Plasma levels of cortisol were sampled for 24 hours in 32 endogenously depressed (ED) patients and 72 normal controls who also underwent the dexamethasone suppression test. The ED patients had significantly higher mean 24-hour plasma levels of cortisol (means 24h PC). However, means 24h PC values of subjects in both groups were normally distributed, with a marked overlap between the two. Only seven ED patients had means 24h PC values higher than 2 SDs from the normal mean (greater than 10 micrograms/dL). An abnormal dexamethasone suppression test result was only partially related to basal cortisol levels. The mean plasma level of cortisol between 1 and 4 PM was found to be highly correlated with the means 24h PC value in ED patients, as has been previously reported in normal subjects and patients with various other diseases (in which it also powerfully discriminated between hypersecretors and normosecretors). This finding supports the use of mean cortisol levels between 1 and 4 PM as a reliable and convenient indication of cortisol secretion.
"The HPA axis consists of the interactions among the hypothalamus, the pituitary gland, and the adrenal cortex, and is a major part of the neuroendocrine system that controls reactions to stress . The clinical manifestation of its dysfunction in depression includes basal hypercortisolemia , elevated cortisol secretion in the dexamethasone suppression test , and increased cortisol release in the combined dexamethasone suppression-corticotropine releasing hormone stimulation test [17,18]. "
[Show abstract][Hide abstract] ABSTRACT: The efficacy of physical exercise as an augmentation to pharmacotherapy with antidepressants for depressive patients has been documented. However, to clarify the effectiveness of exercise in the treatment of depression, it is necessary to distinguish the effect of the exercise itself from the effect of group dynamics. Furthermore, an objective measurement for estimation of the effect is needed. Previous reports adopted a series of group exercises as the exercise intervention and mainly psychometric instruments for the measurement of effectiveness. Therefore, this clinical study was done to examine the effectiveness of a single round of individual exercise on depressive symptoms by assessing the change in saliva free cortisol levels, which reflect hypothalamic-pituitary-adrenocortical axis function that is disturbed in depressive patients.
Eighteen medicated patients, who met the DSM-[unknown][unknown]-TR criteria for major depressive disorder, were examined for the change in saliva free cortisol levels and the change in subjective depressive symptoms before and after pedaling a bicycle ergometer for fifteen minutes. Within a month after the exercise session, participants conducted a non-exercise control session, which was sitting quietly at the same time of day as the exercise session.
Depressed patients who participated in this study were in remission or in a mild depressive state. However, they suffered chronic depression and had a disturbed quality of life. The saliva free cortisol level and subjective depressive symptoms significantly decreased after the exercise session. Moreover, the changes in these variables were significantly, positively correlated. On the other hand, although the subjective depressive symptoms improved in the control session, the saliva free cortisol level did not change.
For the first time in depressive patients, we were able to show a decrease in the saliva free cortisol level due to physical exercise, accompanied by the improvement of subjective depressive symptoms. This identified a possible influence of exercise on the hypothalamic-pituitary-adrenal axis in depression.These results suggest the utility of assessing the effect of physical exercise by saliva free cortisol levels in depressive patients who suffer from bio-psycho-social disability.
BioPsychoSocial Medicine 12/2013; 7(1):18. DOI:10.1186/1751-0759-7-18
"The negative feedback of corticosteroids on the HPA system occurs at the level of the hypothalamus and the anterior pituitary via the glucocorticoid receptors (Thomson and Craighead, 2008; Pariante and Lightman, 2008). Dysregulation of this negative feedback mechanism is reported in patients with major depressive disease, which results in hyperactivity of the HPA system and higher basal levels of serum corticosterone (Carroll et al., 1976; Holsboer et al., 1984; Nemeroff et al., 1984; Halbreich et al., 1985a, b; Schatzberg et al., 1985; Gold et al., 1986a; Young et al., 1993). In addition, many clinical cases demonstrate that elevated corticosterone levels trigger depressive symptoms (Schatzberg et al., 1985; Gold et al., 1986b; Chu et al., 2001). "
"The hippocampus is a critical structure in the pathophysiology of depressive disorders. Depressed patients show characteristic hippocampal atrophy (Sheline et al., 1999; Frodl et al., 2002), as well as dysregulation of many hippocampus-related systems, such as stress coping and memory (Halbreich et al., 1985; McEwen, 2003; Gallassi et al., 2006). Moreover, loss of hippocampal dendritic spines and synaptic inputs to spines are observed in animal models of depression (Hajszan et al., 2005, 2009, 2010). "
[Show abstract][Hide abstract] ABSTRACT: The prevalence of major depression has increased in recent decades; however, the underlying causes of this phenomenon remain unspecified. One environmental change that has coincided with elevated rates of depression is increased exposure to artificial light at night. Shift workers and others chronically exposed to light at night are at increased risk of mood disorders, suggesting that nighttime illumination may influence brain mechanisms mediating affect. We tested the hypothesis that exposure to dim light at night may impact affective responses and alter morphology of hippocampal neurons. Ovariectomized adult female Siberian hamsters (Phodopus sungorus) were housed for 8 weeks in either a light/dark cycle (LD) or a light/dim light cycle (DM), and then behavior was assayed. DM-hamsters displayed more depression-like responses in the forced swim and the sucrose anhedonia tests compared with LD-hamsters. Conversely, in the elevated plus maze DM-hamsters reduced anxiety-like behaviors. Brains from the same animals were processed using the Golgi-Cox method and hippocampal neurons within CA1, CA3, and the dentate gyrus were analyzed for morphological characteristics. In CA1, DM-hamsters significantly reduced dendritic spine density on both apical and basilar dendrites, an effect which was not mediated by baseline cortisol, as concentrations were equivalent between groups. These results demonstrate dim light at night is sufficient to reduce synaptic spine connections to CA1. Importantly, the present results suggest that night-time low level illumination, comparable to levels that are pervasive in North America and Europe, may contribute to the increasing prevalence of mood disorders.
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