Understanding Asexuality

The exposure to hormones prenatally (in the womb) contributes to male and female sexual differentiation of both the body and brain. In other words, prenatal hormones (e.g., testosterone) will help to create male internal and external genitalia in male fetuses, while an absence of these hormones will help to create female internal and external genitalia. There is a critical time during gestation when this occurs, when fetal body tissues are sensitive to the levels of these hormones. Prenatal testosterone also affects the brain and potentially helps to create a gender role/identity and a sexual orientation. There is also a critical time during gestation when this occurs, when fetal brain tissues are sensitive to the level of these hormones. Thus, male (XY) or female (XX) fetuses exposed to atypical levels of this hormone during critical time periods of prenatal development can have altered differentiation of the body (e.g., intersex characteristics). Similarly, atypical levels of these hormones during critical time periods may also alter brain development, thus leading to atypical gender identity (e.g., transgendered) and sexual attractions (e.g., being gay or lesbian). If so, one might also speculate that male (XY) or female (XX) fetuses exposed to atypical levels of prenatal hormones, again at critical time periods, may develop an atypical gender identity (not feeling “male” or “female”), in addition to a lack of sexual attraction (i.e., asexuality).

The traditional scientific wisdom was that female sexual differentiation, including brain differentiation, would occur if these male hormones (e.g., testosterone) were absent. Indeed, females were once seen as the “default” sex, with typical female development occurring as long as male hormones were absent. Recent evidence suggests that sexual differentiation is more complex. Male and female sexual differentiation, including brain differentiation, is indeed related to the presence or absence of male hormones, but it is also related to other prenatal mechanisms (Arnold, 2004; Kopsida, Stergiakouli, Lynn, Wilkinson, & Davies, 2009). For example, there are specific genes on the Y and X chromosomes that affect male or female brain development directly (without, for instance, affecting male hormone levels). Thus, without these additional gene-based mechanisms, male and female sexual development, including brain differentiation, would not occur in a typical fashion. If so, male (XY) or female (XX) fetuses having one or more of these genes inactivated may have altered differentiation of the body (e.g., intersex). Similarly, if it is a gene very specific to the brain, any variation or mutation of this gene may alter neural development, leading to atypical gender identity (such as being transgendered) and atypical sexual attractions, including being gay, lesbian, or asexual.

One related possibility is that altered X- or Y-linked genes or prenatal hormones, or their combination, create a form of genderlessness in some asexuals. In other words, some asexuals may lack sexual attraction to both males and females—a genderless sexual orientation—and lack a male or female gender identity—a genderless identity—because these biological processes have a unique effect on brain development. For example, asexuality in women may occur because of an absence/alteration of male hormones (de-masculinization) in combination with an inactivation of one or more (X) female-specific genes affecting the brain (de-feminization). Thus, some asexual women may have brains that are neither “masculine” nor “feminine.” In contrast, the sexual orientations and identities of gays and lesbians may be the result of some “reversal” of a typical masculinization or feminization process. For example, prenatal exposure to a higher-than-typical level of male hormones has been argued to masculinize lesbians, including their sexual/romantic attractions (Ellis & Ames, 1987; Grimbos, Dawood, Burriss, Zucker, & Puts, 2010).