Biology and sexual orientation
The relationship between biology and sexual orientation is a subject of research. While scientists do not know the exact cause of sexual orientation, they theorize that it is caused by a complex interplay of genetic, hormonal, and environmental influences.[1][2][3] Hypotheses for the impact of the post-natal social environment on sexual orientation, however, are weak, especially for males.[4]
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Biological theories for explaining the causes of sexual orientation are favored by scientists.[1] These factors, which may be related to the development of a sexual orientation, include genes, the early uterine environment (such as prenatal hormones), and brain structure.
Empirical studies
Genetic influences
Multiple genes have been found to play a role in sexual orientation. Scientists caution that many people misconstrue the meanings of genetic and environmental.[4] Environmental influence does not automatically imply that the social environment influences or contributes to the development of sexual orientation. Hypotheses for the impact of the post-natal social environment on sexual orientation are weak, especially for males.[4] There is, however, a vast non-social environment that is non-genetic yet still biological, such as prenatal development, that likely helps shape sexual orientation.[4]:76
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 male 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]
A 2008 study of all adult twins in Sweden (more than 7,600 twins)[9] found that same-sex behaviour was explained by both heritable genetic factors and unique environmental factors (which can include the prenatal environment during gestation, exposure to illness in early life, peer groups not shared with a twin, etc), although a twin study cannot identify which factor is at play. Influences of the shared environment (influences including the family environment, rearing, shared peer groups, culture and societal views, and sharing the same school and community) had no effect for men, and a weak effect for women. This is consistent with the common finding that parenting and culture appears to play no role in male sexual orientation, but may play some small role in women. The study concludes that genetic influences on any lifetime same-sex partner were stronger for men than women, and that "it has been suggested individual differences in heterosexual and homosexual behavior result from unique environmental factors such as prenatal exposure to sex hormones, progressive maternal immunization to sex-specific proteins, or neurodevelopmental factors", although does not rule out other variables. 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.[9]
Chromosome linkage studies
Chromosome | Location | Associated genes | Sex | Study1 | Origin | Note |
---|---|---|---|---|---|---|
X chromosome | Xq28 | male only | Hamer et al. 1993 | genetic | ||
Chromosome 1 | 1p36 | both sexes | Ellis et al. 2008 | potential genetic linkage2 | ||
Chromosome 4 | 4p14 | female only | Ganna et al. 2019 | |||
Chromosome 7 | 7q31 | both sexes | Ganna et al. 2019 | [10][11] | ||
Chromosome 8 | 8p12 | Unknown | male only | Mustanski et al. 2005 | ||
Chromosome 9 | 9q34 | ABO | both sexes | Ellis et al. 2008 | potential genetic linkage2 | |
Chromosome 11 | 11q12 | OR51A7 (speculative) | male only | Ganna et al. 2019 | Olfactory system in mating preferences[10][11] | |
Chromosome 12 | 12q21 | both sexes | Ganna et al. 2019 | [10][11] | ||
Chromosome 13 | 13q31 | SLITRK6 | male only | Sanders et al. 2017 | Diencephalon-associated gene | |
Chromosome 14 | 14q31 | TSHR | male only | Sanders et al. 2017 | ||
Chromosome 15 | 15q21 | TCF12 | male only | Ganna et al. 2019 |
2Not believed to be causal.
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 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.[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] 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] 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.[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. In the full sample they did not find linkage to Xq28.[17]
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.[18] 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 lab's 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,[14][19] though it does appear moderately heritable.[20]
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.[21][22]
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.[23] In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred a female mice specifically lacking a particular gene related to sexual 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.[24]
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.[25][26]
In 2017, Scientific Reports published an article with a genome wide association study on male sexual orientation. The research consisted of 1,077 homosexual men and 1,231 heterosexual men. A gene named SLITRK6 on chromosome 13 was identified.[27] The research supports another study which had been done by the neuroscientist Simon LeVay. LeVay's research suggested that the hypothalamus of gay men is different from straight men.[28] The SLITRK6 is active in the mid-brain where the hypothalamus is. The researchers found that the thyroid stimulating hormone receptor (TSHR) on chromosome 14 shows sequence differences between gay and straight men.[27] Graves' disease is associated with TSHR abnormalities, with previous research indicating that Graves' disease is more common in gay men than in straight men.[29] Research indicated that gay people have lower body weight than straight people. It had been suggested that the overactive TSHR hormone lowered body weight in gay people, though this remains unproven.[30][31]
In 2018, Ganna et al. performed another genome wide association study on sexual orientation of men and women with data from 26,890 people who had at least one same-sex partner and 450,939 controls. The data in the study was meta-analyzed and obtained from the UK Biobank study and 23andMe. The researchers identified four variants more common in people who reported at least one same-sex experience on chromosomes 7, 11, 12, and 15. The variants on chromosomes 11 and 15 were specific to men, with the variant on chromosome 11 located in an olfactory gene and the variant on chromosome 15 having previously been linked to male-pattern baldness. The four variants were also correlated with mood and mental health disorders; major depressive disorder and schizophrenia in men and women, and bipolar disorder in women. However, none of the four variants could reliably predict sexual orientation.[32]
In August 2019, a genome-wide association study of 493,001 individuals concluded that hundreds or thousands of genetic variants underlie homosexual behavior in both sexes, with 5 variants in particular being significantly associated. Some of these variants had sex-specific effects, and two of these variants suggested links to biological pathways that involve sex hormone regulation and olfaction. All the variants together captured between 8 and 25% of the variation in individual differences in homosexual behavior. These genes partly overlap with those for several other traits, including openness to experience and risk-taking behavior. Additional analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced by a similar set of genetic variants. They also found that the genetic effects that differentiate heterosexual from homosexual behavior are not the same as those that differ among nonheterosexuals with lower versus higher proportions of same-sex partners, which suggests that there is no single continuum from heterosexual to homosexual preference, as suggested by the Kinsey scale.[33]
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.[34]
Birth order
Blanchard and Klassen (1997) reported that each additional older brother increases the odds of a man being gay by 33%.[35][36] This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation".[37] 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.[38] 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.[38] 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 masculinization.[35]
In 2017, researchers discovered a biological mechanism of gay people who tend to have older brothers. They think Neuroligin 4 Y-linked protein is responsible for a later son being gay. They found that women had significantly higher anti-NLGN4Y levels than men. In addition, mothers of gay sons, particularly those with older brothers, had significantly higher anti-NLGN4Y levels than did the control samples of women, including mothers of heterosexual sons. The results suggest an association between a maternal immune response to NLGN4Y and subsequent sexual orientation in male offspring.[39]
The fraternal birth order effect, however, does not apply to instances where a firstborn is homosexual.[40][41]
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.[42][43]
Pheromone studies
Research conducted in Sweden[44] 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.[45] 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.[46] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure,[47] but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.[48][49][50]
Research on the physiologic differences between male and female brains are based on the idea that people have male or a female brain, and this mirrors the behavioral differences between the two sexes. Some researchers state that solid scientific support for this is lacking. Although consistent differences have been identified, including the size of the brain and of specific brain regions, male and female brains are very similar.[51][52]
Sexually dimorphic nuclei in the anterior hypothalamus
LeVay also 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.[53]
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.[53]
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".[53]
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.
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.[54]
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.[54]
LeVay has said that Byne replicated his work, but that he employed a two-tailed statistical analysis, which is typically reserved for when no previous findings had employed the difference. LeVay has said that "given that my study had already reported a INAH3 to be smaller in gay men, a one tailed approach would have been more appropriate, and it would have yielded a significant difference [between heterosexual and homosexual men]".[55]:110
J. Michael Bailey has criticized LeVay's critics – describing the claim that the INAH-3 difference could be attributable to AIDS as "aggravating", since the "INAH-3 did not differ between the brains of straight men who died of AIDS and those who did not have the disease".[56]:120 Bailey has further criticized the second objection that was raised, that being gay might have somehow caused the difference in INAH-3, and not vice-versa, saying "the problem with this idea is that the hypothalamus appears to develop early. Not a single expert I have ever asked about LeVay’s study thought it was plausible that sexual behavior caused the INAH-3 differences."[56]:120
The SCN of homosexual males has been demonstrated to be larger (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.[57]
A 2010 study by Garcia-Falgueras and Swaab stated 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."[58]
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.[59]
Boys who were surgically reassigned female
Between the 1960s and 2000, many newborn and infant boys were surgically reassigned as females if they were born with malformed penises, or if they lost their penises in accidents.[4]:72–73 Many surgeons believed such males would be happier being socially and surgically reassigned female. In all seven published cases that have provided sexual orientation information, the subjects grew up to be attracted to females. Six cases were exclusively attracted to females, with one case 'predominantly' attracted to females. In a review article in the journal Psychological Science in the Public Interest, six researchers including J. Michael Bailey state this establishes a strong case that male sexual orientation is partly established before birth:
"This is the result we would expect if male sexual orientation were entirely due to nature, and it is opposite of the result expected if it were due to nurture, in which case we would expect that none of these individuals would be predominantly attracted to women. They show how difficult it is to derail the development of male sexual orientation by psychosocial means."
They further argue that this raises questions about the significance of the social environment on sexual orientation, stating, "If one cannot reliably make a male human become attracted to other males by cutting off his penis in infancy and rearing him as a girl, then what other psychosocial intervention could plausibly have that effect?" It is further stated that neither cloacal exstrophy (resulting in a malformed penis), nor surgical accidents, are associated with abnormalities of prenatal androgens, thus, the brains of these individuals were male-organized at birth. Six of the seven identified as heterosexual males at follow up, despite being surgically altered and reared as females, with researchers adding: "available evidence indicates that in such instances, parents are deeply committed to raising these children as girls and in as gender-typical a manner as possible." Bailey et al. describe these sex reassignments as 'the near-perfect quasi-experiment' in measuring the impact of 'nature' versus 'nurture' with regards to male homosexuality.[4]
Childhood gender nonconformity
Studies frequently find 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.[60] 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.[61]
Biological theories of cause of sexual orientation
Prenatal brain development
The prenatal brain development hypothesis involves research into biological factors that control masculinization of the developing brain. Some studies have seen pre-natal hormone exposures as the primary factor involved in determining sexual orientation.[62][63][64] 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 connected to the well-measured effect of fraternal birth order on 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 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.[65] Wetherell et al. state that Bem "does not intend his model as an absolute prescription for all individuals, but rather as a modal or average explanation."[66]
Two critiques of Bem's theory in the journal Psychological Review concluded that "studies cited by Bem and additional research show that [the] Exotic Becomes Erotic theory is not supported by scientific evidence."[67] Bem was criticized for relying on a non-random sample of gay men from the 1970s (rather than collecting new data) and for drawing conclusions that appear to contradict the original data. An "examination of the original data showed virtually all respondents were familiar with children of both sexes", and that only 9% of gay men said that "none or only a few" of their friends were male, and most gay men (74%) reported having "an especially close friend of the same sex" during grade school.[67] Further, "71% of gay men reported feeling different from other boys, but so did 38% of heterosexual men. The difference for gay men is larger, but still indicates that feeling different from same-sex peers was common for heterosexual men." Bem also acknowledged that gay men were more likely to have older brothers (the fraternal birth order effect), which appeared to contradict an unfamiliarity with males. Bem cited cross-cultural studies which also "appear to contradict the EBE theory assertion", such as the Sambia tribe in Papua New Guinea, which ritually enforced homosexual acts among teenagers; yet once these boys reached adulthood, only a small proportion of men continued to engage in homosexual behaviour - similar to levels observed in the United States.[67] Additionally, Bem's model could be interpreted as implying that if one could change a child's behavior, one could change their sexual orientation, but most psychologists doubt this would be possible.[68]
Neuroscientist Simon LeVay said that while Bem's theory was arranged in a "believable temporal order",[55]:65 that it ultimately "lacks empirical support".[55]:164 Social psychologist Justin LehMiller stated that "Bem's theory has received a lot of praise for the way it seamlessly links biological and environmental influences" and that there "is also some support for the model in the sense that childhood gender nonconformity is indeed one of the strongest predicators of adult homosexuality", but that the validity of the model "has been questioned on numerous grounds and scientists have largely rejected it."[68]
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.[69]
Some scholars[69] have suggested that homosexuality is indirectly adaptive, by conferring a reproductive advantage in a non-obvious way on heterosexual siblings or their children, a hypothesised instance of kin selection. 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).[70]
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.[71]
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".[72] 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. The study acknowledges 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".[72]
The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men.[42][43] As originally pointed out by Hamer,[73] 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.[43]
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.[74]
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.[75] 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. Vasey and VanderLaan 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.[76][77]
The hypothesis is consistent with other studies on homosexuality, which show that it is more prevalent amongst both siblings and twins.[76][77]
Vasey 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.[78]
Biological differences in gay men and lesbian women
Anatomical
Some studies have found correlations between physiology of people and their sexuality; these studies provide evidence which suggests that:
- 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.[79]
- The suprachiasmatic nucleus of the hypothalamus was found by Swaab and Hopffman to be larger in gay men than in non-gay men,[80] the suprachiasmatic nucleus is also known to be larger in men than in women.[81][82]
- Gay men report, on average, slightly longer and thicker penises than non-gay men.[83]
- 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.[53]
- The anterior commissure is larger in women than men and was reported to be larger in gay men than in non-gay men,[47] but a subsequent study found no such difference.[84]
- 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).[85]
- The startle response (eyeblink following a loud sound) is similarly masculinized in lesbians and bisexual women.[86]
- 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).[44][87][88]
- The amygdala, a region of the brain, is more active in gay men than non-gay men when exposed to sexually arousing material.[89]
- Finger length ratios between the index and ring fingers have been reported to differ, on average, between non-gay and lesbian women.[90][91][92][93][94][95][96][97][98][99]
- Gay men and lesbians are significantly more likely to be left-handed or ambidextrous than non-gay men and women;[100][101][102] Simon LeVay argues that because "[h]and preference is observable before birth...[103] [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.[53]
- A study of over 50 gay men found that about 23% had counterclockwise hair whorl, as opposed to 8% in the general population. This may correlate with left-handedness.[104]
- Gay men have increased ridge density in the fingerprints on their left thumbs and little fingers.[104]
- Length of limbs and hands of gay men is smaller compared to height than the general population, but only among white men.[104]
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".[105] 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".[106][107]
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.[108]
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.[109][110][111]
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.[112] 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."[113]
Some advocates for the rights of sexual minorities resist what they perceive as attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm.[112] The journalist 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."[114] 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".[112]
See also
Notes
- 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.
- Mary Ann Lamanna; Agnes Riedmann; Susan D Stewart (2014). Marriages, Families, and Relationships: Making Choices in a Diverse Society. Cengage Learning. p. 82. ISBN 978-1305176898. 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).
- Gail Wiscarz Stuart (2014). Principles and Practice of Psychiatric Nursing. Elsevier Health Sciences. p. 502. ISBN 978-0323294126. 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.
- Bailey JM, Vasey PL, Diamond LM, Breedlove SM, Vilain E, Epprecht M (2016). "Sexual Orientation, Controversy, and Science". Psychological Science in the Public Interest. 17 (21): 45–101. doi:10.1177/1529100616637616. PMID 27113562.
- Bailey JM, Pillard, RC (1991). "A Genetic Study of Male Sexual Orientation". Archives of General Psychiatry. 48 (12): 1089–96. doi:10.1001/archpsyc.1991.01810360053008. PMID 1845227.
- 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. PMID 8494487.
- 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. CiteSeerX 10.1.1.519.4486. doi:10.1037/0022-3514.78.3.524. PMID 10743878.
- 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.
- 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. doi:10.1007/s10508-008-9386-1. PMID 18536986.
- PriceOct. 20, Michael; 2018; Pm, 10:25 (2018-10-19). "Giant study links DNA variants to same-sex behavior". Science | AAAS. Retrieved 2019-08-04.CS1 maint: numeric names: authors list (link)
- Saey, Tina Hesman (2018-10-31). "These DNA differences may be linked to having same-sex partners". Science News. Retrieved 2019-08-04.
- 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.
- Wilson, Glenn; Rahman, Qazi (2008). Born Gay: The Psychobiology of Sex Orientation (2nd ed.). Peter Owen Publishers. ISBN 9780720613094.
- 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. (Submitted manuscript). 11 (3): 248–56. doi:10.1038/ng1195-248. PMID 7581447.
- Vilain E (2000). "Genetics of sexual development". Annu Rev Sex Res. 11: 1–25. PMID 11351829.
- Hamer DH; Rice G; Risch N; Ebers G (1999). "Genetics and Male Sexual Orientation". Science. 285 (5429): 803. doi:10.1126/science.285.5429.803a.
- Mustanski BS, Dupree MG, Nievergelt CM, Bocklandt S, Schork NJ, Hamer DH (March 2005). "A genomewide scan of male sexual orientation" (PDF). Hum. Genet. 116 (4): 272–8. doi:10.1007/s00439-004-1241-4. PMID 15645181. Archived from the original (PDF) on 2005-04-15.
- Sanders AR, Martin ER, Beecham GW, Guo S, Dawood K, Rieger G, Badner JA, Gershon ES, Krishnappa RS, Kolundzija AB, Duan J, Gejman PV, Bailey JM (November 2014). "Genome-wide scan demonstrates significant linkage for male sexual orientation". Psychological Medicine. 45 (7): 1379–88. doi:10.1017/S0033291714002451. PMID 25399360.
- Ngun TC; Vilain E (2014). The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics? (PDF). Advances in Genetics. 86. pp. 167–84. doi:10.1016/B978-0-12-800222-3.00008-5. ISBN 9780128002223. ISSN 0065-2660. PMID 25172350. Archived from the original (PDF) on 2016-03-31. Retrieved 20 March 2016.
- Sanders AR; Martin ER; Beecham GW; Guo S; Dawood K; Rieger G; Badner JA; Gershon ES; Krishnappa RS; Kolundzija AB; Duan J; Gejman PV; Bailey JM (2014). "Genome-wide scan demonstrates significant linkage for male sexual orientation". Psychol Med. 45 (7): 1379–88. doi:10.1017/S0033291714002451. PMID 25399360.
- Ellis L; Ficek C; Burke D; Das S (2008). "Eye Color, Hair Color, Blood Type, and the Rhesus Factor: Exploring Possible Genetic Links to Sexual Orientation". Arch. Sex. Behav. 37 (1): 145–9. doi:10.1007/s10508-007-9274-0. ISSN 1573-2800. PMID 18074215.
- Aldo Poiani (2010). Animal Homosexuality: A Biosocial Perspective. Cambridge University Press. pp. 55–96. ISBN 978-1139490382.
- Pavlou HJ, Goodwin SF (February 2013). "Courtship behavior in Drosophila melanogaster: towards a 'courtship connectome'". Current Opinion in Neurobiology. 23 (1): 76–83. doi:10.1016/j.conb.2012.09.002. PMC 3563961. PMID 23021897.
- Park, D; Choi, D; Lee, J; Lim, DS; Park, C (2010). "Male-like sexual behavior of female mouse lacking fucose mutarotase". BMC Genetics. 11: 62. doi:10.1186/1471-2156-11-62. PMC 2912782. PMID 20609214.
- Connor, Steve (31 October 1995). "The 'gay gene' is back on the scene". The Independent.
- Knapton, Sarah (13 February 2014). "Being homosexual is only partly due to gay gene, research finds". The Telegraph. Telegraph Media Group.
- Sanders, Alan R.; Beecham, Gary W.; Guo, Shengru; Dawood, Khytam; Rieger, Gerulf; Badner, Judith A.; Gershon, Elliot S.; Krishnappa, Ritesha S.; Kolundzija, Alana B.; Duan, Jubao; Gejman, Pablo V.; Bailey, J. Michael; Martin, Eden R. (December 2017). "Genome-Wide Association Study of Male Sexual Orientation". Scientific Reports. 7 (1): 16950. doi:10.1038/s41598-017-15736-4. ISSN 2045-2322. PMC 5721098. PMID 29217827.
- LeVay, S. (30 August 1991). "A difference in hypothalamic structure between heterosexual and homosexual men". Science. 253 (5023): 1034–1037. doi:10.1126/science.1887219. ISSN 0036-8075. PMID 1887219.
- Frisch, Morten; Nielsen, Nete Munk; Pedersen, Bo Vestergaard (2013). "Same-sex marriage, autoimmune thyroid gland dysfunction and other autoimmune diseases in Denmark 1989-2008". European Journal of Epidemiology. 29 (1): 63–71. doi:10.1007/s10654-013-9869-9. ISSN 1573-7284. PMID 24306355.
- Deputy, Nicholas P; Boehmer, Ulrike (1 August 2010). "Determinants of body weight among men of different sexual orientation". Preventive Medicine. 51 (2): 129–131. doi:10.1016/j.ypmed.2010.05.010. ISSN 0091-7435. PMID 20510272.
- Blanchard, Ray; Bogaert, Anthony F. (December 1996). "Biodemographic comparisons of homosexual and heterosexual men in the kinsey interview data". Archives of Sexual Behavior. 25 (6): 551–579. doi:10.1007/BF02437839. PMID 8931880.
- Price, Michael (2018-10-19). "Giant study links DNA variants to same-sex behavior". Science | AAAS. Retrieved 2019-01-21.
-
- Zietsch, Brendan P.; Neale, Benjamin M.; Perry, John R. B.; Sanders, Alan R.; Martin, Eden R.; Beecham, Gary W.; Harris, Kathleen Mullan; Auton, Adam; Långström, Niklas; Lundström, Sebastian; Lichtenstein, Paul; Team16, Paul; Sathirapongsasuti, J. Fah; Guo, Shengru; Abdellaoui, Abdel; Busch, Alexander S.; Wedow, Robbee; Maier, Robert; Nivard, Michel G.; Verweij, Karin J. H.; Ganna, Andrea (30 August 2019). "Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior". Science. 365 (6456): eaat7693. doi:10.1126/science.aat7693. ISSN 0036-8075. PMC 7082777. PMID 31467194.
- "Genetics of Sexual Behavior". Genetics of Sexual Behavior. geneticsexbehavior.info. 28 February 2018. Retrieved 30 August 2019.
- Bocklandt S, Horvath S, Vilain E, Hamer DH (February 2006). "Extreme skewing of X chromosome inactivation in mothers of homosexual men". Hum. Genet. 118 (6): 691–4. CiteSeerX 10.1.1.533.4517. doi:10.1007/s00439-005-0119-4. PMID 16369763. Archived from the original on 2007-06-09. Retrieved 2008-05-28.
- Blanchard R, Klassen P (April 1997). "H-Y antigen and homosexuality in men" (PDF). J. Theor. Biol. 185 (3): 373–8. CiteSeerX 10.1.1.602.8423. doi:10.1006/jtbi.1996.0315. PMID 9156085. Archived from the original (PDF) on 2012-09-15. Retrieved 2017-11-01.
- Wade, Nicholas (10 April 2007). "Pas de Deux of Sexuality Is Written in the Genes". The New York Times.
- Blanchard R (1997). "Birth order and sibling sex ratio in homosexual versus heterosexual males and females". Annu Rev Sex Res. 8: 27–67. PMID 10051890.
- Anthony F. Bogaert & Malvina Skorska (April 2011). "Sexual orientation, fraternal birth order, and the maternal immune hypothesis: a review". Frontiers in Neuroendocrinology. 32 (2): 247–254. doi:10.1016/j.yfrne.2011.02.004. PMID 21315103.
- Bogaert, Anthony F.; Skorska, Malvina N.; Wang, Chao; Gabrie, José; MacNeil, Adam J.; Hoffarth, Mark R.; VanderLaan, Doug P.; Zucker, Kenneth J.; Blanchard, Ray (9 January 2018). "Male homosexuality and maternal immune responsivity to the Y-linked protein NLGN4Y". Proceedings of the National Academy of Sciences. 115 (2): 302–306. doi:10.1073/pnas.1705895114. ISSN 0027-8424. PMC 5777026. PMID 29229842.
- Cantor, Blanchard, Paterson, & Bogaert, 2002; Blanchard & Bogaert, 2004
- Blanchard, 2011; Rieger et al., 2012
- Camperio-Ciani A, Corna F, Capiluppi C (November 2004). "Evidence for maternally inherited factors favouring male homosexuality and promoting female fecundity". Proc. Biol. Sci. 271 (1554): 2217–21. doi:10.1098/rspb.2004.2872. PMC 1691850. PMID 15539346.
- A. Camperio Ciani; P. Cermelli; G. Zanzotto (2008). "Sexually Antagonistic Selection in Human Male Homosexuality". PLOS ONE. 3 (6): e2282. doi:10.1371/journal.pone.0002282. PMC 2427196. PMID 18560521.
- Savic I, Berglund H, Lindström P (May 2005). "Brain response to putative pheromones in homosexual men". Proc. Natl. Acad. Sci. U.S.A. 102 (20): 7356–61. doi:10.1073/pnas.0407998102. PMC 1129091. PMID 15883379.
- Wade, Nicholas. (May 9, 2005). "Gay Men Are Found to Have Different Scent of Attraction." New York Times.
- Swaab DF, Hofman MA (December 1990). "An enlarged suprachiasmatic nucleus in homosexual men" (PDF). Brain Res. 537 (1–2): 141–8. doi:10.1016/0006-8993(90)90350-K. PMID 2085769.
- Allen, L. S.; Gorski, R. A. (1992). "Sexual orientation and the size of the anterior commissure in the human brain". Proceedings of the National Academy of Sciences. 89 (15): 7199–7202. doi:10.1073/pnas.89.15.7199. ISSN 0027-8424. PMC 49673. PMID 1496013.
- Byne W.; Parsons B. (1993). "Human sexual orientation: The biological theories reappraised". Archives of General Psychiatry. 50 (3): 228–239. doi:10.1001/archpsyc.1993.01820150078009. PMID 8439245.
- Byne William; Tobet Stuart; Mattiace Linda A.; Lasco Mitchell S.; Kemether Eileen; Edgar Mark A.; Morgello Susan; Buchsbaum Monte S.; Jones Liesl B. (2001). "The Interstitial Nuclei of the Human Anterior Hypothalamus: An Investigation of Variation with Sex, Sexual Orientation, and HIV Status". Hormones and Behavior. 40 (2): 86–92. doi:10.1006/hbeh.2001.1680. PMID 11534967. S2CID 3175414.
- Lasco MS, Jordan TJ, Edgar MA, Petito CK, Byne W (May 2002). "A lack of dimorphism of sex or sexual orientation in the human anterior commissure". Brain Res. 936 (1–2): 95–8. doi:10.1016/s0006-8993(02)02590-8. PMID 11988236.
- Cahill, 2006; Lenroot and Giedd, 2010; McCarthy et al., 2009; Sakuma, 2009
- Berenbaum and Beltz, 2016.
- LeVay, Simon (1991). "A difference in hypothalamic structure between heterosexual and homosexual men". Science. 253 (5023): 1034–1037. doi:10.1126/science.1887219. ISSN 0036-8075. PMID 1887219.
- Byne W, Tobet S, Mattiace LA, et al. (September 2001). "The interstitial nuclei of the human anterior hypothalamus: an investigation of variation with sex, sexual orientation, and HIV status". Horm Behav. 40 (2): 86–92. doi:10.1006/hbeh.2001.1680. PMID 11534967. S2CID 3175414.
- LeVay, Simon (2016-08-01). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press. ISBN 978-0-19-029738-1.
- Bailey, J. (2003-03-10). The Man Who Would Be Queen. ISBN 978-0-309-08418-5.
- Swaab, D. F.; Gooren, L. J.; Hofman, M. A. (1992). "Gender and sexual orientation in relation to hypothalamic structures". Horm Res (Submitted manuscript). 38 Suppl 2 (2): 51–61. doi:10.1159/000182597. hdl:20.500.11755/7cb8b769-4329-407a-b0ee-13e011017f68. PMID 1292983.
- Garcia-Falgueras A, Swaab DF (2010). Sexual Hormones and the Brain: An Essential Alliance for Sexual Identity and Sexual Orientation. Endocr Dev. Endocrine Development. 17. pp. 22–35. doi:10.1159/000262525. ISBN 978-3-8055-9302-1. PMID 19955753.
- C. E. Roselli & F. Stormshak (March 2009). "Prenatal programming of sexual partner preference: the ram model". Journal of Neuroendocrinology. 21 (4): 359–364. doi:10.1111/j.1365-2826.2009.01828.x. PMC 2668810. PMID 19207819.
- Bailey, J.M.; Zucker, K.J. (1995). "Childhood sex-typed behavior and sexual orientation: A conceptual analysis and quantitative review" (PDF). Developmental Psychology. 31 (1): 43–55. doi:10.1037/0012-1649.31.1.43.
- 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.
- Garcia-Falgueras, Alicia, & Swaab, Dick F., Sexual Hormones and the Brain: An Essential Alliance for Sexual Identity and Sexual Orientation, in Endocrine Development, vol. 17, pp. 22–35 (2010) (ISSN 1421-7082) (authors are of Netherlands Institute for Neuroscience, of Royal Netherlands Academy of Arts and Sciences) (author contact is 2d author) (vol. 17 is Sandro Loche, Marco Cappa, Lucia Ghizzoni, Mohamad Maghnie, & Martin O. Savage, eds., Pediatric Neuroendocrinology).
- Wilson, G.D. & Rahman, Q (2005) Born Gay: The Psychobiology of Sex Orientation, Peter Owen, London
- Brodie HK, Gartrell N, Doering C, Rhue T (January 1974). "Plasma testosterone levels in heterosexual and homosexual men". Am J Psychiatry. 131 (1): 82–3. doi:10.1176/ajp.131.1.82. PMID 4808435.
- Bem DJ, Herdt G, McClintock M (December 2000). "Exotic becomes erotic: interpreting the biological correlates of sexual orientation" (PDF). Arch Sex Behav. 29 (6): 531–48. doi:10.1023/A:1002050303320. PMID 11100261. PDF Archived 2007-04-11 at the Wayback Machine
- Wetherell, Margaret; Talpade Mohanty, Chandra (2010). The SAGE Handbook of Identities. Sage Publications. p. 177. ISBN 1446248372.
- Peplau, Letitia A.; Garnets, Linda D.; Spalding, Leah R; Conley, Terri D.; Veniegas, Rosemary C. (May 1998). "A Critique of Bern's "Exotic Becomes Erotic" Theory of Sexual Orientation" (PDF). Psychological Review. 105 (2): 387–394. doi:10.1037/0033-295X.105.2.387. PMID 9577243 – via PubMed.
- Lehmiller, Justin J. (2017-12-26). The Psychology of Human Sexuality. John Wiley & Sons. pp. 156–157. ISBN 978-1-119-16471-5.
- MacIntyre F, Estep KW (1993). "Sperm competition and the persistence of genes for male homosexuality". BioSystems. 31 (2–3): 223–33. doi:10.1016/0303-2647(93)90051-D. PMID 8155854.
- Baker, Robin (1996) Sperm Wars: The Science of Sex, p.241 ff.
- "Gender bending". The Economist. 2008-10-23.
- Zietsch, B.; Morley, K.; Shekar, S.; Verweij, K.; Keller, M.; Macgregor, S.; et al. (November 2008). "Genetic factors predisposing to homosexuality may increase mating success in heterosexuals". Evolution and Human Behavior. 29 (6): 424–433. doi:10.1016/j.evolhumbehav.2008.07.002.
- Hamer, D., Copeland, P. The Science of Desire: The Search for the Gay Gene and the Biology of Behavior (Simon and Schuster, 1994) ISBN 0-684-80446-8
- February 2010, Clara Moskowitz 11. "How Gay Uncles Pass Down Genes". livescience.com. Retrieved 22 July 2020.
- Mayr, E. (1982). The Growth of Biological Thought: Diversity, Evolution, and Inheritance. Cambridge: Harvard University Press. p 598.
- "The development and evolution of male androphilia in Samoan fa'afafine". 2011.
- "Study Supports Gay Super Uncles Theory". 2010-02-05.
- Vasey, Paul L; Vanderlaan, Doug P (2011). "Sexual Orientation in Men and Avuncularity in Japan: Implications for the Kin Selection Hypothesis". Archives of Sexual Behavior. 41 (1): 209–215. doi:10.1007/s10508-011-9763-z. PMID 21656333.
- "BBC NEWS - Health - Scans see 'gay brain differences'". 2008-06-16.
- http://www.dafml.unito.it/anatomy/panzica/pubblicazioni/pdf/1995PanzicaJEI.pdf
- Swaab DF, Zhou JN, Ehlhart T, Hofman MA (1994). "Development of vasoactive intestinal polypeptide neurons in the human suprachiasmatic nucleus in relation to birth and sex". Brain Res. Dev. Brain Res. 79 (2): 249–59. doi:10.1016/0165-3806(94)90129-5. PMID 7955323.
- Roughgarden, Joan (2004). Evolution's Rainbow: Diversity, Gender, and Sexuality in Nature and People. Berkeley, CA: University of California Press. p. 245. ISBN 9780520240735.
- Bogaert AF, Hershberger S (1999). "The relation between sexual orientation and penile size". Arch Sex Behav. 28 (3): 213–21. doi:10.1023/A:1018780108597. PMID 10410197.
- Lasco, M. S.; Jordan, T. J.; Edgar, M. A.; Petito, C. K.; Byne, W. (2002). "A lack of dimorphism of sex or sexual orientation in the human anterior commissure". Brain Research. 936 (1–2): 95–98. doi:10.1016/S0006-8993(02)02590-8. PMID 11988236.
- McFadden D (2002). "Masculinization effects in the auditory system". Arch Sex Behav. 31 (1): 99–111. doi:10.1023/A:1014087319682. PMID 11910797.
- Rahman Q, Kumari V, Wilson GD (2003). "Sexual orientation-related differences in prepulse inhibition of the human startle response". Behav. Neurosci. 117 (5): 1096–102. doi:10.1037/0735-7044.117.5.1096. PMID 14570558.
- Savic I, Berglund H, Gulyas B, Roland P (2001). "Smelling of odorous sex hormone-like compounds causes sex-differentiated hypothalamic activations in humans". Neuron. 31 (4): 661–8. doi:10.1016/S0896-6273(01)00390-7. PMID 11545724.
- Berglund H, Lindström P, Savic I (2006). "Brain response to putative pheromones in lesbian women". Proc. Natl. Acad. Sci. U.S.A. 103 (21): 8269–74. doi:10.1073/pnas.0600331103. PMC 1570103. PMID 16705035.
- Safron A, Barch B, Bailey JM, Gitelman DR, Parrish TB, Reber PJ (2007). "Neural correlates of sexual arousal in homosexual and heterosexual men". Behav. Neurosci. 121 (2): 237–48. doi:10.1037/0735-7044.121.2.237. PMID 17469913.. The authors of the study caution that any interpretation of this finding must take into account that the group difference in brain activation between heterosexual men and homosexual men in the amygdala region is not large and that the most robust finding is that both heterosexual and homosexual men used the same areas when they reacted to sexually preferred stimuli. "For the most part, homosexual and heterosexual men showed very similar patterns of activation (albeit to different erotic stimuli). One possible exception was the amygdala, in which homosexual men showed greater activational differences between preferred and nonpreferred erotic stimuli compared with heterosexual men. However, this difference was not hypothesized a priori, was not large, and was the only group difference found out of many tested. Thus, this finding needs replication."(Debra A. Hope (editor), What is Sexual Orientation and Do Women Have One? (presentation by J.M. Bailey), Nebraska Symposium on Motivation, Volume 54 p. 47, Springer Science, 2009.)
- Williams TJ; Pepitone ME; Christensen SE; et al. (March 2000). "Finger-length ratios and sexual orientation" (PDF). Nature. 404 (6777): 455–6. doi:10.1038/35006555. PMID 10761903. Archived from the original (PDF) on 2015-06-26. Retrieved 2014-04-23.
- Tortorice JL (2002), Written on the body: butch vs. femme lesbian gender identity and biological correlates of low digit ratio, Rutgers University, OCLC 80234273
- Hall LS, Love CT (February 2003). "Finger-length ratios in female monozygotic twins discordant for sexual orientation". Archives of Sexual Behavior. 32 (1): 23–8. doi:10.1023/A:1021837211630. PMID 12597269.
- Rahman Q, Wilson GD (April 2003). "Sexual orientation and the 2nd to 4th finger length ratio: evidence for organising effects of sex hormones or developmental instability?". Psychoneuroendocrinology. 28 (3): 288–303. doi:10.1016/S0306-4530(02)00022-7. PMID 12573297.
- Putz, David A.; Gaulin, Steven J. C.; Sporter, Robert J.; McBurney, Donald H. (May 2004). "Sex hormones and finger length: What does 2D:4D indicate?" (PDF). Evolution and Human Behavior. 25 (3): 182–99. doi:10.1016/j.evolhumbehav.2004.03.005. Archived from the original (PDF) on 2010-01-07.
- Rahman Q (May 2005). "Fluctuating asymmetry, second to fourth finger length ratios and human sexual orientation". Psychoneuroendocrinology. 30 (4): 382–91. doi:10.1016/j.psyneuen.2004.10.006. PMID 15694118.
- Kraemer B, Noll T, Delsignore A, Milos G, Schnyder U, Hepp U (2006). "Finger length ratio (2D:4D) and dimensions of sexual orientation". Neuropsychobiology. 53 (4): 210–4. doi:10.1159/000094730. PMID 16874008.
- Wallien MS, Zucker KJ, Steensma TD, Cohen-Kettenis PT (August 2008). "2D:4D finger-length ratios in children and adults with gender identity disorder". Hormones and Behavior. 54 (3): 450–4. doi:10.1016/j.yhbeh.2008.05.002. PMID 18585715.
- Grimbos T, Dawood K, Burriss RP, Zucker KJ, Puts DA (2010). "Sexual orientation and the second to fourth finger length ratio: a meta-analysis in men and women". Behav Neurosci. 124 (2): 278–287. doi:10.1037/a0018764. PMID 20364887. S2CID 2777884.
- Hirashi K, Sasaki S, Shikishima C, Ando J (Jun 2012). "The second to fourth digit ratio (2D:4D) in a Japanese twin sample: heritability, prenatal hormone transfer, and association with sexual orientation". Arch Sex Behav. 41 (3): 711–24. doi:10.1007/s10508-011-9889-z. PMID 22270254.
- Lalumière ML, Blanchard R, Zucker KJ (2000). "Sexual orientation and handedness in men and women: a meta-analysis". Psychol Bull. 126 (4): 575–92. doi:10.1037/0033-2909.126.4.575. PMID 10900997.
- Mustanski BS, Bailey JM, Kaspar S (2002). "Dermatoglyphics, handedness, sex, and sexual orientation". Arch Sex Behav. 31 (1): 113–22. doi:10.1023/A:1014039403752. PMID 11910784.
- Lippa RA (2003). "Handedness, sexual orientation, and gender-related personality traits in men and women". Arch Sex Behav. 32 (2): 103–14. doi:10.1023/A:1022444223812. PMID 12710825.
- Hepper PG, Shahidullah S, White R (1991). "Handedness in the human fetus". Neuropsychologia. 29 (11): 1107–11. doi:10.1016/0028-3932(91)90080-R. PMID 1775228.
- The Science of Gaydar by David France. New York Magazine. 18 June 2007.
- The Advocate (1996, February 6). Advocate Poll Results. p. 8.
- Ernulf KE, Innala SM, Whitam FL (December 1989). "Biological explanation, psychological explanation, and tolerance of homosexuals: a cross-national analysis of beliefs and attitudes". Psychol Rep. 65 (3 Pt 1): 1003–10. doi:10.2466/pr0.1989.65.3.1003. PMID 2608821.
- 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 (2): 369–377. doi:10.1177/0146167290162016.
- Leslie, Christopher R. (2017). "The Geography of Equal Protection" (PDF). Minnesota Law Review. 101 (4): 1580. Archived from the original (PDF) on 2018-12-23. Retrieved 2019-12-22.
Thus, because the level of scrutiny is often outcome determinative, the probability of courts protecting gay Americans from discrimination is often a function of whether judges conclude that sexual orientation is a suspect classification. To determine this, courts generally consider four factors: whether the members of the group: (1) have historically been subjected to discrimination; (2) share a defining characteristic unrelated to their ability to perform or contribute to society; (3) share a defining immutable characteristic; and (4) lack political power.
- Balog, Kari (2005–2006) "Equal Protection for Homosexuals: Why the Immutability Argument is Necessary and How it is Met.", Cleveland St. L. Rev. 545–573.
- "Is Sexuality Immutable?", Margaret Talbot, The New Yorker, January 25, 2010.
- "Prop. 8 trial: defenders of gay-marriage ban make their case". Christian Science Monitor. 2010-01-26. Retrieved 27 January 2010.
- What Makes People Gay? By Neil Swidey. The Boston Globe. Published August 14, 2005. Accessed June 18, 2009.
- Card, Orson Scott (August 7, 2008). "Science on gays falls short". Deseret Morning News. Archived from the original on December 4, 2010. Retrieved June 12, 2010.
- Homosexuality and Biology. By Chandler Burr. The Atlantic Monthly. June 2007.
References
- 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
- Byne, William (1994). "The Biological Evidence Challenged". Scientific American. 270 (5): 50–55. doi:10.1038/scientificamerican0594-50. PMID 8197445.
- 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" (PDF). Neuroendocrinology Letters. 22 (6): 393–400. PMID 11781535. Archived from the original (PDF) on 2018-10-05. Retrieved 2007-05-16.
- 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 JP, vom Saal FS (June 1984). "Fetal effects on sexual behavior and aggression in young and old female mice treated with estrogen and testosterone". Horm Behav. 18 (2): 117–29. doi:10.1016/0018-506X(84)90037-0. PMID 6539747.
- Veniegas, Rosemary C.; Conley, Terri D. (2000). "Biological Research on Women's Sexual Orientations: Evaluating the Scientific Evidence". Journal of Social Issues. 56 (2): 267–282. doi:10.1111/0022-4537.00165.
- Ryan BC, Vandenbergh JG (October 2002). "Intrauterine position effects". Neurosci Biobehav Rev. 26 (6): 665–78. doi:10.1016/S0149-7634(02)00038-6. PMID 12479841.
- LeVay, Simon; Hamer, Dean H. (1994). "Evidence for a Biological Influence in Male Homosexuality". Scientific American. 270 (5): 44–49. doi:10.1038/scientificamerican0594-44. PMID 8197444.
- T. J. Taylor (1992). Twin Studies of Homosexuality. Part II Experimental Psychology Dissertation (unpublished), University of Cambridge, UK.
- vom Saal FS (July 1989). "Sexual differentiation in litter-bearing mammals: influence of sex of adjacent fetuses in utero". J. Anim. Sci. 67 (7): 1824–40. doi:10.2527/jas1989.6771824x. PMID 2670873.
- vom Saal FS, Bronson FH (May 1980). "Sexual characteristics of adult female mice are correlated with their blood testosterone levels during prenatal development". Science. 208 (4444): 597–9. doi:10.1126/science.7367881. PMID 7367881.
- 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 December 2007 .
- Begley, Sharon. "Nature plus nurture." Newsweek 126.n20 (Nov 13, 1995): 72(1). Expanded Academic ASAP. Gale. UC Santa Barbara. 10 December 2007 .
- Jones, Steve. "Ys and wherefores." New Statesman & Society 6.n256 (June 11, 1993): 30(2). Expanded Academic ASAP. Gale. UC Santa Barbara. 10 December 2007 .
- LeVay, Simon (2011). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press.