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Homosexuality: The Sophistication of Natural Selection

Homosexuality is a hot and controversial topic in the current socio political sphere, but a different area of controversy has been gathering a substantial amount of debate. The persistence and prevalence of homosexuality shakes the foundation of basic evolutionary concepts, and implies fundamental inconsistencies in our classical understanding of natural selection and reproductive success. Recent research has made sexual orientation a nearly tangible substance. Strong correlates to sexual preference have been found in the anatomical and genetic makeup of the individual. Homosexuals as a group have a lower reproductive fitness than their heterosexual peers because homosexual partnering do not typically produce offspring, though the reproductive fitness of homosexuals is notably not zero due to the use of alternative methods. That a trait such as homosexuality hinders individual reproductive success, yet persists throughout a population subject to evolutionary pressures, is counterintuitive. Many researchers speculate over what has been dubbed a Darwinian paradox, a phenomenon that should, but does not seem to be, subject to Darwinian evolutionary pressure. The evolutionary and biological means by which this paradox exists are still being determined but the current research in homosexuality has managed to highlight the complexity and sophistication of natural selection. Many hypothetical mechanisms are supported by empirical evidence, and others remain hypotheses. I propose that these mechanisms, in particular polygenic traits, sexual antagonism, and in utero immunological reactions, can work concurrently to promote homosexuality in the individual, while also serving to fill in reproduction through indirect benefits to kin.

Introduction – A Darwinian Paradox

Why does homosexuality shake the foundations of natural selection theory?

The topic of homosexuality has been in the cultural spotlight for decades. Research into the origins of sexual orientation traces back to the 19th century and is shaded by moralistic beliefs that homosexuality is a choice or culturally influenced. It has been considered a Darwinian paradox since evidence began accumulating regarding the reduced reproductive fitness (Moran, 1972) and implications of a genetic basis for sexual orientation through family studies (Pillard, Poumadere, & Carretta 1981; 1982; Pillard & Weinrich 1986). Homosexuality has been considered a hole in Darwin’s logic and conversely Darwin’s theory of evolution has been used to argue against the heritability of homosexuality (Moran, 1972).

Darwin’s theory of evolution was established in the 19th century and modified as the mechanisms of heredity came to light. According to resulting synthesis, natural selection acts on phenotypes that affect reproductive fitness, or overall success at producing offspring, when variation in traits is heritable. Variation in reproductive fitness causes a difference in reproduction which could be small for individuals, but can have massive impacts over many generations. Traits that improve reproductive fitness will be selected for by producing more offspring, which will increase the trait’s frequency in the population. Traits that are disadvantageous to reproduction are weeded out and thus their genetic contribution is reduced.

For homosexuality to have a genetic basis, it must be subject to the same selection pressures as other heritable phenotypes. Yet, counter-intuitively, homosexuality persists. As evidence indicating a genetic aspect to homosexuality has accumulated, the peculiarity of this persistence has become more and more apparent. Rather than devastating evolutionary theory, new discoveries and conceptual evolutionary models by which homosexuality benefits a population have highlighted the complexity and sophistication of natural selection.

Homosexuality is not the only situation where traits that reduce personal reproductive fitness somehow escape the grasp of natural selection and manage to maintain a roughly stable frequency in the population. Some females select for the production of “sexy sons,” choosing mates by attractiveness instead of parental contribution (Weatherhead & Robertson, 1979) and thus reducing her immediate fecundity. Alleles for sickle cell anemia persist despite the devastating effect they have on individual survival, due to the health benefit they provide to heterozygous carriers in a malaria-ridden environment (Stearns & Hoekstra, 2005). These examples illustrate the degree to which a simplistic version of natural selection theory underestimates the subtleties of evolution. Complex dynamics can maintain individually disadvantageous traits in the population.

Sexual Dimorphisms

Empirical evidence accumulated during the past decades indicate that human sexuality is reflected in our biological framework. In basic terms, a fundamental attraction to women would be essential to the reproductive success of men, and vice versa. Influential brain structures for sexual behavior have repeatedly diverged from the gender norm in homosexual individuals. Indeed, much research has established that sexual dimorphisms, or structural differences in the brain, occur both between genders and between sexual orientations. Homosexual males have a significantly larger suprachiasmatic nucleus and anterior commissure, substructures within the hypothalamus, an influential brain structure for sexual behavior, than their heterosexual peers (Swaab & Hofman, 1990; Allen & Gorski, 1992). The anterior portion of the hypothalamus of homosexual males, similar to heterosexual females, is significantly smaller than heterosexual males (LeVay, 1991). To cement the significance of these patterns, sexual orientation dimorphisms have been shown to occur in animal models demonstrating homosexual behavior (Roseli et al., 2004).

Research has shown that, when exposed to different visual stimuli, individuals of similar sexual orientation exhibit characteristic neural patterns of sexual arousal (Safron et al., 2007; Hu et al., 2008). Similarly, the hypothalamic response of homosexual men to odorous pheromones is more similar to the response of heterosexual females than that of heterosexual men (Berglund, Lindstrom, & Savic, 2006). Thus, these patterns of neural activation can be used to predict orientation (Safron et al., 2007; Hu et al., 2008).

Taken together, these findings suggest that the brains of homosexual individuals not only have significantly different dimorphisms, but also process visual and olfactory stimuli differently from their heterosexual peers. The homosexual anatomical structure of specific brain regions correspond to a female brain more so than a male brain. From an evolutionary perspective this correspondence is not strikingly out of place. Frequently sexual dimorphisms that occur in organisms are due to competition among males for female mates (Krebs & Davies, 1997; Darwin, 1871). Thus homosexual men do not seem to fit along this classical construct anatomically or behaviorally.

These patterns in brain activity and structure that occur with sexual orientation and gender cannot be claimed to be causal; another common factor may influence the emergence of homosexuality and these neurological differences. One cannot neglect the plasticity of the brain, the ability to reorganize neural pathways, according to life experiences. It is conceivable that, through repeated experiences and strengthening of neural connections, brain activity patterns could come to match that of a homosexual activation patterns, but empirical evidence in this area would be difficult to demonstrate and is currently lacking. The amount of hormones circulating in the blood has also been shown to modify mammalian brain structures to become more similar in size to the opposite gender (Cooke, Tabibnia, & Breedlove, 1999). The hypothalamus is responsible for the production of some of these neurohormones and the development of the hypothalamus in utero is influenced by the presence of these neurohormones (Swaab, 2005). In utero hormone experience could cause the sexual dimorphisms in the anatomical structures or by an atypical hypothalamus could produce hormones that result in sexual dimorphisms creating a chicken or the egg situation.

There could very well be a genetic basis controlling the structural development of the brain, hormone concentration, or susceptibility to experience. The precise biological mechanisms have yet to be untangled. But the neural similarities between individuals who are attracted to men, regardless of their gender, provide the possibility of biological substrates for sexual orientation whether genetically innate or acquired.

Prevalence, persistence, heritability:

Natural selection, if selecting by the reproductive success of individual’s phenotype, would not lend itself to supporting a genetic explanations of homosexuality. Homosexual individuals lack the natural opportunity to reproduce that attraction to the opposite sex provides heterosexual individuals. This disinclination to reproduce heterosexually produces a significantly lower reproductive fitness in homosexual individuals, as compared to heterosexual individuals. Homosexual men produce offspring at a tenth to a fifth the rate of heterosexual men (Moran, 1971; Bell & Weinberg 1978; Van de Ven et al., 1997; Saghir & Robins, 1972). Thus there is a significant gap between the reproductive fitness of a heterosexual and homosexual individual. It seems natural that heritable traits associated with that low reproductive success would be subject to selection pressures, and eventually eliminated from a population.

Yet homosexuality has persisted, and homosexual individuals make up a substantial minority of the population. Estimates of the percentage of self-reporting homosexuals vary between 1 – 5%, depending on location and definition (Gates, 2006; ONS, 2010; Laumann et al., 1994, Black et al., 2011; Diamond, 1993). Due to social stigma, other cultural influences, and differing definitions, it is difficult to definitively determine a demographic estimate of the occurrence of homosexuality. Purely for descriptive purposes, arbitrarily choosing an estimate from the US population of 1% and extending it to the world population of 6.8 billion would mean 68 million homosexual individuals. This is a substantial population in and of itself, further indicating the persistence of this trait.

Despite the theoretical improbability of the persistence of homosexuality, evidence has accrued that firmly establishes its heritability. Homosexuality runs in families (Pillard, Poumadere, & Carretta, 1981). Brothers of homosexual males are significantly more likely (7-11%) to be homosexual (Pillard & Weinrich, 1986; Bailey & Bell, 1993; Bailey et al., 1999). Most studies used self report of the sexual orientation of relatives, which could confound the results. It is possible to misinterpret the orientation of a relative. Outright underestimation of individuals at some varying degree of attraction to the same sex but do not identify as homosexual is another dangerous confound to achieving a representative estimate.

A variety of twin studies have found a concordance rate of homosexual incidence between twins to be roughly 20 – 50% for monozygotic twins, compared to a 20% concordance rate for dizygotic twins. Heritability, the genetic variance among individuals which accounts for the phenotypic variation, is responsible for approximately 30% of the occurrence of homosexuality in twins. A large portion of the variance of phenotypic expression of homosexuality remains open for interpretation, potentially including effects due to environmental factors. Still 30% is a significant portion to be explained by genetic variation. (Bailey & Pillard, 1991; Bailey & Zucker, 1995; Bailey et al., 2000; Kendler et al., 2000; Langstrom et al., 2010). Concordance rates differ in statistical significance according to the 2000 Bailey study. Set against the rest of the evidence for genetic bases for homosexuality, it is possible to give some credit to these past studies so long as it is done with caution. Further studies should work on replicating and improving twin study methodology and rigor. Incorporating brain scans for characteristic neural patterns of sexual orientation could avoid the bias of self-report and confounds from inference made about siblings in a survey.

Pedigree analysis shows that more maternal than paternal relatives of homosexual individuals are also homosexual (Camperio-Ciani et al., Hamer et al., 1993; Hu et al., 1995; Ciani, Cermelli, & Zanzotto, 2008). The asymmetrical inheritance pattern in family line for homosexuality further implicates a genetic basis for homosexuality, and more specifically the X chromosome. Though X–linkage is implicated and there is a particular gene is of interest (Hammer et al., 1993), control of homosexuality or even brain structure size by a single gene on one chromosome is highly unlikely. The specific role of a gene in development and transcription factor cascades is difficult to determine. Still the X-linked pattern provides further evidence for a genetic mechanism for homosexuality.

Evolutionary Mechanisms

The reproductive gap between heterosexuals and homosexuals is filled by means of several different evolutionary mechanisms: kin selection, polygenic traits, sexual antagonism, and immunological reactions. These models address the persistence of homosexuality by emphasizing potential benefits that make up for loss of reproductive success. Each model offers an origin or source of homosexuality coupled with potential positives given to a larger cohort which provide the necessary reduction in the reproductive gap to avoid a situation contrary to evolution theory. None of the models must function in isolation. If they act together, the combined benefits are better able to even out the costs of homosexuality at a population wide level. These evolutionary models can coexist and complement each other.

Kin Selection

Selection may act on the individual phenotype but the fitness of the genotype in a population depends on the averaged fitness of individuals hosting that genotype. This population wide view of genetic fitness could decrease the reduction of reproductive fitness. For a gene to survive, it needs to maintain frequency in the population whether the phenotype is present in the individual or not. Thus Wilson (1975) proposed the concept of inclusive fitness, the sum of direct reproductive fitness from the individual and their indirect affect on their relative’s reproductive success, as opposed to purely reproductive success being effect by evolution. Wilson also championed kin selection as the solution to the paradox of homosexuality (1975).

Kin selection attempts to explain the evolution of altruism, but the theory faces some major challenges. Due to greater genetic variation, reproductive fitness, and a shorter generation time, the individual rather than the group has the advantage. One selfish mutant can take advantage of the situation, invade, and outbreed the altruistics. This picture of altruism functions when the recipient shares some genetic relation to the altruistic individual. Thus perhaps increased benevolence to kin could provide the benefits offsetting the costs of the genes.

Wilson applied kin selection, paired with his concept of homosexuality, to help explain the reproductive gap. As he described it, homosexual individuals, free of the burdens of caring for their own children, are able to provide more resources, time, and care to family as a whole that would otherwise have been allocated to their own offspring. In this manner homosexuality increases the reproductive success and thus the frequency of their family’s genes in the gene pool. The same genes that cause an individual to be sexually attracted to the same gender could cause the bearer to behave more altruistically, empathetically and possibly even more nurturing. Gender atypical behavior is commonly present from childhood for homosexual individuals (). Are homosexual individuals hyper benevolent to their kin?

Empirical evidence does not support this theory. A series of behavioral and psychological studies found no difference in altruism of heterosexual or homosexual single men (Rahman & Hull, 2004). However, the measures used to assess the level of reproductive contribution from homosexual individuals to their kin were an odd conglomeration, including the desire to have children and monetary contributions to siblings. It does not encompass the entirety of one’s role in a family and is easily confounded. I am skeptical of the attitudes measured being indicative of the inclusive reproductive contribution of a single homosexual sibling.

Rather than trying to measure some intangible reproductive contribution, further research could demographically track the resulting reproductive fitness of siblings of heterosexual and homosexual individuals. There is an interesting pattern of increased fecundity for female relatives, as will later be discussed, and it could cause confounding results. A special sample of families with an adopted homosexual sibling compared against families with an adopted heterosexual sibling has the potential to remove the genetic aspect when calculating fecundity in kin and thus isolate the true contribution.

As this analysis of kin selection demonstrates, if the homosexual sibling offsets his own reproductive fitness loss by improving the reproductive fitness of kin, then an entire brood of children with one homosexual sibling maintains reproductive fitness. The benefit would have to be uncharacteristically high, if this were the only mechanism functioning. Still the social mores and stereotypes could obscure a representative measure of behavior and confound the proposed natural advantage of homosexual individuals provide to their kin. It is difficult to reach a conclusive end with kin selection, but this initial research allowed further research into other mechanisms by which a homosexual individual benefits kin.

Advantageous Polygenic Trait

(Rice 1998 balance)

Perhaps homosexual individuals’ indirect contribution to kin’s fitness is a lot more subtle than the provision of monetary or other forms of support. Rather, the indirect contribution could come from the genes they share with kin which confer a benefit to others that is does not to homosexual siblings. The proposed “feminization” of genes associated with homosexual men could increase the reproductive advantage of heterosexual men if they are kept outside the threshold which causes homosexuality. With these polymorphisms, or variation among alleles, comes more genetic diversity which improves the fitness of the entire group. A more feminized male is a more attractive mate (McKnight, 1997; Penton-Voak at al., 1999). Feminized men would be less competitive and tend to be more caring and nurturing and provide a better chance of survival for the woman’s offspring. This phenotypic gradient, also proposed by Miller (2000), could result from an accrual of these alleles in a polygenic fashion each contributing a small amount to a “feminizing” shift in a manner similar to the role of genes in the development of height. In this situation, once past a certain threshold in the individual the traits become deleterious to reproductive success due to the occurrence of homosexuality. Thus the “feminizing” alleles are under stabilizing selection which maintains the genetic frequency and diversity but does not allow it to reach either fixation of extinction.

Pleiotropic genes and overdominance are other evolutionary mechanisms by which stabilizing selection maintains genetic frequency. The polymorphisms in pleiotropic genes are a mixed bag of benefits and costs; they influence many other genes connected to a variety of traits. Miller (2000) suggests pleiotropic genes could control personality, sexual orientation, and behavior through the structural development of the brain and thus feminizing one would feminize the others. A more female typical personality may make the individual a more attractive mate but, if personality is matched with a more feminized sexual orientation, the feminization could end up damaging reproductive success. Overdominance allows the maintenance of reproductively detrimental traits in a population when the heterozygous state of a gene is the most fit. The feminizing factors of heterozygous genes allow an advantage to be gained from the same genes that cause homosexuality without being overblown into homosexuality that they could result from the homozygous state. Gavrilet and Rice (2006) purpose the mathematical model of accumulation of overdominant genes provides the best explanation whether or not the genes are x-linked or for the majority autosomal.

These feminizing genes could code for hormone producing structures, the hypothalamus, changing brain development and normal activity for homosexual individuals. If the polymorphisms do code for this we would note amongst heterosexual men that as the brain structure varies closer and closer to that of homosexual men there should be a clustering of genes that that have been proposed to “feminize.” This continuum should be visible at a neurological and if not a genetic level. Future research should follow up structural differences in the SCN and hypothalamus to determine if a “feminizing” continuum is present in heterosexual men and matched with an accrual of particular forms genes.

I hesitate to refer to the alleles and other mechanisms as feminizing because the mind is not perfectly “feminized.” The empirical data measuring more feminine traits in the Rahman and Hull (2004) study did not find any significant difference with homosexual and heterosexual men in altruism and affinity to children. Still similarities between heterosexual women and homosexual men do exist in brain structure and neural activity patterns. This view should be taken with caution and only the verified locations where homosexual males match more closely with heterosexual females should be used.

The different evolutionary mechanisms reviewed here do not necessarily act in isolation. In fact if homosexuality were a polygenic trait the individual genes could be an accumulation of overdominant genes, pleiotropic genes, overdominant pleiotropic genes, or some combination of each. A pleiotropic model has already been corroborated with heterosexual relatives of homosexuals enjoying higher fecundity and associated with gender atypical behavior in youth (Zietsch et al., 2008). It would be interesting to observe if femininity of heterosexual men varies along with the accrual of homozygous genes and if there was a tipping point at which carriers of these genes atypical sexual orientation.

This balancing act of benefits and costs assumes the genetic benefit of reproductive success to the heterosexual male carriers of these feminizing traits is significant enough to offset the reproductive loss due to homosexuality. This extreme demand would be necessary to maintain the trait in the population if it were the only mechanism at play. Women may also receive a reproductive benefit for being the host of the genetic factors which result in homosexuality and thus also contribute to the benefits gained from sharing genes with a homosexual sibling.

Maternal Fecundity

Female kin of homosexual men show a consistent pattern of increased fecundity (Ciani, Corna, & Capiluppi 2004; Iemmola & Ciani 2009; Vasey & VanderLaan 2007). The increase in fecundity by female relatives could supplement some portion of the fitness loss the genes cause to homosexual males. This balance of advantages given to female carriers of the same alleles compared to the disadvantages possible for in males resulting in homosexuality is called sexual antagonism. When analyzing diverse genetic models one locus sexual antagonism was found to be the best fit (Ciani, Cermelli, Zanzotto 2008). Genetic modeling has analyzed the plausibility of a couple of combinations and confirms scenarios of fitness gains by females outstripping fitness loss by males (Jain Sharma & Sharma 2008). Homosexual individuals tend to come from larger families and their maternal relatives tend to produce larger families (Baily & Pillard 1991, Bailey & Bell, 1993, Pattatucci & Hamer 1995; Rahman et al, 2008). These “feminizing alleles” discussed previously could have a similar effect on women resulting the hyperfertility, sexual proclivity, or ability to attract mates. This competitive pattern between the sexes could emerge through either X linkage or genomic imprinting.

This inheritance pattern of increased fecundity among maternal relatives indicates an X linked gene involved with the genetic mechanism that influences sexuality. Multiple studies have identified a candidate gene on the X chromosome as contributing or coocurring in a significantly high percentage of homosexual individuals (Hammer et al 1993; Hu et al. 1995, Hammer & Copeland 1993), though some research has found no correlation (King 2005). Should future research find this feminizing trait X linked, there is more chance to counterbalance a disadvantage in females than in males whether or not the genes are overdominant. The model proposed by Gavrilets and Rice promotes overdominance in both conditions even though typical models encourage sexually antagonistic relations when x linked.

A more detailed analysis of maternal line homosexuality has revealed a higher rate of homosexuality in the offspring of females than in the offspring of males in that maternal line (CANT FIND THIS PAPER - IMPORTANT). This poses problems for the x linkage and instead promotes the role of genomic imprinting and prenatal hormones in the development of homosexuality. Genomic imprinting has an important role in sex determination (McCarthy et al., 2009). Maternal factors packed in the egg that compete to control the expression of genetic traits would be passed on through a daughter but could not get into the next generation through a son (Miller Gavrilets and Rice 2006). The occurrence of homosexuality and increased fecundity could be explained by the inherited factors and genomic imprinting occurring at fertilization and through development of the zygote.

This is a difficult topic and I need to learn more about the intricacies of genomic imprinting and its relationship with genetics when considering heritability

Maternal Selection??? In Stat analysis paper

If heritable maternal effects influence homosexuality, then the distinction between autosomal versus sex-linked inheritance is eliminated and the parameter space supporting polymorphism is reduced. As a consequence, the fact that empirical evidence indicates that maternal effects can influence the expression of at least male homosexuality (Blanchard & Klassen 1997; Blanchard 2004) does not appear to create a context that expands the opportunity for polymorphism of genes influencing homosexuality. In the 1990s, there was a surge of interest in finding – Gavrilets and Rice 2006

Fraternal Birth Order

Blanchard (2004) found homosexuality becomes much more probable the more brothers a male has. In contrast the number of older females was not significantly correlated. It is known that homosexual individuals come from larger families (). These findings have lead to claims that larger families, and thus the benefit of higher fecundity in the previously proposed models, could be a mere correlate of birth order effect instead of higher fecundity (Zietsch et al, 2008). This extrapolation seems a bit far reaching, it fails to explain larger families of aunts related to homosexual individuals who do not themselves have a homosexual child. Fraternal birth order does not function on its own but is a contributing factor to the development of homosexuality.

Blanchard theorized some form of immunization reaction to proteins introduced into the mother’s system with every subsequent male child has a serial effect on fetal development. Though the precise biological mechanism is unknown, both the probability of having a homosexual child and smaller brain size increase the further a child is in the fraternal birth order (). The neurohormonal changes affect neurodevelopment and, as can be seen by the anatomical differences between homosexual brains and heterosexual brains, such changes could have a strong effect on sexual orientation.

Why would this immunological reaction persist? A mother that is susceptible to this kind of reaction when bearing her male offspring and thus decreasing the fecundity of her offspring would have a disadvantage compared to a mother who could tolerate the male proteins. Most of the previous mechanisms discussed have provided some indirect benefit to unaffected carriers of similar genetic makeup, aka siblings and kin. Is it somehow advantageous to have a higher frequency of homosexuality for sons lower in the birth order? I would purpose a couple of possible routes by which this could occur. Competition amongst sons could be reduced by increasing feminization. Diversity of personalities would be increased. Perhaps where the youngest sons suffer reproductive fitness losses the eldest enjoy advantage provided to the first born sons through minimized competition and genetic benefits. For further insight into the way in which these different mechanisms interact, further research should be performed.

Future Research

Possible Study Proposals Need more formalized formatting here – Can I just extrapolate on these proposed studies like I have in other portions of paper. Perhaps a paragraph for each. Should they be here at the end or integrated into the paper where their topic comes up?

Q: Does the immunological effect on sons damage the reproductive success of the brood or sacrifice the fitness of the youngest for the fitness of the eldest maintaining solid reproductive success of the brood

Q: Does the immunological effect on sons cause an increasing “feminization” the further down the fraternal birth order

Q: Can we isolate the genetic effect from the immunological effect. Identical twins: One gay, what is percentage with gay brother. DZ twins: One gay, what si percentage with gay brother. Does this change as a function of birth order? Maintaining constancy across birthorders (and thus immunological effects) what is the genetic impact of reoccurrence comparing siblings 100% identical genetically and 50% genetically related?

Conclusion

There is a reproductive gap that must be filled for homosexuality to dodge natural selection. Though scientists are still discussing the evolutionary mechanisms no one has been able to resolve the Darwinian Paradox of homosexuality. Sexual orientation is similar to height in that it is multifactorial (). Human beings are a product of a complex interplay of our genes but of every experience during and after conception. A genetic predisposition could succumb to feminizing shifts from a smaller a maternal immunological response. Thus the brain develops in such a way that a child not already genetically predisposed to have an atypical sexual orientation would not have developed a smaller anterior portion of the hypothalamus or other biological predictors. Conversely a strong immunological response could shift the neural development of a fetus not genetically predisposed. Nevertheless additive effects of all these mechanisms result in a continuum of possible phenotypes, some of which may suffer reproductive fitness loss but many more that gain a reproductive advantage through the many different mechanisms. The taboo nature of atypical sexual orientation causes difficulties for empirical testing; however with better techniques we will be able to make these measures more precise.

-...you can then develop your proposed combination of mechanisms (and further research) that can explain the persistence of homosexual traits

-...and finally combine/restate your proposed mechanisms, hypothetical results from your proposed research, AND those examples you mentioned earlier in a closing section of your paper where you can discuss, as you say, the "implications that homosexuality [and other counter-intuitive traits] have for our classical understanding of natural selection and reproductive success"

(wrapping the key bits of earlier sections with a nice bow can make for some

great closing paragraphs).

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6V8K-4R7NPWM-8&_user=483702&_coverDate=05%2F31%2F2008&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_searchStrId=1690682918&_rerunOrigin=scholar.google&_acct=C000022720&_version=1&_urlVersion=0&_userid=483702&md5=f0632f45d8ba3b8666572fdad96812f6&searchtype=a#tbl1

Research Question

Introduction/Thesis Question

What evolutionary and genetic mechanism(s) have allowed homosexuality to persist in the human population at low frequencies despite a lower reproductive fitness compared to heterosexual individuals?

Revised outline

Homosexuality is a hot and controversial topic in the current socio political sphere, but a different area of controversy has been gathering a substantial amount of debate. The persistence and prevalence of homosexuality shakes the foundation of the basic evolutionary concepts. What implications does homosexuality have for our classical understanding of natural selection and reproductive success? Research has explored and empirically established a level of biological and genetic foundation for homosexuality. Homosexual individuals have a lower reproductive fitness than their heterosexual peers since homosexual couplings are not viable to produce offspring unless they use alternative methods. The fact that such a damaging trait to individual reproductive success persists throughout a population subject to evolutionary pressures is counterintuitive. Many researchers speculate over what has been dubbed Darwin’s Paradox. The evolutionary and biological means by which this is possible are still being developed and refined. Many mechanisms have been proposed, some have been supported by empirical evidence others remain hypotheses but most seem to explain the origin and fill the reproductive gap in non mutually exclusive ways.

Introduction

Why is this important?

Homosexuality has biological foundations

Hypothalamus

Structure sizes

Brain Activity

Pheromones

Lowered Reproductive Fitness and Clear Persistence make it weird to consider as genetically linked

But it has, at least partially, genetic foundations

Familiarity Effect

Twin Studies

X Linked

But what mechanisms maintain this?

Group Selection

Kin Selection

How would it work

Empirical Study says no significant difference in feelings of affinity to kids, altruism, etc (Rahman & Hull, 2005)

Issues with the studies

What about running it on the practical time spent with respective family members rather than feelings of affinity?

Is monetary support of neice/nephew a sign of affinity from any population?

Not Traditional Group Selection: Advantages held for population with polygenic traits

Advantage to male carriers: Feminizing/Masculinizing Polymorphism

Rare (Provide Data)

Genetic fitness of group with high variability

Population Genetics – provides models (Jain, Sharma, & Sharma, 2009)

Presence of hormones in the developing brain – male/female neural phenotype (Remage & Bass, 2010)

Empirical Study says no significant difference in feelings of affinity to kids, altruism, etc{Please_Select_Citation_From_Mendeley_Desktop} (Rahman & Hull, 2005) (COUNTERS FEMINIZING POLYMORPHISM ARGUMENT)

A lot is drawn from affinity scales, could it conceivably be that

Advantage to female carriers: Higher Fecundity in Maternal Line

X-linked

Fecundity – potential reproductive capacity of an individual or population, both under genetic and environmental control, affecting fitness

Sexual antagonism: Female reproductive advantage Male reproductive disadvantage

Advantage and compensation by older brothers: Fraternal Birth Order Effect

Immunization effect (Blanchard)

Reduction of Competition

Purpose Study

Conclusion

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