Biological Causes of Male Homosexuality
by Jennifer McCreight
Both the general public and scientists have questioned the cause of homosexuality for many years. The debate effectively is one of nature versus nurture: Are homosexuals born that way, or do they learn or choose the behavior later in life? Many researchers believe that homosexuality has a biological basis that can be molded somewhat by experience. Some people feel that the causes of homosexuality are not important, and the larger concern is how society treats these people. However, the study of sexual orientation is not solely for the pursuit of science itself. One study showed that people who attributed homosexuality to controllable causes had more negative attitudes towards homosexuals, while those who attributed it to natural causes had more positive attitudes (Whitley 369). In addition, a poll conducted in 1996 by The Advocate, a gay and lesbian news magazine, reported that 61% of its readers thought “it would mostly help gay and lesbian rights if homosexuality were found to be biologically determined” (Advocate 8). These results demonstrate how researching the biological basis of homosexuality can be beneficial for society as a whole.
Studies that first alerted researchers to biological causes of homosexuality were done with twins. Twin studies are used to determine the heritability of a certain trait. If the trait has a genetic basis, monozygotic (MZ) twins would have a higher rate of concordance than dizygotic (DZ) twins. DZ twins would also have a higher rate of concordance than unrelated adopted siblings; this control is to account for environmental influences (Cummings 121-123). One study done by Bailey and Pillard showed the concordance for homosexuality to be 52% for MZ twins, 22% for DZ twins, and 11% for unrelated adopted siblings. These heritability estimates are also found in the Minnesota Twin Project, which studied monozygotic twins separated at birth (Cummings 413). An additional study by Whitam, Diamond, and Martin found concordance to be 65% in MZ twins and 29% in DZ twins. These two studies combined place the estimated overall heritability of homosexuality between 50 and 60% (Rahman 1341). This information suggests that homosexual behavior involves many genes in addition to environmental factors (Cummings 413).
Some genes relating to homosexual behavior are thought to be found on the X chromosome. A pedigree analysis of 38 families that contained two homosexual brothers was conducted by Hamer. This research showed that the maternal line of homosexuals had an elevated rate of homosexuality while there was an absence of paternal transmission (Cummings 414). In addition, men with extra X chromosomes are more likely to be gay (Ridley 264). Hamer’s study also showed DNA linkage from the distal region of the long arm in the Xq28 region. While these results were statistically significant, not all brothers showed the linkage, and some heterosexual brothers did. This implies that there are other genetic and environmental factors influencing homosexuality (Cummings 414).
More support for the X chromosome’s role in homosexual behavior comes from a study on X inactivation. Since female cells contain two X chromosomes compared to the one that males have, one chromosome becomes inactivated. Usually the act of inactivation is random, resulting in half of the cells in tissue having the maternal X activated and the other half having the paternal X activated. Skewed patterns of inactivation are due to various epigenetic effects, some of which may effect fetal sexual differentiation. Bocklandt’s study of 97 mothers of homosexual men and 103 mothers of heterosexual children showed extreme skewing in the mothers with gay sons. 4% of the mothers of heterosexuals and 13% of the mothers of gay men showed the extreme skewing. The percentage increased when the mothers had two or more gay sons. This research supports the idea that the X chromosome plays an important role in homosexual behavior through direct or epigenetic factors (Bocklandt 691-694).
Other research, however, suggests that mitochondrial genes may be the key. Mitochondrial genes are also passed maternally and would show inheritance patterns as X-linked traits. Hurst and Haig of Oxford University suggest that the mitochondrial gene could be like a “male killer” gene found in other species. Simply put, these genes sterilize males in order to pass wealth to female offspring, increasing the breeding success of these females. This would explain how a “gay gene” could persist in a population even though homosexuals usually do not reproduce (Ridley 280).
Different evolutionary theories have also been formulated to explain this phenomenon. Camperio-Ciani conducted a study of 98 homosexual and 100 heterosexual men and over 4000 of their relatives. The study confirmed previous signs of increased number of homosexual males in the maternal lineage of homosexuals. More importantly, however, the study showed that female maternal relatives of homosexuals had significantly higher reproductive rates than the female maternal relatives of heterosexuals, and no differences were observed in the paternal relatives. A gene or set of genes can have different effects in different sexes. The increase of fecundity in females evolutionarily “makes up for” the loss of reproduction in males. As long as the advantage for females was worth more than the disadvantage for males, the gene would persist in a population (Camperio-Ciani 2217-2220).
Another theory dealing with reproductive rate advantages is that of adaptive bisexuality. In a study by Baker and Bellis, bisexual women were found to be more fecund than heterosexual women. Male homosexuality could possibly be a maladaptive side effect of this system. An additional theory proposed by Miller is based on female mate choice. The sexual selection of nurturing personalities would increase feminizing alleles that could lead to homosexuality. Miller’s research showed women prefer feminine qualities in men, and gay men were more emphatic and less aggressive. Another theory is that of kin altruism. Homosexual men, while not producing children of their own, could help siblings rear their children, thus indirectly passing down shared genes. This is supported by the increased empathy of gay men and similar altruism found in other species. Also, homosexuality could be a maladaptive extreme of same-sex affiliation that reduces violence between males. Studies of primates have shown that same-sex bonds increase survival, supporting this theory (Rahman 1343-1347).
However, some of the most compelling biological causes lie not in genes, but in the womb. The microenvironment created in the uterus and separate amniotic sacs of twins can account for much of the “environmental” difference witnessed in homosexuals. Even MZ twins, who share an amniotic sac, can experience differences due to differing amounts of blood flow. The differences between male and female brains are due to testosterone release from the testicles that takes place during male development. Addition of testosterone to the blood of adult gay men does not make them more heterosexual. Dorner conducted studies which illustrated that castrated rats were more likely to attempt to mate with other males, and the likelihood increased the earlier they were castrated. Multiple other studies in the
Evidence of differing levels of testosterone during development in homosexual men can be seen by other visible differences. One telling difference occurs in the hypothalamus, which helps regulate male-typical sexual behavior. The third portion of the interstitial nuclei of the anterior hypothalamus was twice as big in heterosexual males as in females. This portion was also twice as big in heterosexual males as in homosexual males (LeVay 1034). A female-like hypothalamus results in lower testosterone response, which as discussed earlier, increases the chance of homosexual behavior. Another study has found similar results in the anterior commissure (Blanchard 374). Additionally, spatial, verbal, and visuo-motor performance in homosexuals is typically female-like. Homosexual men also tended to be more female-like in that they tended to be lighter weight and shorter and have and earlier onset of puberty than heterosexual men (Rahman 1352-1365). Handedness is also influenced by prenatal sex hormones, and homosexuals are more likely to be left-handed than heterosexuals (Ridley 265).
Some of the most promising research so far has been done regarding fraternal birth order. A study by Blanchard showed that sexual orientation has a significant correlation with the number of older brothers an individual has. The chance of homosexuality increases 33% with each additional brother, regardless of cultural, psychological, and demographic differences. Average male to female sibling ratios in white populations is 106 per 100, while the ratios in homosexual men range from 98 to 126 per 100. Extremely feminine homosexuals produced ratios ranging from 131 to 157 per 100. These trends are explained in Blanchard’s maternal immune hypothesis. Male fetuses produce Y-linked minor histocompatibility (H-Y) antigens. H-Y antigens are found in all heterogametic vertebrates and are involved in neural sexual differentiation. They are found in high amounts on brain tissue, and are not necessary for proper genitalia formation. Because the mother lacks a Y chromosome, her body does not recognize this substance and treats it as an invader. Progressive immune responses to male fetuses can lead to increased antibody effects on the sexual differentiation of the brain in the next male fetus. This hypothesis is supported by the fact that number of older sisters has no apparent effect on sexual orientation; this would be because female fetuses would not produce an immune response. Also, preemptive immunization of female mice produced male offspring with less successful reproductive performance. These males would only perform 10% of their matings successfully, compared to the 100% performed by sons of control mothers (Blanchard 373-378).
This variety of studies helps to illustrate the incredible complexity of how homosexual behavior is caused. There is likely no single gene, or even set of genes, that acts as the sole determinant of homosexuality; however, various twin studies have demonstrated that there are likely some genetic influences. The X chromosome is a promising location for future research due to maternal inheritance patterns that have been discovered. This pattern also helped to formulate various theories on how homosexuality can be genetically maintained in a population at all and how it can be a beneficial trait to others. Studies done on the effects of testosterone deprivation on different areas of the brain also shed light on biological factors. Research on H-Y antigens appears to be a very promising explanation of at least one factor that contributes to homosexuality. It is obvious by the vast amounts of evidence and data that homosexual behavior is caused by various biological as well as environmental factors; no simple explanation exists. Most importantly, however, people should not use this data to try and “cure” homosexuals of some biological “ailment.” Rather, this research should illustrate how homosexuality is no different that skin color or height: intrinsically human, no matter the exact causes.
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