SIDS: Low DHEA in utero and after birth
Copyright 2004, James Michael Howard, Fayetteville,
Arkansas, U.S.A.
In 1985, I first suggested sudden infant death syndrome
(SIDS) may result from low dehydroepiandrosterone (DHEA)
during sleep. (This is derived from my sleep mechanism; "New
Sleep Mechanism and SIDS."
www.anthropogeny.com/physiology.html ) Basically, this says
that the levels of DHEA at night are insufficient to
maintain brainstem function in SIDS. (DHEA is very high
during consciousness but is reduced at night which produces
sleep. These low levels of DHEA of sleep fluctuate between
higher levels during REM sleep and lower levels during slow
wave sleep.) When DHEA levels are too low, brainstem
function cannot be maintained. Death may occur.
Some my other work suggests DHEA levels in utero affect
brain development which subsequently affects brain function
later in life. (One of these is schizophrenia;
"Schizophrenia." www.anthropogeny.com/physiology.html There
are others including "premature infants" and "small for
gestational age infants; "Prematurity,"
www.anthropogeny.com/research.html .) Well, as things turn
out, it appears that low DHEA may still explain SIDS, but
the "lesion" of SIDS apparently occurs in utero just like
the foregoing examples.
The following abstract includes the information which
supports the foregoing. My explanation and the connection
with the effects of maternal testosterone follows this
abstract. (High maternal testosterone is not a good thing!
J Perinatol. 2004 May 27 [Epub ahead of print]
Sudden Infant Death Syndrome among Twin Births: United
States, 1995-1998.
Getahun D, Demissie K, Lu SE, Rhoads GG.
1Department of Family Medicine (D.G.), UMDNJ-RWJMS, New
Brunswick, NJ, USA.
OBJECTIVES:: To compare the incidence and risk factors for
sudden infant death syndrome (SIDS) in twin and singleton
births and to estimate the concordance of SIDS in twins.
STUDY DESIGN:: A cohort analysis using the National Center
for Health Statistics Linked Birth and Infant Death files
(1995-1998). RESULTS:: Twins had higher SIDS rate (1.3/1000
live births) compared to singletons (.7/1000 live births),
relative risk: 1.9, 95% confidence interval: 1.68, 2.01.
Male and small- for-gestational age infants as well as
infants of black, unmarried, and smoking mothers were at
increased risk for SIDS in both twins and singletons.
Placental abnormalities also were associated with SIDS in
singletons and twins, although this association failed to
achieve statistical significance in twins. There is a higher
rate of SIDS in the second twin after a first twin SIDS.
CONCLUSIONS:: Twins are at higher risk of SIDS than are
singletons. Overall, the epidemiology of SIDS in twins is
quite similar to that seen in singletons. Journal of
Perinatology advance online publication, 27 May 2004;
doi:10.1038/sj.jp.7211140
The mother produces DHEA for herself and her fetus/es.
Therefore, what the mother does with her DHEA affects her
fetus. Testosterone inhibits the conversion of the
background source, DHEAS (DHEA sulfate), to DHEA. Black
mothers produce more testosterone than white mothers (Cancer
Causes Control. 2003 May;14(4):347-55). Therefore, the
increased testosterone of black mothers and male fetuses
reduces overall DHEA. I suggest this accounts for the
findings above as well as "small for gestational age
infants." That is, this explains the connection of black
mothers and male fetuses with increased incidence of SIDS.
Smoking is also known to increase DHEAS and testosterone in
women. (That is, smoking reduces available DHEA.) I suggest
this also explains the connection of maternal smoking with
increased incidence of SIDS.
The increased incidence of SIDS among twins is the data
which caused me to place the "lesion of low DHEA of SIDS"
in utero. You see, Getahun, et al., found that the
incidence of SIDS in twins verses singletons is
approximately two times higher. If the source of DHEA is
from a single entity, the mother, twins will have to share
available DHEA. This would reduce exposure to DHEA and
adversely affect growth and development of the brain,
including the brain stem. During sleep when DHEA is low,
the brain stem would be less able to respond.