The twisting road to a scientific breakthrough often includes a period of resistance—and sometimes even open hostility—from those who are still wedded to the mainstream view.
This was certainly the experience of three Northeastern researchers—Kim Lewis, Jonathan Tilly and Lisa Feldman Barrett—all of whom have made major discoveries in their respective fields. For each one, the journey began with something that simply didn’t make sense; something that others in the discipline were unable to explain, or chose to ignore.
But a streak of stubbornness, independence, and unquenchable curiosity compelled them to persist, and in doing so, they accomplished what others could not.
What follows is a look at three scientific odysseys, and the roller coaster of frustration and success that, in the end, led to discovery.
Seek and Destroy
By Bill Ibelle
Photography by Brooks Canaday
Kim Lewis’ 13-year scientific journey began with a paradox—and climaxed with a potential cure for MRSA, the so-called “superbug” that kills more than 10,000 Americans each year because of its ability to elude conventional antibiotics.
If his discovery makes it to market, it will provide a cure for hundreds of thousands of potentially fatal infections in the heart, lungs, and bones. In addition, Lewis is applying his breakthrough to parallel research he’s conducting on Lyme disease and antibiotic-resistant tuberculosis, as well as the development of new antibiotics.
As the director of Northeastern’s Antimicrobial Discovery Center, Lewis has dedicated his career to tracking and killing the elusive “persister cell” that makes chronic infections nearly impossible to treat. You could think of the cells as the Bin Laden of infectious disease, hiding until the coast is clear, and then reemerging to wreak havoc of catastrophic proportions.
The paradox Lewis encountered more than a decade ago was this: Traditional antibiotics killed the new superbugs in a petri dish, yet couldn’t touch them in humans. It didn’t make sense. Furthermore, the paradox had become a medical crisis as the number of superbug infections rose dramatically. MRSA (Methicillin-resistant Staphylococcus aureus) infections, which more than doubled from 2003 to 2008, cause more than 18,000 deaths per year, according to the Centers for Disease Control and Prevention.
The explanation, widely accepted in the medical community, was that the antibiotics couldn’t reach the superbugs because they lived within the protective fortress of biofilms—a sort of microbial slime that forms around surfaces within the body. This biofilm, according to conventional wisdom, had unknown properties that made infections impervious to antibiotics.
“These pathogens seemed invincible,” says Lewis, a University Distinguished Professor of Biology. “The standard drugs were not working. It looked like a problem without a solution.”
Which is exactly what attracted Lewis.
“It was the ultimate tough problem,” he says. “I had always been attracted to puzzles and paradoxes.”
The superbug seemed like the perfect focus—complex, extremely important, and enigmatic to scientists.
“Instead of solving the problem, the scientific community was sweeping it under the rug,” says Lewis.
Convinced that the biofilm “wasn’t the real culprit,” he staged a series of experiments to test the theory and quickly demonstrated that conventional antibiotics did, in fact, kill most of the bacteria within the biofilm. So why did the infections keep coming back?
“The reason appeared to be connected to a small subpopulation of cells that seemed invincible,” he says.
But if this was true, why hadn’t others reached this same conclusion?
So Lewis printed out every study he could find on biofilms, divided the foot-high stack with his postdoc, and found four papers that described a similar experiment. Every one of them ignored the subpopulation.
Lewis, who has uncanny recall, remembered a paper he had once read that was published by an Irish microbiologist in 1944. The author had been trying to kill staph infections with penicillin and was frustrated that a small subset of cells survived no matter how much penicillin he used. The author named his discovery “persister cells” and, to Lewis, they sounded exactly like what he was up against.
“The only purpose of persisters is to survive,” he says. “They don’t do anything else.”
As soon as antibiotic treatments are applied, the persister cells go dormant. Since antibiotics only attack active cells, the persisters survive, and when the antibiotic treatment is completed, they come out of their sporelike state and the infection resumes its growth.
“So we had met our ultimate adversary,” says Lewis. “We had found the culprit that had been overlooked. I was very excited.”
As it turned out, the scientific community was far from excited about an iconoclastic theory that would turn decades of scientific research on its head.
Lewis sent his paper to the prestigious journal Science. They weren’t interested. So he soldiered on, publishing his paper in another journal and eagerly awaiting the reaction from his fellow scientists.
“It was completely ignored,” he says. “It was like it never happened.”
So a year later, in 2001, he published a similar paper with a more confrontational title that he was sure the scientific community could not ignore. The paper, he recalls, “caused quite a commotion.” When a graduate student who worked in Lewis’ lab asked about it, he responded, “You have just helped to close an important field of science.”
A few months later, Lewis was slated to chair a session at the annual conference of the American Society for Microbiology. His session was the day after one that focused on biofilms.
“So I went to that session and waited for my opportunity,” he recalls. “During the Q&A, I said, ‘There is nothing unique about the biofilm’s resistance to antibiotics.’” He told the audience he had the research to prove it and invited them to attend his presentation the next day.
“They came and there was a vigorous discussion. I told them, ‘Look, this is a very simple experiment,’ and challenged them to reproduce it and see if they got the same results.”
Apparently they did, because quietly over the next several years, the field of biofilm resistance to antibiotics disappeared and Lewis received substantial funding in government grants for his research.
In spite of his years in the scientific wilderness, Lewis says he never doubted that he would win the battle against persister cells and the resistance of the scientific community.
“Science does not treat wimps kindly,” he says. “You must have a thick skin and an enormous tolerance for defeat.”
Lewis was no longer in scientific exile. He had identified the enemy and had a well-financed lab at Northeastern, with a team of dedicated graduate students and postdocs to help him with his research.
The first step was to isolate the persister cells—a difficult task because they were “slippery” and no one knew much about them. But by 2006, he had succeeded in isolating some and published several papers on this. This time, his work was widely accepted.
Lewis was on a roll and says he “naively” thought the next step would be relatively straightforward. All he had to do was determine the mechanism used by persister cells to shut down, and then find a compound to interrupt that process.
“This is one of the dangers of science,” he says. “It’s like a chess puzzle that seduces you with a solution that is simple, but wrong.”
What Lewis soon discovered is that persister cells don’t have a mechanism that shuts them down; they have at least 10.
“It was like a Hydra head—cut off one and two more grow back,” he says. “It looked like we had hit a dead end. The persister cells were invincible. There was nothing that could touch them.”
The scientist’s enemy
It appeared that Lewis had just completed a decade-long wild goose chase. There was only one thing to do.
“This is part of what I teach my students—how to shut down your common sense,” he says. “You have to start looking for a perfect solution and ignore whether it’s realistic. That mindset helps you battle your ‘common sense,’ which is what prevents you from inventing new things.”
»Sidebar: The Diffusion Chamber
Lewis started to think about the problem differently. What would an ideal solution look like? First, he would need something to activate an important process in the dormant cell. Next, he would need a compound that would corrupt that process, and in doing so, kill the cell.
“That’s the solution—but of course, it sounds far-fetched,” he admits.
So Lewis started looking for such a magical compound. He recalled a compound discovered and discarded by Eli Lilly in 1985.
“They didn’t even publish a paper about it,” says Lewis. “I read about it in a patent.”
Lewis was intrigued because the compound, ADEP, takes a different route to cell destruction. It activates an enzyme (ClpP) within the cell that causes the cell to cannibalize itself. This looked promising.
He investigated further and he found that ADEP was picked up by a second pharmaceutical company, Bayer, but soon dropped because cells quickly developed ADEP-resistant strains. Experiments performed by other researchers also indicated ADEP only worked on rapidly growing cells. If this was true, he had hit another dead end. But Lewis didn’t buy it.
“I knew that nature doesn’t make junk—and this compound sounded like junk. It only hits growing cells, it hits an unessential target, and resistance develops quickly. Why would nature bother making something like that?”
Lewis looked into these studies and noticed the hole he was looking for—exposure times. They were too short. So Lewis and his postdoc, Brian Conlon, reran the experiments with a 24-hour exposure time and it worked. ADEP killed persisters.
“We were revved up,” he says. “ADEP is now going to activate ClpP, chop up every protein in the cell, and force the cell to commit suicide by self-digestion. They were committing suicide. It’s a beautiful mechanism.”
But there was still the issue of the ADEP-resistant mutants Bayer had identified. Again, Lewis had a theory.
He paired ADEP with a conventional antibiotic and, just as he had hoped, the antibiotics that couldn’t touch dormant persister cells could easily kill the mutants. “It turns out that these ADEP-resistant mutants are wimpy,” he says. So as long as you hit them hard with an antibiotic right away, they never get the chance to propagate. Tests in Lewis’ lab killed 100 percent of the pathogens in test tubes and in mice. Then Lewis worked with Steve Leonard, an assistant professor at Northeastern who specializes in pharmacology, to test the combination in a model emulating human infections. The result?
The results were published in Nature in November 2013. Lewis had solved the puzzle.
Bill Ibelle is executive editor.
By John Ombelets
Research Proves Fertile
For decades, the idea that women—in fact, all female mammals—are born with all the eggs they would ever have was considered a settled fact in the field of biology, nearly as certain as death and taxes.
But in 2004, biologist Jonathan Tilly and his research team at Massachusetts General Hospital, in Boston, published a watershed paper in the journal Nature, reporting data from microscopic studies of mouse ovarian tissue that overturned the orthodoxy.
The finding was hailed by the president of the American Society for Reproductive Medicine as potentially the most significant breakthrough in the field since the advent of in vitro fertilization in 1978.
In 2012, Tilly’s team followed up that stunner with new research, published in Nature Medicine, showing that women, just like the female mice they’d studied a decade earlier, have oogonial stem cells in their ovaries. Those “egg precursor cells,” Tilly posited, enable adult mice and adult humans alike to produce viable new eggs.
This year marks the 10th anniversary of the pivotal paper in Nature. But Tilly, who joined Northeastern last July as chair of the biology department, sees it not as an opportunity for celebration so much as an occasion to reflect on the purpose of science.
“I want to tell science students that just because they read something in a textbook does not mean that it’s inviolate,” he says. “Science is supposed to break the boundaries of knowledge.”
The point seems obvious. But sometimes, the scientist doing the breaking gets cuffed around in the process. That was Tilly’s experience, and it made for some difficult years.
“If I was a young scientist just starting out, if I hadn’t had more than a decade of running my own lab under my belt, I’m not sure we’d be having this conversation,” he says. “Because I might not have had the confidence to stay with it; I might have put the findings away in a drawer somewhere.”
Uncovering a mystery
Tilly never set out to shake the foundation of his field.
It was the result of “serendipity,” he says, and came about because he wanted to get to the bottom of a mystery that had always intrigued him: Why does the female body make so many eggs only to kill off all but a tiny fraction?
The numbers are striking. During gestation, the human female fetus develops about 7 million immature egg cells. By the time of birth, her ovaries contain about 1 million egg cells, and at puberty, the total has dropped to 200,000.
The average woman will ovulate about 400 eggs before she reaches menopause—the point at which her egg supply is totally depleted and her ovaries shut down functionally.
If his lab could determine why and how this happened, Tilly reasoned, they might be able to alter the process. That would have major implications not only for fertility, but for women’s health in general, because menopause is associated with a variety of conditions, such as increased risk for cardiovascular disease and osteoporosis.
If menopause could be delayed, perhaps those associated health issues could be as well, increasing what Tilly calls “women’s health span.”
Starting in 1993, Tilly and his research team spent the better part of a decade entirely focused on exploring what drives egg-cell loss. As a result, they were able to draw up a molecular and genetic blueprint showing how and why eggs die.
The research spun off significant findings: how to create a “no-menopause mouse,” how ovaries moderate women’s health, and how pathological “insults”—such as chemotherapy drugs or environmental toxicants—accelerate egg-cell death and cause premature menopause.
By the numbers
But the truly pathbreaking discovery came in 2001, when Tilly used his new cell-mapping techniques to calculate egg-cell death in mice. What he found was shocking. The math didn’t add up. When he counted the total number of eggs at point A and subtracted the number of eggs that had died by point B, there were substantially more live eggs than there were supposed to be.
The only plausible explanation, says Tilly, is that his mice had manufactured a significant number of new eggs. He and his team set to work, confirming the data and trying to determine the mechanism for egg renewal—the research that became the basis for the 2004 paper in Nature. And Tilly decided his lab immediately needed to change its mission, from investigating how egg cells die to how new ones are made.
Research labs don’t recast their focus lightly. It means losing talented doctoral students and postdoctoral researchers. It also means walking away from millions of dollars in grants that were awarded to support the lab’s original mission.
»Sidebar: From the Lab to the Marketplace
At the time, the risk seemed worthwhile. “We didn’t know for certain that [our thesis] was true,” says Tilly. “But we had so much compelling evidence that we had to follow it up” with a total commitment.
Tilly says he should have known what he and his lab mates were in for when one reviewer at Science magazine reacted to their initial paper by writing, “The authors dare to assume they can overturn the dogma.” Tilly felt the comment was unprofessional and, as a scientist, unanswerable, so he withdrew the paper and submitted it to Nature.
When the article first came out, the initial reaction was mixed, but “the criticism just kept building,” he says. “I expected criticism; I did not expect it would be so harsh and personal in tone. We took a lot of guff for a long time.”
He was damned as publicity-seeking and accused of brashly exaggerating the importance and meaning of the data. Other reproductive biology labs claimed that they were unable to replicate some of his findings.
Tilly says that those other researchers were not adhering to his lab’s protocols—the precise approach and methodology used in the research—and that many of his critics misrepresented his team’s work in their comments. “
At first, I was answering every commentary, because I wanted to set the record straight,” says Tilly. “After a while, I told my lab, ‘We’re just going to have to ignore it. I’m not responding any more.’”
The controversy affected Tilly’s lab in real ways: It was harder to get grant proposals and research papers reviewed. Invitations to present at academic conferences dried up.
The turning point came in 2009, when a research group at Shanghai Jiao Tong University reported that they had independently isolated oogonial stem cells from mouse ovarian tissue. When the stem cells were tagged and transplanted into infertile mice, they matured into fertilizable eggs and eventually, healthy pups.
“That’s when I felt like we finally had some breathing room,” Tilly says. And right after that, one of his more vocal critics reached out to acknowledge that Tilly was on to something after all.
Evelyn Telfer, a professor of reproductive biology at the University of Edinburgh in Scotland, called Tilly to make peace. Later that year, they co-authored an article in the journal Molecular Human Reproduction.
The title alone—“Purification of germline stem cells from adult mammalian ovaries: a step closer towards control of the female biological clock?”—illustrated the shift in Telfer’s thinking. The co-authors confidently concluded, “If equivalent (stem) cells can be found in human ovaries, stem cell-based rejuvenation of the oocyte reserve in ovaries on the verge of failure may one day be realized.”
Subsequently, Tilly’s lab succeeded in isolating those equivalent stem cells from human ovaries and using them to generate human egg cells in an immunodeficient mouse with a human ovary graft—the advancement they reported in the 2012 Nature Medicine article.
The holy grail
Today, Tilly is focused on the potential impacts of his breakthrough, not on the storm of controversy that it set off. The criticism has not entirely ceased, but it no longer dominates the discussion.
Increased credibility has attracted new collaborators—a list that now includes Telfer, who has used a sample of human oogonial stem cells taken from Tilly’s lab to grow apparent egg cells in vitro, and the National Institutes of Health, which is working with Tilly and his protocols to replicate the stem-cell research in female rhesus monkeys.
They are asking the same questions he is. Do women in fact produce viable new eggs in vivo, and are oogonial stem cells the source? Can that process be manipulated? Is it possible to create an environment outside the body—in effect, an artificial ovary—where scientists could grow fertile eggs? Could the mitochondrial material in a woman’s oogonial stem cells be injected into her own eggs to “energize” them—improving the chances for conception and decreasing the likelihood of birth defects such as Down syndrome?
And then there is what Tilly refers to as “the Holy Grail,” his personal priority: the ability to delay menopause and thereby postpone the onset of menopause-related health conditions for all women.
The original question, the one that set Tilly on his path—why women’s bodies make and then kill off so many more eggs than they will ever use—remains a puzzle. But that is science—start with one question, and if you persist, who knows what will come across your field of vision?
Tilly says the way is now open to pursue the new answers and questions that have come into his view. “Getting to a fundamental change in this field took almost 10 years, and it’s still not 100 percent accepted,” he says. “But clearly things have changed for the better.”
John Ombelets is senior managing editor.
The New Face of EmotionBy Angela Herring
It seemed like a simple enough question: Do you feel anxious or depressed? Back in 1992, Lisa Feldman Barrett was a doctoral student at the University of Waterloo in Canada, working on research that involved self-esteem. Her research was based, in part, on the universally accepted theory that anxiety was a response to external forces (fear of other people’s expectations), while depression was a response to internal forces (sadness caused by not living up to your own expectations).
But when she attempted to replicate the experiments that established that theory, she failed … eight times.
“When my subjects reported feeling anxious, they also reported feeling depressed,” she says. And vice versa.
“Part of me was thinking maybe I’m not cut out to be a scientist, and I should just focus on being a therapist,” says Barrett, now a University Distinguished Professor at Northeastern. But she couldn’t. She’s a puzzle person, a persistent one, and here was a puzzle to be solved.
Her initial hypothesis was that her subjects were bad at distinguishing among their emotions. If she could get an objective measure of emotion—something that was biological, irrefutable—she’d be able to test this hypothesis. That turned out to be much harder than it sounded.
Two decades later, it’s clear that the puzzle she uncovered back then only scratched the surface of a much larger issue—the “emotion paradox,” as she now calls it, has come to define her entire career. It has forced her to question the very foundations of emotion psychology and a couple of multibillion-dollar government programs that are based on it.
She now contends that emotions are neither universal nor purely biological, and that we reconstruct emotions throughout our lives, based on our culture and personal experience.
In 2007, Barrett’s game-changing research earned her a prestigious Pioneer Award from the National Institutes of Health, making her only the second psychologist to win the agency’s top award.
“Clearly, Dr. Barrett proposed something that could change the paradigm of how people think about emotions,” says Ravi Basavappa, director for the NIH Pioneer Program. “She has broken new ground, definitely, and is trying to expand this into the human subjective experience as a whole.”
As far back as Plato, people have argued over the origin of emotions. Are they fixed entities that are the same every time we experience them (the “basic emotion” view)? Or do we construct them anew each time, based on our culture and personal experience (Barrett’s “constructionist” view)?
Over the past 50 years, consensus has been growing steadily in favor of the former argument and, in recent decades, it has become virtual gospel. So it comes as little surprise that the scientific community treated Barrett with a combination of skepticism and hostility when she challenged the prevailing theory.
“If you’ve been schooled in a particular set of assumptions and then somebody comes along and violates those assumptions, it’s very hard to actually understand what they’re saying,” she says.
This may explain why she’s received insulting reviews that focused more on her character than her data, or why her work went largely uncited by the field’s top researchers, or even why she was physically intimidated by a senior scientist a foot taller than her to “demonstrate that anger really is biologically based.”
Barrett readily admits that the hostility gets to her at times. “I’m not a duck—things don’t roll off my back,” she says.
But while she may be hurt at times, she refuses to be intimidated.
“If you have a question,” she tells her students, “you have to doggedly pursue the answer until you’re convinced. You can’t let other people’s criticisms, or your uncertainty, or the fact that you don’t understand the answer yet, stop you.”
Barrett never set out to be an iconoclast. At first, she was merely trying to explain why her subjects couldn’t distinguish between fear and sadness. She had no reason to question these were two entirely distinct emotions with origins in different parts of the brain and distinct patterns of bodily expression. But she began to have doubts when she couldn’t find any reliable research findings to support the standard hypothesis.
“I believe in the power of data,” she says. “That’s the bottom line for me.”
She looked first to William James, the father of American psychology. In 1894, he reportedly wrote that each emotion has its pattern of physiology—things like sweaty hands or a racing heart. But when Barrett read his actual writings, she found that he wrote the exact opposite. Indeed, James explicitly wrote that emotions are not individual entities, nor do they have a specific pattern of expression. The textbooks had gotten it wrong.
So Barrett turned to Plan B. This time she decided to measure emotions through facial expressions.
In 1972, a psychologist named Paul Ekman rocketed to science stardom when he published Emotion in the Human Face, a seminal work that identifies six basic human emotions—anger, sadness, fear, happiness, surprise, and disgust. Ekman contended that these emotions are expressed and recognized the same way whether a person is raised in downtown Manhattan or the remote jungles of Borneo.
To prove his theory, Ekman traveled to the South Sea island of New Guinea, to find people who had no contact with Western culture. When he showed them photographs of people making exaggerated scowls, frowns, and smiles, then asked them to label each, drawing from a list of basic emotions, they did so with remarkable accuracy, producing the same results as Western test groups.
Ekman’s work appeared to settle the debate about emotions: By showing they are universally recognizable, he proved they are universally hardwired in the human brain. For the next 40 years, his theory served as the foundation for the emerging field of emotion psychology. At first, Barrett had no reason to doubt this work.
“Everybody knew there were six universal facial expressions,” says Barrett. “All I needed to do was measure people’s facial muscle movements, and then I’d know what emotion they were having.”
But again, what she found in the scientific literature didn’t match what she’d been taught in school. Upon deeper review, she realized that no one had ever tested the actual facial muscle movements associated with emotion—Ekman had only looked at how we recognize emotion on others’ faces, Furthermore, when Ekman’s videographer repeated Ekman’s experiments without the list of emotions—just asked the participants to freely label the photos—the evidence completely fell apart.
Barrett’s team recently tested Ekman’s findings themselves. Armed with a pile of photographs depicting more realistic facial expressions, they traveled to sub-Saharan Africa, where they administered the test to members of the Himba tribe in Namibia. The results confirmed those of the videographer. There was minor consistency with a couple of emotions—happiness and fear—but responses on the others were all over the map.
The emotion paradox
Based on the data, Barrett had become skeptical that any objective markers existed for emotion. So she turned to that final frontier—the human brain—to set the record straight.
The same theories that assigned distinct facial expressions to the six emotions also said those emotions could be localized to specific parts of the brain. Fear was supposed to reside in the amygdala, disgust in the insula, and anger in the prefrontal cortex. The original brain-imaging data—which seemed to provide unyielding proof of Ekman’s basic emotion theory—were based on initial neuroimaging studies that looked at an individual part of the brain.
But knowing that little else was universal about emotion, Barrett’s skepticism compelled her to learn neuroscience so that she could take a look for herself. Instead of focusing on one brain region at a time, she looked at the entire brain at once.
Her studies yielded considerably different results. Yes, sometimes amygdala activity increased when a person reported feeling fear, but sometimes it didn’t. And often activity increased when the subject reported a different emotion entirely. She also noted that more than one area of the brain was engaged when a subject reported fear, further discrediting the theory that each emotion originates in a particular part of the brain.
Once again, the science didn’t match the accepted truth.
Barrett’s own experiments show that the brain contains networks that work together to produce emotions, but that no single network is solely responsible for a particular emotion. Most importantly, her research has shown that emotions are not physical entities—people feel different types of anger—and the brain data bear this out.
“The evidence was there,” says Barrett. “But nobody saw it because they weren’t expecting to see it.”
Here was the paradox: We clearly feel emotions; we recognize them in ourselves and in others. But scientists have never found the biological markers that allow us to objectively distinguish between different emotional states.
While Barrett isn’t the first to notice this—people have been observing phenomena that can’t be explained by the basic emotion view for centuries—her brain data settled the score. If individual emotions don’t universally map to the same brain regions, then they simply can’t be unique biological entities.
To some, it may seem obvious to say that each time we feel an emotion we experience it a bit differently. But despite our intuitive understanding that there are countless varieties of happiness and that no two fears are exactly the same, that’s not the direction modern emotion psychology has gone.
Barrett, however, has offered an alternate theory, which she calls the “conceptual act theory.” It’s a bit like the rainbow. We know red when we see it, because we’ve seen it before. We think of it as a discrete entity, wholly separate from blue or green. But the visible light spectrum that defines color is continuous. Just like emotion, red is a real thing—it exists, roughly, between the wavelengths of 620 and 740 nanometers—but there are myriad versions of red, and each one consists of a unique subset of that broader spectrum. We name them based on our previous experience each time we see them.
Emotions work the same way, according to Barrett. What’s the spectrum defining this “psychological rainbow”? In 1999, Barrett and her colleague James Russell gave it a name: core affect. When we experience a feeling as “anger” or “sadness,” she says, we call on our cultural backgrounds, our personal histories, to give a label to that particular “wavelength” of emotion on the core affect spectrum.
Why it matters
Barrett’s theory has caused a dramatic shift in the way psychological science is conducted and taught; her model has become a foundational element in psychology courses around the globe. It has even generated new funding opportunities from the federal government, which recently announced a program focused on affective science based on Barrett’s consulting work.
But it’s also providing real solutions. Those same problems that have plagued the basic emotions view for centuries keep coming up, and now there’s finally a scientific approach to deal with them. For instance, recent animal studies have shown that stress acts like fertilizer for diseased cells to thrive. If emotions were biologically innate, this work would easily translate to human studies—just trigger people’s fear circuits and you’ll see the same effects. But that hasn’t worked.
The problem, Barrett says, is that the one-to-one relationship between physical conditions and nervous system response, which is seen in animals, is not seen in humans.
“It all comes down to how people experience the situation,” she says. “Every time you measure anger, depending on the context, you might see a different physical response. Basic emotion theory can’t explain why.”
But Barrett’s theory can. In fact, it could lend a sort of “personalized medicine” approach to the problem by studying each individual’s profile of emotional experience in context.
“It’s very possible that if you studied one person long enough, you’d be able to find what their characteristic expressions are,” she says. “So it’s not that it’s impossible to find reliable expressions, it’s just that they might be very person-specific and they’re definitely context-specific.”
Barrett’s work could also have implications for national security, since the FBI, CIA, Homeland Security, and Transportation Security Administration have all based policies on the basic emotion theory. The TSA alone has spent nearly $1 billion training security personnel to identify potential terrorists based, in part, on Paul Ekman’s facial recognition techniques.
Yet in November 2013, the federal Government Accountability Office recommended the program be defunded, stating there is no evidence that these techniques are any better than random guesswork at identifying terrorists.
“New theories are best evaluated not by the answers they deliver, but by the questions they get people to ask,” says Barrett. “Our theory is young. It has been around less than 10 years. So far, its real value has been showing that the current ‘facts’ about emotion are not scientific facts at all.”
Angela Herring is a staff science writer.