Hormonal theory of sexuality
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.
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. Prenatal factors that affect or interfere with the interaction of these hormones on the developing brain can influence later sex-typed behavior in children. This hypothesis is originated from 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. Recent studies, however, have provided evidence in support of prenatal androgen exposure influencing childhood sex-typed behavior.
Fetal hormones may be seen as either the primary influence upon adult sexual orientation or as a co-factor interacting with genes. 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. 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. 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.
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." 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."
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. In a female, on the other hand, absence of these levels of androgens results in development of typically female genitals. Following this, sexual differentiation of the brain occurs; sex hormones exert organizational effects on the brain that will be activated in puberty. As a result of these two processes occurring separately, the degree of genital masculinization does not necessarily relate to the masculinization of the brain. Sex differences in the brain have been found in many structures, most notably the hypothalamus and the amygdala. 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. 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.
Most extensively studied in organizational effects of hormones is congenital adrenal hyperplasia (CAH). 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. 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. 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.
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.
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.
Some studies do suggest that prenatal stress significantly increases the likelihood of homosexuality or bisexuality, although varying evidence exists for which trimester is most important. 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.
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. 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."
Fraternal birth order.
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. 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." 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."
Maternal antibodies against Y-chromosome neuroligin have been implicated in this effect, among other evidence that favours this theory. ;ref name="Blanchard/Lippa cite" ; ;/ref ; Further, while percentages of the likelihood of homosexuality have been estimated to be increased by 15–48% 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. Most, 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, including large, nationally representative studies in the US and Denmark. However, Blanchard reanalyzed Frisch's 2006 Danish study and found the birth order effect was in-fact present.
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. 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. 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.
Implicated genes in fraternal birth order.
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. 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.
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.
There is evidence that mutations in NLGN4X and NLGN4Y are linked to autism spectrum conditions and such conditions may be elevated in asexual people. 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. The extremely significant relationship between the two conditions suggested an independent model, named as "Prenatal Thyroid Model of Homosexuality". According to Turkish child &amp; 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, 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). Furthermore, 9 additional cases were reported in IACAPAP Congress, Rio de Janeiro (Sabuncuoglu, 2024).
The findings from previous research in LGBT populations had called for attention to be paid to thyroid system. A commentary by Jeffrey Mullen, published shortly after the 2015 article, underlined the importance of "Prenatal Thyroid Model" and supported developments in this field. Afterwards, several authors have emphasized the role of thyroid system in sexuality while citing the "Prenatal Thyroid Model." 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. 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. 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. This is apparently a big support to the "Prenatal Thyroid Model."
Male homosexuality