Friday, 3 December 2010

The Puzzle - an Overview as of 2009

This article reviews research on biological and psychosocial factors relevant to the etiology of gender-variant identities. There is evidence for a genetic component of gender-variant identities through studies of twins and other within-family concordance and through studies of specific genes. Evidence that prenatal androgens play a role comes from studies that have examined finger length ratios (2D:4D), prevalence of polycystic ovary syndrome among female-to-male transsexuals, and individuals with intersex and related conditions who are more likely to have reassigned genders. There is also evidence that transsexuals have parts of their brain structure that is typical of the opposite birth-assigned gender. A greater likelihood of non-right-handedness suggests developmental instability may also contribute as a biological factor. There is a greater tendency for persons with gender-variant identities to report childhood abuse and a poor or absent relationship with parents. It is unclear if this is a cause or effect of a gender-variant identity. Parental encouragement of gender-variance is more common among individuals who later develop a gender-variant identity. We conclude that biological factors, especially prenatal androgen levels, play a role in the development of a gender-variant identity and it is likely that psychosocial variables play a role in interaction with these factors.

A very useful meta-study indeed, summarising what we knew as of 2009, and in particular, the limits of our knowledge.

I don't agree with some parts - the finger-length ratio evidence is thin (to say the least), I don't see the very real differences in gross lateralisation as being evidence of "instability" in neurological development, and there was nothing on the body map, comparing experiences of "phantom limb syndrome" and "missing limb syndrome".

The quality of the papers studied varies enormously. They have all been given equal weight, leading to some conclusions that are dubious. Nonetheless, I'd far rather have no filtering at all than too much, even if the results are squiffy.

There's some confirmation of my hypothesis about bi-gender.
Veale et al. (2008b) analyzed these outcomes using a logistic regression and found that prenatal androgen exposure and sex of assignment at birth equally predicted adult gender identity among this population. They also found that sex chromosomes and time delayed before sex assignment were not significant predictors of adult gender identity, although these variables had a restricted range with the population tested.
In other words, while 1/3 are male, 1/3 female, the remaining third can be assigned an arbitrary gender with little harm.

So you only kill 1/3 of patients if you do that (rather than half). Or at least, cause severe psychological problems, so that some will suicide, and the rest just pray for an early death. And that "one third" figure will vary with the exact condition - assign a child with cloacal dysgenesis as female, and you'll be wrong far more often if they have 46XY chromosomes than merely 1 in 3. Assign a 46XX child with CAH a female form, and you'll be right 80% of the time.

Oh and chromosomes don't matter - except inasmuch as foetal androgen exposure strongly tends to be caused by chromosomal type. But when this tendency doesn't tend, it's only the foetal hormone mix that matters.
Clearly, further independent research using larger samples is needed to assess the BSTc as a proposed neurobiological basis as an explanation of transsexualism
AGH! It can't be causal, it's symptomatic, a result, not a cause! But as a symptom, it's pretty reliable. Yes, we need more research of course, more data is always better, but they've made an unwarranted assumption about causality. Never mind.

Because of its breadth, dealing with handedness ratios, memory tests, 2D visualisation tests etc from a variety of sources, it's very useful as a reference. The methodology of agglutinating all gender-variant behaviour, from transvestitic fetishism to transsexuality, obscures rather than reveals though. For example:
One study has shown that gender clinic patients were more likely than psychiatric patients to report parent death – especially fathers and during adolescence and early adulthood (Bernstein, Steiner, Glaister, & Muir, 1981). Among a population sample,
Långstrom and Zucker (2005) found an increased likelihood of separation from parents during childhood among males reporting transvestic fetishism. However, studies of NGV populations have not found any evidence for an absent father having an effect on gender development (Stevens, Golombok, Beveridge, & ALSPAC Study Team, 2002; Stevenson & Black, 1988) and two further studies have found that MF transsexuals transvestites, and NGV males did not differ in their reported parent relations to each other or likelihood of living with both parents during their childhood (Hogan-Finlay, 1995; Veale et al., 2008a).
All over the shop, not enough variables shackled.

Nonetheless, one I'll refer to in future. Some parts because of their pristine science, other parts as Horrible Examples to learn from.

There is evidence that biological factors, especially prenatal androgen exposure, play a significant role in the etiology of gender-variant identities. While there is also evidence for other biological correlates, this does not necessarily imply more than one biological factor plays a role – it is likely that they are related and share a common precursor. For instance, it is entirely plausible that there is a causal pathway from genes causing atypical prenatal hormones levels causing neuroanatomical differences and an adult gender-variant identity.

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