Homosexual behavior--论文代写范文精选

男性的性取向可能由睾酮,在胎儿期开始发育。例如,罗宾逊和曼宁的目前证据表明高水平的睾酮会导致同性恋和双性恋取向。下面的essay代写范文进行详述。

Abstract 
Hormone research on sexual orientation has focused on testosterone and estrogen. A common hypothesis has been that homosexual men have more elevated levels of estrogen and depressed levels of testosterone than heterosexual men [e.g., 30, 31, 32, 33, 34]. However, the results of these studies have been inconsistent (see for review [35]). The fact that sexual behavior in rodents [36] and primates [37] can be altered by early exposure to sex hormones has raised the possibility that variation in exposure to hormones might be the basis for variation in sexual orientation also in humans [38]. Clinical studies of the sexuality of individuals who experienced biological conditions which alter the usual prenatal hormonal processes (e.g., congenital adrenal hyperplasia) strongly suggest that some aspects of human sexual orientation and behavior are due to hormonal mechanisms [39]. 

From this perspective, male homosexuality is considered as only one expression of sexual behavior from a continuum of sexual variation that may be signifi cantly infl uenced by hormonal changes. Male sexual preference may be dictated by testosterone action on the brain, which begins in the prenatal period and continues during a critical postnatal period [40, 41]. For example, Robinson and Manning [42] present evidence suggesting that exposure to high levels of prenatal testosterone contributes to homosexual and bisexual orientations. They measured the 2nd to 4th digit ratios of heterosexual, homosexual and bisexual men. This ratio is believed to be affected by prenatal exposure to testosterone and is set early in prenatal development. There is also an established sex difference in the ratio with men showing less of a ratio than women [43].

Robinson and Manning [42] found that, among men, the ratio was greatest in heterosexual men, less in homosexual men, and least in bisexual men. They indicate that this suggests greater exposure to prenatal testosterone for homosexual and bisexual men. Robinson and Manning argue that this could be interpreted as an alternative explanation to some adaptive value associated with homosexuality. In the male fetus there may be strong selection for high testosterone for sexual differentiation of systems associated with effective male survival and reproduction. The cost of this may be that some males are exposed to over-optimal levels of testosterone. 

This contributes to deviation from a heterosexual orientation and to a variety of other biologically deleterious effects. However, their fi nding that bisexual males may have had greater exposure to prenatal testosterone than homosexual males does appear to be inconsistent with their own interpretation. They imply that with increasing exposure to testosterone there is increasing deviation from a heterosexual orientation. 

If this were true, the increasing testosterone-heterosexual deviation pattern should be as follows: heterosexual, bisexual, and homosexual. Robinson and Manning’s argument that a homosexual orientation results from exposure to too much testosterone suggests that a homosexual orientation is due to an over-masculinized brain. The conclusion is contradictory to Miller’s [25] work suggesting that it is due to a feminized brain. However, Rahman and Wilson [44] have suggested that homosexual preferences may be due to high levels of unbinded testosterone during prenatal development that results from a lack of receptors at particular brain sites. From this perspective, the brain could be feminized while other features of the developing fetus, for example 2nd to 4th digit ratio, could be over-masculinized. 

Two major neurohormonal theories of sexual orientation development hold that prenatal hormonal effects upon brain differentiation actually involve complex patterns of masculinization, unmasculinization, feminization, and defeminization associated with particular patterns of sexual orientation [45, 46]. Feierman [47] has extended the neurohormonal theory for the development of sexual orientation. He states that patterns of sexual differentiation of the brain can be associated with particular patterns of preferred partner characteristics based on evaluation of features of the target relative to self. 

For example, he suggests that a masculinized and defeminized brain leads to attraction to targets that are younger and more feminine than the self. In this category would fall, heterosexual adult men, but also, heterosexual and homosexual pedophiles, men attracted to adolescent females, and men attracted to adolescent males. On the other hand, he speculates that brains which are masculinized and feminized direct attraction to targets younger and more masculine than the self, and homosexual men would fall in this category. There is some evidence that gay men are strongly attracted to masculine looking men [48] and to men slightly more masculine than themselves [49].

A speculated genetic-endocrine basis for homosexual behavior 

In an attempt to explain a genetic-endocrine basis for selection for homosexual behavior, Rahman and Wilson [44] have proposed the following scenario. They believe that during human evolution intrasexual aggression constituted an adaptive problem because it led to reduced individual survival and infanticide [50, 51]. Rahman and Wilson [44] speculate that there were genetic mutations that took advantage of evolutionarily based neuroendocrine plasticity. By plasticity they mean a mechanism conserved among vertebrates, upon which selection can act and generate variation in sexual phenotypes. Rahman and Wilson [44] base their theorizing on Grober’s [52] work with teleost fi sh, which exhibit a variety of sexual phenotypes. Specifi cally, according to Rahman (personal communication), there are shifts in the sex of the fi sh (i.e. sexually active males and females regularly transform into an alternative reproductive morph) with accompanying changes in sexual behavior. 

The neuroendocrine mechanism, which permits this is plastic in its ability to change structure and function (see also [53]) and involves changes in the hormones produced by the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-gonadal (HPG) axis. Rahman (pers. comm.) speculates that social cues affect the neural substrates, which change the level of sex hormones through the feedback loops associated with each neural axis. Indeed, Grober and Sunobe [54] demonstrated that socially mediated serial sex change in the marine goby (Trimma okinawae) involves signifi cant and reversible changes in the size of arginine vasotocin-producing forebrain cells. Changes in these sex hormones cause structural and functional changes in neural structures associated with sexual behavior such as the preoptic area of the hypothalamus and the supra-chiasmatic nucleus. These are the same areas that are believed to be associated with sexual orientation in mammals, including humans.

Brain differentiation as an evolutionary adaptation 
Rahman and Wilson [44] agree in principal with the idea that homosexual behavior may have been adaptive because it contributed to alliance formation. Frank Muscarella, Bernhard Fink, Karl Grammer, Michael Kirk-Smith Neuroendocrinology Letters ISSN 0172–780X Copyright © 2001 Neuroendocrinology Letters 397 However, they disagree that humans are essentially bisexual and argue that evidence supports a bimodal male sexual orientation and possibly trimodal female sexual orientation. They also point out that Kirkpatrick [5] and Muscarella [6, 29] have failed to theorize on the genetic-endocrine basis for selection for homosexual behavior. Based upon research on the sex shift of fi sh and Miller’s [25] theory of selection for feminine traits in men, Rahman and Wilson [44] propose that variations in genotypes produced hominid males who were more feminine in behavioral traits and bisexual in sexual preferences. These characteristics contributed to same-sex affi liation and females were attracted to these traits because they were associated with decreased aggression and infanticide, and increased parenting behavior. Over time, females chose increasingly feminine traits in males, which led to the evolution of alleles associated with exclusive homosexual interest. 

The contribution of the feminine traits to parenting and the viability offspring offset the reproductively deleterious effects in males. In this way, alleles for bimodal homosexuality are maintained in a balanced polymorphism. However, there appears to be a signifi cant inconsistency in the argument made by Rahman and Wilson [44]. They speculate that particular genotypes present among hominids made males more feminine in behavioral traits and bisexual in sexual preferences. Thus, bisexuality was a successful survival and reproductive strategy for ancestral males, and there was selection for it. If this were the case, then the majority of human males would be expected to be bisexual or at least have the potential for bisexuality under certain conditions. 

This is what both Kirkpatrick [5] and Muscarella [6, 29] have argued. However, Rahman and Wilson [44] disagree with the contention that human males are essentially bisexual. It is not at all clear how a population of human males would have evolved to be essentially heterosexual when selection was for bisexual traits. According to a recent U. S. survey, only .8% of men were categorized as bisexual and 96.9% were categorized as heterosexual [55]. It does seem reasonable that a small percentage of men could be genetically predisposed to an exclusively homosexual orientation due to normal variation in the genotype regulating same sex preferences. However, it is not clear how a genotype for sexual preference theorized to be the most adaptive would disappear during the course of human evolution leaving genotypes for the less adaptive alternatives. It is possible that although contemporary surveys show a bimodal distribution of sexual orientation this refl ects the effects of cultural constraints and not actual genotypic variation. 

For example, a dictum of evolutionary psychology is that males evolved to be sexually promiscuous (e.g., [56]), but the majority of married American men remain faithful to their wives [55] appearing essentially monogamous. Most ethological observers would agree that this apparent monogamy is best explained as the result of culture constraints upon evolutionary predispositions. In a similar light, it would be scientifi cally reckless to assume that the incidence of a behavior as complex and poorly understood as human sexual orientation refl ected genotypic variation devoid of cultural and societal infl uences. From this perspective, Rahman and Wilson’s [44] theory of selection for bisexual traits in human evolution may be more similar than it appears to that proposed by Kirkpatrick [5] and Muscarella [6, 29].

Conclusion 
The minds of scientists, and the questions they ask, are shaped by the cultures in which they live. Contemporary Western culture has been shaped by Judeo-Christian beliefs, foremost among which has been that the purpose of sex is procreation. This driving assumption is the reason that, historically, the study of the cause of homosexuality has generated such a preponderance of research in the area of human sexuality [1]. Twentieth century advances in research technology have not altered the underlying assumption. Thus, sophisticated methods for identifying and measuring hormones and genes are still used to try to answer the question what causes homosexuality? There are also more nefarious implications to this search because the identifi cation of a cause implies the existence of an intervention, which will allow successful elimination of the behavior. Thus, the scientifi c quest for the cause of homosexuality continues to have compelling implications for those men and women whose sexual orientation has been deemed by society as requiring explanation. Even evolutionary psychology, which promised different insights into human nature, relied heavily upon unquestioned assumptions about homosexual behavior [6].（essay代写)

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