bladder exstrophy or penile agenesis) and who have been assigned to the female gender.
The likelihood of gender dysphoria is furthe r enhanced by additional, prolonged, highly
gender-atypical postnatal androgen exposure with somatic virilization as may occur in fe-
male-raised and noncastrated 46,XY individu als with 5-alpha reductase-2 deficiency or
17-beta-hydroxysteroid dehydrog enase-3 deficiency or in female-raised 46,XX individuals
with classical congenital adrenal hyperplasi a with prolonged periods of non-adherence to
glucocorticoid replacement therapy. Howeve r, the prenatal androgen milieu is more
closely related to gendered behavior than to gender identity. Many individuals with dis-
orders of sex development and markedly gend er-atypical behavior do not develop gender
dysphoria. Thus, gender-atypical behavior by itself should not be interpreted as an indi-
cator of current or future gend er dysphoria. There appears to be a higher rate of gender
dysphoria and patient-initiated gender change from assigned female to male than from as-
signed male to female in 46,XY individu als with a disorder of sex development.
Culture-Related Diagnostic Issues
Individuals with gender dysphoria have be en reported across many countries and cul-
tures. The equivalent of gender dysphoria ha s also been reported in individuals living in
cultures with institutionalized gender categories other than ma le or female. It is unclear
whether with these individuals the diagnostic criteria for gender dysphoria would be met.
Diagnostic Markers 
Individuals with a somatic disorder of sex development show some correlation of final
gender identity outcome with the degree of prenatal androgen production and utilization.