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Several hypotheses may explain the association between substance use, posttraumatic stress disorder (PTSD), and depression. However, few studies have utilized a large multisite dataset to understand this complex relationship. Our study assessed the relationship between alcohol and cannabis use trajectories and PTSD and depression symptoms across 3 months in recently trauma-exposed civilians.
In total, 1618 (1037 female) participants provided self-report data on past 30-day alcohol and cannabis use and PTSD and depression symptoms during their emergency department (baseline) visit. We reassessed participant's substance use and clinical symptoms 2, 8, and 12 weeks posttrauma. Latent class mixture modeling determined alcohol and cannabis use trajectories in the sample. Changes in PTSD and depression symptoms were assessed across alcohol and cannabis use trajectories via a mixed-model repeated-measures analysis of variance.
Three trajectory classes (low, high, increasing use) provided the best model fit for alcohol and cannabis use. The low alcohol use class exhibited lower PTSD symptoms at baseline than the high use class; the low cannabis use class exhibited lower PTSD and depression symptoms at baseline than the high and increasing use classes; these symptoms greatly increased at week 8 and declined at week 12. Participants who already use alcohol and cannabis exhibited greater PTSD and depression symptoms at baseline that increased at week 8 with a decrease in symptoms at week 12.
Our findings suggest that alcohol and cannabis use trajectories are associated with the intensity of posttrauma psychopathology. These findings could potentially inform the timing of therapeutic strategies.
Psychological trauma exposure and posttraumatic stress disorder (PTSD) have been associated with advanced epigenetic age. However, whether epigenetic aging measured at the time of trauma predicts the subsequent development of PTSD outcomes is unknown. Moreover, the neural substrates underlying posttraumatic outcomes associated with epigenetic aging are unclear.
We examined a multi-ancestry cohort of women and men (n = 289) who presented to the emergency department (ED) after trauma. Blood DNA was collected at ED presentation, and EPIC DNA methylation arrays were used to assess four widely used metrics of epigenetic aging (HorvathAge, HannumAge, PhenoAge, and GrimAge). PTSD symptoms were evaluated longitudinally at the time of ED presentation and over the ensuing 6 months. Structural and functional neuroimaging was performed 2 weeks after trauma.
After covariate adjustment and correction for multiple comparisons, advanced ED GrimAge predicted increased risk for 6-month probable PTSD diagnosis. Secondary analyses suggested that the prediction of PTSD by GrimAge was driven by worse trajectories for intrusive memories and nightmares. Advanced ED GrimAge was also associated with reduced volume of the whole amygdala and specific amygdala subregions, including the cortico-amygdaloid transition and the cortical and accessory basal nuclei.
Our findings shed new light on the relation between biological aging and trauma-related phenotypes, suggesting that GrimAge measured at the time of trauma predicts PTSD trajectories and is associated with relevant brain alterations. Furthering these findings has the potential to enhance early prevention and treatment of posttraumatic psychiatric sequelae.
Causes of childhood behavior problems remain poorly understood. Enriched family environments and corresponding brain development may reduce the risk of their onset, but research investigating white matter neurodevelopmental pathways explaining associations between the family environment and behavior remains limited. We hypothesized that more positive prenatal and mid-childhood family functioning – a measure of a family's problem solving and supportive capacity – would be associated with two markers of preadolescent white matter neurodevelopment related to reduced behavior problems: higher global fractional anisotropy (FA) and lower global mean diffusivity (MD).
Data are from 2727 families in the Generation R Study, the Netherlands. Mothers reported family functioning (McMaster Family Assessment Device, range 1–4, higher scores indicate healthier functioning) prenatally and in mid-childhood (mean age 6.1 years). In preadolescence (mean age 10.1), the study collected diffusion-weighted scans. We computed standardized global MD and FA values by averaging metrics from 27 white matter tracts, and we fit linear models adjusting for possible confounders to examine global and tract-specific outcomes.
Prenatal and mid-childhood family functioning scores were moderately correlated, r = 0.38. However, only prenatal family functioning – and not mid-childhood functioning – was associated with higher global FA and lower global MD in preadolescence in fully adjusted models: βglobal FA = 0.11 (95% CI 0.00, 0.21) and βglobal MD = −0.15 (95% CI −0.28, −0.03) per one-unit increase in functioning score. Sensitivity and tract-specific analyses supported these global findings.
These results suggest high-functioning prenatal or perinatal family environments may confer lasting white matter neurodevelopmental benefits into preadolescence.
This is the first report on the association between trauma exposure and depression from the Advancing Understanding of RecOvery afteR traumA(AURORA) multisite longitudinal study of adverse post-traumatic neuropsychiatric sequelae (APNS) among participants seeking emergency department (ED) treatment in the aftermath of a traumatic life experience.
We focus on participants presenting at EDs after a motor vehicle collision (MVC), which characterizes most AURORA participants, and examine associations of participant socio-demographics and MVC characteristics with 8-week depression as mediated through peritraumatic symptoms and 2-week depression.
Eight-week depression prevalence was relatively high (27.8%) and associated with several MVC characteristics (being passenger v. driver; injuries to other people). Peritraumatic distress was associated with 2-week but not 8-week depression. Most of these associations held when controlling for peritraumatic symptoms and, to a lesser degree, depressive symptoms at 2-weeks post-trauma.
These observations, coupled with substantial variation in the relative strength of the mediating pathways across predictors, raises the possibility of diverse and potentially complex underlying biological and psychological processes that remain to be elucidated in more in-depth analyses of the rich and evolving AURORA database to find new targets for intervention and new tools for risk-based stratification following trauma exposure.
The ability to understand others’ mental states carries profound consequences for mental and physical health, making efforts at validly and reliably assessing mental state understanding (MSU) of utmost importance. However, the most widely used and current NIMH-recommended task for assessing MSU – the Reading the Mind in the Eyes Task (RMET) – suffers from potential assessment issues, including reliance on a participant's vocabulary/intelligence and the use of culturally biased stimuli. Here, we evaluate the impact of demographic and sociocultural factors (age, gender, education, ethnicity, race) on the RMET and other social and non-social cognitive tasks in an effort to determine the extent to which the RMET may be unduly influenced by participant characteristics.
In total, 40 248 international, native-/primarily English-speaking participants between the ages of 10 and 70 completed one of five measures on TestMyBrain.org: RMET, a shortened version of RMET, a multiracial emotion identification task, an emotion discrimination task, and a non-social/non-verbal processing speed task (digit symbol matching).
Contrary to other tasks, performance on the RMET increased across the lifespan. Education, race, and ethnicity explained more variance in RMET performance than the other tasks, and differences between levels of education, race, and ethnicity were more pronounced for the RMET than the other tasks such that more highly educated, non-Hispanic, and White/Caucasian individuals performed best.
These data suggest that the RMET may be unduly influenced by social class and culture, posing a serious challenge to assessing MSU in clinical populations given shared variance between social status and psychiatric illness.
The last decade has witnessed remarkable progress in the understanding of the mammalian cannabinoid system, from the cloning of the endogenous cannabinoid receptor to the discovery of new pharmacologic compounds acting on this receptor. Current and planned studies in humans include compounds with effects ranging from direct antagonists to inhibitors of reuptake and breakdown. This progress has been accompanied by a much greater understanding of the role of the cannabinoid system in modulating the neural circuitry that mediates anxiety and fear responses. This review focuses on the neural circuitry and pharmacology of the cannabinoid system as it relates to the acquisition, expression, and extinction of conditioned fear as a model of human anxiety. Preclinical studies suggest that these may provide important emerging targets for new treatments of anxiety disorders.
The concatenation of convergent lines of evidence from basic to clinical research continues to reveal that norepinephrine (NE) is a crucial regulator of a myriad of behaviors ranging from stress response to memory formation. Furthermore, many neuropsychiatric disorders involve neurocircuitry that is directly modulated by NE. This report summarizes the physiological roles of NE, as well as the main findings implicating a role for NE system dysfunction in mood and anxiety disorders, posttraumatic stress disorder, attention-deficit/hyperactivity disorder, and Alzheimer's disease. In each of these disorders, there appears to be a complex dysregulation of NE function, with changes in locus ceruleus firing, NE availability, and both pre- and postsynaptic receptor regulation. Many symptoms of these disorders are attributable to abnormalities within distributed neural circuits regulated by NE. Appreciation of NE's role in modulating the neural circuitry mediating cognition and affect should help elucidate the pathophysiology of a variety of neuropsychiatric disorders and the development of novel treatments.
Anxiety disorders are a common focus of clinical concern and certain forms of anxiety may be conceptualized as disorders of emotional learning. Behavior therapies effective in the treatment of anxiety are modeled on extinction training as a means of reducing pathological anxiety. The present understanding of human anxiety has been informed by preclinical research using rodent models to study the acquisition and extinction of fear. Glutamate appears to have a central role in both of these processes. The authors review this literature and discuss novel applications of D-cycloserine, a partial N-methyl-D-aspartate agonist, for the treatment of anxiety.
Clinically, the principles of extinction learning form much of the foundation for the most effective behavioral therapies for fear-related anxiety disorders. Within the general class of anxiety disorders, posttraumatic stress disorder (PTSD) is unique in the sense that the precipitating traumatic event may provide the opportunity for acute intervention before the onset of symptoms and before memories have been consolidated. The use of propranolol to treat individuals with posttraumatic stress symptoms was initially described in a case series of physically and sexually abused children with severe symptoms of agitation. An alternative consolidation-blockade approach to the use of propranolol involves the administration of glucocorticoids to trauma-exposed patients. Finally, clinically directed interference with initial memory consolidation through the use of beta-blockers or glucocorticoids following acute trauma exposure could prevent or attenuate the formation of traumatic emotional memory and reduce risk of PTSD.
The chapter by Kim Huhman, “Social Stress as a Formative Experience: Neurobiology of Conditioned Defeat,” is a very interesting description of conditioned defeat in Syrian hamsters as a model of understanding the neurobiology of social stress and its effects on stress-related disorders in humans. This commentary will describe recent data from a large sample of inner-city at-risk subjects who have experienced an enormous amount of inter-personal violence. We find that these traumatic experiences, both in adulthood and childhood, contribute greatly to adult posttraumatic stress disorder (PTSD) and depression. Furthermore, we will describe data suggesting that early unstable family environments in this population are a significant risk factor for these adult stress-related disorders, whereas nurturing caregiving appears to be protective. Finally, we refer to recent data that social support in adulthood appears to be a resiliency factor helping to mediate against the effects of child abuse on adult depression.
IMPORTANCE OF INTERPERSONAL VIOLENCE AS A CRITICAL MEDIATOR OF STRESS-RELATED DISORDERS
Among civilians, inner-city minority populations appear to be exposed to extreme amounts of trauma (Breslau et al., 1998; Alim, Charney, & Mellman, 2006). For example, economically disadvantaged African Americans living within urban environments experience high levels of inter-personal violence and trauma (Breslau, Davis, Andreski, & Peterson, 1991; Shakoor & Chalmers, 1991; Fitzpatrick & Boldizar, 1993; Breslau et al., 1998; Selner-O'Hagan, Kindlon, Buka, Raudenbush, & Earls, 1998). Furthermore, a large amount of this exposure occurs during youth (Shakoor et al., 1991; Fitzpatrick et al., 1993; Selner-O'Hagan et al., 1998).
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