Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Sumner JA

PROVIDER: S-EPMC5857414 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Sumner Jennifer A JA Chen Qixuan Q Roberts Andrea L AL Winning Ashley A Rimm Eric B EB Gilsanz Paola P Glymour M Maria MM Tworoger Shelley S SS Koenen Karestan C KC Kubzansky Laura D LD

Brain, behavior, and immunity 20171120

<h4>Background</h4>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.<h4>Methods</h4>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- ...[more]

PMID: 29157934

Similar Datasets

Project description: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.

Project description:BackgroundCurrent research in behavioral cardiology reveals a significant association between posttraumatic stress disorder (PTSD) and increased risk for cardiovascular disease and mortality; however, the underlying mechanisms remain poorly understood. We hypothesized that patients with PTSD would exhibit endothelial dysfunction, a potential mechanism involved in the development and progression of cardiovascular disease.Methods and resultsA total of 214 outpatients treated at the San Francisco Veterans Affairs Medical Center underwent tests of endothelial function and evaluation for PTSD. Flow-mediated vasodilation of the brachial artery was performed to assess endothelial function, and current PTSD status was defined by the PTSD Checklist, based on the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition), with a score ≥40. Multivariable linear regression models were used to estimate the association between PTSD status and endothelial function. Patients with PTSD (n=67) were more likely to be male (99% versus 91%, P=0.04) and to have depression (58% versus 8%, P<0.0001) and were less likely to be on an angiotensin-converting enzyme inhibitor (17% versus 36%, P=0.007) or β-blocker treatment (25% versus 41%, P=0.03). Univariate analysis demonstrated that patients with PTSD had significantly lower flow-mediated vasodilation (5.8±3.4% versus 7.5±3.7%; P=0.003); furthermore, lower flow-mediated vasodilation was associated with increasing age (P=0.008), decreasing estimated glomerular filtration rate (P=0.003), hypertension (P=0.002), aspirin (P=0.03), and β-blocker treatments (P=0.01). In multivariable analysis, PTSD remained independently associated with lower flow-mediated vasodilation (P=0.0005).ConclusionsAfter adjusting for demographic, comorbidity, and treatment characteristics, PTSD remained associated with worse endothelial function in an outpatient population. Whether poor endothelial function contributes to the higher risk of cardiovascular disease in patients with PTSD deserves further study.

Project description:BACKGROUND:Posttraumatic stress disorder (PTSD) is associated with disturbed sleep and elevated levels of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Studies in animals and healthy humans have also shown that disrupted sleep elevates pro-inflammatory cytokines, including IL-6 and TNF-α. A better understanding of overnight cytokine levels and sleep might shed light on possible mechanisms for elevated inflammation in PTSD. Thus, we investigated overnight levels of IL-6 and TNF-α in individuals with and without PTSD while recording sleep polysomnography (PSG). METHOD:Serum samples were collected from otherwise healthy, medication-free participants with chronic PTSD (n = 44; 50% female; M age = 30.34 ± 8.11) and matched controls (n = 49; 53% female; M age = 30.53 ± 6.57) during laboratory PSG. Levels of IL-6 and TNF-α were measured at hours 0, 2, 4, 6, and 8 after typical sleep onset time using serial serum samples. Plasma IL-6 and TNF-α levels were quantified using enzyme-linked immunosorbent assays. RESULTS:Growth model analysis indicated a significantgroup by time interaction for IL-6 (t[247] = -2.92, p = .005) and a significant group by sex by time interaction for TNF-α (t[275] = 2.02, p = .04). PTSD positive men and women initially had higher IL-6 and TNF-α at sleep onset, but not at the end of their sleep cycle. Men with PTSD showed a peak of TNF-α at the end of the sleep cycle, whereas male control subjects demonstrated an inverted U-shaped profile. There were no significant differences in TNF-α levels overnight between women with and without PTSD. CONCLUSION:To our knowledge, this is the largest study to examine IL-6 overnight in a PTSD sample and the first study to examine overnight TNF-α in PTSD. Overnight IL-6 and TNF-α levels may be altered in individuals with PTSD compared to those without PTSD, and TNF-α trajectories also differed by sex. The current findings highlight the need to consider sex, sleep, time of day, and circadian variation when examining inflammation in PTSD. Additional research in broader study samples will be necessary to clarify associations between disrupted sleep, cytokines, and increased risk for disease in PTSD.

Project description:BackgroundComorbidity between posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) has been commonly overlooked by studies examining resting-state functional connectivity patterns in PTSD. The current study used a data-driven approach to identify resting-state functional connectivity biomarkers to 1) differentiate individuals with PTSD (with or without MDD) from trauma-exposed healthy control subjects (TEHCs), 2) compare individuals with PTSD alone with those with comorbid PTSD+MDD, and 3) explore the clinical utility of the identified biomarkers by testing their associations with clinical symptoms and treatment response.MethodsResting-state magnetic resonance images were obtained from 51 individuals with PTSD alone, 52 individuals with PTSD+MDD, and 76 TEHCs. Of the 103 individuals with PTSD, 55 were enrolled in prolonged exposure treatment. A support vector machine model was used to identify resting-state functional connectivity biomarkers differentiating individuals with PTSD (with or without MDD) from TEHCs and differentiating individuals with PTSD alone from those with PTSD+MDD. The associations between the identified features and symptomatology were tested with Pearson correlations.ResultsThe support vector machine model achieved 70.6% accuracy in discriminating between individuals with PTSD and TEHCs and achieved 76.7% accuracy in discriminating between individuals with PTSD alone and those with PTSD+MDD for out-of-sample prediction. Within-network connectivity in the executive control network, prefrontal network, and salience network discriminated individuals with PTSD from TEHCs. The basal ganglia network played an important role in differentiating individuals with PTSD alone from those with PTSD+MDD. PTSD scores were inversely correlated with within-executive control network connectivity (p < .001), and executive control network connectivity was positively correlated with treatment response (p < .001).ConclusionsResults suggest that unique brain-based abnormalities differentiate individuals with PTSD from TEHCs, differentiate individuals with PTSD from those with PTSD+MDD, and demonstrate clinical utility in predicting levels of symptomatology and treatment response.

Project description:BackgroundPosttraumatic stress disorder (PTSD) has been associated with increased cardiovascular risk, however, underlying mechanisms have not been fully specified. PTSD is associated with stress-related hormones, including dysregulated glucocorticoid activity. Dysregulation of aldosterone, a mineralocorticoid activated by psychological stress and implicated in cardiovascular damage, may be a relevant pathway linking PTSD and cardiovascular risk. Few studies to date have evaluated the association between PTSD and aldosterone, none with repeated measures of aldosterone. We examined if trauma and PTSD were associated with altered aldosterone levels relative to women unexposed to trauma.MethodsThe association of trauma exposure and chronic PTSD with plasma aldosterone levels was investigated in 521 middle-aged women in the Nurses' Health Study II. Aldosterone was assessed at two time points, 10-16 years apart, and trauma exposure and PTSD were also ascertained for both time points. Regarding exposure assessment, women were characterized based on a structured diagnostic interview as: having chronic PTSD (PTSD at both time points; n = 174); being trauma-exposed (trauma exposure at first time point but no PTSD; n = 174); and being unexposed (no trauma exposure at either time point; reference group for all analyses; n = 173). Linear mixed models examined associations of trauma and PTSD status with log-transformed aldosterone levels, adjusting for covariates and health-related variables that may confound or lie on the pathway between PTSD and altered aldosterone levels.ResultsAcross the sample, mean aldosterone concentration decreased over time. Adjusting for covariates, women with chronic PTSD had significantly lower aldosterone levels averaged over time, compared to women unexposed to trauma (β = - 0.08, p = 0.04). Interactions between trauma/PTSD group and time were not significant, indicating change in aldosterone over time did not differ by trauma/PTSD status. Post-hoc exploratory analyses suggested that menopausal status partially mediated the relationship between chronic PTSD status and aldosterone level, such that postmenopausal status explained 7% of the effect of PTSD on aldosterone.ConclusionsThese findings indicate that PTSD is associated with lower levels of aldosterone. Further work is needed to understand implications of this type of dysregulation in a key biological stress system for cardiovascular and other health outcomes previously linked with PTSD.

Dataset Information

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

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets