The Ethics of the Gay Gene
How it works
Homosexuality has existed in societies around the world for nearly all of recorded history. From indigenous tribes, to the Romans, Greeks, and even early Americans, a degree of fluid sexuality has permeated cultures around the globe. While homosexual behavior did not pose a large problem in society for much of history, cultural and religious shifts began to fixate upon that which did not fit neatly into boxes established by those in power. Thus, throughout the last several centuries, homosexuality has become demonized, criminalized, and attempts to convert or eradicate homosexuality have been numerous.
As the science of human genetics has progressed, several 20th century researchers made substantial contributions to our biological understanding of homosexuality. Locating a particular gene present exclusively in homosexual people would have a considerable effect on society’s perception of sexuality, and those in favor of the continued research of the “gay gene” claim it could liberate gay people from the idea that sexuality is a choice. However, this research has received a great deal of criticism, particularly for its questionable ethicality. Before exploring the arguments surrounding the genetic research of human sexuality, it is important to observe the history of such research completed on sexuality, and how both psychological and biological studies contributed to the eventual pursuit of the “gay gene.”
Early sexologists Richard von Krafft-Ebing and Magnus Hirschfeld believed that homosexuality (particularly male) was partially inherited. Hirschfeld proposed the idea that homosexuality arises in humans as a result of the weakening of one’s genetics through, disease, alcoholism, and similar factors. He (so kindly) coined this concept “degeneracy.” Hirschfeld later rejected this point of view but remained confident in the idea that genetic factors played a role in homosexuality. This led to the development of his familial theories, in which he asserted that homosexuality “clustered” in families, and that the sibling of a gay person is far more likely to be gay themselves than those without gay siblings, crediting several studies of gay siblings and a few cases of identical gay twins. This theory, however, lacked a distinction between genetic factors and other potential explanations of clustering, such as a mother’s inclination to treat all of her children in a manner that may have predisposed them to being gay (Fisher 78).
Following Krafft-Ebing, in 1952 Franz Kallmann became the first psychiatrist and geneticist to present what seemed, at the time, to be the most dramatically convincing evidence in favor of the genetic determination of sexual orientation. Kallmann investigated the distribution of sexual orientation (using the Kinsey scale) among monozygotic twins (identical twins who share the same genes) and dizygotic twins (fraternal twins sharing only about half of their genes). The results indicated that 25 of the 30 identical twins selected fell within a 5 or 6 on the scale, while none of the fraternal twins scored higher than a 3 or 4 on the scale (LeVay Queer Science 174). A German twin study published ten years later produced very similar data, but Kallmann’s research methods soon fell under severe criticism (175). No substantial developments were made in the field of genetic influence on sexuality during the next twenty years, but interest was revived during the 1980s. Fundamental to this new surge of research was Richard Pillard, who sought to understand homosexuality’s presence in a family line by conducting several studies designed to indicate whether gay people were more likely to have gay siblings than straight people. The results of the studies confirmed Pillard’s theories of clustering, with nearly 25% of the siblings of gay people reporting to also be gay (LeVay, Gay, Straight 159). This study, and others like it, paved the way for more definitive genetic research to take place. By the early 1990’s, human genes were being researched and compared to gather information pertaining to the cause of sexuality, and here we arrive at the search for the “gay gene.”
In 1993, Dean Hamer collected a sample of gay males and deduced that male relatives of the gay man in the sample had a stronger likelihood of being gay only if they were connected to the subject in question through a maternal line (maternal aunts, sons of maternal aunts, etc.). This pattern of inheritance typically points to genes on the X chromosome, which encouraged Hamer to focus his molecular studies on the X chromosome. In this study using forty pairs of two gay brothers, Hamer and his team discovered the significance of the region of the X chromosome named Xq28. If the brothers in each pair were gay because of a gene present on the X chromosome, then they both should have inherited the same genetic material from the same maternal X chromosome (the chromosome that carries the “gay gene”). After examining 22 DNA markers scattered along the X chromosome in what is called a “linkage study,” Hamer interpreted that the Xq28 region contained the genes that predisposed people to homosexuality.