Explanation of Preterm and Reduced Growth and Development

Copyright 2013, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that evolution selected dehydroepiandrosterone 
(DHEA) because it optimizes replication and transcription of DNA. 
Therefore DHEA levels affect all tissues and life span.  It is also my 
hypothesis that evolution selected increased testosterone during 
evolution of primates and humans.  ("Androgens in Human Evolution," 
Rivista di Biologia / Biology Forum 2001; 94: 345-362)  This occurred 
because testosterone increases androgen receptor production which 
increases absorption and use of dehydroepiandrosterone (DHEA).  (Mammals 
evolved because of selection for DHEA: "Hormones in Mammalian 
Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184.)  The 
effect of increased testosterone in primates / humans occurred because 
of increased maternal testosterone.  This increased androgen receptors 
within fetal brains which increased growth and development, hence, 
bigger brains.  This reached a maximum in humans with the selection by 
evolution of females of very high testosterone.  (Human male and female 
testosterone is higher than chimpanzee male and females; human and 
chimpanzee estrogen are approximately equivalent.)

The extra use of DHEA by our bigger brains changes the use of our DHEA 
by our bodies.  Bigger brains produced the changes in our bodies that 
differentiate us from the other primates because of competition between 
the brain and other tissues for DHEA.

Fetal and maternal testosterone, therefore, will affect growth and 
development of a fetus by affecting androgen receptor deposition within 
the brain and body.  A woman of high testosterone, therefore, will 
produce more competition between herself and a fetus for DHEA for growth 
and development.

Since preterm neonates exhibit reduced cerebral and body growth, I 
suggest this is caused by reduced availability of DHEA for the fetus as 
a result of the mother's androgen receptors.  The midbrain of the fetus 
will develop more rapidly during this exposure to testosterone because 
of earlier formation of androgen receptors within the midbrain compared 
to the later development of the cerebrum. Therefore, the fetus will 
exhibit less growth and development in the cerebrum and the body as a 
result of reduced overall DHEA.  The midbrain will benefit from a 
relative increase in its competition with the body and the cerebrum.

From above, I suggest all tissues compete for DHEA and some tissues 
actually participate in stimulation of DHEA production, also, more than 
others.  As I have suggested, above, the midbrain in these fetuses 
produce more androgen receptors than the cerebrum, therefore, the 
midbrain should participate more in the production of end-term, fetal 
DHEA production which initiates birth.

This early stimulation of DHEA by the midbrain of these fetuses should 
stimulate birth, that is, maternal DHEA and fetal DHEA combine to 
stimulate birth as a signal of midbrain development necessary for life 
separate from the mother.  This could explain why gestation is reduced 
in these neonates.

(I recently responded to Sci Transl Med 2013: "Slower postnatal growth is 
associated with delayed cerebral cortical maturation in preterm 
newborns," Vinall, et al.  This is derived from that response.}