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Same Mechanism Involved in Male and Female Homosexuality

James Michael Howard jmhoward at anthropogeny.com
Sun Sep 5 13:33:06 EST 2004


Same Mechanism Involved in Male and Female Homosexuality

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

In 1985, I first suggested male homosexuality results from reduced
availability of DHEA in utero (copyrighted).  (I learned later that,
in fact, DHEA is low, on average, in male homosexuals.)  I think low
DHEA in males in utero reduces "male" orientation because of low
growth and development of the pertinent part of the brain.
Subsequently, I decided that testosterone "intensifies" the effects of
DHEA.  Therefore, if enough DHEA is present, the "hit" of testosterone
produced by male fetuses accentuates the direction of sexuality
established by DHEA.  Female fetuses lack this "hit" of testosterone.
(Our brains are all "female" until this occurs.)  If a male fetus
experiences low DHEA at the time of development of the pertinent part
of the brain, the testosterone cannot change the orientation.  When
puberty and the increase in testosterone arrives, the orientation is
intensified and sexual activity corresponds with the direction
established in utero.

Female homosexuality eluded my hypothesis until recently.  Congenital
adrenal hyperplasia (CAH) is often associated with increased DHEA.  It
was reported that "among women with CAH, we found that recalled
male-typical play in childhood correlated with reduced satisfaction
with the female gender and reduced heterosexual interest in adulthood.
Although prospective studies are needed, these results suggest that
those girls with CAH who show the greatest alterations in childhood
play behavior may be the most likely to develop a bisexual or
homosexual orientation as adults and to be dissatisfied with the
female sex of assignment."  (J Sex Res 2004; 41: 78-81).  I suggest
this fits my hypothesis, that is, that increased DHEA in utero
increases "male" orientation, growth and development of the pertinent
part of the brain, in these girls.  (While DHEA is a weaker "androgen"
than testosterone, enough DHEA may produce comparable growth and
development of the brain.)  These girls are like boys in early play
and later sexual orientation.  The testosterone of puberty in these
girls will simply intensify their orientation.  Testosterone levels,
on average, do not differ between heterosexual and homosexual women
(Horm Behav 1987; 21: 347-57).  The difference occurs in utero.  (A
male with extra DHEA in utero would simply have more "male"
orientation.)  No differences in CAH male childhood play or sexual
orientation were found (J Sex Res 2004; 41: 75-81).

The same mechanism is in effect.  Low DHEA in males in utero reduces
"male" orientation and high DHEA in females in utero increases "male"
orientation.  A man who produces small amounts of testosterone from
puberty but experienced normal DHEA in utero may be "effeminate" but
is heterosexual.  Conversely, an adult male of high testosterone but
low DHEA in utero may be very "masculine" but homosexual.  A woman of
high DHEA in utero but low testosterone may be homosexual while a
women of normal DHEA in utero but who produces a lot of testosterone
may be heterosexual.  The first would be appropriately "feminine" but
homosexual while the second would be "masculine" while heterosexual.

These conditions are not chosen.  Homosexual people should not be
refused equal rights under the law.




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