Of the dozens of hormones found in the human body, oxytocin might just be the most overrated. Linked to the pleasures of romance, orgasms, philanthropy, and more, the chemical has been endlessly billed as the “hug hormone,” the “moral molecule,” even “the source of love and prosperity.” It has inspired popular books and TED Talks. Scientists and writers have insisted that spritzing it up 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’s said about the hormone is, at best, hyperbole. Sniffing the chemical doesn’t reliably make people more collaborative or trusting; trials testing it as a treatment for children with autism spectrum disorder have delivered lackluster results. And although decades of great research have shown that the versatile molecule can at times spark warm fuzzies in all sorts of species–cooperation in meerkats, monogamy in prairie voles, parental care in marmosets and sheep–under other circumstances, oxytocin can turn creatures from rodents to humans aggressive, fearful, even prejudiced. Now researchers have discovered that oxytocin is not sufficient to forge strong bonds. A new genetic study hints that prairie voles–fluffy, fist-size rodents that have long been poster children for oxytocin’s snuggly effects–can permanently partner up without it. This revelation may shake foundations in a whole neuroscience sub-field and force scientists to reexamine some of the older evidence which once suggested that oxytocin is the only way to animal affection. Cuddles, it turns out, can probably happen without the classic cuddle hormone–even in the most classically cuddly creatures of all.
Oxytocin isn’t necessarily obsolete. Lindsay Sailer from Cornell University, neuroscientist, says that this shouldn’t be taken to mean, “Oh, oxytocin does nothing.” But researchers have good reason to be a bit gobsmacked. For all the messy, inconsistent, even shady data that have been gathered from human studies of the hormone, the evidence from prairie voles has always been considered rock-solid. The little rodents, native to the midwestern United States, are famous for being one of the few mammal species that monogamously mate for life and co-parent their young. Over many decades and across geographies, researchers have documented how the rodents nuzzle each other in their nests and console each other when stressed, how they aggressively rebuff the advances of other voles that attempt to homewreck. And every time they checked, “there was oxytocin, sitting in the middle of the story, over and over again,” says Sue Carter, a behavioral neurobiologist who pioneered some of the first studies on prairie-vole bonds. The molecular pathways driving the behaviors seemed just as clear-cut: When triggered by a social behavior, such as snuggling or sex, a region of the brain called the hypothalamus pumped out oxytocin; the hormone then latched on to its receptor, sparking a slew of lovey-dovey effects.
Years of follow-up studies continued to bear that thinking out. When scientists gave prairie voles drugs that kept oxytocin from linking up with its receptor, the rodents started snubbing their partners after any tryst. Meanwhile, simply stimulating the oxytocin receptor was enough to coax voles into settling down with strangers that they’d never mated with. It was so clear, repeatable and undisputed that the connection between oxytocin, pair bonding, became a dogma. Zoe Donaldson, a neuroscientist at the University of Colorado at Boulder who studies the hormone, recalls once receiving dismissive feedback on a grant because, in the words of the reviewer, “We already know everything that there is to know about prairie voles and oxytocin.”
So more than 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 figured that their experiments would be a slam dunk. Shah explained that part of their goal was proof of principle. Researchers still have not developed genetic tools to cleave the oxytocin receptor in prairie voles like they do for mice and other common lab animals. Shah predicted that if the manipulations were successful, the rodents would be able to produce a new line of mice that is immune to the effects of oxytocin. This would prove that CRISPR had succeeded in its mission.
That’s not what happened. The rodents continued to snuggle up with their families, as if nothing had changed. It was quite amazing. At first, the team wondered if the experiment had simply failed. “I distinctly remember sitting there and just being like, Wait a sec; how is there not a difference? ” Kristen Berendzen, a neurobiologist and psychiatrist at UC San Francisco who led the study, told me. The same result was seen again when the three different teams of researchers tried the same manipulations. It was as if they had successfully removed a car’s gas tank and still witnessed the engine roaring to life after an infusion of fuel. It is possible that something went wrong during the experiment. However, it seems unlikely that this is the case, according to Larry Young, Emory University neuroscientist who was not involved in the new research. Young told me that his team has achieved almost identical results in his laboratory.
The explanations for how decades of oxytocin research could be upended are still being sussed out. Maybe oxytocin can attach to more than one hormone receptor–something that studies have hinted at over the years, Carter told me. But some researchers, Young among them, suspect a more radical possibility. Perhaps oxytocin stops working at its normal receptor and the brain instead uses the new pathway to affection. “I think other things pick up the slack,” Young told me.
This idea doesn’t completely reject the older research. Devanand Manoli at UCSF, a neuroscientist and psychiatrist, said that other prairie-vole studies using drugs with oxytocin receptors to stimulate the brain were also done. These rodent brains were wired to react to oxytocin throughout development and couldn’t adjust for the sudden loss later in life. But the Stanford-UCSF team bred animals that lacked the oxytocin receptor from birth, which could have prompted some other molecule, capable of binding to another receptor, to step in. Maybe the car never needed gas to run: Stripped of its tank from the get-go, it went all electric instead.
It would be easy to view this study as yet another blow to the oxytocin propaganda machine. The results, according to the scientists I talked with, are far more interesting than this. Carter said that this proves how crucial pair bonding can be to prairie voles and us. Partnering up for social mammals is more than a sentimental act. It’s an essential piece of how we construct communities, survive past childhood, and ensure that future generations can do the same. “These are some of the most important relationships that any mammal can have,” says Bianca Jones Marlin, a neuroscientist at Columbia University. If oxytocin is present, that’s likely to be the reason for your intimacy. And if it’s not? “Evolution is not going to have a single point of failure for something that’s absolutely critical,” Manoli told me. Knocking oxytocin off its pedestal may feel like a letdown. It’s comforting to know that the desire to form a bond with your partner is unbreakable.
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