Is “Gender Identity” biological? For most people, the answer is intuitively obvious, “duh!”. Of course, for these people, they usually also insist that the markers for such identity is some privileged and testable characteristic, like genitalia, which is easy to observe, or karyotype (sex chromosome configuration) which requires a microscope. But for people with Disorders of Sexual Development (DSD), these markers may not be all that clear. Further, what are we to make of the gender identities of transsexual and transgendered people, people whose experienced / stated gender identity is at odds with all currently known sex markers? IS there a biological etiology? And is that etiology the same as that that gives rise to the gender identity of non-trans people? A recent review article attempts to answer these very questions. Sadly, I believe that it falls far short of a conclusive answer. In fact, as I will show, it invokes conclusions from several papers as evidence that are quite questionable. Further, the authors failed to note the very probable multiple etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality. First, they reviewed evidence for a biological basis for the phenomenological existence of “gender identity” in non-transfolk which comes from those with certain DSDs,
A seminal study by Meyer-Bahlburg et al involving outcomes of XY individuals raised as females due to severe non-hormonal, anatomic abnormalities of sex development has provided the most convincing evidence that gender identity is fixed. These congenital abnormalities include penile agenesis, cloacal exstrophy, and penile ablation. For many years, female gender assignment along with surgical feminization was the dominant approach for these patients. In this study, it was observed that 78% of all female-assigned 46 XY patients were living as females. While the majority of these patients did not initiate a gender change to male, none of the 15 male raised 46 XY patients initiated a gender change to female. Thus, risk of questioning gender identity was higher in those patients raised as females than in those raised as males among 46 XY subjects with one of these conditions. A study by the same group that examined the degree of satisfaction with surgical intervention reported by patients with 46 XY genotype also found that those subjects raised as boys were considerably more comfortable with their gender identity. – Another seminal study relevant to this topic was by Reiner and Gearhart in their review of 16 XY genotype subjects with cloacal exstrophy who underwent female gender reassignment surgery. Out of the 14 individuals raised as girls, 4 announced they were male and 4 later chose to live as boys when they became aware of their genotype. The 2 individuals who were raised as males identified as males throughout life. The sexual behavior and attitudes of all 16 subjects ultimately reflected strong masculine characteristics regardless of gender assignment. Thus, children who were born genetically and hormonally male identified as males despite being raised as females and undergoing feminizing genitoplasty at birth. Although cohort size in these studies is small, these data provide the strongest evidence for biological underpinnings of gender identity. … In a study of affected subjects, gender role changes were reported in 56-63% of cases with 5 alpha-reductase-2 and 39-64% of cases with 17-beta-hydroxy-steroid dehydrogenase-3 who were raised as girls (6). These data support the concept that gender identity might be attributed to hormone milieu during intrauterine development on some occasions.
These studies are indeed very strong evidence. Looking at the data, we see that of those raised as girls, 22% of of these subjects in the first study and 57% in the second study, while in the third study, those with hormonal abnormalities, 56-63%, chose to socially transition from female-to-male. Compare that to the very, very small number of 46XX individuals in the general population who experience severe gender dysphoria and choose to transition. As an aside, the fact that not all chose to transition should not be taken as proof that gender identity is all that malleable, but should probably be taken as a demonstration that social transition has very high social costs and is not undertaken lightly. Strangely, this paper did not explicitly mention that the majority of these individuals, whether they experienced gender dysphoria or not, were exclusively gynephilic, but they did allude to it. Also puzzling was their failure to include the converse situation of individuals with 46XY and complete androgen insensitivity syndrome (CAIS), all raised as female, who are extremely unlikely to experience gender dysphoria or sex reassignment, and are universally exclusively androphilic. Or the even more interesting case of 46XX progestin influenced females raised as male, 50% of whom transitioned from male to female and all are exclusively androphilic.
Thus, they failed to explicitly show the very high correlation of brain sex with gender identity, gendered behavior, and sexual orientation. Having shown that there is indeed very strong evidence that “gender identity might be attributed to hormone milieu during intrauterine development on some occasions”, which supports the notion that gender identity has a basis in biology (as opposed to being purely a social construct overlain on observable sex differences), it is tempting to say that transsexuality, all transsexuality and transgender identity, is also the result of mismatched hormonal milieu. In fact, many transsexuals hold to just such a position.
But they would be dead wrong.
The logical leap that all transsexuals have such an etiology is not supported by the above evidence. In fact, given the very probable differing etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality, at least one of these types must NOT have been caused by such. Blanchard went on to predict that this would be born out by studies of the sexually dimorphic structures in the brain, predicting that the exclusively androphilic MTF transsexual would show shifts toward the female morphology, while the other type would not. It is here that this recent paper has its biggest failings, in that not only did they not discuss this issue, but included very problematic studies by Swaab that purported to have shown female like shifts in non-exclusively androphilic transwomen. These papers did show the shifts in the BSTc and INAH3, but incorrectly concluded that they had existed prior to exogenous HRT and incorrectly concluded that these features in the brain were organization effects of endogenous hormones in utero, when the data clearly demonstrated the opposite, that these shifts were purely activational effects from exogenous estrogenic and anti-androgenic HRT. To be fair, they did mention that the BSTc was potentially questionable, but completely failed with regards to the INAH3, which demonstrably is not evidence for a biological basis of gender identity.
In reviewing the recent grey and white matter studies, they failed to note that it fits and supports Blanchard’s prediction, which had they done so, would have strengthened their argument for a biological basis for a conventional gender identity in exclusively androphilic MTF transsexuals. That is to say, that they experience the same feminine “gender identity” as females because their brains are female like. Conversely, they would also have evidence for a biological underpinning to autogynephiles sexuality, a non-sexually-dimporphic one, which lead to an epiphenomically generated “female gender identity” later in adulthood. (See my essay on the different origins of cross-gender identity in transsexuals.)
The authors reviewed the literature on possible genetic factors that could lead to transsexuality, noting that they were inconclusive. Totally absent in this paper was any mention of the papers that document the fraternal birth order effect found in exclusively androphilic MTF transsexuals. All in all, I was disappointed in this paper.
I found it shallow, lacking in both depth and breadth, and literally out of step with much of the literature on the cutting edge of the science.
(Addendum 7/7/2015: I got suspicious of this paper as it reads like a cherry-picked list of papers that support the brain sex hypothesis for all transsexuals, including “late onset” transwomen, so I checked into the background of the authors. Sure enough, one of the authors is transgendered. While that alone is NOT damning (after all, so am I), it does explain why this paper only referenced the studies it did, and did not include those studies that when considered as a whole, would show that while one subset of the larger transsexual population could possibly be explained by the brain sex hypothesis, most transwomen could not. This paper then can and should be considered part of the ongoing effort by some in the transgender community to deny the evidence of the two type taxonomy.)
Aruna Saraswat, MD, Jamie D. Weinand, BA, BS; Joshua D. Safer, MD, “Evidence Supporting the Biological Basis of Gender Identity” (2015) DOI:10.4158/EP14351.RA