Scientists have suspected since 1800s that sexual orientation may be innate. Different theories about instincts, drives, unconscious impulses, hormones, interhemispheric brain function, and evolutionary aims were proposed by various scientists, including Darwin, Krafft-Ebing, Freud and Ellis. In 1936 Magnus Hirschfeld noted that both male and female sexual orientations tend to run in families (gay men have more gay brothers and lesbians have more lesbian sisters than heterosexuals do), and recent research has borne this out (Pillard 233). Contemporary science has focused on genes and brain function to explain why, but this work is controversial both for its methodology and its relevance to moral or political values. Even as biologists are formulating deterministic models for sexual behavior, cultural anthropologists and sociologists, observing disparate social groups worldwide, argue that sexuality may be as much a product of history, culture, and ideology as it is of nature.

The nature/nurture debate has a number of implications, not the least of which is the simplistic binary itself. Is it even possible to decide which aspects of sexuality are innate and which parts are learned when biological systems are so responsive to environmental conditions and when the hypotheses science tests contain concepts that are themselves socially constructed? If sexuality is a cultural product, its expression may be part of a larger system of meaning science cannot reduce to a manageable focus. We may find ourselves caught in a paradox: deciding the origin of sexuality may require us first to admit that we cannot observe how biology or culture works independent of the terms each imposes upon our observations (Allen 243).

The largest genetic study to date, by psychiatrist Richard C. Pillard (Boston University) and psychologist Michael Bailey (Northwestern University) in 1991, included not only identical and fraternal twins, but a third group, homosexual subjects with adoptive same-sex siblings, genetically unrelated but raised in the same family environment. In the male study, identical twins had a 52% chance of both being gay, compared to a 22% rate for their fraternal twins and only 11% for their adopted brothers. In the study of females, identical twins had a 48% chance of both being lesbian, compared to a 16% rate for sororal twins and only a 6% rate for adopted sisters. Such a result, Pillard and Bailey concluded, shows that genes have a significant influence over sexual orientation, while growing up with a homosexual sibling does not. Moreover, different genes are involved in men than in women; gay men do not have a greater incidence of lesbian sisters; thus, it is hypothesized, two separate and independent genetic influences seem to be operating (Pillard and Bailey, “Innateness”; Pattatucci et al.). In 1993, Bailey et al. conducted a similar study on female twins and found a comparable concordance rate that declined as the degree of genetic relatedness declined (Allen 252).

Such studies encouraged Dean Hamer, a molecular geneticist at the National Institutes of Health, to look for a genetic marker for homosexuality. Recruiting volunteers through advertisements in gay publications, Hamer et al. studied DNA from 40 pairs of gay brothers and found that 33 shared five different patches of genetic material grouped around a particular area on the X chromosome, specifically the 28th region on the X's long arm. This is unusual because the genes on a son's X chromosome are a highly variable combination of the genes on the mother's two X's, and so the sequence of genes varies greatly from one brother to another. As Richard Pillard explains:

Each son gets one of the mother's X chromosomes at random, so the chance of both brothers getting the same chromosome (or the piece of it containing the relevant gene) is 50 percent. The chance of a second pair of gay brothers sharing a marker at the same locus is one in four (one half times one half), the probability generated by flipping pairs of coins. To build a statistically convincing case, the pairs of coins (markers) need to be the same (both heads or both tails) more often than chance predicts…. (236)

Out of 40 pairs of brothers, Hamer found 33 twins with similar DNA markers in the Xq28 region. Subsequent studies of heterosexual brothers revealed that most of them did not share these markers, and no linkage was found for pairs of lesbian sisters. So much overlap between brothers who also share a sexual orientation is unlikely to be just coincidence (Henry 37). Hamer concluded that the odds that his results are only random are less than 200 to 1. Homosexuality was the only trait that all 33 pairs shared; the brothers did not all share the same eye color or shoe size or any other obvious characteristic. Nor were they all identifiably effeminate or hypermasculine. They were diverse except for sexual orientation (Hamer et al.; Henry 37; Angier, “Report”). Hamer recently completed two more studies of the Xq28 gene, both of which confirm his original findings (Burr 197), but he has failed to show a similar genetic linkage for lesbianism (Hu et al.).

If homosexuality is hereditary, why does the trait not gradually disappear, as gay males and lesbians are less likely than heterosexuals to have children? Hamer hypothesizes that the genes specific for male homosexuality can be carried and passed on to children by heterosexual women because these “male” genes do not cause the women who inherit them to be homosexual. Simon LeVay (a neuroanatomist at the Salk Institute of Biological Studies) adds that it is possible “gay genes” confer other traits insuring survival, as is the case for the gene for sickle-cell anemia which confers a resistance to malaria (“Sexual” 69). The overwhelming majority of homosexual children are produced by heterosexual parents, parents who may carry the same genes but do not express them, or they may express them in non-homosexual ways: genes that produce same-sex desires or identifications in one individual may produce heterosexual desires or identifications in others (Henry 37). Moreover, the seven subjects who were gay but did not share DNA patterns in Xq28 suggest that other genes may work to enhance or even substitute for Xq28's actions. It may be impossible to determine which genes produce “gay” traits, under what circumstances, and in what stages of an individual's development. Geneticist Jeremy Nathans at Johns Hopkins is currently collecting a large bank of DNA samples from subjects with identifiable sexual histories, but it will be years before the results are known.

One way genes might affect sexual orientation is by producing enzymes and proteins that determine the structure and function of the brain. Although preliminary and highly controversial, a recent anatomical study suggests that some homosexual brains may be different from heterosexual brains in one of the areas that mediate sexual desire. In autopsies of 41 people, 19 of whom were retrospectively categorized as gay men, 16 straight men, and 6 straight women, LeVay measured the size of a group of cells in the hypothalamus. It was already known that two of the cell-groups were larger in men than in women, and LeVay found the same difference in size when he compared heterosexual men to homosexual men. This area in the hypothalamus of gay men was as small as it was in heterosexual women (“Difference”).

It is important to note that the differences in size were statistical rather than absolute; some gay men and heterosexual women had cell-groups as large as those in most heterosexual men. Perhaps they were bisexual, or perhaps the hypothalamus is not the only part of the brain involved in sexual orientation. It is also possible that brain structure changes in response to behavior, rather than preceding and causing it (Rosario 6). Brain cells can rearrange their neuronal connections in response to environmental demands, although how much is unknown. In general, younger brains are more plastic, and while some adjustments continue throughout the life cycle, other neural pathways are optimized before adolescence ends. Same-sex desires are most often reported by gays and lesbians to occur in adolescence, but whether this reflects a developing brain influencing behavior or behavior influencing brain development is unclear (Burr 69; Satinover 101; Pillard and Bailey, “Genetic”; Eric Marcus 10-11; Kandel and Hawkins).

Similar structural differences may occur in the brains of transgendered men who report feeling like “women trapped in men's bodies.” Researchers in the Netherlands discovered that a small region (the central subdivision of the bed nucleus of the stria terminalis) of the hypothalamus is about 50% larger in non-TG men than in women, but it is almost 60% larger in non-TG men than in MTF transsexuals. Animal studies indicate that this part of  the hypothalamus may help coordinate sexual behavior and the release of essential reproductive hormones. In heterosexual and homosexual men, the bed nucleus measures about 2.6 cubic millimeters; in women it averages 1.73; but in MTF transsexuals it averages only 1.3. This is a substantial difference, suggesting that the smaller the bed nucleus, the more “female” the individual feels (Angier, “Study”). This may not be the only etiology for transsexuality. Some forms (such as the XXY syndrome) are clearly genetic, while others may be associated with an area of the brain called the “Sexually Dimorphic Nucleus” (Bill Stuart, “faq2TS”). It is known that human embryos develop recognizably male or female genitalia in the 12th week of pregnancy, but it is not until the 16th week that the SDN is differentiated. Some researchers believe that, depending on the hormonal mix during this four week gap, gender identity may not develop along the same lines as the genitalia (Brown and Rounsley 22).

Some neuroendocrinologists believe that sexual orientation may also be influenced by the early (even prenatal) effects of androgens on the brain cells that control sexual desire. The theory is that if the infant's brain is exposed to high levels of androgens, then the child will become masculinized and feel attracted to women in adulthood. If the brain is not exposed to high levels of androgens, or if hormonal effects are blunted by some other condition, the brain does not masculinize and attraction to men will result. Studies of rodents have shown that some sex-typical sexual behavior can be affected by altering early androgen levels. Female rhesus monkeys exposed prenatally to high levels of androgen subsequently show elevated rates of male-typical (rough-and-tumble) play behavior (Pillard and Bailey, “Innateness”; Berenbaum and Snyder; Meyer-Bahlburg et al.). Whether or not these mechanisms work the same way in human beings is not known. . .