RESUMO
La Transexualidad según el ICD-10 (Clasificación Internacional de Enfermedades, décima edición), o Disforia de Género en adolescentes y adultos en el DSM-5 (Manual Diagnóstico y Estadístico de Desórdenes Mentales, quinta edición), se caracteriza por una marcada incongruencia entre género y sexo biológico. La etiología de la Disforia de Género (DG) o Transexualidad es compleja. Algunas hipótesis señalan una discrepancia entre sexo cerebral y sexo biológico. Otras evidencias sugieren una vulnerabilidad genética. Henningsson y col, (2004) encontraron diferencias estadísticamente significativas cuando examinaron el receptor de estrógenos Beta (ERß) y el receptor de andrógenos (AR) en una población MtF (del inglés male-to-female). Los autores sugieren que en la población MtF son más frecuentes las formas largas de los genes ERBeta y AR. Hare y col, (2009) también encontraron una asociación significativa entre el tamaño del gen AR y la DG. Nuestro grupo replicó los trabajos de Henningsson y col, (2004) y Hare y col, (2009) en una de las poblaciones con DG más grande analizada hasta el momento, confirmando la implicación de los receptores de estrógenos formas alfa y Beta) y el receptor de andrógenos, en la base genética de la DG. Nuestros datos apoyan la existencia de una vulnerabilidad genética de la DG tanto en la población MtF como en la FtM. Corroboran la implicación de los receptores de estrógenos alfa y beta y el receptor de andrógenos en la masculinización del cerebro en humanos. Confirman así mismo que la identidad sexual no es una opción, sino que viene determinada genéticamente, aunque posee un componente hormonal muy importante. Su substrato por tanto, no es ideológico, sino cerebral
Transsexualism in the ICD-10 (International Classification of Diseases, Tenth Revision), Gender Dysphoria in adolescents and adults in the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition), is characterized by a marked incongruence between ones experienced gender and biological sex. The etiology is complex, but some hypotheses suggest that Gender Dysphoria (GD) arises from discrepant cerebral and biological sexual differentiation. Increasingevidence supports the idea of genetic vulnerability. Henningsson et al, (2004) found significant differences when they examined estrogen receptor Beta (ER Beta) in a male-to-female (MtF) population. They suggested that a long ER Beta polymorphism is more common in MtFs. Hare et al, (2009) also examined an MtF population and found a significant association between the androgen receptor (AR) and GD. Our group analyzed the same polymorphisms and found an association between ER alfa, ER Beta and AR in GD. Our results suggest a genetic basis of GD in MtF and FtM populations. Our data corroborate the implication of the two estrogen receptors, ERalfa and Beta, and the androgen receptor in the genetic basis of GD, and advise the importance of estrogens and androgens in cerebral masculinization. Our data also confirm that sexual identity is not optional, but is determined prenatally by the genes, although it has a very importanthormonal component. Therefore, its substrate is cerebral, not ideological
Assuntos
Humanos , Transexualidade/genética , Disforia de Gênero/genética , Receptores de Estrogênio/análise , Receptores Androgênicos/análise , Pessoas Transgênero/psicologia , Identidade de Gênero , Procedimentos de Readequação Sexual/éticaRESUMO
Transsexualism in the ICD-10 (International Classification of Diseases, Tenth Revision), Gender Dysphoria in adolescents and adults in the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition), is characterized by a marked incongruence between one's experienced gender and biological sex. The etiology is complex, but some hypotheses suggest that Gender Dysphoria (GD) arises from discrepant cerebral and biological sexual differentiation. Increasing evidence supports the idea of genetic vulnerability. Henningsson et al, (2004) found significant differences when they examined estrogen receptor ß (ERß) in a male-to- female (MtF) population. They suggested that a long ERß polymorphism is more common in MtFs. Hare et al, (2009) also examined an MtF population and found a significant association between the androgen receptor (AR) and GD. Our group analyzed the same polymorphisms and found an association between ERα, ERß and AR in GD. Our results suggest a genetic basis of GD in MtF and FtM populations. Our data corroborate the implication of the two estrogen receptors, ERα and ß, and the androgen receptor in the genetic basis of GD, and advise the importance of estrogens and androgens in cerebral masculinization. Our data also confirm that sexual identity is not optional, but is determined prenatally by the genes, although it has a very important hormonal component. Therefore, its substrate is cerebral, not ideological.