Share to: share facebook share twitter share wa share telegram print page

Causes of gender incongruence

Part of a series on
Transgender topics
     
Gender identities
Health care practices
Rights and legal status
Society and culture
Events and awareness
Culture
Theory and concepts
By country
Rights
History
See also
 Category

Gender incongruence is the state of having a gender identity that does not correspond to one's sex assigned at birth. This is experienced by people who identify as transgender or transsexual, and often results in gender dysphoria.[1] The causes of gender incongruence have been studied for decades.

Transgender brain studies,[2] especially those on trans women attracted to women (gynephilic), and those on trans men attracted to men (androphilic), are limited, as they include only a small number of tested individuals.[3] Studies conducted on twins suggest that there are likely genetic causes of gender incongruence, although the precise genes involved are not known or fully understood.[4][5][6]

Genetics

A 2008 study compared the genes of 112 trans women who were mostly already undergoing hormone treatment, with 258 cisgender male controls. Trans women were more likely than cisgender males to have a longer version of a receptor gene (longer repetitions of the gene) for the sex hormone androgen, which reduced its effectiveness at binding testosterone.[7][non-primary source needed] The androgen receptor (NR3C4) is activated by the binding of testosterone or dihydrotestosterone, where it plays a critical role in the forming of primary and secondary male sex characteristics. The research weakly suggests reduced androgen and androgen signaling contributes to trans women's identity. The authors say that a decrease in testosterone levels in the brain during development might prevent complete masculinization of trans women's brains, thereby causing a more feminized brain and a female gender identity.[7][8][non-primary source needed]

A variant genotype for the CYP17 gene, which acts on the sex hormones pregnenolone and progesterone, has been found to be linked to transsexuality in trans men but not in trans women. Most notably, transmasculine subjects not only had the variant genotype more frequently, but had an allele distribution equivalent to cisgender male controls, unlike the cisgender female controls. The paper concluded that the loss of a female-specific CYP17 T -34C allele distribution pattern is associated with transmasculinity.[9][non-primary source needed]

Gender incongruence among twins

In 2013, a twin study combined a survey of pairs of twins where one or both had undergone, or had plans and medical approval to undergo, gender transition, with a literature review of published reports of transgender twins. The study found that one third of identical twin pairs in the sample were both transgender: 13 of 39 (33%) monozygotic or identical pairs of assigned males and 8 of 35 (22.8%) pairs of assigned females. Among dizygotic or genetically non-identical twin pairs, there was only 1 of 38 (2.6%) pairs where both twins were trans.[10] The significant percentage of identical twin pairs in which both twins are trans and the virtual absence of dizygotic twins (raised in the same family at the same time) in which both were trans would provide evidence that transgender identity is significantly influenced by genetics if both sets were raised in different families.[10]

Prenatal hormonal environment

Sex hormones in the prenatal environment differentiate the male and female brain. One hypothesis proposes that transgender individuals may have been exposed to atypical levels of sex hormones during later stages of fetal development, leading to brain structures atypical of their sex assigned at birth.[6]

In people with XX chromosomes, congenital adrenal hyperplasia (CAH) results in heightened exposure to prenatal androgens, resulting in masculinization of the genitalia. Individuals with CAH are typically subjected to medical interventions including prenatal hormone treatment[11] and postnatal genital reconstructive surgeries.[12] Such treatments are sometimes criticized by intersex rights organizations as non-consensual, invasive, and unnecessary interventions. Individuals with CAH are usually assigned female and tend to develop similar cognitive abilities to the typical females, including spatial ability, verbal ability, language lateralization, handedness and aggression. Research has shown that people with CAH and XX chromosomes will be more likely to experience same-sex attraction,[11] and at least 5.2% of these individuals develop serious gender dysphoria.[13]

In males with 5-alpha-reductase deficiency, conversion of testosterone to dihydrotestosterone is disrupted, decreasing the masculinization of genitalia. Individuals with this condition are typically assigned female and raised as girls due to their feminine appearance at a young age. However, more than half of males with this condition raised as females come to identify as male later in life. Scientists speculate that the definition of masculine characteristics during puberty and the increased social status afforded to men are two possible motivations for a female-to-male transition.[13]

Brain structure

General

Transgender brain studies, especially those on trans women attracted to women (gynephilic), and those on trans men attracted to men (androphilic), are limited, as they include only a small number of tested individuals.[3]

Several studies have found a correlation between gender identity and brain structure.[2][14] A first-of-its-kind study by Zhou et al. (1995) found that in the bed nucleus of the stria terminalis (BSTc), a region of the brain known for sex and anxiety responses (and which is affected by prenatal androgens),[15] cadavers of six trans women had female-normal BSTc size, similar to the study's cadavers of cisgender women. While the trans women had undergone hormone therapy, and all but one had undergone sex reassignment surgery, this was accounted for by including cadavers of cisgender men and cisgender women as controls who, for a variety of medical reasons, had experienced hormone reversal. The controls still had sizes typical for their sex. No relationship to sexual orientation was found.[16][non-primary source needed]

In a follow-up study, Kruijver et al. (2000) looked at the number of neurons in BSTc instead of volumes. They found the same results as Zhou et al. (1995), but with even more dramatic differences. One transfeminine subject who had never received hormone therapy was also included, and nonetheless matched up with the female neuron counts.[17][non-primary source needed]

In 2002, a follow-up study by Chung et al. found that significant sexual dimorphism in BSTc did not establish until adulthood. Chung et al. theorized that changes in fetal hormone levels produce changes in BSTc synaptic density, neuronal activity, or neurochemical content which later lead to size and neuron count changes in BSTc, or alternatively, that the size of BSTc is affected by the generation of a gender identity inconsistent with one's assigned sex.[18][non-primary source needed]

It has been suggested that the BSTc differences may be a result of hormone replacement therapy. It has also been suggested that because pedophilic offenders have also been found to have a reduced BSTc, a feminine BSTc may be a marker for paraphilias rather than transgender identity.[3]

In a review of the evidence in 2006, Gooren considered the earlier research as supporting the concept of gender incongruence as a "sexual differentiation disorder" of the sexually dimorphic brain.[19] Dick Swaab (2004) concurred.[20]

In 2008, Garcia-Falgueras & Swaab discovered that the interstitial nucleus of the anterior hypothalamus (INAH-3), part of the hypothalamic uncinate nucleus, had properties similar to the BSTc with respect to sexual dimorphism and gender incongruence. The same method of controlling for hormone usage was used as in Zhou et al. (1995) and Kruijver et al. (2000). The differences were even more pronounced than with BSTc; control males averaged 1.9 times the volume and 2.3 times the neurons as control females, yet regardless of hormone exposure, trans women were within the female range and the trans men within the male range.[21][non-primary source needed]

A 2009 MRI study by Luders et al. found that among 24 trans women not treated with hormone therapy, regional gray matter concentrations were more similar to those of cisgender men than of cisgender women, but there was a significantly greater volume of gray matter in the right putamen compared to cisgender men. Like earlier studies, researchers concluded that transgender identity was associated with a distinct cerebral pattern.[22][non-primary source needed] MRI scanning allows easier study of larger brain structures, but independent nuclei are not visible due to lack of contrast between different neurological tissue types, hence other studies on e.g. BSTc were done by dissecting brains post-mortem.[scientific citation needed]

Rametti et al. (2011) studied 18 trans men who had not undergone hormone therapy using diffusion tensor imaging (DTI), an MRI technique which allows visualizing white matter, the structure of which is sexually dimorphic. Rametti et al. discovered that the trans men's white matter, compared to 19 cisgender gynephilic females, showed higher fractional anisotropy values in posterior part of the right SLF, the forceps minor and corticospinal tract". Compared to 24 cisgender males, they showed only lower FA values in the corticospinal tract. The white matter patterns in trans men were found to be shifted in the direction of cis men.[23][non-primary source needed]

Hulshoff Pol et al. (2006) studied gross brain volume in 8 trans men and in 6 trans women undergoing hormone therapy. They found that hormones altered the sizes of the hypothalamus in a gender-consistent manner: treatment with masculinizing hormones shifted the hypothalamus towards the male direction in the same way as in male controls, and treatment with feminizing hormones shifted the hypothalamus towards the female direction in the same way as female controls. They concluded: "The findings suggest that, throughout life, gonadal hormones remain essential for maintaining aspects of sex-specific differences in the human brain."[24][unreliable medical source?]

A 2011 review published in Frontiers in Neuroendocrinology found that "Female INAH3 and BSTc have been found in MtF transsexual persons. The only female-to-male (FtM) transsexual person available to us for study so far had a BSTc and INAH3 with clear male characteristics. (...) These sex reversals were found not to be influenced by circulating hormone levels in adulthood, and seem thus to have arisen during development" and that "All observations that support the neurobiological theory about the origin of transsexuality, i.e. that it is the sizes, the neuron numbers, and the functions and connectivity of brain structures, not the sex of their sexual organs, birth certificates or passports, that match their gender identities".[25]

A 2015 review reported that two studies found a pattern of white matter microstructure differences away from a transgender person's birth sex, and toward their desired sex. In one of these studies, sexual orientation had no effect on the diffusivity measured.[26]

A 2016 review reported that, for androphilic trans women and gynephilic trans men, hormone treatment may have large effects on the brain, and that cortical thickness, which is generally thicker in cisgender women's brains than in cisgender men's brains, may also be thicker in trans women's brains, but is present in a different location to cisgender women's brains.[3] It also stated that for both trans women and trans men, "cross-sex hormone treatment affects the gross morphology as well as the white matter microstructure of the brain. Changes are to be expected when hormones reach the brain in pharmacological doses. Consequently, one cannot take hormone-treated transsexual brain patterns as evidence of the transsexual brain phenotype because the treatment alters brain morphology and obscures the pre-treatment brain pattern."[3]

A 2019 review in Neuropsychopharmacology found that among transgender individuals meeting diagnostic criteria for gender dysphoria, "cortical thickness, gray matter volume, white matter microstructure, structural connectivity, and corpus callosum shape have been found to be more similar to cisgender control subjects of the same preferred gender compared with those of the same natal sex."[27]

A 2020 paper[28][non-primary source needed] tried to investigate and differentiate between the two competing hypotheses of a neurodevelopmental cortical hypothesis that suggests the existence of different brain phenotypes vs a functional-based hypothesis in relation to regions involved in the own body perception.[28] Trans men, trans women, and cisgender women all had decreased connectivity compared with cisgender men in superior parietal regions, as part of the salience (SN) and the executive control (ECN) networks.[28] Trans men also had weaker connectivity compared with cisgender men between intra-SN regions and weaker inter-network connectivity between regions of the SN, the default mode network (DMN), the ECN and the sensorimotor network.[28] Trans women had lower small-worldness[clarification needed], modularity and clustering coefficient than cisgender men.[28][non-primary source needed]

A 2021 review of brain studies published in the Archives of Sexual Behavior found that "although the majority of neuroanatomical, neurophysiological, and neurometabolic features" in transgender people "resemble those of their natal sex rather than those of their experienced gender", for trans women they found feminine and demasculinized traits, and vice versa for trans men. They stated that due to limitations and conflicting results in the studies that had been done, they could not draw general conclusions or identify-specific features that consistently differed between cisgender and transgender people. The review also found differences when comparing cisgender homosexual and heterosexual people, with the same limitations applying.[29]

Androphilic vs. gynephilic trans women

A 2016 review reported that early-onset androphilic transgender women have a brain structure similar to cisgender women's and unlike cisgender men's, but that they have their own brain phenotype.[3] It also reported that gynephilic trans women differ from both cisgender female and male controls in non-dimorphic brain areas.[3]

The available research indicates that the brain structure of androphilic trans women with early-onset gender dysphoria is closer to that of cisgender women than that of cisgender men.[3] It also reports that gynephilic trans women differ from both cisgender female and male controls in non-dimorphic brain areas.[3] Cortical thickness, which is generally thicker in cisgender women's brains than in cisgender men's brains, may also be thicker in trans women's brains, but is present in a different location to cisgender women's brains.[3] For trans men, research indicates that those with early-onset gender dysphoria and who are gynephilic have brains that generally correspond to their assigned sex, but that they have their own phenotype with respect to cortical thickness, subcortical structures, and white matter microstructure, especially in the right hemisphere.[3] Hormone therapy can also affect transgender people's brain structure; estrogen can cause transgender women's brains to become closer to those of cisgender women, and morphological changes observed in the brains of trans men might be due to the anabolic effects of testosterone.[3]

While MRI taken on gynephilic trans women have likewise shown differences in the brain from non-trans people, no feminization of the brain's structure has been identified.[3]

Gynephilic trans men

Fewer brain structure studies have been performed on transgender men than on transgender women.[3] A team of neuroscientists, led by Nawata in Japan, used a technique called single-photon emission computed tomography (SPECT) to compare the regional cerebral blood flow (rCBF) of 11 gynephilic trans men with that of 9 androphilic cis women. Although the study did not include a sample of cisgender males so that a conclusion of "male shift" could be made, the study did reveal that the gynephilic trans men showed significant decrease in blood flow in the left anterior cingulate cortex and a significant increase in the right insula, two brain regions known to respond during sexual arousal.[30][non-primary source needed]

A 2016 review reported that the brain structure of early-onset gynephilic trans men generally corresponds to their assigned sex, but that they have their own phenotype with respect to cortical thickness, subcortical structures, and white matter microstructure, especially in the right hemisphere.[3] Morphological increments observed in the brains of trans men might be due to the anabolic effects of testosterone.[3]

Onset

According to the DSM-5, gender dysphoria in those assigned male at birth tends to follow one of two broad trajectories: early-onset or late-onset. Early-onset gender dysphoria is behaviorally visible in childhood. Sometimes, gender dysphoria may stop for a while in this group, and they may identify as gay or homosexual for a period of time, followed by recurrence of gender dysphoria. This group is usually androphilic in adulthood. Late-onset gender dysphoria does not include visible signs in early childhood, but some report having had wishes to be the opposite sex in childhood that they did not report to others. Trans women who experience late-onset gender dysphoria are more likely be attracted to women and may identify as lesbians or bisexual. It is common for people assigned male at birth who have late-onset gender dysphoria to experience sexual excitement from cross-dressing. In those assigned female at birth, early-onset gender dysphoria is the most common course. This group is usually sexually attracted to women. Trans men who experience late-onset gender dysphoria will usually be sexually attracted to men and may identify as gay.[31]

Blanchard's typology

Further information: Blanchard's transsexualism typology

In the 1980s and 1990s, sexologist Ray Blanchard developed a taxonomy of male-to-female transsexualism[32][non-primary source needed] built upon the work of his colleague Kurt Freund,[33][non-primary source needed] which argues that trans women have one of two primary causes of gender dysphoria.[34][35][36] Blanchard theorized that "homosexual transsexuals" (a taxonomic category referring to trans women attracted to men) are attracted to men and develop gender dysphoria typically during childhood, and characterizes them as displaying overt and obvious femininity since childhood; he characterizes "non-homosexual transsexuals" (trans women who are sexually attracted to women) as developing gender dysphoria primarily due to autogynephilia (sexual arousal by the thought or image of themselves as a woman[32][non-primary source needed]), and as attracted to women, attracted to both women and men (Blanchard calls this "pseudo-bisexuality", believing attraction to males to be not genuine, but part of the performance of an autogynephilic sexual fantasy), or asexual.[citation needed]

Blanchard's theory has received support from J. Michael Bailey, Anne Lawrence, and James Cantor. Blanchard argued that there are significant differences between the two groups, including sexuality, age of transition, ethnicity, IQ, fetishism, and quality of adjustment.[37][38][non-primary source needed][32][non-primary source needed][39][non-primary source needed] However, the theory has been criticized in papers from Veale, Nuttbrock, Moser, and others who argue that it is poorly representative of trans women and non-instructive, and that the experiments behind it are poorly controlled and/or contradicted by other data.[40][non-primary source needed][41][42][non-primary source needed] A 2009 study by Charles Moser of 29 cisgender women in the healthcare field based on Blanchard's methods for identifying autogynephilia found that 93% of respondents qualified as autogynephiles based on their own responses.[43][non-primary source needed]

See also

References

  1. ^ Curtis R, Levy A, Martin J, Playdon ZJ, Wylie K, Reed R, Reed R (March 2009). "Transgender experiences – Information and support" (PDF). NHS. p. 12. Archived from the original (PDF) on 6 January 2012. Retrieved 2012-07-01.
  2. ^ a b Altinay, Murat; Anand, Amit (2020). "Neuroimaging gender dysphoria: a novel psychobiological model". Review. Brain Imaging and Behavior. 14 (4): 1281–1297. doi:10.1007/s11682-019-00121-8. ISSN 1931-7565. PMID 31134582. S2CID 167207854.
  3. ^ a b c d e f g h i j k l m n o p Guillamon A, Junque C, Gómez-Gil E (October 2016). "A Review of the Status of Brain Structure Research in Transsexualism". Archives of Sexual Behavior. 45 (7): 1615–48. doi:10.1007/s10508-016-0768-5. PMC 4987404. PMID 27255307.
  4. ^ Heylens G, De Cuypere G, Zucker KJ, Schelfaut C, Elaut E, Vanden Bossche H, et al. (March 2012). "Gender identity disorder in twins: a review of the case report literature". The Journal of Sexual Medicine. 9 (3): 751–7. doi:10.1111/j.1743-6109.2011.02567.x. PMID 22146048. Of 23 monozygotic female and male twins, nine (39.1%) were concordant for GID; in contrast, none of the 21 same‐sex dizygotic female and male twins were concordant for GID, a statistically significant difference (P = 0.005)... These findings suggest a role for genetic factors in the development of GID.
  5. ^ Diamond M (2013). "Transsexuality Among Twins: Identity Concordance, Transition, Rearing, and Orientation". International Journal of Transgenderism. 14 (1): 24–38. doi:10.1080/15532739.2013.750222. S2CID 144330783. Combining data from the present survey with those from past-published reports, 20% of all male and female monozygotic twin pairs were found concordant for transsexual identity... The responses of our twins relative to their rearing, along with our findings regarding some of their experiences during childhood and adolescence show their identity was much more influenced by their genetics than their rearing.
  6. ^ a b Besser M, Carr S, Cohen-Kettenis P, Connolly P, de Sutter P, Diamond M, Di Ceglie D, Higashi Y, Jones L, Kruijver F, Martin J, Playdon Z, Ralph D, Reed T, Reid R, Reiner W, Swaab D, Terry T, Wilson P, Wylie K (2006). "Atypical Gender Development – A Review". International Journal of Transgenderism. 9 (1): 29–44. doi:10.1300/J485v09n01_04. ISSN 1553-2739.
  7. ^ a b Hare L, Bernard P, Sánchez FJ, Baird PN, Vilain E, Kennedy T, Harley VR (January 2009). "Androgen receptor repeat length polymorphism associated with male-to-female transsexualism". Biological Psychiatry. 65 (1): 93–6. doi:10.1016/j.biopsych.2008.08.033. PMC 3402034. PMID 18962445.
  8. ^ Carter, Helen (27 October 2008). "Transsexual study reveals genetic link". Australian Broadcasting Corporation.
  9. ^ Bentz EK, Hefler LA, Kaufmann U, Huber JC, Kolbus A, Tempfer CB (July 2008). "A polymorphism of the CYP17 gene related to sex steroid metabolism is associated with female-to-male but not male-to-female transsexualism". Fertility and Sterility. 90 (1): 56–9. doi:10.1016/j.fertnstert.2007.05.056. PMID 17765230.
  10. ^ a b Diamond M (2013). "Transsexuality Among Twins: Identity Concordance, Transition, Rearing, and Orientation". International Journal of Transgenderism. 14 (1): 24–38. doi:10.1080/15532739.2013.750222. S2CID 144330783. Combining data from the present survey with those from past-published reports, 20% of all male and female monozygotic twin pairs were found concordant for transsexual identity... The responses of our twins relative to their rearing, along with our findings regarding some of their experiences during childhood and adolescence show their identity was much more influenced by their genetics than their rearing.
  11. ^ a b Dreger A, Feder EK, Tamar-Mattis A (September 2012). "Prenatal Dexamethasone for Congenital Adrenal Hyperplasia: An Ethics Canary in the Modern Medical Mine". Journal of Bioethical Inquiry. 9 (3): 277–294. doi:10.1007/s11673-012-9384-9. PMC 3416978. PMID 22904609.
  12. ^ Clayton PE, Miller WL, Oberfield SE, Ritzén EM, Sippell WG, Speiser PW (2002). "Consensus statement on 21-hydroxylase deficiency from the European Society for Paediatric Endocrinology and the Lawson Wilkins Pediatric Endocrine Society". Hormone Research. 58 (4): 188–95. doi:10.1159/000065490 (inactive 1 November 2024). PMID 12324718. S2CID 41346214.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  13. ^ a b Erickson-Schroth L (2013). "Update on the Biology of Transgender Identity". Review. Journal of Gay & Lesbian Mental Health. 17 (2): 150–74. doi:10.1080/19359705.2013.753393. S2CID 216136930.
  14. ^ For a survey, see Swaab DF, Castellanos-Cruz L, Bao AM (2016). "The Human Brain and Gender: Sexual Differentiation of Our Brains.". In Schreiber G (ed.). Transsexuality in Theology and Neuroscience. Findings, Controversies, and Perspectives. Berlin and Boston: Walter de Gruyter. pp. 23–42. ISBN 978-3-11-044080-5.
  15. ^ Carlson NR (2010). Psychology: The Science of Behavior (7th ed.). Pearson Education. p. 418. ISBN 9780205547869.
  16. ^ Zhou JN, Hofman MA, Gooren LJ, Swaab DF (November 1995). "A sex difference in the human brain and its relation to transsexuality". Nature. 378 (6552): 68–70. Bibcode:1995Natur.378...68Z. doi:10.1038/378068a0. hdl:20.500.11755/9da6a0a1-f622-44f3-ac4f-fec297a7c6c2. PMID 7477289. S2CID 4344570.
  17. ^ Kruijver FP, Zhou JN, Pool CW, Hofman MA, Gooren LJ, Swaab DF (May 2000). "Male-to-female transsexuals have female neuron numbers in a limbic nucleus". The Journal of Clinical Endocrinology and Metabolism. 85 (5): 2034–41. doi:10.1210/jcem.85.5.6564. PMID 10843193.
  18. ^ Chung WC, De Vries GJ, Swaab DF (February 2002). "Sexual differentiation of the bed nucleus of the stria terminalis in humans may extend into adulthood". The Journal of Neuroscience. 22 (3): 1027–33. doi:10.1523/jneurosci.22-03-01027.2002. PMC 6758506. PMID 11826131.
  19. ^ Gooren L (November 2006). "The biology of human psychosexual differentiation". Review. Hormones and Behavior. 50 (4): 589–601. doi:10.1016/j.yhbeh.2006.06.011. PMID 16870186. S2CID 21060826.
  20. ^ Swaab DF (December 2004). "Sexual differentiation of the human brain: relevance for gender identity, transsexualism and sexual orientation". Review. Gynecological Endocrinology. 19 (6): 301–12. doi:10.1080/09513590400018231. PMID 15724806. S2CID 1410435.
  21. ^ Garcia-Falgueras A, Swaab DF (December 2008). "A sex difference in the hypothalamic uncinate nucleus: relationship to gender identity". Brain. 131 (Pt 12): 3132–46. doi:10.1093/brain/awn276. PMID 18980961.
  22. ^ Luders E, Sánchez FJ, Gaser C, Toga AW, Narr KL, Hamilton LS, Vilain E (July 2009). "Regional gray matter variation in male-to-female transsexualism". NeuroImage. 46 (4): 904–7. doi:10.1016/j.neuroimage.2009.03.048. PMC 2754583. PMID 19341803.
  23. ^ Rametti G, Carrillo B, Gómez-Gil E, Junque C, Segovia S, Gomez Á, Guillamon A (February 2011). "White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study". Journal of Psychiatric Research. 45 (2): 199–204. doi:10.1016/j.jpsychires.2010.05.006. PMID 20562024.
  24. ^ Pol HE, Cohen-Kettenis PT, Van Haren NE, Peper JS, Brans RG, Cahn W, Schnack HG, Gooren LJ, Kahn RS (2006). "Changing your sex changes your brain: influences of testosterone and estrogen on adult human brain structure". European Journal of Endocrinology. 155: S107–S114. doi:10.1530/eje.1.02248.
  25. ^ Bao, Ai-Min; Swaab, Dick (February 18, 2011). "Sexual differentiation of the human brain: relation to gender identity, sexual orientation and neuropsychiatric disorders". Review. Frontiers in Neuroendocrinology. 32 (2): 214–226. doi:10.1016/j.yfrne.2011.02.007. PMID 21334362. S2CID 8735185.
  26. ^ Smith, Elke Stefanie; Junger, Jessica; Derntl, Birgit; Habel, Ute (1 December 2015). "The transsexual brain – A review of findings on the neural basis of transsexualism". Review. Neuroscience & Biobehavioral Reviews. 59: 251–266. doi:10.1016/j.neubiorev.2015.09.008. ISSN 0149-7634. PMID 26429593. S2CID 23913935. Retrieved 4 October 2021.
  27. ^ Nguyen, Hillary B.; Loughead, James; Lipner, Emily; Hantsoo, Liisa; Kornfield, Sara L.; Epperson, C. Neill (January 2019). "What has sex got to do with it? The role of hormones in the transgender brain". Review. Neuropsychopharmacology. 44 (1): 22–37. doi:10.1038/s41386-018-0140-7. ISSN 1740-634X. PMC 6235900. PMID 30082887.
  28. ^ a b c d e Uribe, Carme; Junque, Carme; Gómez-Gil, Esther; Abos, Alexandra; Mueller, Sven C.; Guillamon, Antonio (2020-05-01). "Brain network interactions in transgender individuals with gender incongruence". NeuroImage. 211: 116613. doi:10.1016/j.neuroimage.2020.116613. hdl:2445/183973. ISSN 1053-8119. PMID 32057995. S2CID 211068133.
  29. ^ Frigerio, Alberto; Ballerini, Lucia; Valdes-Hernandez, Maria (2021). "Structural, Functional, and Metabolic Brain Differences as a Function of Gender Identity or Sexual Orientation: A Systematic Review of the Human Neuroimaging Literature". Archives of Sexual Behavior. 50 (8): 3329–3352. doi:10.1007/s10508-021-02005-9. hdl:20.500.11820/7258d49f-d222-4094-a40f-dc564d163ea7. PMC 8604863. PMID 33956296. S2CID 233870640. Results suggest that, although the majority of neuroanatomical, neurophysiological, and neurometabolic features in transgenders resemble those of their natal sex rather than those of their experienced gender,...in the gender identity investigation, in MtF it was possible to find traits which are "feminine and demasculinized" and in FtM it was possible to find traits which are "masculine and defeminized" (Kreukels & Guillamon, 2016)....Due to conflicting results, it was, however, not possible to identify specific brain features which consistently differ between cisgender and transgender nor between heterosexual and homosexual groups. Very small brain changes, to date undetectable using the current neuroimaging tools, may affect behavior. The small number of studies, the small sample size of each study, the heterogeneity of investigations, the lack of negative results reported by some studies, and the fact that some studies did not report the sexual orientation of the individuals that composed their sample did not allow drawing general conclusions. Moreover, as the samples of the publications involved are not representative of the population analyzed, caution should be taken in the interpretation of the results of this review.
  30. ^ Nawata H, Ogomori K, Tanaka M, Nishimura R, Urashima H, Yano R, et al. (April 2010). "Regional cerebral blood flow changes in female to male gender identity disorder". Psychiatry and Clinical Neurosciences. 64 (2): 157–61. doi:10.1111/j.1440-1819.2009.02059.x. PMID 20132527.
  31. ^ Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. 2013. pp. 451–460. ISBN 978-0-89042-554-1.
  32. ^ a b c Blanchard R (October 1989). "The concept of autogynephilia and the typology of male gender dysphoria". The Journal of Nervous and Mental Disease. 177 (10): 616–23. doi:10.1097/00005053-198910000-00004. PMID 2794988.
  33. ^ Freund K, Steiner BW, Chan S (February 1982). "Two types of cross-gender identity". Archives of Sexual Behavior. 11 (1): 49–63. doi:10.1007/BF01541365. PMID 7073469. S2CID 42131695.
  34. ^ Bailey JM (2003). The Man Who Would Be Queen: The Science of Gender-Bending and Transsexualism. Washington, D.C.: Joseph Henry Press. p. 170. ISBN 978-0-309-08418-5. OCLC 52779246.
  35. ^ Blanchard R (August 2005). "Early history of the concept of autogynephilia". Archives of Sexual Behavior. 34 (4): 439–46. doi:10.1007/s10508-005-4343-8. PMID 16010466. S2CID 15986011.
  36. ^ Smith YL, van Goozen SH, Kuiper AJ, Cohen-Kettenis PT (December 2005). "Transsexual subtypes: clinical and theoretical significance". Psychiatry Research. 137 (3): 151–60. doi:10.1016/j.psychres.2005.01.008. PMID 16298429. S2CID 207445960.
  37. ^ Blanchard R (August 1989). "The classification and labeling of nonhomosexual gender dysphorias". Review. Archives of Sexual Behavior. 18 (4): 315–34. doi:10.1007/BF01541951. PMID 2673136. S2CID 43151898.
  38. ^ Blanchard R (January 1988). "Nonhomosexual gender dysphoria". Journal of Sex Research. 24 (1): 188–93. doi:10.1080/00224498809551410. PMID 22375647.
  39. ^ Blanchard R (Winter 1991). "Clinical observations and systematic studies of autogynephilia". Journal of Sex & Marital Therapy. 17 (4): 235–51. doi:10.1080/00926239108404348. PMID 1815090.
  40. ^ Veale JF, Clarke DE, Lomax TC (August 2008). "Sexuality of male-to-female transsexuals". Archives of Sexual Behavior. 37 (4): 586–97. doi:10.1007/s10508-007-9306-9. PMID 18299976. S2CID 207089236.
  41. ^ Moser C (2010). "Blanchard's Autogynephilia Theory: a critique". Journal of Homosexuality. 57 (6): 790–809. doi:10.1080/00918369.2010.486241. PMID 20582803. S2CID 8765340.
  42. ^ Nuttbrock L, Bockting W, Mason M, Hwahng S, Rosenblum A, Macri M, Becker J (April 2011). "A further assessment of Blanchard's typology of homosexual versus non-homosexual or autogynephilic gender dysphoria". Archives of Sexual Behavior. 40 (2): 247–57. doi:10.1007/s10508-009-9579-2. PMC 2894986. PMID 20039113.
  43. ^ Moser C (2009). "Autogynephilia in women". Journal of Homosexuality. 56 (5): 539–47. doi:10.1080/00918360903005212. PMID 19591032. S2CID 14368724.
Kembali kehalaman sebelumnya