What Is The Modern Fountain Of Youth? | Fountain Of Youth

Unlock the mysteries of aging with our fascinating guest, Dr. Nir Barzilai, as we embark on a journey through the science of longevity. This episode promises to reveal the biological secrets that could redefine your approach to living a long, healthy life. Dr. Barzilai, with his wealth of knowledge, decodes the process of antagonistic pleiotropy where the very mechanisms that protect us in youth may become our foes in old age. Together we scrutinize inflammation's role in aging, explore the intertwining of nutrition and longevity, and ponder the potential of targeting aging to preempt age-related diseases. Our conversation navigates through the nuances of intermittent fasting and the surprising health benefits of a 16:8 fasting routine, offering personal insights and strategies that have become integral to our lives.

Some of the topics we will discuss are:

- Secrets of Longevity
- Tips on how to slow down aging
- Does intermittent fasting help with longevity?

When it comes to the tapestry of longevity, the threads are as complex as they are colorful. Dr. Barzilai sheds light on the unexpected shifts in personality among centenarians and the enigmatic cerebellum, which suggests a mind-boggling 400-year lifespan prediction according to epigenetic markers. We traverse the landscape of aging biomarkers, debating the merits of proteomics over methylation and the transformative potential of metformin beyond its conventional uses. The episode is studded with revelations—from the role of the TAME trial in ushering in a new era of gerotherapeutics to the promise held by mitochondrial derived peptides and hyperbaric oxygen therapy. This is the frontier of science where the aging process itself is the adversary we learn to outmaneuver.

Lastly, we venture into the realm of personal health strategies, where sleep, fasting, and the judicious use of supplements play starring roles. With Dr. Barzilai's guidance, we confront the challenges of achieving ketosis and navigate the complexities of the supplement industry in search of reliable data. Through the lens of the Healthy Longevity Medicine Society, we glimpse into the future of longevity biotech—a future rife with opportunities for both medical professionals and investors. This episode isn't merely a treasure trove of information; it's a call to action for anyone intent on curating a healthier, more vibrant life. Join us as we map out the steps toward not just a lon

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Transcript

Speaker 1: 0:02

Welcome back to the Health Long-Empathy Secret Show, and I'm your host, dr Robert Lufkin. Today we get to unlock the mysteries of longevity with Dr Nir Barzali, a leading expert from the Albert Einstein College of Medicine, who brings his groundbreaking insights to our conversation. We're going to be talking about the science of aging and the quest for a life full of vitality. With Dr Barzali's guidance, we'll uncover how targeting the aging process itself could revolutionize the way we prevent age-related diseases, which would open a new chapter in whom human health and longevity. Our journey with Dr Barzali takes us deep into the connections between inflammation, nutrition and living a longer life. He enlightens us on the principle of antagonistic pleotrophy and shares personal experiences with intermittent fasting that just might hold the secret to extended lifespan. I certainly feel that way.

Speaker 1: 1:02

Dr Barzali doesn't just share knowledge. He gives us a glimpse into his own longevity practices, including his approach to sleep and skepticism towards supplements, ending with a peek into the future of longevity science. We provide a roadmap for anyone eager to be a part of the longevity revolution. So please join us for this transformative discussion that could very well change the way you think about aging and health. This episode is brought to you by L Nutra, maker of the prolonged fasting mimicking diet. If you'd like to try it, use the link in the show notes for 20% off. You can support this podcast by checking out their website and taking a look at all their other innovative products. And now please enjoy this week's episode.

Speaker 2: 1:56

Today we're very pleased and honored to be joined by Dr Nir Barzali, a chair and scientist and a chair professor of medicine and genetics at Albert Einstein Nathan Shock Center and the Glenn Center for Excellence in Biology of Aging, and joining me today is Dr Rob Lufkin, my co-host. Rob welcome.

Speaker 1: 2:20

Hey, hey, steve, hi everybody. It's great to be here today. I can't wait to talk to Nir Barzali and hear about centenarians and the TAIM trial and all sorts of great stuff.

Speaker 2: 2:33

That's great. So, without further ado, let's bring on Dr Barzali. Welcome, nir, to our program. It's a pleasure to have you with us. We'd like to start and welcome Rob, my co-host.

Speaker 1: 2:54

Hey, it's great to be here and here. I'm really looking forward to this conversation, me too.

Speaker 2: 3:01

We would like to begin by having you just give us a little bit about what got you into this field of longevity and aging.

Speaker 3: 3:10

Yeah, terrific, and it actually happens early on. And I'll tell you why it happened to me early on and not to others. Because, steve, I don't know if you have grandkids, but the grandkids look at their grandparents and they don't see themselves becoming that. Where did you come from? I mean, what happened to you and for me when I walked, I was 13 years old, I remember, and I walked with my grandfather every Saturday and he would tell me his life story it's a life of pioneer and I would look at this old man, heavy, bold, walking in such a low speed, and I said just what happened. And then I became a medic and I became a doctor and throughout everything, it was the biggest question. I mean, when I learned about cholesterol and when I learned about hypertension, I said, well, or diabetes? I don't know who in this crowd has diabetes and blood pressure and high cholesterol, but I know who's old and who's young. Isn't that the most important thing to figure out? And maybe, if we figure out, we can do something about that?

Speaker 1: 4:31

Yeah, that's great. One thing I love to ask our guests is that is kind of what's your overall view kind of the big picture on longevity and aging and because surprisingly everybody has a little bit of a different take on it. Is it just wear and tear, is it programmed, is it quasi-programmed? What's your take on it, nier?

Speaker 3: 4:54

So maybe let me qualify. I just talked a second ago about the fact that aging has a biology right, because we know who's old and who's young. But the second thing that we have to realize at this biology is what drives the age related diseases. Okay, it's not that we get diseases and we got old. It's the other way we got old and this aging drives the diseases. For example, you can be born with a genetic change, genetic variants. That's called apoE4. That means that when you're 70, you're likely to have Alzheimer and at 80, you're likely to be dead. You don't get Alzheimer when you're born or when you're one year or 10 year or 20 year. You need the aging biology in order to actually start the disease, to get the disease. So this is really very important because if we want to do something about preventing diseases, we have to do a prevention of aging, and this is what the field is trying to do. I mean, we can treat aging when it happens, but we want to prevent it. Sorry.

Speaker 1: 6:07

Oh, that's me, and I just had a follow up question to that. Go ahead, finish your thought.

Speaker 3: 6:16

I have a last point, but if you want to ask about, that Go ahead, go ahead yeah. So the last point, that is the most important point, is that aging can be targeted. Okay, we can delay aging. We can even stop it and reverse it in several situations. So we have to do it. From many reasons we have to do it, but we can do it. So we have to move now and start doing it in humans.

Speaker 1: 6:49

Yeah, an interesting point Just to follow up on that, the underscore which you make that we have these hallmarks of aging you mentioned, and then just the signs of aging the gray hair, the baldness, the wrinkles, all those things that indicate that an organism is getting older. But it's interesting that the longevity actually what determines our point of death is driven by these chronic diseases. Like, nobody dies of wrinkles, nobody dies of gray hair, but it's when they get one of these chronic diseases that are the greatest risk factors. Aging, as you say, right.

Speaker 3: 7:26

And the greatest risk when you get the first disease, it's the greatest risk for you getting the second disease. And between ages 60 and 80, we're getting disease upon disease, a combination of bed diseases, sometimes treatments and sometimes interaction with treatments. So this is really a bad story. Look, during evolution 100,000 years of evolution. I know there's a lot of controversies of how many years was our evolution, but life expectancy was somewhere between 20 and 30 years. I know there were some old people all the time, but in the last 150 years we succeeded in getting lifespan. I mean it's 76 now in the United States. It's dropping Okay, most of the world is past 80. But we basically tripled our lifespan and we did it by prevention getting harness the agriculture, clean the water source, immunization there are other things Surgery I shouldn't ignore surgery and antibiotics. But what did it get? What did it get us? It got us that now we have those age-related diseases and my point is we can target them and prevent them and have aging look very, very different.

Speaker 1: 8:55

That's an interesting point you make, just to follow up. One last follow up on that is that, yeah, we increased our lifespan so dramatically over the last few hundred years but we did it through, as you say, public health measures, infectious disease things. It's interesting those didn't really target longevity per se, but rather public health and infectious disease and all Even though we tripled our lifespan. The way we did it wasn't by getting at any of the basic mechanisms of aging necessarily. Like you say, there were plenty of old people back then. It's just that, on the average, people don't die in childbirth or of infectious disease earlier on.

Speaker 2: 9:45

There's so much we don't know.

Speaker 3: 9:46

You're absolutely right, but on the same token, some of the things that we can do have to do with things that we can do in our environment, such as exercise right, that is crucial at any age. Any sex to exercise is crucial. Diet, which I can talk about what I mean in other time but not being obese, for example, right, sleep and keeping a good mood those are old things that are going to affect our health substantially. This is without talking about gerotherapeutics, drugs, right.

Speaker 2: 10:23

Yeah, Nier, I've read your comments in one place where you talk about the brain being where aging begins. Can you explain what you mean by that?

Speaker 3: 10:36

Yes, I don't know where I wrote it. You'll probably and probably during my career. I said the liver is where aging begins and the pancreas. But I actually returned in my career. I turned to brain and I did a lot of research targeting the hypothalamus.

Speaker 3: 11:04

I think the hypothalamus is a crucial organ that is related to lifespan. It controls metabolism and metabolism is one of the big hallmarks for aging. One of the earliest things that happens in the hypothalamus is inflammation. There's actually glyosis and we are researching that. I actually have a faculty, sandra Alexich, who's doing the MRIs on people in my study to identify these glyosis and to see the relationship.

Speaker 3: 11:41

But from animal models and from human, we think that the hypothalamus could lead a lot of the aspects of aging in particular that are related to metabolism. But the hypothalamus is important for heat regulation, it's important for reproduction, so of course, appetite control, but I think in this sense the hypothalamus is very central. The hypothalamus also communicate with the rest of the brain and with the rest of the body and it's interesting that in my research I could give an insulin to animals in order to show that the insulin clears their glucose. I could give the insulin to the hypothalamus and it would do the same. I didn't need the insulin in the periphery, so it's a kind of a degenerate system and we are arguing which is more important. But certainly the brain has an oversight of all the aspects and there's in and out through there.

Speaker 2: 12:48

Right yeah, right Okay. So many things just to add that in my own research I've done a lot of work on studying the hippocampus and its role, so I agree that there's a lot of places we can begin with in the brain.

Speaker 1: 13:06

Yeah, certainly to follow up on that. The like in the yeah and the hippocampus, that with Alzheimer's disease and with exercise and diet and even reversal on MR scans. It's amazing that these areas of brain like the hypothalamus and the hippocampus have have dramatic effects that we're just beginning to understand here. Maybe a follow up question on the age related diseases near what? How do you think the biology of aging drives these various age related diseases that ultimately determine our longevity? Like you know, it's a heart attack, stroke, alzheimer's, cancer, what's? How does aging turn those on? What's going on so?

Speaker 3: 13:52

so. So look, they're there. The mechanisms of aging, what we call hallmarks, are a are in every cell there. The up regulation is in almost every cell in the body and in in body that age sooner rather than later. This biology will be on all organs, but one organ will lead the aging in each individual. So if you had a diabetic mother and you're obese, you're going to get diabetes. This will be maybe the first disease. If you have genetics for diabetes, that's what will happen. If you have genetics for cancer, that's what will happen. So we individually carry the proponent to get the first disease that the you know, before we get the next one. This is determined by by genetics, by the environment, but the overall mechanism that can be targeted to prevent that is aging.

Speaker 2: 15:04

Can you say a little bit about the inflammation biomarkers and how they relate to aging?

Speaker 3: 15:11

Yeah. So you know and I guess you wanted me before to say what happens. You know what's my definition of aging, which is is really hard, it's hard to do a consensus, a consensus about it, but I think most of us agree that what drives our life Initially is reproduction. Okay, everything that helps reproduction is going to help us transfer whatever we had to get to reproduction to our offspring. Okay, and then evolution really didn't plan our retirement party, okay so. So some of the things that happened before might help us and some of them might be antagonistic to us. But what happens at a certain point let's say 50, but it's very individual, but at 50, we start going from this reproduction stage to a breakdown, and I think it's breakdown that leads aging, and I think that probably inflammation is secondary to the breakdown.

Speaker 3: 16:24

You know there is a hypothesis of aging that's called antagonistic pleotrophy. Never mind the name, but what it means is things that are good to you, for you when you're young, turn against you where you're old. You know, cholesterol is very important for us, for the cells, for the brain, for the, the brain, for the gonads. But if we have high cholesterol metabolism when we're old, we know that it's not good. Okay, so what?

Speaker 3: 16:50

One of the things that really we discovered and and and we kind of proved recently in one of my my papers, is the, the syntagonistic pleotrophy that has to do with growth hormone. And, by the way, when I say growth hormone, there's one growth hormone but there are many growth hormones, so I'm not really meaning the one hormone, that's growth hormone. But when growth hormones are always good when you're young, okay, you have less mortality, you have less diseases. When you're old, it switches Okay, the more growth hormone you have, the more mortality you have, the more diseases you have. And intuitively, you can understand that we, at a certain age, we don't want to spend energy on growth, we want to spare. They spend the energy on repair. Okay, and that's why some of the drugs that are we're using later on are things that are actually decreasing the growth hormones and pathways associated with it.

Speaker 1: 17:57

Yeah, that's. That's such a great point, and our audience is going to be hearing about antagonistic pleotrophy and the hyperfunction theory from Misha blogoskone, and plenty about mTOR too, so this is all going to be be tying together with them here. I wanted to go back and invite you to talk about one thing you hinted at before, and that is targeting aging with nutrition. Everybody is starting to recognize that eating the right diet is healthy for a lot of reasons, but also for longevity. The question is, though nobody can agree on what the right diet is. What? What is the right diet in your mind?

Speaker 3: 18:41

So I'll give you my own example and I should tell you diets are also personalized and people, there are many 50 ways to leave your lovers those of you who remember this song okay, but I'll just give you an example, because this is an example that comes from my lab pretty much, and when I started doing aging studies, we used to put animals and no matter what we were checking. Our positive control was this we took half of the animals and let them eat whatever they want we call it ad libidum feeding and their brothers. We used to figure out what the ad libidum animal have and give only 60% of that to their brothers and their brothers their calorico-stricted one ended up living healthier, much healthier and longer by about 40%, and this was taken for many people. This translation was you have to have less for breakfast, less for lunch, less for dinner. But this was wrong, because what we were doing was actually giving the food to those calorico-stricted animals first thing in the morning. Now they were hungry, so they would eat everything within 20 minutes and then they'll spend 23 hours more fasting. When we give the food throughout the day, they actually don't live much longer.

Speaker 3: 20:17

Okay, and that's where intermittent fasting came from. Okay and, by the way, that's what I'm doing since before COVID. Okay, so it's three and a half years that I'm intermittently fasting and it has been tremendous for me personally. Okay, on many ways. Initially I lost some of the extra pounds that I had, but in many other ways it was terrific for me. And so basically what I do is I skip breakfast but only don't cheat for 16 hours and then at the eight hours that I can eat, I basically can eat whatever I want. So it's not hard.

Speaker 3: 21:02

If I'm hungry in 15th hour, what I'm not going to stay an hour. I mean, if you'd give me a diet for three months, I could break any day, but I'm not going to break for an hour and actually it's not a problem anymore. I usually fast for much more than 16 hours because by then I have some ketones, I'm not so hungry anyhow. So this is an example. The 16 eight has variation. People are doing it several times a week or once a week. There are people who are fasting once a week. There are people who are fasting three days every four months. There's a lot of variation of what you can do from your fasting. But I think there's a lot of support to the fact that a prolonged fasting has health benefit Also. I think overall I'm eating less. Okay, I'm never picking up what I would have had anyhow, but I also I don't have the need for that, like when you eat all day, you kind of get a positive feedback to eat more and that doesn't happen.

Speaker 2: 22:12

That's great. I'm actually doing the 16 hours as well, niren, and I'm finding that it makes me feel better also, so we're in alignment here. Can you talk about some of the maybe surprises you have found in your research with centenarians and super centenarians?

Speaker 3: 22:37

Yes, well, first of all, the opposite of the surprise would be if I found out that they got sick when all of us got sick and now they are sick for longer time. Right, that would be the least attractive. And we actually found two things. First of all, their health spend and lifespan go together. In other words, they're getting diseases 20, 30 years after others are getting their diseases. So health spend and longevity goes together. But there's an additional point they have what we call a contraction of morbidity. They spend less time sick at the end of their lives. That happens to be a huge part of what we're trying to do and frame it as the longevity dividend. And in our studies and also by the CDC, the CDC have shown since 1993 that the medical cost in the last two years of life of some of you dies over after the age of 100 is third of those who dies when they are 70. Okay, so that's a huge cost.

Speaker 3: 23:49

But this is not the whole picture. In fact there is an economist by the name of Andrew Scott in London School of Economy that published in Nature Aging this year or last year. He said you know, you're totally underestimating, because it's not only that, the guy is not in the hospital, okay. But what is he doing? He's traveling, he's shopping, he's buying for his grandkids. So the economical value of that is incredible. I mean, since healthcare is like 40% of expenses, the longevity dividend is, he calculates, I think, something like $380 trillion in the next 10 years.

Speaker 3: 24:33

He said even 10% of that would do a lot for global warming. You know, if you had $36 trillion for global warming? So the point is we cannot afford not to do that and our centenarians have shown that. There's an example. We have it within our capacity. In fact, maximum life, human lifespan and this is a statistical term, okay is 115. You know, we kind of argue about that because somebody lived to be 122. But statistically this is kind of our lifespan and we die, as I said, at age 76 now in the United States. There's really a lot that we can potentially do for those 35, 40 years that we don't utilize now.

Speaker 2: 25:22

Yeah, yeah that's on that same on that same note about those populations From a psychological perspective, an emotional perspective, do you notice anything in particular about those centenarians, super centenarians, that may have to do with social contact, emotional health?

Speaker 3: 25:45

Yeah, it's, it's. It's very difficult. Let me give you an example, but, but, but I'll tell you, first of all, it's very difficult because they leave the hundred years in different social circumstances every time and it's hard for them to even reconstruct that. So how do you deal with somebody with social construction? But, and you know, they, they write, they retire, they lose a spouse, they go to a different home, they go to another different home.

Speaker 3: 26:19

Okay, there's also changes in the brain, not Alzheimer, but changes in the brain that are doing lots of things, changes in their body, that feedback to the brain. So so, so to take a hundred year old and ask him what's your social thing is a problem. So I'll tell you I met this, you know, and many times people are saying you have to see the centenarian, because I'm not seeing all of them. You have to see the centenarians. You have to see the centenarians, I see them. So I go to this hundred and four year old person and I sit with him and he's just lovely. He's lovely, he's reflectful, he has nothing better to say about his daughter in law or, you know, anyone, anyone else, and it was just a joy, you know, just enjoyed sitting with this guy.

Speaker 3: 27:10

So I'm going out of the meeting and I'm bumping into his son. Mind you, his son is 82, right, and, and and I'm telling his son what I just told you. You know, he's like the greatest guy, and the sun looks in my eyes and said you should have seen the son of a beach when he was my age. He was a terrible, terrible person. Okay, so, so then you realize we know about personality. We say personality doesn't change. If you look at the studies until 60, okay, and there are things that are changing, there are things they're not changing. There are people who are changing and people are not changing. But go to a hundred year old and ask him something. You're not going to get reflection of his lifetime exposures.

Speaker 2: 28:00

Yes, it's like as you started that story, I would have reflected back to you. Oh, a positive mindset. So we published him into the picture.

Speaker 3: 28:12

Look, we published that. We published three papers on that. We had an instrument and they were very positive personalities, extrovert, you know, and optimistic and all that but but but people took it to say that that's what led them there. And I'm saying not necessarily, you know, sometimes they become that person.

Speaker 1: 28:38

I want to reach back and touch on one thing you said about the point on the epigenetic or on the maximum age for humans. It was a great paper I just saw from Steve Horvath and about 100 other collaborators about calculating maximum by a lot, or maximum age based on epigenetic markers across different animals, and for humans it was about 120, and other animals it was appropriate to the ages they'd experienced. But one thing struck me in the article. There was one cell type which was the cerebellum and they look at humans. It was 400 years old and that help. Any idea why? Why that would be.

Speaker 3: 29:18

Right, and actually the female breast is 10 years older really than others. Now, you know. No, I think there's still a lot of things. I think epigenetics is really important and it's a really good. You can do really well in identifying the biological age of a person in a simple blood test. It's good to kind of see predictions of diseases.

Speaker 3: 29:57

But the thing I'm most interested is in biomarkers that will reflect successful therapy. If we intervene with aging and we're not there yet with them. And in fact I think methylation is, it takes a while for it to change. I'm quoting Horvath it's nine months, more than a year, until you change methylation and I'd like to know in two months if I'm on the right track. Right, and in this sense there are many other biomarkers. I'm actually very interested in proteomics and in the proteomics. I have lots of inflammatory proteins as much as lots of breakdown proteins and I think no matter what we do, no matter what drugs we'll use, we'll need to stop the breakdown, and that's why I think proteomic is going to be more important than methylation, at least to follow up if you're doing something well.

Speaker 1: 30:59

Yeah, I'd like to follow up on that, speaking of one area that you're very well known for and working in metformin, and also touch on the TAME trial. There's just been an article about metformin use in diabetics with reduction in biological age based on DNA epigenetic methylation markers. But metformin is such a fascinating longevity drug it's been in round for a long time and used Before we talk about the TAME trial. Maybe you could just update us on what's the latest thinking about the mechanism of metformin. I mean, with rapamycin it's clear it's mTOR, but with metformin it's like ampicinase or it's the gut microbiome. There's so many different things. What's the latest thinking on that?

Speaker 3: 31:50

So for every gerotherapeutics, including rapamycin, what we mentioned before, that there are hallmarks of aging. Those two, for example, metformin and rapamycin, hit all the hallmarks of aging. If you can follow any one of the hallmarks of aging, it changes them. Now people are saying are you out of your mind? So all those drugs have nine different mechanisms of action by accident? No, the mechanism of action is actually delaying aging.

Speaker 3: 32:25

But if you take an old cell or an old organ or an old body and make it young, you're going to fix lots of things and that's why we captured it. And it was terrible for us because we used to fight about what's the real mechanism, because there are so many things that we can monitor and I think we just have we, as a geroscientist, we have to know if you have a real good drug, it's going to affect everything. Now, what does it do primarily? I think metformin is primarily MTOR and metformin has more to do with its actions in the mitochondria, in the complexes of the mitochondria, as primary things. But what you see as far as mechanisms is that you're attacking everything because you just improved aging.

Speaker 1: 33:18

Maybe you could just follow up on that and just tell everyone a little bit about the TAME trial and the current status of it. Any late breaking news.

Speaker 3: 33:27

Yeah, look, the TAME trial is. By the way, it stands for targeting aging with metformin, but it's not about metformin, because we already know that metformin prevents mortality significantly. We already know that it prevents diabetes, it prevents cardiovascular disease, it prevents cognitive decline and it's associated with less cancers and less Alzheimer's. So we know all that. Metformin is a tool for us to go to the FDA and prove to them and get indication for the fact that aging can be preventable. Okay, that's why we're doing TAME. That's why TAME is very important for the industry. Tame is very important so that pharmaceuticals that are on the sideline now will jump in and start thinking of how to do better drugs, combination of drugs, and really get us much more ahead of where we are in the quality of aging that we're going to have.

Speaker 1: 34:29

Let me see if I understand that. Just one follow-up. So the important fact is that right now aging is not considered a disease. So by having aging be defined by the FDA as a disease, then the CMS and billing organizations would be able to and companies would be able to develop drugs that specifically target that. So that would mean a lot of investment, venture capital, in the aging space, rather than having to be in the Alzheimer's space or the stroke space or the heart attack space.

Speaker 3: 35:02

Is that correct? Well, but I want to immediately attack one point. I think aging is the mother of diseases. Right, it drives diseases, but I don't think aging should be called a disease for other reasons. You know, if everybody over 60 is sick, you know what happened in COVID we isolated them, we made them lonely. They're doing poorly From a social perspective. There's no need and it's not going to interfere for us.

Speaker 3: 35:32

What the FDA agrees, that we have a cluster of disease and we're going to delay this cluster of diseases and they're okay. If we can show that we don't need to name names, okay, we don't need to go into the political argument. I think aging will be eventually recognized as a disease. But now the people who want to help more the elderly, they don't want to be called sick and there's no reason for us to do that. But otherwise you're right. But you know that's also what people don't understand is how do you do a study like that? Because in a way you can come up with any disease to this study.

Speaker 3: 36:15

But what disease you're going to get? We're agnostic. Okay, we don't care which disease. Whatever you're going to get next is driven by aging. As I said, if you came in and your mother was diabetic and you're obese, you'll get diabetes. You get one point for that. If you get cardiovascular disease, you get one point and we're going to show the trend. The trend is significant. Okay, the trend is significant. That was aging for us. We're going to prevent a whole cluster of diseases which, for us, represent the word aging and we're agnostic to what it is. We're just going to delay that.

Speaker 2: 36:55

Nier, this is a fascinating conversation. I appreciate it very much. I'm wondering if you can identify one or two exciting things happening in the field of longevity that we haven't touched on yet.

Speaker 3: 37:13

Well, there are two things that were unexpected, which is why science is so amazing. One thing is really part of my research. My friend and collaborator, hassi Koyn, who's the Dean of USC School of Gerontology, have discovered what we call mitochondrial derived peptide. In other words, we are all talking about the genome that we have in our cells, but we also have those energy factors, mitochondria and their ancient bacteria, and they have their own genome. This genome is very active and we have hundreds of peptides that are coming from those genome interacting with us. This is a whole new field. That is a regularly field that is really related to aging, because when we give those peptides to a variety of animals, they live healthy and longer. This is something to watch out. There's another genome we didn't know. The microbiome is also an example of another genome that we ignored.

Speaker 3: 38:20

The second thing that has more clinical relevance is something that I heard about several years ago and it shocked me hyperbaric oxygen therapy. Now we know that oxidative stress is not a major regulator of aging. We knew it's still debatable for different diseases, but we knew that that's not a major thing. But I certainly didn't think that having 100% oxygen under pressure is going to be good for biology, but there are clinical studies that are quite convincing that shows that it's a potent treatment. Actually, I purchased a hyperbaric oxygen chamber in my lab to understand more the biology. But there are two things that changed my mind, simply as I can say that, first of all, our blood vessels volume declined by about 40% with aging. We have less vessels, which means that there's a lot of cells in our body that don't see oxygen anymore. If you give them several repeated treatment of 100% oxygen, oxygen will diffuse and wake up some of those cells and there'll be functional benefits from that.

Speaker 3: 39:52

The second thing is actually, when you're hypoxic, when your oxygen level is low, you upregulate your biology with lots of things. That seems to be good for aging. And what happens when you do those treatment with high oxygen pressure but then go to normal? The cells feel relatively hypoxic, so they upregulate those mechanisms as well. So there's at least two mechanisms that could be of benefit, even if oxygen I mean the whole idea of the mitochondria coming to the cell is to protect us from oxygen and harness energy. But it's much more complex and so I would watch it there. It's out there. It's commercial. Okay, people can get treatment. Lots of indication, growing amounts of indication, but watch the cognitive decline is really impressive results in my mind.

Speaker 2: 40:52

Just to follow up on that what would you think is the frequency of use of that? That could make a difference.

Speaker 3: 41:00

I don't know that it's determined. I think part of the issue is they're in centers, they were trying to do protocols and they stuck in the protocol. That's working, but how many times, for how long? And repeating treatment. Is repeating treatment going to help or you have just one chance to do it? Those are all. It's too young to really tell you that, but it's one of those things that's out there that people will use and I hope they'll use responsibly. And I hope that we'll have more data, because this is kind of a cool biology in my mind.

Speaker 1: 41:41

If you had to make a recommendation to people or a suggestion, what are the one or two things that everybody in our audience could do that would most to do right today to help with their longevity and help?

Speaker 3: 41:55

Yeah, well, I'll tell you what I'm doing. First of all, I'm exercising every day, even when I travel. I mean, there are gyms everywhere, and it's even not always about exercising, but moving. The best thing is to have a Fitbit or Ring or something, and if you reach 7,000, preferably 10,000, you've done good for a day, even if you're just walking, but you need to exercise overall, basically. Second thing, as I said, is the diet, and the most simple advice is not to be obese. But I'm doing the intermittent fasting and I think it's easy for a lot of people not for everyone and more for men than women, but if you could do it, I think it's of benefit.

Speaker 3: 42:46

The third thing is sleep. Now, sleep is more complicated, because but what I'm doing is I'm spending eight hours in a dark room, without technology. I'm sleeping between six and seven hours out of that, okay, but if I'm not dead, I'm sleeping even less so, and this is without drugs, right? So this is really crucial. The last thing I'm doing is I'm actually on metformin, and I got metformin because I was pre-diabetic. I'm not even close to it anymore, but I wouldn't give it up. And, by the way, the doctor my doctor, but he's not, but I begged him to stay on that and I believe it has a major. All those things together have major. Did I tell you I'm 100 years old, by the way?

Speaker 3: 43:41

I think it has good effects on me.

Speaker 2: 43:44

You look very good for your age.

Speaker 1: 43:48

Well, you mentioned diet Nier and you said you were in ketosis from the fasting portion. Certainly I didn't say that, oh.

Speaker 3: 43:58

I'm actually not. It happens that I'm not, you know, I'm not sure that. I think ketosis doesn't happen to everyone and I'm not sure how much it's important. I think that probably the low insulin is the most important important thing. I certainly don't get to ketosis, but it's a little bit complicated by metformin because it switches the acetoacetate and beta hydroxybutyric and so I might be falsely not in ketones, but I think it's the intermittent fasting mechanisms yet to be discovered.

Speaker 1: 44:38

Sure, yeah, nobody really knows. There's so many questions here. Well, you mentioned metformin, but any of the other drugs, acarbose, rapamycin, disatinib, any of the other longevity drugs that you're looking at nutrients or supplements, for that matter?

Speaker 3: 44:57

So I'll tell you, okay. So first of all, about drugs, I'll tell you that I'm experimenting other drugs carefully. I take relevant blood tests before and after. So I do that. But I don't care to tell you what I do, because this is for me to be educated personally, okay, so I don't care to talk about any of those things.

Speaker 3: 45:24

The supplements have started scratching my head because my line about supplement was that it's good for the economy. You know, buy a lot, it supports the economy. Because I also felt that many of the supplements first of all, many of the supplements are okay. Many of the supplements more supplements are even don't have what they say they have because it's not regulated. And what I started being worried now is that there's a lot of companies that are doing supplements and those supplements are actually quite potent and they might be helpful. But then you have many supplements that are potent and there's an interaction and I heard a talk, but by a longevity doctor who did biomarkers for aging and showed two people were on 30 supplements and their biological age has increased by six years.

Speaker 3: 46:30

And I think so I think now it's actually could be quite dangerous to take the supplements and I think. I think you just take whatever you need to take, not whatever is out there on the web. I certainly you know there's one example of Mars. You know the Candy Bar Mars, the company which is Mars something had a trial with 20,000 people on flavonoids, cocoa, okay and and the results were very impressive with, you know, 20 30% declining mortality and in cardiovascular events and stuff like that. And I think this is the kind of data that we need. And the FDA, by the way, they cannot say that that's what it does, although they did it as good as drug drug company would do it, but they cannot say it because the FDA doesn't allow that. My view is the FDA should open the possibility for companies getting data and safety data and outcomes data so that we can understand better what's going on.

Speaker 1: 47:47

Otherwise it's the Wild West yeah, that that's so, so important. Maybe you could tell people how can we reach you on social media and also following up your thoughts on medications for health longevity. You're involved with a new, a new project on that that may provide some of that information that the FDA is not willing to get yes, so we started the healthy longevity medicine society.

Speaker 3: 48:20

If you put it on the web, you'll find it and I think there's information. You know, really the information is for doctors, right, not for it's really to train doctors, it's a medical society. So for the doctors of you are interested in longevity, definitely. My tweet is near barzilla MD and and I'm also the scientific director of the American Federation of Aging Research and a lot of information you can find on the on the far side. I should also say another thing. I'm also one of the executives of a longevity biotech association that's trying to standardize the biotech company and get also data for the investment.

Speaker 3: 49:09

If you're investor and you say, wow, it's interesting and and, by the way, people, I was just an investor a meeting in Switzerland with 150 investors, mainly multi-millionaires and billionaires, that are there because they feel the young people feel like it's before the crypto happened and they should be early on, and the old one thing, it's like the web. People know that longevity is coming and they want to be early on. And what my role is basically if, if you want to be there and you say where should I be, I could match you with people who you want to talk with and and get the information. But I think we should all be prepared to longer. Really not longer, I meant to say healthier. You know, by the way, not everybody can afford it, so the side effect might be longer life. You know, I don't know if it's always better for people, but certainly healthier life good point.

Speaker 2: 50:20

Thank you near very much. We've really enjoyed our conversation with you and thank you for the leads to where people can get some additional information.

Speaker 1: 50:29

Thank you very much thank you very much, was fun, good luck if you are enjoying this program, please hit that subscribe button or, even better, leave a review. Your support makes it possible for us to create the quality programming that we're continually striving for. Also, let us know if there is a certain topic that you would like to see covered or a particular guest that you would like to hear from can I start?

Speaker 4: 50:58

it's already recording sorry, this is for general information and educational purposes only and it's not intended to constitute or substitute for medical advice or counseling, the practice of medicine or the provision of health care, diagnosis or treatment, or the creation of a physician, patient or clinical relationship. The use of this information is at their own users risk. If you find this to be on the value, please hit that like button to subscribe to support the work that we do on this channel and we take the your suggestions and advice very seriously, so please let us know what you like to see on this channel. Thanks for watching and we hope to see you next time.

Speaker 1: 51:46

You should say that's good for you, to say that's good, you like it, you want to do it one more time. Or say good.

Speaker 4: 51:55

I think it was good. You need to say it through recording very good.