Defeminization and masculinization are the processes that a fetus goes through to become a male.
Sexual differentiation in mammals is biased towards developing as a female, so that it has often been said that female is the "default" developmental pathway, in the sense that elimination of any of several gene actions necessary for formation of male genitalia leads to the development of external female genitalia (though development of functional ovaries requires effective action of several less understood sex-specific genes). Two processes: defeminization, and masculinization, are involved in producing male typical morphology and behavior. Disruption of either of these processes in males produces female-typical development. The opposite is not true, disruption of normal sexual development in females does not lead to male-typical endpoints.
Defeminization involves the suppression of the development of female typical morphology (development of the Mullerian ducts into the fallopian tubes, uterus and vagina) and behavioural predispositions. Masculinization involves the production of male typical morphology (development of the Wolffian ducts into male reproductive structures) and behavioural predispositions. Both defeminization and masculinization are required for a mammalian zygote to become a fully reproductively functional male.
A brief version of the female default paradigm can be stated as follows:
##The SRY, SOX9, and SF1 genes must be present and functional. ##Functional Leydig cells must form in the gonads. ##The Leydig cells must be able to produce testosterone. ##The target cells must have the hormone receptors to respond to the testosterone. The target cells of the external genitalia must have functional 5-alpha-reductase enzyme to convert some of the testosterone to more active dihydrotestosterone. ##There is some evidence that the brain must be exposed and respond to androgens either prenatally or early in life to produce characteristic mating behavior. This is well demonstrated in many animal species but remains mostly speculative with respect to humans.
This paradigm dates back to the 1950s. Even stronger versions were commonly stated in the 1960s and 1970s. One version, perhaps most associated with John Money, (who termed it the Adam principle), held that additional steps in the cascade to male identity were the recognition by parents and doctor that the external genitalia were male, which resulted in a male sex assignment, which in turn resulted in a male sex of rearing by parents and society, which in turn (coupled with the reinforcing appearance of male genitalia) resulted in a male gender identity. At least by implication, female gender identity simply required a female sex of rearing and lack of an obvious penis.
In Germany in the 1970s, Günter Dörner extrapolated the cascade to include direct testosterone effect on the brain as necessary for a male gender identity and sexual orientation, proposing that transsexualism and or homosexuality in biological males could result from deficiency of prenatal or early postnatal testosterone effect on the brain.
In the 1970s, Money's version was widely accepted in liberal academic circles and Dörner's was fiercely denounced, especially in the gay and transsexual communities. The last decade has seen somewhat of a reversal of appeal in similar circles. This turnabout perhaps illustrates the difficulties of investigating these relationships in humans rather than rodents, the complexities of attempting to explain core aspects of the human psyche, perhaps the influence of intellectual and political fashion in the application of scientific knowledge to human affairs. (Baum 2006; Crouch 1998; Wilson and Reiner 1998)
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