Stop Pretending Transphobia is Scientific Debate

Phony Science with a side of Insidious Rhetoric

Several years ago, in response to an alarming rise in “scientifically” justified anti-trans rhetoric I published an article Stop Using Phony Science to Justify Transphobia in Scientific American. Since then, I have seen many responses ranging from gratitude to - unsurprisingly - transphobia using the exact tactics I lampooned. These amusing retorts are often accompanied by a YouTube video/transcript from a “Paradox Institute.” I have seen it enough that I thought it warranted some response for several reasons:

  1. It’s filled with factual errors.

  2. It’s a great example of The Bullshit Asymmetry Principle.

  3. It’s shows how this fabricated debate about “sex is binary” harms the fight for trans liberation

I will respond to points made, “indicated in quotes.”

The only individual credited in the video is Zach Elliot, so I will refer to Elliot when referring to the video.


The author writes that three subjects help explain the transgender experience: (1) genetics, (2) neurobiology and (3) endocrinology.

I never claimed that these subjects help explain the trans experience, but instead help us better understand it. These small differences in meaning are important: the former implies that the etiology of transness is primarily biological, while the latter acknowledges that these fields of study provide limited but useful insights on a complex phenomenon. Rhetorical tricks like this are exploited by right-wing activists to push for anti-trans policy (Miyagi et al., 2021) and occur repeatedly in Elliot’s response.


Nearly everyone in middle school biology learned that if you’ve got XX chromosomes, you’re a female; if you’ve got XY, you’re a male.” The author claims this is a tired simplification. But even with the existence of X or XXY, is this a simplification?

Maybe “tired” simplification is a dramatic flourish, but yes, the idea that sex determination occurs by the possession of either XX or XY is a simplification. It presents sex determination as tied only to “sex” chromosomes and not to specific genes, hormones, or environmental triggers. In reality, all three of these, and their interactions, can play a role in sex determination (Bachtrog et al., 2014).

The designation of the 23rd pair of chromosomes in humans as the “sex chromosomes” comes with it’s own contentious scientific history. X and Y have been known as allosomes, heterochromosomes, idiochromosomes, gonosomes. “Sex chromosome” is a recent creation and arguably comes with it’s own scientific problems (Richardson, 2013).


First, using atypical karyotypes (like X or XXY) in arguments to support trans identities is disingenuous. Why? Because trans individuals almost always have typical XX or XY karyotypes. How do we know? Because we’ve done the karyotype tests. In one study, conducted with over 300 trans individuals, 97.55% had typical karyotypes of XX or XY, matching their birth sex. Only 3 out of 368 had Klinefelter syndrome (Inoubli et al., 2011).

It is important to note what Elliot does not mention about this study: the context in which the results exist. Inoubli et al. are keen to point out that their observed frequency of atypical karyotypes in transsexual people - 2.45% - is 4 times higher than the general population, which can range between 0.53%-0.63% in the study cited by Inoubli et al.  Additionally, citing “only 3 out of 368 patients had Klinefelter syndrome” is misleading; it’s typically reported within the proportion of male births. A proper comparison would be 3 of 251 live male births, which is significantly higher than the general population rate of 1-2 in 500 live male births. Again, Inoubli et al. are right to point out that this might be a spurious result, due to the limited sample size. It is also interesting to note that intersex people have gender dysphoria at a higher rate than the general population, 8.5-20%. Notably, individuals with intersex conditions related to steroidogenesis (5ɑ-RD2 deficiency, and 17β-HSD3 deficiency) have the highest rate of gender dysphoria (Furtado et al., 2012). What’s even more curious is that these conditions arise from autosomal mutations, not on the sex chromosomes! I don’t use these data to “support trans identities”, but to point out that there is a complex relationship between sex and gender, particularly related to genetic and hormonal interactions. Karyotypes are one piece of that relationship.


Such studies show us that using chromosomal anomalies to explain trans experience is ignorant or dishonest.

This is the insidious rhetoric of the sort I mentioned previously. I am not claiming that chromosomal anomalies explain transness. I only say that they provide important insights into understanding the biology of sex and gender. Studies like Inoubli et al. suggest that there may be a genetic component that contributes to transness. Furthermore, karyotyping provides limited genetic information – a bird’s eye view. It does not indicate what or how specific genes or gene regulatory mechanisms have changed. The emphasis on sex chromosomal abnormalities adds to the dishonesty. As my original article points out, many genes necessary for sex-related traits are on the autosomes, or non-sex chromosomes. Even intersex individuals may not exhibit karyotypic variation; certain intersex varieties arise from mutations of genes in autosomes, like the previously mentioned 5ɑ-RD2 and 17β-HSD3 deficiencies. And though karyotyping is of limited practical use and comes with significant issues concerning medical ethics, results like these are interesting to consider when trying to understand how sex characteristics interact with gender identity.


Second, 99.98% of births are unambiguously male or female (Sax, 2002).

Ah yes, this citation. There are several problems with presenting this statement as proof of binary sex. First, it is not a research paper, it’s an opinion in response to a perspective piece (Blackless et al., 2000) that illuminates the difficulties of intersex as a label. Second, it is an opinion piece written by one author, who is not a biologist but a psychologist and physician. I don’t say this to preclude Sax from the conversation about what does and doesn’t constitute an intersex categorization, but to illustrate how scientific discourse can be bent to suit one’s rhetorical needs and political goals. Third, so what if ambiguous births are rare? The infrequency of ambiguous births does not prove that sex is best explained as a binary system. Life in the universe is infrequent, so do we ignore its rare occurrence and say that the universe is lifeless?


Even in cases of chromosomal anomalies like X or XXY, the fetus still develops a reproductive system organized to support ova (in X cases) or a system organized to support sperm (in XXY cases). The reason why chromosomal anomalies still produce a female or male is thanks to the activation of the SRY gene (usually found on the short arm of the Y chromosome). If the SRY gene is present and active, it initiates a complex set of gene cascades causing male development. Fetuses with only one X do not have the SRY gene, and thus develop as females. Fetuses with XXY DO have the SRY gene, and thus develop as males. This genetic system is so consistent that even in cases of XXX or XXXY, the fetus still develops as a female or male, respectively.

So Elliot agrees, the Y chromosome is not the genetic factor that initiates “male” development.


The author then brings up additional congenital medical conditions to argue against the sex binary: “XX individuals could present with male gonads. XY individuals can have ovaries,” he [sic] writes.

My pronouns are she/they, thank you for being so respectful.


Those unfamiliar with sex development might be confused. How does this happen? Simple: the activation or inactivation [sic] SRY gene. For XX individuals with testes, this occurs when the SRY gene moves onto an X chromosome, causing male development. And for XY individuals with ovaries, this occurs when the SRY gene is not activated, causing female development. Thus, despite the author’s claims that sex does not arise from chromosomal makeup alone, sex [sic] is indeed largely determined by the activation or inactivation of the SRY gene.

The SRY gene is not inactivated in the scenarios relevant to this discussion. This imprecise description of SRY betrays the lack of real understanding Elliot has of genetics. This is wrong because this implies that ovaries arise because SRY is activated and then turned off. It also reveals the ulterior motive to portray the function of SRY as a strict all-or-nothing binary. Gene expression is incredibly variable and can exhibit states more than just activation or inactivation. They can be activated and expressed at high or low levels. They can be repressed. They can be primed. They could be rendered inaccessible to gene expression machinery. They can be expressed but then blocked or interfered. They can be alternatively spliced into different forms to play contextually specific biological roles. Biology is a messy world, and this complexity makes genetics so interesting (but difficult)! With regards to SRY, it does not determine sex, it determines testes. If it is present in XX individuals and activated in a narrow time window, it will initiate testicular differentiation of the bipotential primordium. However, it’s clear that SRY is not all that is needed to result in “maleness” as individuals with XX SRY-positive genotypes may need hormone therapy and other healthcare to develop other male characteristics, if they desire. Additionally, XY SRY-negative genotype results in atypical female development and may also need hormone therapy. “Largely” isn’t looking so binary, is it?


Next, the author discusses how SRY activation initiates additional genes such as DMRT1 and FOXL2, which help and maintain testicular tissue [sic]. This is true [sic].

This is false. I did not say SRY activation initiates DMRT1 and FOXL2. As far as I’m aware, SRY’s only known target at the sex determination stage is SOX9 (Huang et al., 2017). FOXL2 activation does not help or maintain testicular tissue (Uhlenhaut et al., 2009).


If these genes are not present [sic] during fetal development, the testes may not develop, and you will develop as a female. But again, you might ask, what do these congenital conditions of the reproductive tract (DSDs) have to do with trans individuals, who almost always develop with typical chromosomes and typical reproductive systems? Perhaps these DSDs are being used for ideological means?

Again, wrong. These genes (DMRT1, FOXL2) are present in all humans, regardless of sex or age. It’s whether or not these genes are expressed at certain times and in specific tissues is what determines testes or ovary development or maintenance. I leave it up to the reader to determine who is using scientific knowledge for ideological means though I would remind them that Elliot’s presentation is riddled with errors.


PART TWO–Neurobiology.
Here, the author uses neuroscience in brain differences to argue that male and female cannot be clearly defined [sic]: “A half century of empirical research has repeatedly challenged the idea that brain biology is simply XY = male brain or XX = female brain.”

I did not say “male and female cannot be clearly defined.” In fact, I believe that these designations require more precision and clarity.


It is true that there are indeed no black and white “male” and “female” brains. But this variation in brain differences does not mean there is no clearly defined ‘male’ or ‘female,’ because we define sex through one of two evolved reproductive anatomies.

Elliot (and Geoff Parker in discussion of gamete evolution) define sex that way. This definition is useful in specific contexts, like when attempting to understand the evolution of sexual reproduction, but not in others. Sex is complicated and its conceptual usefulness depends on the situation (Richardson, 2021, 2013).

I invite you to react to what Elliot wrote, with the following slight modifications: It is true that there are indeed no black and white “male” and “female” brains. But this variation in brain differences does not mean there is no clearly defined ‘male’ black or ‘female,’ white, because we define sex race through one of two evolved reproductive anatomies.


Rather, there are average differences in the brain within and between males and females that, when aggregated together, allow us to predict someone’s sex [sic] with up to 97% accuracy. This is specifically done through analyzing the overall morphology of the cerebral cortex.

Best not to misquote your sources. They were predicting a person’s gender, not sex. It’s nice that Luo et al. designed an algorithm to correctly predict an individual’s gender from cortical morphology most of the time. What does that tell us about sex differences in the brain? What does that tell us about the neuroscience of gender? What is this useful for?

Also, the success rate of an algorithm isn’t the only important aspect to consider. Knowing when and how an algorithm is wrong can be illuminating! To illustrate this point: I invite you to inspect the usefulness of this algorithm, which can identify cats with up to 97% accuracy.


It is true that trans individuals may have specific structures in the brain that are similar to that typically seen in the opposite sex. As the author mentions, some specific regions in gay men are similar to straight women. But these similarities do not change one’s sex.

I never said anything about changing one’s sex in this article. But if you want or need to change your sex, there are many ways to do that.


The existence of subtle brain similarities to the opposite sex does not mean that such individuals ARE the opposite sex.

Oh definitely not. I would never tell a cis man with a smaller-than-male-average sdnPOA that they are female. That’s rude.


It just means that one might have specific structures that are atypical. This does not change your sex class any more than other physical differences.

What’s “sex class?” Is that the one with the condom and the banana? I thought conservatives were attempting to ban those.


Using brain similarities and differences to argue that someone IS the opposite sex is akin to using sex differences in height to argue that a short male who falls in the typical female range IS a female. Variation does not make someone ‘less male’ or ‘less female’

All I’m arguing is that observable sex and gender differences in the brain show that a binary model of sex is wrong about the human brain. It seems Elliot’s the one arguing (with himself?) about whether variation makes someone ‘less male’ or ‘less female.”


PART THREE–Hormones
The author uses hormone levels to ‘disprove’ the sex binary: “But like all things biology, hormones cannot be limited to the pubescent idea of “estrogen = female and testosterone = male.” This is true, as males and females are both exposed [sic] to testosterone and estrogen.

Thanks for saying I’m right! That’s nice. But why are we talking about exposure to hormones? Hormones are in the body and can originate from endogenous and exogenous sources.


These hormone levels, like differences in the brain, exist as bimodal distributions [sic], an average for males and an average for females.

Wait, really? Someone showed that hormone levels are bimodal? There are reference ranges used for standard medical practice. Did someone really have the money, time, and resources, to sample enough people efficiently and accurately to make a population distribution that was useful? Was this for all hormones? Did they separate estrone, estradiol, and estriol? What about testosterone and dihydrotestosterone? Who did they sample? When? What time of day? Was the stage of the menstrual cycle controlled for? Were some of them taking hormonal birth control? How old were they? Were they pregnant? Wait… were they mice?

It’s easy to just make bullshit up, isn’t it?


But variance in hormones, even extreme variance, does not disprove the sex binary. For example, a male who has less T than the average male does not become ‘less male’ or ‘more female.’ He is still a male, as his body is organized around small gametes.

I thought we were talking about hormones. What’s this about gametes again?


So to conclude, you may notice a pattern in all three aspects: (1) genetics, (2) neurobiology, and (3) neuroendocrinology. In all three categories, variation does not mean sex is on a spectrum, but rather, that sex-related traits are on a spectrum, a bimodal distribution [sic].

I mentioned spectrum to convey that specific traits exist within some range of values. Who’s putting the entirety of sex on a spectrum? Elliot continuously refers to some bimodal distribution without a citation, though in the video he puts up some pretty normal distributions without any axes or labels. Check out these hypothetical distributions I made for a textbook chapter! I think it illustrates the complexity of how hormones regulate gene expression in the brain pretty well. However, in reality even this cartoon is an oversimplification. Each of these distributions are high-dimensional, over many factors of, say, gene expression or aspects of neural activity.


Sex differences within and between males and females exist as bimodal distributions [sic]. There is variation of hormone production, brain structure, and external appearance, but this does not make a ‘sex spectrum.’ Rather, it makes a spectrum of anatomy and physiology. The reason why we can place traits such as hormone levels on bimodal distributions is BECAUSE of the sex binary...

At this point Elliot states “sex binary”, two this, two that, ad nauseum. He refers to this “sex binary” but what he fails to acknowledge is that this binary is a socially constructed definition (science depends on social constructs). He even has to fabricate data to support his binary sex construct. Truth is, the categories of male and female come from people making observations and drawing boxes around those observations. The phenomena we call “sex” exist in many different forms and ways. Even when studying the biology of sex differences, a binary model (researchers sometimes refer to this as “qualitative sexual dimorphism”) only captures a small part of what “sex” is (McCarthy et al., 2012). Elliot can say “sex binary” all he wants, but it doesn’t make sex a binary phenomenon.


But I have a different request: when will activists and authors of major publications stop using complex medical conditions such as DSDs in arguments about unrelated identities? And finally, when will activists stop using the beautiful complexity and diversity of biology to justify the dismantling of male and female under the guise of ‘science’?

Running out of phony science to make up? No one is “dismantling” male and female. They are useful labels in specific scientific, medical, and political contexts. Some people find them helpful in describing themselves. I can only speak for myself: I will stop when anti-trans activists stop using the aesthetic of “scientific truth” to perpetuate the societal and political oppression of trans and gender diverse people.

A closing note:

“Paradox institute” appears to be something similar to “PragerU”, a politically conservative nonprofit group masquerading as an academic institution to provide the allure of academic expertise to right wing talking points. Like PragerU, Paradox has no institutional backing, no academic credentials of any sort, nor has it contributed anything of note to peer-reviewed scientific research on sex, sex differences, or general biology. It was “founded” by Zach Elliot, (at time of video publication) an undergraduate architect student who appears to be this “institute’s” only member.

Conservative ideology is intrinsically anti-academic and anti-science and needs to disingenuously appropriate the aesthetics of intellectualism to mask its political positions with the allure of scientific legitimacy. This “debate” never resolves because one side is fueled by a political goal: to perpetuate the systemic oppression of trans people. They will not stop using “science” in this way until, frankly, trans people are eliminated. It’s why Elliot et al. (more than just him this time!) responded similarly to another short piece I and some colleagues published calling out this strategy. I know that what I’ve written here will not end this cycle of propagandistic trolling, and sadly will perpetuate it. So let this be a “closing statement” if you will:

“Sex is binary” is not a scientific debate. It is a political debate that exists because anti-trans activists cannot abide the existence of trans people, much less trans scientists. However, the great thing about the scientific enterprise is that it is a light that dissolves the illusions of pretenders and illuminates the truth - that nature is beautiful in its creativity and diversity and that all forms of life are worth understanding for what and who they are.