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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.

Aim: Given reports of increased prevalence of PTSD symptoms at COVID-19 pandemic onset, we aimed to assess the prevalence of posttraumatic stress disorder (PTSD) symptoms at pandemic onset in individuals with and without systemic autoimmune rheumatic disease (SARD)., Methods: In May 2020, we invited 6678 patients to complete the Brief Trauma Questionnaire and the Posttraumatic Stress Disorder Checklist (PCL-5), validated PTSD symptom screenings. We compared responses from patients with and without SARD using multivariable logistic regression., Results: We received 1473 responses (22% response rate) from 5/2020 to 9/2021 (63 with prior PTSD diagnoses, 138 with SARD history). The SARD population was more female (p .0001) and had a higher baseline prevalence of stress disorders (56% vs. 43%, p .004). SARD subjects reported more experiences with life-threatening illness, 60%, versus 53% among those without SARD (p .13), and more antidepressant or anxiolytic medication use pre-pandemic (78% vs. 59%, p .0001). Adjusting for pre-pandemic PTSD diagnosis, younger age and history of stress disorder were the most significant predictors of PCL-5 positivity. There were no significant differences in PCL-5 score or positivity among those with or without SARD., Conclusion: In this population, patients with SARD had a higher pre-COVID-19 prevalence of stress-related conditions, but it was not the case that they had an increased risk of PTSD symptoms in the early pandemic. Younger individuals, those with baseline depression, anxiety, or adjustment disorders, and those taking antidepressant or anxiolytic medications were more likely to have PTSD symptoms in the first waves of the COVID-19 pandemic., (© 2023 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.)

Background: Few modifiable risk factors for epithelial ovarian cancer have been identified. We and other investigators have found that individual psychosocial factors related to distress are associated with higher risk of ovarian cancer. The present study examined whether co-occurring distress-related factors are associated with ovarian cancer risk., Methods: Five distress-related factors were measured repeatedly over 21 years of follow-up: depression, anxiety, social isolation, widowhood, and, in a subset or women, posttraumatic stress disorder (PTSD). Cox proportional hazards models estimate relative risks (RR) and 95% confidence intervals (CI) of ovarian cancer for a time-updated count of distress-related factors, in age-adjusted models, then further adjusted for ovarian cancer risk factors and behavior-related health risk factors., Results: Across 1,193,927 person-years of follow-up, 526 incident ovarian cancers occurred. Women with ≥3 versus no distress-related psychosocial factors demonstrated increased ovarian cancer risk (HR age-adjusted  = 1.71; 95% CI = 1.16, 2.52). No significant difference in ovarian cancer risk was observed in women with one or two versus no distress-related psychosocial factors. In the subsample with PTSD assessed, ≥3 versus no distress-related psychosocial factors was associated with twofold greater ovarian cancer risk (HR age-adjusted  = 2.08, 95% CI = 1.01, 4.29). Further analysis suggested that women at highest ovarian cancer risk had PTSD co-occurring with any other distress-related factor (HR = 2.19, 95% CI = 1.20, 4.01). Adjusting for cancer risk factors and health behaviors minimally impacted risk estimates., Conclusions: Presence of multiple indicators of distress was associated with risk of ovarian cancer. When including PTSD as an indicator of distress, the association was strengthened., (© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

Systemic lupus erythematosus (SLE) is a heterogeneous, multisystem autoimmune disorder characterized by unpredictable disease flares. Although the pathogenesis of SLE is complex, an epidemiologic link between posttraumatic stress disorder (PTSD) and the development of SLE has been identified, suggesting that stress-related disorders alter the susceptibility to SLE. Despite the strong epidemiologic evidence connecting PTSD and SLE, gaps remain in our understanding of how the two may be connected. Perturbations in the autonomic nervous system, neuroendocrine system, and at the genomic level may cause and sustain immune dysregulation that could lower the threshold for the development and propagation of SLE. We first describe shared risk factors for SLE and PTSD. We then describe potential biological pathways which may facilitate excessive inflammation in the context of PTSD. Among those genetically predisposed to SLE, systemic inflammation that accompanies chronic stress may fan the flames of smoldering SLE by priming immune pathways. Further studies on the connection between trauma and inflammation will provide important data on pathogenesis, risk factors, and novel treatments for SLE., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Objective: We studied posttraumatic stress disorder (PTSD), a severe trauma-related mental disorder, and systemic lupus erythematosus (SLE) risk in a large, diverse population enrolled in Medicaid, a US government-sponsored health insurance program for low-income individuals., Methods: We identified SLE cases and controls among patients ages 18-65 years enrolled in Medicaid for ≥12 months in the 29 most populated US states from 2007 to 2010. SLE and PTSD case statuses were defined based on validated patterns of International Classification of Diseases, Ninth Revision codes. Index date was the date of the first SLE code. Controls had no SLE codes but had another inpatient or outpatient code on the index date and were matched 1:10 to cases by age, sex, and race. Conditional logistic regressions calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for the association of PTSD with incident SLE, adjusting for smoking, obesity, oral contraceptive use, and other covariates., Results: A total of 10,942 incident SLE cases were matched to 109,420 controls. The prevalence of PTSD was higher in SLE cases, at 10.74 cases of PTSD per 1,000 person-years (95% CI 9.37-12.31) versus 7.83 cases (95% CI 7.42-8.27) in controls. The multivariable-adjusted OR for SLE among those with PTSD was 2.00 (95% CI 1.64-2.46)., Conclusion: In this large, racially and sociodemographically diverse US population, we found patients with a prior PTSD diagnosis had twice the odds of a subsequent diagnosis of SLE. Studies are necessary to clarify the mechanisms driving the observed association and to inform possible interventions., (© 2021 American College of Rheumatology.)

Psychological distress can be conceptualized as an umbrella term encompassing symptoms of depression, anxiety, posttraumatic stress disorder (PTSD), or stress more generally. A systematic review of metabolomic markers associated with distress has the potential to reveal underlying molecular mechanisms linking distress to adverse health outcomes. The current systematic review extends prior reviews of clinical depressive disorders by synthesizing 39 existing studies that examined metabolomic markers for PTSD, anxiety disorders, and subclinical psychological distress in biological specimens. Most studies were based on small sets of pre-selected candidate metabolites, with few metabolites overlapping between studies. Vast heterogeneity was observed in study design and inconsistent patterns of association emerged between distress and metabolites. To gain a more robust understanding of distress and its metabolomic signatures, future research should include 1) large, population-based samples and longitudinal assessments, 2) replication and validation in diverse populations, 3) and agnostic metabolomic strategies profiling hundreds of targeted and nontargeted metabolites. Addressing these research priorities will improve the scope and reproducibility of future metabolomic studies of psychological distress., Competing Interests: Conflict of interest None., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Background: Prior evidence links posttraumatic stress disorder (PTSD) and depression, separately, with chronic inflammation. However, whether effects are similar across each independently or potentiated when both are present is understudied. We evaluated combined measures of PTSD and depression in relation to inflammatory biomarker concentrations., Methods: Data are from women (n's ranging 628-2797) in the Nurses' Health Study II. Trauma exposure, PTSD, and depression symptoms were ascertained using validated questionnaires. We examined (a) a continuous combined psychological distress score summing symptoms for PTSD and depression, and (b) a categorical cross-classified measure of trauma/PTSD symptoms/depressed mood status (reference group: no trauma or depressed mood). Three inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], tumor necrosis factor alpha receptor 2 [TNFR2]) were assayed from at least one of two blood samples collected 10-16 years apart. We examined associations of our exposures with levels of each biomarker concentration (log-transformed and batch-corrected) as available across the two time points (cross-sectional analyses; CRP, IL-6 and TNFR2) and with rate of change in biomarkers across time (longitudinal analyses; CRP and IL-6) using separate linear mixed effects models., Results: In sociodemographic-adjusted models accounting for trauma exposure, a one standard deviation increase in the continuous combined psychological distress score was associated with 10.2% (95% confidence interval (CI): 5.2-15.4%) higher CRP and 1.5% (95% CI: 0.5-2.5%) higher TNFR2 concentrations cross-sectionally. For the categorical exposure, women with trauma/PTSD symptoms/ depressed mood versus those with no trauma or depressed mood had 29.5% (95% CI: 13.3-47.9%) higher CRP and 13.1% (95% CI: 5.1-21.7%) higher IL-6 cross-sectionally. In longitudinal analysis, trauma/PTSD symptoms/depressed mood was associated with increasing CRP levels over time., Conclusions: High psychological distress levels with trauma exposure is associated with elevated inflammation and is a potential biologic pathway by which distress can impact development of inflammatory-related chronic diseases, such as cardiovascular disease. Considering multiple forms of distress in relation to these pathways may provide greater insight into who is at risk for biologic dysregulation and later susceptibility to chronic diseases., Competing Interests: Declarations of interest None, (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Background: Earlier menopause, either natural or through gynecologic surgeries, has been associated with various negative health sequelae. While posttraumatic stress disorder (PTSD) has been linked to dysregulated biological processes, including reproductive system changes that could alter menopausal timing, little work has examined whether trauma and PTSD are associated with greater risk of early cessation of menses., Methods: Data are from 46,639 women in the Nurses' Health Study II, a prospective cohort study of women followed for up to 26 years. Lifetime trauma and PTSD symptoms were assessed with the Brief Trauma Questionnaire and a PTSD symptom screener in 2008. Age at cessation of menses and reason for cessation of menses (i.e., natural menopause, gynecologic surgery including hysterectomy and/or bilateral salpingo-oophorectomy [BSO]) were assessed. Cox proportional hazards models estimated hazards ratios (HR) of cessation of menses (separately for naturally or surgically) associated with trauma alone or PTSD symptoms, relative to no trauma, adjusting for covariates., Results: Trauma/PTSD status was associated with earlier cessation of menses due to surgery, but not natural menopause. Women with trauma exposure, low, and high PTSD symptoms had higher hazard of cessation of menses due to surgery relative to those with no trauma exposure (HR trauma  = 1.16, 95%CI 1.07-1.26; HR low PTSD  = 1.25, 95%CI 1.15-1.36; HR high PTSD  = 1.29, 95%CI 1.17-1.42). Trauma exposure and PTSD symptoms were associated with similarly increased risk of hysterectomy and BSO surgeries., Conclusions: Women who experienced trauma and PTSD may be at elevated risk for common gynecological surgeries premenopausally, potentially due to increased clinical indications or gynecological conditions., (Published by Elsevier Inc.)

Importance: Posttraumatic stress disorder (PTSD) has been hypothesized to lead to impaired cognitive function. However, no large-scale studies have assessed whether PTSD is prospectively associated with cognitive decline in middle-aged adults., Objective: To assess the association between PTSD and decline in cognitive function over time., Design, Setting, and Participants: This cohort study included participants from the Nurses' Health Study II, an ongoing longitudinal cohort study involving community-dwelling middle-aged female nurses residing in the US who had at least a 2-year nursing degree at the time of enrollment in 1989. The present study included 12 270 trauma-exposed women who were enrolled in the PTSD substudy of the Nurses' Health Study II and completed 1 to 5 cognitive assessments. Data were collected from March 1, 2008, to July 30, 2019., Exposures: Lifetime PTSD symptoms, assessed using a validated questionnaire between March 1, 2008, and February 28, 2010., Main Outcomes and Measures: The main outcome was evaluated using the Cogstate Brief Battery, a self-administered online cognitive battery. Cognitive function was measured by a psychomotor speed and attention composite score and a learning and working memory composite score. Women completed the Cogstate Brief Battery every 6 or 12 months (up to 24 months) from October 3, 2014, to July 30, 2019. Linear mixed-effects models were used to evaluate the association of PTSD symptoms with the rate of change in cognition over follow-up, considering a broad range of relevant covariates, including the presence of depression symptoms and history of clinician-diagnosed depression. The rate of cognitive change was adjusted for potential practice effects (ie, potential changes in test results that occur when a test is taken more than once) by including indicators for the number of previous tests taken., Results: Among 12 270 women, the mean (SD) age at the baseline cognitive assessment was 61.1 (4.6) years; 125 women (1.0%) were Asian, 75 (0.6%) were Black, 156 (1.3%) were Hispanic, 11 767 (95.9%) were non-Hispanic White, and 147 (1.2%) were of other race and/or ethnicity. A higher number of PTSD symptoms was associated with worse cognitive trajectories. Compared with women with no PTSD symptoms, women with the highest symptom level (6-7 symptoms) had a significantly worse rate of change in both learning and working memory (β = -0.08 SD/y; 95% CI, -0.11 to -0.04 SD/y; P < .001) and psychomotor speed and attention (β = -0.05 SD/y; 95% CI, -0.09 to -0.01 SD/y; P = .02), adjusted for demographic characteristics. Associations were unchanged when additionally adjusted for behavioral factors (eg, 6-7 symptoms in the analysis of learning and working memory: β = -0.08 SD/y; 95% CI, -0.11 to -0.04 SD/y; P < .001) and health conditions (eg, 6-7 symptoms in the analysis of learning and working memory: β = -0.08 SD/y; 95% CI, -0.11 to -0.04 SD/y; P < .001) and were partially attenuated but still evident when further adjusted for practice effects (eg, 6-7 symptoms in the analysis of learning and working memory: β = -0.07 SD/y; 95% CI, -0.10 to -0.03 SD/y; P < .001) and comorbid depression (eg, 6-7 symptoms in the analysis of learning and working memory: β = -0.07 SD/y; 95% CI, -0.11 to -0.03 SD/y; P < .001)., Conclusions and Relevance: In this large-scale prospective cohort study, PTSD was associated with accelerated cognitive decline in middle-aged women, suggesting that earlier cognitive screening among women with PTSD may be warranted. Given that cognitive decline is strongly associated with subsequent Alzheimer disease and related dementias, better understanding of this association may be important to promote healthy aging.

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., Competing Interests: Disclosure LS is supported by the National Institutes of Health (T32 HL098048). SCJ, RBL, ALR, AR, JHK, LDK, KCK, and EBR are supported by the National Institutes of Health (R01 MH101269). KN is supported by the Department of Veterans Affairs Office of Academic Affiliations Advanced Fellowship Program in Mental Illness Research and Treatment, the Medical Research Service of the San Francisco Veterans Affairs Healthcare System (SFVAHCS), and the Department of Veterans Affairs Sierra-Pacific Mental Illness Research, Education, and Clinical Center (MIRECC). The Nurses' Health Study II cohort infrastructure is supported by the National Institutes of Health (U01 CA176726). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. In the past three years, LS received support from the National Institutes of Health (R01 MH119193 and R01 MH107641), the U.S. Department of Justice (2017-MU-GX-K144), and the U.S. Department of Defense (W81XWH-15-1-0080). In the past three years, KN was supported by the National Institutes of Health (T32 MH017119). In the past three years, JHK received support from the National Institutes of Health (R21 AG051001). In the past three years, JAS received consulting fees from Unilever and was supported by the National Institutes of Health (K01 HL130650 and R01 HL139614) and the U.S. Department of Defense (DOD PR171210). In the past three years, KCK received royalties from Guilford Press, consulting fees from Discovery LTD, Baker Hostetler, and Capita, and speaking honoraria from the Coverys, Sigmund Freud University, University of Southern California and the European Central Bank. No other authors report any other disclosures. Data and/or research tools used in the preparation of this manuscript were submitted to the National Institute of Mental Health (NIMH) Data Archive (NDA). NDA is a collaborative informatics system created by the National Institutes of Health to provide a national resource to support and accelerate research in mental health. Dataset identifier: 10.15154/1522677. This manuscript reflects the views of the authors and may not reflect the opinions or views of the NIH or of the Submitters submitting original data to NDA., (Copyright © 2021 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.)

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 ( β  = -.15, p = .001) and learning/working memory ( β  = -.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., (© 2021 Wiley Periodicals LLC.)

Background: Posttraumatic 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., Methods: The 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., Results: Across 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., Conclusions: These 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., (Published by Elsevier Ltd.)

Background: Posttraumatic stress disorder (PTSD) is associated with higher risk of certain chronic diseases, including ovarian cancer, but underlying mechanisms remain unclear. Although prior work has linked menopausal hormone therapy (MHT) use with elevated ovarian cancer risk, little research considers PTSD to likelihood of MHT use. We examined whether PTSD was prospectively associated with greater likelihood of initiating MHT use over 26 years., Methods: Using data from the Nurses' Health Study II, with trauma and PTSD (symptoms and onset date) assessed by screener in 2008 and MHT assessed via biennial survey (from 1989), we performed Cox proportional regression models with women contributing person-years from age 36 years. Relevant covariates were assessed at biennial surveys. We considered potential effect modification by race/ethnicity, age at baseline, and period (1989-2002 vs. 2003-2015)., Results: Over follow-up, 22,352 of 43,025 women reported initiating MHT use. For example, compared with women with no trauma, the HR for initiating MHT was 1.18 for those with trauma/1-3 PTSD symptoms [95% confidence interval (CI), 1.13-1.22] and 1.31 for those with trauma/4-7 PTSD symptoms (95% CI, 1.25-1.36; P trend < 0.001), adjusting for sociodemographic factors. Associations were maintained when adjusting for reproductive factors and health conditions. We found evidence of effect modification by age at baseline., Conclusions: Trauma and number of PTSD symptoms were associated with greater likelihood of initiating MHT use in a dose-response manner., Impact: MHT may be a pathway linking PTSD to altered chronic disease risk. It is important to understand why women with PTSD initiate MHT use., (©2020 American Association for Cancer Research.)

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.

Importance: Consistent evidence has found associations between posttraumatic stress disorder (PTSD) and increased risk of chronic disease and greater prevalence of health risk factors. However, the association between PTSD and all-cause mortality has not been thoroughly investigated in civilians., Objective: To investigate the association between PTSD symptoms, with or without comorbid depressive symptoms, and risk of death., Design, Setting, and Participants: This prospective cohort study was conducted using data on female US nurses in the Nurses' Health Study II followed up from 2008 to 2017. Women who responded to a 2008 questionnaire querying PTSD and depressive symptoms were included. Data were analyzed from September 2018 to November 2020., Exposures: Symptoms of PTSD, measured using the short screening scale for Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) PTSD, and depression symptoms, measured using the Center for Epidemiologic Studies Depression Scale-10 in 2008., Main Outcomes and Measures: All-cause mortality was determined via National Death Index, US Postal Service, or report of participant's family. The hypothesis being tested was formulated after data collection. Trauma exposure and PTSD symptoms were jointly coded as no trauma exposure (reference), trauma and no PTSD symptoms, 1 to 3 PTSD symptoms (subclinical), 4 to 5 PTSD symptoms (moderate), and 6 to 7 PTSD symptoms (high)., Results: Among 51 602 women (50 137 [97.2%] White individuals), the mean (range) age was 53.3 (43-64) years at study baseline in 2008. PTSD and probable depression were comorbid; of 4019 women with high PTSD symptoms, 2093 women (52.1%) had probable depression, while of 10 105 women with no trauma exposure, 1215 women (12.0%) had probable depression. Women with high PTSD symptoms and probable depression were at nearly 4-fold greater risk of death compared with women with no trauma exposure and no depression (hazard ratio [HR], 3.80; 95% CI, 2.65-5.45; P < .001). After adjustment for health factors, women with these conditions had a more than 3-fold increased risk (HR, 3.11; 95% CI, 2.16-4.47, P < .001). Women with subclinical PTSD symptoms without probable depression had increased risk of death compared with women with no trauma exposure and no depression (HR, 1.43; 95% CI, 1.06-1.93; P = .02). Among 7565 women with PTSD symptoms and probable depression, 109 deaths (1.4%) occurred for which we obtained cause of death information, compared with 124 such deaths (0.6% ) among 22 215 women with no depression or PTSD symptoms. Women with PTSD symptoms and probable depression, compared with women with no PTSD or depression, had higher rates of death from cardiovascular disease (17 women [0.22%] vs 11 women [0.05%]; P < .001), diabetes (4 women [0.05%] vs 0 women; P < .001), unintentional injury (7 women [0.09%] vs 7 women [0.03%]; P = .03), suicide (9 women [0.12%] vs 1 woman [<0.01%]; P < .001), and other causes of death (14 women [0.19%] vs 17 women [0.08%]; P = .01)., Conclusions and Relevance: These findings suggest that at midlife, women with high PTSD symptoms and co-occurring probable depression are at increased risk of death compared with women without these disorders. Treatment of PTSD and depression in women with symptoms of both disorders and efforts to improve their health behaviors may reduce their increased risk of mortality.

Posttraumatic stress disorder (PTSD) has increasingly been linked to heightened systemic inflammation. It matters whether this association is causal (and either bidirectional or unidirectional) or correlational. Investigators have hypothesized that chronic systemic low-grade inflammation may contribute to greater risk of developing PTSD after experiencing trauma and/or serve as a mechanism linking PTSD to adverse physical health outcomes. However, if the PTSD-inflammation relation is correlational, it may not warrant further research aimed at understanding inflammation as a PTSD risk factor or as a pathway linking PTSD with poor health. In this review, we first assess the longitudinal evidence related to PTSD and inflammation to understand more clearly the directionality and causal nature of this relation. Overall, few longitudinal studies rigorously assess the direction of the PTSD-inflammation relation. Some of the evidence indicates that elevated inflammation assessed pretrauma or in the acute aftermath of trauma increases risk for developing PTSD. Fewer studies evaluate the influence of PTSD on subsequent inflammation levels, and findings are mixed. Sample characteristics and study designs, and also the type of inflammation-related measure, vary widely across studies. Based on current evidence, we then recommend several statistical and study design approaches that may help untangle issues of bidirectionality and aid in determining the direction of causality between PTSD and inflammation. Last, we conclude with future research directions and consider potential implications for interventions or treatment approaches based on this growing body of literature., (Copyright © 2019 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

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.

Ovarian cancer is the deadliest gynecologic cancer. Chronic stress accelerates tumor growth in animal models of ovarian cancer. We therefore postulated that posttraumatic stress disorder (PTSD) may be associated with increased risk of ovarian cancer. We used data from the Nurses' Health Study II, a longitudinal cohort study with 26 years of follow-up, conducted from 1989 to 2015 with 54,710 subjects. Lifetime PTSD symptoms were measured in 2008. Self-reported ovarian cancer was validated with medical records. Risk of ovarian cancer was estimated with Cox proportional hazards models and further adjusted for known ovarian cancer risk factors (e.g., hormonal factors) and health risk factors (e.g., smoking). Fully prospective secondary analyses examined incident ovarian cancer occurring after PTSD assessment in 2008. In addition, we examined associations by menopausal status. During follow-up, 110 ovarian cancers were identified. Women with high PTSD symptoms had 2-fold greater risk of ovarian cancer versus women with no trauma exposure [age-adjusted HR = 2.10; 95% confidence interval (CI), 1.12-3.95]. Adjustment for health and ovarian cancer risk factors moderately attenuated this association (HR = 1.86; 95% CI, 0.98-3.51). Associations were similar or moderately stronger in fully prospective analyses (age-adjusted HR = 2.38; 95% CI, 0.98-5.76, N cases = 50) and in premenopausal women (HR = 3.42; 95% CI, 1.08-10.85). In conclusion, we show that PTSD symptoms are associated with increased risk of ovarian cancer. Better understanding of the underlying molecular mechanisms could lead to interventions that reduce ovarian cancer risk in women with PTSD and other stress-related mental disorders. SIGNIFICANCE: PTSD is associated with ovarian cancer risk, particularly in premenopausal women. Understanding the underlying molecular mechanisms will aid in formulating ways to reduce ovarian cancer risk associated with chronic stress., (©2019 American Association for Cancer Research.)

Introduction: The relation between TV viewing and posttraumatic stress disorder (PTSD) is controversial; prior work focused exclusively on whether TV viewing of disaster events constitutes a traumatic stressor that causes PTSD. This study evaluates a possible bidirectional relation between PTSD and TV viewing in community-dwelling women., Methods: Data are from the PTSD subsample of the Nurses' Health II study, an ongoing prospective study of women aged 24-42 years at enrollment and who have been followed biennially (N = 50,020). Trauma exposure and PTSD symptoms (including date of onset) were assessed via the Brief Trauma Questionnaire and the Short Screening Scale for DSM-IV PTSD. Average TV viewing was reported at 5 times over 18 years of follow-up. Linear mixed models assessed differences in TV viewing patterns by trauma/PTSD status. Among women with trauma/PTSD onset during follow-up (N = 14,374), linear spline mixed models assessed differences in TV viewing patterns before and after PTSD onset., Results: Women with high PTSD symptoms reported more TV viewing (hours/wk) compared to trauma-unexposed women at all follow-up assessments (β = 0.14, SE = 0.01, p < .001). Among the women who experienced trauma during follow-up, significant increases in TV viewing (hours/day) prior to onset of high PTSD symptom levels were evident (β = 0.15, SE = 0.02, p < .001)., Conclusions: TV viewing following trauma exposure may be a marker of vulnerability for developing PTSD and also a consequence of having PTSD. High TV viewing levels may be linked with ineffective coping strategies or social isolation, which increase risk of developing PTSD., Competing Interests: The authors have declared that no competing interests exist.

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., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD., Methods: We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses' Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease-free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n = 174). The reference group was women without trauma., Results: In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05)., Conclusions: Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk., (Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Objective: To conduct the first longitudinal study examining whether trauma exposure and posttraumatic stress disorder (PTSD) are associated with increased risk of incident systemic lupus erythematosus (SLE) in a civilian cohort., Methods: We examined the association of trauma exposure and PTSD symptoms with SLE incidence over 24 years of follow-up in a US longitudinal cohort of women (n = 54,763). Incident SLE in women meeting ≥4 American College of Rheumatology criteria was ascertained by self-report and confirmed by medical record review. PTSD and trauma exposure were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition PTSD and the Brief Trauma Questionnaire, respectively. Women were categorized as having no trauma, trauma and no PTSD symptoms, subclinical PTSD (1-3 symptoms), or probable PTSD (4-7 symptoms). We examined whether longitudinally assessed health risk factors (e.g., smoking, body mass index [BMI], oral contraceptive use) accounted for increased SLE risk among women with trauma exposure and PTSD versus those without., Results: During follow-up, 73 cases of SLE occurred. Compared to women with no trauma, probable PTSD was associated with increased SLE risk (for 4-7 symptoms, hazard ratio [HR] 2.94 [95% confidence interval {95% CI} 1.19-7.26], P < 0.05). Subclinical PTSD was associated with increased SLE risk, although this did not reach statistical significance (for 1-3 symptoms, HR 1.83 [95% CI 0.74-4.56], P = 0.19). Smoking, BMI, and oral contraceptive use slightly attenuated the associations (e.g., for 4-7 symptoms, adjusted HR 2.62 [95% CI 1.09-6.48], P < 0.05). Trauma exposure, regardless of PTSD symptoms, was strongly associated with incident SLE (HR 2.83 [95% CI 1.29-6.21], P < 0.01)., Conclusion: This study contributes to growing evidence that psychosocial trauma and associated stress responses may lead to autoimmune disease., (© 2017, American College of Rheumatology.)

Introduction: Post-traumatic stress disorder (PTSD) may be associated with physical inactivity, a modifiable lifestyle factor that contributes to risk of cardiovascular and other chronic diseases; however, no study has evaluated the association between PTSD onset and subsequent physical activity (PA) changes., Method: Analyses were conducted between October 2014 and April 2016, using data from the ongoing Nurses' Health Study II (N=50,327). Trauma exposure and PTSD symptoms were assessed using two previously validated measures, the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD. Average PA (hours/week) was assessed using self-report measures at six time points across 20 years (1989-2009). Linear mixed models with time-updated PTSD assessed differences in PA trajectories by trauma/PTSD status. Among a subsample of women whose trauma/PTSD onset during follow-up, group differences in PA patterns before and after onset were assessed using linear spline models., Results: PA decreased more steeply over time among trauma-exposed women reporting four or five (β= -2.5E -3 , SE=1.0E -3 , p=0.007) or six or seven PTSD symptoms (β= -6.7E -3 , SE=1.1E -3 , p<0.001) versus women without trauma exposure, adjusting for potential confounders. Among a subsample of women whose trauma/PTSD symptoms onset during follow-up, no differences in PA were observed prior to onset; after onset, women with six or seven PTSD symptoms had a steeper decline (β= -17.1E -3 , SE=4.2E -3 , p<0.001) in PA over time than trauma-exposed women without PTSD., Conclusions: Decreases in PA associated with PTSD symptoms may be a pathway through which PTSD influences cardiovascular and other chronic diseases., (Copyright © 2017 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.)

Background: Prior studies suggest that post-traumatic stress disorder (PTSD) is associated with elevated cardiovascular disease (CVD) risk, but effects of duration and remission of PTSD symptoms have rarely been evaluated., Method: We examined the association of time-updated PTSD symptom severity, remission and duration with incident CVD risk (552 confirmed myocardial infarctions or strokes) over 20 years in 49 859 women in the Nurses' Health Study II. Among women who reported trauma on the Brief Trauma Questionnaire, PTSD symptoms, assessed by a screener, were classified by symptom severity and chronicity: (a) no symptoms, (b) 1-3 ongoing, (c) 4-5 ongoing, (d) 6-7 ongoing, (e) 1-3 remitted, (f) 4-7 remitted symptoms. Inverse probability weighting was used to estimate marginal structural logistic regression models, adjusting for time-varying and time-invariant confounders., Results: Compared with women with no trauma exposure, women with trauma/no PTSD [odds ratio (OR) 1.30, 95% confidence interval (CI) 1.03-1.65] and women with trauma/6-7 symptoms (OR 1.69, 95% CI 1.08-2.63) had elevated risk of CVD; women with remitted symptoms did not have elevated CVD risk. Among women exposed to trauma, every 5 additional years of PTSD symptomology was associated with 9% higher CVD incidence compared with women with trauma/no PTSD., Conclusions: The findings suggest that alleviating PTSD symptoms shortly after onset may attenuate CVD risk.

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 (β = -.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., (© 2017 Wiley Periodicals, Inc.)

Post-traumatic stress disorder (PTSD) has been declared 'a life sentence' based on evidence that the disorder leads to a host of physical health problems. Some of the strongest empirical research - in terms of methodology and findings - has shown that PTSD predicts higher risk of cardiometabolic diseases, specifically cardiovascular disease (CVD) and type 2 diabetes (T2D). Despite mounting evidence, PTSD is not currently acknowledged as a risk factor by cardiovascular or endocrinological medicine. This view is unlikely to change absent compelling evidence that PTSD causally contributes to cardiometabolic disease. This review suggests that with developments in methods for epidemiological research and the rapidly expanding knowledge of the behavioral and biological effects of PTSD the field is poised to provide more definitive answers to questions of causality. First, we discuss methods to improve causal inference using the observational data most often used in studies of PTSD and health, with particular reference to issues of temporality and confounding. Second, we consider recent work linking PTSD with specific behaviors and biological processes, and evaluate whether these may plausibly serve as mechanisms by which PTSD leads to cardiometabolic disease. Third, we evaluate how looking more comprehensively into the PTSD phenotype provides insight into whether specific aspects of PTSD phenomenology are particularly relevant to cardiometabolic disease. Finally, we discuss new areas of research that are feasible and could enhance understanding of the PTSD-cardiometabolic relationship, such as testing whether treatment of PTSD can halt or even reverse the cardiometabolic risk factors causally related to CVD and T2D., Competing Interests: “None”

Background: Post-traumatic stress disorder (PTSD) has been linked to hypertension, but most research on PTSD and hypertension is cross-sectional, and potential mediators have not been clearly identified. Moreover, PTSD is twice as common in women as in men, but understanding of the PTSD-hypertension relationship in women is limited. We examined trauma exposure and PTSD symptoms in relation to incident hypertension over 22 years in 47 514 civilian women in the Nurses' Health Study II., Method: We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for new-onset hypertension (N = 15 837)., Results: PTSD symptoms assessed with a screen were modestly associated with incident hypertension in a dose-response fashion after adjusting for potential confounders. Compared to women with no trauma exposure, women with 6-7 PTSD symptoms had the highest risk of developing hypertension (HR 1.20, 95% CI 1.12-1.30), followed by women with 4-5 symptoms (HR 1.17, 95% CI 1.10-1.25), women with 1-3 symptoms (HR 1.12, 95% CI 1.06-1.18), and trauma-exposed women with no symptoms (HR 1.04, 95% CI 1.00-1.09). Findings were maintained, although attenuated, adjusting for hypertension-relevant medications, medical risk factors, and health behaviors. Higher body mass index and antidepressant use accounted for 30% and 21% of the PTSD symptom-hypertension association, respectively., Conclusions: Screening for hypertension and reducing unhealthy lifestyle factors, particularly obesity, in women with PTSD may hold promise for offsetting cardiovascular risk.

Background: Trauma exposure and posttraumatic stress disorder (PTSD) have been linked to myocardial infarction and stroke in women, with biological and behavioral mechanisms implicated in underlying risk. The third most common cardiovascular illness, venous thromboembolism (VTE), is a specific health risk for women. Given previous associations with other cardiovascular diseases, we hypothesized that high levels of trauma and PTSD symptoms would be associated with higher risk of incident VTE in younger and middle-aged women., Methods and Results: We used proportional hazards models to estimate hazard ratios (HRs) and 95% CIs for new-onset VTE (960 events) over 22 years in 49 296 women in the Nurses' Health Study II. Compared to no trauma exposure, both trauma exposure and PTSD symptoms were significantly associated with increased risk of developing VTE, adjusting for demographics, family history, and childhood adiposity. Women with the most PTSD symptoms exhibited the greatest risk elevation: trauma/6 to 7 symptoms: HR=2.42 (95% CI, 1.83-3.20); trauma/4 to 5 symptoms: HR=2.00 (95% CI, 1.55-2.59); trauma/1 to 3 symptoms: HR=1.44 (95% CI, 1.12-1.84); trauma/no symptoms: HR=1.72 (95% CI, 1.43-2.08). Results were similar, although attenuated, when adjusting for VTE-relevant medications, medical conditions, and health behaviors., Conclusions: Women with the highest PTSD symptom levels had nearly a 2-fold increased risk of VTE compared to women without trauma exposure in fully adjusted models. Trauma exposure alone was also associated with elevated VTE risk. Trauma and PTSD symptoms may be associated with a hypercoagulable state. Treatment providers should be aware that women with trauma exposure and PTSD symptoms may be vulnerable to VTE., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Objective: To examine the association between symptoms of post-traumatic stress disorder (PTSD) and rheumatoid arthritis (RA) risk in a prospective cohort and to characterize the role of smoking in this relationship., Methods: A subset (n = 54,224) of the Nurses' Health Study II, a prospective cohort of female nurses, completed the Brief Trauma Questionnaire and a screen for PTSD symptoms. Participants were categorized based on trauma exposure and number of PTSD symptoms. Incident RA cases (n = 239) from 1989 to 2011 were identified. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) between PTSD symptoms and incident RA. To identify the impact of smoking, secondary and subgroup analyses were performed. In all analyses, PTSD and smoking were lagged 2 years before the development of RA., Results: Compared to no history of trauma/PTSD symptoms, the HR for ≥4 PTSD symptoms and incident RA was 1.76 (95% CI 1.16-2.67) in models adjusted for age, race, and socioeconomic status. The risk for RA increased with an increasing number of PTSD symptoms (P = 0.01). When smoking was added to the model, the HR for RA remained elevated (HR 1.60 [95% CI 1.05-2.43]). In a subgroup analysis, excluding women who smoked before PTSD onset, results were unchanged (HR 1.68 [95% CI 1.04-2.70])., Conclusion: This study suggests that women with high PTSD symptomatology have an elevated risk for RA, independent of smoking, adding to emerging evidence that stress is an important determinant of physical health., (© 2016, American College of Rheumatology.)

Background: Psychological 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 Results: We 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., Conclusion: Trauma 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., (© 2015 American Heart Association, Inc.)

Importance: Posttraumatic stress disorder (PTSD) is a common, debilitating mental disorder that has been associated with type 2 diabetes mellitus (T2D) and its risk factors, including obesity, in cross-sectional studies. If PTSD increases risk of incident T2D, enhanced surveillance in high-risk populations may be warranted., Objective: To conduct one of the first longitudinal studies of PTSD and incidence of T2D in a civilian sample of women., Design, Setting, and Participants: The Nurses' Health Study II, a US longitudinal cohort of women (N = 49,739). We examined the association between PTSD symptoms and T2D incidence over a 22-year follow-up period., Main Outcomes and Measures: Type 2 diabetes, self-reported and confirmed with self-report of diagnostic test results, symptoms, and medications, a method previously validated by physician medical record review. Posttraumatic stress disorder was assessed by the Short Screening Scale for DSM-IV PTSD. We examined longitudinal assessments of body mass index, smoking, alcohol intake, diet quality, physical activity, and antidepressant use as mediators of possible increased risk of T2D for women with PTSD. The study hypothesis was formulated prior to PTSD ascertainment., Results: Symptoms of PTSD were associated in a dose-response fashion with T2D incidence (1-3 symptoms: hazard ratio, 1.4 [95% CI, 1.2-1.6]; 4 or 5 symptoms; hazard ratio, 1.5 [95% CI, 1.3-1.7]; 6 or 7 symptoms: hazard ratio, 1.8 [95% CI, 1.5-2.1]). Antidepressant use and a higher body mass index associated with PTSD accounted for nearly half of the increased risk of T2D for women with PTSD. Smoking, diet quality, alcohol intake, and physical activity did not further account for increased risk of T2D for women with PTSD., Conclusions and Relevance: Women with the highest number of PTSD symptoms had a nearly 2-fold increased risk of T2D over follow-up than women with no trauma exposure. Health professionals treating women with PTSD should be aware that these patients are at risk of increased body mass index and T2D. Comprehensive PTSD treatment should be expanded to address the health behaviors that contribute to obesity and chronic disease in affected populations.

Importance: Posttraumatic stress disorder (PTSD) indicates a chronic stress reaction in response to trauma. This prevalent condition has been identified as a possible risk factor for obesity. Whether PTSD symptoms alter the trajectory of weight gain or constitute a comorbid condition has not been established., Objective: To determine whether women who develop PTSD symptoms are subsequently more likely to gain weight and become obese relative to trauma-exposed women who do not develop PTSD symptoms or women with no trauma exposure or PTSD symptoms and whether the effects are independent of depression., Design, Setting, and Participants: The Nurses' Health Study II, a prospective observational study initiated in 1989 with follow-up to 2005, using a PTSD screener to measure PTSD symptoms and time of onset. We included the subsample of the Nurses' Health Study II (54 224 participants; ages 24-44 years in 1989) in whom trauma and PTSD symptoms were measured., Exposures: Trauma and PTSD symptoms., Main Outcomes and Measures: Development of overweight and obesity using body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) cut points 25.0 and 30.0, respectively; change in BMI during follow-up among women reporting PTSD symptom onset before 1989; and BMI trajectory before and after PTSD symptom onset among women who developed PTSD symptoms in 1989 or during follow-up., Results: Among women with at least 4 PTSD symptoms before 1989 (cohort initiation), BMI increased more steeply (b = 0.09 [SE = 0.01]; P < .001) during the follow-up. Among women who developed PTSD symptoms in 1989 or later, BMI trajectory did not differ by PTSD status before PTSD onset. After PTSD symptom onset, women with at least 4 symptoms had a faster rise in BMI (b = 0.08 [SE = 0.02]; P < .001). The onset of at least 4 PTSD symptoms in 1989 or later was also associated with an increased risk of becoming overweight or obese (odds ratio, 1.36 [95% CI, 1.19-1.56]) among women with a normal BMI in 1989. Effects were maintained after adjusting for depression., Conclusions and Relevance: Experience of PTSD symptoms is associated with an increased risk of becoming overweight or obese, and PTSD symptom onset alters BMI trajectories over time. The presence of PTSD symptoms should raise clinician concerns about physical health problems that may develop and prompt closer attention to weight status.

It has long been hypothesized that posttraumatic stress disorder (PTSD) increases coronary heart disease (CHD) risk; however, empirical evidence is limited. In the first prospective study to date, individuals with higher PTSD symptom levels had a significantly increased risk for CHD, after controlling for known coronary risk factors. PTSD indicates a chronic stress reaction and is hypothesized to influence CHD either by causing biological alterations that lead to cardiovascular damage, or by leading to adverse health behaviors that increase CHD risk. A key issue is whether PTSD contributes to the development of CHD, if PTSD and CHD share common pathways, or if CHD causes PTSD. Research combined across different disciplines suggests that prolonged or chronic stress does influence the development of CHD. A better understanding of the relationship will increase prevention and intervention efforts. Cardiologists may be most effective when they can recognize and manage emotional distress in practice.

Objective: Posttraumatic stress disorder (PTSD) reflects a prolonged stress reaction and dysregulation of the stress response system and is hypothesized to increase risk of developing coronary heart disease (CHD). No study has tested this hypothesis in women even though PTSD is more prevalent among women than men. This study aims to examine whether higher levels of PTSD symptoms are associated with increased risk of incident CHD among women., Design: A prospective study using data from women participating in the Baltimore cohort of the Epidemiologic Catchment Area study (n = 1059). Past year trauma and associated PTSD symptoms were assessed using the NIMH Diagnostic Interview Schedule., Main Outcome Measures: Incident CHD occurring during the 14-year follow-up through 1996., Results: Women with five or more symptoms were at over three times the risk of incident CHD compared with those with no symptoms (age-adjusted OR = 3.21, 95% CI: 1.29-7.98). Findings were maintained after controlling for standard coronary risk factors as well as depression or trait anxiety., Conclusion: PTSD symptoms may have damaging effects on physical health for civilian community-dwelling women, with high levels of PTSD symptoms associated with increased risk of CHD-related morbidity and mortality., ((c) 2009 APA, all rights reserved.)

Context: Various correlates of posttraumatic stress disorder (PTSD), such as high levels of sympathetic activation and hypothalamic-pituitary-adrenal axis dysregulation, have been linked to arterial damage and coronary heart disease (CHD) risk. While psychological disturbance is frequently found among patients with cardiac disease, whether psychological problems precede or occur as a result of having a potentially fatal disease is not clear. To our knowledge, no prospective studies to date have evaluated whether PTSD is associated with increased risk of CHD., Objective: To test the hypothesis that high levels of PTSD symptoms may increase CHD risk, using 2 different measures of PTSD., Design: Prospective cohort study., Setting: Community-dwelling men from the Greater Boston, Mass, area who served in the military., Participants: Data are from the Veterans Affairs Normative Aging Study. Men who completed either the Mississippi Scale for Combat-Related PTSD in 1990 (n = 1002) or the Keane PTSD scale in 1986 (n = 944) were included in the study., Main Outcome Measure: Incident CHD occurring during follow-up through May 2001., Results: Levels of PTSD symptoms in this cohort were low to moderate. Men with preexisting CHD at baseline were excluded, and PTSD was measured with the Mississippi Scale for Combat-Related PTSD. For each SD increase in symptom level, men had age-adjusted relative risks of 1.26 (95% confidence interval, 1.05-1.51) for nonfatal myocardial infarction and fatal CHD combined and 1.21 (95% confidence interval, 1.05-1.41) for all of the CHD outcomes combined (nonfatal myocardial infarction, fatal CHD, and angina). Findings were replicated using the Keane PTSD scale and somewhat strengthened after controlling for levels of depressive symptoms., Conclusions: To our knowledge, this is the first study to demonstrate a prospective association between PTSD symptoms and CHD even after controlling for depressive symptoms. These results suggest that a higher level of PTSD symptoms may increase the risk of incident CHD in older men.