Post-traumatic stress disorder symptom remission and cognition in a large cohort of civilian women.

BACKGROUND: Post-traumatic stress disorder (PTSD) is associated with cognitive impairments. It is unclear whether problems persist after PTSD symptoms remit. METHODS: Data came from 12 270 trauma-exposed women in the Nurses' Health Study II. Trauma and PTSD symptoms were assessed using validated scales to determine PTSD status as of 2008 (trauma/no PTSD, remitted PTSD, unresolved PTSD) and symptom severity (lifetime and past-month). Starting in 2014, cognitive function was assessed using the Cogstate Brief Battery every 6 or 12 months for up to 24 months. PTSD associations with baseline cognition and longitudinal cognitive changes were estimated by covariate-adjusted linear regression and linear mixed-effects models, respectively. RESULTS: Compared to women with trauma/no PTSD, women with remitted PTSD symptoms had a similar cognitive function at baseline, while women with unresolved PTSD symptoms had worse psychomotor speed/attention and learning/working memory. In women with unresolved PTSD symptoms, past-month PTSD symptom severity was inversely associated with baseline cognition. Over follow-up, both women with remitted and unresolved PTSD symptoms in 2008, especially those with high levels of symptoms, had a faster decline in learning/working memory than women with trauma/no PTSD. In women with remitted PTSD symptoms, higher lifetime PTSD symptom severity was associated with a faster decline in learning/working memory. Results were robust to the adjustment for sociodemographic, biobehavioral, and health factors and were partially attenuated when adjusted for depression. CONCLUSION: Unresolved but not remitted PTSD was associated with worse cognitive function assessed six years later. Accelerated cognitive decline was observed among women with either unresolved or remitted PTSD symptoms.

Salivary inflammatory biomarkers as a predictor of post-traumatic stress disorder and depressive symptom severity in trauma patients: A prospective study.

BACKGROUND: Although post-traumatic stress disorder (PTSD) and depression screening are recommended for traumatic injury patients, routine screening is still uncommon. Salivary inflammatory biomarkers have biological plausibility and potential feasibility and acceptability for screening. This study tested prospective associations between several salivary inflammatory biomarkers (proinflammatory cytokines interleukin-1ß, interleukin-6, tumor necrosis factor-α; and C-reactive protein), collected during hospitalization and PTSD and depressive symptoms at 5-month follow-up. METHODS: Adult traumatic injury patients (N = 696) at a major urban Level 1 trauma center provided salivary samples and completed PTSD and depressive symptom measures during days 0-13 of inpatient hospitalization. At 5-month follow-up, 368 patients (77 % male, 23 % female) completed the Clinician-Administered PTSD Scale for DSM-IV and the Self-rated Inventory of Depressive Symptomatology. Analyses focused on a latent inflammatory cytokine factor and C-reactive protein at baseline predicting 5-month PTSD and depression symptom outcomes and included baseline symptom levels as covariates. RESULTS: A latent factor representing proinflammatory cytokines was not related to 5-month PTSD or depressive symptom severity. Higher salivary CRP was related to greater PTSD symptom severity (ß = .10, p = .03) at 5-month follow-up and more severity in the following depressive symptoms: changes in weight and appetite, bodily complaints, and constipation/diarrhea (ß's from .14 to .16, p's from .004 -.03). CONCLUSION: In a primarily Latine and Black trauma patient sample, salivary CRP measured after traumatic injury was related to greater PTSD symptom severity and severity in several depressive symptom clusters. Our preliminary findings suggest that salivary or systemic CRP may be useful to include in models predicting post-trauma psychopathology.

Migraine headache in patients with spontaneous coronary artery dissection: A report of the iSCAD Registry.

INTRODUCTION: Spontaneous coronary artery dissection (SCAD) is a nonatherosclerotic cause of myocardial infarction. Migraine headache has been reported to be common among patients with SCAD, but the degree of migraine-related disability has not been quantified. METHODS: Clinical data and headache variables were obtained from the baseline assessment of the prospective, multicenter iSCAD Registry. Migraine-related disability was quantified using the self-reported Migraine Disability Assessment (MIDAS). Demographic, clinical, psychosocial, and medical characteristics from data entry forms were compared between patients with and without migraine. RESULTS: Of the 773 patients with available data, 46% reported previous or current migraines. Those with migraines were more likely to be women (96.9% vs 90.3%, p = 0.0003). The presence of underlying carotid fibromuscular dysplasia was associated with migraine (35% vs 27%, p = 0.0175). There was not a significant association with carotid artery dissection and migraine. Current migraine frequency was less than monthly (58%), monthly (24%), weekly (16%), and daily (3%). Triptan use was reported in 32.5% of patients, and 17.5% used daily migraine prophylactic medications. Using the MIDAS to quantify disability related to migraine, 60.2% reported little or no disability, 14.4% mild, 12.7% moderate, and 12.7% severe. The mean MIDAS score was 9.9 (mild to moderate disability). Patients with SCAD had higher rates of depression and anxiety (28.2% vs 17.7% [p = 0.0004] and 35.3% vs 26.7% [p = 0.0099], respectively). CONCLUSIONS: Migraines are common, frequent, and a source of disability in patients with SCAD. The association between female sex, anxiety, and depression may provide some insight for potential treatment modalities.

Anhedonic Depression Is Not Associated With Risk of Recurrent Major Adverse Cardiac Events and All-Cause Mortality in Acute Coronary Syndrome Patients.

BACKGROUND: Depression after acute coronary syndrome (ACS) is common and increases risks of adverse outcomes, but it remains unclear which depression features are most associated with major adverse cardiac events (MACE) and all-cause mortality (ACM). PURPOSE: To examine whether a subtype of depression characterized by anhedonia and major depressive disorder (MDD) predicts 1-year MACE/ACM occurrence in ACS patients compared to no MDD history. We also consider other depression features in the literature as predictors. METHODS: Patients (N = 1,087) presenting to a hospital with ACS completed a self-report measure of current depressive symptoms in-hospital and a diagnostic interview assessing MDD within 1 week post-hospitalization. MACE/ACM events were assessed at 1-, 6-, and 12-month follow-ups. Cox regression models were used to examine the association of the anhedonic depression subtype and MDD without anhedonia with time to MACE/ACM, adjusting for sociodemographic and clinical covariates. RESULTS: There were 142 MACE/ACM events over the 12-month follow-up. The 1-year MACE/ACM in patients with anhedonic depression, compared to those with no MDD, was somewhat higher in an age-adjusted model (hazard ratio [HR] = 1.63, p = .08), but was not significant after further covariate adjustment (HR = 1.24, p = .47). Of the additional depression features, moderate-to-severe self-reported depressive symptoms significantly predicted the risk of MACE/ACM, even in covariate-adjusted models (HR = 1.72, p = .04), but the continuous measure of self-reported depressive symptoms did not. CONCLUSION: The anhedonic depression subtype did not uniquely predict MACE/ACM as hypothesized. Moderate-to-severe levels of total self-reported depressive symptoms, however, may be associated with increased MACE/ACM risk, even after accounting for potential sociodemographic and clinical confounders.

Introduction to the Special Section on the International Society for Traumatic Stress Studies 38th Annual Meeting: Trauma as a transdiagnostic risk factor across the lifespan.

This article serves as an introduction to the special section in the Journal of Traumatic Stress related to the 38th annual meeting of the International Society for Traumatic Stress Studies, held in Atlanta, Georgia (USA) in November 2022. The theme of this meeting, "Trauma as a Transdiagnostic Risk Factor Across the Lifespan," provided an opportunity to recognize the far-reaching impact of trauma and how traumatic experiences can become embedded into the mind, body, and societal spirit. This introductory article outlines the importance of harnessing multiple perspectives to address these wide-ranging sequelae of trauma and provides an overview of the series of contributions to the special section.

Trauma, Post-Traumatic Stress Disorder, and Treatment Among Middle-Aged and Older Women in the Nurses' Health Study II.

OBJECTIVE: Trauma and post-traumatic stress disorder (PTSD) are common among women and associated with negative health outcomes across the life course. Relatively few studies, however, have examined the epidemiology of trauma, PTSD, and treatment among middle-aged and older civilian women, who are at elevated risk for adverse health outcomes. We aimed to characterize trauma, PTSD, and trauma-related treatment prevalence and correlates in a large cohort of middle-aged and older women. DESIGN: Cross-sectional, nested substudy within the Nurses' Health Study II cohort. SETTING: United States, 2018-2020. PARTICIPANTS: 33,327 current or former nurses, aged 53-74 years. MEASUREMENTS: 16-item modified version of the Brief Trauma Questionnaire; modified PTSD Checklist for the Diagnostic and Statistical Manual, Version 5. RESULTS: The majority (82.2%) of women reported one or more lifetime traumas. The most common trauma types were unexpected death of a loved one (44.9%) and interpersonal violence (43.5%). Almost 30% reported occupational (nursing-related) trauma. Among the trauma-exposed, 10.5% met criteria for lifetime PTSD and 1.5% had past-month PTSD. One-third of lifetime PTSD cases were due to interpersonal violence event types. One-third of women with lifetime PTSD-and nearly half of those with PTSD from a nursing-related trauma-reported never receiving trauma-related treatment. Women aged 65 years and older with PTSD were less likely to be in treatment than those aged less than 65 years. CONCLUSION: History of trauma and PTSD is prevalent in this population, and a treatment gap persists. Addressing this treatment gap is warranted, particularly among older women and those with nursing-related trauma.

The association of posttraumatic stress disorder, depression, and head injury with mid-life cognitive function in civilian women.

BACKGROUND: Despite evidence linking posttraumatic stress disorder (PTSD), depression, and head injury, separately, with worse cognitive performance, investigations of their combined effects on cognition are limited in civilian women. METHODS: The Cogstate Brief Battery assessment was administered in 10,681 women from the Nurses' Health Study II cohort, mean age 64.9 years (SD = 4.6). Psychological trauma, PTSD, depression, and head injury were assessed using online questionnaires. In this cross-sectional analysis, we used linear regression models to estimate mean differences in cognition by PTSD/depression status and stratified by history of head injury. RESULTS: History of head injury was prevalent (36%), and significantly more prevalent among women with PTSD and depression (57% of women with PTSD and depression, 21% of women with no psychological trauma or depression). Compared to having no psychological trauma or depression, having combined PTSD and depression was associated with worse performance on psychomotor speed/attention ( ß = -.15, p = .001) and learning/working memory ( ß = -.15, p < .001). The joint association of PTSD and depression on worse cognitive function was strongest among women with past head injury, particularly among those with multiple head injuries. CONCLUSIONS: Head injury, like PTSD and depression, was highly prevalent in this sample of civilian women. In combination, these factors were associated with poorer performance on cognitive tasks, a possible marker of future cognitive health. Head injury should be further explored in future studies of PTSD, depression and cognition in women.

Posttraumatic Stress Disorder (PTSD) as a Risk Factor for Cardiovascular Disease: Implications for Future Research and Clinical Care.

PURPOSE OF REVIEW: Posttraumatic stress disorder (PTSD) may be an important risk factor for cardiovascular disease (CVD). We explore the literature linking PTSD to CVD, potential mechanisms, interventions, and clinical implications. We outline gaps in current literature and highlight necessary future research. RECENT FINDINGS: PTSD has been independently associated with deleterious effects on cardiovascular health through biological, behavioral, and societal pathways. There are evidence-based psychotherapeutic interventions and pharmacotherapies for PTSD that may mitigate its impact on CVD. However, there are limited studies that rigorously analyze the impact of treating PTSD on cardiovascular outcomes. Trauma-informed CVD risk stratification, education, and treatment offer opportunities to improve patient care. These approaches can include a brief validated screening tool for PTSD identification and treatment. Pragmatic trials are needed to test PTSD interventions among people with CVD and evaluate for improved outcomes.

Posttraumatic stress disorder and changes in diet quality over 20 years among US women.

BACKGROUND: Individuals with posttraumatic stress disorder (PTSD) are at increased risk of various chronic diseases. One hypothesized pathway is via changes in diet quality. This study evaluated whether PTSD was associated with deterioration in diet quality over time. METHODS: Data were from 51 965 women in the Nurses' Health Study II PTSD sub-study followed over 20 years. Diet, assessed at 4-year intervals, was characterized via the Alternative Healthy Eating Index-2010 (AHEI). Based on information from the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD, trauma/PTSD status was classified as no trauma exposure, prevalent exposure (trauma/PTSD onset before study entry), or new-onset (trauma/PTSD onset during follow-up). We further categorized women with prevalent exposure as having trauma with no PTSD symptoms, trauma with low PTSD symptoms, and trauma with high PTSD symptoms, and created similar categories for women with new-onset exposure, resulting in seven comparison groups. Multivariable linear mixed-effects spline models tested differences in diet quality changes by trauma/PTSD status over follow-up. RESULTS: Overall, diet quality improved over time regardless of PTSD status. In age-adjusted models, compared to those with no trauma, women with prevalent high PTSD and women with new-onset high PTSD symptoms had 3.3% and 3.6% lower improvement in diet quality, respectively, during follow-up. Associations remained consistent after adjusting for health conditions, sociodemographics, and behavioral characteristics. CONCLUSIONS: PTSD is associated with less healthy changes in overall diet quality over time. Poor diet quality may be one pathway linking PTSD with a higher risk of chronic disease development.

Not all posttraumatic stress disorder symptoms are equal: fear, dysphoria, and risk of developing hypertension in trauma-exposed women.

BACKGROUND: Posttraumatic 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. METHODS: We 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. RESULTS: Higher 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. CONCLUSIONS: Fear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.

Earlier age at menarche as a transdiagnostic mechanism linking childhood trauma with multiple forms of psychopathology in adolescent girls.

BACKGROUND: Although early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA - threat and deprivation - have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology. METHODS: Data were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders. RESULTS: Greater exposure to threat was associated with earlier AAM (B = -0.1, p = 0.001). Each 1-year increase in AAM was associated with reduced odds of fear, distress, and externalizing disorders post-menarche (ORs = 0.74-0.85). Earlier AAM significantly mediated the association between exposure to threat and post-menarche onset of distress (proportion mediated = 6.2%), fear (proportion mediated = 16.3%), and externalizing disorders (proportion mediated = 2.9%). CONCLUSIONS: Accelerated pubertal development in girls may be one transdiagnostic pathway through which threat-related experiences confer risk for the adolescent onset of mental disorders. Early pubertal maturation is a marker that could be used in both medical and mental health settings to identify trauma-exposed youth that are at risk for developing a mental disorder during adolescence in order to better target early interventions.

Hyperarousal Symptoms in Survivors of Cardiac Arrest Are Associated With 13 Month Risk of Major Adverse Cardiovascular Events and All-Cause Mortality.

BACKGROUND: Key dimensions of cardiac arrest-induced posttraumatic stress disorder (PTSD) symptoms include reexperiencing, avoidance, numbing, and hyperarousal. It remains unknown which dimensions are most predictive of outcome. PURPOSE: To determine which dimensions of cardiac arrest-induced PTSD are predictive of clinical outcome within 13 months posthospital discharge. METHODS: PTSD symptoms were assessed in survivors of cardiac arrest who were able to complete psychological screening measures at hospital discharge via the PTSD Checklist-Specific scale, which queries for 17 symptoms using five levels of severity. Responses on items for each symptom dimension of the four-factor numbing model (reexperiencing, avoidance, numbing, and hyperarousal) were converted to Z-scores and treated as continuous predictors. The combined primary endpoint was all-cause mortality (ACM) or major adverse cardiovascular events (MACE; hospitalization for myocardial infarction, unstable angina, heart failure, emergency coronary revascularization, or urgent defibrillator/pacemaker placements) within 13 months postdischarge. Four bivariate Cox proportional hazards survival models evaluated associations between individual symptom dimensions and ACM/MACE. A multivariable model then evaluated whether significant bivariate predictors remained independent predictors of the primary outcome after adjusting for age, sex, comorbidities, premorbid psychiatric diagnoses, and initial cardiac rhythm. RESULTS: A total of 114 patients (59.6% men, 52.6% white, mean age: 54.6 ± 13 years) were included. In bivariate analyses, only hyperarousal was significantly associated with ACM/MACE. In a fully adjusted model, 1 standard deviation increase in hyperarousal symptoms corresponded to a two-times increased risk of experiencing ACM/MACE. CONCLUSIONS: Greater level of hyperarousal symptoms was associated with a higher risk of ACM/MACE within 13 months postcardiac arrest. This initial evidence should be further investigated in a larger sample.

Childhood and Adolescent Adversity and Cardiometabolic Outcomes: A Scientific Statement From the American Heart Association.

Adverse experiences in childhood and adolescence, defined as subjectively perceived threats to the safety or security of the child's bodily integrity, family, or social structures, are known to be associated with cardiometabolic outcomes over the life course into adulthood. This American Heart Association scientific statement reviews the scientific literature on the influence of childhood adversity on cardiometabolic outcomes that constitute the greatest public health burden in the United States, including obesity, hypertension, type 2 diabetes mellitus, and cardiovascular disease. This statement also conceptually outlines pathways linking adversity to cardiometabolic health, identifies evidence gaps, and provides suggestions for future research to inform practice and policy. We note that, despite a lack of objective agreement on what subjectively qualifies as exposure to childhood adversity and a dearth of prospective studies, substantial evidence documents an association between childhood adversity and cardiometabolic outcomes across the life course. Future studies that focus on mechanisms, resiliency, and vulnerability factors would further strengthen the evidence and provide much-needed information on targets for effective interventions. Given that childhood adversities affect cardiometabolic health and multiple health domains across the life course, interventions that ameliorate these initial upstream exposures may be more appropriate than interventions remediating downstream cardiovascular disease risk factor effects later in life.

Posttraumatic stress disorder and incidence of thyroid dysfunction in women.

BACKGROUND: Abnormal thyroid function is prevalent among women and has been linked to increased risk of chronic disease. Posttraumatic stress disorder (PTSD) has been linked to thyroid dysfunction in some studies; however, the results have been inconsistent. Thus, we evaluated trauma exposure and PTSD symptoms in relation to incident thyroid dysfunction in a large longitudinal cohort of civilian women. METHODS: We used data from 45 992 women from the ongoing Nurses' Health Study II, a longitudinal US cohort study that began in 1989. In 2008, history of trauma and PTSD were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, fourth edition, PTSD, and incident thyroid dysfunction was determined by participants' self-report in biennial questionnaires of physician-diagnosed hypothyroidism and Graves' hyperthyroidism. The study period was from 1989 to 2013. Proportional hazard models were used to estimate multivariable-adjusted hazard ratios and 95% confidence intervals (CIs) for incident hypothyroidism and Graves' hyperthyroidism. RESULTS: In multivariable-adjusted models, we found significant associations for PTSD only with hypothyroidism [p-trend <0.001; trauma with no PTSD symptoms, 1.08 (95% CI 1.02-1.15); 1-3 PTSD symptoms, 1.12 (95% CI 1.04-1.21); 4-5 PTSD symptoms, 1.23 (95% CI 1.13-1.34); and 6-7 PTSD symptoms, 1.26 (95% CI 1.14-1.40)]. PTSD was not associated with risk of Graves' hyperthyroidism (p-trend = 0.34). Associations were similar in sensitivity analyses restricted to outcomes with onset after 2008, when PTSD was assessed. CONCLUSIONS: PTSD was associated with higher risk of hypothyroidism in a dose-dependent fashion. Highlighted awareness for thyroid dysfunction may be especially important in women with PTSD.

The Association of Posttraumatic Stress Disorder With Clinic and Ambulatory Blood Pressure in Healthy Adults.

OBJECTIVE: Posttraumatic stress disorder (PTSD) is associated with incident cardiovascular risk. We tested the association of PTSD with clinic and ambulatory blood pressure (ABP) in a sample of healthy participants and tested ABP reactivity to anxiety as a mechanism by which PTSD may influence blood pressure (BP). METHODS: Participants were originally enrolled during workplace BP screenings at three sites; approximately 6 years (standard deviation = 1.0) later, they completed nine clinic BP assessments within three visits, 1 week apart. Before the third visit, participants were screened for PTSD (≥33 on the PTSD Checklist-Civilian) and depression (Beck Depression Inventory) and then completed 24-hour ABP monitoring with electronic diary assessment of anxiety (0-100) at each awake reading. RESULTS: Of 440 participants, 92 (21%) screened positive for PTSD. In regression models adjusted for depression and demographic and clinical variables, PTSD was associated with greater mean systolic BP (3.8 mm Hg clinic [95% confidence interval {CI}] = 1.1-6.5, p = .006), 3.0 mm Hg awake ABP [95% CI = 0.1-5.9, p = .04], and a nonsignificant 2.1 mm Hg ABP during sleep [95% CI = -1.0 to 5.1, p = .18]). PTSD was associated with greater 24-hour median anxiety (p < .001), and changes in anxiety were positively associated with concurrent systolic ABP (p < .001). ABP reactivity to anxiety was greater in participants with PTSD, which partially explained the association of PTSD with ABP. CONCLUSIONS: PTSD is associated with greater systolic BP, partly because of greater anxiety, and systolic BP reactivity to anxiety throughout the day. Daily anxiety and related BP reactivity may be targets for interventions to reduce the cardiovascular risk associated with PTSD.

Posttraumatic stress disorder onset and inflammatory and endothelial function biomarkers in women.

BACKGROUND: Research has linked posttraumatic stress disorder (PTSD) with higher circulating levels of inflammatory and endothelial function (EF) biomarkers, and effects may be bidirectional. We conducted the first investigation of new-onset PTSD and changes in inflammatory and EF biomarkers. METHODS: Data were from women in the Nurses' Health Study II. Biomarkers obtained at two blood draws, 10-16 years apart, included C-reactive protein (CRP), tumor necrosis factor-alpha receptor-II (TNFRII), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). PTSD was assessed via interview. Analyses compared biomarker levels in women with PTSD that onset between draws (n = 175) to women with no history of trauma (n = 175) and to women with history of trauma at draw 1 and no PTSD at either draw (n = 175). We examined if PTSD onset was associated with biomarker change over time and if pre-PTSD-onset biomarker levels indicated risk of subsequent PTSD using linear mixed models and linear regression, respectively. Biomarkers were log-transformed. RESULTS: Compared to women without trauma, women in the PTSD onset group had larger increases in VCAM-1 over time (b = 0.003, p = .068). They also had higher TNFRII (b = 0.05, p = .049) and ICAM-1 (b = 0.04, p = .060) levels at draw 1 (prior to trauma and PTSD onset). However, pre-PTSD-onset biomarker levels did not predict onset of more severe PTSD. CONCLUSIONS: PTSD onset (vs. no trauma) was associated with increases in one inflammation-related biomarker. Effects may be small and cumulative; longer follow-up periods with larger samples are needed. We did not observe strong support that pre-PTSD-onset biomarkers predicted risk of subsequent PTSD.

The role of perceived threat during emergency department cardiac evaluation and the age-posttraumatic stress disorder link.

Evaluation for acute coronary syndrome (ACS) can trigger posttraumatic stress symptoms (PSS). Research suggests that younger, versus older, individuals may be at elevated risk for PSS after ACS evaluation. It has been proposed that younger individuals may be at greater risk because they perceive the suspected ACS event as more threatening than their older counterparts; however, this has yet to be tested. We examined whether perceived threat during ACS evaluation mediated the association between age and PSS after ACS evaluation in an observational cohort study of patients presenting to the emergency department (ED) with suspected ACS. Demographics and perceived threat were assessed in the ED. PSS were measured upon inpatient transfer or by phone 3 days later. The analytic sample comprised 871 adult participants. Multiple linear regression was used to examine (1) associations of age and perceived threat with PSS and (2) whether perceived threat mediated the association. Bootstrapping with percentile-based confidence intervals (CIs) was used to test the indirect effect. Each year of age was associated with lower PSS (b = - 0.12, p < .001), independent of covariates. Older age was associated with lower perceived threat during ACS evaluation (b = - 0.05, p < .001). Greater threat perceptions predicted greater PSS (b = 0.94, p < .0001). The indirect effect (- 0.04) was statistically significant (95% CI - 0.07, - 0.02). Younger, versus older, individuals are at risk for greater PSS after ACS evaluation, and elevated perceived threat partially mediated this association. Understanding age differences in PSS development risk and the potential impact of age on threat perceptions may help inform ED treatment.

Posttraumatic stress disorder symptoms and cognitive function in a large cohort of middle-aged women.

BACKGROUND: Posttraumatic stress disorder (PTSD) has been linked to cognitive decline, but research in women is generally lacking. We examined whether trauma and elevated PTSD symptoms were associated with worse cognitive function in middle-aged civilian women. A secondary objective was to investigate the possible role of depression in the relation of PTSD symptoms to cognitive function. METHODS: The sample comprised 14,029 middle-aged women in the Nurses' Health Study II. Lifetime trauma exposure, lifetime PTSD symptoms, and past-week depressive symptoms were measured in 2008. Cognitive function was measured in 2014-2016 using the Cogstate Brief Battery, a self-administered online cognitive battery that assesses psychomotor speed, attention, learning, and working memory. We used linear regression models to estimate mean differences in cognition across PTSD symptom levels. RESULTS: Compared to no trauma, elevated PTSD symptoms consistent with probable PTSD (i.e., 4+ symptoms on a screening questionnaire) were associated with worse performance on psychomotor speed/attention (b = -0.08 standard units, p = .001) and learning/working memory (b = -0.09, p < .001) composites, after adjusting for sociodemographics. Although attenuated, associations remained significant when adjusted for depressive symptoms and other cognitive risk factors. We found the strongest associations among women with comorbid probable PTSD and depression. CONCLUSIONS: PTSD symptoms were negatively related to measures of psychomotor speed/attention and learning/working memory in middle-aged women. Our study adds to a growing literature that suggests that mental disorders are associated with worse cognitive function over the life course.

Posttraumatic stress disorder and accelerated aging: PTSD and leukocyte telomere length in a sample of civilian women.

BACKGROUND: Studies in male combat veterans have suggested posttraumatic stress disorder (PTSD) is associated with shorter telomere length (TL). We examined the cross-sectional association of PTSD with TL in women exposed to traumas common in civilian life. METHODS: Data are from a substudy of the Nurses' Health Study II (N = 116). PTSD and subclinical PTSD were assessed in trauma-exposed women using diagnostic interviews. An array of health behaviors and conditions were assessed. DNA was extracted from peripheral blood leukocytes (collected 1996-1999). Telomere repeat copy number to single gene copy number (T/S) was determined by quantitative real-time PCR telomere assay. We used linear regression models to assess associations and examine whether a range of important health behaviors (e.g., cigarette smoking) and medical conditions (e.g., hypertension) previously associated with TL might explain a PTSD-TL association. We further examined whether type of trauma exposure (e.g., interpersonal violence) was associated with TL and whether trauma type might explain a PTSD-TL association. RESULTS: Relative to not having PTSD, women with a PTSD diagnosis had shorter log-transformed TL (ß = -.112, 95% confidence interval (CI) = -0.196, -0.028). Adjustment for health behaviors and medical conditions did not attenuate this association. Trauma type was not associated with TL and did not account for the association of PTSD with TL. CONCLUSIONS: Our results add to growing evidence that PTSD may be associated with more rapid cellular aging as measured by telomere erosion. Moreover, the association could not be explained by health behaviors and medical conditions assessed in this study, nor by type of trauma exposure.