Quote from: stldrmgrl on December 11, 2011, 04:21:13 PM
I mean, seriously. There is no evidence to support anything as to the source or cause of transsexualism, thus it just is.
Biol Psychiatry. 2009 Jan 1;65(1):93-6. Epub 2008 Oct 28.
Androgen receptor repeat length polymorphism associated with male-to-female transsexualism.
Hare L, Bernard P, Sánchez FJ, Baird PN, Vilain E, Kennedy T, Harley VR.
Source
Human Molecular Genetics Laboratory, Prince Henry's Institute of Medical Research, Melbourne, Australia.
Abstract
BACKGROUND:
There is a likely genetic component to transsexualism, and genes involved in sex steroidogenesis are good candidates. We explored the specific hypothesis that male-to-female transsexualism is associated with gene variants responsible for undermasculinization and/or feminization. Specifically, we assessed the role of disease-associated repeat length polymorphisms in the androgen receptor (AR), estrogen receptor beta (ERbeta), and aromatase (CYP19) genes.
METHODS:
Subject-control analysis included 112 male-to-female transsexuals and 258 non-transsexual males. Associations and interactions were investigated between CAG repeat length in the AR gene, CA repeat length in the ERbeta gene, and TTTA repeat length in the CYP19 gene and male-to-female transsexualism.
RESULTS:
A significant association was identified between transsexualism and the AR allele, with transsexuals having longer AR repeat lengths than non-transsexual male control subjects (p=.04). No associations for transsexualism were evident in repeat lengths for CYP19 or ERbeta genes. Individuals were then classified as short or long for each gene polymorphism on the basis of control median polymorphism lengths in order to further elucidate possible combined effects. No interaction associations between the three genes and transsexualism were identified.
CONCLUSIONS:
This study provides evidence that male gender identity might be partly mediated through the androgen receptor.
Androgen Receptor Repeat Length Polymorphism
Associated with Male-to-Female Transsexualism
Lauren Hare, Pascal Bernard, Francisco J. Sánchez, Paul N. Baird, Eric Vilain, Trudy Kennedy,
and Vincent R. Harley. BIOL PSYCHIATRY 2009;65:93–96
Background: There is a likely genetic component to transsexualism, and genes involved in sex steroidogenesis are good candidates. We
explored the specific hypothesis that male-to-female transsexualism is associated with gene variants responsible for undermasculinization
and/or feminization. Specifically, we assessed the role of disease-associated repeat length polymorphisms in the androgen receptor (AR),
estrogen receptor _ (ER_), and aromatase (CYP19) genes.
Methods: Subject-control analysis included 112 male-to-female transsexuals and 258 non-transsexual males. Associations and interactions
were investigated between CAG repeat length in the AR gene, CA repeat length in the ER_ gene, and TTTA repeat length in the CYP19 gene
and male-to-female transsexualism.
Results: A significant association was identified between transsexualism and the AR allele, with transsexuals having longer AR repeat
lengths than non-transsexual male control subjects (p_.04). No associations for transsexualism were evident in repeat lengths for CYP19 or
ER_ genes. Individuals were then classified as short or long for each gene polymorphism on the basis of control median polymorphism
lengths in order to further elucidate possible combined effects. No interaction associations between the three genes and transsexualism
were identified.
Conclusions: This study provides evidence that male gender identity might be partly mediated through the androgen receptor.
Sex steroid-related genes and male-to-female Transsexualism
Susanne Henningssona, Lars Westberga, Staffan Nilssonb,
Bengt Lundstro¨mc, Lisa Ekseliusd, Owe Bodlunde, Eva Lindstro¨md,
Monika Hellstranda, Roland Rosmondf, Elias Erikssona, Mikael Lande´ng,*
Department of Pharmacology, Institute of Physiology and Pharmacology, Go¨teborg University,
Go¨teborg, Sweden Department of Mathematical Statistics, Chalmers University of Technology, Go¨teborg, Sweden Section of Psychiatry, Institute of Clinical Neuroscience, Go¨teborg University, Go¨teborg, Sweden Department of Neuroscience, Uppsala University, Uppsala, Sweden
eDepartment of Psychiatry, UmeaUniversity, Umea, Sweden
fDepartment of Heart and Lung Diseases, Go¨teborg University, Go¨teborg, Sweden
gDepartment of Clinical Neuroscience, Section of Psychiatry S:t Go¨ran, Karolinska Institutet,
Stockholm 112 81, Sweden
Received 16 November 2004; received in revised form 12 February 2005; accepted 14 February 2005
Summary Transsexualism is characterised by lifelong discomfort with the
assigned sex and a strong identiÞcation with the opposite sex. The cause of
transsexualism is unknown, but it has been suggested that an aberration in the early
sexual differentiation of various brain structures may be involved. Animal
experiments have revealed that the sexual differentiation of the brain is mainly
due to an inßuence of testosterone, acting both via androgen receptors (ARs) andÑ
after aromatase-catalyzed conversion to estradiolÑvia estrogen receptors (ERs). The
present study examined the possible importance of three polymorphisms and their
pairwise interactions for the development of male-to-female transsexualism: a CAG
repeat sequence in the Þrst exon of the AR gene, a tetra nucleotide repeat
polymorphism in intron 4 of the aromatase gene, and a CA repeat polymorphism in
intron 5 of the ERb gene. Subjects were 29 Caucasian male-to-female transsexuals
and 229 healthy male controls. Transsexuals differed from controls with respect to
the mean length of the ERb repeat polymorphism, but not with respect to the length
of the other two studied polymorphisms. However, binary logistic regression analysis
revealed signiÞcant partial effects for all three polymorphisms, as well as for the
interaction between the AR and aromatase gene polymorphisms, on the risk of
developing transsexualism. Given the small number of transsexuals in the study,
the results should be interpreted with the utmost caution. Further study of the
putative role of these and other sex steroid-related genes for the development of
transsexualism may, however, be worthwhile.
2005 Elsevier Ltd. All
