Who Qualifies as an “Expert” And How Can We Decide Who Is Trustworthy?
Discerning a real expert from a charlatan is crucial during the COVID-19 pandemic and beyond.
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.
Expertise is a slippery concept. Who has it, who claims it, and who attributes or yields it to whom is a culturally specific, sociological process. During the COVID-19 pandemic, we have witnessed a remarkable emergence of legitimate and not-so-legitimate scientists publicly claiming or being attributed to have academic expertise in precisely my field: infectious disease epidemiology. From any vantage point, it is clear that charlatans abound out there, garnering TV coverage and hundreds of thousands of Twitter followers based on loud opinions despite flimsy credentials. What is more interesting as an insider is the gradient of expertise beyond these obvious fakers.
A person's expertise is not a fixed attribute; it is a hierarchical trait defined relative to others. Despite my protestations, I am the go-to expert on every aspect of the pandemic to my family. To a reporter, I might do my best to answer a question about the immune response to SARS-CoV-2, noting that I'm not an immunologist. Among other academic scientists, my expertise is more well-defined as a subfield of epidemiology, and within that as a particular area within infectious disease epidemiology. There's a fractal quality to it; as you zoom in on a particular subject, a differentiation of expertise emerges among scientists who, from farther out, appear to be interchangeable.
We all have our scientific domain and are less knowledgeable outside it, of course, and we are often asked to comment on a broad range of topics. But many scientists without a track record in the field have become favorites among university administrators, senior faculty in unrelated fields, policymakers, and science journalists, using institutional prestige or social connections to promote themselves. This phenomenon leads to a distorted representation of science—and of academic scientists—in the public realm.
Trustworthy experts will direct you to others in their field who know more about particular topics, and will tend to be honest about what is and what isn't "in their lane."
Predictably, white male voices have been disproportionately amplified, and men are certainly over-represented in the category of those who use their connections to inappropriately claim expertise. Generally speaking, we are missing women, racial minorities, and global perspectives. This is not only important because it misrepresents who scientists are and reinforces outdated stereotypes that place white men in the Global North at the top of a credibility hierarchy. It also matters because it can promote bad science, and it passes over scientists who can lend nuance to the scientific discourse and give global perspectives on this quintessentially global crisis.
Also at work, in my opinion, are two biases within academia: the conflation of institutional prestige with individual expertise, and the bizarre hierarchy among scientists that attributes greater credibility to those in quantitative fields like physics. Regardless of mathematical expertise or institutional affiliation, lack of experience working with epidemiological data can lead to over-confidence in the deceptively simple mathematical models that we use to understand epidemics, as well as the inappropriate use of uncertain data to inform them. Prominent and vocal scientists from different quantitative fields have misapplied the methods of infectious disease epidemiology during the COVID-19 pandemic so far, creating enormous confusion among policymakers and the public. Early forecasts that predicted the epidemic would be over by now, for example, led to a sense that epidemiological models were all unreliable.
Meanwhile, legitimate scientific uncertainties and differences of opinion, as well as fundamentally different epidemic dynamics arising in diverse global contexts and in different demographic groups, appear in the press as an indistinguishable part of this general chaos. This leads many people to question whether the field has anything worthwhile to contribute, and muddies the facts about COVID-19 policies for reducing transmission that most experts agree on, like wearing masks and avoiding large indoor gatherings.
So how do we distinguish an expert from a charlatan? I believe a willingness to say "I don't know" and to openly describe uncertainties, nuances, and limitations of science are all good signs. Thoughtful engagement with questions and new ideas is also an indication of expertise, as opposed to arrogant bluster or a bullish insistence on a particular policy strategy regardless of context (which is almost always an attempt to hide a lack of depth of understanding). Trustworthy experts will direct you to others in their field who know more about particular topics, and will tend to be honest about what is and what isn't "in their lane." For example, some expertise is quite specific to a given subfield: epidemiologists who study non-infectious conditions or nutrition, for example, use different methods from those of infectious disease experts, because they generally don't need to account for the exponential growth that is inherent to a contagion process.
Academic scientists have a specific, technical contribution to make in containing the COVID-19 pandemic and in communicating research findings as they emerge. But the liminal space between scientists and the public is subject to the same undercurrents of sexism, racism, and opportunism that society and the academy have always suffered from. Although none of the proxies for expertise described above are fool-proof, they are at least indicative of integrity and humility—two traits the world is in dire need of at this moment in history.
[Editor's Note: To read other articles in this special magazine issue, visit the beautifully designed e-reader version.]
Catching colds may help protect kids from Covid
A new study shows that the immune system's response to colds can help prepare it to defend against COVID-19 - but only in the very young.
A common cold virus causes the immune system to produce T cells that also provide protection against SARS-CoV-2, according to new research. The study, published last month in PNAS, shows that this effect is most pronounced in young children. The finding may help explain why most young people who have been exposed to the cold-causing coronavirus have not developed serious cases of COVID-19.
One curiosity stood out in the early days of the COVID-19 pandemic – why were so few kids getting sick. Generally young children and the elderly are the most vulnerable to disease outbreaks, particularly viral infections, either because their immune systems are not fully developed or they are starting to fail.
But solid information on the new infection was so scarce that many public health officials acted on the precautionary principle, assumed a worst-case scenario, and applied the broadest, most restrictive policies to all people to try to contain the coronavirus SARS-CoV-2.
One early thought was that lockdowns worked and kids (ages 6 months to 17 years) simply were not being exposed to the virus. So it was a shock when data started to come in showing that well over half of them carried antibodies to the virus, indicating exposure without getting sick. That trend grew over time and the latest tracking data from the CDC shows that 96.3 percent of kids in the U.S. now carry those antibodies.
Antibodies are relatively quick and easy to measure, but some scientists are exploring whether the reactions of T cells could serve as a more useful measure of immune protection.
But that couldn't be the whole story because antibody protection fades, sometimes as early as a month after exposure and usually within a year. Additionally, SARS-CoV-2 has been spewing out waves of different variants that were more resistant to antibodies generated by their predecessors. The resistance was so significant that over time the FDA withdrew its emergency use authorization for a handful of monoclonal antibodies with earlier approval to treat the infection because they no longer worked.
Antibodies got most of the attention early on because they are part of the first line response of the immune system. Antibodies can bind to viruses and neutralize them, preventing infection. They are relatively quick and easy to measure and even manufacture, but as SARS-CoV-2 showed us, often viruses can quickly evolve to become more resistant to them. Some scientists are exploring whether the reactions of T cells could serve as a more useful measure of immune protection.
Kids, colds and T cells
T cells are part of the immune system that deals with cells once they have become infected. But working with T cells is much more difficult, takes longer, and is more expensive than working with antibodies. So studies often lags behind on this part of the immune system.
A group of researchers led by Annika Karlsson at the Karolinska Institute in Sweden focuses on T cells targeting virus-infected cells and, unsurprisingly, saw that they can play a role in SARS-CoV-2 infection. Other labs have shown that vaccination and natural exposure to the virus generates different patterns of T cell responses.
The Swedes also looked at another member of the coronavirus family, OC43, which circulates widely and is one of several causes of the common cold. The molecular structure of OC43 is similar to its more deadly cousin SARS-CoV-2. Sometimes a T cell response to one virus can produce a cross-reactive response to a similar protein structure in another virus, meaning that T cells will identify and respond to the two viruses in much the same way. Karlsson looked to see if T cells for OC43 from a wide age range of patients were cross-reactive to SARS-CoV-2.
And that is what they found, as reported in the PNAS study last month; there was cross-reactive activity, but it depended on a person’s age. A subset of a certain type of T cells, called mCD4+,, that recognized various protein parts of the cold-causing virus, OC43, expressed on the surface of an infected cell – also recognized those same protein parts from SARS-CoV-2. The T cell response was lower than that generated by natural exposure to SARS-CoV-2, but it was functional and thus could help limit the severity of COVID-19.
“One of the most politicized aspects of our pandemic response was not accepting that children are so much less at risk for severe disease with COVID-19,” because usually young children are among the most vulnerable to pathogens, says Monica Gandhi, professor of medicine at the University of California San Francisco.
“The cross-reactivity peaked at age six when more than half the people tested have a cross-reactive immune response,” says Karlsson, though their sample is too small to say if this finding applies more broadly across the population. The vast majority of children as young as two years had OC43-specific mCD4+ T cell responses. In adulthood, the functionality of both the OC43-specific and the cross-reactive T cells wane significantly, especially with advanced age.
“Considering that the mortality rate in children is the lowest from ages five to nine, and higher in younger children, our results imply that cross-reactive mCD4+ T cells may have a role in the control of SARS-CoV-2 infection in children,” the authors wrote in their paper.
“One of the most politicized aspects of our pandemic response was not accepting that children are so much less at risk for severe disease with COVID-19,” because usually young children are among the most vulnerable to pathogens, says Monica Gandhi, professor of medicine at the University of California San Francisco and author of the book, Endemic: A Post-Pandemic Playbook, to be released by the Mayo Clinic Press this summer. The immune response of kids to SARS-CoV-2 stood our expectations on their head. “We just haven't seen this before, so knowing the mechanism of protection is really important.”
Why the T cell immune response can fade with age is largely unknown. With some viruses such as measles, a single vaccination or infection generates life-long protection. But respiratory tract infections, like SARS-CoV-2, cause a localized infection - specific to certain organs - and that response tends to be shorter lived than systemic infections that affect the entire body. Karlsson suspects the elderly might be exposed to these localized types of viruses less often. Also, frequent continued exposure to a virus that results in reactivation of the memory T cell pool might eventually result in “a kind of immunosenescence or immune exhaustion that is associated with aging,” Karlsson says. https://leaps.org/scientists-just-started-testing-a-new-class-of-drugs-to-slow-and-even-reverse-aging/particle-3 This fading protection is why older people need to be repeatedly vaccinated against SARS-CoV-2.
Policy implications
Following the numbers on COVID-19 infections and severity over the last three years have shown us that healthy young people without risk factors are not likely to develop serious disease. This latest study points to a mechanism that helps explain why. But the inertia of existing policies remains. How should we adjust policy recommendations based on what we know today?
The World Health Organization (WHO) updated their COVID-19 vaccination guidance on March 28. It calls for a focus on vaccinating and boosting those at risk for developing serious disease. The guidance basically shrugged its shoulders when it came to healthy children and young adults receiving vaccinations and boosters against COVID-19. It said the priority should be to administer the “traditional essential vaccines for children,” such as those that protect against measles, rubella, and mumps.
“As an immunologist and a mother, I think that catching a cold or two when you are a kid and otherwise healthy is not that bad for you. Children have a much lower risk of becoming severely ill with SARS-CoV-2,” says Karlsson. She has followed public health guidance in Sweden, which means that her young children have not been vaccinated, but being older, she has received the vaccine and boosters. Gandhi and her children have been vaccinated, but they do not plan on additional boosters.
The WHO got it right in “concentrating on what matters,” which is getting traditional childhood immunizations back on track after their dramatic decline over the last three years, says Gandhi. Nor is there a need for masking in schools, according to a study from the Catalonia region of Spain. It found “no difference in masking and spread in schools,” particularly since tracking data indicate that nearly all young people have been exposed to SARS-CoV-2.
Both researchers lament that public discussion has overemphasized the quickly fading antibody part of the immune response to SARS-CoV-2 compared with the more durable T cell component. They say developing an efficient measure of T cell response for doctors to use in the clinic would help to monitor immunity in people at risk for severe cases of COVID-19 compared with the current method of toting up potential risk factors.
In this week's Friday Five: The eyes are the windows to the soul - and biological aging?
Plus, what bean genes mean for health and the planet, a breathing practice that could lower levels of tau proteins in the brain, AI beats humans at assessing heart health, and the benefits of "nature prescriptions"
The Friday Five covers five stories in research that you may have missed this week. There are plenty of controversies and troubling ethical issues in science – and we get into many of them in our online magazine – but this news roundup focuses on new scientific theories and progress to give you a therapeutic dose of inspiration headed into the weekend.
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Here are the stories covered this week:
- The eyes are the windows to the soul - and biological aging?
- What bean genes mean for health and the planet
- This breathing practice could lower levels of tau proteins
- AI beats humans at assessing heart health
- Should you get a nature prescription?