Homosexual behavior is largely shaped by genetics and random environmental factors, according to findings from the world’s largest study of twins.

Writing in the scientific journal Archives of Sexual Behavior, researchers from Queen Mary’s School of Biological and Chemical Sciences, and Karolinska Institutet in Stockholm report that genetics and environmental factors (which are specific to an individual, and may include biological processes such as different hormone exposure in the womb), are important determinants of homosexual behavior.

Dr Qazi Rahman, study co-author and a leading scientist on human sexual orientation, explains: “This study puts cold water on any concerns that we are looking for a single ‘gay gene’ or a single environmental variable which could be used to ’select out’ homosexuality - the factors which influence sexual orientation are complex. And we are not simply talking about homosexuality here - heterosexual behaviour is also influenced by a mixture of genetic and environmental factors.

The team led by Dr Niklas Långström at Karolinska Institutet conducted the first truly population-based survey of all adult (20-47 years old) twins in Sweden. Studies of identical twins and non-identical, or fraternal, twins are often used to untangle the genetic and environmental factors responsible for a trait. While identical twins share all of their genes and their entire environment, fraternal twins share only half of their genes and their entire environment. Therefore, greater similarity in a trait between identical twins compared to fraternal twins shows that genetic factors are partly responsible for the trait.

This study looked at 3,826 same-gender twin pairs (7,652 individuals), who were asked about the total numbers of opposite sex and same sex partners they had ever had. The findings showed that 35 per cent of the differences between men in same-sex behavior (that is, that some men have no same sex partners, and some have one or more) is accounted for by genetics. Rahman explains:

“Overall, genetics accounted for around 35 per cent of the differences between men in homosexual behavior and other individual-specific environmental factors (that is, not societal attitudes, family or parenting which are shared by twins) accounted for around 64 per cent. In other words, men become gay or straight because of different developmental pathways, not just one pathway.”

For women, genetics explained roughly 18 per cent of the variation in same-sex behavior, non-shared environment roughly 64 per cent and shared factors, or the family environment, explained 16 per cent.

The study shows that genetic influences are important but modest, and that non-shared environmental factors, which may include factors operating during fetal development, dominate. Importantly, heredity had roughly the same influence as shared environmental factors in women, whereas the latter had no impact on sexual behavior in men.

Dr Rahman adds: “The study is not without its limitations - we used a behavioral measure of sexual orientation which might be ok to use for men (men’s psychological orientation, sexual behavior, and sexual responses are highly related) but less so for women (who show a clearer separation between these elements of sexuality). Despite this, our study provides the most unbiased estimates presented so far of genetic and non-genetic contributions to sexual orientation.”

Source: Queen Mary, University of London

Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden. Niklas Långström, Qazi Rahman, Eva Carlström and Paul Lichtenstein. Archives of Sexual Behavior.

Josh says:

I’m glad studies like this are coming out (pun not intended). Once someone’s neurological structure is such that they’re gay, then it cannot be changed; the same goes for someone who is straight. I think many aspects of intelligence work this way as well - there is a proportionally smaller genetic component, but environmental factors during neurological development play the largest role.

Reporting in this week’s PLoS ONE, an Italian research team, consisting of Andrea Camperio Ciani and Giovanni Zanzotto at the University of Padova and Paolo Cermelli at the University of Torino, found that the evolutionary origin and maintenance of male homosexuality in human populations could be explained by a model based around the idea of sexually antagonistic selection, in which genetic factors spread in the population by giving a reproductive advantage to one sex while disadvantaging the other.

Male homosexuality is thought to be influenced by psycho-social factors, as well as having a genetic component. This is suggested by the high concordance of sexual orientation in identical twins and the fact that homosexuality is more common in males belonging to the maternal line of male homosexuals. These effects have not been shown for female homosexuality, indicating that these two phenomena may have very different origins and dynamics.

Male homosexuality is difficult to explain under Darwinian evolutionary models, because carriers of genes predisposing towards male homosexuality would be likely to reproduce less than average, suggesting that alleles influencing homosexuality should progressively disappear from a population. This changed when previous work by Camperio Ciani and collaborators, published in 2004, showed that females in the maternal line of male homosexuals were more fertile than average.

Challenged by all these empirical data, the authors of the new study published in PLoS ONE considered a range of different hypotheses for the genetic diffusion of male homosexuality. These included: the genetic maternal effects on sons, the heterozygote advantage (as is found in malaria resistance), and “sexually antagonistic selection.” The latter is a particular aspect of Darwinian evolution, in which genetic factors spread in the population by giving a reproductive advantage to one sex while disadvantaging the other. This type of evolution has been previously found in insects, birds, and some mammals, but never in humans.

To discover and clarify the dynamics of the genetic factors for homosexuality, the researchers had to screen a large set of models and exclude them one by one. They concluded that the only possible model was that of sexually antagonistic selection. The other models did not fit the empirical data, either implying that the alleles would become extinct too easily or invade the population, or failing to describe the distribution patterns of male homosexuality and female fecundity observed in the families of homosexuals. Only the model of sexually antagonistic selection involving at least two genes – at least one of which must be on the X chromosome (inherited in males only through their mother) – accounted for all the known data.

The results of this model show the interaction of male homosexuality with increased female fecundity within human populations, in a complex dynamic, resulting in the maintenance of male homosexuality at stable and relatively low frequencies, and highlighting the effects of heredity through the maternal line.

These findings provide new insights into male homosexuality in humans. In particular, they promote a focus shift in which homosexuality should not be viewed as a detrimental trait (due to the reduced male fecundity it entails), but, rather, should be considered within the wider evolutionary framework of a characteristic with gender-specific benefits, and which promotes female fecundity. This may well be the evolutionary origin of this genetic trait in human beings.

The possible widespread occurrence of sexually antagonistic characteristics in evolutionary processes, which play their evolutionary game by giving a fecundity benefit to one sex while disadvantaging the other, has only recently begun to be appreciated. This is understood as a key mechanism through which high levels of genetic variation are maintained in biological populations. Male homosexuality is just the first example of an unknown number of sexually antagonistic traits, which contribute to the maintenance of the natural genetic variability of humans. The new perspectives opened by the models developed for sexually antagonistic selection may also contribute to a better understanding of most genetically-based sexual conflicts, which are, at present, poorly understood in humans.

An unexpected implication of the new models concerns the impact that the sexually antagonistic genetic factors for male homosexuality have on the overall fecundity of a population. The findings suggest that the proportion of male homosexuals may signal a corresponding proportion of females with higher fecundity. Consequently, these factors always contribute, all else being equal, a positive net increase of the fecundity of the whole population, when compared to populations in which such factors are lower or absent. This increase grows as the population baseline fecundity decreases; this means that the genes influencing male homosexuality end up playing the role of a buffer effect on any external factors lowering the overall fecundity of the whole population.

Source: Public Library of Science

Camperio Ciani A, Cermelli P, Zanzotto G (2008) Sexually Antagonistic Selection in Human Male Homosexuality. PLoS ONE 3(6): e2282. doi:10.1371/journal.pone.0002282

Josh says:

Wow. While they did not actually find a gene mutation linked to this, the data fits the model. Certainly it provides an explanation, and I personally like it better than many other explanations. However, whether a male is homosexual or heterosexual cannot be solely genetic, but rather is more likely a genetic predisposition (though I could be wrong). So what about this type of mutation would create such a predisposition?

Note: For those not familiar with the term, fecundity refers to how fertile a female is or how many offspring are produced.