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.