I usually don’t comment publically on new papers outside my main field but have to in this case. This is because Gliske (2019): “A new theory of gender dysphoria incorporating the distress, social behavioral, and body-ownership networks” manages to combine a lot of useful literature (I have to reread it in preparation for future planned work) and make the 180 degree wrong conclusion, in a way clearly motivated by a desire of the author for there not to be trans people.
In absolute brevity this is a literature review summarizing how sparse imaging data indicates trans people are atypical with regards to brain networks linked to the main components of clinical dysphoria: 1) distress, 2) (reduced) sense of body ownership, and 3) perception/awareness of socially gendered behaviour. The author’s hypothesis is that this atypicality causes dysphoria, and consequently suggests treating the brain networks directly could “cure” it, going so far as to urge for ceasing to carry out currently accepted standard affirming care.
The author acknowledges as possible, but never engages with, the far more immediate interpretation that a sense of gender incongruency causes 1) distress, 2) (reduced) sense of body ownership, and 3) (intense) perception/awareness of socially gendered behaviour, reflected over a lifetime in these networks. The author even cites how treatment, including hormone treatment, both alleviates these symptoms and reduces (to the extent it is studied) the signal from these networks. If they were causal, why would transitioning reduce these symptoms? Why would they not remain equally in play with instead good congruence with the target gender?
His (single author, who here can be assumed to be a cis man) only real response to this is the suggestion that both transfeminine and transmasculine HRT increases effective estrogen impact on the brain, and that it simply is that estrogen “cures” this network damage, whether supplied in circulation (in trans women) or through aromatization (in trans men). But if the circulating levels trans women on HRT receive are sufficient to do so, then why would not the same levels do so in pre-HRT trans men? One can construct scenarios but all in all this seems highly to overcomplicate.
The author even gets close to pet theories of mine that both gender and orientation are keyed off assessment of others as “same” vs “different”, but goes off into a speculative Blanchardian rant rather than to explore how own-body-as-“different” would make ample sense as a source of the brain signatures he has just summarized. Discussion on vasopressin receptors as underlying this “same” vs “different” response in sexual orientation is interesting and I must follow that literaure more, but I don’t think it will lead near the conclusions the author wants to draw.
Again, he is arguing to “fix the brain of trans people” and to stop promoting gender affirming care. He does this based a summary of what is known of the neural correlates of dysphoria, but clings to an interpretation of those correlates as causes rather than effects. This is contrasted against a strawman of “male/female brain” theory, with ideas of a subtler network for gender identity glossed over – but if we wanted to find something like that, we should look at that which determines whether a male/female body/person is interpreted as same/different than oneself, which would not be there on the level of large structures, but on connections between other parts which might otherwise look identical between men and women because they are equally used in both, only in different direction.
I am not opposed to studies into this field at all. This paper was useful to me in terms of sources also. But a quack summarizing literature, deciding symptoms must be causes, then advocating and hoping for medical conversion therapy because he does not want there to be people transitioning, is not good science at all.