Dena BodianFor years scientists have been attempting to ascertain whether or not homosexual behavior can be linked to a biological catalyst. From Alfred Kinsey's revolutionary survey in 1947 to the current media upheaval about a prospective "gay gene," the desire to pinpoint a cause for the personalities and behaviors associated with homosexuality has reached new plateaux. The scientific community is constantly developing more and more evidence to suggest that there may well be a neurological explanation for homosexuality. Although historical studies and purposed treatments have ranged from group counseling to shock therapy, recent research suggests that exposure to an abnormally high or low amount of certain hormones could potentially affect sexual behavior.
Just as there is no gene for heterosexuality, there can be no "gay gene." Genes are not responsible for an individual's actions; they simply guide the "sequence of a particular protein that may influence behavior" ( 1 ). However, it is possible that there is a genetic factor which is responsible for a protein synthesis resulting in particular sex hormone levels (namely testosterone and estrogen) which could augment certain sex-typical characteristics, and might explain sexual behavior ( 1 ). This paper will discuss various studies which examine the effects of male and female hormones in an attempt to develop a potential correlation between biological foundations and homosexual behavior.
According to Fred Delcomyn (2), mammals naturally develop as females "in the absence of sex hormones." Without the intervention of androgens (testicular hormones, specifically testosterone), all mammals develop in utero as female. Not only are the genitals identical in early fetal development ( see fig. 1 ), but the hypothalami are the same size. In humans, the influx of testosterone occurs between the second and fifth month of pregnancy. Prenatal hormonal exposure in rats (the major subjects of sex studies both because they are readily available and because their brains remain in a sex-neutral stage for a few days after their birth) occurs a few days before birth ( 3 ).
Hormones are responsible for activating specific neural circuits which in turn cause sex-specific behavior. In males, testosterone induces physical traits as well as "malelike behavior." Without testosterone, estrogen serves as the "default" hormone and causes female development (2). The term sex-specific behavior refers to gender-typical traits, whether the actions are themselves sexual (like rats mounting) or simply social (like young boys typically playing in a more aggressive manner than do girls).
Although both males and females produce the sex hormone testosterone, human production rates can differ by a factor as large as 100, making the effect of this hormone significantly more crucial to attain a balance in the male body than in the female ( 4 ). In the absence of testosterone, estrogen causes female development; in the presence of testosterone, testes will develop — regardless of genetic sex. It has been established ( 3 ) that at a certain prenatal period, the infiltration of superfluous testosterone has a masculinizing effect on female fetuses. An overactive adrenal gland (either in the mother or fetus) or the usage of anti-miscarriage drugs (which mimic testosterone) are presumed responsible for a testosterone excess.
Adrenalgenital Syndrome ( see figure 2 ), or AGS, is a "metabolic error which causes overproduction of androgens (e.g. testosterone)," resulting not only in "partial masculinization of the external genitalia of female patients," but also "causes a partial masculinisation of human female behavior" ( 5 ).
Prenatal hormone exposure also has effeminizing or emasculating effects on rats. In one study ( 5 ), adult male rats displayed lordosis (the typically female act of submitting to being mounted) if they had been castrated at birth and perinatally injected with estrogen ( see figure 3 ). These rats' chemical make-ups therefore differed from normal male rats in two ways. First, they were deprived of the appropriate amount of testosterone which would have normally been produced in their testes during infancy. Secondly, the amount of estrogen (a primary female sex organ) which the rats were given would not have come close to the amount of estrogen naturally produced in male rats.
Normal male rats displayed normal mounting behaviors as adults, regardless of whether or not estrogen was administered. The male rats which produced testosterone appeared to be "immune" to the estrogen injected into their systems. Only the castrated rats (whose bodies had no testosterone) were affected by the estrogen. Thus, one can deduce that the presence of sex hormones appears to determine certain sexual behaviors in rats, particularly in relation to mounting or attempting to be mounted. This is particularly true of testosterone, since it was shown that only in the absence of testosterone did estrogen have any effect on the male rats. In this study, testosterone exposure was also deemed responsible for certain other behaviors, including "aggression and taste preferences"( 5 ). This shows that sex-specific behavior is manifested in more ways than simply sexual activity.
In a similar study at Cornell University ( 6 ), researchers examining a variety of birds (of which only the males sing) discovered certain brain regions which are "as much as five times larger in males than in females." It was determined that hormones had particular effects on the brain regions which correlate to the birds' ability to sing, both in infancy and adulthood. One of the most significant discoveries suggested that "giving testosterone to adult females can cause the formation of millions of new synapses in these brain areas, and the females begin to sing"( 6 ). Hence, the introduction of the male sex hormone testosterone caused the otherwise normal female birds to exhibit an activity whose behavior is typical of males.
These studies of hormones on animal behavior imply that an animal will exhibit heterotypical sexual behaviors (i.e. those characteristic of the opposite sex) when sex hormones of the other gender are administered. These observations can be directly correlated to human activity through the conclusions of Corrine Hutt (7 ), a researcher of education. Her observations of pre-school children led her to determine that boys were twice as aggressive as girls because of the amount of testosterone in their systems. "The action of testosterone on the central nervous system apparently contributes to the elevated aggressiveness of males compared to females" ( 8 ). A logical experiment to prove this hypothesis would consist of administering testosterone to young girls and comparing their actions with those of their male peers. However, no such tests were done and Hutt's correlation remains speculative.
Similarly, Daryl Bem ( 9 ), a professor of psychology at Cornell University, asserted his theory that hormonal levels (and hence, sexual behaviors) are the causes of homosexuality. He stated that an aggressive child (with a higher amount of testosterone) would be more interested in typical "boy games," such as sports, while a passive child (with lower amounts of testosterone) might be more interested in quieter activities. Bem continues by showing a correlation between participation in sex-typical or atypical activities and perception of the opposite as "exotic." Finally, he hypothesizes that opposites attract -- or, the attraction of the foreign "produces heightened physiological arousal that subsequently gets eroticized to that...class of (others): Exotic becomes erotic." While Bem’s hypothesis presents a biological explanation for the basis of homosexuality, his conclusions have yet to be tested.
The research team of Vom Saal, Grant, McMullen and Laves ( 10 ) offers another potential cause whose basis is also rooted in prenatal hormones. Fetal female rats were seen to have higher levels of testosterone if they had been situated between two male embryos in utero . The reception of testosterone from adjacent brothers was enough "to alter (a female rat's) behavioral phenotype"( 10 ). According to Edward Miller ( 11 ), the same occurs in humans: women who had male twins (and were therefore exposed to testosterone in utero ) exhibited slightly more masculine characteristics than did women who had not been exposed to testosterone before birth.
A recent study (see figure 4) done by Dennis McFadden and Edward Pasanen at the University of Texas (12) has implications for prenatal testosterone exposure both physically and in terms of homosexuality. A test consisting of series of click-evoked otoacoustic emissions (CEOAEs) showed that the cochleas of heterosexual women are nearly three times as sensitive as that of men (there was no notable discrepancy found between the sensitivity of homosexual and heterosexual men). However, it was shown that lesbians’ inner ears are a third as sensitive as those of heterosexual women; their responses are closer to those of males. Cochlear development occurs before birth, and sensitivity is "established at birth and remains constant through life" (12). Cochlear development and consequent sensitivity are attributed to prenatal androgen exposure -- fetal males "are exposed to successively higher levels (of androgens)...and their responses (in terms of sensitivity levels) are correspondingly reduced."
Because the physical trait of sensitivity is linked to androgen exposure and lesbian cochlear sensitivity is more similar to men than to heterosexual women, "...the auditory systems of homosexual...females, and the brain structures responsible for their sexual orientation, have been partially masculinized by exposure to high levels of androgen prenatally "(12).
Severe ramifications pervade the search for a genetic cause for homosexuality. Scientists are faced with many moral and ethical questions. A discovery leading to the belief that homosexuality is an inborn characteristic would probably give gays protection under many of the same laws that protect racial minorities and the physically disabled. However, it is equally possible that the ability to detect potential causes for homosexuality would also cause people to actively prevent such occurrences and thus turn into a lesson in eugenics -- enabling parental carriers to terminate pregnancies of potential homosexual offspring.
It is crucial to consider that personality and behavior are more than simple chemical reactions. While prenatal over-androgenization or estrogenization could potentially be one of the many underlying causes of homosexuality, this has only been shown in certain cases, largely those in which chemical abnormalities have caused effeminate or masculinizing behavioral (and in some cases physical) traits. The studies discussed herein cannot account for the physiological characteristics of every member of the gay, lesbian, bisexual and transgendered community. It is also possible that the amounts of hormones studied are not abnormal, but fall somewhere in the spectrum of human sexuality.
2. Delcomyn, Fred. Foundations of Neurobiology. New York: W.H. Freeman & Co. 1998
7. Beth Rieke
Contains bibliography information: Trends in Education. Hutt, Corrine. "Why do Girls Underachieve." Vol.4 1979. Pp. 24-28.
12. McFadden, D. & Pasanen, E. “Comparisons of the Auditory Systems of Heterosexuals and Homosexuals: Click-Evoked Otoacoustic Emissions. Proceedings of the National Academy of Science. Vol. 95, pp. 2709-2713. March 1998
Comments made prior to 2007
I just read a great article on pathophysiological theories to homosexuality. It was extremely enlightening and really answered by question as to what we currently know about the subject. As a healthcare professional currently undergoing family issues surrounding homosexuality, it really helped to have the scientific support ... Audrey Suh, 10 April 2006