[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.
