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It’s Biological, Duh!

If you’ve read my blog, you’ve probably realized that I’m not one of those people who likes to go around stating unproblematically that transness is “inborn” or due to “nature”. If you’ve ever read my Twitter account, this becomes even more clear that I dislike ‘innate-ness’ explanations.

So when there’s a person going around reddit posting some “masterpost” of how trans identity is biological, it’s sure to arouse some suspicion in me. In my previous post, I addressed the political, scientific and sociological aspects of “brainsex” within trans politics. But the “neuro”-origin myths about being trans are not the only ones that exist: There are also the hormonal ones & the genetic ones. “Biotroofs” are present in all sorts of manners, trying to inscribe identity, lived experience & group differences to various aspects of the body.

Not One, But Two?

One of the most common appeals is to mythical “genes”. Milton Diamond’s paper (forgive the constant misgendering) is especially famous for this, as he examined trans identity among twins. The problem with his study is that not only did he calculate heritability coefficients by using the MZ (monozygotic – identical twins) and DZ (dizygotic – fraternal twins) data that he collected, but he uses a scientific methodology that has been torn to pieces.

For those not acquainted with twin studies, they are a methodology originally created by Francis Galton to ‘determine’ the relative contributions of ‘genetics’ and ‘environment’ to his measures of intelligence. Essentially, they compare the similarity among MZ twins (their concordance rate) and their similarity among DZ twins (their concordance rate) and use that to estimate the genetic contribution. The typical model for this study involves the analysis of variances. Variance, V, of the population is presumed to be a combination of the variances in genes & environments; V=G+E. The way to calculate “G” and “E” was like this: we assume that the variances of twin phenotypes is simply the addition of genes and environment. Monozygotic twins, by virtue of sharing all their genes, had their correlation $r_{MZ}=E+G$. Dizygotic twins had the equation $r_{DZ}=E+G/2$ because they shared only half of their genes. Solving the set of simultaneously equations yields $G=2(r_{MZ}-r_{DZ})$, so $r_{MZ}=E+G \implies r_{MZ}= E+2(r_{MZ}-r_{DZ})$ $\implies E=2r_{DZ}-r_{MZ}$.

This is the original model that psychologists and eugenicists used in the early 1900s, but it has since been the subject of numerous critiques and some advancements. Notably, it has been noted that the “environment” is typically divided into two parts: shared environment (anything that makes twins more similar) and non-shared environment (anything that makes twins less similar). Researchers have also noted the interaction of genes and environment: a gene that “codes” for a particular phenotype may only do so in the presence of an environmental influence. This is typically denoted by GxE and has been the subject of a burgeoning literature, alongside statistical problems. It has been centered within the discussion of the controversial MAOA gene, allegedly* demonstrating that the gene only affects mental health outcomes in the presence of abusive environments.

While twin studies have been one of the most-used paradigms within the ‘heritability study’ scheme because they claim to be able to partition genes and environment, they have been subject to extensive critiques due to their inability to adequately control for confounds, as well as their uselessness in isolating the specific origins of a particular phenotype. Contrary to popular belief, the effects of genes and environment are not separable. As Lickliter so succinctly describes the heritability study methods, it is a fallacy of partitioning. Or as my friend always puts it “development doesn’t work that way“.

Beyond the conceptual disputes over what a heritability statistic means, there are some relevant biases that twin studies face. Most notably is known as the “equal environment assumption”. The equal environment assumption (or EEA) states that MZ twins and DZ twins share equal correlations in environment (i.e. that the environment will be no more similar for MZ twins than DZ twins). We have substantial reasons to believe that this is untrue, however. As a 2001 paper pointed out, one can potentially explain the entire difference in concordance rates between monozygotic twins and dizygotic twins by environmental similarity.

If we again review Diamond’s ‘transsexual twin’ study, we can note a few things. First: that he strangely refused to calculate the heritability statistic (from the naive traditional twin model), which from his Table 3, would be $h^2=2(r_{MZ}-r_{DZ}) \implies h^2=2(.41-.10)=.62$ for ‘males’ and $h^2=2(.36-0)=.72$ for ‘females’, from the bibliographic search. From Table 4, the survey search demonstrates $h^2=2(.27-.0)=.54$ for ‘males’, $h^2=2(.14-0)=.28$ for ‘females’. And from Table 5, the overall aggregated data implies $h^2=2(.33-.05)=.56$ for ‘males’ and $h^2=2(.23-0)=.46$. Interestingly, when we go to calculate the “shared environment” contribution to the phenotype, we get a model violation: $c^2=r_{MZ}-h^2$, which for ‘males’ is $c^2=.33-.56=-0.23$ and for ‘females’ is $.23-.46=-.23$. The ACE model described above does not permit for negative contributions, meaning that the computation of the statistic is meaningless. Regardless, if we calculate the ‘non-shared portion’ ($E=1-A-C=1-r_{MZ}$) we get $E=1-.33=.67$ for ‘males’ and $E=1-.23=.77$ for ‘females’. This would seemingly imply a very large non-shared environment contribution to the trait, but alas the statistic is meaningless. But as many recognize (note that this primer is uncritical of twins reared apart studies that have numerous problems), finding a negative estimate for $c^2$ would imply that either the EEA (equal environments assumption) or NNE (no non-additive effects) are false.

Second: there is another assumption that is almost certain to be violated: random selection & attrition, that is, ascertainment bias. When ‘gathering’ the twin data, especially for such rare identities like being trans, there is a gigantic problem with how data is collected. Because trans people are so rare, the methods that researchers use to identify them are already a huge issue in regular trans research, but in twin research, this problem is compounded: many times. Because twins that are both trans are much more noteworthy (and perhaps, because of the shared identity, the twins could have maintained a closer relationship during adulthood), it is certain that twins that are both trans (i.e. concordant) are more likely to be found by researchers & respond to surveys. This violation of ascertainment bias has been shown to upwardly bias estimates of heritability. Even more, the lack of zygosity testing (i.e. that more similar twins are more likely to consider themselves MZ when they are in actuality DZ) and the circular assumption of zygosity from narratives (i.e. presuming that similarity is a result of genetics and then concluded as such) are two more mechanisms by which the correlations of monozygotic twins are overestimated and dizygotic twins are underestimated.

And, of course, this circles right back to the underlying incoherence of the twin model. Development doesn’t work that way! Peter Taylor has demonstrated at length how underlying developmental heterogeneity invalidates the assumptions of heritability studies, while a review of the research in criminology has sparked a call for their abandonment. What is clear is that the research into the ‘genes’ of trans identity is inherently complex, politically fraught & not going to come to an end any time soon.

It’s Still In The Genes!

Despite the launch of attacks upon twin study methods I’ve alluded to, a careful reader might note that there have been reports of ‘transsexual genes‘ in the news, perhaps rebuking my critical analysis of the twins that Diamond has presented. A closer look, however, will note that it’s part of another failed tool from the hereditarian toolkit: the “candidate gene”. After decades of ‘heritability studies’ purportedly demonstrated that every trait in existence was, in part, genetic, the wave of genomics ushered in a new era of psychologist, geneticist and behavioral scientist alike, all hoping to ‘find the genes’. Their methodology was to identify a ‘locus’ involved in a particular body process. For depression, it was the 5-HTTLPR gene. For various personality traits, it was the DRD4 gene. For aggression, researchers presumed that MAOA gene may be involved. The entire ‘candidate gene’ shtick was nothing but a house of cards, with a recent psychiatric study making waves within genetics communities and the general public alike. Similar null results have been shown for the MAOA gene, and a review of the entire candidate gene literature found nothing but inconsistency and internal contradictions. The minuscule sample sizes (leading to both random and systematic error) for testing effects along with researcher degrees of freedom, p-hacking and publication bias have produced a research environment where non-existent genetic effects have been able to be touted as having large influences.

The paper in question is not much better. Along with the small sample size (N=112, 258), the association detected was only barely significantly at p=0.04Right under the 0.05 margin. You’ll note that once classified into subgroups of ‘long’ and ‘short’, the difference between the cis & trans groups is entirely insignificant:

The AR genotype, being X-linked, is hemizygous, and thus the comparison undertaken was between short and long genotypes. An independent samples t-test revealed no significant association for the AR gene when sub-classified (p > .05).

(Emphasis mine)

I noticed that they had an outlier: a trans individual with 36 CAG repeats, so I did a quick and dirty recomputation without. Following the methodology in the studies I will discuss afterwards, I didn’t calculate the base pairs (as this could artificially inflate significance and because I have yet to hear back from the authors on how to calculate these figures & even more, the following literature doesn’t do so), but rather just the number of repeats (note that this is a rough reconstruction from their Figure 1A).

Number of Repeats Trans Controls
12 0 1
13 0 1
14 0 2
15 0 1
16 2 3
17 9 5
18 9 8
19 9 14
20 17 20
21 12 11
22 9 8
23 13 13
24 7 7
25 2 2
26 5 4
27 1 2
28 5 1
29 0 1
30 0 1
32 0 1
36 2 0

I performed a basic one-tailed Student’s t-test for the sake of ease and got a t-value of 1.31906 and a p-value of .094307. Thus, the number of repeats between the groups was not significant. My suspicion is that the difference found was an artifact of converting the number of repeats into the number of base pairs. See Appendix B for input data & more information about the calculation.

Fascinatingly, there are not only one, but two subsequent papers disconfirming the link. A 2014 paper in Spain tested all of the purported candidate genes (ERβ, AR, and CYP19A1) in the largest sample size yet (N=915) and found no relationship. The study found marginal significance for repeat length and the CYP19A1 gene, finally completing the “significant” result for the trio. But as all previous and subsequent research has not found any association, it is certainly a spurious result. A 2009 study also tested the purported candidate genes for both trans men and trans women with relatively high sample sizes & failed to replicate the AR & ERβ results from previous research. They also found no associations for any of the testosterone/estrogen-related genes they tested (increasing the total number of candidate genes from previous research). We should also note that other studies purporting to link CAG repeats to reproductive/sex-related phenotypes have come up with contradictions and publication bias. I think this qualifies as a robust falsification of the hypothetical aetiology, at least until the gene people break out GWA and start making more bullshit developmentally-ignorant associations.

From Phrenology to Fingerology

Next-up in the never-ending train of purported biological influences on trans identity are the fingers. One might question the relevance of one’s digits to the seemingly neurologically grounded (at least according to the trans-essentialists!) trans identity, but researchers have ‘shown’ (to use the word lightly since this thesis has been challenged numerous times and the relationship to various gender attributes rarely replicates) that the ratio of one’s second finger to their fourth finger is associated with the prenatal level of testosterone, at least purportedly. This result has been thrown up as “evidence” that trans people’s identities are determinisically caused by prenatal hormone exposure, despite the data being so mixed. Let’s take a look.

After a 2017 study (which was both of little value and performed by a doctor that is known to be harmful to trans people) tested the widely reported, sometimes replicated and sometimes not, relationship between 2D:4D and trans identity, there was a comment on the paper. One was from a set of researchers I trust highly, who performed a meta-analysis on the disparate literature on the topic. They found that trans women had 2D:4D ratios that were significantly more “feminized” in their right-hand, while the difference in the left-hand was not significant (although it’s p-value was marginally above the significance level). Trans men did not have “masculinized” ratios on either of their hands (although the g effect sizes were trending in the ‘correct’ direction). Despite the claims of other papers, it did not seem that measurement method affected the results in the meta-analysis. The heterogeneity among studies, then, seems to result from sampling characteristics (perhaps things like ascertainment bias). Most notably, the results indicated that even in the case that the small positive among trans women’s right-hand was not driven by things like developmental heterogeneity (a correlation produced by the fact that the link between 2D:4D and prenatal androgen exposure is weak in the first place), publication bias, ascertainment bias or other sampling biases, this still indicates an overlap of somewhere from 92-98%. If we frame this in terms of diagnostic accuracy, it would only give 51.7-55.3%, only marginally above the random guess of 50%.

Rebuilding Transness

I can already hear people wondering that if I don’t think that transness is biologically inborn, then where do I think that transness arises from? To be honest, I don’t think it’s a very interesting or politically relevant question. Because trans identity is historically and socially contingent and the irrelevance of a ‘biological’/’genetic’ grounding to a trans-affirmative politics, whether or not transness (as formulated by medical gatekeepers) is ‘biological’ just seems like a non-sequitur to every issue facing trans people. As Canguilhem has demonstrated in The Normal and the Pathological, to investigate the cause of something is to pathologize it by casting it as abnormal and need of investigation. Why is it that we have never searched for the cause of cisgenderism, of heterosexuality, of gender-normative behavior? It is precisely because these are norms, the ideal upon which non-cisheteronormative individuals are compared to: to create difference.

Despite the many affirmations that biological explanations are favorable to trans (and LGBQA) people, it’s unclear why this form of biologism would convince anyone. As any cursory engagement with philosophy would tell us, one cannot derive an ought (a moral/normative/ethical/evaluative statement) from a set of is statements (descriptive/empirical statements) alone. Due to this fact, it is quite easy for an anti-trans individual to reject any narrative affirming trans people based solely on vacuous appeals to biological and psychiatric authority (which, of course, ends up reinscribing transmisic oppression). All they have to do is point out that any purported biological influences are not inconsistent with the right-wing’s favorite “mental illness model” (warning: transmisia & homomisia). They could also just deny that a biological grounding of the ever-illusory ‘gender identity’ has any bearing on their privileging of ‘sex’ based on ontological or normative grounds. This realization that a trans-affirmationist politics cannot be based solely on empirical results helps us question the relevance of these findings overall: if the efficacy of the research in debates inevitably reduces to an ontological, ethical and metaphysical debate, why not just start there in the first place?

Now that I’ve avoided presenting my model of gender identity long enough, I’ll release the pressure. For a long time, I just ignored any ‘model’ of gender identity since I didn’t (and still really don’t) believe it’s a coherent, unitary or separable construct. Despite my persistent concerns, it may be better to adopt a tenuous model: one that can be deployed only for those who are insistent that we have to have some idea of where gender identity comes from. One of my favorite authors is Anne Fausto-Sterling, a biologist, feminist & gender studies scholar (she is also known as a leading expert on the development of gender identity!). She is most renowned for her oft-cited book Sexing the Body. In her 2008 work, Sex/Gender: Biology in a Social World, she analyzes the evidence as to what biological factors are associated with gender identity development. She concludes that chromosomes, gonads, reproductive organs, genitalia, prenatal & pubertal hormones do not have much, if any, evidence for a causal influence on gender identity. After reviewing the psychological literature on gender identity formation in early childhood (as well as the literature on intersex individuals), she concludes that gender identity is the result of a complex developmental process involving early postnatal gendered experiences and individual embodiment. I highly recommend reading the entire chapter (chapter 5: Am I A Boy Or A Girl? —The Emergence of Gender Identity). Since I follow her on Twitter, I noticed when she published a new article this year titled: Gender/Sex, Sexual Orientation, and Identity Are in the Body: How Did They Get There? Most of the article is focused on applying a phenomenological perspective to gender/sex, sexual orientation and identity, and in doing so, she develops a more thorough theory of embodied development: how sex/gender and sexual orientation arise and become a part of the body.

Appendix A

Because the focus of this article was on the alleged biological causes of trans identity, I didn’t focus on several other of the points that the reddit user drewiepoodle that sparked this ‘anti-genetics’ (to quote some famous hereditarian redditors) tirade made in their copypasta.

First up is the monkey myth:

A growing body of research is showing how biology influences gender expression, sexual orientation and gender identity — characteristics that can also fall outside of strict, socially defined categories. Toy-preference tests, a popular gauge of gender expression, have long shown that cis boys and cis girls will typically gravitate to toys that are stereotypically associated with their gender (cars and guns for boys, for instance, or plush toys for girls). While one might argue that this could be the by-product of a child’s environment — parental influence at play or an internalization of societal norms — Melissa Hines, a former UCLA researcher and current professor of psychology at the University of Cambridge, in England, has shown otherwise. In 2008, she demonstrated that monkeys showed the same sex-based toy preferences as humans — absent societal influence.

The “monkey studies” have been weaponized against the “gender feminists” (to borrow Christina Hoff Sommers’ term) who point out the pivotal role of socialization and gender roles in the development and expression of gendered preferences for various social features. Here the user is referencing Melissa Hines (who is, funnily enough, a critic of the brain organization thesis in many ways) and her team’s study on vervet monkeys. The study tested whether male or female vervet monkeys would have sex-typed preferences for toys, presumably because monkeys are free from social influence. They tested 6 toys, 2 ‘masculine’ (police car & ball), 2 ‘neutral’ (picture book & stuffed dog) and 2 ‘feminine’ (doll & cooking pan). Interesting, the toy of a ‘ball’ has previously been classified a ‘neutral’ toy in previously studies testing sex differentiation in toy preferences. Overall, male monkeys spent the most time with the dog (neutral) and equal amounts of time with the ball, police car (masculine) and cooking pan (feminine). The female monkeys spent the most time with the cooking pan (feminine), dog (neutral), then doll (feminine) and then less time with the police car and ball (masculine). While there was an overall statistical difference between male and female monkeys in their choices of ‘masculine’ vs ‘feminine’ toys, it doesn’t exactly explain why there were such heterogeneous results: why neutral toys dominated and why there were ‘cross-sex’ results for some toys. This is only compounded by looking at the other monkey study on toys, which is reviewed in Gina Rippon’s The Gendered Brain (pages 194-195), Rebecca Jordan-Young’s Brain Storm (pages 234-236), and Cordelia Fine’s Delusions of Gender (pages 123-129).

Not only do the actual results raise questions about what the actual preferences among monkeys is, it raises questions about monkeys themselves. People often assume that, no, animals don’t have complex social structure. The assumption is that since an animal exhibits a sex difference, the corresponding sex difference in humans is not only natural, but intractable. (Un)fortunately, this is a naive way of looking at development. Just like humans, many primate species have complex social structures with varying hierarchies. It might be anathema to some, but it has been shown that primates and other animals alike have forms of social learning, what some term “socialization”. Some research has even indicated that primates have a form of gender roles and perhaps even gender identity. This research has come alongside with a review of our anthropological concepts of culture and the realization that primates (and other animals!) indeed do have what can be termed ‘culture’. Because there are varying developmental experiences and trajectories among male and female primates, the fact that a difference emerged (however self-contradictory) is not evidence for an innate sex difference, it hints towards a complex developmental origin. In fact, a friend of mine has noted that the only thing that these ‘monkey studies’ can show is the particular troop dynamics.

Next up, a few lessons to anyone (including the subject of my critique) who may read this. Behavioral traits are, if genetic at all, polygenic, meaning originating from numerous genes. In fact, nearly all traits are polygenic, with the exception with a minuscule number of allele substitutions which produce strong changes in phenotype (sickle cell disease, for example). The claim that:

We have no idea what the details are (a gene, multiple genes, etc?) but we have pretty strong data that it’s something durable and biological.

indicates an underlying misunderstanding of the way that not only scientific research (and norms) work, but of how developmental genetics works. If there are going to be any genes that influence trans identity, it isn’t going to be gene or multiple genes, it’s going to be numerous. Estimates of polygenicity (a numerical quantification of how many genes are involved in the development of a phenotype) for traits such as Alzheimer’s disease and schizophrenia have estimated numbers of genes into the thousands, simply for a single trait. And again, to the extent that genes are purported to exist, they are very likely to be mediated, moderated and interact with environmental factors.

Of the final extraneous points I wanted to make is the discussion of intersex people & their gender identities;

Also, the attempts by the medical establishment to surgically change body parts of intersex children based on what seemed easiest surgically was not always in line with the person’s actual gender. The thinking back then(and even today) was that gender identity was not biological. When the data was carefully collected, a majority of kids treated this way have a gender identity at odds with their surgically created body parts and upbringing(socialized as male/female). This is proof that we cannot change the gender identity someone already has innately.

Rebecca Jordan-Young has reviewed the literature (in the aforementioned book Brain Storm) on a variety of research progammes investigating sex differences in various traits, mostly related to the purported causal link between hormones (testosterone, estrogen), brain development and the aforementioned social traits. One of those programmes of research has focused on the development of gender identity in intersex individuals. She has thoroughly demonstrated that the typical consensus that intersex individuals will ‘revert’ to their ‘biological gender identity’ is not back-up by the data (this still doesn’t mean we ought to mutilate intersex children).

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Appendix B

Because I was lazy and my computer doesn’t like to install software these days, I just used an online t-test calculator.

For Treatment 1, I input: 16, 16, 17, 17, 17, 17, 17, 17, 17, 17, 17, 18, 18, 18, 18, 18, 18, 18, 18, 18, 19, 19, 19, 19, 19, 19, 19, 19, 19, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 21, 21, 21, 21, 21, 21, 21, 21, 21, 21, 21, 21, 22, 22, 22, 22, 22, 22, 22, 22, 22, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 24, 24, 24, 24, 24, 24, 24, 25, 25, 26, 26, 26, 26, 26, 27, 28, 28, 28, 28, 28, 36, 36

And for Treatment 2, I input: 12, 13, 14, 14, 15, 16, 16, 16, 17, 17, 17, 17, 17, 18, 18, 18, 18, 18, 18, 18, 18, 19, 19, 19, 19, 19, 19, 19, 19, 19, 19, 19, 19, 19, 19, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 20, 21, 21, 21, 21, 21, 21, 21, 21, 21, 21, 21, 22, 22, 22, 22, 22, 22, 22, 22, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 23, 24, 24, 24, 24, 24, 24, 24, 25, 25, 26, 26, 26, 26, 27, 27, 28, 29, 30, 32

Note that these don’t actually reflect the actual numbers of the sample as these were reconstructed from frequency data. Because I didn’t want to go through the mess of multiplying the frequencies by the sample sizes for the trans & control groups, I just essentially ‘normalized’ the Ns to ~100 (the actual sizes were both slightly above 100 because of errors in estimating the frequency from the graph).

Uncategorized

Radical Feminist Conceptualizations of Sex-Gender

Catherine MacKinnon

MacKinnon rejected the sex/gender distinction, referring to Ortner’s critique Is Male to Female as Nature Is to Culture?:

Much has been made of a supposed distinction between sex and gender. Sex is thought to be the more biological, gender the more social; the relation of each to sexuality varies. I see sexuality as fundamental to gender and as fundamentally social. Biology becomes the social meaning of biology within the system of sex inequality much as race becomes ethnicity within a system of racial inequality. Both are social and political in a system that does not rest independently on biological differences in any respect. In this light, the sex/gender distinction looks like a nature/culture distinction in the sense criticized by Sherry Ortner in “Is Female to Male as Nature Is to Culture?” Feminist Studies 8 (Fall 1982). I use sex and gender relatively interchangeably.

In her view, it isn’t precultural bodies that produce gendered distinctions via some mechanism of reproductive roles or bodily features. While important in determining the phylogeny of the regulatory apparatus of sexuality, they are instead postcultural justifications for the system of sexuality that produces sexual difference itself. By individuals’ roles in sexual intercourse (taking from Dworkin’s Intercourse), MacKinnon elaborates the way that it is social concepts of sexuality that themselves produce female subjects:

To make a theory feminist, it is not enough that it be authored by a biological female, nor that it describe female sexuality as different from (if equal to) male sexuality, or as if sexuality in women ineluctably exists in some realm beyond, beneath, above,
behind-in any event, fundamentally untouched and unmoved by an unequal social order. A theory of sexuality becomes feminist methodologically, meaning feminist in the post-marxist sense, to the extent it treats sexuality as a social construct of male power: defined by men, forced on women, and constitutive of the meaning of gender.

and further:

Sexuality, in feminist light, is not a discrete sphere of interaction or feeling or sensation or behavior in which preexisting social divisions may or may not be played out. It is a pervasive dimension of social life, one that permeates the whole, a dimension along which gender occurs and through which gender is socially constituted; it is a dimension along which other social divisions, like race and class, partly play themselves out

and finally:

This approach identifies not just a sexuality that is shaped under conditions of gender inequality but reveals this sexuality itself to be the dynamic of the inequality of the sexes. It is to argue that the excitement at reduction of a person to a thing, to less than a human being, as socially defined, is its fundamental motive force. It is to argue that sexual difference is a function of sexual dominance. It is to argue a sexual theory of the distribution of social power by gender, in which this sexuality that is sexuality is substantially what makes the gender division be what it is, which is male dominant, wherever it is, which is nearly everywhere.

In the same way that (cis) women’s sexualities are regulated, trans (women’s) sexualities are rendered unintelligible, either by casting any sexual feelings as some form of ‘autogynephilia’ or by reducing sexual expression to ‘male sexuality’. Even more, MacKinnon’s analysis of the pornography industry can be extended with an analysis of the regulatory discourses that produce the transsexual subject. In porn, the oft-recognized fetishization that ‘consumers’ have for the trans body itself is reminiscent of the way that black bodies and disabled bodies are considered within the pornographic sphere. Within MacKinnon’s framework, it would be ludicrous to ignore the harm done to trans subjectivity by trans pornography as an act of violence, exactly why she specifically included transsexuals as a class of individuals able to bring a class-action lawsuit against pornographers for the harm done against them as a sex class.

Dworkin

Dworkin, in contrast, took a much more traditional analytical route in analyzing sexual difference. In her magnum opus Woman Hating, Dworkin analyzed the way sexual difference as a continuum is reduced to a cultural dichotomy between male and female. She incorporated the psycho-sociological analyses of Money’s six aspects of sex (genetic, hormonal, gonadal, internal, external and psychosexual), her contemporaries’ developments in the analysis of intersex bodies and the crosscultural ways sexual differences are represented to present sexual difference not as opposition, but as a spectrum upon which individuals vary in their location. For her, the idea of polarized ‘men’ and ‘women’ were simply caricatured fictions by which androgynous individuality is transformed into oppressive norms:

The discovery is, of course, that “man” and “woman” are fictions, caricatures, cultural constructs. As models they are reductive, totalitarian, inappropriate to human becoming. As roles they are static, demeaning to the female, dead-ended for male and female both. Culture as we know it legislates those fictive roles as normalcy.

While one might interpret this as simply the ‘gender role’ vs ‘sex’ disjunction feminists have made over the years, Dworkin suggests something much more radical. She argues that gender roles arises from the idea of sex as binary & fixed so that feminists are required to challenge this ideal:

There are, after all, men and women. They are different, demonstrably so. We are each of one sex or the other. If there are two discrete biological sexes, then it is not hard to argue that there are two discrete modes of human behavior, sex-related, sex-determined. One might argue for a liberalization of sex-based roles, but one cannot justifiably argue for their total redefinition

But just like feminist scientists in the 21st century, Dworkin draws upon a compendium of research demonstrating the opposite: that sex as a binary is a fiction:

… research … provide[s] basic information which challenges the notion that there are two discrete biological sexes. That information threatens to transform the traditional biology of sex difference into the radical biology of sex similarity. That is not to say that there is one sex, but that there are many. The evidence which is germane here is simple. The words “male” and “female, ” “man” and “woman, ” are used only because as yet there are no others.

We can presume then that there is a great deal about human sexuality to be discovered, and that our notion of two discrete biological sexes cannot remain intact. We can presume then that we will discover cross-sexed phenomena in proportion to our ability to see them. In addition, we can account for the relative rarity of hermaphrodites in the general population, for the consistency o f male-female somatotypes that we do find, and for the relative rarity of cross-sexed characteristics in the general population (though they occur with more frequency than we are now willing to imagine) by recognizing that there is a process of cultural selection which, for people, supersedes natural selection in
importance. Cultural selection, as opposed to natural selection, does not necessarily serve to improve the species or to ensure survival. It does necessarily serve to uphold cultural norms and to ensure that deviant somatotypes and cross-sexed characteristics are systematically bred out of the population.

I highly recommend read the entire chapter Sexuality in Woman Hatingthen comparing it to Anne Fausto-Sterling’s Sexing the Body and then comparing those to Joan Roughgarden’s Evolution’s Rainbow.

Stoltenberg

Continuing upon Dworkin’s cogent analysis, John Stoltenberg (himself Dworkin’s lifelong partner) analyzed the fiction of ‘sex’ and the multisexed nature of humanity in his book Refusing to Be a Man. Stoltenberg was moved by Dworkin’s analysis of sex-gender, and elaborated upon the specifics of the ideology of male sexuality & the male sex itself. For Stoltenberg, the male sex is an ideologically constructed fiction used to maintain dominance of men over women (sex classes):

The idea of the male sex is like the idea of an Aryan race. The Nazis believed in the idea of an Aryan race—they believed that the Aryan race really exists, physically, in nature—and they put a great deal of effort into making it real. The Nazis believed that from the blond hair and blue eyes occurring naturally in the human species, they could construe the existence of a separate race—a distinct category of human beings that was unambiguously rooted in the natural order of things. But traits do not a race make; traits only make traits

His distinction between bodily features, which may be precultural [or perhaps the body is itself constructed as Butler suggests], and the categories that traits are socially transformed into grounds his analysis of sex as an oppressive dichotomy:

Penises and ejaculate and prostate glands occur in nature, but the notion that these anatomical traits comprise a sex—a discrete class, separate and distinct, metaphysically divisible from some other sex, the “other sex” —is simply that: a notion, an idea. The penises exist; the male sex does not. The male sex is socially constructed. It is a political entity that flourishes only through acts of force and sexual terrorism. Apart from the global inferiorization and subordination of those who are defined as “nonmale,” the idea of personal membership in the male sex class would have no recognizable meaning. It would make no sense. No one could be a member of it and no one would think they should be a member of it. There would be no male sex to belong to. That doesn’t mean there wouldn’t still be penises and ejaculate and prostate glands and such. It simply means that the center of our selfhood would not be required to reside inside an utterly fictitious category—a category that only seems real to the extent that those outside it are put down

He shares MacKinnon’s view that it is not sexuality that is gendered but that sexuality produces gender.

Frye

Marilyn Frye’s analysis of sex classes was far and few in her work, but perhaps her most relevant discussion of sex-gender was in her work Sexism. Frye takes perhaps the more traditional view of sex-gender in that sex is made culturally relevant via social processes that themselves constitute patriarchy. She discusses the instances where male dominance is produced in a sexless, genderless sphere of existence as a means of elucidating how reality itself becomes sexed/gendered. But as for Dworkin and Stoltenberg, sexual reality is not dichotomous nor sharp and opposing: it is instead variation ‘along the physical dimensions we think of as associated with maleness and femaleness’:

The pressure on each of us to guess or determine the sex of everybody else both generates and is exhibited in a great pressure on each of us to inform everybody all the time of our sex. For, if you strip humans of most of their cultural trappings, it is not always easy to tell without close inspection which are female, which are male. The tangible and visible physical differences between the sexes are not particularly sharp or numerous. Individual variation along the physical dimensions we think of as associated with maleness and femaleness are great, and the differences between the sexes could easily be obscured by bodily decoration, hair removal and the like.

Frye analyzes the way that we are obligated to announce and assert our sex(es) in a way that itself constitutes sexual dimorphism, in contrast to the ‘biological spectrum between two not-so-sharply defined poles’. The exemplaries of this analysis are intersex individuals, whose biological reality does not fit into the regulatory ideals that define sexual reality. Social processes reinforce preexisting differential averages to (re)produce, exaggerate and dichotomize sexual difference like genital reformation, dietary and exercise regimens and so on:

The intense demand for marking and for asserting what sex each person is adds up to a strenuous requirement that there be two distinct and sharply dimorphic sexes. But, in reality, there are not. There are people who fit on a biological spectrum between two not-so-sharply defined poles. In about 5 percent of live births, possibly more, the babies are in some degree not perfect exemplars of male and female. There are individuals with chromosomal patterns other than XX and XY and individuals whose external genitalia at birth exhibit some degree of ambiguity. There are people who are chromosomally “normal” who are the far ends of normal spectra of secondary sex characteristics-height, musculature, hairiness, body density, distribution of fat, breast size, etc.-whose overall appearance fits the norm of people whose chromosomal sex is the opposite of theirs.

These variations not withstanding, persons (mainly men, of course) with the power to do so actually construct a world in which men are men and women are women and there is nothing in between and nothing ambiguous; they do it by chemically and/or surgically altering people whose bodies are indeterminate or ambiguous with respect to sex. Newborns with “imperfectly formed” genitals are immediately “corrected” by chemical or surgical means, children and adolescents are given hormone “therapies” if their bodies seem not to be developing according to what physicians and others declare to be the norm for what has been declared to be that individual’s sex. Persons with authority recommend and supply cosmetics and cosmetic regimens, diets, exercises, and all manner clothing to revise or disguise the too-hairy lip, the too-large breast, the too-slender stature, the too-large feet, the too-great or too-slight stature. Individuals whose bodies do not fit the picture of exactly two sharply dimorphic sexes are often quite willing to be altered or veiled for the obvious reason that the world punishes them severely for their failure to be the “facts” which would verify the doctrine of two sexes. The demand that the world be a world in which there are exactly two sexes is inexorable, and we are all compelled to answer to it empathetically, unconditionally, repetitiously and unambiguously.

For Frye, the fact that we do not mistake men for women and vice versa (very often at least!) is not because of naturally inborn and biological distinctions, but because of cultural processes that demand ambiguous individuals (perhaps Dworkin’s androgyny) not only signal their ‘true’ sex with cultural markers like clothing, jewelry and hairstyles, but physically alter, modify and mutilate their bodies in accordance with these sexual ideals. Feminism is thought of as a project to blur sexual difference, to break down that of which sexed ontology, sexed reality is even thought of. The liberal feminist’s reactionary defense of a dimorphically sexed society, for Frye, is not grounded in any theoretical or conceptual devotion, but rather in the very physical and ‘behavioral patterns’ that produce sexual difference.

Editorial

The Illusion of “Neurosex”: Your Brain Is Not “Male” nor “Female”

There’s been an unfortunately increasingly popular tendency among many trans communities to rely on some notion of “brain sex“, “subconscious sex“, etc, to provide justificatory accounts of trans womanhood/manhood. The most obvious manifestation of this historically ignorant & sociologically uninformed way of thinking about trans-liberation is the appeal to “neuroscientific” studies that purportedly demonstrate that transness is intrinsic, “biological”, and in a way that trans people are scientifically their true gender (we are, of course, falling right into a naturalistic fallacy).

While this justificatory account of the production of scientific knowledge may be a fascinating sociology of science question, it’s more immediately a political question. The discourse about “male brains” and “female brains” has underpinned a large host of misogynist bioessentialist thought over the last few centuries, including & especially within the scientific sphere. This has elicited a quite justified* reaction from the host of radical, cultural, materialist, lesbian, queer, scientific and radical (trans)feminists who have given radical accounts of sex-gender based not in illusory biology (aside from cultural feminists), but in the material (re)production of difference.

What are the bases for this purported “neurosex”? There is a small, but growing, literature of sex difference research that is aimed at interrogating the purportedly neurobiological foundation of ‘transsexuality’. It is important to recognize that this burgeoning literature does not originate from a trans-inclusive or feminist perspective, but from a classificatory, pathologizing way of constraining trans subjectivity under the microscope of the scientific interlocutor. The transsexual becomes the subject of the scientist, for her (the subject is nearly always a trans woman) brain is a site for knowledge production. She is not considered as a person to be cared for, but as a subject to be poked, prodded & studied.

The “Science”

The ‘original’ study in the this line of literature purporting to demonstrate that ‘transsexuals’ have ‘female’/’male’ brains was a 1996 study done by Zhou et. al. It looked at the bed nucleus of the stria terminalis of the brain of 6 postmortem ‘male-to-female’ transsexuals in comparison with cis ‘male’ and ‘female’ brains. The way that gender norms have infested scientific knowledge production is quite apparent from the start. Brains are presupposed to be dimorphically (that is ‘having two forms) sexed as “male” or “female” so that the finding that ‘transsexuals’ have ‘male’ or ‘female’ brains is either a justificatory or delegitimatizing account of their true sex-gender. But, as we will see later, it is not obvious, and in fact false, that brains are organized dimorphically.

This initial study has been cited 872 times, including in other literatures like explicitly bioessentialist work such as Lippa’s “Gender, nature and nurture”. It is perhaps the most focused upon within the entire literature, meaning it has been the subject of a number of critiques: the horrific sample size (n=6 for the trans individuals), the comparison group(s), sexuality composition, analyzing brain structure postmortem, whether or not the subjects had taken hormones. To  me, all of these critiques have important points to them, especially situating the sample size of the group within the replication crisis within neuroscience.

Whose Science?

Here we ought to consider the parent field of this series of studies: neuroscience. Neuroscience has received increased attention & funding as a revolutionary “neurocognitive” turn in many sciences (behavioral, psychological, etc). This “turn” has been the subject of a number of criticisms, not least by William Uttal. In his book “The New Phrenology“, he critiqued the notion that we can localize psychological processes to a particular region of the brain. That is, the very  subsets of the whole brain that are being interrogated for their sex differences, may not prove very useful in determining the behavioral consequences of these differences, whatever they may be. This idea that a person’s psychological attributes (emotions, intelligence) can be “located” in a particular region of the brain reminds many of the pseudoscience of phrenology, hence the title. Not only is there a theoretical objection to the knowledge that is asserted to be produced by neuroscientific studies, but there’s an empirical one. Despite the valorization of neuroscience in the media as another “biology” to ground the “nature” of the human body, it has a lower replication rate than psychology; famously affected by the replication crisis. In Uttal’s Reliability in Cognitive Neuroscience: A Meta-Meta Analysis, he analyzes the findings from the field and finds them very wanting in terms of empirical support. Other works critiquing naive neuroscience are Rees & Rose’s The New Brain Sciences, De Vos & Pluth’s Neuroscience and Critique: The Limits of the Neurological Turn, and Satel & Lilienfeld’s Brainwashed.

Scan, Compare, Contradict, Deny and Repeat

Returning back to the ‘transsexual brain studies’, a later set of studies after Zhou et. al have produced mixed findings. Some find that the sexuality composition of the ‘transsexual’ selection produces differing results as to the ‘grouping’ that ‘transsexuals’ fit into (i.e. straight [androphilic] trans women have ‘female’ brains in contrast to lesbian [gynephilic] trans women who have ‘male’ brains). Some find that it is not that ‘transsexuals’ have ‘male‘ or ‘female‘ brains, but brains intermediate between the ‘male’ and ‘female’ groupings. And still others confirm the initial finding that trans women have ‘female’ brains and trans men have ‘male’ brains.

For example, a 2000 study by Krujiver et. al again studied the “bed nucleus of the stria terminalis” and discovered that, in a sample of 42 individuals total, that ‘female-to-male’ transsexuals have a ‘male’ number of neurons while ‘male-to-female transsexuals’ have a ‘female’ number of neurons. They also reported that sexuality & hormone treatment did not affect the results. This cannot be considered a replication as 26 of the patients (most of whom were not trans) came from the original Zhou et. al ’96 study. Just as in the other study, all of the postmortem brains analyzed were medical deaths: they had died from a disease or other medical condition. This makes it difficult to interpret the results, especially in light of the inclusion of a large number of AIDS patients & the complex etiology and effects of these diseases. Indeed, one trans female patient had “cytomegaly of the brain”, along with one of the lowest brain weights in the entire study! It is also unclear as to how the authors made the inference that hormone therapy was irrelevant, as they included only one individual that was not on hormone therapy. This individual also happened to be 84 years old! They reported that they did not find an age interaction in any of the numbers, but this is severely limited by the small sample size & methodological heterogeneity.

To delve into the long list of poorly conducted studies would require too much space in this already lengthy article, so I will save this task for another period. There is, however, a useful review of the heterogeneity among study results here.

The “Female Brain”?

Let’s take a moment to consider what the findings that trans women have ‘a female brain’ means. In these studies, there is a comparison group of ‘normal‘ (i.e. cis) women who the ‘abnormal‘ (i.e. ‘transsexual’) women is compared to. The variability within cis women is elided and collapsed into a single ‘average’ value, an awfully unfruitful way of thinking about differences in brain structure. If we are to call a particular brain “size” of a specific section that of a “female” or “woman”, what of the other cis women who have “male” values? By sexing/gendering quantities, we are introducing quite an interesting site of (re)sexing the body. Not only do the studies collapse variability among cis control groups, but they completely elide any variability among ‘transsexual’ test subjects. It is not obvious that every trans woman will have a ‘female’ brain: this would be very unusual given that not all cis women do. But if a justificatory account of trans womanhood is supposed to emanate from this science, then how does one consider the trans woman with a ‘male’ brain? The typical correction to the  discussion of the cis woman with a ‘male’ brain is to shy away from sexing the brain, but this response is unintelligible and out of reach for the purportedly justificatory narrative, for both cis & trans women.

This discussion of ‘male’ and ‘female’ brains is awfully reminiscent of the ways that TECFs (trans-exclusionary cultural feminists) and other transphobes have talked about sexual difference: some body part is innately sexed, producing a particular meaning of sex that includes/excludes particular groups. It is not relevant that some individuals that we ought to consider women/men are included/excluded in/out of the wrong category, because there is the presumption that this particular physiological characteristic grounds and defines sex-gender. For the TECF, the intersex body produces a challenge of classification. For trans neuroessentialist, the cis women’s ‘male brain’ is the site of failure. For the traditional conservative bioessentialist, the masculine lesbian defies a particular way of thinking about the sex-gender equivalency. United in their exclusion is the thought that there must be a physiological/physiognomic way of defining a gender-sex that provides justification for a liberatory politics.

But as the discussion of the trans woman with the ‘male brain’ shows, none of these discussions of physiological grounding of sex-gender actually hold up theoretically. The anti-trans cultural feminist has provided a litany of valid objections to the ‘neurosex’ framework, the transfeminist an account of intersex bodies in sexual difference to object to the genital/chromosomal formations of sex-gender, the liberal feminist objects to the conservative account on the questioning of the connection between their theory of ‘sex roles’ and ‘sex’ (this of course may not be a useful distinction after all). If a neuroessentialist account provided meaningful justification for trans womanhood, one ought to see trans women getting their brains tested & compared to ‘female’ values. But we do not see this form of self-validation: scientific knowledge in the form of averages (i.e. the average volume of trans women’s brain structures in comparison to cis women/men) is assumed to apply to all trans women, regardless of what type of ‘bell curve‘ brains are supposed to be distributed on. A trans woman with SD=2 away from the mean is assumed to have just as much of a ‘female’ brain as a trans woman with SD=-2, despite one falling right as ‘hyper-female’ and another as ‘male’ in the original account of ‘brainsex’ (the one formulated by academic institutions).

Do trans women have “female brains” or simply “female ratios”? Often forgotten is that there is an average (as always, the reality of average sex differences exists on a continuum) difference between the size of the brains (and heads) of ‘males’ and ‘females’. On this account, trans women have ‘male’ brains: their average head (and thus brain) size would be firmly within the ‘male’ range, whatever this is supposed to mean. But the cited studies don’t compare total brain volume, but rather the size of particular brain structures corrected for total brain volume. This is supposed to fix the issue about whether sex differences in brain volumes are simply an artifact of total body size. It’s not entirely clear why the neuroessentialist ought to use this ratio standard rather than the ‘total volume’ standard.

The Male Brain is Empty

It must also be questioned what, exactly, a “male” brain is supposed to represent. If, for instance, the finding that trans women have a “female” brain is purportedly not neuroessentialist or reproductive of the gender roles trans people often deconstruct, then it begs the question of what does a ‘male’ brain mean? The typical meaning of ‘male’ brains within scientific spheres is typically within the framework that men & women have different brains, causally related to prenatal hormones & chromosomal differences, which then produces distinct behaviors. If this essentialist formulation of “male” brains is rejected by the trans affirmationist, then it seems there is not much left to a ‘male’ brain. If it is simply a quantitative average, then it is unclear why this would be in any way constitutive of trans women as women & trans men as men any more than the finding women are, on average, shorter than men is constitutive of tall women as ‘men’ and short men as ‘women’. It is interesting to note that the portions of the brain studied by scientists in (in)validating trans gender-sexes are typically the ones involved in the discussion of ‘innate’ gendered preferences: bed nucleus of the stria terminalis INAH3, etc. This review of the “trans brain” literature is filled with claims that sexed behavior is innate, specifically affirming the misogynist “brain organization hypothesis” that has been debunked time and time again.

The Queer Feminist Scientist’s Objection

Even more, the entire concept of a ‘male’ / ‘female’ brain must be questioned on more empirical grounds (rather than the theoretical objection that it provides a basis for pro-trans attitudes). There have been a litany of feminist empirical works seeking to question the mainstream narrative that ‘male’ brains produce ‘male’ behaviors, and ‘female’ brains ‘female’ behaviors. One of the first books (I skip over Ruth Bleier’s important work) attempting to debunk this idea is Anne Fausto-Sterling (whose name one might recognize for producing a book Sexing the Body that is commonly cited & discussed by the very same people trying to push neuroessentialism) and her Myths of Gender. Although the book is partially devoted to disproving the oft-cited ‘greater male variability’ hypothesis that has been revived (in James Damore) and other silly arguments about IQ, innate differences in aggression, it also has an addendum to the second edition discussing sex differences in the brain. She (FS) discusses the aforementioned issue of total brain volume corrected for body size & the illusory corpus callosum. The numerous methodological choices one makes in measuring the body have a profound influence on the results obtained: a point obvious to any scholar of the sociology of science. The particular way that one cuts the corpus callosum will affect the presence or absence of sex differences, the size of the difference, and the qualitative differences one finds. Whether one “scans” the brain with an MRI or “photographs” and “dissects” it with a postmortem analysis is also important. But a point Fausto-Sterling makes earlier in the book, in the chapter on genes, seems most important & most fruitful to me: that brains developed at the interaction of a complex system of genes, cellular environments, biological and social environments. As more & more research has demonstrated, the biological and social are not easily separable, and the ontogeny of found differences, whether or not they meaningful exist, cannot be assumed from the existence of the differences.

Another infamous book on the sex differences in the brain is Cordelia Fine’s Delusions of Gender [apologize for the link]. While her focus is mostly on the connection between purported sex differences in the brain & the behaviors they are supposed to be causally connected to, she does talk about the complex ways that social learning & socialization can manifest themselves literally as biology. In chapters 15 and 16, she discusses the now seemingly obvious finding that behavior, the social world, environmental factors influences development, including of the brain: neuroplasticity. This novel concept is used to help explain sex differences: perhaps it isn’t that sex differences in the brain are determined by one’s genes at birth, but rather by a complex interaction between genes & environment, nature and nurture. Or perhaps, as developmental systems theorists put it, there is no distinction between nature and nurture.

The most recent magnum opus (skipping over Lise Eliot’s Pink Brains, Blue Brains) on “brains” is Gina Rippon’s The Gendered Brain. I have unfortunately been unable to obtain a copy, but she repeats and elaborates on the many arguments formed within Cordelia Fine & other’s books. She argues that brains cannot be gendered dimorphically (or sexed in most cases) because there is more variation within ‘sexes’/’genders’ than between. This is reminiscent of the Lewontin argument against the existence of races on genetic grounds: there is more genetic variability within races than between them. While we may be able to “statistically distinguish” brains based on some overfit machine learning algorithm, how is that supposed to tell us anything about the differences between brains other than that we can create all sorts of hyperpredictive models. That is, statistical abstraction doesn’t inform us about the ontology of sex differences. Most often cited is a 2015 study done by Daphna Joel (who is very trans-affirming: see my post here) that purported to show that brains are not ‘sexed’, they are intersex. In her study, she demonstrated that most brains are not ‘extreme’: they don’t have all of the ‘male’ or ‘female’ characteristics on each side of the ‘dimorphic’ spectrum. Most brains are a heterogeneous composition of differently ‘sexed’ portions: someone may have a ‘male’ amygdala, but a ‘female’ hypothalamus.

Who Benefits

Now we have to return to the issue at hand: whether “neurosex” exists & supports trans narratives. If someone can have parts of their brain that are differently sexed, then how does one “sex” the brain as a whole? Do we privilege specific parts of the brain that we think are most relevant to ‘determining’ sex? That seems like an inevitably social decision that won’t satisfy any critics. I think it has become clear that not only does the neuroessentialist narrative of “trans women have female brains” & “trans men have male brains” not justify a trans-affirming narrative, but that brains aren’t dimorphic enough to even justify classifications of ‘male’ or ‘female’ brains.

Next, we must turn to the consequences of adopting this narrative: how the entire trans community is supposed to fit within it. Obviously, this discussion of ‘male’ brains and ‘female’ brains has already started to adopt an exorsexist conceptualization of gendered difference, privileging binary gender legitimacy over that of nonbinary people. But how are nonbinary people supposed to fit within this “male brain” – “female brain” conceptualization. Some people have suggested we ought to conceive “brainsex” as yet another spectrum. This may seem plausible at first: nonbinary individuals are neither “male” nor “female”, but it immediately raises a few questions. First, what of the nonbinary identities that exist outside the already exorsexist framework of a gender ‘spectrum’ (presuming polarity and opposition)? The myth of nonbinary as “between” male and female has been the subject of numerous critiques for not only being explicitly misrepresentative of nonbinary identity, but exorsexist/transphobic for imposing a particular view of transness onto nonbinary identity. Are agender & bigender people supposed to occupy neither ends of the ‘brainsex’ spectrum or both, respectively? Or are they to be thrown under the bus in a respectability politic in the goal of transsexual legitimacy in the eyes of the broader public & medical establishment? Second, if we are appealing to a spectrum to legitimize transness, then how are we to pick where “male” starts & “nonbinary” begins. If there is a range from -1 to 1, where 1 represents maleness and -1 represents femaleness, then where does femaleness end, nonbinary begin & end & maleness start? Do ‘female brains’ go from -1 to -1/3, nonbinary from -1/3 to 1/3, and ‘male brains’ from 1/3 to 1? This would divide up the spectrum evenly. But then we encounter our earlier objection: given that brains don’t exist in dichotomies, they exist in distributions within groups, there are going to be trans women whose brains are “nonbinary” or “male”, nonbinary people with “male” or “female” brains & trans men with “nonbinary” or “female” brains. Here we have just legitimized a privileged few whose brains were lucky enough to be the “right” size and/or “right” proportions.

Who is “neurosex” serving? Not women, not men, not trans people, not nonbinary people, not feminists nor transfeminists. The only people it “serves” is the academic misogynists, the “sex difference” evolutionary psychologists, the right-wing reactionaries. It’s time for transfeminists to abandon this model.

References

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Uncategorized

GMOs and Reporting on Science

While I appreciate the Genetic Literacy Project’s elucidation of the issues with many science-critical claims (i.e. genetics), their cavalier attitude to the critics of GMOs seems to underlie a more serious issue with the organization: ignorance and hypocrisy. They recently published an article seemingly rebuking an article from Independent Science News on the FDA’s assessment of ‘golden rice’. ‘Golden rice’ is a genetically modified rice that seeks to increase the amount of beta-carotene (a precursor to vitamin A) in the rice in order to alleviate vitamin A deficiencies in several East Asian countries.

The article does offer some important news source and information, but overall paints a pretty misleading image of the entire issue regarding golden rice and fails to rebut many of the vital concerns brought up by the original Independent Science News’ article: external validity of American/Chinese studies, health risks, the actual total content of beta-carotene in the rice, etc.

However, an FDA approval carries a lot of gravitas worldwide, and the decision is being met with attempts by anti-GM groups to discredit the nutritional value and usefulness of Golden Rice.

The nutritional value/usefulness of golden rice is dubious regardless of FDA statement for or against it. It might be helpful to read the literature referenced in the Independent Science News article you allegedly read and responded to; Schaub et. al ’17 and indeed both FDA memos. Interestingly, as the ISN article notes, milled rice has a higher concentration of beta-carotene.

Just after the FDA’s approval, Independent Science News, a website known for its opposition to genetic engineering and recombinant technologies, published an article headlined “GMO Golden Rice Offers no Nutritional Benefits Says FDA.” Sustainable Pulse, another anti-GM organization reprinted the article, focusing on a misleading nutritional fact that both groups (among others) have perpetuated:

Couching the reporting of the websites in detailed descriptions of their heretical views seems to be typical of GLP articles.

This has been a common criticism of golden rice from groups like ISN and Greenpeace, which argue the approved version of Golden Rice doesn’t have enough beta-carotene, the precursor to Vitamin A, to make a nutritional difference. Instead, these groups advocate planting bananas, carrots, spinach or sweet potatoes, none of which are as affordable or even practical in places suffering from Vitamin A deficiency.

Fascinatingly enough, a comment on the ISN article elucidated a huge issue here: this is a blatant lie and the author of this article knows it. So much of a lie that the author, Andrew Porterfield, has linked to empirical research demonstrating that beta-carotene rich foods can and are grown in Southeast Asia. Even more disturbing is the seemingly deliberate exclusion of the alternative mentioned in the ISN article: Asians greens (Chandra-Hioe et. al 2017).

The FDA did state that. Also, Health Canada wrote that “Replacement of all rice and rice products in Canada with GR2E rice would result in a very small 0.8-8% (34 µg-239 µg per day) increase in ß-carotene intake.” But a health claim is not the same thing as a nutrition statement. So the FDA and Health Canada statements don’t translate into “no nutritional value,” nor does it mean that, as Latham and Wilson wrote, “the tradeoff experienced by the Golden Rice project between beta-carotene production and yield in its various GMO rices has not been resolved.”

I’d “concede” that the FDA letter is being partially misrepresented in the ISN article (I don’t work for them nor am I affiliated with them), but there is important information within that helps bolster golden rice’s critics claims; confirmation of relatively low beta carotene levels.

The FDA also has since rebutted Latham and Wilson’s article, saying the claim of “no value” is misleading. In the comments section of the ISN website, this response was posted from Marianna Naum, communications team lead from the FDA’s Office of Food and Veterinary Medicine:

Which was responded to in whole by Latham & Wilson, mostly convincingly. There is still the issue of the semantics of no nutritional claim vs no health claim that is (rightfully) brought up by the GLP article, but the Naum statement in no way ‘rebuts’ the majority of the content of the article, nor some of the interpretation of the FDA letter itself.

It’s Time For Math

Additionally, U.S. consumers eat rice at very low levels compared to consumers in the specific Asian countries with vitamin A deficiency for which golden rice was developed. IRRI reports that consumption of rice by children in Bangladesh is 12.5 g/kg body weight/day, compared to about 0.5 g/kg bw/d for U.S. consumers). Rice is the major staple in those countries and levels of rice consumption are many-fold higher than they are in the U.S. While a U.S Consumer would be unlikely to eat enough of the rice to achieve that value (10-19 % of the NDI or RDA), that does not mean that the level of consumption of golden rice in the targeted countries would be insufficient to accomplish the intended effect of supplementing their very low consumption of vitamin A-containing foods. Consuming rice containing the levels of pro-vitamin A in GR2E rice as a staple of the diet could have a significant public health impact in populations that suffer from vitamin A deficiency.

If we take the FDA figures at face value (dubious) and combine them with figures given earlier in the article (i.e. the Health Canada figures) we can compute the percent increase in beta-carotene that would result from a switch from current rice strains to golden rice. In the Health Canada statement, it notes that:

Replacement of all rice and rice products in Canada with GR2E rice would result in a very small 0.8-8% (34 µg-239 µg per day) increase in ß-carotene intake

We’ll use the entire range here.

In the FDA statement it states:

IRRI reports that consumption of rice by children in Bangladesh is 12.5 g/kg body weight/day, compared to about 0.5 g/kg bw/d for U.S. consumers).

Consequently, Bangladeshi children consume 25 times more rice than Americans per bw/d.

Now we run into some statistical/comparative issues: the Health Canada data is inferring the increase in beta carotene increase in the Canadian population, the FDA data talks about American consumers (presumably including adults) and the Bangladeshi data is about children. We have three incomparable figures that we can’t really use.

But even given the poor figures, we can give an (even rougher) estimate:

A 0.8-8% increase in North American populations * 25 = 20-200% increase in beta-carotene intake in a Bangladeshi population.

The questions now are:

• How does that level of increase of beta carotene translate into vitamin A?
• How much does that level of level of vitamin A increase affect vitamin A deficiency?
• How well do the assumptions used in the Health Canada calculation hold up?
• What is the external validity of Bangladeshi children data to other age populations & other countries?

Back To The GLP Article

In countries throughout Asia that consume up to 300 grams of rice every day, this means a lot more beta-carotene could be consumed than in the United States, where even 45 grams might be a high figure. Rice is a much cheaper stape, and also much more affordable than meat and other animal products, and colored fruits and vegetables like bananas and carrots (the latter which was bred to enhance beta-carotene content, incidentally, in the 14th century).

We finally have some (unsourced) data on the consumption of rice in Asian countries, noticeably using the upper limit of the range.

More Math

Again, we will take (at face value) the ratios of beta carotene in golden rice from the FDA; 0.504-2.35 mg/kg (see the Niederhuth quote from the GLP article).

Lower

0.504 mg/kg * 1 kg/1000 g * 300 g/day = 0.1512 mg beta carotene/day

Upper

2.35 mg/kg * 1 kg / 1000 g * 300 g/day = 0.705 mg beta carotene/day

We now have a figure for how much beta carotene Asians in the countries with the highest levels of rice consumption would consume in a ideal golden rice world.

We can compare this to the calculations Health Canada gave for Canadian rice replacement;

34 µg-239 µg per day

Or in other words; 0.034 mg-0.239 mg per day. This is an elegant confirmation that Canadians consume less rice than Asians.

Now, we must estimate what proportion of the daily amount of beta carotene this is.

We note that the standard amount of Vitamin A in the United States (which obviously isn’t a cross-cultural standard) is 900 mcg of Vitamin A. Beta carotene is a precursor to Vitamin A, meaning that 12 mg of beta carotene of required to produce 1 mg of vitamin A. Thus, the daily required amount of beta carotene is 900 mcg * 12 = 10800 mcg * 1 mg / 1000 mcg = 10.8 mg.

The amount consumed by these Asian countries by rice would be:

Upper

0.1512 mg / 10.8 mg =  1.4%

Lower

0.705 mg / 10.8 mg = 6.5%

This is evidently not very much vitamin A, even under the most generous of assumptions.

It is obvious in the FDA letter than beta carotene levels are considerably higher than that of normal rice. The FDA letter states that beta carotene in the non-Golden Rice controls was below the limit of quantification of 0.07 mg/kg, in Golden Rice it was 0.504 to 2.35 mg/kg…many times higher. Wilson and Latham never actually tell you how much higher Golden Rice’s beta carotene levels compared to equivalent consumed rice varieties. Instead they compare it to older versions of Golden Rrice or other crops like carrots.

While true, the issue at the core of the golden rice debate is one of risk-benefit calculations. As Wilson & Lantham point out, there are issues with the crop yield from golden rice that have to be balanced with whatever potential vitamin A benefits golden rice may yield, alongside concerns of proprietary genomes, health risks, environmental issues, transparency, food sovereignty and cost effectiveness.

These concerns cannot be dismissed simply by appealing to the higher concentration of beta carotene, especially in regards to well-tested native alternatives that have higher concentrations of beta carotene.

Other Calculations

There have been a myriad of calculations estimating how much beta carotene/retinol golden rice would provide a person.

A 2003 study going over the benefits and hazards of golden rice estimated that golden rice would only provide 70 micrograms of retinol per day, far below the required 1080 micrograms.

Greenpeace similarly estimated that an individual would have to eat 3.7 kilograms of golden rice to achieve their daily value.

The Assumptions

Throughout the FDA letter and this piece, a number of assumptions have been taken for granted: that the people who would eat golden rice have enough other macro/micronutrients to digest the beta carotene, that the rice would keep all of the beta carotene when stored, that people would actually adopt and eat the golden rice, that the implementation of golden rice in these countries wouldn’t have negative externalities.

During the whole Chinese golden rice experiment scandal, one of the major critiques of the paper was that the bioavailability of beta carotene is different in healthy Western(ized) populations with proper nutrition than in malnourished unhealthy populations: the very populations that the intervention is supposed to target. Because the individuals who are suffering from VAD (Vitamin A deficiency) are the same ones who do not receive enough fat in their diets: the very molecule necessary for bioconversion of beta carotene into vitamin A. As a result, it is very likely that the systematic malnutrition people with VAD experience will make it very difficult for the beta carotene to be efficacious in treating VAD.

Another issue with golden rice as a solution to vitamin A deficiency is that it rapidly degrades in temperate conditions,  the exact environments in which rice would be need to grown, distributed and stored. Given that vitamin A deficiency is disproportionately concentrated in rural areas, which have poor storage and temperature conditions, we can reasonably infer that large quantities of beta carotene within the rice will degrade. The distributional mechanisms by which golden rice would have to be produced and distributed (season-dependent growth) would mean that the golden rice would only have significant amounts of beta carotene during specific parts of the year, thus succumbing to the seasonal variability that golden rice advocates posit as an issue for native sources of vitamin A.

We also know that cooking rice and similar foods decreases the amount of carotenoids in them.

But even more than the issues influencing the actual quantity of beta carotene that is available and converts to vitamin A, all of that hinges on people accepting the rice and eating it. We know that populations are often picky about the texture and taste of particular foods and would pay premiums for their preferred versions of foods. Consumers do not prefer GM foods & when educated about them, desire them even less. Even exposure to positive information has minimal effect on customer’s willingness to purchase golden rice.

Now we all know that golden rice is yellow. But what does this have to do with the issues of golden rice as a solution for VAD? Well, unbeknownst to most, but there is a fatal disease of rice called “yellow rice disease” (or beriberi) that infects rice with a yellow color. While there are obviously visible physiological differences between golden rice and rice with yellow rice disease, a campaign mounted to promote golden rice would require eradicating the defense mechanism populations in developing countries have against yellow-coloured rice.

Why?

Now, it’s obvious from the calculations of this article that golden rice wouldn’t provide a meaningful solution to vitamin A deficiencies in Asia. But why is it that the FDA and other regulatory agencies are so willing to let products only tested by proprietary corporate labs go right on through the regulatory process?

The FDA

Throughout the article, you may have noticed that I qualified all my collection of data figures from the FDA with statements like “at face value”. The issue with modern food politics is that the regulatory agencies that are supposed to safeguard our food and ensure quality and safety have been compromised by agribusiness. As anyone who’s paid nearly attention to the news lately, this issue isn’t solely confined to the FDA or food regulatory agencies, but is indicative of a broader societal problem of the corporatization of politics.

Politicians get money from corporate donors, “super PACs” and wealthy individuals. By virtue of the politicians role in selecting regulatory agency leaders, government agencies are inherently politicized and beholden to the interests of politicians, and by proxy, the agricultural industry. This presents a huge issue when interpreting the evaluations published by these regulatory agencies, as they rarely, if ever, make their data public.

Moreover, the people that should be playing a central role in the discourse over golden rice, the people directly affected by these decisions, have been excluded and marginalized in this discussion, only ostensibly included as tokens to promote a specific viewpoint. Indigenous concerns about food sovereignty and food colonialism are almost absent.

Alternatives

If golden rice isn’t sufficient to solve the vitamin A deficiency in Southeast Asia, then what is? Well, the current system uses vitamin A tablets (note that artificial vitamin A is just as good as natural), but hasn’t achieved widespread success. This is likely a result of the inherent problems of widespread distribution of any type of medicine, as well as the contributing factors of imperialist impotence and malice. Let us suppose that a proper vitamin A supplementation programme would not suffice. What other alternatives could we substitute to supplement diets?

Let’s start with the foods: Vandana Shiva, for all her flaws, has listed a number of traditional Indian foods alongside their vitamin A value. For Micronesia, bananas have been mentioned as a major source. Other yellow and green leafy vegetables have been noted for their high amounts of carotene.

What programmes could policymakers implement, one might ask.

There’s a whole literature of results on this! A 2002 review of how micronutrition deficiencies can be addressed covered most of the classical ones, but others have included home gardening (the follow-up study is here),  nutrient education, and fighting parasites. A 2017 review in the journal World Nutrition demonstrated the high efficacy of interventions with fortification, while a 2000 review emphasized the broad consensus that food-based strategies that center indigenous foods & education.

Conclusion

While there are problems with the rabid anti-GMO view that some corners of the internet have professed, it is equally anti-scientific to espouse the view that there are no concerns to be had. Much of the scientific journalism on the GMO question has uncritically espouse one view or the other. This is not a call for ‘both side-ism’, but for critical engagement with opposing arguments rather than the ideological dismissal we have seen here.

Rant 5/5/19

starting this new thing where i just have my unorganized thoughts w/o any type of proper grammar, sentence structuring or organization. just a stream of thought.

(initially came from a sort of response to someone)

actually, i really don’t like that escalante piece that responds to contra. it has like a good critique of some things, but it has this whole ‘you cannot do pragmatism about gender, it’s just impossible’. i don’t take a pragmatist & contextualist stance on gender, but escalante’s argument is just sooooo weak.

“As I have already hinted at, I find this view to be insufficient because it cannot provide strategic insight into what views are useful in which situations. Without a comprehensive theory of gender, we cannot possibly determine what social changes need to be enacted to lead to women’s liberation. An eclectic mix of incompatible feminist theories does not offer us anything if we don’t have an underlying unified theory to tell us which views to deploy in which instances.”

the first one seems p. false: natalie gave examples as to which views to deploy in which circumstances. why do we need some totalizing theory to tell us which view to use in which context when we can just decide which view is most fruitful for analysis. like it’s not like philosophers don’t do that lol

second sentence is just false period. not even going to mount an attack against that.

3rd one mostly addressed in my rebuttal to the first sentence, but again want to emphasize where a universal theory for deployment is necessary

other issues w/ the piece:

• doesn’t challenge natalie’s misinterpretation of butler, despite escalante knowing quite well what butler believed about gender. in a way, escalante almost perpetuates this misinterpretation (though i’ve started having doubts as to whether escalante understands foucault & butler – the gender nihilism piece, specifically escalante’s use of the word ‘power’ betrays a naive understanding / poor deployment of ‘power’ to say the least [takes the traditional leftist pov on power being a one-way thing that just like throws out all of foucault’s project on power]

• one thing i want to note is that i think escalante shares the view of ‘essentialism’ that i do: the one put to use in basically all of feminist gender theory’s discourse on essentialism about gender: essentialism is taken as kind essentialism

• then when i reread the piece, escalante literally throws materialist feminism out the window in embracing a pure marxist feminism with only minimal insight from wittig. she talks about the ‘base producing gender’. like just shut up, that’s the economism/class reductionism/reduction of the material to the economic that materialist feminists (guillaumin & jackson) have challenged for ages… so that’s where upon my rereading, i started to question whether escalante had ever read any materialist feminist work

• then i find it hilarious that escalante implies we ought to reject universal definitions of gender and then 2 sentences later chastises contra for rejecting a universal theory of gender. like, hmmm, what’s the meaningful distinction between the two (other than that one account of gender may be true)

• escalante’s reading of contra, specifically escalante’s discussion of the role butler plays within contra’s discussion of gender makes me want to pound the walls. like contra’s (mis)interpretation of butler is the disgusting one that tecfs appropriated to hate on trans people & one that she wholeheartedly rejects in like all of her work given contra bothered to read it

• escalante also just ‘as a matter of fact’ tries to state that the justine & tabby views can’t coexist. like sis aren’t you a marxist. you know what a dialectic is? you wanna think how contra’s videos are set up (always like dialectics) and see how like maybe they can ‘coexist’ in one sense

• only other positive comment is the discussion of coloniality/race in the piece, but that’s like much better covered by the piece escalante linked to

• she goes on to like admit she wants to ‘provide an account of gender which … Marixst method of historical materialism. I have … to be understood in material and economic terms’. great, you want to discuss materiality. i like derridean language/foucaultian discourse discussions quite a bit & don’t want to see those erased as i know the marxist pov always ends up doing. but then we know escalante doesn’t just want material terms, she wants to reduce those material terms to economic terms.
so my tl;dr used to think this piece was a 9/10, now it’s a 3/10

extended tl;dr fuck the ortho-marxists who never read the frankfurt school and bothered to stop privileging the base over the superstructure.

p.s. fuck marxism-leninism
(just my comment on mari mikkola specifically her page here)

mikkola:

so mikkola is the person who organizes the “stanford encyclopedia for philosophy” page on “feminist ideas on sex/gender” or whatever, and is literally a philosopher in that area. and yet, somehow, thinks that a sex/gender distinction underlies mackinnon’s theorization of gender. like hmmmm, did you bother to open up her book or just read some critique of it somewhere on a blog