SIDS in Twins: Low DHEA in utero
James Michael Howard
jmhoward at arkansas.net
Tue Jun 1 15:02:06 EST 2004
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
(0.7/1000 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;
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.
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