Biological Explanations GID

• Biological explanations for gender identity disorder have found differences in the brain associated with sexual behaviour.
• One biological explanation for gender dysphoria has a basis in brain structure, in particular with the size of the bed nucleus of the stria terminalis (BNST).
• The bed nucleus of the stria terminalis (BNST) is a structure in the brain involved in emotional responses.
• There is some suggestion that the bed nucleus of the stria terminalis (BNST) is implicated in the biological explanation of gender dysphoria. It is believed that people with gender dysphoria have a BNST which is the size of the gender they identify with, not their biological sex.
• Research has found that the BNST, which is a part of the hypothalamus in the brain, is larger in typical males than those with gender identity disorder.
• Kruijver et al (2000) found the BNST area of the brain to be larger in men than women and suggest it has been found to be female sized in transgender women.
• Zhou et al (1995) suggested problems with the BNST fits with reports made by people who are transgender that feel from an early age they are born the wrong sex.
• Zhou et al (1995) found that in a small sample of male to female transsexuals there was evidence of brain activity more typical of females than males.
• Garcia-Falgueras & Swaab (2008) found that in male to female transsexuals there was an area of the hypothalamus that was more similar to the same area in female controls. This suggests that brain structure may resemble the gender they feel they are.
• There are many challenges made to the brain sex theory of gender dysphoria, which limits its credibility as an explanation.
• Hulshoff Pol et al (2006) studied changes in transgender individuals' brains using MRI scans taken during hormone treatment. The scans showed the size of the BNST changed significantly over a period of time.
• Most of the studies investigating the structural differences in the brain of individuals with gender dysphoria are the result of post-mortem examinations. These are less reliable than brain scans where patients are alive.
• Some research evidence suggests there may be other brain differences associated with gender dysphoria.
• Rametti et al (2011) studied the white matter in the brains of males and females. This is the deeper tissue of the brain. They found that the amount and distribution of white matter corresponded more closely to the gender individuals identified as, rather than their biological sex.
• Much of the research into biological factors associated with gender identity disorder focus on genes and hormones.
• Research into the influence of prenatal hormones have shown issues with the production of the male hormone androgen, in determining gender dysphoria.
• Zucker & Green (1992) suggest that problems with gender dysphoria can arise when androgen is not produced or cell receptors do not respond to it.
• There is evidence that some males with gender identity disorder have inherited androgen receptors that are not sensitive to male hormones such as testosterone.
• Hare et al (2009) found evidence a variant of the androgen receptor gene that caused a reduced effect of testosterone, was seen more often in male to female transsexuals.
• Chung et al (2002) argued that prenatal hormonal influences might remain dormant until adulthood where they subsequently trigger a change within the individual. They suggest this may account for the higher proportion of males diagnosed with gender identity disorder.
• Many individuals with gender dysphoria choose to change their gender identity and often respond well to hormone therapy both before and after surgery.
• The fact that hormones can help people to transition from male to female or female to male, suggests that hormones play a fundamental role in gender identity.
• By studying the influence of hormones in gender dysphoria, more practical applications such as treatments can help individuals in the future.
• Some psychologists suggest there may be a genetic prevalence to gender identity disorder.
• The genetic explanation for gender dysphoria looks for inherited characteristics that run in families or in the concordance rate of twins studies.
• Coolidge et al (2002) assessed 157 twin pairs for evidence of gender dysphoria. They found that 62% of the variance could be accounted for by genetic factors, suggesting a strong heritable component.
• Heylens et al (2012) compared 23 MZ twins with 21 DZ twins where one of each pair was diagnosed with gender dysphoria. They found 39% of the MZ twins were concordant for gender dysphoria compared to none of the DZ twins.
• Bennett (2006) reported that genetic processes involved in gender identity disorder, were found in 2% of the sample in more than 300 MZ and DZ twins.
• Pool et al (2000) found evidence for a neurobiological basis for gender dysphoria. They claim that men have twice as many somatostatin neurons than women.
• According to Pool et al (2000) somatostatin neurons promote certain behaviours, specifically risk-taking, exploration/ adventure, and decision making. This might explain why men have more of these skills than women.
• Pool et al (2000) found that in both male to female transsexuals and female to male transsexuals, the number of somatostatin neurons corresponded to their gender of choice.
• The biological explanation of gender identity disorder ignores the role that social or psychological factors play in the feelings of gender confusion.
• The biological explanation of gender identity disorder is reductionist as it fails to take into account other factors which may play a part in gender identity.
• Males appear to be 5 times more prone to gender identity disorder than females, this could be the result of biological vulnerability and provides strong support for the biological explanation.
• Many research studies today have shown that cross-gender behaviour starts very early in childhood, suggesting a strong social or cultural link to gender identity disorder.