Background
Callous‐unemotional behaviors identify children at risk for severe and chronic antisocial behavior. Research is needed to establish pathways from temperament and parenting factors that ...give rise to callous‐unemotional behaviors, including interactions of positive versus harsh parenting with child fearlessness.
Methods
Multimethod data, including parent reports and observations of parent and child behavior, were drawn from a prospective, longitudinal sample of low‐income boys (N = 310) with assessments at 18, 24, and 42 months, and at ages 10–12 years old.
Results
Parent‐reported callous‐unemotional, oppositional, and attention‐deficit factors were separable at 42 months. Callous‐unemotional behaviors at 42 months predicted callous‐unemotional behaviors at ages 10–12, accounting for earlier oppositional and attention‐deficit behaviors and self‐reported child delinquency at ages 10–12. Observations of fearlessness at 24 months predicted callous‐unemotional behaviors at 42 months, but only when parents exhibited low observed levels of positive parenting. The interaction of fearlessness and low positive parenting indirectly predicted callous‐unemotional behaviors at 10–12 via callous‐unemotional behaviors at 42 months.
Conclusions
Early fearlessness interacts with low positive parenting to predict early callous‐unemotional behaviors, with lasting effects of this person‐by‐context interaction on callous‐unemotional behaviors into late childhood.
The emerging field of neurogenetics seeks to model the complex pathways from gene to brain to behavior. This field has focused on imaging genetics techniques that examine how variability in common ...genetic polymorphisms predict differences in brain structure and function. These studies are informed by other complimentary techniques (e.g., animal models and multimodal imaging) and have recently begun to incorporate the environment through examination of Imaging Gene × Environment interactions. Though neurogenetics has the potential to inform our understanding of the development of psychopathology, there has been little integration between principles of neurogenetics and developmental psychopathology. The paper describes a neurogenetics and Imaging Gene × Environment approach and how these approaches have been usefully applied to the study of psychopathology. Six tenets of developmental psychopathology (the structure of phenotypes, the importance of exploring mechanisms, the conditional nature of risk, the complexity of multilevel pathways, the role of development, and the importance of who is studied) are identified, and how these principles can further neurogenetics applications to understanding the development of psychopathology is discussed. A major issue of this piece is how neurogenetics and current imaging and molecular genetics approaches can be incorporated into developmental psychopathology perspectives with a goal of providing models for better understanding pathways from among genes, environments, the brain, and behavior.
Antisocial Behavior (AB) has a tremendous societal cost, motivating investigation of the mechanisms that cause individuals to engage and persist in AB. Recent theories of AB emphasize the role of ...reward-related neural processes in the etiology of severe and chronic forms of AB, including antisocial personality disorder and psychopathy. However, no systematic reviews have evaluated the hypothesis that reward-related neural dysfunction is an etiologic factor in AB in adult samples. Moreover, it is unclear whether AB is linked to a hyper- or hyposensitive reward system and whether AB is related to neural sensitivity to losses. Thus, the current systematic review examined whether AB (including antisocial personality disorder) and psychopathic traits are related to neural reactivity during reward processing, loss processing, or both. Our review identified seven task-based functional MRI or functional connectivity studies that examined associations between neural response to reward and loss, and dimensional and categorical measures of adult AB and/or psychopathy. Across studies, there was evidence that AB is associated with variability in neural functioning during both reward and loss processing. In particular, impulsive-antisocial traits appeared to be specifically associated with hypersensitivity in the ventral striatum during the anticipation, but not the receipt, of rewards.
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Psychological disorders co-occur often in children, but little has been done to document the types of conjoint pathways internalizing and externalizing symptoms may take from the crucial early period ...of toddlerhood or how harsh parenting may overlap with early symptom codevelopment. To examine symptom codevelopment trajectories, we identified latent classes of individuals based on internalizing and externalizing symptoms across ages 3-9 and found three symptom codevelopment classes: normative symptoms (low), severe-decreasing symptoms (initially high but rapidly declining), and severe symptoms (high) trajectories. Next, joint models examined how parenting trajectories overlapped with internalizing and externalizing symptom trajectories. These trajectory classes demonstrated that, normatively, harsh parenting increased after toddlerhood, but the severe symptoms class was characterized by a higher level and a steeper increase in harsh parenting and the severe-decreasing class by high, stable harsh parenting. In addition, a transactional model examined the bidirectional relationships among internalizing and externalizing symptoms and harsh parenting because they may cascade over time in this early period. Harsh parenting uniquely contributed to externalizing symptoms, controlling for internalizing symptoms, but not vice versa. In addition, internalizing symptoms appeared to be a mechanism by which externalizing symptoms increase. Results highlight the importance of accounting for both internalizing and externalizing symptoms from an early age to understand risk for developing psychopathology and the role harsh parenting plays in influencing these trajectories.
Objective:Callous-unemotional behaviors in early childhood signal higher risk for trajectories of antisocial behavior and callous-unemotional traits that culminate in later diagnoses of conduct ...disorder, antisocial personality disorder, and psychopathy. Studies demonstrate high heritability of callous-unemotional traits, but little research has examined specific heritable pathways to early callous-unemotional behaviors. Studies also indicate that positive parenting protects against the development of callous-unemotional traits, but genetically informed designs have not been used to confirm that these relationships are not the product of gene-environment correlations. In a sample of adopted children and their biological and adoptive mothers, the authors tested novel heritable and nonheritable pathways to preschool callous-unemotional behaviors.Method:In an adoption cohort of 561 families, history of severe antisocial behavior assessed in biological mothers and observations of adoptive mother positive reinforcement at 18 months were examined as predictors of callous-unemotional behaviors at 27 months.Results:Despite limited or no contact with offspring, biological mother antisocial behavior predicted early callous-unemotional behaviors. Adoptive mother positive reinforcement protected against early callous-unemotional behaviors. High levels of adoptive mother positive reinforcement buffered the effects of heritable risk for callous-unemotional behaviors posed by biological mother antisocial behavior.Conclusions:The findings elucidate heritable and nonheritable pathways to early callous-unemotional behaviors. The results provide a specific heritable pathway to callous-unemotional behaviors and compelling evidence that parenting is an important nonheritable factor in the development of callous-unemotional behaviors. The finding that positive reinforcement buffered heritable risk for callous-unemotional behaviors has important translational implications for the prevention of trajectories to serious antisocial behavior.
We describe an ecological approach to understanding the developing brain, with a focus on the effects of poverty-related adversity on brain function. We articulate how combining multilevel ecological ...models from developmental science and developmental psychopathology with human neuroscience can inform our approach to understanding the developmental neuroscience of risk and resilience. To illustrate this approach, we focus on associations between poverty and brain function, the roles parents and neighborhoods play in this context, and the potential impact of developmental timing. We also describe the major challenges and needed advances in these areas of research to better understand how and why poverty-related adversity may impact the developing brain, including the need for: a population neuroscience approach with greater attention to sampling and representation, genetically informed and causal designs, advances in assessing context and brain function, caution in interpretation of effects, and a focus on resilience. Work in this area has major implications for policy and prevention, which are discussed.
Public Significance Statement
Millions of youth grow up in poverty and are exposed to an unequal share of adversity which impacts brain and behavior development. An ecological approach to developmental neuroscience can help to articulate the active ingredients associated with poverty that impact brain development. Better understanding how and why various adversities, including harsh parenting and neighborhood poverty, impact brain development can inform policies to prevent negative outcomes.
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CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
The last decades of neuroscience research have produced immense progress in the methods available to understand brain structure and function. Social, cognitive, clinical, affective, economic, ...communication, and developmental neurosciences have begun to map the relationships between neuro-psychological processes and behavioral outcomes, yielding a new understanding of human behavior and promising interventions. However, a limitation of this fast moving research is that most findings are based on small samples of convenience. Furthermore, our understanding of individual differences may be distorted by unrepresentative samples, undermining findings regarding brain–behavior mechanisms. These limitations are issues that social demographers, epidemiologists, and other population scientists have tackled, with solutions that can be applied to neuroscience. By contrast, nearly all social science disciplines, including social demography, sociology, political science, economics, communication science, and psychology, make assumptions about processes that involve the brain, but have incorporated neural measures to differing, and often limited, degrees; many still treat the brain as a black box. In this article, we describe and promote a perspective—population neuroscience—that leverages interdisciplinary expertise to (i) emphasize the importance of sampling to more clearly define the relevant populations and sampling strategies needed when using neuroscience methods to address such questions; and (ii) deepen understanding of mechanisms within population science by providing insight regarding underlying neural mechanisms. Doing so will increase our confidence in the generalizability of the findings. We provide examples to illustrate the population neuroscience approach for specific types of research questions and discuss the potential for theoretical and applied advances from this approach across areas.
The family stress model (FSM) is an influential family process model that posits that socioeconomic disadvantage impacts child outcomes via its effects on the parents. Existing evaluations of the FSM ...are constrained by limited measures of socioeconomic disadvantage, cross‐sectional research designs, and reliance on non‐population‐based samples. The current study tested the FSM in a subsample of the Fragile Families and Child Wellbeing Study (N = 2,918), a large population‐based study of children followed from birth through the age of nine. We employed a longitudinal framework and used measures of socioeconomic disadvantage beyond economic resources. Although the hypothesized FSM pathways were identified in the longitudinal model (e.g., economic pressure at the age of one was associated with maternal distress at the age of three, maternal distress at the age of three was associated with parenting behaviors at the age of five), the effects of socioeconomic disadvantage at childbirth on youth socioemotional outcomes at the age of nine did not operate through all of the hypothesized mediators. In longitudinal change models that accounted for the stability in constructs, multiple indicators of socioeconomic disadvantage at childbirth were indirectly associated with youth externalizing behaviors at the age of nine via either economic pressure at the age of one or changes in maternal warmth from ages 3 to 5. Greater economic pressure at the age of one, increases in maternal distress from ages 1 to 3, and decreases/increases in maternal warmth/harshness from ages 3 to 5 were also directly associated with increases in externalizing behaviors from ages 5 to 9. Results provide partial support for the FSM across the first decade of life.
•We evaluate neuroimaging studies of youth antisocial behavior (AB).•We examine these studies from a developmental psychopathology standpoint.•Differences in amygdala and prefrontal cortex ...functioning are correlated with AB.•Details of studies (e.g., fMRI task, type of AB measured) impact results.•There is some evidence for two subgroups of youth based on neural reactivity.
Youth antisocial behavior (AB) is an important public health concern impacting perpetrators, victims, and society. Functional neuroimaging is becoming a more common and useful modality for understanding neural correlates of youth AB. Although there has been a recent increase in neuroimaging studies of youth AB and corresponding theoretical articles on the neurobiology of AB, there has been little work critically examining the strengths and weaknesses of individual studies and using this knowledge to inform the design of future studies. Additionally, research on neuroimaging and youth AB has not been integrated within the broader framework of developmental psychopathology. Thus, this paper provides an in-depth review of the youth AB functional neuroimaging literature with the following goals: (1) to evaluate how this literature has informed our understanding of youth AB, (2) to evaluate current neuroimaging studies of youth AB from a developmental psychopathology perspective with a focus on integrating research from neuroscience and developmental psychopathology, as well as placing this research in the context of other related areas (e.g., psychopathy, molecular genetics), and (3) to examine strengths and weaknesses of neuroimaging and behavioral studies of youth AB to suggest how future studies can develop a more informed and integrated understanding of youth AB.
Background
Early‐starting child conduct problems (CP) are linked to the development of persistent antisocial behavior. Researchers have theorized multiple pathways to CP and that CP comprise ...separable domains, marked by callous‐unemotional (CU) behavior, oppositional behavior, or ADHD symptoms. However, a lack of empirical evidence exists from studies that have examined whether there are unique correlates of these domains.
Methods
We examined differential correlates of CU, oppositional, and ADHD behaviors during the preschool years to test their potentially distinct nomological networks. Multimethod data, including parent and teacher reports and observations of child behavior, were drawn from a prospective, longitudinal study of children assessed at age 3 and age 6 (N = 240; 48% female).
Results
Dimensions of CU, oppositional, and ADHD behaviors were separable within Confirmatory Factor Analyses across mother and father reports. There were differential associations between CU, oppositional, and ADHD behaviors and socioemotional, cognitive, and behavioral outcomes: CU behavior was uniquely related to lower moral regulation, guilt, and empathy. ADHD was uniquely related to lower attentional focusing and observed effortful control. Finally, CU behavior uniquely predicted increases in teacher‐reported externalizing from ages 3–6 over and above covariates, and ADHD and oppositional behavior.
Conclusions
Consistent with theory, dimensions of CU, ADHD, and oppositional behavior demonstrated separable nomological networks representing separable facets within early‐starting CP.
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