David Price / Destiny "Dee" Price / MangudiaForce - Crazy Mean Ugly Tranny from SC who spergs about Blaire White and Tommy Tooter

blablabla said:
i went to college, what about you dave? and no your retard fantasies about how you are an idiot savant doesnt count
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I went to college. And better yet I was due to the math placement exam a math prodigy and due to the first major exams a science prodigy.

I have a record in academics that include a very high up test from the 9th grade that was above a four year college level where I scored 2nd in the nation.

You are no able to comprehend medical science. it is Dee Dee and that is fact.

I am a transsexual yes but trans woman are women.

trans women are women.jpg


So there is a TRUE AND HONEST stating clearly trans women are in fact women.

So that makes you TRANSPHOBIC. By @Dyn comment. I am a trans woman and was diagnosed as a transsexual in 1982.
 
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Dee Price said:
I went to college. And better yet I was due to the math placement exam a math prodigy and due to the first major exams a science prodigy.

I have a record in academics that include a very high up test from the 9th grade that was above a four year college level where I scored 2nd in the nation.

You are no able to comprehend medical science. it is Dee Dee and that is fact.

I am a transsexual yes but trans woman are women.

View attachment 2754857

So there is a TRUE AND HONEST stating clearly trans women are in fact women.

So that makes you TRANSPHOBIC. By @Dyn comment. I am a trans woman and was diagnosed as a transsexual in 1982.
Click to expand...
>taking dyn seriously
 
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Dead Wayne said:
proof >taking dyn seriously
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Are you mad at Dyn And Dyn is correct. See there is a lot medical science that says Dyn is correct. None that even remotely backs blablabla or yourself.

Now see shit like blablabla say they went to college but will never show proof but want others to show proof so they can dox them.

I am not that stupid and also I know blablabla is totally incorrect and has no clue about biology beyond a high school level.
 
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Dee Price said:
Are you mad at Dyn And Dyn is correct. See there is a lot medical science that says Dyn is correct. None that even remotely backs blablabla or yourself.

Now see shit like blablabla say they went to college but will never show proof but want others to show proof so they can dox them.

I am not that stupid and also I know blablabla is totally incorrect and has no clue about biology beyond a high school level.
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I don't care, I'm just saying citing the site's most prolific provocateur like it's some sort of slam dunk in your favor isn't a good look. I don't know what kind of headspace you need to be in to think screenshotting some random post that ostensibly agrees with you in any way supports your argument
 
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Reactions: secret watcher
Dee Price said:
I went to college. And better yet I was due to the math placement exam a math prodigy and due to the first major exams a science prodigy.
Click to expand...
Going to college and graduating from it are two very different things. And that fractured English in that sentence speaks for itself.
 
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Reactions: secret watcher
Dyn said:
don't at me faggot
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Well here is the thing I am a transsexual diagnosed in 1980 and first went on HRT in 1984.

trans women are women.jpg


so now you are transphobic as well?
Boom Boss said:
Proof?

@Dyn I'm breaking the law.
Click to expand...
Proof it is from 1978 and it was at Aiken Prep. but here lets show you a lot of proof.

Comparative Study

J Clin Endocrinol Metab

. 2000 May;85(5):2034-41.
doi: 10.1210/jcem.85.5.6564.

Male-to-female transsexuals have female neuron numbers in a limbic nucleus​

F P Kruijver 1, J N Zhou, C W Pool, M A Hofman, L J Gooren, D F Swaab
Affiliations collapse

Affiliation​

  • 1Graduate School Neurosciences Amsterdam, The Netherlands Institute for Brain Research. F.Kruijver@nih.knaw.nl

Abstract​

Transsexuals experience themselves as being of the opposite sex, despite having the biological characteristics of one sex. A crucial question resulting from a previous brain study in male-to-female transsexuals was whether the reported difference according to gender identity in the central part of the bed nucleus of the stria terminalis (BSTc) was based on a neuronal difference in the BSTc itself or just a reflection of a difference in vasoactive intestinal polypeptide innervation from the amygdala, which was used as a marker. Therefore, we determined in 42 subjects the number of somatostatin-expressing neurons in the BSTc in relation to sex, sexual orientation, gender identity, and past or present hormonal status. Regardless of sexual orientation, men had almost twice as many somatostatin neurons as women (P < 0.006). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of the females (P = 0.83). In contrast, the neuron number of a female-to-male transsexual was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood did not seem to have influenced BSTc neuron numbers. The present findings of somatostatin neuronal sex differences in the BSTc and its sex reversal in the transsexual brain clearly support the paradigm that in transsexuals sexual differentiation of the brain and genitals may go into opposite directions and point to a neurobiological basis of gender identity disorder.

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  • Comparative Study

pubmed.ncbi.nlm.nih.gov

Male-to-female transsexuals have female neuron numbers in a limbic nucleus - PubMed

Transsexuals experience themselves as being of the opposite sex, despite having the biological characteristics of one sex. A crucial question resulting from a previous brain study in male-to-female transsexuals was whether the reported difference according to gender identity in the central part...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov

Regional gray matter variation in male-to-female transsexualism​

Eileen Luders,1 Francisco J. Sánchez,2 Christian Gaser,3 Arthur W. Toga,1,* Katherine L. Narr,1 Liberty S. Hamilton,1 and Eric Vilain2
Author information Copyright and License information Disclaimer
1Laboratory of Neuro Imaging, Department of Neurology, UCLA School of Medicine, 635 Charles Young Drive South, Suite 225, Los Angeles, CA 90095-7334, USA
2Center for Gender-Based Biology, Department of Human Genetics, UCLA School of Medicine, Gonda 5524, Los Angeles, CA 90095, USA
3Department of Psychiatry, University of Jena, Philosophenweg 3, 07740 Jena, Germany
Correspondence should be addressed to: Dr. Arthur W. Toga Laboratory of Neuro Imaging, Department of Neurology, UCLA School of Medicine 635 Charles Young Drive South, Suite 225, Los Angeles, CA 90095-7334 Phone: 001-310 / 206.2101 Fax: 001-310 / 206.5518 ude.alcu.inol@agot

The publisher's final edited version of this article is available at Neuroimage
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Associated Data​

Supplementary Materials
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Abstract​

Gender identity—one's sense of being a man or a woman—is a fundamental perception experienced by all individuals that extends beyond biological sex. Yet, what contributes to our sense of gender remains uncertain. Since individuals who identify as transsexual report strong feelings of being the opposite sex and a belief that their sexual characteristics do not reflect their true gender, they constitute an invaluable model to understand the biological underpinnings of gender identity. We analyzed MRI data of 24 male-to-female (MTF) transsexuals not yet treated with cross-sex hormones in order to determine whether gray matter volumes in MTF transsexuals more closely resemble people who share their biological sex (30 control men), or people who share their gender identity (30 control women). Results revealed that regional gray matter variation in MTF transsexuals is more similar to the pattern found in men than in women. However, MTF transsexuals show a significantly larger volume of regional gray matter in the right putamen compared to men. These findings provide new evidence that transsexualism is associated with distinct cerebral pattern, which supports the assumption that brain anatomy plays a role in gender identity.
Keywords: Brain, Gender Identity, MRI, Transgender, VBM
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Introduction​

Individuals who identify as transsexual report a history of persistent discomfort with the sex they were assigned at birth and a strong identification with the opposite sex. Many describe significant symptoms of psychological distress (Sánchez and Vilain, 2009) and take steps to alter features of their bodies (e.g., through the use of sex hormones and plastic surgery) to make them congruent with their sense of gender. While no formal epidemiological study has been conducted in the United States, reports from European and Asian countries estimate that the prevalence of transsexualism ranges from 1:100,000 to 1:2,900 (DeCuypere G. et al., 2007).
Despite increased public awareness of transsexualism, our scientific understanding of the development of gender identity is limited. Both environmental events (Eagly and Wood, 1999; Wood and Eagly, 2002) and innate differences (Breedlove, 1994; Dorner, 1985; Gooren, 2006) have been implicated as influencing this fundamental human characteristic. Regarding transsexualism, it has been suggested that sexual differentiation of the brain during embryonic development deviates from the sexual differentiation of the rest of the body (Zhou et al., 1995). This hypothesis implies that neuroanatomy plays a critical role in determining gender identity. Thus, the study of the underlying correlates of transsexualism may help to further identify the mechanisms that contribute to the development of gender identity.
To explore this hypothesis, several studies examined brain structures in male-to-female (MTF) transsexuals. One early in vivo study did not detect any associations between transsexualism and the anatomy of the corpus callosum (Emory et al., 1991). However, two subsequent post mortem brain analyses revealed that MTF transsexuals had a female-like central subdivision of the bed nucleus of the stria terminalis (BSTc) with respect to its size (Zhou et al., 1995) and number of neurons (Kruijver et al., 2000). Another post mortem study published recently reported female-like volumes and neuronal densities of the interstitial nucleus of the anterior hypothalamus (INAH3) in MTF transsexuals (Garcia-Falgueras and Swaab, 2008). These three post mortem studies seem to support the hypothesis that brain anatomy is associated with transsexualism. Yet, the generalization of these findings is limited by the inherent pitfalls of post mortem studies, the relatively small number of MTF transsexuals examined (n1=6; n2=6; n3=11), as well as the subjects' long-term treatment with estrogen. Granted, some argue that estrogen treatment does not alter certain brain structures (Garcia-Falgueras and Swaab, 2008). Nevertheless, other studies have shown that treatment with anti-androgen and estrogen decreases brain volumes of MTF transsexuals subjects towards female proportions (Hulshoff Pol et al., 2006).
To extend these prior findings while overcoming some of their limitations, we investigated variations in brain structure in 60 control subjects (30 males, 30 females) and 24 male-to-female (MTF) transsexuals who had not been treated with female hormones. More specifically, we used magnetic resonance imaging (MRI) to investigate neuroanatomy at high-resolution in vivo, and applied a sophisticated computational image analysis approach to compare regional volumes of gray matter throughout the brain.
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Materials and Methods​

Subjects​

Twenty-four MTF transsexuals were recruited through fliers provided to local transsexual community organizations and to professionals who offer services to the transsexual community. Thirty male and thirty female control subjects were selected from the International Consortium for Brain Mapping (ICBM) database of normal adults (http://www.loni.ucla.edu/ICBM/Databases/). The mean age (SD) of the MTF transsexuals was 46.73 (13.18) years with an age range between 23 and 72 years. Male and female control subjects were closely age-matched (males 46.57±12.45, 23-69 years; females 46.77±12.88, 23-73 years). Transsexual subjects were 76% dextral, control males were 93% dextral, and control females were 90% dextral, where handedness was determined based on self-reports of hand preference for selected activities. For study inclusion, transsexual subjects needed to self-identify as a MTF transsexual, report no history of hormonal treatment, and declare the intention of undergoing estrogen replacement therapy. MTF transsexuals were evaluated to be free of psychosis according to a standardized diagnostic interview (Robins et al., 1989) and confirmed to be genetic males as defined by the presence of the SRY gene in their genome (Jordan et al., 2002). All control subjects had to pass a physical and neurological screening examination performed by a neurologist. All subjects gave informed consent according to guidelines from the Institutional Review Board of the University of Los Angeles, California (UCLA), and were compensated for their participation in this study.

Image acquisition​

Brain images were acquired on a 1.5-T MRI system (Siemens Sonata, Erlangen, Germany) using a 3D T1-weighted sequence (MPRAGE) with the following parameters: TR = 1900 ms; TE = 4.38 ms; flip angle = 15°; 160 contiguous 1 mm sagittal slices; FOV = 256 mm × 256 mm2; matrix size = 256 × 256, voxel size = 1.0 × 1.0 × 1.0 mm.

Image Analysis​

Data were preprocessed and examined using SPM5 software (Wellcome Department of Imaging Neuroscience Group, London, UK; http://www.fil.ion.ucl.ac.uk/spm). Analyses were performed on gray matter segments (Ashburner and Friston, 2005) that were multiplied by the non-linear components derived from the normalization matrix (modulated gray matter volumes) and smoothed with a Gaussian kernel of 12 mm full width at half maximum. These smoothed modulated gray matter volumes are hereafter referred to as gray matter to simplify matters.
We used the general linear model (GLM) and applied analyses of covariance (ANCOVA) to examine voxel-wise gray matter differences between MTF transsexuals, males, and females, while removing the variance associated with age. Statistical outcomes were corrected for multiple comparisons, using false discovery rate (FDR) (Benjamini and Hochberg, 1995) at p<0.001. Significant findings were mapped onto the average 3D cortical model and restricted to clusters exceeding a minimum of 123 voxels (the expected number of voxels per cluster), calculated according to the theory of Gaussian random fields (Fig. 1). Finally, to gain a better understanding of how significance profiles from different sets of comparisons are spatially related to each other, we performed additional post hoc t-tests and overlaid significant group differences as maximum intensity projections on the SPM standard glass brain template in three orthogonal planes. These exploratory outcomes are also presented at p<0.001, corrected for multiple comparisons using FDR (Fig. 2).

[IMG alt="An external file that holds a picture, illustration, etc.
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Fig. 1
Analysis of variance (ANOVA) between samples. The color-coded brain maps illustrate the brain regions where gray matter volumes differ significantly between the three groups (MTF transsexuals, males, females), after removing the variance associated with age. Statistical outcomes are corrected for multiple comparisons, using FDR at p<0.001. Shown are clusters exceeding a spatial extent threshold of 123 voxels. The two box plots display the estimated parameters for clusters located in the region of the left and right putamen, where MTF transsexuals (TR) had more gray matter than males (MA) and females (FE).

[IMG alt="An external file that holds a picture, illustration, etc.
Object name is nihms-123153-f0002.jpg"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754583/bin/nihms-123153-f0002.jpg[/IMG]
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Fig. 2
T-tests between samples. The overlay maps on the SPM standard glass brain template (sagittal, axial, and coronal view) illustrate where independent-sample group comparisons revealed significant gray matter volume differences between females and males (Panel A), between females and MTF transsexuals (Panel B), as well as between males and MTF transsexuals (Panel C), after removing the variance associated with age. Panel D depicts the overlay of significance profiles from different sets of comparisons. Findings are significant at p<0.001, FDR-corrected.
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Results​

As demonstrated in Fig. 1, we detected significant differences between MTF transsexuals, males, and females in a large number of regions across the brain. More specifically, within the frontal lobe, we observed gray matter volume differences bilaterally in the superior frontal gyrus, close to midline and also at the frontal pole, as well as within the right orbital gyrus. Furthermore, we noticed pronounced gray matter volume differences bilaterally across the occipital and posterior temporal lobes, as well as in the parietal lobe, near the intraparietal sulcus, and closer to midline (left). Additional group effects on regional gray matter volume were detected subcallosally in both hemispheres at the brain midline. These regions constitute part of the basal ganglia (i.e., the caudate nucleus and putamen) and limbic system (i.e., the subcallosal gyrus, mammillary body, amygdala, thalamus and hypothalamus). Moreover, we identified two clusters indicating group differences on the basal surface of the right temporal lobe and left frontal lobe.
For each of 22 significantly different regions (twelve within the right hemisphere and ten within the left hemisphere), cluster-specific box plots were generated to illustrate the magnitude and direction of gray matter volume differences between groups (see supplement 1 and 2). Altogether, females had the largest gray matter volumes in all but two significant clusters, which were located in the left and right putamen. Here, MTF transsexuals had the largest gray matter volumes (see Fig. 1). For the remaining clusters, MTF transsexuals had the smallest gray matter volumes, but their data spectrum largely overlapped with that of males.
As illustrated in the spatial profiles of significant group differences (Fig. 2), females had more gray matter than males in large portions of the brain (Females > Males; red clusters in Panel A). Similarly, females had more gray matter than MTF transsexuals (Females > Transsexuals; red clusters in Panel B). Although the differences between females and MTF transsexuals did partly overlap with the difference between females and males (Females > Males / Transsexuals; yellow clusters in Panel D), they were spatially more extended, and also evident in a few regions where females and males did not differ (Females > Transsexuals; green clusters in Panel D). There was no region where females had significantly less gray matter than males (Panel A) or MTF transsexuals (Panel B). Similarly, there was no region where MTF transsexuals had significantly less gray matter than males (Panel C). MTF transsexuals, however, showed significantly more gray matter than males in the right putamen (Transsexuals > Males; red clusters in Panel C; blue clusters in Panel D). MTF transsexuals also showed significantly more gray matter than males in the left putamen when findings were not corrected for multiple comparisons (p<0.001, maps not shown).
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Discussion​

Overall, our study provides evidence that MTF transsexuals possess regional gray matter volumes mostly consistent with control males. However, the putamen was found to be “feminized” in MTF transsexuals. That is, the gray matter volume of this particular structure in the MTF transsexual group was both larger than in males and within the average range of females. Interestingly, in a positron emission tomography (PET) study, it was demonstrated that the left putamen in a sample of MTF transsexuals (n=12), who had no history of estrogen treatment, activated differently to odorous steroids when compared to control males (Berglund et al., 2008). Taken together, these findings lend support to the hypothesis that specific neuroanatomical features are associated with transsexual identity, where the particular role of the putamen requires investigation in future studies.
Further research needs to resolve whether the observed distinct features in the brains of transsexuals influence their gender identity or possibly are a consequence of being transsexual. Alternatively, other variables may be independently affecting both the expression of a transsexual identity and the neuroanatomy in transsexuals that led to the observed association between both. Some possible candidates include genetic predisposition, psychosocial and environmental influences, hormonal exposures, or most likely an interplay between these variables. In support of the influence of genetics and environment, multiple cases of transsexualism occurring within families have been reported (Green, 2000) as well as studies on heritability in twins (Coolidge et al., 2002) and preliminary findings on specific genetic variations in MTF transsexuals (Hare et al., 2009; Henningsson et al., 2005). Furthermore, both genes and environmental demands have been demonstrated to determine brain anatomy (e.g., regional gray matter) (Draganski et al., 2004; Thompson et al., 2001). Finally, hormones have been shown to affect brain development (Arnold and Gorski, 1984), and neuroanatomical alterations in MTF transsexuals (Kruijver et al., 2000; Zhou et al., 1995) have been detected in cerebral structures shown to significantly change in response to hormonal exposure (Del et al., 1987; Guillamon et al., 1988). The MTF transsexuals of the current study had no history of hormonal treatment. Thus, we can exclude the potential effects of administered female hormones as a confounding factor for our findings. Moreover, it has been demonstrated that naturally circulating hormones in adult MTF transsexuals at baseline do not differ significantly from hormonal levels in male control subjects (Goodman et al., 1985; Meyer, III et al., 1986; Spijkstra et al., 1988). However, it remains to be established whether pre-, peri-, or postnatal hormonal effects in early childhood could foster transsexualism. Further studies will need to resolve the degree to which genetic variability and environmental factors influence the development of gender identity (Schweizer et al., 2009), possibly (but not necessarily) via affecting brain structures.
A limitation of the current study is that MTF transsexuals are considered as one homogeneous group rather than dividing them into MTF transsexuals who are sexually attracted (a) to males, (b) to females, (c) to both sexes, or (d) to neither sex. Based on self-report, a common yet limited method of assessing sexual orientation (Moradi et al., 2009), our transsexual sample (n=24) consisted of 6 male-oriented and 18 female-oriented subjects. Given this unequal distribution and given that information on sexual orientation was unavailable for control subjects, we abstained from conducting analyses for different subtypes. However, a number of previous findings appear to indicate brain-structural alterations associated with sexual orientation (Allen and Gorski, 1992; Byne et al., 2001; LeVay, 1991; Ponseti et al., 2007; Savic and Lindstrom, 2008; Swaab and Hofman, 1990; Witelson et al., 2008). Moreover, a highly controversial line of research has suggested that homosexual and non-homosexual MTF transsexualism are etiologically heterogeneous (Blanchard, 1989a; Blanchard, 1989b), which may be associated with differences in neuroanatomy. Therefore, future studies that take into consideration sexual orientation will not only further reveal the underlying determinants of gender identity in general, but also possibly advance our understanding of different transsexual subtypes.
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Supplementary Material​

01​

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02​

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Acknowledgments​

This work was supported by the National Institutes of Health through the NIH Roadmap for Medical Research, grant U54 RR021813 entitled Center for Computational Biology (CCB). Information on the National Centers for Biomedical Computing can be obtained from <http://nihroadmap.nih.gov/bioinformatics>. Additional support was provided by the NIH/NCRR resource grant P41 RR013642, Dr. Sánchez's NIH training grant 5 T32 HD07228: 26, Dr. Gaser's BMBF grant 01EV0709, and Dr. Narr's NIH K-award MH073990.
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Footnotes​


Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Reference List​

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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
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Human Molecular Genetics Laboratory (LH, PB, VRH), Prince Henry's Institute of Medical Research; Department of Genetics (LH, VRH), Monash University; Centre for Eye Research Australia (PNB), University of Melbourne and Royal Victorian Eye and Ear Hospital; Monash Gender Dysphoria Clinic (TK), Moorabbin, Melbourne, Australia; and the Department of Human Genetics (FJS, EV), University of California, Los Angeles, California
Address reprint requests to Vincent R. Harley, BSc(PhD), Human Molecular Genetics Laboratory, Prince Henry's Institute of Medical Research, Melbourne, Australia; gro.syrnehecnirp@yelraH.tnecniV

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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 β (ERβ), 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 ERβ 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 ERβ 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.
Keywords: Androgen receptor, AR, aromatase, CYP19, ERβ, estrogen receptor β, gender identity disorder, transsexualism

​

From an early age, people develop an inner sense of being male or female. Transsexuals however, identify with a physical sex opposite to their biological sex. Such individuals might seek to alleviate their distress by altering their bodies through hormone therapy and sex reassignment surgery (1). The prevalence of transsexualism ranges from 1:2,900 to 1:100,000; and little is known about the etiology of this condition (2–4). Some theories have suggested that psychosocial factors— including dysfunctional family dynamics (5) and traumatic childhood experiences (6)—lead to the development of a transsexual identity.
Increasingly, biomedical research is implicating biological factors. Co-occurrence among twin pairs, father-son pairs, and brother-sister pairs (7,8) raises the question of whether gender dysphoria is heritable. Anatomical studies show that certain brain structures in male-to-female transsexuals are more “female-like” in volume and neuronal density (9,10). Furthermore, the response to the odor of male and female steroids in male-to-female transsexuals was more similar to that of control women than control men (11). Other studies suggest that sex steroids influence gender identity. Female-to-male transsexuality has been associated with polycystic ovary syndrome and hyperandrogenemia (12). Moreover, female subjects with the disorder of sex development called congenital adrenal hyperplasia are exposed to high levels of androgens prenatally and seem to be at much higher risk of gender identity disorder than the general population (13). A significant association was identified between female-to-male transsexualism and the CYP17 gene (which encodes 17α-hydroxylase, the enzyme deficient in some virilized congenital adrenal hyperplasia patients) (14). Aromatase (CYP19), the enzyme that converts testosterone to estrogen, has also been implicated in female gender identity. A 46, XX woman with congenital adrenal hyperplasia carried a null CYP19 mutation, was born with phallic enlargement, a uterus, and ovaries, and exhibited a persistent male gender identity and male gender role behavior (15).
There are few genetic association studies of male-to-female transsexualism. A study of 29 Swedish male-to-female transsexuals identified a significant association with a dinucleotide CA polymorphism in the estrogen receptor β (ERβ) gene (p = .03) (16). It has been suggested that ERβ has a defeminization role in male brain and behavior, on the basis of knockout mouse studies (17). Altogether, genetic studies on transsexuals suggest that both androgen and estrogen might play a role in gender identity.
We sought to investigate whether sex steroidogenesis genes are associated with male-to-female transsexualism in the largest cohort collected to date. We analyzed the variable polymorphism lengths of three genes—androgen receptor (AR), ERβ, and CYP19—in Caucasian transsexuals and compared these with non-transsexual male control subjects.
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Methods and Materials​

Participants​

One hundred and twelve Caucasian male-to-female transsexuals, pre- and post-operative, were recruited from Monash Medical Centre (MMC), Victoria, Australia (n = 76) and from University of California, Los Angeles (UCLA) (n = 36) as per criteria in the DSM-IV—some of whom had reports of gender dysphoria in childhood. Almost all transsexual individuals were receiving hormone treatment. Two hundred and fifty-eight Caucasian male control subjects were also recruited from MMC. Ethical approvals for this study were obtained from MMC and UCLA, and consent procedures adhered to the tenets of the Declaration of Helsinki. The sexuality is only known for approximately 40% of patients, because some patients did not wish to discuss or disclose this information or the patient's sexuality was flexible and not easily classified.

Genotyping​

Genomic DNA was extracted from whole blood (18) or saliva (OrageneT). Androgen receptor exon 1 CAG repeat was amplified with polymerase chain reaction with VIC-labelled 5′-TCTGGAT-CACTTCGCGCAC-3′ and 5′-GTTCCTCATCCAGGACCAGGTA-3′. The ERβ intron 5 CA repeat was amplified with FAM-labelled 5′-GGTACAGACCATGGTTTACC-3′, and 5′-AACAAAATGTT-GAATGAGTGGG-3. The CYP19 intron 4 TTTA repeat was amplified with NED-labelled 5′-GGTACTTAGTTAGCTACAATC-3′, and 5′-GGGTGATAGAGTCAGAGCCT-3′. Polymerase chain re action was 95°C for 30 sec, 30 sec at 59°C for AR, 55°C for ERβ, and 58°C for CYP19, and extension at 72°C for 30 sec for 35 cycles. The polymerase chain reaction products from the three genes were then mixed for each individual with Genescan LIZ-500 size standard and analyzed on an ABI Prism 3130xl (Applied Biosystems, Foster City, California). Successful genotyping was achieved for at least 101 of the 112 transsexual individuals across the three gene polymorphisms (101 for AR, 111 for ERβ, and 104 for CYP19) and 258 control subjects.

Statistics​

To evaluate the repeat length polymorphism data for possible associations with male-to-female transsexualism, independent samples t tests were used. Interactions between the three gene polymorphisms were evaluated with a binary logistic regression model. Analyses were performed with Statistical Package for the Social Sciences 12.0 software (SPSS, Chicago, Illinois). A p value < .05 was considered significant. The primary analysis performed was of the association between male-to-female transsexualism and AR, ERβ, and CYP19 genotypes.
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Results​

Polymorphic fragment lengths for 258 male subjects and 112 transsexuals were obtained. Twenty-one different alleles were identified for the AR gene polymorphism, 14 for the ERβ gene polymorphism, and 8 for the CYP19 gene polymorphism. The percentages of each allele in the control and transsexual populations are shown in Figure 1. For the AR gene, a difference in the mean repeat length was identified, with transsexuals having significantly longer mean repeat lengths (243.2 base pairs) than control subjects (245.1 base pairs, p = .04).

[IMG alt="An external file that holds a picture, illustration, etc.
Object name is nihms369145f1.jpg"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402034/bin/nihms369145f1.jpg[/IMG]
 
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Dee Price said:
I went to college. And better yet I was due to the math placement exam a math prodigy and due to the first major exams a science prodigy.

I have a record in academics that include a very high up test from the 9th grade that was above a four year college level where I scored 2nd in the nation.
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I asked for your college credentials. Not a bunch of trans information.
 
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Boom Boss said:
Looking more feminine than Tommy Tooter is such an easy thing to do. Dee Price is still a ragetard.
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Especially since I don't try, but you know what? Most people have no trouble relating to me as a female person. i don't even get misgendered in the real world by strangers much any more.
 
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Anybody else get angry DM's from @Dee Price? I've been getting them for a week straight, and I guess she rage quit because she stopped submitting them, and continued to submit rage posts on the forums. Here is the multiple part conversation that I just screenshotted. Enjoy the rage, insults, threats, lectures, and false claims.

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