F. Perry Wilson: The Formula for Medical Misinformation

Harlan Krumholz: Welcome to Health & Veritas. I’m Harlan Krumholz.

Howard Forman: And I’m Howie Forman. We are physicians and professors at Yale University. We’re trying to get closer to the truth about health and healthcare. This week we’ll be speaking with Dr. F. Perry Wilson, but first I usually ask what’s got your attention, Harlan, but all of us are paying a lot of attention to the native son of Pittsburgh, the Buffalo Bills defensive back Damar Hamlin, who seems to remain in the ICU at this moment that we’re taping this, after suffering cardiac arrest, after something of a usual tackle. Can you set this up for us, Harlan, and tell us what likely happened?

Harlan Krumholz: Well, and I think it’s hard to say, let’s first say that our thoughts are with this family and we’re hoping for a full recovery by this young football player. And yeah, this was something that riveted America. Many of us were watching the game, and I grew up in Dayton, Ohio, so I’m a Cincinnati Bengals fan. They were playing the Buffalo Bills. And in the course of the game, he made a tackle and apparently got up from the tackle. I mean, he did get up from the tackle and then started staggering and fell to the ground and then was surrounded by teammates. We didn’t have a real good view in it, but soon it was reported that he was receiving CPR. And this of course shook everyone who was there and everyone who was watching.

And it didn’t take long before the news outlets were reporting this broadly healthy, young, vibrant individual—and now it turns out someone highly invested in his community and a person that was widely loved—who was involved in merely a tackle that ended up threatening his life. Now there’s a whole dialogue here about what’s going on in the NFL and about the injuries and the concussions. We’ve talked about concussions on the show. But this was a situation where actually what has been reported is that this is someone who as a result of a tackle, it seems, developed a cardiac arrest. This has elicited a lot of discussion.

I’ll say, we can get into some questions about this, but I think that one of the most important messages that I hope everyone who has seen this is besides the fact that just the mere hope that he has recovery is the recognition of how important it is when something like this happens and someone has a cardiac arrest to intervene immediately and to use cardiopulmonary resuscitation. Any lay person can have these skills to bridge someone to a point where they can get shocked and defibrillated and potentially saved. My hope is that out of this tragedy that there will be a lot of education that’s taking place that may end up saving a lot of other lives.

Howard Forman: I’m curious, everybody has talked a lot about the so-called commotio cordis, which is sort of the arrest of the heart of the ventricular fibrillation that may occur in the setting of a direct blow to the chest in the area of the heart. Can you talk a little bit about what that means and why that might be the mechanism that we’re talking about here?

Harlan Krumholz: Sure. There are a lot of reasons that someone might have a cardiac arrest, a sudden death event within the context of a sporting event. There’s lots of discussions about screening and so forth. But one of the ideas, one of the thoughts about what might have happened here was something as you said is called commotio cordis. And this is really a phenomenon in which a sudden blunt impact to the chest can cause this sort of sudden death, a cardiac arrest in the absence of cardiac damage. And this has been described for hundreds of years in the context I think originally of chest trauma that could occur among workers. But it’s been seen a lot in sports. And when I say a lot, let me just say as physicians—I’m a cardiologist—as a cardiologist, we’re highly aware of it. I don’t mean that it occurs every day, every week. Maybe there are a handful of these that may occur within a year.

And it is generally described as a situation where an object, usually of a circular shape and pretty hard and a small diameter, hits someone directly in the chest, maybe at a speed of 40 miles per hour or greater. And you may say, how do you know all this about this? Well, actually, they developed animal models. I mean, people may cringe when they hear this, but pigs who were set up to get blunt force trauma to the chest and to see whether or not they could elicit this arrhythmia in other animals as well. Then what they found was usually it was like a small ball, like a baseball that—pretty hard, pretty small diameter—and when thrown at a certain speed could actually cause the heart to spasm, to develop this thing that we call ventricular fibrillation, where the heart’s just sort of not really beating effectively. There’s no effective circulation.

That’s what makes this a little odd. We haven’t really seen it in a situation of a football injury. And that’s because it’s not like that small force to a very small place within the chest, right in the middle. But I guess anything’s possible. When you look at the tackle, he did get hit hard in the middle of the chest. That’s why a lot of people are thinking that this might be the mechanism of what happened to him.

Howard Forman: Yeah, they’ve described this I think as you said with baseballs and described it with hockey pucks theoretically happening. I saw a recent report around a lacrosse game, but I wonder in this setting, you said that we’re hopeful he’s going to do well, and I am certainly hopeful that he’s going to do well, but what is the recovery from this like for somebody? He was intubated immediately. He had a second arrest apparently after he got to the hospital. I’m not trying to get us to speculate, but just explaining to the audience how much uncertainty there is and how little information we have to go on to better understand this.

Harlan Krumholz: For a long time people thought that this almost invariably resulted in death, that there was little that we could do when the arrhythmia, the heart rhythm became deranged like this as a result of a blow to the chest. I think it’s probably, as we’ve gotten better at CPR and first response to something like this, the sense now is that as many as 30% to 40% of people actually can be brought back like he was. And you could see the NFL’s primed for this, they’ve got people on the sidelines, someone’s down. I think the reason that two thirds of people may die is because this happens on the field and everyone’s just so shocked, nobody moves. The one thing is, can you get somebody out of the original rhythm that’s really going to lead to sudden death unless there’s an intervention? They did that.

Now, the beautiful thing about CPR and defibrillation is if you can get in and fix the rhythm, there’s no reason somebody can’t make a full recovery. The only variables at stake now are how much damage was done when his heart wasn’t beating effectively? How actually many minutes passed and how well did his body cope with that? And as a world-class athlete, somebody playing professional sports, there’s a hope that his body will in fact be able to recover this because they moved in quickly. But you never know. We’re in this moment now where it’s hard to know exactly, but I retained kind of an optimism that maybe they got in there fast enough and his body is strong enough and that he in fact will come back. And that’s what I’m hoping, at least.

Howard Forman: Let’s hope, and I think just one final question for you, Harlan. In the grand scheme of things, are you more concerned about concussions than you are about something like this for both young athletes as well as professional athletes?

Harlan Krumholz: Yeah. I mean, I think that we always have to be prepared for something like this. And it could be from a blow to the chest. It could be because somebody falls through the cracks and actually has some sort of congenital heart condition or there’s an issue that may lead to it. Cardiopulmonary resuscitation and supporting people and reducing that remains important. But I think the bigger problem in football right now are all these blows to the head. The sport has a lot of work to do to protect the people who are participating.

Howard Forman: We have an upcoming guest who will talk more about that, so we’ll give our audience a little more information about that in the coming weeks. But I really appreciate your expertise on this, Harlan.

Harlan Krumholz: No, no, these are great questions. And like I said, I hope that people will remember, what would I do in this situation if I saw someone go down and how can I help? And recognize that that rapid action can provide dramatic effect in terms of helping someone to get through what would otherwise inevitably lead to their death.

Howard Forman: Yeah, we’re all praying for his recovery, so let’s hope that we’ll have that soon.

Harlan Krumholz: Great. Okay, let’s pivot and get to our guest.

Howard Forman: Dr. F. Perry Wilson is a nephrologist, epidemiologist, and associate professor at Yale School of Medicine. His research focuses on using data and analytics to personalize medicine for each individual. He is the director of Yale Clinical and Translational Research Accelerator (CTRA), dedicated to applying discoveries from the lab to the development of clinical studies. He is the co-director of the Yale Section of Nephrology Human Genetics and Clinical Research Core, which provides services to enhance translational studies in kidney disease. He’s a columnist at Medscape where he hosts a highly popular series called “The Impact Factor,” which analyzes the strengths and weaknesses of published studies.

Dr. Wilson received a bachelor’s degree in biochemistry from Harvard University and his medical degree from Columbia University. He completed his internship, residency, and fellowship at the University of Pennsylvania, where he also received a master’s degree in clinical epidemiology. Most important today, I want to say is that sometime in the next couple of weeks you have a book coming out that’s entitled How Medicine Works and When It Doesn’t, and I’ve read this book now and I think it’s a fantastic distillation of sort of narrative about patient care as well as science and how we could use it better to inform patient care.

And one of the things that struck me right from the beginning is how much you’re able to use experiences from COVID in exploring that narrative. And you have one quote that I want you to respond to, and you said, “It is far, far easier in medicine to simply do something—treat a bunch of patients with a medication—than to study something. And the space between those actions can be measured in lives.” And Harlan and I have talked many times about ivermectin, how it doesn’t work. You talk in the book about hydroxychloroquine. Can you give us a little understanding about why these problems persist and why misinformation particularly seems to perpetuate this?

F. Perry Wilson: Sure. Thank you, Howie and Harlan, for having me. This is a real treat. I’ve been big fans of both of yours for a long time, so this is a great opportunity for me, and I appreciate the kind introduction. A real motivation for the book, it began as a consideration of why people are susceptible to misinformation and disinformation in the medical space. And one of the problems that you’re alluding to is that when you’re in a desperate situation, as we were in the beginning of COVID, I’ll cast you back to the time pre=vaccine when we had people dying, it seemed like the entire hospital was full of people incredibly ill, many of whom were dying with COVID. We had no treatments. We had no vaccine. There was a real desire on all of our parts to find something that might work. And I think our culture has a narrative that the answer is out there.

There’s almost this fairytale thing that happens where the princess has been poisoned and somewhere we go on a quest and we find the one magical thing growing in the forest and that wakes the princess up. We have that. It’s in our DNA. And part of what I wanted to write about in this book was that unfortunately medical research is quite a bit harder than that. In fact, it’s very rare that you’re going to find something on your shelf that treats any new disease. In fact, for any given disease, you’ve got thousands of compounds that are tested at various stages from cell culture up through humans, the vast majority of which failed to have any effect whatsoever, and many of which prove to be harmful. It is really, really hard. And part of what we need to tell people is that these quick fixes, these easy fixes, “aren’t we lucky that this global pandemic happened and we happen to have a cure”—as some people were reporting online—“sitting in our medicine shelves this whole time.”

That just kind of luck doesn’t exist, I’m afraid.

Harlan Krumholz: I want to echo what Howie said. I really enjoyed the book also and appreciate that you shared it with us before it was on sale. And one of the things I thought you did really well was interweave your own clinical experience in with the issues that arose as a result of seeing patients and put it in the context of evidence and evidence generation and did so in a way that I think is really going to be accessible to laypeople, that they really will begin to understand what some of these tensions are and also what are the sort of ways that people are led astray, and really did appreciate the way you thought about this. I was wondering, what was your work process in this? Because the book is so full of useful information that really did require you to pull together so many different sources and to harmonize it into a single coherent book. I mean, how did you do it? You were on sabbatical, I think you told me, and did you just sit down every morning and write, or how did you do it?

F. Perry Wilson: Yeah, I’m more of a nighttime writer, actually. It was sort of the way I managed. I get the kids off to bed and then head down. I had a little spot in the basement, which was relatively quiet. I’m a big believer that people are better editors than creators. My process is very much get whatever I can onto the page, just write, and I’ll worry about editing it later, so that helps remove some of the paralysis. I appreciate you noticing the references in the book. They appear at the end and you’ll see that I think there’s barely a fact that goes unreferenced. And obviously that was quite deliberate because a lot of things that are purported to be facts are rarely referenced out there in the real world. But I think the bigger meta-process for me in writing the book and conceiving of the book was that what began as sort of the theory of why disinformation is successful evolved into, for me, a more deeper understanding of some of the struggles our patients go through.

And I think so much of the you might call it the debunking stuff that goes on today, the fact-checkers and the doctors who get out there and appropriately say, “Hey, ivermectin doesn’t work. The studies don’t show that” neglects one of the main reasons that people are susceptible to these types of misinformation, and that is the medical system itself is doing a really bad job when it comes to certain fundamental things in the care of our patients. One of the things I talk about in the book that I think is so important and under-recognized is the impact of social isolation on patients’ health. This is something that doctors are simply not trained to address. We don’t ask our patients if they’re lonely, we ask them ... we might ask them if they’ve thought of hurting themselves or if their mood is depressed, but we don’t touch on that fundamental problem of our times, the social isolation.

And part of why people are susceptible to things propagating through social media is because that is your social outlet right now. In trying to understand why people might believe that vaccines contain nanochips, I came to understand that part of the problem is us, is even the people who pat ourselves in the back and say, “Oh, we’re the scientists. We follow the science,” what we’re not appreciating is the struggles our patients are facing in their personal lives, with their pharmaceutical companies, with their insurance company, with the healthcare system itself. And part of their desire to reach out to these other voices is because they’re so frustrated, frankly, with all of us, and we need to recognize that too.

Howard Forman: You had two separate narratives about fraud. Maybe you had more, but two that are very strongly burned in my memory right now about fraud in medical research. Two examples that were published in peer-reviewed journals. I wonder if you want to just say a word about both of them. I’m thinking of the one with praying and the one with vaccines.

F. Perry Wilson: Sure.

Howard Forman: Then just reassure our audience what you’ve said in the book, which is this does exist, but there are guardrails that prevent it from getting out of hand.

F. Perry Wilson: Yeah, I mean, one of the things I wanted to do with this book is to say, yeah, there are problems. I’m not a medicine apologist. I see real problems in how we deliver healthcare and medical science in this country, and I think we can’t begin to win people’s trust back without an acknowledgment. Yeah, there are problems here. These for-profit companies want to make money. That is a problem, but it doesn’t mean that the whole system is out to get you or kill you or you don’t throw the baby out with the bathwater. We need a little nuance here. These two cases of fraud, I think, are both telling. One is a fascinating case of how the media can go awry. This was a study that purported to randomize women undergoing in vitro fertilization to either usual care or, unbeknownst to them, a group of people would be praying for their pregnancy to be successful.

A study, a randomized trial of prayer, and they found about a doubling of the pregnancy rate, successful pregnancy rate from 25% to 50% in the prayer group. The lead author was the chair of OB-GYN at Columbia Medical, which was my alma mater. The study was published in the science section of The New York Times. Well, it’s published in The Journal of Reproductive Medicine, but it was reported on in the science section of The New York Times. This is a big deal. It turned out that the entire study was made up of whole cloth. It was written by a guy named Daniel Wirth. Daniel Wirth was subsequently convicted, I mean, more or less seems to be a con artist. Subsequently convicted for check fraud and cashing his dead father’s social security checks, that kind of thing. The study never really happened, but it shows how the media’s kind of desperate for these narratives, these breakthroughs that can lead people astray and even the best-quality study, a randomized trial, the thing we elevate as the pinnacle of evidence, if you just make it up, you’ve got problems there.

The other one, though, that didn’t do too much damage, I don’t think, but the one that really did of course was Andrew Wakefield’s study on the MMR [mumps-measles-rubella] vaccine. And this is the study that purported to show in 12 kids, I believe, who had received the MMR vaccine that within two weeks they developed this regressive form of autism. The ones who could stopped being able to talk, the ones who could walk stopped being able to walk, they got worse and worse. It’s published in The Lancet, one of the premier medical journals in the world, and Wakefield had a press conference even before it was published, saying the MMR vaccine needs to be taken off the market. It subsequently came to light that Wakefield had a financial interest undisclosed in this article, which was that he was starting a company that was founded for the purpose of litigating vaccine harms.

The idea, I think, would be that you patent a blood test that you could use on your kid to show somehow that the vaccine had caused their autism. There’s messaging of him to a friend saying he thinks this is a multimillion-dollar company, but of course it depends on that link actually existing in the first place. Some subsequent sleuthing from a reporter named Leaf—Andrew Leaf, I believe—investigated the medical records of these kids showing that in fact, none of them had regressive autism. And I believe only one or two developed any symptoms after the MMR vaccine. What’s worse, it wasn’t a random sample of kids, it was kids who were recruited from a network of parents who had thought that the vaccines harmed their children. They had sort of selected a group that already had a preexisting belief that there was a problem here. The study was subsequently retracted by The Lancet, but not for 10 years after its initial publication. And it really is the birth of the modern anti-vax movement. This type of thing can do a lot of harm.

Harlan Krumholz: One of the things that’s on my mind is that we have these black-and-white cases, but in science today, there’s just so much disagreement and lack of consensus around areas where you may think that the evidence is actually quite clear. And it really is the pandemic that has brought this, I think, into bright relief. You read your book, and I think anyone who reads a book will develop some good critical thinking skills about the kind of information that they may encounter in medicine, but what they’ll encounter in the real world. There are many experts who are promoting ideas that if they employ your critical thinking skills that you may think that they have without basis, but yet they’re very loud. You can talk about misinformation, but it’s actually in my mind that science wants to encourage active disagreement and struggle around ideas.

But there are places where we should be able to come together with consensus and say, “Given the evidence we have, this is highly likely to be true.” That doesn’t mean that one day we won’t learn something new. But for today, this seems highly likely to be true. And we seem to be in a moment where that’s getting increasingly difficult to come to, to bring together that kind of consensus. I wonder what you think about how this is going to evolve and where it’s going to lead for us because it’s reaching a very difficult moment for patients to know what to do.

F. Perry Wilson: Absolutely. Consensus requires humility. That’s sort of the central issue. And social media is not for the humble. People who are going to do well on Twitter and Instagram and Facebook, which is where a lot of patients frankly are getting this type of information from, are people who express certainty. And what you’re getting at, Harlan, is fundamentally science, especially medical science, and I write this in the book, it is an uncertain science. It’s a science of playing the percentages. I wish we had the type of accuracy that you can get with Einstein’s equations or Maxwell’s field equations, that kind of thing. We don’t have that. What we have is, well, we’re 80% to 90% sure that taking this is better than doing nothing. And that’s good. You’re going to Vegas, you’ll take those odds. But that level of nuance is lost because the people that get promoted and retweeted are the people who say, “I am certain that this thing cures you” or “I am certain that this thing kills you,” because that is exciting.

Howard Forman: To Harlan’s great credit, he has very early in my career, taught me a lot about thinking about individual risk versus population risk and how we can educate patients and inform them and make decisions with them. You spend a lot of time on that in this book, but you’re also a medical educator. You’re teaching medical students this as well. Are we teaching this well enough right now to our medical students? Are we communicating this well enough to the population at large? Because to me, I think we spend way too much time talking about population risk and not enough time talking about individual risk.

F. Perry Wilson: We’re clearly not teaching this well enough. I mean, there’s objective evidence of this. Just for the listeners to talk about the difference here, when we study something, we do a randomized trial of 10,000 people and we have a drug that lowers your blood pressure versus a placebo. And we show, “Oh, there’s less strokes in the people that got the blood pressure drug.” We pat ourselves on the back. That is a population assessment. What is the effect of this drug if you give it to 10,000 people? And that’s important to us because we treat a lot of people and on a national level, we treat millions and millions of people with high blood pressure and we’ll save lives by giving this medication. That’s the population basis. But for an individual, the chance that they’re going to have a stroke is relatively low, at least in the short term.

The chance that the medication will benefit them, well, not zero, slightly greater than zero, but it’s not very high because the chances are, nothing’s going to happen to you. That’s the individual benefit. And we can actually measure these things. There are statistical ways to get a sense of the individual benefit of a medication versus the population benefit. They really aren’t taught. It’s not well discussed. I think doctors do have a bit of an intuitive sense of this where they’ll say, “Hey, the data says you should take this medication, but you know what, Bob, you look fine, if you want to wait a couple months and we’ll come and discuss it again, that’s fine.” That’s actually an evidence-based decision. That is good doctoring there. We shouldn’t treat all patients like they are a homogenous piece of a pool of homogenized population, because they’re not.

Harlan Krumholz: I wanted to just make a note that I think we all really owe you a debt of gratitude for the time you take to educate the public and for the platforms you’re on. I know that some people may look and think this is easy, but it’s a tremendous amount of time to prepare for these pieces that you do—I know. And as you note in the book, it can lead you to be someone that others target that who disagree with you and take you on. It’s not easy. I was just wondering if you could just share a little bit about how did this evolve for you. I mean, this isn’t something when you’re a faculty member that anyone asked you to do. You sort of take it on yourself, say it’s kind of my responsibility as someone who’s in medical research and clinical care. What led you to it, and what keeps you in it?

F. Perry Wilson: Oh, that’s a great question. I mean, I come from a family of teachers. My mom was a teacher. My three older sisters are all teachers, and that’s always been a passion of mine. And I think you want to teach what you know, and once I became a clinical researcher and sort of immersed myself in the design of clinical trials and other types of studies and saw the difficulties and the challenges and the weirdnesses that pop up epidemiologically, it just became something that was really fun to teach. Once I started doing more public-facing stuff, particularly in the past couple of years with COVID, it certainly exposed me to more downsides than I think I would’ve anticipated In the past. I’ve been very surprised at what people will get upset about, particularly in some cases where I’m the messenger, I’m reporting on a study that I find interesting, but I didn’t conceive of it or execute it or even do the statistical analysis for, and yet I’ve received—

Harlan Krumholz: Somebody thinks you own it, they’re going after you because it’s your study, right?

F. Perry Wilson: It’s my study. There are things that have surprised me. For example, there was a study that I thought was very clever, randomized trial in patients with HIV, and they were trying to get them to be good about taking their antiviral medications, an important thing. And basically they randomized people to just the usual care, “Hey, please take your meds” versus “We’re going to test your urine at the end of the month and if we detect the medication in your urine, we’re going to pay you 30 bucks. We’re going to pay 30 bucks a month to make sure you stay on your meds.” Their outcome was viral load. It wasn’t just “Was your urine positive?,” it was to see if, “Was HIV suppressed?” They showed a significantly higher level of viral load suppression in the people that they paid 30 bucks a month.

“Oh, that’s interesting,” I thought. This is 30 bucks a month, that’s actually probably pretty cheap considering the public health benefit. And I reported on that study. I had nothing to do with the study, and I received several—I don’t want to say death threats, it wasn’t like, “You should die”—but it wasn’t far off. It was, “You’re what’s wrong with America.”

Harlan Krumholz: Oh, my goodness.

F. Perry Wilson: It was sort of like, “This is emblematic of the decline of civilization.” Basically, “Why should we have to pay people to do the right thing?” And I get the philosophical argument, I suppose, and I’d even be willing to have it, but the threats and the, “If you keep doing this, you’ll what’s coming to you” language.

Harlan Krumholz: Oh, my gosh.

F. Perry Wilson: I do get surprised. That said, the positives far outweigh the negatives, I believe. I think. I hope I’m not fooling myself too much that it makes some impact. I’m hopeful that the book makes an even larger impact because it’s really written for people who aren’t medical. They’re people who, like me, are fascinated by medicine, who think medical science is cool and science is cool and want to learn more about how it works and of course, when it doesn’t, and to be a little more skeptical in their life, but not cynical.

Howard Forman: Well, I want to remind our listeners that you can pre-order the book on Amazon now. I think it’s officially for sale in the next couple of weeks. It’s titled How Medicine Works and When It Doesn’t: Learning Who to Trust to Get And Stay Healthy by F. Perry Wilson. We’re going to link this in our website also so people can see it that way. And I personally just want to thank you. I think there are so many great stories and specific advice to people about how to do exactly what you say, who to trust to get and stay healthy. Thank you.

F. Perry Wilson: Thank you guys. It’s been a pleasure.

Harlan Krumholz: Terrific job, Perry. Really terrific. And thanks for joining us today. It’s really great to talk with you.

F. Perry Wilson: Oh, my pleasure, guys. Thanks.

Harlan Krumholz: Well, Howie, that was a terrific, terrific interview. I’m so glad that Perry took the time to join us, and I hope his book does very well. Okay, let’s turn to the section where you start to talk about a little bit what’s on your mind this week.

Howard Forman: Yeah, so you and I have already talked about this a little bit, but XBB.1.5 is a variant of interest representing a recombination—and we can talk more about what that means—of two different lineages, of the original Omicron variant of concern. Put that aside, the technical details. It is showing immune evasion to a serious degree, meaning that our most recent boosters are no longer expected to provide the same level of protection that we had hoped for. It’s becoming the dominant variant in most regions. It’s certainly getting there in areas where it’s not dominant already. And we’re seeing cases grow even as we track them less well.

We have huge spikes in our sewage count in New Haven, in particular, reaching levels just below the Omicron peak and higher than other measured peaks. This is serious. We also have more patients in the hospital with COVID than at any time since the Omicron peak. But what I’m seeing in the emergency room seems to indicate that while respiratory tract symptoms are present in most, severe lung disease is decidedly absent from the vast majority. This doesn’t mean people should ignore this wave, but it does mean that our collective immunity through prior infection, vaccination, and boosters may in fact be protecting us more than the laboratory results would indicate. What are your thoughts about this?

Harlan Krumholz: Yeah, it doesn’t feel, Howie, like we’re in a prize fight, and we get through one round and there’s still more rounds ahead and maybe we’re trading out opponents. That first opponent that we had, the one that got us particularly in the northeast in the beginning, was a big and powerful and strong one that inflicted a lot of damage. The subsequent opponents that we’re facing, these other variants, while causing considerable harm, aren’t quite at the same level, especially as the virus and the variants started to affect the upper respiratory system more than the lower respiratory system. We aren’t seeing people gasping for air and lacking oxygen and requiring artificial means to be able to oxygenate the blood. I see this one as getting better and better at being transmissible. It’s figuring out how to go through the population better, but it doesn’t seem to what we would call have been increasing its pathogenicity, its ability to inflict harm.

By the way, if I’m the virus—this is a completely anthropomorphic view—if I’m the virus, I want to survive. If I start killing my host, that’s not good for me. What I actually want to do is get better at jumping from host to host and I want that host to live so I can jump back again. If I just make this sort of… think about evolution, I think I’m probably better off as a virus to get better and better at hopping and to be more and more benign so that people stick around, so I can jump back. But I think we’re going to have to see what happens. And one of the things that is important, I’ll make this one more point about this, is that we really are lacking a good way to link the genomic information with the epidemiologic data at a broad scale.

We’ve got some information about this and we’re seeing, we report on genomics—40%, 50% are of this new variant, but we’re still not good enough in this country linking our systems of information to be able to understand exactly in real time what’s going on with the pathogenicity. I hope that we’ll get better with that, but that’s a challenge for us ahead as we deal with these waves after waves after waves. We want to know really rapidly what’s the story with this, and we’re going to need to be able to bring together these disparate sources of information.

Howard Forman: Yeah, and I’ll just make a shout out to our former guest and our friend Eric Topol, who two points that he’s made repeatedly. One is that the bivalent booster probably still does improve people’s protections, so it’s still worth going for that, particularly if you’re in high-risk groups. But the other point that he made today from an article, I think in Nature or Science, is that Paxlovid really works and it continues to work irrespective of variants seemingly, and it’s being completely underused. 13% of infections in the United States are being treated with Paxlovid. You need to be treated early, you can’t decide you’re going to try to ride this out and only when it gets severe try Paxlovid because it just doesn’t work that way. Somehow we’ve got to do a better job communicating to people that if you’re eligible for Paxlovid, if you don’t have a contraindication to it, you really should seek a consultation with a physician or pharmacist to get it sooner than later.

Harlan Krumholz: You’ve been listening to Health & Veritas with Harlan Krumholz and Howie Forman.

Howard Forman: How did we do? To give us your feedback or to keep the conversation going, you can find us on Twitter.

Harlan Krumholz: Yep. Still on Twitter. I’m @hmkyale. That’s HMK-Yale.

Howard Forman: And I’m @thehowie. That’s @T-H-E-H-O-W-I-E. You can also email us at health.veritas@yale.edu. Aside from Twitter and our podcast, I’m fortunate to be the faculty director of the healthcare track and founder of the MBA for Executives program at the Yale School of Management. Feel free to reach out via email for more information on our innovative programs, or you can check out our website at som.yale.edu/emba.

Harlan Krumholz: And we didn’t say Howie, happy New Year, right? Happy New—

Howard Forman: Happy New Year to all.

Harlan Krumholz: ... Year to everybody. Happy New Year to all. Health & Veritas is produced with the Yale School of Management. Thanks to our researcher, Jenny Tan, and to our producer, Miranda Shafer. They are amazing. Talk to you soon, Howie, I am looking forward to a really great 2023.

Howard Forman: Thanks very much, Harlan. Happy New Year. Healthy New Year to everybody. Talk to you soon.