We examined whether maltreatment experienced in childhood and/or adolescence prospectively predicts young adult functioning in a diverse and well-characterized sample of females with childhood-diagnosed attention-deficit/hyperactivity disorder (N = 140). Participants were part of a longitudinal study and carefully evaluated in childhood, adolescence, and young adulthood (Mage = 9.6, 14.3, and 19.7 years, respectively), with high retention rates across time. A thorough review of multisource data reliably established maltreatment status for each participant (Mκ = 0.78). Thirty-two (22.9%) participants experienced at least one maltreatment type (physical abuse, sexual abuse, or neglect). Criterion variables included a broad array of young adult measures of functioning gleaned from multiple-source, multiple-informant instruments. With stringent statistical control of demographic, prenatal, and family status characteristics as well as baseline levels of the criterion variable in question, maltreated participants were significantly more impaired than nonmaltreated participants with respect to self-harm (suicide attempts), internalizing symptomatology (anxiety and depression), eating disorder symptomatology, and well-being (lower overall self-worth). Effect sizes were medium. Comprising the first longitudinal evidence linking maltreatment with key young adult life impairments among a carefully diagnosed and followed sample of females with attention-deficit/hyperactivity disorder, these findings underscore the clinical importance of trauma experiences within this population.

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.

The quality of the environment experienced by an individual across his or her lifespan can result in a unique developmental trajectory with consequences for adult phenotype and reproductive success. However, it is also evident that these experiences can impact the development of offspring with continued effect on subsequent generations. Epigenetic mechanisms have been proposed as a mediator of both these within- and across-generation effects, and there is increasing evidence to support the role of environmentally induced changes in DNA methylation, posttranslational histone modifications, and noncoding RNAs in predicting these outcomes. Advances in our understanding of these molecular modifications contribute to increasingly nuanced perspectives on plasticity and transmission of phenotypes across generations. A challenge that emerges from this research is in how we integrate these “new” perspectives with traditional views of development, reproduction, and inheritance. This paper will highlight evidence suggestive of an epigenetic impact of the environment on mothers, fathers, and their offspring, and illustrate the importance of considering the dynamic nature of reproduction and development and inclusive views of inheritance within the evolving field of behavioral and environmental epigenetics.

Understanding factors increasing susceptibility to social contexts and predicting psychopathology can help identify targets for prevention. Persistently high externalizing behavior in adolescence is predictive of psychopathology in adulthood. Parental monitoring predicts low externalizing behavior, yet youth likely vary in the degree to which they are affected by parents. Genetic variants of GABA receptor subunit alpha-2 (GABRA2) may increase susceptibility to parental monitoring, thus impacting externalizing trajectories. We had several objectives: (a) to determine whether GABRA2 (rs279827, rs279826, rs279858) moderates the relationship between a component of parental monitoring, parental knowledge, and externalizing trajectories; (b) to test the form of this interaction to assess whether GABRA2 variants reflect risk (diathesis–stress) or susceptibility (differential susceptibility) factors; and (c) to clarify GABRA2 associations on the development of problem behavior. This prospective study (N = 504) identified three externalizing trajectory classes (i.e., low, decreasing, and high) across adolescence. A GABRA2 × Parental Monitoring effect on class membership was observed, such that A-carriers were largely unaffected by parental monitoring, whereas class membership for those with the GG genotype was affected by parental monitoring. Findings support differential susceptibility in GABRA2.

Associations between infants' frontal EEG asymmetry and temperamental negative affectivity (NA) across infants' first year of life and the potential moderating role of maternal prenatal depressive symptoms were examined prospectively in infants (n = 242) of mothers at elevated risk for perinatal depression. In predicting EEG, in the context of high prenatal depressive symptoms, infant NA and frontal EEG asymmetry were negatively associated at 3 months of age and positively associated by 12 months of age. By contrast, for low depression mothers, infant NA and EEG were not significantly associated at any age. Postnatal depressive symptoms did not add significantly to the models. Dose of infants' exposure to maternal depression mattered: infants exposed either pre- or postnatally shifted from a positive association at 3 months to a negative association at 12 months; those exposed both pre- and postnatally shifted from a negative association at 3 months to a positive association at 12 months. Prenatal relative to postnatal exposure did not matter for patterns of association between NA and EEG. The findings highlight the importance of exploring how vulnerabilities at two levels of analysis, behavioral and psychophysiological, co-occur over the course of infancy and in the context of mothers' depressive symptomatology.

In the present study, we used separate measures of parental monitoring and parental knowledge and compared their associations with youths’ antisocial behavior during preadolescence, between the ages of 10 and 12. Parental monitoring and knowledge were reported by mothers, fathers, and youths taking part in the Environmental Risk (E-Risk) Longitudinal Twin Study that follows 1,116 families with twins. Information on youths’ antisocial behavior was obtained from mothers as well as teachers. We report two main findings. First, longitudinal cross-lagged models revealed that greater parental monitoring did not predict less antisocial behavior later, once family characteristics were taken into account. Second, greater youth antisocial behavior predicted less parental knowledge later. This effect of youths’ behavior on parents’ knowledge was consistent across mothers’, fathers’, youths’, and teachers’ reports, and robust to controls for family confounders. The association was partially genetically mediated according to a Cholesky decomposition twin model; youths’ genetically influenced antisocial behavior led to a decrease in parents’ knowledge of youths’ activities. These two findings question the assumption that greater parental monitoring can reduce preadolescents’ antisocial behavior. They also indicate that parents’ knowledge of their children's activities is influenced by youths’ behavior.

A heightened synchrony between the mother's and infant's facial affect predicts adverse infant development. We know that maternal psychopathology is related to mother–infant facial affect synchrony, but it is unclear how maternal psychopathology is transmitted to mother–infant synchrony. One pathway might be maternal emotion dysregulation. We examined (a) whether maternal emotion dysregulation is positively related to facial affect synchrony and (b) whether maternal emotion dysregulation mediates the effect of maternal psychopathology on mother–infant facial affect synchrony. We observed 68 mothers with mood disorders and their 4- to 9-month-old infants in the Still-Face paradigm during two play interactions. The mother's and infant's facial affect were rated from high negative to high positive, and the degree of synchrony between the mother's and infant's facial affect was computed with a time-series analysis. Emotion dysregulation was measured with the Difficulties in Emotion Regulation Scale, and psychopathology was assessed with the Symptom Checklist–90–Revised. Higher maternal emotion dysregulation was significantly associated with higher facial affect synchrony; emotion dysregulation fully mediated the effect of maternal psychopathology on facial affect synchrony. Our findings demonstrate that maternal emotion dysregulation rather than maternal psychopathology per se places mothers and infants at risk for heightened facial affect synchrony.

The genetic and environmental etiology of individual differences was examined in initial level and change in psychopathic personality from ages 9 to 18 years. A piecewise growth curve model, in which the first change score (G1) influenced all ages (9–10, 11–13, 14–15, and 16–18 years) and the second change score (G2) only influenced ages 14–15 and 16–18 years, fit the data better did than the standard single slope model, suggesting a turning point from childhood to adolescence. The results indicated that variations in levels and both change scores were mainly due to genetic (A) and nonshared environmental (E) influences (i.e., AE structure for G0, G1, and G2). No sex differences were found except on the mean values of level and change scores. Based on caregiver ratings, about 81% of variance in G0, 89% of variance in G1, and 94% of variance in G2 were explained by genetic factors, whereas for youth self-reports, these three proportions were 94%, 71%, and 66%, respectively. The larger contribution of genetic variance and covariance in caregiver ratings than in youth self-reports may suggest that caregivers considered the changes in their children to be more similar as compared to how the children viewed themselves.

Environmental risk predicts disrupted basal cortisol levels in preschool children. However, little is known about the stability or variability of diurnal cortisol morning levels or slope patterns over time in young children. This study used latent profile analysis to identify patterns of the hypothalamic–pituitary–adrenal axis activity during the preschool period. Using a community sample (N = 306), this study measured income, cumulative risk, and children's diurnal cortisol (morning level and slope) four times across 2.5 years, starting when children were 36 months old. Latent profile analysis profiles indicated that there were predominantly stable patterns of diurnal cortisol level and slope over time and that these patterns were predicted by income and cumulative risk. In addition, there were curvilinear relations of income and cumulative risk to profiles of low morning cortisol level and flattened diurnal slope across time, suggesting that both lower and higher levels of income and cumulative risk were associated with a stress-sensitive physiological system. Overall, this study provides initial evidence for the role of environmental risk in predicting lower, flattened basal cortisol patterns that remain stable over time.

The development of adult personality disorder symptoms, including transactional processes of relationship representational and behavioral experience from infancy to early adolescence, was examined using longitudinal data from a risk sample (N = 162). Significant preliminary correlations were found between early caregiving experience and adult personality disorder symptoms and between representational and behavioral indices across time and adult symptomatology. Significant correlations were also found among diverse representational assessments (e.g., interview, drawing, and projective narrative) and between concurrent representational and observational measures of relationship functioning. Path models were analyzed to investigate the combined relations of caregiving experience in infancy; relationship representation and experience in early childhood, middle childhood, and early adolescence; and personality disorder symptoms in adulthood. The hypothesized model representing interactive contributions of representational and behavioral experience represented the data significantly better than competing models representing noninteractive contributions. Representational and behavioral indicators mediated the link between early caregiving quality and personality disorder symptoms. The findings extend previous studies of normative development and support an organizational developmental view that early relationship experiences contribute to socioemotional maladaptation as well as adaptation through the progressive transaction of mutually informing expectations and experience.

There is increasing interest among developmental psychopathologists in broad transdiagnostic factors that give rise to a wide array of clinical presentations (multifinality), but little is known about how these processes lead to particular psychopathological manifestations over the course of development. We examined whether individual differences in the error-related negativity (ΔERN), a neural indicator of error monitoring, predicts whether early persistent irritability, a prototypical transdiagnostic construct, is associated with later internalizing versus externalizing outcomes. When children were 3 years old, mothers were interviewed about children's persistent irritability and completed questionnaires about their children's psychopathology. Three years later, EEG was recorded while children performed a go/no-go task to measure the ΔERN. When children were approximately 9 years old, mothers again completed questionnaires about their children's psychopathology. The results indicated that among children who were persistently irritable at age 3, an enhanced or more negative ΔERN at age 6 predicted the development of internalizing symptoms at age 9, whereas a blunted or smaller ΔERN at age 6 predicted the development of externalizing symptoms. Our results suggest that variation in error monitoring predicts, and may even shape, the expression of persistent irritability and differentiates developmental trajectories from preschool persistent irritability to internalizing versus externalizing outcomes in middle to late childhood.

The efforts of many neuroscientists are directed toward understanding the appreciable plasticity of the brain and behavior. In recent years, epigenetics has become a core of this focus as a prime mechanistic candidate for behavioral modifications. Animal models have been instrumental in advancing our understanding of environmentally driven changes to the epigenome in the developing and adult brain. This review focuses mainly on such discoveries driven by adverse environments along with their associated behavioral outcomes. While much of the evidence discussed focuses on epigenetics within the central nervous system, several peripheral studies in humans who have experienced significant adversity are also highlighted. As we continue to unravel the link between epigenetics and phenotype, discerning the complexity and specificity of epigenetic changes induced by environments is an important step toward understanding optimal development and how to prevent or ameliorate behavioral deficits bred by disruptive environments.

This study examined the transactional interplay among dimensions of destructive interparental conflict (i.e., hostility and dysphoria), children's emotional insecurity, and their psychological problems from middle childhood and adolescence. Participants were 232 families, with the first of five measurement occasions occurring when children were in first grade (M age = 7 years). Cross-lagged, autoregressive models were conducted with a multiple-method, multiple-informant measurement approach to identify developmental cascades of interparental and child cascades. Results indicated that emotional insecurity was a particularly powerful mediator of prospective associations between interparental conflict (i.e., dysphoria and hostility) and child adjustment during adolescence rather than childhood. In reflecting bidirectionality in relationships between interparental and child functioning, children's psychological problems predicted increases in interparental dysphoria during childhood and adolescence. Although emotional insecurity was not identified as a proximal predictor of interparental difficulties, an indirect cascade was identified whereby insecurity in early adolescence was associated with increases in teen psychological problems, which in turn predicted greater interparental dysphoria over time. Results are interpreted in the context of how they advance transactional formulation of emotional security theory and its resulting translational implications for clinical initiatives.

Although the negative impact of marital conflict on children has been amply documented, few studies have examined the process of risk in a long-term, longitudinal design. We examined parent–child attachment security as a mechanism that may account for the impact of interparental conflict on children's long-term risk of internalizing problems. Sixty-two community mothers, fathers, and children were followed from ages 2 to 10. Parents reported on their conflicts when their children were 2. Trained observers produced parent–child attachment security scores (Attachment Q-Set, Waters, 1987), based on lengthy naturalistic observations of the child with each parent. Parents rated children's internalizing problems at age 10. A conditional process model and bootstrap approach were implemented to examine conditional indirect effects of conflict on child internalizing problems through attachment security for girls versus boys. Maladaptive marital conflict (destructive strategies, severity of arguments) increased internalizing problems 8 years later due to the undermined security for girls, whereas negative emotional aftermath of conflict (unresolved, lingering tension) increased internalizing problems for both boys and girls. The emotional aftermath of conflict is often overlooked, yet it appears to be a key dimension influencing emotional security in the family system, with significant consequences for children's development.

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.

Guided by emotional security theory, this study examined the temperamental precursors of distinctive profiles of children's responses to interparental conflict. Participants included 243 children (M = 4.6 years) and their parents across two annual measurement occasions. Temperamental constructs of frustration proneness, approach, positive affect, activity level, and effortful control were assessed through multiple methods, informants, and contexts. Behavioral observations of children's responses to interparental conflict at each wave yielded four profiles: secure (i.e., efficiently address direct threat), mobilizing (i.e., vigilance to potential threat and social opportunities), dominant (i.e., directly defeat threat), and demobilizing (i.e., reduce salience as a target of hostility). Results supported hypotheses on the distinct constellations of temperament in predicting subsequent change in the four security profiles.

In response to rapidly growing rates of comorbidity among psychiatric disorders, clinical scientists have become interested in identifying transdiagnostic processes that can help explain dysfunction across diagnostic categories (e.g., Kring & Sloan, 2009). One factor that has received a great deal of attention is that of emotion regulation, namely, the ability to modulate the intensity and/or duration of emotional states (e.g., Cicchetti, Ackerman, & Izard, 1995; Gross, 1998). Recent theoretical and empirical work has begun to emphasize the role that emotion regulation plays in the temporal comorbidity between internalizing and externalizing conditions (e.g., Aldao & De Los Reyes, 2015; De Los Reyes & Aldao, 2015; Drabick & Kendall, 2010; Jarrett & Ollendick, 2008; Patrick & Hajcak, 2016). However, close inspection of this work reveals two very pertinent areas of growth: (a) this literature is characterized by mixed findings that are likely explained, in part, by methodological heterogeneity; and (b) emotion regulation tends to be studied in relatively narrow terms. To address these issues, we provide a series of recommendations for facilitating cross-study comparisons and leveraging multifaceted approaches to studying emotion regulation processes within a developmental psychopathology framework. We hope that our perspective can enhance the organization and growth of this very important area of inquiry, and ultimately result in more effective prevention and treatment programs.