The discussion above places a heavy emphasis on prenatal mechanisms, such as hormones organizing brain structures during fetal development.{We can add to this evidence the research mentioned in chapter 6 showing that asexual women have atypical menarche onset (Bogaert, 2004). There is also evidence that asexual people may be somewhat shorter than sexual people (Bogaert, 2004). Atypical menarche and stature are both potential markers of altered biological development, including an altered prenatal development. Interestingly, there is evidence of atypical height patterns in gays and lesbians, although this research is not consistent and may be subject to non-biological interpretations (Bogaert & McCreary, 2011).} What about current or circulating hormones affecting asexuality? Do asexual people have low circulating hormones that reduce sex drive, and minimize their sexual attractions?
As mentioned in chapter 2, prior to the 1970s, gay men were sometimes administered high levels of testosterone. This was done because “reparative-oriented” clinicians felt that this hormone treatment could change gay men’s orientation. Yet it did not make them attracted to women; it just made them horny for more sex with men! The problem with this approach, aside from the ethics of it, was that gay men’s orientation was already determined, perhaps even before birth, and thus administering testosterone in adolescence and adulthood just “activated” or stimulated their sex drives. So the testosterone worked like fuel on the fire of whatever disposition (i.e., brain organization) was already there in the first place.
By the same token, it is unlikely that we can change many asexual people’s orientation by administering sex hormones. Thus, like gay men, asexual people’s underlying attractions (to no one, in this case) are unlikely to be changed by such interventions, although they may make the masturbating asexuals masturbate even more (see chapter 5)! Indeed, the fact that some asexual people are masturbating already (and some do so frequently) means that, at least for these asexual people, their asexuality is not a sex-drive issue, and thus their underlying sexual connection to others is unlikely to change with added hormones. Finally, as mentioned in chapter 3, there is little evidence that asexuality in animals (the so-called duds in rodents or NORs in rams) is the result of low levels of circulating or activating hormones (Adkins-Reagan, 2005; Perkins, Fitzgerald, & Price, 1992).{Does this mean that no asexual person would ever become sexual (e.g., develop sexual attractions) by taking testosterone? Not necessarily. Although the majority of asexual people likely do not have a “hormone deficiency,” there is always a possibility that some asexual people have lower-than-average testosterone or other hormones relative to sexual people. For example, low hormone levels in some asexual people may occur because of a health condition (for some evidence of this, see my original article published in 2004). Also, it is possible that some asexual people with average hormone levels who take abnormally high testosterone could raise their sex drive and, perhaps, develop some level of sexual attraction for others. There are at least two issues here, though: First, as mentioned, there is currently little evidence that asexual people, as a whole, have lower testosterone levels than average sexual people. Second, is it ethical to administer abnormally high hormones to an asexual person if asexuality, arguably, is not a disorder (see also chapters 8 and 9)?}
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Research suggests that some atypical sexual attractions partly result from atypical rearing events, including sexual abuse (Seto, 2008). This fact raises the possibility that asexuality—as it is also an unusual form of sexual attraction—may be caused by such events. These traumatic events may be experienced very negatively and disrupt any sexual interest or attraction that normally arises in an individual. Thus, traumatic events could shut down an emerging sexuality. These events may also be coupled with (or interact with) other predisposing factors—such as prenatal influences—that could seal the deal on an individual’s asexuality.