2. Can gender identity & behavior be
modified by hormones?
Note the similarity in the chemical structure of these molecules!
3. YES
• Successful case of male to female gender
reassignment, initiated because of a circumcision injury
(ablatio penis)
• Surgical castration at 7 months
• Hormone (estrogen) replacement therapy (HRT) at 11
years
• Occupation involved a male-typical job
• No dissatisfaction with sex of rearing & assignment
• Two interviews during adolescence and young
adulthood found that this individual
―was living socially as a woman and denied any uncertainty about
being a female‖ although childhood gender preferences
involved male-typical activities and toys (Bradley, Oliver,
Chernick, & Zucker, 1998, p. 1).
4. NO
• Case remarkably similar to that described by Bradley et al.
• David Reimer also suffered a botched circumcision and was
raised female as a means of managing the injury
• Received HRT treatment as well
• Never felt like he was a female or fit into the female gender
role
• Rejected sex of rearing & assignment as a teenager, had
reconstructive surgery and assumed a male-typical gender
role (Colapinto, 2001)
• Possible reason for failed reassignment?
– Reimer was reassigned at age 17 mos, and underwent
surgical castration and reconstructive surgery (vaginoplasty)
at age 21 mos., much later than the case previously
described (Bradley et al.,1998)
5. MAYBE
The following studies highlight the mixed outcome of
a variety of hormone-related disorders and
exposure to elevated levels of prenatal
testosterone.
6. Hormonal Influences on Behavior:
Testosterone
• Elevated levels of prenatal testosterone increases
male-typical behavior for both males and females
• Behavior/hormonal linkage more pronounced for
females than males
• Presence of male-typical behavior measured with
the Pre-School Activities Inventory (PSAI)
• Correlation between PSAI scores and
testosterone levels was .42 for girls and .20 for
boys (p < 0.05)
Auyeung et al., 2009
7. Hormonal Influences on Behavior:
Congenital Adrenal Hyperplasia
• Congenital adrenal hyperplasia (CAH) occurs when the body lacks an
enzyme necessary for producing aldosterone and cortisol. This results in an
elevated androgen level. This condition affects both genetic males and
females (MedlinePlus, 2011)
• In one study, 5/16 women (46, XX karyotype) with CAH reported that they
had experienced a desire to be male over the past twelve months.
• No women from the control group (15) or men from both the CAH and
control groups (9 and 10, respectively) experienced gender dysphoria.
• 5 women with CAH also reported engaging in homosexual or bisexual
behavior in the past twelve months
• Control group reported exclusive or nearly exclusive heterosexual behavior
• Women with CAH who completed the PSAI (14) reported more male-
typical behavior in childhood than women in the control group (11) with an
effect size of 1.60
• No differences were found between the CAH and control groups of men
• Conclusion: androgens appear to more significantly influence women’s
behavior, in comparison to men’s behavior
Hines, Brook, and Conway, 2004
8. CAH cont’d
• Females with CAH have a greater tendency to
– Use physical aggression in conflict
– Prefer male-typical careers and activities
– Demonstrate less interest in mothering
• Females with CAH also
– Generally demonstrate male-typical patterns of
cognitive abilities (spatial and mathematical areas)
Mercke & Bornstein, 2005
9. CAH cont’d: Socialization
• Differences in toy preferences between girls with
and without CAH cannot be explained by parental
socialization
• One study found that parents actually reinforce
female-typical play more when daughters have
CAH, as compared to normal daughters
• Girls without CAH in this study engaged in more
female-typical play when alone than when
accompanied by either parent
• Girls with CAH showed no difference between
solo and parent-present play
Pasterski et al., 2005
10. Androgen Insensitivity Syndrome
(AIS)
• Individuals with AIS have a 46, XY karyotype—they are genetically male
• Feminine secondary sex characteristics develop as a result of insensitivity to
androgen; breast development indicates estrogen sensitivity (Rider, 2005)
• Experiences of individuals with partial & complete AIS:
– Psychological complications, feelings of a compromised womanhood
• Lack of reproductive capabilities and/or masculine appearance
– Sense of devaluation
• Fear of others’ negative perceptions
• Rejection
• Lessened value as a partner
– The most salient finding is that individuals with AIS view themselves as
women, but experience difficulties because of fear that society’s
perception will not match their self-perceptions.
Alderson, Madill, and Balen, 2004
11. AIS: Incongruence between Self-
Identity & Society’s Perspective
• Problem of ethical treatment of female athletes
– Female Olympic athletes were required to take a sex chromatin test that
detected their 46, XY karyotype, although these individuals were
described as ―undeniably female‖
– Clinical assessment required to remain in the competition (Genel and
Ljungvist, 2005, S41)
– Genetic testing only discontinued in the year 2000
– One female athlete was pressured to drop out of the competition and
refused. Her experience of discrimination and humiliation of because of
AIS:
• When I crossed the line first in the 60 m hurdles, my story was
leaked to the press. I was expelled from our athletes’ residence, my
sports scholarship was revoked, and my running times were erased
from my country’s athletics records. I felt ashamed and
embarrassed. I lost friends, my fiancé, hope, and energy. But I knew
that I was a woman, and that my genetic difference gave me no
unfair physical advantage. I could hardly pretend to be a man; I have
breasts and a vagina. I never cheated. I fought my disqualification
(Martinez-Patino, 2005, S38).
12. Androgen Biosynthesis Deficiencies:
5-ARD-2 & 17BHSD3
• Individuals with 5-Alpha Reductase-2 Deficiency (5-ARD-2) are genetically
male, that is, they have a karyotype of 46, XY.
• Male gender identity reported to develop at puberty, although sex of rearing
was female (Rider, 2005).
• The gene responsible for the presence of 5-ARD-2 is named the 5a-reductase
type 2 gene or SRD5A2 (Thigpen et al., 1992).
• Thigpen et al. (1992) found that depending on the specific mutation of
SRD5A2, individuals with 5-ARD-2 might demonstrate a more feminine
or masculine phenotype.
– Substitution of arginine for glycine at position 34 in SRD5A2 ―resulted in
a female phenotype with only minor virilization expected at puberty‖ (p.
802).
– Another participant in this study had a mutation in SRD5A2 involving a
serine existing where glycine would normally be present at position 196.
This resulted in ―a predominantly male phenotype‖ (p. 802).
• These results ―suggested a correlation between clinical expression and
severity of the impairment of enzyme [5-alpha reductase] function‖ (p.
804).
•
13. 5-ARD-2: Gender Identity
• Thigpen et al., 1992:
• Some participants were raised as female and
retained a female gender identity
• Some raised as female and adopted a male
gender identity
• Some raised as male and retained male identity
• Participants also received varying combinations
of surgery and female hormones
– Difficult to separate effects of disease from effects of
treatment
14. 5-ARD-2 Gender Identity cont’d
Older comparison study conducted by Imperato-McGinley, Peterson, Gautier, and
Sturla (1979) in two villages in the Dominican Republic:
• Without hormonal and surgical interventions , most individuals spontaneously
adopt a male gender identity.
– 18 subjects raised as girls, 17 adopted a male gender identity.
– Development of a male gender identity occurred at age 7-12,
– Gradual development of male gender identity, not a one-time event
– One subject maintain a female gender identity and female-typical
behavior through adulthood, and desired corrective surgery to increase
her body’s congruence with her gender identity.
• Meyer-Bahlburg (1999) noted that such cases of female to male gender
changes in cases of androgen biosynthesis deficiency occur in
underdeveloped countries
• Difficult to live as a female with the onset of ―dramatic virilizing changes of
puberty‖ without medical intervention (p. 3457)
• In these situations, ―the male role confers a clear social advantage‖ (p. 3457).
• Hormonal influences on identity and behavior confounded with social and
environmental variables
15. 5-ARD-2 & 17BHSD3 Gender Identity
• A study by Schweizer, Brunner, Schtzmann, Schonbucker, and
Richter-Appelt (2009) included female-identifying participants with a
male (46, XY) karyotype who were diagnosed with either 5-ARD-2 or
a similar disorder also involving deficiency in androgen biosynthesis,
17beta-hydroxysteroid dehydrogenase-3 (17BHSD3).
• All 7 participants had developed female gender identity,
• All also received gonadectomies and hormone replacement therapy.
• All but two participants had also received clitoris reduction, vaginal
surgery, or both.
• Two participants had a female-self experience
• Four participants varied between a male and a female experience of
the self.
• One participant reported feeling ―sometimes as a woman, sometimes
neither nor‖ (Schweizer, et al., 2009, p. 196).
16. Summary
• Gender identity and gender role development are COMPLEX!
• Numerous factors, including hormonal influences, must be
considered if it is necessary to assign or reassign a child to a
particular gender
• Among individuals who have PAIS, androgen biosynthesis
deficiency, and incomplete gonadal dysgenesis, about 25%
express dissatisfaction with their sex of rearing (Hughes,
Houk, Ahmed, Lee, & LWPES/ESPE Consensus Group,
2006).
• In light of inconclusive findings from both psychology and the
sciences, caution and an open mind are required to provide
ethical treatment for individuals who do not fit neatly into a
dichotomous gender category.
17. References
Alderson, J., Madill, A., & Balen, A. (2004). Fear of devaluation: Understanding the
experience of intersexed women with androgen insensitivity syndrome. British Journal of
Health Psychology, 9, 81-100.
Auyeung, B., Baron-Cohen, S., Ashwin, E., Knickmeyer, R., Taylor, K., Hackett, G., & Hines,
M. (2009). Fetal testosterone predicts sexually differentiated behavior in both girls and in
boys. Psychological Science, 20(2), 144-148.
Bradley, S., Oliver, G., Chernick, A., & Zucker, K. (1998). Experiment of nurture: Ablatio penis
at 2 Months, sex Reassignment at 7 months, and a psychosexual follow-up in young
adulthood. Pediatrics, 102, 1-5.
Colapinto, J. (2001). As nature made him: The boy who was raised as a girl. New York, NY:
HarperCollins.
Genel, M., & Ljunqvist, A (2005). Gender verification of female athletes. Lancet, 366, S41.
Hines, M., Brook, C., & Conway, G. (2004). Androgen and psychosexual development: Core
gender identity, sexual orientation, and recalled childhood gender role behavior in women
and men with congenital adrenal hyperplasia The Journal of Sex Research, 41(1), 75-81.
Hughes, I., Houk, C., Ahmed, S., Lee, P., & LWPES/ESPE Consensus Group. (2006).
Consensus statement on management of intersex disorders. Archives of Disease in
Childhood, 1-10.
18. References cont’d
Imperato-McGinley, J., Peterson, R., Gautier, T., & Sturla, E. (1979). Androgens and the
evolution of male-gender identity among male pseudohermaphrodites with 5-α reductase
deficiency. The New England Journal of Medicine, 300(22), 1232-1237.
Martinez-Patino, M. (2005). A woman tried and tested. Lancet, 366, S38.
MedlinePlus, 2011. Congenital adrenal hyperplasia. Retrieved from
http://www.nlm.nih.gov/medlineplus/ency/article/000411.htm
Mercke, D., & Bornstein, S. (2005). Congenital adrenal hyperplasia. Lancet, 365, 2125-2135.
Pasterski, V., Geffner, M., Brain, C., Hindmarsh, P., Brook, C., & Hines, M. (2005). Prenatal
hormones and postnatal socialization by parents as determinants of male-typical toy play
in girls with congenital adrenal hyperplasia. Child Development, 76(1), 264-278.
Rider, E. (2005). Our voices: Psychology of women (2nd ed.). Hoboken, NJ: John Wiley &
Sons.
Schweizer, K., Brunner, F., Schtzmann, K., Schonbucker, V., & Richter-Appelt, H. (2009)
Gender identity and coping in female 46, XY adults with androgen biosynthesis deficiency
(intersexuality/DSD). Journal of Counseling Psychology, 56(1), 189-201.
Thigpen, A., Davis, D., Milatovich, A., Mendonca, B., Imperato-McGinley, J., Griffin, J.,
Francke, U., Wilson, J., & Russell, D. (1992). Molecular Genetics of steroid 5a-reductase
2 deficiency. Journal of Clinical Investigation, 90, 799-809.
