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. On grounds of evolutionary plausibility, Gavrilets, Friberg and Rice argue that all mechanisms for exclusive homosexual orientations likely trace back to their epigenetic model. A model proposed by evolutionary geneticist William R. Rice argues that a misexpressed epigenetic modifier of testosterone sensitivity or insensitivity that affected development of the brain can explain homosexuality, and can best explain twin discordance. These males were then reared and raised as females without telling them, but contrary to expectations, this did not make them feminine nor attracted to men. Socialization theories, which were dominant in the 1900s, favored the idea that children were born "undifferentiated" and were socialized into gender roles and sexual orientation. This effect is estimated to account for between 15 and 29% of gay men, while other gay and bisexual men are thought to owe sexual orientation to genetic and hormonal interactions. 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. Dissection studies found that gay men had significantly smaller INAH-3 than heterosexual men, a shift in the female direction, as first demonstrated by neuroscientist Simon LeVay, which has been replicated. Also, the INAH-3 region is bigger in males than in females, and is known to be critical for sexual behavior. Controlled experiments in animals, where scientists manipulate exposure to sex hormones during gestation, can also induce lifelong male-typical behavior and mounting in females, and female-typical behavior in males. In women, if INAH3 receives more testosterone than is normal for females, INAH3 may enlarge somewhat or even to the size that is normal for males, increasing the likelihood of same sex attraction. Some of those epi‐marks are sex‐specific (i.e. different in XX vs. XY embryos) and help protect against atypical androgen exposure (too much in XX, too little in XY). These genes partly overlap with those for several other traits, including openness to experience and risk-taking behavior. 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. Subsequently, INAH3 may function as female or partially female, potentially causing same-sex attraction to males. The influence of hormones on the developing fetus has been the most influential causal hypothesis of the development of sexual orientation. 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. However, modern science shows that the hormone’s role is far more complex and integral to health across genders. It induces the development of male secondary sexual characteristics, such as increased muscle mass, deeper voice, and facial hair growth, aiding in the alignment of their physical appearance with their gender identity. For transgender men (individuals assigned female at birth but who identify as male), testosterone therapy is a key component of gender-affirming treatment. Testosterone is the primary male sex hormone and is critical for the development and maintenance of male reproductive tissues, such as the testes and prostate.
