Understanding Asexuality

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.