The Effects of Posttraumatic Stress and Trauma-Focused Disclosure on Experimental Pain Sensitivity Among Trauma-Exposed Women.
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SUBMITTER: Hood CO
PROVIDER: S-EPMC7725999 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPosttraumatic stress disorder (PTSD) is associated with higher risk of incident hypertension, but it is unclear whether specific aspects of PTSD are particularly cardiotoxic. PTSD is a heterogeneous disorder, comprising dimensions of fear and dysphoria. Because elevated fear after trauma may promote autonomic nervous system dysregulation, we hypothesized fear would predict hypertension onset, and associations with hypertension would be stronger with fear than dysphoria.MethodsWe examined fear and dysphoria symptom dimensions in relation to incident hypertension over 24 years in 2709 trauma-exposed women in the Nurses' Health Study II. Posttraumatic fear and dysphoria symptom scores were derived from a PTSD diagnostic interview. We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each symptom dimension (quintiles) with new-onset hypertension events (N = 925), using separate models. We also considered lower-order symptom dimensions of fear and dysphoria.ResultsHigher levels of fear (P-trend = 0.02), but not dysphoria (P-trend = 0.22), symptoms were significantly associated with increased hypertension risk after adjusting for socio-demographics and family history of hypertension. Women in the highest v. lowest fear quintile had a 26% higher rate of developing hypertension [HR = 1.26 (95% CI 1.02-1.57)]; the increased incidence associated with greater fear was similar when further adjusted for biomedical and health behavior covariates (P-trend = 0.04) and dysphoria symptoms (P-trend = 0.04). Lower-order symptom dimension analyses provided preliminary evidence that the re-experiencing and avoidance components of fear were particularly associated with hypertension.ConclusionsFear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.
| S-EPMC6609506 | biostudies-literature
Project description:OBJECTIVE:Inadequate immunoregulation and elevated inflammation may be risk factors for posttraumatic stress disorder (PTSD), and microbial inputs are important determinants of immunoregulation; however, the association between the gut microbiota and PTSD is unknown. This study investigated the gut microbiome in a South African sample of PTSD-affected individuals and trauma-exposed (TE) controls to identify potential differences in microbial diversity or microbial community structure. METHODS:The Clinician-Administered PTSD Scale for DSM-5 was used to diagnose PTSD according to Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria. Microbial DNA was extracted from stool samples obtained from 18 individuals with PTSD and 12 TE control participants. Bacterial 16S ribosomal RNA gene V3/V4 amplicons were generated and sequenced. Microbial community structure, ?-diversity, and ?-diversity were analyzed; random forest analysis was used to identify associations between bacterial taxa and PTSD. RESULTS:There were no differences between PTSD and TE control groups in ?- or ?-diversity measures (e.g., ?-diversity: Shannon index, t = 0.386, p = .70; ?-diversity, on the basis of analysis of similarities: Bray-Curtis test statistic = -0.033, p = .70); however, random forest analysis highlighted three phyla as important to distinguish PTSD status: Actinobacteria, Lentisphaerae, and Verrucomicrobia. Decreased total abundance of these taxa was associated with higher Clinician-Administered PTSD Scale scores (r = -0.387, p = .035). CONCLUSIONS:In this exploratory study, measures of overall microbial diversity were similar among individuals with PTSD and TE controls; however, decreased total abundance of Actinobacteria, Lentisphaerae, and Verrucomicrobia was associated with PTSD status.
| S-EPMC5763914 | biostudies-literature
Project description:BACKGROUND:Genetic polymorphisms that influence serotonin (5-hydroxytryptamine, 5HT) neurotransmission are candidates for contributing to susceptibility to posttraumatic stress disorder (PTSD). The objective of our study was to determine if a variable length polymorphism for the promoter regions of the 5HT transporter (5HTTLPR), and/or a substitution polymorphism in the promoter region for the 5HT2A receptor, would be associated with PTSD in a trauma exposed population of adult African-Americans. METHODS:Using a case control design, 118 participants recruited from the primary care clinics and the campus of a historically black university who met inclusion criteria including trauma exposure provided blood samples for genomic DNA. PTSD criteria were determined by the Clinician Assessment of PTSD Scale (CAPS) and criteria for other psychiatric disorders by the Structured Clinical Interview for DSM-IV (SCID). 5HTTLPR and 5HT2A-1438A/G were genotyped using established methods. Associations of genotypes with lifetime PTSD, and models testing associations of allele "dose", were analyzed. RESULTS:Fifty-five (47%) participants met lifetime criteria for PTSD and 26 (22%) met criteria for (mostly comorbid) major depression. The 5HT2A (lower expressing) G allele was significantly associated with PTSD. We did not find significant associations with 5HTTLPR. CONCLUSIONS:Our findings suggest a relationship between genetic variation in the 5HT2A promoter region and PTSD.
| S-EPMC2963151 | biostudies-literature
Project description:ImportancePosttraumatic stress disorder (PTSD) is marked by the contrasting symptoms of hyperemotional reactivity and emotional numbing (ie, reduced emotional reactivity). Comprehending the mechanism that governs the transition between neutral and negative emotional states is crucial for developing targeted therapeutic strategies.ObjectivesTo explore whether individuals with PTSD experience a more pronounced shift between neutral and negative emotional states and how the intensity of emotional numbing symptoms impacts this shift.Design, setting, and participantsThis cross-sectional study used hierarchical bayesian modeling to fit a 5-parameter logistic regression to analyze the valence ratings of images. The aim was to compare the curve's slope between groups and explore its association with the severity of emotional numbing symptoms. The study was conducted online, using 35 images with a valence range from highly negative to neutral. The rating of these images was used to assess the emotional responses of the participants. The study recruited trauma-exposed individuals (witnessed or experienced life-threatening incident, violent assault, or someone being killed) between January 17 and March 8, 2023. Participants completed the PTSD Checklist for the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (DSM-5) (PCL-5).ExposureOn the basis of DSM-5 criteria (endorsing at least 1 symptom from clusters B and C and 2 from D and E), participants were categorized as having probable PTSD (pPTSD) or as trauma-exposed controls (TECs).Main outcomes and measuresThe main outcome was the slope parameter (b) of the logistic curve fitted to the valence rating. The slope parameter indicates the rate at which emotional response intensity changes with stimulus valence, reflecting how quickly the transition occurs between neutral and negatively valenced states. The secondary outcome was the association between emotional numbing (PCL-5 items 12-14) and the slope parameter.ResultsA total of 1440 trauma-exposed individuals were included. The pPTSD group (n = 445) was younger (mean [SD] age, 36.1 [10.9] years) compared with the TEC group (mean [SD] age, 41.5 [13.3] years; P < .001). Sex distribution (427 women in the TEC group vs 230 in the pPTSD group) did not significantly differ between groups (P = .67). The pPTSD group exhibited a steeper slope (mean slope difference, -0.255; 89% highest posterior density [HPD], -0.340 to -0.171) compared with the controls. Across all individuals (n = 1440), a robust association was found between the slope and emotional numbing severity (mean [SD] additive value, 0.100 [0.031]; 89% HPD, 0.051-0.15). Additional analysis controlling for age confirmed the association between emotional numbing and transition sharpness (mean [SD] additive value, 0.108 [0.032]; 89% HPD, 0.056-0.159), without evidence of an age-related association (mean [SD] additive value, 0.031 [0.033]; 89% HPD, -0.022 to 0.083).Conclusions and relevanceThese findings support that individuals with PTSD undergo rapid transitions between neutral and negative emotional states, a phenomenon intensified by the severity of emotional numbing symptoms. Therapeutic interventions aimed at moderating these swift emotional transitions could potentially alleviate PTSD symptoms.
| S-EPMC11022112 | biostudies-literature
Project description:BackgroundPosttraumatic stress disorder (PTSD) has been associated with increased cardiovascular risk, however, underlying mechanisms have not been fully specified. PTSD is associated with stress-related hormones, including dysregulated glucocorticoid activity. Dysregulation of aldosterone, a mineralocorticoid activated by psychological stress and implicated in cardiovascular damage, may be a relevant pathway linking PTSD and cardiovascular risk. Few studies to date have evaluated the association between PTSD and aldosterone, none with repeated measures of aldosterone. We examined if trauma and PTSD were associated with altered aldosterone levels relative to women unexposed to trauma.MethodsThe association of trauma exposure and chronic PTSD with plasma aldosterone levels was investigated in 521 middle-aged women in the Nurses' Health Study II. Aldosterone was assessed at two time points, 10-16 years apart, and trauma exposure and PTSD were also ascertained for both time points. Regarding exposure assessment, women were characterized based on a structured diagnostic interview as: having chronic PTSD (PTSD at both time points; n = 174); being trauma-exposed (trauma exposure at first time point but no PTSD; n = 174); and being unexposed (no trauma exposure at either time point; reference group for all analyses; n = 173). Linear mixed models examined associations of trauma and PTSD status with log-transformed aldosterone levels, adjusting for covariates and health-related variables that may confound or lie on the pathway between PTSD and altered aldosterone levels.ResultsAcross the sample, mean aldosterone concentration decreased over time. Adjusting for covariates, women with chronic PTSD had significantly lower aldosterone levels averaged over time, compared to women unexposed to trauma (β = - 0.08, p = 0.04). Interactions between trauma/PTSD group and time were not significant, indicating change in aldosterone over time did not differ by trauma/PTSD status. Post-hoc exploratory analyses suggested that menopausal status partially mediated the relationship between chronic PTSD status and aldosterone level, such that postmenopausal status explained 7% of the effect of PTSD on aldosterone.ConclusionsThese findings indicate that PTSD is associated with lower levels of aldosterone. Further work is needed to understand implications of this type of dysregulation in a key biological stress system for cardiovascular and other health outcomes previously linked with PTSD.
| S-EPMC8487934 | biostudies-literature
Project description:This study investigated group differences and longitudinal changes in brain volume before and after trauma-focused cognitive behavioral therapy (TF-CBT) in 20 unmedicated youth with maltreatment-related posttraumatic stress disorder (PTSD) and 20 non-trauma-exposed healthy control (HC) participants. We collected MRI scans of brain anatomy before and after 5 months of TF-CBT or the same time interval for the HC group. FreeSurfer software was used to segment brain images into 95 cortical and subcortical volumes, which were submitted to optimal scaling regression with lasso variable selection. The resulting model of group differences at baseline included larger right medial orbital frontal and left posterior cingulate corticies and smaller right midcingulate and right precuneus corticies in the PTSD relative to the HC group, R2 = .67. The model of group differences in pre- to posttreatment change included greater longitudinal changes in right rostral middle frontal, left pars triangularis, right entorhinal, and left cuneus corticies in the PTSD relative to the HC group, R2 = .69. Within the PTSD group, pre- to posttreatment symptom improvement was modeled by longitudinal decreases in the left posterior cingulate cortex, R2 = .45, and predicted by baseline measures of a smaller right isthmus (retrosplenial) cingulate and larger left caudate, R2 = .77. In sum, treatment was associated with longitudinal changes in brain regions that support executive functioning but not those that discriminated PTSD from HC participants at baseline. Additionally, results confirm a role for the posterior/retrosplenial cingulate as a correlate of PTSD symptom improvement and predictor of treatment outcome.
| S-EPMC9676083 | biostudies-literature
Project description:BackgroundCognitive processing therapy (CPT) and prolonged exposure (PE) delivered in an individual setting are efficacious and effective treatments for veterans with posttraumatic stress disorder (PTSD). Group CPT has been shown to be less efficacious than individual CPT, however, evidence regarding real-world effectiveness is limited.MethodsWe conducted a retrospective, observational, comparative effectiveness study including veterans that received at least eight sessions of group CPT, individual CPT, or individual PE, and were discharged from PTSD residential treatment at the Department of Veterans Affairs between 1 October 2015, and 30 September 2020. PTSD symptom severity was assessed with the PTSD Checklist for DSM-5 (PCL-5) and treatments delivered in a group (CPT) or individual (CPT or PE) setting were compared at discharge and 4-month post-discharge follow-up.ResultsOf 6735 veterans, 3888 [653 women (17%), median (IQR) age 45 (35-55) years] received individual and 2847 [206 women (7.2%), median (IQR) age 42 (34-54)] received group therapy. At discharge, improvement in PTSD severity was statistically greater among those treated individually (mean difference on the PCL-5, 2.55 (95% CI 1.61-3.49); p = <0.001]. However, the difference was smaller than the minimal clinically important difference of 7.9 points. The groups did not differ significantly at 4-month follow-up [mean difference on the PCL-5, 0.37 (95% CI -0.86 to 1.60); p = 0.551].ConclusionGroup CPT was associated with a slightly smaller reduction of PTSD symptom severity than individual CPT or PE in veterans at the end of residential treatment. There were no differences at 4-month follow-up.
| S-EPMC10388318 | biostudies-literature
Project description:INTRODUCTION:Trauma-exposed individuals with and without posttraumatic stress disorder (PTSD) are more likely to smoke and less successful in quit attempts than individuals without psychopathology. Contingency management (CM) techniques (i.e., incentives for abstinence) have demonstrable efficacy for smoking cessation in some populations with psychopathology, but have not been well tested in PTSD. This pilot study examined the feasibility of CM plus brief cognitive behavioral therapy (CBT) in promoting smoking cessation among trauma-exposed individuals with and without PTSD. METHODS:Fifty trauma-exposed smokers (18 with PTSD) were asked to abstain from tobacco and nicotine replacement therapy for one month. During week one of cessation, CBT was provided daily and increasing CM stipends were paid for each continuous day of biochemically-verified abstinence; CM stipends were withheld in response to smoking lapses and reset to the initial payment level upon abstinence resumption. CBT and fixed payments for study visits were provided during the subsequent three weeks. RESULTS:Of the 50 eligible participants who attended at least one pre-quit visit (49% female, 35% current PTSD), 43 (86%) attended the first post-quit study visit, 32 (64%) completed the first week of CM/CBT treatment, and 26 (52%) completed the study. Post-quit seven-day point prevalence abstinence rates for participants with and without PTSD, respectively, were similar: 39% vs. 38% (1?week), 33% vs. 28% (2?weeks), 22% vs. 19% (3?weeks), and 22% vs. 13% (4?weeks). CONCLUSIONS:Use of CM?+?CBT to support tobacco abstinence is a promising intervention for trauma-exposed smokers with and without PTSD.
| S-EPMC6324961 | biostudies-literature
Project description:A growing literature indicates that genetic variation, in combination with adverse early life experiences, shapes risk for later mental illness. Recent work also suggests that molecular variation at the ADCYAP1R1 locus is associated with posttraumatic stress disorder (PTSD) in women. We sought to test whether childhood maltreatment (CM) interacts with ADCYAP1R1 genotype to predict PTSD in women.Data were obtained from 495 adult female participants from the Detroit Neighborhood Health Study. Genotyping of rs2267735, an ADCYAP1R1 variant, was conducted via TaqMan assay. PTSD, depression, and CM exposure were assessed via structured interviews. Main and interacting effects of ADCYAP1R1 and CM levels on past month PTSD and posttraumatic stress (PTS) severity were examined using logistic regression and a general linear model, respectively. As a secondary analysis, we also assessed main and interacting effects of ADCYAP1R1 and CM variation on risk of past-month depression diagnosis and symptom severity.No significant main effects were observed for ADCYAP1R1 genotype on either PTSD/PTS severity. In contrast, a significant ADCYAP1R1 × CM interaction was observed for both past month PTSD and PTS severity, with carriers of the "C" allele showing enhanced risk for these outcomes among women exposed to CM. No significant main or interaction effects were observed for past month depression/depression severity.Genetic variation at the ADCYAP1R1 locus interacts with CM to shape risk of later PTSD, but not depression, among women. The molecular mechanisms contributing to this interaction require further investigation.
| S-EPMC4081452 | biostudies-literature
Project description:BackgroundPsychological stress is a proposed risk factor for cardiovascular disease (CVD), and posttraumatic stress disorder (PTSD), the sentinel stress-related mental disorder, occurs twice as frequently in women as men. However, whether PTSD contributes to CVD risk in women is not established.Methods and resultsWe examined trauma exposure and PTSD symptoms in relation to incident CVD over a 20-year period in 49 978 women in the Nurses' Health Study II. Proportional hazards models estimated hazard ratios and 95% confidence intervals for CVD events confirmed by additional information or medical record review (n=548, including myocardial infarction [n=277] and stroke [n=271]). Trauma exposure and PTSD symptoms were assessed by using the Brief Trauma Questionnaire and a PTSD screen. In comparison with no trauma exposure, endorsing ≥4 PTSD symptoms was associated with increased CVD risk after adjusting for age, family history, and childhood factors (hazard ratio,1.60; 95% confidence interval, 1.20-2.13). Being trauma-exposed and endorsing no PTSD symptoms was associated with elevated CVD risk (hazard ratio, 1.45; 95% confidence interval, 1.15-1.83), although being trauma-exposed and endorsing 1 to 3 PTSD symptoms was not. After adjusting for adult health behaviors and medical risk factors, this pattern of findings was maintained. Health behaviors and medical risk factors accounted for 14% of the trauma/no symptoms-CVD association and 47% of the trauma/4+ symptoms-CVD association.ConclusionTrauma exposure and elevated PTSD symptoms may increase the risk of CVD in this population of women. These findings suggest that screening for CVD risk and reducing health risk behaviors in trauma-exposed women may be promising avenues for prevention and intervention.
| S-EPMC4519406 | biostudies-literature