Effect of current and lifetime posttraumatic stress disorder on 24-h urinary catecholamines and cortisol: results from the Mind Your Heart Study (original) (raw)
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Implications of Hypothalamic-Pituitary-Adrenal Axis Functioning in Posttraumatic Stress Disorder
Journal of the American Psychiatric Nurses Association, 2011
BACkgrounD: Cortisol secretions serve as the barometer of the hypothalamic-pituitary-adrenal (HPA) axis, which regulates and controls responses to stress. Studies of cortisol secretions in patients with posttraumatic stress disorder (PTSD) reveal inconsistent results. PurPoSe: Current research on HPA axis functioning in PTSD is examined to elucidate the neuroendocrine contributions in the disorder, identify current treatment's impact on the HPA axis, and consider implications for nursing care and areas for future research. FInDIngS: There is evidence for HPA dysregulation in PTSD, which contributes to widespread impairment in functions such as memory and stress reactivity and to physical morbidity via processes such as allostatic load. There is limited, but building, evidence that dehydroepiandrosterone (DHEA), which is released simultaneously with cortisol, may provide anti-glucocorticoid and neuroprotective effects. ConCluSIon: Current treatments such as selective serotonin reuptake inhibitors and psychotherapy may have a beneficial impact on the HPA axis in PTSD populations. Somatic approaches to treating PTSD have not yet been studied in relation to their impact on HPA axis parameters in PTSD patients. Treatment studies of DHEA or glucocorticoids have not yet used HPA axis endpoints. PTSD treatment studies that include measures of HPA axis target mechanisms and consider HPA axis regulation as an additional treatment outcome are warranted.
Sensitization of the Hypothalamic-Pituitary-Adrenal Axis in Posttraumatic Stress Disorder
Annals of the New York Academy of Sciences, 1997
Posttraumatic stress disorder (PTSD) is a psychiatric condition that can occur in individuals who have experienced traumatic events. The symptoms of PTSD were initially conceptualized as reflecting a natural process of adaptation to extraordinarily adverse life event~.l-~ However, in recent years prevalence studies have clarified that PTSD only occurs in a percentage of those exposed to trauma."' Furthermore, among trauma survivors who develop this disorder, a substantial proportion appear to show full remission of their symptoms over time.6 This observation demonstrates that chronic PTSD represents a specific type of adaptation to trauma, which may not necessarily reflect typical or even normative stress responsiveness.1°
Sustained urinary norepinephrine and epinephrine elevation in post-traumatic stress disorder
Psychoneuroendocrinology, 1987
Urinary norepinephrine and epinephrine levels (lag/day) were measured at two-week intervals during the course of hospitalization in the following patient groups: post-traumatic stress disorder (PTSD); major depressive disorder (MDD); bipolar 1, manic (BP); paranoid schizophrenia (PS); and undifferentiated schizophrenia (US). The mean norepinephrine level during hospitalization was significantly higher in PTSD (76 +_ 10.4 I.tg/day) than in BP (60.6 + 8.4 lag/day), MDD (41.2 4.7 I.tg/day), PS (33.4 ± 4.9 lag/day) and US (34.3 + 5.9 p_g/day) groups, according to Duncan's multiple range test, (F(4,39) = 6.94, p < 0.0003). The norepinephrine elevations in the PTSD group were sustained throughout hospitalization. The only other group to show mean levels in this range was the BP group in the first sample after hospital admission. This finding supports prior psychophysiological studies indicating increased sympathetic nervous system activity in PTSD patients. The mean epinephrine level during hospitalization was also significantly higher in PTSD (22.7 + 2.4 lag/day) than in MDD (13.6 + 1.7 p.g/day), PS (14.7 + 2.4 p_g/day), and US (18.9 ~: 1.8 lag/day), but not higher than in BP (21.5 * 2.7 lag/day). The relationship of epinephrine levels among diagnostic groups was sustained throughout hospitalization. It appears likely that the main underlying mechanisms for elevations of both hormones are psychological, but further work will be required to establish the exact nature of these mechanisms.
Journal of Traumatic Stress, 2010
. It is unclear whether trauma exposure during adulthood in the absence of psychopathology is also associated with HPA-axis dysregulation. Thirty-six trauma-exposed peacekeepers, 23 nonexposed peacekeepers, and 25 nonexposed civilians, all without lifetime psychopathology were studied. Basal HPA-axis functioning was assessed with salivary cortisol samples obtained over 2 days. HPA-axis reactivity was assessed with the dexamethasone/corticotropin-releasing hormone test. Lower afternoon salivary cortisol levels were found in both veteran groups versus controls after adjustment for confounders. The authors concluded that this study does not support the idea that HPA-axis functioning is durably altered by trauma exposure during adulthood in men. The hypothalamic-pituitary-adrenal (HPA) axis is involved in stress-related disorders, with cortisol being the predominant corticosteroid secreted from the adrenal cortex. Since Mason, Giller, Kosten, Ostroff, and Podd (1986) first reported on low urinary free-cortisol levels in patients with posttraumatic stress disorder (PTSD), many studies on cortisol under basal and challenged conditions in patients with this disorder have been published. Thus far, most studies have focused on individuals with current or remitted stress-related disorders, making it impossible to discriminate between the possible effects of psychiatric morbidity and trauma exposure on HPA-axis functioning. In a review, reported increased salivary cortisol levels in response to a cognitive challenge, as well as more plasma cortisol suppression after administration of 0.5 mg of dexamethasone in PTSD patients versus controls without PTSD or trauma exposure. However, it was concluded that interpretation of the results The authors kindly thank the Dutch Veterans Institute, Doorn, the Netherlands for providing the opportunity to recruit the Veterans.
Journal of Affective Disorders, 2010
Background: Chronic posttraumatic stress disorder (PTSD) has been associated with perturbed hypothalamic-pituitary-adrenal (HPA) axis function and a hyperadrenergic state. We hypothesized that patients with PTSD attributable to myocardial infarction (MI) would show peripheral hypocortisolemia and increased norepinephrine levels, whereby taking into account that depressive symptoms would affect this relationship. Methods: We investigated 15 patients with interviewer-rated PTSD caused by myocardial infarction (MI) and 29 post-MI patients with no PTSD. Patients also completed the depression subscale of the Hospital Anxiety and Depression Scale and had blood collected to determine plasma cortisol and norepinephrine levels. Results: In bivariate correlation analysis PTSD and depressive symptoms were not significantly associated with cortisol levels. However, patients with PTSD had lower mean± SEM cortisol levels than patients with no PTSD when controlling for depressive symptoms (77 ± 11 vs. 110 ± 7 ng/ml, p = .035). In turn, depressive symptoms correlated with cortisol levels when taking PTSD into account (r = .36, p = .019). In all patients cortisol levels correlated with total PTSD symptoms (r = − .43, p = .005) and hyperarousal symptoms (r = − .45, p = .002) after controlling for depressive symptoms. Depression correlated with cortisol levels after controlling for total PTSD symptoms (r = .45, p = .002). Posttraumatic stress disorder and depressive symptoms were not significantly associated with norepinephrine levels. Conclusions: In post-MI patients we found peripheral hypocortisolemia related to PTSD, respectively hypercortisolemia related to depressive symptoms, when taking joint effects of PTSD and depression into account. No evidence was found for a hyperadrenergic state. Comorbid depressive symptoms ought to be considered to disentangle the unique associations of PTSD with HPA axis dysfunction in cardiac patients.
Neuroendocrine activity and memory-related impairments in posttraumatic stress disorder
Development and Psychopathology, 1998
This article reviews memory-related impairments in trauma survivors with posttraumatic stress disorder and their possible association to neuroendocrine alterations seen in this disorder. The neuroendocrine profile in PTSD first described in chronically ill combat veterans is characterized by lower basal cortisol levels, higher glucocorticoid receptor number, enhanced sensitivity to exogenous steroids, and increased variation in basal cortisol levels over the diurnal cycle. The generalizability and time course of these neuroendocrine alterations are explored in longitudinal studies and studies in other traumatized populations. These studies suggest that at least some aspects of this neuroendocrine profile can also be seen in other populations, including women, children, and victims of childhood trauma. Additionally, the alterations may be present early in the course of illness, perhaps even in the immediate aftermath of trauma, and may continue to be manifest in elderly trauma survivors. The mechanisms by which these neuroendocrine alterations may influence the formation and processing of traumatic memories are discussed.
Clinical psychology review, 2016
Individuals with posttraumatic stress disorder (PTSD) typically exhibit altered hypothalamic-pituitary-adrenal (HPA) function and sympathetic nervous system (SNS) activity. The goals of this study were to determine whether HPA and SNS alterations in the immediate aftermath of trauma predict subsequent PTSD symptom development and whether inconsistencies observed between studies can be explained by key demographic and methodological factors. This work informs secondary prevention of PTSD by identifying subgroups of trauma survivors at risk for PTSD. This meta-analysis (26 studies, N=5186 individuals) revealed that higher heart rate measured soon after trauma exposure was associated with higher PTSD symptoms subsequently (r=0.13). Neither cortisol (r=-0.07) nor blood pressure (diastolic: r=-0.01; systolic: r=0.02) were associated with PTSD symptoms which may be influenced by methodological limitations. Associations between risk markers (heart rate, cortisol, systolic blood pressure) a...
Revista brasileira de psiquiatria (São Paulo, Brazil : 1999)
To compare afternoon serum/plasma levels of hormones in four groups: (A) veterans with posttraumatic stress disorder (PTSD), (B) offspring of PTSD veterans, (C) veterans without PTSD, and (D) offspring of non-PTSD veterans. Evaluation consisted of a semi-structured interview for axis I and II diagnoses, followed by measurement of afternoon serum cortisol and plasma epinephrine and norepinephrine by ELISA (Diametra) and LND (LDN Labor Diagnostika Nord GmbH & Co. KG) respectively. Data were analyzed using descriptive statistics and the Student t, Kolmogorov-Smirnov, and nonparametric Mann-Whitney tests. One hundred and sixty-eight volunteers were investigated across the four groups. The groups were similar in terms of demographic characteristics, war experience and traumatization, and psychiatric and medical conditions other than PTSD (group A was similar to group C and group B was similar to group D). Between-groups comparisons did not yield statistically significant differences. Pos...