Machine Learning Transsexual Brains = Garbage In: Garbage Out

If one spends any time reading science papers about transsexuality, one finds good science, mediocre science, poor science, bad science, and bogus science. But here is an example of garbage science. A paper came out last year that baldy stated that using machine learning and brain imaging, they could, somewhat accurately, determine an individual’s gender identity. This sounded like really exciting results. But after reading the paper, I’m calling BULLSHIT! It’s a harsh characterization, I know. But please follow along to see why I had no other choice.

First, let me state that I’m not an expert on Machine Learning and Deep Neural Net coding. But I have, in my capacity as an engineering executive, managed such experts. I’ve also, in my capacity as a Venture Capitalist (VC) technology advisor, conducted due dilligence research on start-up companies developing ML and NN technology. So I have just enough knowledge to be dangerous… that is to say, I know bullshit when I see it. And I see it here.

The bullshit consists of three elements.

The first is that researchers failed to tell us how many of their subjects were in the training set and how many were in the testing set. But first, let my tell you an anecdote about the time I was in the audience at a technical conference where a young researcher was presenting almost unbelievably high classification accuracy from his new computer vision algorithm. Finally, the first question from the audience during the post-presentation Q&A was how many examples were in the training set and how many in the test set? The young man then acknowledged that he had used the training set to test his algorithm. You could hear the visceral disgust sweep across the room at this basic error. Question is, did the authors make the same mistake? They said that 95% of the DATA was used in training and 5% in the “validation” of the model. Umm…. something is not right. There were less than 25 subjects in each category. Five percent of 25 is one. There was no way they could have used different subjects to have gotten a percentage accuracy of classification without having used the same subjects to provide both training and accuracy tests. So, what was the data split? Different parts of the brain scans of the same subjects? Seriously, something is very wrong here. One cannot do that.

The second garbage element is that they knowingly ignored prior science that there is very clear evidence that there are two separate taxons, at least for the Male-To-Female transsexuals, that have notably different brain phenotypes. We know that they knew because they referenced the Guillamon review paper on that very topic. But, since they didn’t bother to identify and segregate the two taxons for separate analysis, they were knowingly conflating the two, which would dilute the signals of both. The basic rule of thumb is never ascribe to conspiracy what can be explained by incompetence. Given the above issue of questionable Machine Learning validation, incompetence may have been the reason. The second possibility is that they knew this conflation was occuring, but felt, for non-scientific reasons, that they wanted this to occur. (I’ve seen this happen in other papers.)

The third garbage element is actually the most egregious. They claim that they identified nine “cardinal” gender related vectors in their study. But did they? I will argue that no they did not. This is where garbage in, garbage out really applies. They used the Bem Sex Role Inventory and cross correlated it with the brain scan data, claiming that the Bem inventory provides a window to gender. Flat out, it does not. It is an inventory of circa 1970s gender stereotypes! The most enraging thing about this is that the authors KNOW that, fully acknowledge that, but decided to use it anyways.

All in all, the Clemens paper is garbage. So the next question is how could such a paper pass peer review? The answer is where it was published. Cerebral Cortex would have reviewers who were experts in the brain science, but NOT sexology nor in machine learning. They just would have looked at the material that was in their field of expertise and allowed the other material to get a pass, unquestioned.

Further Reading:

Silly Stereotypes: Essay on the BEM inventory

Brainstorm: Essay about the Guillamon brain scan review

Reference:

Clemens, B. et. al., “Predictive Pattern Classification Can Distinquish Gender Identity Subtypes From Behavior And Brain Imaging”, Cerebral Cortex, (2020), https://doi.org/10.1093/cercor/bhz272

Because Boys Must Be Boys…

…Its a Fact of Human Nature, and Girls Must Grow Up to Be Mothers!

Over the years that I’ve been writing this blog, I’ve deliberately avoided using the popular term “gender non-conforming”, using the term “gender atypical” instead.  It may have struck some of my readers as odd and idiosyncratic, given that so many others use the “GNC” term.  But, I have done so for several important reasons, some based on science, some on political-philosophical grounds.

The scientific reasons are easier to explain.  There is no “standard” to which behavior should “conform”.  There is only behavior, period.  However, if we look at, study in depth as scientists, a species we can say that there are behaviors that are far more commonly performed by them than other behaviors seen in other species.  These we can label as “typical” for that species.  If we see a behavior in a given individual of a species that is uncommon for that species, we may label it “atypical”; but we would never label it “non-conforming” since we can’t really say what standard that a given species should “conform” to.  Behaviors are selected by evolution depending upon whether they increase the reproductive ‘fitness’ of the individuals exhibiting them.  The same logic applies to sexes within a given species.  We may observe sexually dimorphic behaviors in a given species.  That is, we will label a behavior sexually dimorphic if we see that it is much more commonly performed in one sex than the other.  If we see an individual performing such a behavior that is uncommon in that given sex, we may label it “atypical” for that sex; but to label it “non-conforming”?  That’s smacks of invoking an outside agency which has the authority to define a standard for such behavior that the theory of natural selection does not provide.  Just as with non-human species, humans do not stand outside of nature.  There is no agency that defines for our species a standard by which to judge whether a given behavior does or does not “conform”.

The political reasons include my personal objection to the very notion that there should be such a “standard”.  But even deeper, is my objection to the post-modernist idea that there are no intrinsic sexually dimorphic behaviors in humans, that there are only socially constructed roles.  This notion would state that since all differences in behavior observed between the human sexes are socially constructed and maintained, there must be a socially defined standard to which we can conform or not.  Another idea that I object to is that of a divinely ordained standard that we must conform to, which has the same effect.  Thus, both of these ideas reduce any behavior that is seen in an individual that is uncommon in that person’s sex to an act of “gender non-conformity” either by accident or by will… but never by nature.  I find both the notion that we stand outside of nature to be scientifically preposterous and philosophically offensive.   Further, those who seek humane treatment for gender atypical individuals will find that they must contend with those who hold these ideas often falling back on unquestioned prejudices, the nature of which is determined by which value system through which they view such gender atypical individuals, post-modernist or religious.

Before going into details about the nature of the prejudices and what we must contend, let’s explore how we know that human beings do have sexually dimorphic behaviors that have both neural correlates and developmental pathways leading to them.  It’s important to differentiate between behaviors that are demonstrably sexually dimorphic because of neural correlates and those that are merely cultural role enactments and false gender stereotypes.  Thus, for purposes of this essay, I differentiate between a strong social construction hypothesis which says that all differences in behavior are purely from culture and a weak social construction hypothesis that says that some behaviors and gender roles are socially constructed around truly sexually dimorphic behaviors and gender role limitations built around cultural prejudice and false stereotypes.  It is the strong social construction hypothesis that I will show is not supported by the evidence.

In other pages of this blog, I’ve made reference to the single most sexually dimorphic behavior in humans: androphilia (sexual attraction to adult males).  In female humans, it is extremely common to be attracted to men.  Approximately 98% of women are attracted to men while only approximately 5-10% of men were attracted to men.  One could object to this being a ‘natural’ phenomena and say that social expectations have defined this.  But it would not fit the evidence that has been amassing that sexual orientation is neither “chosen” nor “taught”.  Further, why should humans be unique in the world?  Most mammalian species are sexually dimorphic in their sexual attractions.  (No, I’m not denying that same sex behavior occurs in non-human species… only saying it is not as common as other sex attraction.)  But, this isn’t the end of the story.

Sexual orientation in adults is presaged by gendered behavior as young children.  That is to say, that humans have sexually dimorphic behaviors as young children and that sexual orientation is highly correlated with those behaviors.  Children that grow up to be homosexual evince notable gender atypicality.  The key behaviors that are noted to be gender atypical in boys are avoidance of rough and tumble play, avoidance of physical aggression, preference for female playmates and play style, etc.  But here is where we start to see the issue of having to contend with those prejudices.  Some cultures attach serious negative stigma to gender atypicality while others do not.  Most of my readers will likely live in cultures that do and will recognize the ugly recriminations in the song, “Boys Will Be Boys”; “You bloody sissy, who said you could cry?” down to the call to an authority defining the standard to which a child must conform, “Doctor, Doctor, tell me where did we go wrong?”.

But we in our enlightened age know that the parents did nothing wrong… (yes, you may take that to be sarcasm).

In other essays on this blog, I’ve explored some of the science that shows that sexual orientation is correlated with childhood gender atypicality, the Fraternal Birth Order Effect, etc.  I’ve discussed possible etiological hypothesis.  I have in the past written about the disappointment with using the 2D:4D digit ratios as a means of exploring the possible effect of varying androgens as being correlated with sexual orientation.  But now, I want to share a really amazing bit of evidence that shows that perinatal exposure to androgens is likely to be responsible for masculinizing the human brain and its absence affecting early childhood gender atypicality, as Vicky Pasterski puts it,

By now, the majority of scientists studying the topic likely agree that homosexuality is definitely not a choice and probably not due to socioenvironmental factors. At the same time, there appear to be no physical indicators of disrupted fetal sexual differentiation in homosexual men that would fit with the basic premise of the hormone theory of sex development. However, it is possible that alterations in the androgen surge that occurs in the early postnatal period, also called mini-puberty, could have effects that are not immediately or physically obvious. Based on the finding that penile growth in the first three months of life correlates with a concomitant surge in serum testosterone levels considered the possibility that penile growth may act as a proxy for neonatal androgen exposure and that change measurements may be related to later neurobehavioral outcomes. In a longitudinal study of 81 typically developing boys, we found that the strength of the early postnatal androgen surge, from birth to approximately three months of age, predicted masculine behavior at 4 years old. By controlling for effects of prenatal androgen exposure using measurements of penile length and anogenital distance (AGD; sexually dimorphic and roughly twice as long in males compared to females) at birth, we showed that penile growth in the first three months of life, but not thereafter, accounted for significant variance in later sex-typed behavior. In the overall regression analysis, which controlled for various factors, penile length at birth was not related to sex-typed behavior. This suggests that disruption to male mini-puberty could have implications for future sex-related outcomes that are masked by a typical appearance at birth. Further, this provides support for the hypothesis that early (postnatal) hormone exposure influences aspects of sex-typed development in men, in a similar fashion to prenatal hormone exposure that is presumed to affect women.

In Pasterski’s research, she divided the boys into three groups (tertiles) based on their gendered behavior from the Pre-School Activities Inventory and mapped against the growth rate of their genitals in the first months after birth, which has been shown to correlate with androgen exposure.  (Though to be complete, it may also correlate with androgen receptor sensitivity, but for my purposes, that would have the same epistemic value.)  The results are dramatic, we see with no ambiguity that the rate of growth of genitalia is positively correlated with gender typical behavior.   That also means that the inverse is true.  Gender atypical behavior is inversely correlated with perinatal genital growth.

Had the strong social construction hypothesis of all gendered behavior been true, there would have been no correlation.  We can reject this hypothesis.  At best, we have a weak social construction hypothesis of gender roles around very real sexually dimorphic differences.  Those that lampoon this conclusion by calling it “Lady Brain” theory are just plain wrong.

It has been previously noted that gender atypically behaving children have differences in facial “attractiveness”.  This fits well with the above research as male children who have not had this intense “mini-puberty” would likely remain neotenous and thus feminine in appearance.  This likely also extends past adolescence to explain the rather dramatic differences in passability between androphilic transwomen and gynephilic transwomen.  Being gender atypical in brain organization, it would naturally lead to later androphilia, gender atypical motor skills (feminine walk and hand gestures), and gender atypical vocal production (feminine or “gay lisp”).

Given the religious (or related social views of gender) prejudice, one can easily see how children who exhibit these gender atypical behaviors are placed under tremendous pressure to “conform” to gender behavior standards that tend to skew to the gender typical, or even an exageration of typical behavior.  Children who meet this standard are prized and praised above other children.  That is to say, extreme gender typicality is valorized as well as held as the gender normitive standard and granted privilege over children who fail to meet this standard.

Here I opine, perhaps even hypothesize, that this pressure to conform to normative gender role standards has distorted what would be the natural course of development of gender atypical children and has led to the creation of the artificial gender normative role of Western Gay and Lesbian culture, especially the “Straight Looking / Straight Acting” Gay male standard to which otherwise gender atypical male children are required to adhere.  To the non-gay community members, the benefit of artificial standard was originally to force gay people to remain deep in the closet.  As the Western Gay Liberation movement gained ground, those who had tacitly accepted this standard began to subtly and not so subtly enforce it.

One would, at first glance, believe that those who hold the strong social construction hypothesis as true would then have no qualms about accepting gender atypical children and adults without reservation as breaking stereotypes.  But, as we can easily discern, they often do not, as demonstrated by the minority movement within the gay and lesbian (mostly lesbian) communities of being “gender critical”.  They philosophically approve of people being gender atypical… but only to a very specified point, accepting the gender normative roles that were established during the early Gay Liberation Movement.  The moment that an individual steps past that point, there will be those who will denounce them as hewing to the very stereotypes that they break, but in the opposite gendered sense, denying that underlying sexually dimorphic behavior as valid.  In some cases, public denouncements of the very existence of gender atypical males have been made (e.g. Jean O’Leary’s public denouncement of Silvia Rivera, and other early androphilic transactivists, as “mocking women” at the 1973 Stonewall commemoriation for wearing feminine clothing).  On the internet today, this same gender role proscription is made where androphilic transwomen are chastised in the ugliest terms, “just because you’re a gay man doesn’t mean that you can be excused for objectifying women (by looking and acting like one).”  Thus, we see that gender role policing based on accepting gender normative standards exists even in the modern LGB communities.

Further Reading:

Essay on motor movement in gender atypical males.

Essay on vocal production in gender atypical people.

Essay on passability differences between gynephilic vs. androphilic transsexuals.

Article on Gender Difference by Olivia Goldhill

References:

Pasterski, V., “Fetal Androgens and Human Sexual Orientation: Searching for the Elusive Link”, (2017) Archives of Sexual Behavior
https://link.springer.com/article/10.1007/s10508-017-1021-6

Pasterski, V., et al., “Postnatal penile growth concurrent with mini-puberty predicts later sex-typed play behavior: Evidence for neurobehavioral effects of the postnatal androgen surge in typically developing boys”, (2015) Hormones and Behavior
http://www.sciencedirect.com/science/article/pii/S0018506X15000033#f0005

Song Reference:

Boys Will Be Boys
(Leon Rosselson)

Boys will be boys, it’s a fact of human nature
And girls will grow up to be mothers

Look at little Peter, isn’t he a terror?
Shooting all the neighbors with his cowboy gun
Screaming like a jet plane, always throwing something
I just can’t control him. Trouble – he’s the one.

Ah but boys will be boys, it’s a fact of human nature
And girls will grow up to be mothers

Look at little Janie, Doesn’t she look pretty?
Playing with her dolly, proper little mum
Never getting dirty, never being naughty
Don’t punch your sister Peter, now look at what you’ve done

Ah but boys will be boys, it’s a fact of human nature
And girls will grow up to be mothers

What’s come over Janie, Janie’s turning nasty
Left hook to the body, right hook in the eye
Vicious little hussy, now Peter’s started bawling
What a bloody sissy, who said you could cry?

Because boys must be boys, it’s a fact of human nature
And girls must grow up to be mothers

Now things are topsy turvy. Janie wants a football
Peter just seems happy pushing prams along
Makes you feel so guilty. Kids are such a worry
Doctor, doctor, tell me, where did we go wrong?
Because boys must be boys, it’s a fact of human nature

 

Audio Sex Perception

I don’t suppose it would surprise anyone that straight men and women respond differently to men’s and women’s voices.  In fact, I think we would be surprised if we didn’t.  After all, straight men are attracted to women and their voices, and straight women are attracted to men and men’s voices.  But that’s only the obvious part.  They also tend to be different in their ability to perceive them, with both sexes responding stronger and faster to opposite sex voices.  They also differ in the amount of cognitive resources used in the task, the amount of effort applied.  Women use fewer resources than men… they are just better at it.

Now, before one says… OH, a sexually dimorphic difference in the brain!  Whoa!  Hold on!  That may not be true at all.  Other research into perception of other signals, ohh… such as emotional expressions have also shown sexually dimorphic difference in ability.  But in that case, we also know that wealth and power differences also show up.  Rich and/or powerful people are significantly and robustly less able to read emotions on other’s faces than poor and/or less socially privileged people.  Further, practice at reading people’s emotional expressions significantly improves this skill.  So, is that a built in, sexually dimorphic brain difference between men and women?  Or does is simply reflect that women, as a class, have less wealth, power, and privilege than men?  I’m betting on the latter.

And so it is with the amount of effort it takes to “read” one’s sex by listening to their voice.  Is this built in?  Or is it that women NEED to read voices better, just as they NEED to read faces better?  I’m betting on the latter.

Now we come to transwomen (MTF transsexuals).  In a study conducted in Germany, transsexuals seemed to be unique in some ways, like men in some, and like women in others.  One thing that they did find is that during fMRI scanning of the brains of transwomen, they showed that they were using very little effort to determine which sex a given speaker was, similar to women.  Interestingly, they analyzed both androphilic and gynephilic transwomen together and separately, though didn’t report them separately, instead they focused on testing pre-HRT and current HRT.  They found little difference between the two populations, androphilic vs. gynephilic and pre-HRT and HRT.  I’m not surprised by this.  In fact, it supports my hypothesis that this is NOT an innate sexually dimorphic trait, nor mediated by hormones, but the result of the social differences in privilege and experience / learning.  The two MTF populations have the same basic experiences regarding their own vocal history and needs, as the authors put it,

“Since we found no differences in accuracy between women and MtFs, decreased activation in MtFs might suggest that they need less effort to achieve levels of performance similar to women. This might be due to the fact that MtFs are more attuned to issues related to voice gender perception in everyday life.  … In line with the behavioral results, MtFs showed differences (compared to men and women) in neuronal response patterns with respect to male vs. female voices. Presumably, a different strategy is used in MtFs’ voice gender identification due to early processing differences. They also might more intensively examine their own and aspired vocal characteristics during gender alignment, resulting in a certain expertise. In this sense, attentional differences due to automatized processing could lead to less brain activation in MtFs.”

Reference:

Junger, J., Habel, U., Bröhr, S., Neulen, J., Neuschaefer-Rube, C., Birkholz, P., … Pauly, K. (2014). More than Just Two Sexes: The Neural Correlates of Voice Gender Perception in Gender Dysphoria.(11), e111672. doi:10.1371/journal.pone.0111672

 

 

Gender Allusions

Is “Gender Identity” biological?  For most people, the answer is intuitively obvious, “duh!”.  Of course, for these people, they usually also insist that the markers for such identity is some privileged and testable characteristic, like genitalia, which is easy to observe, or karyotype (sex chromosome configuration) which requires a microscope.  But for people with Disorders of Sexual Development (DSD), these markers may not be all that clear.  Further, what are we to make of the gender identities of transsexual and transgendered people, people whose experienced / stated gender identity is at odds with all currently known sex markers?  IS there a biological etiology?  And is that etiology the same as that that gives rise to the gender identity of non-trans people? A recent review article attempts to answer these very questions.  Sadly, I believe that it falls far short of a conclusive answer.  In fact, as I will show, it invokes conclusions from several papers as evidence that are quite questionable.  Further, the authors failed to note the very probable multiple etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality. First, they reviewed evidence for a biological basis for the phenomenological existence of “gender identity” in non-transfolk which comes from those with certain DSDs,

A seminal study by Meyer-Bahlburg et al involving outcomes of XY individuals raised as females due to severe non-hormonal, anatomic abnormalities of sex development has provided the most convincing evidence that gender identity is fixed. These congenital abnormalities include penile agenesis, cloacal exstrophy, and penile ablation. For many years, female gender assignment along with surgical feminization was the dominant approach for these patients. In this study, it was observed that 78% of all female-assigned 46 XY patients were living as females. While the majority of these patients did not initiate a gender change to male, none of the 15 male raised 46 XY patients initiated a gender change to female. Thus, risk of questioning gender identity was higher in those patients raised as females than in those raised as males among 46 XY subjects with one of these conditions. A study by the same group that examined the degree of satisfaction with surgical intervention reported by patients with 46 XY genotype also found that those subjects raised as boys were considerably more comfortable with their gender identity. – Another seminal study relevant to this topic was by Reiner and Gearhart in their review of 16 XY genotype subjects with cloacal exstrophy who underwent female gender reassignment surgery. Out of the 14 individuals raised as girls, 4 announced they were male and 4 later chose to live as boys when they became aware of their genotype. The 2 individuals who were raised as males identified as males throughout life. The sexual behavior and attitudes of all 16 subjects ultimately reflected strong masculine characteristics regardless of gender assignment. Thus, children who were born genetically and hormonally male identified as males despite being raised as females and undergoing feminizing genitoplasty at birth. Although cohort size in these studies is small, these data provide the strongest evidence for biological underpinnings of gender identity.  …  In a study of affected subjects, gender role changes were reported in 56-63% of cases with 5 alpha-reductase-2 and 39-64% of cases with 17-beta-hydroxy-steroid dehydrogenase-3 who were raised as girls (6). These data support the concept that gender identity might be attributed to hormone milieu during intrauterine development on some occasions.

These studies are indeed very strong evidence.  Looking at the data, we see that of those raised as girls, 22% of of these subjects in the first study and 57% in the second study, while in the third study, those with hormonal abnormalities, 56-63%, chose to socially transition from female-to-male.  Compare that to the very, very small number of 46XX individuals in the general population who experience severe gender dysphoria and choose to transition.  As an aside, the fact that not all chose to transition should not be taken as proof that gender identity is all that malleable, but should probably be taken as a demonstration that social transition has very high social costs and is not undertaken lightly. Strangely, this paper did not explicitly mention that the majority of these individuals, whether they experienced gender dysphoria or not, were exclusively gynephilic, but they did allude to it.  Also puzzling was their failure to include the converse situation of individuals with 46XY and complete androgen insensitivity syndrome (CAIS), all raised as female, who are extremely unlikely to experience gender dysphoria or sex reassignment, and are universally exclusively androphilic.  Or the even more interesting case of 46XX progestin influenced females raised as male, 50% of whom transitioned from male to female and all are exclusively androphilic.

Thus, they failed to explicitly show the very high correlation of brain sex with gender identity, gendered behavior, and sexual orientation. Having shown that there is indeed very strong evidence that “gender identity might be attributed to hormone milieu during intrauterine development on some occasions”, which supports the notion that gender identity has a basis in biology (as opposed to being purely a social construct overlain on observable sex differences), it is tempting to say that transsexuality, all transsexuality and transgender identity, is also the result of mismatched hormonal milieu.  In fact, many transsexuals hold to just such a position.

But they would be dead wrong.

The logical leap that all transsexuals have such an etiology is not supported by the above evidence.  In fact, given the very probable differing etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality, at least one of these types must NOT have been caused by such.  Blanchard went on to predict that this would be born out by studies of the sexually dimorphic structures in the brain, predicting that the exclusively androphilic MTF transsexual would show shifts toward the female morphology, while the other type would not. It is here that this recent paper has its biggest failings, in that not only did they not discuss this issue, but included very problematic studies by Swaab that purported to have shown female like shifts in non-exclusively androphilic transwomen.  These papers did show the shifts in the BSTc and INAH3, but incorrectly concluded that they had existed prior to exogenous HRT and incorrectly concluded that these features in the brain were organization effects of endogenous hormones in utero, when the data clearly demonstrated the opposite, that these shifts were purely activational effects from exogenous estrogenic and anti-androgenic HRT.  To be fair, they did mention that the BSTc was potentially questionable, but completely failed with regards to the INAH3, which demonstrably is not evidence for a biological basis of gender identity.

In reviewing the recent grey and white matter studies, they failed to note that it fits and supports Blanchard’s prediction, which had they done so, would have strengthened their argument for a biological basis for a conventional gender identity in exclusively androphilic MTF transsexuals.  That is to say, that they experience the same feminine “gender identity” as females because their brains are female like.  Conversely, they would also have evidence for a biological underpinning to autogynephiles sexuality, a non-sexually-dimporphic one, which lead to an epiphenomically generated “female gender identity” later in adulthood.  (See my essay on the different origins of cross-gender identity in transsexuals.)

The authors reviewed the literature on possible genetic factors that could lead to transsexuality, noting that they were inconclusive. Totally absent in this paper was any mention of the papers that document the fraternal birth order effect found in exclusively androphilic MTF transsexuals. All in all, I was disappointed in this paper.

I found it shallow, lacking in both depth and breadth, and literally out of step with much of the literature on the cutting edge of the science.

(Addendum 7/7/2015:  I got suspicious of this paper as it reads like a cherry-picked list of papers that support the brain sex hypothesis for all transsexuals, including “late onset” transwomen, so I checked into the background of the authors.  Sure enough, one of the authors is transgendered.  While that alone is NOT damning (after all, so am I), it does explain why this paper only referenced the studies it did, and did not include those studies that when considered as a whole, would show that while one subset of the larger transsexual population could possibly be explained by the brain sex hypothesis, most transwomen could not.  This paper then can and should be considered part of the ongoing effort by some in the transgender community to deny the evidence of the two type taxonomy.)

Reference:

Aruna Saraswat, MD, Jamie D. Weinand, BA, BS; Joshua D. Safer, MD, “Evidence Supporting the Biological Basis of Gender Identity” (2015) DOI:10.4158/EP14351.RA

 

Autistic Sky

For the past several years, evidence has been accumulating that there is a fairly high comorbitity between transsexuality / transgenderism and the autism spectrum.  Interestingly, and perhaps not totally surprisingly, among MTF transwomen, it appears to be exclusively found in the non-exclusively androphilic population.  This fits the Freund/Blanchard taxonomy and more importantly, Blanchard’s prediction that “non-homosexual” (with respect to natal sex) MTF transwomen would exhibit neurological / brain differences from control males but these differences would NOT be a shift toward female like brains.

Autism and autism spectrum disorders are found in four to five  times as many men as women.  There are a number of theories as to why this happens, including the rather intriguing “hypermasculine brain hypothesis”, in which a link between the slight differences between men and women, as groups, having different cognitive and social behaviors and the apparent similarity, or rather, exaggeration of these differences between men and women, found in those on the autism spectrum.  If autism is a form of hypermasculinization, it would not surprise us to learn that FTM transmen were more autistic-like than most women… and that is what one group of researchers found.

Using a 50 item, Likert scored, instrument called the Autism Spectrum Quotient (AQ), Jones, et Al., found that FTM transmen as a group, scored 23.2, higher than control women AND men!  This puts about half of the FTM onto the high functioning autism spectrum!!   (The lower AQ cut-off for ASD is 23.)  Non-exclusively-androphilic transwomen scored essentially the same as the control men, while exclusively androphilic transwomen scored essentially the same as the control women, and definitely (statistically significant: p<0.03 ) below both the control men and non-androphilic transwomen.

Group:               Men                  Women       FTM                 Non-Androphilic           Androphilic
.                                                                                                     MTF  N=129                   MTF N=69

Score (SD):       17.8 (6.8)        15.4 (5.7)     23.2 (9.1)        17.4 (7.4)                         15.0 (5.6)

The implication is clear, FTM’s are masculine, perhaps even hypermasculine, while the data also supports the Freund/Blanchard two type taxonomy for MTF transwomen.  In the discussion section of the paper, the authors remarked,

“Interestingly, with the 198 transwomen group, there were 6 individuals (i.e. 3%) with a diagnosis of AS. This rate is about 3 times as many as in the general population.”

These authors didn’t state what the sexuality of the six AS individuals were; but if they conform to the greater likelihood that they were non-androphilic, found in other papers, the incidence rate for such non-androphilic transwomen would be closer to five times the rate found in the general population, however, that is only about twice as high as that found in the male population.

(Addendum: 1/21/2017:  Looking at the data again, this time from the perspective of effect sizes with respect to men vs. women and non-androphilic vs. androphilic aids us in understanding how important this difference is.  First, the effect size between men and women is 0.38 a modest but still very noticable difference in the populations.  Now, let’s look at the diffence between non-androphilic and androphilic at 0.37, nearly identical to the difference between men and women.  So, lets compare the difference between men and non-androphilic tranwomen at 0.06 which is tiny.  And similarly, when we compare between women and androphilic transwomen it is only 0.07 which again is very tiny.  That is to say, these statistical tests shows that the difference between men and women is the same size as between non-androphilic and androphilic transwomen, while there is effectly no difference between men & non-androphilic and women & androphilic transwomen respectively.  That is to say, that non-androphilic transwomen are identical to men in general, while androphilic transwomen are essentially the same as women in general.  Further the difference between the two types of transwomen exactly matches the difference between men and women, which strongly supports the Two Type Taxonomy.)

Further Reading:

Autism and Transgender

References:

Jones, et Al, “Female-To-Male Transsexual People and Autistic Traits”, J. Autism Dev. Discord. DOI: 10.1007/s10803-011-1227-8

Annelou L. C. de Vries, Ilse L. J. Noens, Peggy T. Cohen-Kettenis, Ina A. van Berckelaer-Onnes. Theo A. Doreleijers, “Autism Spectrum Disorders in Gender Dysphoric Children and Adolescents” Journal of Autism and Developmental Disorders (2010)
https://link.springer.com/article/10.1007/s10803-010-0935-9

 

 

Drum keeps pounding… ♫♫

♫♫…rhythm to the brain…♫♫

Data keeps coming in regarding brain imaging studies showing differences between MTF and FtM transsexuals and control males and females.  The question still remains, what does it mean?  Two studies, by two different groups, have measured the cortical thicknesses of transwomen before beginning HRT, to ensure that they are measuring potential organizing effects of endogenous hormones, or other effects, without the confounding activational effects of HRT.  However, the two studies looked at the two different MTF populations.  One, the Zubiaurre-Elorza paper examined only androphilic transwomen (N=18). Given that this group came from Spain, which, as Lawrence demonstrated, has a very low Hofstede Individualism index which is correlated with low percentage of gynephilic transwomen, these 18 were likely to have accurately reported their sexuality as exclusively androphilic.   While the Luders study, as an earlier study reported, examined both gynephilic (N=18) and self reported androphilic (N=6) transwomen.  Given that we know from many other studies of transwomen in high Hofstede Individualism societies, and the fact that the youngest of the Luders group was 23, we would expect that not all six of those who reported that they were androphilic were exclusively so.  In fact, I doubt that more than one or two at most is exclusively androphilic, if any.  Thus arises the question, can we use these two studies to get an early test of Blanchard’s prediction that “non-homosexual” transwomen would show brain difference from controls, but not a shift towards the female typical while the “homosexual” will show just such a shift?

First, some background, since I know that not all readers will be thoroughly up to date on the hypothesis being tested, nor the relevant data supporting it.  I recommend reading the FAQ on the is blog before continuing to read this blog entry, as a starting point.  Given that there is now mountains of data supporting the hypothesis that there are two types of MTF tranwomen, one autogynephilic (AGP) and non-homosexual (with respect to natal sex) and one that is non-autogynephilic and exclusively homosexual (HSTS); and that AGP transsexuals were behaviorally masculine since early childhood, and often even after transition and SRS, while HSTS transwomen had been remarkably feminine in behavior, and often in appearance, since early childhood, Blanchard made the prediction that brain studies would show that BOTH populations would be different than control males, but in different ways.  He further made the prediction that HSTS brains would be shifted toward the female morphology in sexually dimorphic areas of the brain, while AGP transsexuals would not.

This prediction is in opposition to the so called, “feminine essence” hypothesis, which is generally popular among AGP transsexuals, in which they posit that despite their obvious lack of naturally feminine behavior, they are still neurologically “female-like”, at least in some important way.

So far, the very limited data supports Blanchard’s hypothesis and NOT the “feminine essence” hypothesis.  Also so far, no formal study has been conducted that would specifically test these two hypothesis together.

I stated earlier that I didn’t believe that the Luders study group contain many exclusively androphilic (HSTS) individuals.  The reasons I believe this are several fold.  First, they collected most of their group by soliciting via transgender organizations.  As was shown in the Veale study on transsexual sexuality, soliciting through such organizations tends to reach only AGP individuals, as HSTS youth do not tend to be members of such.  Second is the age range of the study entire group.  The youngest was 23.  This would be very unusual for a group of that had a sizable portion of HSTS individuals, given that the median age of transition is 20 years old and the top end is typically 25 years old, and even that old is very rare.  If all six HSTS individuals were 23 to 25, this would be odd.  Also given that the mean age of the entire group is 45, which is a bit higher than the typical mean transition age for a group consisting of only AGP transwomen, this would suggest that there were not many of the total group that was in their early 20’s, certainly not six out of 24 individuals.  Thirdly, as Lawrence has shown, in two different study groups, significant numbers of individuals who claim to be androphilic are inaccurately reporting their sexuality.  Added together, I don’t believe that more than one or at most two, of the Luders study group was actually exclusively androphilic.  I suspect that none of them were.

As we explore the data from these two papers, we need to keep in mind that brains, like bodies, come in different shapes and sizes, more or less.  That is to say, although there are differences between male and female brains, on average, it is difficult to point to a part of the brain and say with absolute certainty, this is a male brain vs. a female brain.  Another thing to keep in mind, if we have a mix of two populations, both may have differences unique to each population… and that when mixed, both of those differences will be detected when we average the data, blurring and blunting the differences, but we should still be able to statistically see a signal in the data, provided we have enough data.

So, lets examine the data.  First, if we look at the high level view, it would appear that there are indeed differences between the control men and women and androphilic transwomen.

In general, female brains have thicker cortices (CTh), at least in some areas, as the comparison between male and female controls shows.  As we had expected, MTF  transfolk are different than male controls, but FtM are not that different from female controls.  The authors described the results thus,

“We have found that control females have greater CTh compared with control males in the frontal and parietal regions; in contrast, males have a larger putamen volume than females. With respect to the transsexual groups, we observed that FtMs have greater CTh compared with control males in the parietal and temporal cortices and did not differ from control females. However, FtMs have a larger right putamen than female controls. On the other hand, MtFs did not differ from control females in CTh and had greater CTh than control males in the frontal and occipital regions. In this group, no differences were found in the putamen. All these findings suggest that FtMs have a defeminized putamen, while MtFs have a feminized CTh.

…

With respect to the CTh of MtFs, we found that this group did not differ from female controls but did from male controls.  These findings suggest that MtFs follow the pattern of cortical thinning typically described for females. Whether the cortical feminization of MtFs depends on a differential cortical androgen receptor distribution, a different efficiency in the androgen receptors or other causes remains to be elucidated.  But what seems clear is that in MtFs the cortical developmental process is affected and follows the direction expected for females. This points out that the developmental approach could help to understand the etiology of transsexualism.”

Let’s compare these results with that of the Luders study, which is mostly (and perhaps entirely) non-exclusively androphilic, which being autogynephilic, Blanchard had previously predicted would show differences from control males, but not in the female like direction:

At first blush, we see that they are indeed, as predicted, different than control males.  Some areas of the cortices are thicker, but not the same regions as control females nor androphilic transwomen.  So, it would seem unlikely that these brain difference are caused by a feminization of the brain, given that the regions are not those found in control females.  But what does cause these particular differences?  While we might be tempted to conclude that this is caused by autogynephilia, it could also be caused by another attribute that is common in this population, higher IQ.  It has been noted that higher IQ is correlated with thicker cortices.

So where to do we go from here?  This visual comparison of the two studies can only be described as tentative.  But the need for such comparisons are clearly understood by these researchers, as the Zubiaurre-Elorza paper explained,

“On the basis of chromosomal sex and behavior, Blanchard and co-workers (Blanchard et al. 1987, 1989, 1996; Blanchard 1989; see also Smith et al. 2005) have proposed the existence of 2 types of MtFs: 1) MtFs that are attracted to males (“homosexual” transsexuals in Blanchard terminology), and 2) MtFs that are attracted to women (“heterosexual” transsexuals according to Blanchard). Further, Blanchard (2008) hypothesized that homosexual MtFs would differ from heterosexual males in brain sexually dimorphic structures, while in the heterosexual MtFs, the differences might not implicate sexually dimorphic structures. More recently, Cantor (2011) has noted that our findings on the white matter microstructure of (homosexual) MtFs (Rametti, Carrillo, Gómez-Gil, Junque, Zubiarre-Elorza et al. 2011) and that of Savic and Arver (2011) on the cortical volume of (heterosexual) MtFs would support Blanchard’s hypothesis. In the present report, we studied MtF transsexuals erotically attracted to males that show a feminization of CTh but not in the putamen.  …  Consequently, to verify Blanchard’s hypothesis would require a specific design that is beyond the scope of the present study.”

For more essays on trans-brains see Brain Sex.

References:

Eileen Luders, et al., “Increased Cortical Thickness in Male-to-Female Transsexualism”
Journal of Behavioral and Brain Science, July 2011
http://dbm.neuro.uni-jena.de/pdf-files/Luders-JBBS11.pdf

Leire Zubiaurre-Elorza et al, “Cortical Thickness in Untreated Transsexuals”
Cerebral Cortex, August 2012
http://cercor.oxfordjournals.org/content/early/2012/08/30/cercor.bhs267.abstract

Katherine Narr, et al., Relationships between IQ and Regional Cortical Gray Matter Thickness in Healthy Adults
Cerebral Cortex, November 2006
http://cercor.oxfordjournals.org/content/17/9/2163.abstract

 

The Sound of Your Voice…

♫♫…Oh, how I miss waking up to the sound of your voice…♫♫
-Bare Naked Ladies

Each time we utter a word, we communicate far more than just the lexical unit of speech; we also announce to the listener our native language, our hometown, our age, our gender, and possibly our sexual orientation.  In the transgender field guide videos, I asked the viewer to pay attention to the vocal inflections of each of the transwomen.  If you listened carefully, you probably noted that the HSTS transkids each were distinctly different than the AGPs.  This vocal difference that transkids have, compared to non-gender-atypical boys, is present since childhood.  It is not a recent development, not a conscious attempt to sound like women.  That voice is largely untrained.

Many gay men have a discernibly “gay voice”, but not all.  Interestingly, this voice quality corresponds to the level of gender atypicality that they exhibited as children.  That is to say, that straight sounding gay men report having been typically masculine as boys, but “gay” sounding men report having been gender atypical as boys.  Research also shows that this “gay voice”, far from being a speech defect, the stereotyped “lisp”, it is actually clearer sounding speech.  This speech is also more like how heterosexual women speak, than how straight men speak.  Given this, it shouldn’t surprise anyone that gender atypical boys should sound more like girls than gender typical boys.

A large percentage of boys who were gender atypical grow up to be gay, though some do grow up to be straight identified.  (Given that being gay is still socially stigmatized and discriminated against, I personally suspect that many of these so-called “straight” men are in fact closet homosexuals.)  A number of these gender atypical boys are also gender dysphoric.  And a subset of those that are gender dysphoric will persist being so to become transkids.

In the Crocker and Munson study, they showed that older gender atypical boys had even more feminine voices than younger atypical boys.  As I showed in my essay on persisting and desisting gender dysphoria in children, those who desist in being gender atypical and gender dysphoric seem to be doing so just before the age of 10 or so.  Thus, I believe that we can surmise that Crocker& Munson’s older boys would have a higher percentage of ‘persisters’, transkids, than their younger test group.  So, I hypothesize that the increased perceived femininity of voice production in the older group is an artifact of the desisters having dropped out of the potential pool of older boys, leaving the more naturally feminine transkids.

One working assumption is that a sizable subset of gay men have significantly feminized brain structures that influence both erotic target (sexual orientation) and vocal production.  This is supplanting the hypothesis that the “gay voice” is the result of community wide agreement upon a ‘code’, a voice that helps gay men identify each other.  The evidence supports the former, rather than the latter, as pre-adolescent boys are unlikely to have self-identified as gay, and to have deliberately learned a community code.

I hypothesize that the feminization of the brain is more extensive in ‘persisters’, transkids, and that the voice production is similarly more feminized.  This is in keeping with the conceptualization that (at least some) gay men are somewhat feminized, more like women than straight men, and that HSTS transkids are “so gay they’re women”, as James Cantor has quipped.

I think it would be interesting for researchers to compare the “gay voice” to the “transkid voice”.  From my own experience, they are similar, but not identical.  The gay voice is trending towards the transkid voice, but doesn’t reach it.  The average transkid voice is trending toward the female voice, but also doesn’t quite reach it, though, with just a tiny effort, it can allow the average transkids to pass as female to most listeners.  Some transkids have voices so like the typical female voice that no effort is needed.

Again, as I pointed out in the field guide, the untrained AGP voice is typically masculine.  A great conscious effort must be made if an AGP wishes to achieve a passably female voice.  I think it would be interesting to compare and contrast the HSTS and AGP voice.

Addendum 1/4/2013:

Lal Zimman has conducted an interesting bit of research on FtM transmen’s voice, which I now reference.  He has a couple sound clips that may be of interest.

References:

Crocker, L., & Munson, B., “Speech Patterns of Gender Non-Conforming Boys”
http://www.tc.umn.edu/~munso005/Crocker&Munson_NWAV2006_PostConference.pdf

Peter Renn, “Speech, male sexual orientation, and childhood gender nonconformity”
http://homepage.psy.utexas.edu/homepage/class/psy158h/prevhonors/z111/project.htm

Deborah Günzburger, “Acoustic and perceptual implications of the transsexual voice”
http://link.springer.com/article/10.1007/BF01541604

Lal Zimman, “Pronunciation of ‘s’ sounds impacts perception of gender, CU-Boulder researcher finds”
http://www.colorado.edu/news/releases/2013/01/03/pronunciation-%E2%80%98s%E2%80%99-sounds-impacts-perception-gender-cu-boulder-researcher

 

 

Rolling the Dice…

Alice Dreger, who I deeply admire, has just published a paper regarding the disturbing off label use of powerful steroids… all in the hope of keeping female children from being tomboys, lesbians, and FtM transmen.

Reference:

Alice Dreger & Ellen K. Feder & Anne Tamar-Mattis, “Prenatal Dexamethasone for Congenital Adrenal Hyperplasia: An Ethics Canary in the Modern Medical Mine”
http://dx.doi.org/10.1007/s11673-012-9384-9

And the Beat Goes On…♫♫

♫…Drum keeps pounding rhythm to the brain… ♫ La di da di dee…♫

James Cantor recently published a letter to the editor in the Archives of Sexual Behavior pointing out nearly the same point that I had made earlier, that recent MRI scans of transsexual brains show clear evidence that Blanchard’s two type hypotheses is supported.  One of the papers he referenced is one that I had earlier referenced; The Rametti study in Spain, which showed that MTF  transkids have partially feminized brain structures.  The other paper is new to me; The Savic paper clearly adds yet another confirming MRI study that when combined with the Luders MRI study, shows that gynephilic MTF transsexuals do not have feminized brains.  On top of it, true to another speculative prediction that Blanchard made, the new study confirms the other paper’s finding that gynephilic (AGP) MTF transsexuals show other, non-sexually dimorphic structures, are different from both non-transsexual men and women!

These two papers both noted that the putamen of gynephilic MTF transsexual are different from both non-TS men and women.  This may be the main area to research in the future?

For more essays on trans-brains see Brain Sex

References:

Cantor, James, “New MRI Studies Support the Blanchard Typology of Male-to-Female Transsexualism”
http://www.springerlink.com/content/b52p04306u076623/

Reply to Italiano’s (2012) Comment on Cantor (2011)
JamesM. Cantor  http://link.springer.com/content/pdf/10.1007%2Fs10508-012-0011-y

Rametti G, Carrillo B, Gómez-Gil E, Junque C, Zubiarre-Elorza L, Segovia S, Gomez A, Guillamon A., “The microstructure of white matter in male to female transsexuals before cross-sex hormonal treatment. A DTI study.”
http://www.ncbi.nlm.nih.gov/pubmed/21195418

Ivanka Savic, Stefan Arver, “Sex Dimorphism of the Brain in Male-to-Female Transsexuals”
http://cercor.oxfordjournals.org/content/early/2011/04/05/cercor.bhr032

Luders E, Sánchez FJ, Gaser C, Toga AW, Narr KL, Hamilton LS, Vilain E., “Regional gray matter variation in male-to-female transsexualism.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754583/

 

---

 

Fun Reading:

Sincerity Espinoza didn’t go looking for trouble, it found her. All she wants out of life is the chance to go to the stars but she is caught in a web of misunderstandings, political & legal maneuvering, and the growing threat of terrorist plots by religious fanatics. She has a secret that if found out too soon could mean not only her own death but the ruin of the hope for humanity ever going to the stars. But even amidst momentous events, life is still about the small moments of love, laughter, and sadness.   Available as an ebook at Amazon and Kindle Unlimited.

Seeing the world in Grey and White…

…brain matter

It is exciting to see that neuroimaging science is getting to the point where we needn’t wait until subjects are dead before we can examine their brains in better detail. Exciting recent developments include a pair of papers from Spain in which Diffusion Tensor Imaging (DTI), a form of MRI, was used to compare FtM and MTF transsexuals to control men and women. The results were that transsexual brains exhibit white matter features, that are known to be sexually dimorphic, mid-way between male and female morphologies. The studies are doubly interesting, because the subjects had not yet begun exogenous Hormone Replacement Therapy (HRT) eliminating the possibility that the features were the result of activating effects of HRT.

So, does this mean that we have proven that transsexuals have “intersexed brains”?

Yes… and at the same time… No.

First, in the case of Female-to-Male transsexuals, it has always been noted that the majority were both gynephilic and masculine behaving since early childhood. So, these results are hardly surprising. However, the exact same thing can be said for butch lesbians, who do not necessarily identify as men. So, if we were to image the brains of a population of such butch lesbians, would we see the same masculinized neurological features? Would we see that transmen were more masculinized than butch lesbians, who would in turn be more masculinized than average lesbians? Also, if we imaged the brains of a population of gay identified transmen, would we then see that they do not share such masculinized features? I’m betting we would, and eagerly await the results of such imaging.

Which brings us back to the Male-To-Female subjects in the Spanish DTI study. As Lawrence has pointed out, different cultures have varying prevalence of non-homosexual transsexuality. Spain is one of those cultures where very few of the MTF transsexuals are non-exclusively-androphilic, with only 9% of the MTF transsexuals being non-exclusively-androphilic. In this case, as reported in the paper, there were no such non-exclusively-androphilic subjects. All were described as “early onset” and androphilic. Thus, this study only tells us about one type of transsexual.

Sadly, there wasn’t a gay male control group. It would have been interesting to see if the MTF transsexuals exhibited the same or more feminization (non-masculinization) of these sexually dimorphic brain structures. One hypothesis regarding exclusively androphilic transsexuals is that they are the extreme end of a range of feminine (hypo-masculine) homosexual males, who find that their innate femininity sufficient that living life as women is a better rational as well as emotional choice. (That is to say, that they are so feminine, like women, that they are women at heart.) I eagerly await DTI imaging studies that can test this hypothesis.

Now that we have DTI data on the HSTS population, we must gather data on the non-HSTS population to see if they do or do not exhibit such partially feminized (hypo-masculinized) features. Once again, we have no data that would show, conclusively, one way or the other, that both types of MTF transsexuals share neurologic features that would serve as the basis of a unifying etiology.

It’s not much of a limb to go out on, given the very strong data that shows that there are two types with two separate etiologies, but I’d be willing to bet that that when we do have such DTI images of gynephilic MTF transsexuals, that they will be no different than typical straight men, at least with respect to these particular sexually dimorphic features.

Which brings us to another study (Luders) looking at grey matter instead of white sexually dimorphic brain structure differences between MTF transsexuals and control men and women, this time one that suggests that for a very localized spot, they found a feature in MTF transsexuals that is different and possibly ‘more feminine’ than male controls. However, globally, the MTF brains were shown to more like men, and if anything, perhaps more masculine than control men, as they showed less grey matter then men, who show less grey matter then women. But one spot, the right putamen, is definately different in MTF transsexuals than in control men, showing more grey matter, in fact, more grey matter than the control women.

Sadly, as the researchers themselves point out, they may have included both exclusively androphilic and non-exclusively androphilic transsexuals without analyzing them separately; Of the 24 subjects, six self-reported to be androphilic and 18 reported to be gynephilic. It is heartening that the researchers recognize that in the future, they need to make the distinction and analyze the two types separately. Further, as these TS folk are pre-HRT, their ages may be used as a statistical proxy for our purposes, as MTF transkids usually (>90%) begin transition and HRT before age 25: the mean age was 47 years old, standard deviation of 13 years, with the range from 23 to 72. We know from Lawrence’s re-sorting from the Smith data set that a fair number of MTF transsexuals who self-report being androphilic are not exclusively so, thus it is likely that less than six of the subjects are exclusively androphilic.  A little math will show that that with a normal distribution, only one of the 24 subjects would have been expected to have been 25 or younger, so this 23 year old may be the only one.  Therefor, as Luders et al did find a statistically significant signal, we might infer that it is more likely that it came from the non-exclusively androphilic type, and thus likely also autogynephilic.

While it may be tempting to declare that this feature found in the right putamen proves that MTF transsexuals, in-fact, that gynephilic MTF transsexuals, have a part of their brains that is femininized, this conclusion should not be drawn from this data, at this time. Although it may be a marker of transsexual neurology, it may not be from a feminization of this region, especially given that it shows more grey matter than both control men and women. It may be a marker of an unusual neurological development altogether unrelated to sexual dimorphism. It may in fact be a marker for autogynephilia, or proneness to erotic target location errors. In fact, such a marker is expected to be found. We need further studies.

First, we need to compare the two types of transsexuals to test if this is a marker of a unifying neurological feature of transsexuality. Second, we need to compare both of them to individuals who are sexually aroused at the thought of becoming amputees, to test the hypothesis that this may be a marker of proneness to erotic target location errors.

But, in the mean time, the world is not so much to be understood as black and white, but shades of grey and white.

For more essays on trans-brains see Brain Sex.

Addendum 12/19/2011:

You may wish to read a new blog entry on an additional paper on this topic.

References:

Rametti G, Carrillo B, Gómez-Gil E, Junque C, Segovia S, Gomez A, Guillamon A., “White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study.”
http://www.ncbi.nlm.nih.gov/pubmed/20562024

Rametti G, Carrillo B, Gómez-Gil E, Junque C, Zubiarre-Elorza L, Segovia S, Gomez A, Guillamon A., “The microstructure of white matter in male to female transsexuals before cross-sex hormonal treatment. A DTI study.”
http://www.ncbi.nlm.nih.gov/pubmed/21195418

Luders E, Sánchez FJ, Gaser C, Toga AW, Narr KL, Hamilton LS, Vilain E., “Regional gray matter variation in male-to-female transsexualism.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754583/