Acute Effect of a Glucocorticoid on Normal Human Sleep

Gillin, J. Christian; Jacobs, Laurence S.; Fram, David H.; Snyder, Frederick

doi:10.1038/237398a0

Cited by 123 publications

(44 citation statements)

References 20 publications

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“…67 Nevertheless, another study reported that glucocorticoids acutely decreased REM sleep and increased time spent awake. 68 In Addison's disease, where production of corticosteroids is severely reduced, no major EEG disturbances of sleep have been reported. 69 In contrast, hypercortisolism and disturbed sleep are frequent symptoms in Cushing's disease and in depression.…”

Section: Cortisol Glucocorticoid and Mineralocorticoid Receptor Ligmentioning

confidence: 99%

Hormones, hormonal agents, and neuropeptides involved in the neuroendocrine regulation of sleep in humans

Kotronoulas

Stamatakis²,

Stylianopoulou³

2009

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Sleep is an essential ubiquitous biological process, a periodical state of quiescence in which there is minimal processing of sensory information and no interaction with conspecifics or the environment. Despite relevant research on sleep structure and testing of numerous endogenous sleep-affecting chemicals, questions as to the precise mechanisms and functions of sleep remain without satisfactory responses. The purpose of this review is to report on current evidence as regards the effect of several endogenous and exogenous hormones, hormonal agents, and neuropeptides on sleep onset or wake process, when administered in humans in specific doses and via different routes. The actions of several peptides are presented in detail. Some of them (growth hormone releasing hormone, ghrelin, galanin, neuropeptide Y) seem to promote sleep, whereas others (corticotropin, somatostatin) impair its continuity.

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Section: Cortisol Glucocorticoid and Mineralocorticoid Receptor Ligmentioning

confidence: 99%

Hormones, hormonal agents, and neuropeptides involved in the neuroendocrine regulation of sleep in humans

Kotronoulas

Stamatakis²,

Stylianopoulou³

2009

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“…Cortisol enhances SWS probably by feedback inhibition of CRH (8). High levels of glucocorticoids inhibit rapid eye movement (REM) sleep (4,12). However, GarciaBorreguero and co-workers demonstrated that low cortisol levels also interfered with normal REM sleep in patients with adrenal insufficiency (2).…”

Section: Introductionmentioning

confidence: 99%

“…With the available replacement therapy these patients have marked cortisol deficiency in the late night, which results in an inappropriate rise in adrenocorticotrophic hormone (ACTH), and presumably high corticotrophin-releasing hormone (CRH) levels during these hours of sleep. Some authors recommend replacement with small doses of synthetic glucocorticoids in the evening to mimic the normal nocturnal rise in serum cortisol (3), but the clinical effects are not well documented, and such treatment carries considerable risk of glucocorticoid-induced sleep disturbances (4,5).…”

Section: Introductionmentioning

confidence: 99%

Sleep disturbances in patients with Addison's disease

Løvås

Husebye²,

Holsten³

et al. 2003

Eur J Endocrinol

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Objective: The standard replacement therapy in Addison's disease does not restore normal nocturnal levels of the hormones of the hypothalamic -pituitary-adrenal axis. The aim of the study was to describe the prevalence and characteristics of sleep disturbances in patients with Addison's disease. Methods: Sixty patients completed a self-administered sleep questionnaire and the Epworth Sleepiness Scale (ESS) questionnaire. Activity-based monitoring (actigraph recordings) and sleep diaries were obtained from eight patients. Results: Thirty-four percent reported weekly sleep disturbances (difficulties falling asleep in 13%; repeated awakenings in 14%; early morning awakenings in 20%). The sleep need was 8.21 h (S.D. 1.34; range 6-14 h), and sleep onset latency was 29 min (S.D. 29, range 2-150 min). Forty percent of the patients were tired during daily activities more than once a week, but the scores of the ESS were 6.0 (S.D. 3.5), which is not higher than normal. The actigraph recordings showed higher sleep efficiency than the subjective recordings. Conclusion: We did not identify specific sleep disturbances which were characteristic for patients with Addison's disease. Patients with Addison's disease have increased daytime fatigue, but no more daytime sleepiness than normal.

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“…In humans, most studies on sleep EEG changes induced by acute cortisol administration observed a suppression of rapid-eye movement (REM) sleep and an increase in slowwave sleep as well as stimulation of sleep-associated release of growth hormone (GH) (Gillin et al, 1972;Born et al, 1989Born et al, , 1991Friess et al, 1994). The sleep-promoting effects of an acute cortisol administration were attributed to negative feedback inhibition of endogenous corticotropin-releasing hormone (CRH), shifting the ratio of CRH and GH-releasing hormone (GHRH) towards the latter.…”

Section: Introductionmentioning

confidence: 99%

Acute Cortisol Administration Promotes Sleep Intensity in Man

Frieß

Tagaya

Grethe

et al. 2003

Neuropsychopharmacol

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The neuronal mechanisms of sleep generation, in particular synchronization of brain activity in the process of non-rapid-eye movement (non-REM) sleep, has been elucidated in the past decade. A previous study of our group showed that acute administration of cortisol is known to increase slow-wave sleep and suppress rapid-eye movement (REM) sleep in man. To further elucidate the non-REM sleeppromoting effects of cortisol with respect to the synchronization of cortical activity, it is important to establish a sleep-state-specific quantitative EEG analysis. We therefore investigated the effects of repetitive injections of hydrocortisone on spectral composition of sleep EEG in 10 healthy male young volunteers. In addition, we performed high-frequency blood samplings to assess the relation between changes in the sleep EEG and sleep-associated secretion of growth hormone (GH). Cortisol administration resulted in a significant increase in highly synchronized EEG activity including delta and theta frequencies, according to a higher amount of slow-wave sleep. This effect predominated in the first few hours of night sleep. REM sleep was decreased, which appeared to be secondary to the lengthened first sleep cycle. The cortisol-induced stimulation of GH release did not occur in correspondence with the increased slow-wave activity. In view of the sleep impairing properties of corticotropin-releasing hormone (CRH) and the sleep-promoting function of GH-releasing hormone, it appears likely that a negative feedback inhibition of endogenous CRH was the key mechanism mediating the observed results. The cortisol-induced effects on sleep intensity and sleep-associated GH secretion appeared to be driven by different mechanisms.

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Acute Effect of a Glucocorticoid on Normal Human Sleep

Cited by 123 publications

References 20 publications

Hormones, hormonal agents, and neuropeptides involved in the neuroendocrine regulation of sleep in humans

Hormones, hormonal agents, and neuropeptides involved in the neuroendocrine regulation of sleep in humans

Sleep disturbances in patients with Addison's disease

Acute Cortisol Administration Promotes Sleep Intensity in Man

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