| L Gooren, Frank Kruijver, "Male To Female Transsexual Individuals Have Female Neuron Numbers In The Central Subdivision of the Bed Nucleus of the Stria Terminalis", Journal of Clinical Endocrinology & Metabolism, 85:5 2000, pp. 2034-2041 |
| | The findings indicated that, regardless of sexual orientation, men had almost twice as many SOM neurons as women (P< 0.006). The number of SOM neurons in the BSTc of the transwomen (MFs) was similar to the other women (P= 0.83). In contrast, the neuron number of a transman (FMs) was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood seemed to have no impact on BSTc neuron numbers. The relative volumes of the BSTc were also measured. All of the men, regardless of sexual orientation, had volumes which were similar; the women and the transwomen (MFs) had similar volumes; the transman (FMs) fell into the same range as the other men. The volumes of all men versus all women and transwomen (MFs) were statistically highly significant (P< 0.01) No statistical differences were found for age, post-mortem time, fixation time, storage time or cause of death, nor were any differences found between early, rather than late, recognition of gender dysphoria/transsexualism. The effects of variations in levels of estrogens, testosterone, antiandrogen treatments and orchidectomy were also tested and appeared to have no effect on the BSTc. The finding of SOM neuronal sex differences in the BSTc and the sex reversal of these differences in the brains of gender dysphoric individuals, clearly supports the paradigm that in these individuals, the sex differentiation of the brain and the genitals may go in opposite directions. This points to a neurobiological basis, established during early development, for the condition of gender dysphoria. * somatostatin is a polypeptide hormone, produced in the brain (and also the pancreas), which appears to inhibit the secretion of other hormones. |
| | This study followed one similar piece of research on much of the same brain material, and was thus only the second of its kind to be done on human brains. The research team focussed on a part of the brain understood to be sexually dimorphic, the central subdivision of the bed-nucleus of the stria terminalis BSTc. The main neuron population of the BSTc is somatostatin-expressing SOM neurons.* The team sought to determine the number of SOM neurons in the BSTc (only those with visible nucleolus were counted), in relation to sex, sexual orientation, gender identity and past or present hormonal status. 42 human brains were collected in total: eight (8) gender dysphoric individuals, six (6) of whom were male-to-female individuals ( MFs, transwomen) and had undergone transition, including hormone treatment and surgery, one (1) male-to-female individual who had undergone no treatment whatever, but who had always strongly identified as female, and one (1) female-to-male individual (FMs, transman). The control group of 34 individuals included: nine (9) homosexual men, nine (9) heterosexual men, ten (10) presumed heterosexual women, three (3) women with hormone disorders, three (3) men with hormone disorders. |
| "Gender Bender", The Age Newspaper, 9 October 1999 |
| | Bower has sought for many years to gather evidence that transsexuality is caused by subtle genetic changes after birth or by hormonal fluctuations during pregnancy, but admits that no definite data have emerged, and that his belief is not shared by many in his profession. |
| "Senate Legal and Constitutional References Committee Sexuality discrimination inquiry", Australian Government, 8 August 1996 |
| | Dr. Kennedy: In our clinic all of us have a strong feeling that this is probably a genetic abnormality. The fact is that we have not been able to find out what genetic abnormality it is and we have tried a few things with various gene probes, none of which has come to anything. Nevertheless, people seem to be more or less born with the need to be transgendered. |
| L Gooren, J Zhou, "A sex difference in the human brain and its relation to transsexuality", Nature, 378 1995, pp. 68-70 |
| | Considered together with information from animals, then our study supports the hypothesis that gender identity alterations may develop as a result of an altered interaction between the development of the brain and sex hormones. |
| | Interestingly, the very small BSTc in transsexuals appears to be a very local brain difference. We failed to observe similar changes in three other hypothalamic nuclei, namely, PVN, SDN or SCN in the same individuals (unpublished data). This might be due to the fact that these nuclei do not all develop at the same time, or to a difference between these nuclei and the BST with respect to the presence of sex hormone receptors or aromatase. We are now studying the distribution of sex hormone receptors and the aromatase activity in various hypothalamic nuclei in relation to sexual orientation and gender. |
| Julian Godlewski, "Transsexualism and Anatomic Sex Ratio Reversal in Poland", Archives of Sexual Behavior, 17:6 1988, pp. 547-548 |
| | A genetic explanation would be inappropriate, because the patients observed came from different parts of land and not from an enclave. |
| Richard Fagerstrom, Walter Futterweit, Richard Weiss, "Endocrine Evaluation of Forty Female-to-Male Transsexuals: Increased Frequency of Polycystic Ovarian Disease in Female Transsexualism", Archives of Sexual Behavior, 15:1 1986, p. 69 |
| | Prenatal androgenization of the hypothalamus has been reported to lead to abnormal sexual behavior in animals (Barachlough and Gorski, 1961) and humans (Ehrhardt et al. 1968). Much more must be known about the pathophysiology of PCOD and the effects of the prenatal hormonal environment before any hypotheses may be attempted to explain possible etiologic mechanisms in patients with female transsexualism. |
| Michael Ross, William Walters, "Transsexualism and Sex Reassignment", Oxford University Press, 1986 p55 |
| p55: | So far there is no evidence for a genetic explanation of transsexualism. |
| p19: | There is no evidence to date that endocrinological factors feature among the causes of gender dysphoria or homosexuality. |
| L. Lothstein, "Sex Reassignment Surgery: Historical, Bioethical and Theoretical Issues", Am J Psychiatry, 139:4 April 1982, p. 417 |
| | It is rare to substantiate a neurohormonal disorder for any given case. |
| Anke Ehrhardt, Heino Myer-Bahlburg, "Effects of Parental Sex Hormones on Gender-Related Behavior", Science, 20 March 1981 |
| | Gender identity depends largely on postnatal environmental influences, while sex-dimorphic behavior and temperamental sex differences appear to be modified by prenatal sex hormones. A role of the prenatal endocrine milieu in the development of erotic partner preference, as in hetro-, homo- or bisexual orientation, or of cognitive sex differences has not been conclusively demonstrated. |
| | The evidence for the role of prenatal hormones in the development of sexual orientation is inconclusive. |
| Julianne Imperato-McGinley, "Androgens and the evolution of male-gender identity among male pseudohermaphrodites with 5a reductase deficiency", The New England Journal of Medicine, 300:22 31 May 1979 |
| | Exposure of the brain to normal levels of testosterone in utero, neonatially and at puberty appears to contribute substantially to the formation of male-gender identity. These subjects demonstrate that in the absence of sociocultural factors that could interrupt the natal sequence of events, the effect of testosterone predominates, over-riding the effect of rearing as girls. |
| Toshihiro Aono, "Absence of Positive Feedback Effect of Oestrogen on LH Release in Patients with TFS", Acta Endocrinologica, 87 18 March 1978, pp. 259-267 |
| 259: | The insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. |
| Ira Pauly, "Female Transsexualism Part II", Archives of Sexual Behavior, 3:6 1974, p. 509 |
| | If there are biological determinants which set the stage for subsequent psychosocial forces, these have not been elucidated in the human species. |
| Robert Kolodny, William Masters, "Plasma Testosterone and Semen Analysis in Male Homosexuals", The New England Journal of Medicine, 18 November 1971 |
| | Plasma testosterone levels were significantly below the control for groups of homosexuals . Analysis of variance showed a significant difference in sperm counts according to degree of homosexuality. These findings suggest that further investigation of endocrine variants in homosexuals may be of major value in relation to primary pathogenesis or to secondary hypothalamic response to human homosexual orientation. |