In the coming years we can look forward to research that clarifies specific mechanisms that account for the interplay between genetic and environmental influences on psychological development. Certain misconceptions, arising from research traditions initiated by Francis Galton on the one hand and G. Stanley Hall on the other, may now be set aside in the light of new evidence. Three important findings promise a new synthesis. First, while each of us is born with about 100,000 genes that, under ordinary circumstances, do not change, the expression of these genes on behavior is dynamic. Some genetic influences are expressed early in development, but others are manifest many years later. Second, genetic factors often account not only for some of the individual differences in the measures of adjustments we typically use to monitor development but also for individual differences in environmental experiences that covary with those measures of adjustment. Indeed, genetic factors have been found to account for a surprising amount of covariance between measures of the social environment and of adjustment in young children, adolescents, and adults. Third, the expression of genetic influences are very malleable and responsive to the social environment. These new findings are revealing specific mechanisms for the interplay of genetic and social environmental factors in four domains. First, the social environment may play both a necessary and specific role in the expression of particular genetic influences on a range of behaviors from depression to social responsibility. Second, an understanding of the interplay between the social environment and genetics may lead to a clearer definition of the phenotypic manifestations of particular genetic influences. Third, we will—as a result of these studies—have a clearer fix on the timing of important events and their sequence in development. Fourth, this new genre of work promises to illumine more completely mechanisms by which the social environment influences development independent of genetic influence.

Although the sensitization hypothesis is fundamental to process-oriented explanations of the effects of marital conflict on children, few longitudinal tests of the theory's propositions have been conducted. Hierarchical linear modeling was used in this prospective, longitudinal study (n = 297 families) to assess changes in the dimensions of responding to conflict (i.e., emotional, cognitive, and behavioral) for 3 consecutive years in youths between the ages of 8 and 19 years. Moreover, to test the notion of sensitization, analyses were conducted to examine whether change in marital conflict predicted change in children's responding across middle childhood and adolescence. Supporting the sensitization hypothesis, increases in exposure to hostile marital conflict were associated with increases in children's negative emotionality, threat, self-blame, and skepticism about resolution. With a few exceptions, the effects were largely consistent for boys and girls and for younger and older children.

Early caregiving adversity is associated with increased risk for social difficulties. The ventral striatum and associated corticostriatal circuitry, which have demonstrated vulnerability to early exposures to adversity, are implicated in many aspects of social behavior, including social play, aggression, and valuation of social stimuli across development. Here, we used resting-state functional magnetic resonance imaging to assess the degree to which early caregiving adversity was associated with altered coritocostriatal resting connectivity in previously institutionalized youth (n = 41) relative to youth who were raised with their biological families from birth (n = 47), and the degree to which this connectivity was associated with parent-reported social problems. Using a seed-based approach, we observed increased positive coupling between the ventral striatum and anterior regions of medial prefrontal cortex (mPFC) in previously institutionalized youth. Stronger ventral striatum–mPFC coupling was associated with parent reports of social problems. A moderated-mediation analysis showed that ventral striatal–mPFC connectivity mediated group differences in social problems, and more so with increasing age. These findings show that early institutional care is associated with differences in resting-state connectivity between the ventral striatum and the mPFC, and this connectivity seems to play an increasingly important role in social behaviors as youth enter adolescence.

The long-term sequelae of adolescent depressive symptoms were examined in a multimethod, multireporter study of a diverse community sample of 179 adolescents followed from age 14 to 24. Mild to moderate levels of early adolescent depressive symptoms were found to predict lower maternal relationship quality, less positive interactions with romantic partners, and greater loneliness in adulthood even after accounting for prior levels of social functioning and for concurrent levels of adult depressive symptoms. Predictions were partially mediated via late adolescent avoidance of social interactions and poor maternal relationship quality. Results are interpreted as suggesting the potential impact of depressive symptoms on adolescent social development and the need to consider treatment for even mild symptoms and their social concomitants.

One goal of developmental psychopathology is to understand the origins and course of mental disorders. I argue that pursuit of this goal requires a valid conceptual understanding of disorder and that this understanding can be provided by the “harmful dysfunction” analysis of the concept of disorder. The harmful dysfunction analysis holds that a disorder is a condition that is both harmful according to social values and caused by an internal dysfunction, that is, by a failure of an internal mechanism to perform a function for which it was naturally selected. This analysis explains why many of the distinctive features of developmental psychopathology are appropriate to the study of disorder. It is argued that the harmful dysfunction analysis is a necessary supplement to other proposed criteria for disorder, such as developmental deviation or predictive validity.

Two independent lines of inquiry suggest that growing up under conditions of contextual adversity (e.g., poverty and household chaos) accelerates aging and undermines long-term health. Whereas work addressing the developmental origins of health and disease highlights accelerated-aging effects of contextual adversity on telomere erosion, that informed by an evolutionary analysis of reproductive strategies highlights such effects with regard to pubertal development (in females). That both shorter telomeres early in life and earlier age of menarche are associated with poor health later in life raises the prospect, consistent with evolutionary life-history theory, that these two bodies of theory and research are tapping into the same evolutionary–developmental process whereby longer term health costs are traded off for increased probability of reproducing before dying via a process of accelerated aging. Here we make the case for such a claim, while highlighting biological processes responsible for these effects, as well as unknowns in the epigenetic equation that might instantiate these contextually regulated developmental processes.

Here we tested whether there was genetic moderation of effects of early maternal sensitivity on social–emotional and cognitive–linguistic development from early childhood onward and whether any detected Gene × Environment interaction effects proved consistent with differential-susceptibility or diathesis–stress models of Person × Environment interaction (N = 695). Two new approaches for evaluating models were employed with 12 candidate genes. Whereas maternal sensitivity proved to be a consistent predictor of child functioning across the primary-school years, candidate genes did not show many main effects, nor did they tend to interact with maternal sensitivity/insensitivity. These findings suggest that the developmental benefits of early sensitive mothering and the costs of insensitive mothering look more similar than different across genetically different children in the current sample. Although acknowledgement of this result is important, it is equally important that the generally null Gene × Environment results reported here not be overgeneralized to other samples, other predictors, other outcomes, and other candidate genes.

The present study tested several predictions related to the theory that girls with conduct disorder (CD) follow a single delayed onset pathway. The following hypotheses were tested among a high-risk, stratified random sample of youth who used public services during a 6-month period: boys will be more likely to have childhood onset CD (COCD) than girls; girls with COCD will be less common than girls with adolescent onset CD (AOCD); COCD girls, AOCD girls, and COCD boys will be similar in terms of risk profiles and AOCD boys will have a less severe risk profile than COCD girls; and risk factors that differentiate between COCD and AOCD among males will not differentiate between COCD and AOCD among females. Among those youth who met the criteria for CD, males were significantly more likely to have COCD than females. However, close to half of females with CD met the criteria for the COCD subtype. Of the seven risk factors that were examined, girls with COCD scored higher than COCD boys on three factors and higher than AOCD girls on four factors; however, only one significant difference was found between AOCD girls and COCD boys. Finally, risk factors appeared to differentiate between COCD and AOCD groups in a similar way among males and females. These findings suggest that COCD is not rare among females in public service sectors, COCD girls can be distinguished from AOCD girls in terms of risk factors, and risk factors for COCD among males are also relevant to females.The Patterns of Youth Mental Health Care in Public Service Systems Study is supported by National Institute of Mental Health (NIMH) Grant U01 MH55282. Preparation of this article was supported by Research Scientist Development Awards K01MH01767 and K01MH01924. The authors are most grateful for the comments and suggestions on this manuscript that were provided by Dr. Persephanie Silverthorn and Dr. Theodore Beauchaine.

Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded.

Exposure to high levels of postdivorce interparental conflict is a well-documented risk factor for the development of psychopathology, and there is strong evidence of a subpopulation of families for which conflict persists for many years after divorce. However, existing studies have not elucidated differential trajectories of conflict within families over time, nor have they assessed the risk posed by conflict trajectories for development of psychopathology or evaluated potential protective effects of children's coping to mitigate such risk. We used growth mixture modeling to identify longitudinal trajectories of child-reported conflict over a period of six to eight years following divorce in a sample of 240 children. We related the trajectories to children's mental health problems, substance use, and risky sexual behaviors and assessed how children's coping prospectively predicted psychopathology in the different conflict trajectories. We identified three distinct trajectories of conflict; youth in two high-conflict trajectories showed deleterious effects on measures of psychopathology at baseline and the six-year follow-up. We found both main effects of coping and coping by conflict trajectory interaction effects in predicting problem outcomes at the six-year follow-up. The study supports the notion that improving youth's general capacity to cope adaptively is a potentially modifiable protective factor for all children facing parental divorce and that children in families with high levels of postdivorce conflict are a particularly appropriate group to target for coping-focused preventive interventions.

This study examined changes in adolescents’ perceived relationship quality with mothers and fathers from middle school to high school, gender differences, and associated mental health consequences using longitudinal data from the New England Study of Suburban Youth cohort (n = 262, 48% female) with annual assessments (Grades 6–12). For both parents, alienation increased, and trust and communication decreased from middle school to high school, with greater changes among girls. Overall, closeness to mothers was higher than with fathers. Girls, compared to boys, perceived more trust and communication and similar levels of alienation with mothers at Grade 6. Girls perceived stronger increases in alienation from both parents and stronger declines in trust with mothers during middle school. Increasing alienation from both parents and less trust with mothers at Grade 6 was associated with higher levels of anxiety at Grade 12. Less trust with both parents at Grade 6 and increasing alienation and decreasing trust with mothers in high school were associated with higher levels of depressive symptoms at Grade 12. Overall, girls reported having higher levels of anxiety at Grade 12 compared to boys. Findings on the course of the quality of parent–adolescent relationships over time are discussed in terms of implications for more targeted research and interventions.

The present study examined how changes in child Big Five personality characteristics and overreactive parenting during the transition from childhood to adolescence predict adolescent adjustment problems. The sample included 290 children, aged 8–9 years. At three moments, with 2-year intervals, mothers, fathers, and a teacher reported on the child's personality, and mothers and fathers reported on their parenting behavior. At the third measurement moment, mothers, fathers, and children reported on the child's adjustment problems. Rank-order stability of the personality dimensions and overreactive parenting were high. Univariate latent growth models revealed mean-level decreases for extraversion, conscientiousness, and imagination. Mean levels of benevolence, emotional stability, and overreactive parenting were stable. Multivariate latent growth models revealed that decreases in extraversion and emotional stability predicted internalizing problems, whereas decreases in benevolence, conscientiousness, and emotional stability predicted externalizing problems. Increases in overreactive parenting predicted externalizing, but not internalizing problems. The associations were similar for boys and girls. The results indicate that changes in child personality and overreactive parenting during the transition to adolescence are associated with adolescent adjustment problems. Overall, child personality was more important than overreactive parenting, and children were more likely to “act out” than to “withdraw” in reaction to overreactive parenting.

Adverse early care is associated with attention regulatory problems, but not all so exposed develop attention problems. In a sample of 612 youth (girls = 432, M = 11.82 years, SD = 1.5) adopted from institutions (e.g., orphanages) in 25 countries, we examined whether the Val66Met polymorphism of the brain-derived neurotrophic factor gene moderates attention problems associated with the duration of institutional care. Parent-reported attention problem symptoms were collected using the MacArthur Health and Behavior Questionnaire. DNA was genotyped for the brain-derived neurotrophic factor Val66Met (rs6265) single nucleotide polymorphism. Among youth from Southeast (SE) Asia, the predominant genotype was valine/methionine (Val/Met), whereas among youth from Russia/Europe and Caribbean/South America, the predominant genotype was Val/Val. For analysis, youth were grouped as carrying Val/Val or Met/Met alleles. Being female, being from SE Asia, and being younger when adopted were associated with fewer attention regulatory problem symptoms. Youth carrying at least one copy of the Met allele were more sensitive to the duration of deprivation, yielding an interaction that followed a differential susceptibility pattern. Thus, youth with Val/Met or Met/Met genotypes exhibited fewer symptoms than Val/Val genotypes when adoption was very early and more symptoms when adoption occurred later in development. Similar patterns were observed when SE Asian youth and youth from other parts of the world were analyzed separately.

This study examined the prospective relations of adolescents' perceptions of discrimination and their genetic status with increases in conduct problems. Participants were 461 African American youths residing in rural Georgia (Wave 1 mean age = 15.5 years) who provided three waves of data and a saliva sample from which a polymorphism in the SCL6A4 (serotonin transporter [5-HTT]) gene polymorphism known as the 5-HTT linked promoter region (5-HTTLPR) was genotyped. Data analyses using growth curve modeling indicated that perceived discrimination was significantly related to the slope of conduct problems. As hypothesized, interactions between perceived discrimination and genetic status emerged for male but not female youths. Compared with those carrying two copies of the long allele variant of 5-HTTLPR, male youths carrying one or two copies of its short allele variant evinced higher rates of conduct problems over time when they perceived high levels of racial discrimination. These findings are consistent with resilience and differential susceptibility propositions stating that genes can both foster sensitivity to adverse events and confer protection from those events.

Crittenden has proposed a system for classifying attachment during the preschool years. Ninety-six boys and girls were tested in the Strange Situation at 18 months and 30 months of age. Eighteen-month-olds were coded using the Ainsworth coding system, and the 30-month-olds were coded using Crittenden's preschool attachment coding system. When children changed classification categories, it was not random movement but was in accordance with Crittenden's predictions of reorganization of the child's capacities. Mothers and children were also observed in the home at 18 and 30 months of age, and children were observed in playgroups from 18 to 30 months of age. The children were rated by their teachers on problem behaviors and peer relations and given achievement tests at age 7 years. Parenting of the children and child behaviors at 30 months differed by attachment classification and predicted both children's performance on achievement tests and teacher reports of children's behavior at 7 years. The findings are discussed in terms of reorganization of working models of attachment on the basis of changing child competencies.

When children are exposed to serious life adversities, Ed Zigler believed that developmental scientists must expediently strive to illuminate the most critical directions for beneficial interventions. In this paper, we present a new study on risk and resilience on adolescents during COVID-19, bookended – in introductory and concluding discussions – by descriptions of programmatic work anchored in lessons learned from Zigler. The new study was conducted during the first two months of the pandemic, using a mixed-methods approach with a sample of over 2,000 students across five high schools. Overall, rates of clinically significant symptoms were generally lower as compared to norms documented in 2019. Multivariate regressions showed that the most robust, unique associations with teens’ distress were with feelings of stress around parents and support received from them. Open ended responses to three questions highlighted concerns about schoolwork and college, but equally, emphasized worries about families’ well-being, and positive outreach from school adults. The findings have recurred across subsequent school assessments, and strongly resonate with contemporary perspectives on resilience in science and policy. If serious distress is to be averted among youth under high stress, interventions must attend not just to the children's mental health but that of salient caregiving adults at home and school. The article concludes with some specific recommendations for community-based initiatives to address mental health through continued uncertainties of the pandemic.

Findings of the few psychotherapy outcome studies with depressed children and adolescents raise questions about whether or not treatments are sufficiently sensitive to developmental factors. Here we review the outcome data, then survey potentially relevant research on the cognitions, competencies, and coping behavior of depressed youngsters. Much of the work in each domain is both procedurally and theoretically adevelopmental, and the psychotherapy research does not appear to be well informed by research in the other domains. To help remedy this situation, for each domain we suggest key developmental questions that need to be answered, and we discuss implications for psychotherapy. We also propose a three-way partnership involving basic developmental research linked with research on relations between depression and various cognitive and behavioral processes, with both lines of inquiry informing the development and refinement of interventions.

Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or “programs” postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined.

We evaluate the usefulness of 11 key epigenetic concepts from the behavior genetic research paradigm for advancing the field of developmental psychopathology. Key assumptions, empirical examples, and caveats in interpreting results are presented. We emphasize the usefulness of incorporating both dimensional (e.g., temperament trait) and categorical (e.g., diagnosis) variables, environmental measures, direct behavioral assessments, and multiple, theoretically relevant occasions of study into classic twin and family studies. We highlight contemporary techniques for identifying specific chromosomal regions associated with behavioral patterns, and the importance of considering nonmendelizing genetic influences when discerning the panorama of genetic influences on behavior.

Evidence suggests that the 7-repeat variant of a 48 base pair variable number tandem repeat polymorphism in the dopamine receptor D4 (DRD4) gene may be associated with the development of attention problems. A parallel literature suggests that genes linked to dopaminergic functioning may be associated with differential sensitivity to context, such that the direction of the genetic effect is hypothesized to vary across environmental experience. Guided by these literatures, we used data from the NICHD Study of Early Child Care and Youth Development to consider (a) whether individual differences in children's inattention problems across middle childhood are predicted by gene–environment interactions between the DRD4 gene 7-repeat polymorphism and children's experiences of maternal sensitivity across infancy and early childhood and (b) the degree to which such interactions are consistent with the differential-sensitivity model. Largely consistent with the hypothesized model, gene–environment interactions indicated that, in the context of insensitive early maternal care, the DRD4 7-repeat polymorphism was associated with higher levels of inattention. Although somewhat less consistently, there was also evidence that, in the context of highly sensitive care, the 7-repeat polymorphism was associated with lower levels of inattention. Overall, the magnitude of the absolute genetic effect increased over time, as children's inattention trajectories diverged.