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These Findings May be Explained by Dehydroepiandrosterone (DHEA) Levels

Posted by jamesmhoward on 27 Mar 2014 at 14:28 GMT

I suggest the benefits of sleep are caused by dehydroepiandrosterone (DHEA). Beneficial sleep produces optimal DHEA for daytime function, less so in the elderly, those with pain, and younger individuals who do not sleep well.

Very briefly, it is my hypothesis that the function of sleep is to produce DHEA which stimulates consciousness (http://anthropogeny.com/S... ). My mechanism suggests that the light-dark cycle is involved in stimulating DHEA. This requires melatonin production during the dark phase which then results in the production of DHEA. DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age.

It is my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA. Therefore, DHEA levels affect all tissues and all tissues compete for available DHEA, especially the brain. (I think evolutionary selection of DHEA produced mammalia. "Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184) DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age.

It is part of my explanation of sleep that a background level of DHEA is necessary during sleep to maintain brainstem activity. As DHEA declines at the onset of sleep, it is necessary that brainstem activity be maintained to avoid death, as in sudden infant death syndrome. However, I suggest that in most individuals who cannot sleep, and who have not had stimulants prior to sleep, are kept awake by the brain's natural ability to stimulate DHEA. That is, as these individuals start to sleep, their DHEA begins to decline too deeply, so the brain recruits DHEA which disrupts sleep. Now, aged people do not produce much DHEA, so their DHEA may be declining excessively which will produce insomnia and very less than optimal levels of DHEA during the day. (The reason many elderly cannot sleep at night but can during the day is explained by the foregoing. At night there is not enough DHEA to maintain the brainstem, but, during the day when DHEA has increased, there is sufficient DHEA to maintain the brainstem during sleep.)

Also, it is known that chronic pain has been connected to increased cortisol levels. Some research has found that low DHEA may be involved in pain. It is also my hypothesis that cortisol evolved to counteract the effects of DHEA and is the basis of the "fight or flight" mechanism. ("A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of Dehydroepiandrosterone and the Amygdala," Copyright 1985, James Michael Howard, Fayetteville, Arkansas, U.S.A. (Registered Copyright TXu220580).) The "cortisol to DHEA ratio" appears numerous times in the medical literature; it is becoming an important mechanism. This would indicate that the effects of chronic pain may produce the same negative effects on DHEA that old age causes. Both reduce DHEA.

Low DHEA has also been connected with reduced physical activity. “...lower habitual physical activity is related to lower levels of circulating DHEAS...” (Age Ageing. 1998 Nov;27(6):745-51).

This may explain the findings of Tang and Sanborn.

No competing interests declared.