SIDS: Low DHEA in utero and after birth

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; 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.