Dr. Ania Jastreboff: The Revolution in Obesity Medication

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 will be speaking with Dr. Ania Jastreboff, but first we like to check in on current health news. What’s got your attention this week, Harlan?

Harlan Krumholz: Well, I thought, first of all, I’m just so excited about our guest. This topic has great importance and, for me, endless fascination. And she’s going to present so much information about obesity. So I’m going to keep this short, but there was some big news last week as Illumina, one of the leading companies that sequences genomes, came out and said that they’re going to have a variety of products that is going to drive the cost of sequencing DNA, entirely sequencing DNA, down to $200. Now you got to realize that at the turn of the millennium, in order to sequence even a single genome, it was, I don’t know, I think something like a hundred million dollars, because the NIH had put all this money into the Human Genome Project and were trying to figure out exactly what is the genome made of. And so by the time we got to 2015, it was around, maybe $1000, but going down to $200, this is extraordinary.

And I wanted to just give people a sense of this. Some people may be saying, “Well, but I thought 23andMe is like 99 bucks. What’s the big deal?” There’s a big deal here. There’s a big difference. The 23andMe type of services does genotyping. So they are looking for specific genetic variance that an individual may have, and the genotyping can be performed through a variety of methods, but they’re looking at particular areas of the entire genome in order to find certain things that they report back to you or they may use for other purposes. When we’re talking about sequencing, that’s a method used to determine the exact sequence of the entire genome. And traditionally we could sequence a short piece, but the whole genome and being able to do this for 200 bucks, this is heralding.

Now interestingly, their stock dropped when they announced this. Now how could that be? Well, some people are actually, there’re other companies coming out with inexpensive solutions that some people think may even be better. So time will tell what exactly happens, but the race is on. And I think we’re going to get to an era where it’s going to be extraordinarily inexpensive for people to have their entire genome sequence. Once it’s sequenced, then that data may be available for use in a wide variety of areas in terms of identifying risk or, potentially, response to treatments or tests or a whole range of things. But I just thought this was an important thing to reflect on because $200 would’ve been unimaginable just 20 years ago and now it’s becoming something. It’s akin to Moore’s Law, where every year the price of computing goes down because the computers get more and more powerful. We’re seeing this in sequencing and the competition. The competition in this area is such that it’s really driving everything towards better pricing and better solutions. So anyway, I just wanted to mark that for people listening that that was big news.

Howard Forman: Yeah, a guest two weeks ago talked about this. Jonathan Rothberg and I, he was the first person to ever say to me, probably 17 years ago I think, that we would get to a hundred-dollar genome and that wouldn’t even be the end point. So it is nice to actually see these things happen. It’s an awful lot of people that make promises. It’s nice to see it be delivered.

Today we welcome Professor Ania Jastreboff. Dr. Ania Jastreboff is an associate professor and physician scientist specializing in obesity medicine and is board-certified in adult endocrinology and metabolism, pediatric endocrinology, and obesity medicine. She developed the clinical practice guidelines for the comprehensive care of patients with obesity, serves on the board of directors of the American Board of Obesity Medicine and is a nationally recognized researcher, expert, teacher, and clinician on obesity. Her research focuses on using antiobesity medication and neuroimaging to examine the neurobiology behind obesity. Dr. Jastreboff completed her PhD and fellowships at Yale and before that, her MD and residency at the University of Maryland. First, Ania, welcome to the Health & Veritas podcast. I want to start off by asking you to help our listeners understand how your two focuses—that is, the use of brain imaging in obesity and the treatment with novel molecules—relate to one another and how this has changed the way we must think about obesity. And maybe you can just start off by explaining what neuroimaging is and what these novel drugs are.

Ania Jastreboff: Sure. Thank you so much for having me. It’s my pleasure. So interestingly enough, for decades, obesity was not viewed as a disease. And one of the things that is really critical is really focusing in on the fact that it is a disease. And not only saying that but treating it as a disease. And we can speak to that a little bit more, but the reason why I started out my research using neuroimaging, which is basically using various techniques such as MRI, so magnetic resonance, or PET imaging to look at what may be happening in the brain, is because early on many of us realized, “Well, the brain must control eating behavior. It controls all these other bodily functions.” And so how does it do that in terms of obesity? And specifically, how does it do that in terms of defending a specific amount of fat mass or, basically, energy. We store energy as fat, and so our brain defends a fat mass so that we have enough energy to do the things that we need to do.

And so early on I was using neuroimaging to look at, well, how do individuals who have obesity or individuals who don’t have obesity, how do they respond to viewing pictures of food? So early on we were looking at that. We also looked at how people responded to drinking sugar or drinking fructose or glucose specifically and looking to see whether they had different responses. But all that to say, all of those studies give us insight into what regions of the brain may be involved in controlling eating behavior, but they don’t actually tell us exactly what’s going on.

And so the importance of doing neuroimaging or looking at how the brain may relate to all of this, is to give us insight into how the brain may be doing this. But it doesn’t quite give us all the answers. And so transitioning over to my more recent work, which is looking at various antiobesity medications and who they might work for and how they might work. So I think that in terms of neuroimaging, combining those two things, so combining antiobesity medications with how they’re working in the brain, that is early. We don’t know yet exactly how they work in the brain, but we can speak to the mechanisms of the medications and, potentially down the road, how that might look.

Harlan Krumholz: Howie, you’re burying the lede. Ania’s a rock star here, and what she’s done is nothing short of miraculous. She’s led what, I think, is perhaps the most important study of obesity in a generation. We’ve been going along a track where we’ve started to see medications that have had an effect and then she comes out and blows it out of the water with a combination drug that looks like it might be able to make it so that we don’t need bariatric surgery anymore because people can actually be treated. And not only that, there’s a lot of speculation and some evidence about bariatric surgery and subsequent risk, but these drugs that she’s using have a real prospect of lowering cardiovascular risk.

And Ania, tell us a little bit about these drugs. I was so amazed and proud to see you leading this very important study that is delivering, really, a solution to so many people. And what surprises me is much of the world still doesn’t know about these things. I’m finding people who keep up with lots of things are clueless about the fact that this is actually occurring. I wonder if you could just talk a little bit about the SURMOUNT trial, and what are these drugs, and what do you think of them, now that you’ve had a chance to study them so intensively?

Ania Jastreboff: Sure, absolutely. So for decades, as you said, there have been various agents that we use to treat patients with obesity. They started back in the ’50s and even before that as stimulant medications. And those were effective but not safe. So they worked, but did they work on the appropriate mechanism?

Harlan Krumholz: So, I love this. Anybody who’s watched Mad Men knows that at a certain point, Betty Draper starts to gain weight and she goes to doctors and they just start giving her, what are they, amphetamines at that point?

Ania Jastreboff: Yeah. And now we still have one, and it’s the safest of all of them. It’s used more as an add-on medication in my practice, but that’s phentermine. And so these medications, they do help you lose weight. But again, are they working on the mechanisms that we want them to be working on? Are they working on the innate mechanisms that maintain, that defended body fat mass? And so those are the first generation, let’s say the stimulants. Then the second generation were medications in 2010, 2012, and 2014. So 2012 and 2014, there was several medications that were FDA-approved, and those were effective and safe, but they weren’t highly effective. And then in 2021, semaglutide, which is a GLP-1 [glucagon-like peptide-1] receptor agonist medication, and I’ll talk about that a little bit more, it was FDA-approved for obesity treatment. And then the newest one, the one that you were just referring to, tirzepatide, is a combination of a GIP [glucose-dependent insulinotropic polypeptide] and a GLP-1 receptor agonist. It’s a single molecule.

So what are these new medications, and how effective are they? So this class of medications, they’re nutrient-stimulated, hormone-based medications. So our body naturally makes these hormones that are stimulated when we eat food. So we make these, we release these, we secrete these hormones when we eat food. They’re secreted from our gut, either from our intestine or our pancreas. And what these hormones do naturally is they inform our brain of either what we’re eating or how much fat mass we’re carrying, all these different things. And so it basically, they inform our brain and then they tell us, “Hey, I’m hungry. Hey, I’m full. Hey, I need to eat more. I don’t have enough fat mass, or I have too much fat mass, stop eating.” So they help in terms of meal frequency, meal duration, the amount that you eat at a given meal.

So they help with all these different things. And so these medications mimic those hormones. So GLP-1 and tirzepatide, which is GLP-1 and GIP, they mimic those innate hormones that our body makes, and they signal to our brain, as well as various other tissues in our body, but they signal to our brain that we’ve eaten. And so for example, with semaglutide as well as with tirzepatide, what happens is that patients, they’re eating a meal and then they stop eating earlier; they end up eating less. And this is during the weight reduction phase. So as people are losing weight, they tend to eat less, they tend to feel full more quickly, and they don’t continue to eat, or they don’t go for seconds. They also may change preference for food. And that’s something that we’re looking at. So some patients report that they want to drink less alcohol or maybe that fatty foods exacerbate their symptoms. So they tend to eat fewer fatty foods.

Once they get to a weight plateau—and we’ll talk about that in a second—but once they get to a weight plateau, their repetitive behavior may come back. So their appetite may come back, their hunger may come back, their cravings may come back, but the weight doesn’t. And this is the key here, because when we are treating obesity, we are not treating to lose weight. We are treating to reset or reregulate the body fat mass set point. So these medications, in my opinion and in the opinion of others, they reset that set point to a lower place. And a byproduct or a consequence of that is that you lose weight.

Harlan Krumholz: How does our set point get deranged?

Ania Jastreboff: Yeah, that’s a great question. And I think many things push that set point up. And maybe I should back up. So, basically, our body has this interest in carrying the appropriate amount of fuel and that appropriate amount of fuel is that appropriate amount of fat mass. And that means that having too much of it means we can’t carry out our daily activities, just as having too little of it we can’t carry out our daily activities. And so it sets this defended fat mass set point, as it does with many other things in our body—electrolyte, water balance, temperature, all these other things. And it does this with fat mass. So now superimpose on this the obesogenic environment. And not just highly palatable food that’s readily available 24 hours a day but also stress, lack of sleep, circadian rhythm disruption, all these different things, unhealthy muscle because we don’t have to move to catch our dinner. We can pick up the phone and call Uber Eats.

So there are all these different things that are in the obesogenic environment. And so on a population level, our defended fat mass set point has been pushed up. So let’s say somebody a hundred years ago, their body mass index would have been, let’s say 25, maybe now their body mass index would be 30. So on a population level, this has been pushed up because of the obesogenic environment. And most people tend to gain weight over time. They gain maybe small amounts every year, but over time they tend to gain weight. And so obesity results from an inappropriate regulation of that body fat mass or a dysregulation of that body fat mass. And so obesity treatment requires reregulation of that physiology.

Harlan Krumholz: Can you treat people for a certain amount of time and reset it and stop treating them or they’re going to have to be on that for their entire life?

Ania Jastreboff: So it’s akin to any other chronic treatable disease. So if you have someone who has hypertension and you start an antihypertensive medication and their blood pressure improves, what happens when you stop that medicine? Their blood pressure goes up, and we’re not surprised. So in the same way, if you have someone who has obesity and you treat them with an antiobesity medication, you reregulate that body fat mass set point, you decrease that body fat mass set point. What happens when you stop that medicine? That body fat mass set point goes back up, and we shouldn’t be surprised. And the weight regained before—

Harlan Krumholz: So you guys have seen that. When people withdraw from the treatment, they go back to where they were?

Ania Jastreboff: Yes. So it’s just like any other chronic disease, you have to keep treating it. And here’s the important point, though. Do we want the set point to be immutable? And I would argue not. So let’s say you have a woman and she becomes pregnant, you want that set point to go up because you want the adiposity to go up because she will then be able to carry a healthy child or a healthy baby. So you don’t want the set point to be completely immutable. You just want it to be reregulated to a place that is healthier.

Howard Forman: Can you comment a little bit from the trial itself, from the most recent trial, what is the patient population we’re talking about? And tell us a little more about both the magnitude of the improvement, the weight loss, as well as the safety profile, which to my eyes is amazing.

Ania Jastreboff: Yeah. Two trials and two medications that are highly effective, semaglutide and tirzepatide. And so I’ll speak to the tirzepatide and basically the individuals that were enrolled, there were over 2,500 individuals. They had to have either obesity, so a BMI of greater than 30 or a BMI of greater than 27 with an obesity-related condition such as hypertension or hyperlipidemia, but not type 2 diabetes.

Harlan Krumholz: And just to calibrate people, Ania. So BMI of 30, so for people, that’s your weight divided by your body surface area. And 30 is, if you look around the United States, aren’t about a third of the Americans over 30, it’s a pretty common thing for people to be above 30. Howie excepted, who’s very svelte and maintains a very good body weight. But for those of us who are in average America, what is it? What is the percent?

Ania Jastreboff: So it’s 42% of Americans have a body mass index of greater than or equal to 30. And by 2030 it’s projected that more than 50% will have a body mass index of greater than 30. So half, half—

Harlan Krumholz: Oh my goodness. And the CDC says 30 and above, it represents a classification of a word that they call obesity?

Ania Jastreboff: Yes.

Harlan Krumholz: Is it? Yep.

Ania Jastreboff: That’s correct. And BMI doesn’t actually tell us anything about fat. So we’re defining obesity as an elevated, defended fat mass set point and that adiposity is having some negative consequence on your health. And yet we’re using a measure that was not designed for diagnosis. So BMI is a screening tool, not a diagnostic tool. So as a field, within obesity medicine, we do have to think about how we’re defining obesity and long term, what the goals should be. And they shouldn’t be BMI. But right now that’s what we have. So that’s what we’re using. So it’s a really great point that you bring up. But yes, by the current definition, half of us in the United States will have obesity by 2030. And right now already two-thirds are either overweight or have obesity. So a BMI of greater than 25.

Harlan Krumholz: And sorry, I didn’t mean to interrupt you because I know you were getting to who’s being studied, what the effect was, and the safety. So sorry, I just was curious, wanted to put that in perspective for people that this 30 isn’t a small number of people. It’s actually, maybe, half of Americans soon. So sorry, keep going.

Ania Jastreboff: Yes. So these individuals, they were randomized to either placebo, which included a standard of care and lifestyle intervention or three different doses of tirzepatide. So 5 milligrams, 10 milligrams, and 15 milligrams. And with all of these doses, you have to dose-escalate slowly to mitigate the side effects. And we can talk about that. That’s really, really critical and crucial for, I think, all healthcare providers and for patients to know about. But anyway, they were randomized to these three different doses, and they were followed for 72 weeks.

And after 72 weeks, the group that received the highest dose of tirzepatide, so the 15 milligrams, the ones who were actually on treatment, lost 22.5% of their body weight on average. So that’s an average. And there’s great variability in terms of how much weight people lose. And so some people maybe lost 15 pounds and other people lost over a hundred pounds, but the average weight reduction was 22.5. And when you subtract that from the placebo, from standard of care and lifestyle, the difference was 20.1%. So still, over 20% of your total body weight. Also importantly, patients of course ask us, “Well, what does that translate to in terms of the absolute amount? How many pounds am I going to lose?” So with that highest dose, the average weight reduction was 52 pounds. So again, some people lost 15, some people lost over a hundred. We had one participant at our site who lost 92 pounds. And then the next question is—

Harlan Krumholz: Just one thing about this, just when people are losing this kind of weight, we tend to think about diets as being ones of deprivation. The people that I’ve seen treated with this are changing their habits without a sense of using immense willpower. In fact, what I’ve seen, and you, of course, so much more experience than I, but what I’ve seen is that people don’t have a sense of willpower at all. They’re actually, like you said, a resetting in changing habits without waking up every day and saying, “I really, really wish I could eat something, but I can’t.” They’re losing the appetite. Could you just reflect on that a second? Just what was the experience of people losing? Because many people we’ve seen, like The Big Loser on TV and all that, it’s all about immense effort and immense determination and willpower. That’s not what’s happening here. Is that your experience?

Ania Jastreboff: Yes, absolutely. And that really gets to the crux of the matter, which is that, yet again, we call obesity a disease, but we don’t treat it as such. How do we treat other diseases? We target disease mechanisms. And so these medications are targeting disease mechanisms. Caloric restriction does not target disease mechanisms. Caloric restriction just makes us hungrier and crave more. These medications actually target those brain mechanisms that actually impact obesity and that defended fat mass set point. So I’ll give you a quote. And I ended the presentation at the American Diabetes Association when I was presenting this data for the SURMOUNT-1 study, just back in June. And this is what the participant said to me in the course of the study when she had lost 92 pounds. She said, “Dr. Jastreboff, it’s just as easy to lose weight as it ever was to gain weight.” And to me that says it all.

She basically said, “Look, I’m taking something, you gave me something that is targeting disease mechanisms.” And for years we’ve been saying, “Eat less and move more.” And that is not a viable treatment for obesity. That does not reset your set point. And so for patients who have diabetes, do we say, “Well you need to eat less and move more.” Or do we say, “Here’s some insulin, or here’s some medicine.” And why do we not do that for obesity? And we must. We have to.

Harlan Krumholz: And what about concerns now about access? Because these drugs can be expensive and in some ways the populations that may need the most are going to have the hardest time getting them. How are you thinking about those these days and what do you do for patients who come in who need these meds but can’t get them?

Ania Jastreboff: Yeah, I think that is one of the hardest things that we’re trying to overcome right now. A couple of things with that. One, just note that tirzepatide right now is FDA-approved for type 2 diabetes, not FDA-approved for obesity. So we can try and prescribe it off-label, of course, but it’s not surprising that it’s more difficult to get it covered for that indication. But all the GLP-1 receptor agonists in general are difficult to get covered by insurance, especially Medicaid and Medicare, if a patient doesn’t have type 2 diabetes. And this is very sad, and I’ll tell you why. In terms of the weight reduction, it is significantly—well, it is lower. So people who have type 2 diabetes lose less weight with these medications than people who don’t have type 2 diabetes. And yet we can oftentimes only get them covered if a patient already has type 2 diabetes.

So basically it’s waiting till a patient gets unhealthier in order to be able to get coverage for these medications, which is pretty absurd. And so it’s almost like waiting for your patient to have an hemoglobin A1C of 6.5 so you can get insurance coverage. Liraglutide 1.8 milligrams will be off-patent at the end of 2023. So we’re hoping that that will increase access for some patients. We are lobbying as best as we can on local and national levels. I was telling Howie the other day that I testified in front of the State Senate last March, or a year and a half ago now, March, for Senate Bill 1007, which was a bill that was to cover both bariatric surgery as well as antiobesity medications for individuals with a BMI greater than 40. So greater than 40, but we got to start somewhere, right? That’s nearly 10% of the population. And the committee loved this bill, they were in favor of it, but in appropriations it didn’t pass through because it was deemed to be too expensive. That’s my understanding of why it didn’t pass.

Harlan Krumholz: And when liraglutide becomes generic, do you consider it just as good as semaglutide?

Ania Jastreboff: No, it’s clearly not. It’s a daily injectable instead of a weekly, the weight reduction is not as significant. So with semaglutide you have about 15% depending on how you look, but 15% total body weight reduction. And with semaglutide it’s not nearly that, maybe 70.

Harlan Krumholz: So again, will contribute to disparities and a frontier for us to work on.

Ania Jastreboff: Exactly.

Harlan Krumholz: The crazy thing to me is, if we can get people’s weight under control, we undoubtedly will reduce healthcare utilization and improve health for many of these people. It’s been shown in the trials. Anyway, it just seems like we need to get people to have a sensible strategy about this.

Ania Jastreboff: No, absolutely. And when I speak with healthcare providers or with policymakers, my question is, “Well, let me ask you, what if you could transform your patients’ lives and health by doing one thing? And what if I told you that one thing was treating their obesity and treating it in a way that not only did they lose weight, but they maintain that weight loss.” And by doing that, you’re basically, in essence, treating over 200 obesity-related conditions. And so all those medications that they’re taking for all those other conditions, if we can treat them early enough, they may not need those medicines or maybe they can come off of those medications, but if we wait until the patient has type 2 diabetes or hypertension or hyperlipidemia, they may not be able to come off of all of those medications.

Harlan Krumholz: Yeah. And I’ll just come in, my last thing, because this is just endless fascination for me. But as a cardiologist, the thing I love about this, I’ve been through dexfenfluramine, all of these different things that actually cause problems for people with their hearts or may have increased risk in the end. These drugs, even before the obesity trials, were demonstrating that they were lowering cardiovascular risk. Even if they weren’t affecting weight, you could argue that we should be using them for people at high risk in order to lower their risk. And yet now you’ve got these additional, of course you’re coming out from the obesity angle, I’m coming from cardiovascular risk perspective too, which is people will know that I don’t often come out, I’m a big [proponent of] lifestyle, non-pharmacologic interventions. I think sometimes we’re promoting drugs too much. But I’m endlessly fascinated by this field, by the work you’re doing, the contributions you’re making, and the possibilities that we will be able to make it about not people’s flawed characters, but their deranged biology that’s leading to the health problems that they have.

And for the longest period of time, people who’ve been overweight and more have been the subject of ridicule and shaming and in all sorts of things that make them feel that there’s something wrong with them in terms of their willpower, rather than recognizing them as being in a position where their biology’s been deranged. And I just salute all the work you’re doing. Because I also think in not just treating them but reframing for us how these people have been treated in society and how we need to be thinking about them broadly. So I just thank you so much for everything you’re doing and for your willingness to join us today and for all the wisdom you’ve shared.

Ania Jastreboff: Absolutely. It’s my pleasure. I agree with you a hundred percent. Having obesity is not our patients’ fault, and that is one of the first things that we communicate when they come to see me in clinic. It’s not their fault, it’s not their responsibility to basically account for every morsel of food that they put in their mouth for the rest of their lives. We have to treat their biology, and it’s our job to treat their obesity.

Howard Forman: Thanks very much, Ania. Thanks.

Harlan Krumholz: Thank you.

Ania Jastreboff: Thank you.

Harlan Krumholz: So great. Howie, that was an amazing visit with Ania, and we’ll have to have her back because there’s really actually so much more to talk about. But let’s pivot to your side and what’s on your mind this week?

Howard Forman: Yeah, I’m going to stick to something that’s very current and that is, Tua Tagovailoa is a quarterback with the Miami Dolphins, and I’m not a big sports fan at this point in my life but pay enough attention to something like this when it’s in the news. He appears to have suffered concussions in consecutive games, despite the NFL having concussion protocols to protect the players. The protocols used by the NFL are in broad review now, but 12 players were removed from the game this past Sunday, compared with only three the prior week. Tua was not included the list from the prior week because his first concussion, which everybody seems to now agree was a concussion, was not diagnosed as that. Now this could be just some sampling variation but also could indicate greater caution on the part of the teams. It is way beyond my expertise to opine about how we will eventually manage the concussion and chronic trauma encephalopathy crisis in the NFL.

But here’s where I’m going with this. NFL players are elite athletes, they have enormous income, generally great wealth. They get to make decisions for themselves, they are adults. They have rich owners who may try to push them in one direction or another, but they also have a Players Association and their coaches and others to push back. It’s not an ideal situation. But again, these are adults. There are literally more than 5 million people in our country playing tackle football. Most of them are not nearly as scrutinized or overseen as our elite athletes who are often under the watchful eyes of cameras, thousands of fans, officials, teammates, et cetera. I sincerely doubt we are doing enough to protect the amateur athletes around us and hope that those individuals who manage football and also rugby, soccer, and it’s probably a lot of other sports, lacrosse, are taking this moment to heart and making equally sincere and good-faith efforts to protect these young athletes.

Harlan Krumholz: Well, Howie, you raise a good point about what’s going on and particularly around this issue, around concussion, and concerns about it. I want to just take this in a little bit different direction, quickly, at the end here to say, Mike McDaniel is the coach of the Miami Dolphins, 39 years old, former wide receiver at Yale. Yale undergrad, history major, who’s had a meteoric rise within the NFL and is widely understood and appreciated as a terrific coach. He’s actually, this year, Miami Dolphins have done quite well. This is a really unfortunate event. I’m going back to the Tua episode and the unfortunate consecutive game injuries that he had. McDaniel’s been under a lot of criticism. I’ve seen him in press conferences. I just want to take this to say that, I think this isn’t a case where someone was purposely trying to put someone in jeopardy, but where the medical advice about the initial injury and the discussions about it may have been misunderstood.

Plus, I think that McDaniel himself may be subject to the common approach within the NFL not to give weight to concussions in the same way that you might give a broken leg. And even within a press conference, he said that he was released from the University of Cincinnati Hospital. That second game was in Cincinnati. And he said, fortunately, he only had a concussion. And I think this isn’t about McDaniel as much as it is about the generalized culture, both in amateur and in professional sports where we can readily appreciate what a broken bone is. But when people are hitting their head in these ways and having subsequent symptoms, that we don’t really appreciate the harm that can accrue as a result and aren’t taking quite as seriously as we should.

McDaniel and others throughout the entire ecosystem need to be surrounded by healthcare professionals who are giving that hard truth and making sure that we’re not putting people at risk who are playing sports. And understanding that what can happen downstream can be quite horrific for individuals who are in this position. And you’re very right to call it out, both in the amateurs, but I would say in professionals, we still have ways to go to be able to recognize the importance of these kind of injuries and how to manage people who are at risk for them or have suffered them.

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

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

Harlan Krumholz: 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: Health & Veritas is produced at the Yale School of Management. Thanks to our researcher, Jenny Tan, and to our producer, Miranda Shafer. Talk to you soon, Howie.

Howard Forman: Thanks, Harlan. Talk to you soon.