Cortisol responses to mental arithmetic in acute and remitted depression

Trestman, Robert L.; Coccaro, Emil F.; Bernstein, David P.; Lawrence, T. L. J.; Gabriel, Steven M.; Horvath, Thomas; Siever, Larry J.

doi:10.1016/0006-3223(91)90361-o

Cited by 33 publications

(14 citation statements)

References 3 publications

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“…Finally, several studies have examined the cortisol response to a cognitive stressor in depressed patients, and found elevated pre-stress cortisol but a smaller cortisol response to the cognitive challenge in the depressed patients compared to control subjects. (Trestman et al 1991;Gotthardt et al 1995). It should be noted that the cortisol responses to the cognitive stressors in normal subjects in these studies were much smaller than what we observed with the TSST.…”

Section: Discussioncontrasting

confidence: 66%

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Young

López

Murphy-Weinberg

et al. 2000

Neuropsychopharmacology

136

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In patients with major depression, abnormalities in baseline cortisol secretion and resistance to negative feedback are well established. However, it is unclear if patients with major depression have alterations in the hypothalamicpituitary-adrenal (HPA) response to stressors. While other challenges to the HPA axis have used endocrine stimuli such as insulin-induced hypoglycemia, we now report of the response to a social stressor in patients withOver the last two decades, an extensive body of work has pointed to a close relationship between stress and major depression. Studies by numerous investigators including Frank et al. (1994) and Brown et al. (1994) have documented the role of stressful life events in the precipitation of depressive episodes. Studies in twins by Kendler et al. (1993) have demonstrated a clear interaction between genetic substrate and a recent stressful life event in the precipitation of a depressive episode. In addition, abnormalities in the hypothalamic-pituitary adrenal (HPA) axis are seen during depression. HPA measures have demonstrated different types of dysregulation at rest or following various endocrine challenges. For example, patients with major depression demonstrate elevated plasma cortisol levels at rest, a finding observed in approximately 50% of depressed patients. This increase in plasma cortisol is particularly evident in the evening, at the nadir of the circadian rhythm (Sachar et al. 1973; Carroll et al. 1976;Rubin et al. 1987;Halbreich et al. 1985;Pfohl et al. 1985). Furthermore, a number of studies have investigated abnormal glucocorticoid feedback, typically using the synthetic steroid dexamethasone but also using the naturally occurring glucocorticoid cortisol (Carroll et al. 1981;Young et al. 1993Young et al. , 1991. These studies generally support the view that there is significant dysregulation of NO . 4 steroid negative feedback mechanisms in major depression. Fewer studies have examined the activational circuits of the LHPA axis in depression, and these studies have been limited to endocrine challenges such as metyrapone, or insulin-induced hypoglycemia (Young et al. 1994;von Bardeleben et al. 1988;Kathol et al. 1992;Lopez et al. 1987). The metyrapone studies suggested increased central drive in the evening (Young et al. 1994), while insulin-induced hypoglycemia revealed elevated basal cortisol and an attenuated ACTH response to the challenge (Kathol et al. 1992;Lopez et al. 1987). Finally, there is evidence that corticotropin-releasinghormone, CRH, which represents the final common path of stress responsiveness in the brain, is elevated in CSF and hypothalamus, and that this elevation may contribute both to the endocrine and psychological profile seen in severe depression (Nemeroff et al. 1984;Roy et al. 1987;Raadsheer et al. 1995Raadsheer et al. , 1994Nemeroff, 1988;Nemeroff et al. 1988).In spite of these findings, it remains difficult to determine what these endocrine changes tell us about the alterations in key neuronal circuits which mediate stress resp...

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Section: Discussioncontrasting

confidence: 66%

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Young

López

Murphy-Weinberg

et al. 2000

Neuropsychopharmacology

136

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“…We also expected depression to be associated with a reduced cortisol response to the stressor. This pattern of "blunting" has been documented in a number of studies (41,42), including a recent meta-analysis of the literature in this area (43). Because depression is not generally associated with abnormalities in leukocyte distribution (44), we did not expect to find differences in cell mobilization following the stressor.…”

Section: Introductionmentioning

confidence: 64%

“…First, other studies have documented this pattern, in both lab and field settings (41,42). Moreover, a recent meta-analysis reported that across the published literature, there was a significant reduction in cortisol response to stress among depressed people (43).…”

Section: G E Miller Et Almentioning

confidence: 91%

Clinical Depression and Regulation of the Inflammatory Response During Acute Stress

Miller

Rohleder

Stetler

et al. 2005

Psychosomatic Medicine

230

157

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“…In fact, numerous research groups used either task to induce a psychological ly distressing situation [9][10][11][12][13][14][15]. However, with respect to HPA-axis activity these protocols led only to small or moderate increases in cortisol and/or ACTH values.…”

Section: Discussionmentioning

confidence: 99%

The ‘Trier Social Stress Test’ – A Tool for Investigating Psychobiological Stress Responses in a Laboratory Setting

1993

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This paper describes a protocol for induction of moderate psychological stress in a laboratory setting and evaluates its effects on physiological responses. The ‘Trier Social Stress Test’ (TSST) mainly consists of an anticipation period (10 min) and a test period (10 min) in which the subjects have to deliver a free speech and perform mental arithmetic in front of an audience. In six independent studies this protocol has been found to induce considerable changes in the concentration of ACTH, cortisol (serum and saliva), GH, prolactin as well as significant increases in heart rate. As for salivary cortisol levels, the TSST reliably led to 2- to 4-fold elevations above baseline with similar peak cortisol concentrations. Studies are summarized in which TSST-induced cortisol increases elucidated some of the multiple variables contributing to the interindividual variation in adrenocortical stress responses. The results suggest that gender, genetics and nicotine consumption can influence the individual’s stress responsiveness to psychological stress while personality traits showed no correlation with cortisol responses to TSST stimulation. From these data we conclude that the TSST can serve as a tool for psychobiological research.

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Cortisol responses to mental arithmetic in acute and remitted depression

Cited by 33 publications

References 3 publications

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Clinical Depression and Regulation of the Inflammatory Response During Acute Stress

The ‘Trier Social Stress Test’ – A Tool for Investigating Psychobiological Stress Responses in a Laboratory Setting

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