Cognitive deficits in schizophrenia are increasingly accepted as core features of this disorder that play a role as vulnerability indicators, as enduring abnormalities during clinical remission, and as critical rate-limiting factors in functional recovery. This article demonstrates the lasting influence of Norman Garmezy through his impact on one graduate student and then through his later collaborative research with colleagues. The promise of core cognitive deficits as vulnerability indicators or endophenotypes was demonstrated in research with children born to a parent with schizophrenia as well as with biological parents and siblings of individuals with schizophrenia. In studies of patients with a recent onset of schizophrenia, cognitive deficits were found to endure across psychotic and clinically remitted periods and to have a strong predictive influence on likelihood of returning successfully to work or school. Converging lines of evidence for the enduring core role of cognitive deficit in schizophrenia have led in recent years to a burgeoning interest in developing new interventions that target cognition as a means of improving functional recovery in this disorder.

Self-inflicted injury (SII) in adolescence is a serious public health concern that portends prospective vulnerability to internalizing and externalizing psychopathology, borderline personality development, suicide attempts, and suicide. To date, however, our understanding of neurobiological vulnerabilities to SII is limited. Behaviorally, affect dysregulation is common among those who self-injure. This suggests ineffective cortical modulation of emotion, as observed among adults with borderline personality disorder. In borderline samples, structural and functional abnormalities are observed in several frontal regions that subserve emotion regulation (e.g., anterior cingulate, insula, dorsolateral prefrontal cortex). However, no volumetric analyses of cortical brain regions have been conducted among self-injuring adolescents. We used voxel-based morphometry to compare cortical gray matter volumes between self-injuring adolescent girls, ages 13–19 years (n = 20), and controls (n = 20). Whole-brain analyses revealed reduced gray matter volumes among self-injurers in the insular cortex bilaterally, and in the right inferior frontal gyrus, an adjacent neural structure also implicated in emotion and self-regulation. Insular and inferior frontal gyrus gray matter volumes correlated inversely with self-reported emotion dysregulation, over-and-above effects of psychopathology. Findings are consistent with an emotion dysregulation construal of SII, and indicate structural abnormalities in some but not all cortical brain regions implicated in borderline personality disorder among adults.

We utilized a longitudinal twin study (N = 2,510) to identify the child characteristics present prior to initiation of substance use that best predicted later substance use disorders. Two independent traits accounted for the majority of premorbid risk: socialization (conformity to rules and conventional values) and boldness (sociability and social assurance, stress resilience, and thrill seeking). Low socialization was associated with disruptive behavior disorders, parental externalizing disorders, and environmental adversity and exhibited moderate genetic (0.45) and shared environmental influences (0.30). Boldness was highly heritable (0.71) and associated with less internalizing distress and environmental adversity. In combination, these traits exhibited robust associations with adolescent and young adult substance use disorders (R = .48 and .50, respectively) and incremental prediction over disruptive behavior disorders, parental externalizing disorders, and environmental adversity. The results were replicated in an independent sample. Socialization and boldness offer a novel conceptualization of underlying risk for substance use disorders that has the potential to improve prediction and theory with implications for basic research, prevention, and intervention.

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.

Exposure to childhood adversity has been linked to accelerated telomere shortening, a marker of cellular aging and an indicator of physical health risk. In the current study, we examined whether adult attachment representation moderated the association between childhood adversity and telomere length. Participants included 78 young adults (M age = 20.46, SD = 1.57), who reported on their exposure to adverse childhood experiences (ACE) and were administered the Adult Attachment Interview, which was coded for attachment state of mind. Relative telomere length was assayed from buccal cells. Multiple regression analyses revealed a significant interaction between attachment state of mind and ACE in predicting telomere length. Whereas the association between number of ACE and telomere length was nonsignificant for secure–autonomous, r (50) = –.15, p = .31, and insecure–preoccupied young adults, r (9) = –.15, p = .71, there was a strong negative association between number of ACE and telomere length for insecure–dismissing young adults, r (19) = –.59, p = .007. This study is novel in demonstrating that attachment may affect biological resilience following childhood adversity, contributing to the growing literature about the role of the quality of early caregiving experiences and their representations in shaping biological processes and physical health.

Determinants of individual differences in the sensitivity of parenting attitudes were investigated in mothers with schizophrenic or major mood disorders. Constructs from the major domains of the mother's childhood relational experiences, personality, social context, and child characteristics were evaluated in a developmental model to predict differences in parenting attitudes. Two pathways were identified. An index of the severity and chronicity of the mother's disorder was shown to predict less-adaptive parenting attitudes. A second pathway revealed that emotional support from network members influenced self-esteem, which predicted more adaptive parenting attitudes. However, perceptions of childhood relational experiences, particularly maternal uninvolvement, predicted parenting attitudes as well as accounted for relationships among emotional support, self-esteem, and parenting. The results were discussed from an attachment theory perspective. The implications of individual differences in maternal functioning for both the mother and the child's adaptation were discussed, and treatment issues were addressed.

We examined the nature and directionality of associations between interparental discord and parenting practices in a sample of 227 mothers and fathers of kindergarten children over two measurement waves spaced 1 year apart. Cross-lagged models indicated that associations between interparental discord and maternal and paternal parenting practices (i.e., acceptance, discipline) were generally negligible with one exception: interparental discord at Time 1 predicted decreases in maternal acceptance from Time 1 to Time 2. However, consistent with the family systems conceptualization of the family as an open system, prospective associations among interparental and parent–child subsystems varied significantly as a function of parental depressive symptoms, interparental relationship insecurity, and child-rearing disagreements. The moderating role of adult characteristics commonly varied across the type of adult vulnerability (e.g., depressive symptoms, interparental relationship insecurity, child-rearing disagreements), dimension of parenting practices (e.g., maternal and paternal acceptance and inconsistent discipline), and the directionality of the paths between interparental and parent–child subsystems.This research was supported by the National Institute of Mental Health (Project R01 MH 57318) awarded to Patrick T. Davies and E. Mark Cummings. Melissa L. Sturge–Apple was supported by a postdoctoral National Research Service Award from the National Institute of Mental Health (F32 MH 66596). The authors are grateful to the children, parents, teachers, and school administrators who participated in this project. Gratitude is also expressed to the staff who assisted with the project, including Courtney Forbes, Marcie Goeke–Morey, Amy Keller, Michelle Sutton, and the graduate and undergraduate students at the University of Rochester and the University of Notre Dame.

A structured childhood history interview was administered to 50 low-income mothers of infants. Three levels of risk for infant maltreatment were represented in the sample, including 10 maltreatment cases. Maternal behavior at home was rated and factor analyzed when the infants were 12 months and 18 months old, yielding separate factors labelled maternal involvement and hostile-intrusiveness. Risk for maltreatment was strongly correlated with the overall adversity of the mother's childhood history. Maternal hostile-intrusive behavior was best accounted for by psychiatric disorder in the mother's own mother and poor peer relationships in childhood. Maternal involvement was negatively associated with a separate cluster of variables indexing family disruption and lack of supervision. The emergence of two separate clusters of associations — positive affective involvement and negative affective involvement — is related to similar two-dimensional results in studies of self-reported mood, infant attachment relationships, and peer relationships. Implications of a two-dimensional affective construct for future theorizing in developmental psychopathology are discussed.

Children of depressed parents are significantly more likely to develop depression and other mental health disorders than are children of never-depressed parents. Investigations of the physiological mechanisms underlying this elevated risk have generally focused on basal functioning. It is important to note, however, that physiological reactivity or responses to stress are also critical determinants of mental and physical health. In the current study, we examined whether children of depressed parents exhibit altered physiological responses to stress. In two studies, never-depressed adolescent daughters of either recurrently depressed mothers (RISK) or never-depressed mothers (CTL) underwent social stressors while their physiological responses were measured (cortisol in Study 1, heart rate in Study 2). In both studies, affective responses to the stressors predicted physiological responses in RISK girls, but not in never-depressed girls. For RISK girls, decreased positive affect in response to stress predicted increased cortisol reactivity; in addition, decreased positive affect and increased negative affect were associated with poorer heart rate recovery and habituation, respectively. Future research is needed to examine explicitly whether this coherence between affect and physiology is a mechanism underlying the increased risk for psychopathology in children of depressed parents.

Despite recent emphasis on the profound importance of the fetal environment in “programming” postnatal development, measurement of offspring development typically begins after birth. Using a novel coding strategy combining direct fetal observation via ultrasound and actocardiography, we investigated the impact of maternal smoking during pregnancy (MSDP) on fetal neurobehavior; we also investigated links between fetal and infant neurobehavior. Participants were 90 pregnant mothers and their infants (52 MSDP-exposed; 51% minorities; ages 18–40). Fetal neurobehavior at baseline and in response to vibro-acoustic stimulus was assessed via ultrasound and actocardiography at M = 35 weeks gestation and coded via the Fetal Neurobehavioral Assessment System (FENS). After delivery, the NICU Network Neurobehavioral Scale was administered up to seven times over the first postnatal month. MSDP was associated with increased fetal activity and fetal limb movements. Fetal activity, complex body movements, and cardiac–somatic coupling were associated with infants' ability to attend to stimuli and to self-regulate over the first postnatal month. Furthermore, differential associations emerged by MSDP group between fetal activity, complex body movements, quality of movement, and coupling, and infant attention and self-regulation. The present study adds to a growing literature establishing the validity of fetal neurobehavioral measures in elucidating fetal programming pathways.

The extent to which indices of maternal physiological arousal (skin conductance augmentation) and regulation (vagal withdrawal) while parenting predict infant attachment disorganization and behavior problems directly or indirectly via maternal sensitivity was examined in a sample of 259 mothers and their infants. Two covariates, maternal self-reported emotional risk and Adult Attachment Interview attachment coherence were assessed prenatally. Mothers' physiological arousal and regulation were measured during parenting tasks when infants were 6 months old. Maternal sensitivity was observed during distress-eliciting tasks when infants were 6 and 14 months old, and an average sensitivity score was calculated. Attachment disorganization was observed during the Strange Situation when infants were 14 months old, and mothers reported on infants' behavior problems when infants were 27 months old. Over and above covariates, mothers' arousal and regulation while parenting interacted to predict infant attachment disorganization and behavior problems such that maternal arousal was associated with higher attachment disorganization and behavior problems when maternal regulation was low but not when maternal regulation was high. This effect was direct and not explained by maternal sensitivity. The results suggest that maternal physiological dysregulation while parenting places infants at risk for psychopathology.

The parent–child attachment relationship plays an important role in the development of the infant's stress regulation system. However, genetic and epigenetic factors such as FK506 binding protein 51 (FKBP5) genotype and DNA methylation have also been associated with hypothalamus–pituitary–adrenal axis functioning. In the current study, we examined how parent–child dyadic regulation works in concert with genetic and epigenetic aspects of stress regulation. We study the associations of attachment, extreme maternal insensitivity, FKBP5 single nucleotide polymorphism 1360780, and FKBP5 methylation, with cortisol reactivity to the Strange Situation Procedure in 298 14-month-old infants. The results indicate that FKBP5 methylation moderates the associations of FKBP5 genotype and resistant attachment with cortisol reactivity. We conclude that the inclusion of epigenetics in the field of developmental psychopathology may lead to a more precise picture of the interplay between genetic makeup and parenting in shaping stress reactivity.

Childhood abuse and neglect (CAN) is considered as a risk factor for substance use disorder (SUD). Based on the drinking to cope model, this study investigated the association of two trauma-relevant emotions (shame and sadness) and substance use. Using ecological momentary assessment we compared real-time emotion regulation in situations with high and low intensity of shame and sadness in currently abstinent patients with CAN and lifetime SUD (traumaSUD group), healthy controls with CAN (traumaHC group), and without CAN (nontraumaHC group). Multilevel analysis showed a positive linear relationship between high intensity of both emotions and substance use for all groups. The traumaSUD group showed heightened substance use in low, as well as in high, intensity of shame and sadness. In addition, we found an interaction between type of emotion, intensity, and group: the traumaHC group exhibited a fourfold increased risk for substance use in high intense shame situations relative to the traumaSUD group. Our findings provide evidence for the drinking to cope model. The traumaSUD group showed a reduced distress tolerance for variable intensity of negative emotions. The differential effect of intense shame for the traumaHC group emphazises its potential role in the development of SUD following CAN. In addition, shame can be considered a relevant focus for therapeutic preinterventions and interventions for SUD after CAN.

This study examined family-level and child-level influences on diversity in depression and aggression among children at risk. Data were from 144 children aged 7–14 years. A procedure introduced by Lavori, Keller, Beardslee, and Dorer (1988) was used to correct for the inclusion of more than one child from each family. Family-level influences examined were maltreatment and parental psychopathology. Maladjustment was highest in children of psychiatrically ill parents from maltreating homes and lowest in children of psychiatrically ill parents from nonmaltreating homes. Child-level influences examined were social cognition, intelligence, early developmental difficulties, sex, and age. Independent of family risk status, younger male children with high social-cognitive skills and no early developmental difficulties were least depressed. Child characteristics were less predictive of aggression. Overall, this study shows that efforts to explain diversity in high-risk children's development benefit from attending to all the offspring of high-risk parents and to multiple interacting family risk factors.

The quality of adolescents' relationships with peers can have a lasting impact on later psychosocial adjustment, mental health, and behavior. However, the effect of peer relations on later problem behavior is not uniformly strong, and genetic factors might influence this association. This study used four-wave longitudinal (11–19 years) data (n = 1,151) from the Tracking Adolescents' Individual Lives Survey, a Dutch cohort study into adolescent development to test whether the dopamine receptor D4 polymorphism moderates the impact of negative (i.e., victimization) and positive peer experiences (i.e., social well-being) on later delinquency. Contrary to our expectations, results showed that carriers of the dopamine receptor D4 gene 4-repeat homozygous variant instead of those carrying the 7-repeat allele were more susceptible to the effects of both peer victimization and social well-being on delinquency later in adolescence. Findings of our study are discussed in light of other studies into genetic moderation of peer effects on adolescent development and the possibility that developmental specifics in adolescence, such as maturation processes in brain structure and functioning, may affect the interplay of environmental and genetic factors in this period in life.

Two longitudinal studies were used to examine the occurrence and consequences of peer deviancy training during childhood and the relative role of early covert antisocial behavior in risk for antisocial behavior in early adolescence. Peer deviancy training was apparent in a sample of at-risk first grade children, and it showed persistence and increased prevalence across the school year. Peer deviancy training, peer rejection, and unskilled parenting made additive contributions to the development of antisocial behavior during kindergarten and first grade and to antisocial behavior in fourth grade. Skilled parenting partially mitigated the association of peer deviancy training with antisocial behavior for boys. The appearance and growth of covert antisocial behavior was a predictor of fourth grade antisocial for boys and girls, more so than aggressive and overt antisocial behavior. Peer deviancy training and early covert antisocial behavior were key pathways to girls' antisocial behavior in fourth grade, and they complemented the roles of peer rejection and overt antisocial behavior for boys. The relationships of parenting and peer processes to trajectories of antisocial behavior were similar for boys and girls; but boys showed higher levels of antisocial behavior, were more involved in peer deviancy training, and were more likely to experience peer rejection.

The most commonly reported socially aberrant behavior in postinstitutionalized (PI) children is disinhibited social engagement (DSE; also known as indiscriminate friendliness). There is no gold standard for measurement of this phenomenon nor agreement on how to differentiate it from normative behavior. We adopted a developmental psychopathology approach (Cicchetti, 1984) to study this phenomenon by comparing it to normative social development and by studying its patterns over time in 50 newly adopted PI children (16–36 months at adoption) compared with 41 children adopted early from foster care overseas and 47 nonadopted (NA) controls. Using coded behavioral observations of the child's interaction with an unfamiliar adult, atypical behaviors were differentiated from normative behaviors. Principal components analysis identified two dimensions of social disinhibition. The nonphysical social dimension (e.g., initiations, proximity) showed wide variation in NA children and is therefore considered a typical form of sociability. Displays of physical contact and intimacy were rare in NA children, suggesting that they represent an atypical pattern of behavior. Both adopted groups demonstrated more physical DSE behavior than NA children. There were no group differences on the nonphysical factor, and it increased over time in all groups. Implications for understanding the etiology of DSE and future directions are discussed.

The ability to talk about the internal states (IS) of self and other is an age-typicaldevelopment of early childhood that is thought to reflect young children's emergentself–other understanding. This study examined the emergence of an IS lexicon in across-sectional sample of young children with Down syndrome (DS) and a cognitively anddemographically comparable group of normally developing (ND) children. Children's ISlexicons were derived from transcripts of their spontaneous utterances during two laboratorycontexts: a mother–child emotions picture book task and semistructured play. Childrenwith DS produced significantly fewer IS words and fewer IS word types than their MA-matchedcounterparts. Controlling for corpus size, children with DS also were less likely to attributeinternal states to themselves and were more context bound in their use of IS language. Inaddition, children with DS also differed from ND children in the semantic content of their ISlanguage, with proportionately higher rates of affective words and lower rates for words aboutvolition, ability, and cognition. For both the DS and ND groups, individual differences in ISlanguage production were significantly related to general expressive language skills. However,dissociations were observed for the relation between children's IS word production andnonverbal symbolic play skills in the two groups. These findings suggest some degree ofdisorganization at the interface among symbolic domains for children with DS. Because ISlanguage is critical to the regulation of social interaction and an early index of self–otherdifferentiation and understanding, children with DS may be at risk for later compromises inself-organization.

The last decade has been marked by an increased interest in relating epigenetic mechanisms to complex human behaviors, although this interest has not been balanced, accentuating various types of affective and primarily ignoring cognitive functioning. Recent animal model data support the view that epigenetic processes play a role in learning and memory consolidation and help transmit acquired memories even across generations. In this review, we provide an overview of various types of epigenetic mechanisms in the brain (DNA methylation, histone modification, and noncoding RNA action) and discuss their impact proximally on gene transcription, protein synthesis, and synaptic plasticity and distally on learning, memory, and other cognitive functions. Of particular importance are observations that neuronal activation regulates the dynamics of the epigenome's functioning under precise timing, with subsequent alterations in the gene expression profile. In turn, epigenetic regulation impacts neuronal action, closing the circle and substantiating the signaling pathways that underlie, at least partially, learning, memory, and other cognitive processes.

Previous research suggests that the experience of abuse and neglect in childhood has negative implications for physical health in adulthood. Using data from the Minnesota Longitudinal Study of Risk and Adaptation (N = 115), the present research examined the predictive significance of childhood physical abuse, sexual abuse, and physical/cognitive neglect for multilevel assessments of physical health at midlife (age 37–39 years), including biomarkers of cardiometabolic risk, self-reports of quality of health, and a number of health problems. Analyses revealed that childhood physical/cognitive neglect, but not physical or sexual abuse, predicted all three health outcomes in middle adulthood, even when controlling for demographic risk factors and adult health maintenance behaviors. We discuss possible explanations for the unique significance of neglect in this study and suggest future research that could clarify previous findings regarding the differential impact of different types of abuse and neglect on adult health.