Download Gender Identity Disorder

Gender identity refers to an individual’s self perception as male or female,
according to the DSM-IV-TR (American Psychiatric Association, 2000). Gender
identity is typically consolidated by the age of three to four years and is usually
accompanied by gender role behaviour, a behaviour that is consistent with the cultural
definition of masculine and feminine roles (Bradley & Zucker, 1997). Gender identity
disorder (GID), is defined by the DSM-IV-TR as strong and persistent cross-gender
identification, such as fostering behaviour stereotypical of the other sex or the belief
that one is of the opposite sex, accompanied by constant discomfort about one’s
assigned sex. In addition, to meet criteria for GID diagnosis, the symptoms must not
include physical intersex condition and the individual must suffer significant clinical
discomfort or impairment in important area of functioning. Transsexualism, a sex
reassignment surgery, is considered to be an extreme form of GID, however the
prevalence of adults seeking the surgery is low, 1:10,000-30,000 men and 1:30,000100,000 women in Europe and Singapore (American Psychiatric Association, 2000;
Cohen-Kettenis & Gooren, 1999).
The aetiology of GID is not entirely known at this stage. Research on GID
aetiology is focused on biological and psychosocial, mainly familial, factors. Bradley
and Zucker (1997) have proposed a model for the aetiology of GID, suggesting that
early attachment problems and reactivity to stress together with unstable familial
environment increase the anxiety level of the child. The child chooses GID as a relief
from anxiety due to factors within the child such as activity level and sensitivity and
as parents initially tolerated cross gender behaviour. The present paper critically
examines biological and psychosocial evidence for the Bradley and Zucker model and
also suggests that factors within the child mentioned by the model include
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predisposition to GID, such as genetic factors. It also reviews the model shortcomings
and briefly presents alternative theories of GID aetiology.
Several researches have believed that gender identity might be biologically
innate. Evidence for this can be seen in the case of a boy whose sex was reassigned to
female in infancy due to damage to his penis. Although raised and treated by parents
and the environment as a girl, the child adopted stereotypically male behaviour
(Slijper, Drop, Molenaar & de Muinck Keizer-Schrama, 1998).
One area of biological research of GID aetiology examines the effects of genetic
factors on the development of atypical gender behaviour. Bailey, Dunne and Martin
(2000) in a retrospective study of a large sample of an Australian male and female
monozygotic (MZ) and dizygotic (DZ) twins population, examined the genetic
influences on childhood gender non-conformity and continuous gender identity in
adulthood. Childhood gender non-conformity and continuous gender identity
measured the preference of children and adults, respectively, for cross sex typical
behaviour or feelings, without necessarily meeting the clinical criteria for GID. Bailey
et al. (2000) found that childhood gender non-conformity was inherited for both males
(.50) and females (.37), however the results for adult continuous gender identity were
not significant. A survey of parents responses in a study of 314 MZ and DZ twins
from a normal population of children and adolescents, ages 4 – 17 years, Coolidge,
Thede and Young (2002) found that the heritability of GID was .62, however the
authors emphasised the numbers may be inflated due to a relatively small sample.
More recently, Knafo, Iervolino and Plomin (2005) examined, by parents’ ratings, the
genetic influences on the development of gender atypical 5,799 three and four years
old male and female MZ and DZ twins. Gender atypical boys were the ones rated as
relatively more feminine while gender atypical girls were the ones rated as relatively
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more masculine. Knafo et al. found moderate, yet significant, heritability for boys
(.26-.27) and for girls (.42-.50) and large heritability for masculine girls who were
also low on femininity (.65-.76). The differences between these findings to the
Coolidge et al. (2002) study can be explained by the differences in sample size,
participants’ age or the fact that Knafo et al. (2005) did not measure whether their
subjects met clinical diagnosis of GID. The genetic studies show at least moderate
inheritance for gender non-conformity in children and adolescents, suggesting genetic
predisposition to GID for children and adolescents, but not for adults. These findings
are consistent with the Bradley and Zucker (1997), which suggested factors within the
child contribute to development of GID. It is important to note that the moderate
inheritance suggests there are other factors involved in GID aetiology, as mentioned
below.
Other biological studies hypothesised that excess of prenatal androgens causes
masculinity in girls while deficit causes femininity in boys. The immunohormonal
theory of GID in boys suggests that women pregnant with male foetus produce
antibodies to androgens that pass from the mother to the foetus through the placenta.
The antibodies may reduce the androgen’s biological activity and thus compromise
the masculinity of the male foetus (Ellis & Ames, 1987). They also noted that the
maternal immune response may develop over several pregnancies. Consistent with the
immunohormonal theory, researches found that boys with GID had a later birth order
and a larger ratio of brothers to sisters compared to boys without GID (Blanchard,
Zucker, Bradley & Hume, 1995; Bradley & Zucker, 1997). However, as discussed
later, the birth order and excess number of older brothers relationship with GID can
also be explained by the mother’s wish to have a girl after many boys (Blanchard et
al., 1995).
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Support for the theory that prenatal excess of androgen is related to masculinity
of girls comes from studies of girls with congenital adrenal hyperplasia (CAH)
(Bradley & Zucker, 1997). Chromosomal females with CAH are prenatally exposed
to increased levels of adrenal androgens‚ causing various degrees of masculinisation
of the genitalia (Slijper et al. 1998). Even with surgically created full female genitalia,
girls with CAH appear more masculine, display more masculine behaviour and higher
percentage of them have GID than girls from normal population (Dessens, Slijper &
Drop, 2005). It is important to note that most girls with CAH do not develop GID and
that girls with CAH who were assigned to female gender at birth and treated as
females by family and the environment were less likely to be diagnosed with GID and
displayed less masculine behaviour than CAH girls who were assigned to female sex
later in life (Slijper et al., 1998), suggesting environment factors have also an
influence on development of gender identity in CAH girls.
The literature also associates with prenatal androgen exposure theory the
findings that compare to control groups, boys with GID displayed less rough-andtumble play, lower activity levels and higher sensitivity and girls with GID displayed
more rough-and-tumble play and higher activity levels (Bradley & Zucker, 1997),
boys with GID were rated as more attractive, with more feminine facial features
(Zucker, Wild, Bradley & Lowry, 1993) and girls with GID were rated as less
attractive, with less feminine facial features (Fridell, Zucker, Bradley, & Maing,
1996). Post-mortem brain studies showed the size of the bed nucleus of the stria
terminalis in male-to-female transsexuals was closer to typical female size than to
typical male size (Green, 2000) and the volume and number of neurons of female-tomale transsexuals was closer to that of a typical male (Segal, 2006).
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The researches linking prenatal androgen exposure with increased masculinity in
girls and decreased masculinity or increased femininity in boys suggest predisposition
to GID and to cross gender behaviour for males and females, supporting the Bradley
and Zucker (1997) model regarding predisposition to GID.
Other studies have linked GID with predisposition to stress. Children and adults
with GID were found to have other psychiatric disorders, especially internalised
disorders such as separation anxiety and depression, in higher rates than normal
population (Hepp, Kraemer, Schnyder, Miller & Delsignore, 2005; Zucker, 2005).
Zucker, Bradley, & Lowry Sullivan (1996) found that young boys who met full
criteria for GID were more likely to suffer separation anxiety than boys who engaged
in cross gender behaviour but did not meet full criteria for GID. Coolidge et al.
(2002), however, found that more girls and boys with GID suffered comorbid
depression but not separation anxiety when compared with normal population. As
depression and anxiety suggest predisposition to stress (Tiet et al., 2001), the rates of
comorbidity of GID with depression and possibly with separation anxiety support the
suggestion of Bradley and Zucker (1997) model that predisposition to stress is a factor
in the development of GID. However, the high comorbidity can be attributed to
distress of not being accepted by society and parents. Some clinicians claimed that
symptoms of comorbidity as well as GID symptoms were reduced with increased
acceptance of oneself and parents (Pickstone-Taylor, 2003; Rosenberg, 2002),
suggesting environmental influences on the development of GID.
Several researches found non-shared environment influences on atypical gender
behaviour and GID in childhood, adolescence and adulthood for both male and
female, ranging from .50 - .69 (Bailey et al., 2000; Coolidge et al., 2002). Others
found shared environment effects on atypical gender behaviour in three and four year
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old boys and girls ranging from .33 - .57, but not for girls who were low in femininity
as well as high on masculinity (Knafo et al., 2005). These studies suggest
environment effects play an important role in the development of GID. Research was
done to examine what are the environmental factors associated with the development
of GID.
Bradley and Zucker (1997) suggested that parents of children who later
developed GID, initially tolerated the cross gender behaviour. Further more, they
suggested that GID and cross gender behaviour of boys are linked to mother’s
encouragement of feminine behaviour and discouragement of masculine behaviour.
Some support for that theory may come from Zucker et al. (1994) who found that
mothers’ wish for having a girl increased with the number of only male children they
had and from Blanchard et al. (1995) who found that boys with GID and cross-gender
behaviour had relatively higher number of older brothers than control boys. Combined
together it is possible that mothers wish for a girl after having already several boys
causes the mother to encourage feminine behaviour and discourage masculine
behaviour, and subsequently the development of GID. This theory, however, is yet to
be empirically tested.
Parents of GID children were found to have higher levels of psychopathology
than parents of normal children (Cohen-Kettenis & Gooren, 1999). Mothers to
children with GID suffered more depression, borderline and other psychiatric
problems and fathers suffered more substance abuse compared to control (Bradley &
Zucker, 1997). Boys with GID tended to have atypically close mothers and distant
fathers while girls with GID tended to have two distant parents (Segal, 2006). The
parents’ distance suggests attachment problems while the high psychopathology of
parents suggests unstable familial environment, both supporting the Bradley and
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Zucker (1997) that links attachment problems and insecure environment with GID.
However, a direct connection between parenting style and GID is yet to be established
and it may be that the parental distance from GID children is influenced by parents’
frustration of the child’s atypical behaviour.
Another important factor in the understanding of GID is the differences between
referral rates of boys and girls with GID to clinical treatment versus the prevalence of
GID in the general population. Coolidge et al. (2002) found that the .7% of boys and
3.7% of girls in general population met clinical diagnosis for GID but the boys to girls
ratio of referral to clinical treatment was 6.6:1 (Zucker, Bradley & Sanikhani, 1997).
An explanation for the higher referral of boys is offered by the social constuctionist
approach (Gottschalk, 2003) suggesting that GID is basically a social construct, stems
from society’s assumed roles for males and females. Social constuctionism claims that
adults and children who engage in cross gender behaviour simply express a valid
preference. The difference in referral rates, according to social constructionism,
simply reflects that cross gender behaviour is more tolerated by society in females
than in males. Bradley and Zucker (1997) model does not offer an explanation for the
different referral rates.
Another aspect of GID that is not explained by Bradley and Zucker (1997)
model is that only 20% of children with GID continue to display gender dysphoria in
adulthood. One possibility is that GID is simply an early manifestation of
homosexuality (Blanchard et al., 1995). Support to that approach is found in clinical
reports that symptoms of GID in male adolescents reduced once they assumed a
homosexual sexual orientation (Rosenberg, 2002) and by the DSM-IV-TR description
that by adulthood 75% of boys with GID become homosexuals or bisexuals without
GID and that almost all adult females with GID are sexually attracted to females
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(American Psychiatric Association, 2000). The view that GID is early manifestation
of homosexuality does not take into account that in adulthood only half of males with
GID are sexually attracted males while the other half is sexually attracted to females.
The later group tends to have later onset of GID than the former (Zucker et al., 1996),
which might suggest different aetiology for the two groups. Further study is required
to explore that possibility.
Conclusion
The Bradley and Zucker model suggests that the aetiology of GID involves
predisposition to GID, high reactivity to stress and early attachment problems together
with stressful familial environment and initial tolerance of cross gender behaviour by
parents. The literature supports the model with a range of biological and psychosocial
evidence found to be associated with the development of GID. The biological
evidence, genetic and prenatal androgen exposure, are consistent with factors within
the child or predisposition to GID, suggested by Bradley and Zucker model. The high
comorbidity of GID with internalised disorders suggests high reactivity to stress. The
psychosocial factors that found to be associated with GID are stressful familial
environment, possibly caused by parents high psychopathology and early attachments
problems with distant father for boys and two parents for girls are also consistent with
the model. The Bradley and Zucker model fails to explain the low prevalence of adult
GID compare to childhood GID, the different referral rates of boys and girls and the
two different types of male GID, sexual attraction to males and sexual attraction to
females. The aetiology of adult GID and the different types of sexual attractions
among adult males with GID are worthy of further study.
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