Research on the origins of sexual orientation has received much public attention in recent years, especially findings consistent with the notion of relatively simple links between genes and sexual orientation. Investigation into the causes of same-sex attraction has, however, been ongoing for more than one hundred years. Claims that such inquiry is dangerous, especially in certain social and political climates, are as old as the research itself In this paper, we show that such genetic research in particular gives rise to serious ethical issues.
Scientific research on sexual orientation has taken many forms. One early idea was to find evidence of a person's sexual orientation in such bodily features as amount of facial hair, size of external genitalia, and the ratio of shoulder width to hip width. Today's seemingly more sophisticated morphological research looks instead at neuroanatomical structures. Such inquiry usually assumes sexual orientation is a trait with two forms, one typically associated with males and the other typically associated with females. Researchers who accept this assumption expect particular aspects of an individual's brain or physiology to conform to either a male type that causes sexual attraction to women (shared by heterosexual men and lesbians) or a female type that causes sexual attraction to men (shared by heterosexual women and gay men). This assumption is scientifically unsupported and there are alternatives to it.
Another early approach was to find evidence of a person's sexual orientation in his or her endocrine system. The idea was that gay men would have less androgenic hormones (the so-called male-typical hormones) or more estrogenic hormones (the so-called female-typical sex hormones) than straight men and that lesbians would have more androgenic and less estrogenic sex hormones than straight women. However, an overwhelming majority, of studies failed to demonstrate any correlation between sexual orientation and adult hormonal constitution. According to current hormonal theories of sexual orientation, lesbians and gay men were exposed to atypical hormone levels early in their development. Such theories draw heavily on the observation that, in rodents, hormonal exposure in early development exerts organizational influences on the brain that determine the balance between male and female patterns of mating behaviors in adulthood. Extrapolating from behaviors in rodents to psychological phenomena in humans is, however, quite problematic. In rodents, a male who allows himself to be mounted by another male is counted as homosexual, while a male that mounts another male is considered heterosexual. This model defines sexual orientation in terms of specific postures and behaviors. In contrast, in the human case, sexual orientation is defined not by what "position" one takes in sexual intercourse but by ones pattern of erotic responsiveness and the sex of one's preferred sex partner.
Although early sex researchers reported that homosexuality runs in families, careful studies of this hypothesis are only beginning to be done. Several studies suggest that male homosexuality runs in families, but they are not helpful in distinguishing between genetic and environmental influences because most related individuals share both genes and environmental variables. Further disentanglement of genetic and environmental influences requires adoption studies.
The only heritability study of male homosexuality that includes an adoption component is the highly publicized study of Bailey and Pillard. The study suggests a significant environmental contribution to the development of sexual orientation in men in addition to a moderate genetic influence. This study assessed sexual orientation not only in the identical and fraternal twins, but also in the nontwin biological brothers and the unrelated adopted brothers of the gay men who volunteered for the study. …