Prairie voles are monogamous. Their close cousins, the montane voles, tend to sleep around. But, tweak a hormone receptor or two, and you can practically re-program each vole’s sexual proclivities. When their vasopressin hormone receptors are blocked, prairie voles turn from homebodies into home-wreckers who cheat. And when the vasopressin hormone flows freely in the montane vole bloodstream, even the most sexually liberated rodents settle down and start families.
The implication is clear — genetics can, under some circumstances, mediate sexual and social behavior. But is there really a gene linked to promiscuity? Will voles be voles? And, if genetics determine sexual behavior, do the also excuse human infidelity on some level? The short answer: probably not. Indeed, after Dr. Richard Friedman, professor of clinical psychiatry at Weill Cornell Medical College, raised the possibility of an “infidelity gene,” Scientific American’s John Horgan responded with skepticism. “This claim — like virtually all reported linkages of complex human traits and disorders to specific genes —is based on flimsy, contradictory evidence,” he wrote.
To be fair, it’s not just rodent trials. A handful of studies in humans have suggested that genes and hormones may predispose some men and women to infidelity. The consistent culprit seems to be vasopressin, a hormone that impacts trust, empathy, and sexual bonding. One Finnish study found that women who carry variants of the vasopressin receptor gene are more likely to self-report sexual promiscuity. Although no such observation was found in men, the study suggests that some women are “biologically inclined to wander,” Friedman wrote in the New York Times. “Women who carry certain variants of the vasopressin receptor gene are much more likely to engage in ‘extra pair bonding,’ the scientific euphemism for sexual infidelity.”
At the same time, the vast majority of research into potential infidelity genes has come up empty. Horgan cites a 2004 study, a 2008 study, and a handful of other studies that have failed to find any connection between vasopressin receptors and infidelity. And while other studies have suggested a link between oxytocin receptors and promiscuity, the Finnish study itself found no such link. In a word, none of the studies seem to agree upon a consistent receptor or gene that even correlates with — let alone mediates — unfaithful or promiscuous behavior in humans.
The authors of the Finnish study know how it looks. “Problems with the replicability of candidate-gene associations for behavioral traits are well documented,” they write.
And with good reason. “The literature on candidate gene associations is full of reports that have not stood up to rigorous replication. This is the case both for straightforward main effects and for candidate gene-by-environment interactions,” according to a 2012 editorial published in the journal Behavior Genetics. “As a result, the psychiatric and behavior genetics literature has become confusing and it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge.”
Is there an infidelity gene? Maybe. Future studies will surely chip away at this question. But if prior work in the field of behavior genetics is any indication, it’s safe to say the answer is no.