The concept of resilience has as its starting point the recognition that there is huge heterogeneity in people's responses to all manner of environmental adversities. Resilience is an inference based on evidence that some individuals have a better outcome than others who have experienced a comparable level of adversity; moreover, the negative experience may have either a sensitizing effect or a strengthening “steeling” effect in relation to the response to later stress or adversity. After noting the crucial importance of first testing for the environmental mediation of risk through “natural experiments,” findings are reviewed on “steeling effects” in animal models and humans. Gene–environment interaction findings are considered, and it is noted that there is some evidence that the genetic influences concerns responsivity to all environments and not just bad ones. Life course effects are reviewed in relation to evidence on turning point effects associated with experiences that increase opportunities and enhance coping. Attention is drawn to both research implications and substantive findings as features that foster resilience.

Without even knowing of their existence, Mendel discovered how genes operate when they are completely penetrant, although they rarely are, at least with respect to human personality and psychopathology; yet quantitative genetics results have conclusively demonstrated their substantial macrolevel influence. Now we need to understand just how incompletely penetrant genes make their contributions to psychopathology. Exciting new developments in molecular genetics and epigenetics provide new insight into gene action in principle but have been of limited value so far in understanding the emergence of psychopathology. Some of the most helpful postulates might come from evolutionary and developmental biology and agricultural breeding experiments. I describe the all but forgotten evolutionary mechanisms articulated by Schmalhausen, a Russian evolutionary biologist whose work was suppressed by Stalin in the 1940s. I focus on Schmalhausen's law, the observation that organisms living in conditions at the boundary of their tolerance in any one aspect of existence will be vulnerable to expression of genetic liabilities related to all other aspects of existence. I show how Schmalhausen's ideas are relevant to the results of a century-long corn-breeding experiment and the current concepts of facilitated variation and cryptic genetic variation. I then discuss the relevance of all of these to understanding genetic influences on personality and psychopathology.

We report a graded relationship between neighborhood socioeconomic status (SES) and children's antisocial behavior that (a) can be observed at school entry, (b) widens across childhood, (c) remains after controlling for family-level SES and risk, and (d) is completely mediated by maternal warmth and parental monitoring (defined throughout as supportive parenting). The children were participants in the Environmental Risk Longitudinal Twin Study (N = 2,232), which prospectively tracked the development of children and their neighborhoods across childhood. Direct and independent effects of neighborhood-level SES on children's antisocial behavior were observed as early as age 5, and the gap between children living in deprived versus more affluent neighborhoods widened as children approached adolescence. By age 12, the effect of neighborhood SES on children's antisocial behavior was as large as the effect observed for our most robust predictor of antisocial behavior: sex (Cohen d = 0.51 when comparing children growing up in deprived vs. more affluent neighborhoods in comparison to Cohen d = 0.53 when comparing antisocial behavior among boys vs. girls). However, these relatively large differences in children's levels and rate of change in antisocial behavior across deprived versus more affluent neighborhoods were completely mediated by supportive parenting practices. The implications of our findings for studying and reducing socioeconomic disparities in antisocial behavior among children are discussed.

The construct of emotional availability (EA) refers to the capacity of a dyad to share an emotional connection and to enjoy a mutually fulfilling and healthy relationship. The EA Scales were designed to assess multiple components of a relationship from the perspective of both partners. The four caregiver components include sensitivity, structuring, nonintrusiveness, and nonhostility; two scales measure the child's responsiveness to the caregiver and involvement of the caregiver. We describe the EA construct and introduce the papers in this issue, focusing on the contributions of this Special Section to a developmental psychopathology framework.

Contributions of the Project Competence Longitudinal Study (PCLS) to resilience science and developmental psychopathology are highlighted in this article. Initiated by Norman Garmezy, the PCLS contributed models, measures, and methods, as well as working definitions of concepts like competence, developmental tasks, protective factors, and resilience. Findings from the study corroborated the feasibility of studying adaptation in a normative group of school children, identifying patterns of resilience, competence without major adversity, and maladaptive paths through life. Competence was multidimensional, showing continuity and change over time. Cascading effects across domains indicated that competence and problems spread over time. Thus, adult achievements in developmental tasks were rooted in childhood and adolescence. Young people who showed resilience had much in common with similarly successful peers who experienced less adversity over time, including high-quality relationships with parents and other adults, and good cognitive, as well as social–emotional, skills. Maladaptive youth in the study often faced high adversity with little adaptive capacity (internal or external) and tended to generate stressful experiences. Resilience often emerged in childhood and endured, but there also were late bloomers whose lives turned around in the transition to adulthood. The role of collaboration and mentorship in the PCLS is also discussed.

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

Despite substantial recent advancements in psychiatric genetic research, progress in identifying the genetic basis of anxiety disorders has been limited. We review the candidate gene and genome-wide literatures in anxiety, which have made limited progress to date. We discuss several reasons for this hindered progress, including small samples sizes, heterogeneity, complicated comorbidity profiles, and blurred lines between normative and pathological anxiety. To address many of these challenges, we suggest a developmental, multivariate framework that can inform and enhance anxiety phenotypes for genetic research. We review the psychiatric and genetic epidemiological evidence that supports such a framework, including the early onset and chronic course of anxiety disorders, shared genetic risk factors among disorders both within and across time, and developmentally dynamic genetic influences. We propose three strategies for developmentally sensitive phenotyping: examination of early temperamental risk factors, use of latent factors to model underlying anxiety liability, and use of developmental trajectories as phenotypes. Expanding the range of phenotypic approaches will be important for advancing studies of the genetic architecture of anxiety disorders.

This study examined the links between mothers' frontal EEG asymmetry at rest and during videos of their 5- to 8-month-old infants expressing three emotion states (joy, anger/distress, and neutral interest), mother–infant emotional availability (EA) in the home, mothers' depressive and anxious symptoms, and mothers' emotional experience in response to infant emotion cues. Greater relative right frontal activity at rest was associated with greater maternal anxiety, but was unrelated to EA or mother-reported emotional experience in response to infant emotion cues. A shift toward greater relative right frontal activation in response to infant emotional stimuli was associated with lower maternal anxiety, greater mother–infant EA, and mothers' experience of sadness, concern, irritability, and the absence of joy in response to seeing their own infant in distress. These findings suggest that mothers' in the moment empathetic responding to their infant's emotions, indexed by a shift in frontal EEG asymmetry in response to infant emotional displays, is related to mother–infant EA in the home. Implications for conceptualizing parenting risk are discussed.

According to data from the 1997 NICHD Study of Child Care, center-based child care can have deleterious effects on children's social–emotional development. We hypothesized that training child care professionals to develop positive relationships with children in their care would improve the quality of center-based child care. Thirty-three professional caregiver–child pairs participated in the intervention group and 24 professional caregiver–child pairs were assigned to a care as usual comparison group. The intervention consisted of an informational and a practice component with an emotional availability (EA) coach. The infants and toddlers (ages 11 to 23 months) in the classrooms were enrolled in the project only if they spent at least 20 hr per week in center-based care. The measures included were (a) the EA Scales, (b) the Attachment Q-Sort, and (c) the Classroom Interaction Scale. The intervention group professional caregiver–child relationships showed improvements on the EA Scales, Attachment Q-Sort, and the Classroom Interaction Scale from pre- to posttest, compared to the comparison group, who showed some decrements over a comparable period of time.

This article serves to outline a research paradigm to investigate main effects and interactions of genes, environment, and development on behavior and psychiatric illness. We provide a historical context for candidate gene studies and genome-wide association studies, including benefits, limitations, and expected payoffs. Using substance use and abuse as our driving example, we then turn to the importance of etiological psychological theory in guiding genetic, environmental, and developmental research, as well as the utility of refined phenotypic measures, such as endophenotypes, in the pursuit of etiological understanding and focused tests of genetic and environmental associations. Phenotypic measurement has received considerable attention in the history of psychology and is informed by psychometrics, whereas the environment remains relatively poorly measured and is often confounded with genetic effects (i.e., gene–environment correlation). Genetically informed designs, which are no longer limited to twin and adoption studies thanks to ever-cheaper genotyping, are required to understand environmental influences. Finally, we outline the vast amount of individual difference in structural genomic variation, most of which remains to be leveraged in genetic association tests. Although the genetic data can be massive and burdensome (tens of millions of variants per person), we argue that improved understanding of genomic structure and function will provide investigators with new tools to test specific a priori hypotheses derived from etiological psychological theory, much like current candidate gene research but with less confusion and more payoff than candidate gene research has to date.

Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly because of increased de novo mutations during spermatogenesis with older paternal age. Because severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending. Interlinked Swedish national registers provided information on fathers' age at childbirth and violent criminal convictions in all offspring born from 1958 to 1979 (N = 2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences. In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-family analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.

Norman Garmezy devoted the better part of four decades developing and promoting the construct of resilience for developmental psychopathology. He proposed resilience as a paradigm to guide the understanding of how people can transcend adversity and go on to live healthy, productive lives. This tribute to Norman starts with a look at the early context for his work during his distinguished tenure in the Department of Psychology at the University of Minnesota. Resilience constructs are then compared from interdisciplinary perspectives across a variety of biological and physical sciences. All of these perspectives lead to similar conclusions: resilience is not a thing but a process. Furthermore, the processes are the product of energy-hungry systems. Finally, these insights are applied to difficult to modify maladaptive behaviors raising the question of a dark side to resilience.

Children adopted from institutions (e.g., orphanages) overseas are at increased risk of disturbances in social relationships and social understanding. Not all postinstitutionalized children exhibit these problems, although factors like the severity of deprivation and duration of deprivation increase their risk. To date, few studies have examined whether postadoption parenting might moderate the impact of early adverse care. Three groups were studied: postinstitutionalized and foster care children both adopted internationally and nonadopted children reared in their families of origin. The Emotional Availability (EA) Scales were assessed at 18 months in parent–child dyads. Parent emotional availability was found to predict two aspects of social functioning shown in previous studies to be impaired in postinstitutionalized children. Specifically, EA positively correlated with emotion understanding at 36 months; in interaction with initiation of joint attention at 18 months and group, it predicted indiscriminate friendliness as scored from a parent attachment interview at 30 months. Among the postinstitutionalized children but not among the children in other groups, higher EA scores reduced the negative association between initiation of joint attention and indiscriminate friendliness, thus suggesting that parenting quality may moderate the effects of early institutional deprivation.

Previous research documented a robust link between difficulties in self-regulation and development of externalizing problems (i.e., aggression and delinquency). In this study, we examined the longitudinal additive and interactive genetic and environmental covariation underlying this well-established link using a twin design. The sample included 131 pairs of monozygotic twins and 173 pairs of same-sex dizygotic twins who participated in three waves of annual assessment. Mothers and fathers provided reports of externalizing problems. Teacher report and observer rating were used to assess twin's attention regulation. The etiology underlying the link between externalizing problems and attention regulation shifted from a common genetic mechanism to a common environmental mechanism in the transition across middle childhood. Household chaos moderated the genetic variance of and covariance between externalizing problems and attention regulation. The genetic influence on individual differences in both externalizing problems and attention regulation was stronger in more chaotic households. However, higher levels of household chaos attenuated the genetic link between externalizing problems and attention regulation.

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.

The focus of this article is to present current progress in understanding the interplay among adversity, physiological sensitivity to context, and adaptive functioning, with an emphasis on implications and future directions for resilience researchers. It includes a review of current literature that demonstrates (a) links between various levels of adversity exposure and variability in physiological reactivity, (b) how the interplay between children's physiological reactivity and different sources of risk and adversity relates to variability in adaptive functioning, and (c) various approaches for capturing a more dynamic nature of physiological reactivity and related processes. Throughout, important conceptual and empirical issues are highlighted.