To Sleep, Perchance To Eat

Sleep, along with feeding, reproduction, and self-defense, is intuitively one of the most fundamental requirements for living creatures. Physiological mechanisms involved in sleep regulation are incompletely understood and undoubtedly complex. Pathological disturbances including infectious diseases, inflammation, and sleep deprivation result in excessive sleep, alter hypothalamic-pituitary function, and potentiate cytokine production. These observations have led to the suggestion that cytokines may be involved in normal sleep regulation. Cytokines are small-to-medium size proteins that act as intercellular regulators of cellular changes in metabolism and function. Most cytokines have been well conserved throughout evolution, and many have redundant biological activities, suggesting that cytokines comprise a complex regulatory system for mediation of important physiological processes. Cytokines mediate a wide range of pleiotropic biological responses and regulate neuroendocrine function (1). For example, the known functions of Interleukin (IL)-1 and tumor necrosis factor (TNF) include local induction of adhesion molecules and chemotactic cytokines as well as systemic actions such as fever, the acute phase response, activation of bone marrow (2), and possibly, regulation of sleep. These inflammatory cytokines have been demonstrated to have somnogenic activity (3). TNFα and IL-1β enhance non-rapid-eye movement sleep, increase the amplitude of electroencephalogram slow waves, and suppress rapid-eye-movement sleep in animals (4).