Two Conservative Icons Gave Opposite Advice on COVID-19. Those Misinformed Died in Higher Numbers, New Study Reports.
Sean Hannity (left) and Tucker Carlson each told their audience opposite information about the threat of COVID-19, with serious consequences for those misinformed.
The news sources that you consume can kill you - or save you. That's the fundamental insight of a powerful new study about the impact of watching either Sean Hannity's news show Hannity or Tucker Carlson's Tucker Carlson Tonight. One saved lives and the other resulted in more deaths, due to how each host covered COVID-19.
Carlson took the threat of COVID-19 seriously early on, more so than most media figures on the right or left.
This research illustrates the danger of falling for health-related misinformation due to judgment errors known as cognitive biases. These dangerous mental blindspots stem from the fact that our gut reactions evolved for the ancient savanna environment, not the modern world; yet the vast majority of advice on decision making is to "go with your gut," despite the fact that doing so leads to so many disastrous outcomes. These mental blind spots impact all areas of our life, from health to politics and even shopping, as a survey by a comparison purchasing website reveals. We need to be wary of cognitive biases in order to survive and thrive during this pandemic.
Sean Hannity vs. Tucker Carlson Coverage of COVID-19
Hannity and Tucker Carlson Tonight are the top two U.S. cable news shows, both on Fox News. Hannity and Carlson share very similar ideological profiles and have similar viewership demographics: older adults who lean conservative.
One notable difference, however, relates to how both approached coverage of COVID-19, especially in February and early March 2020. Researchers at the Becker Friedman Institute for Economics at the University of Chicago decided to study the health consequences of this difference.
Carlson took the threat of COVID-19 seriously early on, more so than most media figures on the right or left. Already on January 28, way earlier than most, Carlson spent a significant part of his show highlighting the serious dangers of a global pandemic. He continued his warnings throughout February. On February 25, Carlson told his viewers: "In this country, more than a million would die."
By contrast, Hannity was one of the Fox News hosts who took a more extreme position in downplaying COVID-19, frequently comparing it to the flu. On February 27, he said "And today, thankfully, zero people in the United States of America have died from the coronavirus. Zero. Now, let's put this in perspective. In 2017, 61,000 people in this country died from influenza, the flu. Common flu." Moreover, Hannity explicitly politicized COVID-19, claiming that "[Democrats] are now using the natural fear of a virus as a political weapon. And we have all the evidence to prove it, a shameful politicizing, weaponizing of, yes, the coronavirus."
However, after President Donald Trump declared COVID-19 a national emergency in mid-March, Hannity -- and other Fox News hosts -- changed their tune to align more with Carlson's, acknowledging the serious dangers of the virus.
The Behavior and Health Consequences
The Becker Friedman Institute researchers investigated whether the difference in coverage impacted behaviors. They conducted a nationally representative survey of over 1,000 people who watch Fox News at least once a week, evaluating both viewership and behavior changes in response to the pandemic, such as social distancing and improving hygiene.
Next, the study compared people's behavior changes to viewing patterns. The researchers found that "viewers of Hannity changed their behavior five days later than viewers of other shows, while viewers of Tucker Carlson Tonight changed their behavior three days earlier than viewers of other shows." The statistical difference was more than enough to demonstrate significance; in other words, it was extremely unlikely to occur by chance -- so unlikely as to be negligible.
Did these behavior changes lead to grave consequences? Indeed.
The paper compared the popularity of each show in specific counties to data on COVID-19 infections and deaths. Controlling for a wide variety of potential confounding variables, the study found that areas of the country where Hannity is more popular had more cases and deaths two weeks later, the time that it would take for the virus to start manifesting itself. By March 21st, the researchers found, there were 11 percent more deaths among Hannity's viewership than among Carlson's, again with a high degree of statistical significance.
The study's authors concluded: "Our findings indicate that provision of misinformation in the early stages of a pandemic can have important consequences for health outcomes."
Such outcomes stem from excessive trust that our minds tend to give those we see as having authority, even if they don't possess expertise in the relevant subject era.
Cognitive Biases and COVID-19 Misinformation
It's critically important to recognize that the study's authors did not seek to score any ideological points, given the broadly similar ideological profiles of the two hosts. The researchers simply explored the impact of accurate and inaccurate information about COVID-19 on the viewership. Clearly, the false information had deadly consequences.
Such outcomes stem from excessive trust that our minds tend to give those we see as having authority, even if they don't possess expertise in the relevant subject era -- such as media figures that we follow. This excessive trust - and consequent obedience - is called the "authority bias."
A related mental pattern is called "emotional contagion," in which we are unwittingly infected with the emotions of those we see as leaders. Emotions can motivate action even in the absence of formal authority, and are particularly important for those with informal authority, including thought leaders like Carlson and Hannity.
Thus, Hannity telling his audience that Democrats used anxiety about the virus as a political weapon led his audience to reject fears of COVID-19, even though such a reaction and consequent behavioral changes were the right response. Carlson's emphasis on the deadly nature of this illness motivated his audience to take appropriate precautions.
Authority bias and emotional contagion facilitate the spread of misinformation and its dangers, at least when we don't take the steps necessary to figure out the facts. Such steps can range from following best fact-checking practices to getting your information from news sources that commit publicly to being held accountable for truthfulness. Remember, the more important and impactful such information may be for your life, the more important it is to take the time to evaluate it accurately to help you make the best decisions.
Gene Transfer Leads to Longer Life and Healthspan
In August, a study provided the first proof-of-principle that genetic material transferred from one species to another can increase both longevity and healthspan in the recipient animal.
The naked mole rat won’t win any beauty contests, but it could possibly win in the talent category. Its superpower: fighting the aging process to live several times longer than other animals its size, in a state of youthful vigor.
It’s believed that naked mole rats experience all the normal processes of wear and tear over their lifespan, but that they’re exceptionally good at repairing the damage from oxygen free radicals and the DNA errors that accumulate over time. Even though they possess genes that make them vulnerable to cancer, they rarely develop the disease, or any other age-related disease, for that matter. Naked mole rats are known to live for over 40 years without any signs of aging, whereas mice live on average about two years and are highly prone to cancer.
Now, these remarkable animals may be able to share their superpower with other species. In August, a study provided what may be the first proof-of-principle that genetic material transferred from one species can increase both longevity and healthspan in a recipient animal.
There are several theories to explain the naked mole rat’s longevity, but the one explored in the study, published in Nature, is based on the abundance of large-molecule high-molecular mass hyaluronic acid (HMM-HA).
A small molecule version of hyaluronic acid is commonly added to skin moisturizers and cosmetics that are marketed as ways to keep skin youthful, but this version, just applied to the skin, won’t have a dramatic anti-aging effect. The naked mole rat has an abundance of the much-larger molecule, HMM-HA, in the chemical-rich solution between cells throughout its body. But does the HMM-HA actually govern the extraordinary longevity and healthspan of the naked mole rat?
To answer this question, Dr. Vera Gorbunova, a professor of biology and oncology at the University of Rochester, and her team created a mouse model containing the naked mole rat gene hyaluronic acid synthase 2, or nmrHas2. It turned out that the mice receiving this gene during their early developmental stage also expressed HMM-HA.
The researchers found that the effects of the HMM-HA molecule in the mice were marked and diverse, exceeding the expectations of the study’s co-authors. High-molecular mass hyaluronic acid was more abundant in kidneys, muscles and other organs of the Has2 mice compared to control mice.
In addition, the altered mice had a much lower incidence of cancer. Seventy percent of the control mice eventually developed cancer, compared to only 57 percent of the altered mice, even after several techniques were used to induce the disease. The biggest difference occurred in the oldest mice, where the cancer incidence for the Has2 mice and the controls was 47 percent and 83 percent, respectively.
With regard to longevity, Has2 males increased their lifespan by more than 16 percent and the females added 9 percent. “Somehow the effect is much more pronounced in male mice, and we don’t have a perfect answer as to why,” says Dr. Gorbunova. Another improvement was in the healthspan of the altered mice: the number of years they spent in a state of relative youth. There’s a frailty index for mice, which includes body weight, mobility, grip strength, vision and hearing, in addition to overall conditions such as the health of the coat and body temperature. The Has2 mice scored lower in frailty than the controls by all measures. They also performed better in tests of locomotion and coordination, and in bone density.
Gorbunova’s results show that a gene artificially transferred from one species can have a beneficial effect on another species for longevity, something that had never been demonstrated before. This finding is “quite spectacular,” said Steven Austad, a biologist at the University of Alabama at Birmingham, who was not involved in the study.
Just as in lifespan, the effects in various organs and systems varied between the sexes, a common occurrence in longevity research, according to Austad, who authored the book Methuselah’s Zoo and specializes in the biological differences between species. “We have ten drugs that we can give to mice to make them live longer,” he says, “and all of them work better in one sex than in the other.” This suggests that more attention needs to be paid to the different effects of anti-aging strategies between the sexes, as well as gender differences in healthspan.
According to the study authors, the HMM-HA molecule delivered these benefits by reducing inflammation and senescence (cell dysfunction and death). The molecule also caused a variety of other benefits, including an upregulation of genes involved in the function of mitochondria, the powerhouses of the cells. These mechanisms are implicated in the aging process, and in human disease. In humans, virtually all noncommunicable diseases entail an acceleration of the aging process.
So, would the gene that creates HMM-HA have similar benefits for longevity in humans? “We think about these questions a lot,” Gorbunova says. “It’s been done by injections in certain patients, but it has a local effect in the treatment of organs affected by disease,” which could offer some benefits, she added.
“Mice are very short-lived and cancer-prone, and the effects are small,” says Steven Austad, a biologist at the University of Alabama at Birmingham. “But they did live longer and stay healthy longer, which is remarkable.”
As for a gene therapy to introduce the nmrHas2 gene into humans to obtain a global result, she’s skeptical because of the complexity involved. Gorbunova notes that there are potential dangers in introducing an animal gene into humans, such as immune responses or allergic reactions.
Austad is equally cautious about a gene therapy. “What this study says is that you can take something a species does well and transfer at least some of that into a new species. It opens up the way, but you may need to transfer six or eight or ten genes into a human” to get the large effect desired. Humans are much more complex and contain many more genes than mice, and all systems in a biological organism are intricately connected. One naked mole rat gene may not make a big difference when it interacts with human genes, metabolism and physiology.
Still, Austad thinks the possibilities are tantalizing. “Mice are very short-lived and cancer-prone, and the effects are small,” he says. “But they did live longer and stay healthy longer, which is remarkable.”
As for further research, says Austad, “The first place to look is the skin” to see if the nmrHas2 gene and the HMM-HA it produces can reduce the chance of cancer. Austad added that it would be straightforward to use the gene to try to prevent cancer in skin cells in a dish to see if it prevents cancer. It would not be hard to do. “We don’t know of any downsides to hyaluronic acid in skin, because it’s already used in skin products, and you could look at this fairly quickly.”
“Aging mechanisms evolved over a long time,” says Gorbunova, “so in aging there are multiple mechanisms working together that affect each other.” All of these processes could play a part and almost certainly differ from one species to the next.
“HMM-HA molecules are large, but we’re now looking for a small-molecule drug that would slow it’s breakdown,” she says. “And we’re looking for inhibitors, now being tested in mice, that would hinder the breakdown of hyaluronic acid.” Gorbunova has found a natural, plant-based product that acts as an inhibitor and could potentially be taken as a supplement. Ultimately, though, she thinks that drug development will be the safest and most effective approach to delivering HMM-HA for anti-aging.
A new study provides key insights in what causes Alzheimer's: a breakdown in the brain’s system for clearing waste.
In recent years, researchers of Alzheimer’s have made progress in figuring out the complex factors that lead to the disease. Yet, the root cause, or causes, of Alzheimer’s are still pretty much a mystery.
In fact, many people get Alzheimer’s even though they lack the gene variant we know can play a role in the disease. This is a critical knowledge gap for research to address because the vast majority of Alzheimer’s patients don’t have this variant.
A new study provides key insights into what’s causing the disease. The research, published in Nature Communications, points to a breakdown over time in the brain’s system for clearing waste, an issue that seems to happen in some people as they get older.
Michael Glickman, a biologist at Technion – Israel Institute of Technology, helped lead this research. I asked him to tell me about his approach to studying how this breakdown occurs in the brain, and how he tested a treatment that has potential to fix the problem at its earliest stages.
Dr. Michael Glickman is internationally renowned for his research on the ubiquitin-proteasome system (UPS), the brain's system for clearing the waste that is involved in diseases such as Huntington's, Alzheimer's, and Parkinson's. He is the head of the Lab for Protein Characterization in the Faculty of Biology at the Technion – Israel Institute of Technology. In the lab, Michael and his team focus on protein recycling and the ubiquitin-proteasome system, which protects against serious diseases like Alzheimer’s, Parkinson’s, cystic fibrosis, and diabetes. After earning his PhD at the University of California at Berkeley in 1994, Michael joined the Technion as a Senior Lecturer in 1998 and has served as a full professor since 2009.
Dr. Michael Glickman