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Of the dozens of hormones in the human body, oxytocin may be the most overrated. Linked to the pleasures of romance, orgasm, philanthropy, and more, the chemical has been endlessly described as the “cuddle hormone,” the “moral molecule,” and even the “source of love and prosperity.” She has inspired popular books and TED Talks. Scientists and writers have insisted that sprinkling it on a person’s nostrils can instill compassion and generosity; Online vendors have marketed their snake oil oxytocin formulations as a “liquid box.”
But as my colleague Ed Young and others have written repeatedly, most of what is said about the hormone is, at best, exaggeration. Inhaling the chemical does not make people more cooperative or trusting; The experiments I have tested as a treatment for children with autism spectrum disorder have given lackluster results. And while decades of great research have shown that the versatile molecule can occasionally stir up a warm haze in all sorts of species—cooperation in meerkats, monogamy in prairie voles, parental care in monkeys and sheep—under other circumstances, oxytocin can. It turns creatures ranging from rodents to humans into aggressive, fearful, even prejudiced.
Now researchers are finding that oxytocin may not only be enough to form strong bonds, but it’s also unnecessary. A new genetic study suggests that voles — fluffy, fist-sized rodents that have long inspired children to the endearing effects of oxytocin — can sustainably cooperate without it. This revelation could shake the foundations of an entire sub-field of neuroscience, and prompt scientists to revisit some of the oldest evidence that once seemed to show that oxytocin is the ultimate and ultimate factor of everything to animal affection. It turns out that cuddling can probably happen without the classic cuddling hormone—even in the most cuddly classic critter ever.
Oxytocin is not necessarily old. “This shouldn’t be taken as, ‘Oh, oxytocin doesn’t do anything,'” says Lindsey Seiler, a Cornell University neuroscientist. But researchers have good reason to be a little dumbfounded. For all the messy, inconsistent, and even suspicious data that’s been gathered from human studies of the hormone, , the evidence from prairie voles has always been considered solid.The small rodent, which lives in the Midwestern United States, is famous for being one of the few species of mammals that mates monogamously for life and co-cares for its young.Over many decades and across geographic regions, it has been documented They investigated how the rodents lulled each other into their nests and comforted each other when pressed, and how they forcefully rejected the advances of other mice trying to destroy the house.Every time they checked, “there was oxytocin, sitting in the middle of the story, over and over,” says Su. Carter, the behavioral neurobiologist who pioneered some of the first studies on the associations of prairie and vol. The molecular pathways that drive behaviors seemed quite straightforward: when triggered by a social behavior, such as For snuggling or sex, an area of the brain called the hypothalamus pumps out oxytocin. The hormone then attaches to its receptors, triggering a plethora of stimulating effects.
Years of follow-up studies bear out this thinking. When scientists gave the prairie mice drugs that prevent oxytocin from binding to its receptors, the rodents began to ignore their partners after any attempt. Meanwhile, simply stimulating the oxytocin receptor was enough to coax the rats into settling down with strangers they’d never mated with. The connection between oxytocin and pair bonding was so strong, so frequent, that it has no doubt become a dogma. Zoe Donaldson, a neuroscientist at the University of Colorado at Boulder who studies the hormone, recalls receiving dismissive reactions to the grant because, in the words of the reviewer, “we already know everything there is to know about prairie voles and oxytocin.”
So more than a decade ago, when Nirau Shah, a neurogeneticist and psychiatrist at Stanford, and his colleagues set out to sever the oxytocin receptor from prairie mice using a genetic technology called CRISPR, they discovered their experiments would be a severe blow. Part of the goal, Shah told me, was a proof-of-principle: Researchers haven’t yet mastered the genetic tools of mice the way they have in more common lab animals, like rats. Shah reasoned that if the team’s manipulations worked, they would produce a strain of rodents that were immune to the effects of oxytocin, leaving them unfaithful to their mates and indifferent to their young—proving that the CRISPR mechanism had done its job.
This is not what happened. The ferrets continued to snuggle up to their families, as if nothing had changed. The discovery was baffling. At first, the team wondered if the experiment had simply failed. “I distinctly remember sitting there and saying, wait a moment; How is there no difference?Kristen Berndzen, a neurobiologist and psychiatrist at UC San Francisco who led the study, told me. But when three separate teams of researchers repeated the manipulations, the same thing happened again. It was as if they had successfully removed the car’s gas tank and still saw the engine roaring to life after pumping fuel. Maybe something went wrong with the experiments. That seems unlikely, though, says Larry Young, a neuroscientist at Emory University who was not involved in the new study: Young’s team had produced nearly identical results in his lab, he tells me.
Explanations of how decades of oxytocin research turned upside down remain to be seen. Perhaps oxytocin could bind to more than one receptor for the hormone—something studies have indicated over the years, Carter tells me. But some researchers, Young among them, suspect a more radical possibility. Perhaps, in the absence of its usual receptor, oxytocin no longer does anything at all — forcing the brain to carve out an alternate route to affection. “I think there are other things that benefit from the recession,” Young told me.
This idea is not a complete rejection of ancient research. Other prairie foley experiments that used the drug to latch on to oxytocin receptors were conducted on adult animals raised with the hormone, says Devanand Manuli, a psychiatrist and neuroscientist at the University of California, San Francisco, who helped lead the new study. Wired to respond to oxytocin through evolution, these rodents’ brains were unable to compensate for their sudden loss late in life. But the Stanford University and University of California, San Francisco team bred animals that lacked oxytocin receptors since birth, which would have prompted another molecule, able to bind to another receptor, to intervene. The car probably never needed gas to run: It was stripped from its tank from the start, and it went all-electric instead.
It would be easy to see this study as yet another hit on the oxytocin propaganda machine. But the researchers I spoke with believe the findings reveal more than that. “What this shows us is how important pair bonding is” — for prairie voles, but potentially also for us, Carter told me. For social mammals, partnership isn’t just a matter of affection. It is an essential part of how societies are built, survive past childhoods, and ensure that future generations can do the same. “These are some of the most important relationships any mammal can have,” says Bianca Jones-Marlin, a Columbia University neuroscientist. When oxytocin is present, it likely provides the underlying attraction to that intimacy. And if not? “Evolution will not have a single point of failure for something critical,” Manoli told me. Throwing oxytocin off its base can feel like a disappointment. But it is almost comforting to consider that the impulse to interdependence is unbreakable.