Developmental psychopathology as a meta-paradigm: From zero-sum science to epistemological pluralism in theory and research.

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.

A Monte Carlo evaluation of growth mixture modeling.

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.

Internalizing-externalizing comorbidity and regional brain volumes in the ABCD study.

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.

Serotonergic sensitivity alleles moderate relations between attachment security at age three and socioemotional competence at age five.

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.

Paternal antisociality and growth in child delinquent behaviors: Moderating effects of child sex and respiratory sinus arrhythmia.

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.

Longitudinal associations of callous-unemotional and oppositional defiant behaviors over a three-year interval for Spanish children.

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.

RDoC and Psychopathology among Youth: Misplaced Assumptions and an Agenda for Future Research.

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).

Moving beyond Ordinary Factor Analysis in Studies of Personality and Personality Disorder: A Computational Modeling Perspective.

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.

Correction to: Delay Discounting of Protected Sex: Relationship Type and Sexual Orientation Influence Sexual Risk Behavior.

In the original publication of the article, the corresponding author was processed incorrectly. The corresponding author for this article should be: Woo-Young Ahn.

Delay Discounting of Protected Sex: Relationship Type and Sexual Orientation Influence Sexual Risk Behavior.

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.

Self-injuring adolescent girls exhibit insular cortex volumetric abnormalities that are similar to those seen in adults with borderline personality 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.

Using automated computer vision and machine learning to code facial expressions of affect and arousal: Implications for emotion dysregulation research.

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.

Psychiatry and developmental psychopathology: Unifying themes and future directions.

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.

Mechanisms of child behavior change in parent training: Comment on Weeland et al. (2018).

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.

Quantifying respiratory sinus arrhythmia: Effects of misspecifying breathing frequencies across development.

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.

Patterns of psychological health problems and family maltreatment among United States Air Force members.

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.

Trait Impulsivity and the Externalizing Spectrum.

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.

Neural substrates of trait impulsivity, anhedonia, and irritability: Mechanisms of heterotypic comorbidity between externalizing disorders and unipolar depression.

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.

Neural responses to monetary incentives among self-injuring adolescent girls.

Rates of self-inflicted injury among adolescents have risen in recent years, yet much remains to be learned about the pathophysiology of such conduct. Self-injuring adolescents report high levels of both impulsivity and depression behaviorally. Aberrant neural responding to incentives, particularly in striatal and prefrontal regions, is observed among both impulsive and depressed adolescents, and may mark common vulnerability to symptoms of anhedonia, irritability, and low positive affectivity. To date, however, no studies have examined associations between central nervous system reward responding and self-injury. In the current study, self-injuring (n = 19) and control (n = 19) adolescent females, ages 13-19 years, participated in a monetary incentive delay task in which rewards were obtained on some trials and losses were incurred on others. Consistent with previous findings from impulsive and depressed samples, self-injuring adolescents exhibited less activation in both striatal and orbitofrontal cortex regions during anticipation of reward than did controls. Self-injuring adolescents also exhibited reduced bilateral amygdala activation during reward anticipation. Although few studies to date have examined amygdala activity during reward tasks, such findings are common among adults with mood disorders and borderline personality disorder. Implications for neural models of impulsivity, depression, heterotypic comorbidity, and development of both self-injury and borderline personality traits are discussed.