Explanation of Neurodevelopmental Progress of Premature Infants: A response to journal article...

James Michael Howard jmhoward at arkansas.net
Mon Feb 23 15:12:42 EST 2004


The following is my response to "The neurodevelopmental progress of infants less
than 33 weeks into adolescence" Archives of Disease in Childhood 2004;89:207-211
(http://adc.bmjjournals.com/cgi/content/abstract/archdischild%3b89/3/207).  In
my response, you may read my mechanism in detail along with pertinent citations.

"It is my hypothesis that most prematurity results from reduced availability of
maternal dehydroepiandrosterone (DHEA).  The mother is the source of DHEA for
herself and her developing fetus.  I suggest the major cause of reduced maternal
DHEA is increased maternal testosterone.  Later in life, the testosterone of
puberty, may again, adversely affect the child.  This mechanism may explain the
findings of O'Brien, et al.  (see "prematurity" at
www.anthropogeny.com/research.html )

"DHEA is the "active" form, derived from the large background source,
dehydroepiandrosterone sulfate (DHEAS).  Testosterone inhibits steroid sulfatase
(J Steroid Biochem Mol Biol. 2000; 73: 251-6) which converts DHEAS to DHEA.  It
is my hypothesis that all growth and development is optimized by DHEA,
especially the brain.  Therefore, reduced DHEA decreases growth and development.
Blacks exhibit disproportionate levels of prematurity than whites with or
without prenatal care (Am J Obstet Gynecol. 2002 Nov;187(5):1254-7) and black
mothers produce more testosterone than white mothers (Cancer Causes Control.
2003 May;14(4):347-55).  It has been determined that high DHEAS is most commonly
associated with "small for gestational age" infants with a much smaller
association with low DHEAS (Pediatr Res. 1997 Mar;41(3):440-2).  I suggest
individuals exist whose reserve DHEAS is low so a "normal" conversion to DHEA
would be low.  However, high DHEAS is, by far, connected with reduced fetal
growth and I suggest this is the result of increased maternal testosterone.

Neonates produce their own DHEA.  Therefore, neonates should exhibit varying
degrees of "recovery growth" from the negative effects of maternal testosterone.
This should continue until near puberty when adolescent testosterone production
begins.  In children, abnormally high levels of testosterone have been
associated with learning disabilities (Physiol Behav. 1993; 53: 583-6) and
children exhibiting early puberty frequently exhibit problems with learning.  I
suggest this results from a decrease in available DHEA from DHEAS because of the
testosterone.

O'Brien, et al., found "an apparent deterioation in neurodevelopmental outcome
category, cognitive function, and [necessary] extra educational support" in
"very preterm survivors at school age compared with controls. "  I suggest these
findings result from diminished neurodevelopment in utero as a result of high
DHEAS caused by high maternal testosterone, or simply low maternal DHEA in some
mothers, both of which are later exacerbated by the effects of increasing
testosterone of puberty.  In those children who exhibit early puberty, this
situation would manifest itself earlier and be worsened by high testosterone."


Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.



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