How did homosexuality evolve? There might be a clue in our genes

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Photo by christian buehner on Unsplash
Photo by christian buehner on Unsplash

An Australian led study of genetic variation has identified a possible reason why same-sex sexual behaviour may have persisted throughout human evolution. The study found that genetic variations linked to same-sex behaviour are also found in 'straight' people and when they do occur, those 'straight people' tend to have more sexual partners.  This could mean that 'straight' people with these genes may have had more children in our evolutionary past. A linked article says if this mating boost is enough to outweigh the ‘loss’ of reproduction among the same-sex group, this could resolve the evolutionary puzzle. The authors note that their findings should be interpreted with caution as the data is only from people with European ancestry in the UK and the US and the number of straight sexual partners people report today may not reflect what happened in the past.

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From: Springer Nature

­Evolution: Insights into the evolutionary continuity of same-sex sexual behaviour (N&V)

Genetic effects associated with same-sex sexual behaviour are also associated with a mating advantage among people who engage only in opposite-sex sexual behaviour, according to a study involving participants from the United States and United Kingdom published in Nature Human Behaviour. However, the authors caution that the genetic differences studied here are small, are spread throughout the human DNA sequence and capture only a small portion of the heritability of same-sex sexual behaviour. Further research is needed to confirm whether these findings apply to the wider human population.

Brendan Zietsch and colleagues analysed genetic effects for same-sex sexual behaviour (versus never having had sex with someone of the same sex) in a genome-wide association study (GWAS) of 477,522 people from the UK and the US. They also estimated genetic effects for opposite-sex sexual behaviour in a GWAS of 358,426 people from the same countries, who had only ever had opposite-sex partners and who also reported how many partners they had had in their lifetime. The authors found that genetic effects associated with same-sex sexual behaviour were also associated with having more opposite-sex sexual partners among individuals who had only ever had opposite-sex partners. The authors suggest that number of opposite-sex sexual partners is an indicator of mating success, which during evolution would have led to more children. The genetic effects Zietsch and colleagues identify may help to explain why same-sex sexual behaviour has persisted throughout the evolution of the human species: these genetic effects may have been favoured by evolution as they are associated with more children.

The authors note that there are a number of limitations to this study and their findings should be interpreted with caution. First, the data used in this study are only from individuals of European ancestry in the UK and the US and therefore capture a fraction of human genetic and behavioural diversity. This is likely to affect the results, as both same-sex sexual behaviour and number of opposite-sex sexual partners are highly societally regulated behaviours. Second, the number of opposite-sex sexual partners reported in individuals today may not be associated with a reproductive advantage in our evolutionary past.

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conference:
Nature Human Behaviour
Research:Paper
Organisation/s: The University of Queensland
Funder: A.R.S. received funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development specifically to investigate the genetics of sexual orientation: R01HD041563 (A.R.S. PI) and R21HD080410 (A.R.S., E.R.M. MPI). E.R.M., G.W.B. and S.G. are also supported by R21HD080410. No other member of the group received funding specifically for this study, but members of our team received salary funding from organizations as well as their own universities. B.P.Z. received funding from The Australian Research Council (FT160100298). A.A. is supported by ZonMw grant 849200011 from The Netherlands Organisation for Health Research and Development. Study-specific acknowledgements: This research uses data from Add Health, a programme project directed by K.M. Harris (PI) and designed by J.R. Udry, P.S. Bearman and K.M. Harris at the University of North Carolina at Chapel Hill, and funded by grant P01-HD031921 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, with cooperative funding from 23 other federal agencies and foundations. Information on how to obtain the Add Health data files is available on the Add Health website (http://www.cpc.unc.edu/addhealth). This research uses Add Health GWAS data funded by Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) grants R01 HD073342 to K. M. Harris (PI) and R01 HD060726 to K.M. Harris, J.D. Boardman and M.B. McQueen (MPIs).
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