Luke W. Hyde

The Relations among Cumulative Risk, Parenting, and Behavior Problems during Early Childhood.

BACKGROUND This study examined relations among cumulative risk, nurturant and involved parenting, and behavior problems across early childhood. METHODS Cumulative risk, parenting, and behavior problems were measured in a sample of low-income toddlers participating in a family-centered program to prevent conduct problems. RESULTS Path analysis was utilized to examine longitudinal relations among these constructs, with results supporting an indirect effect of cumulative risk on externalizing and internalizing problems through nurturant and involved parenting. CONCLUSION Results highlight the importance of cumulative risk during early childhood, and particularly the effect that the level of contextual risk can have on the parenting context during this developmental period.

Divergent Effects of Genetic Variation in Endocannabinoid Signaling on Human Threat- and Reward-Related Brain Function

BACKGROUND Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. A common single nucleotide polymorphism (C385A) in the human FAAH gene has been associated with increased risk for addiction and obesity. METHODS Using imaging genetics in 82 healthy adult volunteers, we examined the effects of FAAH C385A on threat- and reward-related human brain function. RESULTS Carriers of FAAH 385A, associated with reduced enzyme and possibly increased eCB signaling, had decreased threat-related amygdala reactivity but increased reward-related ventral striatal reactivity in comparison with C385 homozygotes. Similarly divergent effects of FAAH C385A genotype were manifest at the level of brain-behavior relationships. The 385A carriers showed decreased correlation between amygdala reactivity and trait anxiety but increased correlation between ventral striatal reactivity and delay discounting, an index of impulsivity. CONCLUSIONS Our results parallel pharmacologic and genetic dissection of eCB signaling, are consistent with the psychotropic effects of Delta(9)-tetrahydrocannabinol, and highlight specific neural mechanisms through which variability in eCB signaling impacts complex behavioral processes related to risk for addiction and obesity.

Effects of HTR1A C(-1019)G on amygdala reactivity and trait anxiety.

CONTEXT Serotonin 1A (5-hydroxytryptamine 1A [5-HT(1A)]) autoreceptors mediate negative feedback inhibition of serotonergic neurons and play a critical role in regulating serotonin signaling involved in shaping the functional response of major forebrain targets, such as the amygdala, supporting complex behavioral processes. A common functional variation (C[-1019]G) in the human 5-HT(1A) gene (HTR1A) represents 1 potential source of such interindividual variability. Both in vitro and in vivo, -1019G blocks transcriptional repression, leading to increased autoreceptor expression. Thus, -1019G may contribute to relatively decreased serotonin signaling at postsynaptic forebrain target sites via increased negative feedback. OBJECTIVES To evaluate the effects of HTR1A C(-1019)G on amygdala reactivity and to use path analyses to explore the impact of HTR1A-mediated variability in amygdala reactivity on individual differences in trait anxiety. We hypothesized that -1019G, which potentially results in decreased serotonin signaling, would be associated with relatively decreased amygdala reactivity and related trait anxiety. DESIGN Imaging genetics in participants from an archival database. PARTICIPANTS Eighty-nine healthy adults. RESULTS Consistent with prior findings, -1019G was associated with significantly decreased threat-related amygdala reactivity. Importantly, this effect was independent of that associated with another common functional polymorphism that affects serotonin signaling, 5-HTTLPR. While there were no direct genotype effects on trait anxiety, HTR1A C(-1019)G indirectly predicted 9.2% of interindividual variability in trait anxiety through its effects on amygdala reactivity. CONCLUSIONS Our findings further implicate relatively increased serotonin signaling, associated with a genetic variation that mediates increased 5-HT(1A) autoreceptors, in driving amygdala reactivity and trait anxiety. Moreover, they provide empirical documentation of the basic premise that genetic variation indirectly affects emergent behavioral processes related to psychiatric disease risk by biasing the response of underlying neural circuitries.

What are the associations between parenting, callous-unemotional traits, and antisocial behavior in youth? A systematic review of evidence.

A growing body of research has examined callous-unemotional (CU) traits among samples of antisocial youth. Debate surrounds the malleability of CU traits and their responsiveness to parenting and parent-focused interventions. This review examines evidence from studies that have investigated various relationships between parenting, CU traits, and antisocial behavior (AB). Studies were categorized according to five distinct research questions each addressing associations among parenting, CU traits, and AB in a different way. The results suggest that dimensions of parenting are prospectively related to changes in CU traits. Subgroups of youth with both high levels of CU traits and AB also appear to have experienced negative parenting practices. However, negative parenting is not consistently related to AB in cross-sectional studies for youth with high levels of CU traits. At the same time, parenting-focused interventions appear effective in reducing the level of AB and CU traits in youth. The findings and implications for future studies are critically discussed as they pose challenges for current etiological theories of AB.

The neural signatures of distinct psychopathic traits.

Recent studies suggest that psychopathy may be associated with dysfunction in the neural circuitry supporting both threat- and reward-related processes. However, these studies have involved small samples and often focused on extreme groups. Thus, it is unclear to what extent current findings may generalize to psychopathic traits in the general population. Furthermore, no studies have systematically and simultaneously assessed associations between distinct psychopathy facets and both threat- and reward-related brain function in the same sample of participants. Here, we examined the relationship between threat-related amygdala reactivity and reward-related ventral striatum (VS) reactivity and variation in four facets of self-reported psychopathy in a sample of 200 young adults. Path models indicated that amygdala reactivity to fearful facial expressions is negatively associated with the interpersonal facet of psychopathy, whereas amygdala reactivity to angry facial expressions is positively associated with the lifestyle facet. Furthermore, these models revealed that differential VS reactivity to positive versus negative feedback is negatively associated with the lifestyle facet. There was suggestive evidence for gender-specific patterns of association between brain function and psychopathy facets. Our findings are the first to document differential associations between both threat- and reward-related neural processes and distinct facets of psychopathy and thus provide a more comprehensive picture of the pattern of neural vulnerabilities that may predispose to maladaptive outcomes associated with psychopathy.

Developmental Precursors of Moral Disengagement and the Role of Moral Disengagement in the Development of Antisocial Behavior

The purpose of the study was to advance our understanding of the developmental precursors of Moral Disengagement (MD) and the role of MD in the development of antisocial behavior from early risk among an ethnically diverse sample of 187 low-income boys followed prospectively from ages 1.5 to 17. Results indicated associations between early rejecting parenting, neighborhood impoverishment, and child empathy and later MD. The link between some of these early constructs and later antisocial behavior was mediated by MD. Finally, in an exploratory path model both MD and biases in social information processing were found to mediate separate paths from early risk factors to later antisocial behavior. Results were partially consistent with the notion that adolescent MD was predicted by a combination of early family, neighborhood, and child risk factors, and that MD may be a mechanism underlying some boys’ risk of antisocial behavior.

Early predictors of boys' antisocial trajectories.

Despite the large number of studies tracing patterns of youth antisocial behavior (AB) during adolescence, few have prospective data on the developmental precursors of AB beginning during infancy. Using a cohort of 268 low-income boys first assessed at 18 months, the current study examined predictors of early- and late-starting trajectories of AB assessed during early childhood and early adolescence. Four trajectory groups were identified, including early- and late-starting groups, a low stable group, and a high decreasing group, characterized by multiple risk factors during early childhood and early adolescence. During early childhood, parenting and maternal depression discriminated two AB trajectory groups, an early-starting and a high decreasing group, who would go on to demonstrate a high preponderance of juvenile court involvement (60% to 79%) and elevated rates of clinical depression 13 to 15 years later. The results were discussed in reference to targeting malleable family risk factors during early childhood associated with patterns of AB and mental health disorders during adolescence.

Do harsh and positive parenting predict parent reports of deceitful-callous behavior in early childhood?

BACKGROUND The relationship between parenting and the development of antisocial behavior in children is well established. However, evidence for associations between dimensions of parenting and callous-unemotional (CU) traits is mixed. As CU traits appear critical to understanding a subgroup of youth with antisocial behavior, more research addressing the link between early parenting and CU traits is needed. METHODS The current study investigated longitudinal predictions between measures of harsh and positive parenting, and early CU behavior. Data from mother-child dyads (N = 731; 49% female) were collected from a multi-ethnic, high-risk sample with young children, and included self-reported and multi-method observed parenting. CU behavior was assessed using a previously validated measure of deceitful-callous behavior (Hyde et al., 2011). RESULTS   Results suggest that dimensions of harsh parenting, but not positive parenting, contribute to the development of child deceitful-callous behavior. Nevertheless, deceitful-callous behavior showed strong stability over time and the effects of harsh parenting, especially observed harshness, were modest. CONCLUSIONS The current findings have implications for developmental psychopathology and early interventions for antisocial behavior. The results also raise a number of issues about measuring emerging CU behavior in very young children, including the interrelation between parent perceptions and reports of child behavior, parent reactions, and the subsequent development of severe antisocial behavior.

Understanding risk for psychopathology through imaging gene-environment interactions

Examining the interplay of genes, experience and the brain is crucial to understanding psychopathology. We review the recent gene-environment interaction (G×E) and imaging genetics literature with the goal of developing models to bridge these approaches within single imaging gene-environment interaction (IG×E) studies. We explore challenges inherent in both G×E and imaging genetics and highlight studies that address these limitations. In specifying IG×E models, we examine statistical methods for combining these approaches, and explore plausible biological mechanisms (e.g. epigenetics) through which these conditional mechanisms can be understood. Finally, we discuss the potential contribution that IG×E studies can make to understanding psychopathology and developing more personalized and effective prevention and treatment.

Perceived social support moderates the link between threat-related amygdala reactivity and trait anxiety.

Several lines of research have illustrated that negative environments can precipitate psychopathology, particularly in the context of relatively increased biological risk, while social resources can buffer the effects of these environments. However, little research has examined how social resources might buffer proximal biological risk for psychopathology or the neurobiological pathways through which such buffering may be mediated. Here we report that the expression of trait anxiety as a function of threat-related amygdala reactivity is moderated by perceived social support, a resource for coping with adversity. A significant positive correlation between amygdala reactivity and trait anxiety was evident in individuals reporting below average levels of support but not in those reporting average or above average levels. These results were consistent across multiple measures of trait anxiety and were specific to anxiety in that they did not extend to measures of broad negative or positive affect. Our findings illuminate a biological pathway, namely moderation of amygdala-related anxiety, through which social support may confer resilience to psychopathology. Moreover, our results indicate that links between neural reactivity and behavior are not static but rather may be contingent on social resources.