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Objective: To examine sex differences in autonomic nervous system functioning in children and adolescents with conduct problems and to evaluate the role of aggression in predicting autonomic nervous system functioning, over and above the effects of disruptive behavior. Although deficiencies in autonomic responding among boys with oppositional defiant disorder and/or conduct disorder are well documented, it remains unclear whether such findings extend to girls or apply only to children with aggressive forms of conduct problems.Method: Electrodermal responding, cardiac pre-ejection period, and respiratory sinus arrhythmia were recorded while boys (n = 110; 53 with conduct problems, 57 controls) and girls (n = 65; 33 with conduct problems, 32 controls) between the ages of 8 and 12 sat for an extended baseline, then played a game with conditions of reward and frustrative nonreward.Results: Both sex effects and aggression effects were found. Aggressive boys with conduct problems demonstrated reduced autonomic functioning, consistent with previous research. In contrast, aggressive girls with conduct problems exhibited greater electrodermal responding than controls, with no differences in cardiovascular reactivity to incentives.Conclusions: Observed sex differences in the autonomic correlates of conduct problems and aggression may suggest different etiological mechanisms of externalizing psychopathology for girls compared with boys. [ABSTRACT FROM AUTHOR]

Suicide rates are rising among U.S. youth, yet our understanding of developmental mechanisms associated with increased suicide risk is limited. One high-risk pathway involves an interaction between heritable trait impulsivity and emotion dysregulation (ED). Together, these confer increased vulnerability to nonsuicidal self-injury (NSSI), suicide ideation (SI), and suicide attempts (SAs). Previous work, however, has been limited to homogeneous samples. We extend the Impulsivity × ED hypothesis to a more diverse sample of adolescents ( N = 344, ages 12-15 at Baseline, 107 males and 237 females) who were treated for major depression and assessed four times over two years. In multilevel models, the impulsivity × ED interaction was associated with higher levels and worse trajectories of NSSI, SI, and SAs. As expected, stressful life events were also associated with poorer trajectories for all outcomes, and NSSI was associated with future and concurrent SI and SAs. These findings extend one developmental pathway of risk for self-harming and suicidal behaviors to more diverse adolescents, with potential implications for prevention.

In a thoughtful commentary in this journal a decade ago, Michael Rutter reviewed 25 years of progress in the field before concluding that developmental psychopathology (DP) initiated a paradigm shift in clinical science. This deduction requires that DP itself be a paradigm. According to Thomas Kuhn, canonical paradigms in the physical sciences serve unifying functions by consolidating scientists' thinking and scholarship around single, closed sets of discipline-defining epistemological assumptions and methods. Paradigm shifts replace these assumptions and methods with a new field-defining framework. In contrast, the social sciences are multiparadigmatic , with thinking and scholarship unified locally around open sets of epistemological assumptions and methods with varying degrees of inter-, intra-, and subdisciplinary reach. DP challenges few if any of these local paradigms. Instead, DP serves an essential pluralizing function, and is therefore better construed as a metaparadigm. Seen in this way, DP holds tremendous untapped potential to move the field from zero-sum thinking and scholarship to positive-sum science and epistemological pluralism . This integrative vision, which furthers Dante Cicchetti's legacy of interdisciplinarity, requires broad commitment among scientists to reject zero-sum scholarship in which portending theories, useful principles, and effective interventions are jettisoned based on confirmation bias, errors in logic, and ideology.

This study investigated whether oppositional defiant disorder (ODD) with the DSM-5 limited prosocial emotions (LPE) specifier marks a more severe clinical presentation than ODD alone. Mothers, fathers, and teachers of 2,142 Spanish children (49.49% girls; ages 8 to 13 years) completed measures of ODD, LPE, ADHD-hyperactivity/impulsivity (HI), ADHD-inattention (IN), cognitive disengagement syndrome (CDS), anxiety, depression, social impairment, academic impairment, and peer rejection (teacher only measure). Scores greater or less than 1.50 SDs above the ODD and LPE means were used to create ODD-only (5.89-7.22% of the sample, depending on informant), LPE-only (7.61-8.25%), ODD + LPE (1.69-2.20%), and comparison groups (82.96-84.68%) for each source. For all three sources, the LPE-only group scored higher than the comparison group on social impairment, peer rejection, and academic impairment but did not differ significantly on anxiety. Although the ODD-only and ODD + LPE groups scored higher than the LPE-only group on all symptom and most impairment dimensions, the ODD + LPE group did not show a consistent pattern of higher scores than the ODD-only group. There were no differences on mother ratings, and higher scores for the ODD + LPE group emerged on only three of seven father-report measures (depression, CDS, and ADHD-IN) and three of eight teacher-report measures (peer rejection, social impairment, and academic impairment). Limited differences between the ODD + LPE and ODD-only groups raise questions about the usefulness of LPE as a severity specifier for ODD among children. Future studies need to address this issue with adolescents and clinical samples., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Symmetrical bifactor models are frequently applied to diverse symptoms of psychopathology to identify a general P factor. This factor is assumed to mark shared liability across all psychopathology dimensions and mental disorders. Despite their popularity, however, symmetrical bifactor models of P often yield anomalous results, including but not limited to nonsignificant or negative specific factor variances and nonsignificant or negative factor loadings. To date, these anomalies have often been treated as nuisances to be explained away. In this article, we demonstrate why these anomalies alter the substantive meaning of P such that it (a) does not reflect general liability to psychopathology and (b) differs in meaning across studies. We then describe an alternative modeling framework, the bifactor-( S -1) approach. This method avoids anomalous results, provides a framework for explaining unexpected findings in published symmetrical bifactor studies, and yields a well-defined general factor that can be compared across studies when researchers hypothesize what construct they consider "transdiagnostically meaningful" and measure it directly. We present an empirical example to illustrate these points and provide concrete recommendations to help researchers decide for or against specific variants of bifactor structure.

Studies of 16p11.2 copy number variants (CNVs) provide an avenue to identify mechanisms of impairment and develop targeted treatments for individuals with neurodevelopmental disorders. 16p11.2 deletion and duplication phenotypes are currently being ascertained; however, sleep disturbances are minimally described. In this study, we examine sleep disturbance in a well-characterized national sample of 16p11.2 CNVs, the Simons Foundation Autism Research Initiative (SFARI) database of youth and adults (n = 692). Factor analyses and multilevel models of derived sleep questionnaires for youth (n = 345) and adults (n = 347) indicate that 16p11.2 carriers show elevated sleep disturbance relative to community controls. Non-carrier family members also show elevated sleep disturbance. However, sleep duration does not differ between carriers and controls. Further studies of sleep in 16p11.2 are needed., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Growth mixture modeling (GMM) and its variants, which group individuals based on similar longitudinal growth trajectories, are quite popular in developmental and clinical science. However, research addressing the validity of GMM-identified latent subgroupings is limited. This Monte Carlo simulation tests the efficiency of GMM in identifying known subgroups ( k = 1-4) across various combinations of distributional characteristics, including skew, kurtosis, sample size, intercept effect size, patterns of growth (none, linear, quadratic, exponential), and proportions of observations within each group. In total, 1,955 combinations of distributional parameters were examined, each with 1,000 replications (1,955,000 simulations). Using standard fit indices, GMM often identified the wrong number of groups. When one group was simulated with varying skew and kurtosis, GMM often identified multiple groups. When two groups were simulated, GMM performed well only when one group had steep growth (whether linear, quadratic, or exponential). When three to four groups were simulated, GMM was effective primarily when intercept effect sizes and sample sizes were large, an uncommon state of affairs in real-world applications. When conditions were less ideal, GMM often underestimated the correct number of groups when the true number was between two and four. Results suggest caution in interpreting GMM results, which sometimes get reified in the literature.

Objective: To test differential prospective prediction of growth in externalizing behavior, including oppositional defiant disorder, conduct disorder, and substance use disorders, by earlier hyperactive-impulsive (HI) vs inattentive (IN) symptoms of attention-deficit/hyperactivity disorder (ADHD)., Method: Participants in the Longitudinal Assessment of Manic Symptoms (LAMS) Study (N = 685 at study entry), including 458 boys and 227 girls ages 6-12, completed full parent report and self-report assessments every year for 8 years on the Schedule for Affective Disorders and Schizophrenia for School-Age Children. Three sets of analyses were conducted. First, hierarchal regression (block entry) was used to test independent associations between HI symptoms and later externalizing outcomes, controlling for IN symptoms, and IN symptoms and later externalizing outcomes, controlling for HI symptoms. Second, logistic regression was used to test progression of DSM externalizing disorders. Third, tests of mediation were used to assess potentiation of externalizing progression through environmental risk mediators (eg, family environment, neighborhood violence)., Results: Consistent with hypotheses derived from trait impulsivity theories of externalizing behavior, HI symptoms of ADHD were associated independently with long-term externalizing outcomes, whereas IN symptoms were not. Between months 48 and 96, ADHD-HI/combined symptom subtype diagnoses predicted later oppositional defiant disorder diagnoses, oppositional defiant disorder diagnoses predicted later conduct disorder diagnoses, and conduct disorder diagnoses predicted later substance use disorder diagnoses. Evidence for environmental risk mediation (eg, parental monitoring, neighborhood violence) was also found., Conclusion: Findings support trait impulsivity models of externalizing progression, whereby ADHD-HI/combined symptoms subtypes predispose to increasingly severe externalizing behaviors, which are magnified in contexts of environmental risk., (Copyright © 2021 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)

Despite nonoverlapping diagnostic criteria, internalizing and externalizing disorders show substantial comorbidity. This comorbidity is attributable, at least in part, to transdiagnostic neuroaffective mechanisms. Both unipolar depression and externalizing disorders are characterized by structural and functional compromises in the striatum and its projections to the anterior cingulate cortex (ACC) and other frontal regions. Smaller volumes and dampened reward responding in these regions are associated with anhedonia and irritability - mood states that cut across the internalizing and externalizing spectra. In contrast, smaller amygdala volumes and dampened amygdala function differentiate externalizing disorders from internalizing disorders. Little is known, however, about associations between internalizing-externalizing comorbidity and brain volumes in these regions, or whether such patterns differ by sex. Using a transdiagnostic, research domain criteria (RDoC)-informed approach, we evaluate associations between heterotypic (Internalizing × Externalizing) symptom interactions and striatal, amygdalar, and ACC volumes among participants in the Adolescent Brain Cognitive Development study ( N = 6,971, mean age 9.9 years, 51.6% female). Heterotypic symptoms were associated with ACC volumes for both sexes, over and above the main effects of internalizing and externalizing alone. However, heterotypic comorbidity was associated with larger ACC volumes for girls, but with smaller ACC volumes for boys. These findings suggest a need for further studies and transdiagnostic assessment by sex., Competing Interests: Conflicts of Interest. None.

Children of fathers with antisocial personality disorder (ASPD) are at risk for developing delinquency, and both biological and environmental mechanisms contribute. In this study, we test parasympathetic nervous system (PNS) function as a vulnerability/sensitivity attribute in predicting intergenerational associations between fathers' antisociality and children's delinquency scores. We followed 207 children (ages 8-12 years at intake; 139 boys) across three annual assessments. Fathers' antisociality was measured via maternal reports on the Family Interview for Genetic Studies (FIGS). At Year 1, children's resting respiratory sinus arrhythmia (RSA) was measured. At Years 1, 2, and 3, child delinquent behaviors were assessed using the delinquency subscale of the Youth Self-Report. At age 8, boys' delinquency scores were associated weakly with paternal antisocial behaviors. However, boys' delinquency scores increased steeply thereafter specifically for those who had fathers with higher antisocial symptoms. In addition, associations between delinquency and paternal antisociality were largest for boys with higher resting RSA. For girls, growth in delinquency was unrelated to both father antisociality and resting RSA. These findings (a) suggest moderating effects of children's age, sex, and PNS function on associations between father antisocial behavior and offspring delinquency; and (b) provide insights into differential vulnerability among children of fathers with ASPD., (© 2020 Wiley Periodicals LLC.)

Children with higher socioemotional competence are more likely to build constructive relationships with others and experience more positive adjustment outcomes in later periods. Securely attached children are likely to develop better socioemotional competence, but genetic moderation of associations between attachment and later socioemotional competence has received less attention. Using structural equation modeling, this study analyzed data collected from 1,337 children (51% male) born from 1998 to 2000 in the Fragile Families and Child Wellbeing study. The results demonstrated that relations between attachment security at age 3 years and their social competence at age 5 years differed by two serotonin transporter variants (5-HTTLPR, STin2). Effect sizes of these interactions were larger than effect sizes of main effects and the benefit of having sensitive alleles was consistently supported. This implies that having more secure attachment in the early developmental period is advantageous especially for children with minor alleles who have greater environmental sensitivity., (© 2020 Wiley Periodicals LLC.)

Several studies show altered heart rate variability (HRV) in autism spectrum disorder (ASD), but findings are neither universal nor specific to ASD. We apply a set of linear and nonlinear HRV measures-including phase rectified signal averaging-to segments of resting ECG data collected from school-age children with ASD, age-matched typically developing controls, and children with other psychiatric conditions characterized by altered HRV (conduct disorder, depression). We use machine learning to identify time, frequency, and geometric signal-analytical domains that are specific to ASD (receiver operating curve area = 0.89). This is the first study to differentiate children with ASD from other disorders characterized by altered HRV. Despite a small cohort and lack of external validation, results warrant larger prospective studies.

Attention-deficit/hyperactivity disorder (ADHD) exerts lifelong impairment, including difficulty sustaining employment, poor credit, and suicide risk. To date, however, studies have assessed selected samples, often via self-report. Using mental health data from the entire Swedish population ( N = 11.55 million) and a random sample of credit data ( N = 189,267), we provide the first study of objective financial outcomes among adults with ADHD, including associations with suicide. Controlling for psychiatric comorbidities, substance use, education, and income, those with ADHD start adulthood with normal credit demand and default rates. However, in middle age, their default rates grow exponentially, yielding poor credit scores and diminished credit access despite high demand. Sympathomimetic prescriptions are unassociated with improved financial behaviors. Last, financial distress is associated with fourfold higher risk of suicide among those with ADHD. For men but not women with ADHD who suicide, outstanding debt increases in the 3 years prior. No such pattern exists for others who suicide., (Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).)

Sleep problems are common among children with neurodevelopmental disorders (NDDs). We review sleep disturbance in three major NDDs: autism spectrum disorder, Down syndrome, and fetal alcohol spectrum disorder (FASD). We review associations with functional impairment, discuss how patterns of sleep disturbance inform understanding of etiology, and theorize about mechanisms of impairment. Sleep disturbance is a transdiagnostic feature of NDDs. Caregivers report high rates of sleep problems, including difficulty falling or staying asleep. Polysomnography data reveal differences in sleep architecture and increased rates of sleep disorders. Sleep disturbance is associated with functional impairment and stress among families. Further research is needed to elucidate mechanisms of impairment and develop more effective interventions. Despite significant sleep disturbance in FASD, limited research is available., Competing Interests: Conflict of Interest: The authors declare they have no conflict of interest.

The commentaries by Burke and Johnston (this issue), Eid (this issue), Junghänel et al. (this issue), and Willoughby (this issue) on Burns et al. (this issue) provide useful context for comparing three latent variable modeling approaches to understanding psychopathology-the correlated first-order syndrome-specific factors model, the bifactor S - 1 model, and the symmetrical bifactor model. The correlated first-order syndrome-specific factors model has proven useful in constructing explanatory models of psychopathology. The bifactor S - 1 model is also useful for examining the latent structure of psychopathology, especially in contexts with clear theoretical predictions. Joint use of correlated first-order syndrome-specific model and bifactor S - 1 model provides leverage for explaining psychopathology, and both models can also guide individual clinical assessment. In this reply, we further clarify reasons why the symmetrical bifactor model should not be used to study the latent structure of psychopathology and also discuss a restricted bifactor S - 1 model that is equivalent to the first-order syndrome-specific factors model.

The symmetrical bifactor model is often applied to attention-deficit/hyperactivity disorder (ADHD)-hyperactive/impulsive (HI), ADHD-inattentive (IN), and oppositional defiant disorder (ODD) symptoms, but this model frequently yields anomalous or inadmissible results. An alternative model, the bifactor S - 1 model, is more appropriate for examining the hierarchical structure of ADHD/ODD symptoms. Both models were applied to ADHD-HI, ADHD-IN, and ODD symptom ratings by mothers, fathers, and teachers for 2142 Spanish children (49.49% girls; ages 8-13 years). The symmetrical bifactor model yielded the typical anomalous loadings, with a weakly defined ADHD-HI specific factor and difficult to interpret associations of general and specific factors with correlates. In contrast, the bifactor S - 1 model with ADHD-HI symptoms as general reference factor produced clearly interpretable results. For mothers and fathers, slightly more than 50% of true score variance in ADHD-IN and ODD symptoms represented specific residual variance not shared with the general ADHD-HI reference factor. For teachers, approximately 69% and 39% of true score variance in ADHD-IN and ODD symptoms, respectively, represented specific residual variance not shared with the general ADHD-HI reference factor. The general ADHD-HI reference factor and specific ADHD-IN and ODD residual factors showed convergent and discriminant validity across sources, along with unique associations with peer rejection, social impairment, and academic impairment factors. The bifactor S - 1 model also yielded results consistent with predictions from trait-impulsivity theory of ADHD/ODD development. Researchers should use the bifactor S - 1 model rather than the symmetrical bifactor model if hypotheses involve the latent hierarchical structure of ADHD/ODD symptoms.

The objective was to determine the longitudinal associations between callous-unemotional (CU) and oppositional defiant (OD) behaviors from the first to fourth grades for Spanish children. Four possible outcomes were evaluated: (a) CU behaviors in the first grade predict increases in OD behaviors in the fourth grade, controlling for OD behaviors in the first grade; (b) OD behaviors in the first grade predict increases in CU behaviors in the fourth grade, controlling for CU behaviors in the first grade; (c) both unique effects are significant; and (d) neither unique effect is significant. A longitudinal panel model with two latent variables (CU and OD behaviors), three sources (mothers, fathers, teachers), and two occasions (spring of the first and fourth grades) was used to evaluate the four possibilities among 758 (54% boys) first grade and 469 (53% boys) fourth grade Spanish children. For mother-, father-, and teacher-reports, OD behaviors in the first grade predicted increases in CU behaviors in the fourth grade, after controlling for CU behaviors in the first grade, whereas CU behaviors in the first grade did not predict increases in OD behaviors in the fourth grade, after controlling for OD behaviors in the first grade. OD behaviors thus conferred independent vulnerability to increases in CU behaviors 3 years later among young children.

Now over 10 years old, the Research Domain Criteria (RDoC) has gained impressive traction in the adult psychopathology literature, but enthusiasm among child and adolescent psychopathologists lags somewhat behind. We consider possible reasons why RDoC has not been embraced fully in the child and adolescent literatures. We emphasize common, interrelated, and sometimes outdated assumptions that impede scientific progress that RDoC could facilitate. Traditionally, child and adolescent psychopathologists have used behavioral syndromes as gold standards against which biological markers are validated, even though behavioral syndromes are often measured with less precision; sought to identify large main effects of single biological functions on single behavioral syndromes, thereby ignoring (even if implicitly) the overwhelming etiological complexity of psychopathology; expected 1:1 correspondencies between biological functions and behaviors, despite evidence that core biological systems subserving behavior are functionally interdependent (i.e., modulate one another); and failed to consider neurobiological mechanisms of homotypic and heterotypic comorbidity and continuity. Using examples from our work, we show how a developmental, RDoC-informed approach to externalizing behavior enriches our understanding of psychopathology. We also provide an agenda for future research, which includes calls to (1) adopt neural-systems-first approaches over disorder-first approaches when studying psychopathology, (2) eschew biological reductionism by integrating environmental risk mediators into our etiopathophysiological models, (3) integrate neural vulnerabilities into the empirical latent structure of psychopathology, and (4) replace null hypothesis significance testing with computational approaches that accommodate etiological complexity by evaluating functional dependencies among RDoC constructs, including positive valence systems (approach), negative valence systems (avoidance), and arousal/regulatory systems (self-regulation).

In recent years, irritability has received increasing attention among mental health professionals given its transdiagnostic associations with diverse forms of psychopathology. In contrast to other emotional states and traits, however, literature addressing associations between irritability and related temperament and personality constructs is limited. In addition, those who study irritability have diverse perspectives on its neurobiological substrates. In this comment, we situate irritability in the literatures on child temperament and adult personality, and describe a model in which irritability derives from low tonic dopamine (DA) levels and low phasic DA reactivity in subcortical neural structures implicated in appetitive responding. We note that different findings often emerge in neuroimaging studies when irritability is assessed in circumscribed diagnostic groups versus representative samples. We conclude with directions for future research, and propose that more authors use hierarchical Bayesian modeling, which captures functional dependencies between irritability and other dispositional traits (e.g., trait anxiety) that standard regression models are insensitive too. Treatment implications are also considered., (Copyright © 2019. Published by Elsevier Ltd.)

Almost all forms of psychopathology, including personality disorders, are arrived at through complex interactions among neurobiological vulnerabilities and environmental risk factors across development. Yet despite increasing recognition of etiological complexity, psychopathology research is still dominated by searches for large main effects causes. This derives in part from reliance on traditional inferential methods, including ordinary factor analysis, regression, ANCOVA, and other techniques that use statistical partialing to isolate unique effects. In principle, some of these methods can accommodate etiological complexity, yet as typically applied they are insensitive to interactive functional dependencies (modulating effects) among etiological influences. Here, we use our developmental model of antisocial and borderline traits to illustrate challenges faced when modeling complex etiological mechanisms of psychopathology. We then consider how computational models, which are rarely used in the personality disorders literature, remedy some of these challenges when combined with hierarchical Bayesian analysis., (© 2020 S. Karger AG, Basel.)

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.

Sexual discounting, which describes delay discounting of later protected sex vs. immediate unprotected sex (e.g., sex now without a condom vs. waiting an hour to have sex with a condom), is consistently linked to sexual risk behavior. Estimates suggest that over two-thirds of HIV transmissions occur between individuals in committed relationships, but current sexual discounting tasks examine sexual discounting only with hypothetical strangers, leaving a gap in our understanding of sexual discounting with committed sexual partners. We used the Sexual Discounting Task (SDT) to compare discounting rates between men who have sex with men (MSM; n = 99) and heterosexual men (n = 144) and tested a new SDT condition evaluating sexual discounting with main partners. MSM in committed relationships discounted protected sex with their main partner at higher rates than heterosexual men, and discounting rates correlated with self-report measures of condom use, impulsivity/sensation seeking, and substance use. These findings suggest that sexual discounting is a critical factor potentially related to increased HIV transmission between MSM in committed relationships and may be an important target for intervention and prevention.

As early as infancy, caregivers' facial expressions shape children's behaviors, help them regulate their emotions, and encourage or dissuade their interpersonal agency. In childhood and adolescence, proficiencies in producing and decoding facial expressions promote social competence, whereas deficiencies characterize several forms of psychopathology. To date, however, studying facial expressions has been hampered by the labor-intensive, time-consuming nature of human coding. We describe a partial solution: automated facial expression coding (AFEC), which combines computer vision and machine learning to code facial expressions in real time. Although AFEC cannot capture the full complexity of human emotion, it codes positive affect, negative affect, and arousal-core Research Domain Criteria constructs-as accurately as humans, and it characterizes emotion dysregulation with greater specificity than other objective measures such as autonomic responding. We provide an example in which we use AFEC to evaluate emotion dynamics in mother-daughter dyads engaged in conflict. Among other findings, AFEC (a) shows convergent validity with a validated human coding scheme, (b) distinguishes among risk groups, and (c) detects developmental increases in positive dyadic affect correspondence as teen daughters age. Although more research is needed to realize the full potential of AFEC, findings demonstrate its current utility in research on emotion dysregulation.

Although emotion dysregulation (ED) is a core symptom of borderline personality disorder (BPD), tests of associations between ED and aggression and violence-which are common to BPD-are sparse. The authors evaluated mediating effects of an autonomic vulnerability to ED on links between BPD symptoms and (a) reactive aggression, (b) proactive aggression, and (c) histories of interpersonal violence in a sample of young adults ( N = 104), ages 18-22 years. Low baseline respiratory sinus arrhythmia (RSA) mediated the association between BPD symptoms and reactive aggression. In contrast, although BPD symptoms were correlated with proactive aggression, no mediational effect was found. In addition, low RSA mediated the association between BPD symptoms and histories of interpersonal violence. Collectively, these findings add evidence that neurobiological vulnerability to ED contributes to aggressive and violent behavior among those with BPD.

Non-suicidal self-injury (NSSI) affects 15-20% of adolescents-disproportionately girls-and is a strong predictor of eventual suicide attempts and suicide. Many girls now initiate NSSI before age 10. These early-starters exhibit greater frequency of NSSI, use more diverse methods, and are hospitalized more often, yet there are no empirically supported prevention programs for preadolescents. Obstacles to prevention include ascertaining who is sufficiently vulnerable and specifying mechanistic intervention targets. Recent research indicates that (1) preadolescent girls with ADHD who are also maltreated are at alarming risk for NSSI and suicide attempts by adolescence, and (2) the conjoint effects of these vulnerabilities are sufficiently potent for targeted prevention. Research also indicates that existing interventions are effective in altering child- and family-level mechanisms of NSSI. These interventions alter neurobiological markers of vulnerability, which can be used as proximal efficacy signals of prevention response, without waiting for NSSI and suicide attempts to emerge.

Low resting respiratory sinus arrhythmia (RSA) is observed in many mental health conditions, including anxiety disorders, mood disorders, schizophrenia spectrum disorders, disruptive behavior disorders, and nonsuicidal self-injury, among others. Findings for RSA reactivity are more mixed. We evaluate associations between RSA reactivity and empirically derived structural categories of psychopathology-including internalizing, externalizing, and thought problems-among physically healthy adults. We searched multiple electronic databases for studies of RSA among participants who were assessed either dimensionally using well-validated measures or diagnostically using structured interviews. Strict inclusion criteria were used to screen 3,605 published reports, which yielded 37 studies including 2,347 participants and 76 effect sizes. We performed a meta-analysis, with meta-analytic regressions of potential moderators, including psychopathology subtypes. The sample-wide meta-analytic association between RSA reactivity and psychopathology was quite small, but heterogeneity was considerable. Moderation analyses revealed significant RSA reactivity (withdrawal) specifically in externalizing samples. Additional moderators included (a) stimulus conditions used to elicit RSA reactivity (only negative emotion inductions were effective), (b) sex (women showed greater RSA reactivity than men), and (c) adherence to established methodological guidelines (e.g., higher electrocardiographic sampling rates yielded greater RSA reactivity). These findings indicate that associations between RSA reactivity and psychopathology are complex and suggest that future studies should include more standardized RSA assessments to increase external validity and decrease measurement error., (© 2019 Society for Psychophysiological Research.)

In the past 35 years, developmental psychopathology has grown into a flourishing discipline that shares a scientific agenda with contemporary psychiatry. In this editorial, which introduces the special issue, we describe the history of developmental psychopathology, including core principles that bridge allied disciplines. These include (1) emphasis on interdisciplinary research, (2) elucidation of multicausal pathways to seemingly single disorders (phenocopies), (3) description of divergent multifinal outcomes from common etiological start points (pathoplasticity), and (4) research conducted across multiple levels of analysis spanning genes to environments. Next, we discuss neurodevelopmental models of psychopathology, and provide selected examples. We emphasize differential neuromaturation of subcortical and cortical neural networks and connectivity, and how both acute and protracted environmental insults can compromise neural structure and function. To date, developmental psychopathology has placed greater emphasis than psychiatry on neuromaturational models of mental illness. However, this gap is closing rapidly as advances in technology render etiopathophysiologies of psychopathology more interrogable. We end with suggestions for future interdisciplinary research, including the need to evaluate measurement invariance across development, and to construct more valid assessment methods where indicated., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Recently in this journal, Weeland et al. (2018) published a thought-provoking article reporting moderating effects of children's serotonin transporter-linked polymorphisms (5-HTTLPR) on negative parenting during prevention with the Incredible Years series. Participants were parents and young children of 387 families enrolled in the Observational Randomized Control Trial of Childhood Differential Susceptibility study. An equally important finding, which we focus on in this comment, involved null effects for all tests of parenting as a mediator of prevention-induced improvements in children's externalizing behavior. Although such findings may seem surprising, both confirmations of and failures to confirm parenting change as a mediator of child behavior change are common in the prevention and intervention literatures. In this comment, we explore likely reasons for heterogeneity in findings, including both moderators of treatment effect size and methods used to test mediation. Common moderators of prevention and intervention response to Incredible Years include dose, parenting problems at intake, high-risk versus clinical nature of samples, how parenting is measured, and whether child training is included with parent training. All of these moderators affect power to detect mediation. We then discuss conceptual criteria for testing mediation in randomized clinical trials, and problems with interpreting mediating paths in cross-lag panel models. Although the gene effect reported by Weeland et al. is important, their cross-lag panel models do not provide strong tests of parenting as a mediator of child behavior change. We conclude with recommendations for testing mediation in randomized clinical trials.

Objectives: We sought to identify subgroups of individuals based on patterns of psychological health problems (PH; e.g., depressive symptoms, hazardous drinking) and family maltreatment (FM; e.g., child and partner abuse)., Method: We analyzed data from very large surveys of United States Air Force active duty members with romantic partners and children., Results: Latent class analyses indicated six replicable patterns of PH problems and FM. Five of these classes, representing ∼98% of survey participants, were arrayed ordinally, with increasing risk of multiple PH problems and FM. A sixth group defied this ordinal pattern, with pronounced rates of FM and externalizing PH problems, but without correspondingly high rates/levels of internalizing PH problems., Conclusions: Ramifications of these results for intervention are discussed., (© 2018 Wiley Periodicals, Inc.)

Despite nonoverlapping criterion sets, conduct disorder and depression co-occur at much higher rates than expected by chance. Contemporary model-based approaches to explaining heterotypic comorbidity use factor analysis and its variants to evaluate interrelations among symptoms in large population-based and twin samples. These analyses invariably yield broadband internalizing and externalizing factors, which load on a higher-order general liability factor-findings that are robust across age and informant. Although model-based approaches elucidate structural aspects of comorbidity, they are variable-centered, and usually cross-sectional. Most therefore do not assess developmental continuity of comorbidity, or whether noncomorbid individuals are prospectively vulnerable to heterotypic comorbidity. We use an accelerated longitudinal design to evaluate growth in parent-reported conduct problems (CPs) and depression among children, ages 8-15 years, who were recruited at study entry into depressed only (n = 27), CPs only (n = 28), comorbid (n = 81), and control (n = 70) groups based on levels of symptoms. Consistent with normative developmental trends across this age range, steep growth in depression was exhibited by all groups, including those who reported only CPs at study entry. In contrast, growth in CPs was restricted to those who reported high symptoms at intake (with or without comorbid depression), compared with low and stable among depressed only and control participants. To our knowledge, this is the first study to demonstrate, using carefully ascertained "pure" versus comorbid groups who were followed naturalistically, that comorbid depression is likely to develop among those with pure CPs, but comorbid CPs are not likely to develop among those with pure depression. (PsycINFO Database Record, ((c) 2018 APA, all rights reserved).)

Rates of autism spectrum disorder (ASD) and age at first diagnosis vary considerably across the United States and are moderated by children's sex, race, ethnicity, and availability of services. We additionally suggest that degree of caregiver-clinician agreement on ASD symptoms may play a role in ASD assessment. Since gold standard ASD assessment integrates caregiver-reported developmental history with clinician observations, differential agreement between reporters across demographic groups may contribute to a host of detrimental outcomes. Here, we investigate whether caregiver-clinician agreement on ASD symptoms varies according to child and family characteristics. Comprehensive data from 2,759 families in the Simons Simplex Collection were analyzed. Linear models were created with caregiver reports predicting clinician reports, and moderating effects of child characteristics and family factors were examined. Poorer reporter correspondence was observed when children had higher IQ scores, stronger adaptive behavior, and more behavioral difficulties. Greater disagreement was also associated with African American racial status (for younger children), lower household income, and paternal social difficulties (for older children). Children's biological sex did not moderate caregiver-clinician agreement. Marked disagreement between caregivers and clinicians could lead to suboptimal or insufficient intervention services and negative experiences for families throughout development. Such families may also be less likely to qualify for research studies, and therefore be underrepresented in the ASD literature. Modified assessment procedures may be required to improve assessment accuracy and family experiences. Autism Res 2018, 11: 476-487. © 2017 International Society for Autism Research, Wiley Periodicals, Inc., Lay Summary: Evaluation of autism spectrum disorder (ASD) incorporates both caregiver and clinician perspectives of symptoms, and disagreement between these perspectives could lead to poorer outcomes for families. Using data from 2,759 families, we show that caregiver-clinician agreement on ASD symptoms is poorer for children with higher cognitive and adaptive skills, more behavioral difficulties, lower household income, and African American racial status. These children may be at higher risk for misdiagnosis, poorer family experiences during evaluations, and poorer representation in ASD research., (© 2017 International Society for Autism Research, Wiley Periodicals, Inc.)

This phase of the NIH Science of Behavior Change program emphasizes an "experimental medicine approach to behavior change," that seeks to identify targets related to stress reactivity, self-regulation, and social processes for maximal effects on multiple health outcomes. Within this framework, our project focuses on interpersonal processes associated with health: coercive couple and parent-child conflict. Diabetes and poor oral health portend pain, distress, expense, loss of productivity, and even mortality. They share overlapping medical regimens, are driven by overlapping proximal health behaviors, and affect a wide developmental span, from early childhood to late adulthood. Coercive couple and parent-child conflict constitute potent and destructive influences on a wide range of adult and child health outcomes. Such interaction patterns give rise to disturbed environmental stress reactivity (e.g., disrupted sympathetic nervous and parasympathetic nervous systems) and a wide range of adverse health outcomes in children and adults, including dental caries, obesity, and diabetes-related metabolic markers. In this work, we seek to identify/develop/validate assays assessing coercion, identify/develop and test brief interventions to reduce coercion, and test whether changes in coercion trigger changes in health behaviors., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Low resting respiratory sinus arrhythmia (RSA), and to a lesser extent excessive RSA reactivity to emotion evocation, are observed in many psychiatric disorders characterized by emotion dysregulation, including syndromes spanning the internalizing and externalizing spectra, and other conditions such as nonsuicidal self-injury. Nevertheless, some inconsistencies exist. For example, null outcomes in studies of RSA-emotion dysregulation relations are sometimes observed among younger participants. Such findings may derive from use of age inappropriate frequency bands in calculating RSA. We combine data from five published samples (N = 559) spanning ages 4 to 17 years, and reanalyze RSA data using age-appropriate respiratory frequencies. Misspecifying respiratory frequencies results in overestimates of resting RSA and underestimates of RSA reactivity, particularly among young children. Underestimates of developmental shifts in RSA and RSA reactivity from preschool to adolescence were also observed. Although correlational analyses revealed weak negative associations between resting RSA and aggression, those with clinical levels of externalizing exhibited lower resting RSA than their peers. No associations between RSA reactivity and externalizing were observed. Results confirm that age-corrected frequency bands should be used when estimating RSA, and that literature-wide overestimates of resting RSA, underestimates of RSA reactivity, and underestimates of developmental shifts in RSA and RSA reactivity may exist.

Abnormal patterns of sympathetic- and parasympathetic- linked cardiac activity and reactivity are observed among externalizing children, and mark deficiencies in central nervous system regulation of behavior and emotion. Although changes in these biomarkers have been observed following treatment, mechanisms remain unexplored. We used MEMORE-a new approach to analyzing intervening variable effects-to evaluate improvements in parenting as mediators of changes in SNS- and PNS-linked cardiac activity and reactivity among 99 preschoolers with attention-deficit hyperactivity disorder who were treated using an empirically supported intervention. Decreases in negative parenting (criticism, negative commands, physical intrusions) were associated with increases in resting RSA and PEP reactivity to incentives from pre- to post-intervention. Increases in positive parenting were not associated with changes in autonomic function. These findings suggest socially-induced plasticity in peripheral biomarkers of behavior and emotion regulation, and underscore the importance of reducing aversive interactions between parents and children when treating externalizing behavior., Competing Interests: Carolyn Webster-Stratton has disclosed a potential conflict of interest because she disseminates these treatments and stands to gain from favorable reports. She has voluntarily agreed to distance herself from certain critical research activities, including recruitment, consenting, primary data handling, and data analysis. The University of Washington has approved these arrangements. M. Jamila Reid performs Incredible Years interventions as an independent contractor.

Motivational models of psychopathology have long been advanced by psychophysiologists, and have provided key insights into neurobiological mechanisms of a wide range of psychiatric disorders. These accounts emphasize individual differences in activity and reactivity of bottom-up, subcortical neural systems of approach and avoidance in affecting behavior. Largely independent literatures emphasize the roles of top-down, cortical deficits in emotion regulation and executive function in conferring vulnerability to psychopathology. To date however, few models effectively integrate functions performed by bottom-up emotion generation system with those performed by top-down emotion regulation systems in accounting for alternative expressions of psychopathology. In this article, we present such a model, and describe how it accommodates the well replicated bifactor structure of psychopathology. We describe how excessive approach motivation maps directly into externalizing liability, how excessive passive avoidance motivation maps directly into internalizing liability, and how emotion dysregulation and executive function map onto general liability. This approach is consistent with the Research Domain Criteria initiative, which assumes that a limited number of brain systems interact to confer vulnerability to many if not most forms of psychopathology., (Copyright © 2017 Elsevier B.V. All rights reserved.)

In psychopathology research, endophenotypes are a subset of biomarkers that indicate genetic vulnerability independent of clinical state. To date, an explicit expectation is that endophenotypes be specific to single disorders. We evaluate this expectation considering recent advances in psychiatric genetics, recognition that transdiagnostic vulnerability traits are often more useful than clinical diagnoses in psychiatric genetics, and appreciation for etiological complexity across genetic, neural, hormonal and environmental levels of analysis. We suggest that the disorder-specificity requirement of endophenotypes be relaxed, that neural functions are preferable to behaviors as starting points in searches for endophenotypes, and that future research should focus on interactive effects of multiple endophenotypes on complex psychiatric disorders, some of which are 'phenocopies' with distinct etiologies.

Delay discounting-often referred to as hyperbolic discounting in the financial literature-is defined by a consistent preference for smaller, immediate rewards over larger, delayed rewards, and by failure of future consequences to curtail current consummatory behaviors. Previous research demonstrates (1) excessive delay discounting among individuals with attention-deficit/hyperactivity disorder (ADHD), (2) common neural substrates of delay discounting and hyperactive-impulsive symptoms of ADHD, and (3) associations between delay discounting and both debt burden and high interest rate borrowing. This study extends prior research by examining associations between ADHD symptoms, delay discounting, and an array of previously unevaluated financial outcomes among 544 individuals (mean age 35 years). Controlling for age, income, sex, education, and substance use, ADHD symptoms were associated with delay discounting, late credit card payments, credit card balances, use of pawn services, personal debt, and employment histories (less time spent at more jobs). Consistent with neural models of reward processing and associative learning, more of these relations were attributable to hyperactive-impulsive symptoms than inattentive symptoms. Implications for financial decision-making and directions for future research are discussed.

This article reviews evidence that trait impulsivity-expressed early in life as the hyperactive-impulsive and combined presentations of attention-deficit/hyperactivity disorder (ADHD)-is a bottom-up, subcortically mediated vulnerability to all externalizing disorders. This vulnerability arises from deficient mesolimbic dopamine responding, which imbues psychological states (irritability, discontentment) that motivate excessive approach behavior (hyperactivity, impulsivity). Through complex interactions with (a) aversive motivational states that arise from largely independent subcortical systems, (b) emotion regulatory mechanisms that arise from top-down, cortical modulation of subcortical neural function, and (c) environmental risk factors that shape and maintain emotion dysregulation, trait impulsivity confers vulnerability to increasingly severe externalizing behaviors across development. This perspective highlights the importance of identifying transdiagnostic neural vulnerabilities to psychopathology; dovetails with the hierarchical, latent structure of psychopathology; and suggests that progression along the externalizing spectrum is an ontogenic process whereby a common, multifactorially inherited trait interacts with endogenous and exogenous influences to yield increasingly intractable externalizing behaviors across development.

Previous studies have examined the neural correlates of emotion regulation and the neural changes that are evoked by music exposure. However, the link between music and emotion regulation is poorly understood. The objectives of this review are to (1) synthesize what is known about the neural correlates of emotion regulation and music-evoked emotions, and (2) consider the possibility of therapeutic effects of music on emotion dysregulation. Music-evoked emotions can modulate activities in both cortical and subcortical systems, and across cortical-subcortical networks. Functions within these networks are integral to generation and regulation of emotions. Since dysfunction in these networks are observed in numerous psychiatric disorders, a better understanding of neural correlates of music exposure may lead to more systematic and effective use of music therapy in emotion dysregulation.

Borderline personality disorder (BPD) and antisocial personality disorder (ASPD) are among the most debilitating psychiatric conditions. Behaviors and traits associated with these disorders can have profound influences on those surrounding the affected individual. Accordingly, researchers have begun to examine effects of these symptoms on parent-child relationships. Theoretical and empirical work suggests that one mechanism linking maternal psychopathology to child symptoms is familial transmission of emotion dysregulation. The authors examined children's emotion regulation difficulties as a mediator between maternal BPD/ASPD symptoms and child behavior problems 1 year later. Analyses revealed that a composite of maternal BPD/ASPD symptoms had a direct effect on child internalizing, externalizing, and total symptoms. Associations between maternal BPD/ASPD symptoms and youth problems were partially mediated by child emotion regulation difficulties, even with maternal depression and other relevant covariates included in the models. Thus, maternal BPD/ASPD symptoms and child emotion regulation difficulties represent potential targets for prevention of psychopathology among youth.

High sensitivity and reactivity to behaviors of family members characterizes several forms of psychopathology, including self-inflicted injury (SII). We examined mother-daughter behavioral and psychophysiological reactivity during a conflict discussion using nonlinear dynamics to assess asymmetrical associations within time-series data. Depressed, SII, and control adolescents and their mothers participated ( n= 76 dyads). We expected that (1) mothers' evocative behaviors would affect behavioral and psychophysiological reactivity among depressed and, especially, SII adolescents, (2) adolescents' behaviors would not evoke mothers' behavioral or physiological reactivity, and (3) control teens and mothers would be less reactive, with no dynamic associations in either direction. Convergent cross-mapping with dewdrop regression, which identifies directional associations, indicated that mothers' behaviors evoked behavioral responses among depressed and SII participants, but psychophysiological reactivity for SII teens only. There were no effects of adolescents' behavior on mothers' reactivity. Results are interpreted based upon sensitivity theories and directions for further research are outlined.

Trait impulsivity, which is often defined as a strong preference for immediate over delayed rewards and results in behaviors that are socially inappropriate, maladaptive, and short-sighted, is a predisposing vulnerability to all externalizing spectrum disorders. In contrast, anhedonia is characterized by chronically low motivation and reduced capacity to experience pleasure, and is common to depressive disorders. Although externalizing and depressive disorders have virtually nonoverlapping diagnostic criteria in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, heterotypic comorbidity between them is common. Here, we review common neural substrates of trait impulsivity, anhedonia, and irritability, which include both low tonic mesolimbic dopamine activity and low phasic mesolimbic dopamine responding to incentives during reward anticipation and associative learning. We also consider how other neural networks, including bottom-up emotion generation systems and top-down emotion regulation systems, interact with mesolimbic dysfunction to result in alternative manifestations of psychiatric illness. Finally, we present a model that emphasizes a translational, transdiagnostic approach to understanding externalizing/depression comorbidity. This model should refine ways in which internalizing and externalizing disorders are studied, classified, and treated.