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One of the most interesting parts of transgender science is the continuing search for an identifiable biological cause of gender dysphoria. Is transgender a case of nature or nurture? Is it in our brain, or just in our mind? 

A couple of publications coming out this month debate one such possible cause: altered levels of brain-derived neurotrophic factor (BDNF), a protein that plays a part in growing and maintaining the nervous system. A quick search of PubMed shows that just in 2013 scientists have published studies connecting this vital protein with everything from schizophrenia to obesity to Parkinson’s disease. Apparently BDNF is a BFD in the human body.    

Serum concentrations of brain-derived neurotrophic factor in patients with gender identity disorder” by Fontinari, et al, explores the hypothesis that BDNF levels in the brain could correlate with and possibly even contribute to feelings of gender dysphoria, as “[a]ltered BDNF-signaling is thought to contribute to the pathogenesis of psychiatric disorders and is related to traumatic life events.”  In other words, the hypothesis is altered BDNF levels may be a biomarker of GD, suggesting that GD is not wholly something biological, but biochemical — the result of altered brain chemicals brought about by psychological trauma and abuse that in turn affect the perception of gender identity. The current study, however, only went so far as to measure serum BDNF levels (i.e. amount of BDNF in the blood).

As hypothesized, the study did find that, compared to a control group of healthy cismales, the transwomen in the study had “significantly lower” (about 15%) serum BDNF levels, suggesting that BDNF levels may indeed be a biomarker of GD. In the follow-up discussion, the authors write, 

According to previous studies, lower levels of BDNF were reported in many psychiatric disorders (Begliuomini et al, 2007). Moreover, decreased serum BDNF levels were associated with childhood traumatic events in parents with bipolar disorder […] Few clinical studies have investigated the impact of traumatic childhood experiences on sexual identity and GID. Recent studies reported that children with GID are at high risk for developing psychiatric problems in childhood and that the lifetime psychiatric comorbidity in GID patients is high (Matsumoto et al., 2009; Wallien, 2007). Kersting et al. (2003) found a high prevalence of childhood trauma, especially emotional abuse and emotional neglect, in the transsexual sample (Kersting et al., 2003). GID patients are a group affected by stigma and discrimination (Infante et al., 2009; Meyer, 1995, 2003). Stigma, prejudice, and discrimination create a hostile and stressful social environment that causes mental health problems (Meyer, 2003).The concept of social stress extends stress theory by suggesting that conditions in the social environment, not only personal events, are sources of stress that may lead to mental and physical ill effects [such as GID].

In short, the authors are suggesting that further study may discover a causal link between GD and childhood psychological trauma. They are not saying that their study proves this, nor that they have discovered a definite link between childhood trauma and GD; only that there may be a link and that further study is needed.  

Due to the nature of journal publication, Fontinari et al, has been online for several months now.. As such, it has already generated a response, “On the quest for a biomechanism of transsexualism: Is there a role for BDNF?” by Fuss et al. Their concern is, in short, that individuals with GD have far too many physical and psychological variables that were unaccounted for that may affect BDNF levels regardless of GD. At the most basic level is the chicken-or-egg conundrum. Since altered BDNF levels are known markers of psychological distress, and since people with GD experience a lot of psychological distress because of social stigma (depression, isolation, abuse, etc.), what comes first, the trauma or the GD? Transwomen in particular are also known to have weight issues (a result of HRT) and to participate in fewer highly physical activities like sports. Both weight and activity levels have been found in prior studies to affect BDNF levels. As such, the authors suggest that the findings of Fontinari et al, are far too preliminary to draw anything more than the most basic correlative conclusions. 

Going beyond these two articles, it strikes me that there’s another factor not considered here: the affect that actual brain physiology may play in the way BDNF levels affect the brain. As we’ve reported on Transgender Science before, there could be actual physical differences in the brains of transgender people. In such a scenario, BDNF levels almost certainly would not be a cause of GD, though BDNF levels could possibly enhance the level of GD expression.  

The quest for a biological explanation for transgender is far from over. This pair of recent publications only highlights exactly how much we still don’t know about gender, gender identity, and GD. 


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