Gay Men’s Hands Tell Us About Their Erotic Role

Thirteen years ago, I wrote an essay on how scientists had been frustrated using the 2D:4D digit ratio to demonstrate that gays and transsexuals had anomalous pre-natal exposure to androgens. They had gotten very confusing, contradictory results. I’ve been following the research hoping that some headway would be made. Well, maybe we have.

First was the confusion of not segregating and analyzing transsexual subjects data based on etiology / sexual orientation. We may now have found a similar issue with looking at gay men. There is strong evidence that there is an etiological difference between subsets of androphilic males that has correlates with preferred erotic role, specifically, preferring receptive anal sex vs. everything else.

There have also had some scientists questioning whether the 2D:4D is really about androgen exposure at all. Some data suggests that the differences within, but not across the sexes, may be due to other factors such as stress induced cortisol exposure, etc. But for our purposes, that does not matter. What matters is that when we see data that differentiates between populations and correlates with other markers for those populations, we have something interesting to note and explore. Such is the case with the Swift-Gallant paper on 2D:4D difference between tops and bottoms.

“A growing body of work indicates that anal sex role (ASR) preferences may serve as a proxy for subgroups of gay men who differ in development and gender conformity. Thus, in the present study we asked whether gay men with different ASR preferences may differ in 2D:4D. We hypothesized that gay men with a Bottom ASR (receptive), who tend to be more gender nonconforming (GNC), would have a higher (more female-typical) average digit ratio than ASR Tops (insertive), who tend to be more gender conforming. We predicted that gay men with a Versatile ASR preference (i.e., preference for insertive and receptive) would be intermediate between these two groups in both GNC and 2D:4D.”

The data they gathered is remarkable. The statistical difference between the tops and bottoms was d=0.63 for their right hands. Compare this to the difference between control men and women (from another study) at d=0.76. Thus the difference is nearly as large as that between men and women. This is a dramatic result!

They found that versatiles, those that both top and bottom were intermediate between the two. There are two hypotheses that would explain this. One is that this is a dimensional trait that smoothly varies between tops and bottoms. The other is that this is in fact, taxonic, and those that self-labeled as “versatile” were in fact an admixture of the taxonomically distinct tops and bottoms. The data presented does not allow us to determine this.

I’m predicting that the later hypothesis is correct, based on the fact that earlier work supported that, especially since the obligate bottoms appear to be the only subset of androphilic males who exhibit the Fraternal Birth Order Effect.

Further Reading:

2010 Essay on 2D:4D frustrations

Essay on Etiological Differences between Tops & Bottoms

Essay on Socio-Economic Status effecting 2D:4D differences

Essay on 2D:4D study that supports transsexual taxonomy.

References:

Swift-Gallant, A., Di Rita, V., Major, C.A. et al. Differences in digit ratios between gay men who prefer receptive versus insertive sex roles indicate a role for prenatal androgen. Sci Rep 11, 8102 (2021). https://doi.org/10.1038/s41598-021-87338-0

Gaming Transsexual Brain Sex Research

Another study done by Luders research group on MTF transsexual brains comparing them to control men and women shows a shift toward female brain phenotype. I’m sure this will be picked up by many transwomen and lauded as proof that they are “women inside”. Ummm… not quite so fast.

There are several issues to be addressed first. When I first learned of the study, I was dismayed that they had lumped the two types together. At this point in research history, this is inexcusable. In fact, the Luders group does know better, as they had cited Guillamon who specifically called out this mistake in past studies and recommended that they always be separated. Further, they didn’t look at sexual orientation in the control groups either.

This last may not have been that egregious, in that the control groups only included 24 subjects in each. The likelihood of including gay men and lesbians in such a small group is small and would not push or pull the results very far if there is a difference in brain phenotype from heterosexual subjects.

But lumping androphilic and non-androphilic transwomen together is not only a mistake, but given our current understanding based on previous brain sex research, which as Guillamon showed that only the androphilic type had female shifted phenotypes, guarantees that the whole will show a shift toward female phenotype for the whole subject group; which is likely the desired result of this current study, depending upon the ratio of androphilic to non-androphilic subjects, as the paper details,

Twenty-four transgender women (biological sex: male; perceived gender: female) were recruited through local community organizations and through professionals who offer services to the transgender community. To be included in this study, participants needed to self-identify as transgender women, report no history of hormone therapy, and declare the intention of undergoing estrogen replacement therapy. Moreover, participants were confirmed to be genetic males as defined by the presence of the SRY gene in their genome [53]. Six transgender women reported to be androphile (attracted to men) and 18 transgender women stated to be gynephile (attracted to women). The mean age of the transgender sample was 45.7 ± 13.8 years (range 23–72 years).

One might excuse this failure to examine the two types separately based upon the argument that the were already so few transsexual subjects and thus less likely to be statistically powered enough. But this is NOT a valid excuse. One could have done the analysis both ways. But I strongly suspect that would have defeated the ideological aim of the authors, as it would have demonstrated what those earlier studies also showed, that only the androphilic group had a female shifted phenotype. Instead, by lumping them together, one could give the false impression that MTF transsexuals as a whole show such a shift, if slight.

When I realized that they had lumped the two types together, I made a silent bet with myself, predicting that there would be a bimodal distribution, two “humps” in the data, indicative of two types, taxa, being lumped together. Sure enough, the violin plot of the transwomen shows exactly that!

Further Reading:

Essay on Guillamon Meta Analysis

References:

Kurth, F.; Gaser, C.; Sánchez, F.J.; Luders, E. “Brain Sex in Transgender Women Is Shifted towards Gender Identity” J. Clin. Med. 2022, 11, 1582. https://doi.org/10.3390/jcm11061582

Guillamon, A et al., “A Review of the Status of Brain Structure Research in Transsexualism” Arch Sex Behav (2016). doi:10.1007/s10508-016-0768-5

Lack of In Utero & Perinatal Testosterone Exposure Leads to Childhood Gender Atypicality in Males

In a sad “experiment of nature” in which phenotypically normal appearing males are unable to produce gonadotropin, essentially naturally duplicating the effect of puberty blockers, but experiencing this lack since the beginning of the second trimester in the womb. Most importantly, these males do not experience the so called, “mini-puberty” that occurs perinatally, the time just before birth and the first three months after birth.

Given that we have already seen data from a proxy measure of the level of testosterone production and exposure during this developmentally critical period correlates with later childhood gender typicality / atypicality, (Pasterski 2015) we would predict that these individuals would also report having been more gender atypical than control men. That is exactly what we see in the recently published study by Shirazi, et al. This was especially true of those who had cryptochordia (undescended testicle) at birth, indicating even lower T production in utero. Thus, indicating that T exposure before the birth is also important for brain masculinization.

Demographic Statistics Variable Control (n = 463) IGD-clinical (n = 30) IGD-Web (n = 35)
Mean childhood gender atypicality –0.04 (0.33) 0.24 (0.44) 0.34 (0.59)

Mean sexual orientation (Kinsey 0-6) 0.25 (0.94) 0.31 (0.71) 0.94 (1.48)

Interestingly, the effect sizes were not as large as one might expect. To me, this suggests that fetal gonadotropin levels alone may not truly indicate just how much T is being produced given that the fetal adrenal glands are unaffected. Alternatively, it may be that there are Y chromosome canalization effects that we haven’t discovered and accounted for.

It is odd that given that the earlier Pasterski study concerns the same exact subject, and comes to the same conclusion, it wasn’t referenced by Shirazi.

Further Reading:

Essay on Effect of Mini-Puberty on Childhood Gendered Behavior in Boys

References:

Shirazi, et al., “Low Perinatal Androgens Predict Recalled Childhood Gender Non-Conformity in Men”, Psychological Science (2022) https://doi.org/10.1177%2F09567976211036075

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”, Hormones and Behavior (2015)
http://www.sciencedirect.com/science/article/pii/S0018506X15000033#f0005

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

Sex Chromosomes Expression Associated With Brain Sex?

There has been a long term assumption that sexually dimorphic brain features developed solely from hormonal difference, both organizational and activational.  Some have long suspected that at least some of the sexually dimorphic features were from differential expression of the sex chromosomes themselves.  An association between such features and differential expression has now been found in a recent study.

There is a great essay at Wired that I would recommend you read before continuing to read my essay here.  (Link)

A few comments are warranted here.

First, the hormonal hypothesis is not negated, only modified.  There remain several possibilities, first that the hormonal influence simply triggers which genes are expressed in the brain at and that it is only coincidental that some are on the sex chromosomes; second, that hormonal influence works independently from the sex chromosome expression control.  Of course, it could even be some combination of the two (and my bet is on this third possibility).  Remember, many of the genes differentially expressed are NOT on the sex chromosomes, and even those on the X chromosome, available to both sexes, are differentially expressed.

Please note:  Genes on the X chromosome are NOT all automatically expressed in women nor are they automatically repressed in men.  Further, not all of the genes found on the X chromosome relate to sexually dimorphic development (e.g. color vision receptor).

Second, we don’t know what the FUNCTIONAL differences the sex chromosomes mediate vs. the autosomal chromosomes.  We don’t know how different the behaviors would really be with such differential expression.  These difference could be related not to behaviors but to immune responses for example.  When one is confronted with ignorance, it is important to recognize it and not make conclusions that the data doesn’t support.

Third, a reminder that these differences can NOT be directly associated with important cognitive mechanisms, else females would be at an extreme disadvantage not able to express genes that lie only on the Y chromosome.  We know this because men and women have shown only tiny differences in cognitive performance of specific tasks and that general cognitive ability (IQ – g factor) do not differ between the sexes.  (Male chauvinists be damned!)

Fourth, speculating on what effect this might have on gender atypicality and the degree to which such atypical individuals may resemble the opposite sex in brain sexual dimorphism is inescapable.  Most of it will likely be found wrong later.

One can imagine certain transphobic groups using this material to show that gender atypical transsexuals (HSTS) aren’t “really” a man or a woman… cause… “biology” (essentialism based on karyotype).  But that is not the germain issue as we KNOW that other mechanisms are also involved.

Further Reading:

Essay on hormonal effects on sexually dimorphic brain development

Essay on gene control of sexually dimorphic behaviors

Further External Reading:

Wired Article

Reference:

Liu, et Al.,”Integrative structural, functional, and transcriptomic analyses of sex-biased brain organization in humans”, PNAS (2020)
https://doi.org/10.1073/pnas.1919091117

2D:4D Evidence Supports Transexual Taxonomy

A new paper provided both new direct evidence and a meta-analysis of measurements of 2D:4D finger ratios in transsexuals, both FtM and MTF.  Such measurements are interesting because it is known to be influenced by testosterone levels in utero and thus an indirect measure of testosterone exposure that might influence brain sexual dimorphism.

What is doubly exciting about this paper is that the authors fully comprehend the overwhelming evidence for the two type taxonomy and of the (mild) scientific controversy regarding sexual orientation vs. age of onset as the best clinical markers for the two taxons.  The study is open access so I highly recommend following the link to it and reading it for yourself.  The study is also interesting because of where it was conducted; Iran.

Iran is a Muslim country which while being extremely homophobic, both culturally and legally, treats transsexuals fairly well, at least legally and medically.  Make no mistake, culturally, it is far from truly accepting.  Further, Iran is considered a “Collectivist Society” according to the Hofstede Individualism vs. Collectivism Index.  Lawrence has shown that this index highly correlates with the percentage of non-androphilic (and thus likely autogynephilic / late onset) transwomen transitioning in a given culture.  Thus, we would expect that there were fewer such transwomen in the study and the reported data bear this out.

Let’s look at the new data they provide:

Table 1

Means (and SD) for 2D:4D in the left and right hand for transmen, transwomen, control women, and control men

	Transmen	Control women	Transwomen	Control men
Left 2D:4D	0.991 (0.034)	0.991 (0.032)	0.981 (0.033)	0.974 (0.029)
	n = 104	n = 53	n = 88	n = 56
Right 2D:4D	0.981 (0.030)	0.983 (0.033)	0.972 (0.029)	0.959 (0.033)
	n = 104	n = 53	n = 89	n = 56

Table 2

Means (and SD) for 2D:4D in transsexuals’ left and right hand as a function of early or late onset of gender dysphoria

	Transwomen		Transmen
	Early onset	Late onset	Early onset	Late onset
Left 2D:4D	0.982 (0.034)	0.975 (0.022)	0.988 (0.033)	1.009 (0.031)
	n = 80	n = 8	n = 92	n = 12
Right 2D:4D	0.973 (0.029)	0.963 (0.026)	0.977 (0.028)	1.007 (0.027)
	n = 81	n = 8	n = 92	n = 12

Before the analysis of transfolk, it would be a good idea to scale the effect by looking at the effect size between the controls.  The difference between control women and men is d= 0.56 for the left hand and d= 0.76 for the right. This is only a moderate effect size.

Although the number of late onset is small, and thus must be viewed with caution, the analysis is still very interesting and would seem to confirm (agree) with the two type hypothesis.  Consider that the two MTF types have a small but distinct difference of d= 0.24 for the left hand and d= 0.22 for the right.  When we compare early onset type to the male controls we get d= 0.25 and d= 0.45 for the right.   When we compare early onset to female controls we get d= -0.27 for the left and d= -0.32 on the right.  This shows that early onset transwomen are roughly halfway between the controls, and if anything a bit closer to the female controls.

But even more intriguing, and the reason for trusting this interpretation is that when we compare the late onset population to the male controls we see that it exactly agrees with the hypothesis that the late onset type is essentially like the majority heterosexual male population and not at all feminized, with effect sizes that are, statistically speaking, non-existent at d= 0.04 and d= 0.12 for the left and right hands respectively.

This shows that early onset MTF type has notably hypomasculine (feminized) hands while the late onset MTF type does not, and thus in agreement with other data that supports the two type MTF taxonomy.

But what about the FtM transmen?  Here we see an even more intriguing set of data.

The two FtM types have a moderate to substantial, very notable, difference of d= -0.66 for the left hand and d = -1.07 for the right, indicating that early onset transmen are far more masculine than late onset.  When we compare the early onset FtM to female controls we find effect sizes of d= -0.09 for the left hand and d= -0.20 for the right indicating a non-existent to small masculinization signal.

However when we compare the late onset FtM to female controls we see a very different pattern with effect sizes of d= 0.57 for the left and d= 0.80 for the right.  The positive sign indicates that late onset transmen have a more feminine 2D:4D ratio than control women (!!).  And the effect size difference between early and late onset transmen is far greater than the difference between control men and women (!!!).

This, if replicated, is very big news.  It would support the notion that transmen also exhibit two taxons as has long been suspected, one that is masculinized in both behavior, sexual orientation, and very mildly in appearance, the other that is very feminine, androphilic, and autoandrophilic, the mirror image of late onset transwomen.

Further Reading:

Essay on 2D:4D History

Essay on Cultural Difference in Percentage of HSTS vs. AGP Transwomen

Essay on Androphilic Transmen

Reference:

Sadr, M., Khorashad, B.S., Talaei, A. et al. “2D:4D Suggests a Role of Prenatal Testosterone in Gender Dysphoria” Archives of Sexual Behavior (2020)
https://doi.org/10.1007/s10508-020-01630-0

(Cherry) Picking The Transgender Brain

Or, How To Ignore Brain Science That Tells A Story You Don’t Like

Psychology graduate student and computer coding instructor Sophie Searcy, responding to the recent over-hyped study of transkids brains (mentioned in previous post) has produced an excellent example of transgender brain science cherry picking.  The one that REALLY stands out as egregious is that she cites the Joel study that she claims… well… let Searcy tell it,

“Indeed, not only is the existing literature on sex differences in brain imaging likely biased, but recent work does significant damage to the idea that there are distinct, separate, “male brains” and “female brains” at all. A research group led by Daphna Joel summarizes the findings of their meta-analysis that included brain images from 1,400 participants: “Brains with features that are consistently at one end of the ‘maleness-femaleness’ continuum are rare. Rather, most brains are comprised of unique ‘mosaics’ of features, some more common in females compared with males, some more common in males compared with females, and some common in both females and males.”

So what’s the problem?  Well, it’s dishonest cherry picking to cite a study that another group (Chekrouda, et. al) responded in the same journal with a similar study that showed that if Joel had conducted a multi-variate analysis they would have found out that male and female brains scans WERE in fact differentiable by a mathematical model at 93% accuracy.  As I explained previously I did a bit of calculation and found much to my amazement, that to “guess” the sex of the brain to 93% accuracy means that the effect size (Cohen’s d) would, if it were a single dimorphic feature, be a whopping 3.0 !!!!  That’s an over the top value.  Thus, as we get better imaging tools to see the fine details, we are learning that the human brain, in terms of multivariate statistics of multiple measurements at all points of the brain, is in fact extremely sexually dimorphic.  The problem is that no one area is all that dimorphic, but in aggregate, they are quite dimorphic.  That is to say, if one area is slightly dimorphic, giving a small statistical clue as to the sex of the individual, and a second area is also slightly dimorphic, giving a small clue as the sex of the individual, the two can be used together to give a medium-sized clue to increase the accuracy… and with many many areas, each additively pointing towards one sex or the other, the accuracy gets quite good.

Searcy should have noticed this second paper which shows that Joel’s paper does NOT debunk the hypothesis that discernible male and female brains exist.

So, why did she write this article and cherry pick the science?  Perhaps we can get a clue from another statement she makes,

“In a 2017 paper, Bakker and colleagues summarized similar work on adults as finding that “adults with GD [gender dysphoria] differ from both cis-gender [sic] men and women.” In other words, adult trans brains appear to be distinct from adult cis brains of either sex. Should trans adults be worried? In that same paper, the researchers actually found mixed results for adolescents. They looked at nine brain regions each for trans girls and trans boys. Of those 18 regions, the researchers reported significant differences in only four out of 18 areas. One area where trans girls differ from both cis girls and cis boys, two areas where trans girls are similar to cis girls, and one area where trans boys are similar to cis boys. What does this mixed bag suggest if we are to believe that trans brains must be similar to cis brains in order to be seen as legitimately transgender?

Ummm… this result is in complete agreement with another hypothesis that many transwomen find uncomfortable, one made by Ray Blanchard, in which he hypothesized that late transitioning transwomen would have brain structure differences from both men and women that would NOT be sexually dimorphic; while young (“homosexual”) transsexuals would show shifts in sexually dimorphic structures toward female morphologies.  There was an earlier review of previous studies (which I also wrote a post about) that had shown that hypothesis to be supported.

Searcy is likely to have written her article in an attempt to discount the growing evidence from transgender brain scan research that shows that the two type taxonomy for transwomen is supported.  Where once older transitioning transwomen cherry picked the brain structure research in an attempt to spin it such that all transwomen had female brains.  She is spinning the science to lead us to believe that brain structure research is unimportant and should be ignored, first by saying that there is no brain structure sexual dimorphism of any consequence and then say that what differences between transgender folk and nontransfolk is unimportant anyway.  I believe it represents a growing fear by autogynephilic transwomen that the brain scan science will undermine their own identity as transwomen if the public were to become aware of what the evidence means.

Further Reading:

Essay on Chekrouda paper

Essay on Transgender Brain Sex Review

Essay on Cherry Picking Brain Research to Prove All Transwomen Have Female Brains

References:

https://www.them.us/story/brain-scans-transgender-identity

Chekrouda, et al., “Patterns in the human brain mosaic discriminate
males from females”  http://www.pnas.org/content/113/14/E1968.full.pdf

 

Autism and Transgender

Co-Morbidity of Gender Dysphoria and Autism Spectrum

More studies show that there is a higher than expected by random chance of co-morbidity of gender dysphoria and autism spectrum disorders.  It’s seems to be true for both MTF and FtM.  There are hints that it may be more likely in “nonhomosexual” individuals.  The question not yet answered is whether this is an independent path to gender dysphoria in adults or is co-morbid with autogynephilia and autoandrophilia, though we have seen adolescents with and without autogynephilia in earlier studies.

From the Shumer study abstract:

“There is evolving evidence that children and adolescents with gender dysphoria have higher-than-expected rates of autism spectrum disorder (ASD)… We conducted a retrospective review of patient chart data from 39 consecutive youth ages 8 to 20 years (mean age 15.8 years, natal male: n = 22, natal female: n = 17) presenting for evaluation at a multidisciplinary gender clinic in a large U.S. pediatric hospital from 2007 to 2011 to evaluate the prevalence of ASD in this patient population. … Overall, 23.1% of patients (9/39) presenting with gender dysphoria had possible, likely, or very likely Asperger syndrome as measured by the Asperger Syndrome Diagnostic Scale.”

From the Pasterski study abstract:

“The current study examined this co-occurrence of GD and autistic traits in an adult population, to see whether this heightened prevalence persisted from childhood as well as to provide further comparison of MtF versus FtM transsexuals and homosexual versus nonhomosexual individuals. Using the Autistic Spectrum Quotient (AQ), 91 GD adults (63 male-to-female [MtF] and 28 female-to-male [FtM]) undertaking treatment at a gender clinic completed the AQ. The prevalence of autistic traits consistent with a clinical diagnosis for an autism spectrum disorder (ASD) was 5.5 % (n = 3 MtF and n = 2 FtM) compared to reports of clinical diagnoses of 0.5–2.0 % in the general population. In contrast to the single previous report in adults, there was no significant difference between MtF and FtM on AQ scores; however, all of those who scored above the clinical cut-off were classified as nonhomosexual with respect to natal sex. Results were considered in the context of emerging theories for the observed co-occurrence of GD and autistic traits.”

This was not a very large enough sample size given the small number of individuals found on the spectrum, but note that all five were nonhomosexual.

Further Reading:

Autistic Sky

Further External Reading:

Why we need to respect sexual orientation, gender diversity in autism by John Strang

Large study finds significant overlap between “transgender” identity and autism

References:

Pasterski, et al., “Traits of Autism Spectrum Disorders in Adults with Gender Dysphoria”, Archives of Sexual Behavior (2013)
https://doi.org/10.1007/s10508-013-0154-5

Shumer et al., “Evaluation of Asperger Syndrome in Youth Presenting to a Gender Dysphoria Clinic”, LGBT Health (2016)
https://doi.org/10.1089/lgbt.2015.0070

van der Meisen, et al., “Prevalence of the Wish to be the Opposite Gender in Adolescents and Adults with Autism Sprectrum Disorder”, Archives of Sexual Behavior (2018)
https://doi.org/10.1007/s10508-018-1218-3

Brain Maps…

Or Searching for the Lost Continent of Atlantis

A recently popular counter argument to evidence of the two type taxonomy that arises in the transgender communities is that transsexuals brains have cross-sexed maps of the body.  It sounds so reasonable doesn’t it?  That is to say, if our bodies are sexually dimorphic with respect to genitalia and secondary sexual characteristics, shouldn’t our brains be as well?  And if the sexes have sexually dimorphic brain mapping of those body parts, could it not be that transsexuals have been “cross-wired”?  And further, couldn’t that explain all transsexuals and maybe even non-gender-dysphoric transgender people?

Trusting “truthiness” gut feelings is how we form false beliefs.  We need to look at this issue objectively, both open-mindedly to see if true, and skeptically to find the flaws in this hypothesis to prove it wrong if it is wrong.  So let’s look at the evidence shall we?

First, this idea seems to have cropped up BEFORE any supporting evidence.  Thus, it may be that when this idea is being explored, it will be subject to strong confirmation bias.  I’ve already written about such an incident in a previous essay when, ten years ago, Vilayanur Subramanian Ramachandran tried to pass off experimentally and statistically flawed data to support this hypothesis by comparing the experience of phantom limb sensations of a small group of control men who had penectomies with post-op MTF transwomen.  The study was roundly and rightly criticized by Anne Lawrence for not showing what it purported to show.  When writing about it, I discussed the theoretical objections to the notion of sexually dimorphic neural maps of the genitalia in the brain,

“First and foremost of which is that the genitalia are not really all that different in quality… and only superficially different in quantity.  Nearly each feature of the external and even of some of the internal structures are homologous.  That is, for each feature found in a male, there is a feature that matches it in the female, which is only different in degree, not in kind.  The most obvious example is the glans of the penis is homologous with the glans of the clitoris.  Inside of the penis, and down into its root inside of the body, is spongy tissue that expands when blood pressure fills it with blood.  Inside of the clitoris and down into its root inside of the body, is spongy tissue that expands when blood pressure fills it with blood.  Quite literally, a penis is a very large clitoris; And a clitoris is a very small penis.  Oh there are differences in how the urethra is routed, but even there, they start in the same place.  In men there are two glands called the Cowper’s, which produce a clear fluid that aids in lubrication during sex.  In women there are two glands called the Bartholin’s which produce a clear fluid that aids in lubrication during sex.  Why are they called two different names?  Finally, the scrotal sac is the same tissue as the labia majora, but have fused together.  Thus, the two sexes, which seem so different to a naive observer, are really very nearly the same to a student of anatomy.  So, given that the two are really very nearly the same, shouldn’t the neural maps be the same?”

I stand by my objections with regard to genitalia being sexually dimorphically represented in the brain.  But could there be other areas that are sexually dimorphically represented in the brain?  There could be, in fact… there SHOULD be.  To be specific, those areas of the body which are not homologous between the sexes should be expressed non-homologously in the brain.  Specifically, the uterus and fallopian tubes.  Further, these areas of female anatomy are not served by the pudendal nerves like the genitalia so may experience quite different representation in the brain.

Consider also the phenomena of neural atrophy.  If the brain is not stimulated by external events… for example someone born blind, the portion of the brain not stimulated does not fully develop while it may also be “repurposed” for another function.  That is to say, it is remapped and recruited by neurologically nearby functions.  So, we would expect to find sexually dimorphic maps of the somatic sensation processing functions associated with organs which are non-homologous.

However, under this analysis, we would NOT expect to find a section of a male-to-female transsexual’s brain waiting for input from non-existent non-homologous female anatomy!  That is the equivalent of searching for the Lost Continent of Atlantis.  You can put it one your paper map of the globe, but that won’t mean that you can find it on the real earth.  It sank into mythology a long time ago.

So, can there be sexually dimorphic brain development involving somatic maps where the opposite happens?  That is, can the brain fail to develop a map for a somatically sexually dimorphic feature that does exist?  This might be possible in theory.

Consider breast tissue.  This is superficially sexually dimorphic after puberty, but largely homologous.  But we have evidence from studies in mice that certain nerves leading to the milk glands begin to form in both sexes, but later atrophy in males in utero.  I haven’t been able to find data on humans regarding the same phenomena.  Mice, being rodents, are close cousins of primates, and thus humans.  But evolution does not always conserve every detail.  So we may or may not have the same phenomena.  However, lets for the moment entertain such a notion.  This would suggest that males would fail to develop brain functions that respond to the sensation of milk gland fullness, fail to develop the needed sensory map for the signals from an infant needing to nurse, and fail to send the needed signals back from other unconscious functions to “let down” the milk to an awaiting baby.  This let down signal is triggered by the sight, sound, and feel of a baby wanting to nurse.  It is thought that originally, only the sensations on the nipple bring about ‘let down’, but soon a mother learns by association the sight and sounds (baby hunger cry) that precede nursing.  It is theoretically possible that we could find the location of this somatic sensorium map and how it feeds the let down function in the human brain and see if it is a) sexually dimorphic and b) anomalous in transsexuals.

It is also possible, though I’m not totally convinced, that the maps that allow one to experience touch on the nipples as erotic are also sexually dimorphic.  Interestingly we have discovered that the neural map on the neocortex between the genitalia and the nipples are contiguous and overlapping.  But it turns out, that the very same areas also map for the penis and nipples in males.  Thus, the maps are all in the same place on the sensory cortex.  Both men and women have reported that nipple simulation adds to sexual arousal.  This suggests that this is NOT very sexually dimorphic and is homologous between the sexes.

However, hypothesis were meant to be tested and there is a new paper from Case, et al. that deals with FtM transmen and the possibility of anomalous neurological findings regarding somatic representation.

But before I discus that aspect of the study, I have to share a pet peeve of mine that this paper is guilty of.  It peeves me when I see paper after paper by authors making reference to earlier papers that have clearly been shown to not support a given thesis, especially if those earlier refuted papers are their own.  For example, Swaab’s later papers keep referencing his earlier one regarding transsexuals and BSTc as though that study still had any validity regarding transsexual etiology.  As a reminder, it was Swaab himself that proved it didn’t… but you would never know that from his later papers which keep referring to it as though it did.  In this new paper that also includes Ramachandran as a co-author it references his earlier paper regarding phantom penises as though it supported the notion that MTF transwomen experience fewer of them than control men with penectomies.  But as I mentioned earlier, Lawrence demolished that paper showing that it showed no such thing, not passing even the simplest statistical ‘sniff test’ while I showed not only theoretical problems with the notion but that his purported controls did not qualify as such.  I can forgive not having read my blog, but not of ignoring Lawrence’s reply published in the same journal as the original paper.  My pet peeve is that authors of papers, when they make these references without also referencing those later papers that cast their conclusions into doubt, are guilty of the worst sin of bad science, cherry picking.

Further, the Case paper references xenomelia and observes that this may be similar to transgender, but ascribes it to somatic mapping issues while failing to note that we have another name for xenomelia, “apotemnophilia”, the erotic desire to be an amputee and how that desire arises out of an Erotic Target Location Error (ETLE) for the primary erotic target of amputees.  The authors thus sweep the well documented erotic motivations of both amputation “wannabees” and of autogynephilic transwomen under the rug in order to further their thesis of transgender as a brain mapping issue alone.

But for the moment, lets put these transgressions aside and look at the actual study.  Actually… not much to say about it.  They noted that FtM’s seem to have a reduced somatic awareness of their pre-top-surgery chests as shown by functional brain scans.  And although the authors offer a nod to the notion that their higher level conscious aversion to their breasts, i.e. somatic gender dysphoria, might mean that they repress awareness of touch sensations that announced that they have breasts, they bend over backwards to posit that the direction of causality is reversed.

Ummm… No.

That would mean that non-transmen would also have to have less awareness of their chests… and that has never been noted to happen.

All in all, this paper has interesting details on how psychophysical experiments can be conducted using brain scanning, a topic that is very much of interest to me as one whose career has been in applied psychophysics.  It also discloses sexually dimorphic differences in white matter distribution in parts of the brain in which the FtM subjects differed from female controls, thus adding to the growing pool of data that show that gynephilic transmen are, like androphilic transwomen, gender atypical in brain development.  But it does not show any convincing data for a somato-sensory brain map issue as being causitive of transsexuality.

Further Reading:

Essay on phantom penises

Essay on xenomelia / apotemnophilia and its relationship to autogynephilia

References:

Case, et al., “Altered White Matter and Sensory Response to Bodily Sensation in Female-to-Male Transgender Individuals” (2017) Archives of Sexual Behavior
https://link.springer.com/article/10.1007/s10508-016-0850-z

 

An Issue Whose Time Has Come:

Sex/Gender Influences on Nervous System Function

The recent spring issue of the Journal of Neuroscience Research was wholely dedicated to papers on sexual dimorphism of the brain.  Of course, many will debate that there is in fact any influence of sex, much less gender (identity), on nervous system function.  I’ve written about this before, how the politics can lead some to make the charge of “neurosexism”, deserved or not.

Larry Cahill, the editor remarked about it thus,

” “Be careful, it’s the third rail.” I received this strong advice to steer clear of studying sex differences from a senior colleague around the year 2000 when my research into brain mechanisms of emotional memory began drawing me into the issue of sex differences—or better yet, sex influences—on brain function. And in a way, he was right. For the vast majority of his long and distinguished neuroscience career, exploring sex influences was indeed a terrific way for a brain scientist not studying reproductive functions to lose credibility at best, and at worst, become a pariah in the eyes of the neuroscience mainstream.  …  Fortunately, times are changing. The past 15 to 20 years in particular witnessed an explosion of research (despite the prevailing biases against the topic) documenting sex influences at all levels of brain function. So overpowering is the wave of research that the standard ways of dismissing sex influences (e.g., “They are all small and unreliable,” “They are all due to circulating hormones,” “They are all due to human culture,” and “They don’t exist on the molecular level”) have all been swept away, at least for those cognizant of the research.”

This is an exciting development and this issue is full of great information.  The best thing about it?  It is NOT behind a paywall.  The entire issue is free to read.  And read it you must if you are to remain at the cutting edge of sex influences on the nervous system.

The papers discuss a wide range of topics including the neurology of people with Disorders of Sexual Development (i.e. “intersex”) to the rather dry and esoteric.  I’ve been enjoying reading them and will likely be referencing them in future.

Further Reading:

Essay on the effects of HRT on Transsexual’s Brains and the politics of Brain Sex

“Two minds – The cognitive differences between men and women” By Bruce Goldman

Reference:

Journal of Neuroscience Research
An Issue Whose Time Has Come: Sex/Gender Influences on Nervous System Function
January/February 2017, Volume 95, Issue 1-2
Version of Record online: 7 NOV 2016 | DOI: 10.1002/jnr.23934