What Motivates Creativity?

The ultimate goal of any education system should be to give people the opportunity to find and bring to life that which motivates them intrinsically. 

What Motivates Creativity?

In 1981, Arthur Leonard Schawlow won the Nobel prize in physics for his contributions to laser spectroscopy. When asked what made the difference between highly creative and less creative scientists he responded: "The labor of love aspect is important. The most successful scientists often are not the most talented. But they are the ones who are impelled by curiosity. They've got to know what the answer is."


Schawlow was describing what the psychologist Teresa Amabile calls the “Intrinsic Motivation Principle of Creativity,” or the propensity for human creativity to flourish when people are motivated by the personal enjoyment of the work itself. Athletes call it a “love of the game;” artists refer to it as an unrelenting need to express. For academics like Schawlow, it’s the pure joy of discovering something new.

Extrinsic motivation, in contrast, is the daily pressure we feel from outside incentives – grades, salaries, and promotions – put in place to encourage output. Here’s the question: Is creative output the product of intrinsic or extrinsic motivation? Do we need a reason to work? Or is passion enough?

In the 1970s, Mark Lepper, David Greene and Richard Nisbett conducted a classic study involving a group of preschoolers who liked to draw. The researchers separated the kids into three groups. The first was told that if they continued to draw they would receive a big blue ribbon with their name on it (reward condition). The second wasn’t told about the reward but given a blue ribbon after they finished drawing (unexpected reward condition). The third group wasn’t given a blue ribbon ribbon (no award condition).

They ran the experiment for two weeks and found that the kids in the “no award” and “unexpected reward” conditions continued to enthusiastically draw just like they did initially. However, their peers in the award condition showed a drastic reduction in interest. Sadly, they no longer found pleasure in drawing – their intrinsic motivation was destroyed by an extrinsic reward, the blue ribbon.

A study conducted more recently by Teresa Amabile of the Harvard Business School demonstrated similar results. Amabile’s subjects, unlike Lepper's et al, were college women. In one experiment Amabile asked the women to make paper collages. She told half of them graduate art students would judge their collages; the other half was told that researchers “were studying their mood and had no interest in the collages themselves.” A panel of artists evaluated the collages and Amabile found that those who expected to be judged were significantly less creative. Drawing on this study and other research, Amabile concluded that, “The intrinsically motivated state is conducive to creativity, whereas the extrinsically motivated state is detrimental.”

Are all extrinsic motivators creativity killers? Not exactly. This research doesn’t rule out the important role extrinsic motivation plays in the creative process. Consider the following examples, brought to life by Geoff Colvin in his book Talent is Overrated:

Intrinsic motivation may dominate the big picture, but everyone, even the greatest achievers, has responded to extrinsic forces at critical moments. When Waton and Crick were struggling to find the structure of DNA, they worked almost nonstop because they knew they were in a race with other research teams. Alexander Graham Bell worked similarly on the telephone, knowing he was in competition with Elisha Gray, whom he beat to the patent office by just hours. Such people are driven by much more than fascination or joy.

Colvin concludes that extrinsic motivators are good as long as they are directed at delivering constructive feedback. Here’s what he means:

While the mere expectation of being judged [tends] to reduce creativity, personal feedback could actually enhance creativity if it was the right kind… That is, feedback that [helps] a person do what he or she [feels] compelled to do [is] effective. Even the prospect of direct rewards, normally suffocating to creativity, could be helpful if they were the right kinds of rewards… [As such] intrinsic motivation is still best, and extrinsic motivation that’s controlling is still detrimental to creativity, but extrinsic motivators that reinforce intrinsic drives can be highly effective.

Given the connection between motivation and achievement and creativity, it’s worth asking if the United States education system is doing a good job of balancing intrinsic and extrinsic motivators. The short answer is not really. A new report from the Center on Education Policy outlines new strategies schools are creating to boost student motivation, suggests that many schools still do a poor job of understanding student motivation and describes the inherent problem of motivating a student who seems steadfast in his or her unwillingness to engage the material. Here’s a recent Atlantic article on the study:

Schools nationwide are experimenting with initiatives aimed at boosting student motivation, incorporating new programs aimed at piquing their interest or helping them feel more connected to the material they are being taught. In some instances, and not without controversy, schools have resorted to outright bribery, offering students cash and other rewards in exchange for greater effort and achievement….

[But] even the best school, program, and teacher can't make a dent in improving academic achievement when a student isn't motivated to learn. There are several elements to motivating students successfully, and as more of these triggers are activated, an initiative becomes more likely to work… if students see a direct connection between what they are learning and their own interests and goals, they are likely to be more motivated. Additionally, how schools are organized, and how teachers teach, are all factors in student motivation.

The article and CEP study suggests that schools in the United States should make pedagogical adjustments that consider what we know and don’t know about motivation. I think there’s no doubt that this is true.

For one, too much weight is put on extrinsic motivators - grades, tests, final examples, etc. They’re important – no need to throw the baby out with the bathwater - but the ultimate goal of any education system should be to give people the opportunity to find and bring to life that which motivates them intrinsically. Ideally, all students will find, at some point in their educational careers, a domain where their labor is love, just as Schawlow did. 

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This article was originally published on our sister site, Freethink.

"I was intrigued," says Ron Fouchier, in his rich, Dutch-accented English, "in how little things could kill large animals and humans."

It's late evening in Rotterdam as darkness slowly drapes our Skype conversation.

This fascination led the silver-haired virologist to venture into controversial gain-of-function mutation research — work by scientists that adds abilities to pathogens, including experiments that focus on SARS and MERS, the coronavirus cousins of the COVID-19 agent.

If we are to avoid another influenza pandemic, we will need to understand the kinds of flu viruses that could cause it. Gain-of-function mutation research can help us with that, says Fouchier, by telling us what kind of mutations might allow a virus to jump across species or evolve into more virulent strains. It could help us prepare and, in doing so, save lives.

Many of his scientific peers, however, disagree; they say his experiments are not worth the risks they pose to society.

A virus and a firestorm

The Dutch virologist, based at Erasmus Medical Center in Rotterdam, caused a firestorm of controversy about a decade ago, when he and Yoshihiro Kawaoka at the University of Wisconsin-Madison announced that they had successfully mutated H5N1, a strain of bird flu, to pass through the air between ferrets, in two separate experiments. Ferrets are considered the best flu models because their respiratory systems react to the flu much like humans.

The mutations that gave the virus its ability to be airborne transmissible are gain-of-function (GOF) mutations. GOF research is when scientists purposefully cause mutations that give viruses new abilities in an attempt to better understand the pathogen. In Fouchier's experiments, they wanted to see if it could be made airborne transmissible so that they could catch potentially dangerous strains early and develop new treatments and vaccines ahead of time.

The problem is: their mutated H5N1 could also cause a pandemic if it ever left the lab. In Science magazine, Fouchier himself called it "probably one of the most dangerous viruses you can make."

Just three special traits

Recreated 1918 influenza virionsCredit: Cynthia Goldsmith / CDC / Dr. Terrence Tumpey / Public domain via Wikipedia

For H5N1, Fouchier identified five mutations that could cause three special traits needed to trigger an avian flu to become airborne in mammals. Those traits are (1) the ability to attach to cells of the throat and nose, (2) the ability to survive the colder temperatures found in those places, and (3) the ability to survive in adverse environments.

A minimum of three mutations may be all that's needed for a virus in the wild to make the leap through the air in mammals. If it does, it could spread. Fast.

Fouchier calculates the odds of this happening to be fairly low, for any given virus. Each mutation has the potential to cripple the virus on its own. They need to be perfectly aligned for the flu to jump. But these mutations can — and do — happen.

"In 2013, a new virus popped up in China," says Fouchier. "H7N9."

H7N9 is another kind of avian flu, like H5N1. The CDC considers it the most likely flu strain to cause a pandemic. In the human outbreaks that occurred between 2013 and 2015, it killed a staggering 39% of known cases; if H7N9 were to have all five of the gain-of-function mutations Fouchier had identified in his work with H5N1, it could make COVID-19 look like a kitten in comparison.

H7N9 had three of those mutations in 2013.

Gain-of-function mutation: creating our fears to (possibly) prevent them

Flu viruses are basically eight pieces of RNA wrapped up in a ball. To create the gain-of-function mutations, the research used a DNA template for each piece, called a plasmid. Making a single mutation in the plasmid is easy, Fouchier says, and it's commonly done in genetics labs.

If you insert all eight plasmids into a mammalian cell, they hijack the cell's machinery to create flu virus RNA.

"Now you can start to assemble a new virus particle in that cell," Fouchier says.

One infected cell is enough to grow many new virus particles — from one to a thousand to a million; viruses are replication machines. And because they mutate so readily during their replication, the new viruses have to be checked to make sure it only has the mutations the lab caused.

The virus then goes into the ferrets, passing through them to generate new viruses until, on the 10th generation, it infected ferrets through the air. By analyzing the virus's genes in each generation, they can figure out what exact five mutations lead to H5N1 bird flu being airborne between ferrets.

And, potentially, people.

"This work should never have been done"

The potential for the modified H5N1 strain to cause a human pandemic if it ever slipped out of containment has sparked sharp criticism and no shortage of controversy. Rutgers molecular biologist Richard Ebright summed up the far end of the opposition when he told Science that the research "should never have been done."

"When I first heard about the experiments that make highly pathogenic avian influenza transmissible," says Philip Dormitzer, vice president and chief scientific officer of viral vaccines at Pfizer, "I was interested in the science but concerned about the risks of both the viruses themselves and of the consequences of the reaction to the experiments."

In 2014, in response to researchers' fears and some lab incidents, the federal government imposed a moratorium on all GOF research, freezing the work.

Some scientists believe gain-of-function mutation experiments could be extremely valuable in understanding the potential risks we face from wild influenza strains, but only if they are done right. Dormitzer says that a careful and thoughtful examination of the issue could lead to processes that make gain-of-function mutation research with viruses safer.

But in the meantime, the moratorium stifled some research into influenzas — and coronaviruses.

The National Academy of Science whipped up some new guidelines, and in December of 2017, the call went out: GOF studies could apply to be funded again. A panel formed by Health and Human Services (HHS) would review applications and make the decision of which studies to fund.

As of right now, only Kawaoka and Fouchier's studies have been approved, getting the green light last winter. They are resuming where they left off.

Pandora's locks: how to contain gain-of-function flu

Here's the thing: the work is indeed potentially dangerous. But there are layers upon layers of safety measures at both Fouchier's and Kawaoka's labs.

"You really need to think about it like an onion," says Rebecca Moritz of the University of Wisconsin-Madison. Moritz is the select agent responsible for Kawaoka's lab. Her job is to ensure that all safety standards are met and that protocols are created and drilled; basically, she's there to prevent viruses from escaping. And this virus has some extra-special considerations.

The specific H5N1 strain Kawaoka's lab uses is on a list called the Federal Select Agent Program. Pathogens on this list need to meet special safety considerations. The GOF experiments have even more stringent guidelines because the research is deemed "dual-use research of concern."

There was debate over whether Fouchier and Kawaoka's work should even be published.

"Dual-use research of concern is legitimate research that could potentially be used for nefarious purposes," Moritz says. At one time, there was debate over whether Fouchier and Kawaoka's work should even be published.

While the insights they found would help scientists, they could also be used to create bioweapons. The papers had to pass through a review by the U.S. National Science Board for Biosecurity, but they were eventually published.

Intentional biowarfare and terrorism aside, the gain-of-function mutation flu must be contained even from accidents. At Wisconsin, that begins with the building itself. The labs are specially designed to be able to contain pathogens (BSL-3 agricultural, for you Inside Baseball types).

They are essentially an airtight cement bunker, negatively pressurized so that air will only flow into the lab in case of any breach — keeping the viruses pushed in. And all air in and out of the lap passes through multiple HEPA filters.

Inside the lab, researchers wear special protective equipment, including respirators. Anyone coming or going into the lab must go through an intricate dance involving stripping and putting on various articles of clothing and passing through showers and decontamination.

And the most dangerous parts of the experiment are performed inside primary containment. For example, a biocontainment cabinet, which acts like an extra high-security box, inside the already highly-secure lab (kind of like the radiation glove box Homer Simpson is working in during the opening credits).

"Many people behind the institution are working to make sure this research can be done safely and securely." — REBECCA MORITZ

The Federal Select Agent program can come and inspect you at any time with no warning, Moritz says. At the bare minimum, the whole thing gets shaken down every three years.

There are numerous potential dangers — a vial of virus gets dropped; a needle prick; a ferret bite — but Moritz is confident that the safety measures and guidelines will prevent any catastrophe.

"The institution and many people behind the institution are working to make sure this research can be done safely and securely," Moritz says.

No human harm has come of the work yet, but the potential for it is real.

"Nature will continue to do this"

They were dead on the beaches.

In the spring of 2014, another type of bird flu, H10N7, swept through the harbor seal population of northern Europe. Starting in Sweden, the virus moved south and west, across Denmark, Germany, and the Netherlands. It is estimated that 10% of the entire seal population was killed.

The virus's evolution could be tracked through time and space, Fouchier says, as it progressed down the coast. Natural selection pushed through gain-of-function mutations in the seals, similarly to how H5N1 evolved to better jump between ferrets in his lab — his lab which, at the time, was shuttered.

"We did our work in the lab," Fouchier says, with a high level of safety and security. "But the same thing was happening on the beach here in the Netherlands. And so you can tell me to stop doing this research, but nature will continue to do this day in, day out."

Critics argue that the knowledge gained from the experiments is either non-existent or not worth the risk; Fouchier argues that GOF experiments are the only way to learn crucial information on what makes a flu virus a pandemic candidate.

"If these three traits could be caused by hundreds of combinations of five mutations, then that increases the risk of these things happening in nature immensely," Fouchier says.

"With something as crucial as flu, we need to investigate everything that we can," Fouchier says, hoping to find "a new Achilles' heel of the flu that we can use to stop the impact of it."

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