93% of your longevity is determined by lifestyle factors. Only 7% by genetics, what you've been hearing. Some colleagues used to say that to live old, you have to choose your parents well. But the data doesn't say this.  Hey everyone, I'm Raif Derrazy and in this video I have the great pleasure of interviewing our special guest, Eric Verdin. We're going to talk about the Buck Institute, which focuses its research on aging. Part of that focus includes HIV and aging, and what that means for you and I. We'll cover some of their latest research findings as well. I'm here for the annual HOPE Collaboratory Conference, a meeting of all the scientists from around the world working on the block lock stop, previously I've mentioned it as block lock excise, modality of preclinical research for an HIV cure. So a little bit about Eric. Eric Verdin is the president and chief executive officer of the Buck Institute for Research on Aging. A native of Belgium, Dr. Verdin received his doctorate of medicine from the University of Liege and completed additional clinical and research training at Harvard Medical School. He's held faculty positions at the University of Brussels, the National Institutes of Health, NIH, and the Pickhower Institute for Medical Research. Dr. Verdin is also a professor of medicine at University of California, San Francisco. Dr. Verdin joined the Buck in 2016 after spending the previous 20 years as a senior investigator at the Gladstone Institutes where he served as associate director from 2004 to 2016. Dr. Verdin's laboratory focuses on the role of epigenetic regulators in the aging process. His laboratory was the first to clone a family of enzymes called HDACs, which regulate histone acetylation. Dr. Verdin studies how metabolism, diet, and small molecules regulate the activity of HDACs and sirtuins, and thereby the aging process itself and its associated diseases, including Alzheimer's. If you didn't understand what I just said, that's okay. Just know that he studies how metabolism, diet, and small molecules impact the aging process and its associated diseases. He has published more than 210 scientific papers and holds more than 15 patents. He is a highly cited scientist and has been recognized for his research with a Glenn Award for Research in Biological Mechanisms of Aging and a Senior Scholarship from the Ellison Medical Foundation. He is an elected member of several scientific organizations, including the American Association for the Advancement of Science, the American Society for Clinical Investigation, and the Association of American Physicians. He also serves on the advisory council of the National Institute on Drug Abuse at the NIH. Welcome, Eric. Thank you for sitting through that with me. There's a lot to cover. How are you? It's very good, how are you? I'm excellent. First of all, when I read your bio, I was in awe and reminded just how much a person can accomplish in one lifetime with the right amount of focus, a sense for purpose, and a true passion. I'll start with a general question that I ask all my guests, and that is, what is your current assessment of the global HIV AIDS epidemic? Well, we've reached a really interesting stage in which because of all the work that's been invested in and by friends and colleagues, we have drugs that actually work. And that by itself is a remarkable achievement and I went to medical school. We were told that the 20th century would be looked at the century of when we conquered bacterial diseases, but we also were told that there would never be treatments for viral infections, except for vaccines. And in some way, the HIV pandemic really showed us the way that now we have drugs targeting HIV, we can suppress it, but not only HIV, we can cure hepatitis C and the list goes on. So there's been an incredible paradigm shift. That being said, we all recognize the incredible success of these drugs in allowing patients to survive and to thrive. We all recognize that this is far from a cure. So I think that the reason we're here this weekend at the Buc is really to work and part of the HOPE Collaboratory is really to go to the next stage. And we have six patients who have been cured from HIV. Everyone recognizes this is a momentous achievement, but we also recognize that the treatment that have been used are heavy, risky, and certainly not something that we can implement in the millions of people who are living with HIV. So I think the next stage is really, can we bring the same knowledge, the same hard work and a little bit of luck maybe to bring a cure to everyone who's infected with HIV. And I'm really, I'm an optimist. I think the power of science has showed us what we can do when we focus and we tackle. So this whole topic of HIV cure is really, is the frontier right now of HIV research. And hopefully, we can come back in five years and say we did it. So really excited by what's happening. Yeah, and isn't it true that HIV research also informs research into other diseases as well? Like vaccines for COVID even? Absolutely. I think there's, it's hard for people who are not in the field to understand this, but there is no research in any field that does not impact other fields. For example, through our work on HIV, we ended up cloning the HDACs. Now, your audience may not be familiar with the HDACs, but you probably have heard about those treatments that were initially proposed for a cure, which was the idea of reactivating the virus. What that was based on are cloning the HDACs and showing that the HDAC inhibitors were actually able to force the reactivation of the virus. Is that the reservoirs awakening? Exactly. And now, you know, the field, at least this hope collaboratory is switching in a slightly different direction. We're not sure that reactivating the virus is the best way. We think just locking it in is going to be key. And believe it or not, the enzymes, the HDACs and the whole epigenetic regulation, we think points the way, points to the levers that we have in cells that will allow us to lock the virus in. Okay, great. So basically, I mean, there's, you know, research in any field, research in cancer has helped us advance work on HIV and work on viruses has helped us in many other directions. So it's a whole intricate sort of web of work. And so, you know, the best scientists actually stay attuned to what's happening in many different fields because you never know what you're going to be learning from colleagues who are studying a completely different process. That's such a great insight. Okay, well, I'm sure everyone at home or on the other side of the screen is excited to hear what you have to say about aging. But before we dive into that, I would love to learn a little bit more about you personally. Can you tell us what drew you specifically into the work of aging? Was there like a moment? Was there an experience that you went through? Yes, there were a couple. First, the personal history of my father who was, you know, smoking for a big part of his life.  And so, and we saw indeed, you know, some of his close friends die in their 50s for heart attacks. And so, this is something that sort of collared my youth, the idea that feeling your father being vulnerable to a fatal heart attack. So that was something, and eventually, you know, he did die from lung cancer, which was directly linked to smoking, but he died at 77 and I really could not help to think that, you know, had he not smoked, he could have lived an extra 15 years and he would still be here today. So that there's a part of me that thought, okay, lifestyle, the way you choose your life really will have an enormous impact on your longevity. And we know this. This is what the data says. 93% of your longevity is determined by lifestyle factors. Only 7% by genetics, what you've been hearing. You know, some colleagues used to say that to live old, you have to choose your parents well. But, you know, the data doesn't say this.  Now, the other, so that was the personal aspect. The more professional aspect is we ended up cloning this family of proteins, the HDACs, you mentioned in your introduction, that played a key role in the regulation of HIV and it's silencing. And it turns out these proteins are so involved in the aging process. And so about 20 years ago, 25 years ago, when we discovered these proteins, I realized, you know, there was another side to the HDACs, not just HIV, and by the way, we're still working on HDACs and HIV to this day. But the aging just drew me because there was a personal connection from my father and just I started focusing a part of my lab on studying aging. And eventually, we made a number of discoveries that would let me to being recruited here to direct this institute, which allowed me to sort of bring my work, I continue to run a lab here, but also to bring my work to a bigger stage, basically the idea of directing an organization and becoming sort of a leader in the field of aging research. Great. Yeah, I can certainly relate to your father. My stepfather was also smoking most of his life and he died at 54 of a heart attack, so, you know. And the percentage, 93%, I bet, I'm sure a lot of people watching are shocked to hear that that big of a percentage is based on lifestyle. My question would be, can lifestyle actually manipulate genes turning on and off switches also? Yes, completely. And actually I always tell people that, so this is a field called epigenetics. So think about your DNA is the code, I know how it's written. We cannot change this. You're born with the genes from your parents and that plays a role in your longevity to some degree, only about 7% for most of us. There's some exception to this, the centenarians, for example, we can discuss this, but on top of this layer of genetics, there's epigenetics, which regulates how these genes that you inherit are actually expressed. And our epigenome is highly sensitive to the environment and this is how the environment basically, so you think about the genetics or the genetic code as a score for a piece of music. We know that on top for the same score, you can give it to 20 conductors, they will play a different music. They will all have their own interpretation. And so our epigenome, epigenetics really is highly attuned to the environment and that includes if you have a meal, if you have, and people don't realize it, if you have a meal, your pattern of gene expression will change. So all of these genes that are fixed will start expressing a different level depending on what you eat. For example, if you choose to have a greasy meal, your epigenome will go in one direction and if you have a healthy meal, it will go in another direction. And so our focus of our work is understanding all of the, there's a term for this, it's called the exposome. All of these external influences, the air you breathe, the toxins you are exposed to, exercising, the food you eat, everything will eventually affect the expression of your genes and thereby your health and your longevity. I think that's really empowering to hear for people living with HIV when you start to hear that there are comorbidities associated with having chronic inflammation that you can really take back a lot of that initiative, the power. And I think what I've just told you for the general population, I would say applies even more to people with HIV who are already at increased risk. So I would say the potential positive effect of modulating these risk factors by lifestyle is even greater. And one of the, so that's one layer of the whole aging field right now is really understanding what are the factors that are affecting your longevity? And everyone knows them, if I named them, you'll say, yes, I've heard this nutrition, physical activity or exercise, stress and sleep, human connections, which is a great example of what we have here at this meeting where there's a lot of community buildings or having friends being loved. All of these things actually do affect your epigenome, which is frontier in science. This is the hardest thing to study because our laboratory animals, we don't know how they feel about each other, but we know in humans, all of these variables affect your lifespan and your health span. So one of the focus of our work here at the Institute is really to try to bring some molecular details, understanding what is it about food that actually can make you either sick or healthy? Food is the same potential. What forms of exercise will give you the biggest benefit? What forms of, how much sleep do you need? And so on and so on. Fascinating. I'm curious, I wanted to ask you, maybe this is a little bit of a personal question for me. What drives you to accomplish so much? And most importantly, what's the secret to managing so many things? And having that, what you said is so important, the human connection. What drives me? I think it's a really good question. And actually, by the way, having a sense of purpose is one of the most important thing that you can do for your longevity. The people who are driven, who have the feeling they're here for a reason, tend to live longer and they're more happy. So what drives me? I would like you to consider for one second the likelihood that you would be alive. And so when you look at where you're coming from, if any of your ancestors in the last three billion years had been eaten a little too early, you would not be here. So the fact that we are a unique product of a chain of events that goes back three billion years ago, and for which there could have been so many events, a car accident, or someone eating your ancestor, or your ancestor going to war and not coming back. So the likelihood that each of us would be alive is an incredible miracle. And I felt this since the first day, I mean, not since the first day, but since very young, we only have one life, we're here for a short time and I love living as we all do. So why not make the best of this very precious time that you have and actually try to contribute? So to me, that's really the sense of all that I'm so lucky to be here, to be alive, and let's make the very, very best that I can. And every day that I wake up, I start thinking, oh my God, gratitude for being here, let's make this a very special day. Where do you think that comes from? Because you said you felt that at a very early age. I don't know. I don't know. That's something to study maybe is how. I think it comes from reflection, it comes from having been lucky to have good parents who raised me well. You know, it comes from many, many different things, but it's also something that can be taught. Just sharing this simple negative information, think about how unlikely it is that you would be here. Most people don't spend any time thinking about this, but once you realize, they say, wow, I'm here and it's finite, I'm 66, which means that this is an age at which you start sensing your mortality in a bit of a more acute way. And that even accelerates my desire to really make the best of it. The second thing is you mentioned how, where do you find the energy? I think, or the drive, part of it for me has been that the more I pay attention to my well-being, my physical ability, the more I can do. And I have more energy, I claim this and I probably will make some 20-year-old love, but I claim that I have more energy and more drive today than I had in my whole entire life. And I think part of it being driven by the fact that I pay more attention to how I live, sort of living consciously about your body and trying to really optimize what you can do with it. Perfect answer. So another secret to managing so many moving parts, as you ask, is the fact that I hear from a lot of people when I tell them you have to optimize your lifespan, you have to start being physically active while people tell me I don't have the time to exercise. And my argument is exactly the opposite. Once you start exercising or just spending time on yourself, you will find that your resources, your efficiency, your enthusiasm, your positivity, all of this is going to be increased. So I can mope around at home and feeling sorry for myself and being tired and not accomplish anything, or you can drive yourself a little bit, pay attention to the machine, which is ourselves, and then your productivity will increase. And so in some way and never by the argument, I talk to a lot of people about physical activity and they tell me, well, I just can't do this. I say, well, yes, you can. It just has to be number one priority. And once that is a priority, everything else becomes easier. Absolutely. So well said, couldn't agree more. I'm actually a competitive natural bodybuilder. And that was part of my journey when I, after being diagnosed with AIDS, was reclaiming my body and not being a victim anymore. And yeah, once you make the time and it starts to give you energy, once you give it, in the beginning it's an investment and then after a while it starts to give you energy and it's like...  Thank you. And after a while when you're in this business and you talk to people, I can recognize someone who is... 38 years old. Fantastic. Well, fantastic. You're doing a good job. Okay, I read on the website, the buck is the first independent biomedical research institute in the world focused solely on aging. The mission is to end the threat of age-related disease for this and future generations. I'm curious, what does that mean that it's an independent institute? Well, independent simply means that we're not affiliated to a big university. We collaborate with UCSF, Berkeley, Stanford, all of the UC Davis, the organizations that are part of our ecosystem here and actually across the country and across the world, but we are independently managed. We have our own grants and which gives us, I think some degree of nimbleness that you might not have if you're part of a giant institution. So that's all it means. Okay. Regarding our aging bodies, you mentioned in your talk a distinction between intrinsic aging and immune aging and that HIV impacts one more than the other. Can you speak to what each type of aging is and how HIV impacts each differently? Yes, so it's a bit of a difficult question to answer, but I'll try to simplify it. There have been a number of papers claiming that HIV, people with HIV actually age and an accelerated rate. And this has been based on markers that people call epigenetic clocks. And so recently, and so I've always accepted it, okay, we know patients, people with HIV on average, tend to live a little shorter. They also tend to show an increase in what we call the chronic disease of aging, the comorbidities, heart attacks, and some other complications. But when the clocks were used to measure aging, and we have these tools that allow you to determine not only what is your chronological age, how many years you've lived, but where is your biological age? Where are you? Are you in person with aging faster or slower? So these clocks actually are being used in the setting of our research. But I was always a little bit wary of the data that claimed that HIV infected people were showing true accelerated aging. And there's some degree of skepticism from other people. So what we have found is we have generated a new clock which measures real aging. And I'll come to say what I mean by real aging. And this clock actually shows a very minimal acceleration in HIV and people with HIV about two years. Thinking about a year, a life expectancy of 80, two years is almost negligible. I mean, it's smaller than the genetic variation. So what is it that the old clocks was measuring? And we've come to, through our work here at the Institute, we've come to realize that the traditional epigenetic clocks are not really measuring, that they're a mixture of multiple things. They're measuring multiple things. What we call intrinsic aging and extrinsic aging. So intrinsic aging, the core of aging is not changed during HIV infection. What is changed is chronic inflammation. And we think that the existing clocks are a mixture of the two together. So we've been able to split them. And so we know, another example, there have been some papers recently published saying that COVID infection is associated with a seven year or actually 15 year acceleration of aging. And typical COVID infection is three weeks. From a biological standpoint, it just doesn't make any sense that you would age 15 years in three weeks. This is not how biology works. And actually our new clock, the one that I mentioned, the intrinsic clock shows no change in intrinsic aging. However, COVID, acute COVID infection and untreated HIV infection have two things in common. One thing in common, which is they're both associated with a massive activation of the immune system. And so our other disease, rheumatoid arthritis, many autoimmune diseases, all of these diseases have been reported to show an acceleration of the clock. So I think our work is trying to really dissect whether these clocks really tell us. And so what they tell us is that there is no change of aging rate, intrinsic aging rate during HIV infection, but there's definitely a massive chronic immune activation which is suppressed by the treatment by the way. So I think our message is one of positive message that we should focus on this chronic immune activation by suppressing the virus. And we know, for example, that even in patients who are in people who are infected but treated, there's still some degree of virus churning. This is why you cannot stop the therapy. So the whole block in luck by suppressing this remaining virus, I predict will also eliminate this little remaining chronic immune activation and might enhance the health of people. So as it makes sense, it's a bit of a complicated concept, but for me, it's one that's positive because it means you can really affect chronic immune activation by lifestyle factors and so on. And if you can target that chronic inflammation, you could potentially reverse that aging process. Down to zero. Amazing. That's, we will get there, I'm convinced. Okay, okay. What does the future hold for the possibility of elongating our lives? And in some respects, more importantly, enriching the experience of the life that we are living. No one wants to live until they're 150, knowing they're gonna spend the last 50 years without mobility or being able to do or experience the things that they love. Yes. So the future is actually, it's quite bright. Our lifespan has increased, as you know, in 1840, we were living to 38 on average, 30 ages. Just let this thing in for one second. This is only 150, 170 years ago. And what we've done through sanitation, medicine, vaccination, antibiotics and all of this is essentially eliminate most of infectious disease, obviously not HIV. And so this has resulted in people living much longer. And in this country, it's 78, approximately. I mean, between 76 and 80. But along with this increase in lifespan, we've seen a massive increase in what we call the chronic disease of aging and heart attack, stroke, Parkinson's, Alzheimer's. What else is there? Immaculate degeneration, loss of sarcopenia, loss of muscle mass, hearing loss, glaucoma. I mean, the list goes on and we see this around in our parents or in our families, really the grades, even though we have all these extra years, the grades, the quality of what we live. And if you reach 65, 70% of people carry at least one of these disease. By 70, most people carry two of these chronic diseases. So we equate aging with getting sick. And what we have found through our work is that the same factors, the dials, that were the levers that we've identified that allow us to regulate the rate of aging also regulate the rate at which you get sick. And so the promise of our field in our work is really to help people live better longer. This is like the tagline from the book. And the reason we chose this is this is something that we can do in the laboratory setting. When we tinker with aging pathways that we've identified, animals live longer, but they also live healthier. And that's the promise for humans. Now I imagine living to 100 and instead of spending 15% of your lifespan afflicted by all these disease, you would spend 5%. This is what the centenarians today do. They live to 100 and they live to 95 in good health. So they have five years of rapid decline and then they pass away. Most of us, as I mentioned, we live to 80 or 78 and we start getting 65, that's 15% of our life. So we know today also there's incredible health disparities. Some people are living on average, like there's a community here in Marin County that lives to 88 on average. That could be done today. And I can tell you that whole town is not all optimized in terms of lifespan. So despite this, they're living to 88 on average. But we have other communities here in California who live to 68 on average, all determined by lifespan. So the promise of our field and what we're trying to accomplish is really increasing health span, making people not only live longer, but also living better. And it's done in the laboratory setting and I predict that we will do it in humans as well. Is there also an observational component, especially with now we have a whole cohort of people that are aging with HIV. Is there research that's done simply observing their lifestyle and the way that they age? Exactly. So typically, I mean, if you think about how the aging field works, is typically you start with observation or study. You try to see, okay, these people are living short and these people are living old. What's the difference between them? And you try to tease out the factors that are associated. Now, association is not causation. The fact that, for example, people who floss their teeth live five years on average, that people who don't floss, that's a typical example. That doesn't mean that flossing your teeth will make you live five years longer, but it indicates that if you're flossing your teeth, you're likely are the type of person who pays attention to everything else. And that's typically the headline that you'll see in online is people who floss live five years longer and people make the incorrect connection. So correlation is not causation. The hard part of the job, so it's easy to find all these associations. Vegetarians live a little later. Is it because they're vegetarians or is it because it reflects, again, predisposition to paying attention? So a lot of our work right now here at the buck is really focused on proving the causation and identifying interventions that will have the maximum impact on people's health. And in this case, exercise, I hate to go back to this, physical activity. Physical activity, and I'm using that term deliberately instead of physical exercise, because a lot of people will tell you, I don't like to sweat, I don't like to exercise, therefore I don't do anything. I'll take the car to go to a store where it would be a 10 minutes walk and I'll take the car. So physical activity is the biggest intervention that we have today if you want to maximize your health span and your lifespan. Yeah, you mentioned an example earlier of someone garden, rigorously gardening, that's considered, because I don't think people think of it. Like you said, it's been trained in our minds to think of fitness, of exercise, of working out, not perhaps day-to-day activities or hobbies, things that we love to do as well. You know, there are studies showing that if you walk 25 minutes a day and 25 minutes a day, I'll split it in two. That's 12 minutes in the morning, 12 minutes in the evening, which I would venture to say anybody can make the time for this. No matter how stressed you are, that those 15 minutes in the morning or 15 minutes at night, that will result in a 40% decrease in heart attacks, stroke, type 2 diabetes, Alzheimer's, Parkinson, everything, year over year, 40% decrease. So to me, this is a number and despite this 80% of the American population does not do any physical activity. So again, for your audience, if I can leave you with one message for today, starting tomorrow, just spend that 30 minutes, that will be the best investment you can possibly make for your own health. And like you said, paying attention means planning, planning for it. Sometimes you have to plan. Okay, I give myself 12, 15 minutes in the morning before I do whatever and then at night. Wake up a little earlier. Routine. For me, the routine, for example, I do exercise, I do more than 30 minutes because the effect doesn't stop at 40%. The more you exercise up to a certain point, the better the benefits. But you get a big jump just by that first 30 minutes. But for example, a trick, no one wants to exercise in the morning. When I get up, the last thing I want is to do physical activity. I wanna sit down and have coffee, read the newspaper and so on. So first thing, like the night before, I'll prepare my bag to go to the gym. And so there's no decision to be made in the morning. The only decision I have to do is to carry my bag, get in the car and go to the gym. Yeah, the preparation. The preparation that these little tricks, actually really go a long way. And then once you're doing, you get into a routine, you will see that you will benefit from it. And then it becomes somewhat addictive in a way. I feel so much better. Why should I do not more? Yeah, I agree 100%. COVID showed us the level of distrust that exists between community and between science researchers and healthcare. How can we rebuild and continue to strengthen that trust? This is a great question. And it's one that really preoccupies me. We saw COVID vaccines were a miracle of modern medicine. Developed in one year, actually allowed us to get control of the pandemic and the way we live today is a reflection of this. Not the virus getting tired. But it also showed an incredible disparity in terms of which communities trusted us. The name of Dr. Fauci being demonized. I mean, these are things that I take personally. So the politicization of the whole scientific discourse. All of these are really troubling. I want to finish on a positive sign, which is the work that the HIV community has actually done. First, at the beginning, I remember ACT UP 30 years ago. The first reaction was, wow, I mean, these people are crazy. As a scientist at that point, I thought they're not with us. And I've credited Tony Fauci for his willingness and his ability to engage the community and to actually work with them and to actually get to the point where HIV is showing their way. The fact at this scientific meeting, the HOPE meeting, we have a very strong community presence. You and engaging with the scientists. The scientists listening to the community. It's not enough for us to be standing in our ivory towers and to design treatment and to hand them down to the populace. This is an old model. It's paternalistic. It doesn't engage. So we're confronted with the same thing in the aging field. We now know today many interventions that will make you live longer. And I'm dumbfounded when I go in the community and I talk to people and I hear, well, you gotta dive something. Like my father used to say. Or you know, I don't want any anti-aging medicine just because people don't understand what we're trying to do, what is the purpose. So I think as scientists, as physicians, it is extremely important that we engage with the community and build the support. Now, is it easy, am I delusional that this is going to happen? But I think it has been accomplished for HIV in a remarkable, it might not be perfect, but it is, I can guarantee you that, so Melanie Yacht, who's also my wife, was planning this meeting and planning the grants. She is taking this to heart. And I think there's nothing more satisfying for me as a scientist to participate to a meeting with the community and trying to engage, learn from them. We heard two talks yesterday last evening from two people with HIV.  So I think, I hope we will be able to do this on a broader scale. I'm inspired. I was telling Melanie yesterday and the other two PIs that when I came on, I really wanted to not just be the voice for community, for you all and the scientists and researchers, but also to be able to learn at least enough of the science that I can translate it into a way that's understandable for community. And I was heartened because all the scientists and researchers are so open and willing to talk just as you are right now. And I think that is also important, you sitting here and explaining things, but then also more importantly, realizing that you're not just a lab coat, you're a human being and you have your personal life and your personal passions and your concerns and fears and things affect you just like they do everyone else. So when people know that there are humans really fighting every day, countless humans for our community, I think that helps. It helps solidify the bond and it also prevents us from running in the direction that we think we know what's good for you, but we don't. We're not living these problems. We're not confronted with them on a daily basis. That's why the two talks from the cured people was so inspiring, describing everything that they went through and what they want, what they don't want. So I think it's a model for not only for HIV, but pretty much healthcare in general. I think there's no way, I mean again, another example of this is the fact that we know what you should be doing for your health and people are not doing it. Right, it's not a logical decision. No, it's an emotional decision. And it's one that's built on human connections and also seeing examples, you know? Culture. Culture, so we've got a lot of work to do, but I think that shouldn't stop us from trying. Exactly, as we start to bring the ship into shore here, what does Eric do when he's done at the end of the day, kicks off his shoes, and it's time for you for yourself? Well, I really look at physical activity and sport as one of the joys, but also I have a family, I have three children, a wife, a spouse, so I love friends, so I love spending time with them. I think human connections is a great thing. We thrive on this and we've seen what happens when we actually get taken away during COVID. As a hobby, I also am a passion race car driver. Wow, cool. So it doesn't really seem compatible with longevity, but in my case, it just forces me to stay fit because it's very physically demanding. It also stimulates my brain, forces me to really stay on top of my game. And so that's what Eric does on the weekend. So you're definitely an example living what you espouse in your work. Trying to, and it's not always easy.  Well, you have to work hard at it, and life is just not a given. I mean, it is a given, you're lucky to be here, but what you make of it is at the end of the day is depending on you. Is there anything you'd like to share or discuss today that we haven't covered? No, I think a sense, maybe the last thing for me is I was stunned when I saw the study that showed the relative proportion of the effect of genetics versus lifestyle because it's an empowering message. It means it's on you, it's on me. You can choose the type of life that you're going to have. I mean, it's easy to say it's personal responsibility and so on, but I really view it as a journey and I can tell you from my personal journey, the more I work at being healthy, the more I derive joy from life and HIV should not be in the way of this today with the therapies. If you get the therapies that medical care brought us and then you add on top of it an optimization of your health span and your lifespan using lifestyle factors, you're going to find yourself more and more wanting to live basically. And so to me it's an empowering and positive message and it applies to everyone. Absolutely, perfectly said. Where can folks go to follow you and or your work? Well, probably the easiest would be the Back Institute has a website which actually could serve as an introduction. It's backinstitute.org or you can look for Back Institutes for Research on Aging. We have a pretty nice website which is a mixture of signs but also outreach to the public. We have a newsletter. We have a podcast. So we have ways that you can sign up to come and visit the back. We have docent tours. There are many ways and I hope maybe a post-production you will be able to add a few links. I'll get all those links to all the things he mentioned and have it in the description box below the video. Wonderful. I invite you to join us. I think we are, again, a not-for-profit organization, academic, driven by trying to improve health for everybody. And we need your support. We need your help. We need your, not only financial but also spreading the word about what we're trying to do, visiting, bringing your friends and so on. Well, I would love to bring you back on and or anyone that you recommend who works with you here at Buck at some point in the future, new research, new findings or if you just want to go dive deeper into something. This was a fascinating conversation. I feel like we could talk for hours but I'm going to respect your time and your energy. So to everyone on the other side of the screen, thank you so much for watching. Drop your thoughts, comments and questions below. I'm happy to follow up as well. Like this video if you liked it. Subscribe if you haven't already and hit that bell so you get a notification every time a new video comes out and please share this with anyone who you think might find value in this content. Until next time. Thank you. It was great to be here. All right, thank you. Thank you.


Hey guys, I'm Els Marshall, and welcome to Hey Guys. This is a brand new show where we talk about what's been going on on the internet this week. Let's get into it. So KSI versus Joe Weller. So basically, they're sort of a boxing match, but just before that, I'm gonna tell you the backstory of it. So obviously Joe Weller was fighting his friend, you know, he posted it on YouTube. And KSI, you know, obviously commented on Instagram, oh, I'll fight the winner.  But obviously it turned a bit serious, because you know, Joe Weller went on YouTube. Like dissing KSI, madman. I was like, what's going on? Like when he was dissing him, I was like, raw. Is this guy actually serious? He's actually dissing him. Obviously now they're both big YouTubers. He was like, you know what?  And a press conference came up. I'm on upload.  The crowd was going mad. So in my opinion, yeah, Weller, you know, I know he's a bit ancient. Like, oh, I need to go with Jim too, as KSI is looking strong though. So I reckon KSI maybe just, I don't know if it's going to be a knockout, maybe decision, but maybe just win that fight. So it will be live streamed on KSI and Joe Weller's channel from 4pm GMT time, English. You know, I've been in America. You're not going to get the same time. So don't blame me if you're missing the fight. Yeah, 4pm GMT on both channels on the 3rd of February, Saturday. So comment below. I want to see who you guys think is going to win. Don't miss it. It's going to be a matting. Next. Logan Paul is still more popular than Joe Weller. How? After the suicide video, what's going on? Let's go out in public and see what you guys think about this. What do you think about Logan Paul having more subscribers than Joe Weller? Oh, I didn't knew that information, but it's a bit sad. Logan Paul. Okay, we're just going to go over anyway. See how it goes. Hello, are you okay? Yeah. No, not you, not the cameraman. The cameraman's like, I am good. How's it going? Are you good? Yeah, fine. Yeah, yeah, yeah, I know. He's video. Yeah, yeah. Yeah, the guy. Don't put the **** like that up on YouTube. Yeah, for real. Kids watch, kids watch. Yeah, kids watch. He has a huge, like, young audience. So basically, talk about Logan Paul. No, I'll pass to him. He's like, I don't know what to talk about. What did you just, I don't understand. Okay, that was very fast. Do you rap? They're the propagation of youth culture that I think stereotypes and characterizes young people to be a certain way and to be a certain thing and a certain model in effect that has greater damage too. Okay, cool. Anyway, so don't you think Zoella should have more subscribers on makeup videos? Absolutely amazing. I don't think she knows what I'm talking about. But anyway, we're going to be on to the next question. Where you going? Speaking of Zoella, she's actually looking for a social media manager and photographer. Hmm. I, no, I don't need, no, I'm not doing that. Chill, I'm not applying to nothing. Don't worry, I'm not, Zoella, I'm not a fan. No, stop, stop filming, please. No, outside. No, please. Why is Zoella gets like, ill-assigned? I'm just about stepping in. I don't know anything about makeup. I would just be like, oh, yeah, the eyeshadow was good, the green, yeah, eyelashes, you go, you get the eyelashes up, fake ones, yeah. Get them, link in description, you know, the foundation things, yeah, you put that in your face and that. I'll just be chatting like makeup language, but I'll just be saying the makeups and not making sense. So I'll be like, you know what? Forget all the makeup stuff, forget all of that.  I'll get a more subscribers, definitely. You know what I'm saying?  All right, let's move on. YouTuber, it's Arya, posted a water prank video. He went out in public, on the streets, with a water bowl, and squirted on people. Very smart, you know what I'm saying? That was a good idea. You know, if that happened to me, I wouldn't really be happy. I don't, I don't really understand, it's funny. You know what I mean? Like, just squirting more and then for no reason. They're just literally doing their business. And obviously they don't know if it's water or not, so. And then he used that same running music every time he ran away from the people. Black flag. Changed the music, bro. You know, smacking drinks at our people's hands. Bro, why? Just why? So obviously I was scrolling through Snapchat, Instagram, and I see on Arya's social media that his channel shut down. So I was like, right. All right, so some career advice for Arya, you know, Dr. Marshall's here to help. There's loads of things you can do on YouTube. Please don't do pranks to our people. You know what I'm saying?  Oh, you can see a coin and stuff. And then they're squirting and they're like the one I've seen on Vine or Instagram and stuff like that when they actually get a bottle of water and they squeeze it in the cubicles, in the toilets, and that like is a weave. See, that's a prank. You know what I'm saying? Like, the other ones are not really pranks. They're just, I know you. There's always like Sainsbury's and Tesco. Could be both, maybe, I don't know. You could maybe do a bit of, you know, Sainsbury's and that maybe fish and chip shop down the road. No, I'm saying. There's jobs out there, so don't worry, man. Anyway, next. So apparently, whales can speak. Wait, what? Hello? Oh, it actually said hello. I don't know what's going on, but I feel like I'm in a science lesson. This is really educational. Is that done? I don't know. I need a wall like that, man. I need a wall. I know I can't have it in my house, but you know, I still get one somehow. That's crazy. Animal speaking now. Hey, no, it said hello. No, it said hello. It's like the world's improving. So these all-car whales imitate human speech. I don't know how that's happening. I don't know how humans can get whales to speak. Maybe they're just like, hello, hello. Like, they just keep saying words to them and they just, the world's just running. Be like, you know what? I've had enough. I've had enough of you speaking human speech to me. Human language. I'm just gonna join in. So I'm imagining like, whales in the ocean. They speak to each other. Like, what are you saying? Are you going to get some fish?   Like, it's like going to the shop. No one to be with saying, you go to your friend. You're like, I don't wanna go shop. They're like, say it in the world language. They're like, hey, oh, come and get some fish, man. Oh, let me get some fish. Oh, I thought, what was that? I thought, maybe that happens in the ocean. You don't know, maybe. Do I say maybe? No one knows. You know what I mean? Come and go to some party, man. Nobody's just bare whales there, just don't, okay. What happens in the ocean stays in the ocean. But anyway, I'm just going on and on. Let's go to the next one. Boop! Dumb water bottle pranks on YouTube. YouTubers fighting, Logan Paul, Zoella, and Talking Whales. The internet's gone mad this week. Anyway, let me know what you guys think in the comments. Make sure you follow us at MTV UK and at L's Martial One. I'll see you guys next week.


Do you think more enterprises from the traditional sort of cyber security space will jump into this market and what do you think the impact of that will be as sort of mainstay technology companies not just Facebook and facecoin but folks like Symantec, RSA, McAfee sort of jump into this area what do you think the impact of that will be? The traditional model of security is one on protecting concentric circles of access based on firewalls based on access controls based on procedural process and operational controls. That model assumes that there is a privileged center that has access to all of the information and then you have concentric layers which are more and more open which have less and less valuable information. The problem with that model is that the internet destroyed that model the reason it destroyed it is because the center has the most stale uninteresting information possible and all of the collaboration and contents building and the great richness of our information society operates in the public sphere on the outermost circle and worse if you build these types of security mechanisms you end up isolating the people inside those walls and making it difficult for them to access these services. I don't know if you have tried from a corporate environment to access certain websites that you know are wealth of information they have this wonderful resource that you want to download and it pops up a little message that says your administrator has blocked access to this website because it contains objectionable material well that is the story of modern security in a nutshell that little message right there and this idea of turning inwards and building walls and keeping out the hordes keeping out the barbarians of the big open public internet is reflected in our society it's a medieval idea it's a medieval idea of castle walls and the problem is that you have to open the gates every now and then to let traders and food in otherwise you starve and in the information age you starve by irrelevance and lack of access to information so traditional security companies are welcome to come into this new space of open public blockchains and what they can learn is we have a new model and this new model is an open public platform that ensures security not by restricting access but by collaboration through game theory through mechanisms that have game theoretic output or outcomes based on incentives and punishments that operate through an embedded monetary system that ensures that people behave according to both self interest and in alignment with the consensus rules this is an incredibly powerful new security model for open access to information as well we can use it to read decentralize the web we can use it to open information that needs to be open it puts the ultimate control and responsibility over security into the hands of the individual key holders who control their own destiny and moves that data back into their hands it is a non custodial model for security which also means a non custodial model for identity and non custodial model for your personal data we can use this new security model to fix the web which has lost some of its original promise but don't fret because out of the compromise surveillance laden web that we have today out popped the black swan of bitcoin it's still capable of delivering surprises it's still capable of delivering freedom in disruptive viral packages that you cannot stop and it will do it again and again and again and now bitcoin has popped out another two thousand systems that emulate that model and is exploding that space of innovation security has also been massively disrupted by this model


Hi, my name is Thomas from Kenya. I am one of the young innovators for 2013. So we've developed a platform called Nduru App. So basically Nduru App is a mobile application that empowers road users to take charge of their road safety. So using the platform, users are able to monitor how fast a vehicle is moving. So once a vehicle over speeds, you're able to report that to the relevant authorities. And it also provides a basic first aid guide. So in case of any emergencies, users are able to administer first aid to any injured victim. Thank you.


So if there isn't any operations happening, we are just waking up, eating breakfast, walking around, getting some fresh air maybe, and running through gear inspection. You kind of got to go at the gym's time because if you go during the times when you have off but everybody else has off, then the gym is like really packed. So sometimes you have to go at crazy hours so like one or two in the morning, ship saves you tons of money unless you spend it at the ship store on snacks and energy drinks which I don't drink energy drinks so that was definite benefit for me but I saved at minimum $2,000. $2,000 I saved, well you can always watch movies, just talk to anybody and you can get movies from people so you can always do that. If you're more in like a relaxation mode I guess, for me anyway I would take my guitar out to the catwalks when they didn't have flight operations going on and I would just sit out there and play my guitar because you just listen to the water, listen to the ship, it's very relaxing. The training that you'll get to do is, it's not like training you'll do back where you're stationed at like backyard field ops, you get to do field ops in like different countries, I get real like good training in. You can be like radio and you can work on the heli, like be on the helicopter, the recon, you know, be cool stuff or some people just stay on the ship and just they had a karaoke night that was pretty cool. Coin and patch night because there's so many like so many different units you can get so creative like with the patches and coins and some of them are like personal so you can't really trade them like that so like some of them you get from like a general or like you got it from like this op that you went on and you get from like this McMac class that you did that was really hard. You can look back on that and enjoy that, enjoy that memory. If you have opportunity to do it do it, it's like it's an opportunity of a lifetime.


In the end of section 1.5, we are going to introduce a little bit of vocabulary. We're going to talk about the echelon form of a matrix. So in a matrix, if you have a row which every scalar is zero, we call that a zero row. It's kind of obvious, but we should clarify with a formal definition. Therefore, if a row is not a zero row, we call it a non-zero row. And in a matrix, if you have a non-zero row, the leading entry of the row is going to be the leftmost non-zero number in that row. Since the row is non-zero, some number in that row is non-zero, and therefore there is a leftmost non-zero entry. We call that the leading entry of that row. So with that terminology in mind, we're now ready to talk about the echelon form of a matrix. This is specifically what we call the row echelon form of a matrix. You could talk about column echelon forms, but we won't in this series. Therefore, when I say echelon form, that'll be meaning row echelon form. So we say that a matrix is an echelon form if the following three conditions happen. First, there is no zero row that's above a non-zero row. So all the zero rows are in the bottom of the system. That's the thing. So all the zeros are in the bottom. Next, each leading entry in a column is to the right of any leading entry in a row above it. And then the last one is all entries in a column below a leading entry are zero. So in other words, we're trying to construct matrices that have the following sort of prototype. We have something here, something here, something here. We have a zero, something here, something here. We have a zero, we have a zero, we have something here. This would be an example of a matrix in echelon form. So you'll notice that this matrix doesn't have any rows of zeros. So maybe we tweak it a little bit. I mean, it doesn't, if you don't have any rows of zeros, then the first condition satisfied automatically. But let's just add a row of zeros for the sake of it. The row of zeros are at the bottom. If you look at the leading entries of the matrix, there's a leading entry here, here and here. Notice the leading entries make this downward staircase. That is, if you take a leading entry, it's to the right of the entries that are above it. It makes this downward staircase. And everything that's below a leading entry is called a, well, it's just a zero, right? This would be an example of an echelon matrix. Now let me actually explain what this word echelon actually means here. It derives from a French word, which would translate as staircase or ladder. And so a matrix is an echelon form. If we're building this ladder of zeros, we can climb down the matrix along these leading entries. Like here, we take the steps down, right? These leading entries are also sometimes called pivots, a pivot position. And the terminology pivot position makes more sense when we introduce the elimination algorithm. We'll talk about in section 1.6, excuse me. We say that a matrix is in row reduced echelon form. If it's an echelon form, we sometimes call it REF for short. We say that a matrix is in row reduced echelon form. If in addition to being an echelon form, we also have the condition that every leading entry, every pivot position is a one. And every pivot entry is a one. And all entries above a leading entry are zero. So to be an echelon form, everything below a pivot must be zero. To be in row reduced echelon form, everything above and below the pivots have to be zero. And also to be an echelon, to row reduced echelon form, the leading entries have to be one. No stipulation is on that for echelon form. So every matrix which is in row reduced echelon form is in row echelon form, but the converse is not necessarily true. Like I said, when a matrix is an echelon form, those leading entries we call the pivot positions or the pivot itself. If a row that has a pivot in it, we call it pivot row, a column that has a pivot in it, we call it pivot column. Not every row or column has pivots in them necessarily. So we might have a non pivot column or a non pivot row. The number of pivots in a matrix we call the rank of the matrix. And this will be denoted as a rank of A where A is the matrix here. Let me give you some quick examples of such a thing. Our first matrix is a matrix with complex entries here. This would be, its coefficient matrix is three by three. The augmented matrix itself is three by four. This is an example of a matrix in echelon form. Let's actually check to see what's going on here. You'll notice it has a row of zeros that's on the bottom. When you have an augmented matrix and you're asking, is that matrix in echelon form or not? Ignore the augmented column. That's why we put this vertical line here. In terms of determining whether it's echelon form or not, anything past the augmented line there doesn't matter. No one cares about what's on the right of the vinculum. We only care about what's in the coefficient matrix. So it has a row of zeros, it's in the bottom. That's the first condition. Notice that the pivots make a downward staircase, right? This pivot is to the right of the pivot above it. That's fine. The fact that there's a gap here is not a problem whatsoever. That's acceptable for an echelon form. And every element below a pivot is zero. Notice in column two, it doesn't matter because there's no pivots in that column. So there's no condition violated right there. So this is a matrix in echelon form. Is it in row reduced echelon form? Well, let's double check that. To be in row reduced echelon form, the pivots have to be one, which they are. And everything above a pivot has to be zero. Uh-oh, this is at zero. So this matrix is not in row reduced echelon form. It's an echelon form, but it's not row reduced. All right. It's not already enough. On the other hand, take a look at this matrix right here. Notice there's no rows of zeros. So condition one is checked automatically. The pivots make a downward staircase. There are zeros below the pivots. So this is an echelon form. It's now an echelon form. It's in a row reduced echelon form. Each pivot is a one. So that's great. And every number above a pivot is also one. Again, the augmented column doesn't matter in this consideration here. So this matrix is in row reduced echelon form. Every RREF is an echelon matrix, but not every echelon matrix is RREF. And so that distinction, hopefully we can see here. So this gives examples of matrices which are in echelon form. Most matrices are not an echelon form. But I do want to point out to you that as we've been solving systems of equations, this matrix right here is an echelon form. Here are your pivots right here. This matrix is an echelon form. You have a downward staircase of pivots. There's a row of zeros at the bottom. Everything below a pivot is zero. It's not in row reduced echelon form because there's a nonzero entry above the pivot, although the pivots are one, which is great, but not required. So this matrix was in echelon form. And one of the keys about solving this system of equations, basically if we summarize things as we want to convert using row operations, we want to convert an augmented matrix into echelon form, and then we can solve that matrix using back substitution. That in a nutshell is what one means by Gaussian elimination, which we'll introduce formally in the next section, 1.6.