Gender identity and sexual preference
Resolution of the mechanisms underlying gender self-identity, transsexuality, and homosexuality remains a major challenge. A vast array of genetic and hormonal factors could lead to gender identity problems . Twin and family studies have shown that genetic factors are important. For example, rare chromosomal abnormalities may lead to transsexuality, and polymorphisms of genes encoding estrogen and androgen receptors as well as aromatase also carried an increased risk. Abnormal hormone levels during early development also appear to play a role. This is suggested by the high frequency of androgen-producing polycystic ovaries, oligomenorrhea, and amenorrhea in female-to-male (FtM) transsexuals, indicating that an early intrauterine exposure of a female fetus to abnormally high levels of testosterone may be a causative factor, although this issue remains controversial. There is also a higher prevalence of hyper- androgenism in FtM transsexuals, supporting the possible involvement of high testosterone levels with transsexuality. Girls with congenital adrenal hyperplasia (CAH), who are exposed to extreme levels of testosterone in utero, also have an increased probability of being transsexual. Although the likelihood of developing transsexuality in such cases is 300-1,000 greater than normal, the risk for transsexuality in CAH is only l%-3%, whereas the probability of serious gender problems in the general population is 5.2%. The consensus is that girls with CAH should be raised as girls, even when they are masculinized.
Sexual preference is a complex, sexually dimorphic trait found across animal species. Recent studies with mice revealed an association of sexual preference with DA in the nucleus accumbens . The study used genetically engineered male mice that lack a functioning vomeronasal organ, a scent-sensing olfactory structure that responds to pheromones. These males showed no aggression toward other males and were equally interested in mating with males and females. When exposed to negative conditioning against female pheromones, the mutant male mice avoided mating with females while displaying sexual behavior toward other males. Importantly, female pheromones presented to intact males activated a reward mechanism linked to DA release from the nucleus accumbens, the so-called "pleasure center" in the basal forebrain. In the absence of this stimulus, males showed no preference for females. In spite of the interesting association of DA with sexual preference in rodents, there are no published records to support a dopaminergic association with homosexuality or gender identify in humans.