Most contemporary accounts of psychopathology acknowledge the importance of both biological and environmental influences on behavior. In developmental psychopathology, multiple etiological mechanisms for psychiatric disturbance are well recognized, including those operating at genetic, neurobiological, and environmental levels of analysis. However, neuroscientific principles are rarely considered in current approaches to prevention or intervention. In this article, we explain why a deeper understanding of the genetic and neural substrates of behavior is essential for the next generation of preventive interventions, and we outline 10 specific reasons why considering biological processes can improve treatment efficacy. Among these, we discuss (a) the role of biomarkers and endophenotypes in identifying those most in need of prevention; (b) implications for treatment of genetic and neural mechanisms of homotypic comorbidity, heterotypic comorbidity, and heterotypic continuity; (c) ways in which biological vulnerabilities moderate the effects of environmental experience; (d) situations in which Biology x Environment interactions account for more variance in key outcomes than main effects; and (e) sensitivity of neural systems, via epigenesis, programming, and neural plasticity, to environmental moderation across the life span. For each of the 10 reasons outlined we present an example from current literature and discuss critical implications for prevention.

In this study, we evaluated predictors of resilience among 8-to 12-year-old children recruited from primarily low socioeconomic status neighborhoods, 117 of whom suffered from clinical levels of conduct problems and/or depression, and 63 of whom suffered from no significant symptoms. Tests of interactions were conducted between (a) paternal antisocial behavior and maternal depression and (b) several physiological indices of child temperament and emotionality in predicting (c) children's conduct problems and depression. Both internalizing and externalizing outcomes among children were associated specifically with maternal melancholic depression, and not with nonmelancholic depression. In addition, low levels of respiratory sinus arrhythmia (RSA) among children conferred significant risk for depression, regardless of maternal melancholia, whereas high RSA offered partial protection. Furthermore, high levels of maternal melancholia conferred significant risk for child depression, regardless of paternal antisocial behavior, whereas low levels of maternal melancholia offered partial protection. Finally, low levels of electrodermal responding (EDR) conferred significant risk for conduct problems, regardless of paternal antisocial behavior, whereas high EDR offered partial protection. None of the identified protective factors offered complete immunity from psychopathology. These findings underscore the complexity of resilience and resilience-related processes, and suggest several potential avenues for future longitudinal research.Several alternative definitions of resilience have been proposed by developmental psychopathologists, yet all include some form of adaptive functioning following significant exposure to adversity (see Luthar, Cicchetti, & Becker, 2000). Adverse risk exposure is central to any definition of resilience because without such experiences, psychopathological outcomes are far less likely, so the construct loses much of its meaning (Curtis & Cicchetti, 2003;Luthar, 2006). Accordingly, most researchers agree that some form of risk exposure is necessary to infer resilience or resilience-related processes. Nevertheless, both adaptation and adversity are often defined very differently across studies, sometimes quite broadly and other times quite specifically. For example, adaptation has been defined as a set of general competencies across multiple domains of functioning including social, occupational, and psychopathological; yet it has also been defined as the absence of a specific psychiatric condition such as major depression despite a strong familial loading for mood disorders (see Luthar, 2006). From a developmental psychopathology perspective, more broad definitions of adaptation are preferred because most adversities confer risk that extends to a wide range of multifinal outcomes. For example, in addition to increasing the risk for mood disorders among offspring, maternal depression also confers risk for conduct problems, delinquency, and antisocial behavior (Boyle & Pickles, 1997;Kim-Cohen,...

Objective To evaluate measures of cardiac activity and reactivity as prospective biomarkers of treatment response to an empirically-supported behavioral intervention for attention-deficit/hyperactivity disorder (ADHD). Method Cardiac pre-ejection period (PEP), an index of sympathetic-linked cardiac activity, and respiratory sinus arrhythmia (RSA), and index of parasympathetic-linked cardiac activity, were assessed among 99 preschool children (ages 4–6 years) with ADHD both at rest and in response to behavioral challenge, before participants and their parents completed one of two versions of the Incredible Years parent and child interventions. Results Main effects of PEP activity and reactivity, and of RSA activity and reactivity were found. Although sample-wide improvements in behavior were observed at post treatment, those who exhibited lengthened cardiac PEP at rest and reduced PEP reactivity to incentives scored higher on measures of conduct problems and aggression both before and after treatment. In contrast, children who exhibited lower baseline RSA and greater RSA withdrawal scored lower on prosocial behavior before and after treatment. Finally, children who exhibited greater RSA withdrawal scored lower on emotion regulation before and after treatment. Conclusions We discuss these findings in terms of (a) individual differences in underlying neurobiological systems subserving appetitive (i.e., approach) motivation, emotion regulation, and social affiliation, and (b) the need to develop more intensive interventions targeting neurobiologically vulnerable children.

The term allostasis, which is defined as stability through change, has been invoked repeatedly by developmental psychopathologists to describe long-lasting and in some cases permanent functional alterations in limbic-hypothalamic-pituitary-adrenal axis responding following recurrent and/or prolonged exposure to stress. Increasingly, allostatic load models have also been invoked to describe psychological sequelae of abuse, neglect, and other forms of maltreatment. In contrast, neural adaptations to stress, including those incurred by monoamine systems implicated in (a) mood and emotion regulation, (b) behavioral approach, and (c) social affiliation and attachment, are usually not included in models of allostasis. Rather, structural and functional alterations in these systems, which are exquisitely sensitive to prolonged stress exposure, are usually explained as stress mediators, neural plasticity, and/or programming effects. Considering these mechanisms as distinct from allostasis is somewhat artificial given overlapping functions and intricate coregulation of monoamines and the limbic-hypothalamic-pituitary-adrenal axis. It also fractionates literatures that should be mutually informative. In this article, we describe structural and functional alterations in serotonergic, dopaminergic, and noradrenergic neural systems following both acute and prolonged exposure to stress. Through increases in behavioral impulsivity, trait anxiety, mood and emotion dysregulation, and asociality, alterations in monoamine functioning have profound effects on personality, attachment relationships, and the emergence of psychopathology.

Theoretical and empirical models describe respiratory sinus arrhythmia (RSA) as a peripheral biomarker of emotion regulation and social competence. Recent findings also link RSA to individual differences in social functioning within autism spectrum disorder (ASD). However, associations between RSA and symptoms of internalizing/externalizing psychopathology in ASD have not been explored. We assessed RSA, social functioning, and internalizing/externalizing symptoms among boys with and without ASD. Compared with controls, participants with ASD evidenced reduced parasympathetic cardiac control, which correlated with social behavior. Symptoms were associated with deficiencies in RSA, over-and-above the contribution of social functioning. These findings yield a more nuanced understanding of parasympathetic function in ASD, and suggest a role for integrative intervention strategies that address socioemotional difficulties.