Elevations in Blood Pressure Associated with Exposure to Violence are Mitigated by Pro-gun-Carrying Attitudes among Street-Identified Black Males and Females.

Living in neighborhoods with elevated rates of violent crime, such as in many poor Black American communities, is a risk factor for a range of physical and mental health challenges. However, the individual different factors that influence health outcomes in these stressful environments remain poorly understood. This study examined relations between exposure to violence, gun-carrying attitudes, and blood pressure in a community sample of street-identified Black American boys/men and girls/women. Survey data and blood pressure were collected from 329 participants (ages 16-54; 57.1% male) recruited from two small urban neighborhoods with high rates of violence using street participatory action research methodology. Results revealed that systolic blood pressure was elevated in the sample as was exposure to severe forms of direct and vicarious violence (e.g., shootings, assault). Attitudes about carrying guns moderated associations between the degree of violence exposure endorsed by participants and both systolic and diastolic blood pressure. Specifically, the positive association between exposure to violence and both systolic and diastolic blood pressure at low levels of pro-gun-carrying attitudes was no longer apparent at high levels of pro-gun attitudes. Furthermore, pro-gun attitudes appeared to moderate the association between exposure to violence and systolic pressure for older participants but not younger participants. Results suggest that positive attitudes about carrying guns (presumably indicative of pro-gun-carrying behavior) weakened the link between violence exposure and blood pressure. These novel findings suggest that carrying a gun may protect against the harmful effects of chronic stress from violence exposure on physical health outcomes (i.e., hypertension) among street-identified Black Americans.

Emotional reactivity linking assaultive trauma and risky behavior: Evidence of differences between cisgender women and men.

Accumulating evidence suggests that trauma exposure is positively associated with future engagement in risky behavior, such as substance misuse, aggression, risky sex, and self-harm. However, the psychological factors driving this association and their relevance across gender groups require further clarification. In a community sample of 375 adults with a high rate of trauma exposure (age range: 18-55 years, M = 32.98 years, SD = 10.64; 76.3% assaultive trauma exposure), we examined whether emotional reactivity linked lifetime assaultive trauma exposure with past-month risky behavior. We also explored whether this model differed for cisgender women (n = 178, 47.6%) and men (n = 197, 52.5%). As hypothesized, assaultive trauma was positively related to emotional reactivity, ß = .20, SE = 0.03, t(369) = 3.65, p < .001, which, in turn, partially accounted for the association between assaultive trauma and past-month risky behavior, indirect effect: ß = .03, SE = 0.01, 95% bootstrapped CI [0.01, 0.06]. Gender moderated this association such that assaultive trauma was indirectly associated with risky behavior via emotional reactivity for women but not for men, index moderation: B = -0.03, SE = 0.02, 95% bootstrapped CI [-0.07, -0.01]. Cross-sectional results suggest that emotional reactivity may be a proximal target for clinical intervention to aid in the reduction of risky behavior among women.

Structural barriers explain the link between negative community re-entry experiences and motives for illegal behavior in street-identified Black men and women.

This study examines how the re-entry process is related to structural barriers in the community and to motives for engaging in illegal behavior-two key risk factors for recidivism. We analyzed survey data collected on perceptions of community re-entry, employment opportunities, neighborhood violence, and illegal behavior motives from 379 formerly incarcerated and street-identified Black-American community members residing in Wilmington, Delaware (Mage = 32.3/8.9 years old; 77.0% men; 100% Black) by employing Street Participatory Action Research (Street PAR) methodology. We found that negative perceptions of re-entry correlated positively with (i) hardship caused by structural barriers in the community, specifically blocked employment opportunities and neighborhood violence, and (ii) motives for engaging in illegal behavior. Notably, the link between negative perceptions of re-entry and motives for illegal behavior became significantly weaker when the influence of structural barriers on these individual-level factors was included in a multivariate model. Results suggest negative views of the re-entry process reflect the resource-scarce and stressful environments people are living in, and structural barriers can account for the relationship between negative re-entry experiences and why individuals are motivated to engage in illegal behavior. Findings underscore the importance of improving the economic conditions of communities with high numbers of returning citizens.

Development of a cortical delay discounting assay: a potential biomarker of externalizing disorders.

BACKGROUND: People who tend to impulsively choose smaller, sooner rewards over larger, later rewards are at increased risk for addiction and psychiatric disorders. A neurobiological measure of the tendency to overvalue immediate gratification could facilitate the study of individuals who are susceptible to these mental disorders. The objective of this research was to develop a cortical assay of impulsive choice for immediate rewards. METHODS: A cortex-based assay of impulsive choice was developed using 1105 healthy adults from the Human Connectome Project, and then cross-validated in two independent samples of adults with elevated rates of psychiatric disorders. RESULTS: Study 1: Cortical delay discounting (C-DD) was developed using a multivariate additive model of gray matter thickness across both hemispheres. Higher C-DD corresponded to thinner cortex and greater impulsive choice for immediate rewards. It also predicted cannabis use beyond established risk factors for drug use, including familial substance use, childhood conduct problems, personality traits, and cognitive functioning. Study 2: C-DD replicated the association with delay discounting performance from study 1. Structural equation modeling showed C-DD covaried with symptoms of externalizing, but not internalizing disorders. Study 3: C-DD positively predicted future delay discounting behavior (6-34 months later). CONCLUSIONS: Across three studies, a cortical assay of impulsive choice evidenced consistent associations with drug use and delay discounting task performance. It was also uniquely associated with psychiatric disorders that share impulsivity as a core feature. Together, findings support the utility of C-DD as a neurobiological assay of impulsive decision-making and a possible biomarker of externalizing disorders.

Clarifying the synergistic effects of emotion dysregulation and inhibitory control on physical aggression.

Rising rates of violence underscore the need to better understand how systems that regulate distress and impulse control jointly modulate aggression risk. The goals of the current study were to investigate the unique and interactive effects of emotional dysregulation and inhibitory control on the perpetration of physical aggression. We recruited a high-risk community sample of 206 adults (M/SDage  = 33.55/10.89 years old; 47.1% female) who reported a range of physically aggressive behaviors. All participants completed a self-report measure (Difficulties in Emotion Regulation Scale), neuropsychological testing (Color Word Interference Test), and clinical interviewing (Lifetime History of Aggression Interview), and a subset of individuals (n = 134) underwent a neuroanatomical scan. As expected, the interplay of emotional and inhibitory control explained unique variance in physical aggression above and beyond their main effects. The positive association between emotion dysregulation and aggression strengthened as inhibitory control decreased. Cortical thickness in two right prefrontal clusters, one that peaked in the superior frontal gyrus and one that peaked in the caudal middle frontal gyrus, was also associated with the interactive effects of emotional dysregulation and inhibitory control. Notably, thickness in the superior frontal gyrus mediated the association between emotion dysregulation and physical aggression at low levels of inhibitory control. Using a multilevel and multimethod approach, the present study revealed neuroanatomical correlates of emotion-cognition interactions that have translational relevance to violence perpetration. These findings extend previous work primarily focused on functional-based neural assessments and point to the utility of examining neuroanatomical correlates of emotion-cognition interactions for understanding human aggression.

Childhood trauma moderates morphometric associations between orbitofrontal cortex and amygdala: implications for pathological personality traits.

BACKGROUND: Research has demonstrated that chronic stress exposure early in development can lead to detrimental alterations in the orbitofrontal cortex (OFC)-amygdala circuit. However, the majority of this research uses functional neuroimaging methods, and thus the extent to which childhood trauma corresponds to morphometric alterations in this limbic-cortical network has not yet been investigated. This study had two primary objectives: (i) to test whether anatomical associations between OFC-amygdala differed between adults as a function of exposure to chronic childhood assaultive trauma and (ii) to test how these environment-by-neurobiological effects relate to pathological personality traits. METHODS: Participants were 137 ethnically diverse adults (48.1% female) recruited from the community who completed a clinical diagnostic interview, a self-report measure of pathological personality traits, and anatomical MRI scans. RESULTS: Findings revealed that childhood trauma moderated bilateral OFC-amygdala volumetric associations. Specifically, adults with childhood trauma exposure showed a positive association between medial OFC volume and amygdalar volume, whereas adults with no childhood exposure showed the negative OFC-amygdala structural association observed in prior research with healthy samples. Examination of the translational relevance of trauma-related alterations in OFC-amygdala volumetric associations for disordered personality traits revealed that trauma exposure moderated the association of OFC volume with antagonistic and disinhibited phenotypes, traits characteristic of Cluster B personality disorders. CONCLUSIONS: The OFC-amygdala circuit is a potential anatomical pathway through which early traumatic experiences perpetuate emotional dysregulation into adulthood and confer risk for personality pathology. Results provide novel evidence of divergent neuroanatomical pathways to similar personality phenotypes depending on early trauma exposure.

Validation of the Motivational Inventory Underlying Substance Use Engagement (MI-USE).

Given the growing number of fatalities associated with the use of multiple types of drugs, there is an urgent need for a tool that allows clinicians and researchers to quickly assess diverse reasons for substance use. Here, we sought to validate the Motivational Inventory Underlying Substance Engagement (MI-USE), a new measure that assesses motivations for use across different types of substances. Participants were 538 adults ages 18-60 (48% women) who reported substance use problems and past-year drug or alcohol use. Analyses were conducted to discover and validate the factor structure of the MI-USE and evaluate its construct validity. A 30-item model best fit the MI-USE, with one General Factor capturing overall motivation to engage in substance use and eight motive-specific factors that indexed unique motivations for substance use: Emotional Coping (relief from unpleasant emotions), Pleasure-Seeking (feel pleasurable or exciting emotions and sensations), Dependence Severity (avoid withdrawal and cravings), Expansion (enhance self-insight and spirituality), Social Coping (increase confidence and attractiveness), Advantage (gain a physical or mental advantage), Physical Coping (relief from unpleasant bodily sensations), and Sleep (mitigate sleep problems). Evaluation of the measure's construct validity and internal consistency support the chosen model and interpretation of the motive-specific factors. Results provide initial validation of the MI-USE as a reliable and valid tool for assessing diverse substance use motivations. It improves upon existing measures by allowing clinicians and researchers to simultaneously evaluate motivations for multiple forms of substance use, which facilitates personalized treatment planning and research on polysubstance use.

Linking genes, circuits, and behavior: network connectivity as a novel endophenotype of externalizing.

BACKGROUND: Externalizing disorders are known to be partly heritable, but the biological pathways linking genetic risk to the manifestation of these costly behaviors remain under investigation. This study sought to identify neural phenotypes associated with genomic vulnerability for externalizing disorders. METHODS: One-hundred fifty-five White, non-Hispanic veterans were genotyped using a genome-wide array and underwent resting-state functional magnetic resonance imaging. Genetic susceptibility was assessed using an independently developed polygenic score (PS) for externalizing, and functional neural networks were identified using graph theory based network analysis. Tasks of inhibitory control and psychiatric diagnosis (alcohol/substance use disorders) were used to measure externalizing phenotypes. RESULTS: A polygenic externalizing disorder score (PS) predicted connectivity in a brain circuit (10 nodes, nine links) centered on left amygdala that included several cortical [bilateral inferior frontal gyrus (IFG) pars triangularis, left rostral anterior cingulate cortex (rACC)] and subcortical (bilateral amygdala, hippocampus, and striatum) regions. Directional analyses revealed that bilateral amygdala influenced left prefrontal cortex (IFG) in participants scoring higher on the externalizing PS, whereas the opposite direction of influence was observed for those scoring lower on the PS. Polygenic variation was also associated with higher Participation Coefficient for bilateral amygdala and left rACC, suggesting that genes related to externalizing modulated the extent to which these nodes functioned as communication hubs. CONCLUSIONS: Findings suggest that externalizing polygenic risk is associated with disrupted connectivity in a neural network implicated in emotion regulation, impulse control, and reinforcement learning. Results provide evidence that this network represents a genetically associated neurobiological vulnerability for externalizing disorders.

Contextualizing pubertal development: The combination of sexual partners' age and girls' pubertal development confers risk for externalizing but not internalizing symptoms among girls in therapeutic day schools.

OBJECTIVE: Early pubertal development is associated with negative health and mental health outcomes. Research on the influence of puberty on mental health underscores a need to examine the interplay between puberty and exposure to environmental risk. This study investigates a more rarely studied aspect of girls' environments - romantic relationships with boyfriends. Specifically, this study examined sexual partner age and the timing of girls' pubertal development in relation to externalizing and internalizing symptoms among female students attending therapeutic day schools in the United States, a population at elevated risk for negative mental health outcomes. METHODS: A total of 121 13 to 19-year-old adolescent girls (Mean age = 15.4; SD = 1.5) reported on the relative age of their past 3 sexual partners, their age of pubertal onset, and mental health challenges via clinical assessments of externalizing and internalizing symptoms. RESULTS: Forty-three percent of participants qualified for at least one mental health diagnosis. Earlier pubertal onset predicted greater internalizing symptoms, and this effect did not depend on the age of girls' sexual partners. However, early-developing girls who also reported having a sexual partner more than 2 years older than them were at increased risk for externalizing symptoms. CONCLUSIONS: Findings underscore that sexual relationships are an important risk factor for early-developing girls already at risk for mental health problems. Early developing girls with older partners may experience stronger social pressure to stay in relationships that expose them to partner violence and delinquency-related pressure, which combine with interpersonal stress to predict externalizing symptoms.

Psychopathic Traits, Pubertal Timing, & Mental Health Functioning in Justice-Involved Adolescents.

Although psychopathic traits and pubertal timing have garnered a great deal of attention as potent risk factors for antisocial trajectories, very little research has examined how these processes may be related. We investigated whether psychopathic traits were related to deviations in pubertal onset in a clinically-relevant sample of youth detained in juvenile detention facilities. One-hundred and thirty-seven adolescents (ages 12-17) completed surveys of pubertal timing, psychopathic traits, and mental health functioning. As predicted, psychopathic traits were found to be associated with pubertal timing, and the psychopathy facets evidenced differential associations with the onset of puberty. Trait disinhibition was associated with relatively earlier pubertal timing, whereas trait boldness appeared to confer protection against early pubertal onset in this sample. Symptoms of alcohol/ substance use and anger/ irritability were positively related to psychopathic traits, but only among youth who reported average-/late-pubertal development. These findings implicate psychopathic personality traits as individual difference variables that may influence the onset of pubertal timing and interact with pubertal timing to place justice-involved youth at risk for poor mental health.

Accelerated DNA Methylation Age: Associations With Posttraumatic Stress Disorder and Mortality.

OBJECTIVE: Recently developed indices of cellular age based on DNA methylation (DNAm) data, referred to as DNAm age, are being used to study factors that influence the rate of aging and the health correlates of these metrics of the epigenetic clock. This study evaluated associations between trauma exposure, posttraumatic stress disorder (PTSD) symptoms, and accelerated versus decelerated DNAm age among military veterans. We also examined whether accelerated DNAm age predicted mortality over the course of a 6.5-year medical record review period. METHODS: Three hundred thirty-nine genotype-confirmed white, non-Hispanic, middle-aged, trauma-exposed veterans underwent psychiatric assessment and genome-wide DNAm analysis. DNAm age was calculated using a previously validated algorithm. Medical records were available for a subset of 241 veterans and were reviewed approximately 6.5 years after DNA collection and PTSD assessment. RESULTS: PTSD hyperarousal symptoms were associated with accelerated DNAm age (ß = 0.20, p = .009) but trauma exposure and total PTSD severity were not. Accelerated DNAm age was also associated with 13% increased risk for all-cause mortality (hazard ratio = 1.13, 95% confidence interval = 1.01-1.26) during the medical record review period. CONCLUSIONS: Findings of this study replicate the association between PTSD and accelerated DNAm age and suggest that this effect may be specific to the hyperarousal symptom cluster. Results point to the potential utility of DNAm age algorithms for identifying individuals who are aging at an accelerated rate and for determining the factors that influence this process.

Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer's disease.

Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. Whole-genome polygenic risk scores for the development of Alzheimer's disease were calculated using summary statistics from the largest Alzheimer's disease genome-wide association study to date. Results showed that mild traumatic brain injury moderated the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions. Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease was associated with cortical thinning as a function of time since injury. A moderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced episodic memory performance through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechanism for reduced memory performance. Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of causal effects cannot be inferred from cross-sectional studies. These results underscore the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.

Higher serum cholesterol is associated with intensified age-related neural network decoupling and cognitive decline in early- to mid-life.

Mounting evidence indicates that serum cholesterol and other risk factors for cardiovascular disease intensify normative trajectories of age-related cognitive decline. However, the neural mechanisms by which this occurs remain largely unknown. To understand the impact of cholesterol on brain networks, we applied graph theory to resting-state fMRI in a large sample of early- to mid-life Veterans (N = 206, Meanage = 32). A network emerged (centered on the banks of the superior temporal sulcus) that evidenced age-related decoupling (i.e., decreased network connectivity with age), but only in participants with clinically-elevated total cholesterol (≥180 mg/dL). Crucially, decoupling in this network corresponded to greater day-to-day disability and mediated age-related declines in psychomotor speed. Finally, examination of network organization revealed a pattern of age-related dedifferentiation for the banks of the superior temporal sulcus, again present only with higher cholesterol. More specifically, age was related to decreasing within-module communication (indexed by Within-Module Degree Z-Score) and increasing between-module communication (indexed by Participation Coefficient), but only in participants with clinically-elevated cholesterol. Follow-up analyses indicated that all findings were driven by low-density lipoprotein (LDL) levels, rather than high-density lipoprotein (HDL) or triglycerides, which is interesting as LDL levels have been linked to increased risk for cardiovascular disease, whereas HDL levels appear inversely related to such disease. These findings provide novel insight into the deleterious effects of cholesterol on brain health and suggest that cholesterol accelerates the impact of age on neural trajectories by disrupting connectivity in circuits implicated in integrative processes and behavioral control. Hum Brain Mapp 38:3249-3261, 2017. © 2017 Wiley Periodicals, Inc.

COMT Val158Met polymorphism moderates the association between PTSD symptom severity and hippocampal volume.

BACKGROUND: Memory-based alterations are among the hallmark symptoms of posttraumatic stress disorder (PTSD) and may be associated with the integrity of the hippocampus. However, neuroimaging studies of hippocampal volume in individuals with PTSD have yielded inconsistent results, raising the possibility that various moderators, such as genetic factors, may influence this association. We examined whether the catechol-O-methyltransferase (COMT) Val158Met polymorphism, which has previously been shown to be associated with hippocampal volume in healthy individuals, moderates the association between PTSD and hippocampal volume. METHODS: Recent war veterans underwent structural MRI on a 3 T scanner. We extracted volumes of the right and left hippocampus using FreeSurfer and adjusted them for individual differences in intracranial volume. We assessed PTSD severity using the Clinician-Administered PTSD Scale. Hierarchical linear regression was used to model the genotype (Val158Met polymorphism) × PTSD severity interaction and its association with hippocampal volume. RESULTS: We included 146 white, non-Hispanic recent war veterans (90% male, 53% with diagnosed PTSD) in our analyses. A significant genotype × PTSD symptom severity interaction emerged such that individuals with greater current PTSD symptom severity who were homozygous for the Val allele showed significant reductions in left hippocampal volume. LIMITATIONS: The direction of proposed effects is unknown, thus precluding definitive assessment of whether differences in hippocampal volume reflect a consequence of PTSD, a pre-existing characteristic, or both. CONCLUSION: Our findings suggest that the COMT polymorphism moderates the association between PTSD and hippocampal volume. These results highlight the role that the dopaminergic system has in brain structure and suggest a possible mechanism for memory disturbance in individuals with PTSD.

Reckless Self-Destructive Behavior and PTSD in Veterans: The Mediating Role of New Adverse Events.

The addition of self-destructive and reckless behavior as a symptom of posttraumatic stress disorder (PTSD) in DSM-5 has stimulated renewed interest in understanding relationships between these behaviors and trauma-related psychopathology. This study examined the relationship between reckless and self-destructive behaviors (RSDB), intervening exposure to new adverse events, and later PTSD severity in a sample of trauma-exposed veterans. At baseline, participants were assessed for RSDB (past 5 years) and current PTSD severity (N = 222). PTSD severity was then reassessed approximately 4 years later (N = 148). Overall, RSDB were reported by 74.4% of the sample, with 61.3% engaging in multiple forms of RSDB. The most commonly endorsed behaviors included alcohol/drug abuse (42.8%), driving while intoxicated (29.4%), gambling (24.7%), and aggression (23.1%). There was a positive correlation between RSDB and PTSD severity at both the baseline (r = .16, p = .031) and follow-up assessment (r = .24, p = .005). Path models indicated that exposure to new adverse events fully mediated the effect of Time 1 RSDB on PTSD symptoms at Time 2 (indirect association: ß = .05, p = .046). Results suggest that RSDB are common among trauma-exposed veterans and may perpetuate PTSD symptoms by increasing exposure to new adverse events.

Affect recognition among adolescents in therapeutic schools: relationships with posttraumatic stress disorder and conduct disorder symptoms.

BACKGROUND: Posttraumatic stress disorder (PTSD) and conduct disorder (CD) symptoms often co-occur in adolescence, but little is known about whether they show common or distinct emotional processing deficits. METHOD: We examined the effects of PTSD and CD symptoms on facial affect processing in youth with emotional and behavior problems. Teens enrolled in therapeutic day schools (N = 371; ages 13-19) completed a structured diagnostic assessment and the Diagnostic Analysis of Nonverbal Accuracy-2 facial affect recognition task. RESULTS: PTSD symptoms were associated with deficits in the recognition of angry facial expressions, specifically the false identification of angry faces as fearful. CD symptoms were associated with greater difficulty correctly identifying sadness. CONCLUSIONS: Findings suggest specificity in the relationships of PTSD and CD symptoms with emotional processing.

EPIGENETIC VARIATION AT SKA2 PREDICTS SUICIDE PHENOTYPES AND INTERNALIZING PSYCHOPATHOLOGY.

BACKGROUND: DNA methylation of the SKA2 gene has recently been implicated as a biomarker of suicide risk and posttraumatic stress disorder (PTSD). To examine the specificity and reliability of these findings, we examined associations between SKA2 DNA methylation, broad dimensions of psychiatric symptoms, and suicide phenotypes in adults with high levels of trauma exposure. METHODS: A total of 466 White, non-Hispanic veterans and their intimate partners (65% male) underwent clinical assessment and had blood drawn for genotyping and methylation analysis. DNA methylation of the CpG locus cg13989295 and genotype at the methylation-associated single-nucleotide polymorphism (SNP) rs7208505 were examined in relation to current and lifetime PTSD, internalizing and externalizing psychopathology, and suicide phenotypes (ideation, plans, and attempts). RESULTS: DNA methylation at the previously implicated SKA2 CpG locus (cg13989295) was associated with current and lifetime symptoms of internalizing (but not externalizing) disorders. SKA2 methylation levels also predicted higher rates of current suicidal thoughts and behaviors, even after including well-established psychiatric risk factors for suicide in the model. Associations between PTSD and SKA2 were not significant, and genetic variation at the methylation-associated SNP (rs7208505) was not related to any of the phenotypes examined. CONCLUSIONS: SKA2 methylation may index a general propensity to experience stress-related psychopathology, including internalizing disorders and suicidal thoughts and behaviors. This study demonstrates that SKA2 methylation levels explain unique variance in suicide risk not captured by clinical symptom interviews, providing further evidence of its potential utility as a biomarker of suicide risk and stress-related psychopathology.

Neurobiological indicators of disinhibition in posttraumatic stress disorder.

Deficits in impulse control are increasingly recognized in association with posttraumatic stress disorder (PTSD). To our further understanding of the neurobiology of PTSD-related disinhibition, we examined alterations in brain morphology and network connectivity associated with response inhibition failures and PTSD severity. The sample consisted of 189 trauma-exposed Operation Enduring Freedom/Operation Iraqi Freedom veterans (89% male, ages 19-62) presenting with a range of current PTSD severity. Disinhibition was measured using commission errors on a Go/No-Go (GNG) task with emotional stimuli, and PTSD was assessed using a measure of current symptom severity. Whole-brain vertex-wise analyses of cortical thickness revealed two clusters associated with PTSD-related disinhibition (Monte Carlo cluster corrected P < 0.05). The first cluster included portions of right inferior and middle frontal gyri and frontal pole. The second cluster spanned portions of left medial orbital frontal, rostral anterior cingulate, and superior frontal gyrus. In both clusters, commission errors were associated with reduced cortical thickness at higher (but not lower) levels of PTSD symptoms. Resting-state functional magnetic resonance imaging analyses revealed alterations in the functional connectivity of the right frontal cluster. Together, study findings suggest that reductions in cortical thickness in regions involved in flexible decision-making, emotion regulation, and response inhibition contribute to impulse control deficits in PTSD. Furthermore, aberrant coupling between frontal regions and networks involved in selective attention, memory/learning, and response preparation suggest disruptions in functional connectivity may also play a role.

Recent victimization increases risk for violence in justice-involved persons with mental illness.

A large body of research has examined relationships between distal experiences of victimization and the likelihood of engaging in violence later in life. Less is known about the influence of recent violent victimization on risk for violence perpetration. To our knowledge, this is the first study to examine prospectively whether recent victimization in adulthood increases the risk of future violence. Specifically, the present study assessed the incremental validity of recent violent victimization in the prediction of future violence in a sample of justice-involved adults with serious mental illness. The study examined (a) whether recent experiences of violent victimization (i.e., within 6 months of the baseline assessment) predicted a greater likelihood of perpetrating violence in the next year, and (b) whether inclusion of recent victimization enhanced the predictive validity of a model of violence risk in a sample of justice-involved adults with severe mental illness (N = 167). Hierarchical logistic regression analyses indicated that exposure to recent violent victimization at the baseline assessment predicted a greater likelihood of engaging in violent behavior during the year follow-up period. Additionally, recent exposure to violence at the baseline assessment continued to explain a significant amount of variance in a model of future violence perpetration above the variance accounted for by well-established violence risk factors. Taken together, the findings suggest that recent victimization is important to consider in understanding and evaluating risk of violence by persons with mental disorders who are involved in the criminal justice system.

Impulsive Decision-Making, Affective Experiences, and Parental History of Self-Injurious Thoughts and Behaviors within Parent-Adolescent Dyads.

Impulsive decision-making, particularly during states of affective intensity, is associated with greater risk of engagement in self-injurious thoughts and behaviors (SITBs) during adolescence. The proximal (dyadic parent-adolescent affect and impulsivity) and distal (family history of SITBs) risk factors that occur within the family system could be relevant processes at stake in the intergenerational transmission of risk. The current study tests the interdependence of parent-adolescent factors associated with risk for SITBs and probes the extent to which parent-adolescent affective states influence their own (actor-effects) and each other's (partner-effects) impulsive decision-making, and further whether these relationships are moderated by a parent's history of SITBs. Participants included 212 (106 dyads) community parents and their adolescents who completed self-report and behavioral tasks related to positive and negative affective states, impulsive decision-making, and lifetime history of SITBs. Application of the Actor-Partner Interdependence Model (APIM) revealed a partner-effect where greater parent negative affect in the past week was associated with elevated adolescent impulsive decision-making among families with a history of SITBs (Estimate = 0.66, Standard Error = 0.13, p < 0.001). In addition, a significant actor-effect was observed where greater positive affect was associated with decreased impulsive decision-making among adolescents (Estimate = -0.21, Standard Error = 0.10, p = 0.03), however, moderating effects of parent history of SITBs were not detected. Findings from the present study shed light on the interdependence of affect and impulsivity within parent-adolescent dyads, and the extent to which these interactions may be particularly salient for families with known vulnerabilities for SITBs.