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An avalanche of information besets us on what to eat. It comes from the news, from influencers of every ilk, from scientists, from government, and of course from the food companies. Super foods? Ultra-processed foods? How does one find a source of trust and make intelligent choices for both us as individuals and for the society as a whole. A new book helps in this quest, a book entitled Food Intelligence: the Science of How Food Both Nourishes and Harms Us. It is written by two highly credible and thoughtful people who join us today.Julia Belluz is a journalist and a contributing opinion writer for the New York Times. She reports on medicine, nutrition, and public health. She's been a Knight Science Journalism Fellow at MIT and holds a master's in science degree from the London School of Economics and Political Science. Dr. Kevin Hall trained as a physicist as best known for pioneering work on nutrition, including research he did as senior investigator and section chief at the National Institutes of Health. His work is highly regarded. He's won awards from the NIH, from the American Society of Nutrition, the Obesity Society and the American Physiological Society. Interview Transcript Thank you both very much for being with us. And not only for being with us, but writing such an interesting book. I was really eager to read it and there's a lot in there that people don't usually come across in their normal journeys through the nutrition world. So, Julia, start off if you wouldn't mind telling us what the impetus was for you and Kevin to do this book with everything else that's out there. Yes, so there's just, I think, an absolute avalanche of information as you say about nutrition and people making claims about how to optimize diet and how best to lose or manage weight. And I think what we both felt was missing from that conversation was a real examination of how do we know what we know and kind of foundational ideas in this space. You hear a lot about how to boost or speed up your metabolism, but people don't know what metabolism is anyway. You hear a lot about how you need to maximize your protein, but what is protein doing in the body and where did that idea come from? And so, we were trying to really pair back. And I think this is where Kevin's physics training was so wonderful. We were trying to look at like what are these fundamental laws and truths. Things that we know about food and nutrition and how it works in us, and what can we tell people about them. And as we kind of went through that journey it very quickly ended up in an argument about the food environment, which I know we're going to get to. We will. It's really interesting. This idea of how do we know what we know is really fascinating because when you go out there, people kind of tell us what we know. Or at least what they think what we know. But very few people go through that journey of how did we get there. And so people can decide on their own is this a credible form of knowledge that I'm being told to pursue. So Kevin, what do you mean by food intelligence? Coming from a completely different background in physics where even as we learn about the fundamental laws of physics, it's always in this historical context about how we know what we know and what were the kind of key experiments along the way. And even with that sort of background, I had almost no idea about what happened to food once we ate it inside our bodies. I only got into this field by a happenstance series of events, which is probably too long to talk about this podcast. But to get people to have an appreciation from the basic science about what is going on inside our bodies when we eat. What is food made out of? As best as we can understand at this current time, how does our body deal with. Our food and with that sort of basic knowledge about how we know what we know. How to not be fooled by these various sound bites that we'll hear from social media influencers telling you that everything that you knew about nutrition is wrong. And they've been hiding this one secret from you that's been keeping you sick for so long to basically be able to see through those kinds of claims and have a bedrock of knowledge upon which to kind of evaluate those things. That's what we mean by food intelligence. It makes sense. Now, I'm assuming that food intelligence is sort of psychological and biological at the same time, isn't it? Because that there's what you're being told and how do you process that information and make wise choices. But there's also an intelligence the body has and how to deal with the food that it's receiving. And that can get fooled too by different things that are coming at it from different types of foods and stuff. We'll get to that in a minute, but it's a very interesting concept you have, and wouldn't it be great if we could all make intelligent choices? Julia, you mentioned the food environment. How would you describe the modern food environment and how does it shape the choices we make? It's almost embarrassing to have this question coming from you because so much of our understanding and thinking about this idea came from you. So, thank you for your work. I feel like you should be answering this question. But I think one of the big aha moments I had in the book research was talking to a neuroscientist, who said the problem in and of itself isn't like the brownies and the pizza and the chips. It's the ubiquity of them. It's that they're most of what's available, along with other less nutritious ultra-processed foods. They're the most accessible. They're the cheapest. They're kind of heavily marketed. They're in our face and the stuff that we really ought to be eating more of, we all know we ought to be eating more of, the fruits and vegetables, fresh or frozen. The legumes, whole grains. They're the least available. They're the hardest to come by. They're the least accessible. They're the most expensive. And so that I think kind of sums up what it means to live in the modern food environment. The deck is stacked against most of us. The least healthy options are the ones that we're inundated by. And to kind of navigate that, you need a lot of resources, wherewithal, a lot of thought, a lot of time. And I think that's kind of where we came out thinking about it. But if anyone is interested in knowing more, they need to read your book Food Fight, because I think that's a great encapsulation of where we still are basically. Well, Julie, it's nice of you to say that. You know what you reminded me one time I was on a panel and a speaker asks the audience, how many minutes do you live from a Dunkin Donuts? And people sort of thought about it and nobody was more than about five minutes from a Dunkin Donuts. And if I think about where I live in North Carolina, a typical place to live, I'm assuming in America. And boy, within about five minutes, 10 minutes from my house, there's so many fast-food places. And then if you add to that the gas stations that have foods and the drug store that has foods. Not to mention the supermarkets. It's just a remarkable environment out there. And boy, you have to have kind of iron willpower to not stop and want that food. And then once it hits your body, then all heck breaks loose. It's a crazy, crazy environment, isn't it? Kevin, talk to us, if you will, about when this food environment collides with human biology. And what happens to normal biological processes that tell us how much we should eat, when we should stop, what we should eat, and things like that. I think that that is one of the newer pieces that we're really just getting a handle on some of the science. It's been observed for long periods of time that if you change a rat's food environment like Tony Sclafani did many, many years ago. That rats aren't trying to maintain their weight. They're not trying to do anything other than eat whatever they feel like. And, he was having a hard time getting rats to fatten up on a high fat diet. And he gave them this so-called supermarket diet or cafeteria diet composed of mainly human foods. And they gained a ton of weight. And I think that pointed to the fact that it's not that these rats lacked willpower or something like that. That they weren't making these conscious choices in the same way that we often think humans are entirely under their conscious control about what we're doing when we make our food choices. And therefore, we criticize people as having weak willpower when they're not able to choose a healthier diet in the face of the food environment. I think the newer piece that we're sort of only beginning to understand is how is it that that food environment and the foods that we eat might be changing this internal symphony of signals that's coming from our guts, from the hormones in our blood, to our brains and the understanding that of food intake. While you might have control over an individual meal and how much you eat in that individual meal is under biological control. And what are the neural systems and how do they work inside our brains in communicating with our bodies and our environment as a whole to shift the sort of balance point where body weight is being regulated. To try to better understand this really intricate interconnection or interaction between our genes, which are very different between people. And thousands of different genes contributing to determining heritability of body size in a given environment and how those genes are making us more or less susceptible to these differences in the food environment. And what's the underlying biology? I'd be lying to say if that we have that worked out. I think we're really beginning to understand that, but I hope what the book can give people is an appreciation for the complexity of those internal signals and that they exist. And that food intake isn't entirely under our control. And that we're beginning to unpack the science of how those interactions work. It's incredibly interesting. I agree with you on that. I have a slide that I bet I've shown a thousand times in talks that I think Tony Sclafani gave me decades ago that shows laboratory rats standing in front of a pile of these supermarket foods. And people would say, well, of course you're going to get overweight if that's all you eat. But animals would eat a healthy diet if access to it. But what they did was they had the pellets of the healthy rat chow sitting right in that pile. Exactly. And the animals ignore that and overeat the unhealthy food. And then you have this metabolic havoc occur. So, it seems like the biology we've all inherited works pretty well if you have foods that we've inherited from the natural environment. But when things become pretty unnatural and we have all these concoctions and chemicals that comprise the modern food environment the system really breaks down, doesn't it? Yeah. And I think that a lot of people are often swayed by the idea as well. Those foods just taste better and that might be part of it. But I think that what we've come to realize, even in our human experiments where we change people's food environments... not to the same extent that Tony Sclafani did with his rats, but for a month at a time where we ask people to not be trying to gain or lose weight. And we match certain food environments for various nutrients of concern. You know, they overeat diets that are higher in these so-called ultra-processed foods and they'd spontaneously lose weight when we remove those from the diet. And they're not saying that the foods are any more or less pleasant to eat. There's this underlying sort of the liking of foods is somewhat separate from the wanting of foods as neuroscientists are beginning to understand the different neural pathways that are involved in motivation and reward as opposed to the sort of just the hedonic liking of foods. Even the simple explanation of 'oh yeah, the rats just like the food more' that doesn't seem to be fully explaining why we have these behaviors. Why it's more complicated than a lot of people make out. Let's talk about ultra-processed foods and boy, I've got two wonderful people to talk to about that topic. Julia, let's start with your opinion on this. So tell us about ultra-processed foods and how much of the modern diet do they occupy? So ultra-processed foods. Obviously there's an academic definition and there's a lot of debate about defining this category of foods, including in the US by the Health and Human Services. But the way I think about it is like, these are foods that contain ingredients that you don't use in your home kitchen. They're typically cooked. Concocted in factories. And they now make up, I think it's like 60% of the calories that are consumed in America and in other similar high-income countries. And a lot of these foods are what researchers would also call hyper palatable. They're crossing these pairs of nutrient thresholds like carbohydrate, salt, sugar, fat. These pairs that don't typically exist in nature. So, for the reasons you were just discussing they seem to be particularly alluring to people. They're again just like absolutely ubiquitous and in these more developed contexts, like in the US and in the UK in particular. They've displaced a lot of what we would think of as more traditional food ways or ways that people were eating. So that's sort of how I think about them. You know, if you go to a supermarket these days, it's pretty hard to find a part of the supermarket that doesn't have these foods. You know, whole entire aisles of processed cereals and candies and chips and soft drinks and yogurts, frozen foods, yogurts. I mean, it's just, it's all over the place. And you know, given that if the average is 60% of calories, and there are plenty of people out there who aren't eating any of that stuff at all. For the other people who are, the number is way higher. And that, of course, is of great concern. So there have been hundreds of studies now on ultra-processed foods. It was a concept born not that long ago. And there's been an explosion of science and that's all for the good, I think, on these ultra-processed foods. And perhaps of all those studies, the one discussed most is one that you did, Kevin. And because it was exquisitely controlled and it also produced pretty striking findings. Would you describe that original study you did and what you found? Sure. So, the basic idea was one of the challenges that we have in nutrition science is accurately measuring how many calories people eat. And the best way to do that is to basically bring people into a laboratory and measure. Give them a test meal and measure how many calories they eat. Most studies of that sort last for maybe a day or two. But I always suspected that people could game the system if for a day or two, it's probably not that hard to behave the way that the researcher wants, or the subject wants to deceive the researcher. We decided that what we wanted to do was bring people into the NIH Clinical Center. Live with us for a month. And in two two-week blocks, we decided that we would present them with two different food environments essentially that both provided double the number of calories that they would require to maintain their body weight. Give them very simple instructions. Eat as much or as little as you'd like. Don't be trying to change your weight. We're not going to tell you necessarily what the study's about. We're going to measure lots of different things. And they're blinded to their weight measurements and they're wearing loose fitting scrubs and things like that, so they can't tell if their clothes are getting tighter or looser. And so, what we did is in for one two-week block, we presented people with the same number of calories, the same amount of sugar and fat and carbs and fiber. And we gave them a diet that was composed of 80% of calories coming from these ultra-processed foods. And the other case, we gave them a diet that was composed of 0% of calories from ultra-processed food and 80% of the so-called minimally processed food group. And what we then did was just measured people's leftovers essentially. And I say we, it was really the chefs and the dieticians at the clinical center who are doing all the legwork on this. But what we found was pretty striking, which was that when people were exposed to this highly ultra-processed food environment, despite being matched for these various nutrients of concern, they overate calories. Eating about 500 calories per day on average, more than the same people in the minimally processed diet condition. And they gained weight and gained body fat. And, when they were in the minimally processed diet condition, they spontaneously lost weight and lost body fat without trying in either case, right? They're just eating to the same level of hunger and fullness and overall appetite. And not reporting liking the meals any more or less in one diet versus the other. Something kind of more fundamental seemed to have been going on that we didn't fully understand at the time. What was it about these ultra-processed foods? And we were clearly getting rid of many of the things that promote their intake in the real world, which is that they're convenient, they're cheap, they're easy to obtain, they're heavily marketed. None of that was at work here. It was something really about the meals themselves that we were providing to people. And our subsequent research has been trying to figure out, okay, well what were the properties of those meals that we were giving to these folks that were composed primarily of ultra-processed foods that were driving people to consume excess calories? You know, I've presented your study a lot when I give talks. It's nice hearing it coming from you rather than me. But a couple of things that interest me here. You use people as their own controls. Each person had two weeks of one diet and two weeks of another. That's a pretty powerful way of providing experimental control. Could you say just a little bit more about that? Yeah, sure. So, when you design a study, you're trying to maximize the efficiency of the study to get the answers that you want with the least number of participants while still having good control and being able to design the study that's robust enough to detect a meaningful effect if it exists. One of the things that you do when you analyze studies like that or design studies like that, you could just randomize people to two different groups. But given how noisy and how different between people the measurement of food intake is we would've required hundreds of people in each group to detect an effect like the one that we discovered using the same person acting as their own control. We would still be doing the study 10 years later as opposed to what we were able to do in this particular case, which is completed in a year or so for that first study. And so, yeah, when you kind of design a study that way it's not always the case that you get that kind of improvement in statistical power. But for a measurement like food intake, it really is necessary to kind of do these sorts of crossover type studies where each person acts as their own control. So put the 500 calorie increment in context. Using the old fashioned numbers, 3,500 calories equals a pound. That'd be about a pound a week or a lot of pounds over a year. But of course, you don't know what would happen if people were followed chronically and all that. But still 500 calories is a whopping increase, it seems to me. It sure is. And there's no way that we would expect it to stay at that constant level for many, many weeks on end. And I think that's one of the key questions going forward is how persistent is that change. And how does something that we've known about and we discuss in our books the basic physiology of how both energy expenditure changes as people gain and lose weight, as well as how does appetite change in a given environment when they gain and lose weight? And how do those two processes eventually equate at a new sort of stable body weight in this case. Either higher or lower than when people started the program of this diet manipulation. And so, it's really hard to make those kinds of extrapolations. And that's of course, the need for further research where you have longer periods of time and you, probably have an even better control over their food environment as a result. I was surprised when I first read your study that you were able to detect a difference in percent body fat in such a short study. Did that surprise you as well? Certainly the study was not powered to detect body fat changes. In other words, we didn't know even if there were real body fat changes whether or not we would have the statistical capabilities to do that. We did use a method, DXA, which is probably one of the most precise and therefore, if we had a chance to measure it, we had the ability to detect it as opposed to other methods. There are other methods that are even more precise, but much more expensive. So, we thought that we had a chance to detect differences there. Other things that we use that we also didn't think that we necessarily would have a chance to detect were things like liver fat or something like that. Those have a much less of an ability. It's something that we're exploring now with our current study. But, again, it's all exploratory at that point. So what can you tell us about your current study? We just wrapped it up, thankfully. What we were doing was basically re-engineering two new ultra-processed diets along parameters that we think are most likely the mechanisms by which ultra-processed meals drove increased energy intake in that study. One was the non-beverage energy density. In other words, how many calories per gram of food on the plate, not counting the beverages. Something that we noticed in the first study was that ultra-processed foods, because they're essentially dried out in the processing for reasons of food safety to prevent bacterial growth and increased shelf life, they end up concentrating the foods. They're disrupting the natural food matrix. They last a lot longer, but as a result, they're a more concentrated form of calories. Despite being, by design, we chose the overall macronutrients to be the same. They weren't necessarily higher fat as we often think of as higher energy density. What we did was we designed an ultra-processed diet that was low in energy density to kind of match the minimally processed diet. And then we also varied the number of individual foods that were deemed hyper palatable according to kind of what Julia said that crossed these pairs of thresholds for fat and sugar or fat and salt or carbs and salt. What we noticed in the first study was that we presented people with more individual foods on the plate that had these hyper palatable combinations. And I wrestle with the term terminology a little bit because I don't necessarily think that they're working through the normal palatability that they necessarily like these foods anymore because again, we asked people to rate the meals and they didn't report differences. But something about those combinations, regardless of what you call them, seemed to be driving that in our exploratory analysis of the first study. We designed a diet that was high in energy density, but low in hyper palatable foods, similar to the minimally processed. And then their fourth diet is with basically low in energy density and hyper palatable foods. And so, we presented some preliminary results last year and what we were able to show is that when we reduced both energy density and the number of hyper palatable foods, but still had 80% of calories from ultra-processed foods, that people more or less ate the same number of calories now as they did when they were the same people were exposed to the minimally processed diet. In fact they lost weight, to a similar extent as the minimally processed diet. And that suggests to me that we can really understand mechanisms at least when it comes to calorie intake in these foods. And that might give regulators, policy makers, the sort of information that they need in order to target which ultra-processed foods and what context are they really problematic. It might give manufacturers if they have the desire to kind of reformulate these foods to understand which ones are more or less likely to cause over consumption. So, who knows? We'll see how people respond to that and we'll see what the final results are with the entire study group that, like I said, just finished, weeks ago. I respond very positively to the idea of the study. The fact that if people assume ultra-processed foods are bad actors, then trying to find out what it is about them that's making the bad actors becomes really important. And you're exactly right, there's a lot of pressure on the food companies now. Some coming from public opinion, some coming from parts of the political world. Some from the scientific world. And my guess is that litigation is going to become a real actor here too. And the question is, what do you want the food industry to do differently? And your study can really help inform that question. So incredibly valuable research. I can't wait to see the final study, and I'm really delighted that you did that. Let's turn our attention for a minute to food marketing. Julia, where does food marketing fit in all this? Julia - What I was very surprised to find while we were researching the book was this deep, long history of calls against marketing junk food in particular to kids. I think from like the 1950s, you have pediatrician groups and other public health professionals saying, stop this. And anyone who has spent any time around small children knows that it works. We covered just like a little, it was from an advocacy group in the UK that exposed aid adolescents to something called Triple Dip Chicken. And then asked them later, pick off of this menu, I think it was like 50 items, which food you want to order. And they all chose Triple Dip chicken, which is, as the name suggests, wasn't the healthiest thing to choose on the menu. I think we know obviously that it works. Companies invest a huge amount of money in marketing. It works even in ways like these subliminal ways that you can't fully appreciate to guide our food choices. Kevin raised something really interesting was that in his studies it was the foods. So, it's a tricky one because it's the food environment, but it's also the properties of the foods themselves beyond just the marketing. Kevin, how do you think about that piece? I'm curious like. Kevin - I think that even if our first study and our second study had turned out there's no real difference between these artificial environments that we've put together where highly ultra-processed diets lead to excess calorie intake. If that doesn't happen, if it was just the same, it wouldn't rule out the fact that because these foods are so heavily marketed, because they're so ubiquitous. They're cheap and convenient. And you know, they're engineered for many people to incorporate into their day-to-day life that could still promote over consumption of calories. We just remove those aspects in our very artificial food environment. But of course, the real food environment, we're bombarded by these advertisements and the ubiquity of the food in every place that you sort of turn. And how they've displaced healthy alternatives, which is another mechanism by which they could cause harm, right? It doesn't even have to be the foods themselves that are harmful. What do they displace? Right? We only have a certain amount the marketers called stomach share, right? And so, your harm might not be necessarily the foods that you're eating, but the foods that they displaced. So even if our experimental studies about the ultra-processed meals themselves didn't show excess calorie intake, which they clearly did, there's still all these other mechanisms to explore about how they might play a part in the real world. You know, the food industry will say that they're agnostic about what foods they sell. They just respond to demand. That seems utter nonsense to me because people don't overconsume healthy foods, but they do overconsume the unhealthy ones. And you've shown that to be the case. So, it seems to me that idea that they can just switch from this portfolio of highly processed foods to more healthy foods just doesn't work out for them financially. Do you think that's right? I honestly don't have that same sort of knee jerk reaction. Or at least I perceive it as a knee jerk reaction, kind of attributing malice in some sense to the food industry. I think that they'd be equally happy if they could get you to buy a lot and have the same sort of profit margins, a lot of a group of foods that was just as just as cheap to produce and they could market. I think that you could kind of turn the levers in a way that that would be beneficial. I mean, setting aside for example, that diet soda beverages are probably from every randomized control trial that we've seen, they don't lead to the same amount of weight gain as the sugar sweetened alternatives. They're just as profitable to the beverage manufacturers. They sell just as many of them. Now they might have other deleterious consequences, but I don't think that it's necessarily the case that food manufacturers have to have these deleterious or unhealthy foods as their sole means of attaining profit. Thanks for that. So, Julia, back to you. You and Kevin point out in your book some of the biggest myths about nutrition. What would you say some of them are? I think one big, fundamental, overarching myth is this idea that the problem is in us. That this rise of diet related diseases, this explosion that we've seen is either because of a lack of willpower. Which you have some very elegant research on this that we cite in the book showing willpower did not collapse in the last 30, 40 years of this epidemic of diet related disease. But it's even broader than that. It's a slow metabolism. It's our genes. Like we put the problem on ourselves, and we don't look at the way that the environment has changed enough. And I think as individuals we don't do that. And so much of the messaging is about what you Kevin, or you Kelly, or you Julia, could be doing better. you know, do resistance training. Like that's the big thing, like if you open any social media feed, it's like, do more resistance training, eat more protein, cut out the ultra-processed foods. What about the food environment? What about the leaders that should be held accountable for helping to perpetuate these toxic food environments? I think that that's this kind of overarching, this pegging it and also the rise of personalized nutrition. This like pegging it to individual biology instead of for whatever the claim is, instead of thinking about how did environments and don't want to have as part of our lives. So that's kind of a big overarching thing that I think about. It makes sense. So, let's end on a positive note. There's a lot of reason to be concerned about the modern food environment. Do you see a helpful way forward and what might be done about this? Julia, let's stay with you. What do you think? I think so. We spent a lot of time researching history for this book. And a lot of things that seem impossible are suddenly possible when you have enough public demand and enough political will and pressure. There are so many instances and even in the history of food. We spend time with this character Harvey Wiley, who around the turn of the century, his research was one of the reasons we have something like the FDA protecting the food supply. That gives me a lot of hope. And we are in this moment where a lot of awareness is being raised about the toxic food environment and all these negative attributes of food that people are surrounded by. I think with enough organization and enough pressure, we can see change. And we can see this kind of flip in the food environment that I think we all want to see where healthier foods become more accessible, available, affordable, and the rest of it. Sounds good. Kevin, what are your thoughts? Yes, I just extend that to saying that for the first time in history, we sort of know what the population of the planet is going to be that we have to feed in the future. We're not under this sort of Malthusian threat of not being able to know where the population growth is going to go. We know it's going to be roughly 10 billion people within the next century. And we know we've got to change the way that we produce and grow food for the planet as well as for the health of people. We know we've got to make changes anyway. And we're starting from a position where per capita, we're producing more protein and calories than any other time in human history, and we're wasting more food. We actually know we're in a position of strength. We don't have to worry so acutely that we won't be able to provide enough food for everybody. It's what kind of food are we going to produce? How are we going to produce it in the way that's sustainable for both people and the planet? We have to tackle that anyway. And for the folks who had experienced the obesity epidemic or finally have drugs to help them and other kinds of interventions to help them. That absolve them from this idea that it's just a matter of weak willpower if we finally have some pharmaceutical interventions that are useful. So, I do see a path forward. Whether or not we take that is another question. Bios Dr. Kevin Hall is the section chief of Integrative Physiology Section in the Laboratory of Biological Modeling at the NIH National Institute of Diabetes and Digestive and Kidney Diseases. Kevin's laboratory investigates the integrative physiology of macronutrient metabolism, body composition, energy expenditure, and control of food intake. His main goal is to better understand how the food environment affects what we eat and how what we eat affects our physiology. He performs clinical research studies as well as developing mathematical models and computer simulations to better understand physiology, integrate data, and make predictions. In recent years, he has conducted randomized clinical trials to study how diets high in ultra-processed food may cause obesity and other chronic diseases. He holds a Ph.D. from McGill University. Julia Belluz is a Paris-based journalist and a contributing opinion writer to the New York Times, she has reported extensively on medicine, nutrition, and global public health from Canada, the US, and Europe. Previously, Julia was Vox's senior health correspondent in Washington, DC, a Knight Science Journalism fellow at the Massachusetts Institute of Technology in Cambridge, and she worked as a reporter in Toronto and London. Her writing has appeared in a range of international publications, including the BMJ, the Chicago Tribune, the Economist, the Globe and Mail, Maclean's, the New York Times, ProPublica, and the Times of London. Her work has also had an impact, helping improve policies on maternal health and mental healthcare for first responders at the hospital- and state-level, as well as inspiring everything from scientific studies to an opera. Julia has been honored with numerous journalism awards, including the 2016 Balles Prize in Critical Thinking, the 2017 American Society of Nutrition Journalism Award, and three Canadian National Magazine Awards (in 2007 and 2013). In 2019, she was a National Academies of Sciences, Engineering, and Medicine Communications Award finalist. She contributed chapters on public health journalism in the Tactical Guide to Science Journalism, To Save Humanity: What Matters Most for a Healthy Future, and was a commissioner for the Global Commission on Evidence to Address Societal Challenges.

Christina Badaracco, MPH, RDN, LDN, works as a healthcare consultant, author, and thought leader, seeking to advance the role of nutrition in healthcare. She applies her expertise in healthcare and public health research, policy, and practice to support leading institutions and organizations across the world to improve care delivery and health outcomes. She also regularly writes, teaches, and develops training and programs about nutrition, culinary medicine, and sustainable agriculture—including designing and directing award-winning and innovative culinary medicine training and programs for various healthcare institutions and professional associations and coauthoring The Farm Bill: A Citizen's Guide and Mix It Up: The Culinary Medicine Cookbook for Mixing Things up in the Kitchen. Christina previously worked for Avalere, a healthcare advisory firm, as well as the U.S. Environmental Protection Agency, Teaching Kitchen Collaborative, Oakland Unified School District, and NIH Clinical Center. Christina holds various leadership roles within the Academy of Nutrition and Dietetics and Slow Food and she is actively engaged in her local food and healthcare systems. Pertinent links: Food As Medicine Network Live 2025 in Chicago on 5/7: https://www.foodasmedicinenetwork.com/masterclassSociety for Nutrition Education and Behavior in Indianapolis on 7/11: https://raybourn.my.site.com/SNEB/s/lt-event?id=a1YVs000000r8nRMAQ#/Agendahttps://www.linkedin.com/in/christina-badaracco/https://www.christinabadaracco.com/eventshttps://www.oliviathomasrd.com/book https://www.rewire-health.com/blog/cooking-up-behavior-change-omas-pre-conference-culinary-medicine-workshophttps://www.healthaffairs.org/content/forefront/food-vital-ingredient-transforming-obesity-carehttps://www.instagram.com/cbadarac/Support the showThe Gaining Health Podcast will release a new episode monthly, every second or third Wednesday of the month. Episodes including interviews with obesity experts as well as scientific updates and new guidelines for the management of obesity.If you're a clinician or organization looking to start or optimize an obesity management program, and you want additional support and resources, check out the Gaining Health website! We offer a Roadmap to starting an obesity program or practice, pre-recorded Master Classes, digital resources including patient education materials and office forms, and much more! Check out our resources on our Gaining Health Shop! If you are loving this podcast, please consider supporting us on Patreon

The Trump administration has begun mass layoffs of federal employees, with more than 10,000 workers terminated across multiple agencies. Many of those affected were recently hired and still on probationary status, according to officials speaking anonymously to NPR. Nearly 300 employees were fired from the Federal Aviation Administration (FAA), while the Department of Energy cut up to 2,000 positions, including staff at the National Nuclear Security Administration. The Department of Health and Human Services saw thousands of job losses at the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH), including nurses at the NIH Clinical Center. The Department of Homeland Security lost over 400 employees, while the Department of Veterans Affairs terminated 1,000 workers. The IRS is expected to lay off thousands more next week, which could impact tax processing. Learn more about your ad choices. Visit megaphone.fm/adchoices

A leader for conducting rigorous randomized trials of humans along with animal models for understanding nutrition and metabolism, Dr. Kevin Hall is a Senior Investigator at the National Institutes of Health, and Section Chief of the Integrative Physiology Section, NIDDK. In this podcast, we reviewed his prolific body of research a recent publications. The timing of optimizing our diet and nutrition seems apropos, now that we're in in the midst of the holiday season!Below is a video snippet of our conversation on his ultra-processed food randomized trial.Full videos of all Ground Truths podcasts can be seen on YouTube here. The current one is here. If you like the YouTube format, please subscribe! The audios are also available on Apple and Spotify.Note: I'll be doing a Ground Truths Live Chat on December 11th at 12 N EST, 9 AM PST, so please mark your calendar and join!Transcript with links to publications and audioEric Topol (00:05):Well, hello. This is Eric Topol with Ground Truths, and I'm really delighted to have with me today, Dr. Kevin Hall from the NIH. I think everybody knows that nutrition is so important and Kevin is a leader in doing rigorous randomized trials, which is not like what we usually see with large epidemiologic studies of nutrition that rely on food diaries and the memory of participants. So Kevin, it's really terrific to have you here.Kevin Hall (00:34):Thanks so much for the invitation.Ultra-Processed FoodsEric Topol (00:36):Yeah. Well, you've been prolific and certainly one of the leaders in nutrition science who I look to. And what I thought we could do is go through some of your seminal papers. There are many, but I picked a few and I thought we'd first go back to the one that you published in Cell Metabolism. This is ultra-processed diets cause excessive caloric intake and weight gain. (Main results in graph below.) So maybe you can take us through the principle findings from that trial.Kevin Hall (01:10):Yeah, sure. So that was a really interesting study because it's the first randomized control trial that's investigated the role of ultra-processed foods in potentially causing obesity. So we've got, as you mentioned, lots and lots of epidemiological data that have made these associations between people who consume diets that are very high in ultra-processed foods as having greater risk for obesity. But those trials are not demonstrating causation. I mean, they suggest a strong link. And in fact, the idea of ultra-processed foods is kind of a new idea. It's really sort of appeared on the nutrition science stage probably most prominently in the past 10 years or so. And I first learned about this idea of ultra-processed foods, which is really kind of antithetical to the way most nutrition scientists think about foods. We often think about foods as nutrient delivery vehicles, and we kind of view foods as being the fraction of carbohydrates versus fats in them or how much sodium or fiber is in the foods.Kevin Hall (02:17):And along came this group in Brazil who introduced this new way of classifying foods that completely ignores the nutrient composition and says what we should be doing is classifying foods based on the extent and purpose of processing of foods. And so, they categorize these four different categories. And in the fourth category of this so-called NOVA classification scheme (see graphic below) , they identified something called ultra-processed foods. There's a long formal definition and it's evolved a little bit over the years and continues to evolve. But the basic ideas that these are foods that are manufactured by industries that contain a lot of purified ingredients made from relatively cheap agricultural commodity products that basically undergo a variety of processes and include additives and ingredients that are not typically found in home kitchens, but are typically exclusively in manufactured products to create the wide variety of mostly packaged goods that we see in our supermarkets.Kevin Hall (03:22):And so, I was really skeptical that there was much more about the effects of these foods. Other than that they typically have high amounts of sugar and saturated fat and salt, and they're pretty low in fiber. And so, the purpose of this study was to say, okay, well if there's something more about the foods themselves that is causing people to overconsume calories and gain weight and eventually get obesity, then we should do a study that's trying to test for two diets that are matched for these various nutrients of concern. So they should be matched for the macronutrients, they should be matched for the sugar content, the fat, the sodium, the fiber, and people should just be allowed to eat whatever they want and they shouldn't be trying to change their weight in any way. And so, the way that we did this was, as you mentioned, we can't just ask people to report what they're eating.Kevin Hall (04:19):So what we did was we admitted these folks to the NIH Clinical Center and to our metabolic ward, and it's a very artificial environment, but it's an environment that we can control very carefully. And so, what we basically did is take control over their food environment and we gave them three meals a day and snacks, and basically for a two-week period, they had access to meals that were more than 80% of calories coming from ultra-processed foods. And then in random order, they either received that diet first and give them simple instructions, eat as much as little as you want. We're going to measure lots of stuff. You shouldn't be trying to change your weight or weight that gave them a diet that had no calories from ultra-processed foods. In fact, 80% from minimally processed foods. But again, both of these two sort of food environments were matched for these nutrients that we typically think of as playing a major role in how many calories people choose to eat.Kevin Hall (05:13):And so, the basic idea was, okay, well let's measure what these folks eat. We gave them more than double the calories that they would require to maintain their weight, and what they didn't know was that in the basement of the clinical center where the metabolic kitchen is, we had all of our really talented nutrition staff measuring the leftovers to see what it was that they didn't eat. So we knew exactly what we provided to them and all the foods had to be in our nutrition database and when we compute what they actually ate by difference, so we have a very precise estimate about not only what foods they chose to ate, but also how many calories they chose to eat, as well as the nutrient composition.And the main upshot of all that was that when these folks were exposed to this highly ultra-processed food environment, they spontaneously chose to eat about 500 calories per day more over the two-week period they were in that environment then when the same folks were in the environment that had no ultra-processed foods, but just minimally processed foods. They not surprisingly gained weight during the ultra-processed food environment and lost weight and lost body fat during the minimally processed food environment. And because those diets were overall matched for these different nutrients, it didn't seem to be that those were the things that were driving this big effect. So I think there's a couple of big take homes here. One is that the food environment really does have a profound effect on just the biology of how our food intake is controlled at least over relatively short periods of time, like the two-week periods that we were looking at. And secondly, that there's something about ultra-processed foods that seem to be driving this excess calorie intake that we now know has been linked with increased risk of obesity, and now we're starting to put some of the causal pieces together that really there might be something in this ultra-processed food environment that's driving the increased rates of obesity that we've seen over the past many decades.Eric Topol (07:18):Yeah, I mean I think the epidemiologic studies that make the link between ultra-processed foods and higher risk of cancer, cardiovascular disease, type 2 diabetes, neurodegenerative disease. They're pretty darn strong and they're backed up by this very rigorous study. Now you mentioned it short term, do you have any reason to think that adding 500 calories a day by eating these bad foods, which by the way in the American diet is about 60% or more of the average American diet, do you have any inkling that it would change after a few weeks?Kevin Hall (07:54):Well, I don't know about after a few weeks, but I think that one of the things that we do know about body weight regulation and how it changes in body weight impact both metabolism, how many calories were burning as well as our appetite. We would expect some degree of moderation of that effect eventually settling in at a new steady state, that's probably going to take months and years to achieve. And so the question is, I certainly don't believe that it would be a 500 calorie a day difference indefinitely. The question is when would that difference converge and how much weight would've been gained or lost when people eventually reached that new plateau? And so, that's I think a really interesting question. Some folks have suggested that maybe if you extrapolated the lines a little bit, you could predict when those two curves might eventually converge. That's an interesting thought experiment, but I think we do need some longer studies to investigate how persistent are these effects. Can that fully explain the rise in average body weight and obesity rates that have occurred over the past several decades? Those are open questions.Eric Topol (09:03):Yeah. Well, I mean, I had the chance to interview Chris van Tulleken who wrote the book, Ultra-Processed People and I think you might remember in the book he talked about how he went on an ultra-processed diet and gained some 20, 30 pounds in a short time in a month. And his brother, his identical twin brother gained 50, 60 pounds, and so it doesn't look good. Do you look at all the labels and avoid all this junk and ultra-processed food now or are you still thinking that maybe it's not as bad as it looks?Kevin Hall (09:38):Well, I mean I think that I certainly learned a lot from our studies, and we are continuing to follow this up to try to figure out what are the mechanisms by which this happen. But at the same time, I don't think we can throw out everything else we know about nutrition science. So just because we match these various nutrients in this particular study, I think one of the dangers here is that as you mentioned, there's 60% of the food environment in the US and Great Britain and other places consist of these foods, and so they're unavoidable to some extent, right? Unless you're one of these privileged folks who have your backyard garden and your personal chef who can make all of your foods, I'm certainly not one of those people, but for the vast majority of us, we're going to have to incorporate some degree of ultra-processed foods in our day-to-day diet.Kevin Hall (10:24):The way I sort of view it is, we really need to understand the mechanisms and before we understand the mechanisms, we have to make good choices based on what we already know about nutrition science, that we should avoid the foods that have a lot of sugar in them. We should avoid foods that have a lot of saturated fat and sodium. We should try to choose products that contain lots of whole grains and legumes and fruits and vegetables and things like that. And there's some of those, even in the ultra-processed food category. I pretty regularly consume a microwavable ready meal for lunch. It tends to be pretty high in whole grains and legumes and low in saturated fat and sugar and things like that. But to engineer a food that can heat up properly in a microwave in four minutes has some ultra-processing technology involved there. I would be pretty skeptical that that's going to cause me to have really poor health consequences as compared to if I had the means to eat homemade French fries every day in tallow. But that's the kind of comparison that we have to think about.Eric Topol (11:36):But I think what you're touching on and maybe inadvertently is in that NOVA class four, the bad ultra-processed foods, there's a long, long list of course, and some of those may be worse than others, and we haven't seen an individual ranking of these constituents. So as you're alluding to what's in that microwave lunch probably could be much less concerning than what's in these packaged snacks that are eaten widely. But I would certainly agree that we don't know everything about this, but your study is one of the most quoted studies ever in the ultra-processed food world. Now, let me move on to another trial that was really important. This was published in Nature Medicine and it's about a plant-based diet, which is of course a very interesting diet, low-fat versus an animal-based ketogenic diet. Also looking at energy intake. Can you take us through that trial?Plant-Based, Low Fat Diet vs Animal-Based, Low Carbohydrate Ketogenic DietKevin Hall (12:33):Sure. So it's actually interesting to consider that trial in the context of the trial we just talked about because both of these diets that we tested in this trial were relatively low in ultra-processed foods, and so both of them contained more than a kilogram of non-starchy vegetables as a base for designing these, again, two different food environments. Very similar overall study design where people again were exposed to either diets that were vegan plant-based diet that was really high in starches and was designed to kind of cause big insulin increases in the blood after eating the meals. And the other diet had very, very few carbohydrates of less than 10% in total, and we built on that kind of non-starchy vegetable base, a lot of animal-based products to kind of get a pretty high amount of fat and having very low carbohydrates. Both diets in this case, like I mentioned, were pretty low in ultra-processed foods, but what we were really interested in here was testing this idea that has come to prominence recently, that high carbohydrate diets that lead to really large glucose excursions after meals that cause very high insulin levels after meals are particularly obesogenic and should cause you to be hungrier than compared to a diet that doesn't lead to those large swings in glucose and insulin and the prototypical case being one that's very low in carbohydrate and might increase the level of ketones that are floating around in your blood, which are hypothesized to be an appetite suppressant. Same sort of design, these minimally processed diets that one was very high in carbs and causes large swings in insulin and the other that's very low in carbs and causes increases in ketones.Kevin Hall (14:22):We ask people, again, while you're in one food environment or the other, don't be trying to gain weight or lose weight, eat as much or as little as you'd like, and we're going to basically measure a lot of things. They again, don't know what the primary outcome of the study is. We're measuring their leftovers afterwards. And so, the surprise in this particular case was that the diet that caused the big swings in glucose and insulin did not lead to more calorie consumption. In fact, it led to about 700 calories per day less than when the same people were exposed to the ketogenic diet. Interestingly, both food environments caused people to lose weight, so it wasn't that we didn't see the effect of people over consuming calories on either diet, so they were reading fewer calories in general than they were when they came in, right. They're probably eating a pretty ultra-processed food diet when they came in. We put them on these two diets that varied very much in terms of the macronutrients that they were eating, but both were pretty minimally processed. They lost weight. They ended up losing more body fat on the very low-fat high carb diet than the ketogenic diet, but actually more weight on the ketogenic diet than the low-fat diet. So there's a little bit of a dissociation between body fat loss and weight loss in this study, which was kind of interesting.Eric Topol (15:49):Interesting. Yeah, I thought that was a fascinating trial because plant-based diet, they both have their kind of camps, you know.Kevin Hall (15:57):Right. No, exactly.Immune System Signatures for Vegan vs Ketogenic DietsEric Topol (15:58):There are people who aren't giving up on ketogenic diet. Of course, there's some risks and some benefits and there's a lot of interest of course with the plant-based diet. So it was really interesting and potentially the additive effects of plant-based with avoidance or lowering of ultra-processed food. Now, the more recent trial that you did also was very interesting, and of course I'm only selecting ones that I think are particularly, there are a lot of trials you've done, but this one is more recent in this year where you looked at vegan versus ketogenic diets for the immune signature, immune response, which is really important. It's underplayed as its effect, and so maybe you can take us through that one.[Link to a recent Nature feature on this topic, citing Dr. Hall's work]Kevin Hall (16:43):Yeah, so just to be clear, it's actually the same study, the one that we just talked about. This is a secondary sort of analysis from a collaboration we had with some folks at NIAID here at the NIH to try to evaluate immune systems signatures in these same folks who wonder what these two changes in their food environment. One is vegan, high carbohydrate low-fat diet and the other, the animal-based ketogenic diet. And again, it was pretty interesting to me that we were able to see really substantial changes in how the immune system was responding. First of all, both diets again seem to have improved immune function, both adaptive and innate immune function as compared to their baseline measurements when they came into the study. So when they're reading their habitual diet, whatever that is typically high in ultra-processed foods, they switched to both of these diets.Kevin Hall (17:39):We saw market changes in their immune system even compared to baseline. But when we then went and compared the two diets, they were actually divergent also, in other words, the vegan diet seemed to stimulate the innate immune system and the ketogenic diet seemed to stimulate the adaptive immune system. So these are the innate immune system can be thought of. Again, I'm not an immunologist. My understanding is that this is the first line defense against pathogens. It happens very quickly and then obviously the adaptive immune system then adapts to a specific pathogen over time. And so, this ability of our diet to change the immune system is intriguing and how much of that has to do with influencing the gut microbiota, which obviously the gut plays a huge role in steering our immune system in one direction versus another. I think those are some really intriguing mechanistic questions that are really good fodder for future research.Eric Topol (18:42):Yeah, I think it may have implications for treatment of autoimmune diseases. You may want to comment about that.Kevin Hall (18:51):Yeah, it's fascinating to think about that the idea that you could change your diet and manipulate your microbiota and manipulate your gut function in a way to influence your immune system to steer you away from a response that may actually be causing your body damage in your typical diet. It's a fascinating area of science and we're really interested to follow that up. I mean, it kind of supports these more anecdotal reports of people with lupus, for example, who've reported that when they try to clean up their diet for a period of time and eliminate certain foods and eliminate perhaps even ultra-processed food products, that they feel so much better that their symptoms alleviate at least for some period of time. Obviously, it doesn't take the place of the therapeutics that they need to take, but yeah, we're really interested in following this up to see what this interaction might be.Eric Topol (19:46):Yeah, it's fascinating. It also gets to the fact that certain people have interesting responses. For example, those with epilepsy can respond very well to a ketogenic diet. There's also been diet proposed for cancer. In fact, I think there's some even ongoing trials for cancer of specific diets. Any comments about that?Kevin Hall (20:10):Yeah, again, it's a really fascinating area. I mean, I think we kind of underappreciate and view diet in this lens of weight loss, which is not surprising because that's kind of where it's been popularized. But I think the role of nutrition and how you can manipulate your diet and still you can have a very healthy version of a ketogenic diet. You can have a very healthy version of a low-fat, high carb diet and how they can be used in individual cases to kind of manipulate factors that might be of concern. So for example, if you're concerned about blood glucose levels, clearly a ketogenic diet is moderating those glucose levels over time, reducing insulin levels, and that might have some positive downstream consequences and there's some potential downsides. Your apoB levels might go up. So, you have to kind of tune these things to the problems and the situations that individuals may face. And similarly, if you have issues with blood glucose control, maybe a high carbohydrate diet might not be for you, but if that's not an issue and you want to reduce apoB levels, it seems like that is a relatively effective way to do that, although it does tend to increase fasting triglyceride levels.Kevin Hall (21:27):So again, there's all of these things to consider, and then when you open the door beyond traditional metabolic health markers to things like inflammation and autoimmune disease as well as some of these other things like moderating how cancer therapeutics might work inside the body. I think it's a really fascinating and interesting area to pursue.Eric Topol (21:55):No question about it. And that also brings in the dimension of the gut microbiome, which obviously your diet has a big influence, and it has an influence on your brain, brain-gut axis, and the immune system. It's all very intricate, a lot of feedback loops and interactions that are not so easy to dissect, right?Kevin Hall (22:16):Absolutely. Yeah, especially in humans. That's why we rely on our basic science colleagues to kind of figure out these individual steps in these chains. And of course, we do need human experiments and carefully controlled experiments to see how much of that really translates to humans, so we need this close sort of translational partnership.On the Pathogenesis of Obesity, Calories In and Calories OutEric Topol (22:35):Yeah. Now, you've also written with colleagues, other experts in the field about understanding the mechanisms of pathogenesis of obesity and papers that we'll link to. We're going to link to everything for what we've been discussing about calories in, calories out, and that's been the longstanding adage about this. Can you enlighten us, what is really driving obesity and calories story?Kevin Hall (23:05):Well, I co-organized a meeting for the Royal Society, I guess about a year and a half ago, and we got together all these experts from around the world, and the basic message is that we have lots of competing theories about what is driving obesity. There's a few things that we all agree on. One is that there is a genetic component. That adiposity in a given environment is somewhere between 40% to 70% heritable, so our genes play a huge role. It seems like there's certain genes that can play a major role. Like if you have a mutation in leptin, for example, or the leptin receptor, then this can have a monogenic cause of obesity, but that's very, very rare. What seems to be the case is that it's a highly polygenic disease with individual gene variants contributing a very, very small amount to increased adiposity. But our genes have not changed that much as obesity prevalence has increased over the past 50 years. And so, something in the environment has been driving that, and that's where the real debates sort of starts, right?Kevin Hall (24:14):I happen to be in the camp that thinks that the food environment is probably one of the major drivers and our food have changed substantially, and we're trying to better understand, for example, how ultra-processed foods which have risen kind of in parallel with the increased prevalence of obesity. What is it about ultra-processed foods that tend to drive us to overconsume calories? Other folks focus maybe more on what signals from the body have been altered by the foods that we're eating. They might say that the adipose tissue because of excess insulin secretion for example, is basically driven into a storage mode and that sends downstream signals that are eventually sensed by the brain to change our appetite and things like that. There's a lot of debate about that, but again, I think that these are complementary hypotheses that are important to sort out for sure and important to design experiments to try to figure out what is more likely. But there is a lot of agreement on the idea that there's something in our environment has changed.Kevin Hall (25:17):I think there's even maybe a little bit less agreement of exactly what that is. I think that there's probably a little bit more emphasis on the food environment as opposed to there are other folks who think increased pollution might be driving some of this, especially endocrine disrupting chemicals that have increased in prevalence. I think that's a viable hypothesis. I think we have to try to rank order what we think are the most likely and largest contributors. They could all be contributing to some extent and maybe more so in some people rather than others, but our goal is to try to, maybe that's a little simple minded, but let's take the what I think is the most important thing and let's figure out the mechanisms of that most important thing and we'll, number one, determine if it is the most important thing. In my case, I think something about ultra-processed foods that are driving much of what we're seeing. If we could better understand that, then we could both advise consumers to avoid certain kinds of foods because of certain mechanisms and still be able to consume some degree of ultra-processed foods. They are convenient and tasty and relatively inexpensive and don't require a lot of skill and equipment to prepare. But then if we focus on the true bad guys in that category because we really understand the mechanisms, then I think that would be a major step forward. But that's just my hypothesis.Eric Topol (26:43):Well, I'm with you actually. Everything I've read, everything I've reviewed on ultra-processed food is highly incriminating, and I also get frustrated that nothing is getting done about it, at least in this country. But on the other hand, it doesn't have to be either or, right? It could be both these, the glycemic index story also playing a role. Now, when you think about this and you're trying to sort out calories in and calories out, and let's say it's one of your classic experiments where you have isocaloric proteins and fat and carbohydrate exactly nailed in the different diets you're examining. Is it really about calories or is it really about what is comprising the calorie?Kevin Hall (27:29):Yeah, so I think this is the amazing thing, even in our ultra-processed food study, if we asked the question across those people, did the people who ate more calories even in the ultra-processed diet, did they gain more weight? The answer is yes.Kevin Hall (27:44):There's a very strong linear correlation between calorie intake and weight change. I tend to think that I started my career in this space focusing more on the metabolism side of the equation, how the body's using the calories and how much does energy expenditure change when you vary the proportion of carbs versus fat, for example. The effect size is there, they might be there, but they're really tiny of the order of a hundred calories per day. What really struck me is that when we just kind of changed people's food environments, the magnitude of the effects are like we mentioned, 500 to 700 calories per day differences. So I think that the real trick is to figure out how is it that the brain is regulating our body weight in some way that we are beginning to understand from a molecular perspective? What I think is less well understood is, how is that food intake control system altered by the food environment that we find ourselves in?The Brain and GLP-1 DrugsKevin Hall (28:42):There are a few studies now in mice that are beginning to look at how pathways in the brain that have been believed to be related to reward and not necessarily homeostatic control of food intake. They talk to the regions of the brain that are related to homeostatic control of food intake, and it's a reciprocal sort of feedback loop there, and we're beginning to understand that. And I think if we get more details about what it is in our foods that are modulating that system, then we'll have a better understanding of what's really driving obesity and is it different in different people? Are there subcategories of obesity where certain aspects of the food environment are more important than others, and that might be completely flipped in another person. I don't know the answer to that question yet, but it seems like there are certain common factors that might be driving overall changes in obesity prevalence and how they impact this reward versus homeostatic control systems in the brain, I think are really fascinating questions.Eric Topol (29:43):And I think we're getting much more insight about this circuit of the reward in the brain with the food intake, things like optogenetics, many ways that we're getting at this. And so, it's fascinating. Now, that gets me to the miracle drug class GLP-1, which obviously has a big interaction with obesity, but of course much more than that. And you've written about this as well regarding this topic of sarcopenic obesity whereby you lose a lot of weight, but do you lose muscle mass or as you referred to earlier, you lose body fat and maybe not so much muscle mass. Can you comment about your views about the GLP-1 family of drugs and also about this concern of muscle mass loss?Kevin Hall (30:34):Yeah, so I think it's a really fascinating question, and we've been trying to develop mathematical models about how our body composition changes with weight gain and weight loss for decades now. And this has been a long topic, one of the things that many people may not realize is that people with obesity don't just have elevated adiposity, they also have elevated muscle mass and lean tissue mass overall. So when folks with obesity lose weight, and this was initially a pretty big concern with bariatric surgery, which has been the grandfather of ways that people have lost a lot of weight. The question has been is there a real concern about people losing too much weight and thereby becoming what you call sarcopenic? They have too little muscle mass and then they have difficulties moving around. And of course, there are probably some people like that, but I think what people need to realize is that folks with obesity tend to start with much higher amounts of lean tissue mass as well as adiposity, and they start off with about 50% of your fat-free mass, and the non-fat component of your body is skeletal muscle.Kevin Hall (31:45):So you're already starting off with quite a lot. And so, the question then is when you lose a lot of weight with the GLP-1 receptor agonist or with bariatric surgery, how much of that weight loss is coming from fat-free mass and skeletal muscle versus fat mass? And so, we've been trying to simulate that using what we've known about bariatric surgery and what we've known about just intentional weight loss or weight gain over the years. And one of the things that we found was that our sort of expectations for what's expected for the loss of fat-free mass with these different drugs as well as bariatric surgery, for the most part, they match our expectations. In other words, the expected amount of fat loss and fat free mass loss. The one outlier interestingly, was the semaglutide study, and in that case, they lost more fat-free mass than would be expected.Kevin Hall (32:44):Now, again, that's just raising a little bit of a flag that for whatever reason, from a body composition perspective, it's about a hundred people underwent these repeated DEXA scans in that study sponsored by Novo Nordisk. So it's not a huge number of people, but it's enough to really get a good estimate about the proportion of weight loss. Whether or not that has functional consequences, I think is the open question. There's not a lot of reports of people losing weight with semaglutide saying, you know what? I'm really having trouble actually physically moving around. I feel like I've lost a lot of strength. In fact, it seems to be the opposite, right, that the quality of the muscle there seems to be improved. They seem to have more physical mobility because they've lost so much more weight, that weight had been inhibiting their physical movement in the past.Kevin Hall (33:38):So it's something to keep an eye on. It's an open question whether or not we need additional therapies in certain categories of patients, whether that be pharmacological, there are drugs that are interesting that tend to increase muscle mass. There's also other things that we know increase muscle mass, right? Resistance exercise training, increase this muscle mass. And so, if you're really concerned about this, I certainly, I'm not a physician, but I think it's something to consider that if you go on one of these drugs, you might want to think about increasing your resistance exercise training, maybe increasing the protein content of your diet, which then can support that muscle building. But I think it's a really interesting open question about what the consequences of this might be in certain patient populations, especially over longer periods of time.Dietary Protein, Resistance Exercise, DEXA ScansEric Topol (34:30):Yeah, you've just emphasized some really key points here. Firstly, that resistance exercise is good for you anyway. And get on one of these drugs, why don't you amp it up or get it going? The second is about the protein diet, which it'd be interesting to get your thoughts on that, but we generally have too low of a protein diet, but then there are some who are advocating very high protein diets like one gram per pound, not just one gram per kilogram. And there have been studies to suggest that that very high protein diet could be harmful, but amping up the protein diet, that would be a countering thing. But the other thing you mentioned is a DEXA scan, which can be obtained very inexpensively, and because there's a variability in this muscle mass loss if it's occurring, I wonder if that's a prudent thing or if you just empirically would just do the things that you mentioned. Do you have any thoughts about that?Kevin Hall (35:32):Yeah, that's really a clinical question that I don't deal with on a day-to-day basis. And yeah, I think there's probably better people suited to that. DEXA scans, they're relatively inexpensive, but they're not readily accessible to everyone. I certainly wouldn't want to scare people away from using drugs that are now known to be very effective for weight loss and pretty darn safe as far as we can tell, just because they don't have access to a DEXA scanner or something like that.Eric Topol (36:00):Sure. No, that makes a lot of sense. I mean, the only reason I thought it might be useful is if you're concerned about this and you want to track, for example, how much is that resistant training doing?Kevin Hall (36:13):But I think for people who have the means to do that, sure. I can't see any harm in it for sure.Continuous Glucose Sensors?Eric Topol (36:19):Yeah. That gets me to another metric that you've written about, which is continuous glucose tracking. As you know, this is getting used, I think much more routinely in type one insulin diabetics and people with type 2 that are taking insulin or difficult to manage. And now in recent months there have been consumer approved that is no prescription needed, just go to the drugstore and pick up your continuous glucose sensor. And you've written about that as well. Can you summarize your thoughts on it?Kevin Hall (36:57):Yeah, sure. I mean, yeah, first of all, these tools have been amazing for people with diabetes and who obviously are diagnosed as having a relative inability to regulate their glucose levels. And so, these are critical tools for people in that population. I think the question is are they useful for people who don't have diabetes and is having this one metric and where you target all this energy into this one thing that you can now measure, is that really a viable way to kind of modulate your lifestyle and your diet? And how reliable are these CGM measurements anyway? In other words, do they give the same response to the same meal on repeated occasions? Does one monitor give the same response as another monitor? And those are the kinds of experiments that we've done. Again, secondary analysis, these trials that we talked about before, we have people wearing continuous glucose monitors all the time and we know exactly what they ate.Kevin Hall (37:59):And so, in a previous publication several years ago, we basically had two different monitors. One basically is on the arm, which is the manufacturer's recommendation, the other is on the abdomen, which is the manufacturer's recommendation. They're wearing them simultaneously. And we decided just to compare what were the responses to the same meals in simultaneous measurements. And they were correlated with each other thankfully, but they weren't as well predictive as you might expect. In other words, one device might give a very high glucose reading to consuming one meal and the other might barely budge, whereas the reverse might happen for a different meal. And so, we asked the question, if we were to rank the glucose spikes by one meal, so we have all these meals, let's rank them according to the glucose spikes of one device. Let's do the simultaneous measurements with the other device.Kevin Hall (38:53):Do we get a different set of rankings? And again, they're related to each other, but they're not overlapping. They're somewhat discordant. And so, then the question becomes, okay, well if I was basically using this one metric to kind of make my food decisions by one device, I actually start making different decisions compared to if I happen to have been wearing a different device. So what does this really mean? And I think this sort of foundational research on how much of a difference you would need to make a meaningful assessment about, yeah, this is actionable from a lifestyle perspective, even if that is the one metric that you're interested in. That sort of foundational research I don't think has really been done yet. More recently, we asked the question, okay, let's ignore the two different devices. Let's stick to the one where we put it on our arm, and let's ask the question.Kevin Hall (39:43):We've got repeated meals and we've got them in this very highly regimented and controlled environment, so we know exactly what people ate previously. We know the timing of the meals, we know when they did their exercise, we know how much they were moving around, how well they slept the night before. All of these factors we could kind of control. And the question that we asked in that study was, do people respond similarly to the same meal on repeated occasions? Is that better than when you actually give them very different meals? But they match overall for macronutrient content, for example. And the answer to that was surprisingly no. We had as much variability in the glucose response to the same person consuming the same meal on two occasions as a whole bunch of different meals. Which suggests again, that there's enough variability that it makes it difficult to then recommend on for just two repeats of a meal that this is going to be a meal that's going to cause your blood glucose to be moderate or blood glucose to be very high. You're going to have to potentially do this on many, many different occasions to kind of figure out what's the reliable response of these measurements. And again, that foundational research is typically not done. And I think if we're really going to use this metric as something that is going to change our lifestyles and make us choose some meals other than others, then I think we need that foundational research. And all we know now is that two repeats of the same meal is not going to do it.Eric Topol (41:21):Well, were you using the current biosensors of 2024 or were you using ones from years ago on that?Kevin Hall (41:27):No, we were using ones from several years ago when these studies were completed. But interestingly, the variability in the venous measurements to meal tests is also very, very different. So it's probably not the devices per se that are highly variable. It's that we don't really know on average how to predict these glucose responses unless there's huge differences in the glycemic load. So glycemic load is a very old concept that when you have very big differences in glycemic load, yeah, you can on average predict that one kind of meal is going to give rise to a much larger glucose excursion than another. But typically these kind of comparisons are now being made within a particular person. And we're comparing meals that might have quite similar glycemic loads with the claim that there's something specific about that person that causes them to have a much bigger glucose spike than another person. And that we can assess that with a couple different meals.Eric Topol (42:31):But also, we know that the spikes or the glucose regulation, it's very much affected by so many things like stress, like sleep, like exercise. And so, it wouldn't be at all surprising that if you had the exact same food, but all these other factors were modulated that it might not have the same response. But the other thing, just to get your comment on. Multiple groups, particularly starting in Israel, the Weizmann Institute, Eran Segal and his colleagues, and many subsequent have shown that if you give the exact same amount of that food, the exact same time to a person, they eat the exact same amount. Their glucose response is highly heterogeneous and variable between people. Do you think that that's true? That in fact that our metabolism varies considerably and that the glucose in some will spike with certain food and some won't.Kevin Hall (43:29):Well, of course that's been known for a long time that there's varying degrees of glucose tolerance. Just oral glucose tolerance tests that we've been doing for decades and decades we know is actually diagnostic, that we use variability in that response as diagnostic of type 2 diabetes.Eric Topol (43:49):I'm talking about within healthy people.Kevin Hall (43:53):But again, it's not too surprising that varying people. I mean, first of all, we have a huge increase in pre-diabetes, right? So there's various degrees of glucose tolerance that are being observed. But yeah, that is important physiology. I think the question then is within a given person, what kind of advice do we give to somebody about their lifestyle that is going to modulate those glucose responses? And if that's the only thing that you look at, then it seems like what ends up happening, even in the trials that use continuous glucose monitors, well big surprise, they end up recommending low carbohydrate diets, right? So that's the precision sort of nutrition advice because if that's the main metric that's being used, then of course we've all known for a very long time that lower carbohydrate diets lead to a moderated glucose response compared to higher carbohydrate diets. I think the real question is when you kind of ask the issue of if you normalize for glycemic load of these different diets, and there are some people that respond very differently to the same glycemic load meal compared to another person, is that consistent number one within that person?Kevin Hall (45:05):And our data suggests that you're going to have to repeat that same test multiple times to kind of get a consistent response and be able to make a sensible recommendation about that person should eat that meal in the future or not eat that meal in the future. And then second, what are you missing when that becomes your only metric, right? If you're very narrowly focused on that, then you're going to drive everybody to consume a very low carbohydrate diet. And as we know, that might be great for a huge number of people, but there are those that actually have some deleterious effects of that kind of diet. And if you're not measuring those other things or not considering those other things and put so much emphasis on the glucose side of the equation, I worry that there could be people that are being negatively impacted. Not to mention what if that one occasion, they ate their favorite food and they happen to get this huge glucose spike and they never eat it again, their life is worse. It might've been a complete aberration.Eric Topol (46:05):I think your practical impact point, it's excellent. And I think one of the, I don't know if you agree, Kevin, but one of the missing links here is we see these glucose spikes in healthy people, not just pre-diabetic, but people with no evidence of glucose dysregulation. And we don't know, they could be up to 180, 200, they could be prolonged. We don't know if the health significance of that, and I guess someday we'll learn about it. Right?Kevin Hall (46:36):Well, I mean that's the one nice thing is that now that we have these devices to measure these things, we can start to make these correlations. We can start to do real science to say, what a lot of people now presume is the case that these spikes can't be good for you. They must lead to increased risk of diabetes. It's certainly a plausible hypothesis, but that's what it is. We actually need good data to actually analyze that. And at least that's now on the table.Eric Topol (47:04):I think you're absolutely right on that. Well, Kevin, this has been a fun discussion. You've been just a great leader in nutrition science. I hope you'll keep up your momentum because it's pretty profound and I think we touched on a lot of the uncertainties. Is there anything that I didn't ask you that you wish I did?Kevin Hall (47:23):I mean, we could go on for hours, I'm sure, Eric, but this has been a fascinating conversation. I really appreciate your interest. Thank you.Eric Topol (47:30):Alright, well keep up the great stuff. We'll be following all your work in the years ahead, and thanks for joining us on Ground Truths today.**************************************Footnote, Stay Tuned: Julia Belluz and Kevin Hall have a book coming out next September titled “WHY WE EAT? Thank you for reading, listening and subscribing to Ground Truths.If you found this fun and informative please share it!All content on Ground Truths—its newsletters, analyses, and podcasts, are free, open-access.Paid subscriptions are voluntary. All proceeds from them go to support Scripps Research. Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. I welcome all comments from paid subscribers and will do my best to respond to them and any questions.Thanks to my producer Jessica Nguyen and to Sinjun Balabanoff for audio and video support at Scripps Research.Note on Mass Exodus from X/twitter:Many of you have abandoned the X platform for reasons that I fully understand. While I intend to continue to post there because of its reach to the biomedical community, I will post anything material here in the Notes section of Ground Truths on a daily basis and cover important topics in the newsletter/analyses. You can also find my posts at Bluesky: @erictopol.bsky.social, which is emerging as an outstanding platform for sharing life science. Get full access to Ground Truths at erictopol.substack.com/subscribe

Dr. Michael Keller is a Staff Clinician in the Critical Care Medicine Department at the NIH Clinical Center and Instructor of Medicine in Pulmonary and Critical Care Medicine at Johns Hopkins Hospital. He presents a lecture entitled "Heart-Lung Interactions in Spontaneous and Mechanical Ventilation" as part of the DC5 lecture series.

I have a front row seat watching my sister's, Sharon @shaydplace, journey with sickle cell. Today, she's sharing HER story on the pod. This episode is personal. But I wouldn't share it if I didn't think it would help someone in some way. Her resilience and self advocacy are inspiring. This episode, I'm in conversation with my sister as well as NIH physician scientist, Dr. Nicole Farner, and Professor and biologist, Dr. Fatimah Jackson. We talk about sickle cell - what it is, its origins, and the healing power of plants to help manage symptoms.It's a great conversation for anyone, but if you know someone with sickle cell, please share with them.About My GuestsDr. Fatimah JacksonDr. Fatimah Jackson received her Ph.D., M.A., and B.A. from Cornell University. Her doctoral dissertation research was on The Relationship of Certain Genetic Traits to the Incidence and Intensity of Malaria in Liberia, West Africa. She has conducted research on and is particularly interested in: human-plant coevolution and population substructure in peoples of African descent. Trained as a human biologist, Dr. Jackson has published extensively in journals and her research has been funded by multiple organizations. Jackson has taught at Cornell University, University of California - Berkeley, University of Florida, University of Maryland - College Park, University of North Carolina - Chapel Hill and now at Howard University. Dr. Nicole FarmerDr. Nicole Farmer is currently a Physician Scientist at the NIH Clinical Center and the Acting Section Chief of the Dietary Behaviors and Biopsychosocial Health Section. Dr. Farmer is involved in both community-based and patient research exploring the role of cooking in chronic disease prevention and psychosocial health. Prior to joining the NIH, she was a well-established primary care clinician and routinely engaged her patients in nutrition education through cooking classes. Dr. Farmer is an alumnus of Howard University College of Medicine, received her internal medicine training from Thomas Jefferson University Hospital, and held a prior appointment at Johns Hopkins University Hospital. She has also completed fellowship training in Integrative Medicine from University of Arizona and Duke University. In addition, Dr. Farmer was named a Harvard Macy Fellow in 2021 for her work on incorporating humanities into culinary medicine education and research. Sharon MartinMom. Wife. Sister. Friend. Sickle Cell Warrior. At 48 years old, Sharon has learned to thrive with her sickle-beta thalassemia diagnosis.Sickle Cell Study: Dietary Intake and Dietary Behaviors in Adults With Sickle Cell DiseaseAbout the Study: https://clinicaltrials.gov/ct2/show/NCT05170412To participate, contact: Nicole.Farmer@nih.govGrown and Growing Podcast -- Like. Follow. Share. Website: grownandgrowing.buzzsprout.comFacebook: @GrownandgrowingpodcastInstagram: @GrownandgrowingpodcastEmail: grown.growingpodcast@gmail.com

As women, there is no shortage of things that we worry about. But we're no good to others if we're not at the top of the list.  On the podcast, I talk a lot about being in a good mental space, but our physical health is just as important.  In this episode, I'm talking to Dr. Nicole Farmer, NIH physician scientist and internal medicine doctor, about women's health and how we can ensure we're health-conscious. And because she's a researcher, I ask her about the importance of medical research, and how history prevents Black Americans from fully benefiting from clinical advancements. About My Guest:Dr. Nicole Farmer is currently a Physician Scientist at the NIH Clinical Center and the Acting Section Chief of the Dietary Behaviors and Biopsychosocial Health Section. Dr. Farmer is involved in both community-based and patient research exploring the role of cooking in chronic disease prevention and psychosocial health. Prior to joining the NIH, she was a well-established primary care clinician and routinely engaged her patients in nutrition education through cooking classes. Dr. Farmer is an alumnus of Howard University College of Medicine, received her internal medicine training from Thomas Jefferson University Hospital, and held a prior appointment at Johns Hopkins University Hospital. She has also completed fellowship training in Integrative Medicine from University of Arizona and Duke University. In addition, Dr. Farmer was named a Harvard Macy Fellow in 2021 for her work on incorporating humanities into culinary medicine education and research. Grown and Growing Podcast: Like. Follow. Share. Connect with me:Website: grownandgrowing.buzzsprout.comFacebook: @GrownandgrowingpodcastInstagram: @GrownandgrowingpodcastEmail: grown.growingpodcast@gmail.com

On this episode, Dr. Nicole Farmer joins us to talk about her research on cooking frequency in non-Hispanic households and highlights the advantages of home cooking for better diet quality, mental health, and prevention of chronic disease. Dr. Nicole Farmer is currently a Staff Scientist at the NIH Clinical Center and the Acting Section Chief of the Dietary Behaviors and Biopsychosocial Health Section within The Translational Biobehavioral and Health Disparities Branch (TBHD). In the intramural research position, Dr. Farmer is involved in both community-based and patient research exploring the role of cooking in chronic disease prevention and psychosocial health. Question of the Day: What's your favorite go-to home-cooked meal to make? In this episode you will learn: Non-Hispanic Black Households & Dinner Cooking Balanced Meal Preparation at Home Home Cooking in Post-COVID World Cooking and Mental Health Perceptions Connect with Yumlish: Website Instagram Twitter Facebook LinkedIn Connect with Dr. Nicole Farmer Website Twitter 00:00 Intro with Shireen 00:32 Welcome Dr. Nicole Farmer 02:39 Lower cooking frequency 06:08 Promoting Cooking Frequency in Higher Income Non-Hispanic Blacks 08:15 Correlation between Low-Income and High-Income Individuals and Cooking Habits 09:51 Advice for Healthy Home Cooked Meals on a Time Budget 14:14 Good Intentions in Home Cooking and Potential for Poor Nutritional Choices 17:26 How to Audit Your Meal: Identifying Nutrient-Dense vs Non-Nutrient Dense Foods 18:48 The Benefits of Cooking for Mental Health in a Post-COVID World 22:09 The Importance of Home Cooking in Chronic Disease Prevention 25:22 Outro with Shireen --- Send in a voice message: https://anchor.fm/yumlish/message

This week, please join authors Jonas Oldgren and Signild Åsberg as they discuss the article "Early Versus Delayed Non–Vitamin K Antagonist Oral Anticoagulant Therapy After Acute Ischemic Stroke in Atrial Fibrillation (TIMING): A Registry-Based Randomized Controlled Noninferiority Study." Dr. Carolyn Lam: Welcome to Circulation on The Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, Associate Editor, Director of the Poly Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Today's featured paper is a very important discussion, and in fact, the first study to compare early versus delayed NOACs after acute ischemic stroke in patients with atrial fibrillation. The timing study. You're not going to want to miss this, but you're going to have to wait for it, because we're going to discuss all the papers in today's issue. Can I start, Greg? Because I want to start, or is it too early to start with a Greg quiz? With the quiz question being, what is cell-free DNA? Dr. Greg Hundley: Oh, thank you Dr. Lam. I really appreciate your wonderment into the world of preclinical science. So something maybe short DNA fragments, but I'm not sure. Dr. Carolyn Lam: Aw, you're absolutely right. It's circulating DNA fragments predominantly from mononuclear zones that represent cell injury and/or turnover. So what we know is elevated total cell-free DNA concentration has been associated with worse prognosis in a variety of conditions such as sepsis, trauma, malignancy. In addition, and this may be where a lot of us have heard of cell-free DNA, it's become clinically relevant as a noninvasive marker of solid organ transplant rejection as well as a tool for genotyping and surveillance in oncology. However, in today's paper, given the parallels in the pathogenesis of pulmonary artery hypertension, two of the diseases I've talked about before that are characterized by increased cell proliferation and turnover, like the cancers and inflammatory mediated tissue injury. Now this particular study sought to determine if plasma cell-free DNA concentrations were elevated in pulmonary artery hypertension, and if those levels would correlate with disease severity or predict outcomes. Dr. Greg Hundley: Oh wow, Carolyn, this sounds really informative. So what did they find? Dr. Carolyn Lam: Well, this study from corresponding authors, Dr. Solomon from NIH Clinical Center and Dr. Agbor-Enoh from NHLBI in Bethesda and their team found that circulating cell-free DNA is elevated in patients with pulmonary arterial hypertension compared to healthy controls. In two independent PAH patient cohorts, cell-free DNA concentrations increased with severity of disease and predicted transplant free survival in the larger of the two cohorts. Interestingly, methylation patterns revealed increased cell-free DNA originating from biologically plausible sites including erythrocyte progenator and myeloid lineage inflammatory cells, vascular endothelium, and cardiac myocytes. So the implications are that in pulmonary arterial hypertension, cell-free DNA concentrations could serve as a non-invasive biomarker of underlying disease activity, may add prognostic value to currently use risk scores, and may provide a unique noninvasive window into its pathogenesis. Dr. Greg Hundley: Wow, Carolyn. So another interesting technique and pathophysiologic study highlighting the utility of circulating cell-free DNA. Wow. Well, Carolyn, how about I start in with my first study and it comes to us from the world of clinical science and refers to the paradise MI echocardiographic substudy. So Carolyn, the prospective RNE versus ACE inhibitor trial to determine superiority in reducing heart failure events after myocardial infarction. So the Paradise MI echo study tested the effect of Sacubitril/Valsartan compared to Ramipril on LV function and adverse remodeling following high risk acute myocardial infarction. So this substudy included 544 Paradise MI participants that underwent echocardiography at randomization, and then again later at eight months. Patients were randomized within a half to seven days of their presentation with their index, myocardial infarction, to receive a target dose of Sacubitril/Valsartan of 200 milligrams or Ramipril five milligrams twice daily. Dr. Carolyn Lam: All right. So the Paradise MI echo substudy, what did they find? Dr. Greg Hundley: Right Carolyn, so treatment with Sacubitril/Valsartan compared to Ramipril following acute myocardial infarction did not result in changes in left ventricular ejection fraction or left atrial volume at eight months. Patients randomized to Sacubitril/Valsartan had less LV enlargement and greater improvement in filling pressure, and thus there are new insights here in that treatment with Sacubitril/Valsartan compared to Ramipril early following acute myocardial infarction may beneficially impact LV size and diastolic properties possibly due to reductions in LV filling pressure. Dr. Carolyn Lam: Oh, very nice, Greg. Thank you. Another clinical study here, and this time a paper aimed to evaluate the influence of sex on the effects of empagliflozin in patients with HFpEF enrolled in the Emperor Preserved trial. Dr. Greg Hundley: Ah, Carolyn, two of your favorite things, sex differences and SGLT2 inhibitors. So Carolyn, remind us, what did Emperor Preserved show us? Dr. Carolyn Lam: Ah, so Emperor Preserved studied the sodium glucose cotransporter 2 or SGLT2 inhibitor empagliflozin in patients with HFpEF, which is an ejection fraction above 40%, and showed a significant reduction in the risk of cardiovascular death or heart failure hospitalization. In the current paper, corresponding author Dr. Javed Butler from University of Mississippi Medical Center and colleagues found that empagliflozin reduced the risk of the primary outcome of cardiovascular death or hospitalization for heart failure to a similar degree in both women and men with HFpEF irrespective of baseline left ventricular ejection fraction. Empagliflozin produced comparable benefits for the pre-specified secondary outcomes of total heart failure hospitalizations, cardiovascular death, and all-cause mortality, as well as physiologic measures and health status. The pattern of the effects of empagliflozin and HFpEF in both sexes in EMPEROR- Preserved stands in contrast to the influence of sex on the response to neprilysin inhibition. So very interesting paper. I encourage everyone to pick it up, of course, because it's two of my favorite topics. Dr. Greg Hundley: Very nice, Carolyn. Well, my next paper comes to us from the world of pre-clinical science, and it's from Dr. Chunyu Zeng from Diping Hospital, the third military medical university. Carolyn, adverse environmental exposure during the prenatal period can lead to diseases in offspring, including hypertension. Now whether or not the hypertensive phenotype can be trans-generationally transmitted is really not new. Dr. Carolyn Lam: Wow, that's interesting. So what did this paper find? Dr. Greg Hundley: Carolyn, this was really interesting. So these authors in a rat model, they found that prenatal lipopolysaccharide exposure can impair the ability to excrete a salt load and induce hypertension from the first to the third generations, with the fourth and fifth generations inducing salt-sensitive hypertension. And Carolyn, really interestingly, and based on these findings, they treated lipopolysaccharide exposed pregnant rats with the reactive oxygen species scavenger temple, which successfully prevented hypertension in the first-generation offspring and the transgenerational inheritance of hypertension. So Carolyn, these findings show that adverse prenatal exposure induces transgenerational hypertension through an epigenetic regulated mechanism. And these findings identify potentially preventive and therapeutic strategies for this form of generationally transmitted hypertension. Really interesting. Dr. Carolyn Lam: Wow, that sounds wild. Very, very interesting. Well, let's go through the other things that are in today's issue. There's a research letter by Dr. Moayedi on anteroposterior pacer pad position is more likely to capture than anterolateral for transcutaneous cardiac pacing. Dr. Greg Hundley: Great, Carolyn. And I've got a research letter from Professor Porrello entitled, “Defining the Fetal Gene Program at Single Cell Resolution in Pediatric Dilated Cardiomyopathy.” And then lastly, there's an ECG Challenge from Dr. Chen entitled, “A Shark Thin Electric Cardiogram in the Intensive Care Unit.” Well Carolyn, how about we get onto that featured discussion and learn more about non-vitamin K antagonists after acute ischemic stroke? Dr. Carolyn Lam: Yep. In patients with EF, here we go. Today's feature discussion is all about atrial fibrillation, how it's a risk factor for stroke, but also about how we've never known really how soon after an acute stroke can we start oral anticoagulation to prevent recurrent strokes? Today we're going to talk about the timing study. It's the first randomized controlled study to evaluate the efficacy and safety of initiation of treatment with NOACs within 10 days of acute ischemic stroke in patients with atrial fibrillation. Wow. What an exciting study, and also how exciting that we have two co-first authors. We have Dr. Jonas Oldgren and Dr. Signild Åsberg from Uppsala University in Sweden, and this represents a partnership between neurology and cardiology. I mean really unique in many aspects as well as the way this study was performed, which is truly, truly a feat in itself. May I ask you both please to tell me the story of how this study came to be in the first place? Dr. Signild Åsberg: Well, we like to mention the late Professor Gesteruen student who actually was the first to bring this question to the table. Together we talked with the cardiology department and Jonas Oldgren to see if we can collaborate to solve this important question for us that works with stroke patient, because it's on a weekly or even a daily basis, troublesome question. Dr. Jonas Oldgren: My background is as a cardiologist and professor of coagulation research. I've been very interested in anticoagulants, antithrombotic treatments, and had the pleasure and privilege to be part of the development of the novel oral anticoagulants. And in all those pivotal trials, we excluded patients with a recent stroke at least seven days from the stroke, sometimes even 30 days from the acute stroke we excluded them from the studies. So when we found the exciting results with at least as good efficacy as warfarin and at least as good safety as warfarin and the tremendous reduction in intracerebral or intracranial bleeds, that was a finding which was not evaluated in acute stroke patients with atrial fibrillation. And when Signild approached me with this idea, I said, "Well this is absolutely a very important question and why hasn't it been resolved earlier?" And the problem is, of course, that these are patients who are in a sensible setting earlier after the acute ischemic stroke, and when are we able to safely start an effective treatment? Dr. Carolyn Lam: Oh, I couldn't agree more with you about how important that is. I mean, when we have an acute stroke patient, we just don't know whether we should start the NOAC early or delay it and we definitely need that evidence gap filled. But I'm also so intrigued with the way you did it with the Swedish Stroke Register. I mean, what a powerful way to look at important questions like this. Could you tell us a bit more about the method used? Dr. Jonas Oldgren: Yeah, so in cardiology we started rather early by using our national health registries for doing randomized controlled trials. We did a lot of observational studies in our registries, both in stroke and in cardiovascular medicine, otherwise in every other area of medicine. But in the end we realized that we could at best be hypothesis generating, but we still needed to add randomized controlled studies to have the last piece of the puzzle to provide good evidence. And then we ran a lot of studies in cardiologists, especially in myocardial infarction patients, by just adding to simplify, by adding a randomization module, and then follow the patients in the registries because we know that we have high quality data in the registry. For instance, in the stroke registry. So we anyway collect every important data on each and every patient in the register. So by adding a randomization module, we can facilitate the conduct of a clinical study. Dr. Carolyn Lam: Wow. The way you say it, you make it sound so simple, but I can tell you what you have there in Sweden is like the envy of the whole world, and everybody's thinking about how to do a registry based trial like that. So maybe after you tell us the results, you could also share a little bit of how difficult and challenging it can be as well. But would either of you like to share the results? Dr. Signild Åsberg: Well, the major result from our trial is that initiating NOAC within four days is non-inferior to starting in a delayed phase of up to 10 days. So that's our key finding. But equally important is that we didn't have any patients explaining as symptomatic and terrible hemorrhage, and that is extremely good news for us who worked with these patients. Dr. Carolyn Lam: That is such an important message. The early initiation was non-inferior. Could you expand on non-inferior in terms of what primary outcome? Dr. Jonas Oldgren: Yeah, so the primary outcome was really a clinically important outcome we think, both from the cardiac perspective but also from stroke specialists. So we had a combination composite of symptomatic intracerebral hemorrhages, ischemic strokes and death. And this is what matters to patients and to doctors. We would like to avoid strokes, and it doesn't matter if it's an ischemic stroke or if it's a hemorrhagic stroke. We would like to avoid them. And of course we would not like to have an increased mortality as well. So it's a relevant endpoint. And when we designed the study, the main drug used was warfarin, and there we knew that there was a lot of hemorrhagic transformations and a lot of intracerebral hemorrhages. So we designed the trial to look at these three endpoints to prevent ischemic strokes, but to avoid hemorrhagic strokes. And that is why we choose to have a non-inferiority design, because we also have the advantage of starting early if we can make the decision to start with the stroke specialists sometimes in collaboration with the cardiologist, and then we can have the patient step down unit earlier if the treatment is already started. So that was the choice of a non-inferiority design. We of course also tested for superiority, but unfortunately we didn't meet that superiority testing endpoint. But as Signal mentioned, I think thrilling results is to have no symptomatic intracerebral hemorrhage in any of the groups. That really speaks in favor of the safety of this drug or these drugs that we used, but also the concept to start early. We can also note that we had some ... I mean there were numerically lower rates of both ischemic strokes and deaths in the early group, albeit not meeting the significance for superiority, but it's important. And as we see also the events tend to occur very early. So we really gain with treating our patients earlier with this intervention. Dr. Carolyn Lam: Oh indeed. And to all the listeners, do pick up the paper because if you look at the Kaplan-Meier curves, they're really impressive, exactly like you said, numerical differences, although the trial did demonstrate non-inferiority and could not demonstrate the superiority. But have a look at those figures. And if I could just clarify the comparator arm, notice that we've been saying NOACs, not a particular NOACs. So could you expand on that a bit? Dr. Signild Åsberg: We used all the four NOACs that we have in Sweden, so that was to the physician's discretion to choose between them. So that was not a part of the randomization. So we only randomized the timing to the early phase or the delayed phase. Dr. Carolyn Lam: I love that. And then if you could please educate the cardiologist in me, please. There are symptomatic intracerebral hemorrhages, and then there are all kinds of little things that you can pick up if you image the brain and hemorrhagic transformation and microbleeds and all these things. So I think one of the things here was their systematic imaging and does it matter? Could you teach us a little bit more about these different types of bleeds? Dr. Signild Åsberg: We did not have a systematic imaging, but in Sweden that is performed mostly by CT on admission. So that was for all patients. And then on events, the imaging was performed and reported through the registry. And yes, there were hemorrhagic transformation actually in three patients, two in the early phase, and one in the delayed phase, but only one before day 10. So all blood that was seen on imaging was reported, but we used symptomatic criteria from the stroke severity scale. Dr. Carolyn Lam: Thank you. That's a good clarification. And then the study aimed for a larger number, and here perhaps if either of you could tell us the story, the struggles, and how you ended up with these beautiful results. Dr. Signild Åsberg: Yeah, struggle is the word. It was troublesome and we had long talks. So why was this happening? Why didn't science recruit more? But I think one issue might have been that NOACs had been on the market for a while once we started, and even the stroke physicians were getting used to it and had trouble not to start. Before the timing study started, we did a observational pre-timing study just to see how we were doing in Sweden at this stage. Because we didn't really know that. We know that a lot of patients were discharged with oral anticoagulation, but we didn't really know when they started. And so by that study we could see that in median time to initiation was five days, already before the timing study. So one thought was that this was for some physicians then had to delay their start. They were getting used to start early. So that could have been one explanation. Dr. Jonas Oldgren: And of course there has been a lot of observational studies looking at the safety of NOACs or other oral anticoagulants in the early setting after acute ischemic stroke in patients with atrial fibrillation. And of course with the evidence from such studies, albeit observational doctors felt perhaps more confident starting very early despite the lack of evidence from randomized control trials. So we had the opportunity to follow those patients as well in the stroke registry. Every patient with an acute stroke in Sweden attending a stroke unit is registered. So we have in the supplement of the paper in circulation, we have observational data from the centers participating in stroke, but patients not randomized in the timing study. And we also have observational data from all stroke centers in Sweden. So we can see that many start very earlier with NOACs based on observational data, based on experiences. And perhaps we're more and more reluctant to randomize the patient in the study because as Signal says, that means there is a 50% chance of delayed treatment by randomization. And when we started this study, there were no evidence from randomized controlled trials within the first 14 days. But while running the study for a couple of years, you start to believe that there seemed to be safety because no one saw any symptomatic intracerebral hemorrhage. And we discussed that, of course, at investigative meetings that this seemed to be a very good treatment, which is bad for running a clinical study, but it's of course good for the patients. Dr. Carolyn Lam: Interesting. So echo points kind of may have shifted a little bit even during the course of the trial. So just thank you so much all the more. Thank you for seeing this to completion in the sense of a beautiful manuscript with very meaningful results. If I could ask you both to each summarize just very quickly what the take home message is for clinical practice from neurologist's point of view and cardiologist's point of view? Dr. Signild Åsberg: Yeah, what I would say, it seems both safe and reasonable to initiate NOAC earlier after an acute ischemic stroke. So I think that's the key take home message that really to consider the acute secondary prevention. Dr. Jonas Oldgren: I may bring that from another perspective. I think when there's lack of data in collaboration, we can do a lot. So in this case, we had a great collaboration in the student committee, cardiologist and stroke specialists collaborating to run such a study. And we are extremely grateful for all the sites and all the investigators at the sites participating in the study. And then of course grateful to circulation for publishing it because we are very proud of this study. Dr. Carolyn Lam: And we are proud to be publishing this. So ladies and gentlemen, you heard it right here in Circulation On The Run. Remember this is about early versus delayed initiation of NOACs in patients after an acute stroke who also have atrial fibrillation. And this is a very, very, I think, important study that fills an important evidence gap. We're so grateful to both of you for being here to discuss it, and to the audience for listening today. You've been listening to Circulation On The Run. And don't forget to tune in again next week. Dr. Greg Hundley: This program is Copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit AHAjournals.org.

PSC Partners Seeking a Cure is pleased to present Living With PSC, a podcast moderated by Niall McKay. Each month, this podcast explores the latest research and knowledge about primary sclerosing cholangitis (PSC), a rare liver disease. From patient stories, to the latest research updates from PSC experts, to collaborations that are necessary to find better treatments and a cure, this podcast has it all! In episode 33 of the Living with PSC Podcast, Host Niall McKay talks with Hepatologist and Senior Research Clinician Theo Heller, MD, and Hepatology Fellow Gracia Viana, MD, National Institute for Health (NIH) Clinical Center, about their primary sclerosing cholangitis (PSC) study. "We want to study the evolution of PSC," says Dr. Heller. "We're proposing a study that has the potential of unraveling some of the most fundamental aspects of the disease." Information about this study will be sent to PSC Partners Registry participants. If you are a PSC patient but have not yet joined the Patient Registry, now would be a good time. www.pscpartnersregistry.org Questions about the Registry? Email: registrycoordinator@pscpartners.org

Captain Daniel S. Chertow MD, MPH is an investigator in the Critical Care Medicine Department at the NIH Clinical Center and in the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases. He serves as a senior officer in the United States Public Health Service (USPHS). He presents an interactive lecture on viral illness in the ICU with current and emerging threats as part of DC5 lecture series.

Join NETEC and host Lauren Sauer as they welcome Dr. Sameer Kadri, author of the article "Association Between Caseload Surge and COVID-19 Survival in 558 U.S. Hospitals, March to August 2020," recently published in the Annals of Internal Medicine.Dr. Kadri is an ICU physician and associate research physician at NIH. He serves as the head of the Clinical Epidemiology Section in the NIH Clinical Center's Critical Care Medicine Department.In this episode of Transmission Interrupted, Dr. Kadri discusses his findings from a study that sought to understand the relationship between the COVID-19 surge and its impact on the mortality risk of patients admitted to these hospitals. Additional topics discussed in this episode include surge index, a metric designed to help measure the strain of hospital overcrowding.Questions or comments for NETEC? Contact us: info@netec.orgFind us on the web: netec.orgGuestSameer S. Kadri, MD, MSDr. Sameer S. Kadri is currently an associate research physician and head of the Clinical Epidemiology Section in the Clinical Center's Critical Care Medicine Department.Dr. Kadri earned his degree in Medicine from the Seth G. S. Medical College and King Edward Memorial Hospital in Mumbai, India. He went on to complete internship and residency training in Internal Medicine at the New York-Presbyterian Hospital and Weill Cornell Medical Center and obtained a Masters degree in Clinical Epidemiology at the Harvard T.H. Chan School of Public Health.Following his fellowship training in Critical Care Medicine at the NIH and in Infectious Diseases at Massachusetts General Hospital and Harvard Medical School, Dr. Kadri was appointed to Staff Clinician in the Critical Care Medicine Department at the NIH in 2014. In this role, he splits his time between attending in the Intensive Care Unit at the NIH Clinical Center, conducting clinical research and training clinical and research fellows in the Critical Care Medicine Department.His primary research interest lies in infections in the critically ill. He leverages large datasets for epidemiologic investigations on antimicrobial resistance, sepsis, procalcitonin use, smoke inhalation acute lung injury and the role of IVIG in necrotizing fasciitis and granulocyte transfusions in invasive mycoses. His ongoing work includes use of large electronic health record-based repositories to understand the market size for new antibiotics (in collaboration with the US FDA), the impact of early discontinuation of antibiotics in culture negative sepsis and identify more objective candidate ICU performance measures.He founded and leads the NIH Antimicrobial Resistance Outcomes Research Initiative (NIH–ARORI), a collaborative between the NIH Clinical Center, Intramural NIAID, the CDC and Harvard Medical School. Through this initiative he developed and tested a simple but clinically relevant bedside classification scheme for antimicrobial resistance called “Difficult-to-treat Resistance” or DTR that focuses on non-susceptibility to all first-line antibiotics. He is a peer reviewer for several subspecialty journals and has served as an editor for the Infectious Diseases Clinics of North America issue titled Complex Infectious Disease Issues in the Intensive Care Unit. He has spearheaded investigations that underscore the benefits of dually training in critical care medicine and infectious diseases and is promoting the unique role of critical care providers in combating antimicrobial resistance.HostLauren Sauer, MScLauren is an Associate Professor in the College of Public Health, Department of Environmental, Agricultural, and Occupational Health, at the University of Nebraska Medical Center and Core Faculty of the UNMC Global...

In Episode 35, Melissa talks with Christina Martin who recently returned to pharmacy practice at NIH Clinical Center and previously served as Director, Office of Member Relations at the American ...

Sunil Aggarwal, MD, PhD, FAAPMR is a Board-Certified Physician in Hospice and Palliative Medicine and Physical Medicine and Rehabilitation and Medical Geographer and serves as the Past Chair of the American Academy of Hospice and Palliative Medicine (AAHPM) Integrative Medicine Special Interest Group and an inaugural member of the Safe Use in Psychedelic-Assisted Therapies Forum. He was recently named as a Top 20 Emerging Leader by the AAHPM. He is an Affiliate Assistant Clinical Professor in Rehabilitation Medicine at the University of Washington School of Medicine, an Affiliate Assistant Professor in the Department of Geography, and an Affiliate Clinical Faculty with Bastyr University. He completed his MD and PhD degrees at the University of Washington and Residency and Fellowship at Virginia Mason Medical Center, NYU Langone Health, and the NIH Clinical Center. He is a Co-founder, Co-director and practitioner at the Advanced Integrative Medical Science (AIMS) Institute in Seattle, a multispecialty teaching clinic and research institute offering cutting edge care in oncology, psychiatry, neurology, rehabilitation, pain, and palliative care. He also serves as an Associate Hospice Medicine Director and On-Call Palliative Physician for MultiCare Health System. He has published over three dozen peer-reviewed article and book chapters that have been cited over 800 times per Google Scholar. 8:32 Dr. Aggarwal describes the unique cancer care at the Advanced Integrative Medical Science (AIMS) Institute in Seattle. 13:50 Dr. Diva's take on how this approach is revolutionary compared to the standard of cancer care. 18:48 How AIMS Institute's approach translates to treating chronic conditions beyond cancer. 21:24 Dr. Aggarwal's approaches to psycho-spiritual healing. 27:05 Dr. Aggarwal explains his utilization of ketamine-assisted therapies, and his legal efforts to expand patients' access to other psychedelics including psilocybin. 32:58 Dr. Aggarwal's perspective on how psychedelic therapies assist in overall healing and wellbeing. 36:59 The power of psychedelics as psychoplastogens—and the psychology of awe. 41:10 Discussing dosages for ketamine-assisted therapy. 44:13 The ongoing efforts to track how AIMS' integrative approach compares to the current standards of care. 48:17 Contact info, and how to utilize the services of the AIMS Institute. Links mentioned in this episode: https://www.aimsinstitute.net/ (AIMS Institute Website) https://www.facebook.com/aimsinstitutepllc/posts_to_page/ (Facebook) https://www.instagram.com/aimsinstituteseattle/ (Instagram) This episode is sponsored by http://www.getchews.com/ (TotumVos Collagen Chews). You can find TotumVos at www.getchews.com. *Use code DRDIVA for an additional 10% off your first order.

Dr. Nitin Seam, MD, Associate Chief and Fellowship Director of the Critical Care Medicine Department at NIH Clinical Center, presents on how to effectively consume medical information in a social media world.

Dr. Ron Waksman interviews Dr. Daniel S. Chertow, an investigator with the Emerging Pathogens Section of the NIH Clinical Center, about the state of research into COVID-19 pathophysiology and treatment. Watch the interview videos on CRTonline

We've been keeping tabs on a New Jersey lab called BioAegis because of their work with the protein Gelsolin, which they say has potential to be an effective therapy for very ill COVID-19 patients. When we found out that Dr. John Gallin, Chief Scientific Officer of the NIH Clinical Center and the NIH Associate Director for Clinical Research was also studying the protein, we asked him to join KYW In Depth to talk about what he thinks the possibilities are and why he wanted to take a closer look. We're also joined by Dr. Susan Levinson, co-founder and CEO of BioAegis Therapeutics to break down where their treatment stands in the regulatory approval process and how they see Gelsolin being used if it's approved by the FDA. More information about the NIH Clinical Center: https://clinicalcenter.nih.gov/ And about BioAegis: https://www.bioaegistherapeutics.com/

Social distancing is the best way to curtail the spread of COVID-19, but if innumerable days of isolation start to feel like they’re taking a toll on your mental welfare, there might be some solace waiting in the kitchen. According to mental health experts, cooking can reduce anxiety and alleviate mental distress. Dr. Nicole Farmer is a clinical researcher studying many facets of how diet affects human biology and behavior, including the effects of cooking interventions on mental well-being. Dr. Farmer is a staff scientist at the NIH Clinical Center and a 2020 recipient of the William G. Coleman Jr. Minority Health and Health Disparities Research Innovation Award from the National Institute of Minority Health and Health Disparities (NIMHD). Learn more about her research at https://www.nimhd.nih.gov/programs/intramural/research-award/2020-awardees/farmer.html

By Michael Tetreault & Dr. Stephen C Schimpff, MD, MACP Today we sit down for a very special interview with our good friend Dr. Stephen C Schimpff, MD, MACP. Former CEO of the University of Maryland Medical Center, author of the books shown above, former senior investigator at the National Cancer Institute; former head of infectious diseases and director of the University of Maryland Greenabaum Cancer Center, Professor of Medicine and Public Policy at the University of Maryland, former chair Board of Governors of NIH Clinical Center, -- along with a life long love of nature and a frequent visitor to Canaan Valley in West Virginia with my wife of 53 years. Stephen C Schimpff, MD, MACP. Blog: Medical Megatrends and the Future of Medicine http://medicalmegatrends.blogspot.com Other Resources & Citations Mentioned: www.ConciergeMedicineToday.com www.DirectPrimaryCare.com www.ConciergeMedicineFORUM.com

When people refer to the NIH as the “National Institutes of Hope,” Dr. Bill Gahl is one of the many people who come to mind. Dr. Gahl is a medical geneticist working to help patients with rare and undiagnosed diseases. His research group focuses on inborn errors of metabolism, which include defects in the body’s biochemical processes caused by rare genetic disorders, such as cystinosis, Hermansky-Pudlak syndrome, alkaptonuria, and ciliopathies. Transcending biomedical boundaries to take advantage of the IRP’s unique team-science environment, Dr. Gahl led the creation of the NIH’s Undiagnosed Diseases Program to provide answers and possible treatments for people with mysterious conditions that have long eluded diagnosis. Since seeing their first patient at the NIH Clinical Center in July of 2008, the Program has expanded to become the Undiagnosed Diseases Network, which now includes 12 clinical sites along with supporting scientific facilities around the country. Even when no concrete answer or cure can be found, each patient shares new information that may in the future help other people facing similar health problems, and such hope can provide powerful meaning for people’s struggles that seem to occur without reason. William Gahl, M.D., Ph.D., is a Senior Investigator in the Medical Genetics Branch of the NIH's National Human Genome Research Institute (NHGRI). Learn more about Dr. Gahl and his research at https://irp.nih.gov/pi/william-gahl

In 2011, the NIH Clinical Center had a cluster of infections of a pathogen that tops the CDC's list of urgent threats: antibiotic-resistant Klebsiella pneumoniae. This bacteria, which can cause bloodstream and other infections, has recently developed resistance to the class of antibiotics known as carbapenems. The outbreak at NIH started with a single infected patient who was discharged weeks before any other cases were detected. This story of antibiotic-resistant infections is becoming more common around the world, and is especially dangerous in hospitals. Dr. Julie Segre, a senior investigator at the National Human Genome Research Institute, discuses how the outbreak was traced using state-of-the-art DNA sequencing.

In 2011, the NIH Clinical Center had a cluster of infections of a pathogen that tops the CDC's list of urgent threats: antibiotic-resistant Klebsiella pneumoniae. This bacteria, which can cause bloodstream and other infections, has recently developed resistance to the class of antibiotics known as carbapenems. The outbreak at NIH started with a single infected patient who was discharged weeks before any other cases were detected. This story of antibiotic-resistant infections is becoming more common around the world, and is especially dangerous in hospitals. Dr. Julie Segre, a senior investigator at the National Human Genome Research Institute, discuses how the outbreak was traced using state-of-the-art DNA sequencing.

In 2011, the NIH Clinical Center had a cluster of infections of a pathogen that tops the CDC's list of urgent threats: antibiotic-resistant Klebsiella pneumoniae. This bacteria, which can cause bloodstream and other infections, has recently developed resistance to the class of antibiotics known as carbapenems. The outbreak at NIH started with a single infected patient who was discharged weeks before any other cases were detected. This story of antibiotic-resistant infections is becoming more common around the world, and is especially dangerous in hospitals. Dr. Julie Segre, a senior investigator at the National Human Genome Research Institute, discuses how the outbreak was traced using state-of-the-art DNA sequencing.

SCCM President Frederick P. Ognibene, MD, FCCM, shares his experiences and accomplishments as president, offers his vision for the Society and discusses current topics in critical care. Dr. Ognibene is director of the office of clinical research training and medical education at the National Institutes of Health (NIH) Clinical Center and the director of clinical research training program. He also is an attending in the medical intensive care unit at the NIH Clinical Center.

Frederick P. Ognibene, MD, FCCM, discusses his goals as the Society's president for 2007 as well as his decades-long involvement in SCCM and the critical care community. Dr. Ognibene is director of the office of clinical research training and medical education at the National Institutes of Health (NIH) Clinical Center and the director of clinical research training program, OIR. He also is an attending in the medical intensive care unit at the NIH Clinical Center.