Letter from the Editor
Staff Articles
- Women and HIV: A Discourse of Necessary Interventions
- Aspects of Gender Identity Development: Searching for an Explanation in the Brain
- The Relationship between Parental Involvement and Mathematics Achievement in Struggling Mathematics Learners
- Reflections on Moral Decision-Making: A Qualitative Analysis of Holocaust Survivors
- Predictors of Happiness among LGBQ College Students
- Discrimination and Social Support: Impact on Behavior Outcomes of Children of Immigrants
- Mothers’ Book Sharing Styles and Children’s School Readiness Skills
- Internalizing Symptoms and Social Aggression Victimization among Early Adolescent Girls: Where Does Academic Achievement Fit In?
- Paternal Support of Emergent Literacy Development: Latino Fathers and Their Children
- Sociopolitical Identity of Turkish Emerging Adults: The Role of Gender, Religious Sect, and Political Party Affiliation
Elizabeth Glaeser
Psychologists consider some individual characteristics to be fixed while others are understood as flexible, such as preferences and intellectual ability. Professionals in the field of child development do not often put gender identity development in a category apt for much variation. However, sometimes gender identity is not so cut and dry. A small percentage of our population feels that their “brain” is one gender while their “body” is another, a phenomenon known as Gender Identity Disorder (GID). This variation from the norm creates immense discomfort and inhibits some children from developing a strong, confident sense of self (Hepp, Kraemer, Schnyder, Miller & Delsignore, 2005). In fact, past research has demonstrated that when is GID experienced in childhood, it has been correlated with low self-esteem and has been disruptive of healthy identity development (Hepp et al., 2005).
Recently, inclusion of GID in the upcoming DSM-V has been a subject of debate. As the DSM currently stands, GID is considered an illness that can be “treated,” and many psychologists argue that considering only one form of gender identity development to be “healthy” may define gender in a heteronormative way (Zucker, 2006). The lack of understanding about the true causes and considerations involved in GID only leaves room for discriminatory, stereotyped classification of individuals developing gender identities. Society passes judgment in the face of uncertainty and the mystery of sex and gender is no exception. However, a neurological understanding of gender identity as it relates to sexual identity may allow both clinicians and the public increased exposure to constructs related to sex and gender. By increasing public knowledge about gender identity development beyond the hetero-normative tradition, we may be able to improve social acceptance for both children and adults diagnosed with GID, who do not fall in the traditional gender paradigm.
Society’s Medical Model
The medical model of our society has created a dualism in which infants, children, and adults are either male or female. Nothing apart from this dichotomy is typically tolerated, as society does not leave room for ambiguous gender expression or genderless people. For example, infants born with intersex conditions like congenital adrenal hyperplasia in genetic females and steroid 5- reductase 2 deficiency in genetic males undergo near immediate surgery to “correct” the condition by sculpting the child as a male or female (Zucker, 2002). The assumption in these cases is that the human brain is organized in a sexually dimorphic manner and gender identity is not taken into account separately from sexual identity. Therefore, the current model advocates that an individuals’ gender identity should never deviate from physical or genetic sex. However, it does happen and when it does, these individuals are labeled with a “disorder:” GID as described in the DSM-IV-TR is defined as:
[E]vidence of a strong and persistent cross- gender identification, which is the desire to
be, or the insistence that one is, of the other sex. […] To make the diagnosis, there must
be evidence of clinically significant distress or impairment in social, occupational, of
other important areas of functioning (APA, 2000).
Classifying GID this way assumes that the gender identity development of individuals with GID is maladaptive and dangerous. In turn, these individuals internalize that very societal under- standing of their situation, often feeling that they do not belong in the body assigned to them by nature. This thought process might lead to a lack of self-confidence and uncertain sense of self (Zucker, 2002). Furthermore, the comorbidity of psychiatric and personality disorders is extremely high for those diagnosed with GID.
Society’s medical model has further defined transsexualism as a disorder based on the desire of individuals to “correct” GID with surgery. Transsexualism is defined as “desire to live and be accepted as a member of the opposite sex, usually accompanied by a sense of discomfort with, or inappropriateness of one’s anatomic sex, and a wish to have surgery and hormonal treatment to make one’s body as congruent as possible with one’s preferred sex” (APA, 2000). The 1 out of 30,000 adult males and 1 out of 100,000 adult females who identify as transsexual often undergo major hormone therapy, surgery, and lifelong complications that, despite their desires, do not “fix” the psychological problem of not fitting into society’s mold (APA, 2000). Despite the presence of corrective surgery in the Western world, social norms indicate that no person can ever completely be a member of the other sex.
The Need for Neurological Answers
Currently, there is a significant lack of neurological evidence that defends or disputes the idea that the brain is sexually dimorphic, and if so, where exactly “gender” and “sexual” identities are located. The brain structures speculated to be the home of gender and sexual identity, are acted upon by hormonal activation at both puberty and prenatally. These activation periods are relatively well understood, yet they do not account for all of our gendered behavior. Further, genetic sex remains unaccounted for. If society and the medical profession insist on diagnosing the small percentage of the population that do not fit into assumed, socially constructed roles then evidence must be found to defend the belief that gender is neurologically determined.
However, the question of the origin of gender identity remains. The term “gender identity” was coined in the 1960’s by Hooker and Stoller, who defined it as “ a young child’s developing a fundamental sense of belonging to one sex, and not the other” (Hooker & Stoller as quoted in Zucker, 2002). Hooker goes on to say that gender identity is assessed using a structured verbal interview in children. However, this study shows that most children do not have a sense of their own gender identity unless it is somewhat confused against the “normal” (Zucker, 2002). Therefore, if gender identity, like all assumed human characteristics, is based in the brain, how would a verbal interview possibly aid neurological classification? Gender is fundamental to the human experience, and society has created such a distinction between the two that the lack neurological information regarding the differences between the developing sexes creates a remarkable paradox. With more research in the field of gender identity development, early detection and intervention will be possible to assist children in developing a strong sense of identity and to reduce the number of comorbid psychological conditions associated with gender identity disorder in any stage of life.
When a scholarly study refers to gender identity confusion, there is no blood test, MRI, or combination of answers to a questionnaire that can make a diagnosis. Instead, the diagnosis refers specifically to a detailed interview and psychiatric evaluation adhering to DSM-IV-TR criteria. When a neurological site is found for gender identity that is different from biological sex an argument can be made against simple biological sexual dichotomy and the legitimacy of GID as a disorder can be debated. In the present time, people afflicted with so-called GID are treated with hormones dictated by the medical model and current knowledge of clinicians and live in emotional turmoil because they are unable to forge a complete identity in the eye of society.
Gender Identity “Disorder” Damage throughout the Lifetime
Naturally, the preoccupation with a desire to be a different gender starts early in life and as a result many psychiatric disorders develop due to lack of understanding, acceptance, and professional care. It would seem then, that a study of children and their comprehension of their gender conflict would provide answers to how gender identity is perceived at a young age. The damage associated with labeling these children as “disordered” further inhibits children’s ability to develop a strong sense of self. The intense stress of a “disorder” in childhood impacts this damaged sense of self throughout the lifetime and is intensified by the lack of knowledge around gender identity in the brain.
Current research attempts to isolate gender identity from biological sex in children in order to determine the validity of GID, and therefore lessen or even eliminate the stress and damage associated with the labeling as gender disordered. Research conducted by Simonelli, Rossi, Tripodi, Stasio, and Petruccelli (2007) attempts to isolate gender identity in children as its own separate entity apart from sex differentiation and sexual orientation. However, since a child is often unaware of his/her development, it can be difficult to decipher how a child feels about his/her gender unless he/she feels something is wrong (Simonelli et al., 2007). Through this study, Simonelli et al (2007) found that only 11 out of the 246 children had any atypical gender answers, but none were more atypical than typical (Simonelli et al., 2007). In other words, no child answered questions outside of his/her biological sex more times than in congruence with his/her biological sex. These few atypical profiles, all of which were female, showed gender non-conformity, aggression, and low conscientiousness (Simonelli et al., 2007). The majority of children reported being satisfied with their gender, and none of the atypical profiles met the diagnostic criteria for GID (Simonelli et al., 2007). Interestingly, over 40% of the children could not find positive attributes to their gender indicating that children age 9 to 13 often do not understand their own gender in comparison with others (Simonelli et al., 2007). Due to the lack of concrete evidence for GID in children, generalizations about how children feel about their gender identity under “normal” circum- stances are almost impossible (Simonelli et al., 2007). Although first of its kind, this study paves the way for researchers and clinicians to begin to understand that gender identity may be complex and fluid.
Though children may experience discomfort with their gender during their childhood years, not all individuals who display atypical gendered behaviors in childhood go on to identify as transsexual as adults. In fact, many people who prefer to identify as the opposite gender during childhood no longer feel that way after puberty. Though 5% of girls and 2.6% of boys show opposite sex behaviors during childhood, this percentage shrinks to 2% of girl and 1% of boys in adolescence (Asscheman, 2009). However, for those individuals who continue to experience gender discomfort after puberty, the damage done by peers and violations of social norms is perpetual. As a result of this damage, the number of referrals of adolescents with possible GID has tripled in the last 30 years (Asscheman, 2009). As many as 25-27% of adolescents who felt discomfort with their gender in childhood continue this behavior through adolescents and beyond, while 75% identify as homosexual or bisexual (Asschemann, 2009). These statistics suggest that childhood identification of gender is not an indicator of adult transexualism, lending support to the notion that gender is not necessarily hard-wired at birth. In fact, the gender constructions of these children may be centered on their ability to adapt to their environment. Though childhood gender role association develops into gender identity, which is located in the brain (Zucker 2002), there is no formula of understanding whether children who identify as gender dysmorphic will eventually identify as transsexual.
As it stands, the damage done by this early diagnosis and “treatment” or lack of proper management of individuals with GID is well reflected in adults with the condition. In a study done by Hepp et al. (2005) it was found that 45% of GID adults had been diagnosed with a mood disorder in their lifetime, compared with 12.9% of the general population. Futhermore, 45% of GID adults have also been diagnosed with a substance abuse disorder, compared with 9.7% of the general population (Hepp et al, 2005). These remarkable statistics may indicate that diagnoses may fail to properly address gender identity concerns instead exacerbating them.
Hormones
Hormones also play a role in developing gender identity at two distinct time periods in our lives. Prenatal hormones cause hard-wired, permanent brain organization. GID theoretically roots itself in the idea that individuals are prenatally wired for one sex, but identify as another in childhood. However, the hormones that aid in the neurological hard wiring of biological sex have a second activation at the onset of puberty, meaning that many children who felt that they were the wrong gender pre-puberty now feel gender satisfied as the hormones activate to create secondary sex characteristics. These new roles are “right” in 73-93% of gender-confused children (Zucker 2002; Asschemann, 2009). Because of the very small percentage of people feel lifelong gender dysmorphic, it seems that some individuals are born with a biological sex that his/her gender identity contradicts, while others grow up feeling unsatisfied with their gender until puberty sways the hormonal influence back toward their assigned sex in accordance with gender identity. Therefore, hormonal activation in the brain does not independently create gender identity, but it is a reliable predictor of gender identity confusion if the confusion extends into adolescent and into adulthood (Asschemann, 2009).
A recent study by Swaab (2007) reviews what is currently known about the sexual differentiation of the brain areas and what areas are responsible for gender identity, sex, and sexual orientation, including the effects of hormones. Sexual differentiation brings about permanent prenatal changes in brain structures and functions. This is due to interactions of the developing neurons with the environment—formed by surrounding nerve cells, hormones, nutrients, medication, and other chemical substances in utero (Swaab, 2007, p. 431). Specifically, testicles and ovaries develop in the 6th week of pregnancy due to genetic sex of the fetus. It is thought that hormonal influences at this time have a direct effect on the brain’s gender identity while biological sex is developing. Specifically, androgens produced by the Y chromosome account for the sexual differentiation between 6-12 week of pregnancy, while female development is based on the absence of androgens (Swaab, 2007).
Brain differentiation is due to influence of androgens on the developing brain that is permanent and organizational. In utero, hormonal influences on the brain peak at 34-41 weeks, then again 3 months after birth. The three month post birth period is considered arbitrary considering many sex-defining surgeries in cases of ambiguity are done right after birth with no further gender confusion. These two hormonal peaks organize and program the brain sexually for life with the presence/absence of testosterone (Swaab, 2007). Later, during puberty, brain circuits are activated by sex hormones and secondary sex character- istics develop. The rising hormone levels “activate” circuits that were built during development, and behavioral patterns and dis- orders that originate much earlier in development, such as schizophrenia, are expressed (Swaab, 2007). Sexual differentiation occurs in two independent processes that can result when people with male sexual organs feel female and vice versa in the brain (Swaab, 2007). Since there are two distinct activation periods of gendered hormones, Swaab’s research states that a discrepancy in gender identity and sex are routed in the brain’s chemistry.
Swaab (2007) generalizes these hormonal processes in brain structure and function:
Different brain structures that result from interaction between hormones and
developing brain cells are thought to be the basis of sex differences in the structure of
the brain, and thus of behavior, gender identity, gender role, sexual orientation, and sex
differences regarding cognition and aggression. (p. 433)
Thus, Swaab (2007) asserts that hormonal influence creates our biological sex as well as our gender identity and sexual orientation during development, but they are distinct in both development and identification. Therefore, there is no proof that social environment has any effect on gender identity or sexual orientation. While research does not yet completely explain the process by which gender identity is developed in the brain, such examples using specific intersex conditions offer possible future research findings.
Learning from Intersex Conditions and Socialization
Scholars researching gender indentify disorder and its possible causes and solutions learn from the information on the biologically concrete intersex conditions. Intersex individuals’ have an anatomical difference in their sexual organs different from individuals that are typically male or female (Zucker, 2002). In genetic boys with steroid 5-reductase 2 deficiency, a disorder that prevents testosterone from producing male genitalia, a “girl” with a large clitoris is born. These children, subsequently, are raised as girls and there is no cause to think otherwise until puberty when testosterone production increases and this “clitoris” grows to penis size, the testicles descend, and the child begins to appear masculine. 60% of these children choose to live as heterosexual men, even though they were raised as girls due to the brain organization that testosterone inflicts on the brain prenatally (Swaab, 2007). The remaining 40% of people with steroid 5-reductase 2 deficiency continue to live as women. Without taking sexual orientation into account, that is a significant percentage. Thus, the influence of hormones may not be strong enough to sway all brain organization toward one gender expression at any given time. Evidence from these cases of “explained” gender identity dysmorphia offers insight to GID itself, which is not associated with any type of physical difference to typically developing males and females.
In line with Swaab’s (2007) findings and the theories of John Money in the 1950’s, 40% of individuals with steroid 5-reductase 2 deficiency live as their socially constructed gender (Zucker 2002). Money spent his life trying to prove that gender identity was a product of society, a learned way of life. His famous John/Joan experiment involved a genetic male whose penis was damaged during circumcision and was subsequently raised as a girl. Much to John Money’s dismay, after childhood, “Joan” chose to live as a man and eventually committed suicide in May 2004. Therefore, gender identity is at least in part socially constructed, but there are clearly other factors at play.
As with steroid 5-reductase 2 deficiency, genetic girls who possess excess testosterone in the womb, or congenital adrenal hyperplasia do not always go on to identify as females when adults. Yet, they do not always go on to identify as male either. These girls tend to be “tomboys” as children, prefer boys as playmates, and are more aggressive than other girls (Zucker, 2002). These girls are also more likely to identify as lesbians or transsexuals than the rest of the population, but neither are always the case. The risk of transexuality in these girls is only 1-3% and those with serious gender problems are 5.2% leading to the consensus that these girls should be raised as girls despite the high levels of testosterone in utero (Swaab, 2007). Based on the current research, it is clear that neither hormones nor socialization create a definitive gender identity in the brain that can be used to predict gender from one case to the next.
Gender Identity in the Brain
Swaab & Garcia-Falgueras, (2008) believe the have isolated specific structures that may be responsible for gender identity in the brain. According to their research, this network of structures in the brain is responsible for gender and sexual orientation as both genetically and socially expressed (Swaab & Garcia-Falgueras, 2008). While differences in the number of neurons and size of the INAH-3 and BSTc were originally thought to be just sex differences, now with more careful analysis they can be viewed as the discrepancy between biological sex and gender identity.
These structures responsible for biological sex and gender identity are all separate parts in the brain, each with a different component and developmental trajectory. Such research supports the idea that gender identity and biological sex can be thought of as separate from individual identity. The structures, all of which are related to the SDN-POA (Sexually Dimorphic Network), include the INAH1 and 2, which are related to the SCN, the BSTc, and the INAH3 and 4, which are all located in the hypothalamus of the brain (2008). Each of these structure differs from person to person based on lifestyle lived. For example, adult Male- to- Female transgender individuals who receive no hormone injections or surgery in their lifetime have an INAH-3 volume of a male, but a neuron number of a female. On the other hand, hormone-treated Male-to-female transgender individuals have an intermediate value and a BSTc the size of typical female. However, the hormone treatments are not believed to have caused this change (Swaab & Garcia-Falgueras, 2008). Swaab and Garcia-Falgueras’s (2008) findings indicate that the brain chemistry of individuals who identify as transgender is different from those individuals who do not, regardless of the presence of hormone treatment.
An individual who is exclusively attracted to women has an INAH-3 volume of a male because it is believe that the volume of the INAH-3 structure displays that of sexual orientation and has no correlation to the size of the BSTc, which is believed to be representative of personal gender identity (Swaab & Garcia-Falgueras, 2008). Therefore, these structural differences cannot be accounted for by hormone treatment or castration later in life. Instead, the differences are representative of early developmental abnormalities and differences during the critical fetal periods opposed to non-transsexuals. Therefore, the possible cause of atypical gender presentation presumes a combination of genetic background and early organizational effect on the interaction of sex hormones with the developing brain during critical fetal periods (Green & Keverne quoted in Swaab & Garcia-Falgueras, 2008). Individuals who have lifelong GID experience different hormonal breakdown, different gender role transition, and different sexual organizational effects in their brains than individuals without GID. Sexual differentiation of the brain occurs later in development and can be influenced independently of genital differentiations; the resulting modifications in brain structures in transsexual people are hypothesized to be the basis of GID (Swaab & Garcia-Falgueras, 2008). With the tools to differentiate the gender identity structure and the biological sex structure, it is clear that specific measures can be developed to better understand GID. Firstly, both gender identity and biological sex structures remain atypical in transgendered people with or without reassignment therapy throughout the lifespan, suggesting that gender identity is hardwired at birth (Swaab & Garcia-Falgueras, 2008). This finding is the key to understanding that gender identities that are not “normal” are not necessarily unhealthy or physiologically maladaptive.
Conclusion
Researchers in the field of sex and gender are on the brink of understanding a wealth of knowledge about the brain’s gender expression. However, to make decisions about children’s lives based on assumed knowledge is premature. There are several genetic and inborn intersex conditions and syndromes that leave society wanting to “fix” the problem by uprooting natural anatomy, yet similar gender confusions exist without this anatomical disruption. These individuals are labeled gender identity disordered in childhood and many go on to identify as transgender as adults. The “cure” for the gender problem must be related to on a case-by-case basis until more neurological information is available to actually “test” for such a discord between brain and body. There is a great need for more research in the area so that young children do not have to suffer with an identity imposed by society that leads to psychological distress and disorder in addition to not feeling at home in one’s own body. For the first time, neurological findings conclude that there are differences in gender identity in the brain. Swaab’s (2008) findings isolate differences between transgender individuals and those of the assigned and identifying sexes. This research offers the first glance into the richness of a transgendered individual’s brain. Indentifying as one gender and looking like another can one day be a source of pride and insight, yet the lack of dissemination of this information leaves most, if not all, gender deviant children struggling with this completely alone. Their isolation for resources and clinical support leads to poor self identity and self esteem and can even lead to adulthood substance abuse and Axis 1 psychiatric disorders. All of this could result because a child feels he cannot express his or her true self.
Researchers in the field of gender and sexual identity have a responsibility to create effective management models for identity development. Currently, treatment is necessary to help children feel comfortable with their gender expression when it is non-normative. Neurological researchers are still struggling to understand the real difference between people with these afflictions, but during this time it is wrong to call the confusion a disorder before it is fully understood, as scientists did until the 1970’s with homosexuality. Neither the affects of prenatal and puberty hormones nor socialization alone are enough to explain gender identity development, the process must lie in a brain structure. Perhaps someday, when society catches up with research, there will be no need to force a gender upon a child and the desire to live as another gender will not be considered a disorder at all.
References
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.
Asscheman, H. (2009). Gender identity disorder in adolescents. Sexologies, 18, 105-108.
Coolidge, F., Thede, L., & Young, S. (2002). The heritability of gender identity disorder in a child and adolescent twin sample. Behavior Genetics, 22(4), 251-257.
Hepp, U., Kraemer, B., Schnyder, U., Miller, N., & Delsignore, A. (2005). Psychiatric comorbidity in gender identity disorder. Journal of Psychosomatic Research, 58, 259-261.
Simonelli, C., Rossi, R., Tripodi, M. F., DeStasio, S., & Petruccelli, I. (2006). Gender identity disorder and preadolescence: A pilot study. Sexologies, 16, 22-28.
Swaab, D., & Garcia-Falgueras, A. (2008). A sex difference in the hypothalamic uncincate nucleus: Relationship to gender identity. Brain, 131, 3132-3146.
Swaab, D. (2007). Sexual differentiation of the brain and behavior. Best Practice and Research Clinical Endocrinology & Metabolism, 21(3), 431-444.
Zucker, K. (2002). Intersexuality and gender identity differentiation. Journal of Pediatric and Adolescent Gynecology, 15, 3-13.
Zucker, K. (2006). Commentary on Langer and Martin’s (2004) “How dresses can make you mentally ill: Examining gender identity disorder in children.” Child and Adolescent Social Work Journal, 23, 533-555.