Biology and sexual orientation


Biology and sexual orientation
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Biology and sexual orientation is the subject of research into the role of biology in the development of human sexual orientation. No simple, single cause for sexual orientation has been conclusively demonstrated, but research suggests that it is by a combination of genetic, hormonal, and environmental influences,[1] with biological factors involving a complex interplay of genetic factors and the early uterine environment.[2] Biological factors which may be related to the development of a heterosexual, homosexual, bisexual or asexual orientation include genes, prenatal hormones, and brain structure.

Contents

Empirical studies

Twin studies

A number of twin studies have attempted to isolate biological factors in sexual orientation. As Bearman and Bruckner (2002) describe it, early studies concentrated on small, select samples, which showed very high genetic influences;[3] however, they were also criticized for non-representative selection of their subjects.[4] Later studies, performed on increasingly representative samples, showed much lesser concordance among monozygotic (MZ, colloquially "identical") twins, although still significantly larger than among dizygotic (DZ) twins.

For example, a meta-study by Hershberger (2001)[5] compares the results of eight different twin studies: among those, all but two showed MZ twins having much higher concordance of sexual orientation than DZ twins, suggesting a non-negligible genetic component. Two additional examples: Bailey and Pillard (1991) in a study of gay twins found that 52% of monozygotic (MZ) brothers and 22% of the dizygotic (DZ) twins were concordant for homosexuality.[6] Also, Bailey, Dunne and Martin (2000) used the Australian twin registry to obtain a sample of 4,901 twins.[7] Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. MZ twin concordance for homosexuality was found to be 30%.

A recent study of all adult twins in Sweden (more than 7,600 twins)[8] found that same-sex behavior was explained by both heritable factors and individual-specific environmental sources (such as prenatal environment, experience with illness and trauma, as well as peer groups, and sexual experiences), while influences of shared-environment variables such as familial environment and societal attitudes had a weaker, but significant effect. Women showed a statistically non-significant trend to weaker influence of hereditary effects, while men showed no effect of shared environmental effects. The use of all adult twins in Sweden was designed to address the criticism of volunteer studies, in which a potential bias towards participation by gay twin may influence the results (see below).

Overall, the environment shared by twins (including familial and societal attitudes) explained 0–17% of the choice of sexual partner, genetic factors 18–39% and the unique environment 61–66%. The individual's unique environment includes, for example, circumstances during pregnancy and childbirth, physical and psychological trauma (e.g., accidents, violence, and disease), peer groups (other than those shared with a twin), and sexual experiences. [...] In men, genetic effects explained .34–.39 of the variance, the shared environment .00, and the individual-specific environment .61–.66 of the variance. Corresponding estimates among women were .18–.19 for genetic factors, .16–.17 for shared environmental, and .64–.66 for unique environmental factors.

Criticisms

Twin studies have received a number of criticisms including self-selection bias where homosexuals with gay siblings are more likely to volunteer for studies. Nonetheless, it is possible to conclude that, given the difference in sexuality in so many sets of identical twins, sexual orientation cannot be purely caused by genetics.[9]

Another issue is the recent finding that even monozygotic twins can be different and there is a mechanism which might account for monozygotic twins being discordant for homosexuality. Gringas and Chen (2001) describe a number of mechanisms which can lead to differences between monozygotic twins, the most relevant here being chorionicity and amniocity.[10] Dichorionic twins potentially have different hormonal environments and receive maternal blood from separate placenta. Monoamniotic twins share a hormonal environment, but can suffer from the 'twin to twin transfusion syndrome' in which one twin is "relatively stuffed with blood and the other exsanguinated".[11] If one twin receives less testosterone and the other more, this could result in different levels of brain masculinisation.

Chromosome linkage studies

Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993, Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families.[12] Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed as the 'gay gene' in the media, causing significant controversy. Sanders et al. in 1998 reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared to 6% on the paternal side.[13]

A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28.[14] Although two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men,[13] a rigorous replication of the maternal loading was reported on samples in Italy in England.[citation needed] One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[15] Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation.[citation needed] A recent study of 894 heterosexual and 694 homosexual men found no evidence of sex linkage.[16]

Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects.[17] With the larger sample set and complete genome scan, the study found somewhat reduced linkage for Xq28 than reported by Hamer et al. However, they did find other markers with a likelihood score falling just short of significance at 7q36 and likelihood scores approaching significance at 8p12 and 10q26. Interestingly, 10q26 showed highly significant maternal loading, thus further supporting the previous family studies.

Epigenetics studies

A recent study suggests linkage between a mother's genetic make-up and homosexuality of her sons. Women have two X chromosomes, one of which is "switched off". The inactivation of the X chromosome occurs randomly throughout the embryo, resulting in cells that are mosaic with respect to which chromosome is active. In some cases though, it appears that this switching off can occur in a non-random fashion. Bocklandt et al. (2006) reported that, in mothers of homosexual men, the number of women with extreme skewing of X chromosome inactivation is significantly higher than in mothers without gay sons. Thirteen percent of mothers with one gay son, and 23% of mothers with two gay sons showed extreme skewing, compared to 4% percent of mothers without gay sons.[18]

Birth order

Blanchard and Klassen (1997) reported that each older brother increases the odds of a man being gay by 33%.[19][20] This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation."[21] To explain this finding, it has been proposed that male fetuses provoke a maternal immune reaction that becomes stronger with each successive male fetus. Male fetuses produce HY antigens which are "almost certainly involved in the sexual differentiation of vertebrates." It is this antigen which maternal H-Y antibodies are proposed to both react to and 'remember'. Successive male fetuses are then attacked by H-Y antibodies which somehow decrease the ability of H-Y antigens to perform their usual function in brain masculinisation.[19] However the theory has been criticized because symptoms which would be typical of such effects are rare compared with prevalence of homosexuality [22]

Female fertility

In 2004, Italian researchers conducted a study of about 4,600 people who were the relatives of 98 homosexual and 100 heterosexual men. Female relatives of the homosexual men tended to have more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. The researchers concluded that there was genetic material being passed down on the X chromosome which both promotes fertility in the mother and homosexuality in her male offspring. The connections discovered would explain about 20% of the cases studied, indicating that this is a highly significant but not the sole genetic factor determining sexual orientation.[23]

Pheromone studies

Recent research conducted in Sweden[24] has suggested that gay and straight men respond differently to two odors that are believed to be involved in sexual arousal. The research showed that when both heterosexual women (lesbians were included in the study, but the results regarding them were "somewhat confused") and gay men are exposed to a testosterone derivative found in men's sweat, a region in the hypothalamus is activated. Heterosexual men, on the other hand, have a similar response to an estrogen-like compound found in women's urine.[25] The conclusion is that sexual attraction, whether same-sex or opposite-sex oriented, operates similarly on a biological level. Researchers have suggested that this possibility could be further explored by studying young subjects to see if similar responses in the hypothalamus are found and then correlating these data with adult sexual orientation.[citation needed]

Studies of brain structure

A number of sections of the brain have been reported to be sexually dimorphic; that is, they vary between men and women. There have also been reports of variations in brain structure corresponding to sexual orientation. In 1990, Swaab and Hofman reported a difference in the size of the suprachiasmatic nucleus between homosexual and heterosexual men.[26] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure.[27]

Early work of this type was also done by Simon LeVay. LeVay studied four groups of neurons in the hypothalamus, called INAH1, INAH2, INAH3 and INAH4. This was a relevant area of the brain to study, because of evidence that this part of the brain played a role in the regulation of sexual behaviour in animals, and because INAH2 and INAH3 had previously been reported to differ in size between men and women.[28]

He obtained brains from 41 deceased hospital patients. The subjects were classified as follows: 19 gay men who had died of AIDS, 16 presumed heterosexual men (6 of whom had died of AIDS), and 6 presumed heterosexual women (1 of whom had died of AIDS).[28] The AIDS patients in the heterosexual groups were all identified from medical records as intravenous drug abusers or recipients of blood transfusions, though only 2 of the men in this category had specifically denied homosexual activity. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been mostly or all heterosexual "on the basis of the numerical preponderance of heterosexual men in the population."[28] LeVay found no evidence for a difference between the groups in the size of INAH1, INAH2 or INAH4. However, the INAH3 group appeared to be twice as big in the heterosexual male group as in the gay male group; the difference was highly significant, and remained significant when only the 6 AIDS patients were included in the heterosexual group. The size of the INAH3 in the homosexual male brains was similar to that in the heterosexual female brains.

William Byne and colleagues attempted to replicate the differences reported in INAH 1–4 size using a different sample of brains from 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). They found a significant difference in INAH3 size between heterosexual men and women. The INAH3 size of the homosexual men was apparently smaller than that of the heterosexual men and larger than that of the heterosexual women, though neither difference quite reached statistical significance.[29]

Byne and colleagues also weighed and counted numbers of neurons in INAH3, tests not carried out by LeVay. The results for INAH3 weight were similar to those for INAH3 size; that is, the INAH3 weight for the heterosexual male brains was significantly larger than for the heterosexual female brains, while the results for the gay male group were between those of the other two groups but not quite significantly different from either. The neuron count also found a male-female difference in INAH3, but found no trend related to sexual orientation.[29]

A 2010 study stated: "The fetal brain develops during the intrauterine period in the male direction through a direct action of testosterone on the developing nerve cells, or in the female direction through the absence of this hormone surge. In this way, our gender identity (the conviction of belonging to the male or female gender) and sexual orientation are programmed or organized into our brain structures when we are still in the womb. There is no indication that social environment after birth has an effect on gender identity or sexual orientation."[30]

Biological theories of etiology of sexual orientation

Early fixation hypothesis

The early fixation hypothesis includes research into prenatal development and the environmental factors that control masculinization of the brain. Some studies have seen pre-natal hormone exposures as the primary factor involved in determining sexual orientation.[31][32][33] This hypothesis is supported by both the observed differences in brain structure and cognitive processing between homosexual and heterosexual men. One explanation for these differences is the idea that differential exposure to hormone levels in the womb during fetal development may change the masculinization of the brain in homosexual men. The concentrations of these chemicals is thought to be influenced by fetal and maternal immune systems, maternal consumption of certain drugs, maternal stress, and direct injection. This hypothesis is also connected to the fraternal birth order research.

Imprinting/critical period

This type of theory holds that the formation of gender identity occurs in the first few years of life after birth. It argues that individuals can be predisposed to homosexual orientation by biological factors but are triggered in some cases by upbringing. Part of adopting a gender identity involves establishing the gender(s) of sexual attraction. This process is analogous to the "imprinting" process observed in animals. A baby duckling may be genetically programmed to "imprint" on a mother, but what entity it actually imprints upon depends on what objects it sees immediately after hatching. Most importantly, once this process has occurred, it cannot be reversed, any more than the duckling can hatch twice.[citation needed]

A sort of reverse sexual imprinting has been observed in heterosexual humans; see the section on the "Westermarck effect" in Behavioral imprinting.

Several different triggers for imprinting upon a particular sexual orientation have been proposed, but there is no empirical evidence to support any of them.[citation needed]

Exotic becomes erotic

Daryl Bem, a social psychologist at Cornell University, has theorized that the influence of biological factors on sexual orientation may be mediated by experiences in childhood. A child's temperament predisposes the child to prefer certain activities over others. Because of their temperament, which is influenced by biological variables such as genetic factors, some children will be attracted to activities that are commonly enjoyed by other children of the same gender. Others will prefer activities that are typical of another gender. This will make a gender-conforming child feel different from opposite-gender children, while gender-nonconforming children will feel different from children of their own gender. According to Bem, this feeling of difference will evoke physiological arousal when the child is near members of the gender which it considers as being 'different'. Bem theorizes that this physiological arousal will later be transformed into sexual arousal: children will become sexually attracted to the gender which they see as different ("exotic"). This theory is known as Exotic Becomes Erotic theory.[34]

The theory is based in part on the frequent finding that a majority of gay men and lesbians report being gender-nonconforming during their childhood years. A meta-analysis of 48 studies showed childhood gender nonconformity to be the strongest predictor of a homosexual orientation for both men and women.[35] Fourteen studies published since Bailey & Zucker's 1995 also show the same results.[36] In one study by the Kinsey Institute of approximately 1000 gay men and lesbians (and a control group of 500 heterosexual men and women), 63% of both gay men and lesbians reported that they were gender nonconforming in childhood (i.e., did not like activities typical of their sex), compared with only 10–15% of heterosexual men and women. There are also six "prospective" studies—that is longitudinal studies that begin with gender-nonconforming boys at about age 7 and follow them up into adolescence and adulthood. These also show that a majority (63%) of the gender nonconforming boys become gay or bisexual as adults.[37] There are very few prospective studies of gender nonconforming girls.[38][39] In a group of eighteen behaviorally masculine girls (mean age of assessment: 9 years), all reported a homosexual sexual orientation at adolescence, and eight had requested sex reassignment.[40]

William Reiner, a psychiatrist and urologist with the University of Oklahoma has evaluated more than a hundred cases of children born with sexual differentiation disorders. In the 1960s and 70s, it was common in developed countries for doctors to castrate boys born with a micropenis and have them raised as girls. However, this practice has come under attack, because even though these boys were raised as girls, they nearly all report as adults that they are sexually attracted to women. This suggests that their sexual orientation was determined at birth.[citation needed]

Pathogenic hypothesis of homosexuality

The pathogenic hypothesis of homosexuality, also called the 'gay germ' hypothesis, suggests that homosexuality might be caused by an infectious agent. The speculative hypothesis was suggested by Gregory Cochran and Paul Ewald as part of a larger project advocating a number of pathogenic theories of disease. They argue that because of the reduced number of offspring produced by gay and lesbian people, evolution would strongly select against it. They also draw an analogy to diseases that alter brain structure and behavior, such as narcolepsy, which are suspected of being triggered by viral infection.[41] Cochran also argues that the prevalence of homosexuality in urban areas suggests that an infectious disease causes homosexuality.[42] They conclude that it is a "feasible hypothesis... no more and no less."[41] After they were unable to publish this account in a peer-reviewed journal, the idea appeared in the popular press.[43] An American Philosophical Association newsletter the following year stated "there is ultimately very little to be said in favor of these contentions", and criticized the press attention gained, given a lack of peer reviewed publication of the theory, and questioned the general ethics of communication of theories about homosexuality by researchers to the public. [44] In an article in Out Magazine, brain researcher William Byne stated "Cochran and Ewald are guilty of pathologizing homosexuality",[45] while in the same article psychology professor J. Michael Bailey posited that a 'germ theory' did not necessarily mean homosexuality was a disease, but recognised the political ammunition such a belief could give to homophobes.[45]

Sexual orientation and evolution

Sexual practices that significantly reduce the frequency of heterosexual intercourse also significantly decrease the chances of successful reproduction, and for this reason, they would appear to be maladaptive in an evolutionary context following a simple Darwinian model of natural selection—on the assumption that homosexuality would reduce this frequency. Several theories have been advanced to explain this contradiction, and new experimental evidence has demonstrated their feasibility.[46]

Some scholars[46] have suggested that homosexuality is adaptive in a non-obvious way. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia when two copies are present may also confer resistance to malaria with a lesser form of anemia when one copy is present (this is called heterozygous advantage).[47]

The so-called "gay uncle" hypothesis posits that people who themselves do not have children may nonetheless increase the prevalence of their family's genes in future generations by providing resources (food, supervision, defense, shelter, etc.) to the offspring of their closest relatives. This hypothesis is an extension of the theory of kin selection. Kin selection was originally developed to explain apparent altruistic acts which seemed to be maladaptive. The initial concept was suggested by J.B.S. Haldane in 1932 and later elaborated by many others including John Maynard Smith, W. D. Hamilton and Mary Jane West-Eberhard.[48] This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.

Brendan Zietsch of the Queensland Institute of Medical Research proposes the alternative theory that men exhibiting female traits become more attractive to females and are thus more likely to mate, provided the genes involved do not drive them to complete rejection of heterosexuality.[49]

In a 2008 study, its authors stated that "There is considerable evidence that human sexual orientation is genetically influenced, so it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency." They hypothesized that "while genes predisposing to homosexuality reduce homosexuals' reproductive success, they may confer some advantage in heterosexuals who carry them." and their results suggested that "genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could help explain the evolution and maintenance of homosexuality in the population.".[50] However, in the same study, the authors noted that "nongenetic alternative explanations cannot be ruled out" as a reason for the heterosexual in the homosexual-heterosexual twin pair having more partners, specifically citing "social pressure on the other twin to act in a more heterosexual way" (and thus seek out a greater number of sexual partners) as an example of one alternative explanation. Also, the authors of the study acknowledge that a large number of sexual partners may not lead to greater reproductive success, specifically noting there is an "absence of evidence relating the number of sexual partners and actual reproductive success,either in the present or in our evolutionary past."

Important new evidence on a plausible mechanism for the evolution of "gay genes" has emerged from the work of Camperio-Ciani.[23] They found in two large, independent studies that the female relatives of homosexual men tended to have significantly more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. This indicates that females carrying a putative "gay genes" complex are more fecund than women lacking this complex of genes, and thereby can compensate for any decreased fertility of the males carrying the genes. This is a well known phenomenon in evolution known as "sexual antagonism,"[citation needed] and has been widely documented for many traits that are advantageous in one sex but not in the other.[citation needed] This provides solid experimental evidence of how "gay genes" could not only survive but thrive over the course of evolution.[citation needed]

Biological differences in gay men and lesbians

Physiological

Some studies have found correlations between physiology of people and their sexuality. These studies provide evidence which they claim suggests that:

  • Gay men report, on an average, slightly longer and thicker penises than non-gay men.[51]
  • Gay men and straight women have, on average, equally proportioned brain hemispheres. Lesbian women and straight men have, on average, slightly larger right brain hemispheres.[52]
  • The VIP SCN nucleus of the hypothalamus is larger in men than in women, and larger in gay men than in heterosexual men.[53]
  • The average size of the INAH-3 in the brains of gay men is approximately the same size as INAH 3 in women, which is significantly smaller, and the cells more densely packed, than in heterosexual men's brains.[28]
  • The anterior commissure is larger in women than men and was reported to be larger in gay men than in non-gay men,[27] but a subsequent study found no such difference.[54]
  • Gay men's brains respond differently to fluoxetine, a selective serotonin reuptake inhibitor.[55]
  • The functioning of the inner ear and the central auditory system in lesbians and bisexual women are more like the functional properties found in men than in non-gay women (the researchers argued this finding was consistent with the prenatal hormonal theory of sexual orientation).[56]
  • The suprachiasmatic nucleus was found by Swaab and Hopffman to be larger in gay men than in non-gay men,[57] the suprachiasmatic nucleus is also known to be larger in men than in women.[58]
  • The startle response (eyeblink following a loud sound) is similarly masculinized in lesbians and bisexual women.[59]
  • Gay and non-gay people's brains respond differently to two putative sex pheromones (AND, found in male armpit secretions, and EST, found in female urine).[24][60][61]
  • One region of the brain (amygdala) is more active in gay men than non-gay men when exposed to sexually arousing material.[62]
  • Finger length ratios between the index and ring fingers may be different between non-gay and lesbian women.[56][63][64][65][66][67]
  • Gay men and lesbians are significantly more likely to be left-handed or ambidextrous than non-gay men and women;[68][69][70] Simon LeVay argues that because "[h]and preference is observable before birth[71]... [t]he observation of increased non-right-handness in gay people is therefore consistent with the idea that sexual orientation is influenced by prenatal processes," perhaps heredity.[28]
  • A study of 50 gay men found 23% had counterclockwise hair whirl, as opposed to 8% in the general population. This may correlate with left-handedness.[72]
  • Gay men have increased ridge density in the fingerprints on their left thumbs and pinkies.[72]
  • Length of limbs and hands of gay men is smaller compared to height than the general population, but only among white men.[72]

Cognitive

Recent studies suggest the presence of subtle differences in the way gay people and non-gay people process certain kinds of information. Researchers have found that:

  • Gay men[73] and lesbians are more verbally fluent than heterosexuals of the same sex[74][75][76] (but two studies did not find this result).[77][78]
  • Gay men may receive higher scores than non-gay men on tests of object location memory (no difference was found between lesbians and non-gay women).[79]

Political aspects

Whether genetic or other physiological determinants form the basis of sexual orientation is a highly politicized issue. The Advocate, a U.S. gay and lesbian newsmagazine, reported in 1996 that 61% of its readers believed that "it would mostly help gay and lesbian rights if homosexuality were found to be biologically determined".[80] A cross-national study in the United States, the Philippines, and Sweden found that those who believed that "homosexuals are born that way" held significantly more positive attitudes toward homosexuality than those who believed that "homosexuals choose to be that way" or "learn to be that way".[81][82]

Equal protection analysis in U.S. law determines what groups are considered suspect classes and therefore eligible for heightened scrutiny based on several factors, one of which is immutability. Evidence that sexual orientation is biologically determined (and therefore perhaps immutable in the legal sense) would strengthen the legal case for heightened scrutiny of laws discriminating on that basis.[83][84][85]

The perceived causes of sexual orientation have a significant bearing on the status of sexual minorities in the eyes of social conservatives. The Family Research Council, a conservative Christian think tank in Washington, D.C., argues in the book Getting It Straight that finding people are born gay "would advance the idea that sexual orientation is an innate characteristic, like race; that homosexuals, like African-Americans, should be legally protected against 'discrimination;' and that disapproval of homosexuality should be as socially stigmatized as racism. However, it is not true.", but did not give any further explanations. On the other hand, some social conservatives such as Reverend Robert Schenck have argued that people can accept the "inevitable... scientific evidence" while still morally opposing homosexuality.[86] As well, National Organization for Marriage board member and fiction writer Orson Scott Card has supported biological research on homosexuality, writing that "our scientific efforts in regard to homosexuality should be to identify genetic and uterine causes... so that the incidence of this dysfunction can be minimized.... [However, this should not be seen] as an attack on homosexuals, a desire to 'commit genocide' against the homosexual community.... There is no 'cure' for homosexuality because it is not a disease. There are, however, different ways of living with homosexual desires."[87]

Some advocates for the rights of sexual minorities resist linking that cause with the concept that sexuality is biologically determined or fixed at birth. They argue that sexual orientation can shift over the course of a person's life.[88] At the same time, others resist any attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm.[86] Chandler Burr writing for The Atlantic Monthly has stated that "[s]ome, recalling earlier psychiatric "treatments" for homosexuality, discern in the biological quest the seeds of genocide. They conjure up the specter of the surgical or chemical "rewiring" of gay people, or of abortions of fetal homosexuals who have been hunted down in the womb."[89] Simon LeVay has said, in response to letters from gays and lesbians making such criticisms, that the research "has contributed to the status of gay people in society."[86]

See also

References

Notes
  1. ^ Frankowski BL; American Academy of Pediatrics Committee on Adolescence (June 2004). "Sexual orientation and adolescents". Pediatrics 113 (6): 1827–32. doi:10.1542/peds.113.6.1827. PMID 15173519. http://pediatrics.aappublications.org/cgi/content/full/113/6/1827?maxtoshow=&hits=10&RESULTFORMAT=&fulltext=%22Sexual+orientation+and+adolescents%22&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT. 
  2. ^ Royal College of Psychiatrists: Submission to the Church of England’s Listening Exercise on Human Sexuality.
  3. ^ This work was published in the American Journal of Sociology (Bearman, P. S. & Bruckner, H. (2002) Opposite-sex twins and adolescent same-sex attraction. American Journal of Sociology 107, 1179–1205.) and is available only to subscribers. However, a final draft of the paper is available here – there are no significant differences on the points cited between the final draft and the published version.
  4. ^ While inconsistent with modern findings, the first relatively large-scale twin study on sexual orientation was reported by Kallman in 1952. (See: Kallmann FJ (April 1952). "Comparative twin study on the genetic aspects of male homosexuality". J. Nerv. Ment. Dis. 115 (4): 283–97. PMID 14918012. ). Examining only male twin pairs, he found a 100% concordance rate for homosexuality among 37 monozygotic (MZ) twin pairs, compared to a 12%–42% concordance rate among 26 dizygotic (DZ) twin pairs, depending on definition. In other words, every identical twin of a homosexual subject was also homosexual, while this was not the case for non-identical twins. This study was criticised for its vaguely described method of recruiting twins and for a high rate of psychiatric disorders among its subjects. (See Rosenthal, D., "Genetic Theory and Abnormal Behavior" 1970, New York: McGraw-Hill.)
  5. ^ Hershberger, Scott L. 2001. Biological Factors in the Development of Sexual Orientation. Pp. 27–51 in Lesbian, Gay, and Bisexual Identities and Youth: Psychological Perspectives, edited by Anthony R. D’Augelli and Charlotte J. Patterson. Oxford, New York: Oxford University Press. Quoted in Bearman and Bruckner, 2002.
  6. ^ cited in Wilson and Rahman 2005, p47
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  12. ^ Hamer DH, Hu S, Magnuson VL, Hu N, Pattatucci AM (July 1993). "A linkage between DNA markers on the X chromosome and male sexual orientation". Science 261 (5119): 321–7. doi:10.1126/science.8332896. PMID 8332896. http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=8332896. 
  13. ^ a b Wilson, G.D., & Rahman, Q. (2005). Born Gay: The Biology of Sex Orientation. London: Peter Owen Publishers.
  14. ^ Hu S, Pattatucci AM, Patterson C, et al. (November 1995). "Linkage between sexual orientation and chromosome Xq28 in males but not in females". Nat. Genet. 11 (3): 248–56. doi:10.1038/ng1195-248. PMID 7581447. 
  15. ^ Vilain E (2000). "Genetics of sexual development". Annu Rev Sex Res 11: 1–25. PMID 11351829. 
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    Despite some degree of logical plausibility, there is ultimately very little to be said in favor of these contentions. In its focus on the reduced reproductive rates of homosexual men and women, the account ignores other mechanisms by which genetic traits endure across generations. More importantly, the account is offered without any evidence whatsoever about which microbe might work how to generate homosexual interests. A peer-reviewed science journal turned this account away, but it nevertheless found its way into the pages of the public press.... the ease with which theories of homosexuality seep into public discourse raises important ethical questions about the way in which researchers ought to communicate their various theories to the public. Given that an unfounded theory of homosexuality can do more damage than good, researchers should raise the bar in regard to the views they propound about its origin.

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    On the one hand, William Byne, a brain researcher at the Mount Sinai School of Medicine in New York, suspects that Cochran and Ewald are guilty of pathologizing homosexuality. "It's hard for most people to entertain the idea that homosexuality might be a natural variant of human sexual behavior," says Byne. On the other hand, Michael Bailey, a professor of psychology at Northwestern University, gives Cochran and Ewald the benefit of the doubt. Bailey does worry that homophobes could use the germ theory as political ammunition—as "proof" that homosexuality is a disease. But that would be "a totally illegitimate conclusion," in Bailey's opinion. Not everything caused by a germ is a disease, he insists. "Suppose we found that a form of genius was also caused by a virus. Would that mean that genius is a disease?"

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