of behavior problems relate to specific components of socioeconomic status (e.g., income, educational attainment, and occupational prestige) or overall social status. In this study, we conducted a second-order meta-analysis to estimate the average associations of income, education, occupation, and overall socioeconomic status with internalizing and externalizing behavior problems, and to examine if age, sex, and race/ethnicity moderated these associations. Our systematic search in PsycINFO, PubMed, Google Scholar, Web of Science, and ProQuest Dissertations and Theses Global identified 12 meta-analyses (17% unpublished), including approximately 474 primary studies and 327,617 participants. In relation to internalizing, we found small average associations with income, r+ = –.18, 95% confidence interval (CI) [–.31, –.04], and education, r+ = –.12, 95% CI [–.15, –.09]. In relation to externalizing, we found smaller associations with income, r+ = –.02, 95% CI [–.15, .10], education, r+ = –.03, 95% CI [–.16, .10], and overall socioeconomic status, r+ = –.05, 95% CI [–.11, .01], but these CIs included zero. Only sex composition of the samples moderated the latter association. We provide recommendations for best practices and future research directions.

Although some risk taking in adolescence is normative, evidence suggests that adolescents raised in conditions of socioeconomic disadvantage are disproportionately burdened with risk taking and its negative consequences. Using longitudinal data from the NICHD Study of Early Child Care and Youth Development, we investigated quality of the early caregiving environment as a potential prospective buffer against the long-term association between childhood poverty and adolescent risk taking. Multicategorical moderation model results indicated that if raised in poverty across age 1–54 months (average family income to needs ratio ≤ 1.02), relative to affluence (income to needs ratio ≥ 6.16), adolescents with histories of secure attachment to caregivers exhibited two times the number of risk behaviors at age 15, whereas adolescents with insecure–disorganized histories exhibited nearly five times the number of risk behaviors. Both early family economic hardship and history of insecure–disorganized attachment remained significant predictors of increased adolescent risk taking, alongside the interactive effect. Probing the interaction's region of significance revealed that history of secure (vs. insecure–disorganized) attachment is associated with protective reductions in risk taking below a family income to needs ratio of 2.24, or about 220% poverty level. Findings support a diathesis–stress model in which children with secure attachment histories are less deleteriously impacted by early socioeconomic adversity than their insecure–disorganized peers.

The literature on developmental psychopathology has been criticized for its limited integration of culture and, particularly, the lack of research addressing cultural development in relation to psychopathology. In this paper, I present how the study of ethnic–racial identity provides a heuristic model for how culture can be examined developmentally and in relation to psychopathology. In addition, I introduce the Identity Project intervention program and discuss how its findings provide empirical support for the notions that cultural development can be modified with intervention, and that such modifications can lead to psychosocial benefits for adolescents. Finally, I discuss existing challenges to advancing this work and important future directions for both basic and translational research in this area.

Data from the in-school sample of the PROSPER preventive intervention dissemination trial were used to investigate associations between alcohol dehydrogenase genes and alcohol use across adolescence, and whether substance misuse interventions in the 6th and 7th grades (targeting parenting, family functioning, social norms, youth decision making, and peer group affiliations) modified associations between these genes and adolescent use. Primary analyses were run on a sample of 1,885 individuals and included three steps. First, we estimated unconditional growth curve models with separate slopes for alcohol use from 6th to 9th grade and from 9th to 12th grade, as well as the intercept at Grade 9. Second, we used intervention condition and three alcohol dehydrogenase genes, 1B (ADH1B), 1C (ADH1C), and 4 (ADH4) to predict variance in slopes and intercept. Third, we examined whether genetic influences on model slopes and intercepts were moderated by intervention condition. The results indicated that the increase in alcohol use was greater in early adolescence than in middle adolescence; two of the genes, ADH1B and ADH1C, significantly predicted early adolescent slope and Grade 9 intercept, and associations between ADH1C and both early adolescent slope and intercept were significantly different across control and intervention conditions.

Although delinquency, substance use, and sexual activity are established to be highly intercorrelated, the extant research provides minimal evidence in support of one particular sequence of risk behavior or on the cascade effects from maltreatment. The present study tested a longitudinal model incorporating maltreatment, deviant peers, sexual behavior, delinquency, and substance use to elucidate the sequential pathway(s) from maltreatment to each specific risk behavior throughout adolescence. Data came from a longitudinal study on the effects of maltreatment on adolescent development (N = 454) with four study assessments from early (Time 1 M age = 10.98) to late adolescence (Time 4 M age = 18.22). Results from the cross-lagged model showed a sequence from maltreatment to sexual behavior (Time 1), to delinquency (Time 2), to sexual behavior (Time 3), to substance use and delinquency (Time 4). These findings support sexual behavior as the initial risk behavior that is the catalyst for engagement in more advanced risk behaviors across adolescence.

Prenatal programming models have rarely been applied to research on children with prenatal substance exposure, despite evidence suggesting that prenatal drug exposure is a form of stress that impacts neurodevelopmental outcomes and risk for psychopathology. Utilizing data from two longitudinal multisite studies comprising children prenatally exposed to substances as well as a nonexposed comparison group (Maternal Lifestyle Study, n = 1,388; Infant Development, Environment, and Lifestyle study, n = 412), we tested whether early phenotypic indicators of hypothesized programming effects, indexed by growth parameters at birth and infant temperament, served as a link between prenatal substance exposure and internalizing and externalizing behavior at age 5. Latent profile analysis indicated that individual differences in reactivity and regulation for infants prenatally exposed to substances was best characterized by four temperament profiles. These profiles were virtually identical across two independent samples, and demonstrated unique associations with adjustment difficulties nearly 5 years later. Results of path analysis using structural equation modeling also showed that increased prenatal substance exposure was linked to poorer growth parameters at birth, profiles of temperamental reactivity in infancy, and internalizing and externalizing behavior at age 5. This pathway was partially replicated across samples. This study was among the first to link known individual-level correlates of prenatal substance exposure into a specific pathway to childhood problem behavior. Implications for the developmental origins of a child's susceptibility to psychopathology as a result of intrauterine substance exposure are discussed.

Recently in this journal, Weeland et al. (2018) published a thought-provoking article reporting moderating effects of children's serotonin transporter-linked polymorphisms (5-HTTLPR) on negative parenting during prevention with the Incredible Years series. Participants were parents and young children of 387 families enrolled in the Observational Randomized Control Trial of Childhood Differential Susceptibility study. An equally important finding, which we focus on in this comment, involved null effects for all tests of parenting as a mediator of prevention-induced improvements in children's externalizing behavior. Although such findings may seem surprising, both confirmations of and failures to confirm parenting change as a mediator of child behavior change are common in the prevention and intervention literatures. In this comment, we explore likely reasons for heterogeneity in findings, including both moderators of treatment effect size and methods used to test mediation. Common moderators of prevention and intervention response to Incredible Years include dose, parenting problems at intake, high-risk versus clinical nature of samples, how parenting is measured, and whether child training is included with parent training. All of these moderators affect power to detect mediation. We then discuss conceptual criteria for testing mediation in randomized clinical trials, and problems with interpreting mediating paths in cross-lag panel models. Although the gene effect reported by Weeland et al. is important, their cross-lag panel models do not provide strong tests of parenting as a mediator of child behavior change. We conclude with recommendations for testing mediation in randomized clinical trials.

In this prospective study of upper middle class youth, we document frequency of alcohol and drug use, as well as diagnoses of abuse and dependence, during early adulthood. Two cohorts were assessed as high school seniors and then annually across 4 college years (New England Study of Suburban Youth younger cohort [NESSY-Y]), and across ages 23–27 (NESSY older cohort [NESSY-O]; ns = 152 and 183 at final assessments, respectively). Across gender and annual assessments, results showed substantial elevations, relative to norms, for frequency of drunkenness and using marijuana, stimulants, and cocaine. Of more concern were psychiatric diagnoses of alcohol/drug dependence: among women and men, respectively, lifetime rates ranged between 19%–24% and 23%–40% among NESSY-Os at age 26; and 11%–16% and 19%–27% among NESSY-Ys at 22. Relative to norms, these rates among NESSY-O women and men were three and two times as high, respectively, and among NESSY-Y, close to one among women but twice as high among men. Findings also showed the protective power of parents’ containment (anticipated stringency of repercussions for substance use) at age 18; this was inversely associated with frequency of drunkenness and marijuana and stimulant use in adulthood. Results emphasize the need to take seriously the elevated rates of substance documented among adolescents in affluent American school communities.

Following the civil war in Syria, there has been a growing interest in the impact of war, violent conflict, and refuge on the development and mental health of refugee children in general and Syrian refugee children in particular. The objective of this paper is threefold: (a) to critically review the existing literature on the psychological functioning of Syrian refugee children, with a particular focus on those residing in the urban areas or camps in Turkey; (b) to identify the main theoretical and methodological problems of this emerging literature; and (c) to suggest guidelines for how to improve research and practice in this field. The reviewed literature predominantly focuses on psychological trauma, trauma-related symptomatology or other maladaptive functioning in children, and psychosocial interventions conducted toward alleviating these issues. This paper will summarize the research findings in the above-mentioned topics to discern what can be known from the existing literature on Syrian refugee children.

In their commentary, Beauchaine and Slep (2018) raise important issues regarding research on behavioral parenting training (BPT). In this reply we highlight key points of agreement and respond to issues that we feel require clarification. BPT has been repeatedly proven effective in decreasing disruptive child behavior (also in the work of our research team). Yet, there is much to learn about for whom and how BPT is effective. Specifically, assessing the how (i.e., mediation) comes with many challenges. One of these challenges is taking into account the timeline of change, and being able to infer causal mechanisms of change. We argue that cross-lagged panel models (which we, and many other scholars, used) are a valid and valuable method for testing mediation. At the same time, our results raise important questions, specifically about the timing and form of expected changes in parenting and child behavior after BPT. For example, are these changes linear and gradual or do they happen more suddenly? To select the appropriate design, assessment tools, and statistical models to test mediation, we need to state detailed hypotheses on what changes when. An important next step might be to assess multiple putative mediators on different timescales, not only before and after, but specifically also during BPT.

Research shows that childhood dysregulation is associated with later psychiatric disorders. It does not yet resolve discrepancies in the operationalization of dysregulation. It is also far from settled on the origins and implications of individual differences in dysregulation. This study tested several operational definitions of dysregulation using Achenbach attention, anxious/depressed, and aggression subscales. Individual growth curves of dysregulation were computed, and predictors of growth differences were considered. The study also compared the predictive utility of the dysregulation indexes to standard externalizing and internalizing indexes. Dysregulation was indexed annually for 24 years in a community sample (n = 585). Hierarchical linear models considered changes in dysregulation in relation to possible influences from parenting, family stress, child temperament, language, and peer relations. In a test of the meaning of dysregulation, it was related to functional and psychiatric outcomes in adulthood. Dysregulation predictions were further compared to those of the more standard internalizing and externalizing indexes. Growth curve analyses showed strong stability of dysregulation. Initial levels of dysregulation were predicted by temperamental resistance to control, and change in dysregulation was predicted by poor language ability and peer relations. Dysregulation and externalizing problems were associated with negative adult outcomes to a similar extent.

The present review revisits three hypothesized models that potentially could explain how prenatal maternal stress influences fetal development, birth outcomes, and subsequent developmental psychopathology. These models were mostly based on animal models, and new evidence for these models from human studies is evaluated. Furthermore, divergent trajectories from prenatal exposure to adversities to offspring affected outcomes are reviewed, including the comparison of studies on prenatal maternal stress with research on maternal substance use and maternal malnutrition during pregnancy. Finally, new directions in research on the mechanism underlying prenatal stress effects on human offspring is summarized. While it is concluded that there is abundant evidence for the negative associations between prenatal maternal stress and offspring behavioral, brain, and psychopathological outcomes in humans, there is no consistent evidence for specific mechanisms or specific outcomes in relation to stress exposure in utero. Rather, principles of multifinality and equifinality best describe the consequences for the offspring, suggesting a generic vulnerability and different pathways from prenatal adversities to developmental psychopathology, which complicates the search for underlying mechanisms. New and promising directions for research are provided to get a better understanding of how prenatal stress gets under the skin to affect fetal development.

Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action.

Using multilevel models, we examined mother-, father-, and child-reported (N = 1,336 families) externalizing behavior problem trajectories from age 7 to 14 in nine countries (China, Colombia, Italy, Jordan, Kenya, the Philippines, Sweden, Thailand, and the United States). The intercept and slope of children's externalizing behavior trajectories varied both across individuals within culture and across cultures, and the variance was larger at the individual level than at the culture level. Mothers’ and children's endorsement of aggression as well as mothers’ authoritarian attitudes predicted higher age 8 intercepts of child externalizing behaviors. Furthermore, prediction from individual-level endorsement of aggression and authoritarian attitudes to more child externalizing behaviors was augmented by prediction from cultural-level endorsement of aggression and authoritarian attitudes, respectively. Cultures in which father-reported endorsement of aggression was higher and both mother- and father-reported authoritarian attitudes were higher also reported more child externalizing behavior problems at age 8. Among fathers, greater attributions regarding uncontrollable success in caregiving situations were associated with steeper declines in externalizing over time. Understanding cultural-level as well as individual-level correlates of children's externalizing behavior offers potential insights into prevention and intervention efforts that can be more effectively targeted at individual children and parents as well as targeted at changing cultural norms that increase the risk of children's and adolescents’ externalizing behavior.

Adolescents’ appearance-related concerns can provoke increasing emotional, social, and eating-related problems. The aims of this five-wave (2.5-year), multiple-informant longitudinal study were to (a) examine growth trajectories of appearance anxiety symptoms and appearance esteem, (b) identify whether trajectories differed by gender, and (c) examine several launching factors including parent-reported physical maturation, peer-rated physical appearance, body mass index, and appearance teasing by parents and peers. Participants were 387 adolescents (44% boys) aged 10 to 13 years at the first assessment. Steep growth in appearance anxiety symptoms was found for both girls and boys, but there was no average change in appearance esteem. Girls had more elevated appearance anxiety symptoms and lower appearance esteem than boys, girls’ body mass index was associated with symptoms, and earlier physical maturation and teasing about appearance, alone and in combination, were associated with growth in appearance anxiety symptoms for girls and boys. Earlier maturing boys who were highly teased by parents, but even more so when teased by peers, were at utmost risk for elevated appearance anxiety symptoms and increasing symptoms over time. In contrast, all girls exhibited elevated or increasing appearance anxiety symptoms across time, with the exception of girls with the latest maturation who also reported little teasing about their appearance.