The etiology of male homosexuality.
This hypothesis agrees with Le Vay's suggestion that the two phenomena of childhood behavior and adult sexuality are induced by separate events rather than being two events in a single chain. However, it differs from Le Vay in that it includes the postnatal period, as being of crucial importance in the development of adult sexuality. Male homosexuality is portrayed as a biological variation of human sexuality and the hormonal changes which may produce it are described. It is postulated that sexual preference is dictated by testosterone action on the brain possibly commencing prenatally but certainly continuing during a critical postnatal period. It is proposed that reduction in testosterone action results in reduced proliferation of hypothalamic nuclei, which play a vital role in psycho-sexual orientation. The cause of this reduction in testosterone is the prolongation of hyperprolactinemia during this critical postnatal period, which is deemed to be secondary to prolactin microadenomata stimulated to secrete prolactin by high estrogen levels at the end of pregnancy and failing to turn off this secretion until after this critical postnatal period. It is postulated that there is a temporal dissociation between the development of masculine behaviour and psycho-sexual orientation, but that hormonal influences may overlap these periods. Hyperprolactinemia, caused by stress upon the infant, may also influence psycho-sexual orientation.
Roper
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WG
D000328:Adult; D000818:Animals; D001921:Brain / Q000196:embryology / Q000254:growth & development / Q000502:physiology; D002648:Child; D005260:Female; D005333:Fetus / Q000502:physiology; D018451:Homosexuality, Male / Q000523:psychology; D006801:Humans; D008297:Male; D008954:Models, Biological; D011247:Pregnancy; D011388:Prolactin / Q000378:metabolism; D013312:Stress, Physiological / Q000503:physiopathology / Q000523:psychology; D013739:Testosterone / Q000502:physiology
D013739:Testosterone; D011388:Prolactin