Feel Better, Live More with Dr Rangan Chatterjee - The Science of Longevity: Why Healthspan Matters More Than Lifespan with Dr Peter Attia #356

Episode Date: April 25, 2023

No one would argue that smoking is a killer. And no doctor would wait until a patient was showing early signs of cancer or heart disease before advising them to quit. Yet this is one of the few health scenarios where early prevention is given the evidence-based weight it deserves. Today’s guest believes that needs to change. Dr Peter Attia is a medical doctor, a longevity expert and author of the brand new book Outlive: The Science and Art of Longevity. He gained his medical degree at Stanford University, trained in general surgery at Johns Hopkins Hospital, and was a surgical oncology fellow at the US National Cancer Institute. He’s also on the editorial board for the journal Aging and host of The Drive podcast, which covers health, medicine, and longevity. Peter is not interested in reaching unheard-of age milestones or hitting birthdays in triple figures – unless he can do it with full vitality. He believes our focus needs to be on the quality of life we’re living; our healthspan rather than our lifespan. We talk about the evolution of medicine and we discuss the limitations of current practice. Peter calls this ‘medicine 2.0’ and describes it as adept at dealing with ‘fast death' from trauma and infection. But it’s failing to counter our declining life expectancy or deal with the prevalence of chronic disease. Peter shares what he calls the ‘four horsemen’ of the health apocalypse – namely the 4 disease states, that will end up taking most of our lives: atherosclerosis, cancer, neurodegenerative diseases and metabolic dysfunction. Our objective, he says, should be to die ‘with’ disease, not ‘of’ disease and a huge part of Peter’s philosophy is about aggressively taking action to delay the onset of these four horsemen. But, to do that, we will need to take a different approach, which Peter calls, ‘medicine 3.0’. In our wide-ranging conversation, Peter shares which investigations and tests he thinks we should all be doing and he explains why when it comes to longevity, exercise is the most important area to focus on.  We also discuss the vital importance of emotional health and, Peter talks openly about his own struggles with extreme perfectionism and shares some of the tools that he uses daily to help. I loved having the opportunity to connect with Peter during this in-depth and enlightening chat. I hope you enjoy listening. Support the podcast and enjoy Ad-Free episodes. Try FREE for 7 days on Apple Podcasts https://apple.co/feelbetterlivemore. For other podcast platforms go to https://fblm.supercast.com. Thanks to our sponsors: https://www.boncharge.com/livemore https://www.athleticgreens.com/livemore https://www.vivobarefoot.com/livemore Show notes https://drchatterjee.com/356 DISCLAIMER: The content in the podcast and on this webpage is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your doctor or qualified healthcare provider. Never disregard professional medical advice or delay in seeking it because of something you have heard on the podcast or on my website.

These three things doubled human life expectancy in a very short period of time. One was the scientific method. The second thing was the development of the light microscope. The third piece of that was the development of antibiotics. We went from about a life expectancy of 40 to 80 inside of a generation and a half. Today, we're at a point where not only has life expectancy flattened, but in many parts of the developed world, it's actually declining a little bit. And more importantly, quality at the end of life is going down. The question is why?

Hey guys, how you doing? Hope you're having a good week so far. My name is Dr. Rangan Chatterjee, and this is my podcast, Feel Better, Live More. No one would argue that smoking is a killer, and no doctor would wait until the patient was showing early signs of cancer or heart disease before advising them to quit. Yet this is one of the very few health scenarios where early prevention is given the evidence-based weight it deserves. Today's guest believes that needs to change. Dr. Peter Atiyah is a medical doctor, a longevity expert, and author of the brand new book, Outlive, the science and art of longevity. Peter gained his medical degree at Stanford University,

trained in general surgery at Johns Hopkins Hospital, and was a surgical oncology fellow at the US National Cancer Institute. He's also on the editorial board for the journal Aging and host of the Drive podcast, which covers health, medicine, and longevity. Now, Peter is not someone who's interested in reaching unheard-of age milestones or hitting birthdays in triple figures, unless he can do it with full vitality. He believes our focus needs to be on the quality of life we're living, our health span, rather than our lifespan. lifespan. We begin our conversation by talking about the evolution of medicine without being critical of doctors who are all trying to do their best with the models they have been taught. We discuss the limitations of current practice. Peter calls this medicine 2.0 and describes it as adept at dealing with what he calls fast death from trauma and infection,

adept at dealing with what he calls fast death from trauma and infection, but it's failing to counter our declining life expectancy or deal with the prevalence of chronic disease. Peter shares what he calls the four horsemen of the health apocalypse, namely the four disease states that will end up taking most of our lives. Atherosclerosis, cancer, neurodegenerative disease, and metabolic dysfunction. Our objective, he says, should be to die with disease, not off disease. And a huge part of Peter's philosophy is about aggressively taking action to delay the onset of these four horsemen. But to do that, we will need to take a different approach, which Peter calls Medicine 3.0. In our wide-ranging conversation, Peter shares what investigations and tests he thinks we should all be doing. He explains why when it comes to longevity, exercise is the most important area to focus on, and we discuss the important but often underappreciated idea of

context and payoff. What is the cost of your health habit, and do the sums add up? If exercising to extremes causes an injury that puts you out of action for months, was it worth it? If meditation or food prep robs you of quality time spent with loved ones, is that the best choice to make? Of course, Peter and I cannot answer those questions for you, but nonetheless, they are very important questions that we would all benefit from asking ourselves regularly. We also discussed one of my big passions, the vital importance of emotional health. And Peter talks openly about his own struggles with extreme perfectionism and shares some of the tools that he uses daily to help. This really was a fascinating conversation.

Peter is someone who has a very analytical mind and he uses it to take a practical and logical approach to health and wellbeing. I very much enjoyed speaking to him. I hope you enjoyed listening. And now, my conversation with Dr. Peter Atiyah. I wanted to start, Peter, by thinking about our general approach to health and well-being. So if we think about your patient population and we think about

health and longevity, where is it that you see many of us going wrong? Well, I think of it more through the lens of the medical system than perhaps individual physicians. medical system than perhaps individual physicians. And I sort of described this as medicine 2.0, which is the current system that we're in. And medicine 2.0 is obviously something that would have followed medicine 1.0, or I wouldn't have called it that. And it's been a remarkably successful evolution in medicine. And it really solved the jugular problem that our species faced for most of our existence. And that was the problem of fast death. So historically, we have died from things that killed us quickly. And that's namely trauma and infections. And again, we collectively take this for granted today.

But as you know, and anyone who's sort of studied the problem realizes, you know, human life expectancy was relatively short, you know, shy of 40 years up until about 150 years ago. And again, that was largely the result of having very few tools, if any, to cope with trauma and infection or communicable diseases to be more broad. So something really fundamental happened to shift medicine from this 1.0 to 2.0 about 150 years ago, roughly. And it was largely sort of three things. One was a new way of thinking. And that new way of thinking was the scientific method, you know, really proposed initially in the late 17th century. I write a little bit about that. But it was this idea that

diseases were not caused by the gods and things like that, but were actually caused by things that existed in the world. And obviously in terms of infectious diseases, that was microscopic organism. The second thing then was the development of the light microscope. This is something that actually Sid Mukherjee has written about very eloquently in his most recent book, The Cell, where he kind of talks about what a pivotal moment that is in medicine when finally scientists and physicians were able to, with their own eyes, see some of these microscopic agents. Then of course, the third piece of that was developing treatments to combat those things. So the development of antibiotics and later on vaccines.

So again, these three things basically doubled human life expectancy in a very short period of time. We went from about a life expectancy of 40 to 80 inside of a generation and a half. But here's where we are today. Today, we're at a point where not only has life expectancy flattened, but in many parts of the developed world, it's actually declining a little bit. expectancy flattened, but in many parts of the developed world, it's actually declining a little bit. And the question is why, right? Why is it that life expectancy isn't going up? If anything, it's slightly going down. And more importantly, quality at the end of life is going down. And so it's a long answer to a very simple question you asked, but I think it frames the problem, right? Which is, what should we do about this individually? There is no physician who's out there on the front lines,

who's taking care of patients, who doesn't appreciate that the problem is not that we don't have better drugs to lower blood pressure or better drugs to lower cholesterol. We do have all of those things, but we're not really in a system that allows us to use those things correctly. And I think the physician also understands that while at a high level, the obvious things are still obvious. For example, it's important to maintain a normal weight, not to have type 2 diabetes, to be exercising, to sleep well. They don't have the training to inform how to do that for a patient. So let me kind of give you a glib example.

Think about how long it takes to become a medical oncologist. So if you finish medical school, at least in the United States, that would be a five or six year postgraduate fellowship after medical school. Now, a person walking down the street who's never gone to medical school knows that a cancer patient needs chemotherapy. They, you know, they have some sense that if you have, you know, metastatic colon cancer or breast cancer, you probably need chemotherapy. But of course, the person walking down the street has no idea what chemotherapy they need or how many cycles, how many courses, where it should be placed in proximity to surgery, radiation, what biomarkers you would track of that patient as they go into remission and hopefully remain there. That's why the medical

oncologist needs five or six years of training to do that. And now think about the fact that every doctor knows exercise is valuable, but how many of them know your VO2 max? How many of them know how many watts you can produce at your aerobic threshold? How many of them know how strong you are, what your appendicular lean mass index is, how you should train to improve those variables, which by the way, have a greater bearing on your lifespan and healthspan than any other factor we are aware of, inclusive of the absence of or presence of diabetes, hypertension, renal disease, or even smoking. It's a very backward situation if you

view it through such a stark lens. The physician truly has no training in how to, at a granular, nuanced, and individual level, help their patient with nutrition, sleep, exercise, or stress. Yet these things are clearly the most important determinants of our length and quality of life. Yeah, it's fascinating. There has been, I think, a growing movement. You call it Medicine 3.0. In my first book, I called it Progressive Medicine. There's a movement in the UK called Lifestyle Medicine. And I think really all of these different movements are in their own way trying to challenge the status quo and go, wow, listen, we kind of need to update things. We need to improve the tools that we have, think about

our education differently. And what's really interesting in what you said there, Peter, is one of the pushbacks often tends to be, well, just tell patients to eat better and exercise more and sleep more. Yeah, that's obvious. Any good healthcare professional would already be doing that. And I disagree. A, I don't think any good healthcare professional is doing it for a variety of reasons, including the bias we have in our training towards a particular style of medicine. But as you've just pointed out with something just like exercise alone, there's so much nuance, isn't there, into the type of exercise, the intensity of exercise. What exactly are you exercising for? In the book, you made the case that exercise may well be the most potent longevity intervention that exists.

Number one, do you still stand by that since you pressed print and the manuscript went off to the publishers? And if so, why do you put that right at the top? The answer to the first question is very simple. Yes, I certainly do. And the answer to the second question is also quite simple, which is it really is not a matter of opinion. It is simply a matter of the data. The data make it abundantly clear. I kind of alluded to this a moment ago, but maybe for the sake of the audience, we can explain what a hazard ratio is a number that communicates the relative risk of one condition relative to another. So, for example, the hazard ratio associated with all-cause mortality for a smoker versus a non-smoker is about 1.4. And so, statistically, what that means is a smoker is about 40% more likely to die in any given year than a non-smoker, all other things being equal. That's what the 1.4 means.

And, you know, if we were to look at something, some intervention, I'm making this up, but, you know, drinking a certain type of tea, if that had a hazard ratio of 0.91, we would say that that intervention is associated with a 9% relative reduction in risk. If the hazard ratio is one, it means there's no difference. Okay. So that's the math on hazard ratios. So when you look at the hazard ratios associated with all-cause mortality, and of course, all-cause mortality is the gold standard of thinking about lifespan. We're going to talk about healthspan in a moment, but we'll just bracket this on lifespan. Let's consider the known things that rob people of lifespan. Type 2 diabetes, high blood pressure, coronary artery disease, smoking, end-stage renal disease. Those would

be the big ones. What are the hazard ratios associated with each of those conditions? Well, at one end of the spectrum, you'd see hypertension has a hazard ratio of about 1.2. It's about a 20% increase in all-cause mortality, meaning you're 20% more likely in any year to die than someone who's otherwise equal without hypertension. Smoking, as I said, is about 1.4, 1.41. Coronary artery disease, about 1.3. Type 2 diabetes, about the same. End-stage renal disease, about 2.75, somewhere between 1.75 and 2.75. So anywhere from a 75% to 175% increase.

So anywhere from a 75 to 175% increase. But now when you do the same analysis based on different metrics of cardio, respiratory fitness, strength, and muscle mass, the numbers are simply bigger and they're bigger by a lot. So for example, when you look at comparing the VO2 max of somebody in the bottom 25% of the population for their age and sex. So meaning someone in the bottom quarter of their age and sex in terms of maximal oxygen uptake, which is a test that we can readily do on people. It's a measure of peak aerobic capacity. And you compare that to someone in the top 2% of the same age and sex, the hazard ratio is five,

slightly over five, meaning it's a 400% difference in all-cause mortality. In fact, if you just go from being in the bottom 25th percentile to being slightly above average from the 50th to 75th percentile, the hazard ratio difference is 2.75, meaning it's even more significant than having end-stage renal disease. I could go through this analysis all day long and I could do the same thing for muscle mass and I could do the same thing for strength. But across the board, the difference in all-cause mortality is significantly wider when it comes to measures of strength and fitness than it is for any disease condition we

know. And so the corollary of all of this is, by definition, whatever it is you have to do to have that higher VO2 max, greater muscle mass, and greater strength must be hands down the most potent thing we have at our disposal to live longer. And of course, the only way one can have those things is through the right type of exercise. Yeah, I really appreciate how you broke that down, Peter. Very, very clear. I definitely want to dive in here, but let's just clear up a couple of things before we do. You mentioned healthspan and lifespan. I wonder if you could explain exactly what you mean by them. And then I think it would be useful to talk about your four horsemen, because I think

it's such a beautiful concept for people to get their heads around the kind of core philosophy behind your approach. I think it would be quite useful to start here, if that's okay. think it would be quite useful to start here if that's okay. Sure. So the word longevity is kind of a shorthand word that people sort of loosely have an idea what it means, but it's also a word that's been largely bastardized by a sort of, you know, shady collection of people who prey on the fears of, you know, people who are afraid of one of the most frightening things we experience, which is the fear of dying. So I generally don't love the word longevity, despite the fact that it's part of the subtitle of the book. But I use it because, again, it has such an obvious shorthand for what we're talking about.

But if we want to be more technical, what we're really talking about with longevity is two vectors. One is the lifespan vector, and one is the healthspan vector. Now the lifespan vector is the more, you know, call it objective, easier to understand binary, digital, whatever word you want to use, it's on or off. You are either alive or you are dead. And there are certainly going to be some gray areas around brain death, but for the most part, people have a clear understanding of what it means to be respiring versus not. And so, you know, your a Silicon Valley ethos around extending lifespan to, you know, magical numbers. We're going to, everybody's going to live to 150 or 200. And, um, you know, the reality of it is I just think that that's not only far-fetched, um, but,

but I don't think it's really what most people are interested in. I think what most people are interested in, even if they can't articulate it, is the other side of the equation, which is the healthspan side, which is the quality of life piece. I alluded to this earlier. This is the piece that Medicine 2.0 is failing in dramatically. So not only is Medicine 2.0 failing to add much years to lifespan beyond what's already been done, but we're doing so at the great expense of healthspan. And healthspan is harder to explain because it's more nuanced. First of all, I think there are

three components to it, but it's also analog. It's not binary. It's not on or off. It's relative. And it declines in slow, perceptible ways. And at times it declines very quickly. For example, a person that suffers a devastating injury would experience a dramatic reduction in one of the three areas of health span, which is the physical component, right? The body, the exoskeleton. There's also a cognitive piece and an emotional piece. And then further complicating all of this is that two of those three are heavily age dependent, the physical and the cognitive, while the third, the emotional bucket, is actually not age-dependent very much at all. In fact, sometimes we get wiser with age to enhance our emotional health. I mean,

we'll definitely get to emotional health, but I really appreciate you outlining that. How does these four horsemen fit into this conversation around healthspan versus lifespan? So when you want to think about the lifespan side of this equation, it seems only logical that one must have a great understanding of what the impediments are to lifespan. In other words, what takes our life away? And for a non-smoker, this can be pretty easily distilled into the big four. And the big four are the diseases of atherosclerosis, and the big four are the diseases of atherosclerosis. So cardiovascular and cerebrovascular disease, far and away number one, followed by cancer. Of course, as you and your audience know, cancer is not just one disease of cancer of the breast is different from cancer of the colon, but collectively all of cancer. Number three is neurodegenerative disease and related dementias.

So neurodegenerative disease includes Alzheimer's disease, Lewy body dementia, Parkinson's disease, and it also includes other types of dementia, such as vascular dementia, frontotemporal lobe dementia, and things like that nature. And then the fourth horseman is not so much on the list because of the number of lives that it directly takes, but because of the number of lives that it directly takes, but because of the number of lives that it indirectly takes. And that's less a disease and more of a spectrum. The spectrum ranging from insulin resistance and NAFLD or non-alcoholic fatty liver disease, all the way to type two diabetes. It's basically what we think of as the metabolic diseases, which again,

It's basically what we think of as the metabolic diseases, which again, in terms of how often those diseases show up on the death certificate as the proximate cause of death is not that large. We're talking about in the United States, maybe 100,000 or so. I would imagine in the UK, slightly less. But it's how those things amplify the risk of the other three horsemen by typically about twofold. So what we really want to be careful of is understanding that when you have type two diabetes, non-alcoholic fatty liver disease, insulin resistance, your risk of cancer, neurodegenerative disease, and heart disease goes up significantly. And so by understanding everything we can about the four horsemen, we have a chance to delay their onset. And that's really the objective here.

I don't think we are in a situation, barring science fiction, to completely eliminate the horsemen. Certainly, some of these diseases seem somewhat inevitable to our species. Cancer, for example, at the end of the day, is ultimately a tug of war between acquired genetic mutations that alter cellular properties and the ability of our immune system to detect them and evade them. But we can certainly delay these, and we have great proof already that that happens and the proof exists in the long-lived people the so-called centenarians people who live already to the age of 100 or more and we know from studying these people that their superpower is not living longer with the four horsemen. It's living longer without the

four horsemen. Once they come down with the same diseases as the rest of us, the time it takes for them to die is about the same. It's that they get the diseases about two decades later than everybody else. And that's what we have to figure out. Yeah, super interesting. That's else. And that's what we have to figure out. Yeah, super interesting. That's really quite something for us to reflect on that these super centenarians, once they get the same problems that we get, the time to death is pretty similar. It's just trying to delay that. So coming back to the problems with the medical system, the way it's set up, the way we're trained, the way many of us are still practicing, we get involved very, very late. We diagnose type 2 diabetes at some theoretical point that we have defined. For many years, I've been teaching doctors in the UK saying, listen guys, we're still reporting an HbA1c. We have slightly different cutoffs to you guys. So we have 6.5,

yes, as the cutoff for type 2 diabetes, but we call pre-diabetes here from 5.7, where I believe you guys start at 6. But nonetheless, a lot of the time, we're reporting these suboptimal blood sugar levels as normal. And the way it works in the NHS, typically here, the National Health Service, is what will often happen is that you will get your bloods drawn and you will often be told, if you don't hear from us, everything is okay. Now, first of all, that is unsatisfactory on a number of levels. A, it's such a big juggernaut of a system. Things go wrong. Things get missed all the time. So I would always say to my patients, phone up, make sure you've got your result. Make sure someone has said something about that result.

Just don't rely on the fact that nothing's come in the post, so you're okay. But the wider point is that even many doctors are not getting involved with their patient or not taking preemptive action until it's quite far advanced. You know, type 2 diabetes, Alzheimer's, you know, dementia, for example. You know, Dale Bredesen will say that that condition maybe starts in the brain maybe 30 years before you actually get a diagnosis, for example. And so from your perspective, Peter, I know you have quite a bespoke and very targeted practice. You know, what are the things that we should be looking out for? What are the things that we can all start looking at in ourselves to make sure that we're not waiting until these diseases have set in and we've got advanced end-stage disease? What are these key things that maybe we're walking around

with, but we're not aware of them? Well, it certainly varies by disease, but let's take the clearest example of where prevention is unmistakably able to get us to the point where we would be far more likely to die with a disease rather than from it. And that's the ultimate goal, right? So, you know, I'm sure you've shared this with many of your male patients. I mean, any man who lives long enough will die with prostate cancer, but some will die from it, right? But most men do not die from it. They die with it. And so the most broad example of that from a disease perspective is atherosclerosis. Everybody has it to some extent. The goal is to not die as a result of it, not to die of a major

adverse cardiac event, a heart attack, a stroke. So what would be required to delay the onset of atherosclerosis? Something that I argue is probably somewhat inevitable to our species. Well, again, this is where understanding your opponent matters. Now, heart disease, it turns out atherosclerosis, we have a great understanding of its pathogenesis. And we know that while genes play a significant role, those genes play a significant role often through the modification of the following pathways, lipid-related pathways, blood pressure-related pathways, endothelial dysfunction-related pathways. So what are the big risks for heart disease? What are the big risks for heart disease? Smoking, high blood pressure, elevated ApoB,

and metabolic disorders. So the most extreme example being type 2 diabetes, but again, any dysregulation of glucose and insulin is going to be amplifying the risk of type 2 diabetes, pardon me, of cardiovascular disease. So how can we take that information and act on it so that we delay its onset by two decades? Well, this comes down to how you view the world through the lens of prevention. So I can't speak to how it's done in the UK, but I can tell you that in the United States, we tend to view things through a time horizon of about five to 10 years. through a time horizon of about five to 10 years. So we use risk calculators. The risk calculators incorporate information such as your family history, whether you smoke or not, what your lipids look like, your blood pressure, things of that nature. Sometimes they even incorporate information such as a calcium score and they spit out probabilities. They say the probability of you having a major adverse cardiac event, so heart attack, stroke,

death, in the next five years or in the next 10 years is X percent. And the consensus view here in the United States is you do not need to treat a patient for primary prevention unless that number is above some threshold, typically 5%. So if you're talking to a 39-year-old patient, by definition, it is mathematically impossible for them to have a five or 10-year risk above 5%. In fact, most of the risk models don't even allow a calculation if age is below 40. In my case, that was the case. I first began to pay attention to this 15 years ago when I was 35 and there were no risk models. So basically no one would consider having treated me preventatively, even though my family history

was significant. I even had a speck of calcium on my calcium score, which is a symbol of late atherosclerosis. My view is that that's completely backwards logic. It's backwards for two reasons. The first is the time horizon is completely wrong. Yes, it's true that if someone's 10-year risk is high, we need to act dramatically. But to wait until a person's 10-year risk is high is tantamount to driving a car towards the edge of the cliff and telling the driver, you're only allowed to hit the brakes when you actually see the edge of the cliff. As opposed to telling the driver, I can't quite see the edge of the cliff. As opposed to telling the driver, I can't quite see the edge of the cliff now, but I know that there is an edge there.

Let's slow the car down. But the second reason to me is even more frustrating. And I think if I'm going to be critical of the medical establishment in one regard, it's going to be this, which is there's often a failure to appreciate the implication of causality. And causality is a complicated topic because it's so often confounded with correlation and association. But I'll spare the listener kind of all of the details because I write about it at some length. But there is no ambiguity about the causality of ApoB and its effect on atherosclerosis. I don't know how much your listeners are familiar with ApoB and if it's worth explaining what that is. Yeah, Peter, I was going to ask you,

so please do expand because it's also not a test that the NHS offer people in the UK either. So not only is it, I know very well, a very powerful, if not the most powerful predictor, but at the same time, it's something that people, unless they pay privately here, which is a very different model, really don't have access to. So yeah, please do explain. Just taking a quick break to give a shout out to AG1, one of the sponsors of today's show. Now, if you're looking for something at this time of year to kickstart your health, I'd highly recommend that you consider AG1. AG1 has been in my own life for over five years now. It's a science-driven daily health drink with over 70 essential nutrients to support your overall health. It contains vitamin C and zinc, which helps support a healthy immune system, something that

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and five free travel packs with their first order. But until the end of January, they are doubling the five free travel packs to 10. And these packs are perfect for keeping in your backpack, office or car. If you want to take advantage of this limited time offer, all you have to do is go to drinkag1.com forward slash live more. That's drinkag1.com forward slash live more. Okay. Well, the good news is, first of all, it's a very inexpensive test.

Even in the United States with our grossly and disgustingly elevated costs that are artificially inflated, even in the United States, the ApoB test is only on the order of about 20, somewhere between 12 and $25. So I would imagine that in the UK, even if one were to pay out of pocket, we're talking about a test that probably would cost less than, you know, 10 pounds. But putting that aside for a moment, a poor man's substitute for ApoB, which I assume the NHS would cover, would be non-HDL cholesterol. Yeah. Is that something that would be readily available to anybody? Yeah. So non-HDL cholesterol is a poor man's surrogate for ApoB, but what ApoB is,

it's a protein that's wrapped around all of the particles that cause atherosclerosis, of which the most common is the low-density lipoprotein or LDL. And by measuring the ApoB concentration, you are directly measuring the concentration, i.e. the number of particles per unit volume of all the lipoproteins, the LDLs, the VLDLs, IDLs, LP little a's that cause atherosclerosis. And that turns out to be the most powerful predictor of any lipid or lipoprotein as it pertains to cardiovascular disease. And what you want is for that number to be as low as possible. In formal logic, we would describe ApoB as necessary but not sufficient for atherosclerosis.

So you need it to get atherosclerosis, but by itself, it's not sufficient to cause atherosclerosis, which means that there are some people walking around with very high levels of ApoB who do not go on to develop atherosclerosis. But you can't get atherosclerosis without it. on to develop atherosclerosis, but you can't get atherosclerosis without it. So we've established through epidemiologic studies, primary prevention studies, meaning the treatment of people who don't yet have cardiovascular disease, secondary prevention studies, the treatment of people with cardiovascular disease, and Mendelian randomization, perhaps the most powerful of them all. We can explain that if people want in a moment, but I don't

think it's germane. We've established through all of these different levels of evidence that low-density lipoprotein, or ApoB, is causally related to atherosclerosis. This is so important. Again, I don't think there are many doctors worth their salt that would not acknowledge that. So now the question becomes, why would we not reduce dramatically at an early age, the level of this lipoprotein? And I would use an example that I've used before. I think I use it in the book of smoking. And I would use an example that I've used before. I think I use it in the book of smoking. Everybody knows that smoking is causally related to lung cancer, meaning it's not just an association that we see a tenfold higher prevalence of lung cancer in smokers. And by the way, it doesn't

mean that every smoker will get lung cancer or every person who has lung cancer was a smoker. And by the way, it doesn't mean that every smoker will get lung cancer or every person who has lung cancer was a smoker. Neither of those things are true, but neither of those things diminish the causal relationship between smoking and lung cancer. And because we know that smoking is causally related to lung cancer, we take a very simple preventive strategy, which is we tell people out of the gate, do not smoke. And if you do smoke, stop right away. Can you imagine if we used models to predict the likelihood of people getting lung cancer and

waiting until the probability of that event was 10% and then saying, well, listen, Johnny, your risk of lung cancer is now 10%. It's time to stop. Or let's wait until on the chest CT, we see calcified lesions in your lungs that are suspicious for cancer. Now it's time to stop. Or let's wait until on the chest CT, we see calcified lesions in your lungs that are suspicious for cancer. Now it's time to stop. Of course not. Once you've established causality, you remove the causative agent. And yet we don't take that approach in treating atherosclerosis, which is why atherosclerosis is the leading cause of death globally. 19 million people die every year from atherosclerosis. Number two is a distant second, cancer, 11 to 12 million per year. Atherosclerosis not only shouldn't be the leading cause of death, it shouldn't even be in the top 10

based on the tools we have to delay its onset significantly. Yeah, I really appreciate the analogy to smoking. I think it makes it really clear how backward, short-sighted, frustrating, limited our approach currently is to how we look at these things. What's really interesting is that you mentioned APOB, and it's necessary, but not sufficient in and of itself. Of course, there's all kinds of other things. I'm guessing inflammation, immune dysfunction, all kinds of sort of ingredients to put into the mix, really, to combust things up where you actually end up having the atherosclerosis. But you also mentioned you want to bring ApoB down as much as possible,

the lower the better. Now, what's interesting about that for me when I hear that is most things in life, I would say there's upsides and there's downsides, right? And often we just look at the upside and we negate or we fail to take into consideration what is the downside here. So let's say ApoB, let's say we've measured it and it's higher than we would want. And let's say the patient is of a reasonably high risk. I guess you would say by definition, having a high APOB puts them in a risk category of sorts. The question then is, how aggressively do you decide to lower it? What therapeutic intervention do you use to lower it? And then just to add on there, Peter, is

to lower it. And then just to add on there, Peter, is we're talking about these four horsemen that end up bringing life to a close early, right? Atherosclerosis, cancer, neurodegenerative disease, and I think poor metabolic health. It's an ever-evolving scenario where you are aggressively attacking one horseman to bring your risk down of that one that's then inadvertently increasing your risk of one of the other horsemen. Yeah, there is. And I think staying on this example, let's use two examples. So we know that aggressive use of a class of lipid-lowering agents called statins has a small but non-zero risk of increasing insulin resistance in some individuals. on a statin, so a dose like resuvastatin, metorvastatin, things like that, you reduce their ApoB, which is the desired outcome, but you get an undesirable side effect, which is

glucose levels and insulin levels go up. And you are pushing them now further towards the risk side of the spectrum on the metabolic health plane. Well, that's a problem, right? Because to your point, if you're solving one problem and creating another, that's a problem, right? Because to your point, if you're solving one problem and creating another, that's a suboptimal solution. So we have to look for optimal solutions. Now, the good news is where we are today, we have so many tools for reducing ApoB that don't come with those side effects. Now, the good news is most people, and it's hard to quantify this, but it seems to be in the neighborhood of about 90 to 94% of people have no measurable, discernible, subjective, or objective side effects to statins, meaning

they don't have muscle pain, they don't experience elevations in transaminases, they don't have insulin sensitivity issues or anything, but let's just say 10% of people do. We have PCSK9 inhibitors. We have ezetimibe. We have bempendoic acid. These are drugs that really don't seem to come with any side effects. Sometimes when I look at the mechanism of action of a statin, I'm surprised the side effects aren't higher because of where it acts in the inhibition of cholesterol synthesis and how it does so ubiquitously in the body. But when you look at how these other drugs work, and we don't, I think, need to go into

the mechanisms of each of those. I do cover that very briefly in the book. It's intuitive that the mechanism of action of those drugs matches the clinical experience, which is basically virtually nobody has any side effects to these other drugs. They're much cleaner drugs than a statin, if we can use that lingo. So yes, the goal is to get ApoB as low as possible. We'll talk about how low that is. But you have to be able to do that without creating another problem. And I think,

you know, 15 years ago, 20 years ago, that was a much harder proposition than it is today. Before we go further, Peter, just on that point, which I think is a beautiful illustration of some of the kind of upsides and downsides that have to be weighed up. If we move away from pharmaceutical medication for just a moment, and we look at these four horsemen and go, okay, what do we know that is probably playing a role in all of them? Most of them, chronic unresolved inflammation would probably be something that most people would agree on is one of those core root causes that are going to increase the likelihood of each of those four. So therefore, if we can adopt certain lifestyle behaviors that help us to lower chronic

inflammation, then those lifestyle changes are likely to aggressively start to reduce our risk of all four of those. We're probably not having to weigh up lowering risk of one and increasing risk of another. First of all, I wonder if you agree with that perspective or whether you have a slightly different perspective. And then following on from that, is it only typically when we're bringing in foreign agents, let's say a pharmaceutical drug, that these considerations of improvement here, problem here, start to become an issue? Because you mentioned statins, and of course statins are known for some to impair negatively mitochondrial function. Then you write about, beautifully in the exercise section of the book, about the importance of

mitochondrial function for a whole variety of different reasons, which hopefully we'll get to during this conversation. It's kind of these upsides, downsides, upsides, downsides. That appears for many people, if they're listening to this, trying to take ownership of their health. And I know your book's going to help them sort of walk them through this and try to figure out how they do this. It kind of comes across maybe as, man, is this confusing? Am I going to reduce my risk of atherosclerosis, but at the same time increase my risk of type 2 diabetes? So how would you help us kind of, how would you help the general public you know look at these problems and what can they actually you know practically do to sort of manage this risk for themselves if at all they can all right so i think the first question was is the problem of whack-a-mole

where you lower the risk of one only to potentially amplify the risk of another is that a problem we only see in pharmaceuticals and the answer is unfortunately, no. In fact, that's a general problem of life. There is no scenario that I am aware of by which you can take an action that addresses one issue that does not potentially have an impact on another. So let's take two lifestyle examples, quote unquote, lifestyle examples, where you have a clear positive impact in one arena and a clear negative impact in another. The first would be fasting. Okay. So let's just be more, you know, let's just talk about caloric restriction, extreme caloric restriction. So there's only two interventions in the entire literature of geroscience that have

reproducibly extended life in virtually every model organism across which they've been tested. One of those is caloric restriction. When you calorie restrict an organism in a laboratory environment, it generally lives longer. There are some caveats, organism in a laboratory environment, it generally lives longer. There are some caveats, but as a general rule, you calorie restrict mice, rodents, flies, worms, everything. They just tend to live longer. Do we believe calorie restricting humans to 30% of their required caloric intake?

So a person who would normally need 2,500 calories per day, you're going to knock 30 percent of those calories off day in and day out. Do we believe that that is a net positive in their life? And the answer is it is probably not. Because while you will have undoubtedly reduced their risk of diabetes and metabolic disease, and probably by extension, reduced their risk of cancer and maybe heart disease in the process. Less clear on the neurodegenerative side, by the way. You have undoubtedly, and this has been demonstrated in animal models, increased their susceptibility to trauma and infectious diseases. In fact, those people are very likely

to end up in a case of sarcopenia. They're far more susceptible to one of the other great horsemen that doesn't quite rise to the level of being the big four, but it's a very close number five, and that is accidental death, which is virtually entirely dominated by falling once you reach the age of 65. So these are individuals who lack muscle mass, who lack bone mineral density, and the mortality from a hip fracture or pelvic fracture when you reach the age of 65 approaches 30% in the first 12 months. So you solve one problem, you create another. And that's, again, just dealing with something that's as beneficial potentially as caloric restriction.

Let's take another example. If an individual goes from never exercising at all to exercising to an extreme level, they might get injured, right? So they're going to accrue lots of cardiovascular and muscular benefits of exercise. Let's say they take on a very aggressive regimen where they're running an hour a day and lifting weights for two hours a day. There's an enormous benefit to that. But if they injure themselves, and I mean a bad injury, they damage a disc in their back that ultimately requires a two-level fusion. Well, that's going to have a terrible outcome on the duration of their life, not necessarily in terms of how long it is,

but in terms of the quality of life and the pain that they're in. So I just want to make sure that everybody understands that everything we're talking about has a trade-off, and that's why we have to be nuanced, and we have to apply the right tool at the right time. And I think what, you know, what I tend to bristle against is the idea that we would individually or collectively view tools as binary goods or bads, right? You know, and I get this question all the time, of course, I'm sure you do, which is, are statins good or bad? You know, is metformin good or bad? And it's sort of like, that's the wrong question, right? That's like asking a carpenter, is a hammer good or bad? Is a screwdriver good

or bad? Well, it depends what you're using it for. And it depends if you know how to use it. If you try to take a hammer to a Phillips screw, that's a suboptimal use case. If you try to take a Phillips screwdriver to a nail, that's a suboptimal use case. If you try to take a Phillips screwdriver to a nail, that's a suboptimal use case. So we have to get away from kind of what I call paint by numbers into sophisticated, nuanced approaches to pharmacology, exercise, nutrition, sleep, etc. I think that's one of the things I've loved about your book the most is that it isn't a prescription for optimal aging. It's not, if you do the Peter Atiyah plan, you will live to this age or whatever it might be. It's much more nuanced. It's much more aligned with, I think, the philosophy I have as a doctor,

which is different things work for different people. It is very hard to give generic guidelines that work for absolutely everyone. And I think what your book does beautifully is it helps people think differently about their life, about the choices they make. That idea that there's nothing good or bad, really, it depends on the context, I think is, it sort of applies, as you say, to everything in life beyond health. But even if we just stick to health for a minute, as you were explaining those examples of caloric restriction or over-exercising, you know, good sides, bad sides, I was thinking about, okay, what's neutral here? Okay, improving our sleep is probably neutral. Then I thought, well, hold on a minute. What about if you're working hard and the cost of switching off in the evening and going to bed early so that you can get your sleep hours in

to reduce your risk of A, B, and C, if that means that you don't get to spend quality time with your partner because of that, then sure, on one hand, you might be getting more sleep. But on the other hand, you are potentially impacting a really important relationship. And I know that seems like quite an extreme place to go. But I think it has validity. I think everything in life, what we choose, we could be doing something else with that time. And it's something that I think it has validity. I think everything in life, what we choose, we could be doing something else with that time. And it's something that I think a lot of people who are really focused on biohacking and health optimization, I think really need to understand, yeah, but that's another part to life as well. And are you missing out on that? I think I've been guilty of

this at various times in my life for sure. What about walking though, Peter? Walking. at various times in my life, for sure. What about walking though, Peter? Walking, where's the downside? I mean, I guess you could apply what I just said to sleeping to walking, but let's put it like this. In your heads right now, are there any generic health recommendations

you can make to people without knowing their personal history? Yeah, I mean, I think the most obvious ones would certainly be around exercise, adequate sleep, and adequate protein consumption. I mean, I think those are three almost across the board recommendations that can be made. Now, what adequate means will differ for different people. So for me, the amount of exercise that I now need, given my training history, right, I've been exercising, you know, my entire life. So for me to receive what we would call the training effect requires me to do quite a bit. Whereas a person

who doesn't exercise only requires about three hours a week to get an even greater benefit than I'm probably getting incrementally going from say nine hours a week to 12 hours a week if I were to make a change of that magnitude. So the details still matter, but exercise really has shown no upper bound in terms of benefit, at least through the lens of strength, muscle mass, and most importantly, cardiorespiratory fitness. There does not appear to be an upper bound of benefit, but that doesn't mean there isn't an upper bound to what you do in the pursuit of those things, using your example, in terms of time and opportunity cost, and also using injury as a risk. I mean, I do have a patient

who was just hell bent on getting 20,000 steps a day. This became like this person's mission in life. Well, until they developed an injury in their foot from walking so much, because it turns out their mechanics and their shoes weren't really optimally suited for what they were doing. So in pursuit of something that was clearly beneficial, they actually created a little bit of a problem. You made another good point that I think is really worth emphasizing, which is, you know, this biohacking movement, which I've certainly been accused of being a leader of, I think has a couple of problems. And one of them is certainly the failure to appreciate the opportunity cost argument. Now,

many people who partake in sort of the elaborate aspects of biohacking say, look, I don't care about the cost. It's a worthwhile trade-off to me if there's potential upside. But what they're often discounting is the opportunity cost of time. And that's something for which we are all equal, right? We might be disparate in our economic means by which we can pursue crazy ideas, but we're completely equal in that we all have 168 hours in the week. And so to give you one example, I had a patient who said, look, week. And so to give you one example, I had a patient who said, look, I'm really thinking about getting into hyperbaric oxygen. And he gave me all his reasons for it. And I said, well, let's just be clear. None of the data on this topic suggests it's remotely viable for what you're

interested in. There are indications for hyperbaric oxygen, but if your indication is zero protection cognitive enhancement, I've reviewed that literature 10 ways to Sunday, and there appears to be absolutely zero benefit. And he said, well, that might be true, but even if there's a chance it works, I think I want to pursue it. And I said, okay, how far is the chamber from your house? 30 minutes. Okay. You have to sit in the chamber for an hour, six a week that's right and then 30 minutes back okay that's 12 hours a week you're putting into something but i'm telling you has a very low chance of succeeding and you're acknowledging that by the way why not put that time into

something that is demonstrated to succeed, right? Taking that 12 hours and saying, I'm going to spend six of those hours exercising. I'm going to spend, you know, three of those hours socially with people who matter to me, building relationships with my kids or my spouse. I'm going to spend three of those hours out in nature walking. Like, you know, just using that as an example. So this is where I think we have to be very cautious about, you know, sort of taking the shotgun approach to biohacking, because it does come at a cost that is, the

financial cost is the lowest cost, by the way. Yeah, I think it's a great point. And that approach I think is important for people of all income levels, actually. I read about this in my last book a little bit about time. And just to briefly summarize this case that I wrote about, Peter, I was in a practice, an NHS practice in an area of very low socioeconomic status, a lot of low income, a lot of poverty. And there was someone who was coming in, there's all kinds of issues which I was trying to help him with. And he was struggling for time. And he was saying, look, I don't have time to do this. I'm busy, I'm doing this. But when we actually figured it all out and actually went through how he spent his time when he was not at work, he was doing things like going for three or

four shops a week to different shops to save money. He was driving, I think, 20 minutes out of town to get cheaper petrol. And in the context of everything, I won't go through the whole story, but essentially, we figured out that actually he was saving very little money, but spending about four hours a week for that. And so we came up with a, like a four week challenge say, okay, for these four weeks, instead of saving that, and I appreciate that money's tight. And he agreed to this. It wasn't me sort of cajoling him into doing something he didn't want to do. I said, with that time saving, you could go for a walk. You could spend time with your kids. You could do all kinds of other things. And I kid you not, Peter, that one change literally over the course of six to 12 months started to transform his health because he suddenly realized, wait a minute, everything in

life has a cost. And actually the cost of actually just going to the petrol pump down the road, which is a bit more expensive, but actually, it gives me so much more time to look after myself. And a year later, the guy had lost weight. He's got a better relationship with his children, with his wife, simply because he needed somebody outside of him to help him understand that actually, everything in life has a cost. We're often simply not weighing it up. Yeah. Look, that's a beautiful example. And I think it's something that, as you point out, it's not always easy for you to see it yourself when you're the one in it. This is where it really helps. He was lucky that he had a doctor who,

with the limited system of having 10 minutes with a patient, because most, I think most doctors wouldn't have necessarily what the ability you had, which is to say, Hey, I'm going to think beyond the immediate problem in front of me, which is that your blood pressure is too high and you're overweight. And I'm going to start thinking about this from the standpoint of your life. So he's very fortunate that he had that. And, you know, unfortunately, I think that that's probably not common, right? I think many of us go through life making these trade-offs that in the big picture are quite irrational.

So we've mentioned ApoB, right? So in terms of the things that you feel that many of us should be looking at, and then potentially treating aggressively, if it's elevated, or if we have a strong family history, or whatever it might be. And to be clear, you set this out really beautifully in the book for people who want to dive deep. That's one thing that we've mentioned that not everyone can have access to, both in the US, I think, and here. But before we move on from APOB, if someone cannot get that, and all they have available to them is a standard lipid panel of total cholesterol, triglycerides, LDL, and HDL, how would you advise them to look at that with a view to assessing their risk? Well, as I said, non-HDL

cholesterol, which you can calculate by taking total cholesterol and subtracting out HDL cholesterol, that gives you a number. That's a poor man's version of ApoB, and it's a better predictor than LDL cholesterol of risk. And so I assume in the UK, your units are millimole, not milligrams per deciliter. So I'm not familiar with the unit system as well. But there are readily available tables that will demonstrate percentiles. And so what we suggest is that a young person really should be below the 20th percentile, at or below the 20th percentile, at or below the 20th percentile. And the younger you are, the less aggressive you need to be, because this is sort of an area under

the curve problem. So it's really about lifetime exposure, just as blood pressure is, right? If you have high blood pressure, even mildly elevated for a very long period of time, it's going to cause proportionally similar damage to a person who has higher blood pressure, but over a shorter period of time. And similarly with ApoB, if you start lowering this when a person is in their 30s, you don't have to make an enormous change outside of cases where people have familial hypercholesterolemia or things like that versus when somebody shows up in their 50 and they already have evidence of atherosclerosis on a CT scan then you're going to have to be much much more aggressive so you know I mean I would just say directionally somebody who has any evidence of atherosclerosis you're basically now treating

them as a very high risk secondary prevention case, even if they have not had an MI, which is normally what we would use to move into the world of secondary prevention. If a person has calcification on a CT angiogram or coronary CT, that's effectively secondary prevention. We would want that non-HDL cholesterol or LDL cholesterol below the fifth percentile. That's such a good point, Peter, which I think many people haven't really grasped that if you've already got signs, you don't have to wait. It's that smoking analogy again, wait until you're off the cliff, wait until you've had the heart attack. Okay, now we know what we're dealing with. Now we can implement secondary prevention. It's kind of like, no, we don't need to wait for that moment. It's so basic and obvious when you lay it out like that. It is quite remarkable that we seem to have got into a system where we don't treat early. And I

get it. I understand the pressures within the medical system. I understand why we've ended up working like this. Why, of course, you set out the case, we need to upgrade medicine now, rethink medicine. But that's a really, really good point. Do you have numbers that you look for? I know, don't worry about the UK units, people can easily convert. Are there, you know, do you have numbers with these ratios, like triglyceride to HDL ratio? Do you like to see it below a certain amount, for example? Well, it's important to understand that while the ratio of triglyceride to HDL cholesterol is suggestive of insulin resistance, it has no bearing on atherosclerosis risk. In fact, I think we wrote about this in our newsletter. We have a newsletter that

comes out every Sunday and it usually goes pretty deep into these topics. And we did a newsletter on this particular issue around the value of knowing triglyceride level. We certainly pay attention to it and we're alarmed anytime the triglycerides are over about 100 milligrams per deciliter. That tends to be alarming. And certainly if the ratio of triglyceride to HDL cholesterol is above about two, we also tend to think that that's a red flag. Even though most people would say three, four, or even five would be the threshold. We think anything over two is a red flag as a ratio of triglyceride, HDL cholesterol. But here's the interesting thing. Once you normalize for ApoB, there is no residual remaining predictive value

of HDL cholesterol, triglyceride, total cholesterol. Those things completely become irrelevant once you know ApoB and basically non-HDL cholesterol as well. So in other words, and basically non-HDL cholesterol as well. So in other words, once you have the non-HDL cholesterol level pegged, that captures all of your lipid risk. Now, the only exception to that is LP little a, but we can talk about that separately.

So based on what you've just said, in a hypothetical scenario where people were given an option to say, you can have one test to measure your risk of atherosclerosis, one blood test, and you had to pick, and I appreciate we're not in that scenario, but as a thought experiment, you would say that one test should be APOB? Yeah, there's no ambiguity about this. The literature is overwhelmingly... In fact, I'm not aware of a single study that would suggest that there is a superior lipid biomarker to ApoB. There are some studies that would suggest that non-HDL cholesterol is almost as good, but on balance, when you look at the overall body of literature, it is unambiguous that APOB is the superior biomarker.

But I want to be clear, and I don't want us to get hung up on this because I know your audience might not have access to APOB. So I don't want perfect to be the enemy of good. Yeah. If you don't have access to APOB, that's okay. The jugular point here is know your non-HDL cholesterol, know your LDL cholesterol, and manage those aggressively. And the reason that non-HDL cholesterol is better than LDL cholesterol is it includes VLDL cholesterol by proxy. And therefore, it includes the negative impact of excess triglycerides. So you asked a question earlier about triglycerides and you're absolutely correct. Elevated triglycerides are a risk for cardiovascular

disease and they're a risk that is not captured by the LDL cholesterol, but they are captured in the VLDL cholesterol. And that's why ApoB captures them both because ApoB is the concentration of all atherogenic particles. And so as the triglyceride level goes up, so too do the number of lipid transporting lipoproteins because they now have to make way not just for the cholesterol that they're trying to carry back to the liver, but also this high burden of triglyceride. And that's, again, why ApoB is a superior metric. But if you don't know ApoB and you don't know, for some reason, non-HDL cholesterol, then yes, you do need to know triglyceride and LDL cholesterol to capture the full risk. Before we move on from this topic,

thank you for summarizing that, for people who don't have access. But let's say, by whatever means, you found out that you have higher levels of ApoB or non-HDL cholesterol than you would ideally want. You've mentioned there are some pharmaceutical interventions that one can use. What sort of lifestyle interventions can people do to bring that down? The most important ones come down to those that reduce triglycerides. Because of everything I just said a moment ago, namely that the higher the triglyceride, the more lipoproteins you need to carry them.

And namely, that's the VLDL, the very low density lipoprotein, which ultimately becomes an LDL, a low density lipoprotein. So the question then becomes, what do you need to do to lower triglycerides? So the people for whom dietary interventions are most potent at lipid lowering are the people who have the highest triglyceride level as a general rule. So when I see people that show up with very elevated LDL cholesterol, ApoB, and very low to normal triglycerides, we don't waste any time with dietary intervention with one exception, which I'll come back to in a moment. But for the most part, we recognize a genetic defect, usually at the level of the LDL receptor that is responsible for this problem, and it must be addressed pharmacologically. But let's go back to where we still see a lot of room for intervention, which is a person with elevated ApoB or LDL cholesterol, non-HDL cholesterol, and also very elevated triglycerides. So the easiest solution here is typically carbohydrate restriction.

So carbohydrate restriction generally is the quickest path to reducing triglycerides, but it comes with a catch. And that is carbohydrate restriction usually means increasing fat consumption. And in susceptible individuals, increasing fat consumption, especially saturated fat consumption, will, via a totally different mechanism, increase cholesterol production. And that's what I was actually referring to earlier, which is the other dietary thing you have to always be mindful of when you're staring down the barrel of very elevated LDL cholesterol or ApoB is what is this person's consumption of dietary fat and in particular dietary saturated fat. If a person is sensitive to that, they will increase cholesterol synthesis and dietary fat, high degrees of saturated fat will impair LDL clearance

from circulation via the liver. Yeah, it's a great point. And I would agree in my experience as well, that there's nothing faster and more effective to bring triglycerides down than some form of carbohydrate restriction. But as you say, you've got to not just look at the triglycerides in isolation, because you don't know what else might be going on as a consequence of that. of the question you asked earlier. You do something on the lifestyle. You cut carbohydrates and fix the triglyceride problem. But if you do it by mainlining coconut oil or whatever your saturated fat du jour is, you'll drive ApoB up through the roof. You're probably worse net off than you were at the outset. Everything has a yin and a yang. Yeah. And there's obviously this big online debate over how much does that matter on an aggressive, let's say a low carbohydrate diet, for example. I'm sure you have been involved with this, seen it all, like the conversations around how much does this really matter if the HSCRP, the marker of inflammation,

is down? How much do we need to worry about other things potentially going up? I don't think this question is as nuanced as those proponents would argue. It's no more nuanced than you saying, how much should a smoker worry about smoking if they're otherwise healthy and fit? Maybe less than a non-smoker, maybe less than a smoker who is not healthy and fit. But does anything about the fitness of or otherwise good health of that smoker diminish the causality of smoking in respect to cancer? No. And similarly, if you tell me that a person is on a low carbohydrate diet and that they're insulin sensitive and their inflammation is low,

but their ApoB or LDL cholesterol is still through the roof, that doesn't change the fact that they're still at risk as a result of that. So again, this is why causality matters so much. The person that has familial hypercholesterolemia can be completely metabolically healthy. In fact, many of them are. Right? You diagnose this in a child who's 15, 20 years old. They're thin, they're lean, they're healthy, their hemoglobin A1c is 5%. Their biomarkers are pristine, yet they have premature atherosclerosis because of lifetime exposure to LDL cholesterol of 200 milligrams per deciliter. So I think that the people who are suggesting that just because you're on a low carbohydrate diet and your other biomarkers are fine, and you can ignore your LDL cholesterol, I think those people are playing a very dangerous game

of Russian roulette. And I hope that people who are paying attention to those people get a broader aperture on their view of health. attention to those people get a broader aperture on their view of health. Blood pressure, of course, is also a very important metric for us to pay attention to. And of course, for many years now, there's been home blood pressure cuffs available, right? So whether your doctor is doing it or not, of course there are some pretty big limitations of rushing uh getting your car parts rushing in and actually hey yeah take my blood pressure doc but of course there's some real problems there but speak a little bit about blood pressure because what i love about addressing blood pressure is that first of all in terms of us being blind to what is going on inside our bodies and then somehow at 50 or 60 running into

problems. Blood pressure is something that we could get on top of pretty early if we started paying attention. So how do you view blood pressure? How do you frame it with your patients? Yeah, and then we can maybe dig into treatment potentially depending on where we go with this. Yeah, I'm really glad you bring this up. There are a handful of regrets I have in writing the book. Regrets is the wrong word. There's nothing that could have been done about it. But I guess I would say there are a handful of topics that I wanted to go much, much deeper into. But as you know, the book is almost 500 pages. There was simply no margin to go longer. simply no margin to go longer. So this book is 60,000 words shorter than the previous version of this book. In other words, an entire book was stripped out of this book. And one of the topics

that I really wish I could have put more energy into is this exact topic. And I would argue this is just as important as the ApoB discussion, but for a slightly different reason. And the reason is here you have a physiologic parameter that not only shortens your length when it comes to cardiovascular disease, but also does so with respect to Alzheimer's disease and dementia. By the way, we didn't talk about that with ApoB, but ApoB is also probably, lowering ApoB is, I would say, one of the three most potent interventions you have to avoid dementia and Alzheimer's disease. We should maybe bracket that and come back to that. That doesn't get nearly enough attention, right? Along with exercise, reducing lipids is unambiguously

the surest way to prevent Alzheimer's disease and dementia, but so too is lowering blood pressure. And the other thing that doesn't get nearly as much attention is the impact of elevated blood pressure on kidney function and how significant this becomes in an aging population. And while, you know, this rarely gets a 40, 50, or even 60-year-old into trouble, it starts to become very problematic when people are in their 70s and 80s. And when you have very compromised kidney function, one, it makes it much less likely that you're going to live to, say, 90. And also, you become far more susceptible to toxins that your kidney would normally filter out when your kidney is functioning

at a quarter of its capacity. So blood pressure, as you said, is partially complicated by the fact that we as a medical community don't do a great job measuring it in our patients. So you very accurately alluded to the exact problem, right? Which is patient, you know, parks the car, has to run up the stairs, sit in the, you know, reception area, get quickly shuttled back, have their blood pressure checked with an automated cuff. And that number doesn't tell us much. I mean, we know from the sprint trial that there is a really clear protocol for how to measure blood pressure.

And you need to be sitting comfortably with your legs uncrossed, not speaking for five minutes. The automated cuff or the manual cuff needs to be placed in exactly the right way, such that the marking on the cuff aligns with the brachial artery and such that the cuff is at the level of the right atrium, i.e. where the vena cava, superior and inferior, empty into the heart. I think it's interesting, and I do this all the time just to show people, take a blood pressure reading with your arm significantly above or below your heart, and you will be amazed at the difference in pressure. It is very sensitive to this finding. For this reason, we typically recommend that our patients get a very high quality monitor and we typically direct them to two or three that we fancy and let them buy it on Amazon or at their

local drugstore. We give them a log electronically and we ask that they check their blood pressure twice a day in the morning, in the afternoon or evening, according to this protocol. And we don't even make assessments on this until we have at least two weeks of data. But those data now we can believe, we can trust those data. And now we know if those numbers average above 120 over 80, we need to take action. Because again, this is where the largest, most well-conducted blood pressure studies make it abundantly clear that treating either with lifestyle or pharmacology, to better than 120 over 80 has significant benefits in outcomes over even 130 over 85, where we used to historically consider the upper limit of normal.

Yeah, it's such a good point. Measuring it correctly, of course, is really important. Otherwise, people can go out, buy something from the local drugstore, try and take ownership of their health, and then start to stress themselves out that actually, whoa, my blood pressure is really, really high. There's a couple of things there for me to discuss, Peter. One of them is trackers in general. Because certainly, as someone who's observed you online for a number of years, you've been pretty open with what you track. You've shared lots of times about the sort of things that you do track. And of course, not everyone is pro-trackers. And my view is that it often depends on the personality type in terms of, you know, I have had patients in the past, let's say 10 years ago, for example,

I seem to recall that maybe, you know, and I say 50% of patients, this is just, you know, a rough guess, but basically around half of my patients, when they would say, should I get a blood pressure monitor? Would it be helpful? I said, hey, sure, why don't you pick one up and, you know, let's sort of see what happens or, you know, and let's sort of see what happens or measure it at these times. What I found is that maybe half of the patients would measure maybe three or four times a week and they would use it as a way of keeping them on track with lifestyle change. It would help motivate them. Whereas the other half I found would start checking it six times a day. Whereas the other half, I found, would start checking it six times a day. If one of them was slightly elevated, it would make them anxious.

It would probably drive up their blood pressure for the rest of the day. They'd be phoning. And so I thought, okay, is this good or bad? Coming back to what you said previously, Peter, well, it kind of depends, right? It depends on who you are. So I like what you're doing as a practice where you have this set protocol. You're not really looking at those individual numbers. it kind of depends, right? It depends on who you are. So I like what you're doing as a practice where you have this set protocol. You're not really looking at those individual numbers. It's like, just do this for two weeks and then let us have a look and see what the overall pattern is. I think that's useful. So given that many people will get their blood pressure at the doctors in this suboptimal way, or they're going to pick one up from their local

pharmacy. Where do you see trackers here? I know I heard you say in a conversation a little while ago that you were checking out a few of these wrist trackers. You know, I hope we get to CGMs because I think CGMs are one of the most powerful tools I have seen to change behavior in my two decades of practice. I don't think I've seen anything as powerful in real time do that. But just to finish off on blood pressure a little bit, where are you up to with that, with your sort of investigation into this kind of non-invasive monitoring at home? So first of all, I just want to reiterate what you've said. And I agree completely. I do think people tend to major in the minor and minor in the major a little bit. And the tracking is a tool. People tend to get distracted by the tool and they miss the substance. The substance is the insight from the tool and what you do with it. And for some people, tracking is a very valuable insight generating tool. And for some people, it's also a very valuable behavioral tool. Well, as we will talk about with CGM. But when I see the debates between the tracking and the anti-tracking community, it strikes me as religious, political, partisan, and uninformed.

Yeah. And so I actually try to distance myself from that a little bit. I have a point of view on the benefit of these things, but I find myself less interested in debating it because I don't find the debates to be full of merit. They tend to be, again, they just tend to degrade into sort of unhelpful debates. Especially online, right? That's never, in my experience, on Twitter or on Instagram, especially on Twitter, you're very unlikely to get to some sort of meaningful place at the end of it where everyone's learned a little bit, everyone's evolved their understanding. I know as a fellow podcaster, I feel these debates or

these kind of things, long form podcasting, I feel is the best medium to have those conversations because the nuance and context comes out within them. Whereas online, it's just like, as you say, it deteriorates very, very quickly. So like you, I just stay out of them and distance and say what I have to say on this podcast, basically. Yeah, yeah. And I've had really interesting discussions with people about people who might disagree with me on various things. And yeah, these discussions, when you have them properly over the phone or whatever,

they tend to be much more productive. So as it pertains to blood pressure, I would have to guess that even the harshest critic of tracking as a general concept would at least have to maintain some interest in continuous blood pressure monitoring. Because this is something where there are so many limitations of spot checking. So even if you get over the limitations we just described, which are numerous, you still have the limitation of even if

you do it perfectly, you're only looking at two points in time. You don't know what your blood pressure is at night. You don't know what your blood pressure is when you're working, when you're on a phone call and you're stressed out or when you're making dinner or all these other things. And what we really would like to know potentially is what is your average blood pressure over the course of a day. And today, the only way to really do that is with a 24-hour ambulatory blood pressure monitor, what's called an ABPM. And I've worn one of these before. So it's an actual cuff that you wear on your arm that's hooked up to a regular blood pressure machine, except that it's smaller. And it's set to cycle every 15 minutes. And so you wear this thing for a couple of days.

You take it off when you shower. every 15 minutes. And so you wear this thing for a couple of days, you take it off when you shower, but otherwise you're wearing it 24 seven and it's just cycling like a regular blood pressure cuff every 24 hours. But the problem is it's so cumbersome that it doesn't really lend itself to great use. And I, for someone like me who actually doesn't mind being tracked, For someone like me who actually doesn't mind being tracked, I found it so cumbersome that I quickly got rid of it. So there are devices out there now, one of which I played quite a bit with, that measure blood pressure optically off the back of the wrist, and they're calibrated to an automated cuff measurement. It's too soon for me to say what I think of these devices, but I'm very curious and I'm very hopeful and optimistic that these things pan out. Because I really think that that's a piece of information I would like to know for all of my patients. I would really like to know what their

average blood pressure is. And I think that would probably be even more important than knowing what their average blood glucose is. Yeah. I mean, I'm pretty sure we'll solve this problem, won't we, with technology the way it is, whether it's now or in six months or 12 months or two years, it's inconceivable to me that we won't at some point have an excellent non-invasive blood pressure tracker that really gives us that information. I guess in a way that CGM does, right? In a way that that gives us information in a way that you can barely know you're wearing one. Just going back to blood pressure, your target of 120 over 80, as you say, is lower now. It's more aggressive than what we were certainly doing five or 10 years ago in medicine. Is there a specific trial that made you realize? I think there's quite a few, but where- Yeah, I think the most recent sprint trial is where we saw that what was then described as

aggressive management versus standard management. Was there a difference? And the answer was, yeah, there really was a difference. And would you go even lower? So again, lower, you're saying with APOB, you strongly believe is better for your risk of atherosclerosis. Can we say the same thing for blood pressure? What if it goes to 115 to 110, as long as of course you're not getting dizziness or- Well, that's the big if, right? I mean, blood pressure is one of those things where symptoms matter a lot on the low end, They don't matter on the high end. In other words, we're not going to wait until people are symptomatic to say your blood pressure

is too high, but we would certainly back off if the symptoms are low. And that's why, you know, I'm much slower to turn to pharmacologic interventions on blood pressure than I am on lipids because you don't pay as heavy a price on the lipid side, right? You don't need ApoB. This is a big misconception. You have plenty of essential cholesterol in your body floating around without ApoB. Kids have an ApoB concentration of 10 to 20 milligrams per deciliter. It's nothing. And yet kids have no problem with the profound and rapid period of growth that they go through, including in their central nervous system. Yeah. Right. So think about that. All these people who say, oh my God, you can't lower

cholesterol because your brain will starve. I mean, there's categorically nonsense, right? The most aggressive, ravenous appetite that the CNS has for growth is during a period of life when you have the lowest level of cholesterol. So there is no downside to lowering cholesterol except for the side effects of the medicines that you use to do it. And we've discussed those and they're important and you need to understand them. With blood pressure, it's quite different. It's not so much the side effect of the medicine. It's the side effect,

which by the way, there are side effects to those medicines, but the far more dangerous side effects are the dangerous side effects of hypotension and orthostatic hypotension in particular. And so I would much rather use exercise and weight loss and sleep improvements as, you know, and that includes correcting sleep apnea if it's present, as the three first, second,

third line agents to fix hypotension. Because the body is much better at auto-regulation under that setting than if you have to turn to something pharmacologic. And we would really only want to use pharmacologic agents when we have reached the limit of those other three. Yeah, it's such a great point. And any practicing physician will know full well the problems with blood pressure medications, especially with our elderly populations. You know, you put them on a tiny dose and then suddenly, you know, they get dizzy when they're standing up. There's all kinds of things to manage. And so I think that's a really nice way of looking at it.

Your threshold of risk will depend on the downside or the potential downside of that treatment. So that makes a lot of sense. Blood pressure, when you look at, of course, we haven't met in person. So over Zoom, you can't tell how tall I am, but I am six foot six and a half. I'm nearly two meters tall, right? And why that's relevant is when we look at these generic figures like blood pressure, you want to treat to 120 over 80. And this is, of course, when nuance comes into the practice of medicine.

What if someone like me, super tall comes in, you know, and you could make a case potentially that some people at the extremes may, you know, I may need a slightly bigger blood pressure because I've got so much more vasculature to, you know, to pump my blood around my body. I'm not saying I do necessarily, I'm just putting it out there as a theoretical. How much do you take these things into consideration? Or when the data is so clear as it is with blood pressure, do you just go, well, let's still treat aggressively as long as we're not getting negative symptoms? Yeah, no, it's a great question. And it's a question I've been asked before when it comes to especially tall patients. I guess, so the short

answer is I don't know. I don't think I know the answer. One way that I would think about it is considering that as tall as you are, and you're seven, eight inches taller than the average person, the real question is, what is the difference in height between your aortic valve and the vasculature of your brain? Because that's really the part of blood pressure that is working. That's the most important perfusion part of the equation, right? That's the part we're most worried about is are we getting enough central perfusion in you? Because the rest of your body is working a little less off gravity. In other words, that's the part where the heart has to pump against gravity. Obviously, your heart is receiving perfusion, regardless of your systolic blood pressure that's being perfused during diastole. And everything that's kind of below your neck has the aid of gravity to some extent.

which is even though you're eight inches taller than an average person, how much taller are you in an area where your heart is working against gravity? Another way to think about it, and I haven't done this analysis, is to look at the blood pressure of, say, a giraffe versus another large animal that's not quite as long or doesn't have quite as much distance between ventricle and brain. And I'm curious as to, I remember at one point reading that analysis, but I've just forgotten the answer. Yeah, really, really interesting. I love the way you think about this quandary. The sort of looking at giraffes is really interesting, not least because, you know, it has been known for colleagues or friends of mine to call me a giraffe. So, you know, I kind of like what you're doing there without that knowledge. But also this is a wider point for

me that I've been thinking about, particularly, I know you have a movement coach. I think her name is Beth from recollection from the book. And I see a lot of similarities between you and me, Peter, in terms of approach to medicine, certain personality traits that we may currently have, have had, are trying to eliminate or reduce. But I have my equivalent of, I guess, what I perceive to be your relationship with Beth. I have a lady called Helen Hall in the UK who is just one of the most knowledgeable people about the human body and movement I've ever come across. And there's all kinds of things we do together to optimize the efficiency of my movements and my muscle sequencing and efficiency and all kinds of things. But let's take running for example. A lot of people who talk about running will talk about the cadence should be around 180, you know, foot force per minute, something like that.

That should be your cadence. And, you know, I'd read this stuff and I'd absorb it and I'd try and implement it. I'd get metronomes. I'd try and stick to 180. And I'd be like, this is kind of, I'm struggling here. This doesn't feel like I think it should feel. Through my work with Helen, I've been working with her for about three years now. She says, Ron, I just don't think that's the right thing for you. You've got super long legs. It's just a simple example of where generic advice can start to become problematic if we don't put a bit of context in. So currently my cadence, which is beautiful for me, is about 1.62, and she's watched me run,

she's measured me, which is quite a lot different from 1.80, but then I'm also quite a lot different from the average runner. So that's the kind of context behind my question. No, actually it's funny you bring that example up. I was the same way in swimming. I mean, there's really a clear sense of what your cadence should be in swimming in terms of arm turnover.

And my cadence is significantly slower than anybody else's that I've ever swum with. I've never swum alongside people. I've never swum alongside a person who has a lower cadence. swim alongside a person who has a lower cadence. So for whatever reason, my style of swimming was such that it was better for me to turn my arms over less and just pull harder and glide, try to glide further. And anytime I would try to pick up that cadence, it would usually backfire. So there was no rhyme or reason for it. And it frustrated me to no end until I finally just accepted it and said, this is my cadence. One other there were one other point I want to make going back to your particular example, which is, you know, this is where I think we can be more judicious in our use of other biomarkers to help us understand the trade-offs. So for us,

one of the most important biomarkers is cystatin C, which we tend to rely exclusively on that and not on creatinine when it comes to understanding kidney function. We tend to ignore creatinine entirely because it is so influenced by muscle mass, exercise status, things like that, that it always seems to, I mean, I would say without being facetious, 80% of the time, I think it's under or overestimating kidney function to the point of being unhelpful. So we're looking at cystatin C, which I think the literature makes very clear is a far superior biomarker for kidney function. And of course, then we look at, you know, once a year. So we'll look at that every time we look at a person's labs. And then once a year, we'll also look for urinary protein and things of that nature.

And so that might be another thing that you can be tracking if you're saying, look, I'm going to go off the beaten path a little bit by measuring blood pressure and accepting a slightly higher level is saying, well, is my cystatin C very, very, you know, is it low enough that I can say my estimated GFR based on cystatin C is still very high? And if you're seeing any compromise there, the first place we look, of course, is at blood pressure. Yeah. And of course, the benefits are taken around that approach using more than one metric to make decisions, of course, is always going to be a good thing. We didn't sort of cholesterol as a big sort of term.

We mentioned blood pressure. I wonder if we should just finish off trackers a little bit. We've touched on CGM briefly. Of course, one of the four horsemen is metabolic health. So maybe we could just briefly speak to metabolic health. What is it? And why do you think that a CGM, a continuous glucose monitor, is potentially more helpful for us than the standard markers that we have? For example, HbA1c, which is that two to three month average blood sugar measurement that many people have ready access to. many people have ready access to. Before we get back to this week's episode, I just wanted to let you know that I am doing my very first national UK theatre tour. I am planning a really special evening where I share how you can break free from the habits that are holding you back and make meaningful changes

in your life that truly last. It is called the Thrive Tour. Be the architect of your health and happiness. So many people tell me that health feels really complicated, but it really doesn't need to be. In my live event, I'm going to simplify health and together we're going to learn the skill of happiness, the secrets to optimal health, how to break free from the habits that are holding you back in your life. And I'm going to teach you how to make changes that actually last. Sound good? All you have to do is go to drchatterjee.com forward slash tour, and I can't wait to see you there. This episode is also brought to you by the Three Question Journal, the journal that I designed and created in partnership with Intelligent Change.

Now, journaling is something that I've been recommending to my patients for years. It can help improve sleep, lead to better decision-making, and reduce symptoms of anxiety and depression. It's also been shown to decrease emotional stress, make it easier to turn new behaviours into long-term habits and improve our relationships. There are of course many different ways to journal and as with most things it's important that you find the method that works best for you. One method that you may want to consider is the one that I outline

in the three question journal. In it, you will find a really simple and structured way of answering the three most impactful questions I believe that we can all ask ourselves every morning and every evening. Answering these questions will take you less than five minutes, but the practice of answering them regularly will be transformative. Since the journal was published in January, I have received hundreds of messages from people telling me how much it has helped them and how much more in control of their lives they now feel.

Now, if you already have a journal or you don't actually want to buy a journal, that is completely fine. I go through in detail all of the questions within the three-question journal completely free on episode 413 of this podcast. But if you are keen to check it out, all you have to do is go to drchatterjee.com forward slash journal or click on the link in your podcast app. Yeah, so I'm going to guess that your listeners know what a CGM is. It's a device that you wear, it's implanted in you. It has a tiny filament that, like there's a needle that inserts a filament, the needle comes out, but the filament stays in and it stays in the, you know, basically the subcutaneous tissue and it samples interstitial fluid. So it's not actually measuring the glucose level in blood directly, but it is indirectly

doing so by measuring the glucose level in the interstitial fluid of the subcutaneous tissue. And it is calibrated to then know how that translates to glucose. So if it's working well, and that's a big if, it's giving you the real time, maybe delayed by five minutes, reading of your blood glucose. So why is that important? Well, I think first of all, it's important for patients to understand how various factors impact their blood glucose.

And the reason for that, again, comes down to understanding the relationship between average blood glucose and glucose variability and health. And at the extreme levels, this is not disputed. In other words, I have yet to meet a person who has tried to argue, which isn't to say that somebody's not trying to argue that, but I certainly haven't met the person or read the argument that type 2 diabetes is harmful. In other words, that when a person's blood sugar averages more than 140 milligrams per deciliter, which is the cutoff at a 6.5% hemoglobin A1c, deciliter, which is the cutoff at a 6.5% hemoglobin A1c, that poses increased risk to an individual relative to a lower hemoglobin A1c that is beyond outside of the diabetic range.

So the question then becomes, well, what if you don't talk about it through the lens of type 2 diabetes? So if you took a hemoglobin A1c of 5.7% or 5.6%, which would translate to approximately 120 milligrams per deciliter in our units, that's probably about six millimole in your units, right? And then the question becomes, how does that compare to a hemoglobin A1c of 5%? So now we're talking about two people who have neither diabetes nor type 2 or prediabetes. And we're asking, how do two quote unquote normal blood glucoses compare when one is higher than the other? One is say 120 and one is 100. Well, it turns out that that analysis has been done. We've written about that. And the analysis is pretty clear. There is a monotonic decrease in all-cause mortality as average blood glucose goes down, even within the normal range outside of type 2 diabetes.

Similar analysis exists for other parameters of glucose. And so the takeaway here is that things that can result in a lower average blood glucose, even in the normal range, i.e. below the type 2 diabetes threshold, are probably beneficial for all-cause mortality. And so therefore, by measuring those things using a hemoglobin A1c would be the crudest way to do that. There might be an advantage to measuring that. In other words, you would tell a patient whose hemoglobin A1c is 5.6, let's work on getting it down to 5.2, even though both of those patients are considered normal. And can I say, Peter, just that, I just want to highlight for people that that is

what you've just laid out there, for me, is one of the big holes in how we currently practice medicine. It is normal, but not optimal. It's the lack of recognition that these things are on a continuum, and we don't want to wait until it's too late. We want to get involved early. So please continue. I think it's such an important point for us to get, for all of us to understand. No, thank you for making that point. Actually, that's a more eloquent way to say what I was trying to say, which is we tend to confuse normal and optimal, and they should not be. Normal is generally a term that's reserved for being inside the extreme ends of a bell curve, right? So if something is normally distributed on a bell curve, we might say you're normal

if you're above the fifth percentile and below the 95th percentile. You know, the 90% of people that are not at the extremes are quote unquote normal, but that says nothing about being optimal. And this is true with blood glucose. This is true with kidney function. This is true with ApoB. This is true with liver function tests, transaminases. It's true with hormones. It's true with everything. So the CGM is a tool that offers at least a couple of advantages over, I would say three advantages to be clear, I would say three advantages to be clear over measuring something using a hemoglobin A1c. The first is the hemoglobin A1c tends to be inaccurate in any scenario by which red blood cell life is not exactly as predicted by the assay. Just so folks understand, hemoglobin A1c is something that is directly measured. You draw the blood, you measure the amount of glycosylation on the hemoglobin molecule.

That's the number you get. That's the 6.1% or the 5.7%. The average blood glucose is imputed, not measured. It's imputed from the hemoglobin A1c based on a belief that the red blood cell lived about 90 days. But if that red blood cell was in circulation for a much shorter period of time, for example, in a person with low-grade anemia, either due to red cell turnover or bleeding, low-grade bleeding, you're going to get an artificially low estimate of their average blood glucose because the red blood cell hasn't been in circulation long enough to accumulate

the glycosylation. So if it comes back at 5.0 and you assume their average blood glucose is 100, you're grossly underestimating it. Similarly, conditions that lead... You would also see this, by the way, in macrocytic anemia and things lead, but you would also see this by the way in macrocytic anemia and things like that. You would also see the reverse in conditions where the red blood cell sticks around longer. So microcytic conditions such as beta-thal trait and things of that nature that result in small red blood cells that aren't getting chewed up at the same speed through the spleen, you're going to see longer residence time of red blood cell. You're going to see artificially elevated estimates

of hemoglobin A1c or average blood glucose vis-a-vis hemoglobin A1c. So that's the first reason. A calibrated CGM, and I do insist on calibrating them when I use them. I don't rely on the manufacturer's calibration. So I insist on doing calibrations the entire time I would wear a CGM. A calibrated CGM is a far more accurate tool to measure average blood glucose and glucose variability. The second reason is that the person using it, even if they only use it for a month and never put it back on, gets a far more profound relationship or insight relationship to how various factors, most notably what they eat, how they sleep, how they exercise, and what stress is doing. They get to see how those things affect blood glucose. And those are, you know, having now used a CGM on myself and with patients going back eight years, there is simply, I've yet to meet a person who isn't amazed the first time they wear one at those relationships. is different from eating in the morning. How eating after I exercise is different from eating

when I don't exercise. How sleeping six hours a night changes my blood sugar the next day versus sleeping eight hours a night. How being under stress versus not under stress. I mean, the differences are so pronounced that people are really blown away. So there's this phase of what I call insight generation for which there is no substitute and which can't be done without real-time feedback. And then the final reason, and this is more for people who, like me, find value in using this tool beyond the state of insight, it becomes a bit of a behavioral tool. So if I'm wearing a CGM and I go into my pantry and I see a bag of my favorite junk food, I'm less likely to consume it when I'm wearing the CGM.

There's just a gamification that goes on with me where I don't want to see the number go up. I don't want to see the number skyrocket because I ate five cookies. So I'm just going to be better at not eating those cookies. And for some people, that doesn't mean anything. They don't need that. They might have the willpower to do that, to avoid those five cookies without the CGM. But for many people, it is a valuable tool. Opponents to wearing CGMs will often say it could promote disordered eating or an unhealthy relationship with foods. And of course, for some people, it could do. Yeah, I agree. I agree with that completely. I think we are very careful in who we prescribe the CGM to. And if a person has any history of disordered eating, and we do have some patients in our practice who do, we simply don't use CGM as a tool. And we're very careful about other things as well, such as,

you know, macro tracking. Yeah. You know, so, so yes, of course, this is an example of nuance, which again, I think the listener by this point of the podcast understands if there's something that has to underpin everything you're doing in medicine 3.0, it is nuance. Yeah, for sure. And yeah, so you have to be mindful of who you apply the treatment to. You know, I'm currently on my journey with CGMs. I would say I put one on for two weeks every three months or so. I found that for me, that seems to work quite nicely. I get some insights. I then don't wear it. I apply those insights. And then I pop it back on a few months later to see where I'm at. It can help me modify. Often, if I've fallen off, it helps focus me. But again, that's what works for me. And I'm sure for some people, it'll be less. For some people, it might be more. And of course,

for some people, it may be never. But I have yet to see something more powerful in two decades of practice, as you just highlighted at changing behavior. We have mentioned blood pressure. And it's really interesting to me observing your journey and reading your book as to when you came across emotional health as a key part of the health and longevity conversation. And I feel that emotional health for me, both because of struggles I've had personally, but also with patients. I don't know if this rings true to you or not, Peter, but I always used to observe people and go, people say information is power. Okay, great. I don't disagree with that statement. But what I would see is that patients would make changes. Together, we'd help them make some changes to their lifestyle. Again, that term lifestyle, their life

behaviors, let's say, and they would start to feel better. And sometimes that would be one month, sometimes they'd be doing it for four months or six months, and their life would be transformed and they'd feel good, they'd have energy, better relationships, better sleep, whatever it might be. But often people would then flip back to where they were before. And I would observe this with patients and I would think, okay, why is this? It's clearly not an information problem. They know the information. They've not only know the information, they've experienced how they can feel when they apply these things. Why are they going back? Now, of course, there's many different reasons, but this is the sort of topic I covered in my last book was that I thought, well,

is lifestyle really the issue here or is it something further upstream? And I really have come to the conclusion that actually it's something more upstream than that. It's how they approach the world. It's how they deal with conflict. It's how they manage their relationships because when there's problems there with, let's say, emotional health. And I think the chapter you've written on that is brilliant. I think often our lifestyle choices are downstream consequences of them. So one of the reasons I went down this road maybe five, ten years ago is because I thought, I know I need to tackle this. I also feel, Peter, I'm sorry for the long-winded start to this point,

but I'm trying to get a couple of points across. It feels to me that you, throughout your return to medicine, have had access to a lot of testing. So you can do a lot of testing with your patients for whatever reason that may be. Whereas as someone who has typically spent most of his career in the National Health Service, not having had access to testing means that I feel I've had to really pay attention to other things. So I don't have the testing. So what's going on here? Oh, they're telling me these words. What's the story behind their words? And so I feel maybe the different ways in which we practiced have meant we've come to this from slightly different approaches.

So a couple of things there, Peter. I wonder if you could maybe give me your perspective on what I've just said. No, I think what you said is beautiful. And I think that's such an amazing way to think about the differences between, you know, the two ends of, you know, opposite or extreme ends of how, you know, we could talk about two different practices, right? So I'm sitting

here in the United States, which is a private health insurance only, right? There is no national healthcare. And even within private insurance, you know, you can move from insurance to just pure fee for service. And the US is sort of the sky is the limit when it comes to testing, testing, testing. We can do anything and everything. You're at the other end of that spectrum. And yet, you're absolutely correct. I think that our system pays very little attention to the problem that you address. And I think it's very astute. And I'd be curious to know what fraction of physicians within the NHS would recognize what you've recognized, which is, look, I have less at my disposal right now

in terms of fancy tools. So I'm going to rely on more of these human tools, these interpersonal tools, these skills that once made a physician what a physician was. And I'm going to rely on those to try to better understand how I can apply the fewer tools that I have. So no, I think that's really interesting. Of course, my foray into this as an interest was very personal, right? It started through my own experience. And I would say that prior to my own experience with it, I was not necessarily that attentive

to how much of a struggle maybe others had and how much of a role this played in the behavior of other people, especially in the examples that you use around the ability to make changes and then the ability to sustain changes. Peter, you've recently spoken very publicly about a lot of life experiences that you've been through where I guess you were forced to confront some uncomfortable truths. You've spoken about anger, rage, about when your five-week-old baby had a cardiac arrest and you were in New York and you didn't fly back to be with your wife and child. I'm really interested as someone who defines themselves or certainly has defined themselves as a perfectionist. What has it been like for you being so open, being so vulnerable on such a public stage? Well, it's very uncomfortable. I mean, I don't think,

I appreciate you thinking that maybe I'm a former perfectionist. I think I'm a perfectionist in recovery. And, uh, like I think any addict, we, you know, I think we have to have humility around our addictions and, uh, and keep a close eye on them. So, um, I, I think I'm always going to struggle with vulnerability and with, with letting people see my faults and acknowledging my faults and my own humanity to myself. That said, I also realize that I'm very lucky and that, you know, I think to, to whom much is given, much is expected. And so to be sitting here having this discussion to have, you know, survived the ordeal of my,

you know, my past and what I went through in, you know, 2017, 2018, 2019, and 2020 relied on me being very fortunate, meaning I had a lot of people around me. And there have been some people who have commented to that effect, which is, hey, you know, most people don't have the resources you have to get the help that you got, right? You know, you went and spent, you know, I was five weeks collectively in an inpatient residential treatment center. And that's, that's not something our health insurance pays for here in the United States. I mean, that's, I don't even remember what that cost, but it was a lot. And I have access to these incredible therapists. And so that's not lost on me, that there are many people who can't necessarily afford either in time away from work or in financial costs what I have been very fortunate to afford. And while I can't apologize for those things, I'm not going to apologize for my good fortune. What I am going to say is, how can I pay it forward? How can I take my fortune, my blessing and help other people with it? And I

think the best thing that I can do is write a chapter like the last chapter in this book and be open about my story, even though it doesn't feel good. It doesn't feel good to talk about or write about these things the way it feels easy and autonomic to talk about exercise and sleep. Yeah. Thank you for sharing that. Perfectionism is a growing problem, actually. I was reading some research from a psychologist in London recently how perfectionism is growing across the world. There's a particularly dangerous form of perfectionism, social perfectionism, about what we think other people think of us, which if we just break down that, you know, we think what they think about us, it's based upon a lot of assumptions that we may not

know what they think, and we're imagining what people think of us and the link between social perfectionism and suicide. So I would also describe myself as a perfectionist in recovery. I often think about it in terms of, you know, when there's a gap between our ideal self and who we actually are, our actual self, in that gap, the greater that gap, the greater the inner conflict I think we experience. That's how I've been thinking about it recently. But you're right, it is uncomfortable. You know, you mentioned that you think you will always struggle with being vulnerable. I find that interesting. And I've also heard you say in previous conversations, Peter, that given that it's taken me 40, 50 years to get to this point, I can't see this going quickly. It's going to take a long time to go.

As someone who's maybe been on this journey since my father died in 2013, I don't think it necessarily needs to take as long as people think. I really don't. And I really feel that with, again, it depends on access, of course, I've done a form of therapy called internal family systems, Peter, by Dr. Dick Schwartz, which has just been incredible, really incredible about going back into childhood situations, reframing them. And then, you know, when you sleep with consolidation and reconsolidation in the brain, you almost lay down a new memory of what has happened. It's really been quite profound. So as someone who also describes himself as a perfectionist in recovery, I would like as,

you know, as a fellow human to say to you, I don't think necessarily it is something we always have to struggle with. I do believe that we can. I passionately believe that we can get to the roots of these things and rewire them and change. And I've certainly come to the belief, Peter, that a lot of our personality is not who we are, it's simply who we became. And if we apply ourselves to certain practices, we can actually change how we show up in the world. When I say that to you, Peter, or when I share my view with you, Um, when I say that to you, Peter, or when I share my view with you, um, does it hit? Do you push back?

Do you think, nah, I'm a difficult case. It's going to take me a long time. I mean, what, what comes up for you when, when I sort of share insights like that? Oh, no, I, I completely agree. And I, if I think about the progress I've made in three years, um, it's, it's profound. I mean, I'm not the same human being I was three years ago, that there's simply no comparison. And actually, I think I talked about this on the podcast with Andrew Huberman, or maybe it was on with Rich Roll, but it was one of those two where one of the hardest things for me to shed, or one of the first things I had to go after or one of the first things I had to go after was the inner monologue, which was a very,

very destructive inner monologue. And it was something that I had never not known. So there was never, I don't have a conscious memory of not having this harsh, at times violent, awful voice that would speak to me speak to me and and not just silently like it would do so audibly as well so if i made mistakes um you know i was going to berate myself for them and it didn't take a rocket scientist to know that a big part of the problem was was you know what was at the root of that? And then how could we fix that? Because that was then leading to so much other problem and conflict in my life. So without going into the details of it, um, cause I do so on those other podcasts, which, um, we can talk about if you like, but the process of undoing that, which was a, was rooted in a very daily deliberate behavior practice, took maybe six months to undo that voice. So that surprised me because I really did believe that that was a permanent

feature of my existence. That was as permanent as my height or my eye color. And I was very surprised, eye color. And I was very surprised, delighted that, you know, the plasticity of the human mind could allow me to kind of rewire that in only six months. And I admittedly am working very, very hard in those six months. But yeah, that was very pleasant. So no, I'm actually incredibly optimistic that 10 years from now, I'm going to be in far better shape than I am now emotionally. Might not be physically and cognitively as sharp at 60 as I am at 50, but I think emotionally I'll be in a better place. In other words, I think the trajectory is positive. Thank you for sharing that. Going back to what we said earlier on in the conversation, physical, cognitive, emotional. And of course, we were discussing how physical and cognitive get worse with age. And I was sort of saying, yeah, as you were just demonstrating

there, I think emotional can get better with age actually. And I don't know, maybe counteract some of that other stuff potentially, but that's a much deeper and longer discussion. Without sort of going back into the detail you have already shared on those other podcasts, I think what might be useful in terms of a practical tool is simply sharing what you had to do to change the negative voice in your head. Because clearly negative voices in our heads are so common. Yours sounded particularly brutal, I must say, when I heard it. I did recognize elements of it as well in myself. But to see that change dramatically in six months, I think is really empowering. Would you mind sort

of briefly sharing what that exercise was that enabled you to do that? Sure, sure. So the voice was basically the voice of a guy, a very famous college basketball coach, former basketball coach in the US named Bobby Knight. So Bobby Knight was this insanely angry, maniacal savant of a basketball coach, but who ultimately lost his career over his temper. And every game was like witnessing some crazy temper tantrum that he would have. And so the exercise was framed as, you have a board of directors that runs your life, the board of directors in your head. And unfortunately, this guy, Bobby Knight is the chairman of the board and we have to get him out of the boardroom. We have to get him far enough away from the boardroom that you don't hear him talking all the time. So the way we're going to do this is every time you hear him talk. And that's going to happen anytime you do something in the pursuit of

what we would call performance-based esteem. So basically, most things I'm doing in life, I'm doing so that I can generate self-esteem. So just as an alcoholic might turn to a drink, or a gambler might turn to a slot machine. I turn to performance as the drug. That's literally the drug that I need to have the self-esteem. And anytime those performance-based esteem activities fail to generate esteem because I fail in the activity, I turn the rage inward. fail in the activity, I turn the rage inward. Just as an alcoholic would be furious if he walked into a bar and asked for a vodka and received a water, he would be furious at the bartender. That's basically the cycle that's happening. So the exercise was every time you feel that happen, I want you to imagine that it is your closest friend that committed the act in which

you failed, right? So for example, if you're in your driving simulator, and driving is one of my huge passions. So if I'm not on a racetrack, I'm in a simulator, and you're having a bad day, you're just not driving well, you're spinning, you're crashing, your times are slow, whatever it is. Normally, you would get out of the simulator and you'd be yelling and screaming and sometimes even break the simulator. Instead, imagine that your closest friend was the one in the simulator who drove poorly. What would you say to him? And to do this exercise, you have to be able to picture the person. And so for this exercise, I would typically pick a friend of mine named Matt Walker, who you may recognize. Matt Walker wrote the great book on sleep. And Matt's a very, very dear friend who is also a total motorhead gearhead, loves cars. Whenever he comes my eyes, and I would imagine what I was saying to Matt if he drove that poorly. And of course, it would be very kind, very loving, very supportive.

And I would record that discussion on my phone and I would send that recording to my therapist. So two or three times every single day, my therapist would be getting one of these five-minute voice memos from me where I would be talking to one of my friends in this type of situation. And that was simply the exercise. we've had the advice before on this show particularly when i spoke to kristen neff who's done a lot of the research into self-compassion yeah you know talk to yourself as if you were talking to your best friend or a young child and i think we intuitively get that but i think what makes your exercise the one that you were given to do so powerful there's an extra component of accountability. It's not just, oh yeah, I wouldn't say that. Oh, come on, change the record in your head. No, you have to record that message and send it to somebody who is going to hear it.

So maybe you could just speak to what was so powerful about sending it. Was it embarrassing? Will you read it? Will you think, oh man, I have to send this to someone? Like, was the goal that you then play them back to you to sort of subliminally change the messaging you give yourself? Or just give us a little bit more detail there if you can. Well, I think the recording is important because I think when you say it out loud, it's much more powerful than just thinking it. So it's one thing to say, okay, I just, you know, shot poorly with my bow and arrow,

or I drove poorly in the simulator. I'm going to now sort of think nice thoughts. But the reality of it is Bobby's voice is too loud for me to outthink him in silence. I have to outspeak him. Right? The mind works through concentration and there are very few things that can harness your concentration more than the audible sound you make with your own mouth. So I have to outspeak this otherwise very loud force in my mind, who, by the way, sometimes would actually speak to me. I would sometimes actually speak what he was saying. So I have to one-up him in volume. And then secondly, the recording it and sending it is not about being embarrassing. It's, as you said, it's accountability. It's, there's a person who knows that two, three, four times every day,

I engage in some behavior that is demanding of my perfectionism and is a vehicle for which I generate self-esteem. And therefore, I'm going to have commentary. So it's really those two things. And so therefore, by forcing the audible overriding of a historical way of doing things, I'm rewriting. And by having the accountability, I'm making sure that no matter how much I don't want to do it, I do it. Going back to what you said before, Peter, about having the means to pay for a residential inpatient facility to deal with a lot of the inner conflict you were feeling at the time and wanting to pay it forward. I'm just trying to think, is there something there in that

exercise that people at home can actually utilize themselves? For example, of course, it's not the same as having a therapist. I understand that. But just as if, for example, you're recommending to a patient to work out more, whatever that may mean, you may sometimes, I'm guessing, ask them to have an accountability partner who can show up with them to make sure that they're doing it and they can help encourage each other together. Could a version of this be with a close friend, someone you trust, perhaps your partner? Could it be that you go, actually, you know what, I'm going to ask them if for the next month I can do that exercise with them. Would they be willing to be that person for me? Do you think that could be a good thing or do you see any potential

problems with that? I'd have to give it some thought, but my inclination out of the gate is probably not to select a romantic partner for that exercise. I think that probably would introduce some unnecessary strain on a relationship. But I think it could be done with a friend. That might not be as ideal as a therapist because the advantage of doing it with a therapist is, you know, in my case, once a week, I'm going to talk to that person as well. And we're going to process those things. And by the way, some of them were just so significant that she would just call me

right away. She would listen to it and call me an hour later just to check on me or something like that. So there's something to be said for that. But I think if the alternative is not doing it, then doing it with a friend, I think would be a far better option than not doing it. Are there any practices you try and do on a daily basis or at least a regular basis that keep your emotional health in tune? Or is it something you just go to from time to time? No, no. It's a huge deal. And in fact, when I left PCS, which I write about in the book, it's the place I went to in Arizona in 2020, PCS, which I write about in the book, it's the place I went to in Arizona in 2020.

You know, I had a recovery contract that I made and the recovery contract had red light behaviors, yellow light behaviors, green light behaviors. So red light behaviors were things I never, ever, ever wanted to happen again. And if they happened, I understood that that was a trip back to rehab. Yellow light behaviors were warning signs. This was a very important part of the journey. One of the things that frightened me so much in my life was how seemingly unpredictable my meltdowns had appeared. Again, I write about this in the book that I was so paranoid that I was like the space shuttle challenger that just out of nowhere would blow

up over the sky. And the reality of it is that space shuttle challenger, which for people don't remember is the space shuttle that blew up in January of 1986. That turned out to be an entirely predictable disaster had people been paying attention to what the engineers were telling them. And so there were lots of yellow lights that predicted that the space shuttle Challenger was going to blow up that day. It's just people didn't pay attention. And so I had to now identify what my yellow light behaviors were. And they had to be plastered right in front of me in a contract that I looked at twice a day, every day. And whenever those things happened, which they did, that necessitated an increase in therapy and immediate

discussion with somebody. It was all about cooling the flames. And then there were the green light behaviors, which were what you're asking about. What are the things that I have to do every single day? And these are the things that are going to widen my distress tolerance window. That's the sort of figure I include in the book, right? Which is like, I have to widen my operating range as much as possible. This is something kind of through the type of therapy I do called dialectical behavioral therapy. That's really geared towards making me as emotionally resilient to stressors as possible. So it's really through those lenses that I approach the day.

But just to give you an example of some of the green light behaviors, exercise is important. So exercising every day, but doing so in a non-forced way. This is a very important thing for someone like me. Exercise has always been important to me, but what I had to do was not learn to exercise more, but at times learn to exercise less and learn that, you know, if on Sunday you're trying to get a double workout in, but it's ultimately the choice between spending a little bit more time with your kids or getting that second workout in, maybe the better thing to do is actually just spend time with the kids and not get the second workout in and be okay with that. Yeah. And be okay with that being the key thing there. That's right. Yeah. And over time,

that becomes easier and easier and easier. For a long period of time, for about a year, I did not permit myself to score in archery. Meaning in archery, when you do it competitively, you actually have scores. You keep scores of exactly where the arrows are hitting. And for a year, I did not do that. So I still practiced archery, but I didn't score it. In other words, I had to take out some of the performance. I also, for six months, did not ever drive the simulator and do archery on the same day. I know these things sound kind of crazy, but you have to understand for somebody who's recovering in the way that I was, I didn't want to have too many of these performance-based things stacking up.

I also wanted to not look at my phone from the time I woke up for about, you know's say I woke up around 5.30 in the morning. The goal would be to not look at my phone or do any work until my kids left for school at 7.15. So just hang out with my wife, have coffee and play with my kids. That was a very important part of resetting. Anyway, there were about, I don't know, 15 or 16 things on the recovery contract that were part of the green light behaviors. And these things had to be done constantly, right? That was therapy. That was checking in with friends once a week who I asked if they would be supporters for me. That was writing in a journal.

So there were lots of things that I had to do. And it took time. This was a time-consuming process. It was took time. You know, this was a time consuming process. It was as time consuming as, you know, exercise was. Yeah. I really appreciate you sharing that. Again, I think what you just said speaks to personalization. You had to figure out with your team, your helpers, your therapists, what was the right

approach for you? Someone else, you know, not scoring an archery has no relevance to them in their life, but for you, that was something that you had to address. And I think it falls on all of us to find what are those things for us. I found it really interesting when reading that chapter in your book, Peter, when you spoke about the issues in 2017. I know you didn't write about this stuff in 2019. I heard you talk to Rich about that. And then in 2020, so you'd already been through that. You were already on this journey, yet you said something which I underlined, which I found

it really interesting. At the start of March 2020, when things were kicking off everywhere, I let my morning meditation practice go, right? You let something important go to, you know, deal with a crisis. I get that. But it's one of those things, isn't it, that I've learned in my own life. There are certain things, I don't call them non-negotiables anymore because I feel a non-negotiable brings me back to an old pattern of thinking. Yep, yep, agreed. So I no longer use that term, actually. I feel there's a balance between discipline and compassion. And I'm always trying to find the sweet spot between those two. But I really do appreciate you sharing that.

And I think it's going to be helpful for people. Peter, I think you've written a wonderful book. I don't feel I've even scratched the surface of where I really wanted to go with this conversation. But just to finish off, Peter, for people who obviously want to learn more, they can go to your book. But for people who go,

okay, I get it. I get your philosophy. It's about getting stuck in earlier and not waiting till it's too late or very late before I start addressing things around my health and my longevity. I always like to finish the podcast with some sort of actionable take-homes for my audience. So for that person who does feel inspired and goes, okay, right, you've convinced me. I'm going to get on top of this now. I'm 40 years old. It's not going to happen to me what happened to my father or my brother or my granddad or whatever. I want to take control of my life and my health.

What would you say to them? Well, if you're really committed, I would say get the data, right? Let's figure out what your baseline is according to all of those metrics that matter. And again, we do lay them all out in the book, right? So you need to know your VO2 max. You need to have a DEXA scan and know what your ALMI is. I mean, again, if you really want to understand these things, and yeah, you're going to have to invest in doing these things. I mean, whether you're in the UK or in the US, no health insurance company is going to pay for that information. You're going to have to get it on your own. And there are less expensive ways to do it. There are ways to estimate those things beyond measuring them via the gold standard. But what you want to do is take advantage

of the fact that you're 40, right? And take advantage of the fact that you have hopefully four or five decades ahead of you on which to compound benefit. This is a much different proposition than if you're in the last few years of your life, what I call the marginal decade, and you realize, oh, I want to do something about it. There's still value in making change at any point, but you're going to be able to move the needle less. So if you're talking about this through the lens of somebody who's in midlife or even younger, what you want to do is say, what changes can I make consistently? I often say, I'd much rather someone do seven out of 10 work every single day than do 10 out of 10 work some days and zero out of 10 work other days. The ping-ponging back and forth tends to produce

inferior results. As far as what to do once you have those results, I think the results have to drive it, right? So if your VO2 max is at the 25th percentile, that's an enormous opportunity. You have to be doing the type of training that's going to increase VO2 max, both increasing your aerobic efficiency, your base of aerobic fitness and your peak. If by extension, your VO2 max is already at the 80th percentile, but your muscle mass and strength are at the 20th percentile, then that's where you just need to disproportionately train while you do things to maybe maintain your aerobic fitness. Again, the list goes on and on. If your sleep is really the thing that's suffering, then that's where you need to focus. And again, we kind of lay out how to do that. If you're overnourished and under muscle, then you're going to be focusing on strength training, protein and calorie reduction. And that's probably going to be your biggest focus to get back onto a level playing field of health. So I know that's not a very satisfying answer because it, again, is an individual answer.

But unfortunately, I think at this level of medicine 3.0, it's the only way that I can think about talking through these issues. Peter, I think you've been doing fantastic work for so many years. You're helping so many people improve the quality of their lives. I really appreciate you making time to come on this show. Thank you for writing the book.

It's fantastic. I really can't imagine that anyone will read it and at least not take something from it that's going to help them make positive changes for them and their family. Thanks for coming on. I appreciate it. Thank you so much for having me on. And for, as I said, taking the time to read the book and allowing us to have this, you know, I think really nuanced and enjoyable discussion. Really hope you enjoyed that conversation. As always, do think about one thing that you can take away and start applying into your own life. Now, before you go, just wanted to let you know about Friday Five. It's my free weekly email

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