COVID-19 : What causes certain people to stick to their beliefs and act with skepticism despite evidence?


In recent weeks, several conservative media personalities, political and business leaders and other influencers have publicly shrugged off warnings about the dangers of the novel coronavirus, calling it no deadlier than the flu.

While some of them have walked back their comments in the face of rising global and U.S. COVID-19 cases and deaths, many of their fans continue to subscribe to the ideology that the contagion is “fake” or overblown. Meanwhile, many young adults are defying the 6-feet-apart social distancing rules.

A group in Kentucky even threw a coronavirus party, which helped to spread the virus.

What causes certain people to stick to their beliefs and act with skepticism despite overwhelming contradictory evidence? Berkeley News asked Celeste Kidd, a UC Berkeley computational cognitive scientist who studies false beliefs, curiosity and learning. Here is what Kidd has to say:

Berkeley News: So, why do some people ignore scientific or other evidence to follow authoritarian ideology or to confirm their own biases?

Celeste Kidd: As humans, we rely on other people to inform our opinions. It’s the strength of our species and the reason why we have modern medicine and technologies like smartphones and the internet and robots and vaccines.

We especially pay attention to authority figures and majority opinions. We also pay more attention to the beliefs of those we like over those we dislike.

People in positions of authority have a special duty to be careful with their words for this reason. Their words, by nature of their position and stature, are more likely to be adopted as beliefs by people, and at a larger scale, than the words of everyone else.

They can use that power to do a lot of good if they are careful or do a lot of damage if they are not.

For example, recently, President Trump repeatedly and confidently suggested that an old malaria treatment, chloroquine, could treat coronavirus, in the absence of scientific evidence to back that statement.

He said it was “safe,” that he had a “good feeling” about it and that it could be “one of the biggest game changers in the history of medicine,” even after Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, corrected him.

An Arizona man, heeding Trump’s advice, ingested an aquarium cleaner that contained an ingredient called chloroquine, and died. The words of authority figures, like heads of state, hold particular weight in influencing people’s beliefs and can be deadly.

Why do we choose to believe some things and not others?

Most of us like to think of ourselves as rational agents who can make decisions and form beliefs that make sense. But the world is far too big and complex for us to have the time or attentional bandwidth to know about everything, so we have to pick and choose.

The scientific name for this is “sampling,” and it works well in a dynamic world where the approximate truth is usually good enough to make everyday decisions.

We’re also built to favor investigating the things we feel uncertain about. This tendency pushes us to expand and update our knowledge base. Once we feel like we know everything, we disengage and move on to the next thing. This prevents us from wasting time on what we already know so we can learn something new.

The problem arises when we believe that we know everything there is to know, but we are wrong.

When this happens, we are less open to changing our minds based on new information because we don’t seek out new information, and we are more inclined to ignore it when we do encounter it.

Ultimately, who and what influences our beliefs?

If everyone around us appears to believe something, we’re more likely to believe it. And that feedback loop matters, especially early on. For example, if we are forming an opinion about something we’re not completely sure about, we are more likely to make up our minds based on the first pieces of evidence we see. All of this is unconscious, and that’s how learning systems work.

Let’s say your neighbor mentions that she’s on a new activated charcoal diet to rid her body of toxins. Maybe you leave that conversation unsure about whether that diet is legitimate, and you hop online to do some sleuthing.

If you search for the phrase “activated charcoal,” you’re likely to see a bunch of pseudoscientific health and wellness content about how activated charcoal is wonderful for all kinds of things—clearing your skin, curing your hangover, calming indigestion.

If the first couple things you see echo that viewpoint, you tend to quickly adopt that belief with high certainty. In the case of the activated charcoal diet, that may not be prudent.

There is no good evidence that activated charcoal can do any of those things. And believing that it can, at best, robs you of the opportunity to discover other evidence-based methods that would actually help. At worst, it can be dangerous.

Are some personality types more prone than others to sticking to beliefs despite contradictory evidence?

All of us stick to beliefs in the face of contradictory evidence. All of us have beliefs that do not match reality. It is unavoidable. But it’s possible that some people are better or worse than others at keeping an open mind.

Our previous research suggests that uncertainty makes people more willing to change their mind. The downside of that is that constant uncertainty can make us less willing to make decisions and act, which would make it hard to navigate life.

What we do know from work in our lab is that how certain you feel is not a good indicator of how certain you should feel based on the strength of the evidence.

Research led by Louis Martí in our lab measured people’s confidence and accuracy as they were in the process of learning a new concept. What we found was that people’s certainty was not predicted by the strength of the evidence.

Instead, it was predicted by feedback. If people guessed the answer to a question and got it right by some fluke, their confidence remained high even when they got subsequent answers wrong. That early positive feedback created high certainty that couldn’t be shaken.

Let’s say you hear that sunlight heals sick people, and so you spend some time outside next time you get a cold, or open the bedroom blinds, and you do seem to heal quicker.

You tell your friend, he tries it, he says he got better quicker too. Now you feel certain that sunlight cures sickness. But maybe sunlight made you less attentive to your symptoms, or maybe you had a minor cold that ran its course.

But because you are certain about the healing powers of sunlight, you aren’t open to subsequent data. So, if someone suggests that maybe sunlight does not cure illness, you are not really interested. Why should you be? You figured it out.

What kind of leadership is needed right now, given our belief systems and what is at stake?

We all need to be more intellectually humble. We all need to recognize that how certain we feel is irrelevant to how certain we should be. We need to recognize that there are scientists and medical experts out there who have the knowledge and expertise we need to make smart decisions, and they are willing and able to share that information with us.

What causes certain people to stick to their beliefs and act with skepticism despite overwhelming contradictory evidence?

We need our leaders especially right now to understand the role they have in all of this. Words aren’t just words. Words are the basis of beliefs, and beliefs drive our behavior. People who don’t believe the pandemic is real or that it will spread put themselves and everyone else at risk by not doing what needs to be done to stop it.

The media and online platforms that disseminate information also have a critical role to play. A lot of online sites repost and recycle content, which could artificially distort the apparent level of agreement or disagreement that exists in the population.

It’s important that people creating and curating this information, and managing delivery platforms, recognize the profound role they play in shaping beliefs and changing minds. They must be cognizant of the responsibility they bear in times of crisis.

Can people be taught to be more open-minded?

It’s possible. Beliefs are not stable, finished things because we are constantly taking in new data and updating. It may seem disheartening that people shut down once they become certain.

But I see hope in the fact that people are fundamentally social and that they seek to engage with one another. People are sensitive to the beliefs of those around them. When those beliefs change, people may reconsider their positions. That’s why talking about what is happening is important, and informed people who know the most should be talking the loudest.

As for behavioral and cognitive scientists, we don’t yet know if the tendency to hold onto dubious beliefs can be trained out of people. I

t’s something a lot of researchers, including us, are interested in right now. If people are aware of their fallibility, they could be taught to moderate their behavior accordingly. We are investigating the viability of that idea. We’ll test it and see, because that’s how science works.

The World Health Organization (WHO) last week announced a major study to compare treatment strategies in a streamlined clinical trial design that doctors around the world can join.

Other trials are also underway; all told, at least 12 potential COVID-19 treatments are being tested, including drugs already in use for HIV and malaria, experimental compounds that work against an array of viruses in animal experiments, and antibody-rich plasma from people who have recovered from COVID-19.

More than one strategy may prove its worth, and effective treatments may work at different stages of infection, says Thomas Gallagher, a coronavirus researcher at Loyola University Chicago’s Health Sciences Campus. “The big challenge may be at the clinical end determining when to use the drugs.”

Researchers want to avoid repeating the mistakes of the 2014–16 West African Ebola epidemic, in which willy-nilly experiments proliferated but randomized clinical trials were set up so late that many ended up not recruiting enough patients.

“The lesson is you start trials now,” says Arthur Caplan, a bioethicist at New York University’s Langone Medical Center. “Make it a part of what you’re doing so that you can move rapidly to have the most efficacious interventions come to the front.”

To that end, WHO on 20 March announced the launch of SOLIDARITY, an unprecedented, coordinated push to collect robust scientific data rapidly during a pandemic. The study, which could include many thousands of patients in dozens of countries, has emphasized simplicity so that even hospitals overwhelmed by an onslaught of COVID-19 patients can participate.

WHO’s website will randomize patients to local standard care or one of the four drug regimens, using only ones available at the patient’s hospital. Physicians will simply record the day the patient left the hospital or died, the duration of the hospital stay, and whether the patient required oxygen or ventilation.

“That’s all,” says Ana Maria Henao Restrepo, a medical officer at WHO’s Department of Immunization Vaccines and Biologicals.

The design is not blinded: Patients will know they received a drug candidate, and that could cause a placebo effect, Henao Restrepo concedes. But it is in the interest of speed, she says. “We are doing this in record time.” The agency hopes to start to enroll patients this week.

Rather than taking years to develop and test compounds from scratch, WHO and others want to repurpose drugs that are already approved for other diseases and have acceptable safety profiles.

They’re also looking at experimental drugs that have performed well in animal studies against the other two deadly coronaviruses, which cause SARS and Middle East respiratory syndrome (MERS). And they are focusing on compounds plentiful enough to treat a substantial number of patients.

For its study, WHO chose an experimental antiviral called remdesivir; the malaria medication chloroquine (or its chemical cousin hydroxychloroquine); a combination of the HIV drugs lopinavir and ritonavir; and that combination plus interferon-beta, an immune system messenger that can help cripple viruses. The treatments would stop the virus by different mechanisms, but each has drawbacks.

Remdesivir, developed by Gilead Sciences to combat Ebola and related viruses, shuts down viral replication by inhibiting a key viral enzyme, the RNA polymerase. It didn’t help patients with Ebola in a test during the 2019 outbreak in the Democratic Republic of the Congo. But in 2017, researchers showed in test tube and animal studies that the drug can inhibit the SARS and MERS viruses.

The drug, which is given intravenously, has been used in hundreds of COVID-19 patients in the United States and Europe under what’s known as compassionate use, which required Gilead to review patient records; some doctors have reported anecdotal evidence of benefit, but no hard data.

Gilead says it is now starting to supply remdesivir under a simpler “expanded use” designation. Five other clinical trials underway in China and the United States are testing it and may have preliminary results soon. Of the drugs in the SOLIDARITY trial, “remdesivir has the best potential,” says Shibo Jiang of Fudan University, who works on coronavirus therapeutics.

Like most drugs for acute infections, remdesivir may be much more potent if given early, says Stanley Perlman, a coronavirus researcher at the University of Iowa—and that could be a challenge.

“What you really want to do is give a drug like that to people who walk in with mild symptoms,” he says. “And you can’t do that because it’s an [intravenous] drug, it’s expensive, and 85 out of 100 people don’t need it” because they won’t develop severe disease.

Chloroquine and hydroxychloroquine have received intense attention because of positive results from small studies and an endorsement from President Donald Trump, who said, “I feel good about it.”

The drugs decrease acidity in endosomes, compartments that cells use to ingest outside material and that some viruses co-opt during infection. But SARS-CoV- 2’s main entryway is different: It uses its so-called spike protein to attach to a receptor on the surface of human cells.

Studies in cell culture have suggested chloroquine can cripple the virus, but the doses needed are usually high and could cause severe toxicity.

“Researchers have tried this drug on virus after virus, and it never works out in humans,” says Susanne Herold, an expert on pulmonary infections at the University of Giessen.

Results from COVID-19 patients are murky. Chinese researchers who treated more than 100 patients touted chloroquine’s benefits in a letter in BioScience, but they did not publish data. And WHO says “no data has been shared” from more than 20 other COVID-19 studies in China using chloroquine or hydroxychloroquine.

French microbiologist Didier Raoult and colleagues published a study of hydroxychloroquine in 20 COVID-19 patients that concluded the drug had reduced viral load in nasal swabs. (It seemed to work even better with the antibiotic azithromycin.)

But the trial, reported in the International Journal of Antimicrobial Agents, was not randomized, and it didn’t report clinical outcomes such as deaths.

Hydroxychloroquine might actually do more harm than good. It has many side effects and can, in rare cases, harm the heart—and people with heart conditions are at higher risk of severe COVID-19, says David Smith, an infectious disease physician at the University of California, San Diego.

“This is a warning signal, but we still need to do the trial,” he says. There have also been reports of chloroquine poisoning in people who self-medicated.

Many coronavirus researchers are similarly skeptical of the lopinavir-ritonavir combination. Abbott Laboratories developed the drugs to inhibit the protease of HIV, an enzyme that cleaves a long protein chain during assembly of new viruses.

The combination has worked in marmosets infected with the MERS virus, and has also been tested in patients with SARS and MERS, though those results are ambiguous. But the first trial with COVID-19 was not encouraging.

When doctors in Wuhan, China, gave 199 patients standard care with or without lopinavir-ritonavir, the outcomes did not differ significantly, they reported in The New England Journal of Medicine on 15 March. The authors say the patients were very ill and treatment may have started too late.

The fourth arm of SOLIDARITY combines these two antivirals with interferon-beta, a molecule involved in regulating inflammation that has lessened disease severity in marmosets infected with MERS. But interferon-beta might be risky for patients with severe COVID-19, Herold says. “If it is given late in the disease it could easily lead to worse tissue damage, instead of helping patients,” she cautions.

SOLIDARITY is designed to provide a quick, useful verdict, based on the outcomes that are the most relevant for public health, says virologist Christian Drosten of the Charité University Hospital in Berlin. More detailed data could come from an add-on trial in Europe, announced on 23 March by the French biomedical research agency INSERM. To include 3200 patients, it will test the same drugs, including hydroxychloroquine but not chloroquine, and collect additional data such as blood gas levels or lung imaging.

Other approved and experimental treatments are in testing against coronavirus or likely soon to be. They include drugs that can reduce inflammation, such as corticosteroids and baricitinib, a treatment for rheumatoid arthritis. Some researchers have high hopes for camostat mesylate, a drug licensed in Japan for pancreatitis, which inhibits a human protein involved with infection.

Other antivirals will also get a chance, including the influenza drug favipiravir and additional HIV antiretrovirals. Researchers also plan to try to boost immunity with “convalescent” plasma from recovered COVID-19 patients or monoclonal antibodies directed at SARS-CoV-2.

Perlman says the smartest way to test the drugs is in people in early stages of disease who doctors think are most likely to get much worse. How would you determine that? “That is the key question,” he says. Researchers might find a biomarker in blood that helps them predict disease course.

Crucially, doctors and researchers around the world are tackling the problem with urgency, Henao Restrepo says. “This is a crisis like no other and we will have to work together,” she says. “That is the only way perhaps we are going to find a solution.”

UC Berkeley



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