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Attempts to correlate blood levels of brain-derived neurotrophic factor (BDNF) with post-traumatic stress disorder (PTSD) have provided conflicting results. Some studies found a positive association between BDNF and PTSD diagnosis and symptom severity, while others found the association to be negative. The present study investigated whether serum levels of BDNF are different cross-sectionally between combat trauma-exposed veterans with and without PTSD, as well as whether longitudinal changes in serum BDNF differ as a function of PTSD diagnosis over time. We analyzed data of 270 combat trauma-exposed veterans (230 males, 40 females, average age: 33.29 ± 8.28 years) and found that, at the initial cross-sectional assessment (T0), which averaged 6 years after the initial exposure to combat trauma (SD=2.83 years), the PTSD positive group had significantly higher serum BDNF levels than the PTSD negative controls [31.03 vs. 26.95 ng/mL, t(268) = 3.921, p

Sexual dysfunction is not a symptom of PTSD but is a common clinical complaint in trauma survivors with this disorder. In that there are biological parallels in the neuroendocrine processes underlying both PTSD and sexual behavior, we conducted an exploratory investigation of the relationship of PTSD and related neuroendocrine indicators with sexual dysfunction in armed service veterans. Major Depressive Disorder, highly comorbid with PTSD and sexual dysfunction, was also assessed. In veterans with PTSD, sexual problems were associated with plasma DHEA and cortisol, urinary catecholamines, and glucocorticoid sensitivity, even when controlling for the effects of comorbid depression. In a subsample analysis, testosterone levels did not distinguish PTSD or sexual dysfunction, suggesting that sexual problems reported by veterans in this sample were not the result of organic disorder. PTSD did predict higher dihydrotestosterone (DHT) levels, which were associated with sexual problems. More detailed assessment of sexual dysfunction in biologically informed studies of PTSD is warranted to clarify the relationships of PTSD symptomatology and related neurobiology with sexual dysfunction.

Posttraumatic stress disorder (PTSD) is associated with increased risk for Type 2 diabetes and cardiovascular disease (cardiometabolic disease), warranting research into targeted prevention strategies. In the present case–control study of 160 young (mean age 32.7 years) male military veterans, we aimed to assess whether PTSD status predicted increased markers of cardiometabolic risk in otherwise healthy individuals, and further, to explore biological pathways between PTSD and these increased markers of cardiometabolic risk. Toward these aims, we compared measures of cardiometabolic risk, namely insulin resistance (IR) (HOMA-IR), metabolic syndrome (MetS) and prediabetes, between 80 PTSD cases and 80 controls without PTSD. We then determined whether PTSD-associated increases in HOMA-IR were correlated with select biological variables from pathways previously hypothesized to link PTSD with cardiometabolic risk, including systemic inflammation (increased C-reactive protein, interleukin-6, and tumor necrosis factor α), sympathetic over-activity (increased resting heart rate), and neuroendocrine dysregulation (increased plasma cortisol or serum brain-derived neurotrophic factor (BDNF)). We found PTSD diagnosis was associated with substantially higher HOMA-IR (cases 4.3 ± 4.3 vs controls 2.4 ± 2.0; p 0.05). Cases also had increased pro-inflammatory cytokines (p

Summary Background Alterations of hypothalamic–pituitary–adrenal (HPA) axis function and sympathetic-adrenal activity have been proposed as key factors in biological models of posttraumatic stress disorder (PTSD). Methods We examined neuroendocrine function in female survivors of intimate partner violence (IPV) with lifetime (current or remitted) PTSD ( n =29) and in women who were exposed to IPV but never developed PTSD ( n =20). Salivary cortisol was collected as a marker of HPA axis function at 1, 4, 9, and 11 h after awakening. Platelet epinephrine and norepinephrine were assayed as markers of sympathetic-adrenal activation. Results Women with lifetime PTSD had significantly higher cortisol levels across the day compared to abuse-exposed participants without PTSD, after controlling for age, depression, severity, and latency of abuse. There were no significant group differences in levels of platelet catecholamines. Conclusions Elevated cortisol levels may be a biomarker of IPV-related lifetime PTSD, reflecting long-lasting changes associated with trauma-exposure or possibly a reflection of risk for PTSD in women.

This study examines whether pre- or post-dexamethasone salivary cortisol is related to cumulative critical incident exposure, peritraumatic responses, or post-traumatic stress disorder (PTSD) symptom severity. Thirty active duty police officers completed the study protocol, which included measures of peritraumatic emotional distress, peritraumatic dissociation, duty-related trauma exposure, and PTSD symptoms. Salivary cortisol was consolidated into three outcome variables: (1) pre-dexamethasone free cortisol levels at 1, 30, 45, and 60 min after awakening, (2) post-dexamethasone cortisol levels at the identical wake times, and (3) percentage of cortisol suppression. Control variables included age, gender, average daily alcohol use, night shift work, routine work environment stressors, and salivary dexamethasone levels. Zero order correlations showed that greater levels of PTSD symptoms, peritraumatic distress, and peritraumatic dissociation were associated with lower levels of pre-dexamethasone cortisol levels on awakening, but were not associated with the other two cortisol variables. A trend was also noted for older subjects to have lower pre-dexamethasone cortisol on awakening. When these four predictors were entered simultaneously in a regression analysis, only age and PTSD symptom severity significantly predicted pre-dexamethasone awakening cortisol levels. These results replicate previous research indicating a relationship between greater PTSD symptoms and lower levels of basal cortisol on awakening, and extend this finding to a previously unstudied non-treatment seeking population, urban police.

Department of Psychology, University of Pittsburgh Sennott square, 3rd Floor, 210 S. Bouquet Street, Pittsburgh, PA 15260, USA Department of Psychiatry, University of Pittsburgh Medical Center, University of Pittsburgh Cancer Institute, Behavioral Medicine and Oncology, 405 Iroquois Building, 3600 Forbes Avenue, Pittsburgh, PA 15213, USA Department of Veterans Affairs Medical Center, 4150 Clement Street (116P), San Francisco, CA 94121, USA Department of Psychiatry, University of California, San Francisco, CA 94121, USA Department of Psychiatry and Psychotherapy, University Hospital Hamburg-Eppendorf, Martinistrasse 52,20246 Hamburg, Germany Division of Emergency Medicine, Department of Surgery, Southwestern Medical Center, Parkland Memorial Hospital, University of Texas, Dallas, TX 75390-8579, USA Center for Health Equity Research and Promotion, VA Pittsburgh Health care System, University Drive C: Building 28 (151-C), Room 1A109, Pittsburgh, PA 15240, USA