Same Mechanism Involved in Male and Female Homosexuality

James Michael Howard jmhoward at anthropogeny.com
Mon Oct 18 09:35:28 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
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. DHEA does affect
growth of brain areas, even in adult song sparrows, when testosterone
is low. DHEA stimulates "aggression and the size of an entire brain
region [involved in male territorial song]" (Horm Behav 2002; 41:
203-12). Subsequently, I decided testosterone "intensifies" the
effects of brain growth stimulated by 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. (All of our brains are
"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 testosterone
increases at puberty, the orientation is intensified and sexual
activity corresponds with the direction established in utero.

Explaining female homosexuality eluded me until recently. Congenital
adrenal hyperplasia (CAH) is often (90%) associated with increased
DHEA. It was recently 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. 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 are 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. These conditions are not chosen.




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