May 24, 2015


[Now, before you run out and get your prospective partner genotyped for his or her vasopressin and oxytocin receptor genes, two caveats: Correlation is not the same as causation; there are undoubtedly many unmeasured factors that contribute to infidelity. And rarely does a simple genetic variant determine behavior.]

By Richard A. Friedman

AMERICANS disapprove of marital infidelity. Ninety-one percent of them find it morally wrong, more than the number that reject polygamy, human cloning or suicide, according to a 2013 Gallup poll.
Yet the number of Americans who actually cheat on their partners is rather substantial: Over the past two decades, the rate of infidelity has been pretty constant at around 21 percent for married men, and between 10 to 15 percent for married women, according to the General Social Survey at the University of Chicago’s independent research organization, NORC.
We are accustomed to thinking of sexual infidelity as a symptom of an unhappy relationship, a moral flaw or a sign of deteriorating social values. When I was trained as a psychiatrist we were told to look for various emotional and developmental factors — like a history of unstable relationships or a philandering parent — to explain infidelity.
But during my career, many of the questions we asked patients were found to be insufficient because for so much behavior, it turns out that genes, gene expression and hormones matter a lot.
Now that even appears to be the case for infidelity.
We have long known that men have a genetic, evolutionary impulse to cheat, because that increases the odds of having more of their offspring in the world.
But now there is intriguing new research showing that some women, too, are biologically inclined to wander, although not for clear evolutionary benefits. 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.
Brendan P. Zietsch, a psychologist at the University of Queensland, Australia, has tried to determine whether some people are just more inclined toward infidelity. In a study of nearly 7,400 Finnish twins and their siblings who had all been in a relationship for at least one year, Dr. Zietsch looked at the link between promiscuity and specific variants of vasopressin and oxytocin receptor genes. Vasopressin is a hormone that has powerful effects on social behaviors like trust, empathy and sexual bonding in humans and other animals. So it makes sense that mutations in the vasopressin receptor gene — which can alter its function — could affect human sexual behavior.
He found that 9.8 percent of men and 6.4 percent of women reported that they had two or more sexual partners in the previous year. His study, published last year in Evolution and Human Behavior, found a significant association between five different variants of the vasopressin gene and infidelity in women only and no relationship between the oxytocin genes and sexual behavior for either sex. That was impressive: Forty percent of the variation in promiscuous behavior in women could be attributed to genes. That is surprising since, as Dr. Zietsch points out, there are so many other factors that are necessary for promiscuous encounters, like circumstance and the availability of a willing and able partner. Although this is the largest and best study on this, it’s not clear why there was no relationship between the vasopressin gene and promiscuous behavior in men.
Other studies confirm that oxytocin and vasopressin are linked to partner bonding, which bears on the question of promiscuity since emotional bonding is, in a sense, the inverse of promiscuity. Hasse Walum at the Karolinska Institute in Stockholm found that in women, but not in men, there is a significant association between one variant of the oxytocin receptor gene and marital discord and lack of affection for one’s partner. In contrast, there was a significant correlation in men between a specific variant of the vasopressin receptor gene and lower marital quality reported by their spouses.
Now, before you run out and get your prospective partner genotyped for his or her vasopressin and oxytocin receptor genes, two caveats: Correlation is not the same as causation; there are undoubtedly many unmeasured factors that contribute to infidelity. And rarely does a simple genetic variant determine behavior.
Still, there is a good reason to take these findings seriously: Data in animals confirm that these two hormones are significant players when it comes to sexual behavior. An intriguing clue came from the pioneering work of Dr. Thomas R. Insel, now the director of the National Institute of Mental Health, who studied the effects of vasopressin and oxytocin in a little rodent called the vole. It turns out that there are two closely related species of voles: montane voles, which are sexually promiscuous, and prairie voles, which are sexually monogamous and raise their extended families in burrows.
After sex, prairie voles quickly develop a selective and enduring preference for their mate, while mating for montane voles is more of a one-night stand.
What Dr. Insel described is that the strikingly different sexual behavior of these two species of voles reflects the action of vasopressin in their brains. The vasopressin receptors in the montane and prairie voles are in completely different brain regions so that when these receptors are stimulated by vasopressin, there are very different behavioral effects.
When vasopressin is injected directly into the brain of the monogamous male prairie vole, it triggers pair bonding; in contrast, blocking the vasopressin receptors inhibits monogamy, but does nothing to stop sexual activity. In other words, vasopressin promotes social bonding, and blocking the activity of this hormone encourages social promiscuity.
In the monogamous prairie voles, the vasopressin receptors are close to the brain’s reward center, but in the philandering montane voles, these same receptors are mostly found in the amygdala, a brain region that is critical to processing anxiety and fear.
So mating for the prairie voles activates the pleasurable reward pathway, which reinforces mating and promotes attachment and thus monogamy. For the promiscuous montane voles, sex has little effect on attachment; any vole will do.
It is even possible experimentally to take a home-wrecking montane vole and make him behave like a family-oriented prairie vole. Using a virus as a delivery vehicle to transmit the vasopressin receptor gene, it’s easy to artificially boost the number of vasopressin receptors in the brain’s reward center, and make a male vole behave monogamously. The story for female voles is similar except that it is oxytocin, not vasopressin, that triggers monogamous behavior.
We don’t yet know from human studies whether the vasopressin receptor genes that are linked with infidelity actually make the brain less responsive to these hormones, but given the animal data, it is plausible.
EXPERIMENTS in which oxytocin and vasopressin are directly administered to humans show these hormones have effects that go beyond sex; they appear to increase trust and social bonding. In one study, for example, healthy subjects were randomly given either intranasal oxytocin or a placebo and then played a trust game. In this game, the two subjects either act as an investor or a trustee. The investor first has the chance of choosing a costly trusting action by giving money to the trustee. Then the trustee can either honor the trust by returning a portion of the money or violate it by not sharing the money. Those who play under the influence of oxytocin continue to trust and make generous monetary offers in response to betrayal, while subjects getting a placebo become less trusting and stingier after getting burned. Oxytocin appears to make us more socially trusting — even in situations where it may not be in our best interest to do so.
In one study of men, giving vasopressin enhanced the subjects’ memory for both happy and angry faces compared with a placebo, which implies that vasopressin could boost social affiliation and aggressive behavior since it increased social and emotional learning.
These findings also suggest potential therapeutic uses for oxytocin and vasopressin for people who have either a deficit or an excess of trust and social bonding. Autism is an example of a deficit, and indeed there is preliminary evidence that oxytocin may have some beneficial prosocial effects in this disorder. In contrast, Williams syndrome is a rare genetic illness in which kids are pathologically trusting and indiscriminately befriend complete strangers. The disorder is associated with baseline oxytocin levels that are on average three times above normal, so a drug that blocks oxytocin may curb their excessive trust.
If you have an Orwellian bent, you’ve probably already imagined the mischief you might do with these two hormones. You could surreptitiously make a potential investor more trusting or encourage a monogamous impulse in a partner who you suspect is cheating. All you need is aerosolized oxytocin or vasopressin, perhaps in a spiked air freshener or perfume. Kidding, of course, but you get the idea.
Sexual monogamy is distinctly unusual in nature: Humans are among the 3 to 5 percent of mammalian species that practice monogamy, along with the swift fox and beaver — but even in these species, infidelity has been commonly observed.
The evolutionary benefit of promiscuity for men is pretty straightforward: The more sexual partners you have, the greater your potential reproductive success. But women’s reproductive capacity is more limited by biology. So what’s in it for women? There may be no clear evolutionary advantage to female infidelity, but sex has never just been about procreation. Cheating can be intensely pleasurable because, among other things, it involves novelty and a degree of sensation seeking, behaviors that activate the brain’s reward circuit. Sex, money and drugs, among other things, trigger the release of dopamine from this circuit, which conveys not just a sense of pleasure but tells your brain this is an important experience worth remembering and repeating. And, of course, humans vary widely in their taste for novelty.
In a 2010 study of 181 young, healthy adults, Justin R. Garcia, then at Binghamton University, found that subjects who carried a variant of one dopamine receptor subtype, the D4 receptor, were 50 percent more likely to report sexual infidelity. This D4 genetic variant has reduced binding for dopamine, which implies that these individuals walk around at baseline feeling less stimulated and hungrier for novelty than those lacking this genetic variant.
So do we get a moral pass if we happen to carry one of these “infidelity” genes? Hardly. We don’t choose our genes and can’t control them (yet), but we can usually decide what we do with the emotions and impulses they help create. But it is important to acknowledge that we live our lives on a very uneven genetic playing field. A friend of mine, who is a bisexual woman in her early 50s, recently told me about her long history of sexual exploits outside of her marriage. She hadn’t had sex with her partner for many years, although she wanted to — “she just wasn’t into it anymore,” she told me. One day, she ran into a man she had known years earlier and, not long after, struck up an affair with him. “He was really into me and the sex was so exciting that I just went with it and decided not to say anything to my partner.” Here were all the usual factors that we know set the stage for extramarital sex: marital discord, sexual dissatisfaction and emotional alienation in the primary relationship. My friend was well aware of them and this was how she explained the basis of her own infidelity.
But when she told me that she’d cheated early on in her relationship with her partner, at least once when things were going well, I realized that she probably had a propensity for sexual exploration that seemed in some ways independent of the emotional status of her relationships.
For some, there is little innate temptation to cheat; for others, sexual monogamy is an uphill battle against their own biology.
The author is a professor of clinical psychiatry at Weill Cornell Medical College and a contributing opinion writer.