(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
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.
Because direct evidence of such changes is rarely available, researchers often seek indirect “markers” of biological development, particularly those markers that are determined before birth and that are sensitive to atypical womb conditions. One of the most important and well-studied biological markers of prenatal development is handedness.
Did you know that fetuses often suck their thumbs? They do, and ultrasound studies show that the rate of right-handed thumb sucking in fetuses matches relatively closely the rate of right-handedness in adults (Hepper, Shabidullah, & White, 1991). This rather intriguing correspondence in bodily characteristics between fetal and adult life suggests that handedness is determined before birth.
Handedness is linked to genes (and what isn’t?), including the androgen receptor (AR) gene mentioned above (Medland et al., 2005). Elevated non-right-handedness is also associated with atypical pregnancy/birth conditions (e.g., birth stress) (Coren, 1993). Handedness is additionally linked to variations in prenatal hormone levels (Witelson & Nowakowski, 1991). Thus, if a group has a rate of non-right-handedness that differs statistically from, say, 10 percent—the rate seen in many adult populations—it suggests that this group has elevated variations in relevant genes and/or atypical prenatal development (e.g., altered hormone levels). For example, non-right-handedness is elevated in gay men and lesbians (Lalumiere, Blanchard, & Zucker, 2000) and other groups with atypical sexual attractions (Bogaert, 2001).{One of these groups is pedophiles. This fact should not be taken to mean that homosexuality (or asexuality) and thus pedophilia should be seen as linked in a behavioral way—that is, to mean that gay men, lesbians, or asexuals are more likely to abuse children. This is not the case. Instead, this fact should be taken as evidence that sexual attraction, atypical and otherwise, is very likely influenced by prenatal events.} This research suggests that atypical womb events (e.g., variations in prenatal hormones) can alter brain mechanisms affecting both handedness and patterns of sexual attraction in these groups. As such, handedness is also an important biological marker to examine in the context of a possible biological underpinning of asexuality.
Is there any evidence that asexuals have atypical handedness patterns? There is. Perhaps the most intriguing finding related to the etiology of asexuality is that 26 percent of (self-identified) asexual people have been found to be non-right-handed (Yule, 2011). This is a very high percentage in comparison to population norms or to the control group of heterosexual participants (12 percent) in the study itself. The elevated non-right-handedness occurred in both asexual men and asexual women, and is consistent with elevated rates of non-right-handedness in both gay men and lesbians (Lalumiere et al., 2000).
Another potential biological marker of atypical prenatal development is a high number of older brothers. Such a marker is relevant to the biology of men’s sexual orientation and the theory of maternal immune response contributing to male homosexuality mentioned above. An important corollary of this theory is that the immune effect should have a higher likelihood of occurring with each son that a mother gestates. This is because a mother has increased opportunities to develop an immune response against male-specific substances with each male gestation. Each male fetus gestated increases the likelihood that eventually a mother will be exposed to and ultimately react against such a substance as a male-specific protein. So, in other words, we should observe an “older brother effect”—a greater number of older brothers in gay men versus heterosexual men—if a maternal immune effect underlies male homosexuality. There should also be no sibling (e.g., older sister) effect in female homosexuality, because a mother should not develop an immune response against a female-specific substance, given that she herself is female.
Is there an older brother effect in gay men? Yes! On average, gay men have a higher number of older brothers than do heterosexual men. In 1996, psychologist Ray Blanchard and I first demonstrated this effect using a Canadian sample (Blanchard & Bogaert, 1996). However, there is now a large body of research, including cross-cultural studies, showing this effect, but only in men’s sexual orientation (Blanchard, 2004; Bogaert & Skorska, 2011). The fact that this “older brother effect” is indeed a
Interestingly, there is recent evidence of an “older brother effect” in asexual men: Morag Yule (2011), in her
