Objective:Polygenic risk scores (PRS) for posttraumatic stress disorder (PTSD) often account for a low amount of variance. Ancestry-related differences in PRS scale and variance limit cross-group comparisons. This methodological challenge further complicates gene-by-environment (GxE) analyses, given that socioenvironmental exposures are inequitably distributed across ethnoracial groups. We constructed an ancestry-calibrated polygenic risk score (AC-PRS) for PTSD in the largest longitudinal study of trauma survivors to date and investigated GxE interactions. Method:Recent trauma survivors (N=1,801) provided a blood specimen for genotyping. Six PTSD trajectories were previously identified from PTSD Checklist for DSM-5 (PCL-5) scores at 2-weeks, 8-weeks, 3-months, and 6-months post-trauma. Greenspace (normalized difference vegetation index [NDVI) and socioeconomic disadvantage (area deprivation index [ADI]) were derived from residential addresses. Logistic regressions examined interactions between newly developed AC-PRS and neighborhood factors on trajectories after adjusting for sociodemographic and trauma-related covariates. Secondary linear models considered GxE interactions on 6-month PCL-5 scores. Results:AC-PRS performed well across ethnoracial groups, explaining significant variability in PTSD trajectories (R2=.053). ADI moderated the association between AC-PRS and the likelihood of assignment in a high nonremitting trajectory of PTSD symptoms and severity of symptoms at 6-months (ps < .05). There were no NDVI x AC-PRS interactions in any models. Conclusions:AC-PRS captures genetic risk for PTSD in admixed trauma survivors, demonstrating good discrimination between nonremitting and resilient courses of PTSD. However, neighborhood disadvantage may modify utility of PRS for PTSD, warranting careful consideration when applying these scores across contexts.

BackgroundAdverse posttraumatic neuropsychiatric sequelae are common after trauma. Early identification of individuals at risk for these outcomes could enable the deployment of preventive interventions to survivors at greatest risk. Smartphone keystroke biomarkers show promise in identifying individuals with neuropsychiatric symptoms; however, to our knowledge, no research has examined whether they can be used to identify symptoms in the aftermath of trauma. ObjectiveThis study evaluates whether passively collected keystroke data from smartphone use in daily life could identify individuals with high symptom levels, as well as worsening or recovery of symptoms, after trauma exposure. MethodsData from a diverse cohort of individuals presenting to 27 emergency departments after trauma were analyzed. Inclusion criteria were presenting to the emergency department within 72 hours of trauma, age 18-75, and the ability to speak and read English. Exclusion criteria were solid organ injury, significant hemorrhage, operative intervention, or likely admission for over 72 hours. Participants installed an app that passively collected keystroke data during use of any app on their smartphone, beginning in the emergency department. Participants also completed serial symptom assessments over 8 weeks after trauma exposure. ResultsA total of 3445 patients met study criteria, provided informed consent, and completed assessments in the emergency department. Of these, 1072 (mean age 40, SD 13; 616/1072, 57.46%, women; 565/1072, 52.71% non–Hispanic Black) installed the app on their Android smartphone and completed the 8-week assessment and were therefore included in analyses. Keystroke biomarkers related to typing speed, identified using bivariate linear mixed models controlling for false discovery rates, were associated with elevated pain, reexperiencing, and mental fatigue (absolute values of rs=0.22-0.25, Ps=.02). Separate change-of-operation and scrolling keystroke biomarkers were associated with increased reexperiencing symptoms (r=0.18, P=.047) and mental fatigue (rs=0.18-0.19, Ps=.031-.047). Further, changes in specific keystroke biomarkers were associated with worsening or recovery of pain (rs=0.07-0.10, Ps=.02), somatic symptoms (rs=0.02, Ps=.02), mental fatigue (rs=0.02-0.04, Ps=.02), sleep disturbance (absolute rs=0.07-0.09, Ps=.02), reexperiencing (rs=0.02-0.04, Ps=.02), and hyperarousal (rs=0.02-0.04, Ps=.02). ConclusionsIn general, slower typing and scrolling speeds were associated with higher symptom levels, with small to medium effect sizes. Keystroke data passively collected via smartphone use may help identify individuals with significant or changing posttraumatic symptoms. Future research should continue to explore these keystroke biomarkers and whether they can be leveraged to connect vulnerable trauma survivors to appropriate services. Overall, these results add to the literature, indicating that passively collected keystroke data may help identify individuals with neuropsychiatric symptoms or changes and are, to our knowledge, the first to test whether keystroke biomarkers are useful in the aftermath of trauma. This represents a critical period during which preventive interventions could be deployed to reduce the long-term burden of trauma-related sequelae.

Importance:Prior work demonstrates that earlier trauma exposure increases the risk of posttraumatic stress disorder (PTSD) after a subsequent trauma, and cross-sectional work has also identified sexual violence (SV) as the form of traumatic stressor with the greatest conditional risk for PTSD. However, little work explores these findings longitudinally with a comparison group with no history of SV. Objective:To examine the differences in PTSD symptoms after a new incident of trauma exposure in survivors with and without an earlier history of SV. Design, Setting, and Participants:In this case-control study, data from a longitudinal cohort sample of patients enrolled in the Advancing Understanding of Recovery After Trauma (AURORA) study were examined. Participants were admitted to emergency departments due to a traumatic injury (primarily motor vehicle crash), and they were followed up for 1 year after emergency department (ED) admission. They were recruited within 72 hours of ED admission and then assessed at 5 time points (2 weeks, 8 weeks, 3 months, 6 months, 12 months) after their injury. Participants were a diverse and heterogeneous sample of individuals admitted to EDs across the US. Study data were evaluated from January 2025 to March 2026. Exposure:Earlier history of SV as assessed at ED admission using the Childhood Trauma Questionnaire and the Life Events Checklist. Main Outcomes and Measures:Symptoms of PTSD as assessed by the PTSD Checklist for DSM-5. Results:The study sample included 2423 individuals (mean [SD] age, 36 [13] years; 1566 female [64.6%]), 1270 whom (52%) reported an earlier history of SV. At every time point, participants with a history of SV demonstrated significantly elevated symptoms of PTSD (β = 4.62; 95% CI, 3.09-6.21; P < .001) compared with those without a history of SV, even after controlling for earlier nonsexual trauma exposure. Within the group with prior SV, the PTSD symptoms that remained the highest across time points were hypervigilance symptoms (criterion E), although negative alterations in cognition and mood (criterion D) were the symptom cluster that recovered most slowly. Conclusions and Relevance:Results of this case-control study indicate that having a history of SV was associated with elevated symptoms of PTSD and slower symptom recovery after a subsequent nonsexual trauma. These results raise important considerations for clinicians, regardless of whether or not they self-identify as working specifically with survivors of SV.

Chronic pain following traumatic stress exposure (TSE) is common. Increasing evidence suggests inflammatory and immune mechanisms are activated following TSE, play a role in the transition from acute to chronic pain, and may differ by sex. In this study, we tested the hypothesis that elevated levels of the inflammatory marker C-reactive protein (CRP) would be associated with acute and chronic pain in a sex-specific manner. We utilized blood-plasma samples and pain questionnaire data from men (n=116) and women (n=269) enrolled in AURORA, a multi-site emergency department (ED)-based longitudinal study of TSE survivors. CRP levels were measured by ELISA using plasma samples collected in the ED ('peritraumatic CRP') and six-months following TSE. Multivariate models were used to assess the relationship between CRP and pain. Men and women reported similar acute pain levels in the ED; however, pain resolved more rapidly in men over time. Peritraumatic CRP was not associated with acute pain severity in either men or women. However, six-month CRP levels were positively associated with six-month pain severity in both men (r=0.19, p=0.089, non-significant) and women (r=0.21, p=0.0015). In men only, higher peritraumatic CRP predicted lower chronic pain severity (β=-0.36, p=0.024) whereas no association was observed in women (β=0.04, p=0.628). Among men with elevated peritraumatic CRP, decreases in CRP over time were associated with decreases in pain over time (r=-0.38, p=0.0197). These findings suggest sex-specific relationships between CRP and chronic pain following TSE and highlight inflammation as a potential mechanism contributing to differential pain recovery trajectories in men and women. PERSPECTIVE: Longitudinal CRP levels following traumatic stress exposure showed sex-dependent associations with chronic pain outcomes. Unexpectedly, higher early CRP predicted lower chronic pain severity in men, suggesting inflammatory responses may differentially influence pain recovery trajectories in men and women.

Socioenvironmental factors may be associated with patterns of biological age and modify individual vulnerability to trauma- and stress-related psychiatric conditions. We examined whether neighborhood socioeconomic disadvantage is associated with accelerated epigenetic aging in the early aftermath of trauma. Next, we tested whether individual psychological resources, previously shown to attenuate stress-related accelerated aging, moderated the association between neighborhood disadvantage and epigenetic aging. Participants provided blood samples approximately 2 weeks post-trauma (N = 203; 64% female) and completed sociodemographic and psychometric assessments, including a measure of individual psychological resources (Connor-Davidson Resilience Scale [CD-RISC]). Epigenetic aging was assessed using the Horvath, Hannum, GrimAge, PhenoAge, and DunedinPACE clocks. Neighborhood disadvantage (national area deprivation index [ADI]) was derived from participants' home addresses. Linear models evaluated the relationship between ADI and epigenetic aging as well as a subsequent CD-RISC x ADI interaction after covarying for chronological age, income, sex, lifetime trauma, lifetime tobacco and alcohol use, PTSD symptoms, and five estimated cell-type proportions. Higher ADI was associated with accelerated aging in GrimAge, PhenoAge, and DunedinPACE models (pscorrected <0.05) after adjusting for covariates. There was an ADI x CD-RISC interaction on GrimAge, such that the effect of neighborhood disadvantage was not significant among individuals with higher levels of individual psychological resources. Findings underscore a link between neighborhood disadvantage and accelerated biological aging and highlight several modifiable factors at both the neighborhood and individual levels associated with epigenetic age.

BACKGROUND:Systemic inflammation is hypothesized to contribute to post-traumatic stress disorder (PTSD) vulnerability. Few studies have examined inflammation shortly after trauma as a predictor of later PTSD symptoms. We examined whether inflammation from the emergency department (ED) post-trauma is associated with PTSD symptom severity over the following 6 months. METHODS:Our sample included 742 AURORA participants, a longitudinal cohort of patients in 29 EDs across the United States after a traumatic stressor, followed up to 6 months. Plasma cytokines were assessed from a study blood draw in the ED: an inflammatory index (standardized sum of generally pro-inflammatory markers interleukin [IL]-6, IL-8, tumor necrosis factor alpha [TNF-α], interferon gamma [IFN-γ]), and generally anti-inflammatory IL-10. PTSD symptoms were self-reported at 2 weeks, 8 weeks, 3 months, and 6 months post-ED. Covariate-adjusted repeated-measures regressions estimated associations between inflammation and PTSD symptoms, overall and sex-stratified. RESULTS:Among 742 participants (age m = 40.0 [13.7]; 479 [64.6%] female), PTSD symptoms were elevated then modestly decreased over follow-up. Higher ED inflammation was associated with higher PTSD symptoms across follow-up (standardized symptoms β = 0.05, 95% CI: 0.01-0.09), adjusted for potential confounders. Higher pro-inflammatory index levels and IL-6, IL-8, and TNF-α were associated with higher PTSD symptoms in males only, while higher IL-10 was associated with higher PTSD symptoms in females only. CONCLUSIONS:Pro-inflammatory levels shortly after traumatic stress are associated with heightened PTSD symptoms, particularly among males. Inflammatory markers may prove useful additions to prediction models for PTSD following trauma, with attention to sex differences.

OBJECTIVE:Preventing posttraumatic psychopathology (e.g., depression or posttraumatic stress disorder [PTSD]) following an acute traumatic event requires attention to modifiable factors that may protect against such psychopathology. In this study, we aimed to identify the relative contributions of resiliency factors across multiple domains to posttraumatic psychopathology and to delineate subcomponents that may be most influential. METHOD:This study leveraged prospective data from 2,043 trauma-exposed individuals recruited from emergency departments in the Advancing Understanding of RecOvery afteR traumA Study. We first used structural equation modeling to examine higher level regulatory and interpersonal strength domains following acute trauma exposure and their relative associations with symptoms of depression or PTSD at 3 months posttrauma. We then tested which specific factors within these domains were associated with 3-month symptoms. RESULTS:Both regulatory and interpersonal strength domains were linked to fewer symptoms of depression and PTSD 3 months later, though relational strengths were more strongly associated than regulatory strengths when modeled together. Within interpersonal strengths, higher levels of emotional support and supportive networks, but not social engagement, were associated with lower depressive and PTSD symptoms. Within regulatory strengths, trait resilience was associated with lower depressive and PTSD symptoms, and self-efficacy showed mixed associations, whereas mindfulness (measured as nonreactively observing internal experiences) was associated with higher symptoms. CONCLUSIONS:Findings suggest enhancing interpersonal resiliency, above and beyond regulatory strengths, may be crucial in the aftermath of acute trauma, with emotional support and supportive networks as especially strong potential buffers against posttraumatic psychopathology. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Residential segregation is associated with differential exposure to air pollution. Hippocampus structure and function are highly susceptible to pollutants and associated with posttraumatic stress disorder (PTSD) development. Therefore, we investigated associations between residential segregation, air pollutants, hippocampal neurobiology, and PTSD in recent trauma survivors. Participants (N = 278; 34% non-Hispanic white, 46% Non-Hispanic Black, 16% Hispanic) completed multimodal neuroimaging two weeks after trauma. Yearly averages of air pollutants (PM2.5 and NO2) and racial/economic segregation (Index of Concentration at the Extremes) were derived from each participant's address. Linear models assessed if air pollutants mediated associations between segregation and hippocampal volume, threat reactivity, or parahippocampal cingulum fractional anisotropy (FA) after covarying for age, sex, income, and 2-week PTSD symptoms. Further models evaluated if pollutants or segregation prospectively predicted PTSD symptoms six months post-trauma. We found that non-Hispanic Black participants lived in neighborhoods with significantly greater segregation and air pollution compared to Hispanic and non-Hispanic white participants (ps < 0.001). PM2.5 concentration was positively correlated with threat reactivity (r(276) = 0.16, p < 0.006), while NO2 concentration was positively correlated with hippocampus volume (r(276) = 0.17, p < 0.005) and negatively correlated with white matter tract FA (r(276) = -0.18, p < 0.003). There was a significant indirect effect of NO2 between segregation and FA values (β = 0.08, 95% CI[0.01, 0.15]), and an indirect effect of PM2.5 between segregation and threat reactivity (β = -0.08, 95% CI[-0.14, -0.01]). There was no direct effect of segregation on hippocampal features. Pollutants and segregation were not associated with PTSD symptoms. In conclusion, residential segregation is associated with greater air pollution exposure, which is in turn associated with variability in hippocampal features among recent trauma survivors. Further research is needed to assess relationships between other environmental factors and trauma and stress-related disorders.

Background:While social impairment is a hallmark of increasing severity of post-traumatic stress disorder (PTSD), the dynamics between social support and trauma recovery are less clear. Current theories suggest either social support is responsible for reducing PTSD severity (social causation), or worsening PTSD ultimately degrades supportive networks (social erosion). Furthermore, there is a paucity of research on social support and longitudinal trauma recovery within the civilian population. We hypothesized a bidirectional relationship exists between social support and PTSD, such that both social causation and erosion impact the trajectory of recovery at different times post-trauma. Methods:A total of n = 2943 participants were recruited following a traumatic event leading to Emergency Department visit in the AURORA study, reported perceived emotional support (PROMIS) and severity of PTSD symptoms (PCL-5) at 2 weeks, 8 weeks, 3 months, 6 months, and 12 months post trauma. PTSD symptom severity overall and within symptom criteria (B-E) were assessed. Results:A 5-wave cross-lagged panel model showed a statistically significant negative association between emotional support and subsequent PTSD symptoms across the majority of timepoints in the year following trauma. Concurrently, we observed a negative association between PTSD severity and subsequent perceived emotional support. Additional analyses showed emotional support was mainly correlated with subsequent negative mood and feelings, whereas avoidant behavior was most correlated with lower emotional support. Conclusion:Our analyses emphasize the importance of initiating social interventions and establishing robust social networks immediately after a traumatic event.

Social cognition is an important mechanism linking trauma to psychopathology; however, current models fail to explain individual differences in social cognition after trauma exposure. We investigated whether the interpersonal nature of trauma exposure helps to explain variability in social cognitive outcomes. Our sample was derived from the AURORA study, a national initiative involving intensive follow-up of trauma survivors for one year. We analyzed data from 2241 participants (Mage = 35.12, 64% female, 54% Black) who experienced an assault (n = 262) or a motor vehicle collision (n = 1979). Social cognition was assessed with the Multiracial Emotion Identification Task and the Belmont Emotion Sensitivity Test. Overall emotion identification accuracy declined over time among participants who experienced interpersonal trauma (β = -.10, p = .03), but not non-interpersonal trauma (β = .00, p = .83). These results may help to enhance the prediction of psychopathological outcomes following trauma exposure.

Childhood adversity is associated with susceptibility to posttraumatic stress disorder (PTSD) in adulthood. Both PTSD and adverse experiences in childhood are linked to disrupted white matter microstructure, yet the role of white matter as a potential neural mechanism connecting childhood adversity to PTSD remains unclear. The present study investigated the potential moderating role of previous childhood adversity on longitudinal changes in white matter microstructures and posttraumatic stress symptoms following a recent traumatic event in adulthood. As part of the AURORA Study, 114 recent trauma survivors completed diffusion weighted imaging at 2-weeks and 6-months after exposure. Participants reported on prior childhood adversity and PTSD symptoms at 2-weeks, 6-months, and 12-months post-trauma. We performed both region-of-interest (ROI) and whole-brain correlational tractography analyses to index associations between white matter microstructure changes and prior adversity. Whole-brain correlational tractography revealed that greater childhood adversity moderated the changes in quantitative anisotropy (QA) over time across threat and visual processing tracts including the cingulum bundle and inferior fronto-occipital fasciculus (IFOF). Further, QA changes within cingulum bundle, IFOF, and inferior longitudinal fasciculus were associated with changes in PTSD symptoms between 2-weeks and 6-months. Our findings suggest temporal variability in threat and visual white matter tracts may be a potential neural pathway through which childhood adversity confers risk to PTSD symptoms after adulthood trauma. Future studies should take the temporal properties of white matter into consideration to better understand the neurobiology of childhood adversity and PTSD.

PTSD is more prevalent in women than men and associated with autonomic dysfunction. Higher oestradiol levels have been associated with decreased PTSD severity, however, the impact of oestradiol on autonomic function is not well characterised. We examined associations among peritraumatic oestradiol levels and autonomic function in the multi-site AURORA study. Participants (n = 283, 69.6% female) were recruited from the emergency department (ED) following trauma exposure. Skin conductance (SC) was measured during trauma recall at the ED. Oestradiol was assayed from blood collected at ED, 2-week and 6-month. Fear conditioning, including fear potentiated startle (FPS), was completed at 2-week and 6-month. In women, ED oestradiol was significantly positively associated with ED SC and FPS at 6-month. In men, significant negative correlations between ED oestradiol and SC were found. Among women in the study, peritraumatic oestradiol was positively associated with fear responding 6-month. Findings suggest that the protective effects of oestradiol on PTSD may depend on other factors, such as time since trauma. Additional research is needed to elucidate how peritraumatic oestradiol and autonomic function may interact to confer risk for PTSD.

Traumatic stress exposures (TSEs) are common in life. Although most individuals recover after a TSE, a substantial subset develop adverse post-traumatic neuropsychiatric sequelae such as chronic post-traumatic musculoskeletal pain (CPMP). Vulnerability factors for CPMP are poorly understood, which hinders identification of high-risk individuals for targeted interventions. One known vulnerability factor for many pain types is exposure to early life adversity (ELA), but few studies have assessed whether ELA increases risk for CPMP. This study used data from the Advancing Understanding of RecOvery afteR traumA study, a prospective human cohort study of TSE survivors, to test the hypothesis that ELA increases risk for CPMP. In addition, in secondary analyses, we assessed which subtypes of ELA (including childhood bullying) were most predictive of CPMP and whether a rat ELA model consisting of neonatal limited bedding, combined with single prolonged stress (SPS) in adulthood, would accurately model human findings. In Advancing Understanding of RecOvery afteR traumA study participants (n = 2480), using multinomial logistic regression modeling of 4 identified latent pain classes, we found that ELA increased vulnerability to the high unremitting pain class (odds ratio [OR] = 1.047, P < 0.001), the moderate pain class (OR = 1.031, P < 0.001), and the moderate recovery pain class (OR = 1.018, P = 0.004), with physical abuse, emotional abuse, and bullying being the strongest predictors of high pain class assignment. Similarly, in male and female Sprague Dawley rats, in comparison with SPS alone, neonatal limited bedding combined with SPS caused increased baseline sensitivity and prolonged mechanical hypersensitivity (F(11,197) = 3.22, P < 0.001). Further studies in animals and humans are needed to understand mechanisms by which ELA confers vulnerability to CPMP.

Despite extensive of research on sex differences in posttraumatic stress disorder (PTSD), underlying mechanisms are still not fully understood. Here we present a systematic overview of three sex-related risk pathways. We assessed 16 risk factors as well as 3-month PTSD severity in a prospective cohort (n=2924) of acutely traumatized individuals and investigated potential mediators in the pathway between sex and PTSD severity using multiple mediation analysis with regularization. Six risk factors were more prevalent/severe in women, and none was more pronounced in men. Analyses showed that acute stress disorder, neuroticism, lifetime sexual assault exposure, anxiety sensitivity, and pre-trauma anxiety symptoms fully mediated and uniquely contributed to the relationship between sex and PTSD severity. Our results demonstrate different risk mechanisms for women and men. Such knowledge can inform targeted interventions. Our systematic approach to differential risk pathways can be transferred to other mental disorders to guide sex-sensitive mental health research.

Tobacco smoking and drinking alcohol are common substance use behaviors influenced by both genetic risk and environmental exposures. Traumatic events are highly prevalent, affecting about 70% of people in their lifetime. After trauma, it is unclear what role post-traumatic stress disorder (PTSD) symptoms play in substance use behaviors when accounting for this genetic risk. We used data from the Advancing Understanding of RecOvery afteR traumA (AURORA), which included 2973 participants recruited at emergency departments (EDs) within 72 h of a traumatic event and followed over time. We measured PTSD symptoms via PTSD Checklist for the DSM-5. Tobacco and alcohol consumption as frequency, quantity, and quantity-frequency in the past 30 days. We generated polygenic risk scores with continuous shrinkage for cross-ancestry estimation (PRS-CSx). We tested for main effects between PRS-CSx scores and interactions with PTSD using quasipoisson regression, with week 8 PTSD symptoms and month 6 substance use behaviors after the traumatic event. Tobacco PRS-CSx score increased the risk of tobacco use by 14% (95% CI: 1.01, 1.29, p = 0.03), and alcohol PRS-CSx score did not demonstrate consistent associations in the whole cohort (IRR: 1.08, 95% CI: 0.97, 1.19, p = 0.16). When stratified by ancestry group, both tobacco (IRR: 1.36, 95% CI: 1.14, 1.61, p < 0.001) and alcohol (IRR: 1.24, 95% CI: 1.07, 1.44, p = 0.005) PRS-CSx scores were associated with their respective outcomes in the European ancestry subcohort. Participants with lower genetic risk had stronger associations between re-experiencing symptoms and tobacco use, while participants with higher genetic risk demonstrated weaker association between re-experiencing symptoms and tobacco use. A similar pattern was observed for negative alterations in cognition/mood (NACM) symptoms—participants with lower PRS-CSx scores had stronger associations between NACM symptoms with tobacco use, compared to participants with higher PRS-CSx scores. These interactions were both statistically significant, suggesting an antagonistic effect between PRS-CSx scores and PTSD symptoms on tobacco use.

Post-traumatic stress (PTS) symptoms are highly comorbid with substance use (i.e., alcohol, tobacco, and cannabis). Few studies have investigated potential individual-, household-, and neighborhood-level socioeconomic effect modifiers of this comorbidity in longitudinal analyses. We aim to examine interactions between this multi-level environment and PTS symptoms on future substance use behaviors. Data were drawn from the Advancing Understanding of RecOvery afteR traumA (AURORA) study, including 2943 individuals who presented to the emergency department (ED) within 72 h of a traumatic event. Frequency of tobacco, alcohol, cannabis use, and PTS symptoms were reported at 6 timepoints. Mixed effect Poisson models, clustered by state, were used to generate incidence rate ratios (IRRs) substance use, both cross-sectionally and prospectively. Moderation analysis of PTS and substance use, stratified by household income and area deprivation index (ADI), was conducted using mixed effect models and parallel process growth curves. Significant associations were observed between PTS with tobacco, alcohol, and cannabis use frequency cross-sectionally, and for tobacco and alcohol and PTS exposure prospectively. Lower income (P < 0.001) and higher deprivation (P < 0.001) were associated with tobacco use, while higher income (P < 0.001) and less deprivation (P = 0.01) were associated with increased alcohol use. We found modest modification by household income for alcohol and tobacco, and little evidence of modification by neighborhood ADI. Household income had greater evidence of effect modification for substance use, compared to neighborhood-level ADI. Our findings demonstrate that household indicators of socioeconomic status likely modify the relationship between PTS and substance use.

This study examines the association between brain dynamic functional network connectivity (dFNC) and current/future posttraumatic stress (PTS) symptom severity, and the impact of sex on this relationship. By analyzing 275 participants' dFNC data obtained ~2 weeks after trauma exposure, we noted that brain dynamics of an inter-network brain state link negatively with current (r=-0.179, p corrected = 0.021) and future (r=-0.166, p corrected = 0.029) PTS symptom severity. Also, dynamics of an intra-network brain state correlated with future symptom intensity (r = 0.192, p corrected = 0.021). We additionally observed that the association between the network dynamics of the inter-network brain state with symptom severity is more pronounced in females (r=-0.244, p corrected = 0.014). Our findings highlight a potential link between brain network dynamics in the aftermath of trauma with current and future PTSD outcomes, with a stronger protective effect of inter-network brain states against symptom severity in females, underscoring the importance of sex differences.

BACKGROUND:Childhood adversity is associated with susceptibility to posttraumatic stress disorder (PTSD) in adulthood. PTSD and childhood adversity are linked to white matter microstructure, yet the role of white matter as a potential neural mechanism connecting childhood adversity to PTSD remains unclear. In the current study, we investigated the potential moderating role of previous childhood adversity on longitudinal changes in white matter microstructure and posttraumatic stress symptoms following a recent traumatic event in adulthood. METHODS:As part of the AURORA (Advancing Understanding of RecOvery afteR traumA) study, 114 recent trauma survivors completed diffusion-weighted imaging at 2 weeks and 6 months after exposure. Participants reported on prior childhood adversity and PTSD symptoms at 2 weeks, 6 months, and 12 months posttrauma. We performed region of interest (ROI) analysis using fractional anisotropy (FA) and whole-brain correlational tractography using quantitative anisotropy (QA) to index associations between white matter microstructure changes and prior adversity. RESULTS:ROI-based analyses did not identify significant associations between childhood adversity and changes in FA. Whole-brain correlational tractography revealed that greater childhood adversity moderated the QA changes within threat and visual processing tracts including the cingulum bundle and inferior fronto-occipital fasciculus (IFOF). QA changes within the cingulum bundle and IFOF were associated with changes in PTSD symptoms between 2 weeks and 6 months. CONCLUSIONS:Our findings suggest that temporal variability in threat and visual white matter tracts may be a potential neural pathway through which childhood adversity confers risk for PTSD symptoms after adulthood trauma. Future studies should take the temporal properties of white matter into consideration to better understand the neurobiology of childhood adversity and PTSD.

Background and aims Insomnia symptoms are a potential risk factor for alcohol and cannabis use, particularly in trauma-exposed populations. The initial weeks and months after trauma are a period of risk for problematic substance use, however prior research has not examined whether insomnia symptoms predict alcohol or cannabis use after trauma. Design Using a large-scale, multi-site, prospective study of trauma survivors presenting to emergency departments (EDs), the current study tested direct and indirect associations between pre-trauma insomnia symptoms, two-week posttraumatic stress disorder (PTSD) symptoms, and eight-week post-trauma heavy alcohol and cannabis use and binge drinking. Setting Participants were recruited from 23 EDs in the United States and followed up using remote assessments. Participants/cases Participants were from the AURORA study (n = 2449). A slight majority were women (63.8 %) and were an average of 37 years old. Participants were racially and ethnically diverse (50.5 % Black, 11.2 % Hispanic). Measurements Participants completed self-report measures during their ED visit, and two- and eight-weeks post-trauma. Findings Pre-trauma insomnia symptoms significantly predicted eight-week post-trauma heavy alcohol and cannabis use, as well as binge drinking. Associations persisted after covarying for pre-trauma substance use, demographic variables, and trauma severity at the time of emergency care. Further, the association between pre-trauma insomnia symptoms and heavy alcohol and cannabis use at eight-weeks post-trauma was significantly mediated by two-week PTSD symptoms. Conclusions Insomnia symptoms may be an important malleable risk factor for heavy alcohol and cannabis use and binge drinking after trauma. Further research is needed to explore the effectiveness of insomnia interventions to mitigate post-trauma substance use and to better understand the complex relationships between sleep, trauma, PTSD, and substance use.

Language features may reflect underlying cognitive and emotional processes following a traumatic event that portend clinical outcomes. The authors sought to determine whether language features from usual smartphone use were markers associated with concurrent posttraumatic symptoms and worsening or improving posttraumatic symptoms over time following a traumatic exposure. This investigation was a secondary analysis of the Advancing Understanding of RecOvery afteR traumA study, a longitudinal study of traumatic outcomes among survivors recruited from 33 emergency departments across the United States. Adverse posttraumatic sequelae were assessed over the six months following the initial traumatic exposure. Language features were extracted from usual smartphone use in a specialized app. Bivariate linear mixed models were used to identify and validate language features that are markers associated with posttraumatic symptoms. Participants were 1744 trauma survivors, with a mean age of 39 [SD = 13] years old, and 56% were female. Fourteen language features were associated with severity level of posttraumatic symptoms at specific timepoints (cross-sectional markers) and five features were associated with change in severity level of posttraumatic symptoms (longitudinal markers). References to the body and health or illness were predictive of worsening pain, somatic, and thinking/concentration/fatigue symptom severity over time. An increase in references to others was associated with improvement in somatic symptom severity over time and increases in expressions of causation or cognitive processes were associated with improvement in pain symptom severity over time. Language features derived from usual smartphone use can convey important information about health, functioning, and recovery following a traumatic event. Clinicians might utilize such information to determine who may experience a high symptom burden or risk of worsening posttraumatic symptoms.