Q&A with Holden Thorp: Finding Better Ways to Communicate Science
Leaps.org spoke with Holden Thorp, Editor-in-Chief of the prestigious Science family of journals, about ways to improve science journalism, the challenges faced by experts, the lab leak theory and much more.
This month, Leaps.org had a chance to speak with Holden Thorp, Editor-in-Chief of the Science family of journals. We talked about the best ways to communicate science to the public, mistakes by public health officials during the pandemic, the lab leak theory, and bipartisanship for funding science research.
Before becoming editor of the Science journals, Thorp spent six years as provost of Washington University in St. Louis, where he is Rita Levi-Montalcini Distinguished University Professor and holds appointments in both chemistry and medicine. He joined Washington University after spending three decades at the University of North Carolina at Chapel Hill, where he served as the UNC's 10th chancellor from 2008 through 2013.
A North Carolina native, Thorp earned a doctorate in chemistry in 1989 at the California Institute of Technology and completed postdoctoral work at Yale University. He is a fellow of the National Academy of Inventors and the American Association for the Advancement of Science.
Read his full bio here.
This conversation was lightly edited by Leaps.org for style and format.
Matt Fuchs: You're a musician. It seems like many scientists are also musicians. Is there a link between the scientist brain and the musician brain?
Holden Thorp: I think [the overlap is] relatively common. I'm still a gigging bass player. I play in the pits for lots of college musicals. I think that it takes a certain discipline and requires you to learn a lot of rules about how music works, and then you try to be creative within that. That's similar to scientific research. So it makes sense. Music is something I've been able to sustain my whole life. I wouldn't be the same person if I let it go. When you're playing, especially for a musical, where the music is challenging, you can't let your mind wander. It’s like meditation.
MF: I bet it helps to do something totally different from your editing responsibilities. Maybe lets the subconscious take care of tough problems at work.
HT: Right.
MF: There's probably never been a greater need for clear and persuasive science communicators. Do we need more cross specialty training? For example, journalism schools prioritizing science training, and science programs that require more time learning how to communicate effectively?
HT: I think we need both. One of the challenges we've had with COVID has been, especially at the beginning, a lot of reporters who didn’t normally cover scientific topics got put on COVID—and ended up creating things that had to be cleaned up later. This isn't the last science-oriented crisis we're going to have. We've already got climate change, and we'll have another health crisis for sure. So it’d be good for journalism to be a little better prepared next time.
"Scientists are human beings who have ego and bravado and every other human weakness."
But on the other side, maybe it's even more important that scientists learn how to communicate and how likely it is that their findings will be politicized, twisted and miscommunicated. Because one thing that surprised me is how shocked a lot of scientists have been. Every scientific issue that reaches into public policy becomes politicized: climate change, evolution, stem cells.
Once one side decided to be cautious about the pandemic, you could be certain the other side was going to decide not to do that. That's not the fault of science. That’s just life in a political world. That, I think, caught people off guard. They weren't prepared to shape and process their messages in a way that accounted for that—and for the way that social media has intensified all of this.
MF: Early in the pandemic, there was a lack of clarity about public health recommendations, as you’d expect with a virus we hadn’t seen before. Should public officials and scientists have more humility in similar situations in the future? Public officials need to be authoritative for their guidance to be followed, so how do they lead a crisis response while displaying humility about what we don't know?
HS: I think scientists are people who like to have the answer. It's very tempting and common for scientists to kind of oversell what we know right now, while not doing as much as we should to remind people that science is a self-correcting process. And when we fail to do that – after we’ve collected more data and need to change how we're interpreting it – the people who want to undermine us have a perfect weapon to use against us. It's challenging. But I agree that scientists are human beings who have ego and bravado and every other human weakness.
For example, we wanted to tell everybody that we thought the vaccines would provide sterilizing immunity against infection. Well, we don't have too many other respiratory viruses where that's the case. And so it was more likely that we were going to have what we ended up with, which is that the vaccines were excellent in preventing severe disease and death. It would have been great if they provided sterilizing immunity and abruptly ended the pandemic a year ago. But it was overly optimistic to think that was going to be the case in retrospect.
MF: Both in terms of how science is communicated and received by the public, do we need to reform institutions or start new ones to instill the truth-seeking values that are so important to appreciating science?
HS: There are a whole bunch of different factors. I think the biggest one is that the social media algorithms reward their owners financially when they figure out how to keep people in their silos. Users are more likely to click on things that they agree with—and that promote conflict with people that they disagree with. That has caused an acceleration in hostilities that attend some of these disagreements.
But I think the other problem is that we haven’t found a way to explain things to people when it’s not a crisis. So, for example, a strong indicator of whether someone who might otherwise be vaccine hesitant decided to get their vaccine is if they understood how vaccines worked before the pandemic started. Because if you're trying to tell somebody that they're wrong if they don't get a vaccine, at the same time you're trying to explain how it works, that's a lot of explaining to do in a short period of time.
Lack of open-mindedness is a problem, but another issue is that we need more understanding of these issues baked into the culture already. That's partly due the fact that there hasn't been more reform in K through 12 and college teaching. And that scientists are very comfortable talking to each other, and not very comfortable talking to people who don't know all of our jargon and have to be persuaded to spend time listening to and thinking about what we're trying to tell them.
"We're almost to the point where clinging to the lab leak idea is close to being a fringe idea that almost doesn't need to be included in stories."
MF: You mentioned silos. There have been some interesting attempts in recent years to do “both sides journalism,” where websites like AllSides put different views on high profile issues side-by-side. Some people believe that's how the news should be reported. Should we let people see and decide for themselves which side is the most convincing?
HS: It depends if we're talking about science. On scientific issues, when they start, there's legitimate disagreement about among scientists. But eventually, things go back and forth, and people compete with each other and work their way to the answer. At some point, we reach more of a consensus.
For example, on climate change, I think it's gotten to the point now where it's irresponsible, if you're writing a story about climate change, to run a quote from somebody somewhere who's still—probably because of their political views—clinging to the idea that anthropogenic global warming is somehow not damaging the planet.
On things that aren't decided yet, that makes sense to run both. It's more a question of judgment of the journalists. I don't think the solution to it is put stark versions of each side, side-by-side and let people choose. The whole point of journalism is to inform people. If there's a consensus on something, that's part of what you're supposed to be informing them about.
MF: What about reporting on perspectives about the lab leak theory at various times during the pandemic?
HS: We’re the outlet that ran the letter that really restarted the whole debate. A bunch of well-known scientists said we should consider the lab leak theory more carefully. And in the aftermath of that, a bunch of those scientists who signed that letter concluded that the lab leak was very, very unlikely. Interestingly, publishing that letter actually drove us to more of a consensus. I would say now, we're almost to the point where clinging to the lab leak idea is close to being a fringe idea that almost doesn't need to be included in stories. But I would say there's been a lot of evolution on that over the last year since we ran that letter.
MF: Let's talk about bipartisanship in Congress. Research funding for the National Institutes of Health was championed for years by influential Republicans who supported science to advance health breakthroughs. Is that changing? Maybe especially with Sen. Roy Blunt retiring? Has bipartisanship on science funding been eroded by political battles during COVID?
HS: I'm optimistic that that won't be the case. Republican Congresses have usually been good for science funding. And that's because (former Sen.) Arlen Specter and Roy Blunt are two of the political figures who have pushed for science funding over the last couple decades. With Blunt retiring, we don't know who's going to step in for him. That's an interesting question. I hope there will be Republican champions for science funding.
MF: Is there too much conservatism baked into how we research new therapies and bring them to people who are sick, bench-to-bedside? I'm thinking of the criticisms that NIH or the FDA are overly bureaucratic. Are you hopeful about ARPA-H, President Biden’s proposed new agency for health innovation?
HS: I think the challenge hasn't been cracked by the federal government. Maybe DARPA has done this outside of health science, but within health science, the federal government has had limited success at funding things that can be applied quickly, while having overwhelming success at funding basic research that eventually becomes important in applications. Can they do it the other way around? They’ll need people running ARPA-H who are application first. It’s ambitious. The way it was done in Operation Warp Speed is all the money was just given to the companies. If the hypothesis on ARPA-H is for the federal government to actually do what Moderna and BioNTech did for the vaccine, themselves, that's a radical idea. It's going to require thinking very differently than the way they think about dispersing grants for basic research.
MF: You’ve written a number of bold op-eds as editor of the Science journals. Are there any op-eds you're especially proud of as voicing a view that was important but not necessarily popular?
HS: I was one of the first people to come out hard against President Trump['s handling of] the pandemic. Lots of my brothers and sisters came along afterwards. To the extent that I was able to catalyze that, I'm proud of doing it. In the last few weeks, I published a paper objecting to the splitting of the OSTP director from the science advisor and, especially, not awarding the top part of the job to Alondra Nelson, who is a distinguished scientist at black female. And instead, giving part of it to Francis Collins. He’s certainly the most important science policy figure of my lifetime, but somebody who’s been doing this now for decades. I just think we have to push as hard as we can to get a cadre of young people leading us in Washington who represent the future of the country. I think the Biden administration leaned on a lot of figures from the past. I’m pushing them hard to try to stop it.
MF: I want to circle back to the erosion of the public’s trust in experts. Most experts are specialists, and specialists operate in silos that don’t capture the complexity of scientific knowledge. Are some pushbacks to experts and concerns about the perils of specialization valid?
HS: You're on the right track there. What we need is more respect for the generalist. We can't help the fact that you have to be very specialized to do a lot of stuff. But what we need is more partnership between specialists and people who can cross fields, especially into communication and social sciences. That handoff is just not really there right now. It's hard to get a hardcore scientist to respect people who are interested in science, education and science communication, and to treat them as equals. The last two years showed that they're at least as important, if not more so.
MF: I’m grateful that you’re leading the way in this area, Holden. Thank you for sharing your thoughts and your work.
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