The hormonal theory of sexuality holds that, just as exposure to certain hormones plays a role in fetal sex differentiation, such exposure also influences the sexual orientation that emerges later in the individual. Prenatal hormones may be seen as the primary determinant of adult sexual orientation, or a co-factor with genes, biological factors and/or environmental and social conditions.

Sex-typed behavior

The hormonal theory of sexuality holds that, just as exposure to certain hormones plays a role in fetal sex differentiation, such exposure also influences the sexual orientation that emerges later in the adult. Differences in brain structure that come about from chemical messengers and genes interacting on developing brain cells are believed to be the basis of sex differences in countless behaviors, including sexual orientation.[1]: 25  Prenatal factors that affect or interfere with the interaction of these hormones on the developing brain can influence later sex-typed behavior in children.[1]: 24  This hypothesis is originated from countless experimental studies in non-human mammals, yet the argument that similar effects can be seen in human neurobehavioral development is a much debated topic among scholars.[2] Recent studies, however, have provided evidence in support of prenatal androgen exposure influencing childhood sex-typed behavior.[2]

Fetal hormones may be seen as either the primary influence upon adult sexual orientation or as a co-factor interacting with genes and/or environmental and social conditions.[3][page needed] However, Garcia-Falgueras and Dick Swaab disagree that social conditions influence sexual orientation to a large degree. As seen in young children as well as in vervet and rhesus monkeys, sexually differentiated behavior in toy preference is differing in males versus females, where females prefer dolls and males prefer toy balls and cars; these preferences can be seen as early as 3–8 months in humans.[2] It is impossible to completely rule out the social environment or the child's cognitive understanding of gender when discussing sex typed play in androgen-exposed girls.[2] Conversely, children tend towards objects which have been labelled for their own sex, or toys that they have seen members of their sex playing with previously.[2]

An endocrinology study by Garcia-Falgueras and Swaab postulated that "In humans, the main mechanism responsible of [sic] sexual identity and orientation involves a direct effect of testosterone on the developing brain."[1]: 25  Further, their study puts forward that intrauterine exposure to hormones is largely determinative. Sketching the argument briefly here, the authors say that sexual organs are differentiated first, and then the brain is sexually differentiated "under the influence, mainly, of sex hormones such as testosterone, estrogen and progesterone on the developing brain cells and under the presence of different genes as well ... The changes brought about in this stage are permanent. ... Sexual differentiation of the brain is not caused by hormones alone, even though they are very important for gender identity and sexual orientation."[1]: 24 

Organizational aspects

Embryonic gonads develop primarily based on whether there is an SRY gene, normally present on the Y chromosome. If SRY exists, then the gonads develop as testes, and commence the production of androgen hormones, mainly testosterone, dihydrotestosterone (DHT) and androstenedione; production of testosterone and conversion into dihydrotestosterone during weeks 6 to 12 of pregnancy are key factors in the production of a male fetus's penis, scrotum and prostate.[4] In a female, on the other hand, absence of these levels of androgens results in development of typically female genitals.[4] Following this, sexual differentiation of the brain occurs; sex hormones exert organizational effects on the brain that will be activated in puberty.[4] As a result of these two processes occurring separately, the degree of genital masculinization does not necessarily relate to the masculinization of the brain.[1]: 24 [4] Sex differences in the brain have been found in many structures, most notably the hypothalamus and the amygdala.[2] However, few of these have been related to behavioral sex differences, and scientists are still working to establish firm links between early hormones, brain development and behavior.[2] The study of the organizational theory of prenatal hormones can be difficult, as ethically researchers cannot alter hormones in a developing fetus; instead, scholars must rely on naturally occurring abnormalities of development to provide answers.[5]

Most extensively studied in organizational effects of hormones is congenital adrenal hyperplasia (CAH).[6] CAH is a genetic disease that results in exposure to high levels of androgens beginning early in gestation. Girls with CAH are born with masculinized genitalia, which is corrected surgically as soon as possible.[5][6] CAH provides the opportunity for natural experiments, as people with CAH can be compared to people without it. However, "CAH is not a perfect experiment", since, "social responses to masculinized genitalia or factors related to the disease itself" can confound results.[5] Nonetheless several studies have shown that CAH has a clear but not determining influence on sexual orientation; women with CAH are less likely to be exclusively heterosexual than are other women.[6]

Since hormones alone do not determine sexual orientation and differentiation of the brain, the search for other factors that act upon sexual orientation have led genes such as the SRY and ZFY to be implicated.[7]

Prenatal maternal stress

Further information: Prenatal maternal stress

As of 2006 results from studies in humans had found conflicting evidence regarding the effect of prenatal exposure to hormones and psychosexual outcomes; Gooren noted in 2006 that studies in subprimate mammals are invalid measures of human sexual differentiation, as sex hormones follow a more "on-off" role in sex-typed behavior than is found in primates.[8]

Studies do suggest that prenatal stress significantly increases the likelihood of homosexuality or bisexuality, although varying evidence exists for which trimester is most important.[1]: 24  Studies of endocrinology have found implications for amphetamines and thyroid-gland hormones to increase homosexuality in female offspring as well, although it has not been examined in conjunction with prenatal stress levels.[1]: 24 

Some have postulated that postnatal (e.g., social and environmental factors) development can play a role in the sexual orientation of an individual, yet solid evidence of this has yet to be discovered. Children born through artificial insemination with donor sperm and consequently raised by lesbian couples have typically been heterosexually oriented.[1]: 24 [4] Summed up by Bao and Swaab, "The apparent impossibility of getting someone to change their sexual orientation ... is a major argument against the importance of the social environment in the emergence of homosexuality, as well as against the idea that homosexuality is a lifestyle choice."[4]

Fraternal birth order

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According to a multitude of studies over several decades, gay men have more older brothers on average, a phenomenon known as the fraternal birth order effect. It has been suggested that the greater the number of older male siblings the higher the level of androgen fetuses are exposed to. No evidence of birth order effects have been observed in women. The theory holds that the fraternal birth order effect is a result of a maternal immune response that is produced towards a factor of male development over several male pregnancies.[9] Bogaert's hypothesis argues that "the target of the immune response may be male specific molecules on the surface of male fetal brain cells (e.g., including those in the anterior hypothalamus). Anti-male antibodies might bind to these molecules and thus interfere with their role in normal sexual differentiation, leading some later born males to being attracted to men as opposed to women."[9] Garcia-Falgueras and Swaab state that "The ... fraternal birth order effect ... is putatively explained by an immunological response by the mother to a product of the Y chromosome of her sons. The chance of such an immune response to male factors would increase with every pregnancy resulting in the birth of a son."[1]: 24 

Maternal antibodies against Y-chromosome neuroligin have been implicated in this effect,[10] among other evidence that favours this theory.[11] Further, while percentages of the likelihood of homosexuality have been estimated to be increased by 15[11]–48% per older brother, these odds really account for only a few percent of the population; thus, this hypothesis cannot be universally applied to the majority of homosexual men.[8] Most,[12] but not all, studies have been able to reproduce the fraternal birth order effect. Some did not find any statistically significant difference in either the sibling composition or rate of older brothers of gay and straight men,[13][14] including large, nationally representative studies in the US and Denmark.[15][16] However, Blanchard reanalyzed Frisch's 2006 Danish study and found the birth order effect was in-fact present.[17]

In conjunction with fraternal birth order, handedness provides further evidence of prenatal effects on sexual orientation, because handedness is regarded by many as a marker of early neurodevelopment. Other correlates to handedness (e.g., cerebral laterality, prenatal hormonal profiles, spatial ability) have been linked to sexual orientation, either empirically and/or theoretically.[9] In right-handed individuals, the number of older brothers increased the odds of homosexual orientation, but this effect was not seen in left-handed individuals.[9] As with other purported marks indicating higher incidence of homosexuality, however, the link with handedness remains ambiguous and several studies have been unable to replicate it.[18][19][20]

Implicated genes in fraternal birth order

Main article: Fraternal birth order and male sexual orientation

A gene of the Rh system has been discussed as a possible candidate for affecting fraternal birth order, as it has been linked to both handedness and immune system functioning.[9] Gene variants in the Rh system are implicated in a maternal response to what is known as hemolytic disease of the newborn. Rh is a factor in blood, and in cases where the mother is absent of this (Rh-) while carrying an Rh+ fetus, an immune response may develop with deleterious effects. The Rh gene hypothesis is a strong candidate because not only does it involve the maternal immune response, but it has been implicated in handedness as well.[9]

Variants of the androgen receptor (AR) gene have also been discussed, in that non-right-handedness in men has been linked with greater CAG repeats in the AR gene, which in turn is associated with lower testosterone. A theory that high prenatal testosterone leads to neuronal and axonal loss in the corpus callosum is supported by this hypothesis.[21]

There is evidence that mutations in NLGN4X and NLGN4Y are linked to autism spectrum conditions[22][23] and such conditions may be elevated in asexual people.[24] Thus, NLGN4X/Y may affect neurological functioning associated with, broadly, the forming of social connections to others, including sexual/romantic ones.

Prenatal Thyroid Theory of Homosexuality/Gender Dysphoria

Prenatal thyroid theory of same-sex attraction/gender dysphoria has been based on clinical and developmental observations of youngsters presenting to child psychiatry clinics in Istanbul/Turkey. The report of 12 cases with same-sex attraction/gender dysphoria born to mothers with thyroid diseases was first presented in EPA Congress, Vienna (2015) and published as an article in the same year.[25][26] The extremely significant relationship between the two conditions suggested an independent model, named as Prenatal Thyroid Model of Homosexuality. According to Turkish child & adolescent psychiatrist Osman Sabuncuoglu, who generated the theory, maternal thyroid dysfunction may lead to abnormal deviations from gender-specific development in the offspring. Autoimmune destructive process as seen in Hashimoto thyroiditis, diminished supply of thyroid hormones and impacts on prenatal androgen system were all considered as contributing mechanisms. In a follow-up theoretical paper,[27] previous research findings indicating higher rates of  polycystic ovary syndrome (PCOS) in female-to-male transsexuals and lesbian women were conceived as an indication of Prenatal Thyroid Model since PCOS and autoimmune thyroiditis are frequently comorbid diseases. Likewise, increased rates of autism spectrum disorder in children born to mothers with thyroid dysfunction and overrepresentation of ASD individuals in gender dysphoria populations suggest such an association. A second group of young children with this pattern were presented in IACAPAP Congress, Prague (2018).[28]

The findings from previous research in LGBT populations had called for attention to be paid to thyroid system.[29][30] A commentary by Jeffrey Mullen, published shortly after the 2015 article, underlined the importance of Prenatal Thyroid Model and supported developments in this field.[31] Afterwards, several authors have emphasized the role of thyroid system in sexuality while citing the Prenatal Thyroid Model.[32][33][34][35] Among them, Carosa et al. concluded that thyroid hormones, affecting the human sexual function strongly, the thyroid gland must be considered, along with the genitals and the brain, a sexual organ.[32] As a tertiary source, an authoritative book on the subject of interplay between endocrinology, brain and behavior has also cited the thyroid-homosexuality proposal article in the latest edition.[36] Most importantly, a genome-wide genetic association study on male homosexuals identified a significant region on Chromosome 14 which is related to autoimmune thyroid dysfunction in human beings.[37] This is apparently a big support to the Prenatal Thyroid Model.

Male homosexuality as hypermasculine

Main article: Hypermasculinity

There is evidence of a correlation between sexual orientation and traits that are determined in utero.[3][page needed] A study by McFadden in 1998 found that auditory systems in the brain, another physical trait influenced by prenatal hormones is different in those of differing orientations; likewise the suprachiasmatic nucleus (SCN) was found by Swaab and Hofman to be larger in homosexual men than in heterosexual men.[38] The suprachiasmatic nucleus is also known to be larger in men than in women.[39] An analysis of the hypothalamus by Swaab and Hofman (1990;2007) found that the volume of the SCN in homosexual men was 1.7 times larger than a reference group of male subjects, and contained 2.1 times as many cells.[8][40] During development, the volume of the SCN and the cell counts reach peak value at approximately 13 to 16 months after birth; at this age, the SCN contains the same number of cells as was found in adult male homosexuals, yet in a reference group of heterosexual males the cell numbers begin to decline to the adult value of 35% of the peak value.[8] These results were replicated and confirmed the findings.[41] However; there also has yet to be a meaningful interpretation of these results provided in the context of human sexual orientation.[8] Some highly disputed studies suggest gay men have also been shown to have higher levels of circulating androgens[42][43][44] and larger penises,[45] on average, than heterosexual men.

Male homosexuality as hypomasculine

Main article: Hypomasculinity

In a 1991 study, Simon LeVay demonstrated that a tiny clump of neurons of the anterior hypothalamus—which is believed to control sexual behavior and linked to prenatal hormones—known as the interstitial nuclei of the anterior was, on average, more than twice the size in heterosexual men when contrasted to homosexual men. Due to this area also being nearly twice the size in heterosexual men than in heterosexual women, the implication is that the sexual differentiation of the hypothalamus in homosexuals is in a female direction.[8] In 2003 scientists at Oregon State University announced that they had replicated his findings in sheep.

Other evidence pointed to the contrary: 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), contradicting the hypothesis that homosexual males have a "female hypothalamus".[46][41] William 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.[47] Finally, the same research has found that the INAH3 is smaller in volume in homosexual men than in heterosexual men because homosexual men have a higher neuronal packing density in the INAH3 than heterosexual men; there is no difference in the number or cross-sectional area of neurons in the INAH3 of homosexual versus heterosexual men.[48]

Female homosexuality

Most empirical or theoretical research into women's sexual orientation has, historically, been guided by the idea of lesbians as essentially masculine and heterosexual women as essentially feminine.[49] Typically, this belief is traced to the early "inversion theory" of sex researchers who state that homosexuality is a result of biological abnormalities that "invert" sexual attraction and personality.[49] Handedness research has provided implications; because more men than women present a preference for their left hand, the higher proportion of non-right handedness that has been discovered among lesbians when compared to heterosexual women demonstrates a possible link of prenatal masculinization and sexual orientation.[49] Backing this up are reports that lesbians display more masculinized 2D;4D digit ratios than heterosexual women, based on data gathered from at least six different laboratories.[50] This effect has not yet been observed between homosexual and heterosexual males.[50] However, the validity of this measure of digit ratios remains controversial as a predictor of prenatal androgen, as many other prenatal factors may play roles in bone growth in prenatal stages of development.[8] While many studies have found results confirming this hypothesis, others have failed to replicate these findings,[8] leaving the validity of this measure unconfirmed.

Diethylstilbestrol (DES), a drug that has been in the past prescribed to prevent miscarriages, has also been studied in relation to women's sexual orientation. It has been observed to exert a masculinizing/defeminizing effect on the developing brain of the fetus.[49] When compared to controls, higher percentages of DES-exposed women (17% vs 0%) reported that they had engaged in same-sex relations; however, the great majority of DES women stated an exclusively heterosexual orientation.[49]

Girls with congenital adrenal hyperplasia (an autosomal recessive condition which results in high androgen levels during fetal development) have more masculinized sex role identities and are more likely to have a homosexual sexual orientation as adults than controls.[51][52][53][54][55] An alternative explanation for this effect is the fact that girls with this condition are born with masculinized external genitalia, which leads their parents to raise them in a more masculine manner, thus influencing their sexual orientation as adults. However, the degree to which the girls' genitals are masculinized does not correlate with their sexual orientation, suggesting that prenatal hormones are a stronger causal factor, not parental influence.

Together with congenital adrenal hyperplasia, DES studies have provided little support of the prenatal hormone theory of sexual orientation; they do, however, provide the framework for possible pathways to a homosexual orientation for a small number of women.[49]

Gender dysphoria

Main article: Gender dysphoria

In individuals with gender dysphoria, previously known as gender identity disorder (GID), prenatal exposure to testosterone has been hypothesized to have an effect on gender identity differentiation. The 2D;4D finger ratio, or relative lengths of the 2nd "index" and 4th "ring" fingers, has become a popular measure of prenatal androgen because of accumulated evidence suggesting the 2D;4D ratios are related to prenatal exposure to testosterone.[56] Many children with gender dysphoria differentiate a homosexual orientation during adolescence, but not all of them; adults with "early onset", or a childhood history of cross-gender behavior, often have a homosexual orientation. Adults with "late onset", or those without a childhood history of said behavior, are more likely to have a non-homosexual orientation.[56]

Prenatal androgen exposure has been associated with an increased chance of patient-initiated gender reassignment to male after being initially raised as female in early childhood or infancy.[8][57] Gooren found that organizational effects of prenatal androgens are more prevalent in gender role behavior than in gender identity, and that there are preliminary findings that suggest evidence of a male gender identity being more frequent in patients with fully male-typical prenatal androgenization.[8]

Individuals with complete androgen insensitivity syndrome are almost always brought up as females, and the differentiation of gender identity/role is feminine.[8] This example is important in demonstrating that chromosomes and gonads alone do not dictate gender identity and role.[8]


Main article: Transsexualism

Because organ differentiation and brain differentiation occur at different times, in rare cases transsexualism can result.[1]: 24 

Drawing on some transsexualism cases, Garcia-Falgueras and Swaab state that "[f]rom these examples it appears that the direct action of testosterone on the developing brain in boys and the lack of such action on the developing brain in girls are crucial factors in the development of male and female gender identity and sexual orientation".[1]: 26  Countless studies have been run on peripheral levels of sex steroids in male and female homosexuals, a considerable number of which claimed to find "less 'male hormone' and/or more 'female hormone' in male homosexuals and vice versa in female homosexuals".[8] However, these findings have been reviewed and have subsequently been dismissed by Gooren as suffering from faulty design and interpretation.[8]

Factors implicated in the development of transsexuality include chromosomal abnormalities, polymorphisms of certain genes, and variations in aromatase (cytochrome P450 CYP19) and CYP17.[8] Girls with congenital adrenal hyperplasia show an increase in probability of transsexuality later in life; however, this probability is still only 1–3% in CAH.[8] Although historically abnormal sexual differentiation has pointed to androgens as a causal factor, there are codeterminants of gender identity and sexual orientation.[8] These factors are currently unknown, and thus no clear cut answer for the cause of transsexualism and homosexuality exists.[8]

Due to relatively small population sizes, generalizability of studies on transsexuality cannot be assumed.

Endocrine disruptors

Endocrine disrupting chemicals (EDCs) are chemicals that, at certain doses, can interfere with the endocrine system in mammals.[58] Work on possible neurotoxic effects of endocrine disruptors, and their possible effects on sexual orientation when a fetus is exposed to them, is in its infancy: "we mostly know about the relationship between EDC exposure and neurobehavioral function through an examination of outcomes within a limited sphere of questions."[59] While studies have found that xenoestrogens and xenoandrogens can alter the brain's sexual differentiation in a number of species used as animal models,[60] from the data in hand to date, it is "misleading expect EDCs to produce profiles of effects, such as sexually dimorphic behaviors, as literal copies of those produced by native hormones. Such agents are not hormones. They should not be expected to act precisely as hormones."[59]

See also


  1. ^ a b c d e f g h i j k Garcia-Falgueras A, Swaab DF (2010). "Sexual hormones and the brain: an essential alliance for sexual identity and sexual orientation". Pediatric Neuroendocrinology. Endocrine Development. Vol. 17. pp. 22–35. doi:10.1159/000262525. ISBN 978-3-8055-9302-1. PMID 19955753.
  2. ^ a b c d e f g Hines M (October 2010). "Sex-related variation in human behavior and the brain". Trends in Cognitive Sciences. 14 (10): 448–456. doi:10.1016/j.tics.2010.07.005. PMC 2951011. PMID 20724210.
  3. ^ a b Wilson, G., & Q. Rahman, Born Gay: The Psychobiology of Human Sex Orientation, Peter Owen Publishers; 2nd edition (May 1, 2008) ISBN 9780720613094
  4. ^ a b c d e f Bao AM, Swaab DF (April 2011). "Sexual differentiation of the human brain: relation to gender identity, sexual orientation and neuropsychiatric disorders". Frontiers in Neuroendocrinology. 32 (2): 214–226. doi:10.1016/j.yfrne.2011.02.007. PMID 21334362. S2CID 8735185.
  5. ^ a b c Berenbaum SA, Beltz AM (April 2011). "Sexual differentiation of human behavior: effects of prenatal and pubertal organizational hormones". Frontiers in Neuroendocrinology. 32 (2): 183–200. doi:10.1016/j.yfrne.2011.03.001. PMID 21397624. S2CID 205776417.
  6. ^ a b c Hines M (April 2011). "Prenatal endocrine influences on sexual orientation and on sexually differentiated childhood behavior". Frontiers in Neuroendocrinology. 32 (2): 170–182. doi:10.1016/j.yfrne.2011.02.006. PMC 3296090. PMID 21333673.
  7. ^ Ngun TC, Ghahramani N, Sánchez FJ, Bocklandt S, Vilain E (April 2011). "The genetics of sex differences in brain and behavior". Frontiers in Neuroendocrinology. 32 (2): 227–246. doi:10.1016/j.yfrne.2010.10.001. PMC 3030621. PMID 20951723.
  8. ^ a b c d e f g h i j k l m n o p q r Gooren L (November 2006). "The biology of human psychosexual differentiation". Hormones and Behavior. 50 (4): 589–601. doi:10.1016/j.yhbeh.2006.06.011. PMID 16870186. S2CID 21060826.
  9. ^ a b c d e f Bogaert AF, Blanchard R, Crosthwait LE (October 2007). "Interaction of birth order, handedness, and sexual orientation in the Kinsey interview data". Behavioral Neuroscience. 121 (5): 845–853. doi:10.1037/0735-7044.121.5.845. PMID 17907817.
  10. ^ McCarthy MM (January 2019). "Sex differences in neuroimmunity as an inherent risk factor". Neuropsychopharmacology. 44 (1): 38–44. doi:10.1038/s41386-018-0138-1. PMC 6235925. PMID 29977075.
  11. ^ a b Blanchard R, Lippa RA (April 2007). "Birth order, sibling sex ratio, handedness, and sexual orientation of male and female participants in a BBC internet research project". Archives of Sexual Behavior. 36 (2): 163–176. doi:10.1007/s10508-006-9159-7. PMID 17345165. S2CID 18868548.
  12. ^ Blanchard R (January 2018). "Fraternal Birth Order, Family Size, and Male Homosexuality: Meta-Analysis of Studies Spanning 25 Years". Archives of Sexual Behavior. 47 (1): 1–15. doi:10.1007/s10508-017-1007-4. PMID 28608293. S2CID 10517373.
  13. ^ Zietsch BP, Verweij KJ, Heath AC, Madden PA, Martin NG, Nelson EC, Lynskey MT (March 2012). "Do shared etiological factors contribute to the relationship between sexual orientation and depression?". Psychological Medicine. 42 (3): 521–532. doi:10.1017/S0033291711001577. PMC 3594769. PMID 21867592.
  14. ^ Kishida M, Rahman Q (July 2015). "Fraternal Birth Order and Extreme Right-Handedness as Predictors of Sexual Orientation and Gender Nonconformity in Men". Archives of Sexual Behavior. 44 (5): 1493–1501. doi:10.1007/s10508-014-0474-0. PMID 25663238. S2CID 30678785.
  15. ^ Francis AM (2008). "Family and sexual orientation: the family-demographic correlates of homosexuality in men and women". Journal of Sex Research. 45 (4): 371–377. doi:10.1080/00224490802398357. PMID 18937128. S2CID 20471773.
  16. ^ Frisch M, Hviid A (October 2006). "Childhood family correlates of heterosexual and homosexual marriages: a national cohort study of two million Danes". Archives of Sexual Behavior. 35 (5): 533–547. doi:10.1007/s10508-006-9062-2. PMID 17039403. S2CID 21908113.
  17. ^ Frisch M, Hviid A (2007-12-01). "Reply to Blanchard's (2007) "Older-Sibling and Younger-Sibling Sex Ratios in Frisch and Hviid's (2006) National Cohort Study of Two Million Danes"". Archives of Sexual Behavior. 36 (6): 864–867. doi:10.1007/s10508-007-9169-0. ISSN 1573-2800. S2CID 143749001.
  18. ^ Mustanski BS, Bailey JM, Kaspar S (February 2002). "Dermatoglyphics, handedness, sex, and sexual orientation". Archives of Sexual Behavior. 31 (1): 113–122. doi:10.1023/A:1014039403752. PMID 11910784. S2CID 29217315.
  19. ^ Williams TJ, Pepitone ME, Christensen SE, Cooke BM, Huberman AD, Breedlove NJ, et al. (March 2000). "Finger-length ratios and sexual orientation". Nature. 404 (6777): 455–456. Bibcode:2000Natur.404..455W. doi:10.1038/35006555. PMID 10761903. S2CID 205005405.
  20. ^ Rahman Q, Clarke K, Morera T (April 2009). "Hair whorl direction and sexual orientation in human males". Behavioral Neuroscience. 123 (2): 252–256. doi:10.1037/a0014816. PMID 19331448. S2CID 46164333.
  21. ^ Witelson SF, Nowakowski RS (1991). "Left out axons make men right: a hypothesis for the origin of handedness and functional asymmetry". Neuropsychologia. 29 (4): 327–333. doi:10.1016/0028-3932(91)90046-B. PMID 1857504. S2CID 23754055.
  22. ^ Jamain S, Quach H, Catalina B, Maria R, Colineaux, C, Gillberg IC, Soderstrom H, Giros B, Leboyer M, Gillberg C, Bourgeron T (2003). "Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism". Nature Genetics. 34 (1): 27–29. doi:10.1038/ng1136. PMID 12669065. S2CID 4798621.
  23. ^ Ross JL, Tartaglia N, Merry DE, Dalva M, Zinn AR (2015). "Behavioral phenotypes in males with XYY and possible role of increased NLGN4Y expression in autism features". Genes, Brain and Behavior. 14 (2): 137–144. doi:10.1111/gbb.12200. PMID 25558953. S2CID 36755210.
  24. ^ Attanasio M, Masedu F, Quattrini F, Pino MC, Vagnetti R, Valenti M, Mazza M (2022). "Are Autism Spectrum Disorder and Asexuality Connected? features". Archives of Sexual Behavior. 51 (4): 2091–2115. doi:10.1007/s10508-021-02177-4. PMID 34779982. S2CID 244115396.
  25. ^ Sabuncuoglu O (March 2015). "Maternal Thyroid Dysfunction During Pregnancy May Lead to Same-sex Attraction/gender Nonconformity in the Offspring: Proposal of Prenatal Thyroid Model". European Psychiatry. 30: 374. doi:10.1016/s0924-9338(15)30294-7. ISSN 0924-9338. S2CID 143359069.
  26. ^ Sabuncuoglu O (September 2015). "High Rates of Same-Sex Attraction/Gender Nonconformity in the Offspring of Mothers with Thyroid Dysfunction During Pregnancy: Proposal of Prenatal Thyroid Model". Mental Illness. 7 (2): 5810. doi:10.4081/mi.2015.5810. PMC 4620281. PMID 26605033.
  27. ^ Sabuncuoglu O (October 2017). "Towards a further understanding of prenatal thyroid theory of homosexuality: Autoimmune thyroiditis, polycystic ovary syndrome, autism and low birth weight". Mental Illness. 9 (2): 7325. doi:10.4081/mi.2017.7325. PMC 5661141. PMID 29142667.
  28. ^ Sabuncuoglu O (30 August 2022). "A second group of youngsters with gender nonconformity/same-sex attraction born to mothers with thyroid dysfunction in pregnancy".
  29. ^ Ellis, Lee; Hellberg, Jill (January 2005). "Fetal exposure to prescription drugs and adult sexual orientation". Personality and Individual Differences. 38 (1): 225–236. doi:10.1016/j.paid.2004.04.004. ISSN 0191-8869.
  30. ^ Frisch, Morten; Nielsen, Nete Munk; Pedersen, Bo Vestergaard (January 2014). "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. S2CID 11819672.
  31. ^ Mullen, Jeffrey (2016-06-23). "A link between maternal thyroid hormone and sexual orientation?". Mental Illness. 8 (1): 6591. doi:10.4081/mi.2016.6591. ISSN 2036-7465. PMC 4926038. PMID 27403279.
  32. ^ a b Carosa, Eleonora; Lenzi, Andrea; Jannini, Emmanuele A. (May 2018). "Thyroid hormone receptors and ligands, tissue distribution and sexual behavior". Molecular and Cellular Endocrinology. 467: 49–59. doi:10.1016/j.mce.2017.11.006. hdl:11573/1132156. ISSN 0303-7207. PMID 29175529. S2CID 36883213.
  33. ^ Basavanhally, Tara; Fonseca, Renée; Uversky, Vladimir N. (2018-09-06). "Born This Way: Using Intrinsic Disorder to Map the Connections between SLITRKs, TSHR, and Male Sexual Orientation". Proteomics. 18 (21–22): 1800307. doi:10.1002/pmic.201800307. ISSN 1615-9853. PMID 30156382. S2CID 52115603.
  34. ^ Wang, Yan; Wu, Haoda; Sun, Zhong Sheng (October 2019). "The biological basis of sexual orientation: How hormonal, genetic, and environmental factors influence to whom we are sexually attracted". Frontiers in Neuroendocrinology. 55: 100798. doi:10.1016/j.yfrne.2019.100798. ISSN 0091-3022. PMID 31593707. S2CID 203667616.
  35. ^ Roberto Castello; Marco Caputo (2019-09-01). "Thyroid diseases and gender". Italian Journal of Gender-Specific Medicine. 5 (2019September–December): 136–141. doi:10.1723/3245.32148.
  36. ^ Castellanos-Cruz, Laura; Bao, Ai-Min; Swaab, Dick F. (2017), "Sexual Identity and Sexual Orientation", Hormones, Brain and Behavior, Elsevier, pp. 279–290, doi:10.1016/b978-0-12-803592-4.00104-8, ISBN 9780128036082, retrieved 2022-09-07
  37. ^ 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. Bibcode:2017NatSR...716950S. doi:10.1038/s41598-017-15736-4. ISSN 2045-2322. PMC 5721098. PMID 29217827.
  38. ^ Panzica GC, Aste N, Viglietti-Panzica C, Ottinger MA (March 1995). "Structural sex differences in the brain: influence of gonadal steroids and behavioral correlates". Journal of Endocrinological Investigation. 18 (3): 232–252. doi:10.1007/BF03347808. PMID 7615911. S2CID 10435075.
  39. ^ Swaab DF, Zhou JN, Ehlhart T, Hofman MA (June 1994). "Development of vasoactive intestinal polypeptide neurons in the human suprachiasmatic nucleus in relation to birth and sex". Brain Research. Developmental Brain Research. 79 (2): 249–259. doi:10.1016/0165-3806(94)90129-5. PMID 7955323.
  40. ^ Swaab DF, Hofman MA (December 1990). "An enlarged suprachiasmatic nucleus in homosexual men" (PDF). Brain Research. 537 (1–2): 141–148. doi:10.1016/0006-8993(90)90350-K. PMID 2085769. S2CID 13403716.
  41. ^ a b Shao-Hua, Hu "Discovery of new genetic loci for male sexual orientation in Han population" Nature. N.p., 31 October 2021. Web. 31 October 2021.
  42. ^ Brodie HK, Gartrell N, Doering C, Rhue T (January 1974). "Plasma testosterone levels in heterosexual and homosexual men". The American Journal of Psychiatry. 131 (1): 82–83. doi:10.1176/ajp.131.1.82. PMID 4808435.
  43. ^ Doerr P, Pirke KM, Kockott G, Dittmar F (May 1976). "Further studies on sex hormones in male homosexuals". Archives of General Psychiatry. 33 (5): 611–614. doi:10.1001/archpsyc.1976.01770050063010. PMID 1267577.
  44. ^ Neave N, Menaged M, Weightman DR (December 1999). "Sex differences in cognition: the role of testosterone and sexual orientation". Brain and Cognition. 41 (3): 245–262. doi:10.1006/brcg.1999.1125. PMID 10585237. S2CID 44831103.
  45. ^ Bogaert AF, Hershberger S (June 1999). "The relation between sexual orientation and penile size". Archives of Sexual Behavior. 28 (3): 213–221. doi:10.1023/A:1018780108597. PMID 10410197. S2CID 42801275.
  46. ^ Swaab DF, Gooren LJ, Hofman MA (1992). "Gender and sexual orientation in relation to hypothalamic structures". Hormone Research (Submitted manuscript). 38 Suppl 2 (2): 51–61. doi:10.1159/000182597. hdl:20.500.11755/7cb8b769-4329-407a-b0ee-13e011017f68. PMID 1292983.
  47. ^ Byne W, Tobet S, Mattiace LA, Lasco MS, Kemether E, Edgar MA, et al. (September 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. [permanent dead link]
  48. ^ Byne W, Tobet S, Mattiace LA, Lasco MS, Kemether E, Edgar MA, et al. (September 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.
  49. ^ a b c d e f Peplau L, Huppin M (October 2008). "Masculinity, Femininity and the Development of Sexual Orientation in Women". Journal of Gay & Lesbian Mental Health. 12 (1–2): 145–165. doi:10.1300/J529v12n01_09. S2CID 142691272.
  50. ^ a b Gobrogge KL, Breedlove SM, Klump KL (February 2008). "Genetic and environmental influences on 2D:4D finger length ratios: a study of monozygotic and dizygotic male and female twins". Archives of Sexual Behavior. 37 (1): 112–118. doi:10.1007/s10508-007-9272-2. PMID 18074216. S2CID 41921265.
  51. ^ Dittmann V, Dilling H (June 1990). "Chapter V (F) of ICD-10: mental, behavioural and developmental disorders--introduction and overview". Pharmacopsychiatry. 23 (suppl 4): 137–141. doi:10.1055/s-2007-1014552. PMID 2197637. S2CID 34081785.
  52. ^ Dittmann V, von Cranach M, Eckermann G (June 1990). "Abnormalities of adult personality and behaviour (section F 6)--results of the ICD-10 field trial". Pharmacopsychiatry. 23 (Suppl 4): 170–172. doi:10.1055/s-2007-1014559. PMID 2197643. S2CID 24696932.
  53. ^ Dittmann V (August 1992). "[ICD-10 in psychiatric diagnosis. The concept and initial practical experiences]". Versicherungsmedizin (in German). 44 (4): 114–119. PMID 1509643.
  54. ^ Zucker KJ, Bradley SJ, Oliver G, Blake J, Fleming S, Hood J (December 1996). "Psychosexual development of women with congenital adrenal hyperplasia". Hormones and Behavior. 30 (4): 300–318. doi:10.1006/hbeh.1996.0038. PMID 9047259. S2CID 20206538.
  55. ^ Hines M, Brook C, Conway GS (February 2004). "Androgen and psychosexual development: core gender identity, sexual orientation and recalled childhood gender role behavior in women and men with congenital adrenal hyperplasia (CAH)". Journal of Sex Research. 41 (1): 75–81. doi:10.1080/00224490409552215. PMID 15216426. S2CID 33519930.
  56. ^ a b 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): 450–454. doi:10.1016/j.yhbeh.2008.05.002. PMID 18585715. S2CID 6324765.
  57. ^ Meyer-Bahlburg HF (August 2005). "Gender identity outcome in female-raised 46,XY persons with penile agenesis, cloacal exstrophy of the bladder, or penile ablation". Archives of Sexual Behavior. 34 (4): 423–438. doi:10.1007/s10508-005-4342-9. PMID 16010465. S2CID 34971769.
  58. ^ Staff, NIEHS. Last Reviewed, June 05, 2013. Endocrine Disruptors
  59. ^ a b Weiss B (December 2012). "The intersection of neurotoxicology and endocrine disruption". Neurotoxicology. 33 (6): 1410–1419. doi:10.1016/j.neuro.2012.05.014. PMC 3458140. PMID 22659293.
  60. ^ Roselli CE, Stormshak F (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.

Further reading