Complex biological processes that enable optimal foetal growth throughout pregnancy are linked to notable haemodynamic and metabolic changes in the mother's body. An inability to adapt to these changes can affect cardiovascular health. During pregnancy, women may experience mood swings, anxiety, and emotional ambivalence. These symptoms can lead to stress and harm the mental well-being of expectant mothers. It is crucial to know the aspects that can influence the development of cardiovascular problems among pregnant women. Effective management requires identifying risk factors. Applying the PRISMA ScR guidelines, we conducted a scoping review to explore and summarise the evidence regarding the impact of stress and anxiety on cardiovascular health in pregnant women. The following enquiries were looked into as research topics: What effects do anxiety and stress have on a pregnant woman's cardiovascular health? How is it quantifiable? It is essential to comprehend the physiological changes that the body undergoes throughout pregnancy in order to inform and assist both patients and medical professionals. This makes it possible for them to identify any pathological disorders or risk factors that could worsen the health of expectant mothers. Psychological and cardiovascular risk factor screening, either before or during pregnancy, may be able to uncover circumstances that require specific medical and psychological therapies in order to lower maternal morbidity and death from cardiovascular disease. Our findings underscore the need for systematic psychological and cardiovascular screening during prenatal care to mitigate adverse outcomes and improve maternal-foetal health.

This study investigates the impact of single prolonged stress (SPS), a model of post-traumatic stress disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate the mechanisms linking traumatic stress to hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases in blood pressure and heart rate and significantly altered the expression of hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), and FOSL1 in the PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated in the pre-autonomic regions of the PVN, colocalizing with AT1R- and FOSL1-expressing cells, suggesting that oxidative stress may amplify sympathetic activation and stress responses. SPS also increased mRNA levels of pro-inflammatory cytokines (TNFα and IL1β) and inducible nitric oxide synthase (iNOS) in the aorta, and impaired vascular reactivity to vasoconstrictor and vasodilator stimuli, reflecting compromised vascular function. These findings suggest that SPS-sensitize neuroendocrine, autonomic, and vascular pathways create a state of cardiovascular vulnerability that could predispose individuals to hypertension when exposed to additional stressors. Understanding these mechanisms provides critical insights into the pathophysiology of stress-related cardiovascular disorders and underscores the need for targeted therapeutic interventions that address oxidative stress and modulate altered PVN pathways to mitigate the cardiovascular impact of PTSD and related conditions.

This study examines the profound impact of political violence and repression on the mental and physical health of Academics for Peace (AfP) in Turkey. The research combines quantitative and qualitative data to explore the interplay between violence, stigmatization, and health outcomes among the affected academics. This study particularly focuses on the aftermath of the State of Emergency in Turkey in 2016, which led to the dismissal of thousands of academics. We employ the World Health Organization's definition of violence to understand the broad nature of violent acts, encompassing power dynamics and systemic repression. The findings highlight the extensive physical and mental health consequences faced by AfP due to political violence. The prevalence of diagnosed mental illness among respondents is notably high, indicating that exposure to trauma, threats, and repression leads to severe mental distress. Anxiety, depression, post-traumatic stress disorder, and musculoskeletal diseases are among the common health issues reported. The research underscores how political violence disrupts psychosocial pillars including safety and security, bonds and networks, justice, roles and identities, and existential meaning, and explores how these disruptions contribute to communal mental health deterioration. It also identifies the impact on well-being of economic losses, uncertainties, and isolation from social and academic networks.

Young individuals with post-traumatic stress disorder (PTSD) display peripheral vascular and autonomic nervous system dysfunction, two factors potentially stemming from a redox imbalance. It is currently unclear if these aforementioned factors, observed at rest, alter peripheral haemodynamic responses to exercise in this population. This study examined haemodynamic responses to handgrip exercise in young individuals with PTSD following acute antioxidant (AO) supplementation. Thirteen young individuals with PTSD (age 23 ± 3 years), and 13 age- and sex-matched controls (CTRL) participated in the study. Exercise-induced changes to arm blood flow (BF), mean arterial pressure (MAP) and vascular conductance (VC) were evaluated across two workloads of rhythmic handgrip exercise (3 and 6 kg). The PTSD group participated in two visits, consuming either a placebo (PL) or AO prior to their visits. The PTSD group demonstrated significantly lower VC (P = 0.04) across all exercise workloads (vs. CTRL), which was significantly improved following AO supplementation. In the PTSD group, AO supplementation improved VC in participants possessing the lowest VC responses to handgrip exercise, with AO supplementation significantly improving VC responses (3 and 6 kg: P < 0.01) by blunting elevated exercise-induced MAP responses (3 kg: P = 0.01; 6 kg: P < 0.01). Lower VC responses during handgrip exercise were improved following AO supplementation in young individuals with PTSD. AO supplementation was associated with a blunting of exercise-induced MAP responses in individuals with PTSD displaying elevated MAP responses. This study revealed that young individuals with PTSD exhibit abnormal, peripherally mediated exercise responses that may be linked to a redox imbalance.

The ongoing Russian invasion of Ukraine marks a critical juncture in a series of events posing severe threat to the health of Ukrainian citizens. While recent reports reveal higher rates of PTSD in Ukrainian refugees following Russia's invasion - data for Ukrainians remaining at the warfront is inherently difficult to access. A primarily elderly demographic, Ukrainians in previously Russian-occupied areas near the front (UPROANF) are at particular risk.

Data was sourced from screening questionnaires administered between March 2022 and July 2023 by mobile health clinics providing services to UPROANF.

Previously occupied villages in Eastern and Southern Ukraine.

UPROANF attending clinics completed voluntary self-report surveys reporting demographics, prior health diagnoses, and PTSD symptom severity (n = 450; Meanage = 53.66; 72.0% female).

Participants were exposed to Russian occupation of Ukrainian villages.

The PTSD Checklist for the DSM-V (PCL-5) with recommended diagnostic threshold (i.e. 31) was utilized to assess PTSD prevalence and symptom severity. ANCOVA was used to examine hypothesized positive associations between (1) HTN and (2) loneliness and PTSD symptoms (cumulative and by symptom cluster).

Between 47.8% and 51.33% screened positive for PTSD. Though cumulative PTSD symptoms did not differ based on HTN diagnostic status, those with HTN reported significantly higher PTSD re-experiencing symptoms (b = 1.25, SE = 0.60, p = .046). Loneliness was significantly associated with more severe cumulative PTSD symptoms (b = 1.29, SE = 0.31, p < .001), re-experiencing (b = 0.47, SE = 0.12, p < .001), avoidance (b = .18, SE = 0.08, p = .038), and hypervigilance (b = 0.29, SE = 0.13, p = .036).

PTSD prevalence was higher than other war-exposed populations. Findings highlight the urgent mental health burden among UPROANF, emphasizing the need for integrated care models addressing both trauma and physical health. Given the significance of loneliness as a risk factor, findings suggest the potential for group-based, mind-body interventions to holistically address the physical, mental, and social needs of this highly traumatized, underserved population.

Background: Women have twice the lifetime prevalence of posttraumatic stress disorder (PTSD) relative to men, and PTSD is a known risk factor for cardiovascular disease (CVD). Two sex hormones - estradiol and progesterone - have been found to impact both PTSD and CVD symptomatology, but the way in which sex hormones influence cardiovascular physiology among individuals with PTSD is not well understood.Objective: This study sought to clarify the association between sex hormones, PTSD, and CVD among trauma-exposed women.Method: Sixty-six trauma-exposed women (M age = 31.45, SD = 8.92) completed a clinical interview for PTSD and self-reported CVD symptoms; estradiol and progesterone were assayed from blood samples. The association between each sex hormone and CVD symptoms was analyzed, controlling for age, systolic blood pressure (BP), and diastolic BP.Results: Neither estradiol nor the PTSD-by-estradiol interaction was significantly associated with CVD symptoms. Higher progesterone and, relatedly, progesterone-to-estradiol ratio (PE ratio) were each significantly associated with greater CVD symptom severity, but only for individuals with lower relative PTSD severity.Conclusions: The findings indicate that PTSD moderates the relationship between progesterone and CVD symptoms, and further research is warranted to reconcile findings in existing literature regarding the direction of and mechanisms behind this relationship.

Growing evidence supports the impact of psychological factors such as traumatic experiences and Post Traumatic Stress Disorder (PTSD) on the incidence of arterial hypertension (HTN) and cardiovascular diseases (CVD). The war in Ukraine is exposing million inhabitants to traumatic experiences and severe stress. Part of Ukrainians (mostly women and children) left the country to escape war. We report the protocol of a prospective study aiming at the assessment of the impact of war-induced stress on HTN and CVD in women Ukrainian refugees who moved to Poland.

The study will be conducted in 3 stages. Stage 1 will assess the prevalence of HTN and PTSD among Ukrainian refugees and will estimate the impact of war-related trauma exposure on these parameters. Data on office blood pressure (BP) will be compared to data already collected in STEPS data 2019 and May Measurement Month 2021 in Ukraine, matched for age and sex. Stage 2 will involve subjects diagnosed with HTN and/or PTSD referred for management and follow-up of these conditions. Psychologic targeted therapies will be offered to subjects with confirmed PTSD, with a periodical reassessment of the severity of PTSD-associated symptoms and of its impact on HTN and cardiovascular health. Clinical history and characteristics will be compared among three groups: subjects with HTN and PTSD, with HTN without PTSD, with PTSD but without HTN. Stage 3 will involve a subgroup among those screened in Stage 1, with the objective of investigating the biological mechanisms underlying the relation between HTN and trauma exposure, identifying early signs of subclinical target organ damage in subjects with HTN with/without PTSD.

This study will test the hypothesis that trauma exposure and psychological stress contribute to BP elevation and progression of CVD in this population. It will provide new evidence on the effect of an integrated management, including psychological therapy, on BP and cardiovascular risk. Such approach may be further tested and extrapolated to other populations exposed to war and chronic violence, migrants and refugees around the world.

number 2022/45/P/NZ5/02812.

Although the link between trauma, posttraumatic stress disorder (PTSD), and hypertension is established, its underlying mechanisms remain underexplored.

This study tested a theoretical model exploring the moderating influence of psychological (emotion regulation) and interpersonal (social support) factors on the mediation between trauma and hypertension, through PTSD.

We measured these variables through self-reported questionnaire on 212 patients, recruited from internal medicine in a general hospital of Bukavu, a region affected by more than 25 years of armed conflicts. We first evaluated the PTSD mediation in the absence of moderators, before testing each moderator using moderated path analysis.

Results showed that PTSD partially mediates the relationship between human-made trauma and hypertension, whereas social support and maladaptive emotion regulation moderate the relationship between human-made trauma and PTSD.

The relationship between human-made trauma, PTSD, and hypertension might be modulated by psychological and interpersonal factors, which paves the way for new interventions targeting emotion regulation and social support to reduce PTSD and hypertension in populations exposed to human-made violence.

Currently, the efficacy of drug therapy for post-traumatic stress disorder or PTSD leaves much to be desired, making nutraceutical support a promising avenue for treatment. Recent research has identified the protective effects of resveratrol in PTSD. Here, we tested the behavioral and neurobiological effects of combining cheese consumption with resveratrol supplements in an experimental PTSD model. Using the elevated plus maze test, we observed that cheese intake resulted in a shift from anxiety-like behavior to depressive behavior, evident in increased freezing acts. However, no significant changes in the anxiety index value were observed. Interestingly, supplementation with cheese and resveratrol only led to the elimination of freezing behavior in half of the PTSD rats. We further segregated the rats into two groups based on freezing behavior: Freezing+ and Freezing0 phenotypes. Resveratrol ameliorated the abnormalities in Monoamine Oxidize -A and Brain-Derived Neurotrophic Factor gene expression in the hippocampus, but only in the Freezing0 rats. Moreover, a negative correlation was found between the number of freezing acts and the levels of Monoamine Oxidize-A and Brain-Derived Neurotrophic Factor mRNAs in the hippocampus. The study results show promise for resveratrol supplementation in PTSD treatment. Further research is warranted to better understand the underlying mechanisms and optimize the potential benefits of resveratrol supplementation for PTSD.

Posttraumatic stress disorder (PTSD) is associated with heightened emotional responding, avoidance of trauma related stimuli, and physical health concerns (e.g., metabolic syndrome, type 2 diabetes, cardiovascular disease). Existing treatments such as exposure-based therapies (e.g., prolonged exposure) aim to reduce anxiety symptoms triggered by trauma reminders, and are hypothesized to work via mechanisms of extinction learning. However, these conventional gold standard psychotherapies do not address physical health concerns frequently presented in PTSD. In addition to widely documented physical and mental health benefits of exercise, emerging preclinical and clinical evidence supports the hypothesis that precisely timed administration of aerobic exercise can enhance the consolidation and subsequent recall of fear extinction learning. These findings suggest that aerobic exercise may be a promising adjunctive strategy for simultaneously improving physical health while enhancing the effects of exposure therapies, which is desirable given the suboptimal efficacy and remission rates. Accordingly, this review 1) encompasses an overview of preclinical and clinical exercise and fear conditioning studies which form the basis for this claim; 2) discusses several plausible mechanisms for enhanced consolidation of fear extinction memories following exercise, and 3) provides suggestions for future research that could advance the understanding of the potential importance of incorporating exercise into the treatment of PTSD.

The goal of the present study was to investigate the association between PTSD and the onset of hypertension in previously normotensive individuals in a population living in the stressful environment of the urban slums while controlling for risk factors for cardiovascular disease (CVD).

Participants were 320 normotensive individuals who lived in slums and were attending a family doctor program. Measurements included a questionnaire covering sociodemographic characteristics, clinical status and life habits, the Posttraumatic Stress Disorder Checklist - Civilian Version, and the Beck Depression Inventory. Incident hypertension was defined as the first occurrence at the follow-up review of the medical records of (1) systolic blood pressure of 140 mm Hg or higher or diastolic blood pressure of 90 mm Hg or higher, (2) the participant started taking antihypertensive medication, or (3) a new diagnosis of hypertension made by a physician. Differences in sociodemographic, clinical, and lifestyle characteristics between hypertensive and non-hypertensive individuals were compared using the χ² and t tests. Multivariate Cox proportional hazards models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI).

Six variables - age, educational level, body mass, smoking, diabetes, and PTSD diagnosis - showed a statistically significant (p ≤ 0.20) association with the hypertensive status. In the Cox regression, only PTSD diagnosis was significantly associated with incident hypertension (multivariate HR = 1.94; 95% CI 1.11-3.40).

The present findings highlight the importance of considering a diagnostic hypothesis of PTSD in the prevention and treatment of cardiovascular diseases.

Veterans, especially women, are three times more to experience sexual harassment and assault [military sexual trauma (MST)] than civilians. As trauma is associated with elevated cardiovascular risk, we investigated whether MST independently contributes to risk for incident hypertension and whether the effects are distinct among women.

We assessed 788 161 post-9/11 Veterans ( Mage  = 32.14 years, 13% women) who were free of hypertension at baseline, using nationwide Veterans Health Administration data collected 2001-2017. Time-varying, multivariate Cox proportional hazard models were used to examine the independent contribution of MST to new cases of hypertension while sequentially adjusting for demographics, lifestyle and cardiovascular risk factors, including baseline blood pressure, and psychiatric disorders including posttraumatic stress disorder. We then tested for effect modification by sex.

Over 16 years [mean = 10.23 (SD: 3.69)], 35 284 Veterans screened positive for MST (67% were women). In the fully adjusted model, MST was associated with a 15% greater risk of hypertension [95% confidence interval (95% CI) 1.11-1.19]. In sex-specific analyses, men and women with a history of MST showed a 6% (95% CI, 1.00-1.12, P  = 0.042) and 20% greater risk of hypertension (95% CI, 1.15-1.26, P  < 0.001), respectively.

In this large prospective cohort of young and middle-aged Veterans, MST was associated with incident hypertension after controlling for established risk factors, including trauma-related psychiatric disorders. Although MST is disproportionately experienced by women, and the negative cardiovascular impact of MST is demonstrated for both sexes, the association with hypertension may be greater for women. Subsequent research should determine if early MST assessment and treatment attenuates this risk.

3,4-Methylenedioxymethamphetamine (MDMA/"ecstasy") is an empathogen that can give rise to increased pleasure and empathy and may effectively treat post-traumatic stress disorder. Although prior research has demonstrated associations between ecstasy use and favorable mental health outcomes, the associations between ecstasy and physical health have largely been unexplored. Thus, the goal of this study was to examine the associations between ecstasy use and physical health in a population-based survey sample.

This study utilized data from the National Survey on Drug Use and Health (2005-2018), a yearly survey that collects information on substance use and health outcomes in a nationally representative sample of U.S. adults. We used multinomial, ordered, and logistic regression models to test the associations between lifetime ecstasy use and various markers of physical health (self-reported body mass index, overall health, past year heart condition and/or cancer, past year heart disease, past year hypertension, and past year diabetes), controlling for a range of potential confounders.

Lifetime ecstasy use was associated with significantly lower risk of self-reported overweightness and obesity (adjusted relative risk ratio range: 0.55-0.88) and lower odds of self-reported past year heart condition and/or cancer (adjusted odds ratio (aOR): 0.67), hypertension (aOR: 0.85), and diabetes (aOR: 0.58). Ecstasy use was also associated with significantly higher odds of better self-reported overall health (aOR: 1.18).

Ecstasy shares protective associations with various physical health markers. Future longitudinal studies and clinical trials are needed to more rigorously test these associations.

Post-traumatic stress disorder (PTSD), an anxiety-related syndrome, is associated with increased risk for cardiovascular diseases. The present study investigated whether predator scent (PS) stress, a model of PTSD, induces sensitization of hypertension and anxiety-like behaviors and underlying mechanisms related to renin-angiotensin systems (RAS) and inflammation. Coyote urine, as a PS stressor, was used to model PTSD. After PS exposures, separate cohorts of rats were studied for hypertensive response sensitization (HTRS), anxiety-like behaviors, and changes in plasma levels and mRNA expression of several components of the RAS and proinflammatory cytokines (PICs) in the lamina terminalis (LT), paraventricular nucleus (PVN), and amygdala (AMY). Rats exposed to PS as compared to control animals exhibited (1) a significantly greater hypertensive response (i.e., HTRS) when challenged with a slow-pressor dose of angiotensin (ANG) II, (2) significant decrease in locomotor activity and increase in time spent in the closed arms of a plus maze as well as general immobility (i.e., behavioral signs of increased anxiety), (3) upregulated plasma levels of ANG II and interleukin-6, and (4) increased expression of message for components of the RAS and PICs in key brain nuclei. All the PS-induced adverse effects were blocked by pretreatment with either an angiotensin-converting enzyme antagonist or a tumor necrosis factor-α inhibitor. The results suggest that PS, used as an experimental model of PTSD, sensitizes ANG II-induced hypertension and produces behavioral signs of anxiety, probably through upregulation of RAS components and inflammatory markers in plasma and brain areas associated with anxiety and blood pressure control.

Numerous risk factors have been involved in the pathogenesis of hypertension. The contribution of psychological factors, including post-traumatic stress disorder, remains largely underexplored, despite their potential role in hypertension.

We compared the prevalence of trauma, post-traumatic stress and other psychological disorders between hypertensive and normotensive patients from Bukavu (Democratic Republic of Congo), a 25-year war-exposed city.

In this case-control study, we assessed past traumatic events with the Stressful-Events-Scale, post-traumatic stress disorder through the post-traumatic diagnostic scale, depression and alcohol use disorder through the MINI-International-Neuropsychiatric-Interview, and emotion regulation through the Emotion-Regulation-Questionnaire in 106 hypertensive and 106 normotensive patients, enrolled at the Bukavu General Hospital.

Compared with normotensive controls (73% women, age: 43 ± 14 years, BP: 121 ± 10/75 ± 8 mmHg), hypertensive patients (57% women, age: 42 ± 13 years, BP: 141 ± 12/82 ± 7 mmHg, on a median of two antihypertensive drugs) were exposed to more man-made traumas (61 vs. 13%, P < 0.001), used more expressive suppression (P = 0.05) and less cognitive reappraisal (P = 0.02) as emotional regulation strategies. They developed more frequent post-traumatic stress disorder (36 vs. 7%, P < 0.001) and major depressive disorder (37 vs. 13%, P = 0.001), often in association with alcohol use disorder (23 vs. 4%, P < 0.001). In multivariate logistic regression, post-traumatic stress disorder [OR = 3.52 (1.23-6.54)], man-made trauma [OR = 2.24 (1.15-4.12)], family history of hypertension [OR = 2.24 (1.06-4.44)], fasting blood glucose [OR = 1.85 (1.07-3.08)], BMI [OR = 1.28 (1.12-2.92)], expressive suppression [OR = 1.23 (1.11-2.23)] and cognitive reappraisal [OR = 0.76 (0.63-0.98)] were independent predictors of hypertension.

In Congolese populations exposed to war, man-made trauma exposure and post-traumatic stress disorder appear to be more tightly related to hypertension than classical hypertension risk factors.

Much of the literature on hospitalizations post-September 11, 2001 (9/11) focuses on adults but little is known about post-9/11 hospitalizations among children. Data for World Trade Center Health Registry enrollees who were under 18-years old on 9/11 were linked to New York State hospitalization data to identify hospitalizations from enrollment (2003-2004) to December 31, 2016. Logistic regression was used to analyze factors associated with hospitalization. Of the 3151 enrollees under age 18 on 9/11, 243 (7.7%) had at least one 9/11-related physical health hospitalization and 279 (8.9%) had at least one 9/11-related mental health hospitalization. Individuals of non-White race, those living in New York City Housing Authority housing, those exposed to the dust cloud on 9/11, and those with probable 9/11-related PTSD symptoms were more likely to be hospitalized for a 9/11-related physical health condition. Older age and having probable 9/11-related PTSD symptoms at baseline were associated with being hospitalized for a 9/11-related mental health condition. Dust cloud exposure on 9/11 and PTSD symptoms were associated with hospitalizations among those exposed to 9/11 as children. Racial minorities and children living in public housing were at greater risk of hospitalization. Continued monitoring of this population and understanding the interplay of socioeconomic factors and disaster exposure will be important to understanding the long-term effects of 9/11.

Posttraumatic stress disorder (PTSD) is characterized by a persistent maladaptive reaction after exposure to severe psychological trauma. Traumatic events that may precipitate PTSD include violent personal assaults, natural and human-made disasters, and exposure to military combat or warfare. There is a growing body of evidence for associations of PTSD with major risk factors for cardiovascular disease (CVD), such as hypertension and diabetes, as well as with major CVD outcomes, such as myocardial infarction and heart failure. However, it is unclear whether these associations are causal or confounded. Furthermore, the biological and behavioral mechanisms underlying these associations are poorly understood. Here, the available evidence on the association of PTSD with CVD from population, basic, and genomic research as well as from clinical and translational research are reviewed, seeking to identify major research gaps, barriers, and opportunities in knowledge acquisition and technology as well as research tools to support and accelerate critical research for near-term and longer-term translational research directions. Large-scale, well-designed prospective studies, capturing diverse and high-risk populations, are warranted that include uniform phenotyping of PTSD as well as broad assessment of biological and behavioral risk factors and CVD outcomes. Available evidence from functional brain imaging studies demonstrates that PTSD pathophysiology includes changes in specific anatomical brain regions and circuits, and studies of immune system function in individuals with PTSD suggest its association with enhanced immune inflammatory activity. However, establishment of animal models and human tissue biobanks is also warranted to elucidate the potential causal connection of PTSD-induced brain changes and/or inflammation with CVD pathophysiology. Emerging large-scale genome-wide association studies of PTSD will provide an opportunity to conduct mendelian randomization studies that test hypotheses regarding the presence, magnitude, and direction of causal associations between PTSD and CVD outcomes. By identifying research gaps in epidemiology and genomics, animal, and human translational research, opportunities to better justify and design future interventional trials are highlighted that may test whether treatment of PTSD or underlying neurobiological or immune dysregulation may improve or prevent CVD risk or outcomes.

Growing research suggests that posttraumatic stress disorder (PTSD) may be a risk factor for poor cardiovascular health, and yet our understanding of who might be at greatest risk of adverse cardiovascular outcomes after trauma is limited. In this study, we conducted the first examination of the individual and synergistic contributions of PTSD symptoms and blood pressure genetics to continuous blood pressure levels. We harnessed the power of the Psychiatric Genomics Consortium-PTSD Physical Health Working Group and investigated these associations across 11 studies of 72,224 trauma-exposed individuals of European (n = 70,870) and African (n = 1,354) ancestry. Genetic contributions to blood pressure were modeled via polygenic scores (PGS) for systolic blood pressure (SBP) and diastolic blood pressure (DBP) that were derived from a prior trans-ethnic blood pressure genome-wide association study (GWAS). Results of trans-ethnic meta-analyses revealed significant main effects of the PGS on blood pressure levels [SBP: β = 2.83, standard error (SE) = 0.06, p < 1E-20; DBP: β = 1.32, SE = 0.04, p < 1E-20]. Significant main effects of PTSD symptoms were also detected for SBP and DBP in trans-ethnic meta-analyses, though there was significant heterogeneity in these results. When including data from the largest contributing study - United Kingdom Biobank - PTSD symptoms were negatively associated with SBP levels (β = -1.46, SE = 0.44, p = 9.8E-4) and positively associated with DBP levels (β = 0.70, SE = 0.26, p = 8.1E-3). However, when excluding the United Kingdom Biobank cohort in trans-ethnic meta-analyses, there was a nominally significant positive association between PTSD symptoms and SBP levels (β = 2.81, SE = 1.13, p = 0.01); no significant association was observed for DBP (β = 0.43, SE = 0.78, p = 0.58). Blood pressure PGS did not significantly moderate the associations between PTSD symptoms and blood pressure levels in meta-analyses. Additional research is needed to better understand the extent to which PTSD is associated with high blood pressure and how genetic as well as contextual factors may play a role in influencing cardiovascular risk.

Posttraumatic stress disorder (PTSD) has been associated with an increase in risk of cardiovascular disease (CVD). The goal of this study was to determine if peripheral vascular dysfunction, a precursor to CVD, was present in young adults with PTSD, and if an acute antioxidant (AO) supplementation could modify this potential PTSD-induced vascular dysfunction. Thirteen individuals with PTSD were recruited for this investigation and were compared with 35 age- and sex-matched controls (CTRL). The PTSD group participated in two visits, consuming either a placebo (PTSD-PL) or antioxidants (PTSD-AO; vitamins C and E; α-lipoic acid) before their visits, whereas the CTRL subjects only participated in one visit. Upper and lower limb vascular functions were assessed via flow-mediated dilation and passive leg movement technique. Heart rate variability was utilized to assess autonomic nervous system modulation. The PTSD-PL condition, when compared with the CTRL group, reported lower arm and leg microvascular function as well as sympathetic nervous system (SNS) predominance. After acute AO supplementation, arm, but not leg, microvascular function was improved and SNS predominance was lowered to which the prior difference between PTSD group and CTRL was no longer significant. Young individuals with PTSD demonstrated lower arm and leg microvascular function as well as greater SNS predominance when compared with age- and sex-matched controls. Furthermore, this lower vascular/autonomic function was augmented by an acute AO supplementation to the level of the healthy controls, potentially implicating oxidative stress as a contributor to this blunted vascular/autonomic function.

This study tested whether aerobic exercise delivered during the consolidation window following fear extinction learning reduces the return of fear among women with posttraumatic stress disorder (PTSD). Participants (n=35) completed an initial clinical assessment followed by a 3-day fear acquisition, extinction, and recall protocol. On day 1, participants completed a fear acquisition training task in which one geometric shape (conditioning stimulus; CS+) was paired (with 50% probability) with a mild electric shock (unconditioned stimulus; US), while a different shape (CS-) was never paired with the US. On day 2 (24 h later), participants completed a fear extinction training task in which the CS+ no longer predicted administration of the US. Shortly following extinction, participants were randomly assigned to complete either moderate-intensity aerobic exercise (EX) or a light-intensity exercise control (CON) condition. On day 3 (24 h later), participants completed fear recall tests assessing the return of fear (spontaneous recovery, renewal, and reinstatement). Fear responding was assessed via threat expectancy ratings and skin conductance responses (SCR). In the threat expectancy ratings, there were no significant differences between groups in spontaneous recovery; however, EX significantly (p=.02) reduced threat expectancy ratings following reinstatement relative to CON. In SCR measures, there were no significant differences between groups in spontaneous recovery, renewal, or reinstatement. These results support a role for moderate-intensity aerobic exercise during the consolidation window in reducing threat expectations following reinstatement in women with PTSD. Research should continue to examine exercise as a potential method for improving the efficacy of exposure-based therapies. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04113798.

Stroke is a major cause of mortality and disability globally that has multiple risk factors. A risk factor that has recently gained more attention is post-traumatic stress disorder (PTSD). Literature searches were carried out for updated PTSD information and for the relationship between PTSD and stroke. The review was divided into two sections, one exploring PTSD as an independent risk factor for stroke, with a second concentrating on PTSD's influence on stroke risk factors. The study presents accumulating evidence that shows traumatic stress predicts stroke and is also linked to many major stroke risk factors. The review contributes knowledge to stroke aetiology and acts as a reference for understanding the relationship between PTSD and stroke. The information presented indicates that screening and identification of traumatic experience would be beneficial for directing stroke patients to appropriate psychological and lifestyle interventions. In doing so, the burden of stroke may be reduced worldwide.

Mental health conditions are common and can have significant effects during the perinatal period. Our objective was to determine the incidences and predictors of psychiatric conditions during pregnancy and postpartum among universally insured American women.

This was an Institutional Review Board (IRB)-approved protocol using a retrospective cohort of 104,866 deliveries covered by TRICARE from 2005 to 2014. We used TRICARE claims data to identify pregnant women without current psychiatric conditions who developed new psychiatric condition(s) during pregnancy or postpartum compared with those who did not, as identified by International Classification of Diseases (ICD)-9 CM codes. Predictors of psychiatric conditions during pregnancy or postpartum were determined using stepwise logistic regression models.

A total of 104,866 women met the inclusion criteria; of these, 35% (n = 36,192) were diagnosed with a new psychiatric condition during pregnancy or within 1 year of delivery, 15% (n = 15,636) with a psychiatric condition during pregnancy, and 20% (n = 20,556) with a psychiatric condition within 1 year of delivery. We demonstrated that the African-American race (odds ratio [OR] 1.16, 95% CI 1.10-1.22), active duty status (OR 1.20, 95% CI 1.14-1.25), and severe maternal morbidity during delivery (OR 1.18, 95% CI 1.02-1.35) were significantly associated with the occurrence of a psychiatric condition within 1 year of delivery. For Asian women, there was a 28% higher odds of developing a psychiatric disorder during pregnancy (adjusted OR 1.28, 95% CI 1.17-1.40) compared with White women. Active duty women were twice as likely to be diagnosed with post-traumatic stress disorder (adjusted OR 2.31, 95% CI 1.83-2.90).

In a universally insured population, the incidences of psychiatric conditions in pregnancy and within a year of delivery were similar to the American population. Additionally, the development of psychiatric conditions in pregnancy and within a year of delivery may be associated with race, active duty status, and complicated births.

A better understanding of the long-term health effects of combat injury is important for the management of veterans' health in the Department of Defense (DoD) and Veterans Affairs (VA) health care systems and may have implications for primary care management of civilian trauma patients.

To determine the impact of traumatic injury on the subsequent development of hypertension (HTN), diabetes mellitus (DM), and coronary artery disease (CAD) after adjustment for sociodemographic, health behavior, and mental health factors.

Retrospective cohort study of current and former US military personnel with data obtained from both the DoD and VA health care systems.

Combat injured (n = 8727) service members between 1 February 2002 and 14 June 2016 randomly selected from the DoD Trauma Registry matched 1:1 based on year of birth, sex, and branch of service to subjects that deployed to a combat zone but were not injured.

Traumatic injury, stratified by severity, compared with no documented injury. Diagnoses of HTN, DM, and CAD defined by International Classification of Diseases 9th or 10th Revision Clinical Modification codes.

After adjustment, severe traumatic injury was significantly associated with HTN (HR 2.78, 95% CI 2.18-3.55), DM (HR 4.45, 95% CI 2.15-9.18), and CAD (HR 4.87, 95% CI 2.11-11.25), compared with no injury. Less severe injury was associated with HTN (HR 1.14, 95% CI 1.05-1.24) and CAD (HR 1.62, 95% CI 1.11-2.37).

Severe traumatic injury is associated with the subsequent development of HTN, DM, and CAD. These findings have profound implications for the primary care of injured service members in both the DoD/VA health systems and may be applicable to civilian trauma patients as well. Further exploration of pathophysiologic, health behavior, and mental health changes after trauma is warranted to guide future intervention strategies.

Posttraumatic stress disorder (PTSD) is an independent risk factor for the development of hypertension and cardiovascular disease. Patients with PTSD have heightened blood pressure and sympathetic nervous system reactivity; however, it is unclear if patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation that could also contribute to increased blood pressure reactivity. Therefore, we hypothesized that patients with PTSD have increased sensitivity of vascular α₁-adrenergic receptors (α1ARs), the major mediators of vasoconstriction in response to release of norepinephrine at sympathetic nerve terminals. To assess vascular α1AR sensitivity, we measured the degree of venoconstriction in a dorsal hand vein in response to exponentially increasing doses of the selective α1AR agonist, phenylephrine (PE), in 9 patients with PTSD (age = 59 ± 2 yr) and 10 age-matched controls (age = 60 ± 1 yr). Individual dose-response curves were generated to determine the dose of PE that induces 50% of maximal venoconstriction (i.e., PE ED₅₀) reflective of vascular α1AR sensitivity. In support of our hypothesis, PE ED₅₀ values were lower in PTSD compared with controls (245 ± 54 ng/min vs. 1,995 ± 459 ng/min, P = 0.012), indicating increased vascular α₁AR sensitivity in PTSD. The PTSD group also had an increase in slope of rise in venoconstriction, indicative of an altered venoconstrictive reactivity to PE compared with controls (19.8% ± 1.2% vs. 15.1% ± 1.2%, P = 0.009). Heightened vascular α₁AR sensitivity in PTSD may contribute to augmented vasoconstriction and blood pressure reactivity to sympathoexcitation and to increased cardiovascular disease risk in this patient population.

Populations in the global south are disproportionately exposed to the stressors of development, disaster and armed conflict, all of which heighten cardiovascular disease (CVD) risk. We consider how war-related stressors exert a lasting influence upon population health, in particular the cardiovascular health of war survivors now entering older adulthood. Data come from the 2018 Vietnam Health and Aging Study conducted among 2447 northern Vietnamese adults age 60 and older. We conduct survey-adjusted logistic regression analyses to examine the associations among respondents' wartime exposure to combat and physical threat, malevolent environment conditions, and four CVD conditions (hypertension, dyslipidemia, heart disease, and stroke). We examine posttraumatic stress disorder (PTSD) as it mediates the association between wartime stress exposures and late life CVD, and gender as it moderates the relationship between wartime stressors and CVD. We find that exposure to wartime combat and violence, as well as malevolent living conditions, exhibit significant, positive associations with cardiovascular conditions. These associations are mediated by the severity of recent PTSD symptoms. For certain CVD conditions, particularly hypertension, the associations between wartime stressors and late life cardiovascular conditions diverge across gender with women experiencing a greater penalty for their exposure to war-related stressors than their male counterparts. We conclude that the stressors of war and resultant PTSD, widespread in this cohort of Vietnamese older adults who endured myriad forms of war exposure during their young adulthood, exhibit modest, yet significant associations with late-life cardiovascular conditions. Women, especially those exposed to wartime violence and combat, bear this CVD burden alongside men.

The goal of this retrospective cohort study was to determine whether stressors related to military service, determined by a diagnosis of chronic post-traumatic stress disorder (cPTSD) or receiving a Purple Heart (PH), are associated with an increased risk of vascular risk factors and disease, which are of great concern for veterans, who constitute a significant portion of the aging US population. The Veterans Integrated Service Network (VISN) 16 administrative database was searched for individuals 65 years or older between October 1, 1997 to September 30, 1999 who either received a PH but did not have cPTSD (PH+/cPTSD-; n = 1499), had cPTSD without a PH (PH-/cPTSD+; n = 3593), had neither (PH-/cPTSD-; n = 5010), or had both (PH+/cPTSD+; n = 153). In comparison to the control group (PH-/cPTSD-), the PH+/cPTSD- group had increased odds ratios for incidence and prevalence of diabetes mellitus, hypertension, and hyperlipidemia. The PH-/cPTSD+ group had increased odds ratios for prevalence of diabetes mellitus and for the incidence and prevalence of hyperlipidemia. The PH-/cPTSD+ and PH+/cPTSD- groups were associated with ischemic heart disease and cerebrovascular disease, but not independently of the other risk factors. The PH+/cPTSD+ group was associated only with an increase in the incidence and prevalence of hyperlipidemia, though this group's much smaller sample size may limit the reliability of this finding. We conclude that certain physical and psychological stressors related to military service are associated with a greater incidence of several vascular risk factors in veterans aged 65 years or older, which in turn are associated with greater rates of ischemic heart disease and cerebrovascular disease.

Posttraumatic stress disorder (PTSD) is associated with increased risk for cardiometabolic disease. Clinically meaningful PTSD improvement is associated with a lower risk for diabetes, but it is not known if similar associations exist for incident hypertension, hyperlipidemia, and clinically relevant weight loss (i.e., ≥5% loss).

Medical record data from Veterans Health Affairs patients with clinic encounters between fiscal year (FY) 2008 to 2015 were used to identify patients with worsening or no PTSD improvement (i.e., PTSD checklist (PCL) score decrease <10), small (10-19 point PCL decrease), and large (≥20 point PCL decrease) PTSD improvement. To estimate the association between degree of PTSD improvement and incident hypertension (n = 979), incident hyperlipidemia (n = 1,139) and incident ≥5% weight loss (1,330), we computed Cox proportional hazard models, controlling for confounding using inverse probability of exposure weighting (IPEW).

Overall, patients were about 40 years of age, 80% male and 65% White. Worsening or no PCL change occurred in about 60%, small improvement in 20%, and large improvement in 20%. After weighting data, compared with worsening or no change, both small and large PTSD improvements were associated, albeit not significantly, with lower risks for hypertension (HR = 0.68; 95% confidence interval, CI [0.46, 1.01] and HR = 0.79; 95% CI [0.53, 1.18], respectively). In weighted data, PTSD improvement was not associated with incident hyperlipidemia or ≥5% weight loss.

We observed limited evidence for an association between PTSD improvement and decreased hypertension risk. PCL decreases were not associated with hyperlipidemia or ≥5% weight loss. Further studies that measure potential physical health benefits of change in specific PTSD symptoms are needed. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Residential mobility is hypothesized to impact health through changes to the built environment and disruptions in social networks, and may vary by neighborhood deprivation exposure. However, there are few longitudinal investigations of residential mobility in relation to health outcomes. This study examined enrollees from the World Trade Center Health Registry, a longitudinal cohort of first responders and community members in lower Manhattan on September 11, 2001. Enrollees who completed ≥2 health surveys between 2004 and 2016 and did not have diabetes (N = 44,089) or hypertension (N = 35,065) at baseline (i.e., 2004) were included. Using geocoded annual home addresses, residential mobility was examined using two indicators: moving frequency and displacement. Moving frequency was defined as the number of times someone was recorded as living in a different neighborhood; displacement as any moving to a more disadvantaged neighborhood. We fit adjusted Cox proportional hazards models with time-dependent exposures (moving frequency and displacement) and covariates to evaluate associations with incident diabetes and hypertension. From 2004 to 2016, the majority of enrollees never moved (54.5%); 6.5% moved ≥3 times. Those who moved ≥3 times had a similar hazard of diabetes (hazard ratio (HR) = 0.78; 95% Confidence Interval (CI): 0.40, 1.53) and hypertension (HR = 0.99; 95% CI: 0.68, 1.43) compared with those who never moved. Similarly, displacement was not associated with diabetes or hypertension. Residential mobility was not associated with diabetes or hypertension among a cohort of primarily urban-dwelling adults.

The purpose of the study was to assess demographic features, rates of trauma exposure, prevalence of post-traumatic stress and depressive symptoms in a group of urban, low-income, African-American women with type 1 or type 2 diabetes mellitus.

We conducted a survey of (n = 290) low-income, African-American women seeking care in the diabetes clinic of an urban hospital and collected data on the demographic characteristics, childhood and nonchildhood abuse trauma exposure, and the severity of post-traumatic stress and depressive symptoms using the Post-traumatic Stress Disorder (PTSD) Symptom Scale (PSS) and the Beck Depression Inventory (BDI). In a subset of women with type 2 diabetes (n = 96), we assessed haemoglobin A1c to examine the relationship between psychopathology and glycaemic control.

Of the overall sample, 61.7% reported exposure to trauma in their lifetime, and 30.4% and 29.3% had current PTSD and MDD, respectively. Exposure to both childhood and nonchildhood abuse trauma was associated with an increased PTSD and depressive symptom severity (P's < .05). PTSD diagnosis, but not depression, was associated with increased haemoglobin A1c (P = .002).

These data document high levels of trauma exposure, PTSD and depressive symptoms in diabetic African-American women treated in a specialty clinic of an urban hospital setting. Furthermore, these data indicate that the presence of PTSD is negatively associated with glycaemic control.

Posttraumatic stress disorder is a prevalent mental health condition with substantial impact on daily functioning that lacks sufficient treatment options. Here we evaluate six phase 2 trials in a pooled analysis to determine the study design for phase 3 trials of MDMA-assisted psychotherapy for PTSD.

Six randomized, double-blind, controlled clinical trials at five study sites were conducted from April 2004 to February 2017. Active doses of MDMA (75-125 mg, n = 72) or placebo/control doses (0-40 mg, n = 31) were administered to individuals with PTSD during manualized psychotherapy sessions in two or three 8-h sessions spaced a month apart. Three non-drug 90-min therapy sessions preceded the first MDMA exposure, and three to four followed each experimental session.

After two blinded experimental sessions, the active group had significantly greater reductions in CAPS-IV total scores from baseline than the control group [MMRM estimated mean difference (SE) between groups - 22.0 (5.17), P < 0.001]. The between-group Cohen's d effect size was 0.8, indicating a large treatment effect. After two experimental sessions, more participants in the active group (54.2%) did not meet CAPS-IV PTSD diagnostic criteria than the control group (22.6%). Depression symptom improvement on the BDI-II was greatest for the active group compared to the control group, although only trended towards significant group differences [MMRM, estimated mean difference (SE) between groups - 6.0 (3.03), P = 0.053]. All doses of MDMA were well tolerated, with some expected reactions occurring at greater frequency for the active MDMA group during experimental sessions and the 7 days following.

MDMA-assisted psychotherapy was efficacious and well tolerated in a large sample of adults with PTSD. These studies supported expansion into phase 3 trials and led to FDA granting Breakthrough Therapy designation for this promising treatment.

ClinicalTrials.gov Identifier: NCT00090064, NCT00353938, NCT01958593, NCT01211405, NCT01689740, NCT01793610.

Post-traumatic stress disorder (PTSD) is characterized by a disordered stress response and associated with increased cardiovascular disease risk. The present study investigated whether angiotensin (Ang) II-elicited hypertensive response is sensitized in a model of PTSD and whether inhibition of angiotensin-converting enzyme (ACE) or tumor necrosis factor (TNF)-α prior to PTSD blocks this sensitization of Ang II hypertension.

The resident-intruder paradigm was used to model PTSD. Each intruder rat (male Sprague-Dawley) was given normal drinking water or was pretreated with either an ACE inhibitor (captopril) or a TNF-α inhibitor (pentoxifylline) in the drinking water for 2 weeks. Subsequently, they were exposed to a different resident (male Long-Evans) for 2 hours on 3 days with each session separated by 1 day and then received a subcutaneous infusion of Ang II for 2 weeks.

The stressed rats had a significantly enhanced hypertensive response to the Ang II infusion (stressed Δ40.2 ± 3.9 mm Hg vs. unstressed Δ20.5 ± 4.5 mm Hg) and an upregulation of mRNA or protein expression of renin-angiotensin system (RAS) and proinflammatory cytokine (PIC) components and of a microglial marker in the lamina terminalis and hypothalamic paraventricular nucleus when compared with unstressed control rats. Both the sensitized hypertensive response and enhanced gene and protein expression were blocked by pretreatment with either ACE (Δ21.3 ± 3.9 mm Hg) or TNF-α inhibitor (Δ21.4 ± 2.6 mm Hg).

The results indicate that upregulation of the brain RAS and PICs produced by severe stress contributes to traumatic-induced sensitization of hypertensive response to Ang II, and disorders such as PTSD may predispose individuals to development of hypertension.

Mechanisms for the association between posttraumatic stress disorder (PTSD) symptoms and cardiovascular diseases remain poorly understood. The present study examined associations among PTSD symptoms, appraisals of a current stressor, baseline cardiovascular indices, and cardiovascular responses to the stressor, including appraisals as a potential mediator of PTSD symptoms and cardiovascular responses. A sample of 125 undergraduates provided information about demographics, physical health, trauma history, and PTSD symptoms. Weight, height, blood pressure (BP), and heart rate (HR) measurements were obtained. During a modified Trier Social Stress Task, appraisals of the stressor were assessed and BP and HR were measured again. Findings suggest that PTSD symptoms are associated with current physical health (resting BP and HR) and more negative appraisals of the stressor; in turn, more negative appraisals were associated with increases in cardiovascular response. In particular, threat appraisal mediated the relationship between PTSD symptoms and increases in systolic BP response.

This manuscript reviews the epidemiological data linking psychosocial stress to cardiovascular disease (CVD), describes recent advances in understanding the biological pathway between them, discusses potential therapies against stress-related CVD, and identifies future research directions.

Metabolic activity of the amygdala (a neural center that is critically involved in the response to stress) can be measured on ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG-PET/CT) yielding a neurobiological signal that independently predicts subsequent CVD events. Furthermore, a serial pathway from ↑amygdalar activity → ↑hematopoietic tissue activity → ↑arterial inflammation → ↑CVD events has been elucidated, providing new insights into the mechanism linking stress to CVD. Psychosocial stress and stress conditions are independently associated with CVD in a manner that depends on the degree and duration of stress as well as the individual response to a stressor. Nevertheless, the fundamental biology remains incompletely defined, and stress is often confounded by adverse health behaviors. Thus, most clinical guidelines do not yet recognize psychosocial stress as an independent CVD risk factor or advocate for its treatment in CVD prevention. Clarification of this neurobiological pathway provides a better understanding of the underlying pathophysiology and suggests opportunities to develop novel preventive strategies and therapies.

To estimate the rate of sick leave and sick leave diagnosis among employees before and after a work-place targeted terror attack, and to compare sick leave in subgroups of employees based on gender and trauma exposure.

Data on sick leave and diagnosis in ministerial employees from the period 3 years before to 3 years after the 2011 bombing in the governmental district of Oslo was retrieved from the Norwegian Social Insurance Administration Registries.

Prior to the attack, sick leave was twice as high in women as in men. Compared to the period prior to the attack, sick leave increased the first year after the attack, for both women and men that were directly exposed to the event. Sick leave stabilized to the initial level 3 years after the incident. For indirectly exposed employees, i.e., those who were not present at the site of the attack, there was no significant increase in sick leave from before to after the attack. There were no statistical significant changes in diagnoses applied before and after the terrorist attack. However, there was a tendency towards an increase in sick leave due to psychological diagnoses among the directly exposed women.

After a work-place terrorist attack a transient increase in sick leave may occur among employees who were present at the site of the attack. The increase may seem relatively modest and last for 1-3 years.

Posttraumatic stress is associated with elevated risk for cardiovascular disease (CVD). Relatively little research, particularly among women, has documented mechanisms by which PTSD might confer CVD risk during early adulthood. The purpose of the present study was to examine whether the number and relative levels of CVD risk factors are associated with posttraumatic stress symptom severity among young, trauma-exposed women.

Participants were premenopausal women ages 19-49 with varying levels of posttraumatic stress and no history of chronic medical illness (n = 54), and were recruited from mental health clinics and the general community. Posttraumatic stress severity was assessed with a structured clinical interview (Clinician-Administered PTSD Scale). The CVD risk factors assessed were lipids (total cholesterol, triglycerides, high- and low-density lipoproteins), resting blood pressure (BP), body mass index (BMI), no exercise in typical week, and cigarette smoking.

Posttraumatic stress severity was associated with lower high-density lipoprotein levels and higher triglycerides, greater systolic and diastolic BP, greater BMI, and a greater number of total CVD risk factors.

The main limitation is the limited number of participants who displayed clinical levels on some of the CVD risk factors (e.g., BP). Nonetheless, most participants exhibited more than one CVD risk factor, indicating the potential for many of the women in this relatively young sample to progress toward greater risk later in life.

The present results support the contention that, in the absence of medical illness, posttraumatic stress symptom severity among young women is associated with several CVD risk factors early in life.