Dehydroepiandrosterone,
Sleep, and DNA Methylation
Copyright, July 5, 2015, James
Michael Howard, Fayetteville, Arkansas, U.S.A.
I suggest DNA
methylation (DNAmation) is part of an evolutionary selection
mechanism of dehydroepiandrosterone (DHEA) involved in sleep. I
think DNAmation occurs as a result of low DHEA during sleep.
It
is my hypothesis that evolution selected dehydroepiandrosterone
(DHEA) because it optimizes replication and transcription of DNA,
that is, genes. 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. When DHEA is low or decreasing, all tissues are
adversely affected.
Very briefly, it is my hypothesis that the
function of sleep is to produce DHEA which stimulates consciousness
(http://anthropogeny.com/Sleep%20and%20SIDS.htm
). 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. The
function of sleep / circadian rhythm is production of DHEA.
This mechanism eventually produced mammalian evolution.
“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology
Forum 2001; 94: 177-184. If your library does not subscribe to
“Rivista … ,” you may find this at:
http://anthropogeny.com/evolution.html
.
A case may be made that DNAmation increases during sleep.
My explanation of sleep is that DHEA is high during consciousness and
low during sleep.
It is also my hypothesis of 1985 that
the “fight or flight mechanism” is based on the ratio of DHEA to
cortisol. That is, I think DHEA levels determine the amount of
motivation an organism brings to a confrontation and cortisol evolved
to counteract the effects of DHEA. If cortisol is high enough,
then an organism avoids the consequences of a confrontation such as
loss of blood, infection, ...death. Evolution would quickly
select this mechanism as it would promote future reproduction of more
organisms and fighting would reduce reproduction.
This is
derived from my examination of the adrenal hormone pathways in 1984.
It became apparent to me quickly that there really are mainly two
pathways of major amounts of hormone production, that is, DHEA and
cortisol. This ratio directly affects gene activation, so,
physiology and behavior are affected.
A case may be made that
cortisol is connected with increased DNAmation.
In 1985, I
first suggested that low DHEA is involved in depression, HIV AIDS
(not called this at the time), Alzheimer's disease, aging, etc.
All of these express increased DNAmation.
It
is also my hypothesis that low DHEA is involved in cancer initiation.
In 1994, I first suggested that low DHEA is directly involved in
initiation of oncogenes: “An Explanation of Cancer and the Increase
in Cancer: High Testosterone, Low DHEA and Breast Cancer,” at:
http://anthropogeny.com/An%20Explanation%20of%20Cancer%20and%20the%20Increase%20in%20Cancer.htm
which appeared first in publication: (Annals of Internal Medicine
2005; 142: 471-472 .) “It is commonly known that inactivation of
certain tumor-suppressor genes occurs as a consequence of
hypermethylation within the promoter regions and a numerous studies
have demonstrated a broad range of genes silenced by DNA methylation
in different cancer types.” (Adv Genet. 2010;70:27-56)
I
think DHEA was selected by evolution to increase gene expression.
I
suggest that low dehydroepiandrosterone increases DNA methylation.
This mechanism was selected by evolution to reduce gene activity
during sleep.