Edelyn Verona, Ph.D. - US grants

DESCRIPTION (Applicant's abstract): Recent national news reports of incidents of extreme violence, e.g., Columbine, Atlanta shootings, have highlighted the emotional state of the perpetrator, as a precipitant to the violent act. Specifically, such incidents have suggested that negative emotional states arising from environmental stressors, e.g., peer rejection, financial difficulties, can prompt some individuals to act out violently against others not responsible for their distress. Mirroring the above, researchers in the field of human aggression have long been interested in the role of emotion in aggressive behavior. Relevant theory and data suggest that self-reported negative mood is related to greater aggressivity (Berkowitz, 1990; Geen, 1990; Almagor & Ehrlich, 1990), and that negative affect may mediate the aggression observed in those exposed to frustrating or provoking circumstances (Berkowitz, 1989, 1988). Nonetheless, only a limited number of studies have experimentally investigated the effects of negative affect on aggressivity. The limitations of existing research include reliance on negative affect manipulations, i.e., provocation, negative evaluation, that have time-limited effects on emotion, and reliance on self-report measures of negative emotionality. The present investigation will analyze the impact of manipulated negative affect, using a novel on-going aversive stimulus, on laboratory aggressive behavior. As is customary in laboratory aggression studies, a deceptive cover story will be utilized to ensure valid responses on the dependent measure (i.e., aggression). An on-line psychophysiological measure of emotion, the startle probe methodology, will be utilized to index on-going, negative affect, in accordance with theories that predict physiological and behavioral response, consistent with the emotional state of the individual. Moreover, affective individual differences, particularly traits related to emotional reactivity, will be analyzed as moderators of the emotion-aggression effect.

DESCRIPTION (provided by applicant): Recent nationally reported incidents of violence (Columbine, Atlanta) have suggested that negative emotional states arising from environmental stressors (e.g., peer rejection, financial difficulties) can prompt some individuals to act out violently against others not responsible for their distress. Self-report and experimental research has confirmed a general emotional priming of aggression (Berkowitz, 1990; Geen, 1990; Moyer, 1976; Rotton, 1979; Bell & Baron, 1976). Other research supports a relationship between negative emotional traits and reactive forms of aggressive behavior (Caprara et al., 1983; Netter, et al., 1998). Emphasis should be placed on examining cognitive-emotional interactions as mechanisms underlying risk for chronic aggression (Berkowitz, 1994). Preliminary evidence suggests that heightened aggression in stress-reactive individuals may result from the experience of prolonged periods of negative emotions (Verona, Patrick, & Lang, 2002) and the tendency to ruminate or experience recurrent negative thinking about past events (Caprara, et al., 1987; Rusting & Nolen-Hoeksema, 1998). The current project will examine the interacting impact of prolonged emotional and cognitive experiences on laboratory aggressive behavior (via a Buss paradigm) among individuals exhibiting varying levels of negative emotional traits. Simultaneous recording of on-going negative emotional state (indexed via acoustic startle reactivity), autonomic nervous system activity, and aggressive responses will occur during experimental task blocks including a high stress or low stress condition. Participants' autonomic responses will also be recorded during a post-task "recovery" period, and subsequently, aggressive responses will be gauged during a post-recovery final block. Self-report measures of rumination will also be administered. It is expected that highly stress-reactive persons will experience prolonged (tonic) negative emotional arousal when exposed to an on-going stressor, as well as for a period of time after the end of the stressor. It is hypothesized that the tendency to "hold on" to negative emotions and thoughts will be directly related to participants' concurrent (during experimental blocks) and subsequent (during the post-recovery block) aggressive responses toward a confederate.

DESCRIPTION (provided by applicant): It is becoming increasingly clear that risk factors for use and trajectories toward desistance may differ significantly for men and women (e.g., Westermeyer &Boedicker, 2000). For example, recent work has uncovered different effects of monoamine genotypes (e.g., serotonin transporter, MAO-A) on male and female psychopathology and behavior (Sjoberg et al., 2007a;Verona, Joiner, Johnson &Bender, 2006). In addition, there is evidence that pubertal onset, childhood sexual abuse, and intimate partner violence (IPV) constitute unique risk factors for antisocial behavior and drug use among women compared to men (Dick, Rose, Kaprio, &Viken, 2000) and can predict drug relapse in women many years later in adulthood (Hyman, Garcia, &Sinha, 2006). Thus, a primary goal of the present application is to identify gender differences in biological and environmental risk factors for substance use outcomes as a way of advancing nuanced conceptualizations of female drug problems. The current project intends to (1) explore various gene by environment (GxE) effects on drug use outcomes, by examining different monoamine genes (5HTT, DRD4, MAO-A) and incorporating gendered environmental risk factors that are not commonly included in studies of drug use (e.g., intimate partner violence), (2) examine the extent to which GxE effects or individual risk factors are specific to substance use outcomes in women relative to men, and (3) identify multivariate models involving GxE effects and mediators of these effects to predict substance use pathways in men and women. The goal is to examine not only GxE effects (e.g., gene-by-abuse, gene-by-IPV) that directly influence substance use outcomes, but identify potential mediators (pubertal development, internalizing symptoms) in an effort to understand nuanced pathways for female substance use. The ultimate goal is to help in the development of tailored interventions to address gender-specific manifestations and etiologies. PUBLIC HEALTH RELEVANCE: Women's drug arrests have increased in the last two decades, whereas men's arrests have decreased. Thus, women's drug use has become a significant social problem. An innovative aspect of the project is the attempt to identify genetic and environmental factors that are female specific for substance use outcomes. Given important sex differences in biology, gene expression, and motives, this project can inform psychosocial and pharmacological treatments for substance use so that they are tailored to address gender-specific issues.

Project Summary/Abstract Aggressive behavior that co-occurs with mental disorders has been associated with distinct trajectories, manifestations and severity of mental illness, suggesting a distinct etiological process relative to when the disorder is expressed without aggression. Thus, one key to cutting across diagnostic boundaries in the understanding of underlying psychopathological processes is to investigate the biobehavioral mechanisms behind transdiagnostic symptom dimensions like aggression. As such, the current proposal will test a process model of emotional aggression that implicates the functional interplay of biobehavioral systems under at least two of the domains in NIMH?s Research Domain Criteria (RDoc), Negative Valence and Cognitive systems. Given the increasing influence of RDoC in potential shifts in conceptualization of psychopathology, the RDoC mapping of aggression will ensure that processes that propel aggressive behavior across various forms of psychopathology are given due influence in terms of research, intervention and prognostic judgments. The proposed project involves three aims across two sites that leverage availability of samples that vary on aggression proneness (selected community sample and existing pool of high-risk participants) to reveal causal connections between affective and cognitive brain systems and test specific predictions from the model. Event- related brain potential and startle measures of cognition and emotion will be used to obtain temporally precise indices of brain responses to incoming stimuli and how these relate to behavior. The first aim will experimentally identify whether acute and sustained threat exposure actually alter cognitive systems, specifically brain circuits involved in attentional alerting and cognitive inhibition, respectively, among persons with varying levels of aggression proneness. The second aim will examine the extent to which these threat- related alterations of attention or cognitive control actually predict aggressive behavior in the lab and real life instances subsequent to the measurement of these processes. The third aim will explore whether depression symptoms relate to distinct neurocognitive profiles depending on the level of aggression present. The data from this project can be used to further work that compares syndromes on the presence or absence of aggression to identify biological mechanisms that explain differential trajectories in mental illness, a key step to developing treatments that reflect more general processes in psychopathology.