Homosexuality, one of the many different sexual behaviors exhibited by humankind, has been rejected, persecuted, and denied. Are the studies that attempt to find causation moral? Is this search for the "why" of homosexuality a continuation of the heterosexist assumption that heterosexuality is normal and homosexuality abnormal? Are assumptions being made that homosexuality is a disease and should therefore be treated medically? Is the research currently being done heterosexist? Studies that are being performed currently and those done in the recent past have shown that there are strong connections between male homosexuality and biology. By presenting the scientifically significant studies that I have come across, I intend to reduce the ignorance surrounding homosexuality and the behaviors often found with it, and to show some of the correlations between biology and male homosexuality.

Throughout my research of homosexuality, I wavered back and forth, debating the morality of this search for a cause. It seemed that finding a cause for homosexuality was somewhat akin to finding the cause for a disease. Unhappy with the association of homosexuality with abnormality, I wondered why scientists were allowed to place homosexuals at such a level. On one hand, with biology backing up gay men and women, the fight for equality and basic human rights could be won more quickly. Although science and society have progressed significantly since the days of Nazi Germany, when homosexuality was thought to come about through "seduction and mind-traps," critics of the current scientific curiosity with homosexuality consider every study and experiment an effort to strengthen the argument that homosexuals are atypical, abnormal, and have a condition that is disease-like and should be treated as such. On the other hand, scientists who are homosexual themselves have conducted some of the more recent and more scientifically significant studies. This lends a validity to the research that has not been seen in the past. Those who would like to see scientific progress continue are those who would like to see the "born that way" argument validated. In the interests of scientific curiosity, and in the hopes that the evidence gathered will be used appropriately, the following are examples of correlation between biology and homosexuality.

Hormones have, throughout history been touted as the "cause" behind homosexuality. There is currently no scientific evidence to prove this. There are correlations between unusual prenatal hormone levels and abnormal sexual behavior later in life, however, evidence gathered from studies of phenomena such as this can be easily argued away.

Historically speaking, the most common claim relating hormones to homosexuality was that gay men had "lower levels of testosterone and higher levels of estrogen in their bloodstream and urine" when compared to their heterosexual counterparts. (Stein,1999) This theory, which didn't subside until the mid-to-late 1970's, was the driving force for many attempts to cure gay men of their homosexuality. It is now known that there is no distinguishable difference between the testosterone levels found in gay males and those found in heterosexual males. Programs were set up claiming that a cure for homosexuality had been found. Many of these programs incorporated the use of testosterone injections or implants and in the most unusual cases, the implantation of a heterosexual man's testicle, to cure homosexuality. (Stein,1999) I did not find evidence of a single case where these methods were efficacious. Generally, with the increase of testosterone in the bloodstream, most of the men being treated expressed an increased desire for other men. The object of their affections was not changed at all.

Using a different and more permanent approach to those tried before and since, Nazi concentration camps were the sites of many castrations. Rather than cure gay men of their "disease," this operation only succeeded in reducing the sex drive of most of the subjects. The sexual desire for other men did not shift.

Studies done with female rats and guinea pigs have shown a correlation between exposure to androgens (of which testosterone is one) in utero and male-typical behavior later in life. For example, in a study done by C.H. Phoenix in 1959, female guinea pigs were exposed to testosterone while they were still fetuses. This factor led to their defeminization. They no longer expressed a female typical behavior found in rodents. Known as lordosis, this behavior is the lowering of the rump–it allows the male animal to mount the female in order to copulate. When these same female guinea pigs were grown, they were again treated with testosterone. This time, they began showing male typical behavior–mounting other females.

Doing a similar study with rats, Young found that by castrating newborn male rats, the treated animals didn't show male typical sexual behavior, even when supplemented with testosterone later in life. Interestingly, when given estrogen, these castrated male rats were willing to allow non-castrated male rats to mount them. However, rats and guinea pigs are not primates.

Studies done with female macaque monkeys have shown that exposure in utero to hormone baths (in this case, excessive testosterone) have led to the masculinization of female monkeys as adults. In 1981, Robert Goy exposed fetal female macaque monkeys to higher than normal levels of testosterone. Before they had grown fully, these monkeys were already expressing non-female typical sexual and non-sexual behavior. The behavior of the treated females significantly differed from that of their female peers. They engaged in play fighting at a level that was comparable to that of male juveniles, and these females also tended to take the male role in "play-sex". The latter behavior is almost never found in female macaques. Studies like this are helpful in demonstrating that hormones play a factor in organizing the brain. Once the brain is "organized" or set in a certain way, hormones that an animal is exposed to have a negligible effect on changing that organization, if there is at all an effect. In other words, it is likely that sexual orientation is set before birth and in the early stages of development and is reinforced in some way throughout life, making changes later in life extremely difficult to impossible.

But are these animals really homosexual? The behaviors that were documented do not prove that hormone manipulated females prefer mounting other females, or for that matter that hormone manipulated males prefer being mounted. In fact, when these two manipulated sexes are put together, it has been documented that the female will mount the male–a blatantly heterosexual encounter, but with role reversal. Studies involving females mounting males and females and males engaging in sex atypical behavior, all of these being non-human animals, have been criticized. Has the question of "Whom is a person sexually attracted to?" been confused with "What role does a person take when he or she has sex?" I believe that it has to some extent.

Although hormone studies done after birth have not proven (or disproven) the role that hormones play in determining homosexuality, pre-natal studies have been slightly more conclusive. Because performing experiments with hormone levels on human fetuses is unethical and work intensive, science has had to rely on "natural experiments," or situations that arise when a fetus is naturally exposed to atypical levels of hormones while in the uterus. The first of the two studied "natural experiments," congenital adrenal hyperplasia (CAH), involves an XX individual who is exposed to levels of androgens that are normally found with XY fetuses. Symptoms of this disease usually include ambiguous or variant genitalia, and treatment (if reared as a woman) involves hormone therapy and surgery. This disease is important because of the resulting sexual behavior found in those who have CAH later in life. Compared to women who do not have the congenital disorder, a greater percentage of women with this condition report a sexual desire for other women.(Money, Schwartz, and Lewis, 1984) Noting that lesbianism is more common with persons exhibiting CAH, it should also be noted that the environment that CAHers grow up in is likely to be exceedingly different than that in which a normal child would grow up in. For example, when one's external genitalia is significantly different than one's peers, notions of gender and sexuality are often questioned. This should not be overlooked.

The hormones that influence our sexual behavior are not the only factor that makes humans and other vertebrates sexual beings. The brain has been argued to be the most important sexual organ. In the search for biological correlations with homosexuality, the hypothalamus, a small lobe that hangs down at the base of the brain has been found to play a significant role. There are two different areas of the hypothalamus that have been found in rats to correspond with male typical and female typical sexual behavior. For example, the medial preoptic area (more towards the front of the hypothalamus) seems to underlie many male sexual behaviors and sexual behaviors typical to females have been linked with the ventromedial nucleus (more towards the back of the hypothalamus). (A. Soulairac and M.L. Soulairac, 1956) Critics of these studies argue that the hypothalamus plays a very insignificant role in sexuality. When the medial preoptic area is decommissioned in male rats, they are still sexual beings. The express interest in female rats, but appear to be unable to express their interest. It doesn't seem to occur to these rats to mount the female. The case is somewhat similar with primates. Male rhesus monkeys will masturbate, showing an interest in pleasurable stimulation. However, having lost the medial preoptic area, they completely lose interest in females–seemingly forgetting that females can provide a means to the same end. (Slimp, Hart and Goy, 1978)

The hypothalamuses of mammals (rats, gerbils, macaque monkeys and others) have been found to be sexually dimorphic, more specifically in the medial preoptic area. The difference in size has been directly correlated with hormone levels in utero and directly following birth. If testosterone is given to a female rat just prior to and following birth, the size of the medial preoptic area of her hypothalamus will fall within the range of that found in non-treated male rats. (R.A. Gorski, J. H. Gordon, J. E. Shryne, and A. M. Southam, 1978) When female adult rats were given testosterone, there was no change in the size of this area of their brains.

This region is also different in humans, but the research involving hormone levels has not been done on humans (for obvious reasons). However, research, upon death, has delved into the sexually dimorphic regions of the brain. In 1980, Roger Gorski found that the interstitial nuclei of the anterior hypothalamus (INAH), numbers 2 and 3 (there are four of these nuclei, were sexually dimorphic. The size differential between males and females was most apparent in INAH 3. In males, this nucleus can be from two to three times larger than it is in females. This difference spans all age groups, meaning that the differentiation must occur at some time before birth.

Then, in 1991, Simon LeVay set out to find if the sexual dimorphism in INAH2 and 3 could be correlated with sexual orientation. He hypothesized that the size of this region in the brain in homosexual males would be similar in size to that in heterosexual females, and that it would be larger in heterosexual males and lesbians. He dealt mainly with the INAH 3, as it is more significantly different between males and females. He found that male homosexuals had INAH 3's that were comparable in size to heterosexual females. He didn't study lesbians. With results stating that this region of the brain is different in homosexual and heterosexual men, and the knowledge that the size of this same region in rats is determined in utero and directly following birth, the evidence seems to support the theory that homosexuals are "born that way."

This is not the only sexually dimorphic region of the human brain, however. The anterior commissure, which is typically larger in females, was found to be larger in gay males as well. (L.S. Allen and R. A. Gorski, 1992) It is likely, however, that this region is not involved with sexual regulation. It is a group of nerve fibers, not brain cells, which the INAH is.

Significant studies relating heredity to homosexuality began with Richard Pillard and James Weinrich in the 1980's. By comparing the siblings of a sample of homosexual men to those of a comparable group of heterosexual men, Pillard and Weinrich found that of the heterosexual men, only 4 percent had homosexual brothers, and of the homosexual men, 22 percent of them had brothers that were also gay or bisexual.(R. Pillard and J. Weinrich, 1986) Heredity of homosexuality can also be found through twin studies. The numbers vary somewhat, but within the past 10 years, several different studies have been able to point to the incidence of homosexuality in males is approximately twice as high in monozygotic co-twins as in heterozygotic twins. (See Table I)

The search for the genes that cause homosexuality commenced with the work of Dean Hamer in 1992. Hamer began by compiling a sample of gay men who had a significant number of gay men within their pedigrees. Upon the inspection of these pedigrees, Hamer and his colleagues noted that male homosexuality appeared to be inherited through the female line. An hypothetical instance of this inheritance pattern would be a gay man (who has a sister) has a gay nephew through her, and then this gay nephew would in turn have another gay nephew through his sister, and so on down through the family tree. From this part of the study, it seemed apparent that gay men were inheriting the genes fro homosexuality through their mothers, not their fathers. Going on the data received in this first part of the study, Hamer and his team then attempted to close in further on the genes causing homosexuality by performing a statistical study. With a sampling of 76 gay men, Hamer inquired of them of the incidence of homosexuality in their families. He found that there was an above average incidence of homosexuality in brothers (13.5 percent were gay), maternal uncles (7.3% were gay), and cousins who were the sons of maternal aunts (7.7%). Closing in still further in the search for the "gay gene(s)," Hamer then saturating his sample group with gay men who had gay brothers. Hamer's reasoning for choosing families such as these was that there would likely be a high incidence of the gene(s) that cause homosexuality within these families. He was right. Ten percent of the maternal uncles were gay, as well as thirteen percent of the cousins who were sons of maternal aunts. These two percentages were higher than those found in the statistical study. The explanation that Hamer decided was causing homosexuality is a simple one–male homosexuality was being passed through women on the X chromosome of the 26^th pair. Since men only have one X in this pair (the other being Y), the theory states that men in the general populace have either the heterosexual gene(s) or the homosexual gene(s). The gay gene(s) appears to be much less common than that which determines heterosexuality in males. Sharpening the focus even further, Hamer and his team then used molecular genetics to help find how this trait was being passed from mother to son. By taking blood from gay brothers and their mothers, Hamer conducted a linkage study–he looked for linkage markers that had a higher instance than 50 percent of occurring in the familial groups that he tested. He found that in a region called Xq28, these mother/son groups had a statistically significant rate of coinheritance. So significant in fact, that even after replicating this study, the results that Hamer and his colleagues found could have occurred by chance only once every 100,000 times. Hamer's study does not prove that male homosexuality is caused by gene(s) found within the Xq28 region of the 26^th chromosome. He found some families in which this gene seemed to have no effect on sexual orientation. His study does show that for many gay men who have gay brothers, there is a concordance between sharing a genetic marker with their mothers and brothers and being gay. In order to test his theories further, Hamer then looked at families in which there were two gay brothers and one heterosexual brother in order to compare the genes that these brothers were given. They found as they had predicted, that the heterosexual brothers had different markers at the Xq28 region than did the homosexual brothers.

At this point in time, the research done by Hamer has not yet been replicated. It has been attempted in a laboratory in Canada. They failed to reproduce the Hamer's results. (Rice et al., 1995)

With the technology that is currently available, there may soon be an answer to the question of "How?" when it comes to male homosexuality. The human genome project is making significant progress, and scientists have been able to pinpoint distinct differences between gay and straight men on the basis of more than just fashion sense and stereotypes. Studies with female macaque monkeys have shown that exposure in-utero to hormone baths (in this case, excessive testosterone) have led to the masculinization of female monkeys as adults. Yet, there are critics saying that sexuality in lower mammals shouldn't be placed on the same pedestal as human sexual orientation. Human sexual behaviors are much more complex than who mounts who. It doesn't all boil down to sex alone. There are studies that have more validity. LeVay, with his comparisons of brain physiology between heterosexual and homosexual males have shown that there are differences that begin at or before birth. Finally, Hamer's search for the cause of homosexuality on a more molecular level shows that there is a positive correlation between the region Xq28 and being gay. The gene hasn't yet been found, but his study found that many pairs of gay brothers shared a marker at this particular region of their genetic makeup. Also, in finding that homosexuality seemed to be a sex-linked trait, biology again seems to lend causation. Although the exact mechanism is at this point still shrouded in mystery, researchers are continuing to search for the true cause of homosexuality.