To Make Science Engaging, We Need a Sesame Street for Adults
A new kind of television series could establish the baseline narratives for novel science like gene editing, quantum computing, or artificial intelligence.
This article is part of the magazine, "The Future of Science In America: The Election Issue," co-published by LeapsMag, the Aspen Institute Science & Society Program, and GOOD.
In the mid-1960s, a documentary producer in New York City wondered if the addictive jingles, clever visuals, slogans, and repetition of television ads—the ones that were captivating young children of the time—could be harnessed for good. Over the course of three months, she interviewed educators, psychologists, and artists, and the result was a bonanza of ideas.
Perhaps a new TV show could teach children letters and numbers in short animated sequences? Perhaps adults and children could read together with puppets providing comic relief and prompting interaction from the audience? And because it would be broadcast through a device already in almost every home, perhaps this show could reach across socioeconomic divides and close an early education gap?
Soon after Joan Ganz Cooney shared her landmark report, "The Potential Uses of Television in Preschool Education," in 1966, she was prototyping show ideas, attracting funding from The Carnegie Corporation, The Ford Foundation, and The Corporation for Public Broadcasting, and co-founding the Children's Television Workshop with psychologist Lloyd Morrisett. And then, on November 10, 1969, informal learning was transformed forever with the premiere of Sesame Street on public television.
For its first season, Sesame Street won three Emmy Awards and a Peabody Award. Its star, Big Bird, landed on the cover of Time Magazine, which called the show "TV's gift to children." Fifty years later, it's hard to imagine an approach to informal preschool learning that isn't Sesame Street.
And that approach can be boiled down to one word: Entertainment.
Despite decades of evidence from Sesame Street—one of the most studied television shows of all time—and more research from social science, psychology, and media communications, we haven't yet taken Ganz Cooney's concepts to heart in educating adults. Adults have news programs and documentaries and educational YouTube channels, but no Sesame Street. So why don't we? Here's how we can design a new kind of television to make science engaging and accessible for a public that is all too often intimidated by it.
We have to start from the realization that America is a nation of high-school graduates. By the end of high school, students have decided to abandon science because they think it's too difficult, and as a nation, we've made it acceptable for any one of us to say "I'm not good at science" and offload thinking to the ones who might be. So, is it surprising that a large number of Americans are likely to believe in conspiracy theories like the 25% that believe the release of COVID-19 was planned, the one in ten who believe the Moon landing was a hoax, or the 30–40% that think the condensation trails of planes are actually nefarious chemtrails? If we're meeting people where they are, the aim can't be to get the audience from an A to an A+, but from an F to a D, and without judgment of where they are starting from.
There's also a natural compulsion for a well-meaning educator to fill a literacy gap with a barrage of information, but this is what I call "factsplaining," and we know it doesn't work. And worse, it can backfire. In one study from 2014, parents were provided with factual information about vaccine safety, and it was the group that was already the most averse to vaccines that uniquely became even more averse.
Why? Our social identities and cognitive biases are stubborn gatekeepers when it comes to processing new information. We filter ideas through pre-existing beliefs—our values, our religions, our political ideologies. Incongruent ideas are rejected. Congruent ideas, no matter how absurd, are allowed through. We hear what we want to hear, and then our brains justify the input by creating narratives that preserve our identities. Even when we have all the facts, we can use them to support any worldview.
But social science has revealed many mechanisms for hijacking these processes through narrative storytelling, and this can form the foundation of a new kind of educational television.
Could new television series establish the baseline narratives for novel science like gene editing, quantum computing, or artificial intelligence?
As media creators, we can reject factsplaining and instead construct entertaining narratives that disrupt cognitive processes. Two-decade-old research tells us when people are immersed in entertaining fiction narratives, they loosen their defenses, opening a path for new information, editing attitudes, and inspiring new behavior. Where news about hot-button issues like climate change or vaccination might trigger resistance or a backfire effect, fiction can be crafted to be absorbing and, as a result, persuasive.
But the narratives can't be stuffed with information. They must be simplified. If this feels like the opposite of what an educator should be doing, it is possible to reduce the complexity of information, without oversimplification, through "exemplification," a framing device to tell the stories of individuals in specific circumstances that can speak to the greater issue without needing to explain it all. It's a technique you've seen used in biopics. The Discovery Channel true-crime miniseries Manhunt: Unabomber does many things well from a science storytelling perspective, including exemplifying the virtues of the scientific method through a character who argues for a new field of science, forensic linguistics, to catch one of the most notorious domestic terrorists in U.S. history.
We must also appeal to the audience's curiosity. We know curiosity is such a strong driver of human behavior that it can even counteract the biases put up by one's political ideology around subjects like climate change. If we treat science information like a product—and we should—advertising research tells us we can maximize curiosity though a Goldilocks effect. If the information is too complex, your show might as well be a PowerPoint presentation. If it's too simple, it's Sesame Street. There's a sweet spot for creating intrigue about new information when there's a moderate cognitive gap.
The science of "identification" tells us that the more the main character is endearing to a viewer, the more likely the viewer will adopt the character's worldview and journey of change. This insight further provides incentives to craft characters reflective of our audiences. If we accept our biases for what they are, we can understand why the messenger becomes more important than the message, because, without an appropriate messenger, the message becomes faint and ineffective. And research confirms that the stereotype-busting doctor-skeptic Dana Scully of The X-Files, a popular science-fiction series, was an inspiration for a generation of women who pursued science careers.
With these directions, we can start making a new kind of television. But is television itself still the right delivery medium? Americans do spend six hours per day—a quarter of their lives—watching video. And even with the rise of social media and apps, science-themed television shows remain popular, with four out of five adults reporting that they watch shows about science at least sometimes. CBS's The Big Bang Theory was the most-watched show on television in the 2017–2018 season, and Cartoon Network's Rick & Morty is the most popular comedy series among millennials. And medical and forensic dramas continue to be broadcast staples. So yes, it's as true today as it was in the 1980s when George Gerbner, the "cultivation theory" researcher who studied the long-term impacts of television images, wrote, "a single episode on primetime television can reach more people than all science and technology promotional efforts put together."
We know from cultivation theory that media images can shape our views of scientists. Quick, picture a scientist! Was it an old, white man with wild hair in a lab coat? If most Americans don't encounter research science firsthand, it's media that dictates how we perceive science and scientists. Characters like Sheldon Cooper and Rick Sanchez become the model. But we can correct that by representing professionals more accurately on-screen and writing characters more like Dana Scully.
Could new television series establish the baseline narratives for novel science like gene editing, quantum computing, or artificial intelligence? Or could new series counter the misinfodemics surrounding COVID-19 and vaccines through more compelling, corrective narratives? Social science has given us a blueprint suggesting they could. Binge-watching a show like the surreal NBC sitcom The Good Place doesn't replace a Ph.D. in philosophy, but its use of humor plants the seed of continued interest in a new subject. The goal of persuasive entertainment isn't to replace formal education, but it can inspire, shift attitudes, increase confidence in the knowledge of complex issues, and otherwise prime viewers for continued learning.
[Editor's Note: To read other articles in this special magazine issue, visit the beautifully designed e-reader version.]
Researchers at Stanford have found that the virus that causes Covid-19 can infect fat cells, which could help explain why obesity is linked to worse outcomes for those who catch Covid-19.
Obesity is a risk factor for worse outcomes for a variety of medical conditions ranging from cancer to Covid-19. Most experts attribute it simply to underlying low-grade inflammation and added weight that make breathing more difficult.
Now researchers have found a more direct reason: SARS-CoV-2, the virus that causes Covid-19, can infect adipocytes, more commonly known as fat cells, and macrophages, immune cells that are part of the broader matrix of cells that support fat tissue. Stanford University researchers Catherine Blish and Tracey McLaughlin are senior authors of the study.
Most of us think of fat as the spare tire that can accumulate around the middle as we age, but fat also is present closer to most internal organs. McLaughlin's research has focused on epicardial fat, “which sits right on top of the heart with no physical barrier at all,” she says. So if that fat got infected and inflamed, it might directly affect the heart.” That could help explain cardiovascular problems associated with Covid-19 infections.
Looking at tissue taken from autopsy, there was evidence of SARS-CoV-2 virus inside the fat cells as well as surrounding inflammation. In fat cells and immune cells harvested from health humans, infection in the laboratory drove "an inflammatory response, particularly in the macrophages…They secreted proteins that are typically seen in a cytokine storm” where the immune response runs amok with potential life-threatening consequences. This suggests to McLaughlin “that there could be a regional and even a systemic inflammatory response following infection in fat.”
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
The macrophages studied by McLaughlin and Blish were spewing out inflammatory proteins, While the the virus within them was replicating, the new viral particles were not able to replicate within those cells. It was a different story in the fat cells. “When [the virus] gets into the fat cells, it not only replicates, it's a productive infection, which means the resulting viral particles can infect another cell,” including microphages, McLaughlin explains. It seems to be a symbiotic tango of the virus between the two cell types that keeps the cycle going.
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
Macrophages are mobile; they engulf and carry invading pathogens to lymphoid tissue in the lymph nodes, tonsils and elsewhere in the body to alert T cells of the immune system to the pathogen. Perhaps some of them also carry the virus through the bloodstream to more distant tissue.
ACE2 receptors are the means by which SARS-CoV-2 latches on to and enters most cells. They are not thought to be common on fat cells, so initially most researchers thought it unlikely they would become infected.
However, while some cell receptors always sit on the surface of the cell, other receptors are expressed on the surface only under certain conditions. Philipp Scherer, a professor of internal medicine and director of the Touchstone Diabetes Center at the University of Texas Southwestern Medical Center, suggests that, in people who have obesity, “There might be higher levels of dysfunctional [fat cells] that facilitate entry of the virus,” either through transiently expressed ACE2 or other receptors. Inflammatory proteins generated by macrophages might contribute to this process.
Another hypothesis is that viral RNA might be smuggled into fat cells as cargo in small bits of material called extracellular vesicles, or EVs, that can travel between cells. Other researchers have shown that when EVs express ACE2 receptors, they can act as decoys for SARS-CoV-2, where the virus binds to them rather than a cell. These scientists are working to create drugs that mimic this decoy effect as an approach to therapy.
Do fat cells play a role in Long Covid? “Fat cells are a great place to hide. You have all the energy you need and fat cells turn over very slowly; they have a half-life of ten years,” says Scherer. Observational studies suggest that acute Covid-19 can trigger the onset of diabetes especially in people who are overweight, and that patients taking medicines to regulate their diabetes “were actually quite protective” against acute Covid-19. Scherer has funding to study the risks and benefits of those drugs in animal models of Long Covid.
McLaughlin says there are two areas of potential concern with fat tissue and Long Covid. One is that this tissue might serve as a “big reservoir where the virus continues to replicate and is sent out” to other parts of the body. The second is that inflammation due to infected fat cells and macrophages can result in fibrosis or scar tissue forming around organs, inhibiting their function. Once scar tissue forms, the tissue damage becomes more difficult to repair.
Current Covid-19 treatments work by stopping the virus from entering cells through the ACE2 receptor, so they likely would have no effect on virus that uses a different mechanism. That means another approach will have to be developed to complement the treatments we already have. So the best advice McLaughlin can offer today is to keep current on vaccinations and boosters and lose weight to reduce the risk associated with obesity.
Air pollution can lead to lung cancer. The connection suggests new ways to stop cancer in its tracks.
Researchers at Francis Crick Institute found that air pollution can "wake up" existing mutations, triggering them to turn into lung cancer. The scientists used their new understanding about this connection to prevent cancer in mice.
Forget taking a deep breath. Around the world, 99 percent of people breathe air polluted to unsafe levels, according to data from the World Health Organization. Activities such as burning fossil fuels release greenhouse gases that contribute to air pollution, which could lead to heart disease, stroke, asthma, emphysema, and some types of cancer.
“The burden of disease attributable to air pollution is now estimated to be on a par with other major global health risks such as unhealthy diet and tobacco smoking, and air pollution is now recognized as the single biggest environmental threat to human health,” wrote the authors of a 2021 WHO report.
The majority of lung cancer is attributed to smoking. But as pollution levels have increased, and anti-smoking campaigns have discouraged smoking, the proportion of lung cancers diagnosed in non-smokers has grown. The CDC estimates that 10 to 20 percent of lung cancers in the U.S. currently occur in non-smokers.
The mechanism between air pollution and the development of lung cancer has been unclear, but researchers at London’s Francis Crick Institute recently made an important breakthrough in understanding the connection. Lead investigator Charles Swanton presented this research last month at a conference in Paris.
Pollution awakens mutations
The Crick Institute scientists were able to identify a new link between common air pollutants and non-small cell lung cancer (NSCLC). They focused on pollutants called particulate matter, or PM, that are 2.5 microns wide, narrower than human cells.
Most cancer diagnosed in non-smoking people is NSCLC, but this type of cancer hasn’t received the same research attention as more common lung cancers found in smokers, according to Clare Weeden, a cancer researcher at the Crick Institute and a co-author of the study.
“This is a really underserved and under-researched population that we really need to tackle, as well as lung cancers that occur in smokers,” she says. “Lung cancer is the number one cancer killer worldwide.”
In the past, some researchers believed air pollution caused mutations that led to cancer. Others believed these mutations could remain dormant without any detriment to health until pollutants or other stressors triggered them to become cancerous. Reviving the latter hypothesis that carcinogens may activate pre-existing mutations, instead of directly causing them, the Crick researchers analyzed samples from 463,679 people in the UK and parts of Asia, noting mutations and comparing changes in gene expression in mice and human cells.
“The mutation can exist in a nascent clone without causing cancer,” says Emilia Lim, a bioinformatics expert and a co-first author of the Crick study. “It is the carcinogen that promotes a conducive environment for this one little clone to grow and expand into cancer. Through our work, we were able to revive excitement for this hypothesis and bring it to light.”
The study explains a confusing pattern of lung cancer developing, particularly in women, despite a lack of environmental risk factors like smoking, secondhand smoke, or radon exposure. The culprit in these cases may have been too much PM 2.5 exposure.
Other researchers had previously identified a link between mutations in certain genes that control epidermal growth factor receptors, or EGFR mutations, and the development of NSCLC. In a 2019 study of 250 people with this type of cancer, about 32 percent had the mutation. Women are more likely to have EGFR mutations than men.
Not everyone who has the EGFR mutation will develop lung cancer. Respirologist Stephen Lam studies lung cancer at the BC Cancer Research Centre in Vancouver, Canada, but was not involved in the Crick Institute research. He says the study explains a confusing pattern of lung cancer developing, particularly in women, despite a lack of environmental risk factors like smoking, secondhand smoke, or radon exposure. The culprit in these cases may have been too much PM 2.5 exposure.
More exposure leads to inflammation and lesions
The Crick researchers found that an excess of PM 2.5 in the air sparked an inflammatory process in cells within the lung. This inflammation set the stage for NSCLC to develop in people and mice with existing EGFR mutations.
The researchers also exposed mice without EGFR mutations to PM 2.5 pollution—an experiment that couldn’t be ethically conducted in humans—to link pollution exposure to NSCLC. The mice experiments also showed that NSCLC is dose-dependent; higher levels of exposure were associated with higher number of cancerous lesions forming.
Ultimately, the study “fundamentally changed how we view lung cancer in people who have never smoked,” said Swanton in a Crick Institute press release. “Cells with cancer-causing mutations accumulate naturally as we age, but they are normally inactive. We’ve demonstrated that air pollution wakes these cells up in the lungs, encouraging them to grow and potentially form tumors.”
Preventing cancer before it begins
Targeted therapies already exist for people with EGFR mutations who’ve developed NSCLC, but they have many side effects, according to Weeden. Researchers hope that making more definitive links between pollutants and cancer could help prevent people with EGFR or other mutations from developing lung cancer in the first place.
Along those lines, as an additional component of their study presented last month, the Crick researchers were able to prevent cancer in mice that had the EGFR mutations by blocking inflammation. They used an antibody to inhibit a protein called interleukin 1 beta, which plays a key role in inflammation. Scientists could eventually use such antibodies or other therapies to make a drug treatment that people can take to stop cancer in its tracks, even if they live in highly polluted areas.
Such potential could reach beyond lung cancer; in the past, Crick and other researchers have also found associations between exposure to air pollution and mesothelioma, as well as cancers of the small intestine, lip, mouth, and throat. These links could be meaningful to a growing number of people as climate change intensifies, and with increases in air pollution from fossil fuel combustion and natural disasters like forest fires.
Plus, air pollution is just one external condition that can flip the switch of these inflammatory pathways. Identifying a link between pollution and cancer “has wide ramifications for many other environmental factors that may [play] similar roles,” Weedon says. She hopes that the Crick study and future research in this area will offer some hope for non-smokers frustrated by cancer diagnoses.