The Dr. Hyman Show - How Silent Inflammation Accelerates Aging with Dr. David Furman

Episode Date: December 21, 2022

This episode is brought to you by Rupa Health, BiOptimizers, and InsideTracker. If you’re interested in health, you’ve heard the term inflammation quite a bit. But did you know there are different kinds of inflammation? Some of them are more alarming than others. Acute inflammation happens when you cut your finger and it gets red and a little swollen. This is helpful inflammation and usually resolves in about a week. But the inflammation that naturally happens as we age, called sterile-inflammation, sets us up for less resiliency against things like autoimmunity, cancer, and other forms of chronic disease.  Today, I’m excited to dive deep into the topic of inflammation and its role in aging with Dr. David Furman. Dr. David Furman is Associate Professor and Director of the Bioinformatics Core at the Buck Institute for Research on Aging, as well as the Director of the Stanford 1000 Immunomes Project. He obtained his doctoral degree in immunology from the School of Medicine, University of Buenos Aires, Argentina, for his work on cancer immune-surveillance. During his postdoctoral training at the Stanford School of Medicine, Dr. Furman focused on the application of advanced analytics to study the aging of the immune system in humans. This episode is brought to you by Rupa Health, BiOptimizers, and InsideTracker. Rupa Health is a place where Functional Medicine practitioners can access more than 2,000 specialty lab tests from over 20 labs like DUTCH, Vibrant America, Genova, and Great Plains. You can check out a free, live demo with a Q&A or create an account at RupaHealth.com. Magnesium Breakthrough really stands out from the other magnesium supplements out there. BiOptimizers is offering my community 10% off, so just head over to magbreakthrough.com/hyman with code hyman10. InsideTracker is a personalized health and wellness platform like no other. Right now they’re offering my community 20% off at insidetracker.com/drhyman. Here are more details from our interview (audio version / Apple Subscriber version): The origins of Dr. Furman’s unique thinking about the immune system and aging (7:21 / 3:58)  Types of inflammation (11:13 / 8:02)  How systemic chronic inflammation drives all of the hallmarks of aging (13:32 / 10:30)  Causes of inflammation (18:24 / 13:46)  The immunome and the 1000 Immunomes Project (26:31 / 21:14)  How inflammatory age can be used to predict disease (33:13 / 27:12)  Predicting frailty in individuals years before they become frail (35:54 / 30:37)  Newly discovered biomarkers that can be used for early detection of age-related disease (38:54 / 32:02)  How the iAge test will be used in the future (47:58 / 43:42)  Learnings from centenarians (59:24 / 54:12)  Learn more about the 1000 Immunomes Project.

Coming up on this episode of The Doctor's Pharmacy. Every single one of the hallmarks of aging are driven by elevated systemic chronic inflammation in the body as a response to multiple triggers that have to do with how we treat our bodies. Hey everyone, it's Dr. Mark. One of the most important tools I have for helping my patients optimize their health is testing. And that is why I love what Rupa Health is doing. Functional medicine testing can require placing orders with lots of different labs, and it can kind of get really complicated for doctors and their patients to easily access results and keep track of everything.

But Rupa Health has totally streamlined that process. Looking at hormones, organic acids, nutrient levels, inflammatory factors, gut bacteria, and so many other internal variables can help us find the most effective path to health and healing. I'm really excited about that now, and I can finally take advantage of these tests without the hassle of the confusion of going through so many multiple labs. Rupa Health is the place for functional medicine practitioners to access more than 2,000 specialty lab tests from over 20 labs like Dutch, Vibrant America, Genova, Great Plains, and more. It's 90% faster, letting

you simplify the process of getting you the functional tests that you need and giving you more time to focus on your patients. This is really a much needed option in the functional medicine space and it means better service for you and your patients. You can check it out with a free live demo, with a Q&A, or create an account at rupahealth.com. That's R-U-P-A health.com. I'm all about using food first when it comes to nutrition, but there's certain nutrients I recommend everyone supplement with because it's simply impossible to get adequate amounts from your diet alone. One example is magnesium, which our soils, well, they're not too healthy. And because there's no organic matter, they can't extract the magnesium from the soil from industrial farming, which is a drag. And that leads to 50% less of these minerals in our food than there was 50

years ago. And then of course, we're doing things that cause us to lose magnesium, like sugar, caffeine, fluoride, even stress, which none of us have, right? 80% of Americans are actually deficient in magnesium. And that may mean insufficient, not necessarily true deficiency, but just not enough for optimal functioning because magnesium is so important. And it's a huge problem for our health. Considering the pandemic of stress, along with the pandemic of COVID that we're facing, we should all really be conscious about our magnesium intake because it activates the parasympathetic nervous system, which keeps us calmer and more relaxed. Magnesium is crucial for more than 300 other chemical reactions in the body and impacts everything from metabolism

to sleep to neurologic health, energy, pain, muscle function, and lots more. My favorite new magnesium is from a company called BioOptimizers. Their magnesium breakthrough formula contains seven different forms, all of which have different functions in the body. There was truly nothing like it on the market. I really noticed a difference when I started taking it, and I've tried a lot of different magnesium products out there. I also love that all their products are soy-free, gluten-free, lactose-free, non-GMO, free of chemicals, fillers, and made with natural ingredients. Plus, they give back to their community. For every 10 bottles sold, they donate one to someone in need, and there's a lot of those. Right now, you can try BioOptimizers Magnesium Breakthrough for 10% off. Just go to magbreakthrough.com.

That's M-A-G-B-R-E-A-K-T-H-R-O-U-G-H.com slash Hyman and use the code Hyman10 and you'll get 10% off this really great formula. I think you're going to like it as much as I do. And now let's get back to this week's episode of The Doctor's Pharmacy. Welcome to The Doctor's Pharmacy. I'm Dr. Mark Hyman. That's pharmacy with an F, a place for conversations that matter. And if you are wondering about how fast you're aging and if there's a way to test and track it, if there's new science that's telling us how we can identify hidden inflammation that's linked to all the chronic disease of aging, then you're going to love this podcast because I am excited to bring to you Dr. David Furman, who is an expert in immunology. He's a physician. He's an associate professor and

director of the bioinformatics core at the Buck Institute for Research on Aging, as well as the director of the Stanford 100 Immunomes Project. We're going to get deep into what the 100, I mean, sorry, the 1,000 Immunomes Project, what that is. He got his PhD in immunology from School of Medicine, University of Buenos Aires, Argentina. And he also has done postdoctoral work at Stanford School of Medicine. And he's basically looking at how we use artificial intelligence, advanced analytics to study aging of the immune system in humans, which is really an important topic because, as you know, inflammation is a huge driver of all the chronic disease of aging. So he's doing some really amazing work and has developed a number of things, including this test, which we're going to

talk about called the IH test, measures your immunological age. And as you know, I'm all excited about longevity and aging. I've written this new book, Young Forever, which is coming out February. We're going to talk a lot about this. And I do include a lot about this work, about the 1000 Immunos Project in my book. Now, he's got over 30 scientific publications in major journals like Cell, Nature Medicine, Lancet. These are top tier journals. So he's the real deal and we're going to get deep into this. So welcome, David. Thank you so much, Mark, for having me here. Yeah. So it's great. You know, you, you are a very unusual physician and scientist because you think in systems

and you think about how things relate to one another and you are looking for things that most people often ignore. You know, often we go to the doctor and we get a checkup and doctor does like the blood panel and it may be 20, 30, 50, maybe a hundred analytes if you're lucky. And he goes, oh, you're fine. Everything's fine. Your liver's fine. Your kidney's fine. Your electrolytes are good. You know, your cholesterol is all right. And okay, good. You're fine. And send you on your way. And the truth is they may be missing a whole slew of clues about your health and your rate of aging. And you decided you were going to take a very different perspective, which is rather than look at the tests that we're already doing and try to find what is correlated with aging,

you were going to look at the immune system in ways that are only now possible because of advanced analytics and bioinformatics and artificial intelligence. And you are going to take a thousand people ages, I think nine to 96 and look at them over 10 years and correlate all kinds of biomarkers from the immune system, over 50 different cytokines and markers that you didn't know if were relevant or not, but you were going to see if they were correlated with aging and age related disease and how they were important or not. So this is a radically different view. And it's really exciting because you publish this data and you've developed this test, which allows us to

measure our immunological age, which is really important. We're going to talk about why immune age is such an important biomarker of health and aging. And it's sort of exciting. So before we sort of get into the nitty gritty of like what you found and what the science is around this and why the immunology of aging is so important, how did you actually become interested in this? And how did you, as a scientist, begin to think differently than everybody else? Because you were thinking very differently than most scientists out there about this process of aging and longevity. Yeah. Thank you for that question. I think it's a very appropriate one. Just first of all,

let me correct you. I'm not a physician. I studied medicine for four years, but I dropped out to go to Stanford. So I studied medicine for four years. You're a med student dropout. Exactly. That kind of counts. That kind of counts. Maybe you didn't get officially licensed, but you definitely went through medical school. So that's the important part.

Not board certified, but exactly. I went to medical school, got my PhD in immunotherapy against cancer, and then went into Stanford to study immunology in an unbiased fashion. The idea really, Mark, was to conduct research in humans, right? For the most part, what we know about immunology over the past 100, 150 years comes from animal models, namely mice, right? And the big, big problem there is that things do not translate. Just to give an example, for one drug to be successful, you need about 10 to 15 years of research and around $2 billion to make it work, right, to get to the FDA approval. This means that the systems are not working well, right, and mostly because studies in animals do not translate into humans. So we decided to take a very different approach

and start using humans as model organisms, if you will. And one thing that we noticed is that the variation that we see in humans is huge. It's just gigantic, right? We are not inbred. We're not in a controlled environment. Hopefully we're not. Hopefully we're not. And therefore, the variation in immune systems is huge. It's gigantic. So one way to cope with this huge variance that we see in human immune systems is by measuring a lot of different things in an individual or a set of individuals in different cohorts over time, right? And this is what we know, it's one way to study the immune system. And we call that systems biology of immunology.

So we use a systems approach. Why for a number of years this wasn't possible? Because of technology, right? But what we had at Stanford was state-of-the-art technologies including proteomics that measures many, many cytokines and measures other proteins in the blood and also cellular phenotypes and also many genes that we can measure from individuals. And then the premise was, okay, we're going to be using AI and machine learning to really understand and cope with all this data and try to see if the immune system is able to predict rates of aging in these individuals and we can make this generalizable. Yeah, it's fascinating

because, you know, you took a very different approach, which is a systems biology approach. And functional medicine is essentially a clinical model that applies the principles of system biology, which basically hypothesizes that everything is connected, that the body is a system, that you can't just look at one organ or one pathway and try to fix problems. It's sort of whack-a-mole medicine. But if we stand back and we go, what is the relationship between these various sort of networks in our body? And the immune network is such a critical aspect of aging. And I want to get into that in a minute. You know, we can begin to understand

things a little bit better. So, you know, in the work that you're doing, you sort of describe a lot of the hallmarks of aging and inflammation is one of the key hallmarks and is often referred to as inflammaging. In fact, the process of aging itself is a weird process because at one point, at the same time, you're actually getting more sterile inflammation and your immune system isn't working to fight infections. You're also less able to fight cancer and have more autoimmune disease. So it's kind of a weird kind of mishmash of things happening. But at the end of the day, what happens as we age is we get more inflamed. And that's what you're really finding and looking for, right? Exactly. So here I would like to just pause for a moment and try to make a very important distinction between inflammation as the response to an infection,

and that's what we all know as acute inflammation. You know, you cut your finger, it gets red, swollen, warm. All those are signs, cardinal signs of acute inflammation that should be resolved in less than a week or 10 days, right? In this case, we only 20 years ago started to realize that there's other types of inflammation out there, right? The original paper that was published by Franceschi in 2000, talking about this concept of inflammaging, points to this reality that there are multiple types of inflammation, right? And in this case, we're talking about a type of inflammation that increases with age that we call, exactly as you mentioned,

is sterile. That means that these stimuli, that the triggers of inflammation are not infectious, right? And they go back to very multiple things that have to do with how we age, right? So the quality of air, the quality of water, the nutrition that you know very well. Dr. Justin Marchegiani A inflammatory diet, right. Dr. David DeRuwe Exactly. Consumption of gluten, sedentarism, sleep quality, the levels of stress. And we can elaborate on this thing extensively for hours, right? But going back to the hallmarks of aging,

that's a really interesting one. These are hallmarks of aging are found for the most part in animal models. So we're testing these hallmarks of aging as I speak, right? Mostly using worms and flies and mice. So the classical telomere shortening and genomic instability and disruption in different intracellular communication. All these things are actually driven by systemic chronic inflammation. Yes, yes.

And there's more than 5,000 papers showing that every single one of the hallmarks of aging are driven by elevated systemic chronic inflammation in the body as a response to multiple triggers that have to do with how we treat our bodies. Yeah. So it's almost like the final common pathway, right? When you look at the hallmarks of aging, and I was going deep into this in my book, mitochondrial damage, changes to our proteins that are damaged, the changes in nutrient sensing pathways around insulin and protein, mTOR, AMPK, and all these different pathways, the epigenetic changes, the genomic instability, as you mentioned. I sort of added an extra one, the microbiome. I think that's a degradation of the microbiome,

could be even an important additional hallmark of aging. But like you said, all of them are worsened and made worse by inflammation. So the inflammation can both accelerate these, but also these problems can accelerate inflammation. So for example, disorder nutrient sensing, when you have inflammation from eating sugar, then that's going to drive problems with insulin sensing pathways, and then you end up with more inflammation. So it's kind of this big mishmash of everything that ends up with lots of inflammation. That's absolutely right. And oftentimes, I get asked this question, what goes first? Is it inflammation? Or is it the other hallmarks of aging? And it's both, right? As we age, we are exposed to multiple different inflammatory triggers that cause cellular senescence, as you know as well. It's a very important hallmark of aging.

Zombie cells. We call them zombie cells. The zombie cells, exactly. And they produce all these inflammatory products that go around just creating a wildfire like a wildfire throughout your body that accelerate aging even more it's like and then they don't die and they just keep producing making other cells zombie cells and it's just a nightmare exactly exactly but there are ways to cope with that and obviously um the the one thing that uh we both know it's a very powerful um a method method to avoid all these things is just really stop the trigger.

All these are triggers that are pushing inflammation upwards. Well, this is really an important thing because as I began to do the science investigation and look at these hallmarks of aging and look at the research on longevity, a little more detail, it kind of occurred to me that the researchers in a way are stopping short. They're going, okay, these are the hallmarks of aging. These are the things that go wrong. Let's fix these things. And my question is, well, what's causing these things, right? Functional medicine is looking at the cause, the root cause. And if hallmarks are the cause of aging, what's the cause of the hallmarks of aging? And like you said, inflammation is one of the key hallmarks in the final common pathway, but then what's causing the inflammation in the first place that's driving sterile chronic inflammation and

causing acceleration of all these hallmarks of aging? So that's really the question. So I want to ask you about that. And then I want to get into how you kind of mapped out a way of looking at the sterile chronic inflammation in a novel way that gives us a chance to see our rate of aging and where we're headed. Because a lot of the traditional testing doesn't do that. And so I think this is a huge contribution to science. And when I saw this, I was so excited. Because I know that people are inflamed and sometimes the normal tests don't show up

as inflammation but then you found all this other stuff so let's kind of start with okay now we've established that you know these hallmarks of aging and by the way they're all in my book you can read all about them but uh we're gonna it's coming out in February but but I want we're not going to get into all that this this this this podcast but I want to get into the overarching framework of inflammation and what's causing the inflammation. And then we're going to talk about how we identify it and what you've learned about how to identify the right kinds of inflammation that correlate with aging specifically. So take us down the pathway of what we know about the causes. Because if we know the causes, then we can get to the pathway of what we know about the causes, because

if we know the causes, then we can get to the treatment of the root cause, right? That's the key. Yeah, yeah, absolutely. So I've been studying social and exposome determinants of inflammation for about 15 years now, right? And the type of data that it's out there point very clearly to things that most of us know. However, there are certain aspects of the exposome that we do not know. What's the totality of biological, chemical, and social exposures that a person suffers throughout the life course. And what we know about that is that 95% of chronic disease is caused by the exposome, not the genome. Meaning your genes are affected by the exposures that then change the gene's function, which then lead to all these diseases. But it's not the genes that are the problem.

It's the exposome that's the major problem for most of us. That's exactly right. I would like to get at that in a moment. We have the genome, everybody, you and I and everybody in this world, to be able to live 120, 130 years at least, right? That is something we know. Now, the problem is in some countries, people are dying at the age of 70, 75. That's the average lifespan expectancy. Some countries it's 89 or 90 like Monaco Japan, because we figure out ways to extend that

period of healthy living, right? So in essence, what we're trying to achieve is to push that 80 to 90 average life expectancy to 120. Now, tweaking genes is a completely different thing. We're not going to talk about that at this podcast. But I'd like to go to the idea of the exposome. Yeah. Back to the root cause of inflammation. So we do know already today that pollutants in the air, that pollutants in water. Pollution.

Pollution, exactly. Pollution. Pollution, exactly. Pollution are drivers of inflammation. Imbalances in nutrition, such as both macro and micronutrients, right? These cause inflammation by large. Food additives go back to the microbiome. Things like carboxymethyl cellulose or polysorbate 80 that will wipe out your microbiome and will cause inflammation because the mucin layer in your linen of your gut will get very thin. And then you're going to have translocation of different antigens to your periphery, and you're going to develop an inflammatory reaction.

Gluten, you know, gliadin. It's a major- Wait, wait, I just want to hold on. What you said was very important. You just said that basically when you eat these food additives, things that are in our food that we don't even pay attention to,

like polysorbate 80, it damages your gut lining. And then all the poop and bad, like in food particles that are partially digested leak across that. And your immune system is right under the lining of your gut. then your immune system goes hey what's this bad foreign stuff and it starts creating this inflammation so that's why it's bad so food adders are just not bad because they're you know if you're a hippie and you want to eat granola and like this you shouldn't eat

food adders they're really damaging to our bodies right your microbiome yeah exactly they're they're causing this concept of uh dysbiosis right in your gut and then you're going gluten was the next thing you were going into exactly so or plasticizers plastics things that are are stored in in plastics and plasticizers or the plasticizers and plus the resin make a plastic and there's leaching right and there's a leaching of plasticizers that go into our foods. And those are hormone disruptors that also cause inflammation long term. I was going to go to gluten. Gluten, as you know, is highly inflammatory.

Glyadin can bind to certain cells in your gut and cause inflammation, increasing leaky gut, etc. The other one is sedentarism. As you very well are aware, if we're sitting in a chair, we're developing an inflammatory reaction and that it's a perfect correlation between the time sitting in a chair and mortality. There's almost a perfect correlation between those two. Sleep quality, disruption in our circadian rhythm, social stress. There's a very, very compelling evidence

that individuals that are exposed chronically to social stress, social isolation, they develop inflammation, they have more cardiovascular disease, elevated rates and death. And obviously other chemicals that we're exposed to that are surrounding us, just even an example, formaldehyde, right? Paraformaldehyde that serves as a glue for plywood that is often used in furniture and cabinetry. So those are important things. So basically, it's environmental toxins, it's social stresses, it's inflammatory foods like sugar, it's food additives, and even other environmental toxins you didn't even mention like heavy metals, not just plastics. We're exposed to all this stuff and our gut microbiome becomes

disturbed because of a lot of these things and that even creates worse inflammation. So we're in this inflammatory environment, which historically we really didn't have throughout evolution. And the truth is we did a lot of things that naturally combated inflammation. So just as there's an inflammatory lifestyle, there's an anti-inflammatory lifestyle, right? Hey everyone, it's Dr. Mark. Now something I get more and more excited about every year is personalized medicine. Now when I began practicing functional medicine over 20 years ago, it was clear to me we have to look at how unique each body is. Now with technology advancing in amazing ways, we can truly take that concept to the next level. Like one of the tools that I recently discovered that can help us all do this from home is Inside Tracker. Founded in 2009 by top scientists in aging, genetics, and biometric data from MIT,

Tufts, and Harvard, Inside Tracker is a personalized health and wellness platform like no other. It's purpose-built to help you live a longer, more productive life. Their cutting-edge technology analyzes your blood, DNA, your lifestyle to give you highly personalized recommendations. Then, using the app, you can track your progress every day. InsideTracker tells you what to do and why, so your health goals are clear and actionable, and most importantly, based on exactly what your body needs. And now you can connect InsideTracker with your Apple Watch to unlock deeper, more precise insights into your health.

With real-time exercise, resting heart rate, and sleep data synced with your InsideTracker plan, you can truly wear your health on your sleeve. My team took InsideTracker for a spin and really loved it. They discovered some important things about their health that led them to stop procrastinating when it comes to certain parts of their health, like, for example, finally taking a vitamin D supplement after seeing they were deficient, or eating more iron-rich foods due to low ferritin and hemoglobin,

and making an effort to embrace stress reduction techniques after seeing high cortisol levels. Now, health is not black and white. Your wellness plan shouldn't be either. If you're curious about getting your own health program dialed in to your unique needs, I highly recommend checking out InsideTracker. Right now, they're offering my community 20% off at insidetracker.com forward slash Dr. Hyman. That's I-N-S-I-D-E-T-R-A-C-K-E-R.com slash Dr. Hyman. That's me, Dr. Hyman. And you'll see the discount quote in your cart. Now let's get back to this week's episode of The Doctor's Pharmacy. So the beauty of your work, and I want to get into this in a minute, is that you've been able to map out the changes in the immunome. And for those that don't know what that is, it's basically

the sort of immune... Well, why don't you define the immunome? You're the expert. Yeah. I don't want to probably screw it up. I doubt you will. So similar to the concept of exposome, the end and the word some accounts for the totality of it. So when we talk about the immunome, we talk about all the cells, the proteins, and the genes that are in your immune system that are able to communicate between them, right? And so orchestrate an immune response. So we're talking about hundreds of thousands of different parameters that can be measured from blood. And that's what we did in the Thousand Immunomes Project, which is a project that,

as you mentioned, lasted for about now 15 years. We just got another source of funding from NIH, $15 million to continue the study for the next five years. And we've been monitoring these individuals, their immunome. And basically, we focus in blood. So, we take cells, genes, proteins in the blood. And as you mentioned before, the biomarkers that are currently existing for what we believe is inflammation, such as CRP, HSCRP, sedimentation rate, that you can go to the doctor and have those, are very poor predictors of any type of condition, right? CRP, just to give an example, is predictive of cardiovascular events with a power of 0.6. The area under the curve when you're trying to predict cardiovascular events is almost close to random chance, right? So, in studies... It's helpful, but it's not very sensitive. It's not very sensitive.

It's not very sensitive as a measure for systemic chronic inflammation, exactly. And that's where this whole idea of discovering new biomarkers, but looking at the immune system in an unbiased fashion comes into play. And that's what we did. So what we are using is not only technology that help us measure all these things, but also computational analytical tools that are rather novel, including AI ML, right, machine learning, to be able to cope with the data and to derive metrics that are simplified, that take us hundreds of thousands of parameters.

Now we have a metric that can be used in the clinic, right? So it's like finding a needle in the haystack, you know, and it's a way of doing that, which is very hard to do in medicine, right? That's exactly right. That's exactly right. But the medicine and the clinical medicine and also research is changing. So there's now a lot of different groups across the world. Here in the U.S. it's very popular to do transcriptomics, proteomics, and we're measuring 7,000 proteins in the blood, 3,500 metabolites, and it becomes much more normal. It has normalized with time. Yeah.

So when you did the 1,000 Immunomes Project, were you measuring how many analytes? Because I remember reading the paper and there were like 50 cytokines that you looked at. But was there a lot of other stuff you also measured besides those 50? Right. So we measure the expression of genes. And these are roughly 15,000 genes that we measure from a drop of blood, basically. We also measure cells that are circulating in the body. And these are immunological cells, around 25 different cell types. And we also measure metabolites.

And the 50 proteins that we measured across these different years, this is a panel that was expanded now. We're currently measuring 7,000 proteins from individuals. And making sense of that is the challenge here. And it's really a beautiful system that this company has started, I would say maybe 10 years ago or so, in which they can now analyze 7,000 proteins. There are other companies analyzing 35 or 4,000 proteins. And we're measuring all these things to see how those contribute to rates of aging. So in a way, this is something that's never been possible before because you have this convergence of the framework of systems biology, understanding the bodies and network,

where there's these dynamic interactions of thousands and thousands and maybe trillions of chemical reactions every minute. And you can measure through advanced technologies, thousands and thousands of proteins, the expression of thousands of genes, the analytics that help you process that data, which is so hard with bioinformatics and computational tools like AI and machine learning, which really didn't exist before. And so as a doctor, I'm so excited because it's always been really clear to me that we're missing stuff. That we do an exam and we do lab tests pretty much like we've been doing for the last hundred years without a change.

Exactly. You know, it's like, come on guys, there's like more going on here. And we get stuck in the way we do things. But you're kind of blowing the lid off it. And what you did was then correlate things that would be hard for the average, you know, scientist in his lab, like, you know, with graphs and maps and things to figure out, correlate which of these analytes and proteins and cytokines and biomarkers were correlated with different diseases and the rate of aging. So to sort of explain what you found as you begin to sort of unpack the extraordinary amount of data and what were the kind of nuggets that you came up with in terms of

identifying the things that we should be looking at. And there are honestly things I never even heard of as a doctor that I don't even remember. Maybe they taught me medical school, but I don't even think we knew about it then. So it's like, it's so exciting. I'm like, oh, there's this cool thing that is so different that I never even heard about that may be actually more relevant than anything else I've figured out, like, you know, CXCL9, which is a chemokine. Well, I never heard of that, but that may be more important than anything else we're measuring on our blood work, right? Yeah.

So that's a great segue for what I wanted to discuss with regards to how this inflammatory age metric that we build is predictive of diseases, right? So, we can predict the age of individuals by just a selfie. That's easy. We can- Come on, you do a selfie of me? How old do I look? You can also take any blood biomarker and predict the age. Age prediction of age is easy because things change with age. That's not the complicated part. The interesting part is once you take these immune biomarkers and try to predict the age of individuals, so you, in essence,

are you generating a clock, a biological clock, a new clock of aging. And this is an inflammatory clock because we're looking at the immune system and inflammation as our source of data. So we build that inflammatory clock that is able to accurately predict the age of an individual. Nothing very fancy. Now, when we adjust for age, that means that for a given age group, we see those that are deviated upwards versus those that are protected, deviated downwards. So in other words, they have an inflammatory age that is beneficial according to their age. Then we find that those with higher inflammatory age, according to their age, are at risk for developing multimorbidity. That's the first finding. And multimorbidity is what?

Multimorbidity is defined as the sum of multiple diseases, in this case, non-communicable diseases of aging. So, say someone could have a musculoskeletal condition, that's one disease. If that person also suffers from cardiovascular conditions or some events in the cardiovascular system, that's two diseases. And then you add up to 10 diseases. And this is very common, as you know well, in the US and also in other parts of the world, after the age of 65, we're suffering from around 8 to 10 diseases, and we're taking about 14 to 15 different medications. So it's huge, it's huge. So what we're trying to here identify is a biomarker from blood that is focused in the immune system that is able to predict multiple diseases

simultaneously. So this is multi-morbidity, that concept. And then we went ahead and did a whole slew of different studies, right? We looked at frailty in individuals. So frailty is measured by asking individuals whether or not they're independent enough and you take the, you know, a grip strength and the time up and go, different functional measurements in individuals. And we're able to predict with the inflammatory age, seven years before it happens, who's going to become fell? Wow. So that's another big discovery that we did that we published last year in Nature Aging. And also CXCL9, as you just mentioned, one of the most important contributors of inflammatory age of this new metric is a chemokine that is part of the immune system

proteins in the blood that has not been identified before as a marker of systemic chronic inflammation, right? In markers that are usually coming up in the inflammatory reaction against pathogens. That's easy to measure. Interleukin-6, TNF-alpha, interleukin-1-beta, those are well-established canonical markers for acute inflammation. Those are cytokines like we talked about with the cytokine storm with COVID. So those are, yeah, those are the typical cytokines, right? Exactly.

And those allow for cell-to-cell communication. In this case, we're talking about a very different set of proteins that are coming up as being the most predictive. And then we went ahead and looked at a number of different cardiovascular phenotyping measurements in these individuals, and were able to correlate CXCL9 with cardiovascular aging, with cardiovascular health. And then we went ahead and continued this study to look for mechanisms and to explain other morbidities, and we published that last year in 2021. So basically, this iAGE biomarkers, and as I understand, there's a smaller panel, an expanded panel.

So out of these thousands and thousands of things, you found like four key ones that you can measure now on a blood test. And there's others that are an expanded one. Maybe it's seven or eight. I don't remember the number. But there's not an infinite number of these. And in those kind of biomarkers, you're able to identify the rate of aging and also the risk of chronic diseases, whether it's dementia or heart disease or cancer or diabetes. These are all inflammatory diseases, right? Correct. So the understanding of these diseases is very poor, as we know. Otherwise, we wouldn't suffer from those.

And so, only as I mentioned at the beginning of this conversation, 20 years ago, we started looking at the immune system as a major root cause of these diseases. And we are just starting to derive the biomarkers. This is rather new, right? And you're absolutely right. From looking at this extended panel of cytokines and proteins in the blood, we identify core five biomarkers, including this one CXCL9, that is, by the way, largely produced by your endothelium. So it's not just immune cells producing. The endothelium is the cells that are making up your vessels, right? They're lining your blood vessels. Exactly. Your blood vessels, lining of your blood vessels. And those cells can become

inflammatory. So when you, as you get older and we treat our bodies in different ways, those cells become senescence and they start producing CXCL9. And then you have all these downstream effects that we just mentioned a few minutes ago. And so what are these cytokines and chemokines, what are they doing? Like how are they accelerating aging? And are they the cause of heart disease? Are they the cause of dementia? You know, are they just correlated with them?

That's a very, that's a great question. It's a little bit of a loaded question. And I'm saying that because we would need a lot of mechanistic studies to demonstrate the relationship between every one of these proteins and the causal inference in tissues and degradation of organs. We did that for a single one, right? CXCL9. When we take CXCL9 and incubate, that means that we put it in a Petri dish, and we start growing cells in the presence of CXCL9, these endothelial cells are completely dysfunctional. They don't respond well to acetylcholine. They don't contract. They don't have the production of tubes that you need. So these are completely dysfunctional endothelial cells. And then we also see that cardiomyocytes,

which are the cells that are in our heart, are suffering from the presence of CXCL9 in the body. So when we now block, let's say block, right? We block CXCL9 by introducing what we call silencing of the protein. In this case, we use an shRNA, we can restore completely that function of those cells. Exactly. Yeah. Amazing. So really, it opens the door to a different set of therapeutics, because, you know, before, you know, it was very hard to measure metrics that gave us a predictive sense of the rate of aging. There's DNA methylation clocks, which are really important. I've talked about them before on the

podcast, but they're essentially looking at your epigenetics and how your genes change and the marks on your genes change and how that correlates with longevity and aging and your biological age. And for example, I had my DNA methylation test done and I'm 63 this month, but I'm actually 43 according to my biological age, which makes me happy. So then I think the immune age is a little bit different because it sort of looks at a different kind of component of aging, which is not just epigenetic changes, but the immune changes, which may, who knows, may be more important. And what's really important as we start to look at the science of longevity is we need biomarkers or we need metrics to say,

oh, if we do this, this gets better. In other words, if I eat better, do these markers change? Or if I take this vitamin or this herb, does it get better? If I do a sauna, does it fix this problem? Or whatever it is that we're doing, do I take stem cells, is it going to make it better? So we need metrics to sort of look at the interventions that are going to control. And so I know you've done a lot of work and you're doing now a couple of clinical trials, actually using some interventions that are designed to modify these biomarkers that you've identified, and that hopefully will then sort of lead down the road to avoiding some of these age-related diseases or even treating them.

Right. I think what you're bringing is twofold, right? You're talking about ways to evaluate interventional procedures. It could be dietary. It could be other lifestyle procedures. We need those surrogate markers of aging. Inflammatory age is one, epigenetic aging is another one. There's now a metabolic, metabolomics clock. There's a number of clocks out there that will ultimately help address the question, is this intervention helping for the aging process? That's one question. Now, a very different one is, are these biomarkers or clocks, can they be used to identify

interventions? Not interventions that we know could help, like a better quality of sleep or not interventions that we know are anti-inflammatory, like a better diet, but interventions that can actually reverse the clock because you're targeting those biomarkers. So, for example, if you do that with the epigenetic clock, that's very difficult. And why is it difficult because we understand very little about how to change epigenetic landscapes that's very difficult now with the inflammatory age is much easier because we just measure proteins right so i take uh uh uh the way we have building this and let me expand this a little bit in this idea.

We take these five biomarkers, one of them being CXEL9, the other one, eotoxin, other biomarkers that you can find in blood. artificial intelligence and machine learning to pull from the literature hundreds of thousands of compounds that are able to interact with these biomarkers. And then I would ask the algorithm to pull, to take the compounds that are likely to change that in vivo, right? And so that's the basis of the two clinical studies that we have been running. The first one, we identify a compound that is able to decrease your inflammatory age by about two and a half years in two weeks. That's very rapid, very, very quickly. What is that compound? That's a compound that's included in a hot breakfast. I cannot really disclose at the moment because this is a collaboration with a corporate partner. Yeah, yeah, yeah.

What I could tell you, though, is our own clinical trial in 1,000 individuals in which we tested different grass-approved compounds. So these are generally recognized as safe by the FDA. So we can take drugs, we can take bioactive compounds, and we can take also a number of different mapping compounds to food and food ingredients, right? So things like manganese chloride, beta-carotene, iron, other vitamins, ticetanil, quercetin, things that are readily available as a direct-to-consumer OTC. Yeah. Yeah, it was interesting because when I looked at your clinical trial, it's listed on clinicaltrials.gov, you know,

the compounds that you had identified to regulate inflammation, I was a little surprised by some of them, like iron bisglycinate, magnesium chloride, vitamin D2, guar gum. You've got a broccoli extract in there, indole-3-carbinol, methionine, biotin, caffeine, lutein, zinc, beta-carotene. So I'm like, this is an interesting cocktail. I'm like, how did they come up with this? And I guess it was because you used the literature to determine which of these compounds may have mechanistic actions that regulate these pathways of inflammation, right? Exactly. That's exactly right. And you can take drugs to be able to

repurpose drugs. That's not in our business here. Or we can take bioactive compounds that are readily available and also found in foods. So you're absolutely right. Yeah. It's amazing. So these trials are not completed yet. They're still underway. So we're going to find out more. But you have on the website for Edivis Health, which is the company that's sort of behind the IH test. And by the way, is this available, this test now, clinically yet or not yet? It's not available yet. And the reason is to make this available to the public,

we need a couple of milestones, right? One is to finish a trial, be able to add our claims. And preliminary results are looking really interesting. Very, very good. So I'm very happy for that. And we also need a CLIA accreditation. And this is particularly for labs that are taking clinical samples. So we cannot go to market quite yet until we have a CLIA certification in our labs.

So that's part of the undergoing process. Yeah. So we had lunch, right, as COVID was starting in March of 2020. And you were telling me about this. And I was like, wait a minute. It's two plus years ago already. Let's go. I'm waiting.

I'm waiting. I'm waiting. I'm being patient here. But it's exciting. I think it'll come around soon. And then as an individual, you can go, you know, geez, I want to change my diet, or I'm going to take these supplements for a few months, and I'm going to check my test, and I'm going to repeat it and see how it looks, right? And so

we'll be able to sort of, on an NM1 basis, determine what works and what doesn't for us. And I think as a doctor, it's very exciting to me because then I have a metric to use with my patients to determine, you know, is what I'm doing working or not on things that actually really matter, right? So we do things that are, we do that already. Like, oh, we change our diet and improve our cholesterol, or we change our diet and improve our blood pressure. We see a reduction in CRP or inflammation.

And we can do that already. But I think this is going to be a much more profound marker because what you're saying is based on this huge data analytics and thousands and thousands of biomarkers, you're actually finding the things that are maybe the most important. Right. And it's important that you mention the fact that you as a physician that can use this to evaluate how your patients are doing, right, and how effective your interventions of your favorite interventions for a particular patient will work.

And so on that angle, I would like to say that we really need to educate primary care physicians and other healthcare providers about the power of inflammation, about the power of our test. For now, it's a test that is out of pocket, and it will come out as out-of-pocket test. And the reason for that is that we have a long way to get FDA approval. And why is that?

Because aging is not considered a disease. Inflammation is not considered, not yet. Inflammation is also not considered a disease. Inflammation is not considered, not yet. Inflammation is also not considered a disease. So we have a risk factor for multimorbidity, which is also not a disease. How can you go to the FDA and explain to these folks that this needs to be reimbursed and everybody should have access to this. So that's a completely different story. But we do have to map inflammatory age as a risk factor for a particular indication, for a particular disease, and that's one way to go FDA and get that approval. Yeah, it's such a mess though because traditional medicine is so hyper-specialized and reductionist

and it doesn't understand that if you – it's like a unified field theory, right, of medicine. If you understand inflammation, you understand so much about what goes wrong with our bodies and really almost any disease. And it's such a key phenomena. I mean, and it's such a misunderstood and inadequately understood phenomena that the doctors don't know how to identify inflammation properly. They don't know how to treat inflammation properly. They don't know what to do from a lifestyle perspective. And they go, oh, just take Advil.

You know, I remember one study that came out a while ago where they're like, oh, and Alzheimer's is inflammation in the brain. So they did a big study where they gave everybody Advil. I'm like, oh, that's not going to work. It's like, you know, we got to find out the cause of the inflammation. And so from a functional medicine perspective, it's the things you talked about. It's sedentary lifestyle. It's inflammatory diet. It's chronic stress.

It's environmental toxins. It's allergens. It's microbes. It's the gut microbiome. All these things which we actually have ability to control. And it's also the lack of things, right? So, you know, I hear from Argentina and, you know, the world's quite different down there and the foods are different and people live in a more sort of closer to land way.

And like when I came back from Sardinia and Ikaria in Greece and in Italy, I mean, these people were eating these foods that were so rich in phytochemicals and in these compounds that are anti-inflammatory. They didn't even know they were doing it, right? They don't know that they have this wild sage tea every day for breakfast because that's what's growing in their field, you know, that it's full of these catechins that, in fact, modify NF-kappa B and regulate gene expression of inflammatory cytokines and blah, blah, blah. They don't know any of that. They just drink the stuff because it tastes good.

But we've gotten so far away from that. And yet, what's exciting is you're starting to kind of look at these interventions, which are relatively low cost, which are relatively accessible to most people. Like it's what you eat, it's how much exercise, it's how you sleep, it's how you manage stress, it's including some phytochemicals in your diet, maybe a few supplements. And these are the kinds of things that you're looking at. Because when you, I think you realize, and it's exciting to me to kind of hear the way you're thinking about it, is that it's not like we're going to find the drug to, you know, change your immune age. You know, it's like, that's just not a sensible way to think about it because it's not one pathway. There's all these inputs that you have to modify in order to actually allow yourself to age well and to not only, you know, prevent disease, but to reverse your biological age.

So the good example that you have given on taking Advil to combat inflammation for Alzheimer's is a poster child. It's perfect because not only this will not work, but also you would wipe out your microbiome. And in the long term, Advil will cause probably more chronic inflammation. So it's not just... Kidney failure and leaky gut and ulcers and bleeding. But the hope here is that more and more primary care physicians and functional medicine physicians are realizing the importance of inflammation, the important part of using this systems approach, right? We can't treat one disease. You're going to have another disease. What happens if currently you stop today,

you cure cancer in the entire population worldwide. You only extend the lifespan of the humanity by one and a half years, right? We know that because you have all the diseases. And that's where it's important. So the war on cancer doesn't make sense, right? The moonshot for cancer, it should be the moonshot for the root causes of disease, right? Of many diseases, exactly. And we know now that that's possible. And let me tell you something really interesting that's happening in France.

I'm collaborating with a group in Toulouse, and the WHO, very recently, in July of this year, have accepted, has included in the ICD-11, the classification for diseases, a decline in intrinsic capacity as a disease. Yeah, aging. It's not aging, right? Because we can't talk about aging as a disease. That causes a lot of social and political issues. And I think we're talking now about the decline in intrinsic capacity.

It would be something similar to aging, right? But that's very good news because if we now can map or correlate inflammation with that decline in intrinsic capacity, we can present this to the FDA and make it available for everybody, right? And so the French system is really interesting what's happening. Bruno Vela is at the University of Toulouse. He's assembling around 500 people in the Gerontopole University Hospital, and he developed an app that tracks functional domains of aging, namely vision, you know, audition, mobility, et cetera. And what happens if he already has 25,000 or 30,000 individuals that have been filling up these questionnaires in the app, what happens with there is a slight decrease

in some of these functional domains of aging, a red flag calls a nurse, nurse comes in, she makes sure that the input is correct, and that person gets derived to a primary care physician. They're not sick yet. That's not an indication. They're starting to decline in their capacity of their organs and systems. So that's where the whole healthcare systems are actually going to. I think the idea of doing functional organ-specific decline is where everything and everybody should be focused on. We now have a clock of different organs.

That's a completely separate story. But we're trying to define from a single drop of blood how or where you, Mark, where are you in terms of your internal organs? Is it your liver maybe going a little bit off? Maybe my cardiovascular system is off as opposed to my liver. So everything is pointing to functional and to personalized precision health using these different domains. So the IAH test is going to help us map that, right? That's exactly right.

Do you think you're going to be adding more biomarkers to that test, or is there going to be another kind of framework to look at biological aging as you start to learn more? Because you're constantly learning, right? So, aside from the product that we have, inflammatory age, which is these five core proteins, we're measuring on the back thousands of them, right? So, imagine we don't have a very large population, ethnically diverse so far, right? So the study was run at Stanford, Palo Alto individuals, very specific population there. And we're expanding this to African-Americans, to Indians, to Japanese population. So more biomarkers will be added. Absolutely.

No question about it. You know, one of the things I thought was fascinating about your study was that you had a bunch of people who got very old. There were like 19 people who got to 99 or more. What did you learn from that group? So this is a centenarian group that we obtained in collaboration with the University of Bologna in Italy. So they get to be centenarians, right?

A lot of fish, a lot of walking, good quality of lives. And so what we learned was that… A lot of pasta bolognese, right? I would avoid that one. But what we did learn when we did the… In that population, we measured 1,300 proteins, and we derived inflammatory age, and we compared with older adults, 70 to 80 years old. in this very older individual centenarians, I'm saying, it's very, very low as compared to their calendar age. So on average, 40 years below their calendar age.

Wow. That means that for a 105- So assuming that when you look at their eye age test, they were 40 years younger. So if they were 100, they were like 60. On average. Some individuals are closer to their own age and some of them, there's one outlier, very interesting outlier,

super healthy, he's never seen a doctor, 105 year old. He looks like a 25 year old kid. So we're talking about 80 years below his calendar. Oh, you mean not not he looks like his blood work looked like he was exactly yeah it's like maybe he got a birthday wrong there no no no no no i'm look i'm i'm referring to his inflammatory age uh was 80 years below his calendar age

and and he's doing extremely well and still alive. Incredible. And so you found basically that, were there anything unique about these people besides their lower levels of these inflammatory compounds in the IH study? Not in our study. We didn't look in detail, but we know that the microbiome of centenarians is very particular, that the immune system is also particular with very high levels of CD4 naive cells, which usually they exhaust with time. So it looks like they do have a constellation of biomarkers that are associated with immune system function that looks much younger than their chronological age. Wow. Wow. That's quite amazing. And were there any characteristics of their lifestyle, their habits, what they did that were different besides living in Bologna? We were all in Bologna, right? Yeah, we couldn't have access to additional

information. This is a collection that we just had the samples, the blood samples, and we ran our studies. And what we do see, though, is that when you do metabolomics, and metabolomics measures around 4,000 metabolites from blood that can inform what you're eating, actually, right? So the quality of the nutrition. Yeah. Oh, you did that? Yes, we did. Yeah.

What did you find? Well, we do see a very favorable phenotype in the metabolomics. So the metabolomics clock that we built is actually much more beneficial in these individuals that in younger counterparts that are still older, like, so 70 to 70 to 80 years old. So. So this metabolomic clock is a measurement of the metabolites in the blood that are related to what they're eating or related to what? Yeah. So it's yet another clock of aging. So you take metabolomics in large cohorts and you're trying to predict a chronological

age. And after you do so, you look at which metabolites are more informative and then you map that to back to foods. Yes. So we can actually predict what you were eating yesterday, say, based on that metabolic clock. And did you see any things that they were eating that were unique or different in that group? Mostly fish derivatives. Yeah. Fish derivatives. Interesting. Yeah. Yeah. Not surprising though. No. Well, omega-3 fats and selenium and iodine and protein. Yeah. Interesting. I mean,

I did my metabolomics once and it was shocking actually. And it made me change everything. So I found that I had these oxidized byproducts of olive oil because at the time, this was years ago, I was using olive oil to cook, like not just on my salad dressing. And they were basically oxidized, damaged olive oil compounds, which the olive oil is healthy, but when you heat it up to high temperature, it oxidizes. So I was actually harming myself by having cooked olive oil. And I didn't notice that. Completely. Yeah. So it was interesting. So I think what's so exciting is that, you know, people listening, there's this whole new world emerging in medicine that you're really not getting in the clinic that is able to sort of look at massive amounts of data from things that, tens of thousands of genes that are doing all sorts of things, our epigenetics, our immune system, our microbiome. I mean, that's a whole

nother can of worms of what's in there, which is even far greater than our own genome. There's probably 100 to 400 times the amount of genes in our microbiome than there are our own genes. So they're all producing proteins and metabolites. We're absorbing them. They're doing stuff. It's like this incredible ecosystem soup. And so what's exciting about people like David and Dr. Fuhrman, I mean, is that they're actually able to start to make sense of all this kind of stuff that has been hidden below the surface and now is becoming revealed and guiding us into ways of changing our practice of medicine, our diagnostics, and our ability to change our therapies and then measure how our therapies are working in ways that are much more relevant than what we're doing today. Would you say that's fair? It's absolutely fair. And we owe this to technology, right?

Technology has enabled all this to happen. We can now measure what we measure because we have advances in technology. We also have advances in computing power. And that's very, very important. When 10 or 15 years ago, just to run a script that may involve 1,000 people and 50,000 features, it could take a day. Now it's taking milliseconds. computational standpoint, technology has evolved and we're using that at large to try to resolve this issue of information that drives aging. So we know that today, we have mapped that out and we'll continue to do so. Yeah. So what are you most excited about that's coming up for you? What are the things that you're seeing on the horizon that get you really excited and out of bed in the morning?

Yeah. Well, I mentioned this transition, right, from a highly reactive, disease-centered vision of governments and non-for-profit organizations and the whole industry and academics to a much more proactive, a much more preventative, a much more functionally related healthcare system. That is something that I think I'm personally feel like I'm involved in this. I'm taking part of this change, and I'm very excited for this huge change that is very positive for humanity, obviously. That's so exciting. It just reminds me of this patient I had years ago. We came in. His blood sugar was like 110, which is pretty much in the almost diabetic stage, like pre-diabetic. Diabetes is like 126.

And I said, gee, did you see your doctor about this? And what did he say? And he says, well, yeah, he said he saw it. And I said, what did he say? He said, well, he said, watch it until it gets to be diabetes, and then we'll treat it with a medication. And I was like, oh, God. And I think this is the opposite of that it's like before even you have a symptom before even

a disease manifests before even you you can pick it up on most lab work we're going to be you know able to almost like some star trek use a tricorder and kind of figure out what's going on run it through, you know, this incredible computational abilities that are emerging, that we haven't even seen yet, like quantum computing, which allows us to crunch enormous amounts of data. I mean, each one of your, you know, each one of us human beings has literally gigabytes, terabytes of data in us, literally all the time, like trillions of reactions. And it's just beyond the capacity of the human mind to even start to process or think about.

But when you start to combine these technologies with emerging science of systems biology and the work that you're doing at Stanford, and there's a lot of other people doing this in other domains in medicine, and it's all coming together. So the medicine that we see today is really, I would say it's, it's like, you know, we're going to look back and go, God, this is like bloodletting or leeches. And, and I think, I think we're, we're in this incredible moment and I, I'm excited to see about your work with the hundred thousand immunos project, the IH test, which is coming online hopefully soon, and also with the kinds of interventions you're now doing to see what modifies your immunological age. Because, you know, this is kind of an exciting moment where there's like billions of dollars pouring

into longevity science where there's, you know, it was kind of a neglected stepchild of medicine. Like, why study aging? It's inevitable. So what, who cares? Like, you know, let's study cancer. Let's study heart disease. But aging, you know, one of the things that was shocking is like, if you're like 30 years old and you're a smoker and you smoke three packs a day of cigarettes, your risk of cancer is like 50 times less than if you're like 75 years old and don't smoke, right? Something like that, where the idea, I mean, I'm kind of, you know, just making up numbers here,

but I think the idea is that the aging itself is such a bigger risk factor for all these diseases that we're kind of missing the point of like studying aging. So you're studying aging and a lot of other people are doing this. It's an exciting moment. So thank you so much, David, for your work. And at Stanford, we're going to keep track of it. I'll probably have you back on the podcast to talk about what's

next and happening in your horizon. Everybody listening, you can check out more of their work at their website. It's edificehealth.com. And there's information there about the IH test and about the 100,000 Immunos project. And you can read their research, you know, kind of little technical sometimes, but they've got a really great interface to sort of learn more about what they're doing. And I hope you've enjoyed this podcast because I did. And I think it's a very exciting moment in medicine. And David, I hope we continue to collaborate and talk. And for those of you listening to this podcast and you'd love to with your friends and family, we bet they'd love to hear about how to regulate their inflammation. Subscribe to every year podcast and we'll see you next time on The Doctor's Pharmacy.

Hey everybody, it's Dr. Hyman. Thanks for tuning into The Doctor's Pharmacy. I hope you're loving this podcast. It's one of my favorite things to do and introduce to you all the experts that I know and I love and that I've learned so much from. And I want to tell you about something else I'm doing, which is called Mark's Picks. It's my weekly newsletter. And in it, I share my favorite stuff from foods to supplements to gadgets to tools to enhance your health. It's all the cool stuff that I use and that my team uses to optimize and enhance our health. And I'd love you to sign up for the weekly newsletter. I'll only send it to you once a week on Fridays. Nothing else, I promise.

And all you have to do is go to drhyman.com forward slash PICS to sign up. That's drhyman.com forward slash PICS, P-I-C-K-S, and sign up for the newsletter, and I'll share with you my favorite stuff that I use to enhance my health and get healthier and better and live younger longer. Hi, everyone.

I hope you enjoyed this week's episode. Just a reminder that this podcast is for educational purposes only. This podcast is not a substitute for professional care by a doctor or other qualified medical professional. This podcast is provided on the understanding that it does not constitute medical or other professional advice or services. If you're looking for help in your journey, seek out a qualified medical practitioner. If you're looking for a functional medicine practitioner, you can visit ifm.org and search their find a practitioner database. It's important that you have someone

in your corner who's trained, who's a licensed healthcare practitioner, and can help you make changes, especially when it comes to your health.