Anthony Bogaert - Understanding Asexuality

Asexuality may also be an evolutionary puzzle in need of a solution, assuming it also has a genetic basis across time. Perhaps asexuality “genes” are also conserved throughout evolutionary time because of kin-selection mechanisms. Thus, it would be interesting to examine in a research study if asexual people give, on average, elevated care for their siblings’ children, thus potentially offsetting their reduced sexual reproduction by such kin-enhancement strategies. [53] This is not to imply that this would be a “conscious” strategy.

Speaking of genetics and asexuality, no studies thus far have tested for this linkage directly. Indirect evidence is all we can rely on at this point: no studies have ever examined asexuality as a trait and its “concordance” or similarity between identical (as compared to fraternal) twins, a common methodology used to determine if variation in a trait is partly genetically based. Moreover, no one has ever isolated a specific gene directly associated with asexuality.

But let’s discuss some plausible genetic candidates affecting asexuality. In chapter 6, we discussed the role of certain X-linked (female) or Y-linked (male) genes in sexual differentiation. Some of these genes may play a key role in the prenatal development of the brain. Some of these gene effects on prenatal development are also independent of hormonal effects. In other words, they may directly affect the structure or organization of brain cells associated with sexual attraction. These genes, however, are not well studied. Some other sex-linked genes are well studied and have been clearly shown to affect hormones and their impact on sexual differentiation. For example, the SRY gene allows for the development of the testes, which produce hormones during prenatal and postnatal development. There are also other “hormone-related” genes. For example, the androgen receptor (AR) gene is important in determining how hormones affect the body and the brain. As you may recall, receptors are specialized parts of the cell that receive and activate a hormone molecule, and androgens (testosterone in particular) affect sex drive and prenatally organize sites in the lower brain related to gender, sexuality, and attraction. Variation in the AR gene likely affects the person’s level of sensitivity to testosterone. Interestingly, variation in the AR gene has been implicated in male-to-female transsexualism (Hare et al., 2009), and there is evidence that asexuality is associated with elevated rates of atypical gender identity (see also chapter 6). There is also evidence that variation in the AR gene might influence the age at which puberty begins (Comings, Muhleman, Johnson, & MacMurray, 2002), and there is evidence that the age of first menstruation (menarche) is, on average, later in asexual women than in sexual women (Bogaert, 2004). Finally, one of the explanations for asexuality in animals is an alteration in the receptors for testosterone (see also chapter 3). In sum, this research suggests that variations in the AR gene may underlie (or least predispose someone to) asexuality.

Genes underlying receptors for other hormones, including estrogens (e.g., estradiol), may also be involved in the causes of asexuality. Estrogens, among other functions, help regulate women’s menstrual cycle, [54] Estrogens (e.g., estradiol) are sometimes referred to as “female hormones,” but this is a bit simplistic, just as suggesting that testosterone is a male hormone (see the complexity of sex and gender in chapter 6). For example, testosterone itself can be converted to estradiol under the influence of an enzyme (aromatase) and both testosterone and estrogen (e.g., estradiol) are produced in both males and females. but also likely play some role in the sexual differentiation of both male and female fetuses. There is also some evidence that male-to-female transsexuals have an atypical variation in the estrogen receptor (ER) gene (Henningsson et al., 2005).

Recall from chapter 6 that sexual differentiation involves the development of female features (feminization) and male features (masculinization), as well as processes that prevent or remove female features in male fetuses (de-feminization) and prevent or remove male features in female fetuses (de-masculinization). Exploration of the possible role of androgen and/or estrogen receptors in the sexual differentiation process raises the possibility that some asexual people are, partially, neither masculinized nor feminized (see also chapter 6). In other words, instead of an inversion of masculinization and feminization that, at times, may occur in gays and lesbians during prenatal development (Ellis & Ames, 1987), some asexual people may be de-gendered during prenatal development. That asexual people report a high level of atypical gender identity, along with the role of these hormone receptor genes in transsexualism, adds support for this possibility.

Genes are chemicals that provide the codes for proteins, the building blocks of life, which in turn produce parts of the body (e.g., hormones, receptors, and/or brain sites); thus, variations in certain genes may alter typical brain development and affect asexuality. But aside from genes, are there other factors that could cause alterations in typical development of the brain? There are, and these factors have broad applicability to sexual orientation development, including the development of an asexual orientation. Let’s first consider these factors in the context of traditional sexual orientation—that is, in the development of a homosexual versus a heterosexual orientation.

One biological theory of sexual orientation is that homosexuality results when atypical events during pregnancy expose fetuses to variations in prenatal hormones (e.g., Ellis & Ames, 1987). These atypical events may include unusual pregnancies (e.g., carrying twins), a maternal exposure to certain drugs, or stress during pregnancy. Such events may alter the typical hormonal milieu (e.g., raise or lower testosterone levels) of the womb during pregnancy, and consequently alter the course of fetal brain development.

Another biological theory of male homosexuality is that atypical events during pregnancy expose male fetuses to a maternal immune response. In this theory, some pregnant mothers have an immune reaction to a substance important in male fetal development (Blanchard & Bogaert, 1996; Bogaert & Skorska, 2011). For example, male fetuses, because of genes on their Y-chromosome, produce certain male-specific proteins that may be seen as “foreign” to the mother. Thus, the target of a mother’s immune response may be these proteins, some of which are expressed on the surface of male fetal brain cells. Products of a mother’s immune system (e.g., antibodies) might alter the typical function of these proteins and thus alter their role in typical sexual differentiation, leading some males later in life to be attracted to men as opposed to women.

What could cause such an immune reaction, and what factors affect the degree to which such an immune reaction alters the typical development of the fetus? The events mentioned above—unusual pregnancies—may be relevant. For example, some unusual pregnancies may lead to a higher likelihood of products of the mother’s immune system (e.g., antibodies) crossing the placental barrier that separates the fetus and the mother, ultimately affecting fetal development.

In summary, two biological theories of sexual orientation development—variations in prenatal hormones and a maternal immune response—have as a central theme that an atypical womb environment can predispose fetuses to homosexuality. Yet there is often no direct information about atypical events that occurred while a fetus developed in its mother’s womb. A mother may know this about her pregnancy history, but her sons and daughters, when asked in research studies, may not be privy to this information. Moreover, even if there is information about such atypical events, very often little direct evidence exists that these events sufficiently altered the womb environment—such as by producing atypical hormone levels or a maternal immune response—to affect fetal development.