1991).Finally, using structural magnetic resonance imaging, Scamvougeras et al.(1994)
reported that the isthmus of the corpus callosum was larger by 13% in right-handed
homosexual men as compared to heterosexual men. The isthmus is also larger in
women and positively correlated with left-handedness in men (Witelson, 1989;
Witelson & Goldsmith, 1991).
The theory of prenatal androgen exposure originates from a large body of research
demonstrating that the male foetal brain is masculinized by exposure to androgenic
gonadal steroids during critical periods of development. The absence of androgens
results in feminization of the foetal brain. Hormonal exposure at these stages
organizes the brain in a lasting manner and determines patterns of male-typical
versus female-typical behaviors (including sexual preferences, gender identity and
childhood interests), as well as neurocognitive features (Collaer & Hines, 1995).
In this view, homosexuality in males is due to under-masculinisation (the partial
absence of androgenising effects) in women over-masculinization (excess
androgenising effects) during early development (Collaer & Hines, 1995; Ellis & Ames,
1987). Genetic products produce androgen receptor (AR) proteins in most end tissues,
particularly the brain, which mediate the action of steroid hormones ...
The classic model of neurohormonal differentiation has always assumed that female
sexual differentiation develops by default. Recent evidence suggests that estrogenic
products have an active role in feminization, but this mechanism is poorly
understood (Ogawa & Pfaff, 2000). Moreover, the paradox of estrogenic influences in
both female-typical and male-typical reproductive behaviors remains. There may also
be different critical periods for the activation or inhibition of female differentiation.
Thus it is difficult to construct coherent theories for the development of female
sexual preferences in humans. Studies with mice indicate that the action of estrogen
receptor genes depends on the gender in which they are expressed. In female mice,
disruption of the estrogen receptor leads to loss of lordosis and female sexual
behavior, whereas in male mice it results in reduced male-typical sexual behaviors
(Ogawa & Pfaff, 2000) ...
One possible environmental insult during neurodevelopment that could determine
sex-atypical sexual preferences is maternal stress. This longstanding theory suggests
that maternal stress affects the intrauterine hormonal milieu of the foetus, resulting
in homosexuality (Dorner et al., 1980; Dorner, Schenk, Schmiedel, & Ahrens, 1983).
More sophisticated accounts have suggested that stressful maternal experiences may
release high levels of stress hormones which interfere with the functioning of the
hypothalamic-adrenal-gonadal axis in the foetus. This may cause deviations from
normal patterns of sexual differentiation (Ellis & Cole-Harding, 2001). Although some