Gender Identity Disorder (GID)
Mostly men report masculine identities and women feminine identities. There are rare occasions when a person can report feeling very uncomfortable with their gender identity. This is Gender Identity Disorder (GID) and can result in extreme anxiety, distress and even suicide.
Many opt for gender reassignment surgery (not sex change operation) and have their outward appearance surgically altered to fit with their gender identity.
NB: GID does not refer to chromosomal abnormalities such as Turners or Klinefelters and it is also inappropriate to use the case of David Rhymer as an example!
We shall consider biological and psychological explanations:
Biological explanations of GID
Genetics
The concordance rate for MZ twins is 39% compared to 0% for DZ twins. On the face of it this appears to suggest a genetic component. Certainly those sharing 100% of their genes appear to be far more similar in prevalence of GID than ordinary fraternal twins.
However, all the usual arguments apply and just because you’ve used them before in discussions of OCD, anorexia and smoking addiction doesn’t mean they are not going to be credit-worthy here too. Twin studies typically tend to over-estimate the contribution played by genes. They assume that the environments shared by MZ are no more similar than the environments shared by DZ. This is simply and manifestly not true. MZ twins are confused for one another, they dress alike, are often in the same classes at school, it is impossible to disentangle the effects of nature and nurture in respect of their behaviour. In fact, compared to other disorders such as anorexia (56%) and bipolar (72%), the concordance rate appears to be quite low.
In addition to this, GID, being so rare, the number of twins available for study must be very low resulting in a small and therefore unrepresentative sample.
Brain structure
As always any genetic cause of a disorder will have its affect via brain structure or brain chemistry. In the case of GID research has focused on dimorphic brain structures, areas of the brain known to be different in men and in women. One such structure, the bed nucleus of the stria terminalis (call it BSTc) has been shown to be promising.
Typically in men this structure is 40% larger than in women and was once thought to be fully developed by the age of five years. Post-mortems on transgender male to female patients showed that in fact their BSTc, although in a male brain, was typically the same size as that of a woman. There was also a much reduced neuron density in this structure, again more in line with the density found in women. Could it be possible that this structure alone was the cause of GID?
There are many issues with this research. The sample size is tiny, only six participants and these may not be representative of GID patients as a whole. However, there is a far greater issue with cause and effect. The researchers are assuming, that because the structure is fully developed by the age of five, long before GID is apparent, that the abnormal development must pre-date the disorder suggesting a cause rather than a symptom. However, this reasoning appears to be flawed.
Firstly Chung et al (2002) found that although the size of the BSTc appears to be determined by hormones in the womb, these developments do not occur until after puberty. It appears not to be fully developed prior to the possible onset of the disorder. More importantly, many male to female transgender patients receive hormone treatment including the administration of female hormones such as oestrogen and progesterone.
Pol et al (2006) found that such treatment does affect the size of the BSTc. This raises the possibility that treatment of patients might, at a later date, be resulting in a shrinking of this structure. If true, the odd size of the BSTc would be merely a symptom not a cause of GID.
Overall evaluation of biological explanation
As always the model is nomothetic. It provides a one-size fits all explanation for what we’ve seen to be a very complex phenomenon. In failing to recognise other possible socio-psychological influences it is reductionist.
Crucially, as always we have a model that is biologically deterministic. This removes the element of free-will and choice. In the case of a disorder that carries such a stigma as GID and one in which those with the disorder are widely ridiculed, this is ethically important. If GID could be found to be biological, if a gene or abnormal brain structure could be found as a cause then it would help remove that stigma and the blame and humiliation that often comes with it.
Psychological Explanations of GID
Psychodynamic
This is very much in the traditional Freudian, Little Hans-esque mould. According to the theory, GID develops as a result of extreme separation anxiety in the first few years of life and before gender identity has developed. This anxiety causes the child (we’ll assume boy in this case) to fantasise of a symbolic fusion with mother. This causes, according to Ovesey and Person (1973) the boy to identify with mother rather than with father, as would normally be the case during resolution of the Oedipus Complex. Instead of developing a male gender identity, the boy develops a female identity and GID is the outcome.
Support has come in the form of interviews with adult patients who report a very close mother-son relationship during their younger years. Although this does appear to offer support, it is clearly not the most valid measure. Data has been collected retrospectively, requiring recollection of events in very early years. As we saw in the topic of memory, our recall is reconstructed; it changes over time and alters throughout life. Without additional evidence it would be very difficult to draw firm conclusions.
Di Ceglie (2002) reported the case of James. From the age of 6 months to five years James had been cared for by his grandmother whilst mum worked away. He was brought up engaging in mostly traditionally female activities such as cooking and housekeeping. When gran suddenly died James developed all the symptoms of GID. He wanted to be a girl, would play with dolls, wanted to grow up to be a bride and to breast-feed children. He never spoke of his gran’s death. Following psychoanalysis which encouraged him to talk about his gran he made a full recovery.
Clearly, there are issues with this case study and would be difficult to generalise.
Rekers (1986) found that gender identity issues in boys are far more likely due to absence of the father rather than the mother. He studied 36 transgender boys and found that 75% of the most disturbed had an absent father. Later research still, found no association between absent parents and development of gender identity.
As always with psychodynamic theory, we have hypothetical constructs for which there can be no objective evidence. The result is a theory that is non-testable and therefore non-falsifiable. It can offer no empirical evidence and is therefore unscientific.
Cognitive Explanation of GID
Liben and Bigler (2002) proffered an extension of Gender Schema Theory to explain GID, the dual pathway theory.
Normal developmental pathway is for gender schemas to develop which in turn direct gender appropriate behaviour and attitudes.
Personal development route suggests that gender identity is affected by the kinds of activity in which the child engages. For example, a boy playing with toys will come to accept that this behaviour is gender appropriate for boys as well as girls. The result is a non-sex-typed schema for gender resulting in androgynous behaviour and feelings and flexible attitudes about gender. In a minority this may lead to GID.
However, by cognitive standards this explanation is poor and it fails to explain how the initial non-typical play behaviour develops in the first place. As always, it’s a cognitive model that takes the outcomes or symptoms and suggests that these are the cause.
CGS Psychology Blog: Mrs Harris 