Sleep-inducible hormones

Depressive states can alter significantly the basal rates of pituitary hormone secretion and their circadian rhythms. In fact, depression may be related to periods when hormonal rhythms are out of phase with other rhythms in the body. Circulating levels of sleep-inducible hormones (GH, PRL, LH) are lower in depressive states, whereas that of ACTH is elevated. The basal level of ACTH in a depressed individual is elevated to the extent that it flattens the circadian oscillations of the hormone. These changes resemble those seen during disruptive phase shifts (e.g., east-bound trip, altered work schedule, etc.) and emphasize the importance of CNS influence on the release of anterior pituitary hormones. 

Within the European Union there are no restrictions regarding these additives. However, primary fatty-acid amides have been shown to have hormone-like activity, e.g., oleamide (c -9,10-octadecenoamide) is an endogenous bioregulator that acts like a sleep-inducing factor (Cravatt et al., 1995 Bezuglov et al., 1998). 

Colle, M., Rosenzweig, R, Bianchetti, G., Fuseau, E., Ruffle, A., Rue-das, E., and Morselli, P.L. (1991) Nocturnal profile of growth hormone secretion during sleep induced by zolpidem a doubleblind study in young adults and children. Norm Res 35 30-34. 

Because melatonin is sold over the counter and its production is not the subject of strict regulation as is that of prescribed medications, it is in wide use, but insufficient scientifically controlled information is available. Another consequence of the popularity and availability of the hormone is its use in a wide array of situations in which its efficacy has not been proven yet for instance, as treatment for neurodegenerative diseases or as a sleep-inducing medication. It also has been tried as an antidepressant, but that effect is still unclear. The administration of melatonin to patients with bipolar depression, especially to rapid cyclers, is of interest, especially if its use is associated with the presumed decrease in nocturnal hormonal levels and increase in sensitivity to light (Lewy et al. 1985). The possibility that melatonin also serves as a stabilizer of rhythm in these patients is in accord with the homeostatic effect of several other hormones that have been previously discussed here. 

The class III cytokine receptor family includes two TNE receptors, the low affinity NGE receptor and 7-ceU surface recognition sites that appear to play a role in proliferation, apoptosis, and immunodeficiency. TNE-a (- 17, 000 protein) is produced by astrocytes and microglia and can induce fever, induce slow-wave sleep, reduce feeding, stimulate prostaglandin synthesis, stimulate corticotrophin-releasing factor and prolactin secretion, and reduce thyroid hormone secretion. TNE-a stimulates IL-1 release, is cytotoxic to oligodendrocytes, and reduces myelination this has been impHcated in multiple sclerosis and encephalomyelitis. Astrocyte TNE-a receptors mediate effects on IL-6 expression and augment astrocytic expression of MHC in response to other stimulants such as lEN-y. 

IL-1 (17.5) Monocyte/macrophage, lymphocyte, neutrophil, endothelium, fibroblast keratinocyte Activation of T cells, B cells, natural killer cells, osteoblasts, and endothelium. Induces fever, sleep, anorexia, ACTH release, hepatic acute phase protein synthesis and HSPs. Leads to myocardial depression, hypercoagulability, hypotension/sbock, and death. Simulates production of TNF, IL-6, and IL-8 and stress hormone release. Suppression of cytochrome P-450, thyro-globulin, and lipoprotein synthesis. Procoagulant activity. Antiviral activity. 

Opp MR. Corticotropin-releasing hormone involvement in stressor-induced alterations in sleep and in the regulation of waking. Adv Neuroimmunol 1995 5 127-113. 

Mougin F, Bourdin H, Simon-Rigaud ML, Nguyen NU, Kantelip JP, Davenne D. Hormonal responses to exercise after partial sleep deprivation and after a hypnotic drug-induced sleep. J Sports Sci 2001 19 89-97. 

Intracerebral or systemic administration of IL-1 P enhances NREM sleep in mice, rats, rabbits, cats, monkeys, and humans (reviewed in Refs. 40,46), and TNF-a promotes NREM sleep in rabbits, mice, rats, and sheep (reviewed in Refs. 40,46). Both NREM sleep time and intensity (EEG slow-wave activity) increase after IL-1 3 or TNF-a. In rats and cats, only low doses of IL-1 stimulate NREM sleep. In contrast, higher doses decrease NREM sleep, perhaps owing to IL-ip-induced stimulation of corticotropin-releasing hormone (CRH), which is known to suppress NREM sleep (55,56). A correlation is observed between plasma TNF-a concentrations and sleepiness or fatigue in a number of clinical conditions. Thus, TNF-a is... 

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