Etiology of Male Homosexuality and Current Rise of Male Homosexuality -------------------------------------------------------------------------------- Copyright © 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. To All Now I am really sorry but people writing papers like this is just too much of a coincidence with what is happening where adult women with cah is concerned. Things do run their course but often like I said you can't control them. When I read this paper it more or less confirmed things for me. because if boys can be affected in utero by higher levels on androgen in women being converted to estrone, then I guess the female baby actually making masses of androgen (dhea) in utero can have just the same effects. I am not arguing here, merely stating what is out there where thi is concerned. Some of us actually think about these things a great deal and want to broach the issues before they arise for ourselves or help others. Yes men and women have certain levels of both hormones. But there are levels that are considered "normal" and within normal ranges and there are levels which are considered high and excessive or too low. As we know, with cah many children get sick and die with just subtle differences in their levels. So although you post may sound quite reasonable for some, it goes no way to solving what my intuition is telling me. I really believe that in the next few years there will be a better understanding of these issues. Studies have probable already been done. I don't need them published to use my common sense. How can an issue run it's course when there are still questions in parents heads about the long term effects of something. Your post above was almost sounding like you have had enough of this issue and I do not think that your personal feelings should have anything to do with this. Or other parents who just do not want to learn about this. That is there perogative, but parents like I would like to know and raise such issues in such a forum and discuss every aspect of them. I have no idea why parents wish to push people around on this issue when it is a valid one to raise and want to talk about. Shame on you all.