A new study has uncovered a potential evolutionary origin of the female orgasm, using a rabbit model. The findings are published in Proceedings of the National Academy of Sciences.
Why does the female orgasm exist?
Whilst some are likely unopposed to its evolution, female orgasm is not actually necessary for successful human reproduction, despite its underlying neuroendocrine complexity. So why does it happen?
In short – scientists are not entirely sure. Several hypotheses exist, but few of them have empirical support. However, a recent study into one such hypothesis has suggested that female orgasm is the result of an evolutionary mechanism.
In this study, researchers investigated the ovulatory homolog model (OHM), which suggests that female orgasm is an evolutionary “left-over”, a consequence of physiological mechanisms developed to trigger ovulation during copulation. “The OHM posits that the neuroendocrine mechanisms underlying female orgasm are evolutionarily derived from the mechanisms that cause ovulation in animals with copulation induced ovulation (CIO)” says Günter Wagner, co-author of the study.
CIO occurs in many mammalian species, including rabbits, cats and ferrets – but not in humans.1 Since these species exist within the same mammalian subclass, the authors concluded that, if female orgasm evolved according to the OHM, then pharmacological agents that affect human orgasm would also affect ovulation in these species. The agent chosen to investigate was fluoxetine, an SSRI that is widely used as an antidepressant.
On their choice of animal model for these tests, Wagner says: “It is known that fluoxetine causes anorgasmia (inability to reach orgasm) in women. We reasoned that if orgasm and male-induced ovulation are phylogenetically related, fluoxetine would also reduce the rate of ovulation after copulation in rabbits. Rabbits are the animals in which CIO is best documented.”
Over the course of two weeks, female rabbits were given a daily dose of fluoxetine. After this period, copulation was allowed to occur; one day post-copulation, the authors measured the number of ovulations through retrieval of the ovaries.2
In fluoxetine-treated rabbits, the number of ovulations was 30% lower than in the control group. Although this supports the OHM, the authors cautiously mention that this is a relatively modest effect. Why wasn’t ovulation fully suppressed? The authors noted that during the experiment that rabbits are much better than humans at breaking down fluoxetine. This would create difficulties in producing the same side-effects of fluoxetine in rabbits as those occurring in humans. Of this, Wagner concludes: “Maybe other molecules that have SSRI effects would have shown stronger effects. But nevertheless, the effects we found remain statistically significant.”
The researchers also acknowledged further limitations. In a secondary experiment, the fluoxetine regime was repeated, but this time, ovulation was induced by injection of human chorionic gonadotropin (hCG). hCG is structurally similar to luteinizing hormone, the molecule involved in inducing ovulation in humans.3 This time, they discovered that fluoxetine did not have a significant effect on ovulation. These findings suggest that fluoxetine affects ovulation in rabbits via the central nervous system elements of CIO, rather than directly affecting the ovaries.2
Overall, it was concluded that CIO in rabbits and orgasm in female humans are homologous; in other words, they share a common evolutionary origin.
Asked about the route ahead for this research, Wagner says: “There are two directions one should go: There is an argument to repeat similar experiments with other species that have CIO, to test whether our finding in rabbits are representative for CIO in general, plus experiments with animals that have other copulation-induced effects, like the copulation-dependent maintenance of the corpus luteum in mice.”
“The bigger question looming after this positive result is that the research question shifts from “How did the female orgasm evolve?” to “Why is it maintained after its function in ovulation was lost?”. We have some ideas, but these are speculative at this point and might not be a good idea to discuss before we have evidence.”
1. Bakker, J. and Baum, M.J. (2000) Neuroendocrine regulation of GnRH release in induced ovulators. Frontiers in Neuroendocrinology. DOI: https://doi.org/10.1006/frne.2000.0198
2. Pavlicev, M. et al. (2019) An experimental test of the ovulatory homolog model of female orgasm. PNAS. DOI: https://www.pnas.org/cgi/doi/10.1073/pnas.1910295116
3. Choi, J. and Smitz, J. (2014) Luteinizing hormone and human chorionic gonadotropin: Origins of difference. Molecular and Cellular Endocrinology. DOI: https://doi.org/10.1016/j.mce.2013.12.009