Autistic Dawn
— Are gender dysphoric youth prone to being autistic. Or reversing that, are autistic children prone to being gender dysphoric? There has been some clinicians suggesting there is a connection. But does the data support that assertion? There is data that suggests that transmen (FtM transsexuals) do show more autism type characteristics but the data for transwomen is mixed. That is to say, that gynephilic transwomen seem to have the name level of such as control men, while exclusively androphilic (HSTS) transwomen show the same, lower, level as control women. Given that HSTS are far more likely to have been identified as gender dysphoric as youth, we would expect that such male children w/ gender dysphoria would NOT show elevated autistic traits.
But I was challenged on this prediction and given a citation for a 2015 paper by Van der Laan, et al., that purported to show that both male and female gender dysphoric children did show elevated autistic traits.
But did it? Let’s look at the data. The paper is available on SciHub as a downloadable pdf, so you may refer to Table 2. Here is where we begin to see something odd. The researchers do NOT have data on any Autisism Spectrum Disorder (ASD) diagnoses nor have they used the clinically validated Autism Quotient (AQ) instrument as in other studies. Instead they have used only two items in a maternally scored checklist about “obsessions” and “compulsions”. These constructs only weakly map to ASD, and could map to other disorders… or no disorder at all. After all, one child’s “obsession” is another child’s hobby, or even just a keen interest. This alone brings the study’s value for our purposes to near zero. However, data is data.
Of the male children, 54% were scored as having an obsession with a (cross?) gendered theme. While of the sibling controls, only 13% were. Sounds pretty convincing doesn’t it? But is it? But of the controls, 87% were scored as having an obsession with a non-gendered theme. Gee… that doesn’t sound like these gender dysphoric youth were any more likely to have an obsession indicating a likely ASD. The rest of the data for the compulsions and for the female children is similar.
The authors appear to know that this may not reflect a propensity to ASD, as they note,
“Another possibility is that intense cross-sex interests are simply a manifestation of GD. Such interests may lead to a clinical presentation that is ASD-like but only superficially so because the intensity of the interests is due to the GD and not an underlying ASD. If such were the case, then few, if any, additional ASD features should accompany intense cross-sex interests. If few additional ASD features are present, then other circumstances that might influence such interests to be elevated should be considered. For instance, GD children may obsess about cross-sex objects and activities as a way of communicating their strong desire to be the opposite gender. When confronted with resistance about this desire, the child may react by further intensifying these obsessions and, hence, his or her communication of this desire.”
My snarky response is, “Ya think?!?”
Further Reading:
Reference:
VanderLann, et al., “Do Children With Gender Dysphoria Have Intense/Obsessional Interests?”, JOURNAL OF SEX RESEARCH, 52(2), 213–219, 2015, DOI: 10.1080/00224499.2013.860073
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
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Critique of Gliske’s Gender Dysphoria Conjecture
When a radically new conjecture is put forward regarding the etiology of a phenomena that purports to be a new explanitory theory it must explain all of the previous observations, evidence, and data in a better, more compact way to be accepted as a theory, displacing or augmenting a previous one. Stephen V. Gliske claims to have a new explication of the mechanism leading to a unitary theory of gender dysphoria, displacing our current two type taxonomy with its two separate and distinct etiologies, namely extreme gender atypicality vs. Erotic Target Identity Inversion caused by an Erotic Target Location Error.
However, as one digs into Gliske’s recent paper published in eNeuro, one very quickly notes several serious defects. First, he relies on neuro-anatomical studies that have been shown to be purely effects of hormonal treatments. He attempts to recruit xenomelia as a point of argument for his thesis but fails to note that such evidence supports the two type as that phenomena is also highly correlated with apotemnophilia and thus another example of an Erotic Target Location Error. He cites a study which showed reduced activation of part of the brain to sensory touch of transmen’s breasts as evidence that this is a cause of gender dysphoria, rather than an effect of gender dysphoria (attentional suppression of emotionally distasteful experience). Finally, he fails to explain or even directly acknowledge the overwhelming evidence for the role of autogynephilia in the development of gender dysphoria in one of the two types including the studies that concluded that the two types have different brain structural shifts.
Gliske leans very heavily on post-mortem studies of MTF transsexual brains by Swaab’s group in the Netherlands. For a while so did many other researchers and especially the transgender population. Sadly for Gliske’s argument, this effect on areas of the BNST (BSTc & INAH3) was shown to be purely an artifact of these patients being treated for gender dysphoria using female hormones for years. These changes are activational effects of hormones. Perhaps Gliske can be forgiven for not knowing this, given that even Swaab’s group continues to publish papers referencing this earlier work as though it hadn’t been shown to be meaningless as evidence for any etiological arguments.
Gliske proposes a mechanism of gender dysphoria that arises out of a disturbance of sensory networks in the brain. This idea is not new. It was proposed by Ramachandran some years ago but with a different twist. The earlier work suggested it as supporting the sexually dimorphorphic brain hypothesis. That earlier work was shown to be statistically weak and inconclusive. Later work using fMRI scans of transmen while their breasts were touched were interpreted as evidence of an intrinsic neurological difference in the sensory networks involving the breast of transmen. However, as I have argued in the past, this ignores the ability of the attentional networks of the brain to both highlight and suppress sensory experience awareness at multiple levels.
{My reader can test this ability for themselves. While reading the above, were you keenly aware of the exact position of your left foot? Are you now aware of it? Now imagine you hate your left foot and concentrate on your right hand.}
Ramachandran and Case also attempted to cite the example of 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. Gliske commits the same academic sin.
Gliske doesn’t completely ignore the two type taxonomy, but makes a sweeping statement that he does not back up with compelling evidence, that the two types are better characterized by age of onset than sexual orientation, failing to note that once false self reporting for both characteristics are taken into account, the two are in fact merely labels for the same taxons that focus on one or the other of the two very highly correlated items. However, as has been shown repeatedly, sorting for the two taxons on sexual history to determine likely sexual orientation leads to significantly higher statistical signals.
Finally, Gliske ignores that the very studies he cites as evidence for his thesis more properly supports the two type taxonomy, as Guillamon, et al., concluded in a meta-review of the papers.
“The review of the available data seems to support two existing hypotheses: (1) a brain-restricted intersexuality in homosexual MtFs and FtMs and (2) Blanchard’s insight on the existence of two brain phenotypes that differentiate “homosexual” and “nonhomosexual” MtFs”
Gliske ends his paper with a classic Bad Science Journalism(tm) move by suggesting that his work will lead to better therapies for treating gender dysphoria without the slightest evidence or hint of how that might be.
Gliske calls this a “new theory”, but in fact, it is poorly warmed over previous conjecture with very little evidence to support it, certainly not enough to displace the Two Type Taxonomy and Erotic Target Identity Inversion.
Addendum 4/30/2020: Gliske’s paper has been retracted. I guess I’m not the only one who noted that this paper fails to meet basic standards:
Further Reading:
Essay on Swaab’s research on BSTc & INAH3
Essay on Ramachandran’s paper on phantom pain after SRS
Essay on Case & Ramachandran’s paper on Transmen’s responses to breast touch
Essay on Apotemnophilia arising from an Erotic Target Location Error
Essay on Age of Onset vs. Sexual Orientation
Further External Reading:
Essay on Bad Science Journalism(tm)
References:
Stephen V. Gliske, “A new theory of gender dysphoria incorporating the distress, social behavioral, and body-ownership networks” eNeuro 2 December 2019, ENEURO.0183-19.2019; DOI: https://doi.org/10.1523/ENEURO.0183-19.2019
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The Transsexual Brain Sex Gallop
A year ago I wrote an essay in response to an article that clearly cherry picked its citations to argue that recent brain sex research shouldn’t be used in evaluations of transsexual etiology. I pointed out that it represented a change in strategy by autogynephilic transwomen from attempting to use brain sex research to bolster the claim that all transwomen had feminized brains to a strategy of attempting to claim that brains aren’t sexually dimorphic so that no one would notice that the latest brain scan studies on transfolk support the two type taxonomy of transwomen.
Well, it looks like I was right – as another article by Simon(e) D Sun [sic], this time in Scientific American Blogs, attempts to tell the very same misleading story, even right in the subtitle, “Actual Research Shows that Sex is Anything But Binary”.
It reads as a Gish Gallop running headlong away from the two type taxonomy while setting up some amazing strawmen and logical disconnects that the author hopes the reader doesn’t spot,
Let’s just take the most famous example of sexual dimorphism in the brain: the sexually dimorphic nucleus of the preoptic area (sdnPOA). This tiny brain area with a disproportionately sized name is slightly larger in males than in females. But it’s unclear if that size difference indicates distinctly wired sdnPOAs in males versus females, or if—as with the bipotential primordium—the same wiring is functionally weighted toward opposite ends of a spectrum. Throw in the observation that the sdnPOA in gay men is closer to that of straight females than straight males, and the idea of “the male brain” falls apart.
Say What? Ummmm…. So Sun turns a classic example of a sexually dimorphic brain feature that has been feminized in a class of people whose very sexuality has been feminized, who are known to have more female typical gendered behaviors as children… and somehow that gets flipped to demonstrate that the “Idea of the male brain falls apart”. Ummmm… No! Just No. This demonstrates just the opposite, that there is a very strong correlation with a female typical feature and female typical behaviors in both male and female bodied people. That argues for a sexually dimorphic brain with behavioral correlates.
Then, Sun cites studies of transsexual MRI brain scans but completely fails to mention that they are from two separate etiological types and as such do NOT support the thesis of a non-binary, non-sexually dimorphic brain. Sun is counting on the reader not knowing this key fact.
It is disappointing to see articles this poor. Sun, stop using phony science articles to justify ignoring the two type taxonomy.
Further Reading:
(Cherry) Picking The Transgender Brain
Further External Reading:
https://blogs.scientificamerican.com/voices/stop-using-phony-science-to-justify-transphobia/
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The Gender Dysphoria Epidemic in Teens
In the media and in clinical circles, there is a perception that there is a growing epidemic of gender dysphoria in teenagers. But is there really? A recent paper set out to test this perception using a survey of 318 male and 401 female youth participated in 2012–2013, and 326 male and 701 female youth in 2017 with up to 3.6% of the boys reporting gender dysphoria in the later survey. That’s twelve of the boys.
Right from the start, I have to question the utility of this study because these numbers are FAR too small to detect clinical gender dysphoria in statistically valid numbers given that we know that only three out of ten thousand individuals experience gender dysphoria sufficient to drive them to socially transition. And that counts “late onset” gender dysphoria which would not occur in teenagers. If we count only “early onset”, we would expect to see only one out of ten thousand. So, with less than two thousand subjects this study couldn’t possibly detect any change in the incidence of severe gender dysphoria.
Lying on survey instruments is common in the general population. It also occurs in the transsexual population and has been shown to be heavily driven by social desirability bias in which autogynephilia is strongly downplayed or outright denied in the “late transitioning” / gynephilic transsexual population. But another form of misrepresentation occurs, especially in teenagers, as the authors point out,
“Validity screening is a novel approach in GD research. Social desirability has been recognized as a methodological problem resulting in the concealing of information perceived as stigmatizing in clinical encounters and research studies. Anonymous survey studies appear to offer a forum to disclose sensitive information without such inhibition, but particularly among adolescents, surveys have also been shown to be susceptible to exaggeration of such information. The proportion of those who admitted to giving incorrect responses was low, but missing information on this item was decidedly common. Comparisons between those reporting responding honestly with those who were not honest and those omitting to answer the honesty question revealed first that among male youth, admitting incorrect responding was strongly associated with reporting GD as measured by the GIDYQ-A. Unfortunately, no validity screen was included in the earlier data. The prevalence of GD detected among males in the earlier data may also be an overestimation. However, not responding to the honesty question was likewise associated with vastly increased prevalence of GD. This may indicate that adolescents felt uneasy after mispresenting themselves when faced with the honesty question and chose to ignore it. However, it may also be that adolescents exaggerated their gender-related dissatisfaction due to assuming that such feelings are expected. GD has recently attracted extensive media coverage in Finland. Adolescents may perceive that they should problematize their gender, and this may influence their responses. When confronted with the validity question they perhaps nevertheless hesitated.”
The odd thing about this study is that their validity screening was conducted with just a single question item in the survey at the end, “Did you respond honestly?” While one can imagine that some who had previously been dishonest would now admit to “Yeah, I’m just messing with you.” Can we assume that all who had been dishonest would suddenly be totally honest just because they asked? Seriously? Still, answering the question that they had not been honest or not answering that question both correlated with a higher GD score. This tells us that we can not trust these scores.
Simply put, there is no credible evidence that there is such a serious epidemic of gender dysphoria in teenagers. Underpowered studies such as this will not answer the question.
For myself, I don’t see any evidence of any increase in the incidence of severe gender dysphoria, only an increase in the visibility and acceptance of transfolk, and of the trendiness of claiming to be transgender.
Further Reading:
Essay on teenagers falsely claiming to be transgender
References:
Katiala-Heino, R., et al, “Gender dysphoria in adolescent population: A 5-year replication study” Clinical Child Psychology and Psychiatry (2019)
https://doi.org/10.1177%2F1359104519838593
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ROGD Redux
A paper published online today in the Archives of Sexual Behavior by a young transwoman, Arjee Restar, tears apart the Littman paper purporting to be about a phenomena called Rapid Onset Gender Dysphoria which Littman claims is an example of “social contagion” in which teenagers, most of whom are female bodied, develop gender dysphoria purely because of exposure to what many are calling “transgender ideology”. Restar’s paper admirably questions Littman’s paper on it’s poor methodology which failed to follow good science practices. The critique shows that rather than testing a hypothesis, Littman’s entire study was designed to produce a predetermined result and pass it off as science, as Restar explains,
“Participants recruited into a study should never be selected based on a researcher’s a priori knowledge of how the results of the paper would appear and confirm their premise. As noted earlier, Littman recruited specifically on three Web sites solely because these venues are attracting a specific demographic group of parental-respondents who are already subscribed into, are selecting into (i.e., self-selection bias), are promoting the concept of “ROGD,” and agree via consent form with the premise of the study. By choosing a specific population of interest and selecting cases and venues where cases can be found, an a priori motivation that favors the investigator’s premise and specific perspectives is likely to be gathered from the sample and thus likely contributing to systemically biased results.”
Fortunately, both Littman’s revised paper and Restar’s critique are openly published, not behind a paywall, so anyone can read both and come to their own conclusions. However, I do have a few of my own comments to make here.
First, the idea of social contagion of minority human sexual orientation has previously been put forward. In fact, it became a center piece of homophobic political activism that used such slogans as “Save Our Children” from the “homosexual agenda” of “recruitment”. That Littman and her ilk recycle this thoroughly debunked trope in a new guise should be no surprise (ref: Brakefield, 2014).
Second, the idea of social contagion (ROGD as a form of “conversion disorder”) focused on girls smacks of the misogynist concept of “hysterical women” found in sexist medical literature of the past. It’s use here as a “just so” explanation is one that transphobic parents would happily cling to in their denialism.
Third, I’ve already shared my thoughts on transphobic parental denialism in a previous essay.
Finally, I look forward to seeing more of Ms. Restar’s academic work in the future.
References:
Restar, A. J., “Methodological Critique of Littman’s (2018) Parental-Respondents Accounts of “Rapid-Onset Gender Dysphoria” “, Archives of Sexual Behavior (2019)
https://doi.org/10.1007/s10508-019-1453-2
Littman, L. L. “Rapid-onset gender dysphoria in adolescents and young adults: A study of parental reports.” PLoS ONE, 13(8) (2018)
https://doi.org/10.1371/journal.pone.0202330
Brakefield, T. A., et al, “Same-sex sexual attraction does not spread in adolescent social networks.” Archives of Sexual Behavior (2014)
https://doi.org/10.1007/s10508-013-0142-9
https://en.m.wikipedia.org/wiki/Female_hysteria
Further Reading:
Essay on ROGD and Parental Denialism
Further External Reading:
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Autopedophilia
The Love of One’s Self as a Child
With the release of Leaving Neverland documenting the experiences of two men who were sexually abused by Michael Jackson, now seems a good time to talk about how Erotic Target Identity Inversions motivate otherwise difficult to understand behavior. Some time back, I read a comment by Dr. Bailey suggesting that Jackson’s behavior fit the theoretical description of an autopedophilic androphilic pedophile. That is to say, a pedophile, attracted to little boys, who also finds the thought of being a little boy himself sexually arousing and rewarding. Jackson saw himself as Peter Pan, the boy who never grew up, one of the lost boys of Neverland who in his innocence has sex with other little boys. This wasn’t just a metaphor. It was central to his sexual identity.
Hsu and Bailey conducted research to test the hypotheses that pedophiles, who are sexually aroused at the thought of being a child, autopedophiles, will be most aroused by imagining themselves to be the type of child that they are most sexually attracted towards as the Erotic Target Identity Inversion theory would predict. That is to say, if he is attracted to nine-year old boys, he will be most aroused by the thought of being a nine year old boy. Likewise, if he is most attracted to little girls, he will be most aroused by the thought of being a little girl. This prediction was supported by the data gathered.
Interestingly, the data suggests that autopedophilia is COMMON among hebepedophilic men.
This result is important because it adds to the evidentiary support for Erotic Target Identity Inversion theory to explain heterosexual male adults who are aroused at the thought of being or becoming women, to wit, autogynephilic transwomen. It also helps to explain the phenomena of adult men whose gender dysphoria is accompanied by “age dysphoria”… and attempt to live as little girls or young teenaged girls, much to the embarrassment of the transcommunity, as Stephanknee W. shown here has.
But there has also been worse than simple embarrassment caused by others. About little over a decade ago, a young transwoman related to me a set of incidences she witnessed about an individual who showed up in the transcommunity in a mid-western state. This individual first caused consternation in a transgender support group in which some members clearly felt uncomfortable with an individual claiming to be a little girl trapped in the body of an adult man, wearing very age inappropriate female clothing. This individual then caused an even greater upset by showing up in said inappropriate young girl’s clothing at an LGBT Pride event and entering a child-care space, insisting on being treated as a child and allowed to play with the “other children” there. But was ejected when it became impossible to ignore that “she” was very sexually aroused and was rocking back and forth in a manner to add to the self-stimulation and arousal.
Morally, ethically, an autopedophile who wishes to play out one’s fantasies in private or with consenting adults is fine. But the moment that one crosses the line to include minors, as Jackson did, we should all seek to have them prosecuted to the full extent of the law… and to believe the victims.
Further Reading:
References:
Kevin J. Hsu, J. Michael Bailey, “Autopedophilia: Erotic-Target Identity Inversions in Men Sexually Attracted to Children”
https://doi.org/10.1177/0956797616677082
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J. Michael Bailey Video Interview
Excepting Blanchard himself, no one has been more misunderstood nor falsely vilified than J. Michael Bailey, Ph.D. The conservatives have lambasted him for researching sexual orientation. Bisexuals have lambasted him for showing that true bisexuality in men is actually quite rare. Gay people have maligned him for his philosophical stance that if it is “OK” for parents to use genetic screening or manipulation to effect a non-critical trait such as eye or hair color, then it is equality “OK” to select for the equally non-critical trait of sexual orientation (meaning that Bailey sees gay or straight as equally valuable and acceptable outcomes in children), falsely accusing Bailey of supporting anti-gay genocide (ummmm… no… he equally supported chosing FOR being gay… as they were morally the same). But it is his authorship of a book that only incidentally covered Blanchard’s research on the Two Type MTF transsexual taxonomy that got his name on the uninformed LGBT communities black list.
Bailey’s book, The Man Who Would Be Queen is primarily about male androphilia and its deep connection to gender atypicality, to male femininity. But, in order to explain that connection, he needed to show that autogynephilic transwomen were NOT in that taxon. Cue that autogynephilic transwomen’s backlash !
So, let’s hear Bailey in his own words:
Further Reading:
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Blood Lines
I
A recent study regarding cross-sex blood transfusions and subsequent mortality may have implications for Blanchard’s immune factor Fraternal Birth Order Effect etiology hypothesis. In the study, they found that when blood from a previously pregnant woman is transfused in men, their subsequent mortality is increased compared to women who are transfused. Blood from women who had never been pregnant did not increase men’s mortality. The hypothesis is that when women are pregnant with a male child, immune factors are created against “males” that can be transfused into men and cause iatrogenic harm. Note the similarity with the immune factor Fraternal Birth Order Effect hypothesis.
To remind my reader. The Fraternal Birth Order Effect is the now well established fact that androphilic males (both gay and transsexual) have more older brothers than sisters. That is to say, that the odds that a given male baby will be androphilic increases with each male child that their mother had carried previously. This is a cumulative effect.
Further research is called for in this new case of transfusion induced mortality connection, of course. But this suggests a new wrinkle to the immune factor hypothesis. Could the issue of immune factor mediation for the Fraternal Birth Order Effect be one of increased fetal mortality for heterosexual males rather than immune factors interfering with virilization? This too should be researched. If this hypothesis is true, the mothers of gay men would have higher “chemical” pregnancies that did not become clinical pregnancies than mothers of only heterosexual men.
Further Reading:
Essay on Fraternal Birth Order Effect
References:
Camila Caram-Deelder, Aukje L. Kreuger, Dorothea Evers, et al, “Association of Blood Transfusion From Female Donors With and Without a History of Pregnancy With Mortality Among Male and Female Transfusion Recipients” JAMA (2017)
https://jamanetwork.com/journals/jama/article-abstract/2657377
Malvina N. Skorska, Ray Blanchard, Doug P. VanderLaan, Kenneth J. Zucker, Anthony F. Bogaert, “Gay Male Only-Children: Evidence for Low Birth Weight and High Maternal Miscarriage Rates” Archives of Sexual Behavior (2016)
https://link.springer.com/article/10.1007/s10508-016-0829-9
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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 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
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