Hormones and Sleep

Akerstedt, T

doi:10.1007/978-3-642-69554-4_15

Cited by 4 publications

(6 citation statements)

References 50 publications

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“…1,41,[53][54][55][56][57][58][59][60] Catabolic hormones such as serum catecholamines and cortisol, which are elevated following burns, 48,49,52,61 are increased following sleep deprivation as well. [2][3][4][5][6][7][8][9][10]16,17,54,56,[62][63][64][65][66][67][68][69][70][71] In addition, impaired glucose tolerance is reported following both burns [72][73][74] and sleep deprivation. 10,12,[75][76][77] On the other hand, there is reduced secretion of growth hormone (GH) during inadequate sleep, [78][79][80] and GH levels are likewise suboptimal postburn.…”

Section: Discussionmentioning

confidence: 99%

“…There are some indications that disturbed sleep may be associated with increased catecholamine levels. [2][3][4][5][6][7][8]10,[54][55][56]62,67,68 In particular, catecholamines have been linked to wakefulness and have a negative impact on 3+4 and REM sleep. 8,82 This investigation corroborates prior reports of a reciprocal association of the catecholamines and REM sleep.…”

Section: Discussionmentioning

confidence: 99%

“…The most well-established connection between a hormone and sleep is probably that of growth hormone. 2,8,9,[78][79][80][129][130][131][132] Growth hormone is secreted by the anterior pituitary gland. Growth hormone levels are usually low, except for secretory bursts in association with the first few hours of sleep, eating, or exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Growth hormone levels are usually low, except for secretory bursts in association with the first few hours of sleep, eating, or exercise. 2,78,132 Growth hormone elicits immune modulatory and wound-healing benefits, and, therefore, exogenous supplementation is often utilized postburn. [133][134][135][136][137][138][139][140][141] Plasma growth hormone levels were relatively low in this study.…”

Section: Discussionmentioning

confidence: 99%

“…It is well documented in the nonburn literature that sleep is a major modulator of metabolic and endocrine regulation. [1][2][3][4][5][6][7][8][9][10][11][12] There are significant pathophysiological and psychological consequences of sustained sleep deprivation and sleep required the presence of a burn > 20% total body surface area (TBSA) in children 3−18 years of age. Infants and toddlers were excluded due to marked differences in sleep patterns that present in very young children.…”

Section: Methodsmentioning

confidence: 99%

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An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients

Gottschlich

Warden

Kagan

2009

J Parenter Enteral Nutr

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This work characterizes the relationship between sleep deprivation and select endocrine parameters postburn. Drug interventions utilized in this study were either ineffective or insufficient in modulating improved hormonal response. Significance of zolpidem's and haloperidol's effect on serum levels of DHEA is unclear. The inverse correlation of epinephrine with REM may suggest that hypermetabolism associated with burns is partly due to lack of REM sleep. Questions remain regarding the effects of sleep deprivation on metabolism and clinical outcome.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients

Gottschlich

Warden

Kagan

2009

J Parenter Enteral Nutr

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Vasoactive intestinal polypeptide promotes sleep without effects on brain temperature in rats at night

Sáry

Alföldi

Rubicsek

et al. 1986

Neuroscience Letters

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Evolving concepts of sleep cycle generation: From brain centers to neuronal populations

1986

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As neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator.Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence.In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets.Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine.Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.

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Hormones and Sleep

Cited by 4 publications

References 50 publications

An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients

An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients

Vasoactive intestinal polypeptide promotes sleep without effects on brain temperature in rats at night

Evolving concepts of sleep cycle generation: From brain centers to neuronal populations

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