Normal healthy aging is associated with increasing sleep fragmentation, increasingly light sleep (stages 1 and 2), and less slow wave sleep (SWS, stages 3 and 4) (Benca, Obermeyer, Thisted, and Gillin 1992; Ehlers and Kupfer 1997; Van Cauter, Leproult, and Plat 2000). These changes are thought to contribute to daytime fatigue, depression, and impairments in health functioning in older adults. Such changes in sleep parameters may explain why self reported poor sleep is one of the most common complaints in elderly adults. Furthermore, the elderly are at higher risk of developing insomnia than any other age group, and this sleep impairment is independent of medical and psychiatric illness, medication use, circadian rhythm changes, and psychosocial factors which can all contribute to sleep complaints (Ancoli-israel 2000).
As of yet, there are no studies integrating cytokine and sleep assessment in older adults with insomnia. Considering that older adults are particularly vulnerable to insomnia, this would be an important population to study. Elderly persons exhibit many of the prominent immune changes observed after acute or prolonged sleep
□ Insomnia patients
□ Insomnia patients
□ Depressed patients
NK activity deprivation described earlier. Regarding innate immune functions, aging, like sleep deprivation, leads to diminished NK cell activity when considered on a per cell basis (Irwin et al. 1994). There is also evidence that aging is associated with progressive increases in circulating levels of inflammatory cytokines such as IL-6 (Glaser and Kiecolt-Glaser 2005). For example, as compared to young subjects, healthy elderly subjects showed an increased production of interleukin 1 (IL-1) and tumor necrosis factor (TNF) that was particularly pronounced during nocturnal sleep (Born et al. 1997). In younger adults, levels of IL-6 are lower during SWS as compared to stages 1 and 2 sleep; however, aging is associated with progressive decreases in SWS, and this change may be important in explaining the increases in IL-6 seen in older adults. Although these findings are promising, there are some important caveats. Aging-related thymic involution accounts for reduced numbers of circulating lymphocytes in older adults, and this decrease is opposite to what is observed following sleep deprivation. Accordingly, it should be cautioned against considering alterations in immune function in the aged as a consequence of a "chronic sleep deprivation," since the effects of poor sleep in elderly persons interact with a number of other physiological conditions not related to sleep. However, there appears to be a convergence of declines in host defense, increases in systemic low-grade inflammation and poorer sleep in older adults, which suggests that the health consequences of sleep-immune interactions are particularly salient in this population.
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