Biology and sexual orientation

[12]: 107–110  The size of the sheep oSDN has also been demonstrated to be formed in utero, rather than postnatally, underscoring the role of prenatal hormones in masculinization of the brain for sexual attraction.

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.

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.

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.

[24] 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.

[29] Bailey states: What kind of environmental factor can cause genetically identical twins reared in the same family from birth—often dressed alike and given the same toys—to differ in their sexual orientations?

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.

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".

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.

[42] In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred female mice specifically lacking a particular gene related to sexual behavior.

[48][49] 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.

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.

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.

[65] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure,[66] but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.

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.

[47] 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.

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.

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."

[80][4] 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.

[90] Based on research conducted in Japan that found no evidence that homosexual Japanese men exhibited elevated avuncular tendencies compared to heterosexual counterparts, 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.

[91] In 2011 and 2014, the Journal of Cognition and Culture published two studies that found that Canadian homosexual men exhibited significantly greater altruistic tendencies toward kin versus non-kin children relative to heterosexual men and women, but did not find that Canadian homosexual males exhibited significantly higher altruistic behavior towards nieces and nephews over geographic disconnect.

[94] In 2017, Evolutionary Psychological Science published a logistic regression analysis of the results of 17,295 female subjects across 58 countries on World Values Survey questionnaires about attitudes toward homosexuality that found that subjects that were potentially most in need of alloparental support exhibited significantly more positive attitudes towards homosexuals, which the researchers suggested was circumstantial evidence in support of the hypothesis on a global scale.

[98] 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."

[99] The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men.

[100][101] As originally pointed out by Dean Hamer,[102] 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.

[118] In 2012, the Journal of Sexual Medicine published a study examining the phenotypic expression of the genetic factors that influence increased fecundity in female relative carriers that found that as compared with corresponding female relatives of heterosexual men, mothers and maternal aunts of homosexual men had fewer gynecological disorders and complicated pregnancies, had reduced family stability and a higher divorce and spousal separation rate, and self-reported less interest in having children, less emphasis on romantic love within couples, and less importance on their social life, but scored higher on the extraversion scale of a Big Five personality traits questionnaire.

[126] In 2021, Nature Human Behaviour published a study that used the results from a pair of genome-wide association studies (GWAS) that found that opposite-sex behavior individuals that were carriers of genetic variants associated with same-sex behavior had a greater number of opposite-sex sexual partners on average, and that computer simulations suggested that such a mating advantage could explain the maintenance of such genetic variants in human populations.

He argues that gay men are "punished much more than rewarded" for their childhood gender nonconformity, and that such behavior "emerges with no encouragement, and despite opposition", making it "the sine qua non of innateness".

[167] The journalist Chandler Burr has stated that "[s]ome, recalling earlier psychiatric "treatments" for homosexuality, discern in the biological quest the seeds of genocide.

Identical twin studies are a useful mechanism for assessing the role of genes and environment