Same Mechanism Involved in Male and Female Homosexuality
Etiology of Male Homosexuality and Current Rise of Male Homosexuality (follows below)
New: How this mechanism develops into homosexual orientation: How Homosexual Orientation May Form
Same Mechanism Involved in Male and Female Homosexuality
2004, James Michael Howard,
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.
Etiology of Male Homosexuality and Current Rise of Male Homosexuality
Copyright ă 1997 by James Michael Howard
In 1985, I developed an hypothesis (copyrighted) of male homosexuality that produced predictions. These predictions have since been supported. My explanation is very lengthy; for sake of brevity I am including the significant part regarding the predictions. As you read this, you should know that, earlier in my treatise, I said this: "As I have suggested, DHEA is directly responsible for growth and differentiation of the brain." In the context of homosexuality, I was saying that reduced DHEA will reduce growth of specific areas of the brain that determine sexuality. In the fetus, the ratio of DHEA to estrone, which I mention in the following quotation, is determined by the mother, as the adrenal glands of the fetus do not function until birth.
"Results indicate that the fetal adrenal activity increases independently of the maternal adrenal cortex at term and plays an important role in the onset of labour." (Orv. Hetil. 1987; 128: 2153).
Not all human fetuses are exposed to molecules of the type that I have been discussing. I propose that the hormone which induces homosexuality in humans is estrone. This hormone could induce alterations in critical function of the receptors during critical periods. Estrone is only one conversion step away from DHEA in the enzymatic syntheses in the adrenal glands. Remember that DHEA sulfate is the chief precursor molecule of estrone. [Here I meant the mother.] During the genesis of the nervous system, a ratio of DHEA/estrone might occur abnormally in the fetus. This would continue throughout life. The amount of DHEA/estrone would determine the degree of influence from slight to the syndrome of homosexuality. To further clarify this, later in my treatise, I suggested: "It is important to differentiate here between the asexual male and the homosexual. The person of low DHEA without estrone production, might very well become asexual.
For this argument I want to demonstrate that a number of these predictions have been supported, subsequent to 1985. The effects of DHEA on growth and differentiation of neurons was reported in 1987.
"In the present study, using methods of immunocytochemistry, autoradiography, and scanning electron microscopy, we show that a supplement of as little as 10(-8) M DHEA or DHEA-S greatly increases neuronal survival and differentiation and reduces astroglial proliferation rates in mouse brain cells in cultures." (J. Neurosci. Res. 1987; 17(3): 225)
In 1992, a study of homosexual men, during progressive stages of AIDS, determined that DHEA is low and estrone high. As you read the following quotation, notice the use of the word "all." "The serum DHEA sulfate values of all groups of HIV+ patients were lower than those of controls. …The serum E1 [estrone] and E2 [estradiol] were elevated 30-50% (p<0.01) in all groups of HIV+ patients." (J. Acquired Immune Deficiency Syndromes 1992; 5: 841)
So, I suggest that male homosexuality results, in utero, from an increased ratio of estrone to DHEA. This combination results in the increased growth, and reduced growth of other structures, in the male homosexual brain. Furthermore, my hypothesis can be extended to explain the current rise in homosexuality. While I think the current "climate" of increased acceptance of homosexuality may account for more acknowledging their homosexuality, I think the current increase is due to an evolutionary phenomenon.
My theory of human evolution suggests that testosterone is currently rising. I suggest testosterone periodically rises in civilizations, and this increased testosterone causes a number of phenomena, including an increase in homosexuality. If you understood my explanation of increases in estrone in the mother as the cause of male homosexuality, then some connection of testosterone and estrone should exist. This has been confirmed. In the following report, a positive correlation was found between testosterone and "unconjugated and total estrone."
"Serum androgens, estrogens, 'steroid-sensitive proteins', thyroid components, and albumin were measured twice within a 4-5 week interval in 44 cases of early normal pregnancy (gestational weeks 8-18). Positive correlations were found in the total material between dehydroepiandrosterone sulfate (DHAS) and testosterone (T), unconjugated and total estrone, albumin, tetraiodothyronine, and calculated free tetraiodothyronine concentrations and within 2-week intervals between DHAS and T, estradiol-17 beta, and unconjugated and total estrone, and between T and estradiol-17 beta and unconjugated estrone." (Gynecol. Obstet. Invest. 1995; 40(3):145)
I suggest that the current rise in male homosexuality is the result of increased testosterone in women. It is known that the phenomenon known as the "secular trend" is occurring here. The secular trend is characterized by increased size in our children, male and female, and an earlier onset of puberty. I suggest the secular trend is driven by increased testosterone and the rise in male homosexuality is a result of this.