This paper examines the ongoing scientific debate over the biological underpinnings of sexual orientation. Drawing on genetic twin studies, hormonal theories of fetal development, fluctuating asymmetry (FA) research, and birth-order studies, the paper evaluates competing explanations for homosexuality in men and women. It critically assesses the "insufficiently masculinized fetus" hypothesis, the older-brother immune response theory, and evolutionary arguments for gay gene persistence. The paper also highlights methodological and conceptual limitations in this body of research — including rigid binary definitions of sexuality, androcentric framing, and the influence of cultural assumptions on scientific inquiry — concluding that no single biological cause has been established.
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The search for a so-called "gay gene" that conclusively determines an individual's sexual orientation remains elusive — and very likely no such singular gene exists at all. Current genetic studies indicate that while homosexuality appears to have a clear biological component, there is equally compelling evidence that gayness cannot be entirely attributed to an individual's genetic code alone. Even in pairs of identical twins, one twin is often gay while the other is heterosexual. Even the most generous estimates "suggest there is a genetic basis for homosexuality in only 50% of gay men" (Kunzig, 2008). Studies of brain development do suggest a strong biological predisposition for homosexuality, but not a singular cause-and-effect pattern.
"In 2005 a study conducted at the University of Illinois at Chicago and published in Human Genetics indicated there were three different chromosomes that appeared to be linked to sexual orientation" (Graceffo, 2008). These chromosomes are influential in determining sexual orientation, but they only create a tendency — not a final determination of an individual's orientation. Genetics and environmental factors before and after birth interact in complex ways that can be difficult to calculate.
In Sweden, researchers conducted the world's largest twin study of 3,826 same-gender twin pairs focusing on sexual orientation. They "concluded that genetics accounted for around 35% of the difference between men in homosexual behavior. The remainder was due to environmental factors after birth and factors operating during fetal development. For women, genetics explained about 18% of the variation in same-sex behavior" (Graceffo, 2008).
Hormonal theories about genetic and environmental influences upon the developing fetus have been proposed in various forms, but no clear and conclusive evidence has yet emerged to favor one over another. So-called "gay genes" could refer to the genes that control certain hormones, "enzymes that modify hormones, or receptors on the surface of brain cells that bind to those hormones. A mutation in any one of those genes might make a person gay" — or various hormonal influences could arise depending on drugs and other unusual environmental stressors experienced by the mother during pregnancy (Kunzig, 2008).
One prominent theory holds that there is "a gene that helps time the release of testosterone from the testes of a male fetus. Testosterone masculinizes the fetal genitalia — and presumably also the brain. Without it, the fetus stays female. It may be that the brains of gay men don't feel the full effects of testosterone at the right time during fetal development, and so are insufficiently masculinized" (Kunzig, 2008).
Studies of women have shown an "increased incidence of non-heterosexual sexual orientations among women with congenital adrenal hyperplasia (CAH), an inherited disorder which causes higher than normal secretion of adrenal androgens," which also suggests a hormonal influence — in this case, a masculinizing one (Hall & Schaeff, 2008, p. 158). However, female studies of the genetic components of sexuality have proven more difficult for researchers to construct, given that women are more apt to identify as sexually "fluid" than their male heterosexual or homosexual counterparts.
Furthermore, the theory of hormonal influence upon the developing male fetus reflects the fact that the developing male fetus "begins" as female and only becomes male later in gestation, and thus homosexuality is conceptualized as a deviation from the process of masculinization. This framing tends to emphasize the development of male homosexuality over lesbianism in understanding orientation. The phenomenon of under- or over-masculinization of the fetus has also been noted in non-human animals: animals with insufficient masculinizing hormones exhibit same-sex attraction. As Diamond (2009) explains, "the organization-activation theory posits that the nervous system of a developing fetus responds to prenatal androgens so that, at a postnatal time, it will determine how sexual behavior is manifest."
"FA studies link hormonal stress to physical asymmetry in gay individuals"
"Gay offspring may offer evolutionary advantage; immune response hypothesis"
"Binary orientation assumptions and cultural bias skew research"
If these numbers were so different, the question arises as to why left-handedness is more common in female homosexuals than in male homosexuals, and also what criteria researchers use in their categorization of female homosexuality. These invisible, subconscious biases about the nature of homosexuality — and the unexamined acceptance of cultural constructions of sexuality as self-evident fact — underscore that science, particularly the science of sexuality, always takes place within a social context that shapes the perceptions of the researchers themselves.
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