hypothalamus in transsexuals;
http://press.endocrine.org/doi/full/10.1....85.5.6564
'Results
Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 103) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 103) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 103) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 103) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm3, similar to that in homosexual men (5.00 ± 0.39 mm3) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm3) and that of transsexuals (3.58 ± 0.19 mm3) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm3).
Discussion
In the present study, we show regardless of sexual orientation: 1) a sex difference in SOM neuron numbers in the human BSTc, with males having almost twice as many SOM neurons as females; 2) a number of SOM neurons in the BSTc of male-to-female transsexuals in the female range; and 3) an opposite pattern in the BSTc of a female-to-male transsexual with a SOM neuron number in the male range.
Analysis of the total number of SOM neurons of the human BSTc in individual patients with highly different hormone levels does not give any indication that changes in sex hormone levels in adulthood change the neuron numbers. Because the transsexuals had all been treated with estrogens, at least for some time (see Table 2), the reduced neuron numbers of the BSTc could theoretically be due to the presence of high levels of circulating estrogens. Arguments against this possibility come from the finding that transsexuals T2 and T3 both showed a small BSTc (Fig. 1), despite the fact that T2 stopped taking estrogens about 15 months before her death because of hyperprolactinemia, and T3 no longer received hormone treatment when a sarcoma was found about 3 months before she died. T5 continued to take estrogens until 3 months before death and had even more SOM neurons than T3, whereas T1 and T6 continued to take estrogens until death and even had higher SOM neuron numbers than T2 and T3 (Fig. 1). Furthermore, a 31-yr-old man (S2), who suffered for at least 1 yr from a feminizing adrenal tumor that produced high blood levels of estrogens, still had a BSTc neuron number in the normal male range (the latest highest serum estradiol levels before death varied between 577–779 pmol/L; the normal range is 50–200 pmol/L).
Our results might theoretically also be explained by a lack of androgens in the transsexual group because all subjects, except for T4, had been orchiectomized. We, therefore, studied two nontranssexual men (S3 and S5) who had been orchiectomized because of prostate cancer 3 months and 2 yr before death, respectively, and found that the BSTc neuron number of S3 was close to the mean of the male group and that the BSTc number of neurons of S5 was even the highest observed (Fig. 1), indicating that orchiectomy did not cause any decrease in SOM neuron numbers. Not only were five of the transsexuals orchiectomized, they all used the antiandrogen cyproterone acetate (CPA). However, an effect of CPA reducing the number of SOM neurons of the BSTc is highly unlikely because S5 had taken CPA during the last 2 yr of his life and his BSTc neuron number was at the upper end of the male range, whereas T6 had not taken CPA for the past 10 yr, and T3 took no CPA during the last 2 yr before her death, and they still had relatively low numbers of SOM neurons.....(read full article)'
additional information from bennington edu;
http://faculty.bennington.edu/~sherman/s...GENDER.pdf
