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.

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.

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.

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.

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.

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.

A Systematic Review of the Self-Medication Hypothesis in the Context of Posttraumatic Stress Disorder and Comorbid Problematic Alcohol Use.

Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) commonly co-occur and are associated with many negative public health outcomes. There are several etiological models that explain the overlap between PTSD and AUD, including shared genetic risk and phenotypic causality, but the predominant model of etiologic association is the drinking-to-cope self-medication model. Although the self-medication model is conceptually appealing and has been widely accepted within the literature examining alcohol use and anxiety (e.g., PTSD) phenotypes, the findings are inconsistent and there is a lack of rigorous empirical evidence in support of this model. This review, which was, to our knowledge, the first systematic review of the self-medication model in relation to PTSD to date, aimed to synthesize the current literature on the association between PTSD and problematic alcohol use within the context of the self-medication model. In total, 24 studies met the inclusion criteria for the review and assessed the self-medication hypothesis using a variety of measurement instruments and data analytic approaches, such as mediation, moderation, and regression. Overall, the included studies provide evidence for the self-medication hypothesis but are limited in rigor due to methodological limitations. These limitations, which include issues with the operationalization (or lack thereof) of trauma-related drinking to cope, are discussed, and directions for future research are presented.

Examination of a novel measure of trauma-related drinking to cope.

OBJECTIVES: The present study sought to fill a gap in the current literature by developing a concise self-report questionnaire assessing drinking motives specific to coping with symptoms of posttraumatic stress disorder (PTSD). This new four-item questionnaire is called the Trauma Related Drinking questionnaire (TRD). METHOD: Using structural equation modeling, the latent structure of the TRD items and how they relate to other variables of interest were explored among a sample of 1,896 college undergraduates from a large public university. RESULTS: Broadly, we found evidence to suggest that TRD is a more specific measure of drinking to cope motives compared to the commonly used Drinking Motives Questionnaire coping subscale. Additionally, findings demonstrate support for the external validation of TRD, both with regard to PTSD and alcohol consumption and related problems. CONCLUSIONS: Results support the use of TRD in future self-medication research and as a clinically useful screening tool.

Replication of the Interaction of PRKG1 and Trauma Exposure on Alcohol Misuse in an Independent African American Sample.

In the present study, we sought to replicate recent findings of Polimanti et al. (2017), who conducted a genome-wide gene-by-environment interaction study (GEWIS) and identified a gene-by-trauma interaction that predicts alcohol misuse among African Americans.  Consistent with the findings published by Polimanti and colleagues, results of the current study demonstrated an interaction effect, b = 0.41, of trauma exposure and rs1729578 in the intron of PRKG1 on alcohol misuse in a subsample of ancestral African Americans. The minor allele (rs1729578*C) was positively associated with increased alcohol use disorder symptoms in trauma-exposed subjects and negatively associated in non-trauma-exposed subjects.  This effect, however, was only significant for one out of three alcohol outcome measures we investigated, suggesting the interaction may be most salient when predicting higher severity of alcohol misuse. Additionally, the effect did not remain significant after we accounted for testing the effect on three different outcome variables. Also in line with the original study, the gene-by-environment effect was not demonstrated among the ancestral European subsample.  The findings suggest this gene variant may increase an individual's susceptibility to environmental influences, both adverse and supportive.

Associations Between Personality and Distress Tolerance Among Trauma-Exposed Young Adults.

Low distress tolerance (DT) is related to negative mental health outcomes, particularly among trauma-exposed populations, who are at greater risk for mental health problems. However, little is known about potential etiological factors underlying the development of perceived (i.e., self-report) or behaviorally assessed DT. The present study examined associations between Big Five personality factors (i.e., openness, conscientiousness, extraversion, agreeableness, & neuroticism) and multiple measures of DT. Participants were 440 college students (71.4% women) endorsing a history of one or more potentially traumatic events. Participants completed the abbreviated Big Five Inventory (BFI), Distress Tolerance Scale (DTS), Discomfort Intolerance Scale (DIS), breath-holding task, and Paced Auditory Serial Addition Test (PASAT). Results of a series of hierarchical linear regressions indicated that higher levels of neuroticism and lower levels of conscientiousness were significantly associated with lower DTS scores, but no other DT measures. Greater extraversion was significantly associated with greater DT on the DIS and the PASAT. Lower levels of openness were associated with lower DT on the breath-holding task. Individual differences in normal personality traits account for significant variation in multiple measures of DT and may provide insight into the etiology of various forms of DT.

An examination of the etiologic overlap between the genetic and environmental influences on insomnia and common psychopathology.

BACKGROUND: Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders. METHODS: We utilized twin data from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (total n = 7,500). Insomnia, internalizing disorders (major depressive disorder [MDD], generalized anxiety disorder [GAD]), and alcohol abuse or dependence (AAD) were assessed at two time points, while antisocial personality disorder (ASPD) was assessed once. Cholesky decompositions were performed in OpenMx and longitudinal measurement models were run on available phenotypes to reduce measurement error. RESULTS: The latent additive genetic influences on insomnia overlapped significantly (56% for females, 74% for males) with MDD and were shared completely (100%) with GAD. There was significant overlap of latent unique environmental influences, with overlap ranging from 38 to 100% across disorders. In contrast, there was less genetic overlap between insomnia and externalizing disorders, with 18% of insomnia's heritability shared with AAD and 23% with ASPD. Latent unique environmental overlap between insomnia and both externalizing disorders was negligible. CONCLUSIONS: The evidence for substantial genetic overlap between insomnia and stable aspects of both internalizing disorders suggests that there may be few insomnia-specific genes and investigation into unique environmental factors is important for understanding insomnia development. The modest overlap between insomnia and externalizing disorders indicates that these disorders are genetically related, but largely etiologically distinct.

Temporal relations between alcohol use, posttraumatic stress disorder, and internalizing symptoms during the COVID-19 pandemic: An ecological momentary assessment investigation.

OBJECTIVE: COVID-19 is a collective stressor associated with both increased mental health symptoms and increased frequency of alcohol use. These increases highlight the need for investigations into the functional relationships between traumatic stress symptoms and alcohol use in the wake of the pandemic. This study sought to use ecological momentary assessment to examine the temporal association of posttraumatic stress disorder (PTSD) with alcohol use during the COVID-19 pandemic. METHOD: Participants were 21 students (Mage = 21.0; 86% female, 23.9% White) from a large, mid-Atlantic public university. Ecological momentary assessment data on PTSD symptoms, internalizing psychopathology, affect, and alcohol consumption were collected via twice daily surveys for a 14-day period. RESULTS: Increased negative affect predicted an increase in alcohol consumption at the next assessment. Increased alcohol consumption predicted increased subsequent negative affect, anxiety symptoms, and depressive symptoms. Findings did not support a relationship between PTSD symptoms and alcohol consumption in either direction. CONCLUSIONS: Results suggest a bidirectional, cyclical relationship between alcohol consumption and internalizing psychopathology broadly, rather than PTSD specifically, during the pandemic. Interventions for alcohol consumption on college campuses may benefit from targeting internalizing symptoms, such as through facilitating the development of adaptive coping strategies. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

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.

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.

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.

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.

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).

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.

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.