Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans

Citation
L. Redwine et al., Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans, J CLIN END, 85(10), 2000, pp. 3597-3603
Citations number
42
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
10
Year of publication
2000
Pages
3597 - 3603
Database
ISI
SICI code
0021-972X(200010)85:10<3597:EOSASD>2.0.ZU;2-Q
Abstract
The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentra tions of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and pa rtial sleep deprivation-early night (awake until 0300 h). Sleep was measure d by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levels of IL-6 (P < 0. 05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the noc turnal increase in IL-6 occurred in association with stage 1-2 sleep and ra pid eye movement sleep, but levels during slow wave sleep were not differen t from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melato nin showed no concordance with sleep. Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the associ ation between sleep stages and IL-6 levels, depressed or aged populations w ho show increased amounts of REM sleep and a relative loss of slow wave sle ep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.