Val Dobson

I think you’re presenting a neurological mechanism as established fact when it hasn’t actually been demonstrated. Firstly, sexual differentiation of the brain is considerably more complicated than simply developing along a male–female continuum. Much of our mechanistic understanding comes from rodents, where we distinguish four partially independent processes: - masculinisation (development of male-typical characteristics) - defeminisation (suppression of female-typical characteristics) - feminisation (development of female-typical characteristics) - demasculinisation (reduction of male-typical characteristics). These aren’t necessarily reciprocal. Masculinisation doesn’t automatically imply a corresponding defeminisation, for example. In rodents, testosterone is locally aromatised into estrogen within the brain, affecting the structural organisation of specific neural circuits (mainly the hypothalamus). For example, estrogen is known to increase dendritic spine density in the preoptic area (POA) via prostaglandin E2 signalling. We can also experimentally dissociate masculinisation from defeminisation, as male rodents can develop male-typical mounting behaviour while retaining the capacity for lordosis (female-typical sexual receptivity). So, masculinising one characteristic doesn’t necessarily eliminate female-typical ones. Attempting to extrapolate this directly to humans is difficult. Human sexual differentiation appears more dependent on androgen-receptor signalling rather than aromatisation observed in rodents. Natural experiments (such as CAIS, CAH, 5α-reductase deficiency and aromatase deficiency) provide evidence that androgen signalling influences aspects of neurological and psychological development, but none establish a discrete, hardwired male or female “neurological identity”. There’s also an issue with your developmental timeline. Genital differentiation and brain development aren’t two independent processes occurring months apart. Neural development is already underway during genital differentiation, and androgen-sensitive developmental periods overlap considerably. Both tissues are influenced by circulating hormones, although their responses depend on aspects such as receptor expression and localisation. They can certainly develop differently, but that doesn’t mean the body develops as one sex before the brain independently develops according to another “blueprint”. More importantly, wheres the evidence that the human brain develops according to some internal male or female “blueprint”, or that it continuously compares this supposed “blueprint” against the body’s anatomy, generating GD when they don’t match? We know prenatal hormones influence aspects of sex-typical behaviour. But that’s different from demonstrating that GD results from a hardwired mismatch between the brain and body. You’re taking findings about the hormonal organisation of particular neural circuits, largely from rodents, and extrapolating them into a comprehensive explanation for transgender identity. That’s a hypothesis, not an established neurological mechanism. I also think it’s a lot harder to correlate the prenatal environment to GD than for sexual orientation, in terms of an actual mechanistic explanation.