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Speaker 1: Pushkin. On every episode of Decoding Women's Health, we talk about the science behind women's bodies and share stories from leading researchers and clinicians. But now I want to hear your stories and your questions. No question is too complex, awkward, or small. So tell me what kindacologic questions have been on your mind lately. We'll get into everything from entimetriosis to fibroids, pms, pcos, and more. We really want to hear from you, so please send your questions to us at Decoding Women's Health at Pushkin dot fm. That's Decoding Women's Health at Pushkin dot fm, or feel free to leave us a voicemail at four FI five two oh one, three three eight five.
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Speaker 2: This show is not a substitute for professional medical advice, diagnosis, or treatment. It is for informational purposes. Please consult your healthcare professional with any medical questions. Also in this show, we use women as shorthand for people with XX chromosomes. We understand sex and gender are more complex and acknowledge the experiences we describe reach beyond that word.
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Speaker 3: I think everybody knows that aging has a biology because we know who's young and who's old. But we know even more than that. We know that some people age faster than others, or some people are ages much slower than others. In other words, there's a chronological age that's your passport, birth certificate, and then there's your biological age.
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Speaker 1: That's Doctor Neer Barzilai. He's a gyroscientist, which means he focuses on better understanding the biologic mechanisms of aging. For decades, he has been studying the aging process and looking for clues within our own bodies to help us all age better. He's the founding director of the Institute for Aging Research at Albert Einstein College of Medicine, and he's also the scientific director of the American Federation for Aging Research. Doctor Barzilai has been studying centenarians and their families to understand their genes, often referred to as longevity genes. He's hoping to identify interventions that could actually delay the process of aging. He's engaged in some really fascinating work looking at whether existing drugs such as met foreman and rapamycin can be repurposed to delay the hallmarks of aging. Is one that I have been following quite closely for some time. And I was excited to have doctor Barzilai on the show to hear more about his ongoing research, but I also wanted to get his honest thoughts on all the hype surrounding longevity medicine, because that word longevity is everywhere these days. So today we're breaking down what the latest science actually says about living longer and living better, starting with this concept of biologic age, as doctor Barzilai says, there's your chronologic age, how old you are, and then there's your biologic age how your body functions. He told me one of his missions is to be able to define biologic age in a test, just.
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Speaker 3: Like you have cholesterol and you have glucos and you measure blood pressure. We know that there's a biology for aging, and we know that there's a hope because some people do better than others, which means there's flexibility. But there's one additional thing that we have to know, and this biology, this aging, is what drives diseases. Cardiovascar disease and cancer and diabetes and Alzheimer's and more are all driven by this biology of aging. So it's not that you're getting a disease and you're getting old. Okay, you're getting old and that drives disease. It means really that you have to target this aging before you have diseases. You have to think of prevention.
00:04:45
Speaker 1: What is the biology of aging? Can you take us through the biology of aging in a very big strokes kind of fashion.
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Speaker 3: Yeah, very big strokes. We have something that we call the hallmarks of aging, and there are now twelve hallmarks of aging. For example, one of the hallmarks is the decline in the number and faction of mitochondria. Mitochondria is really important because that's the source of energy that we have and a lot of the complain of elderly that they feel that they're losing energy is because of decline in their mitochondrial function. One of our major companies in our Longevity Biotech Association, and actually company that is also using our facilities in Einstein, is a company that can actually take a sell and expand it and take a lot of mitochondria and then infuse it to your vein. So what happens when you infuse mitochondria to the vein, This mitochondria goes into the cells and get inside and replenish the mitochondria and the energy and everything that has to do with it, right, So that's one of the problems and one of the promises. Let me give you another one. There is a process that's called autophogy, and autophogy is a green energy garbage disposal. So, first of all, there's a lot of garbage that accumulates by mistakes in our cells all the time, okay, all the time, so we get garbage, and there is a garbage disposal that's called autophogy. It's a biological process that is quite well understood. This process declines with aging, so your cells are starting to accumulate more garbage. For example, what happens in Alzheimer's when we are accumulating those better amyloid or tao. This is all garbage that cannot be really disposed appropriately. So there's effort to produce a drug. There's actually a drug in biotech that is enhancing autophogy. And when you atophagy and you give it to animals, for example, they live healthier and they live much longer, and in particular models that have Alzheimer's disease. So I'm giving you two examples that are only two of those hallmarks of aging. There's telomeres by the way, people hear a lot about telomeres. That's a hallmark of aging too.
00:07:29
Speaker 1: One other hallmark of aging. Can you speak about inflammation? Can you drill down on that a little bit for us or is it relevant?
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Speaker 3: Yeah, no, it is relevant. Inflammation or as we call it, inflammaging, is another one of the hallmarks of aging that we're trying to address. And you know, in the clinical setup, everybody talks about it because you kind of can measure it with highly sensitive tests. There are good markers for the breakdown.
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Speaker 4: You know, when we go over the age of fifty, we're dealing with breakdown, and in response to this breakdown, there's an inflammation, and so inflammation is a response.
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Speaker 3: So some of it is good, but then it goes bad because it's I'm trying to say that inflammation is not the cause of aging. I think it's a more secondary biomarker. But if we fix everything else with aging will probably decrease inflammation. Two. So inflammation is kind of of a center, but you have to understand that it's both. Okay, inflammation is bad also in the sense that it also drives things worse, but it's not what starts the process of aging.
00:08:42
Speaker 1: How do you measure aging? Are these biologic clocks that are marketed to us of any value? How do you look at aging? How do you measure it?
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Speaker 3: So let me start by saying, I have ten measurements of my biological age, and I'm anywhere between twenty years younger than my age and four years older than my age, and it kind of tells you the problem, although I would also tell you that eight of those ten are pretty much in agreement. So those tools that were developed are kind of good to tell you what's your biological age. What they fail is to change if you do intervention. So what do we want. We want a biomarker that you will take and you will tell you you're two years older than your age, and the doctor will say, well, start exercising and take me for me. Okay, and you want to come in three months and see that you're now two years younger than when you started. Okay, that's what we want because we have to show success. You know. Let's say we stop aging and we ask you after two years, how you are. You said, you know, I'm the same, because you don't know how it would be if you're two years older. Right, it's a problem. So we need the market. It's like with blood pressure and glucose, you wouldn't know unless you're tested, So we need this. We also we need it for the development of drugs. We need in a phase two trial to see if it takes us to the right direction before we spend billion dollar in a phase three trial. My last grant that is with Dan Belsky from Columbia, we're looking at one hundred thousands biomarkers to see not only what's your biological age, but which of those biomarkers have changed in common, right, So we want to find those that are aging biomarkers. That also tells you that you're getting a respond I think once we have those biomarkers, we're going to learn so much for them and going to implement so fast that you can yourself see in your clinic what you're doing that is right or wrong.
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Speaker 1: Sels in essence, can you just define what that is and how that segue is into inflammation because these are all words that are now like all over the internet and on social media, and so I think it's an important for our listeners to understand a little bit about what they are.
00:11:14
Speaker 3: So I have to tell you something that might frighten you. Initially, each one of our cells every day have thousands of basically mutations. Okay. The good thing is that we're pretty good at fixing everything. Okay, it's part of what we do. It was never meant to fix everything, because if we fix all the mutation will never have evolution, right. Evolution is based on the fact that, oh, there's mutation here and there. Some of them are bad, some of them are better. Let's take the better and let's, you know, reproduce with them. So in a way, mutation is why we have evolution. But of course sometimes will fail. So now we have a mutation, and sometimes also very rare, this mutation actually has an effect. It changed something in the cell. It could make this cell a cancer cell. It could make this cell say, you know, I'm committing suicide. Okay. But one of the options, and this option is very common, is that the cell sees that it's stress and it's become what is known as the senescen cell. It stops dividing. And that's fine, except that if you have a lot of those senescence cells, they secrete proteins that could be harmful, and particularly in the area that there's a lot of them when they accumulate, and that's what happened with aging. It accumulates. Then it is a risk actually of cancer and other diseases. And in animal models, when you remove those senescence cell they get healthier. I don't want to say they live longer, but they get healthier. So senesin is one of those hallmarks. It's one of those hallmarks that is out there to find. What are the drugs that you can take in order to remove a bunch senesence cells and improve your health.
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Speaker 1: So are so called gerotherapeutics you mentioned, Matt Foreman, How are they different from other drugs? Like we know that statins, for example, are very effective at preventing heart attacks and stroke, both of which can kill you. How is this class of drugs, the ones that target aging itself? How are they different?
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Speaker 3: Studings are such great drugs, they're so important, they're preventing so much cardiovascular events and cardiovascular mortality. But if you give them to animals, if you give them to cells, they don't change the hallmarks of aging. And if you give them to animals, they don't live longer. Okay, So they are drugs that are very important when you grow. But in my view, you don't call them gero therapeutics. They're not therapeutics for aging. What the statins have shown to do is taking care of cardiovasclar disease, so you can get now all shade or concert or another disease, which is not what we want to do. We want you to do something maybe one drug, and it will delay your aging, which means it will delay many diseases and not just one.
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Speaker 1: The way I look at this and tell me if this is like kind of a basis. Aging is the root cause of cardiac disease or brain health issues or metabolic issues, and so if you target the aging process, then you target all these downstream effects.
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Speaker 3: Of aging exactly. Aging drives the diseases.
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Speaker 1: Right. Do you see a day where we have like one drug or one therapeutic or one intervention or is it going to be a combination of these things? And can you highlight some important ones that you're working on.
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Speaker 3: For the first three questions, the answer is yes, I mean it's everything. What do we need to show to say that this drug is gerotherapeutic A. We want to put it in cells. We want to expose it to cells and show that the cells are getting younger, okay, which really means the hallmarks of aging are changing. Second, we want to give it to animals, all the animals. One of the problems we had in drug development is that people were doing age related disease, were working on young animals, and I just made a lot of effort to say it's different bodies. The young and old are totally different bodies. So you have to give a drug to an old animal and show that it becomes healthier and it lives longer. Okay, that's the pre clinical part. The clinical part is you want to show that the drug that was designated for a specific disease unexpectedly prevented other diseases. You want to show that this drug that was targeting one specific disease is actually changing overall mortality, not disease specific mortality. And if that's the strict definition for gerotherapeutics, we have already four drugs. Now what are the four drugs. One drug is met forming. Met forming it's an extract of the French lilac, but it's modulated, so it's not a nutraceutical. You need a prescription for that. But people notice that it also lowered glucose, and then it was used in diabetes, and in clinical trialing diabetes, it was shown that METFORMI decreased cardiovastri disease, and there's less cancer, and there's less alzheimer and there's less mortality when you take met forming. The latest paper was showing that you're something like twice as likely to get to the age of ninety if you're a diabetic and you're on met forming. So this is one drug. The second drug is the class that is called s GILT two inhibitors. The third classes the GLP one agonist, the ozempiic and manjaro, and the fourth is biphosphonates, which are anti ostroporotic drugs.
00:17:22
Speaker 1: So these are repurpose drugs, right, These are all drugs that are being used for other things. So I just want to back end into a couple of them that I'm really curious about because I've followed this field for a while. Met Foreman, right, mett Foreman was really out there. Then it lost a little favor. Where do you position it in terms of a longevity strategy.
00:17:44
Speaker 3: Losing a little favor is through podcasts of people who just are opinionated. Okay, in my mind. What happened to me for it gained favor, And let me explain to you why I'm claiming that those drugs affect more than one whole mark of aging. Right, met forman You can think it's only for diabetes and only for metabolism, but they're nine studies around the world during COVID that showed that people on metforming had less hospitalization, less mortality, which led to a clinical study. Okay, and that's what we need, clinical studies. And the clinical study was taking patients who just got COVID within the first three days, mostly within first day of COVID, and they gave them metforming and they had less hospitalization, less death, and less long COVID. And the point is metforming is not only metabolism, it's also immunity, it's also inflammation. It also makes the body more resilience to acute the salt. So this idea that metforming lost favor, I think is irresponsible. The second thing that happened that really made me crazy is not everything that's good for young is good for old. Okay. If you have high cholesterol metal when you're young, you're building your go nuts and brains, and it's great but if you have high cholesterol metabolism when you're old, you're clogging your arteries. Right. It's the same with drugs. Not every drug that is good for old people it's good for young. In fact, metformin has a lot of problems if you're let's say, less than fifty and don't have diabetes. There's a lot of things. It's decreasing growth from on the growthrom on igf one, and you don't want to decrease this igf one when you're young. It decreases testosterone in man. So there's a lot of confusion of what metformin is doing and the fact that young people are saying, you know, I noticed that it's not good for me. Well, you should have never been on them.
00:19:56
Speaker 1: Talk to me about the GLP ones and aging.
00:20:00
Speaker 3: If you look what GLP one is doing in cells, it's correcting a lot of the hallmarks of aging. If you give it to animals, even to animals that you make sure or that they are the same weight. Okay, you have to change the amount of the agonists. You have to feed the animals differently, but if you match the animals will still live twenty percent longer. Obesity drives aging, there's no doubt just treating obesity is good. But the point I'm making is that the GLP agonists are taking care of obesity, but that's not even their majority effect. They're affecting other cells directly, other organs and tissues directly. They're doing much more from aging than just the weight loss, which is important on its own. So those drugs were developed for diabetes, okay, because in diabetes they're doing something good. They're increasing insultin secretion, decreasing local goaues. But then they had a strong effect on weight loss also. And now when you give it, you notice that it prevents heart diseases, it prevents kidney diseases, it prevents some cognitive de client. It's not clear if it's pre alzheimer or Alzheimer's, but it's investigated now. In other words, it has effects on aging that are in part weight loss and in part independent.
00:21:26
Speaker 1: What is the mechanism of the best posphonates impacting aging processes?
00:21:32
Speaker 3: So some of it is senolytics, it takes care of the cells. Some other effects we are not sure. But one of our thoughts and their supporting elements is that the biphosphonates are in the bones, and a lot of our stem cells are in the bones, and that they are doing something to make the stem cell both youthful and also go into the periphery and through that improve our health.
00:21:59
Speaker 1: So interesting. So talk a little bit about rapamycin.
00:22:02
Speaker 3: Rapamycin is a drug that increased health span of almost every animal in the world. World and why is it important? Because all animals are aging similarly to us in the sense you know, their skin, their hair, they get diseases, their their muscular skeletal is fading away, not the same diseases, not exactly the same, but it's all aging, and that's why the animals are important. The longest living animal groups of animals has been the combination of rapamizing and metformin. They lived substantially longer, and that's why rapamicin is exciting. Rapamicin is also an FTY approved drugs, but it's approved in very high doses as an immune suppressor for people who got kidney or some transplant. Of course, we don't want to be immune suppressed when we're old or any any time of our life, so the stud these have been done only on those people and not on people who would get you know, tenth of the dose and see what's their effect on aging. There's some clinical, small clinical trials on that, but we just don't have enough evidence to suggest that this is something that we can take. And without clinical studies, we don't know the side effects, we don't know the safety, so we are not there yet. It didn't make it to the fore top.
00:23:46
Speaker 1: Coming up, doctor Barzilai walks us through a longitudinal study that he's co leading called the superager Study, what differentiates most people who live to one hundred from many of us. His answers might surprise you. Let's talk a little bit about the Superasier Family Study. Can you tell me about this study?
00:24:13
Speaker 3: The Superagor study started at Einstein, but now we have an initiative to recruit ten thousand centenarians and their families across the United States so we can find all the longevity genes and develop all drugs that we could to imitate them. And it's very important because we found a lot of genes variants that are different in them than others that had the functional consequences. And in fact, two drugs have been developed in part because of our discovery, and there are others that are on their way. Even more promising. But there's another study. We have a longitudal study on the offspring of centenarians and the people who they are married to. Pretty much if they don't have longevity in the family. And when we look at those people in a longitudal study, we have about fourteen hundred of them. The offspring of centenarians have pretty much half the cardiovascure disease, half the mortality, half the cognitive decline. So just this genetic is making a huge difference for them.
00:25:26
Speaker 1: What if we learn from superagers, what can we adopt? What can we learn from them?
00:25:31
Speaker 3: So listen carefully to what I tell you, because I mean you're asking me as if what was their diet and what was their exercise, and what was their social connectivity and all that, And I'll tell you we were in a way lucky, but that didn't matter to them. That's not what they were about. In other words, it's not that they did what the doctors tell us to do. Fifty percent of them were overweight, over obese, fifty percent of them did not move at all, even moderate exercising, very few vegetarians. So as a group, they're nothing. To tell you, There is this woman I always say, there's a woman who I met when she was one hundred years old and she was smoking, and I said, Helen, nobody told you to stop smoking. And she said, the four doctors who told me to stop smoking, they died, right, And she continued to smoke until she was one hundred and ten. And the argument was for me, is you know, who knows how long you would leave if you don't smoke. She got to one hundred and ten. I don't know what's the answer to that, really, So in this case we don't learn from them. What we learn is the genetic case. What are their longevity genes that slows their aging process and how can we make them a therapy? You know, our maximum lifespan as humans is somewhere like one hundred and fifteen, maybe one hundred and twenty. Okay, half of us died before the age of eighty, so we have thirty five years that we have to realize. And it's not that tomorrow we have the drug to make you one hundred and fifteen. It will be you know, several years in every effort. But that's what we should work on and I think will be successful.
00:27:22
Speaker 1: And are you seeing any gender specific differences when you look at the genetic backgrounds of the superagers. In any difference between men and women.
00:27:31
Speaker 3: Yes, yes, somewhat. But you know we have less men centenarians than women's centenarians. I know that women health is a very important issue, but women are living four years longer than men almost everywhere in the world, between two and four years. Why is that This is a huge difference? Okay, because even if we cure cardiovastar disease from the world, will get only two years, okay, because we'll start dying from another thing. So four years is really a lot. And for every one hundred years old in the world, eighty five are women, so their ability to also get to be a centenarian is much higher. The reason you're concerned is that in those four years you're spending them sicker. My view is that if men could live that long, they will be sicker too. I don't think it's a woman issue. I think it's an aging issue that we have to make sure that we can do. You're asking why. I don't know why. Okay. In fact, the simplest answers have not been confirmed, so we're in the midst of trying to figure out. But when we give animals drugs that we think will target their aging. Sometimes they affect only male and sometimes they affect only female.
00:29:02
Speaker 1: Coming up will delve into the technologies, strategies, therapies and supplements being marketed to decrease mortality and encase longevity, including super hot topics like intermittent fasting, and the popular supplement trend in AD. Back in a minute, Welcome back to the show. Perhaps you've heard of NAD, one of the most talked about supplements out there. It's sometimes given as a pill, injection, topical, or as an infusion, and it's generated a lot of buzz in the media and online as something that can extend your lifespan. So I wanted to hear doctor Barzelaw's take on this trend. But before we get into that, I asked him about the impact new and emerging technologies may have in this field. Where do you land on the usefulness of wearable technologies to improve health span and.
00:30:09
Speaker 3: Health I think of what we would do to keep ourselves healthy has to do with what we learned from wearable technology, Because what's missing in the technology is the app that will talk back to you all the time. It's partially there but you know you did only five thousand steps and it's five o'clock. The technology have to tell you, hey, you have to walk somewhere or jog or go and exercise. Okay. The technology of glucose monitoring is really important because you're finding your weaknesses. You're finding that rise is crazy for you. It takes your glucose so high. You can find out what happened when you exercise to your glucose and decide if you're fasting in the morning or in the evening. I think technology is just going to be a major tool to the extent that the technology will tell you if you need to see a doctor. You don't need to go to a doctor for a follow up. The technology will tell you take blood and will tell you if your cholesterol is I ask you prescription for your doctor. But in my mind, the whole longevity medicine doesn't have to be really a burden on doctors, but rather on you working with the technology, and the doctors are there to prescribe drugs or to do tests or things like that.
00:31:30
Speaker 1: Is AI going to contribute to the discovery of biomarkers.
00:31:34
Speaker 3: Absolutely. AI will help us see you know which biomarkers for which people, and you know, maybe they're different biomarkers for young and old, and maybe there's a different responsor. There's a lot of questions that we're going to ask and AI is going to help us. You need to have enough data to use AI, and that's what we're trying to produce.
00:31:58
Speaker 1: Let's talk about some lifestyle things. Talk to me a little bit about intermittent fasting.
00:32:03
Speaker 3: When I started my career, you know, one of the few that had career in biology of aging. When I was a younger assistant professor, the experiment to do was to take animals brothers, okay, and do to two groups. One just continue, eat whatever you want, and the others we would take to the side and give them sixty percent of what their brothers had. Those experiences were done all over the world in animals and got the same result. I actually did it initially with rats. The rats lived forty percent more and they were healthy for much much longer. Okay, So this was the effect of caloric restriction. And when it hit the media, you know, people were talking, you just need to have less for lunch, less for breakfast, less for dinner. But that's not what we've done. What we've done is we would bring the food early in the morning. The animals will be hungry, so they would eat all the food within an hour, and then they would be fasting for twenty three more hours. So what we saw is not only caloric restriction, it's also fasting. When we started giving the animals food throughout the day, little bits, they were thinner, but they didn't live much longer. Okay, so the fasting was very important. I'm telling you all that because this came from our lab, from my lab, and that's when I realized that fasting is really part of longevity. And that's where a lot of us starting to practice fasting for at least sixteen hours every day, which usually means I finished dinner by eight pm and I'm not having anything but coffee without milk and sugar until noontime the next day. And that has actually improved my health significantly. Of course, not everything is for everyone, but this and met forming I had a major impact on my health that others have noticed too. And I have pictures of me ten years ago. You think that I'm ten years older than.
00:34:31
Speaker 1: Now, So talk to me a little bit about exercise and longevity. Aerobic strength training, mixture of the two.
00:34:40
Speaker 3: I think it's very reasonable to say that you need two things. From a biological perspective, you have to have a good cardiovasular system, so you have to move on a treadmill or you know, find a way to do cardiovassor training. But you also need muscle and just your lean body mass is a good index of your health and your mortality, so you need to do both of them.
00:35:04
Speaker 1: So can I ask a personal question. You've talked a little bit about Mett Foreman and intermittent pasting that you do. What else do you do to do you preserve your health and wellness.
00:35:13
Speaker 3: I'm trying to sleep as good as I can. You know. It's like the recommendation is eight hours. It's something weird. No matter where I go and jet legs and everything, every week, I end up sleeping six hours and forty minutes. But I think I do that because I'm eight hours in a dark room without interruption. Okay, I think if it wasn't that, I would have done less. And six hours and forty minutes is probably enough for me because I'm not feeling tired or not energized or anything like that. So I think it is what it is social connectivity. You know, elderly become lonely, and this is something that have shown taking older people into social activities had outcomes of decreasing cardiovaster disease and other diseases. So it has real biological underpinnings. Every one of them is important.
00:36:08
Speaker 1: Let's talk about some of the popular strategies that are in the media that are in longevity clinics, right, NAD, NMN peptides. Can you just talk a little bit about infusions of NAD Are they useful? Are they harmful?
00:36:26
Speaker 3: I want to say the following thing. People think that if they optimize the nutrition, the exercise and everything, and they need something, it should be nutraceutical or supplements. Then, by the way, for me, supplement means you measured something and it was low and you supplemented. Okay, that's not how it's done. You're getting something in bottles. You even don't know what's in the bottles. But mainly they were not tested for health outcome. Nutraceutical don't have health outcome. So the marketing is about the hope. It's not even about a promise, it's about hope. And that's different than FD approved drugs and you say, oh, FD approved drugs. I see what GLP wants on side effects as well. At least you know what's the side effects. You know that it's safe, you know the efficacy, but you don't know anything about nutrients. So I would warn people against them unless there will be clinical studies that show you that those are good. And it has nothing to do with how you feel. Look the NAD story, which many young people are doing. You know, they're coming from a long flight and they order these fifteen hundred dollars treatment that get them hydrated and they get on petamines. Also, you don't know what you're getting those in those bags, and you're getting an NAD which probably doesn't go anywhere but to your blood cells, but you feel better. That has nothing to do with longevity. Okay, you can do it in a spa, you can do it by drinking more, you can do it by taking on fetamine or whatever. So I would say from a longevity output, there's nothing on those supplements. Is it safe? Well, maybe if you do it one time, it's safe. The question for us is a lot of the studies on NMN. We're on cancer sales and cancer celles love n men. So if you have cancer and you take NMN, I don't know. Okay. On the other end, it might prevent cancer, right, But this has to be figured out. I always say I want to start with good thing. The good thing about supplements is good for the economy, okay, But for you, I don't think so. Look. The example of supplement that is used correctly, okay, is vitamin D. All of us have low vitamin D. All of us are taking vitamin D at least when I ask elderly, okay, eighteen percent are taking vitamin D. So you're basically measuring something and you're supplementing this something. But clinical trial have been so disappointing because vitamin D was associated with other diseases, and so they thought it's good for many diseases. There's no every for that. All the other indication of itamin D has mainly failed, some have been balanced, some a little bit success, some a little bit failure. But here there's a supplement that you're using, right, and even this is not affecting aging. It can affect some things, but not aging.
00:39:28
Speaker 1: How do are your interventions like gene editing or crisper or some of the regenerative medicine strategies, but into the current practice around aging right now.
00:39:38
Speaker 3: They do in relationship to a specific disease. Okay, So for example, there is a rejuvenation effort for glaucoma that really squeeze your nerve to try to rejuvenate that, and there's a company that is approved now for clinical trials and we'll see. But it's not rejuvenation of the whole body. That's a very different issue. And I don't I think you need Crisper for you know, like for the longevity genes that we found, you don't need Chrisper usually need a drug. So I don't see any reason to discuss it now because it's not It's all very important development that will be related to longevity, I hope, but they are not some things that are available now. You know, it's not about older adults. Only people who survive cancer are aging rapidly. People with HIV are ten years older than their cohort, people who are disabled, you know, poor people should be the first in line. So there variety of reasons why we should accelerate our research and why it's so important for so many people.
00:41:06
Speaker 1: There's a negative connotation associated with aging, especially in the United States. But aging is no longer a passive endeavor. It's something that we can influence through our actions, healthy lifestyles, and through science. There was so much from this conversation that has really stayed with me. Doctor Barzilaw's work around interventions that may extend our health span is really exciting stuff. It was quite interesting to hear about the participants in doctor Barzilai's studies who have lived long lives despite some not so healthy lifestyle choices. Of course, their genetics likely play a role here. The data from these studies around centenarians and their offspring are providing us with a better understanding of the biology of aging.
00:41:56
Speaker 2: To zoom out for just a.
00:41:57
Speaker 1: Moment here, I'd argue that the focus shouldn't just be living longer. It's also about your quality of life, making choices that will keep you feeling better, staying active and in community. We also want to mention something important we talked about today, animal studies. These provide interesting insights and give us opportunities to shape human studies. More research always needs to be done to see how those findings and animals translate into humans. And a quick note about intermittent fasting. Studies have shown it may be beneficial for longevity, but as we mentioned, everyone responds differently, and actually some women may not tolerate intermittent fasting. So as always do what feels right for you. There's still so much we don't understand about the biology of aging, but I'm enthusiastic about the field of gyroscience and the secrets at canon Lock for all of us to live longer and healthier lives. Decoding Women's Health is a production of Pushkin Industries and the atrea health and research institute. This episode was produced by Kala Leah. It was edited by Amy Gaines McQuaid, mastering by Sarah Buguer. Our associate producer is Sonia Gerwit. Our executive producer is Alexander Garretton. Our theme song was composed by Hannas Brown. Concept and creative development by Shavan O'Connor. Special thanks to Vicky Marrick, Alan Tish, David Saltzman, Doctor David Dodick, Sarah Nix, Jacob Goldstein, Leah Rose, Jordan McMillan, Morgan Ratner, Owen Miller, Eric Sandler, and Greta Cohne. I'm doctor Elizabeth Pointer. Thanks for listening and until next time
Speaker 1: Pushkin. On every episode of Decoding Women's Health, we talk about the science behind women's bodies and share stories from leading researchers and clinicians. But now I want to hear your stories and your questions. No question is too complex, awkward, or small. So tell me what kindacologic questions have been on your mind lately. We'll get into everything from entimetriosis to fibroids, pms, pcos, and more. We really want to hear from you, so please send your questions to us at Decoding Women's Health at Pushkin dot fm. That's Decoding Women's Health at Pushkin dot fm, or feel free to leave us a voicemail at four FI five two oh one, three three eight five.
00:01:17
Speaker 2: This show is not a substitute for professional medical advice, diagnosis, or treatment. It is for informational purposes. Please consult your healthcare professional with any medical questions. Also in this show, we use women as shorthand for people with XX chromosomes. We understand sex and gender are more complex and acknowledge the experiences we describe reach beyond that word.
00:01:47
Speaker 3: I think everybody knows that aging has a biology because we know who's young and who's old. But we know even more than that. We know that some people age faster than others, or some people are ages much slower than others. In other words, there's a chronological age that's your passport, birth certificate, and then there's your biological age.
00:02:12
Speaker 1: That's Doctor Neer Barzilai. He's a gyroscientist, which means he focuses on better understanding the biologic mechanisms of aging. For decades, he has been studying the aging process and looking for clues within our own bodies to help us all age better. He's the founding director of the Institute for Aging Research at Albert Einstein College of Medicine, and he's also the scientific director of the American Federation for Aging Research. Doctor Barzilai has been studying centenarians and their families to understand their genes, often referred to as longevity genes. He's hoping to identify interventions that could actually delay the process of aging. He's engaged in some really fascinating work looking at whether existing drugs such as met foreman and rapamycin can be repurposed to delay the hallmarks of aging. Is one that I have been following quite closely for some time. And I was excited to have doctor Barzilai on the show to hear more about his ongoing research, but I also wanted to get his honest thoughts on all the hype surrounding longevity medicine, because that word longevity is everywhere these days. So today we're breaking down what the latest science actually says about living longer and living better, starting with this concept of biologic age, as doctor Barzilai says, there's your chronologic age, how old you are, and then there's your biologic age how your body functions. He told me one of his missions is to be able to define biologic age in a test, just.
00:04:00
Speaker 3: Like you have cholesterol and you have glucos and you measure blood pressure. We know that there's a biology for aging, and we know that there's a hope because some people do better than others, which means there's flexibility. But there's one additional thing that we have to know, and this biology, this aging, is what drives diseases. Cardiovascar disease and cancer and diabetes and Alzheimer's and more are all driven by this biology of aging. So it's not that you're getting a disease and you're getting old. Okay, you're getting old and that drives disease. It means really that you have to target this aging before you have diseases. You have to think of prevention.
00:04:45
Speaker 1: What is the biology of aging? Can you take us through the biology of aging in a very big strokes kind of fashion.
00:04:53
Speaker 3: Yeah, very big strokes. We have something that we call the hallmarks of aging, and there are now twelve hallmarks of aging. For example, one of the hallmarks is the decline in the number and faction of mitochondria. Mitochondria is really important because that's the source of energy that we have and a lot of the complain of elderly that they feel that they're losing energy is because of decline in their mitochondrial function. One of our major companies in our Longevity Biotech Association, and actually company that is also using our facilities in Einstein, is a company that can actually take a sell and expand it and take a lot of mitochondria and then infuse it to your vein. So what happens when you infuse mitochondria to the vein, This mitochondria goes into the cells and get inside and replenish the mitochondria and the energy and everything that has to do with it, right, So that's one of the problems and one of the promises. Let me give you another one. There is a process that's called autophogy, and autophogy is a green energy garbage disposal. So, first of all, there's a lot of garbage that accumulates by mistakes in our cells all the time, okay, all the time, so we get garbage, and there is a garbage disposal that's called autophogy. It's a biological process that is quite well understood. This process declines with aging, so your cells are starting to accumulate more garbage. For example, what happens in Alzheimer's when we are accumulating those better amyloid or tao. This is all garbage that cannot be really disposed appropriately. So there's effort to produce a drug. There's actually a drug in biotech that is enhancing autophogy. And when you atophagy and you give it to animals, for example, they live healthier and they live much longer, and in particular models that have Alzheimer's disease. So I'm giving you two examples that are only two of those hallmarks of aging. There's telomeres by the way, people hear a lot about telomeres. That's a hallmark of aging too.
00:07:29
Speaker 1: One other hallmark of aging. Can you speak about inflammation? Can you drill down on that a little bit for us or is it relevant?
00:07:35
Speaker 3: Yeah, no, it is relevant. Inflammation or as we call it, inflammaging, is another one of the hallmarks of aging that we're trying to address. And you know, in the clinical setup, everybody talks about it because you kind of can measure it with highly sensitive tests. There are good markers for the breakdown.
00:07:57
Speaker 4: You know, when we go over the age of fifty, we're dealing with breakdown, and in response to this breakdown, there's an inflammation, and so inflammation is a response.
00:08:08
Speaker 3: So some of it is good, but then it goes bad because it's I'm trying to say that inflammation is not the cause of aging. I think it's a more secondary biomarker. But if we fix everything else with aging will probably decrease inflammation. Two. So inflammation is kind of of a center, but you have to understand that it's both. Okay, inflammation is bad also in the sense that it also drives things worse, but it's not what starts the process of aging.
00:08:42
Speaker 1: How do you measure aging? Are these biologic clocks that are marketed to us of any value? How do you look at aging? How do you measure it?
00:08:50
Speaker 3: So let me start by saying, I have ten measurements of my biological age, and I'm anywhere between twenty years younger than my age and four years older than my age, and it kind of tells you the problem, although I would also tell you that eight of those ten are pretty much in agreement. So those tools that were developed are kind of good to tell you what's your biological age. What they fail is to change if you do intervention. So what do we want. We want a biomarker that you will take and you will tell you you're two years older than your age, and the doctor will say, well, start exercising and take me for me. Okay, and you want to come in three months and see that you're now two years younger than when you started. Okay, that's what we want because we have to show success. You know. Let's say we stop aging and we ask you after two years, how you are. You said, you know, I'm the same, because you don't know how it would be if you're two years older. Right, it's a problem. So we need the market. It's like with blood pressure and glucose, you wouldn't know unless you're tested, So we need this. We also we need it for the development of drugs. We need in a phase two trial to see if it takes us to the right direction before we spend billion dollar in a phase three trial. My last grant that is with Dan Belsky from Columbia, we're looking at one hundred thousands biomarkers to see not only what's your biological age, but which of those biomarkers have changed in common, right, So we want to find those that are aging biomarkers. That also tells you that you're getting a respond I think once we have those biomarkers, we're going to learn so much for them and going to implement so fast that you can yourself see in your clinic what you're doing that is right or wrong.
00:11:00
Speaker 1: Sels in essence, can you just define what that is and how that segue is into inflammation because these are all words that are now like all over the internet and on social media, and so I think it's an important for our listeners to understand a little bit about what they are.
00:11:14
Speaker 3: So I have to tell you something that might frighten you. Initially, each one of our cells every day have thousands of basically mutations. Okay. The good thing is that we're pretty good at fixing everything. Okay, it's part of what we do. It was never meant to fix everything, because if we fix all the mutation will never have evolution, right. Evolution is based on the fact that, oh, there's mutation here and there. Some of them are bad, some of them are better. Let's take the better and let's, you know, reproduce with them. So in a way, mutation is why we have evolution. But of course sometimes will fail. So now we have a mutation, and sometimes also very rare, this mutation actually has an effect. It changed something in the cell. It could make this cell a cancer cell. It could make this cell say, you know, I'm committing suicide. Okay. But one of the options, and this option is very common, is that the cell sees that it's stress and it's become what is known as the senescen cell. It stops dividing. And that's fine, except that if you have a lot of those senescence cells, they secrete proteins that could be harmful, and particularly in the area that there's a lot of them when they accumulate, and that's what happened with aging. It accumulates. Then it is a risk actually of cancer and other diseases. And in animal models, when you remove those senescence cell they get healthier. I don't want to say they live longer, but they get healthier. So senesin is one of those hallmarks. It's one of those hallmarks that is out there to find. What are the drugs that you can take in order to remove a bunch senesence cells and improve your health.
00:13:17
Speaker 1: So are so called gerotherapeutics you mentioned, Matt Foreman, How are they different from other drugs? Like we know that statins, for example, are very effective at preventing heart attacks and stroke, both of which can kill you. How is this class of drugs, the ones that target aging itself? How are they different?
00:13:35
Speaker 3: Studings are such great drugs, they're so important, they're preventing so much cardiovascular events and cardiovascular mortality. But if you give them to animals, if you give them to cells, they don't change the hallmarks of aging. And if you give them to animals, they don't live longer. Okay, So they are drugs that are very important when you grow. But in my view, you don't call them gero therapeutics. They're not therapeutics for aging. What the statins have shown to do is taking care of cardiovasclar disease, so you can get now all shade or concert or another disease, which is not what we want to do. We want you to do something maybe one drug, and it will delay your aging, which means it will delay many diseases and not just one.
00:14:25
Speaker 1: The way I look at this and tell me if this is like kind of a basis. Aging is the root cause of cardiac disease or brain health issues or metabolic issues, and so if you target the aging process, then you target all these downstream effects.
00:14:40
Speaker 3: Of aging exactly. Aging drives the diseases.
00:14:44
Speaker 1: Right. Do you see a day where we have like one drug or one therapeutic or one intervention or is it going to be a combination of these things? And can you highlight some important ones that you're working on.
00:14:56
Speaker 3: For the first three questions, the answer is yes, I mean it's everything. What do we need to show to say that this drug is gerotherapeutic A. We want to put it in cells. We want to expose it to cells and show that the cells are getting younger, okay, which really means the hallmarks of aging are changing. Second, we want to give it to animals, all the animals. One of the problems we had in drug development is that people were doing age related disease, were working on young animals, and I just made a lot of effort to say it's different bodies. The young and old are totally different bodies. So you have to give a drug to an old animal and show that it becomes healthier and it lives longer. Okay, that's the pre clinical part. The clinical part is you want to show that the drug that was designated for a specific disease unexpectedly prevented other diseases. You want to show that this drug that was targeting one specific disease is actually changing overall mortality, not disease specific mortality. And if that's the strict definition for gerotherapeutics, we have already four drugs. Now what are the four drugs. One drug is met forming. Met forming it's an extract of the French lilac, but it's modulated, so it's not a nutraceutical. You need a prescription for that. But people notice that it also lowered glucose, and then it was used in diabetes, and in clinical trialing diabetes, it was shown that METFORMI decreased cardiovastri disease, and there's less cancer, and there's less alzheimer and there's less mortality when you take met forming. The latest paper was showing that you're something like twice as likely to get to the age of ninety if you're a diabetic and you're on met forming. So this is one drug. The second drug is the class that is called s GILT two inhibitors. The third classes the GLP one agonist, the ozempiic and manjaro, and the fourth is biphosphonates, which are anti ostroporotic drugs.
00:17:22
Speaker 1: So these are repurpose drugs, right, These are all drugs that are being used for other things. So I just want to back end into a couple of them that I'm really curious about because I've followed this field for a while. Met Foreman, right, mett Foreman was really out there. Then it lost a little favor. Where do you position it in terms of a longevity strategy.
00:17:44
Speaker 3: Losing a little favor is through podcasts of people who just are opinionated. Okay, in my mind. What happened to me for it gained favor, And let me explain to you why I'm claiming that those drugs affect more than one whole mark of aging. Right, met forman You can think it's only for diabetes and only for metabolism, but they're nine studies around the world during COVID that showed that people on metforming had less hospitalization, less mortality, which led to a clinical study. Okay, and that's what we need, clinical studies. And the clinical study was taking patients who just got COVID within the first three days, mostly within first day of COVID, and they gave them metforming and they had less hospitalization, less death, and less long COVID. And the point is metforming is not only metabolism, it's also immunity, it's also inflammation. It also makes the body more resilience to acute the salt. So this idea that metforming lost favor, I think is irresponsible. The second thing that happened that really made me crazy is not everything that's good for young is good for old. Okay. If you have high cholesterol metal when you're young, you're building your go nuts and brains, and it's great but if you have high cholesterol metabolism when you're old, you're clogging your arteries. Right. It's the same with drugs. Not every drug that is good for old people it's good for young. In fact, metformin has a lot of problems if you're let's say, less than fifty and don't have diabetes. There's a lot of things. It's decreasing growth from on the growthrom on igf one, and you don't want to decrease this igf one when you're young. It decreases testosterone in man. So there's a lot of confusion of what metformin is doing and the fact that young people are saying, you know, I noticed that it's not good for me. Well, you should have never been on them.
00:19:56
Speaker 1: Talk to me about the GLP ones and aging.
00:20:00
Speaker 3: If you look what GLP one is doing in cells, it's correcting a lot of the hallmarks of aging. If you give it to animals, even to animals that you make sure or that they are the same weight. Okay, you have to change the amount of the agonists. You have to feed the animals differently, but if you match the animals will still live twenty percent longer. Obesity drives aging, there's no doubt just treating obesity is good. But the point I'm making is that the GLP agonists are taking care of obesity, but that's not even their majority effect. They're affecting other cells directly, other organs and tissues directly. They're doing much more from aging than just the weight loss, which is important on its own. So those drugs were developed for diabetes, okay, because in diabetes they're doing something good. They're increasing insultin secretion, decreasing local goaues. But then they had a strong effect on weight loss also. And now when you give it, you notice that it prevents heart diseases, it prevents kidney diseases, it prevents some cognitive de client. It's not clear if it's pre alzheimer or Alzheimer's, but it's investigated now. In other words, it has effects on aging that are in part weight loss and in part independent.
00:21:26
Speaker 1: What is the mechanism of the best posphonates impacting aging processes?
00:21:32
Speaker 3: So some of it is senolytics, it takes care of the cells. Some other effects we are not sure. But one of our thoughts and their supporting elements is that the biphosphonates are in the bones, and a lot of our stem cells are in the bones, and that they are doing something to make the stem cell both youthful and also go into the periphery and through that improve our health.
00:21:59
Speaker 1: So interesting. So talk a little bit about rapamycin.
00:22:02
Speaker 3: Rapamycin is a drug that increased health span of almost every animal in the world. World and why is it important? Because all animals are aging similarly to us in the sense you know, their skin, their hair, they get diseases, their their muscular skeletal is fading away, not the same diseases, not exactly the same, but it's all aging, and that's why the animals are important. The longest living animal groups of animals has been the combination of rapamizing and metformin. They lived substantially longer, and that's why rapamicin is exciting. Rapamicin is also an FTY approved drugs, but it's approved in very high doses as an immune suppressor for people who got kidney or some transplant. Of course, we don't want to be immune suppressed when we're old or any any time of our life, so the stud these have been done only on those people and not on people who would get you know, tenth of the dose and see what's their effect on aging. There's some clinical, small clinical trials on that, but we just don't have enough evidence to suggest that this is something that we can take. And without clinical studies, we don't know the side effects, we don't know the safety, so we are not there yet. It didn't make it to the fore top.
00:23:46
Speaker 1: Coming up, doctor Barzilai walks us through a longitudinal study that he's co leading called the superager Study, what differentiates most people who live to one hundred from many of us. His answers might surprise you. Let's talk a little bit about the Superasier Family Study. Can you tell me about this study?
00:24:13
Speaker 3: The Superagor study started at Einstein, but now we have an initiative to recruit ten thousand centenarians and their families across the United States so we can find all the longevity genes and develop all drugs that we could to imitate them. And it's very important because we found a lot of genes variants that are different in them than others that had the functional consequences. And in fact, two drugs have been developed in part because of our discovery, and there are others that are on their way. Even more promising. But there's another study. We have a longitudal study on the offspring of centenarians and the people who they are married to. Pretty much if they don't have longevity in the family. And when we look at those people in a longitudal study, we have about fourteen hundred of them. The offspring of centenarians have pretty much half the cardiovascure disease, half the mortality, half the cognitive decline. So just this genetic is making a huge difference for them.
00:25:26
Speaker 1: What if we learn from superagers, what can we adopt? What can we learn from them?
00:25:31
Speaker 3: So listen carefully to what I tell you, because I mean you're asking me as if what was their diet and what was their exercise, and what was their social connectivity and all that, And I'll tell you we were in a way lucky, but that didn't matter to them. That's not what they were about. In other words, it's not that they did what the doctors tell us to do. Fifty percent of them were overweight, over obese, fifty percent of them did not move at all, even moderate exercising, very few vegetarians. So as a group, they're nothing. To tell you, There is this woman I always say, there's a woman who I met when she was one hundred years old and she was smoking, and I said, Helen, nobody told you to stop smoking. And she said, the four doctors who told me to stop smoking, they died, right, And she continued to smoke until she was one hundred and ten. And the argument was for me, is you know, who knows how long you would leave if you don't smoke. She got to one hundred and ten. I don't know what's the answer to that, really, So in this case we don't learn from them. What we learn is the genetic case. What are their longevity genes that slows their aging process and how can we make them a therapy? You know, our maximum lifespan as humans is somewhere like one hundred and fifteen, maybe one hundred and twenty. Okay, half of us died before the age of eighty, so we have thirty five years that we have to realize. And it's not that tomorrow we have the drug to make you one hundred and fifteen. It will be you know, several years in every effort. But that's what we should work on and I think will be successful.
00:27:22
Speaker 1: And are you seeing any gender specific differences when you look at the genetic backgrounds of the superagers. In any difference between men and women.
00:27:31
Speaker 3: Yes, yes, somewhat. But you know we have less men centenarians than women's centenarians. I know that women health is a very important issue, but women are living four years longer than men almost everywhere in the world, between two and four years. Why is that This is a huge difference? Okay, because even if we cure cardiovastar disease from the world, will get only two years, okay, because we'll start dying from another thing. So four years is really a lot. And for every one hundred years old in the world, eighty five are women, so their ability to also get to be a centenarian is much higher. The reason you're concerned is that in those four years you're spending them sicker. My view is that if men could live that long, they will be sicker too. I don't think it's a woman issue. I think it's an aging issue that we have to make sure that we can do. You're asking why. I don't know why. Okay. In fact, the simplest answers have not been confirmed, so we're in the midst of trying to figure out. But when we give animals drugs that we think will target their aging. Sometimes they affect only male and sometimes they affect only female.
00:29:02
Speaker 1: Coming up will delve into the technologies, strategies, therapies and supplements being marketed to decrease mortality and encase longevity, including super hot topics like intermittent fasting, and the popular supplement trend in AD. Back in a minute, Welcome back to the show. Perhaps you've heard of NAD, one of the most talked about supplements out there. It's sometimes given as a pill, injection, topical, or as an infusion, and it's generated a lot of buzz in the media and online as something that can extend your lifespan. So I wanted to hear doctor Barzelaw's take on this trend. But before we get into that, I asked him about the impact new and emerging technologies may have in this field. Where do you land on the usefulness of wearable technologies to improve health span and.
00:30:09
Speaker 3: Health I think of what we would do to keep ourselves healthy has to do with what we learned from wearable technology, Because what's missing in the technology is the app that will talk back to you all the time. It's partially there but you know you did only five thousand steps and it's five o'clock. The technology have to tell you, hey, you have to walk somewhere or jog or go and exercise. Okay. The technology of glucose monitoring is really important because you're finding your weaknesses. You're finding that rise is crazy for you. It takes your glucose so high. You can find out what happened when you exercise to your glucose and decide if you're fasting in the morning or in the evening. I think technology is just going to be a major tool to the extent that the technology will tell you if you need to see a doctor. You don't need to go to a doctor for a follow up. The technology will tell you take blood and will tell you if your cholesterol is I ask you prescription for your doctor. But in my mind, the whole longevity medicine doesn't have to be really a burden on doctors, but rather on you working with the technology, and the doctors are there to prescribe drugs or to do tests or things like that.
00:31:30
Speaker 1: Is AI going to contribute to the discovery of biomarkers.
00:31:34
Speaker 3: Absolutely. AI will help us see you know which biomarkers for which people, and you know, maybe they're different biomarkers for young and old, and maybe there's a different responsor. There's a lot of questions that we're going to ask and AI is going to help us. You need to have enough data to use AI, and that's what we're trying to produce.
00:31:58
Speaker 1: Let's talk about some lifestyle things. Talk to me a little bit about intermittent fasting.
00:32:03
Speaker 3: When I started my career, you know, one of the few that had career in biology of aging. When I was a younger assistant professor, the experiment to do was to take animals brothers, okay, and do to two groups. One just continue, eat whatever you want, and the others we would take to the side and give them sixty percent of what their brothers had. Those experiences were done all over the world in animals and got the same result. I actually did it initially with rats. The rats lived forty percent more and they were healthy for much much longer. Okay, So this was the effect of caloric restriction. And when it hit the media, you know, people were talking, you just need to have less for lunch, less for breakfast, less for dinner. But that's not what we've done. What we've done is we would bring the food early in the morning. The animals will be hungry, so they would eat all the food within an hour, and then they would be fasting for twenty three more hours. So what we saw is not only caloric restriction, it's also fasting. When we started giving the animals food throughout the day, little bits, they were thinner, but they didn't live much longer. Okay, so the fasting was very important. I'm telling you all that because this came from our lab, from my lab, and that's when I realized that fasting is really part of longevity. And that's where a lot of us starting to practice fasting for at least sixteen hours every day, which usually means I finished dinner by eight pm and I'm not having anything but coffee without milk and sugar until noontime the next day. And that has actually improved my health significantly. Of course, not everything is for everyone, but this and met forming I had a major impact on my health that others have noticed too. And I have pictures of me ten years ago. You think that I'm ten years older than.
00:34:31
Speaker 1: Now, So talk to me a little bit about exercise and longevity. Aerobic strength training, mixture of the two.
00:34:40
Speaker 3: I think it's very reasonable to say that you need two things. From a biological perspective, you have to have a good cardiovasular system, so you have to move on a treadmill or you know, find a way to do cardiovassor training. But you also need muscle and just your lean body mass is a good index of your health and your mortality, so you need to do both of them.
00:35:04
Speaker 1: So can I ask a personal question. You've talked a little bit about Mett Foreman and intermittent pasting that you do. What else do you do to do you preserve your health and wellness.
00:35:13
Speaker 3: I'm trying to sleep as good as I can. You know. It's like the recommendation is eight hours. It's something weird. No matter where I go and jet legs and everything, every week, I end up sleeping six hours and forty minutes. But I think I do that because I'm eight hours in a dark room without interruption. Okay, I think if it wasn't that, I would have done less. And six hours and forty minutes is probably enough for me because I'm not feeling tired or not energized or anything like that. So I think it is what it is social connectivity. You know, elderly become lonely, and this is something that have shown taking older people into social activities had outcomes of decreasing cardiovaster disease and other diseases. So it has real biological underpinnings. Every one of them is important.
00:36:08
Speaker 1: Let's talk about some of the popular strategies that are in the media that are in longevity clinics, right, NAD, NMN peptides. Can you just talk a little bit about infusions of NAD Are they useful? Are they harmful?
00:36:26
Speaker 3: I want to say the following thing. People think that if they optimize the nutrition, the exercise and everything, and they need something, it should be nutraceutical or supplements. Then, by the way, for me, supplement means you measured something and it was low and you supplemented. Okay, that's not how it's done. You're getting something in bottles. You even don't know what's in the bottles. But mainly they were not tested for health outcome. Nutraceutical don't have health outcome. So the marketing is about the hope. It's not even about a promise, it's about hope. And that's different than FD approved drugs and you say, oh, FD approved drugs. I see what GLP wants on side effects as well. At least you know what's the side effects. You know that it's safe, you know the efficacy, but you don't know anything about nutrients. So I would warn people against them unless there will be clinical studies that show you that those are good. And it has nothing to do with how you feel. Look the NAD story, which many young people are doing. You know, they're coming from a long flight and they order these fifteen hundred dollars treatment that get them hydrated and they get on petamines. Also, you don't know what you're getting those in those bags, and you're getting an NAD which probably doesn't go anywhere but to your blood cells, but you feel better. That has nothing to do with longevity. Okay, you can do it in a spa, you can do it by drinking more, you can do it by taking on fetamine or whatever. So I would say from a longevity output, there's nothing on those supplements. Is it safe? Well, maybe if you do it one time, it's safe. The question for us is a lot of the studies on NMN. We're on cancer sales and cancer celles love n men. So if you have cancer and you take NMN, I don't know. Okay. On the other end, it might prevent cancer, right, But this has to be figured out. I always say I want to start with good thing. The good thing about supplements is good for the economy, okay, But for you, I don't think so. Look. The example of supplement that is used correctly, okay, is vitamin D. All of us have low vitamin D. All of us are taking vitamin D at least when I ask elderly, okay, eighteen percent are taking vitamin D. So you're basically measuring something and you're supplementing this something. But clinical trial have been so disappointing because vitamin D was associated with other diseases, and so they thought it's good for many diseases. There's no every for that. All the other indication of itamin D has mainly failed, some have been balanced, some a little bit success, some a little bit failure. But here there's a supplement that you're using, right, and even this is not affecting aging. It can affect some things, but not aging.
00:39:28
Speaker 1: How do are your interventions like gene editing or crisper or some of the regenerative medicine strategies, but into the current practice around aging right now.
00:39:38
Speaker 3: They do in relationship to a specific disease. Okay, So for example, there is a rejuvenation effort for glaucoma that really squeeze your nerve to try to rejuvenate that, and there's a company that is approved now for clinical trials and we'll see. But it's not rejuvenation of the whole body. That's a very different issue. And I don't I think you need Crisper for you know, like for the longevity genes that we found, you don't need Chrisper usually need a drug. So I don't see any reason to discuss it now because it's not It's all very important development that will be related to longevity, I hope, but they are not some things that are available now. You know, it's not about older adults. Only people who survive cancer are aging rapidly. People with HIV are ten years older than their cohort, people who are disabled, you know, poor people should be the first in line. So there variety of reasons why we should accelerate our research and why it's so important for so many people.
00:41:06
Speaker 1: There's a negative connotation associated with aging, especially in the United States. But aging is no longer a passive endeavor. It's something that we can influence through our actions, healthy lifestyles, and through science. There was so much from this conversation that has really stayed with me. Doctor Barzilaw's work around interventions that may extend our health span is really exciting stuff. It was quite interesting to hear about the participants in doctor Barzilai's studies who have lived long lives despite some not so healthy lifestyle choices. Of course, their genetics likely play a role here. The data from these studies around centenarians and their offspring are providing us with a better understanding of the biology of aging.
00:41:56
Speaker 2: To zoom out for just a.
00:41:57
Speaker 1: Moment here, I'd argue that the focus shouldn't just be living longer. It's also about your quality of life, making choices that will keep you feeling better, staying active and in community. We also want to mention something important we talked about today, animal studies. These provide interesting insights and give us opportunities to shape human studies. More research always needs to be done to see how those findings and animals translate into humans. And a quick note about intermittent fasting. Studies have shown it may be beneficial for longevity, but as we mentioned, everyone responds differently, and actually some women may not tolerate intermittent fasting. So as always do what feels right for you. There's still so much we don't understand about the biology of aging, but I'm enthusiastic about the field of gyroscience and the secrets at canon Lock for all of us to live longer and healthier lives. Decoding Women's Health is a production of Pushkin Industries and the atrea health and research institute. This episode was produced by Kala Leah. It was edited by Amy Gaines McQuaid, mastering by Sarah Buguer. Our associate producer is Sonia Gerwit. Our executive producer is Alexander Garretton. Our theme song was composed by Hannas Brown. Concept and creative development by Shavan O'Connor. Special thanks to Vicky Marrick, Alan Tish, David Saltzman, Doctor David Dodick, Sarah Nix, Jacob Goldstein, Leah Rose, Jordan McMillan, Morgan Ratner, Owen Miller, Eric Sandler, and Greta Cohne. I'm doctor Elizabeth Pointer. Thanks for listening and until next time
