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ADC Fetal and Neonatal Edition Letters and ADC Education and Practice Letters
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James M. Howard, Biologist Independent
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jmhoward{at}arkansas.net James M. Howard
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Dear Editor It is my hypothesis (1985) that the sleep-consciousness cycle is controlled by interactions of melatonin and DHEA. (It has been demonstrated that DHEA is involved in melatonin production and melatonin is involved in DHEA production.) Basically, when melatonin is high, sleep occurs, when DHEA is high, consciousness occurs. As is well known, quiet sleep alternates with active sleep. I suggest this cycling is designed to maintain sufficient levels of DHEA during sleep to maintain brainstem function during times of sufficiently low DHEA that allow sleep. When DHEA is very low, quiet sleep occurs, when DHEA is higher, during sleep, active sleep occurs. Prolactin is known to stimulate DHEA production. The cycling of quiet sleep and active sleep involves the reduction of prolactin by melatonin with prolactin rebounding in response to levels of melatonin. The first sleep is the deepest, I suggest, due to the high levels of melatonin at this time. As prolactin rebounds, DHEA is produced which begins to decrease levels of melatonin as sleep progresses. This gradual reduction of melatonin and increase in prolactin eventually reaches a level of DHEA which induces consciousness and stops release of melatonin until DHEA production decreases near nighttime and begins the cycle again. The connection between melatonin and DHEA is prolactin. Breast milk contains prolactin. I suggest prolactin occurs in breast milk to stimulate DHEA. Therefore, prolactin in breast milk would activate DHEA production, but not sufficient to induce arousal. This would combine with an infant's DHEA to increase DHEA during active sleep. It is my hypothesis that sudden infant death syndrome results from insufficient DHEA during quiet sleep to maintain brainstem function. I suggest the evolutionary value of prolactin in breast milk is decreased SIDS. |
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