Misplaced Pages

Biology and sexual orientation: Difference between revisions

Article snapshot taken from Wikipedia with creative commons attribution-sharealike license. Give it a read and then ask your questions in the chat. We can research this topic together.
Browse history interactively← Previous editNext edit →Content deleted Content addedVisualWikitext
Revision as of 17:49, 1 July 2008 editMickMacNee (talk | contribs)23,386 edits re-add more lost information. Summarisation is not duplication.← Previous edit Revision as of 21:14, 1 July 2008 edit undoPeculiar Light (talk | contribs)Extended confirmed users4,281 edits most of this page and most of medical world does not say biology causes homosexuality, just contributes to itNext edit →
Line 1: Line 1:
{{Sexual orientation}} {{Sexual orientation}}
In the topic of '''biology and sexual orientation''', ongoing scientific research is examining the possibility of there existing a specific biological ] to the ultimate development of a specific ] in human beings. In the topic of '''biology and sexual orientation''', ongoing scientific research is examining the possibility of there existing a specific biological contribution to the ultimate development of a specific ] in human beings.


Research to date has identified several biological factors which appear to influence the development of a ], ] or ] orientation in individuals. These include ]s, ], and ] structure. Research to date has identified several biological factors which appear to influence the development of a ], ] or ] orientation in individuals. These include ]s, ], and ] structure.

Revision as of 21:14, 1 July 2008

Sexual orientation
Sexual orientations
Related terms
Research
Animals
Related topics

In the topic of biology and sexual orientation, ongoing scientific research is examining the possibility of there existing a specific biological contribution to the ultimate development of a specific sexual orientation in human beings.

Research to date has identified several biological factors which appear to influence the development of a heterosexual, homosexual or bisexual orientation in individuals. These include genes, prenatal hormones, and brain structure.

No biological silver bullet hypothesis has been conclusively demonstrated, and there is no scientific consensus as to whether the contributory factors are primarily bioligical, environmental, or a combination of the two.

A number of theories have been proposed based on evidence gathered through scientific studies. Conclusive proof of a biological cause of sexual orientation would have significant political, cultural and religious implications.

Empirical studies

Chromosome linkage studies and the "Gay Gene" controversy

In 1993, Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families. 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 an infamous 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 (but inaccurately) dubbed as the 'gay gene' in the media, causing significant controversy.

A later analysis by Hu et al. revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28. Sanders et al. (1998) replicated the study, finding 66% Xq28 marker sharing in 54 pairs of gay brothers. On the other hand, 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. Also, a study by Rice et al. in 1999 failed to replicate the Xq28 linkage results,

Additinally, 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. With the larger sample set and complete genome scan, the study found much weaker link for Xq28 than reported by Hamer et al. However, they did find other markers with significant likelihood scores at 8p12, 7q36 and 10q26, the latter two having approximately equivalent maternal and paternal contributions.

These studies only examined homosexuality in males; they provide little information about female homosexuality.

Other chromosome linkage 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.

Twin studies

Researchers have traditionally used twin studies to try to isolate genetic influences from environmental or other influences. One common type of twin study compares identical twins (known as monozygotic or "MZ twins") who both have a particular trait to non-identical or fraternal twins (known as dizygotic or "DZ twins") with that same trait. Since identical twins have the same genetic makeup (genotype) while non-identical twins share only 50% of their genes, a difference between these types of twins provides evidence of a genetic component. For example, if a high percentage of identical twins both have red hair (while a low percentage of non-identical twins both have red hair), that suggests that red hair has a genetic basis. On the other hand, if identical twins share a characteristic just as often as fraternal twins (such as love of music), that suggests that there is not a genetic basis for that trait.

A number of twin studies have attempted this kind of isolation. As Bearman and Bruckner (2002) describe it, early studies concentrated on small, select samples, which showed very high genetic influences; however, they were also easily criticized for non-representative selection of their subjects. Later studies, performed on increasingly representative samples, showed much lesser concordance among MZ twins, although still significantly larger than among DZ twins.

For example, a recent meta-study by Hershberger (2001) 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. Also, Bailey, Dunne and Martin (2000) used the Australian twin registry to obtain a sample of 4,901 twins. 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%.

As a counter-example, Bearman and Bruckner (2002), analyzed data from a large longitudinal study of adolescents. They found the data did not support genetic influence:

Among twins, 6.7% are concordant . twin pairs are 7.2% concordant. Full-siblings are 5.5% concordant. Clearly, the observed concordance rates do not correspond to degrees of genetic similarity. None of the comparisons between twins and others ... are even remotely significant. If same-sex romantic attraction has a genetic component, it is massively overwhelmed by other factors.

Their conclusion is that the expression of same-sex attraction requires a social environment: "More plausible is the idea that genetic expression is activated only under strongly circumscribed social structural conditions. In contrast to other theories considered below, we assume that the close connection between gender identity and sexual identity is socially constructed."

Conclusions

Twin studies have received a number of criticisms including ascertainment bias where homosexuals with gay siblings are more likely to volunteer for studies. As all the studies show, homosexuality cannot be purely genetic, otherwise, all identical twins would have the identical sexual orientation as their twin.

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. 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". If one twin receives less testosterone and the other more, this could result in different levels of brain masculinisation.

Counter-studies such as Bearman and Bruckner (2002) are also subject to critique, because of their reliance on self-reports from adolescents (ie. between 7th and 12th grade), who have not reached sexual maturity.

Maternal linkage, birth order, and female fertility

Blanchard and Klassen (1997) reported that each older brother increases the odds of being gay by 33%. This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation." 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.

Bocklandt, Horvath, Vilain and Hamer (2006) reported that some mothers of gay babies have extreme skewing of X chromosome inactivation. Using a sample of 97 mothers of homosexual men and 103 mothers of heterosexual men, the pattern of X inactivation was ascertained from blood assays. 4% of the mothers of straight men showed extreme skewing compared to 13% of the mothers of gay men. Mothers of two or more gay babies had extreme skewing of X inactivation of 23%. This extreme skewing may influence male sexual orientation through the fraternal birth order effect.

An alternate theory was proposed by Italian researchers in 2004 supported by 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, however, would explain only 20% of the cases studied, indicating that this might not be the sole genetic factor determining sexual orientation.

Homosexuals of either sex are more likely than the general population to be non-right-handed. (See also Handedness and sexual orientation.)

Pheromones correlation

Recent research conducted in Sweden 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. The conclusion, that sexual attraction, whether same-sex or opposite-sex oriented, operates similarly on a biological level, does not mean that there is necessarily a biological cause for homosexuality. 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 this data with adult sexual orientation.

Early fixation hypothesis

Main article: Prenatal hormones and sexual orientation

The early fixation hypothesis includes research into prenatal development and the environmental factors that control masculinization of the brain. Studies have concluded that there is empirical evidence to support this hypothesis, including 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 block or exaggerate 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.

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.

One hypothesis is that something about what young children see in the gender-roles behavior of adults, or some differences (possibly unconscious) in the way adults treat young children, somehow influences or determines a child's eventual sexual orientation.

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 (EBE) theory.

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. Fourteen studies published since Bailey & Zucker's 1995 also show the same results. 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. There are very few prospective studies of gender nonconforming girls. 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.

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. The only cases Reiner found where children born with a X and Y chromosome are attracted to males as adults were those where testosterone receptors were absent, which prevented the male sex hormones from masculinizing the fetus.

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. In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure.

Early work of this type was also done by Simon LeVay - however, LeVay's assessments have not been replicated. 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.

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). 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." 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. However, he also found some contrary results:

  • Three of the 19 homosexual subjects had a larger group of neurons in the hypothalamus than the average control-group subject.
  • Three of the 16 control-group subjects had a smaller group of neurons in the hypothalamus than the average homosexual subject.

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.

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.

Conclusions

LeVay concluded in his 1991 paper that "The discovery that the nucleus differs in size between heterosexual and homosexual men illustrates that sexual orientation in humans is amenable to study at the biological level, and this discovery opens the door to studies of neurotransmitters or receptors that might be involved in regulating this aspect of personality. Further interpretation of the results of this study must be considered speculative. In particular, the results do not allow one to decide if the size of INAH 3 in an individual is the cause or consequence of that individual's sexual orientation, or if the size of INAH 3 and sexual orientation covary under the influence of some third, unidentified variable."

He later added,

"It's important to stress what I didn't find. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didn't show that gay men are born that way, the most common mistake people make in interpreting my work. Nor did I locate a gay center in the brain. ... Since I look at adult brains, we don't know if the differences I found were there at birth or if they appeared later."

In addition to this, of the men LeVay used in his studies, the sexual histories of the men he assumed to be heterosexual were unknown.

Pathogenic hypothesis of homosexuality

The pathogenic hypothesis of homosexuality, also called the 'gay germ' hypothesis, suggests that homosexuality might be caused by an infectious disease. 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 supposedly 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. Cochran also argues that the prevalence of homosexuality in urban areas suggests that an infectious disease causes homosexuality. They conclude that it is a "feasible hypothesis... no more and no less." After being unable to publish this account in a peer-reviewed journal, the idea appeared in the popular press. An American Psychological Association newsletter the following year stated "there is ultimately very little to be said in favor of these contentions", and criticised 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. . In an article in Out Magazine, brain researhcer William Byne stated "Cochran and Ewald are guilty of pathologizing homosexuality", while in the same article psychology professor 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.

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.

Those who believe that homosexuality is purely genetic argue that maladaptive traits will only be removed from a population if the trait is under simple, direct selection, if it derives from a heritable component of a genotype and if the intensity of selection is greater than other evolutionary forces like genetic drift, or inclusive fitness.

Some scholars 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).

The so-called "gay uncle" theory 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 and West Eberhard. This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.

The primary criticism of this theory has to do with the fact that children share on average 25% of their genes with their uncles and aunts, but on average 50% with their parents. This means that to be adaptive, a "gay uncle" would need to somehow assist an extra two nieces or nephews, on average, to reach adulthood for every one of their own offspring they give up. Critics of the theory find this trade-off to be unlikely to produce a net reproductive gain.

The alleged evolutionary disadvantage of homosexuality has led Amherst College biologist Paul W. Ewald to argue that it might be caused by an as-yet undetected virus working in utero that triggers hormonal responses.

Politics

The issue of genetic or other physiological determinants as the basis of sexual orientation is a highly politicised 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". 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" and/or "learn to be that way".

The perceived causes of sexual orientation have a significant bearing on the status of sexual minorities such as lesbians and gays. 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."

One prominent evangelical leader, Rev. Rob Schenck, who used to advocate conversion therapy, came to believe that homosexuality is not a choice after speaking with scientists, and that conservative Christians need to drop the choice argument in order to continue opposing homosexual sex. He was quoted in the Boston Globe as saying "if it's inevitable that this scientific evidence is coming, we have to be prepared with a loving response. If we don't have one, we won't have any credibility."

Some advocates for the rights of sexual minorities also resist the idea that sexuality is biologically determined, or fixed at birth. They point out that sexual orientation can shift over the course of one's life. Many resist any attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm. Others fear that discoveries about medical causes of sexuality may be used by doctors and parents to eradicate non-heterosexual orientations.

See also

References

  1. American Psychological Association Answers to Your Questions For a Better Understanding of Sexual Orientation & Homosexuality -

    There is no consensus among scientists about the exact reasons that an individual develops a heterosexual, bisexual, gay, or lesbian orientation. Although much research has examined the possible genetic, hormonal, developmental, social, and cultural influences on sexual orientation, no findings have emerged that permit scientists to conclude that sexual orientation is determined by any particular factor or factors. Many think that nature and nurture both play complex roles; most people experience little or no sense of choice about their sexual orientation.

  2. "Gay, Lesbian and Bisexual Issues". Association of Gay and Lesbian Psychiatrics. May 2000.

    No one knows what causes heterosexuality, homosexuality, or bisexuality.... there is a renewed interest in searching for biological etiologies for homosexuality. However, to date there are no replicated scientific studies supporting any specific biological etiology for homosexuality.

  3. Hamer, Hu, Magnuson, Hu and Pattatucci (1993) A linkage between DNA markers on the X chromosome and male sexual orientation. Science 261(5119): 321-7
  4. Hu, S., Pattatucci, A. M. L., Patterson, C., Li, L., Fulker, D. W., Cherny, S. S., Kruglyak, L., & Hamer, D. H. (1995). Linkage between sexual orientation and chromosome Xq28 in males but not in females. Nature Genetics, 11, 248–256.
  5. ^ Wilson, G.D., & Rahman, Q. (2005). Born Gay: The Biology of Sex Orientation. London: Peter Owen Publishers.
  6. Vilain, E. (2000). Genetics of Sexual Development. Annual Review of Sex Research, 11.
  7. Mustanski, B. S., Dupree, M. G., Nievergelt, C. M., Bocklandt, S., Schork, N. J., & Hamer, D. H. (2005). A genomewide scan of male sexual orientation. Human Genetics, 116, 272-278 PDF accessed 2 September 2006.
  8. ^ 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 Postprint of article
  9. ^ 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.
  10. While inconsistent with modern findings, the first relatively large-scale twin study on sexual orientation was reported by Kallman in 1952. (See Kallmann, F. J. 1952. Comparative Twin Study on the Genetic Aspects of Male Homosexuality. J. Nerv. Ment. Dis. 115:283-298). 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.)
  11. 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.
  12. cited in Wilson and Rahman 2005, p47
  13. Bailey, J.M., Dunne, M.P., Martin, N.G. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78(3)
  14. Gringas, P. and Chen, W. (2001). Mechanisms for difference in monozygous twins. Early Human Development, 64, (2), 105-117.
  15. Rutter, M. (2006). Genes and Behavior. Oxford, UK: Blackwell Publishing.
  16. ^ Blanchard and Klassen (1997). H-Y Antigen and Homosexuality in Men. Journal of Theoretical Biology, 185, 373-378.
  17. Pas de Deux of Sexuality Is Written in the Genes
  18. Blanchard, R. (1997). Birth order and sibling sex ratio in homosexual versus heterosexual males and females. Review of Sex Research, Vol. 8
  19. Camperio-Ciani et al. 2004
  20. Lalumière, M. L., Blanchard, R., & Zucker, K. J. (2000). Sexual orientation and handedness in men and women: A meta-analysis. Psychological Bulletin, 126, 575–592.
  21. Savic, Berglund, & Lindström (2005) Brain response to putative pheromones in homosexual men. PNAS, vol. 102, no. 20, 7356-7361.
  22. Wade, Nicholas. (May 9, 2005). "Gay Men Are Found to Have Different Scent of Attraction." New York Times.
  23. Bem, D. J. (1996). Exotic becomes erotic: A developmental theory of sexual orientation. Psychological Review, 103: 320-335.
  24. Bailey, J.M., and Zucker, K.J. (1995). Childhood sex-typed behavior and sexual orientation: A conceptual analysis and quantitative review. Developmental Psychology, 31(1): 43-55.
  25. Zucker, K.J. (2005) Commentary on Gottschalk’s (2003) ‘Same-sex sexuality and childhood gender non-conformity: A spurious connection’ Journal of Gender Studies, 14:55–60.
  26. Zucker, K.J. (1990) Gender identity disorders in children: clinical descriptions and natural history. p.1-23 in R. Blanchard & B.W. Steiner (eds) Clinical management of gender identity disorders in children and adults. Washington DC, American Psychiatric Press.
  27. Green, R. (1979) Childhood cross-gender behavior and subsequent sexual preference, American Journal of Psychiatry, 136, pp. 106–108.
  28. Cohen-Kettenis, P. T. (2001) Gender identity disorder in DSM? , Journal of the American Academy of Child and Adolescent Psychiatry, 40, p. 391.
  29. Cohen-Kettenis, P. T. (2001) Gender identity disorder in DSM? , Journal of the American Academy of Child and Adolescent Psychiatry, 40, p. 391. and comments reported in: Zucker, K.J. (2005) Commentary on Gottschalk’s (2003) ‘Same-sex sexuality and childhood gender non-conformity: A spurious connection’ Journal of Gender Studies, 14:55–60.
  30. Swaab DF & and Hofman, MA (1990), "An Enlarged Suprachiasmatic Nucleus in Homosexual Men", Brain Research, vol. 537, pages 141-148.
  31. Allen LS, Gorski RA (1992): Sexual orientation and the size of the anterior commissure in the human brain. Proc Natl Acad Sci USA 89:7199-­7202.
  32. ^ LeVay, S. (1991). A difference in Hypothalmic structure between heterosexual and homosexual men. Science, 253(5023): 1034-1037
  33. ^ Byne, W. et al. (2001). The Interstitial Nuclei of the Human Anterior Hypothalamus: An Investigation of Variation with Sex, Sexual Orientation, and HIV Status. Hormones and Behavior, 40: 86-92.
  34. Byrd, A. Dean, Shirley E. Cox, and Jeffrey W. Robinson (May 27, 2001), Homosexuality: The Innate-Immutability Argument Finds No Basis in Science. Salt Lake Tribune
  35. ^ Crain, C. "Did a Germ Make You Gay?" in Out Magazine, August 1999.
  36. An Evolutionary Look at Human Homosexuality Greg Cochran, original publication date unknown
  37. http://www.apaonline.org/apa/publications/newsletters/v00n1/lgbt/04.asp
  38. http://www.apaonline.org/apa/publications/newsletters/v00n1/lgbt/04.asp -

    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.

  39. ^ Crain, C. "Did a Germ Make You Gay?" in Out Magazine, August 1999 :

    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?"

  40. Mayr, E. (1982). The Growth of Biological Thought: Diversity, Evolution, and Inheritance. Cambridge: Harvard University Press. p598.
  41. The Advocate (1996, February 6). Advocate Poll Results. p. 8.
  42. Ernulf, K. E., Innala, S. M., & Whitam, F. L. (1989). Biological explanation, psychological explanation, and tolerance of homosexuals: A cross-national analysis of beliefs and attitudes. Psychological Reports, 65, 1003-1010. See also: Whitley, B. E., Jr. (1990). The relationship of heterosexuals' attributions for the causes of homosexuality to attitudes toward lesbians and gay men. Personality and Social Psychology Bulletin, 16, 369-377.

Bibliography

  • BBC (April 23, 1999). Doubt cast on 'gay gene'. BBC News.
  • Articles by Dr. Daryl Bem will be found at , including several on his EBE theory
  • William Byne (May 1994). The Biological Evidence Challenged. Scientific American, vol. 270, pp. 50-55.
  • Simon LeVay (updated at intervals) The Biology of Sexual Orientation, a literature review web page.
  • Trisha Macnair (undated). Genetics and human behaviour. BBC Health.
  • Timothy F. Murphy (Fall 2000). Now What? The Latest Theory of Homosexuality. APA Newsletter on Philosophy and Lesbian, Gay, Bisexual and Transgender Issues.
  • Muscarella, F., Fink, B., Grammer, K., & Kirk-Smith, M. (2001). Homosexual Orientation in Males: Evolutionary and Ethological Aspects. Neuroendocrinology Letters, 22(6), 393-400. Full text
  • Nuffield Council on Bioethics (2002). Genetics and human behaviour. London: Author. Chapter 10 discusses sexual orientation.
  • Out in Nature: Homosexual Behaviour in the Animal Kingdom, a documentary by Stéphane Alexandresco, Bertrand Loyer and Jessica Menendez
  • Rahman Q. (2005). The neurodevelopment of human sexual orientation. Neuroscience and Biobehavioral Reviews 29 :1057–1066.
  • Rines, J.P. & vom Saal, F.S. (1984). Fetal effects on sexual behavior and aggression in young and old female mice treated with estrogen and testosterone. Horm. Behav. 18:117-­12.
  • Rosemary C. Veniegas & Terri D. Conley (2000). Biological Research on Women's Sexual Orientations: Evaluating the Scientific Evidence. Journal of Social Issues, vol. 56, pp. 267-282.
  • Ryan, B.C. & Vandenbergh, J.G. (2002) Intrauterine position effects. Neurosci. Biobehav. Rev. 26:665--678.
  • Simon LeVay & Dean H. Hamer (May 1994). Evidence for a Biological Influence in Male Homosexuality. Scientific American, vol. 270, pp. 44-49.
  • T. J. Taylor (1992). Twin Studies of Homosexuality. Part II Experimental Psychology Dissertation (unpublished), University of Cambridge, UK.
  • vom Saal, F.S. (1989) Sexual differentiation in litter bearing animals: influence of sex of adjacent fetuses in utero. J. Anim. Sci. 67:1824-1840.
  • Vom Saal, F.S. & Bronson, F. (1980). Sexual characteristics of adult female mice are correlated with their blood testosterone levels during prenatal development. Science 208:597-599.
  • McCarty, Linda. "Wearing my identity: a transgender teacher in the classroom." Equity & Excellence in Education 36.2 (June 2003): 170-183. Expanded Academic ASAP. Gale. UC Santa Barbara. 10 Dec. 2007 .
  • Begley, Sharon. "Nature plus nurture." Newsweek 126.n20 (Nov 13, 1995): 72(1). Expanded Academic ASAP. Gale. UC Santa Barbara. 10 Dec. 2007 .
  • Jones, Steve. "Ys and wherefores." New Statesman & Society 6.n256 (June 11, 1993): 30(2). Expanded Academic ASAP. Gale. UC Santa Barbara. 10 Dec. 2007 .
Sex differences in humans
Biology
Medicine and Health
Neuroscience and Psychology
Sociology
Category: