Developmental psychopathology has successfully advanced an understanding of risk and protective factors in multivariate models. However, many areas have relied on top-down approaches that define psychological constructs based largely or solely on their physical form. In this paper, we first describe how top-down approaches have significantly hindered progress by generating generic risk and protective models that yield little more than the conclusion that axiomatically positive and negative factors respectively beget an interchangeable array of positive and negative child sequelae. To advance precision and novelty as central priorities, we describe behavioral systems frameworks rooted in evolutionary theory that infuse both form (i.e., what it looks like) and function (what it is designed to do) into psychological constructs. We further address how this paradigm has generated new growing points for developmental models of interparental relationships and parenting. In the final section, we provide recommendations for expanding this approach to other areas of developmental psychopathology. Throughout the paper, we document how the focus on functional patterns of behavior in well-defined developmental contexts advance precision and novelty in understanding children’s response processes to threats, opportunities, and challenges in associations between their developmental histories and their psychological sequelae.

In this study, we sought to combine two lines of research to better understand risk for the intergenerational transmission of depression. The first focuses on the role of maternal criticism as a potential mechanism of risk for depression in youth while the second builds from interpersonal and stress generation models regarding the potential impact of youth depression on future escalations in maternal criticism. Specifically, we examined the role of maternal criticism within a transactional mediation model using data from a multi-wave study. Participants were 251 mother–offspring pairs consisting of mothers with (n = 129) and without (n = 122) a history of major depressive disorder (MDD) during their child’s lifetime who completed assessments every 6 months for 2 years. We found support for the hypothesized transactional mediational model in which maternal expressed emotion-criticism (EE-Crit) mediated the link between maternal history of MDD and residual change in youth’s depressive symptoms over the previous 6 months and, reciprocally, youth depressive symptoms mediated the relation between maternal MDD history and residual change in EE-Crit 6 months later. These results indicate that maternal criticism and offspring depressive symptoms may contribute to a vicious cycle of depression risk, which should be considered for interventions targeted toward youth at risk of developing MDD.

This study aimed to examine Dispositional, Adaptational, and Environmental (DAE) variables at the intersection of adaptive and maladaptive personality development as a conceptual replication of the DAE-model (Asendorpf & Motti-Stefanidi, European Journal of Personality, 32(3), 167–185, 2018). In a community sample of adolescents (N = 463; Mage = 13.6 years; 51% female) hypotheses-driven cross-lagged panel models were tested. Longitudinal associations between Dispositional (i.e., neuroticism, disagreeableness and unconscientiousness), Adaptational (i.e., social problems), and Environmental (i.e., perceived quality of the parent-child relationship) variables were investigated. The results partially support the DAE hypotheses. High levels of neuroticism, disagreeableness and social problems were found to predict the perceived quality of the parent–child relationship. In turn, the perceived quality of the parent–child relationship was found to predict levels of unconscientiousness and social problems. No mediation effects were found and, in contrast to DAE hypotheses, results did not indicate bidirectional influences between dispositions and adaptations. The results shed light on differential person–environment interactions that shape personality development and the importance of the perceived quality of the parent–child relationship. These findings provide insight in pathways of personality development, that may lead to personality pathology, and demonstrate the value of the DAE model as a structured guideline that provides testable hypotheses.

Autism is associated with challenges in emotion recognition. Yet, little is known about how emotion recognition develops over time in autistic children. This four-wave longitudinal study followed the development of three emotion-recognition abilities regarding four basic emotions in children with and without autism aged 2.5 to 6 years over three years. Behavioral tasks were used to examine whether children could differentiate facial expressions (emotion differentiation), identify facial expressions with verbal labels (emotion identification), and attribute emotions to emotion-provoking situations (emotion attribution). We confirmed previous findings that autistic children experienced more difficulties in emotion recognition than non-autistic children and the group differences were present already from the preschool age. However, the group differences were observed only when children processed emotional information from facial expressions. When emotional information could be deduced from situational cues, most group differences disappeared. Furthermore, this study provided novel longitudinal evidence that emotion recognition improved with age in autistic children: compared to non-autistic children, autistic children showed similar learning curves in emotion discrimination and emotion attribution, and they showed greater improvements in emotion identification. We suggest that inclusion and respect in an environment free of stereotyping are likely to foster the development of emotion recognition among autistic children.

Hot executive functioning (EF) – EF under emotionally or motivationally salient conditions – is a putative etiology of attention-deficit/hyperactivity disorder (ADHD), disruptive behavior problems (DBPs), and their related impairments. Despite two decades of research, the present study is the first review of the construct in youth ADHD, with a particular focus on the role of task design, age, and DBPs, as well as relevant conceptual and methodological considerations. While certain hot EF tasks have been investigated extensively (e.g., choice impulsivity), substantial inconsistency in measurement of the broader construct remains, severely limiting conclusions. Future research should a) consider the extent to which various hot EF tasks relate to one another, a higher order factor, and other related constructs; b) further investigate task design, particularly the elicitation of emotion or motivation and its anticipated effect on EF; and c) incorporate multiple levels of analysis to validate similarities and differences among tasks with regard to the affective experiences and cognitive demands they elicit. With improved measurement and conceptual clarity, hot EF has potential to advance the literature on etiological pathways to ADHD, DBPs and associated impairments and, more broadly, may represent a useful tool for understanding the influence of emotion and motivation on cognition.

The pubertal transition is characterized by pronounced sex hormone fluctuation, refinement of affective neural circuitry, and an increased risk of depression in female adolescents. Sex hormones, including testosterone, exert modulatory effects on frontal-limbic brain networks and are associated with emotion dysregulation and depressive symptoms. Weekly changes in hormones predict affective symptoms in peripubertal female adolescents, particularly in the context of stress; however, the biobehavioral mechanisms underlying hormone change and mood relationships during the pubertal transition have yet to be determined and was the objective of the present study. Forty-three peripubertal female adolescents (ages 11–14) collected 8-weekly salivary hormone (estrone, testosterone) samples and mood assessments to evaluate hormone-mood relationships, followed by a biobehavioral testing session with psychosocial stress and EEG. Within-person correlations between weekly hormone changes and corresponding mood were performed to determine individual differences in mood sensitivity to weekly hormone change. Increased frontal theta activity indexing emotion reactivity, reduced cortisol reactivity, and reduced vagal efficiency predicted the strength of the relationship between testosterone and mood. Further, testosterone-sensitivity strength was associated with the enhancement of negative affect following stress testing. Results identify divergent frontal theta and stress responses as potential biobehavioral mechanisms underlying mood sensitivity to peripubertal testosterone fluctuation.

This study examined co-occurring patterns of mental health among disaster victims using latent profile analysis and assessed the difference between sociodemographic factors and protective factors that affect group classification. The data of 2300 disaster victims from 2019 (4th wave) NDMI (National Disaster Management Research Institute) for Long-term Survey on the Change of Life of Disaster Victims were analyzed. The latent profile analysis revealed that three profiles; High comorbid symptom (HCS) (6.2%), Medium comorbid symptom (MCS) (22.6%), and Low symptom (LS) (71.2%). The factors that explain the difference in this divided profile group were the type of disaster, hurt, income, age, elapsed years, resilience, and community resilience in the multinomial logistic regression. When individual resilience and community resilience are high, more effective in making people belong to the low comorbid symptom group. Therefore, there is a need for a strategy that promotes synergy between the two relationships while maintaining a dual focus point of view that fosters resilience at the individual and community level together.

Difficulty recognizing negative emotions is linked to aggression in children. However, it remains unclear how certain types of emotion recognition (insensitivities vs. biases) are associated with functions of aggression and whether these relations change across childhood. We addressed these gaps in two diverse community samples (study 1: aged 4 and 8; N = 300; study 2: aged 5 to 13, N = 374). Across studies, children performed a behavioral task to assess emotion recognition (sad, fear, angry, and happy facial expressions) while caregivers reported children’s overt proactive and reactive aggression. Difficulty recognizing fear (especially in early childhood) and sadness was associated with greater proactive aggression. Insensitivity to anger – perceiving angry faces as showing no emotion – was associated with increased proactive aggression, especially in middle-to-late childhood. Additionally, greater happiness bias – mistaking negative emotions as being happy – was consistently related to higher reactive aggression only in early childhood. Together, difficulty recognizing negative emotions was related to proactive aggression, however, the strength of these relations varied based on the type of emotion and developmental period assessed. Alternately, difficulty determining emotion valence was related to reactive aggression in early childhood. These findings demonstrate that distinct forms of emotion recognition are important for understanding functions of aggression across development.

Developmental psychopathology started as an intersection of fields and is now a field itself. As we contemplate the future of this field, we consider the ways in which a newer, interdisciplinary field – human developmental neuroscience – can inform, and be informed by, developmental psychopathology. To do so, we outline principles of developmental psychopathology and how they are and/or can be implemented in developmental neuroscience. In turn, we highlight how the collaboration between these fields can lead to richer models and more impactful translation. In doing so, we describe the ways in which models from developmental psychopathology can enrich developmental neuroscience and future directions for developmental psychopathology.

Pre-diagnostic deficits in social motivation are hypothesized to contribute to autism spectrum disorder (ASD), a heritable neurodevelopmental condition. We evaluated psychometric properties of a social motivation index (SMI) using parent-report item-level data from 597 participants in a prospective cohort of infant siblings at high and low familial risk for ASD. We tested whether lower SMI scores at 6, 12, and 24 months were associated with a 24-month ASD diagnosis and whether social motivation’s course differed relative to familial ASD liability. The SMI displayed good internal consistency and temporal stability. Children diagnosed with ASD displayed lower mean SMI T-scores at all ages and a decrease in mean T-scores across age. Lower group-level 6-month scores corresponded with higher familial ASD liability. Among high-risk infants, strong decline in SMI T-scores was associated with 10-fold odds of diagnosis. Infant social motivation is quantifiable by parental report, differentiates children with versus without later ASD by age 6 months, and tracks with familial ASD liability, consistent with a diagnostic and susceptibility marker of ASD. Early decrements and decline in social motivation indicate increased likelihood of ASD, highlighting social motivation’s importance to risk assessment and clarification of the ontogeny of ASD.

This study examined how temporal associations between parents’ physiological and behavioral responses may reflect underlying regulatory difficulties in at-risk parenting. Time-series data of cardiac indices (second-by-second estimates of inter-beat intervals – IBI, and respiratory sinus arrhythmia – RSA) and parenting behaviors were obtained from 204 child welfare-involved parents (88% mothers, Mage = 32.32 years) during child-led play with their 3- to 7-year-old children (45.1% female; Mage = 4.76 years). Known risk factors for maltreatment, including parents’ negative social cognitions, mental health symptoms, and inhibitory control problems, were examined as moderators of intra-individual physiology-behavior associations. Results of ordinary differential equations suggested increases in parents’ cardiac arousal at moments when they showed positive parenting behaviors. In turn, higher arousal was associated with momentary decreases in both positive and negative parenting behaviors. Individual differences in these dynamic processes were identified in association with parental risk factors. In contrast, no sample-wide RSA-behavior associations were evident, but a pattern of increased positive parenting at moments of parasympathetic withdrawal emerged among parents showing more total positive parenting behaviors. This study illustrated an innovative and ecologically-valid approach to examining regulatory patterns that may shape parenting in real-time and identified mechanisms that should be addressed in interventions.

This commentary discusses opportunities for advancing the field of developmental psychopathology through the integration of data science and neuroscience approaches. We first review elements of our research program investigating how early life adversity shapes neurodevelopment and may convey risk for psychopathology. We then illustrate three ways that data science techniques (e.g., machine learning) can support developmental psychopathology research, such as by distinguishing between common and diverse developmental outcomes after stress exposure. Finally, we discuss logistical and conceptual refinements that may aid the field moving forward. Throughout the piece, we underscore the profound impact of Dr Dante Cicchetti, reflecting on how his work influenced our own, and gave rise to the field of developmental psychopathology.

Peer victimization is a developmentally salient stressor that elevates adolescents’ risk for anxiety disorders. However, modifiable mechanisms that explain this link and can be targeted via therapeutic interventions remain poorly understood. Drawing from psychobiological models implicating aberrant threat sensitivity in the development and maintenance of psychopathology, the current study investigated sensitivity to peer-related social threats as a mechanism underlying the association between peer victimization and anxiety. A sample of 197 dyads of early adolescents (Mage = 12.02; 46% female) and parents/guardians (Mage = 41.46; 90% female) completed online surveys assessing peer victimization, sensitivity to potential (i.e., ambiguous) social threats, and anxiety. Controlling for potentially confounding demographic and psychosocial factors, both self- and parent-reported peer victimization were positively associated with adolescent anxiety symptoms. Additionally, there were significant indirect effects from self- and parent-reported peer victimization to anxiety via social threat sensitivity. Supplemental analyses indicated unique effects of covert, but not overt, peer victimization on social threat sensitivity and anxiety. The findings provide initial evidence that peer victimization experiences lower adolescents’ threshold for interpreting threats in ambiguous social situations, which contributes to heightened anxiety. These results implicate social threat sensitivity as a potential therapeutic target for interrupting links from peer victimization to psychological distress.

Aggressive reactions to peer victimization may be tempered by hormone levels. Grounded on the dualhormone hypothesis (DHH), which proposes that testosterone (T) is associated with aggressive behavior only when cortisol (C) is low, this study assessed whether the combination of T and C moderated adolescents’ aggressive responses to peer victimization. The study involved 577 adolescents (50.4% girls, aged 12–17 years), who completed measures of online and offline victimization and perpetration of aggressive behavior in three waves over the course of one year. Moreover, they provided salivary samples to measure T and C levels. Multilevel analyses showed a three-way interaction between T, C, and victimization levels for both online and offline aggressive behaviors. In both cases, the adolescents with high T and high C or low T and low C responded with more aggressive behaviors when victimized or provoked by peers. The T/C ratio was only associated with aggressive behavior in the girls’ sample. The results are opposite to those predicted by the DHH, but they are consistent with the findings of other studies that examined aggressive behaviors as reactions to provocations. These results suggest that some combinations of T and C predict higher aggressive reactions to peer victimization.

Gene-environment interactions (GxE) have been increasingly explored in psychiatry but with low replication rates. Attention-deficit/hyperactivity disorder (ADHD) is a suitable candidate for studying GxE due to its high heritability and well-defined environmental risk factors. Here, we explored GxE using polygenic risk score (PRS) to represent the genetic liability to ADHD (ADHD-PRS) and environmental risk score (ERS) to represent the combined effects of environmental risk factors. We analyzed longitudinal data of 2,046 individuals (6-14 years of age at baseline and 14-23 at the last follow-up) from the Brazilian High-Risk Cohort Study for Psychiatric Disorders. Psychiatric evaluation included the Child Behavior Checklist and the Strength and Difficulties Questionnaire. Statistical analyses were performed using mixed-effects models. We observed statistically significant interactions between ADHD-PRS and ERS, suggesting that environmental and genetic factors act synergistically in the development of ADHD symptoms. These effects were not present for depression or anxiety symptoms. No evidence of GxE correlation was detected. Mechanistically, our findings suggest that environmental stressors modulate the genetic risk for ADHD. Future studies should investigate whether the reduction of environmental risks can prevent the development of symptoms of ADHD, especially in children with a family history of the disorder.

Dante Cicchetti propelled forward the field of developmental psychopathology by advancing this framework and championing new methods, including emphasizing the central role that multilevel analysis holds for explicating pathways of risk and resilience. His work continues to change the face of existing science. It has also paved the way for the formation of new projects, like the Research Domain Criteria initiative. This paper uses our laboratory’s work on multilevel approaches to studying adolescent depression, non-suicidal self-injury, and suicidal thoughts and behaviors to shine a spotlight on Dr Cicchetti’s contributions. In addition, we review recent developments, ongoing challenges, and promising future directions within developmental psychopathology as we endeavor to carry on the tradition of growth in the field.

This study examined parental depression and parental reflective functioning (PRF) as predictors of parental proficiency in relational savoring (RS), the association between RS proficiency and a marker of children’s physiological self-regulation, respiratory sinus arrhythmia (RSA), during a stressor, and indirect effects of parental depression and PRF on children’s RSA via parents’ RS. At Time 1 (T1), parents of 8- to 12-year-old children (N = 139) reported on their depressive symptoms and completed a parenting interview, coded for PRF. After 1.5 years (Time 2; T2), parents savored a positive relational memory that involved their children, which was coded for savoring proficiency. Children’s RSA was measured during a stressful task (a series of impossible puzzles). Depressive symptoms (inversely) and PRF (positively) were associated with RS proficiency. Higher parental RS proficiency was associated with children’s higher mean levels of RSA during the stressor. Indirect effects models supported that T2 RS proficiency mediated the negative association between parental T1 depressive symptoms and children’s T2 RSA, and between T1 PRF and children’s T2 RSA. We discuss these findings in terms of implications for parents’ emotion regulation, children’s emotion regulation, children’s mental health, and intervention.

Attachment theory has played an important role in attempts to understand the “cycle of violence,” where maltreated children are at increased risk for perpetrating violence later in life. However, little is known empirically about whether adult attachment insecurity in close relationships may partly explain the link between childhood maltreatment and violent behavior. This study aimed to address this gap using data from a prospective longitudinal study of documented childhood abuse and neglect cases and demographically matched controls (ages 0–11 years), who were followed into adulthood and interviewed (N = 892). Participants completed the Relationship Scales Questionnaire assessing adult attachment styles at mean age 39.54. Criminal arrest data were used to determine arrests for violence after the assessment of attachment through mean age 50.54. There were significant direct paths from childhood maltreatment and adult attachment insecurity to violent arrests after attachment measurement. Attachment insecurity partly explained the higher levels of violence in individuals with maltreatment histories. Analyses of maltreatment subtypes and attachment styles revealed that attachment anxiety appeared to mediate paths between neglect and physical abuse and later violence. There were no significant indirect paths from neglect or physical abuse to violence via attachment avoidance. Implications and future directions are discussed.

While peer interaction differences are considered a central feature of autism, little is known regarding the nature of these interactions via directly-observed measurement of naturalistic (i.e., minimally-structured) groups of autistic and non-autistic adolescent peers. 148 autistic and non-autistic adolescents (111 male, Mage = 14.22, SDage = 1.90; MIQ = 103.22, SDIQ = 15.80) participated in a 50-minute, minimally-structured, naturalistic peer interaction paradigm with activities of varying social demands: an incidental social demand (eating in a room with peers), a physical social demand (playing a physically-interactive game), and a verbal social demand (playing a verbal game). While autistic youth exhibited fewer overall interaction behaviors than non-autistic youth, the two groups did not differ in amount of positive, negative, and low-level interaction behaviors. Within activities, autistic and non-autistic youth only differed in positive interaction behaviors during the context of a verbal social demand. Youth who displayed more positive interaction behaviors during this same activity had less autism spectrum disorder symptomatology, controlling for nested group effects and relevant covariates. These results point toward subtle differences in social demands across naturalistic settings that can either support or impede prosocial interaction for autistic youth, providing a guidepost for identifying settings that best promote social success for neurodiverse populations.