Biology and sexual orientation

The relationship between biology and sexual orientation is a subject of research. A simple and singular determinant for sexual orientation has not been conclusively demonstrated; various studies point to different, even conflicting positions, but scientists hypothesize that a combination of genetic, hormonal, and social factors determine sexual orientation.[1][2][3]

Biological theories for explaining the causes of sexual orientation are favored by experts[1] and involve a complex interplay of genetic factors, the early uterine environment and brain structure.[4] These factors, which may be related to the development of a heterosexual, homosexual, bisexual or asexual orientation, include genes, prenatal hormones, and brain structure.

Empirical studies

Twin studies

A number of twin studies have attempted to compare the relative importance of genetics and environment in the determination of sexual orientation. In a 1991 study, Bailey and Pillard conducted a study of twins recruited from "homophile publications", and found that 52% of monozygotic (MZ) brothers (of whom 59 were questioned) and 22% of the dizygotic (DZ) twins were concordant for homosexuality.[5] 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In a study of 61 pairs of twins, researchers found among their mostly male subjects a concordance rate for homosexuality of 66% among monozygotic twins and a 30% one among dizygotic twins.[6] In 2000 Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance.[7] They found 20% concordance in the male identical or MZ twins and 24% concordance for the female identical or MZ twins. Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. Other researchers support biological causes for both men and women's sexual orientation.[8]

Bearman and Brückner (2002) criticized early studies concentrating on small, select samples[9] and non-representative selection of their subjects.[10] They studied 289 pairs of identical twins (monozygotic or from one fertilized egg) and 495 pairs of fraternal twins (dizygotic or from two fertilized eggs) and found concordance rates for same-sex attraction of only 7.7% for male identical twins and 5.3% for females, a pattern which they say "does not suggest genetic influence independent of social context."[9]

A 2010 study of all adult twins in Sweden (more than 7,600 twins)[11] 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 social 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 twins may influence the results;

Biometric modeling revealed that, in men, genetic effects explained .34–.39 of the variance [of sexual orientation], 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. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.[11]

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 attributed solely to genetic factors.[12]

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.[13] Dichorionic twins potentially have different hormonal environments because they receive maternal blood from separate placenta, and this could result in different levels of brain masculinisation. 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".[14]

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.[15] 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 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 with 6% on the paternal side.[16]

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.[17] 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.[16] One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[18] 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.[19]

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.[20] 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. 10q26 showed highly significant maternal loading, thus further supporting the previous family studies.

Results from the first large, comprehensive multi-center genetic linkage study of male sexual orientation were reported by an independent group of researchers at the American Society of Human Genetics in 2012.[21] The study population included 409 independent pairs of gay brothers, who were analyzed with over 300,000 single-nucleotide polymorphism markers. The data strongly replicated Hamer's Xq28 findings as determined by both two-point and multipoint (MERLIN) LOD score mapping. Significant linkage was also detected in the pericentromeric region of chromosome 8, overlapping with one of the regions detected in the Hamer labʻs previous genomewide study. The authors concluded that "our findings, taken in context with previous work, suggest that genetic variation in each of these regions contributes to development of the important psychological trait of male sexual orientation." Female sexual orientation does not seem to be linked to Xq28,[17][22] though it does appear moderately heritable.[23]

In addition to sex chromosomal contribution, a potential autosomal genetic contribution to the development of homosexual orientation has also been suggested. In a study population composed of more than 7000 participants, Ellis et al. (2008) found a statistically significant difference in the frequency of blood type A between homosexuals and heterosexuals. They also found that “unusually high” proportions of homosexual males and homosexual females were Rh negative in comparison to heterosexuals. As both blood type and Rh factor are genetically inherited traits controlled by alleles located on chromosome 9 and chromosome 1 respectively, the study indicates a potential link between genes on autosomes and homosexuality.[24][25]

The biology of sexual orientation has been studied in detail in several animal model systems. In the common fruit fly Drosophila melanogaster, the complete pathway of sexual differentiation of the brain and the behaviors it controls is well established in both males and females, providing a concise model of biologically controlled courtship.[26] In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology altered the sexual preferences of female mice by removing a single gene linked to reproductive behavior. Without the gene, the mice exhibited masculine sexual behavior and attraction toward urine of other female mice. Those mice who retained the gene fucose mutarotase (FucM) were attracted to male mice.[27]

In interviews to the press, researchers have pointed that the evidence of genetic influences should not be equated with genetic determinism. According to Dean Hamer and Michael Bailey, genetic aspects are only one of the multiple causes of homosexuality.[28][29]

Epigenetics studies

A 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. 13% of mothers with one gay son, and 23% of mothers with two gay sons showed extreme skewing, compared to 4% of mothers without gay sons.[30]

Birth order

Blanchard and Klassen (1997) reported that each additional older brother increases the odds of a man being gay by 33%.[31][32] This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation."[33] To explain this finding, it has been proposed that male fetuses provoke a maternal immune reaction that becomes stronger with each successive male fetus. This maternal immunization hypothesis (MIH) begins when cells from a male fetus enter the mother's circulation during pregnancy or while giving birth.[34] Male fetuses produce H-Y antigens which are "almost certainly involved in the sexual differentiation of vertebrates." These Y-linked proteins would not be recognized in the mother's immune system because she is female, causing her to develop antibodies which would travel through the placental barrier into the fetal compartment. From here, the anti-male bodies would then cross the blood/brain barrier (BBB) of the developing fetal brain, altering sex-dimorphic brain structures relative to sexual orientation, increasing the likelihood that the exposed son will be more attracted to men than women.[34] 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.[31]

However, the maternal immune hypothesis has been criticized because the prevalence of the type of immune attack proposed is rare compared with the prevalence of homosexuality.[35]

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.[36][37]

Pheromone studies

Research conducted in Sweden[38] 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 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.[39] 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.

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, Dick Swaab and Michel A. Hofman reported a difference in the size of the suprachiasmatic nucleus between homosexual and heterosexual men.[40] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure,[41] but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.[42][43][44]

Sexually dimorphic nuclei in the anterior hypothalamus

Simon LeVay, too, conducted some of these early researches. He 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 it 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.[45]

He obtained brains from 41 deceased hospital patients. The subjects were classified into three groups. The first group comprised 19 gay men who had died of AIDS-related illnesses. The second group comprised 16 men whose sexual orientation was unknown, but whom the researchers presumed to be heterosexual. Six of these men had died of AIDS-related illnesses. The third group was of six women whom the researchers presumed to be heterosexual. One of the women had died of an AIDS-related illness.[45]

The HIV-positive people in the presumably heterosexual patient groups were all identified from medical records as either intravenous drug abusers or recipients of blood transfusions. Two of the men who identified as heterosexual specifically denied ever engaging in a homosexual sex act. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been primarily or exclusively heterosexual "on the basis of the numerical preponderance of heterosexual men in the population."[45]

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 six AIDS patients were included in the heterosexual group. The size of INAH3 in the homosexual men's brains was comparable to the size of INAH3 in the heterosexual women's brains.

However, other studies have shown that the sexually dimorphic nucleus of the preoptic area, which include the INAH3, are of similar size in homosexual males who died of AIDS to heterosexual males, and therefore larger than female. This clearly contradicts the hypothesis that homosexual males have a female hypothalamus. Furthermore, the SCN of homosexual males is extremely large (both the volume and the number of neurons are twice as many as in heterosexual males). These areas of the hypothalamus have not yet been explored in homosexual females nor bisexual males nor females. Although the functional implications of such findings still haven’t been examined in detail, they cast serious doubt over the widely accepted Dörner hypothesis that homosexual males have a "female hypothalamus" and that the key mechanism of differentiating the "male brain from originally female brain" is the epigenetic influence of testosterone during prenatal development.[46][47]

William Byne and colleagues attempted to identify the size differences reported in INAH 1–4 by replicating the experiment using brain sample from other subjects: 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). The researchers found a significant difference in INAH3 size between heterosexual men and heterosexual 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.[48]

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.[48]

A 2010 study, Garcia-Falgueras and Swaab asserted that "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."[49]

Ovine model

The domestic ram is used as an experimental model to study early programming of the neural mechanisms which underlie homosexuality, developing from the observation that approximately 8% of domestic rams are sexually attracted to other rams (male-oriented) when compared to the majority of rams which are female-oriented. In many species, a prominent feature of sexual differentiation is the presence of a sexually dimorphic nucleus (SDN) in the preoptic hypothalamus, which is larger in males than in females.

Roselli et al. discovered an ovine SDN (oSDN) in the preoptic hypothalamus that is smaller in male-oriented rams than in female-oriented rams, but similar in size to the oSDN of females. Neurons of the oSDN show aromatase expression which is also smaller in male-oriented rams versus female-oriented rams, suggesting that sexual orientation is neurologically hard-wired and may be influenced by hormones. However, results failed to associate the role of neural aromatase in the sexual differentiation of brain and behavior in the sheep, due to the lack of defeminization of adult sexual partner preference or oSDN volume as a result of aromatase activity in the brain of the fetuses during the critical period. Having said this, it is more likely that oSDN morphology and homosexuality may be programmed through an androgen receptor that does not involve aromatisation. Most of the data suggests that homosexual rams, like female-oriented rams, are masculinized and defeminized with respect to mounting, receptivity, and gonadotrophin secretion, but are not defeminized for sexual partner preferences, also suggesting that such behaviors may be programmed differently. Although the exact function of the oSDN is not fully known, its volume, length, and cell number seem to correlate with sexual orientation, and a dimorphism in its volume and of cells could bias the processing cues involved in partner selection. More research is needed in order to understand the requirements and timing of the development of the oSDN and how prenatal programming effects the expression of mate choice in adulthood.[50]

Biological theories of cause 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.[51][52][53] 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.

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 psychological arousal when the child is near members of the gender which it considers as being 'different'. Bem theorizes that this psychological arousal will later be transformed into sexual arousal: children will become sexually attracted to the gender which they see as different ("exotic"). This proposal is known as the "exotic becomes erotic" theory.[54]

Bem sought support from published literature but did not present new data testing his theory.[55] Research cited by him as evidence of the "exotic becomes erotic" theory includes the study Sexual Preference by Bell et al. (1981)[55] and studies showing 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.[56] In six "prospective" studies—that is, longitudinal studies that began with gender-nonconforming boys at about age 7 and followed them up into adolescence and adulthood— 63% of the gender nonconforming boys had a homosexual or bisexual orientation as adults.[57]

Sexual orientation and evolution

General

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 (competition amongst individuals) 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.[58]

Some scholars[58] have suggested that homosexuality is indirectly adaptive, by conferring a reproductive advantage in a non-obvious way on heterosexual siblings or their children. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia when two copies are present, also confers resistance to malaria with a lesser form of anemia when one copy is present (this is called heterozygous advantage).[59]

Scholars have also pointed out that Darwin himself described Kin selection in The Origin of Species, so under a Darwinian model of evolution, not only individuals, but family groups (bloodlines) can compete for selection.

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.[60]

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." 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."[61]

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."

The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men.[36][37] As originally pointed out by Hamer,[62] even a modest increase in reproductive capacity in females carrying a "gay gene" could easily account for its maintenance at high levels in the population.[37]

Gay uncle hypothesis

The "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 (e.g. food, supervision, defense, shelter) to the offspring of their closest relatives.

This hypothesis is an extension of the theory of kin selection, which 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.[63] This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.

Vasey and VanderLaan (2010) tested the theory on the Pacific island of Samoa, where they studied women, straight men, and the fa'afafine, men who prefer other men as sexual partners and are accepted within the culture as a distinct third gender category. V&V found that the fa'afafine said they were significantly more willing to help kin, yet much less interested in helping children who aren't family — providing the first evidence to support the ‘kin selection hypothesis,'”.[64][65]

The hypothesis is consistent with other studies on homosexuality, which show that it is more prevalent amongst both siblings and twins.[64][65][66] Since both twins and sibling share genes and therefore have a higher factor of genetic redundancy, there is less genetic familial risk if the strategy is expressed. It is speculated that environmental and hormonal stress factors (linked to resource feedbacks) may act as triggers.

Since the hypothesis solves the problem of why homosexuality has not been selected out over thousands of years, despite it being antithetical to reproduction, many scientists consider it the best explanatory model for non-heterosexual behaviour such as homosexuality and bisexuality. The natural bell curve variation that occurs in biology and sociology everywhere, explains the variable spectrum of expression.

Vasal and VanderLaan (2011) provides evidence that if an adaptively designed avuncular male androphilic phenotype exists and its development is contingent on a particular social environment, then a collectivistic cultural context is insufficient, in and of itself, for the expression of such a phenotype.[67]

Biological differences in gay men and lesbian women

Physiological

Some studies have found correlations between physiology of people and their sexuality; these studies provide evidence which suggests that:

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".[95] 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".[96][97]

Equal protection analysis in U.S. law determines when government requirements create a “suspect classification" of groups 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.[98][99][100]

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." On the other hand, some social conservatives such as Reverend Robert Schenck have argued that people can accept any scientific evidence while still morally opposing homosexuality.[101] 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."[102]

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.[103] 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.[101] Chandler Burr 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."[104] 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."[101]

See also

Notes

  1. 1 2 Frankowski BL; American Academy of Pediatrics Committee on Adolescence (June 2004). "Sexual orientation and adolescents". Pediatrics. 113 (6): 1827–32. PMID 15173519. doi:10.1542/peds.113.6.1827.
  2. ↑ Mary Ann Lamanna, Agnes Riedmann, Susan D Stewart (2014). Marriages, Families, and Relationships: Making Choices in a Diverse Society. Cengage Learning. p. 82. ISBN 1305176898. Retrieved February 11, 2016. The reason some individuals develop a gay sexual identity has not been definitively established  – nor do we yet understand the development of heterosexuality. The American Psychological Association (APA) takes the position that a variety of factors impact a person's sexuality. The most recent literature from the APA says that sexual orientation is not a choice that can be changed at will, and that sexual orientation is most likely the result of a complex interaction of environmental, cognitive and biological factors...is shaped at an early age...[and evidence suggests] biological, including genetic or inborn hormonal factors, play a significant role in a person's sexuality (American Psychological Association 2010).
  3. ↑ Gail Wiscarz Stuart (2014). Principles and Practice of Psychiatric Nursing. Elsevier Health Sciences. p. 502. ISBN 032329412X. Retrieved February 11, 2016. No conclusive evidence supports any one specific cause of homosexuality; however, most researchers agree that biological and social factors influence the development of sexual orientation.
  4. ↑ "Submission to the Church of England’s Listening Exercise on Human Sexuality". The Royal College of Psychiatrists. Retrieved 13 June 2013.
  5. ↑ Bailey JM, Pillard, RC (1991). "A Genetic Study of Male Sexual Orientation". Archives of General Psychiatry. 48 (12): 1089–96. PMID 1845227. doi:10.1001/archpsyc.1991.01810360053008.
  6. ↑ Whitam FL; et al. (1993). "Homosexual orientation in twins: a report on 61 pairs and three triplet sets.". Arch Sex Behav. 22 (3): 187–206. doi:10.1007/bf01541765.
  7. ↑ Bailey JM, Dunne MP, Martin NG (March 2000). "Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample". J Pers Soc Psychol. 78 (3): 524–36. PMID 10743878. doi:10.1037/0022-3514.78.3.524.
  8. ↑ 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.
  9. 1 2 Bearman P. S.; Bruckner H. (2002). "Opposite-sex twins and adolescent same-sex attraction". American Journal of Sociology. 107 (5): 1179–1205. doi:10.1086/341906. Archived from the original on 2011-07-19.
  10. ↑ 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 criticized 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. 1 2 Långström N, Rahman Q, Carlström E, Lichtenstein P (February 2010). "Genetic and environmental effects on same-sex sexual behavior: a population study of twins in Sweden". Arch Sex Behav. 39 (1): 75–80. PMID 18536986. doi:10.1007/s10508-008-9386-1.
  12. ↑ Schacter, Daniel L., Gilbert, Daniel T., and Wegner, Daniel M. (2009) "Psychology". Worth Publishers: 435.
  13. ↑ Gringas, P.; Chen, W. (2001). "Mechanisms for difference in monozygous twins". Early Human Development. 64 (2): 105–117. PMID 11440823. doi:10.1016/S0378-3782(01)00171-2.
  14. ↑ Rutter, M. (2006). Genes and Behavior. Oxford, UK: Blackwell Publishing.
  15. ↑ 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. PMID 8332896. doi:10.1126/science.8332896.
  16. 1 2 Wilson, G.D., & Rahman, Q. (2005). Born Gay: The Biology of Sex Orientation. London: Peter Owen Publishers.
  17. 1 2 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. PMID 7581447. doi:10.1038/ng1195-248.
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References

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