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From the Clinical Research Centers |
Sleep Research and Treatment Center (A.N.V., E.O.B., A.K.), Department of Psychiatry, Pennsylvania State University, Hershey, Pennsylvania 17033; Developmental Endocrinology Branch (D.A.P., A.L., K.Z., G.P.C.), National Institute of Child Health Development, National Institutes of Health, Bethesda, Maryland 20892; Clinical Neuroendocrinology Branch (P.P., M.-L.W., J.L., P.W.G.), National Institute for Mental Health, Bethesda, Maryland 20892; Bioengineering and Chronobiology Laboratories (R.C.H.), ETSI Telecommunications, Campus Universitario Vigo, Pontevedra 36200, Spain; and Endocrine Unit (G.M.), Evgenidion Hospital, Athens University, Athens 11528, Greece
Address all correspondence and requests for reprints to: Alexandros N. Vgontzas, M.D., Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033. E-mail: axv3{at}psu.edu
Patients with pathologically increased daytime sleepiness and fatigue have elevated levels of circulating interleukin-6 (IL-6). The latter is an inflammatory cytokine, which causes sickness manifestations, including somnolence and fatigue, and activation of the hypothalamic-pituitary-adrenal axis. In this study, we examined: 1) the relation between serial measurements of plasma IL-6 and quantity and depth of sleep, evaluated by polysomnography; and 2) the effects of sleep deprivation on the nyctohemeral pattern of IL-6 secretion. Eight healthy young male volunteers were sampled for 24 h twice, at the baseline state, after a normal night’s sleep and after total overnight sleep deprivation. At the baseline state, IL-6 was secreted in a biphasic circadian pattern with two nadirs at 0800 and 2100 and two zeniths at 1900 and 0500 (P < 0.01). The baseline amount of sleep correlated negatively with the overall daytime secretion of the cytokine (P < 0.05). Also, depth of sleep at baseline correlated negatively with the postdeprivation increase of daytime secretion of IL-6 (P < 0.05). Sleep deprivation changed the temporal pattern of circadian IL-6 secretion but not the overall amount. Indeed, during the postdeprivation period, the mean daytime (0800–2200 h) levels of IL-6 were significantly higher (P < 0.05), whereas the nighttime (2200–0600 h) levels were lower than the predeprivation values. Thus, sleep-deprived subjects had daytime oversecretion and nighttime undersecretion of IL-6; the former might be responsible for their daylong somnolence and fatigue, the latter for the better quality (depth) of their sleep. These data suggest that a good night’s sleep is associated with decreased daytime secretion of IL-6 and a good sense of well-being and that good sleep is associated with decreased exposure of tissues to the proinflammatory and potentially detrimental actions of IL-6. Sleep deprivation increases daytime IL-6 and causes somnolence and fatigue during the next day, whereas postdeprivation decreases nighttime IL-6 and is associated with deeper sleep.
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