In addition to genetic theory there have been physiological studies which show some effect in homosexual behaviour. In 1990, LeVay studied four groups of neurones in the hypothalamus (INAH1, INAH2, INAH3, INHA4), known to play a role in the regulation of sexual behaviour in animals. INAH2 and INAH3 differ between men and women. LeVay studied the hypothalamus in autopsy specimens from 19 gay men who died of aids, 16 presumed heterosexual men ( 6 who had died of aids) and 6 presumed heterosexual women (1 had died of aids). INAH3 was twice as big in heterosexual men than in homosexual men. Like Gorski’s results (1978: cited in Hamer & LeVay 1994), LeVay found that INAH3 was twice as large in males than in females. INAH3 in homosexual men’s brains was similar to heterosexual women’s brains. Although the AIDS virus might provide a strong confounding variable, this suggests an physiological basis, as well the earlier genetic ones.
homosexuality is increased by the number of older brothers an individual posses Blanchard and Klassen (1997). As an explanation these results it has been proposed that male foetuses cause a maternal immune reaction that becomes stronger with each successive male foetus (Blanchard and Klassen, 1997). Male foetuses produce HY antigens which are “almost certainly involved in the sexual differentiation of vertebrates” (Blanchard and Klassen, 1997). It is this antigen which maternal H-Y antibodies bind. Successive male foetuses are then attacked by H-Y antibodies which somehow decrease the ability of H-Y antigens to perform their usual function in brain masculinisation.
This does not address the fundamental paradox to the principle of natural selection that homosexuality poses i.e. homosexuals do not produce offspring, so how can this be maintained in the population. However there are several possible hypotheses that address this issue.
One theory proposed by Trivers suggests that, since the (potential) gene is sex linked on the X chromosome, there is a sexually antagonistic effect between the males and females. Since the gene spends twice as long in the female; if it had a trait that benefited female fertility the it would survive in the population, even if it had twice as large a deleterious effect on male fertility (Ridely, 1999). Thus if female ‘carriers’ were more desirable to heterosexual males, then the gene would be propagated in the population regardless of the reduced fitness effect it had on the male offspring, as female offspring would compensate This is confirmed by Corna et al (2004), who shows that female relatives of gay men, on their mother’s side of the family had more children than female relatives of heterosexual men. More recent studies by Bocklandt et al (2006) dealt with the issue of linkage. Since females are homozygous for the X chromosome, then one allele will be “inactive”. Bocklandt et al. shows that the number of women with extreme skewing of X chromosome inactivation is higher in mothers with homosexual offspring than in controls without gay sons. 4% of controls showed extreme skewing compared to 13% of the mothers with gays sons and 23% of mothers with two or more gay sons.
In 1990, LeVay studied four groups of neurones in the hypothalamus (INAH1, INAH2, INAH3, INHA4), which were known to play a role in the regulation of sexual behaviour
in animals. INAH2 and INAH3 differed between men and women. LeVay studied the hypothalamus in autopsy specimens from 19 gay men who died of aids, 16 presumed heterosexual men ( 6 who had died of aids) and 6 presumed heterosexual women (1 had died of aids). INAH3 was twice as big in heterosexual men than in homosexual men. Like Gorski’S (1978: cited in Hamer & LeVay 1994) results, LeVay found that INAH3 was twice as large in males than in females. INAH3 in homosexual men’s brains was similar to heterosexual women’s brains. However one has to be very sceptical about any confounding variable that may influence the results, which would be AIDS in this case. Although a difference was found between the brains, it could be due to the AIDS virus itself, which may damage the brain cells and so cause the reduction in size of INAH3 size in the homosexual men.
This might be linked to the reported effect of HY antibodies on sexuality.
Another theory that might be operating is that of kin selection. Homosexuals altruistically forego reproduction to assist offspring of relatives (Wilson 1975, Weinrich 1987)- lecture notes. If a homosexual increases the reproductive success of his kin, then this may offset his/her lack of offspring, and pass on genes for homosexuality in his/her siblings offspring, thus the homosexual becomes a helper. This suggests that the individuals who are most likely to become homosexual are individuals who are least likely to reproduce, but this is not necessarily the case; in a sample of contemporary British women bisexuals were shown to have a significantly higher fecundity to age 25, and no lifetime difference over this age (Baker and Bellis, 1995: cited in Kirkpatrick 2000). Thus homosexual genes might be passed on latently to these offspring. However, the principle argument against the kin selection theory, however, is that non reproductive individuals who are altruistic benefit their parents reproductive success before being able to benefit their own (Trivers 1974: cited in Kirkpatrick 2000).
An alternative, and more convincing theory to kin selection, is that of the importance of alliance formation in the survival of the individual. Homosexuality has been noted as key in the formation of alliances within bonobo chimps as well as among humans e.g. the K’ekchi’ Mayans of Belieze. Thus one theory is that homosexuality is maintained within a population due to the benefits it has on individuals maintaining alliances and households, allowing offspring to reach reproductive age. In this way the survival of homosexuals who might otherwise be at risk is increased. For example in Melanesian ‘patron/client’ the patron provides food and education, increasing the clients chance of success, while the client provides labour (and sexual services) (van Baal 1966: cited in Kirkpatrick 2000). However, this still means that homosexuality is a maladaptive in Darwinian terms, an done caveat to this is that bisexuals should outnumber homosexuals (Kirkpatrick 2000). Numerous sources, including the Kinsey study (Kinsey 1953: cited in Kirkpatrick 2000) verify this. Thus homosexuality might be adaptive to individual’s survival.
There are also environmental factors suggested about the basis of homosexuality. According to Bieber, a “male child who grows up with a close, over possessive, mother and a detached, indifferent, father lacks a male model to identify with…is sexually over stimulated by the mother and emasculated by her” (cited in Braverman, 1973). Hoever, Bieber’s sample of male homosexuals consisted of many who had pathological parenting and were emotionally ill to start with. Some believe that is impossible to identify “whether the homosexuality is pathological or whether it is the parenting that is pathological” and in fact many psychologists believe that pathological parenting conditions are “neither necessary nor sufficient causes for homosexuality.” (Braverman, 1973). A similar approach to that of Bieber, is Freud’s psychoanalytic theory; he believes that an unconscious hatred of a mother and an envy of a brother’s penis cause girls to become lesbians. Although many retrospective studies indicate that homosexual men have an unusually close relationship with their mothers and a distant relationship with their fathers, it does not automatically mean that parental attitudes influence sexual orientation (no causal relationship). It might be possible that these factors increase the likihood of homosexuality manifesting itself in individividuals with the Xq28 gene. Thus the genetic and environmental theories are not mutually exclusive.
Although there is evidence for both a genetic and environmental cause to homosexuality, is seems that overall there is a basis in the biological approach, which might be affected by the rearing environment. It is possible that the expression of the Xq28 gene on the X chromosome has an effect which increases the susceptibility of the developing fetal brain to the mothers H-Y antigens. This would then cause an increase in the likihood of homosexuality in successive male offspring, explaining the results found by Blanchard and Klassen. This would also explain the high prevalence of homosexuality in the maternal lineage of gay men, which could be operating under Trivers theory that the reduced fitness in the male offspring is offset by the increased fitness gained by female “carriers”. Thus these individuals who have been affected physiologically as a result of their genetic makeup might be more predisposed to homosexuality as a result of their infantile interactions with their parents as per Bieber’s theory. Individuals who do not manifest as homosexuals would still pass the gene on into the gene pool. This would also make sense in terms of the theory of individual survival and alliance formation, which would further act to maintain the trait in amongst individuals within a population behaviorally. A great deal of further work should be done on this.
Corna F, A. Camperio-Ciani and C. Capiluppi, 2004. Evidence for maternally inherited factors favouring male homosexuality and promoting female fecundity.
Bocklandt, S.B., Horvath, S., Vilain, E., Hamer, D.H. (2006). Extreme skewing of X chromosome inactivation in mothers of homosexual men. Human Genetics, 118:691-694
Blanchard and Klassen (1997). H-Y Antigen and Homosexuality in Men. Journal of Theoretical Biology, 185, 373-378
One of the earliest biological explanations of sexual orientation was put forward by Plato around 2,400 years ago.
Corna F, A. Camperio-Ciani and C. Capiluppi, 2004. Evidence for maternally inherited factors favouring male homosexuality and promoting female fecundity.
