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Of the dozens of hormones found in the human body, oxytocin may well be the most overrated. Linked to the pleasures of romance, orgasms, philanthropy, and more, the chemical has been endlessly touted as the “cuddle hormone,” the “moral molecule,” even “the source of love.” and prosperity”. He inspired popular books and TED talks. Scientists and writers have insisted that spraying it into human nostrils can instill compassion and generosity; online sellers have marketed snake oil oxytocin concoctions as «Liquid Trust».
But as my colleague Ed Yong and others have repeatedly written, most of what is said about the hormone is, at best, hyperbole. Sniffing the chemical doesn’t make people more collaborative or confident; trials testing it as a treatment for children with autism spectrum disorders have shown poor results. And while decades of extensive research has shown that the versatile molecule can sometimes trigger warm fluff in all sorts of species — cooperation in meerkats, monogamy in prairie voles, parental care in marmosets and sheep — in d In other circumstances, oxytocin can transform creatures ranging from rodents to aggressive, fearful, even prejudiced humans.
Now researchers are discovering that oxytocin may not only be insufficient to forge strong bonds, but also useless. A new genetic study suggests that prairie voles — fluffy, fist-sized rodents that have long been poster boys for the cozy effects of oxytocin — can associate permanently without it. The revelation could shake the foundations of an entire subfield of neuroscience and cause scientists to reconsider some of the oldest evidence that once seemed to point to oxytocin as the be-all and end-all of animal affection. It turns out hugs can probably happen without the classic hug hormone, even in the most cuddly creatures of all.
Oxytocin is not necessarily obsolete. «It shouldn’t be interpreted as ‘Oh, oxytocin doesn’t do anything,'» says Lindsay Sailer, a neuroscientist at Cornell University. But researchers have good reason to be a little dumbfounded. Despite all the messy, inconsistent, even shady data that has been gathered from human studies of the hormone, the evidence for prairie voles has always been considered rock solid. Small rodents, native to the Midwestern United States, are famous for being one of the few mammalian species that mate monogamously for life and co-parent their young. Over many decades and across geographic regions, researchers have documented how rodents curl up in their nests and console themselves when stressed, how they aggressively fend off the advances of other voles attempting to wreck. And every time they checked, «there was oxytocin, sitting in the middle of the story, over and over,» says Sue Carter, a behavioral neurobiologist who pioneered some of the earliest studies of prairie vole links. The molecular pathways driving the behaviors seemed equally clear: When triggered by social behavior, such as snuggling or making love, a brain region called the hypothalamus pumped out oxytocin; the hormone then latched onto its receptor, triggering a host of amorous effects.
Years of follow-up studies have continued to support this thinking. When scientists gave prairie voles drugs that prevented oxytocin from binding to its receptor, the rodents began to snub their partners after any date. Meanwhile, the mere stimulation of the oxytocin receptor was enough to entice the voles to settle down with strangers they had never mated with. The link between oxytocin and pair bonding was so strong, so reproducible, so indisputable that it became dogma. Zoe Donaldson, a neuroscientist at the University of Colorado at Boulder who studies the hormone, recalls once receiving dismissive comments about a grant because, in the reviewer’s words, «We already know everything there is. there is to know about prairie voles and oxytocin.”
So over a decade ago, when Nirao Shah, a neurogeneticist and psychiatrist at Stanford, and his colleagues set out to cleave the oxytocin receptor from prairie voles using a genetic technique called CRISPR, they thought their experiences would be a slam dunk. Part of the goal was, Shah told me, a proof of principle: Researchers haven’t yet perfected the genetic tools for voles the way they have for more common laboratory animals, like mice. . If the team’s manipulations worked, Shah explained, they would spawn a line of rodents immune to the influence of oxytocin, leaving them unfaithful to their mates and indifferent to their young, proving that the CRISPR machinery had done its job. work.
That’s not what happened. The rodents continued to huddle with their families, as if nothing had changed. The find was puzzling. At first, the team wondered if the experiment had simply failed. «I vividly remember sitting there and being like, Wait a second; how is there no difference?Kristen Berendzen, 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 like s «They had managed to remove the gas tank from a car and still saw the engine roar to life after an infusion of fuel. Something may have gone wrong in the experiments. That seems unlikely, however, states Larry Young, an Emory University neuroscientist who was not involved in the new study: Young’s team, he told me, produced nearly identical results in his lab.
Explanations for how decades of oxytocin research could be turned upside down are still being researched. Perhaps oxytocin can bind to more than one hormone receptor, which studies have suggested over the years, Carter told me. But some researchers, including Young, suspect a more drastic possibility. Perhaps in the absence of its usual receptor, oxytocin no longer does anything at all, forcing the brain to carve an alternate path to affection. “I think other things take over,” Young told me.
This idea is not a total repudiation of the old research. Other experiments on prairie voles that used futz drugs with oxytocin receptors were done on adult animals that grew up on the hormone, says Devanand Manoli, a psychiatrist and neuroscientist at UCSF who helped to lead the new study. Hardwired to respond to oxytocin throughout development, these rodent brains could not compensate for its sudden loss late in life. But the Stanford-UCSF team bred animals that lacked the oxytocin receptor since birthwhich could have prompted another molecule, capable of binding to another receptor, to intervene. Perhaps the car never needed gasoline to run: stripped of its tank from the start, it went all-electric instead.
It would be easy to dismiss this study as yet another blow to the oxytocin propaganda machine. But the researchers I spoke with think the results are more telling than that. “What this shows us is how important pair bonding is,” Carter told me — for prairie voles, but also potentially for us. For social mammals, associating isn’t just sentimental. It is an essential part of how we build communities, survive past childhood 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 neuroscientist at Columbia University. When the oxytocin is there, it probably packs the punch behind that intimacy. And if not? «Evolution won’t have a single point of failure for something absolutely critical,» Manoli told me. Knocking oxytocin off its pedestal may seem like a disappointment. But it’s almost heartwarming to consider that the drive to bond is simply unbreakable.