Endocrine Factors in Stress and Psychiatric Disorders (original) (raw)

High trait anxiety in healthy subjects is associated with low neuroendocrine activity during psychosocial stress

Progress in Neuro-psychopharmacology & Biological Psychiatry, 2004

Altered stress responsiveness has been repeatedly related to mood and anxiety disorders. In a traditional view, a reduction of the stress response has been thought favorable. The goal of the present study was to verify the hypothesis that high anxiety is accompanied by enhanced hormone release during stress. Healthy subjects at the upper (anxious, n=15) and lower (non-anxious, n=12) limits of the normal range of a trait anxiety scale (State trait anxiety inventory) were exposed to psychosocial stress procedure based on public speech. Hormone levels, cardiovascular activation and skin conductance were measured. Exposure to psychosocial stress was associated with significant increases of all parameters measured. During the stress procedure, subjects with high trait anxiety exhibited lower levels of hormones of the hypothalamo-pituitary-adrenocortical axis, namely ACTH and cortisol in plasma, as well as cortisol in saliva. Similarly, the stress-induced activation of epinephrine, norepinephrine and prolactin secretion was significantly lower in anxious subjects in comparison with that in nonanxious subjects. Thus, in contrast to the traditional view, high anxiousness was not associated with exaggerated stress response. Our findings suggest that high trait anxiety may be associated with an inability to respond with adequate hormone release to acute stress stimuli. D

Salivary cortisol as a biomarker in stress research

Psychoneuroendocrinology, 2009

Salivary cortisol is frequently used as a biomarker of psychological stress. However, psychobiological mechanisms, which trigger the hypothalamus-pituitary-adrenal axis (HPAA) can only indirectly be assessed by salivary cortisol measures. The different instances that control HPAA reactivity (hippocampus, hypothalamus, pituitary, adrenals) and their respective modulators, receptors, or binding proteins, may all affect salivary cortisol measures. Thus, a linear relationship with measures of plasma ACTH and cortisol in blood or urine does not necessarily exist. This is particularly true under response conditions. The present paper addresses several psychological and biological variables, which may account for such dissociations, and aims to help researchers to rate the validity and psychobiological significance of salivary cortisol as an HPAA biomarker of stress in their experiments.

Salivary cortisol levels and the 2-year course of depressive and anxiety disorders

Psychoneuroendocrinology, 2013

Introduction: Depression and anxiety disorders have been associated with hyperactivity of the hypothalamic-pituitary adrenal (HPA) axis. However, lower cortisol levels have also been observed in depressed patients. Whether cortisol level predicts the course of these disorders has not been examined in detail. We examined whether salivary cortisol indicators predict the 2-year course of depression and anxiety disorders. Methods: Longitudinal data are obtained from 837 participants of the Netherlands Study of Depression and Anxiety, with a DSM-IV based depressive and/or anxiety disorder at baseline. At baseline, seven saliva samples were obtained, including the 1-h cortisol awakening response, evening cortisol level and a 0.5 mg dexamethasone suppression test. At follow-up, DSM-IV based diagnostic interviews and Life Chart Interview integrating diagnostic and symptom trajectories over 2 years were administered to determine an unfavorable course. Results: 41.5% of the respondents had a 2-year unfavorable course trajectory without remission longer than 3 months. Adjusted analyses showed that a lower awakening response was associated with an unfavorable course (RR = 0.83, p = 0.03). No associations were found between evening cortisol or cortisol suppression after dexamethasone ingestion and an unfavorable course trajectory. Conclusions: Among patients with depressive or anxiety disorders, a lower cortisol awakening response -which may be indicative of underlying exhaustion of the HPA axis -predicted an unfavorable course trajectory. #

An investigation into the relationship between salivary cortisol, stress, anxiety and depression

Biological …, 2003

This study examined the relationship between indices of self-reported emotional distress and absolute versus change in cortisol levels. Fifty-four women attending a diagnostic breast clinic completed scales measuring stress, anxiety and depression and provided five saliva samples over the course of a single day for the measurement of cortisol. No significant relationships were evident between absolute cortisol levels and the distress measures. Analysis of the change in cortisol levels revealed a non-linear interaction effect between stress and anxiety and time of day. There was a non-linear relation between time of day and cortisol levels, but the extent of the non-linearity was dependent upon levels of stress and anxiety, not depression. A relationship was apparent between indices of distress and change in cortisol levels, but not absolute levels of the hormone. # (K. Vedhara). Biological Psychology 62 (2003) 89 Á/96 www.elsevier.com/locate/biopsycho 0301-0511/02/$ -see front matter # 2002 Elsevier Science B.V. All rights reserved. PII: S 0 3 0 1 -0 5 1 1 ( 0 2 ) 0 0 1 2 8 -X

Systemic hormonal and physiological abnormalities in anxiety disorders

Psychoneuroendocrinology, 1988

Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral a2 and B-adrenoreceptor down-regulation, with normal semtonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal pmtiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.

ARTICLE IN PRESS G Model Salivary alpha-amylase and cortisol responsiveness to stress in first episode, drug-naïve patients with panic disorder

Please cite this article in press as: Altamura, M., et al., Salivary alpha-amylase and cortisol responsiveness to stress in first episode, drug-naïve patients with panic disorder. Neurosci. Res. (2018), https://doi. a b s t r a c t Reported findings on reactivity to stress of the sympathetic-adreno-medullar (SAM) and hypothalamic-pituitary-adrenal (HPA) systems in panic disorder (PD) are very variable. This inconsistency may be explained by differences in treatment exposure, illness duration and emotion regulation strategies. The present study examined the reactivity to mental stress of the SAM and HPA axes in a sample of first episode, drug naïve patients with PD which avoids confounds of medications exposure and illness chronic-ity. Activation of the SAM axis was evaluated by dosage of salivary alpha-amylase (sAA) and heart rate. Activation of the HPA axis was tested by dosage of salivary cortisol. Psychological assessments were done by the Self-Rating Depression Scale, the Self-Rating Anxiety Scale, the State-Trait Anxiety Inventory, the Cope Orientation to Problems Experienced (COPE) Inventory and the 16 Personality Factor Questionnaire (16PF). Patients showed reduced sAA stress reactivity, higher baseline cortisol levels and a more rapid decrease in stress cortisol levels as compared with controls. A significant correlation was found between active coping strategies and cortisol levels (response to stress). The findings suggest that blunted SAM stress reactivity and a rapid decrease in stress cortisol levels reflect traits that may enhance vulnerability to psychopathology in patients with PD.

Mental Health and Salivary Cortisol. In The Role of Saliva Cortisol Measurement in Health and Disease

The aim of this chapter was to analyze associations between measures of cortisol in saliva and mental health and to see if divergent results were functions of the methods used. Measures of mental health outcome included Major Depressive Disorder (MDD), symptoms of depression, and symptoms of anxiety, Burnout (BO), and Vital Exhaustion (VE). Only studies on otherwise healthy individuals were included. Cortisol measures were grouped into single time point measures, measures of deviations, laboratory test responses, Area Under the Curve (AUC), and response to dexamethasone. Some consistency is seen for MDD, mainly higher mean levels. The results regarding single measures and depressive mood are less consistent, but the overall picture for depression shows poorer diurnal deviation and response to stress. Inconsistency among papers studying depression seems to be related mainly to the study population. Very few significant findings were found for anxiety, therefore cortisol does not seem...

Stress and the Neuroendocrinology of Anxiety Disorders

Stress is a risk factor for depressive and anxiety disorders. Changes in lifestyle patterns that are associated with increased stress therefore place a greater burden on mental health. Stress challenges the organism’s homeostatic mechanisms, triggering a cascade of events that should, normally, maintain or allow a return to equilibrium. Stressful events are perceived by sensory systems in the brain, facilitating evaluation and comparison of the existing and previous stimuli as well as the activation of hormones responsible for energy mobilization. The limbic system coordinates the release of corticosteroids, the primary stress hormones, by modulating activation of the hypothalamic paraventricular nucleus (PVN). The amygdala, a limbic structure related to emotional behavior, has a putative role in the evaluation of emotional events and formation of fearful memories; it is also a target of the neurochemical and hormonal mediators of stress. Clinical and experimental data have correlated changes in the structure/function of the amygdala with emotional disorders such as anxiety. In this chapter we review the neuroendocrinology of the stress response, focusing on the role of the limbic system in its establishment and supplementing that information with new experimental data that demonstrates the relationship between stress and anxiety disorders; we also discuss the structural changes that occur in the amygdala after stress.