Initial posttraumatic urinary cortisol levels predict subsequent PTSD symptoms in motor vehicle accident victims (original) (raw)
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Journal of Anxiety Disorders, 2003
This study examined the relationship between prior history of traumatic events, life threat, and injury severity experienced during a motor vehicle accident (MVA), and posttraumatic stress disorder (PTSD) assessed 1 month after the accident. In addition, initial urinary cortisol levels after the accident were examined as a possible mediator of this relationship. Fifteenhour urinary cortisol samples were collected from MVAvictims upon admission to the trauma unit. In the hospital, subjective life threat was measured and objective Injury Severity Scores (ISSs) were computed. One month after the accident, participants were assessed for prior history of traumatic experiences, presence of acute PTSD, and levels of intrusive and avoidant thoughts and behaviors. Victims, who met PTSD diagnostic criteria, reported more prior traumatic events, and signi®cantly greater life threat despite receiving signi®cantly lower ISSs than victims who did not develop PTSD. The relationships between ISSs and PTSD symptoms and prior trauma history and PTSD symptoms were mediated by cortisol levels. Results suggest that cortisol levels in the acute aftermath of a traumatic event may serve as a mechanism through which various factors may increase risk for PTSD. #
Psychoneuroendocrinology, 2015
Posttraumatic stress disorder (PTSD) is associated with an increased risk of cardiovascular disease and several other chronic illnesses. Alterations in the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis in PTSD might contribute to these associations but findings regarding SNS and HPA activity in PTSD are heterogeneous. We measured 24-h urinary catecholamines and cortisol in a large cohort of adult outpatients recruited from 2 Veterans Affairs medical centers. 24-h urinary norepinephrine, epinephrine, dopamine and cortisol were measured by tandem mass spectrometry. Lifetime and current PTSD were assessed with the Clinician Administered PTSD Scale using DSM-IV-TR criteria. Out of 613 participants, 199 (32.5%) had current PTSD, 100 (16.3%) had lifetime but not current PTSD, and 314 (51.2%) never had PTSD. Patients with current PTSD had significantly higher norepinephrine secretion compared to those without PTSD. Patients in the lifetime PTSD group ex...
Biological psychiatry, 2007
The hypothalamic-pituitary-adrenal axis and the catecholaminergic system are involved in the pathophysiology of post-traumatic stress disorder (PTSD). This was a prospective and longitudinal study of neuroendocrine physiology in children with PTSD following a motor vehicle accident (MVA). Sixty children aged 7-18 were studied immediately after an MVA and 1 and 6 months later. Fasting morning plasma catecholamine and serum cortisol concentrations were measured. Salivary cortisol concentrations were measured serially five times daily to examine circadian variation in all three assessments. Values were compared between those who did (PTSD) or did not develop PTSD (non-PTSD) after the trauma and a control group at months 1 and 6. Twenty-three of the children had PTSD at the 1-month and 9 children at the 6-month evaluations. 1) Plasma noradrenaline concentrations were higher in the PTSD group than in the other two groups at both months 1 and 6 (p = .001 and p = .001, respectively). Addit...
The Acute Stress Response Following Motor Vehicle Accidents and Its Relation to PTSD
Annals of the New York Academy of Sciences, 1997
This study aimed to identify acute biological stress responses in trauma victims and to determine their contribution to the development of psychiatric illness, especially posttraumatic stress disorder (PTSD). Abnormalities of the hypothalamic-pituitaryadrenal (HPA) axis have been noted in PTSD, with evidence of heightened sensitivity in the negative feedback loop. However, it is not known if some abnormality of stress response occurs at the time of the traumatic event or if the disruption of the HPA axis develops during the course of the illness. An understanding of the acute stress response in accident victims who go on to develop PTSD may provide important information about biological vulnerability to psychiatric illness and may provide a marker of "at risk" individuals.'
Psychoneuroendocrinology, 2003
Preclinical studies show that animals with a history of chronic stress exposure have increased hypothalamic-pituitary-adrenal (HPA) axis reactivity following reexposure to stress. Patients with posttraumatic stress disorder (PTSD) have been found to have normal or decreased function of the HPA axis, however no studies have looked at the HPA response to stress in PTSD. The purpose of this study was to assess cortisol responsivity to a stressful cognitive challenge in patients with PTSD related to childhood abuse. Salivary cortisol levels, as well as heart rate and blood pressure, were measured before and after a stressful cognitive challenge in * Corresponding author. Present address: patients with abuse-related PTSD (N = 23) and healthy comparison subjects (N = 18). PTSD patients had 61% higher group mean cortisol levels in the time period leading up to the cognitive challenge, and 46% higher cortisol levels during the time period of the cognitive challenge, compared to controls. Both PTSD patients and controls had a similar 66-68% increase in cortisol levels from their own baseline with the cognitive challenge. Following the cognitive challenge, cortisol levels fell in both groups and were similar in PTSD and control groups. PTSD patients appeared to have an increased cortisol response in anticipation of a cognitive challenge relative to controls. Although cortisol has been found to be low at baseline, there does not appear to be an impairment in cortisol response to stressors in PTSD. Published by Elsevier Science Ltd.
Systematic Reviews
Background: Posttraumatic stress disorder (PTSD) is a disorder that develops following exposure to severely stressful events. Altered cortisol secretion has been reported in PTSD; however, results have been inconsistent. Previous meta-analyses of cortisol levels in PTSD have combined results of studies that have used different tissue samples (blood, saliva, urine) for cortisol measurement and have not included newer methods of determining cortisol levels (e.g. hair samples). In this systematic review, we will synthesise evidence from studies evaluating basal cortisol levels in PTSD patients versus controls and stratify studies according to tissue type used for cortisol measurement. We will also determine whether results from different tissue types can be pooled and if any specific tissue samples have better utility in research studies on PTSD. Methods: We will perform a systematic review of the scientific literature including all studies that have evaluated basal or baseline cortisol levels in adults with current PTSD versus controls, with and without trauma exposure. Independent reviewers will conduct searches in electronic databases (Medline, CINAHL, PTSDpubs, Web of Science, Scopus, ProQuest Dissertations & Theses A&I, ClinicalTrials.gov, and ICTRP), and additional studies will be obtained by searching the reference lists of articles. Two reviewers (LLvdH and SW) will independently conduct standardised screening, eligibility assessments, data extraction, and quality assessments before qualitative and, if appropriate, quantitative (meta-analysis and meta-regression) synthesis. Disagreements that arise at any stage will be resolved by a third reviewer (ShS). Discussion: In line with previous reviews, we expect that cortisol levels will be lower in PTSD patients than in controls, but that patterns may vary somewhat according to the tissue sample in which cortisol is measured. This systematic review will assist in developing a better understanding of the acute and chronic patterns of basal cortisol secretion in PTSD and will inform future research.
Frontiers in psychology, 2017
Background: Although depression symptoms are often experienced by individuals who develop posttraumatic stress disorder (PTSD) following trauma exposure, little is know about the biological correlates associated with PTSD and depression co-morbidity vs. those associated with PTSD symptoms alone. Methods: Here we examined salivary cortisol responses to trauma activation in a sample of 60 survivors of the World Trade Center attacks on September 11, 2001. Participants recalled the escape from the attacks 7 months post 9/11. Salivary cortisol levels were measured before and after their recollection of the trauma. PTSD, depression, and somatic symptoms were also assessed. From the behavioral assessment scales, the participants were grouped into three conditions: those with comorbid PTSD and depressive symptoms, PTSD alone symptoms, or no-pathology. Results: Baseline and cortisol response levels differed between the comorbid, PTSD alone, and no-pathology groups. Individuals endorsing co-m...
Altered cortisol awakening response in posttraumatic stress disorder
Psychoneuroendocrinology, 2006
An altered function of the hypothalamic-pituitary-adrenal axis is assumed to be characteristic for Posttraumatic Stress Disorder (PTSD), although there is inconsistent empirical evidence. Only few studies examined the awakening cortisol response and a daytime profile in PTSD. Salivary cortisol levels were measured at seven intervals from awakening until 8 PM in trauma-exposed subjects with (NZ29) and without PTSD (NZ19) and in 15 non-exposed controls. While the three groups did not differ with respect to their first cortisol level immediately after awakening, the expected cortisol increase to awakening 15-60 min later was significantly lower in PTSD patients compared to non-PTSD subjects and healthy controls. This effect remained stable when trauma-exposed subjects with comorbid major depression were excluded from the analysis. A significant negative correlation between the overall cortisol secretion (AUC G ) and overall PTSD symptomatology and hyperarousal symptoms was found. The findings are discussed in light of the hypothesis of a counterregulation of hyperarousal symptoms and chronic stress in PTSD. Q