Heavy criticism of such studies has arisen from the questionable recruitment method employed. Hines (2005) points out that since participants were mostly recruited through advertisement in the homosexual press, the group was essentially self-selected, and would likely include a greater proportion of homosexual twin pairs than would be seen in the population at large because the subject would be of particular interest to them. Bailey, Dunne & Martin (2000) rectified this fault by collecting participants from a pre-existing database of MZ and DZ twins in Australia. They found somewhat lower rates of sexual similarity--although, again, identical twins were more likely than fraternal twins to share homosexual feelings.
However the environment could still be a confounding factor in these studies as MZ twins are likely to be treated more similarly than DZ twins which could account for the differences observed. Investigation of MZ twins raised apart allows a genetic link to be singled out since the prenatal environment was the same and the postnatal environment was entirely divergent, so any correlation found must be attributed to either chance or genetics. Eckert et al. (1986) investigated the correlation between 6 pairs of such MZ twins (two pairs being male, four female) and Whitam (1993) of two pairs of male MZ twins. Of the four total male pairs, two were concordant for homosexuality, while a third engaged in an isolated homosexual experience. Of the four female twin pairs no concordance was seen, but one of the ‘second twins’ was bisexual. An obvious criticism of these studies is the small data set and self selecting participants.
Meisel and Ward (1981) use evidence from rats to demonstrate that inter-uterine hormonal levels are not uniform, and that in multiple pregnancies the hormonal levels of rat foetuses affect the hormone levels of the neighbouring rats. If this were true in humans, it would presumably mean that sharing a placenta or amniotic sac and the presence of inter-foetal vascular connections, would lead to increased conformity between hormone levels in inter-uterine environment of MZ twins compared to those who don’t share aspects of this environment.
The basic assumption that the hormonal environment is identical for both twins, is undermined since there is clear evidence that this relates to humans and MZ human twins are likely to have more inter-uterine environmental conformity (Jeanty et al. 2000). This means that all the studies mentioned above are highly questionable since none account for the amniotic and chorionic status of the twins studied as the placenta is the primary conduits of hormones, which may therefore act as potentially confounding variable. Therefore these results cannot isolate possible genetic causes from inter-uterine hormonal causes.
Attempts have been made to isolate genes that predispose males to homosexuality. A study by Mustanski et al. (2005) analysed the genomes of 456 men from 146 families with two or more gay brothers and examined all 22 pairs of non-sex chromosomes. The investigation builds on studies conducted by Hammer et al. (1993) that have suggested that there tend to be clusters of gays within a family. Mustanski found stretches of DNA that appeared to be linked to sexual orientation on three different chromosomes in the nucleus of cells of the human male. "There is no one 'gay' gene," said Mustanski. "Sexual orientation is a complex trait, so it's not surprising that we found several DNA regions involved in its expression. Our best guess is that multiple genes, potentially interacting with environmental influences, explain differences in sexual orientation."
Mustanski claims that earlier studies failed to find a link between DNA and homosexuality because they had focused solely on the X chromosome, where as his study examined all 22 pairs of non-sex chromosomes in addition to the X chromosome. However the frequency of shared markers, chromosomes 7, 8 and 10, of 60% is only 10% higher then that expected by chance, and so is not actually a significant link. An alternative explanation to these results is that the correlation of these genes may not be a direct link to sexual orientation but instead to a confounding variable that is dependant on sexual orientation. An example of this is a gene that does not causes homosexuality when passed on, but alters the hormone production of women (in general, or just during pregnancy) creating a more conducive inter-uterine environment for the development of homosexuality in their children.
Rice et al. (1999a) points out that from an evolutionary perspective, its hard to imagine a ‘gay gene’ or ‘genes’, since there would be strong selective pressures against such a gene. This is in keeping with the laws of natural selection as homosexuals would not be able to reproduce and so couldn’t contribute to the gene pool. However, it seems possible that they gene could be passed on by men who are not yet aware of their homosexuality and realise later in life, after they have produced offspring. There are many cases of this in the news and media, but I don’t think it has been empirically addressed.
Le Vay (1991) investigated the brain structures of males and found an area known as INAH-3 to be an average of 3 times smaller in homosexual mean compared to heterosexual men. To avoid biasing the results, he did the study "blind," without knowing which donors were gay. Le Vay attributed these differences to prenatal cerebral development caused by hormonal differences. However this does not shed light on what stage brain differentiation began; at conception, in the womb or during childhood or adolescences and is consequently of limited use in the debate of whether sexual orientation is inborn.
Bailey and Pillard et al. (1991) demonstrated that when female rats are given male levels of androgens early in development they acquire male sexual preferences, an example being attempts to mount other females. Researchers also observed that male rats, derived of androgens in the inter-uterine, became sexually passive and amiable to the attempts of other rats to mount them. This appears to be strong evidence in the indication that sexual orientation can be affected by hormones and so is not ‘inborn’.
This is further supported in Money, Schwartz, & Lewis’s, (1984) research that women suffering from the rare disorder of Congenital Adrenal Hyperplasia (CAH) who were exposed to high levels of androgens in the inter-uterine were found to be more likely to say they are bisexual or homosexual than female controls with other endocrine disorders. In case one would think that an eviromental influence could still be present, Dittmann, Kappes, & Kappes, (1992) also found women with CAH to score higher on a measure of homosexual interest and lower on a measure of heterosexual interest than their unaffected sisters.This provides compelling evidence of the importance of inter-uterine hormones in influencing sexual orientation.
Further convincing evidence supporting prenatal hormonal influences on the development of sexual orientation is found in a study by Masica et al. (1971), which compared CAH sufferers to Complete Androgen Insensitivity Syndrome (CAIS) sufferers, (genetic men living as females). It was found that the hormonal effect had over ridden gender differences to the extent that the genetic XY’s who were incapable of reacting to androgen were more attracted to men than XX’s who were exposed to androgen in the inter-uterine.
Since the milder form of CAH is often not recognized until a girl fails to menstruate at puberty, treatment may begin after suffers have been masculinised for many years, which casts doubt on the above results since they be confounded by feedback from the masculinised body. However longitudinal research on prepubescent girls with CAH by Ehrhardt (1968) found high levels of homosexuality, again emphasizing the important role of pre-natal hormone levels on sexual orientation.
Children born with ambiguous sexuality; such as boys with XY genes but suffering from partial androgen insensitivity syndrome (PAIS), or boys who’s genitalia were deformed or damaged post-nataly have also been studied with regard to sexual orientation. Money and Ogunro (1974) found that the above suffers who were feminized tended towards heterosexuality, i.e. they desire men as sexual partners, while those raised as boys also tended towards heterosexuality. Similar patterns were found in girls with CAH by Money and Dalery, (1976). In all cases it was reported that post-natal treatment could succeed in manipulating the sexual orientation of patients along with their gender, which provides strong evidence for a post natal influence on sexual orientation.
There are also a variety of social approaches that claim to influence sexual orientation. One that is borrowed from anthropological studies is that of imprinting. It is believed that the brain is programmed to attach an instinctual response to a stimulus whilst in a critical period, just as is seen in goslings that follow the first moving object they see after they hatch (Lorenz, 1935). Irwin and Price (1999) found evidence for sexual imprinting in male Zebra Finches, as they appeared to prefer mates with similar pattern of feathers to the female bird that rears then, rather then mates of their own type. This suggests that the post natal environment can impact sexual orientation, although its dubious that research on animals, can equally apply to humans.
Freud (1905) advocates the social influences on sexual orientation in a similar vain. He felt that all human beings were innately bisexual and during a critical period of 3 to 6 years, sexual orientation is fixed by a complex process of family relations, involving the Oedipus and Electra complexes. Freud lists a number of ways in which imprinting can be disturbed leading to homosexuality. This includes the child witnessing overvaluation of the opposite sex by one of both of the parents, a large number of opposite sex siblings/ role models in the family, if a parent does not demonstrate the usual heterosexual cultural stereotype, such as feminine fathers etc. Likewise, Bieber et al. (1962) claimed homosexuality resulted from pathological family relationships during the oedipal period, and claimed to have observed these patterns in their homosexual patients.
Freud’s assumption of inherent bisexuality is rejected by Rado (1940, 1949) who argues that heterosexuality in inborn and homosexuality is a result of a phobic response to members of the opposite sex. However, no rigorous empirical testing has been applied to either claims as they are based on analysing the clinical observations of patients already known to be homosexual. This means that the analyst’s theoretical orientation, expectations and personal attitude are likely to provide a bias for their observation. This is why the double blind method of empirical studies in now currently used. These theories are also solely based on homosexuals seeking therapy, which is not representative of well adjusted homosexuals at large, which makes it hard to generalize to all or even most cases.
Golombok and Tasker (1996) addressed the commonly held assumption that children brought up by lesbian mothers will themselves grow up to be gay or lesbian, implying the social environment to have a strong influence on sexual orientation. They matched 27 lesbian mothers to a control group of 27 heterosexual single mothers and followed their children from around the ages of 10 to 24. They found no significant difference between the two groups of children with regards to their heterosexual attraction. Furthermore Golombok and Tasker found no association between homosexual interest in adulthood and the number of years the child had been raised in a heterosexual household, the mother’s warmth with the child, the mother’s contentment with her sexual identity, the mother’s attitude towards men and a list of other variables. This lack of empirical evidence suggests that parent’s behaviour does not influence the development of the child’s sexual orientation.
However there were slight differences between the two groups regarding the future possibility of homosexual experiences as, “Significantly more of the young adults from lesbian family backgrounds stated that they had previously considered, or thought it a future possibility that they might experience same-gender attraction or relationship or both”, which makes it hard to entirely rule out the link between sexual orientation and ones home environment, although this could also be explained by a genetic predisposition or prenatal hormonal influences.
This essay has only scratched the surface in explaining the etiology of sexual orientation, and due to word limitations, only a selection of relevant evidence has been discussed. It seems that evidence demonstrating a genetic element to sexuality is limited and appears to be inconsistent with evolutionary theory. Even without this inconsistency, it is clear that homosexuality can not be entirely inborn, which is neatly summed up in a quote by Mann (1994), “The same data that show the effects of genes also point to the enormous influence of non-genetic factors." In the same manner, social theories purporting sexual orientation are even weaker as they have little empirical basis, apart from that which rests upon generalisation from birds to humans, and cannot rule out genetic of prenatal influences. In contrast there is extensive evidence to suggest that prenatal hormone levels cause changes in sexual orientation and even in brain structures such as INAH-3 which have been correlated with homosexuality in men.
I conclude with a summary by the national organization P-FLAG ("Parents and Friends of Lesbians and Gays"), that “to date, no researcher has claimed that genes can determine sexual orientation. At best, researchers believe that there may be a genetic component. Sexuality, like every other behavior, is undoubtedly influenced by both biological and societal factors."
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References:
Bailey, J. M., Pillard, R. C., Dawood, K, Miller, M. B., Farrer, L. A., Trivedi, S., Murphy, R. L. (1999). A family history study of male sexual orientation using three independent samples. Behavior Genetics, 29(2), 79-86,
Bailey & Bell (1993). Familiality of Female and Male Homosexuality. Behavior Genetics 23(4): 313-322.
Bailey, J.M., Dunne, M.P., and Martin, N.G., (2000), Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample: J Pers Soc Psychol, v. 78, p. 524-36.
Bieber, I., Dain, H.J, Dince, P.R., Drellich, M.G., Grand, H.G., Gundlach, R.H., Kremer, M.W., Rifkin, A.H., Wilbur, C.B., & Bieber, T.B. (1962). Homosexuality. New York: Basic Books, Inc.
Bouchard, S. J. (1984). Effects of a self-administered subliminal-relaxation treatment on anxiety. United States International University. Dissertation Abstracts International, 45 (6-B), p. 1906.
Dittmann, Ralf W., Marianne E. Kappes, and Michael H. Kappes. 1992. Sexual behavior in adolescent and adult females with congenital adrenal hyperplasia. Psychoneuroendocrinology 17 (2/3):153-170.
Eckert, E.D., Bouchard, T.J., Bohlen, J., and Heston, L.L., (1986), Homosexuality in monozygotic twins reared apart: Br J Psychiatry, v. 148, p. 421-5.
Ehrhardt, A. A., Epstein, R., Money, J. (1968) Fetal androgens and female gender identity in the early treated adrenogenital syndrome. Johns Hopkins Medical Journal, 122, 165-167.
Ellis, L., & Ames, M. A. (1987). Neurohormonal functioning and sexual orientation: A theory of homosexuality – heterosexuality. Psychological Bulletin, 101, 233–258.
Francoeur, R.T., M. Cornog, T. Perper, N.A. Scherzer, & G. Sellmer. 1991. A Descriptive Dictionary and Atlas of Human Sexuality. New York: Greenwood/Praeger Publishers.
Freud, S. (1905). Three essays on the theory of sexuality. In J. Strachey (Ed. and Trans.), The London: Hogarth Press. (Original work published 1905)
Golombok, S. & Tasker, F. (1996). Do Parents Influence the Sexual Orientation of Their Children ? Findings From a Longitudinal Study of Lesbian Families. Developmental Psychology, 32(1), 3-11.
Hammer, D., Hu, S., Magnuson, V., Hu, N., Pattatucci, A. (1993). The linkage between DNA markers on the X chromosome and male sexual orientation. Science, 26, 321-326.
Hines, M. (2004). Brain Gender. Oxford University Press: New York.
Hines, M. (2005). In Psychobiology of Gender Development Lecture given at City University.
Irwin DE, Price T, (1999). Sexual imprinting, learning and speciation. Heredity 82:347–354.
Kendler K. S., Karkowski L. M, Neale M. C., Prescott C. A. (2000), Illicit psychoactive substance use, heavy use, abuse, and dependence in a US population-based sample of male twins. Arch Gen Psychiatry 57(3):261-269.
Kinsey (1948) Sexual Behavior in the Human Male. p 639 Kinsey, Alfred C. et al. (1948/1998). . Philadelphia: W.B. Saunders; Bloomington: Indiana U. Press. Retrieved from http://www.kinseyinstitute.org/resources/ak-hhscale.html
Le Vay, S. (1991). A difference in hypothalamic structure between heterosexual and homosexual men. Science, 253, 1034-1037.
Le Vay, S. (1993). The Sexual Brain. Cambridge: MIT Press.
Lorenz, K. (1935) Cited in Slagsvold, T., Hanson, B. (2001). Sexual Imprinting and the Origin of Obligate Brood Parasitism in Birds. The American Naturalist, vol 158, No. 4.
Mann, C. (1994). Genes and behavior, Science 264:1687 (1994), pp. 1686-1689.
Masica, D. N., Monry, J., Ehrhardt, A. A. (1971) Fetal feminization and fetal gender identity in the testicular feminizing syndrome of androgen insensitivity. Archives of Sexual Behavior, 1, 131-142.
Meisel, R.L., & Ward, I.L., 1981, Fetal female rats are masculinized by male littermates located caudally in the uterus: Science, v. 213, p. 239-42.
Money, J., Dalery, J., (1976) Hermaphrodism – born with a penis. Three readed as boys four as girls, Journal of Homosexuality, Vol.1(4), p357-371.
Money, J., & Ogunro, C. (1974). Cited in Hines, M. (2004). Brain Gender. Oxford University Press: New York.
Money, J.,Schwartz, M., & Lewis, V. (1984). Cited in Hines, M. (2004). Brain Gender. Oxford University Press: New York.
Mustanski, BS, DuPree, MG, Nievergelt, CM, Bocklandt, S, Schork , NJ , Hamer, DH (2005). A genomewide scan of male sexual orientation. Human Genetics. On line, unpaged.
Pillard, R. & Weinrich, J. (1986). Evidence of familial nature of male homosexuality. Cited in Hines, M. (2004). Brain Gender. Oxford University Press: New York.
Rado, S. (1940). A critical examination of the concept of bisexuality. Psychosomatic Medicine, 2, 459-467.
Rado, S. (1949). An adaptational view of sexual behavior. In P.H. Hoch & J. Zubin (Eds.), Psychosexual development in health and disease (pp. 159-189). New York: Grune and Stratton.
Rice, G., Anderson, C., Risch, N., and Ebers, G., (1999a), Male homosexuality: absence of linkage to microsatellite markers at Xq28: Science, v. 284, p. 665-7.
Sell R. L., (1997), Defining and Measuring Sexual Orientation: A Review. Archives of Sexual Behavior Vol. 26, No 6 pp. 643-658
Whitam F. L., Mathy, R. M.(1991) Childhood cross-gender behavior of homosexual females in Brazil, Peru, the Philippines, and the United States. Arch Sex Behav; 20(2): 151-170.
Zuger, B. (1970). Gender role determination: A critical review of the evidence from hermaphroditism. Pyschomatic Medicine, 32, 449-467.
From the A.P.A.'s booklet, "Answers to Your Questions About Sexual Orientation and Homosexuality"
