Conclusion: lessons from the untaught: the cloacal exstrophy experience Males who were born with cloacal exstrophy, whether raised as male or castrated at birth and raised as female, demonstrate psychosocially and psychosexually dominant male-typical tendencies. It seems that prenatal androgen exposure (and perhaps sex chromosome-specific neuronal properties) influences gender role, and, at least sometimes, creates male sexual identity, even if males are castrated at birth and reared female. These children adapt to their lives with severe somatic anomalies, pathophysiologic vulnerabilities, and complex medical and surgical interventions from birth. They do not observe their lives; they live their lives. The intuitive recognition of male identity by many, whether they experienced sex assignment or not, attests to our own lack of knowledge about the formation of human identity. These children adapt to neonatal surgical castration and feminizing genitoplasty, although data from this study do not imply that clinical indications justify such interventions. Genetic female as well as genetic male children who have cloacal exstrophy require genital construction. Genetic females have normal ovaries; genetic males have normal testes [48]. Surgical castration does not eliminate the need for genital construction; it induces a hypogonadal state that requires life-long exogenous sex hormone administration. Additionally, neonatal castration plus feminizing genitoplasty—coupled with a social and legal assignment to female—does not seem to override the neurobiological underpinnings of male sexual identity and male gender role preferences. Therefore, female sex assignment in genetically- and hormonally-male neonates risks personal internal confusion and social external conflict and contradiction. Studies of males who have cloacal exstrophy underscore our lack of full understanding of the mechanisms of neonatal and childhood male psychosexual development. Yet we argue that evidence-based medicine must be at the core of medical decision-making. Data from these studies highlights the tenuousness of the intellectual foundations of our arguments for sex assignment in children who have cloacal exstrophy. The study data imply an important role for prenatal androgen exposure in male-typical development, including male sexual identity. Clinical algorithms and paradigms in these children need to be re-evaluated. The implications of these data need to be studied in terms of children who have intersex. These children’s inability to circumvent male-typical gender role and their frequent intuitive recognition of male sexual identity provide arguments that contradict the conception that a genetic and hormonal male can be successfully assigned to female.
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