This was a prospective longitudinal multisite study of the effects of prenatal cocaine and/or opiate exposure on temperament in 4-month-olds of the Maternal Lifestyle Study (N = 958: 366 cocaine exposed, 37 opiate exposed, 33 exposed to both drugs, 522 matched comparison). The study evaluated positivity and negativity during The Behavior Assessment of Infant Temperament (Garcia Coll et al., 1988). Parents rated temperament (Infant Behavior Questionnaire; Rothbart, 1981). Cocaine-exposed infants showed less positivity overall, mainly during activity and threshold items, more negativity during sociability items, and less negativity during irritability and threshold items. Latent profile analysis indicated individual temperament patterns were best described by three groups: low/moderate overall reactivity, high social negative reactivity, and high nonsocial negative reactivity. Infants with heavy cocaine exposure were more likely in high social negative reactivity profile, were less negative during threshold items, and required longer soothing intervention. Cocaine- and opiate-exposed infants scored lower on Infant Behavior Questionnaire smiling and laughter and duration of orienting scales. Opiate-exposed infants were rated as less respondent to soothing. By including a multitask measure of temperament we were able to show context-specific behavioral dysregulation in prenatally cocaine-exposed infants. The findings indicate flatter temperament may be specific to nonsocial contexts, whereas social interactions may be more distressing for cocaine-exposed infants.

Current adolescent substance use risk models have inadequately predicted use for African Americans, offering limited knowledge about differential predictability as a function of developmental period. Among a sample of 500 African American youth (ages 11–21), four risk indices (i.e., social risk, attitudinal risk, intrapersonal risk, and racial discrimination risk) were examined in the prediction of alcohol, marijuana, and cigarette initiation during early (ages 11–13), mid (ages 16–18), and late (ages 19–21) adolescence. Results showed that when developmental periods were combined, racial discrimination was the only index that predicted initiation for all three substances. However, when risk models were stratified based on developmental period, variation was found within and across substance types. Results highlight the importance of racial discrimination in understanding substance use initiation among African American youth and the need for tailored interventions based on developmental stage.

One of the central tenets of developmental psychopathology is the belief that we can learn more about normal functioning through the study of psychopathology and arrive at a better understanding of pathological conditions through investigations of normal behavior. Advances in knowledge from one area will inform us regarding mechanisms at work in the other. A similar perspective is the driving force behind recent scientific advances in our understanding of certain developmental disorders. In this paper, molecular findings for four developmental disorders are reviewed: Prader–Willi syndrome, fragile X syndrome, Williams syndrome, and lissencephaly. These disorders were chosen for discussion because putative genes for each of them have been isolated. The ways in which mutations within these genes disrupt normal cognitive and behavioral functioning are discussed. Although considerable progress has been achieved in understanding the genetic mechanisms for these illnesses, much more research is needed to identify the environmental and genetic factors that interact to contribute to the expression of the more complex behavioral disorders.

In sub-Saharan countries, like South Africa, there is scant understanding of adolescent resilience to depression over time; the multisystemic resource combinations that support such resilience; and whether more diverse resource combinations yield better mental health dividends. In response, we conducted a longitudinal concurrent nested mixed methods study with 223 South African adolescents (mean age: 17.16 years, SD = 1.73; 64.60% girls; 81.60% Black). Using longitudinal mixture modeling, the quantitative study identified trajectories of depression and associations between trajectory membership and resource diversity. Using a draw-and-write methodology and reflexive thematic analyses, the qualitative study explored the resource diversity associated with each trajectory. Taken together, these studies identified four depression trajectories (Stable Low; Declining; Worsening; Chronic High) with varying resource diversity at baseline and over time. Resource diversity was inclusive of personal, relational, contextual, and culturally valued resources in both the Stable Low and Declining trajectories, with emphasis on relational supports. Personal resources were emphasized in the Worsening and Chronic High trajectories, and culturally valued and contextual resources de-emphasized. In summary, resource constellations characterized by within and across system diversity and cultural responsiveness are more protective and will be key to advancing sub-Saharan adolescent mental health.

In interventions for at-risk children, Tom Dishion strongly exhorted programs that are short term, cost-effective, and delivered in families’ own communities, just as resilience researchers underscore the need for programs that provide ongoing support for children's primary caregivers, and are implementable on a large scale. Presented here are preliminary results on a short-term intervention for mothers, the Authentic Connections Virtual Groups. A previous randomized trial of the in-person version of this program, conducted with mothers at high risk for stress and burnout, showed significant benefits. There had been zero dropouts across the 3-month program, and participants showed significant improvements on psychological indices as well as cortisol, even 3 months after the program ended. In the present study, virtual groups were conducted with five sets of women, all white-collar professionals with highly stressful, exacting careers, and most also primary caregivers of their children. Again, there were zero dropouts. Mean satisfaction ratings were 9.6 of 10, and the Net Promoter Score (promoters vs. detractors) fell in the “world class” range. To illuminate mechanisms of change, participants’ responses to open-ended questions on the groups’ value are presented verbatim. Recurrently mentioned were the development of new, authentic connections and invaluable ongoing support. These results, with the low costs and ease of women's attendance, attest to the value of expanding offerings such as these, toward benefiting even more highly stressed mothers themselves as well as the children for whose care they are responsible.

Exposure to threat increases the risk for internalizing problems in adolescence. Deficits in integrating bodily cues into representations of emotion are thought to contribute to internalizing problems. Given the role of the medial prefrontal cortex in regulating bodily responses and integrating them into representations of emotional states, coordination between activity in the medial prefrontal cortex and autonomic nervous system responses may be influenced by past threat exposure with consequences for the emergence of internalizing problems. A sample of 179 Mexican-origin adolescents (88 female) reported on neighborhood and school crime, peer victimization, and discrimination when they were 10–16 years old. At age 17, participants underwent a functional neuroimaging scan during which they viewed pictures of emotional faces while respiratory sinus arrhythmia (RSA) and skin conductance responses were measured. Adolescents also reported symptoms of internalizing problems. Greater exposure to threats across adolescence was associated with more internalizing problems. Threat exposure was also associated with stronger negative coupling between the ventromedial prefrontal cortex and RSA. Stronger negative ventromedial prefrontal cortex–RSA coupling was associated with fewer internalizing problems. These results suggest the degree of coordinated activity between the brain and parasympathetic nervous system is both enhanced by threat experiences and decreased in adolescents with more internalizing problems.

This study examined struggles to establish autonomy and relatedness with peers in adolescence and early adulthood as predictors of advanced epigenetic aging assessed at age 30. Participants (N = 154; 67 male and 87 female) were observed repeatedly, along with close friends and romantic partners, from ages 13 through 29. Observed difficulty establishing close friendships characterized by mutual autonomy and relatedness from ages 13 to 18, an interview-assessed attachment state of mind lacking autonomy and valuing of attachment at 24, and self-reported difficulties in social integration across adolescence and adulthood were all linked to greater epigenetic age at 30, after accounting for chronological age, gender, race, and income. Analyses assessing the unique and combined effects of these factors, along with lifetime history of cigarette smoking, indicated that each of these factors, except for adult social integration, contributed uniquely to explaining epigenetic age acceleration. Results are interpreted as evidence that the adolescent preoccupation with peer relationships may be highly functional given the relevance of such relationships to long-term physical outcomes.

A recent article in this journal reported a number of gene × environment interactions involving a serotonin transporter–gene network polygenic score and a composite index of prenatal adversity predicting several problem behavior outcomes at 48 months (e.g., anxious/depressed, pervasive developmental problems) and at 60 months (e.g., withdrawal, internalizing problems), yet did not illuminate the nature or form these genetic × environment interactions took. Here we report results of six additional analyses to evaluate whether these interactions reflected diathesis–stress or differential–susceptibility related processes. Analyses of the regions of significance and proportion of interaction index are consistent with the diathesis–stress model, seemingly because of the truncated nature of the adversity score (which did not extend to supportive/positive prenatal experiences/exposures); in contrast, the proportion (of cases) affected index favors the differential–susceptibility model. These results suggest the need for future studies to extend measurement of the prenatal environment to highly supportive experiences and exposures.

Violence exposure during childhood and adolescence is associated with a range of negative psychosocial outcomes. Research examining the impact of violence exposure has been limited by the compartmentalization into separate bodies of research (e.g., community violence, domestic violence). There is also a paucity of research examining long-term adult outcomes. Using a large and racially diverse sample (n = 754; male = 58%; Black = 46%), the current longitudinal study aimed to elucidate the comparative and cumulative effect of different types of violence exposure (witnessing vs. victimization) across different locations (home, school, neighborhood) in childhood and adolescence (lifetime through Grade 8) on long-term internalizing, externalizing, and attention problems; substance use; and intimate partner violence in adulthood (age 25). Victimization, but not witnessing violence, predicted all five adult outcomes. Specifically, being victimized at home was associated with the widest range of negative outcomes (internalizing, externalizing, and attention problems), while school victimization was associated with substance use. Further, when youth experienced multiple types of violence across multiple locations (cumulative violence exposure), they experienced a more diverse range of negative outcomes in adulthood (composite score). The current study highlights the stronger effects of violence exposure in more proximal contexts, and how these locations are important for emotional and behavioral development.

Child genotype is an important biologically based individual difference conferring differential sensitivity to the effect of parental behavior. This study explored dopaminergic polygenic composite × parental behavior interactions in relation to young children’s executive function. Participants were 135 36-month-old children and their mothers drawn from a prospective cohort followed longitudinally from pregnancy. A polygenic composite was created based on the number of COMT, DAT1, DRD2, and DRD4 alleles associated with increased reward sensitivity children carried. Maternal negative reactivity and responsiveness were coded during a series of structured mother–child interactions. Executive function was operationalized as self-control and working memory/inhibitory control. Path analysis supported a polygenic composite by negative reactivity interaction for self-control. The nature of the interaction was one of diathesis-stress, such that higher negative reactivity was associated with poorer self-control for children with higher polygenic composite scores. This result suggests that children with a higher number of alleles may be more vulnerable to the negative effect of negative reactivity. Negative reactivity may increase the risk for developing behavior problems in this population via an association with poorer self-control. Due to the small sample size, these initial findings should be treated with caution until they are replicated in a larger independent sample.

Childhood adversity is thought to undermine youth socioemotional development via altered neural function within regions that support emotion processing. These effects are hypothesized to be developmentally specific, with adversity in early childhood sculpting subcortical structures (e.g., amygdala) and adversity during adolescence impacting later-developing structures (e.g., prefrontal cortex; PFC). However, little work has tested these theories directly in humans. Using prospectively collected longitudinal data from the Fragile Families and Child Wellbeing Study (FFCWS) (N = 4,144) and neuroimaging data from a subsample of families recruited in adolescence (N = 162), the current study investigated the trajectory of harsh parenting across childhood (i.e., ages 3 to 9) and how initial levels versus changes in harsh parenting across childhood were associated with corticolimbic activation and connectivity during socioemotional processing. Harsh parenting in early childhood (indexed by the intercept term from a linear growth curve model) was associated with less amygdala, but not PFC, reactivity to angry facial expressions. In contrast, change in harsh parenting across childhood (indexed by the slope term) was associated with less PFC, but not amygdala, activation to angry faces. Increases in, but not initial levels of, harsh parenting were also associated with stronger positive amygdala–PFC connectivity during angry face processing.

As championed by the work of Ed Zigler, investing in nurturing environments for all children is a chief tenet of primary prevention that will have far-reaching benefits to the health and welfare of all members of society. Children who endure child maltreatment (CM) are among society's most vulnerable. Prospective longitudinal research aimed at a comprehensive understanding of the mechanisms linking CM to subsequent adverse health consequences is needed to improve outcomes and to strengthen causal inference. This paper outlines the methods of the Child Health Study (CHS), a large, state-wide longitudinal cohort of recently maltreated and nonmaltreated youth aged 8–13 who will be assessed every 2 years. The CHS is designed to include in-depth assessments of multiple environmental, behavioral, neural, physiological, and molecular mechanisms through which CM may impact a broad spectrum of youth development, including behavioral and physical health outcomes. In addition to describing the conceptual framework and methods underlying the CHS, we provide information on valuable “lessons learned” in the hopes of supporting future research efforts facing similar challenges. The ultimate goal of this research is demonstrating how policies regarding CM impact the well-being, resilience and recovery of survivors and that they are worthy of large public investment.

This article presents our response to the comments of Baron-Cohen, Harris, Hobson, and Leslie and Happé. We suggest that a singular cognitive hypothesis does not provide a parsimonious explanation of autism. We argue that certain aspects of autism, including observations of joint-attention deficits and observations of deficits in the prosodic elements of speech, may best be explained in terms of both cognitive and affective factors. We also acknowledge the validity of the criticism of our contingency processing deficit hypothesis (Mundy & Sigman, 1989a). In response to this criticism, we offer a modification of our model of joint-attention skill deficits in autistic children.

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.

Structural and functional magnetic resonance imaging (MRI) are increasingly common research methods among investigators interested in typically and atypically developing populations. However, the effective use of these tools requires an understanding of the basis of the magnetic resonance signal, as well as some of the additional experimental complications that arise when collecting MRI data from developmental populations. This primer provides a foundation for investigators who wish to utilize MRI methods in their research and whose primary interest involves typically and atypically developing populations. The basic concepts of MRI physics are introduced, as well as the typical MRI scanner components and their role in MRI data acquisition. In addition, a variety of scan types (structural, functional, diffusion tensor) are discussed, along with a number of important experimental design factors that can impact the quality and utility of the data collected. Special consideration is given to working with pediatric and special populations.

Four different models have been generally proposed as plausible etiological explanations for the relation between personality and psychopathology, namely, the vulnerability, complication, pathoplasty, and spectrum or continuity model. The current study entails a joint investigation of the continuity, pathoplasty, and complication models to explain the nature of the associations between early maladaptive traits and psychopathology over time in 717 referred and community children (54.4% girls), aged from 8 to 14 years. Across a 2-year time span, maladaptive traits and psychopathology were measured at three different time points, thereby relying on comprehensive and age-specific dimensional operationalizations of both personality symptoms and psychopathology. The results demonstrate overall compelling evidence for the continuity model, finding more focused support for pathoplasty and complication effects for particular combinations of personality symptoms and psychopathology dimensions. As expected, the continuity associations were found to be more robust for those personality–psychopathology associations that are conceptually closer, such as the emotional instability/introversion–internalizing problems association and the disagreeableness–externalizing problems association. Continuity associations were also stronger when personality was considered from a maladaptive rather than from a general trait perspective. The implication of the findings for the treatment of psychopathology and personality symptoms are briefly discussed.

Life course theorists posit that sensitive periods exist during life span development where risk and protective factors may be particularly predictive of psychological outcomes relative to other periods in life. While there have been between-cohort studies trying to examine differences in discrimination and depressive symptoms, these studies have not been designed to identify these sensitive periods, which are best modeled by examining intra-individual change across time. To identify sensitive periods where discrimination and shift-&-persist (S&P) – a coping strategy that may protect against the negative impact of discrimination – are most strongly predictive of depressive symptoms, we employed latent growth curve modeling using an accelerated longitudinal design to track intra-individual change in depressive symptoms from ages 20–69. Participants were 3,685 adults measured at three time points ~10 years apart from the Midlife in the United States study (Mage = 37.93, SD = 6.948 at Wave I). Results identified two sensitive periods in development where high levels of S&P interacted with discrimination to protect against depressive symptoms; during the 30s and a lagged effect where 40's S&P protected against depressive symptoms when participants were in their 50s. Implications for the life course study of discrimination, coping, and depression are discussed.

Translational research focuses on innovation in healthcare settings, but this is a two-way process that may have implications for either treatment or prevention. Smoking and lung cancer and the fetal alcohol syndrome are used as examples. Experimental medicine that budges basic and clinical science often constitutes a key way forward. Areas of scientific progress and challenge are discussed in relation to drug action, social cognition, cognitive neuroscience, molecular genetics, gene–environment interaction, and epigenetics. Key concepts and challenges in relation to stress include toxicity, allostatic load, the hypothalamus–pituitary–adrenal axis, and objectives versus subjective stress. The reasons for the need to test causal inferences are discussed. Various kinds of “natural experiments” are discussed in illustration using the assisted conception design, the discordant monozygotic twin design, and the study of universal exposure. Animal models are discussed in relation to enrichment and deprivation effects and the effects of infant separation experiences, epigenetic effects, and the biological embedding of experiences. Translational issues are discussed in relation to the hypothalamic–pituitary–adrenal axis, epigenetics, and inflammation. In conclusion, it is suggested that there are immediate possibilities for experimental medicine but caution is needed with respect to moving into translation too quickly.

Extremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.

Building on Ellis et al.’s theorization for potent dimensions of environmental adversity, the present work sought to evaluate how environmental harshness and unpredictability might function directly and in interaction with child sensory processing sensitivity (SPS) to shape the development of child socioemotional functioning. Participants were 235 young children (Mage = 2.97 at the first measurement occasion) and their parents, who were followed for two consecutive annual measurement occasions. Child SPS was measured through behavioral observation across multiple tasks within the laboratory setting. Greater environmental unpredictability was significantly associated with the development of children’s externalizing problems over a year only for children with high SPS. Follow-up analyses indicated that the unpredictability-x-SPS interaction was consistent with differential susceptibility, such that high SPS children showed greater increases in externalizing problems under high unpredictability, but also lower increases/greater decreases in externalizing problems under low unpredictability. Such association did not apply to children with low SPS.