Baseline Levels of Rapid Eye Movement Sleep May Protect Against Excessive Activity in Fear-Related Neural Circuitry

I suggest the basis of Lerner, et al., is dehydroepiandrosterone (DHEA).

Very briefly, it is my hypothesis of 1985 that the function of sleep is to produce dehydroepiandrosterone (DHEA) which stimulates consciousness. 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. Melatonin triggers prolactin production which is a direct and specific stimulator of DHEA. As DHEA is literally used during the day, melatonin increases at sleep. During sleep the melatonin - prolactin cycle increases until sufficient levels of DHEA are produced to induce awakening and consciousness during the day. The function of sleep / circadian rhythm is production of DHEA. "Sleep deprivation" is caused by low / insufficient DHEA. During periods of increasing DHEA, I suggest DHEA not only maintains brainstem activity but also causes REM sleep.

It is 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.

Therefore, I submit that the basis of Lerner, et al., is the effects of DHEA during sleep. DHEA, prolactin, melatonin, and cortisol are not mentioned in Lerner, et al.