Originally posted by PaulNik:
I think just the opposite is true.
PaulNik:
you may find this of interest:
"Sexual orientation is a component of human sexual differentiation. Research over the last 15 years has sketched in the major aspects of sexual differentiation in mammals.
Ellis and Ames (1987) have written a very fine tutorial describing the ontogeny of mammalian sexual orientation (300 references):
* Mammalian sexual development usually expresses chromosomal pairing: females have an "XX" pairing of the sex chromosome; males have an "XY" pairing. The chromosomal pairing can be called the karyotypic sex of a person. [The picture of an organism's paired chromosomes arranged from largest to smallest is known as a karyotype.]
* The prototype mammal is female. Male characteristics reflect specific biochemical interventions in the development of the individual. If some or all of the active interventions are blocked, the male characteristics will not occur.
* There are four aspects of sexual differentiation and organization: genital (reproductive organs), neurological (differences in brain structure and functioning), secondary sexual characteristics (breast development, facial hair, etc.), and behavioral (sexual orientation and sex-typical behaviors).
* Each of these aspects may be "inverted" (the individual has the characteristics of the other sex) with respect to the individual's karyotypic sex ("XX" or "XY" chromosome pairing).
* Sexual orientation is revealed by a consistent preference for sexual relations with same-sexed or other-sexed partners. If there is a degree of ambivalence about the partner's sex, the person is bisexual. Sexual orientation is not altered by occasional sexual experiences with noncongruently sexed partners by choice or in the absence of alternative sexual outlets.
* Sexual differentiation relevant to sexual orientation occurs in hypothalamic areas of the brain (in 1987 the preoptic anterior nucleus, ventromedial nucleus, and anterior nucleus were known).
* Brain sexual differentiation develops as "female" unless there are high levels of testosterone (an androgen) in which case "male" brain differentiation occurs. In human beings, hypothalamic differentiation begins about the middle of the second month of gestation and is completed by the middle of the fifth.
* Primate neurological sexual differentiation can be affected by four different interventions: (a) direct manipulation of androgen levels during gestation; (b) pharmacological blocking or augmentation of the effects of androgens; (c) exposure of the pregnant female to stress (which can depress androgen levels); (d) immune-system responses to androgens.
* Inversion of sexual behavior (males presenting to other males) has been produced in rodents and possibly monkeys by rearing in unisex peer groups. Rodent sexual differentiation is not complete at birth; the rearing conditions may have lowered testosterone levels and thus altered the rodent sexual differentiation. The rodent literature is thus not directly generalizable to primate ontogeny. In monkeys, unisexual rearing seems to create a general unease with other-sexed peers and awkwardness in responding to sexual overtures from the other sex. Continued exposure to peers of both sexes "heterosexualizes" the monkeys' behavior.
* Sexual orientation is a continuum from exclusive heterosexuality, through various degrees of bisexuality, to exclusive homosexuality. Sexual orientation is definitely not a binomial or trinomial categorical variable.
* Sexual orientation is permanent and cannot be changed. Therapies that purport to change sexual orientation are, in all likelihood, reporting changes in sexual behavior of bisexual persons--not of the sexual orientation of homosexual persons.
* "To summarize the human evidence ... sexual orientation is mainly the result of neurological factors that are largely determined prenatally, even though they do not fully manifest themselves until adolescence or adulthood." (Ellis & Ames, 1978, p. 248).
* The sexual-differentiation model Ellis & Ames propose suggests that a significant proportion of male homosexual-orientation is a result of maternal stress during the first and second trimesters of pregnancy.
APA (1992). Award for distinguished contribution to psychology in the public interest: Evelyn Hooker. American Psychologist, 47, 501-503.
Burr, C. (1993). Homosexuality and biology. The Atlantic Monthly, 271(3), 47-65.
Byne, W. (1994). The biological evidence challenged. Scientific American, 270, 50-55.
Ellis, L., & Ames, M. A. (1987). Neurohormonal functioning and sexual orientation: A theory of homosexuality-heterosexuality. Psychological Bulletin, 101, 233-258.
Hyde, J. S., Fennema, E., & Lamon, S. J. (1990). Gender differences in mathematics performance: A meta-analysis. Psychological Bulletin, 107, 139-155.
Hyde, J. S. & Linn, M. C. (1988). Gender differences in verbal ability: A meta-analysis Psychological Bulletin, 104, 53-69.
LeVay, S. & Hamer, D. H. (1994). Evidence for a biological influence in male homosexuality. Scientific American, 270, 43-49.
McCormick, C. M. & Witelson, S. F. (1991). A cognitive profile of homosexual men compared to heterosexual men and women. Psychoneuroendocrinology, 16, 459-473.
Money, J. (1988). Gay, Straight, and In-Between: The Sexology of Erotic Orientation. New York: Oxford University Press."
http://www.lemoyne.edu/OTRP/otrpresources/otrp_glb.html