Summary and Conclusions

The physiological necessity of sleep is readily apparent, but besides saying sleep is "restorative" we have not really improved our understanding of why we sleep. The notion that sleep is important for preserving our innate host defense mechanisms, exerting effects on both specific and nonspecific immunity, is an intriguing one, and there is, as has been discussed, some evidence for this notion, in particular work exploring the correlations behind disrupted sleep and infection, both in young and elderly individuals. There is a large body of evidence that suggests that key cytokines produced within the CNS are important in regulating sleep behavior, including IL-1P, TNF-a, and IL-6. Also consistent with this information is the evidence that alterations in expression of these molecules occur in a number of disease states, and in the elderly, and correlate well with disruption of normal sleep patterns. Considerably less evidence is available to suggest that deliberate attempts to modulate expression of those cytokines can prove beneficial to sleep performance. In addition, there are a number of chronic disease states, including cancer and autoimmune disorders, where sleep disruption, and/or altered expression of inflammatory cytokines is known to occur, yet corollary changes in the alternate variables have yet to be investigated. It is not being overly optimistic to anticipate significant advances, both in basic science understanding and in pharmaceutical intervention, in these areas over the next several years.

Acknowledgments. This study was supported by grants from the Canadian Space Agency (#9F007-001142, to R.M.G.); Trillium Therapeutics Inc. (to R.M.G.); the Turkish Science Foundation (to R.M.G. and E.T.); and from Clinique La Prairie, Montreux, Switzerland (to R.M.G.).

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