Alcohol consumption and dependence risk among male and female Veterans: Trajectories and predictors.

BACKGROUND: With few exceptions, previously conducted research on hazardous drinking among Veterans has employed samples in which the majority of participants identify as male. In addition, past studies have solely focused on alcohol consumption, rather than associated risk for dependence. In this study, we expanded upon the extant literature by investigating sex differences in trajectories and predictors of change in alcohol consumption and dependence risk among post-9/11 Veterans. METHODS: A national sample of 1649 Veterans (50.0% female) were recruited in a five-wave longitudinal study that followed Veterans for up to 16 years after deployment. We used growth curve modeling to investigate trajectories of change in alcohol consumption and dependence risk among men and women Veterans. We examined predictors of growth, including demographics, support and resources, psychiatric symptoms, and trauma exposure. RESULTS: Among male Veterans, alcohol consumption and dependence risk remained stagnant, which is in contrast to past work using non-Veteran samples. For female Veterans, consumption exhibited initial reductions that decelerated, and dependence risk reduced at a continuous rate. PTSD diagnosis was a significant predictor of individual differences in growth for men. Psychiatric symptoms (i.e., PTSD diagnosis, probable depression diagnosis, suicidal ideation) and psychosocial functioning were significant predictors of decreasing alcohol use for women. CONCLUSIONS: Results highlight important sex differences in patterns and predictors of change in alcohol consumption and dependence risk among post-9/11 Veterans. Findings are discussed in relation to screening for hazardous alcohol use and intervention strategies in this at-risk population.

An EWAS of dementia biomarkers and their associations with age, African ancestry, and PTSD.

BACKGROUND: Large-scale cohort and epidemiological studies suggest that PTSD confers risk for dementia in later life but the biological mechanisms underlying this association remain unknown. This study examined this question by assessing the influences of PTSD, APOE ε4 genotypes, DNA methylation, and other variables on the age- and dementia-associated biomarkers Aß40, Aß42, GFAP, NfL, and pTau-181 measured in plasma. Our primary hypothesis was that PTSD would be associated with elevated levels of these markers. METHODS: Analyses were based on data from a PTSD-enriched cohort of 849 individuals. We began by performing factor analyses of the biomarkers, the results of which identified a two-factor solution. Drawing from the ATN research framework, we termed the first factor, defined by Aß40 and Aß42, "Factor A" and the second factor, defined by GFAP, NfL and pTau-181, "Factor TN." Next, we performed epigenome-wide association analyses (EWAS) of the two-factor scores. Finally, using structural equation modeling (SEM), we evaluated (a) the influence of PTSD, age, APOE ε4 genotype and other covariates on levels of the ATN factors, and (b) tested the mediating influence of the EWAS-significant DNAm loci on these associations. RESULTS: The Factor A EWAS identified one significant locus, cg13053408, in FANCD2OS. The Factor TN analysis identified 3 EWAS-significant associations: cg26033520 near ASCC1, cg23156469 in FAM20B, and cg15356923 in FAM19A4. The SEM showed age to be related to both factors, more so with Factor TN (ß = 0.581, p < 0.001) than Factor A (ß = 0.330, p < 0.001). Genotype-determined African ancestry was associated with lower Factor A (ß = 0.196, p < 0.001). Contrary to our primary hypothesis, we found a modest negative bivariate correlation between PTSD and the TN factor scores (r = - 0.133, p < 0.001) attributable primarily to reduced levels of GFAP (r = - 0.128, p < 0.001). CONCLUSIONS: This study identified novel epigenetic associations with ATN biomarkers and demonstrated robust age and ancestral associations that will be essential to consider in future efforts to develop the clinical applications of these tests. The association between PTSD and reduced GFAP, which has been reported previously, warrants further investigation.

Trauma exposure and transdiagnostic distress: Examining shared and posttraumatic stress disorder-specific associations.

We examined transdiagnostic and posttraumatic stress disorder (PTSD)-specific associations with multiple forms of trauma exposure within a nationwide U.S. sample (N = 1,649, 50.0% female) of military veterans overselected for PTSD. A higher-order Distress factor was estimated using PTSD, major depressive disorder (MDD), and generalized anxiety disorder (GAD) symptoms as indicators. A structural equation model spanning three assessment points over an average of 3.85 years was constructed to examine the unique roles of higher-order Distress and PTSD-specific variance in accounting for the associations between trauma exposure, measured using the Life Events Checklist (LEC) and Deployment Risk and Resiliency Inventory Combat subscale (DRRI-C), and psychosocial impairment. The results suggest the association between trauma exposure and PTSD symptoms was primarily mediated by higher-order distress (70.7% of LEC effect, 63.2% of DRRI-C effect), but PTSD severity retained a significant association with trauma exposure independent of distress, LEC: ß = .10, 95% CI [.06, .13]; DRRI-C: ß = .11, 95% CI [.07, .14]. Both higher-order distress, ß = .31, and PTSD-specific variance, ß = .36, were necessary to account for the association between trauma exposure and future impairment. Findings suggest that trauma exposure may contribute to comorbidity across a range of internalizing symptoms as well as to PTSD-specific presentations.

MMPI-2-RF Profiles of Treatment-Seeking Veterans in a VA Pain Clinic and Associations with Markers of Physical Performance.

Chronic pain is a debilitating condition for many military Veterans and is associated with posttraumatic stress disorder (PTSD). This study examined the Minnesota Multiphasic Personality Inventory-2-Restructured Form (MMPI-2-RF) in 144 Veterans (88.2% male, mean age = 57.95 years) recruited from a VA outpatient pain clinic and associations with self-reported pain severity, pain-related interference in daily activities, prescription opioid use, and objective metrics of physical performance on tasks impacted by pain (walking, stair climbing, grip strength, indexed by a single latent variable). Among the cohort with valid responses on the MMPI-2-RF (n = 117) and probable PTSD, mean Somatic Complaints (RC1) and Ideas of Persecution (RC6) scores were clinically elevated. All MMPI-2-RF scales were more strongly correlated with self-reported pain interference than severity. Regressions revealed associations between self-rated pain interference (but not pain or PTSD severity) and physical performance scores (ß = .36, p = .001). MMPI-2-RF overreporting Validity and Higher-Order scales contributed incremental variance in predicting physical performance, including Infrequent Psychopathology Responses (ß = .33, p = .002). PTSD severity was associated with prescription opioid use when accounting for the effects of over-reported somatic and cognitive symptoms (odds ratio 1.05, p ≤ .025). Results highlight the role of symptom overreporting and perceptions of functional impairment to observable behaviors among individuals with chronic pain.

Longitudinal study of traumatic-stress related cellular and cognitive aging.

Traumatic stress is associated with both accelerated epigenetic age and increased risk for dementia. Accelerated epigenetic age might link symptoms of traumatic stress to dementia-associated biomarkers, such as amyloid-beta (Aß) proteins, neurofilament light (NFL), and inflammatory molecules. We tested this hypothesis using longitudinal data obtained from 214 trauma-exposed military veterans (85 % male, mean age at baseline: 53 years, 75 % White) who were assessed twice over the course of an average of 5.6 years. Cross-lagged panel mediation models evaluated measures of lifetime posttraumatic stress disorder and internalizing and externalizing comorbidity (assessed at Time 1; T1) in association with T1 epigenetic age (per the GrimAge algorithm) and T1 plasma markers of neuropathology along with bidirectional temporal paths between T1 and T2 epigenetic age and the plasma markers. Results revealed that a measure of externalizing comorbidity was associated with accelerated epigenetic age (ß = 0.30, p <.01), which in turn, was associated with subsequent increases in Aß-40 (ß = 0.20, p <.001), Aß-42 (ß = 0.18, p <.001), and interleukin-6 (ß = 0.18, p <.01). T1 advanced epigenetic age and the T1 neuropathology biomarkers NFL and glial fibrillary acidic protein predicted worse performance on T2 neurocognitive tasks assessing working memory, executive/attentional control, and/or verbal memory (ps = 0.03 to 0.009). Results suggest that advanced GrimAge is predictive of subsequent increases in neuropathology and inflammatory biomarkers as well as worse cognitive function, highlighting the clinical significance of this biomarker with respect to cognitive aging and brain health over time. The finding that advanced GrimAge mediated the association between psychiatric comorbidity and future neuropathology is important for understanding potential pathways to neurodegeneration and early identification of those at greatest risk.

PTSD and Alcohol Use Disorders Predict the Pace of Cellular Aging.

Advanced epigenetic age is associated with psychopathology and may help to explain the link between psychopathology and physical health morbidity and mortality. Using a longitudinal sample of 171 trauma-exposed Veterans, we modeled the rate of change in epigenetic age across two time points (averaging 5.58 years apart) using two epigenetic age algorithms (GrimAge and Horvath) and tested associations with posttraumatic stress disorder (PTSD), alcohol use disorder (AUD), and depression. Results showed that PTSD (ß = .199) and AUD (ß = .186) were associated with a quickened pace of epigenetic aging over time (ps < .021). Results replicate and extend prior work and offer foundational support for identifying interventions that slow the pace of biological aging among those with psychopathology.

Genetic associations between alcohol phenotypes and life satisfaction: a genomic structural equation modelling approach.

Alcohol use (i.e., quantity, frequency) and alcohol use disorder (AUD) are common, associated with adverse outcomes, and genetically-influenced. Genome-wide association studies (GWAS) identified genetic loci associated with both. AUD is positively genetically associated with psychopathology, while alcohol use (e.g., drinks per week) is negatively associated or NS related to psychopathology. We wanted to test if these genetic associations extended to life satisfaction, as there is an interest in understanding the associations between psychopathology-related traits and constructs that are not just the absence of psychopathology, but positive outcomes (e.g., well-being variables). Thus, we used Genomic Structural Equation Modeling (gSEM) to analyze summary-level genomic data (i.e., effects of genetic variants on constructs of interest) from large-scale GWAS of European ancestry individuals. Results suggest that the best-fitting model is a Bifactor Model, in which unique alcohol use, unique AUD, and common alcohol factors are extracted. The genetic correlation (rg) between life satisfaction-AUD specific factor was near zero, the rg with the alcohol use specific factor was positive and significant, and the rg with the common alcohol factor was negative and significant. Findings indicate that life satisfaction shares genetic etiology with typical alcohol use and life dissatisfaction shares genetic etiology with heavy alcohol use.

Neurobiological and genetic correlates of the dissociative subtype of posttraumatic stress disorder.

Approximately 10%-30% of individuals with posttraumatic stress disorder (PTSD) exhibit a dissociative subtype of the condition defined by symptoms of depersonalization and derealization. This study examined the psychometric evidence for the dissociative subtype of PTSD in a sample of young, primarily male post-9/11-era Veterans (n = 374 at baseline and n = 163 at follow-up) and evaluated its biological correlates with respect to resting state functional connectivity (default mode network [DMN]; n = 275), brain morphology (hippocampal subfield volume and cortical thickness; n = 280), neurocognitive functioning (n = 337), and genetic variation (n = 193). Multivariate analyses of PTSD and dissociation items suggested a class structure was superior to dimensional and hybrid ones, with 7.5% of the sample comprising the dissociative class; this group showed stability over 1.5 years. Covarying for age, sex, and PTSD severity, linear regression models revealed that derealization/depersonalization severity was associated with: decreased DMN connectivity between bilateral posterior cingulate cortex and right isthmus (p = .015; adjusted-p [padj] = .097); increased bilateral whole hippocampal, hippocampal head, and molecular layer head volume (p = .010-.034; padj = .032-.053); worse self-monitoring (p = .018; padj = .079); and a candidate genetic variant (rs263232) in the adenylyl cyclase 8 gene (p = .026), previously associated with dissociation. Results converged on biological structures and systems implicated in sensory integration, the neural representation of spatial awareness, and stress-related spatial learning and memory, suggesting possible mechanisms underlying the dissociative subtype of PTSD. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

PTSD, major depression, and advanced transcriptomic age in brain tissue.

BACKGROUND: Psychiatric disorders have been associated with advanced epigenetic age in DNA methylation, yet this relationship has not been studied in the brain transcriptome. We examined transcriptomic age using an RNA-based algorithm recently developed by Ren and Kuan ("RNAAgeCalc") and the associations between posttraumatic stress disorder (PTSD), major depressive disorder (MDD), and alcohol use disorder with age-adjusted RNA age ("RNA age residuals") in three brain regions: dorsolateral prefrontal cortex, ventromedial prefrontal cortex (vmPFC), and motor cortex. METHODS: RNA sequencing was used to measure gene expression in postmortem brain tissue from the VA National PTSD Brain Bank (n = 94; 59% male). RESULTS: Linear models revealed that diagnoses of PTSD and/or MDD were positively associated with RNA age residuals in vmPFC only (p-adj = 0.012). Three genes in the RNAAgeCalc algorithm (KCNJ16, HYAL2, and CEBPB) were also differentially expressed in association with PTSD/MDD in vmPFC (p-adj = 6.45E-05 to 0.02). Enrichment analysis revealed that inflammatory and immune-related pathways were overrepresented (p-adj < 0.05) among the 43 genes in RNAAgeCalc that were also at least nominally associated with PTSD/MDD in vmPFC relative to the 448 RNAAgeCalc genes. Endothelial and mural cells were negatively associated with RNA age residuals in vmPFC (both p-adj = 0.028) and with PTSD/MDD (both p-adj = 0.017). CONCLUSIONS: Results highlight the importance of inflammation and immune system dysregulation in the link between psychopathology and accelerated cellular aging and raise the possibility that blood-brain barrier degradation may play an important role in stress-related accelerated brain aging.

For whom the bell tolls: psychopathological and neurobiological correlates of a DNA methylation index of time-to-death.

Psychopathology is a risk factor for accelerated biological aging and early mortality. We examined associations between broad underlying dimensions of psychopathology (reflecting internalizing and externalizing psychiatric symptoms), PTSD, and age-adjusted GrimAge ("GrimAge residuals"), a DNA methylation biomarker of mortality risk relative to age. We also examined neurobiological correlates of GrimAge residuals, including neurocognitive functioning, blood-based biomarkers (of inflammation, neuropathology, metabolic disease), and cortical thickness. Data from two independent trauma-exposed military cohorts (n = 647 [62.9% male, Mage = 52], n = 434 [90% male, Mage = 32]) were evaluated using linear regression models to test associations between GrimAge residuals, psychopathology, and health correlates. Externalizing psychopathology significantly predicted GrimAge residuals in both cohorts (ps < 0.028). PTSD predicted GrimAge residuals in the younger (p = 0.001) but not the older cohort. GrimAge residuals were associated with several neurobiological variables available in the younger cohort, including cognitive disinhibition (padj = 0.021), poorer memory recall (padj = 0.023), cardiometabolic pathology (padj < 0.001), oxidative stress (padj = 0.003), astrocyte damage (padj = 0.021), inflammation (C-reactive protein: padj < 0.001; IL-6: padj < 0.001), and immune functioning (padj < 0.001). A subset of inflammatory and neuropathology analytes were available in the older cohort and showed associations with GrimAge residuals (IL-6: padj < 0.001; TNF-α: padj < 0.001). GrimAge residuals were also associated with reduced cortical thickness in right lateral orbitofrontal cortex (padj = 0.018) and left fusiform gyrus (padj = 0.030), which are related to emotion regulation and facial recognition, respectively. Psychopathology may be a common risk factor for elevated mortality risk. GrimAge could help identify those at risk for adverse health outcomes and allow for early disease identification and treatment.

An in-depth look at latent classes of DSM-5 psychiatric comorbidity among individuals with PTSD: Clinical indicators and treatment utilization.

OBJECTIVE: Posttraumatic stress disorder (PTSD) is associated with high comorbidity rates across the full range of psychiatric disorders. However, little is known about how psychiatric comorbidity manifests among people with PTSD, particularly with regard to concurrent diagnoses. METHOD: Latent class analysis (LCA) was used to characterize discrete classes of PTSD comorbidity using past year DSM-5 diagnostic standards among a large nationally representative epidemiologic sample of U.S. adults. Follow-up analyses compared participant characteristics across latent classes. RESULTS: The LCA was best characterized by five classes: low comorbidity, distress-fear, distress-externalizing, mania-fear-externalizing, and mania-externalizing. Excluding the low comorbidity class, proportions of borderline and schizotypal personality disorder were high across classes. CONCLUSION: Participant characteristics across classes of past year PTSD comorbidity are explored through the lens of case conceptualization and treatment planning utility.

Conceptualizing traumatic stress and the structure of posttraumatic psychopathology through the lenses of RDoC and HiTOP.

Trauma-related psychopathology, most notably posttraumatic stress disorder (PTSD), poses unique challenges for psychiatric nosology due to the wide range of symptoms and diagnoses associated with trauma and challenges representing the impact of trauma exposure on psychopathology. In this paper, we review the literature on categorical (i.e., Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases systems) versus dimensional conceptualizations of trauma-related symptoms with an emphasis on the Research Domain Criteria (RDoC) and the Hierarchical Taxonomy of Psychopathology (HiTOP) frameworks. We identify strengths of each approach and challenges in accommodating the full range of trauma-related psychopathology and the clinical implications thereof. We discuss several potential approaches for improving the representation of traumatic stress, including the use of PTSD subtypes, trauma-related specifiers for psychiatric diagnoses, and the development of a dimension that we call the traumatic stress spectrum, which spans both adaptive and adverse reactions to trauma. These approaches to representing traumatic stress can be evaluated empirically and further refined. We also discuss how the use of an integrated RDoC-HiTOP approach to reconceptualize traumatic stress might maximize the ability to model valid and reliable trauma-related phenotypes, which would aid in the investigation of clinically relevant biological correlates.

Alcohol use and alcohol use disorder differ in their genetic relationships with PTSD: A genomic structural equation modelling approach.

PURPOSE: Posttraumatic Stress Disorder (PTSD) is associated with increased alcohol use and alcohol use disorder (AUD), which are all moderately heritable. Studies suggest the genetic association between PTSD and alcohol use differs from that of PTSD and AUD, but further analysis is needed. BASIC PROCEDURES: We used genomic Structural Equation Modeling (genomicSEM) to analyze summary statistics from large-scale genome-wide association studies (GWAS) of European Ancestry participants to investigate the genetic relationships between PTSD (both diagnosis and re-experiencing symptom severity) and a range of alcohol use and AUD phenotypes. MAIN FINDINGS: When we differentiated genetic factors for alcohol use and AUD we observed improved model fit relative to models with all alcohol-related indicators loading onto a single factor. The genetic correlations (rG) of PTSD were quite discrepant for the alcohol use and AUD factors. This was true when modeled as a three-correlated-factor model (PTSD-AUD rG:.36, p < .001; PTSD-alcohol use rG: -0.17, p < .001) and as a Bifactor model, in which the common and unique portions of alcohol phenotypes were pulled out into an AUD-specific factor (rG with PTSD:.40, p < .001), AU-specific factor (rG with PTSD: -0.57, p < .001), and a common alcohol factor (rG with PTSD:.16, NS). PRINCIPAL CONCLUSIONS: These results indicate the genetic architecture of alcohol use and AUD are differentially associated with PTSD. When the portions of variance unique to alcohol use and AUD are extracted, their genetic associations with PTSD vary substantially, suggesting different genetic architectures of alcohol phenotypes in people with PTSD.

Methylation of the AIM2 gene: An epigenetic mediator of PTSD-related inflammation and neuropathology plasma biomarkers.

BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with inflammation and various forms of chronic disease. The Absent in Melanoma 2 (AIM2) gene has been implicated in mechanisms of inflammation and anxiety, and methylation at a particular locus in this gene (cg10636246) has previously been shown to influence the association between PTSD and elevated C-reactive protein levels in blood. METHOD: We tested if this association might extend to other indicators of inflammation and to plasma-based measures of neuropathology in a cohort of post-9/11 US military veterans. Using a Bayesian approach, mediation models were tested cross-sectionally (n = 478) and longitudinally (n = 298). Peripheral markers of inflammation and neuropathology were measured with ultra-sensitive Single Molecule Array (Simoa®) technology. RESULTS: Analyses revealed indirect effects of PTSD symptom severity on peripheral indices of both inflammation (interleukin [IL]6, IL-10, tumor necrosis factor-α; indirect standardized [std.] ß range = 0.018-0.023, all p-values adjusted for multiple testing [padj ] < 0.05) and neuropathology (neurofilament light [NFL]; indirect std. ß = -0.018, padj = 0.02) via AIM2 methylation. This indirect effect was also evident when predicting IL-10 at a follow-up assessment (indirect std. ß = -0.018, padj = 0.04) controlling for baseline IL-10. CONCLUSIONS: Given that AIM2 methylation mediated the association between PTSD symptoms and multiple inflammatory and neuropathology markers, our results suggest that AIM2 methylation may offer clinical utility for indexing risk for adverse health outcomes associated with these peripheral indices of inflammation and neuropathology. Results also suggest a possible shared etiology underlying the frequent co-occurrence of inflammation and neuropathology.

Does Prior Civilian Trauma Moderate the Relationship Between Combat Trauma and Post-deployment Mental Health Symptoms?

In addition to combat trauma, childhood and adult non-military, interpersonal trauma exposures have been linked to a range of psychiatric symptoms (e.g., alcohol use problems, posttraumatic stress disorder [PTSD], depression symptoms) in veterans. However, few studies simultaneously explore the associations between these civilian and combat trauma types and mental health outcomes. Using a sample of combat-exposed veterans who were previously deployed to Iraq and Afghanistan (N = 302), this study sought to (a) understand the independent associations of civilian interpersonal trauma (i.e., childhood trauma and non-military adult trauma) and combat-related trauma with post-deployment alcohol use, PTSD symptoms, and depressive symptoms, respectively and (b) to examine the interactive effects of trauma type to test whether childhood and non-military adult trauma moderate the association of combat trauma with these outcomes. A path analytic framework was used to allow for the simultaneous prediction of these associations. In the final model non-military adult trauma and combat trauma were found to be significantly associated with PTSD symptoms and depression symptoms, but not average amount of drinks consumed per drinking day. Childhood trauma was not associated with any outcomes (i.e., PTSD symptoms, depression symptoms, average amount of drinks consumed per day). Only combat trauma was significantly associated with average amount of drinks consumed per day. Results underscore the importance of assessing multiple trauma types and considering trauma as a non-specific risk factor, as different trauma types may differentially predict various mental health outcomes other than PTSD. Further, results highlight the noteworthiness of considering co-occurring outcomes within the veteran community. Limitations, future directions, and implications of diversity are discussed.

Diagnostic validity of the PC-PTSD screen in college students.

Objective: The purpose of this study was to test the diagnostic validity of the Primary Care PTSD screen (PC-PTSD) in a generalizable college sample and to examine potential differences in its predictive efficacy according to sex and racial/ethnic identity. An exploratory aim was to determine whether PC-PTSD symptom items differentially predicted PTSD diagnostic status. Participants: Data from 475 undergraduates were analyzed. Methods: Logistic regressions were conducted to examine the relationship between different PC-PTSD endorsement thresholds and probable PTSD among various subsamples. Follow-up tests of diagnostic accuracy were performed. Results: Results of this study indicated that the PC-PTSD identified PTSD among college students with poor accuracy. Furthermore, the PC-PTSD did not demonstrate equal predictive validity across neither sex nor racial/ethnic identity. Endorsement of reexperiencing symptoms appeared to be the strongest predictor of PTSD. Conclusions: Results highlight the clear need for a validated PTSD screener effective for a diverse college population.

The Associations Between Sexual Victimization and Health Outcomes Among LGBQA College Students: Examining the Moderating Role of Social Support.

Prior studies have demonstrated that sexual minority college students are two to four times more likely to experience sexual victimization (e.g., sexual assault and/or unwanted or uncomfortable sexual experiences) compared to their heterosexual counterparts. However, research that has focused on the detrimental effects of sexual victimization on health outcomes has paid more attention to heterosexual college samples and community-based adults. Understanding how sexual victimization influences mental health and substance use outcomes among lesbian, gay, bisexual, queer, and asexual (LGBQA) emerging adults in college is warranted given that this developmental period represents a critical risk period for trauma exposure, risk behavior, and psychological distress. Thus, the current study tested how sexual victimization was associated with depressive symptoms, post-traumatic stress disorder (PTSD) symptoms, and alcohol use disorder (AUD) symptoms among 234 diverse college students who self-identified as LGBQA. Additionally, social support was tested as a moderator. Findings indicated that sexual victimization was related to greater depressive symptoms, PTSD symptoms, and AUD symptoms. In addition, perceived social support moderated the relation between sexual victimization and depressive symptoms, however, in a direction contrary to hypotheses. In particular, higher sexual victimization was associated with greater depressive symptoms among LGBQA students with higher levels of social support (b = .29, p = .00), and was not significant among LGBQA students with lower levels of social support (b = .13, p = .26). The current study highlights the need to consider the detrimental effects of sexual victimization on health outcomes among LGBQA college students, as well as the mechanisms through which social support may be influencing these relations.

Premorbid traumatic stress and veteran responses to the COVID-19 pandemic.

The COVID-19 pandemic has had unprecedented effects on lifestyle stability and physical and mental health. We examined the impact of preexisting posttraumatic stress disorder (PTSD), alcohol use disorder (AUD), and depression on biopsychosocial responses to the pandemic, including psychiatric symptoms, COVID-19 exposure, and housing/financial stability, among 101 U.S. military veterans enrolled in a longitudinal study of PTSD, a population of particular interest given veterans' trauma histories and defense-readiness training. Participants (83.2% male, 79.2% White, Mage  = 59.28 years) completed prepandemic, clinician-administered psychiatric diagnostic interviews and a phone-based assessment between May and September 2020 using a new measure, the Rapid Assessment of COVID-19-Related Experiences (RACE), which was used to assess pandemic responses and its effects on mental and physical health; COVID-19 diagnosis and testing were also extracted from electronic medical records. Multivariate regressions showed that, controlling for demographic characteristics, prepandemic PTSD, ß = .332; p = .003, and AUD symptoms, ß = .228; p = .028, were associated with increased pandemic-related PTSD symptoms. Prepandemic AUD was associated with increased substance use during the pandemic, ß = .391; p < .001, and higher rates of self-reported or medical record-based COVID-19 diagnosis, ß = .264; p = .019. Minority race was associated with pandemic-related housing/financial instability, ß = -.372; p < .001, raising concerns of population inequities. The results suggest that preexisting PTSD and AUD are markers for adverse pandemic-related psychiatric outcomes and COVID-19 illness. These findings carry implications for the importance of targeting prevention and treatment efforts for the highest-risk individuals.

Efficacy and acceptability of interventions for co-occurring PTSD and SUD: A meta-analysis.

Over the past 20 years, numerous treatments addressing comorbid Posttraumatic Stress Disorder (PTSD) and Substance Use Disorder (SUD) have been developed and tested. The current meta-analysis examined the efficacy and acceptability of the two central treatment types- trauma-focused and non-trauma-focused - compared with all comparators and with cognitive-behavioral manualized SUD treatments immediately post-treatment and at longest follow-up. Twenty-eight randomized clinical trials (N = 3247) were included. There were small to large within-group effects for all forms of active treatment (gs = 0.30-1.11). Trauma-focused but not non-trauma-focused treatments outperformed all comparators on PTSD outcomes at post-treatment. Neither trauma-focused nor non-trauma-focused treatment outperformed all comparators on SUD outcomes at post-treatment. Neither trauma- nor non-trauma-focused treatment outperformed manualized SUD treatments on PTSD outcomes at either time point. Manualized SUD treatments outperformed trauma-focused treatments on SUD outcomes at post-treatment and non-trauma-focused treatments on PTSD outcomes at follow-up. Regarding treatment retention, neither trauma-focused nor non-trauma-focused treatments significantly differed from all comparators or from manualized SUD treatments. Between-group results were largely unchanged in trim-and-fill analyses, but were not robust to fail-safe N. Few moderators were detected. Taken together, results suggest that trauma-focused, non-trauma-focused, and manualized SUD interventions are sound options for individuals with comorbid PTSD/SUD.