Effects of Experimental Sleep Loss

Few clinical studies have studied sleep and immunity in persons with primary insomnia. However, sleep deprivation studies, in which healthy participants are required to undergo extended periods of wakefulness, provide some clues. Partial sleep deprivation studies typically involve 4 h of sleep deprivation and as such, are more closely related to sleep loss in insomnia patients. In studies with healthy participants, partial sleep deprivation results in decreased natural killer (NK) cell activity, independent of changes in actual numbers of natural killer cells, which also decrease (Irwin, McClintick, Costlow, Fortner, White, and Gillin 1996). This subset of cells represent an important line of defense against viral infections and in tumor surveillance (Ben-Eliyahu, Shakhar, Page, Stefanski, and Shakhar 2000). Although the implications of decreased NK activity in healthy participants are unclear, some studies show that decreases NK activity in cancer patients is associated with poorer prognosis (Pross and Lotzova 1993). Cytokine levels also fluctuate in response to partial sleep deprivation. Circulating levels of interleukin 6 (IL-6) are readily detected systemically and this cytokine is thought to exhibit potent systemic inflammatory effects including activation of acute phase proteins (Isomaki and Punnonen 1997). IL-6 is produced by multiple sources including monocytes, fibroblasts, endothelial cells, smooth muscle cells, and adipose tissue. IL-6 is thought to regulate systemic inflammation by stimulating production of acute phase reactants by the liver. It also stimulates both B-cell maturation into plasma cells as well as T-cell differentiation to cytotoxic T cells. However, elevated levels of plasma IL-6 are associated with polyarthritis and rheumatoid arthritis. IL-6 has a circadian rhythm, peaking at night, with lower levels during the day (Bauer et al. 1994). Redwine, Hauger, Gillin, and Irwin (2000) found that in healthy men, levels of IL-6 increased with peak values occurring 2.5 h after sleep onset; however, during partial sleep deprivation, the nocturnal increase of IL-6 was delayed and did not occur until after sleep onset at 3 AM Sleep deprivation did not influence the nocturnal secretion of cortisol or melatonin, which taken together suggest that sleep, rather than a circadian pacemaker, influences nocturnal IL-6 and growth hormone secretion (Redwine et al. 2000). A sleep induced increase in IL-6 is in contrast to findings by Born, Lange, Hansen, Molle, and Fehm (1997), who found that IL-6 concentrations were flat during sleep and during sleep deprivation. However, blood sampling was limited to 3-h intervals. Thus, the frequency of blood sampling may not have been adequate to ascertain nocturnal increases in IL-6 during normal sleep or the effects of sleep deprivation on this cytokine. In contrast, other researchers have found that partial sleep deprivation each night for a week results in increased circulating levels of IL-6 (Vgontzas et al. 2004a).

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