Foresight Medicine

Robert S. Rogers
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Conversations about the future of preventive healthcare with leading experts. foresightmedicine.substack.com

Episodes

  1. Jun 8

    Episode #7: Prevention of Diabetes and Innovation in Metabolic Health with Dr. Robert Gabbay

    Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a systematic framework for leveraging new technology to maintain health for as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties. Today we’ll be talking about the foundational topics of diabetes, obesity, and metabolic health. I am very honored to have as my guest, Dr. Robert Gabbay. Dr. Gabbay is an endocrinologist, physician- scientist, and an inspiring leader in diabetes care, research, and prevention. He has served as both chief scientific and chief medical officer of the American Diabetes Association and the chief medical officer of the Joslin Diabetes Institute, and is Associate Professor of Medicine at Harvard Medical School. He has pioneered innovative care models for diabetes and chronic disease more broadly, and he is a major contributor to the important guidelines clinicians use to provide optimal diabetes care, a prolific and insightful analyst on new developments in the world of pharmacotherapy devices and other technologies for metabolic health. Listeners should note we are recording this on Monday, June 1st, 2026, and this conversation is for general informational purposes only and does not constitute individual medical advice. Bob, welcome. Thank you so much for joining me today on Foresight Medicine. Robert Gabbay: Thanks, Robert. I’m looking forward to our conversation. Robert Rogers: So I’m really looking forward to this conversation, and one thing that I know is that you are a guest with whom we could probably cover any aspect of the broader topic of diabetes, metabolism, obesity with and have a really insightful conversation. But that is a very broad topic. Perhaps it’s the most foundational thing to health today and a place where there’s a lot of focus. And to focus our conversation in the spirit of Foresight Medicine and our focus on prevention and early intervention, what I’d really like us to spend most of our time talking about is not healthcare, and medical care for patients with full-blown, well-established diabetes, significant obesity, and all of those attendant complications that come downstream of that. Hugely important topic, really exciting developments now with better tools to treat those patients. But I think a bit of a already emerging care paradigm, that we have that we really, that we’re really knowing more and more what to do with that population. And what I’d really like to focus on is the millions of Americans who have prediabetes or maybe just a little bit overweight, who are at risk of having, those outcomes but aren’t there yet, where I think the terrain is a little bit less settled, maybe you’ll have something to say about that and really focus our attention there. So maybe just to start, you’re a wonderful writer and analyst of new developments in this field, and I recently read a great series you wrote on the state of prediabetes care in the US, and you pointed out big opportunities for improved care. So why don’t we just lay a little foundation for our guests?What is prediabetes, and what is the sort of benefit of recognizing it as its own entity? Robert Gabbay: Great. Thanks for asking that and so a number of years ago, prediabetes was defined as a subgroup of individuals that in essence, have a very high risk of developing diabetes. And the reason to identify those folks is there are things that could be done to help prevent them from moving from prediabetes to diabetes. Robert Rogers: Yeah, and just say, maybe say a little bit more about that. So prediabetes itself is a marker of some level of risk for poor health outcomes, but it also carries with it an attendant risk of progressing to diabetes. And could you say a little bit more about both of those risks and how we sort of think about their magnitude? Robert Gabbay: Yeah. No, absolutely. So first of all, just to give you the sense of numbers, and your listeners, so there are over ninety million people with prediabetes, so really a large part of the US population, and about thirty-eight million people with actual type two diabetes. And so what determines, first of all, someone with prediabetes moving to diabetes, so the state of prediabetes is a marker for having some typically some significant amount of resistance to insulin. And the development of diabetes, type two diabetes, takes two problems, being resistant to the effects of insulin and not being able to overproduce insulin to compensate. So these people with prediabetes already have the resistance, but they’re able to make a lot of extra insulin to keep their blood glucose normal, or in the case of prediabetes, a little bit above normal, and that’s the zone that puts them at risk. Turns out that having prediabetes in and of itself, and more specifically that resistance to insulin, insulin resistance, increases the risk of cardiovascular disease significantly. So it’s really a marker of high cardiovascular risk and at the same time, a marker for people that are at high risk for developing type two diabetes and all of the other complications that go with type two, like, eye disease, kidney disease, neuropathy, et cetera. Robert Rogers: Great. So that’s a really nice foundation, I think, to start for our listeners, and something that I’ve always thought interesting when I think about the challenge of diabetes and how we define it, is that metabolic health really does exist on a spectrum, and there’s a marker that clinicians use a lot, that’s, best thought of I think, as an average of your blood glucose level over a period of time, called the hemoglobin A1C. And it’s very hard for us to practice medicine without kind of hard definitions, so we have to choose specific cutoffs and say, “This person has prediabetes. This person has diabetes.” But the fact of the matter is that risk exists somewhat continuously along this along this spectrum. And so I think as we think about individualizing and personalizing care, it’s okay to share that level of nuance with patients. One thing I’d like to ask your opinion on is there is this famous project called the Diabetes Prevention Plan, something that you know very well, something that you’ve been involved in and it’s actually known to be quite effective. And maybe you could talk a little bit about what exactly it is but also why has it been so challenging for our healthcare system to implement it at scale? Robert Gabbay: Well, it’s an interesting story. So it started with a sponsored randomized controlled trial that asked the question: Can you prevent the development of type 2 diabetes? You can identify people at high risk with prediabetes, but is there anything you can do about it, or is it inevitable? People randomized to different interventions. One of them was a lifestyle program, and that reduced the risk of developing type 2 diabetes by sixty percent. Another arm looked at a drug, metformin, and that was only half as effective. So we have an intervention that can reduce the risk of developing diabetes by sixty percent, which is quite remarkable when you think of a lot of the other treatments that we use for prevention. That led to a lot of efforts by a number of individuals, and the Center for Disease Control and CMS, ultimately to have coverage for the diabetes prevention program. So Medicare covers a diabetes prevention program. A number of other commercial insurers cover it as well. So here’s an intervention that works, and it has coverage. And at the same time, with those over ninety million people with prediabetes that would be eligible, for being in this program, how many do you think have actually over the last… Oh, it’s been out there for oh, probably close to twenty years now, at least fifteen. How many people do you think out of those ninety million have gone through the program over those years? Robert Rogers: A very small percentage. I can imagine that much. If I was gonna guess a number, I’d say it’d be in the low millions. Robert Gabbay: Yeah, less than a million. Robert Rogers: Is that right? Yeah. Robert Gabbay: Wow. Yeah, despite all of the effort, and something that works, and it’s evidence-based and all of that. So the question is why, and there are probably a number of factors. Some of the sort of administrative challenges of being certified to deliver this program, are challenging. Reimbursement happens after you do it, and so small places, community health centers, which are probably the ideal place to do this because if you think about you need something that will be able to reach ninety million people. So that could happen in primary care or honestly, really probably best in a community environment, just to have the reach that one needs. It is a commitment, and it’s — it’s generally an in-person program. Robert Rogers: Just say a little bit, if you don’t mind, just say a little bit about the actual components of this of this intervention, just so people get a sense of how manageable or cumbersome it is. Robert Gabbay: Yeah. So there are a series of classes that occur, initially weekly and then, a bit less often. And part of the power of the program, is not to just do it with one individual, but to have that peer support, to have a group of people together that are learning together. It’s led by a facilitator that can be taught to do this. Doesn’t have to be in general, it’s not a physician. It may be a nurse, but it doesn’t need to be. It could be a community health worker, and there are programs to train individuals to do this. And so it’s a in large part, a weekly program, that guides individuals on the lifestyle changes and the things that worked. So what did they do in that diabetes prevention program that reduced the risk by

    34 min

  2. Jun 8

    Episode #6: Prevention and Early Intervention for Kidney Disease with Dr. Katherine Tuttle

    Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine podcast at the Foresight Medicine Substack where we are envisioning the future of preventive healthcare as a comprehensive whole body framework for leveraging new technology to maintain health as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties, and today we will be talking about the kidneys. I am very honored to have as my guest, Dr. Katherine Tuttle. Dr. Tuttle is professor of medicine in the Division of Nephrology at the University of Washington and Executive Director of Research at Providence Inland Northwest Health. She is one of today’s most prolific and impactful clinical and translational scientists in the area of kidney disease. She has led foundational research on the pathophysiology of diabetic kidney disease, and her work has been pivotal in establishing the current pillars of therapy for chronic kidney disease more broadly. Her work is broad, and it spans elucidating the mechanisms of those therapies, the clinical trials that have established their benefit, and the interrelationship between kidney disease and cardiovascular and overall health. She’s a leader in many of the major national and international organizations focused on kidney health that shape the practice of nephrology through guidelines and grant making. Listeners should note that we are recording this on Friday, May 22nd 2026, and this conversation is for general informational purposes only and does not constitute individual medical advice. Kathy, welcome. Thank you so much for joining me today. Katherine Tuttle: Well, it’s great to join you. Robert Rogers: So I’m really looking forward to this conversation, and on the Foresight Medicine project, we’re really going organ system by organ system, disease category by disease category, thinking about the future of preventive and proactive health. And for some of the diseases, the tools that we have both from a diagnostic and therapeutic standpoint are really exciting, but they’re almost somewhat aspirational. And I think one of the really cool things, and I think we’re gonna get into this today when it comes to kidney disease, is that of course, the tools in our toolbox are evolving and expanding, and you’re a major participant and leader in those efforts, but they’re actually already quite good in many ways. And so there’s this additional challenge of how can we deploy optimally what we already have. And so I’m really excited to get into both aspects of that. And so I guess I would just like to start out by saying how did you first become particularly interested among your interests in the early identification and prevention of chronic kidney disease? Katherine Tuttle: Well, thanks for that question, Rob because it really goes back a long time. And before I was a nephrologist, I actually did a fellowship in endocrinology and metabolism. And the focus was really on physiology, glucose metabolism, glucose regulation. And there were people who volunteered for these studies. These were the original insulin and glucose clamping studies done some 40 years ago. Mostly people with type 1 diabetes who would spend eight to 10 hours in a room with multiple lines and blood draws. And we had a machine called the Biostator, which was an artificial pancreas. Today, people wear it on their belt, but in those days, it filled an entire room. And when I was doing those experiments, I got to know the study participants really well. We didn’t have helpers then either. I mean, I was drawing the blood, processing the samples, and staying with the patient the entire time while running the Biostator. And I got to know them quite well. We were all about the same age in our late 20s, and it really stunned me one day when one of our study participants, this altruistic volunteer who signed up for these experiments with the hope that it would somehow help people, crashed into dialysis at Barnes Hospital. We didn’t see it coming. We weren’t even looking for kidney disease. We weren’t even thinking about it. We were focused on the physiology of glucose metabolism, really important. I’m still a physiologist. I still do preclinical research. But it occurred to me that we really need to get much more focused on solving problems that matter to patients, and not-- virtually nothing was being done about kidney disease and diabetes in the mid-1980s. We weren’t screening for albuminuria. We had maybe a serum creatinine, but no one knew what to do with it. And I realized that this was an enormous unmet need, and I just decided that something needed to be done about it. I wasn’t sure what I was going to do but I decided I would do something, and then I pivoted to nephrology and went on to train in nephrology. And then I’ve spent most of my career focused on trying to solve problems related to diabetes and the kidney. And thankfully, after decades of work and along with really an army of other people in the field, we now have truly transformative therapies, so I’m glad I’ve been here for the whole journey. Robert Rogers: I just want listeners to appreciate how unique it is to have fully trained in both endocrinology and in nephrology. But it clearly set you up very well because diabetes which we’ll get into is of course one of the major contributors to kidney disease. And so your own training and career trajectory kind of follows along. So I’d like to lay a little bit of foundation and help people understand the scope of the problem that we care about preventing or intervening upon when we talk about kidney disease. And I mentioned to a few friends who were kind enough to listen to this podcast that I was gonna be doing an episode on kidney disease and the first couple of comments that I got were like, “Oh yeah, ending up on dialysis is really terrible.” And that is of course true. When many people think of kidney disease, our minds immediately go to perhaps the most severe or extreme outcome, which is when your kidneys completely fail and you require dialysis or a transplant. And there’s several hundred thousand people in this country, I think about eight hundred thousand, who are currently on dialysis, tens of thousands more who live with a with a transplanted kidney. And so that is of course a problem of significant scope. But in some ways it’s really only the tip of the iceberg. And so maybe you could explain how is it that decrements in kidney function that are well short of complete loss, end-stage kidney disease, really are quite important, significant and a health burden? Katherine Tuttle: Oh, thanks for that question, Rob. I think it’s been the great under-recognized public health crisis, frankly. In fact, The Lancet published an updated global burden of disease study on CKD in November of twenty twenty-five, coincident with American Society of Nephrology’s Kidney Week with new estimates of the global burden of disease. They’re now estimating eight hundred million people worldwide, and half of it is attributable to diabetes, so some four hundred million people with diabetes and kidney disease in this world. The other thing, too, is they projected the death rate squarely attributable to kidney disease. In 2013, it was the nineteenth leading cause of death. By 2023, it’s now... It became the ninth leading cause of death. And if we don’t change the trajectory we’re on by 2040, they’re projecting it’ll be the fifth leading cause of death in the world. So it is an enormous public health problem. And I think that is really the issue. It’s the mortality associated with this. So nine out of ten people who develop chronic kidney disease, particularly if they have diabetes, will die on the road to kidney failure. And the people who make it to dialysis or transplant to the end of the line are a ragtag survivor bunch because of the enormous complications that are highly fatal, and these include cardiovascular complications. And yes, there’s a high burden of conventional cardiovascular risk factors, but it’s the kidney disease that really accelerates the risk. So if you have low kidney function and you spill protein in your urine, above and beyond diabetes, the risk of cardiovascular death is increased thirty, three zero, fold. We published those data over 15 years ago. And so I think people have not recognized how fatal this condition is. The next leading cause of death is infections due to impaired immune response associated with CKD. And the reason it matters is not just scary to statistics, and I imagine we’ll get to this but we now have therapies that reduce mortality, and mortality from both cardiovascular disease and infections in people with chronic kidney disease. So you’re right, it is the tip of the iceberg, and people are very sick, and many will die and never make it to dialysis. So we can say if you get to the point you need kidney replacement therapy, congratulations, you made it. Wow. Yeah. But then, life on dialysis is also very burdensome. And even today, let’s just talk about survival as the starting point. The median survival of a person with diabetes who initiates dialysis is two years, worse than most forms of bad cancer which we fear because of the death risk. So what I wanna call out is we need to recognize that this is a killer. It’s rising in prevalence, and it’s rising in importance of causes of death as we’ve done better with other causes of death at least historically reducing cardiovascular risk and risk from infections because we vaccinated people at least historically. Now what we have emerging is this other cause which has been left unaddressed. Robert Rogers: Yeah. And so in your very compelling answer there, you mentioned a couple of things that I really want us to take a deeper dive on. One is how now we have medicines that really do impact

    54 min
  3. Episode #5: Prevention of Autoimmune Diseases with Dr. Kevin Deane

    May 12

    Episode #5: Prevention of Autoimmune Diseases with Dr. Kevin Deane

    Foresight Medicine Episode #5 Prevention of autoimmune diseases If you enjoy this interview and want to learn more about the frontier of prevention for autoimmune disease, including how you can become involved in a study of prevention for rheumatoid arthritis, please visit the website of the Autoimmune Disease Prevention Center of the University of Colorado, directed by my guest, Dr. Kevin Deane: https://medschool.cuanschutz.edu/centers/adpc Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine Podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a comprehensive, whole-body framework for leveraging new technologies to maintain health for as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties. And today, we will be talking about autoimmune diseases. I’m very honored to have as our guest Dr. Kevin Deane. Dr. Deane is Professor of Medicine in the Division of Rheumatology at the University of Colorado. He is a leading researcher in the field of rheumatoid arthritis, where his many high-impact publications, bridging immunology, epidemiology, and clinical trials, have helped define the concept of preventing or intercepting rheumatoid arthritis and other autoimmune diseases before significant damage occurs. Dr. Deane was the principal investigator of the STOP-RA trial, a landmark rheumatoid arthritis interception study that tested whether treatment in high-risk individuals could prevent or delay the development of clinically apparent rheumatoid arthritis. And he’s a major contributor to guidelines on the identification, risk stratification, and management of people at high risk of rheumatoid arthritis. Listeners should note that we are recording this on Thursday, May 7th, 2026, and this conversation is for general informational purposes only, and does not constitute individual medical advice. Kevin, welcome. Thanks so much for joining me today. Really excited to be chatting with you. Kevin Deane: Great, Robert, thanks for the invitation, and happy to be here. Robert Rogers: So, you know, to kick things off here, this is one of the conversations that I’ve been most excited to have, because I feel like it’s one of the furthest out there frontiers for preventive healthcare. There’s a cadre of people who call themselves preventive cardiologists, preventive neurologists. I think there’s many primary care physicians and others who would consider themselves to be quite conversant in screening and early detection of cancer. But it’s not too many people who call themselves preventive rheumatologists, and I think you’re probably one of the leading people who might be able to change that. And so, first question I always just like to start off with is,how did you become interested in this field, in autoimmune disease and rheumatoid arthritis, but specifically this idea of early detection, intervention, and as you’ve termed it, interception? Kevin Deane: Good, good question. I think part of it was my own personal belief that I’d like to catch people before they get too sick. And I think that underpins a lot of my philosophy now and where I’ve gone with trying to help prevent rheumatoid arthritis. In a bunch of autoimmune diseases, in particular the rheumatic diseases, things like rheumatoid arthritis and lupus, we oftentimes wait until people get quite sick before we even see them for the first time in a rheumatologist’s office and initiate treatment. I got tired of seeing that. I thought, why can’t we get to these people earlier? There was another line of evidence, if you will, as I started my training about 20 years ago, that was coming to the forefront, where blood tests for our autoimmune diseases got a lot better, and in particular, a test came on the market, something called the anti-CCP antibody for rheumatoid arthritis, it was highly accurate for disease. That sort of acted as a game changer, because rheumatologists had a phrase, and they still do to some extent, oh, don’t just treat a lab test. And I get that, but when you have really good lab tests, it may indicate that somebody has not only got a disease now, or maybe at high risk for disease, that can change the game. So, and quick summary of that. My personal belief, let’s try and catch people before they get sick, and then some advances in the field where in rheumatic disease, we had really good blood-based biomarkers that could be predictive of future disease. That got me going down the pathway to prevention. I’ll add one other thing to that. Robert Rogers: That’s so super interesting about how the discovery and really the identification of the anti-CCP antibodies as a really powerful diagnostic tool really leveraged your career in this direction, because I sort of take for granted that blood test has existed. As long as I’ve practiced, it’s always something we send when we’re suspecting rheumatoid arthritis in the workup, but as you said, it really, really opened up this field in a very different way. Kevin Deane: Yeah. And the other line of evidence along those… For years, the disease entity type 1 diabetes has been working on early risk identification and prevention. They’re well ahead of us in, actually, rheumatic diseases, but they’ve been using autoantibodies that are related to type 1 diabetes for years, have had for years very good predictive models, but had really advanced their understanding of how you can use antibodies to predict future disease, about the same time I came along into the career of rheumatology, and I was working with people who had a foot in the epidemiology world of type 1 diabetes, and also knew about rheumatoid arthritis and other autoimmune diseases. So that coming together, the knowledge from type 1 diabetes really informed my thinking. And so those three lines of evidence, me wanting to prevent disease, the new tests in rheumatic diseases, and the work that had been done in type 1 diabetes, all those things came together. Robert Rogers: Yeah, there’s a couple of threads you mentioned there that I really want us to go with here, and I think it’s interesting that you’ve brought up early in our conversation, kind of comparing some autoimmune diseases, and as you mentioned, type 1 diabetes is perhaps, among all the autoimmune diseases, the one where the paradigm of prevention is the farthest advanced, in the sense that there’s actually an approved therapy, and I’ll just say briefly for our listeners, you know, for patients who are at have a family member who’ve had type 1 diabetes, and they have the antibodies that are highly suggestive they’re going to get it, there is actually a therapy that can delay the onset of them getting to the point where they actually have full-blown diabetes and need insulin. And you could imagine, especially for a mostly juvenile disease, when you’re dealing with children, being able to delay for a few years when they might need that level of intervention is hugely, hugely valuable. And I’m glad you brought up that comparison, because I don’t want us to go too deep on this right now, but, you know, when we say… when we think of, for example, preventive cardiology, right, we’re talking mostly about, say, coronary artery disease, atherosclerotic cardiovascular disease, and maybe a few other diseases now we can get into nowadays with the valves and stuff. But when we talk about autoimmune disease, I mean, it is so many diseases, right? I mean, medical textbooks will say there’s about 100 of them, and, you know, there’s probably 10 to 15 that constitute the vast majority of what you see in your clinical practice. And I don’t really want to spend a huge amount of time, because I think it’s a really complicated and time-consuming topic. People can do a little of their own self-education with their own LLM of choice, of sort of, you know, how we describe and classify and group together the many different autoimmune diseases. But since we are going to focus on rheumatoid arthritis, I’m just curious. where do you place RA? And we can… maybe we’ll start using that, introduce that abbreviation so people… we don’t have to keep saying all the time, RA. Where do you place RA in terms of the spectrum of autoimmune diseases, in terms of how preventable or intervenable it might be? Kevin Deane: So, yeah, as you state, there’s a bunch of autoimmune diseases. If you look at each one of them, they’re all, as an individual disease, pretty rare. Like, for example, rheumatoid arthritis affects about 1% of the population. Type 1 diabetes actually affects 1 in 300, so, quite rare, but still very impactful. Lupus is about 1 in 1,000. But when you lump them all together, about 1 in 6 people actually have an autoimmune disease. This is counting them all up. Thyroid disease, some of the things I talked about, RA, or lupus, or type 1 diabetes, you lump them all. So that’s a pretty substantial, substantial portion of the population has some form of autoimmune disease. At a very high level, autoimmune diseases are when your own immune system, which should normally help you fight infections, heal wounds, help clear cancers, goes bad, if I can use that term, and starts attacking you. They can either do it in a very targeted way, like, for example, type 1 diabetes, it attacks the cells in your pancreas that make insulin. Only those cells are attacked, but boy, when those are gone. you’re out of luck, because you don’t have any insulin, and you need insulin. Rheumatoid arthritis, on the other hand, is where your immune system attacks, as the name implies, your joints and causes arthritis. It can also affect other things, including the lung, but the joints are the primary target. Other diseases, such as lupus, can affect almost any organ in the body. Another one that’s a little

    52 min
  4. Episode #4: Screening for Pulmonary Fibrosis with Dr. Anna Podolanczuk

    May 12

    Episode #4: Screening for Pulmonary Fibrosis with Dr. Anna Podolanczuk

    Foresight Medicine Episode #4 Transcript Screening and early intervention for pulmonary fibrosis Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine Podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a systematic and whole-body framework for leveraging new technologies to maintain health for as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties. Today, we will be focusing on the lungs and interstitial lung disease and pulmonary fibrosis. I’m very honored to have as our guest today Dr. Ana Podolanczuk. Dr. Podolanczuk is Associate Professor of Medicine at Weill Cornell, and a nationally recognized expert in interstitial lung disease and pulmonary fibrosis.She is a pulmonologist, critical care physician, a major contributor to the current clinical trials landscape, testing new therapies in interstitial lung disease, and a leading investigator of the earliest detectable stages of this disease. And it is in that capacity that I am most excited to speak with her today. Her work spans imaging, biomarkers, environmental risk factors, and the broader question of how we might identify interstitial lung disease earlier at a stage where intervention could potentially alter outcomes. Anna, welcome. Listeners should note that we are recording this on Thursday, April 23rd, 2026, and as always, this conversation is for general informational purposes only and does not constitute individual medical advice. So, Anna, I’m really excited to have you on today, and one of the reasons is because in some previous episodes of Foresight Medicine, we have had discussions about diseases where there’s really a quite well-established paradigm for what preventive or early intervention care looks like. And when it comes to the lungs and the diseases we’re going to be talking about today, I don’t think there’s an established paradigm, but there’s people who are working on that, and you’re very much one of those. And so this is an exciting new frontier for us. And so, kind of the first question I want to just start out with, and it’s always my first question to our guests is, what inspired you to focus on this area of lung disease? How did you get here? But in the course of your answer, for our listeners, let’s just level set with a couple of important terms. When we say interstitial lung disease, what do we mean? And when we say pulmonary fibrosis, what do we mean? Anna Podolanczuk: Sure, thanks so much for having me, and this is something I feel very passionate about and happy to speak about it. So, let’s start with the definitions. When we’re talking about interstitial lung disease, we are talking about diseases of the lungs that affect the lung parenchyma, the little membranes in the alveoli, where gas exchange occurs. And so that separates those diseases. They’re separate from things like airways diseases, like asthma and COPD, or from vascular diseases like pulmonary hypertension. And so pulmonary fibrosis is a subset of interstitial lung diseases, where there is scarring of the lung interstitium, of the lung parenchyma. And so that makes it really hard for oxygen, to get into the body, and leads to progressive usually progressive symptoms, like shortness of breath and cough,and worsening quality of life for many of our patients. And so, really, it’s that presentation that inspired me to go into this field, because even when I was in medical training as a medical student, as a resident, we saw many patients with pulmonary fibrosis being admitted to the hospital, or I would see them sometimes in clinic, and the thing that inspires me to do what I do now, which is focusing on early detection, is that many of those patients used to present very late in their disease course, and usually by the time they presented to the hospital or to clinic, their disease was very, very advanced, and there was very little that we can do. The thing about pulmonary fibrosis or scarring in the lungs is that it’s not reversible. Or currently, with our current treatments, there’s nothing to reverse it. And so, that makes it very challenging to intervene and to improve quality of life. And so all we can do, if we can diagnose disease earlier, we can hopefully have the biggest impact for our patients in terms of actually improving their quality of life. Robert Rogers: I really like that answer, and there’s two threads in that answer that I want to pick up on. First is you started to already kind of lay the foundation for why we might be interested in early intervention and early detection of pulmonary fibrosis, because when patients present clinically and it’s quite advanced, their prognosis can be challenging. But also, in the course of your answer there, in explaining what interstitial lung disease is, for our listeners, I just want to explain why, among all lung diseases are we focusing on this in this episode of prevention. And I think it’s fair to say, you know, in a pulmonologist’s office, there’s many different diseases you see, but probably the single most common, right, are those diseases of the airways, asthma and COPD. And I think that we sort of have a preventive care paradigm for those airways diseases. For COPD, it is so much dominated by the risk factor of smoking. Really, prevention consists a lot of smoking cessation, and for asthma, asthma is very much a disease where the whole care paradigm is about preventing exacerbations. Another disease that we see a lot in the pulmonary clinic is when people have nodules on their lungs, and we’re concerned if they’re cancer or not. And we had an entire episode of that on episode 1 of this series, and I encourage our listeners to check that out. So I think interstitial lung disease is really, among the pulmonary diseases, one that’s really ripe for our discussion today. So, picking up on what you said there about how, you know, when patients with pulmonary fibrosis present to the hospital, or present clinically, it’s often quite advanced. Let’s just outline a little bit what are the current treatment options, because of course, the logic of intervening early depends very much on what treatments can we offer. Anna Podolanczuk: Yeah, for sure. And so, you know, just to add to a little bit to what you were saying, it’s absolutely right that airways, diseases, nodules, you know, those are common, and those are pretty, you know, significant diseases as well, but what makes pulmonary fibrosis so challenging is that they are some of the sickest patients that we see in pulmonary Clinic are those patients with pulmonary fibrosis. And one of the challenges in taking care of those patients is that treatment options are very limited. Like I said, there’s nothing that reverses lung fibrosis. There are currently, 3 approved, what we call, antifibrotic therapies. And all 3 of those therapies slow disease progression. But they don’t even stop it from progressing. They, you know, at best, they slow the disease, the decline in lung function over time. They have limited efficacy. They don’t make anybody feel better. Two of those drugs have been around since 2014, and the latest drug, was just approved, a few months ago, and all of those drugs have side effects. The newer one has fewer than the older ones, but they all have, you know, they’re challenges with tolerability for patients, they’re difficult to take, they’re pills you have to take every day, and there’s not even a good way of knowing if they’re working, because most patients at some point are going to progress with or without therapy, they just progress a little bit slower without those drugs. And so the only other treatment that we often discuss with patients is lung transplantation, right? And so pulmonary fibrosis is actually the leading indication for lung transplantation. And it’s because it’s such a severe disease with so few treatment options. But lung transplantation is not a cure. Takes care of their fibrosis, when successful, but you’re trading one disease for a set of complications, including the risk of rejection, the risk of infection, and so there’s challenges. And then other things that we use to help patients feel better are things like supplemental oxygen, but again, those are, you know, comes with a quality of life, challenge where patients have to lug oxygen around. It may help them feel better, but it also significantly impacts how they feel and function in the world. And so, it’s just very challenging and we’re constantly doing clinical trials and research to find better treatments for patients, but so far, we have very limited options. Robert Rogers: Yeah, and let’s just double-click a little bit more on those antifibrotic agents, because as you’ve pointed out, they are far from perfect, they are not cures for the disease, they are not medicines that reverse the disease. But they do slow the progression of the disease, but they do that at the cost of certain side effects. And maybe just talk a little bit about, with the current standard of care, how you see the benefits of slowing the disease down versus the side effects you see the patients incurring. Anna Podolanczuk: Yeah, so it’s always a balance, and whenever I see a new patient with a new diagnosis of pulmonary fibrosis, we spend a lot of time talking about those risks and the benefits of when to start therapy. The antifibrotic therapies all have significant gastrointestinal side effects, and so many of them can cause diarrhea, nausea, stomach cramping, weight loss, poor appetite. Again, the newer drug is a little bit better, but none of them are perfect. And so for many patients, they don’t want to start therapy if they’re feeling okay when they still have very early disease. But the challenge there is that if you’re going

    48 min
  5. Episode #3: Prevention and Early Intervention in Parkinson's Disease with Dr. Ray Dorsey

    Mar 31

    Episode #3: Prevention and Early Intervention in Parkinson's Disease with Dr. Ray Dorsey

    Edited Transcript of Foresight Medicine Episode #3 on Prevention and Early Intervention in Parkinson’s Disease with Dr. Ray Dorsey Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine Podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a systematic and whole-body framework for leveraging new technologies to maintain health for as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties. Today, we will be discussing Parkinson’s disease. I am very honored to have as our guest Dr. Ray Dorsey. Dr. Dorsey is Director of the Center for the Brain and Environment at the Atria Health and Research Institute, and part-time professor of neurology at the University of Rochester Medical Center. He is a leading Parkinson’s clinician and researcher with numerous very impactful publications that span the fields of epidemiology, clinical trials of Parkinson’s, as well as Huntington’s disease, and he has pioneered new models of care delivery and clinical trial implementation for neurological diseases. He has shaped our understanding of the growing global burden of Parkinson’s disease, including the concept of a Parkinson’s pandemic and has been a prominent voice in highlighting the role of environmental exposures as targets for prevention. He’s the co-author of two highly acclaimed books on these subjects, Ending Parkinson’s Disease and The Parkinson’s Plan, A New Path to Prevention and Treatment. Listeners should note that we are recording this on Tuesday, March 24th, 2026, and this conversation is for general information purposes only and does not constitute individual medical advice. Ray, welcome. I’m really excited for our conversation. Thank you so much for joining me today. Ray Dorsey: Many thanks for having me, Robert. Delighted to be with you. Robert Rogers: Great. So, in the next 40 minutes or so, I want to cover a lot of ground about the frontiers of prevention and early intervention and detection in Parkinson’s disease, but I’d like to spend the first few minutes laying a little bit of a foundation for our listeners, both about Parkinson’s disease, but also just briefly about you. The question I always start off with is, what drew you to study and take care of patients with Parkinson’s? Ray Dorsey: So both my parents were psychiatrists, so I like to say I rebelled and I became a neurologist. And, during the course of my medical training, as you know, you spend time in different settings, and once we made it to the clinics. I had a wonderful grandmother, and I enjoy being around older people, and got to care for people with Parkinson’s disease, it’s very clinical in its orientation, a lot of it’s based on listening and observation, and you can make people better. And so, I thought that would be a great combination and something that mastered a lot of my interests, and I think I chose wisely. Robert Rogers: I would certainly say so, based on the impact you’re having in the field. We’re going to talk about preventing Parkinson’s, but I want us to make sure we understand what is this terrible disease that we care about preventing in the first place. So, say a patient comes into your office for the first time, and sadly you have to deliver them the news that, yes, they indeed do have Parkinson’s. How do you explain, based on what our current textbook model or understanding is of what is Parkinson’s disease? What is its pathophysiology, its symptoms, and its prognosis? Ray Dorsey: Classically, Parkinson’s disease is a neurological disorder that produces at least two of the following four symptoms. One is a tremor, usually in the hands, usually asymmetric, usually at rest. Second is, slowness of movement takes people longer to do almost everything. Third is stiffness or rigidity, and fourth is difficulties with a balance or a gait. When Dr. Parkinson first described the condition in 1817, he said, I’m describing something that’s not been classified in the medical literature, something that’s not in the medical textbooks of the time, he described 6 individuals with this disease based on just casually observing half the people on the streets of London. Two centuries later, it’s estimated that 6 million people had the disease. So you went from something affecting 6 people on the streets of London that wasn’t part of the medical textbooks to one that’s the world’s fastest-growing disease affecting 6 million people around the world. And it begs the question, why? And we know that our genes don’t change that much in that period of time. We know that it’s growing faster than aging alone can explain, and growing far faster than other age-related diseases, like stroke and Alzheimer’s disease, they really lead you to the conclusion that Parkinson’s disease is being fueled by… not by changes in our DNA, not by things that are going inside of us, but things that are going outside of us in our environment. Chemicals in our food, including certain pesticides, water, including dry cleaning and degreasing chemicals. And outdoor air pollution are likely responsible for the astronomical rise of this disease. Robert Rogers: That’s super interesting about how, you know, it was only 200 years ago that the disease became prominent enough to really make it onto the radar, and here we are with a Parkinson’s pandemic. And I’d like to double-click on that, and maybe just take us a little bit deeper into how how we go about studying and identifying what it is in the environment that is driving the increase in Parkinson’s disease. Ray Dorsey: Yeah, so it’s, it’s, it’s hard, So, since you’re a pulmonologist, do you know how they determined that smoking was linked to lung cancer? Robert Rogers: You, you, go, go ahead, you’ll, you’ll teach, you’ll teach me and our audience. Ray Dorsey: In the late 1800s in Europe, lung cancer starts emerging, and lung cancer was extraordinarily rare. And the German pathologists, being German, said, did we miss this? So they went back to their cadavers and, you know, looked at the lungs more carefully and see if they were missing occult or hidden malignancies, and there wasn’t any. And they were wondering what was causing it. In the U.S, it was so rare in 1900. That was considered a once-in-a-lifetime oddity. All that doctors and medical students would gather around when they saw a case of lung cancer, thinking they would never see one again. But lung cancer kept getting more and more common in the early 1900s, and in Britain, they were wondering what was going on. Some people thought, was this a delayed effect of exposure to gases from World War I? Other people, including a physician, Richard Dahl, thought it was due to asphalt that was being, poured to pave the way for roads in early 20th century England, and then some people thought it was due to these new things, cigarettes, that had been recently introduced into Europe and then the US around 1900. And so Richard Dahl and his friend Bradford Hill, a statistician did something called the British Doctor Study. They mailed postcards to all the British physicians, I think they might have been all men, and asked them, do you smoke? Yes or no? And if you smoke, how much do you smoke? And then they, sat around and waited. They waited for all the doctors to die. And then they looked at those who died from lung cancer and those who died from other causes, and it turned out that those who died from lung cancer were 30 times more likely to smoke cigarettes than those who, than people who didn’t. Ergo, smoking is as strongly as associated with, lung cancer. But Bradford Hill was bothered by this. He said, boy, I have an association, how do I know it’s a causation? Maybe all smokers really enjoy drinking coffee, and maybe it’s coffee that’s causing lung cancer. So, Bradford Hill put forth nine criteria by which you could go from an association to a causation. I can’t give you them all, but one is, like, the strength of a relationship. Is this a small, small thing or a large effect size? Is this been replicated? Does the exposure happen before the disease? Do people smoke the cigarette before they get lung cancer as opposed to getting lung cancer, which might make them more prone to smoke. Is there a dose-response relationship? Is the more exposure to the toxicant, the chemical, the exposure, more cigarette smoking associated with a greater risk of the disease? Is this biologically plausible? Does this make sense? Are there animal models that are consistent with this? Can we, reason by means of analogy? You go through all those criteria, and smoking, you know, checks a lot of those boxes. Well, it turns out that my colleagues have applied those same criteria to some of the environmental risk factors linked to Parkinson’s disease. Chief among them is a weed killer called Paraquat.Over 70 countries have banned it because it’s been used to commit homicide and suicide, and it’s associated with a 150% increased risk of Parkinson’s disease among farmers who use it, associated with a 100% increased risk of Parkinson’s among people who simply live or work near where it’s sprayed, and in the laboratory reproduces the features of the disease. You’re starting to check off a lot of the Bradford Hill criteria, and they pointed out that it largely did check off these. So I think we have lots and lots of evidence for some of these toxicants. For some, we have much less, and quite frankly, I think the fact that we have much less is an indictment of science, indictment of scientists, and indictment of funders. I’ve never been on rounds where we saw a patient who had lung cancer who smoked, where we talked about the genetics, the genetic… underlying genetic predisposition that led this smoker to get lung cancer. H

    42 min
  6. Episode #2: The present and future of genomic screening with Dr. Michael Murray

    Feb 18

    Episode #2: The present and future of genomic screening with Dr. Michael Murray

    Foresight Medicine Episode #2 Transcript Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a systematic and whole-body framework for leveraging new technologies to maintain health for as long as possible. In this podcast series, I interview leading experts at the forefront of prevention and early intervention across medical specialties. I am very honored to have as my guest today Dr. Michael Murray. Dr. Murray is Professor of Medicine at the Icahn School of Medicine at Mount Sinai, where he is Chief of the Division of Genomic Medicine and Clinical Director of the Institute for Genomic Health. He is a foremost expert in and a true pioneer of the field of genomic screening and integrating the burgeoning science of genomics into actual clinical practice. In addition to being a leading researcher in applied genomics, he has shaped the field as an architect of genomic education for medical professionals, journal editor, a key contributor to task force guidelines and policy statements in the area of genomic medicine, and as founding director of Mount Sinai’s Genomic Health Clinic. I also want to add that Dr. Murray is the senior author of a beautiful review of this topic, entitled DNA-Based Population Screening for Adults, published January 27th in the New England Journal of Medicine Evidence, which frames the topic we are discussing today, and I encourage all of our listeners to read it, and hopefully our conversation can lead to even greater understanding of this topic. Listeners should note that we are recording this on Wednesday, February 11th, 2026, and this conversation is for general information purposes only and does not constitute individual medical advice. Michael, welcome, really excited to have you on and to be talking with you today. So, one of the many reasons I’m very, excited to chat with you and have you as a very early guest in this podcast series is that the goal of this whole project is really to envision the future of preventive health across different organ systems and categories of disease. And I believe that advances in genomic screening are the foundation of this whole enterprise. It’s really the general-purpose technology that’s opening up new opportunities to identify disease risk at a personalized level. So, let’s start with a pretty general question. What is genomic screening, or as you’ve recently termed it, DNA-based population screening for adults, and how did you get drawn to the field? Michael Murray: Yeah, so, so we’re trying to get people to adopt, the term DNAPS, D-N-A-P-S, just because saying the longer things is a mouthful. But, I got interested in screening, in, the early 2000s. I had left, internal medicine infectious disease practice to become a, a geneticist and refocus my career, and I was at Brigham and Women’s Hospital, and taking care of adults, with rare genetic disorders, but particularly interested in, in bringing the information we were learning to the, to the greater population. And at that point, it was, it was theoretical. There were a few companies that launched in the early 2000s, Navigenics and, 23andMe, and they were starting to, to think about this from a business perspective, but it was really the ClinSeq project at the NIH in 2007-2008, led by Les Biesecker, that was the first to, to do this at scale. They came out with a paper showing that they were identifying cases of BRCA in patients that had no no personal or family history, that would go along with that, and, got very interested in their paper, and left Harvard a couple years later to go to a cornfield in Pennsylvania, where Geisinger Health System is, to really, launch a large-scale project in screening. Robert Rogers: Very interesting on multiple levels, including how you, early on, saw the power of this field and sort of reoriented your career. Just for our listeners, BRCA is a gene that confers increased risk for multiple cancers, and something that actually has come up on another one of our podcasts when we talk about multi-cancer early detection. So. Nowadays, that’s… it’s actually quite striking to think that these key efforts that enabled this new field are only about 15 to 20 years old. But nowadays, when somebody thinks about DNA-based population screening, tell us what… what are the tests? What is the tests that are available? What is the actual information, the genes and the variants that they contain? Michael Murray: So, there’s a couple different technical processes that can be used to create the dataset for an individual. The two, most common are what’s called a whole exome sequence, or a whole genome sequence. And the reason why, projects are deciding one versus the other is still mostly around cost. A whole genome sequence gives you all the information in between the genes. You have 20,000 genes, and they only make up about 1-2% of all the data. Everything else is in between the genes, and a lot of that is regulatory information, regulating the genes to turn on, turn off. Turn up, turn down. And so with, with an exome, or a whole exome, you can just get the 1% to 2% that has the gene data, which is where most of current efforts are focused. You can do the whole, genome and get all the data, but right now, you basically ignore 98 or so percent of that data, just because we don’t know what to do with it. Robert Rogers: And, at your own clinic, can you tell us a little bit about what’s actually offered? Michael Murray: Sure, so, so at the Genomic Health Clinic, we, we have people that come in, sometimes referred by providers for an indication, meaning that, you know, they, they have a family member with a genetic problem, and they want to be tested for it. So we call that, diagnostic care or indicated care. Others come in for screening. They, some are, very educated about it. You know, we have scientists and geneticists that come in, and doctors, and others just have this correct notion that they could learn more about their health risks if somebody looked at their DNA and screened it for common risks. So, we… the most common test we do there is called, well, it’s a 163 gene panel. I mentioned that we have 20,000, and it just picks out 163 genes that are the ones we know the most about, and that we can do something with the information if we find a problem. So, about 80% of those 163 genes are either for cancer risk or heart disease risk. That’s really where we have the biggest area of knowledge. And then the third category is just miscellaneous. There’s a number of different, conditions that we know enough about to look for a problem and then address it if we, if we find a problem. Robert Rogers: Yeah, so I really want to double-click on that, because I think that’s so interesting. As you said, there are about 20,000 human genes, and the report that a patient gets back, or that someone who’s interested in screening gets back, contains information on 163 of them. So, could you say a little bit more about the criteria that are used to determine if a gene and a variant should be included in the report to patients? Michael Murray: Yeah, so the, you know, the, the data, that can be generated through these processes, doesn’t change. This is called our germline data, so it’s different than some of the other conversations you’re having about, about cancer genes that have, have a mutation. So this is the germline data in an individual, and that can be looked at to see if there is a disease-associated or a pathogenic change that can be recognized within the code of the gene of interest. So, I’ll borrow the, explanation from my genetic counselor, who gives a great, description of what we do. So, a gene is like a paragraph of, letters, and what we do is go through and do a spell check, and we might find a change that changes the meaning or breaks the function of the gene. Or we might find a benign change, meaning, the example I always give is, like, spelling the word gray, G-R-A-Y, versus G-R-E-Y. It’s a different spelling, but it sounds the same and it means the same thing. We’ve got lots of those changes in our genes, and it’s the ones that actually break the function of the gene that we’re interested in. Because then we can predict the risk that’s associated with not having that gene function. Robert Rogers: Right, so there’s at least two important elements, it sounds like, to deciding the genes that comprise the test. One is being able to assess the pathogenicity of a given variant, and another is how actionable, or not actionable that is. And, let’s… talk a little bit more about both of those aspects. So, first of all, in terms of determining the significance or the pathogenicity of a variant. So, the DNA sequencing machine, it reads all the letters of someone’s DNA, but then to determine if that is relevant to health or associated with the disease, we need to have a system for describing that variant, and you’ve written a lot about this. Can you describe a little bit about the system that’s used to grade variants in terms of being benign or pathogenic? Michael Murray: Yeah, so in, about 15 years ago, there were a number of diagnostic labs, and they had their own internal databases that they used, and sort of one of the reasons to use one lab versus another is whoever had the most data about what were the problematic changes in a particular gene. So you had… you had labs built just to look at one gene, and they were the experts in that. As the data set started growing and the interest started growing, it was recognized that there needed to be a common repository for that information. So, rules were set up on what causes a change to be pathogenic, or likely pathogenic, so disease associated. What information you need to categorize something as benign or likely benign, so just, a incidental ch

    1h 11m
  7. Episode #1: Multi-Cancer Early Detection with Dr. Betsy O'Donnell

    Feb 18

    Episode #1: Multi-Cancer Early Detection with Dr. Betsy O'Donnell

    Foresight Medicine Episode #1 Transcript The present and future of multi-cancer early detection with Dr. Betsy O’Donnell Robert Rogers: I’m Robert Rogers, host of the Foresight Medicine Podcast at the Foresight Medicine Substack, where we are envisioning the future of preventive healthcare as a systematic, comprehensive, and whole body framework for leveraging new and emerging technologies to maintain health for as long as possible. In this podcast series I interview leading experts at the forefront of prevention and early intervention across medical specialties. I am very honored to have as our guest today Dr. Betsy O’Donnell. Dr. O’Donnell is Associate Professor of Medicine at Harvard Medical School. She’s an oncologist and a clinician and researcher who’s making big contributions across multiple fields, including multiple myeloma, nutrition, and exercise for cancer survivors. And in recent years, in the burgeoning field of multi cancer early detection. And it is in that capacity that I am most excited to speak with her today. She’s the director of the Multi Cancer Early Detection Clinic at Dana-Farber Cancer Institute, and an innovative thought leader in this field. Betsy. Welcome. Listeners should note that we are recording this on Monday, January 26th, 2026. This is a field with new data being published all the time, and this episode will not air for a few weeks. So if we say something that becomes slightly outdated, we’ll note that in the show notes, but the audio will stand and this conversation is for general information purposes only, and does not constitute individual. Medical advice. Throughout this conversation, you’ll hear us use the word MED, spelled MCED, which is an abbreviation for multi cancer early detection. Robert Rogers: So Betsy, thank you. I’m really excited to have this conversation. Thanks so much for coming on today. Betsy O’Donnell: Thank you so much for having me. It’s truly fun to get to talk about this and, and really go back and forth about such an exciting topic. Robert Rogers: For our listeners, I’ll just give them a little bit of a guide to this conversation where I’d like to take it. In the next 45 minutes or so, we’re gonna do a little bit of a, the sandwich technique. So we’re gonna end with our destination being some of the really new and exciting stuff that’s at the forefront of this exciting field of multi cancer early detection, the data that’s driving the field, what you see coming down the pipeline. But before we get there, I want us to build a little bit of a foundation in understanding the principles of cancer screening and early detection, early intervention. But I would like us to start out with understanding what it is that, that, that we’re gonna really be talking about today. So tell us what is multi cancer early detection, and how did you get interested in, drawn to this field. Betsy O’Donnell: Absolutely. So multi cancer early detection is really an evolving field, trying to think of means by which we can screen for multiple cancers at once. So if we start with what is the state of cancer screening currently? So right now the United States Preventive Task Force Service recommends screening for breast cancer, colorectal cancer, cervical cancer and lung cancer in smokers. So that’s four cancers. But we know that about 70% of the cancers that are diagnosed don’t have screening tests. And so multi cancer early detection is really aimed at trying to find cancer screening tests that can screen for many of the cancers that don’t currently have existing screening tests with a goal of finding more cancers earlier. And one of the challenges - there are many challenges to cancer screening, but one of the important ones is. As we think about screening and the number needed to screen to find a cancer, the more rare it is, the harder it is to justify screening thousand, a thousand patients to find one cancer if you’re that primary care doctor. And not only that, we don’t have good modalities to find those cancers, but if we aggregate cancers into one test. We need to screen fewer people to find a cancer. And the major goal of multi cancer early detection testing again, is to think about novel ways to find more cancers, but also to find them earlier. And so there are a lot of different ways in which people are exploring early cancer detection. I focus primarily on blood-based screening, and the reason I do this is for multiple reasons actually. One, I think most patients are accepting of blood tests as something they’re willing to do. And also they really offer the ability to be done anywhere, any point of care, location. And one of the major goals that I have when I think about the work that I do in multi cancer early detection, is not only. Bettering cancer screening, but making it more accessible. So when I think about multi cancer early detection tests, I’m thinking about it not only for finding more cancers early, but thinking about how that can affect the population and how we can better medical care nationally, potentially globally, um, through enhancing access. You asked me how I became interested in this. So, Robert Rogers: and lemme lemme just say for, for our listeners, you, said that your focus within multi cancer early detection is on blood-based tests. And, implicit in that is in contrast to these whole body imaging approaches, which are another modality. Let’s put a pin in that because that is a, an interesting kind of side story to the, to the MCED [Multi Cancer Early Detection] world, which maybe we’ll get into maybe how that could be combined with blood tests at the end. But I’d love to hear a little bit about your personal history and interest getting into the field. Betsy O’Donnell: Thank you so definitely put a pin. So as a person in general, I’m a very proactive person. I think most of us in our, in our lives are always thinking ahead, um, trying to figure out what we can do to achieve our goals or to prevent things from happening that we don’t wanna have happen. Oncology in general has been primarily been a reactive field. So a lot of that is history. There’s history and so much of what we do in medicine. But you know, I think about when I started my career in 2001, I was a clinical research coordinator at Dana-Farber, and that was really at the start of targeted therapy. All of the cancer therapies that we had historically really targeted the cell cycle, mitosis, cell division, and we had a limited number of chemotherapies that we combined to try to increase the efficacy, but using all of those same drugs in different cancers. And what’s happened over the past two decades is this dramatic revolution of cancer therapies, targeted therapies, small molecule inhibitors, CAR T cells, bispecific, T-cell engagers. I could go on and on. And what we’ve done is we’ve become much better at treating cancers and keeping people alive with cancer, but we really haven’t got it at the front end of the problem, which is finding cancer when it’s earliest, when it can be cut out, when it can be treated, look as a localized process, and that’s when it’s most curable. And so I worked as the director of inpatient operations at MGHI was very involved in just thinking about how we can operate most efficiently. And as you recall, in 2020, you know, the world was shut down by COVID. And what that did to the hospital that you and I were both at, is we had to allocate most of our resources to treating patients with COVID, which meant we stopped doing elective procedures, things like colonoscopies. We put them on hold so we could manage the pandemic. The original publication, the Pathfinder publication of Grail’s Galleri test was presented ASCO in 2021. And this was at a time where our hospital was really trying to get back in action, trying to get back on its feet. But things like, because we had stopped doing elective colonoscopies, there was a backlog. And it was just tremendously challenging in the healthcare system to just get fundamental things done, like colonoscopies for patients who needed them. And so when I first heard about the data. From the Galleri study, which is a multi cancer early detection test. What really excited me as someone who is doing operations, who’s someone who’s forward looking, who someone believes in preventive medicine, is this is something that could be, you know, a win across multiple fronts. We can find cancer early, we can find multiple types of cancer, but maybe also we can mitigate the burden on the healthcare system. And what do I mean by that? I mean that we can keep patients out of chairs. It’s great. That we can treat cancers for longer, but that’s not what people want, and that’s not what the healthcare system needs. We need cure. And so that keeps people out of chairs, that minimizes the burden of resources needed, like blood products, like experts to give these novel therapies. And then also just the economic cost of ongoing cancer care for these very expensive but miraculous drugs. So not only did I think it was a twofer, I thought it was a lot more than that. This idea. That cancer screening could address a very specific problem, but have a lot of downstream impact on the entire operation of medicine. Particularly excited me. Robert Rogers: Wow. That’s, that’s great. Well, we definitely can hear the passion in how you describe it, and I think that’s sets up, the rest of our conversation really well. So I think when you mentioned how there are guideline recommended single organ cancer screening tests, and I think most people are basically familiar with the concept of how those work, what you’re looking for in a mammogram, what they’re looking for in a colonoscopy. Let’s talk a little bit about what the actual tests are when we talk about multi cancer early detection. Generally speaking, the idea here is that cancer cells are

    55 min
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