The influence of Stria Terminalis

This week we continue to review the body of literature that some members of our LGBT (lesbian, gay, bisexual, transgender) community use to argue that gender identity has biological basis.

As we observed in the previous months, this basis must be a normal biological phenomenon to be valid as evidence of the normal state of the “third gender.” Otherwise, the argument will end up supporting the contention that members of the LGBT community are not biologically normal.

As we have seen in our past reviews, the proof in abnormality supports only the idea that they are “abnormal” or, using a medical euphemism, “biologically disordered.” Thus, such an argument is not acceptable if we insist that they must be treated as normal persons.

The next basis that researchers Aruna Saraswat, Jamie Weinand and Joshua Safer reported in the 2015 Endocrine Practice issue involves the bed of nucleus of the stria terminalis (BNST), which is also referred to as “extended amygdala.” “Stria terminalis” means “terminal fibers.” It is located in the basal part of the forebrain (frontal zone of the brain) and the gray-colored portion of the brain (grey matter). This structure is supposedly dimorphic, which means that the BNST of males look different from those of the females, thus differentiating their sex identity.

Saraswat and colleagues mentioned three studies. The first study in 1995 (by Zhou and colleagues) observed that the BNST of six male-to-female (MTF) transgender people showed similarity in quantity and size to those often found in females. However, these transgender people treated themselves with estrogen, a female hormone. Thus, it cannot be safely concluded that the findings were due to biologically determined female BNST development among MTFs or to the long-term use of estrogen. There is an unknown chance that, without the treatment, no female BNST may exist. The second study (by Kruijver and colleagues) simply confirmed adultonset sexual dimorphism in BNST neurons.

The third study of dead brains in 2008 (by Chung and colleagues) noted that this BNST sexual dimorphism develops only in adulthood. This observation con- tradicts the fact that most transgender people experience gender incongruence, which psychiatrists label as “gender identity disorder” (GID), even while still in childhood. This means the BNST sexual dimorphism is not the “cause” of gender identity. Instead, the GID (or its cause) may be the cause of BNST sexual dimorphism or estrogen injection.

Well, the evidence did not point to BNST as the biological determinant of sex identity (because the sexual organs of the person are already differentiated at birth) or gender identity (because change in gender perception already started happening during childhood). Thus, this evidence failed to prove that gender identity has a normal biological basis as claimed.