Tag Archives: gay

Gender Identity Disorder and Anorexia Nervosa in Male Monozygotic Twins – Review

This is a fascinating study of identical twins; one had gender dysphoria and one did not. Both twins developed anorexia.

Both twins were feminine in behavior from a young age and both were sexually attracted to men. Both had a difficult childhood with an abusive father.

Both twins were underweight at birth and needed intensive care. Both had developmental delays.

However, one twin considered himself to be a gay man while one identified as a straight woman.

In this case study, gender dysphoria did not cause the eating disorder.

This case highlights the importance of other factors in eating disorders, including genes, hormones, and trauma.

It raises the question; how important is gender identity as a cause of eating disorders?

This case is different from other case studies where gender dysphoria seems to be intimately linked to the eating disorder.

We can’t look at these two patients and conclude that gender dysphoria never contributes to eating disorders. However, this case is a good reminder to be cautious about drawing conclusions from other case studies. Perhaps there are just some people with eating disorders who also have gender dysphoria. Or perhaps there is some other factor which causes both eating disorders and gender dysphoria.

As always, we need more studies.

More about the Patients:

Eating Disorders

Twin A was diagnosed with AN-purging subtype and Twin B was diagnosed with AN-restricting subtype.

Twin B developed an eating disorder at an earlier age, but Twin A was more underweight and had a more disturbed perception of his body. Furthermore, Twin A was hospitalized for his eating disorder and Twin B was not.

Neither twin seems to have been able to maintain a healthy weight.

At age 16 Twin A “was admitted to a children’s hospital because of AN. Later, he was hospitalized in the psychiatric inpatient unit for adolescents. At first, his eating behavior was restrictive. Then he reported intermittent vomiting (AN binge-purge). His weight decreased to 46 kg/1.79 m (body mass index [BMI] ¼ 14.3 kg/m²). His ideal weight was 44 kg according to a BMI of 13.7 kg/m² , which shows his severe disturbance in body perception. During hospitalization, his behavior was sometimes aggressive. He was emotionally unstable, depressed, and was rarely able to engage in stable relationships. Despite strict dietary rules, he achieved a maximal weight of 55 kg (BMI ¼ 17.2 kg/m²). Soon after being discharged, his weight decreased again.”

Twin B’s eating disorder began at a younger age. “In puberty, he developed severe underweight. At the age of 13, he was 42 kg/1.58 m (BMI ¼ 16.8 kg/m² ). When he was referred to our outpatient unit at the age of 18½ years [for gender dysphoria], his weight was 48 kg and his height was 1.76 m (BMI ¼ 15.5 kg/m² ). He denied deliberate dieting, binging, or purging. Although he regarded himself as too slim, he did not manage to gain weight. Further medical checkups revealed no somatic cause for his underweight. An osteodensitometry yielded an osteopenia of the spine.”

Gender Identity

Twin A was a gender non-conforming gay male:

In childhood, he preferred girls’ games and toys (Barbie dolls) and was very close to his twin brother. His sexual feelings were always for males. Although he started cross-dressing at the age of about 16 years, his gender identification was always male. He considered himself to be a homosexual.”

Twin B was a trans woman:

“As far as he could remember, he had felt he was a girl, preferring girls as playmates and had started cross-dressing at nursery school. In gymnastic lessons, he refused to change with the other boys because he was ashamed of his body. Eventually, he refused to attend sports lessons at all. When he was 9 years old, he started to grow his hair. His class mates seemed to accept him as a girl. When he started to work as a hairdresser, he tried to correspond to the male gender role and did not cross-dress. However, at his professional school and in his free time, he continued to cross-dress. His employer, who realized he was transsexual, permitted and encouraged him to cross-dress at work, which consequently allowed him to live as a young woman. Sexually, he was always attracted to men. However, in contrast to his brother, he never considered himself to be homosexual and viewed this attraction as ‘‘heterosexual.’’ Until this point, he had not engaged in sexual relationships either with men or with women.”

Twin B requested hormonal and surgical sex reassignment.

Childhood

The twins grew up together in a small Swiss city without any other siblings. Their childhood was not easy:

“[Their father] was very authoritarian. He could not accept the sexual orientation and the cross-dressing of his sons and threatened them with assault and even with death.

…In family conflicts, [their mother] took a position between her husband and her sons. At a family consultation, she appeared emotionally unstable.”

Birth 

The birth was a difficult one. Both twins were underweight and spent time in intensive care.

“the mother had been admitted to a hospital with hypertension, edema, and proteinuria at 38 weeks of gestation. The vaginal delivery was induced because of maternal preeclampsia. Twin A weighed 2.17 kg at delivery and his Apgar score was 9/9/9. Because of perinatal acidosis and hypotonia, he was kept in the incubator for 3 days. He was diagnosed with a subependymal hemorrhage with ventricular invasion. Twin B’s birth weight at delivery was 1.95 kg and his Apgar score was 7/9/9. Both twins were admitted immediately to the neonatal intensive care unit.”

Developmental Delays

They both had developmental delays:

“In early childhood, Twin A showed a developmental delay in language and motor skills and had deficits in cognitive and verbal skills. He was socially isolated and his behavior was often aggressive.”

“…Twin B had delays in language and motor development during early childhood. He showed the typical symptoms of attention deficit and hyperactivity disorder. The parents refused further assessment and treatment.”

Other

Twin A was diagnosed with borderline personality disorder and subnormal verbal intelligence.

Twin B was diagnosed with gender dysphoria.

There is no obvious pattern to any of this. Twin A was larger at birth, but had more problems right after birth. Both had developmental delays, and Twin B may have had ADHD as well. Both were feminine in their behavior, but only Twin B developed gender dysphoria. Both were sexually attracted to men. Twin B developed an eating disorder earlier, but Twin A’s eating disorder seems more severe. Twin A has borderline personality disorder and Twin B does not.

Discussion

The authors offer two possible hypotheses about the twins’ gender identity.

Perhaps the twins are on a continuum of gender non-conformity where gender dysphoria is at the extreme end.

Alternatively, perhaps gender dysphoria* in childhood is inherited, but the later development of gender identity is determined by environmental factors and psychiatric comorbidity.

“In childhood, both Twin A and Twin B showed gender atypical behavior and stereotypical feminine traits and interests. In adolescence, their sexual orientation was revealed to be homosexual. Twin A developed effeminate homosexuality with male gender identity, whereas Twin B stabilized his cross-gender identity. Although Twins A and B are concordant for GID in childhood and sexual orientation on a categorical level, they are now discordant for TS. On a more dimensional level, one could argue that Twins A and B show an opposite sex-dimorphic behavior and that they arrived at different points of a continuum. The fact that GID in childhood is a predictor for later homosexuality and TS could support the dimensional view. It could be hypothesized that GID in childhood is mainly hereditary, whereas the development of the later phenotype of the gender identification is determined by environmental factors and psychiatric comorbidity, as any difference between MZ twins provides strong evidence for the role of environmental influences.”

The authors also discuss the relationship between gender and eating disorders. However, they don’t address the fact that the two twins had different gender identities, but both had eating disorders.

Perhaps both gay men and trans women are vulnerable to eating disorders for different reasons, but perhaps genes, hormones, and environment matter more than gender identity.

“Homosexual men seem to have an increased vulnerability to eating disturbance and body dissatisfaction (Williamson & Hartley, 1998), are more dissatisfied with their weight (French, Story, Remafedi, Resnick, & Blum, 1996), and are more concerned about their attractiveness (Siever, 1994). Male AN is associated with disturbed psychosexual and gender identity development, which supports the hypothesis that males with atypical gender role behavior have an increased risk of developing an ED (Fichter & Daser, 1987). Furthermore, feminine gender traits are discussed as a specific risk factor for ED in men and women (Meyer, Blissett, & Oldfield, 2001). Although the role of sexual orientation as a risk factor for ED is well documented, there is hardly any literature about GID and ED. For men with disturbance of gender identity in addition to the aforementioned factors concerning sexual orientation, underweight could be a way to suppress their libido and the expression of their secondary sexual characteristics and, at the same time, correspond to a female ideal of attractiveness (Hepp & Milos, 2002).”

We need more research!

“Further research in eating behavior and body dissatisfaction in patients with GID could provide more insight into the role of gender identity in the development of ED and lead to a better understanding of ED as well as GID.”

 

* In this case, gender non-conformity might be a more fitting phrase. Twin A does not seem to have ever wanted to be a girl.

 

Original Source:

Gender Identity Disorder and Anorexia Nervosa in Male Monozygotic Twins by Urs Hepp, Gabriella Milos, and Hellmuth Braun-Scharm in Int J Eat Disord. 2004 Mar;35(2):239-43.

 

Review – Diverging Eating Psychopathology in Transgendered Eating Disorder Patients: A Report of Two Cases

These are two somewhat unusual case studies from Singapore. Once again, there is a connection between eating disorders and gender identity. Once again, the connection is different from other case studies.

Case 1 – A Fluid Gender Identity and an Eating Disorder

In the first case, the patient had a fluid gender identity; sometimes he identified as a man and sometimes as a woman.

When he identified as a woman, he restricted his food and exercised excessively. He wanted to be thin and felt a kinship with emaciated women because they were infertile like him.

When he identified as a man, he tried to gain weight and muscles, but his exercise and eating habits were still pathological.

The patient was always distressed and dissatisfied with his body.

In other words, his gender identity affected the form his eating disorder took, but it was probably not the cause of it.

Case 2 – Changing Gender Identity, Changing Eating Patterns

In the second case, the patient identified as a woman when he first sought treatment for his eating disorder. However, after a year of treatment, the patient came out to his friends as gay. They were accepting of his sexual orientation and he became more comfortable with a male gender identity.

Similarly to the first case, when the patient wanted to be a woman, he tried to become thin, using restricted eating, excessive exercise, and purging. However, when he began to identify as a male, he tried to build up his muscles and he ate more.

The authors do not comment on whether or not this patient still disliked his body.

The authors suggest that gender identity influences the form of body psychopathology; constructing your gender identity is linked to constructing your body. However, they do not suggest that gender dysphoria caused the eating disorders or that treating the gender dysphoria will cure them.

These two cases support their theory, but it is important to remember that this is a case study of two people. So far, the main conclusion I can draw from various cases studies is that each person’s story is different.

From the Discussion:

“The present case series describes two transgendered biological males seeking treatment for eating disorders, whose intermittent periods of endorsing both masculine and feminine gender identities impacted significantly upon their experience of eating disorder psychopathology. The two patients indicated that during periods of endorsing a feminine gender identity, they experienced an elevated definite drive for thinness, such that their body image psychopathology was oriented towards weight loss, reporting dietary restriction and cardiovascular exercise to lose weight. Furthermore, both patients reported that during periods of masculine gender identity endorsement, their body image psychopathology was oriented towards weight gain with an emphasis on “buff muscularity,” reporting increased food intake and muscle building exercise regimens.

This case series draws attention to the potential role of masculinity and femininity in body image psychopathology amongst males. Both patients depicted reported that the variation in their eating disorder psychopathology was concordant with their preferred gender identity, suggesting that the construction of one’s gender identity and the construction of one’s body may be interrelated.”

More details on the gender shift in the second case study:

At the beginning of treatment,

“…he reported homosexual sexual orientation and described privately wondering whether he was born into the wrong gender from approximately age 6. He reported periodically ‘trying to like girls’ due to the cultural and legal ramifications of homosexuality in his country of origin [probably China], and further stated that on many occasions his sexual orientation resulted in him feeling victimized and bullied. Patient Z reported significant discomfort with his sexual orientation, although he did report a female gender identity, which allowed him to experience his secretive same sex relationships as heterosexual given his assumed female identity.”

Before treatment, when he was restricting his food and purging,

“Patient Z reported immense discomfort surrounding his emerging sexual orientation, and reported strongly endorsing a female identity which enabled Patient Z to experience his same-sex attraction as heterosexual, alleviating the subjective distress and internal conflict he experienced in his homosexual urges. Patient Z described his role models to be female supermodels, stating that he aspired to their thin and feminine frames, adding that his gaunt appearance brought about by dietary restriction ‘accentuated his cheekbones’ and helped him identify with his female role models. Patient Z reported egosynotonicity of eating disorder symptomatology, allowing him to feel ‘small and more like a woman’ which he demonstrated in a collection of drawings depicting emaciated women, which he described as his ideal body.”

But then,

“Approximately 12 months into treatment Patent Z revealed his sexuality to his friends, whose acceptance and support reportedly alleviated the internal conflict he experienced around his same-sex attraction. As a result Patient Z reported reduced ambiguity surrounding his gender identity, describing more comfort in identifying with a male gender identity. During this same period, Patient Z developed a desire for muscular development as opposed to emaciation, and started a muscle building training regimen. Furthermore, this period was also characterized by Patient Z consuming greater quantities of food in support of his desire for greater muscularity.”

Original Source:

Diverging Eating Psychopathology in Transgendered Eating Disorder Patients: A Report of Two Cases by Murray SB, Boon E, Touyz SW in Eat Disord. 2013;21(1):70-4.

Evidence for an Altered Sex Ratio in Clinic-Referred Adolescents with Gender Dysphoria – Review

This is a highly significant study showing that the population of teenagers referred for gender dysphoria is changing. It is noteworthy that this is happening in two different countries.

The sex ratio is changing:

The sex ratio of teenagers seeking help for gender dysphoria has changed at two clinics, one in Canada and one in the Netherlands.

Before 2006, more male than female teenagers sought transition at these clinics. Since 2006, they have seen more female teenagers than male teenagers.

Sex ratio for teenage patients at the Canadian Gender Identity Service:

  • 1999-2005 – 68% male, 32% female
  • 2006-2013 – 36% male, 64% female

Sex ratio for teenage patients at the Dutch Center for Expertise on Gender Dysphoria:

  • 1989-2005 – 59% male, 41% female
  • 2006-2013 – 37% male, 63% female

At the Canadian clinic, there was no change in the sex ratio of teenagers referred for psychiatric issues.* In both time periods, roughly two-thirds of their other patients were male.

According to the authors, “In adult samples [of transitioners], in almost all cases, the number of natal males either exceeds the number of natal females or the sex ratio is near parity.” Poland and Japan are exceptions; in those countries more females transition than males.

In addition, clinics for children with gender dysphoria have found that the number of males exceeds the number of females.

More teenagers are transitioning:

The number of teens of both sexes has increased over time, although the increase is larger for the female teenagers.

Increases at the Canadian clinic:

Female teenagers

  • 46 in 30 years (1976-2005)
  • 129 in 8 years (2006-2013)

Male teenagers

  • 80 in 30 years (1976-2005)
  • 73 in 8 years (2006-2013)

Increases at the Dutch clinic:

Female teenagers

  • 77 in 17 years (1989-2005)
  • 148 in 8 years (2006-2013)

Male teenagers

  • 109 in 17 years (1989-2005)
  • 86 in 8 years (2006-2013)

In other words, the Canadian clinic saw nearly nearly three times as many female teens in the past 8 years as they had seen in the previous thirty. The Dutch clinic saw nearly twice as many female teens in the past 8 years as they had seen in the previous seventeen.

Furthermore, “For many years in the Toronto clinic, the number of adolescent referrals was quite low. Between 1976 and 2003, for example, no more than five adolescents of one biological sex were assessed in a calendar year and, during this period, the number of males exceeded the number of females. Beginning in 2004, however, the number of adolescent referrals began to rise quite dramatically, which appears to be consistent with the observations of clinicians and researchers from other gender identity clinics.”

For earlier data on the increase in Canada, see this article.

Sexual orientation percentages have changed:

The Canadian clinic also looked at sexual orientation.

Sexual orientation of females:

  • 1976-2005 – 89% primarily attracted to females; 11% other
  • 2006-2013 – 64% primarily attracted to females; 36% other

Other could mean primarily attracted to males, bisexual, or asexual.

Sexual orientation of males:

  • 1976-2005 – 67% primarily attracted to males, 33% other
  • 2006-2013 – 44% primarily attracted to males, 56% other

Other could mean primarily attracted to females, bisexual, or asexual.

To put it another way, in the past most of the teenagers would have been gay if they weren’t transgender. If they transitioned, they would live their lives as straight people.

In 2006-2013 most of the male teenagers would have been straight, bisexual, or asexual if they weren’t transgender. If they transition, some of them will live their lives as lesbians.

One-third of the female teenagers in 2006-2013 would have been straight, bisexual, or asexual if they weren’t transgender. If they transition, some of them will live their lives as gay men.

What’s going on?

Why are we seeing more teenagers seeking help for gender dysphoria?

Why is the increase greater among female teens than males?

And why are we seeing a shift in the sexual orientation of these teens? Was it harder in the past to come out as transgender if you were seen as straight? Or is this a group of people who were less likely to have gender dysphoria in the past?

Has something changed in our environment that increases the number of people with gender dysphoria? What would affect more females than males? Why would it affect teenagers more than children (see this earlier article)? How would it fit with the changing percentages related to sexual orientation?

Is it just that there were always this many teenagers with gender dysphoria and now they are able to get care at an earlier age? How does that theory fit with the change in the sex ratio of teens applying to the clinic? with changes in their sexual orientation?

Clearly, we need more research to sort out these questions.

The authors speculate about possible explanations for the change in the sex ratio at their clinics.

They suggest that the general increase in patients might be due to a combination of destigmatization and more awareness of the biomedical treatments available to teens. However, they point out that this does not explain why more females would apply for treatment.

I don’t think we can know why the number of patients has increased without further research – research which is desperately needed.

The increase in the number of female patients at the Toronto clinic was not caused by a change in the severity of cases; they found that there was no significant relationship between severity of dysphoria and year assessed.

However, for male teens in Toronto, there was a weak correlation between severity of dysphoria and year assessed. “More recently assessed cases had moderately higher GD severity.” This only explained 6.7% of the variance. Therefore “it is unlikely that the recent inversion in the sex ratio can be accounted for by a substantive change in severity variation.”

On the other hand, they only have data on the severity of dysphoria starting in 2001 and the number of cases began increasing in 2004.

The change in the sex ratio was not due to females entering puberty at an earlier age; both clinics found no significant difference for the mean ages when females and males came to the clinic.

The sex ratio did not change due to the shift in sexual orientation. A logistical regression analysis did not find evidence for a sex x sexual orientation interaction.**

The authors suggest that perhaps the explanation for the change in the sex ratio is that it is harder for males to transition to a female role than for females to transition to a male one.

I find this unconvincing as this would have been true in the past when more male teenagers than females applied to their clinic. Nor would this hypothesis explain the shift in sexual orientation.

Here is their full explanation:

“Given that there is at least some overlap in the gender-variant developmental histories of early-onset individuals with GD and some gay men and lesbians, it might, therefore, be asked whether or not degree of stigmatization for gender-variant behavior might account for the recent inversion in the sex ratio of GD adolescents. It is well-known that cross-gender behavior in children is subject to more social stigma (e.g., peer rejection and peer teasing) in males than in females, in both clinic-referred adolescents with GD and in the general population[26–30]. Thus, it could be argued that it is easier for adolescent females to “come out” as transgendered than it is for adolescent males to come out as transgendered because masculine behavior is subject to less social sanction than feminine behavior. Some support for this was found in Shiffman’s [31] study of peer relations in adolescents with GD, in which adolescent males with GD reported more “social bullying” than adolescent females with GD. Given that a transgendered identity as an “identity option” has become much more visible over the past decade, it is conceivable, therefore, that such an identity option is easier for females to declare than it is for males because it does not elicit as much of a negative response. Thus, it could be argued that it is this sex difference in degree of stigmatization that accounts for the inversion in the sex ratio that we have identified in the two studies reported here. In other words, there are greater costs for a male to adopt a female gender identity in adolescence than it is for a female to adopt a male gender identity.”

A few more details about this study:

The first study looked at 328 teens (13-19) who were referred to the Toronto clinic between 1976 and 2013. The mean age at the time of referral was 16.66 years with no difference between the ages of males and females.

All of the teens met criteria for Gender Identity Disorder or Gender Identity Disorder Not Otherwise Specified. They were diagnosed using criteria in the relevant version of the DSM – this changed over time. The assessment of severity of dysphoria began in 2001.

The control group was 6,592 teens referred to their general clinic for psychiatric issues between 1999-2013. Eleven teens originally referred for psychiatric issues who were later referred to the Gender Identity Service were not included in this group.

The teens’ sexual orientation was determined by either clinical chart data or measurements on the Erotic Response and Orientation Scale and the Sexual History Questionnaire. This data was not available for five probands (aka people in this study).

The numbers for the sexual orientation of the teens at the Canadian clinic were:

1976-2005 (30 years)

  • 52 males primarily attracted to males
  • 26 males in the “other” category
  • 39 females primarily attracted to females
  • 5 in the “other” category

2006-2013 (8 years)

  • 32 males primarily attracted to males
  • 41 males in the “other” category
  • 82 females primarily attracted to females
  • 46 females in the “other” category

The clinic did not have data on the sexual orientation of five of the teenagers.

The second study looked at data on 420 teenagers (13 and up) referred to the Dutch clinic between 1989-2013.  Their mean age at the time of assessment was 16.14 and there was no significant age difference between males and females.

The second study did not include data on sexual orientation or a control group for comparison.

“The percentage of female adolescents from Amsterdam in the first time period did not differ significantly from the percentage of female adolescents from the Toronto clinic, and the percentage of female adolescents from Amsterdam in the second time period also did not differ from the percentage of female adolescents from the Toronto clinic, both χ2(1) < 1.”

This study is a follow-up to two earlier letters to the editor about changes in the teenage population at the clinic in Toronto: Is Gender Identity Disorder in Adolescents Coming out of the Closet? and Patterns of Referral to a Gender Identity Service for Children and Adolescents (1976–2011): Age, Sex Ratio, and Sexual Orientation.

The first letter discussed a rise in teenagers referred to the Canadian clinic between 2004-2007. The second letter discussed the continued increase in referrals from 2008-2011 and raises the question of a possible change in the sex ratio in 2008-2011.

Original Article:

Evidence for an Altered Sex Ratio in Clinic-Referred Adolescents with Gender Dysphoria by Aitken M1, Steensma TD, Blanchard R, VanderLaan DP, Wood H, Fuentes A, Spegg C, Wasserman L, Ames M, Fitzsimmons CL, Leef JH, Lishak V, Reim E, Takagi A, Vinik J, Wreford J, Cohen-Kettenis PT, de Vries AL, Kreukels BP, Zucker KJ in J Sex Med. 2015 Mar;12(3):756-63. doi: 10.1111/jsm.12817. Epub 2015 Jan 22.

* The Canadian clinic is the Gender Identity Service, within the Child, Youth, and Family Services (CYFS) at the Centre for Addiction and Mental Health in Toronto. The clinic in the Netherlands is the Center of Expertise on Gender Dysphoria at the VU University Medical Center in Amsterdam. This may explain why we have a comparison group for the Canadian patients with gender dysphoria, but not the Dutch ones.

**  “In the cohort examined in Study 1, perhaps it could be argued that, in the first time period, the greater number of biological males than biological females was an artifact of there being two prominent subtypes of GD (androphilic and nonandrophilic) in the former, whereas the latter were predominantly of only one subtype (gynephilic), but that this shifted in the second time period, with a greater number of females with a nongynephilic sexual orientation. However, the logistic regression analysis shown in Table 4 did not provide evidence for a sex × sexual orientation interaction. It only showed that a nonandrophilic or nongynephilic sexual orientation increased the odds that a proband presented in the second time period, but sexual orientation did not interact with probands’ biological sex.”

Patterns of Referral to a Gender Identity Service for Children and Adolescents (1976–2011): Age, Sex Ratio, and Sexual Orientation – Review

This is a follow-up to an earlier letter to the editor calling for research and discussion on the subject of teenagers with gender dysphoria. The authors had seen a sharp increase in the number of teenagers referred to their Toronto clinic between 2004 and 2007.

You can read about some new, related data here.

In this letter, the authors report that:

Cases of teens with gender dysphoria are still increasing.

Between 2008-2011 the number of teenagers referred to their clinic increased even further.

Based on their graph, before 2000, they saw fewer than 20 teenagers in a four year period. From 2004-2007 they saw about 55 teens and from 2008-2011, they saw about 95. In other words, the number of teen patients they saw more than quadrupled.

usmt_a_675022_o_f0001g (1)

By my calculations, about two-thirds of their teenage patients in the last 36 years came to the clinic between 2000 and 2011; over half came to the clinic in the last 8 years between 2004 and 2011.

In contrast, the number of cases of children with gender dysphoria increased sharply in 1988-1991, but has been reasonably stable since then.

Looking at their graph again, between 1988 and 2011 they saw 75 to 90 children in a four year period. The children who came to the clinic between 2004 and 2011 only make up 29% of the child patients they’ve seen in the past 36 years.

In 2008-2011, the number of teenagers at their clinic was larger than the number of children for the first time ever.

From 1976-2004, the number of children at their clinic was much higher than the number of teens. The number of teens increased greatly after 2004, but was still lower than the number of children at their clinic.

The sex ratio of their teenage patients may be changing.

For teenage patients, the sex ratio was close to even, ranging from 1.03:1 boys to girls in 2004-2007 to 3:1 in 1976-1979. There were two time periods when they saw more female teenagers than males: 1988-1991 and the most recent group in 2008-2011.

***Spoiler alert – a 2015 study found that the sex ratio has indeed changed from more boys to more girls. This was true for both this clinic and a Dutch one. More later.***

It is important to remember that the numbers of both male and female teenage patients increased starting in 2004.

The increase in female teenagers is much more striking. Based on the graph below they went from fewer than 10 patients every four years prior to 2000 to nearly 60 patients from 2008-2011.

However, male teenage patients also increased. They went from about 5-15 patients every four years prior to 2000 to about 35 patients from 2008-2011. In 2004-2007 the number of male and female teenage patients was nearly equal.

usmt_a_675022_o_f0002g

The authors also discuss the pattern of sex ratio by age. Putting the data from different time periods together, from ages 12-16, there were slightly more boys than girls. However, at age 17-18, there were more females than males, and at age 19-20, the sex ratio shifted again to 2.4 boys to 1 girl.

Sexual orientation

The authors had data on sexual orientation for 98% of the teenagers they saw.* Of these 76% of their female teenage patients were sexually attracted to females while 56.7% of their male teenage patients were sexually attracted to males.**

The sex ratio for child patients is different than for teenage patients.

The overall sex ratio for children was 4.49 boys to 1 girl. For 3 year olds, the sex ratio was 33 boys for every girl.***

From 1976-1996, over 75% of their child patients were boys, from 2001-2011 the percentage hovered around 75%.

What does this mean?

We don’t know why more teenagers are seeking help at this clinic. Are there more teenagers with gender dysphoria than in the past? If so, why? What would make gender dysphoria increase among teenagers and not among children? Are people with gender dysphoria simply able to get help at an earlier age?

As always, we need more research!

The authors provide some interesting insights:

“Regarding the increase in adolescent referrals, it is, of course, not clear if it reflects a true increase in prevalence (which can only be established via epidemiological studies) or if it simply reflects a greater willingness on the part of youth to come out as transgendered, perhaps because of the influence of social media in which there are dozens, if not hundreds, of websites and blogs that assist youth in understanding their own identity and its concomitant struggles. We have been impressed, for example, in recent years with youth describing to us that they never realized that their feelings could be named in a formal way (gender identity disorder, transgender, trans). One might infer that the Internet has made much more visible terminology used in technical journals. 

Another parameter that has struck us as clinically important is that a number of youth comment that, in some ways, it is easier to be trans than to be gay or lesbian. One adolescent girl, for example, remarked, “If I walk down the street with my girlfriend and I am perceived to be a girl, then people call us all kinds of names, like lezzies or faggots, but if I am perceived to be a guy, then they leave us alone.” To what extent societal and internalized homonegativity pushes such youth to adopt a transgendered identity remains unclear and requires further empirical study. Along similar lines, we have also wondered whether, in some ways, identifying as trans has come to occupy a more valued social status than identifying as gay or lesbian in some youth subcultures. Perhaps, for example, this social force explains the particularly dramatic increase in female adolescent cases in the 2008–2011 cohort.

Another factor that has impressed us in accounting for the increase in adolescent referrals pertains to youth with gender identity disorder who also have an autism spectrum disorder. As noted by others (de Vries, Noens, Cohen-Kettenis, van Berckelaer-Onnes, & Doreleijers, 2010), many clinicians are now reporting a co-occurrence of these two conditions.

More than 10 years or so ago, it was rare in our clinic to see an adolescent with gender identity disorder who also appeared to have an autism spectrum disorder. It is possible, therefore, that the apparent increase in the number of adolescents who present with a co-occurring autism spectrum disorder is contributing to the increase in the number of referrals. Over the past decade, a great deal of media attention has been given to the use of hormonal therapy to treat gender dysphoria in adolescents, including the use of “blockers” to either delay or suppress somatic puberty (Cohen-Kettenis, Steensma, & de Vries, 2011; Zucker et al., 2011). In the province of Ontario, its health care system relisted sex reassignment surgery as an insured medical treatment in 2008 after having been delisted in 1998 (Ministry of Health and Long-Term Care Processing Sites, 2008; Radio Canada, 2008). Perhaps the availability again of insurance coverage has led to more adolescents seeking treatment. Whatever the explanation for the increase in adolescent referrals, it appears that gender identity disorder in adolescents has come out of the closet, although there may be different closets from which to come out.”

A few more details about the data:

The children were significantly more likely to be living in two-parent homes than the teens (66% versus 46%).

Most of the patients were white; 80% of the children and 76% of the teens.****

The study included 577 children (3-12 years old) and 253 teens (13-20 years old).

The study excluded “26 boys referred for fetishistic cross-dressing and referred adolescents who were diagnosed with transvestic fetishism (without co-occurring gender dysphoria), gay youth, and youth who were ‘undifferentiated'”.

Original Source:

Patterns of Referral to a Gender Identity Service for Children and Adolescents (1976–2011): Age, Sex Ratio, and Sexual Orientation by Wood H, Sasaki S, Bradley SJ, Singh D, Fantus S, Owen-Anderson A, Di Giacomo A, Bain J, Zucker KJ. in J Sex Marital Ther. 2013;39(1):1-6.

* 248 teenagers out of 253 total.

** The authors classified the teenagers as homosexual or nonhomosexual in relation to birth sex.

***It may be that parents are more worried about boys who are gender non-conforming than girls so more boys are referred to the clinic. By adolescence the teenagers might play more of a role in coming to the clinic.

**** Yup, we need more research on people with gender dysphoria who aren’t white.

You can read more in the follow-up study, Evidence for an Altered Sex Ratio in Clinic-Referred Adolescents with Gender Dysphoria.

The Science Behind Suicide Contagion – New York Times Article

Reposting this for the holidays. There have been more trans teenagers and adults who committed suicide since I wrote this article. We need to do anything we can to stop this.

“When Marilyn Monroe died in August 1962, with the cause listed as probable suicide, the nation reacted. In the months afterward, there was extensive news coverage, widespread sorrow and a spate of suicides. According to one study, the suicide rate in the United States jumped by 12 percent compared with the same months in the previous year.

Mental illness is not a communicable disease, but there’s a strong body of evidence that suicide is still contagious. Publicity surrounding a suicide has been repeatedly and definitively linked to a subsequent increase in suicide, especially among young people. Analysis suggests that at least 5 percent of youth suicides are influenced by contagion.”

Read more: The Science Behind Suicide Contagion, The New York Times, August 2014.

I am posting this link because last Sunday a transgender teenager committed suicide after posting a suicide note on Tumblr.

This came about a month and a half after another widely discussed case of a transgender teenager who committed suicide after posting a suicide note on Tumblr.

Two days ago another transgender teen posted on Instagram that they were going to commit suicide. They made multiple references to the first two teenagers – they wondered what selfie people would use to talk about them and would they get a hash tag? It is not clear what happened to the third teenager, although they posted a suicide note that was later taken down.

I believe some of my readers are parents of teens. Hug them, love them, compliment them. Talk to them about this issue.

Sources of Help and Information:

Trans Lifeline for trans people:

  • US number: 1-877-565-8860
  • Canadian number: 1-877-330-6366
  • and their website.

The Trevor Lifeline for LGBTQ youth (US) – 1-866-488-7386 and their website.

National Suicide Prevention Lifeline (US): 1-800-273-TALK (8255) and their website.

The International Association for Suicide Prevention – their website has an interactive map with phone numbers and locations of crisis centers.

From Maria Shriver’s blog, Powered by Inspiration.

Two Years After My Suicide Attempt, I’m Still Living and Sharing

“Waking up two years ago gave me opportunities, some of which seem obvious but some of which I’m still discovering. I have the opportunity to continue the life I began and do the things I want to do. I have the opportunity to offer help to people who would have helped me if only I had shared what was going on.”

Read more here.

Finally, some helpful tips from the website Recommendations for Reporting on Suicide:

Suicide Warning Signs

  • Talking about wanting to die
  • Looking for a way to kill oneself
  • Talking about feeling hopeless or
    having no purpose
  • Talking about feeling trapped or
    in unbearable pain
  • Talking about being a burden
    to others
  • Increasing the use of alcohol or drugs
  • Acting anxious, agitated or recklessly
  • Sleeping too little or too much
  • Withdrawing or feeling isolated
  • Showing rage or talking about seeking revenge
  • Displaying extreme mood swings

The more of these signs a person shows, the greater the risk. Warning signs are associated with suicide but may not be what causes a suicide.

What to Do

If someone you know exhibits warning signs of suicide:

  • Do not leave the person alone
  • Remove any firearms, alcohol, drugs or sharp objects that could be used in a suicide attempt
  • Call the U.S. National Suicide Prevention Lifeline at 800-273-TALK (8255)
  • Take the person to an emergency room or seek help from a medical or mental health professional

Study of Gay Brothers Suggests Genetic Basis of Male Homosexuality – Discovery Magazine Article

An interesting and important piece from Discovery magazine.

“Are people born gay or is it a choice? A new study of gay brothers, the largest to date, adds more scientific evidence that there’s a genetic basis for homosexuality.

A genetic analysis of over 409 pairs of gay brothers found that two areas of the human genome, a portion of the X chromosome and a portion of chromosome 8, were associated with the men’s sexual orientation. The findings gel with a smaller study conducted in 1993 that implicated the same area of the X chromosome.”

You can read the rest of the article at Discovery magazine.

So why is this important for research on gender dysphoria?

1) If sexual orientation is influenced by genes, then researchers looking for genes related to gender identity need to control for sexual orientation.

Trans men (born female) are usually attracted to women and about half of trans women (born male) are attracted to men, so they might share genes with cis lesbians or gay men.

Future studies of genes and gender dysphoria need to include cis gay men and lesbians in the control groups.

2) The genes that may be involved in male homosexual orientation were found on the X chromosome and chromosome 8. The researchers looked at the whole genome for 409 pairs of homosexual brothers.

Studies of genes for gender dysphoria have focused on genes known to be related to sex hormones and the X and Y chromosomes (read more in Genes and Gender Dysphoria). This makes sense if you are looking at behavior that is related to sex differences, but perhaps the genes are somewhere else.

So far, researchers have had not luck finding genes related to gender dysphoria in trans women and only some luck finding genes related to gender dysphoria in trans men. Perhaps the genes for gender dysphoria and the mechanism involved are not what we expect.

A whole genome scan for genes related to gender dysphoria would be a great study for someone to do.

Genes and Gender Dysphoria

Twin and family studies suggest that there may be a genetic component to gender dysphoria. Researchers have naturally been trying to find genes linked to gender dysphoria.

Most of the research has focused on genes that are known to be related to sex hormones in some way.

I. Researchers may have found genes related to gender dysphoria in trans men (born female).

A large Spanish study found an association between the gene for Estrogen Receptor β and gender dysphoria, but a medium-sized Japanese study did not.

A small Austrian study found an association between gender dysphoria and a different gene related to converting progesterone into androgens. Nobody else has looked at this gene.

A possible flaw with the Austrian study is that the control females were seeking help with perimenopausal issues; it may be that their genes were different from the general public.

Both of these results need to be replicated.

It is also possible that the genes were related to sexual orientation.

In the Spanish study, all of the trans men were attracted to women; it is likely that 95% of the control women were attracted to men.

The Austrian study does not talk about sexual orientation, but typically most trans men are attracted to women and most women are not.

Many control women also had the genetic variations found in trans men. Some other genes or environmental factors must also be involved.

These results need to be replicated. The Austrian study was relatively small and possibly flawed while the Spanish and Japanese studies contradict each other.

II. Researchers thought they had found genes related to gender dysphoria in trans women (born male), but larger studies did not replicate the results. It is possible, however, that the genes related to gender dysphoria are different in different populations.

Four studies looked at genes related to sex hormones, specifically genes for estrogen receptor β, androgen receptor, and CYP19A1. CYP19A1 encodes aromatase, an enzyme involved in turning androgens into estrogens.

None of the studies found a relationship between gender dysphoria and the gene for CYP19A1.

Three studies found no difference in the gene for estrogen receptor β; the study that found a difference was much smaller than the others.

Three studies found no difference in the gene for androgen receptor, including one study of over 400 trans women.

III. An Italian study that looked at the Y chromosome found no differences between trans women and control males.

IV. An Austrian study that looked at sex chromosomes in trans women and trans men found no significant abnormalities.

V. A Japanese study that looked at genes related to estrogen receptor alpha and progesterone receptor found no differences between the genes of male to female transsexuals and male controls or the genes of female to male transsexuals and female controls. This study also looked at estrogen receptor β, androgen receptor, and CYP19A1 and found no differences for those genes either; this is one of the studies discussed above.

VI. An Austrian study of a gene related to steroid 5-alpha reductase (SRD5A2) found no differences between trans women, trans men, and male and female controls. SRD5A2 is involved in the conversion of testosterone to dihydrotestosterone.

It is important to remember that there may be some other genetic variations that are linked to gender dysphoria in trans women, something that we haven’t studied yet.

At this point, however, we do not seem to have found genes related to gender dysphoria in trans women.

Recommendations for future research:

Look at genes other than the ones related to sex hormones or sex chromosomes. Perhaps the cause of gender dysphoria is different from what we expect.

Control for sexual orientation by including some cis lesbians and gay men in the study.

Study trans people with African ancestry – and other groups that have not yet been studied. Studies so far have looked at people from Spain, Italy, Japan, Austria, America and Australia (Caucasian only), and Sweden.

For more details on the studies, see the links and comments below.

STUDIES OF TRANS MEN (Born female)

2014:

The (CA)n Polymorphism of ERβ Gene is Associated with
FtM Transsexualism – This Spanish study compared the genes of 273 female to male transsexuals and 371 control females. As in the study of trans women below, they focused on three variable regions of genes: estrogen receptor β (ERβ), androgen receptor, and CYP19A1 which encodes aromatase, an enzyme involved in turning androgens into estrogens.

They found no connection between the genes related to androgen receptors or aromatase, but they did find an association between the ERβ gene and gender dysphoria in trans men.

“The repeat numbers in ERβ were significantly higher in FtMs than in control group, and the likelihood of developing transsexualism was higher (odds ratio: 2.001 [1.15-3.46]) in the subjects with the genotype homozygous for long alleles.”

Three caveats:

All the trans men participating in the study had gender dysphoria that began before puberty and were attracted to women (i.e. members of their biological sex). The control females were probably 95% straight. It is possible that the genetic difference they found is related to sexual orientation, not gender identity.

This is not an absolute difference, it is a difference in frequency – 69% of the trans men had the long allele for ERβ, but so did 59% of the control women. Some other genes or environmental factors must also be involved in gender dysphoria (or sexual orientation).

The study below found different results; however, this study was larger.

note: All participants in the study were of Spanish origin.

2009:

Association study of gender identity disorder and sex hormone-related genes.

This Japanese study compared 74 male-to-female transsexuals, 168 female-to-male transsexuals, 106 male controls, and 169 female controls. They looked at genes for androgen receptor, estrogen receptors alpha and beta, aromatase, and progesterone receptor.

They found no differences between the genes of male to female transsexuals and male controls or the genes of female to male transsexuals and female controls. 

“The present findings do not provide any evidence that genetic variants of sex hormone-related genes confer individual susceptibility to MTF or FTM transsexualism.”

The abstract does not provide any information on the demographics of the trans women and trans men.

The results of this study for ERβ contradict the results of the Spanish study. The Spanish study looked at 273 trans men while this study only looked at 74, so it is unlikely that the Spanish study is simply wrong.

It may be, however, that this study is still right, at least in Japan. People in different countries have different genes; they may have different genes for gender dysphoria.

It is possible that cultural differences or medical policies may mean that clinics in different countries are looking at groups of people with different problems.

Finally, gender dysphoria might be caused by different factors or combinations of factors in different cultures. Japanese trans men may be different from Spanish trans men in some important way.

2008:

A polymorphism of the CYP17 gene related to sex steroid metabolism is associated with female-to-male but not male-to-female transsexualism.

This Austrian study compared 102 male to female transsexuals to 756 male controls and 49 female to male transsexuals to 915 female controls.

A possible flaw in this study is that the females controls were women seeking help with perimenopausal disorders; they may have had genes that were different from the general population. The male controls, on the other hand, were “participating in a health prevention program.”

Since the results found that the frequency of a particular mutation was different in female controls from all of the other groups, it matters a great deal if the control females are significantly different in some other way from the other participants.

This study looked at a different gene from the other studies, CYP17. CYP17 encodes cytochrome, an enzyme involved in converting progesterone and pregnenolone into androgens.

The authors found that a particular mutation of this gene, CYP17 −34 T>C, was associated with female to male transsexualism, but not male to female transsexualism.

They also found that, “the CYP17 −34 T>C allele distribution was gender-specific among controls. The MtF transsexuals had an allele distribution equivalent to male controls, whereas the FtM transsexuals did not follow the gender-specific allele distribution of female controls but rather had an allele distribution equivalent to MtF transsexuals and male controls.” 

In other words, trans men and trans women were similar to male controls and not female controls.

They point out, however, that there were women without gender dysphoria who had the mutant allele as well as women with gender dysphoria who did not have it. “Thus, carriage of the mutant CYP17 T−34C SNP C allele is neither necessary nor sufficient for developing transsexualism.”

In other words, there must be other genetic or environmental factors involved.

They do not discuss the sexual orientation of the participants in the study. As discussed above, it is possible that most of the trans men were attracted to women and that this genetic mutation is related to sexual orientation, not gender identity.*

Finally, I keep coming back to the female control group. What if converting progesterone to androgens is related in some way to perimenopausal symptoms? What if the mutant gene protects against problems in menopause somehow and so the female control group includes fewer people with this gene?

2007:

A common polymorphism of the SRD5A2 gene and transsexualism. This Austrian study compared 100 trans women, 47 trans men, 755 control men, and 915 control women. They looked at a mutation of the steroid 5-alpha reductase gene (SRD5A2); this gene produces an enzyme that catalyzes the conversion of testosterone to dihydrotestosterone.

They found no differences between any of the groups. The mutant allele was not associated with transsexualism and its distribution was not gender specific among controls.

This study has the same flaw as the 2008 study listed above; the control females were all seeking help for problems with perimenopause.

2002:

Sex chromosome aberrations and transsexualism. This Austrian study looked at the chromosomes of 30 trans women and 31 trans men. They did not find significant abnormalities, although they suggested further investigation might be worthwhile.

“We could not detect any chromosomal aberrations with the exception of one balanced translocation 46,XY,t(6;17)(p21.3;q23). Importantly, no sex chromosomal aberrations, which would be detectable on the G-banded chromosome level, have been observed.”

They conclude:

“The data described here provide evidence that genetic aberrations detectable on the chromosome level are not significantly associated with transsexualism. In addition, molecular-cytogenetic FISH analyses did not reveal deletions of the androgen receptor gene locus on chromosome Xq12 or of the SRY locus on chromosome Yp11.3. Multiplex PCR analyses demonstrated one AZF deletion in a male-to-female transsexual.”

but:

“However, the detection of one carrier of a Y chromosome microdeletion out of 30 male-to-female transsexuals could argue for further investigations. This is of special interest in light of the recent discussion of gamete banking before hormonal and sex reassignment surgery of transsexuals.”

 

STUDIES OF TRANS WOMEN (Born male)

The Y Chromosome:

2013

Hormone and genetic study in male to female transsexual patients. This Italian study looked at six areas on the Y chromosomes of 30 trans women. They found no abnormalities.

“This gender disorder does not seem to be associated with any molecular mutations of some of the main genes involved in sexual differentiation.”

The trans women were aged 24-39 and had already begun hormone therapy. A little over half of them had already had sex reassignment surgery and the rest were waiting for it.

2002:

Sex chromosome aberrations and transsexualism. This Austrian study looked at the chromosomes of 30 trans women and 31 trans men. They did not find significant abnormalities, although they suggested further investigation might be worthwhile.

For further details, see the description above under trans men.

Genes Related to Sex Hormones:

2007:

A common polymorphism of the SRD5A2 gene and transsexualism. This Austrian study looked at a mutation of the steroid 5-alpha reductase gene (SRD5A2. They found no differences related to gender or gender identity. For more details, see the description above in the section on studies of trans men.

The following studies looked at the same areas of genes related to sex hormones.

Initially, a small Swedish study of trans women (born male) found a difference in the length of the estrogen receptor β repeat polymorphism, but none of the other studies did.

Similarly, an American-Australian study found that trans women had longer repeat lengths for the androgen receptor allele, but none of the other studies did.

It looks like these genes do not affect gender dysphoria in trans women, although it is possible that different genes affect people in different countries.

2014:

Association Study of ERβ, AR, and CYP19A1 Genes and MtF Transsexualism – This Spanish study compared the genes of 442 trans women and 473 control males. They focused on three variable regions of genes: estrogen receptor β, androgen receptor, and CYP19A1 which encodes aromatase, an enzyme involved in turning androgens into estrogens.

They found no connection between these genes and gender dysphoria.

Interestingly, 98% of the trans women had chromosomes that were 46,XY, i.e. normal, but 2% of the group showed aneuploidy, or abnormal chromosomal numbers. This is slightly higher than usual.

The abstract does not go into detail, but presumably the aneuploidies were cases of Klinefelter syndrome; a condition where a person typically has one Y chromosome and two X chromosomes. Most people with Klinefelter’s syndrome identify as male, but there may be a higher than usual occurrence of gender dysphoria among people with Klinefelter’s.

There are no details on the trans women in the abstract; however, the same researchers did a very similar study of trans men (see above). It may be that the participants in the two studies were screened in the same way.

2009:

Association study of gender identity disorder and sex hormone-related genes.

This Japanese study compared 74 male-to-female transsexuals, 168 female-to-male transsexuals, 106 male controls, and 169 female controls. They looked at genes for androgen receptor, estrogen receptors alpha and beta, aromatase, and progesterone receptor.

They found no differences between the genes of male to female transsexuals and male controls or the genes of female to male transsexuals and female controls. 

“The present findings do not provide any evidence that genetic variants of sex hormone-related genes confer individual susceptibility to MTF or FTM transsexualism.”

The abstract does not provide any information on the demographics of the trans women and trans men.

Androgen receptor repeat length polymorphism associated with male-to-female transsexualism.

This Australian and American study compared 112 male to female transsexuals to 258 control males. They looked at genes for androgen receptor, estrogen receptor beta, and aromatase. No differences were found for the estrogen receptor or aromatase, but transsexuals had longer repeat lengths for the androgen receptor allele.

“This study provides evidence that male gender identity might be partly mediated through the androgen receptor.”

This result was not found in the Spanish study or the Japanese study above. The Spanish study was larger than this one. Thus, this result has not been replicated.

However, it is possible that this genetic variation is connected to gender dysphoria for Caucasian trans women in America and Australia, but not in Spain or Sweden and not for Japanese trans women.

It is also possible that the genetic difference found here is related to sexual orientation, not gender identity. The researchers in this study only knew the sexual orientation for about 40% of the participants in the study, but people with gender dysphoria are much more likely to be attracted to people of the same biological sex than people without gender dysphoria.

As in the Spanish, study above, this is not an absolute difference, it is a relative one. There were also cis men who had long AR repeat lengths (Figure 1). Again, some other genes or environmental factors must also be involved in gender dysphoria (or sexual orientation).

The trans women in this study were all Caucasian; 76 of them were from an Australian clinic and 36 of them were from UCLA in America. Almost all of them were on hormones. Some of them had gender dysphoria in childhood. “The sexuality is only known for approximately 40% of patients, because some patients did not wish to discuss or disclose this information or the patient’s sexuality was flexible and not easily classified.”

2005:

Sex steroid-related genes and male-to-female transsexualism.

This Swedish study compared the genes of 24 male to female transsexuals and 229 male controls. They looked at specific areas in the androgen receptor gene, the aromatase gene, and the estrogen receptor β gene.

They did not find a difference between male-to-female transsexuals and men for the first two genes, but they did find a difference related to the gene for estrogen receptor β. “Transsexuals differed from controls with respect to the mean length of the ERβ repeat polymorphism.”

In addition, “binary logistic regression analysis revealed significant partial effects for all three polymorphisms, as well as for the interaction between the AR and aromatase gene polymorphisms, on the risk of developing transsexualism.” 

The study was very small, however, and as the authors said, “results should be interpreted with the utmost caution.”

The three more recent studies above did not replicate the findings of this study. The other studies were much larger than this one, so it is possible that these results were a fluke.

It is also possible, that the genes linked to gender dysphoria in Sweden are different from the genes linked to it in other countries.

The authors of the American-Australian study described above say, “Our sample size was approximately four times larger than that of the Swedish study, so it is possible that the former study was underpowered to detect a false positive. Alternatively, there might be differences between Swedish and non-Swedish populations in this polymorphism. In the Swedish study, the long repeat occurred in 51.8% of control subjects and 67.1% of transsexuals, whereas in the present study the long repeat occurred in 36.5% of control subjects and 44.1% of transsexuals. Thus, although there was a trend in the same direction in both studies, there are major differences in prevalence of these long repeats between the two populations.”

The only data we have on the participants in the study are that the trans women were Caucasian and the vast majority of the controls were also Caucasian. Again, it is likely that there was a higher percentage of people attracted to male in the group of trans women than the general population; this might have affected the results.

As the authors point out, “the gene variants investigated in this study are relatively common, none of the studied variants could hence be assumed to be the primary cause of this condition.” Rather, genes might increase or decrease the chance of developing gender dysphoria.

So, if the results of this study are not a fluke, we are still left with the questions of what other factors contribute to developing gender dysphoria and is this a gene related to gender dysphoria or sexual orientation in Sweden?

The end result of all this:

We have a couple of possible candidates for genetic variations related to gender dysphoria in trans men, but we need further studies. We need to replicate the results and to control for sexual orientation. In the case of the CYP 17 gene, we need to compare trans men to healthy control females instead of women with perimenopausal issues.

We don’t have any strong candidates for genetic variations related to gender dysphoria in trans women. Future studies might do well to look for genes that are not related to sex hormones. As always, they should control for sexual identity. (This should be done by adding lesbians and gay men without gender dysphoria, not by excluding trans women who are attracted to women from the studies. See my rants in articles on brain sex.)

 

*A group of trans women would include many more people attracted to men than a group of control males, but typically about half of trans women are attracted to women while most trans men are attracted to women. Thus this could be a comparison of two groups (control males and trans men) where a large majority of the people are sexually attracted to women, one group where half the people are attracted to women (trans women), and a group where about 5% of the people are attracted to women (control females).