A new study asks an interesting genetics question: if there was a gene that controlled homosexuality—and hence limited reproduction—how could it be favored to exist? If there is a gene that causes one to not reproduce, natural selection would dictate that it cannot survive long in a population, since it is not being passed on to future generations. A new paper in the Proceedings of the Royal Society is using population-genetics modeling to try and answer why a theoretical gene predisposing an individual to homosexuality could spread in a population.

It needs to be mentioned that this is merely a theoretical study, and that there is no known gene that dictates one's sexuality. However, there is evidence that at some level genetics plays a role. It is known that human twins are more likely to both be gay when compared with non-identical siblings. It has also been reported that male homosexuality is often inherited from the maternal line, suggesting that a gene on the X chromosome may play some role. The question then becomes: if a gene existed that caused one to have no desire to reproduce (through heterosexual intercourse), how can this theoretical gene persist throughout generations?

The theoretical study by Gavrilets and Rice looked at a single gene with two alleles (variants) and examines three previously reported hypotheses as to how this gene can persist in a population. It should be noted that this model did not strictly classify an individual as straight or gay, but determined the level of homosexual activity by relating it to the fitness within the model. The first mechanism examined is one of overdominance, where in this scenario if the offspring only receives the 'gay allele' from one parent (heterozygous), then they would have a competitive reproductive advantage over others in the population. Here the 'gay allele' would need to be received from both parents (homozygous) in order for the offspring to exhibit homosexuality and have a reproductive disadvantage. The next hypothesis is one of kin altruism, where homosexuals would help their own family members, thereby increasing the family's fitness and allowing the gene (which would be present in the family group) to be passed on to the next generation. The final previously posited hypothesis, sexually antagonistic selection, is that—in the case of male homosexuality—the allele would result in a fitness loss for male offspring, but a fitness gain in female offspring. The gain in fitness for female offspring would potentially result in more offspring in the next generation having this allele.

Through modeling of classical population-genetics equations, the authors describe the evolution and frequency of these two alleles throughout a large population. The authors find conditions in which overdominace or sexually antagonistic selection hypotheses could lead to a stable population with this homosexual gene in place when it is located on autosomes (non-sexual chromosomes) or on the X chromosome. The models found that under the sexually antagonistic selection, the homosexual allele would become very prevalent, provided that those who carried two alleles of it were generally bisexual. This is an interesting hypothesis, which seems to hearken back to the work of Kinsey in the late 1940's and early 1950's where he suggested that sexuality was a spectrum and people were not fully straight or gay, but existed somewhere in between. This work at hand represents a interesting study into the 'Darwinian paradox of male homosexuality'. Even though the study was only theoretical, it produced some interesting results and shows what can be done with modeling and simulation, a field I am partial to.