Podcast appearances and mentions of Steve Horvath

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Play Episode Listen Later Nov 2, 2024 43:03

Above is a brief video snippet from our conversation. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to audio and external citationsEric Topol (00:06):Well, hello it's Eric Topol with Ground Truths, and I'm really delighted to welcome Dr. Rachael Bedard, who is a physician geriatrician in New York City, and is actually much more multidimensional, if you will. She's a writer. We're going to go over some of her recent writings. She's actually quite prolific. She writes in the New Yorker, New York Magazine, New York Times, New York Review of Books. If it has New York in front of it, she's probably writing there. She's a teacher. She works on human rights, civil rights, criminal justice in the prison system. She's just done so much that makes her truly unique. That's why I really wanted a chance to meet her and talk with her today. So welcome, Rachael.Rachael Bedard (00:52):Thank you, Dr. Topol. It's an honor to be here.Eric Topol (00:55):Well, please call me Eric and it's such a joy to have a chance to get acquainted with you as a person who is into so many different things and doing all of them so well. So maybe we'd start off with, because you're the first geriatrician we've had on this podcast.Practicing Geriatrics and Internal MedicineEric Topol (01:16):And it's especially apropos now. I wanted maybe to talk about your practice, how you got into geriatrics, and then we'll talk about the piece you had earlier this summer on aging.Rachael Bedard (01:32):Sure. I went into medicine to do social justice work and I was always on a funny interdisciplinary track. I got into the Mount Sinai School of Medicine through what was then called the Humanities and Medicine program, which was an early acceptance program for people who were humanities focused undergrads, but wanted to go into medicine. So I always was doing a mix of politics and activist focused work, humanities and writing, that was always interested in being a doctor. And then I did my residency at the Cambridge Health Alliance, which is a social medicine program in Cambridge, Massachusetts, and my chief residency there.(02:23):I loved being an internist, but I especially loved taking care of complex illness and I especially loved taking care of complex illness in situations where the decision making, there was no sort of algorithmic decision-making, where you were doing incredibly sort of complex patient-centered shared decision making around how to come up with treatment plans, what the goals of care were. I liked taking care of patients where the whole family system was sort of part of the care team and part of the patient constellation. I loved running family meetings. I was incredibly lucky when I was senior resident and chief resident. I was very close with Andy Billings, who was one of the founders of palliative care and in the field, but also very much started a program at MGH and he had come to work at Cambridge Hospital in his sort of semi-retirement and we got close and he was a very influential figure for me. So all of those things conspired to make me want to go back to New York to go to the Sinai has an integrated geriatrics and palliative care fellowship where you do both fellowships simultaneously. So I came to do that and just really loved that work and loved that medicine so much. There was a second part to your question.Eric Topol (03:52):Is that where you practice geriatrics now?Rachael Bedard (03:55):No, now I have ever since finishing fellowship had very unusual practice settings for a geriatrician. So right out of fellowship, I went to work on Rikers Island and then New York City jail system, and I was the first jail based geriatrician in the country, which is a sort of uncomfortable distinction because people don't really like to think about there being a substantial geriatric population in jails. But there is, and I was incredibly lucky when I was finishing fellowship, there was a lot of energy around jail healthcare in New York City and I wrote the guy who was then the CMO and said, do you think you have an aging problem? And he said, I'm not sure, but if you want to come find out, we'll make you a job to come find out. And so, that was an incredible opportunity for someone right out of fellowship.(04:55):It meant stepping off the sort of academic track. But I went and worked in jail for six years and took care of older folks and people with serious illness in jail and then left Rikers in 2022. And now I work in a safety net clinic in Brooklyn that takes care of homeless people or people who have serious sort of housing instability. And that is attached to Woodhull Hospital, which is one of the public hospitals in New York City. And there I do a mix of regular internal medicine primary care, but I preferentially see the older folks who come through, which is a really interesting, painful, complicated patient population because I see a fair amount of cognitive impairment in folks who are living in the shelter system. And that's a really hard problem to address.Frailty, The Aged, and LongevityEric Topol (05:54):Well, there's a theme across your medical efforts. It seems to me that you look after the neglected folks, the prisoners, the old folks, the homeless people. I mean that's kind of you. It's pretty impressive. And there's not enough of people like you in the medical field. Now, no less do you do that, but of course you are a very impressive author, writer, and of many topics I want to get into with you, these are some recent essays you've written. The one that piqued my interest to start to understand who you were and kind of discover this body of work was the one that you wrote related to aging and President Biden. And that was in New York Times. And I do want to put in a quote because as you know very well, there's so much interest in longevity now.Eric Topol (06:51):Interrupting the aging process, and this one really stuck with me from that op-ed, “Time marches forward, bodies decline, and the growing expectation that we might all live in perfect health until our 100th birthdays reflects a culture that overprizes longevity to the point of delusion.” So maybe if you could tell us, that was a rich piece, you got into frailty, you related it to the issues that were surrounding President Biden who at that time had not withdrawn from the race. But what were you thinking and what are your thoughts about the ability to change the aging process?Rachael Bedard (07:36):I am very interested in, I mean, I'm incredibly interested in the science of it. And so, I guess I think that there are a few things.(07:49):One thing is that the framework that, the part that gives me pause the most is this framework that anything less than perfect health is not a life worth living. So if you're going to have a long life, life should not just be long and sort of healthy in relative terms to your age cohort, but healthy that when you're 80 you should feel like you have the health of a 45-year-old is my understanding of the culture of longevity science. And while I understand why that's aspirational and everybody worry about my body's decline, I think it's a really problematic thing to say that sick bodies are bodies that have disability or people who have cognitive difference are somehow leading lesser lives or lives that are not meaningful or not worth living. I think it's a very, very slippery slope. It puts you in a place where it sort of comes up against another trend or another emerging cultural trend, which is really thinking a lot about physician-assisted suicide and end of life choices.(09:04):And that in some ways that conversation can also be very focused on this idea that there's just no way that it's worth living if you're sick. And that's just not true, I think, and that's not been true for many, many, many of my patients, some of whom have lived with enormous disability and incredible burden of illness, people who are chronically seriously ill and are still leading lives that for them and for the people who love them are filled with meaning. So that's my concern about the longevity stuff. I'm interested in the science around the longevity stuff for sure. I'm interested in, I think we're living in this really interesting moment where there's so much happening across so many of the chronic disease fields where the things that I think have been leading to body decay over the last several decades for the majority of the population, we're sort of seeing a lot of breakthroughs in multiple fronts all at once. And that's really exciting. I mean, that's really exciting. And so, certainly if it's possible to make it to 100 in wonderful health, that's what I'd wish for all of us. But to hold it up as the standard that we have to achieve, I think is both unrealistic and a little myopic.Eric Topol (10:28):Yeah. Well, I certainly agreed with that and I think that that particular essay resonated so well and you really got into frailty and the idea about how it can be potentially prevented or markedly delayed. And I think before we move on to one of those breakthroughs that you were alluding to, any comments about the inevitability of frailty in people who are older, who at some point start to get the dwindles, if you will, what do you have to say about that?Rachael Bedard (11:11):Well, from a clinical standpoint, I guess the caveat versus that not everybody becomes frail and dwindles exactly. Some people are in really strong health up until sort of their final years of life or year of life and then something happens, they dwindle quickly and that's how they die. Or some people die of acute events, but the vast majority of us are going to become more frail in our final decades than we are in our middle decades. And that is the normal sort of pattern of wear and tear on the body. And it is an extraordinary framework, I think frailty because the idea of this sort of syndrome of things where it's really not a disease framework, it is a syndrome framework and it's a framework that says many, many small injuries or stressors add up to create a lot of stress and change in a body and trauma for our body. And once you are sort of past a tipping point of an amount of stress, it's very hard to undo those things because you are not sort of addressing one pathologic process. You're addressing, you're trying to mitigate many processes all at once.(12:31):When I wrote that piece, it was inspired by the conversation surrounding President Biden's health. And I was particularly struck by, there was a huge amount of clinical speculation about what was going on with him, right? I'm sure you remember there were people, there was all of this talk about whether he had Parkinson's and what his cognitive status was. And it felt to me like there was an opportunity to do some public education around the idea that you need not have one single sort of smoking gun illness to explain decline. What happens to most of us is that we're going to decline in many small ways sort of simultaneously, and it's going to impact function when it tips over a little bit. And that pattern of decline is not going to be steady day over day worsening. It's going to be up and down. And if you slept better the night before, you might have a better day the next day. And if you slept badly, you might have a worse day. And without knowing anything specific about his clinical situation, it felt like a framework that could explain so much of what we were seeing in public. And it was important also, I think to say that nothing was necessarily being hidden from anybody and that this is the kind of thing that, this has accumulated stress over time that then presents suddenly all at once after having been submerged.Eric Topol (14:01):Yeah, you reviewed that so well about the wear and tear and everything related to that. And before I move on to the second topic, I want to just circle back to something you alluded to, which is when Peter Attia wrote about this medicine 3.0 and how you would be compressed and you'd have no comorbidities, you'd have no other illnesses and just fall off the cliff. As a geriatrician, do you think that that is even conceivable?Rachael Bedard (14:35):No. Do you think it is?Eric Topol (14:37):No, but I just wanted to check the reality. I did challenge on an earlier podcast and he came up with his pat answer. But no, there's no evidence of that, that maybe you can delay if there ever was a way to do that. But I think there's this kind of natural phenomena that you just described, and I'll refer people also to that excellent piece that you get into it more.Rachael Bedard (15:06):Peter Attia, I mean, he is certainly the sort of standard bearer in my mind of that movement and that science or that framework of thinking about science. And there's stuff in there that's really valuable. The idea of thinking about lifestyle in your middle decades is having meaningful impact on how you will age, what your final years will look like. That seems intuitively true, I think. And so, thinking about his emphasis on exercise, I mean, his emphasis on exercise is particularly intense and not super achievable for the average person, but the idea that you should sort of be thinking about keeping your body strong because it will decline eventually. And so, you want to do that from a higher peak. That makes a lot of sense to me. The idea that where we sort of draw pathologic disease cutoffs is obviously a little bit arbitrary. And so, wanting to think about optimizing pre-disease states and doing prevention, that's obviously, I think pretty appealing and interesting. It's just really in an evidence free zone.Ozempic for the IndigentEric Topol (16:18):Yeah, that's what I confronted him with, of course, he had a different perspective, but you summed that up really well. Now let's switch to a piece you had in New York magazine. It was entitled, What If Ozempic Is Just a Good Thing? And the reason, of course, this ties into the first thing we're discussing. There's even talk now, the whole GLP-1 family of drugs with the dual triple receptors, pills to come that we're going to be able to interrupt a path towards Alzheimer's and Parkinson's. Obviously you've already seen impact in heart disease, liver disease, kidney disease way before that, diabetes and obesity. So what are your thoughts? Because you wrote a very interesting, you provided a very interesting perspective when you wrote that one.Rachael Bedard (17:11):So that piece I wrote because I have this unbelievably privileged, interesting clinical practice. In New York City, there is public health insurance basically available to anybody here, including folks who are undocumented. And the public hospital system has pharmacies that are outpatient pharmacies that have, and New York Medicaid is very generous and they arranged through some kind of brilliant negotiating. I don't quite know how to make Ozempic to make semaglutide available to people who met criteria which meant diabetes plus obesity, but that we could prescribe it even for our very, very poor patients and that they would be able to get it reliably, that we would have it in stock. And I don't know how many other practices in the country are able to reliably provide GLP-1s to marginalized folks like that. I think it feels like a really rare opportunity and a very distinct perspective.(18:23):And it has just been the most amazing thing, I think to have this class of drugs come along that, as you say, addresses so many problems all at once with at least in my prescribing experience, a relatively mild tolerable side effect profile. I have not had patients who have become incredibly sick with it. And for folks where making that kind of impact on their chronic illness is so critical to not just their longevity, but their disease status interacts so much with their social burden. And so, it's a very meaningful intervention I think around poverty actually.(19:17):I really feel that almost all of the popular press about it has focused very much on use amongst the wealthy and who's getting it off label and how are they getting it and which celebrities are taking it, and what are the implications for eating and diet culture and for people who have eating disorders. And that's a set of questions that's obviously sort of interesting, but it's really interesting in a very rarefied space. There's an unbelievable diabetes epidemic in this country, and the majority of people who have diabetes are not the people who are getting written about over and over again in those pieces. It's the patients that I take care of, and those people are at risk of ending up on dialysis or getting amputations. And so, having a tool this effective is really miraculous feeling to me.Eric Topol (20:10):Well, it really gives me some hope because I don't know any program like that one, which is the people who need it the most. It's getting provided for them. And we have been talking about a drug that costs a thousand dollars a month. It may get down to $500 a month, but that's still a huge cost. And of course, there's not much governmental coverage at this point. There might be some more for Medicare, Medicaid, whatever in the future, but it's really the original criteria of diabetes, and it took almost 20 years to get to where we are right now. So what's so refreshing here is to know that there's at least one program that is helping to bridge the inequities and to not make it as was projected, which was, as you say, for celebrities and wealthy people more exclusively, so that's great. And we still don't know about the diverse breadth of these effects, but as you well know, there's trials in Alzheimer's. I spoke to Steve Horvath recently on the podcast and he talked about how it's reset the epigenetic clock, GLP-1.Rachael Bedard (21:24):Does he think so?Eric Topol (21:26):Whoa. Yeah, there was evidence that was just presented about that. I said, well, if that does correspond to aging, the thing that we spoke about first, that would be very exciting.Rachael Bedard (21:37):It's so wild. I mean, it's so exciting. It's so exciting to me on so many levels. And one of them is it's just exploding my mental model of disease pathogenesis, and it's making me think, oh my goodness, I have zero idea actually how metabolism and the brain and sort of cardiovascular disease, all of those things are obviously, what is happening in the interplay between all of those different systems. It's really so much more complicated and so much more interdependent than I understood it to be. I am really optimistic about the Alzheimer's trial. I am excited for those results, and I think we're going to keep seeing that it prevents different types of tumors.Eric Topol (22:33):Yeah, no, and that's been shown at least certainly in obese people, that there's cancers that gets way reduced, but we never had a potent anti-inflammatory that works at the brain and systemically like this before anyone loses the weight, you already see evidence.Long Covid and ME/CFS(22:50):It is pretty striking. Now, this goes back to the theme that was introduced earlier about looking after people who are neglected, who aren't respected or generally cared for. And I wanted to now get into Long Covid and the piece you wrote in the New Yorker about listening to patients, called “what would it mean for scientists to listen to patients?” And maybe you can talk about myalgic encephalitis/chronic fatigue (ME/CFS), and of course Long Covid because that's the one that is so pervasive right now as to the fact that these people don't get respect from physicians. They don't want to listen to their ailments. There's no blood tests, so there's no way to objectively make a diagnosis supposedly. And they're basically often dismissed, or their suffering is discounted. Maybe you can tell us again what you wrote about earlier this year and any updated thoughts.Rachael Bedard (24:01):Have you had my friend Harlan Krumholz on the show to talk about the LISTEN study?Eric Topol (24:04):Not yet. I know Harlan very well. Yes.Eric Topol (24:11):I know Akiko Iwasaki very well too. They're very, very close.Rachael Bedard (24:14):So, Akiko Iwasaki and Harlan Krumholz at Yale have been running this research effort called the LISTEN study. And I first learned about it sometime in maybe late 2021. And I had been really interested in the emerging discourse around chronic illness in Long Covid in the 2021. So when we were past the most acute phase of the pandemic, and we were seeing this long tail of sequelae in patients, and the conversation had really shifted to one that was about sort of trying to define this new syndrome, trying to understand it, trying to figure out how you could diagnose it, what were we seeing sort of emerge, how are we going to draw boxes around it? And I was so interested in the way that this syndrome was really patient created. It came out of patients identifying their own symptoms and then banning together much, much faster than any kind of institutional science can ever work, getting into message boards together or whatever, and doing their own survey work and then coming up with their own descriptive techniques about what they were experiencing.(25:44):And then beyond that, looking into the literature and thinking about the treatments that they wanted to try for themselves. Patients were sort of at the forefront of every step of recognizing, defining, describing this illness presentation and then thinking about what they wanted to be able to do for themselves to address it. And that was really interesting to me. That was incredibly interesting to me. And it was also really interesting because by, I don't know exactly when 2021 or 2022, it was already a really tense landscape where it felt like there were real factions of folks who were in conflict about what was real and what wasn't real, how things ought to be studied, who ought to be studying them, what would count as evidence in this realm. And all of those questions were just really interesting to me. And the LISTEN study was approaching them in this really thoughtful way, which was Harlan and Akiko sort of partnering really closely with patients who enrolled.(26:57):And it's a decentralized study and people could enroll from all over the world. There's a portion of patients who do have their blood work evaluated, but you can also just complete surveys and have that data count towards, and those folks would be from anywhere in the world. Harlan did this amazing, amazing work to figure out how to collect blood samples from all over the country that would be drawn at home for people. So they were doing this decentralized study where people from their homes, from within the sort of circumstances of their lives around their chronic illness could participate, which that was really amazing to me. And then they were partnering really thoughtfully with these patients just to figure out what questions they wanted to ask, how they wanted to ask them, and to try to capture a lot of multimodal data all at once.(27:47):Survey data, journaling so people could write about their own experience in a freeform journal. They were collecting blood samples, and they were holding these town halls. And the town halls were on a regular basis, Harlan and Akiko, and anybody who was in the study could come on, could log onto a Zoom or whatever, and Harlan and Akiko and their research staff would talk about how things were going, what they were working on, what questions they had, what the roadblocks were, and then they would answer questions from their participants as the study was ongoing. And I didn't think that I had ever heard of something quite like that before. Have you ever heard of anything?Eric Topol (28:32):No. I mean, I think this is important to underscore, this was the first condition that was ever patient led, patient named, and basically the whole path was laid by the patient. So yes, and everything you summarize is so well as to the progress that's been made. Certainly, Harlan and Akiko are some of the people that have really helped lead the way to do this properly as opposed to, unfortunately one and a half billion dollars that have been put to the NIH for the RECOVER efforts that haven't yet led to even a significant clinical trial, no less a validated treatment. But I did think it was great that you spotlighted that just because again, it's thematic. And that gets me to the fourth dimension, which is you're the first prison doctor I've ever spoken to. And you also wrote a piece about that called, “the disillusionment of a Rikers Island Doctor” in the New Yorker, I think it was. And I wonder if you could tell us, firstly, now we're four years into Covid, you were for a good part of that at Rikers Island, I guess.The Rikers Island Prison Doctor During CovidRachael Bedard (30:00):I was, yeah.Eric Topol (30:00):Yeah. And what could be a more worrisome spot to be looking after people with Covid in a prison? So maybe you could just give us some insight about all that.Rachael Bedard (30:17):Yeah, it was really, I mean, it was the wildest time, certainly in my career probably that I'll ever have. In the end of February and beginning of March of 2020, it became very apparent to my colleagues and I that it was inevitable that this virus that was in Wuhan and in Italy was coming to the US. And jails are, we sort of jokingly described them as the worst cruise ships in the world. They are closed systems where everybody is eating, sleeping, going to the bathroom, everything on top of each other. There's an incredible amount of excess human contact in jails and prisons because people don't have freedom of movement and they don't get to do things for themselves. So every single, somebody brings you your mail, somebody brings you your meals, somebody brings you your medications. If you're going to move from point A to point B, an officer has to walk you there. So for a virus that was going to spread through what we initially thought was droplets and then found out was not just droplets but airborne, it was an unbelievably high-risk setting. It's also a setting where folks tend to be sicker than average for their age, that people bring in a lot of comorbidity to the setting.(31:55):And it's not a setting that does well under stress. I mean, jails and prisons are places that are sort of constitutionally violent, and they're not systems that adapt easily to emergency conditions. And the way that they do adapt tends to be through repressive measures, which tends to be violence producing rather than violence quelling. And so, it was just an incredibly scary situation. And in mid-March, Rikers Island, the island itself had the highest Covid prevalence of anywhere in the country because New York City was the epicenter, and Rikers was really the epicenter within New York. It was a wild, wild time. Our first seriously ill patient who ended up getting hospitalized. That was at that time when people were, we really didn't understand very much about what Covid looked like. And there was this guy sitting on the floor and he said, I don't know. I can't really get up.(32:59):I don't feel well. And he had an O2 stat of 75 or something. He was just incredibly hypoxic. It's a very scary setting for that kind of thing, right? It's not a hospital, it's not a place where you can't deliver ICU level care in a place like that. So we were also really worried about the fact that we were going to be transferring all of these patients to the city hospitals, which creates a huge amount of extra burden on them because an incarcerated patient is not just the incarcerated patients, the officers who are with that person, and there are special rules around them. They have to be in special rooms and all of these things. So it was just a huge systems crisis and really painful. And we, early on, our system made a bunch of good guesses, and one of our good guesses was that we should just, or one of our good calls that I entirely credit my bosses with is that they understood that we should advocate really hard to get as many people out as we could get out. Because trying to just manage the population internally by moving people around was not going to be effective enough, that we really need to decant the setting.(34:18):And I had done all of this work, this compassionate release work, which is work to get people who are sick out of jail so that they can get treatment and potentially die in a free setting. And so, I was sort of involved in trying to architect getting folks who were sort of low enough security risks out of jail for this period of time because we thought that they would be safer, and 1500 people left Rikers in the matter of about six weeks.Rachael Bedard (34:50):Which was a wild, wild thing. And it was just a very crazy time.Eric Topol (34:56):Yeah. Well, the word compassion and you go together exceptionally well. I think if we learn about you through your writings, that really shines through and what you've devoted your care for people in these different domains. This is just a sampling of your writings, but I think it gives a good cross section. What makes you write about a particular thing? I mean, obviously the Rikers Island, you had personal experience, but why would you pick Ozempic or why would you pick other things? What stimulates you to go after a topic?Rachael Bedard (35:42):Sometimes a lot of what I write about relates to my personal practice experience in some way, either to geriatrics or death and dying or to the criminal justice system. I've written about people in death row. I've written about geriatrics and palliative care in sort of a bunch of different ways. I am interested in topics in medicine where things are not yet settled, and it feels very of the moment. I'm interested in what the discourse is around medicine and healthcare. And I am interested in places where I think the discourse, not just that I'm taking a side in that discourse, but where I think the framework of the discourse is a little bit wrong. And I certainly feel that way about the Ozempic discourse. And I felt that way about the discourse around President Biden, that we're having not just a conversation that I have a strong opinion about, but a conversation that I think is a little bit askew from the way that we ought to be thinking about it.Eric Topol (36:53):And what I love about each of these is that you bring all that in. You have many different points of view and objective support and they're balanced. They're not just trying to be persuasive about one thing. So, as far as I know, you're extraordinarily unique. I mean, we are all unique, but you are huge standard deviations, Rachael. You cover bases that are, as I mentioned, that are new to me in terms of certainly this podcast just going on for now a couple of years, that is covering a field of both geriatrics and having been on the corrections board and in prison, particularly at the most scary time ever to be working in prison as a physician. And I guess the other thing about you is this drive, this humanitarian theme. I take it you came from Canada.Rachael Bedard (37:59):I did.Eric Topol (37:59):You migrated to a country that has no universal health.Rachael Bedard (38:03):That's right.Eric Topol (38:03):Do you ever think about the fact that this is a pretty pathetic situation here?Rachael Bedard (38:08):I do. I do think about it all the time.Eric Topol (38:10):In our lifetime, we'll probably never see universal healthcare. And then if you just go a few miles up north, you pretty much have that.Rachael Bedard (38:18):Yeah, if you've lived in a place that has universal healthcare and you come here, it's really sort of hard to ever get your mind around. And it has been an absolute possessing obsession of my entire experience in the US. I've now been here for over 20 years and still think it is an unbelievably, especially I think if you work with marginalized patients and how much their lack of access compounds the difficulty of their lives and their inability to sort of stabilize and feel well and take care of themselves, it's really frustrating.Advice for Bringing Humanities to Medicine in a CareerEric Topol (39:14):Yeah, yeah. Well, I guess my last question to you, is you have weaved together a career that brings humanities to medicine, that doesn't happen that often. What's your advice to some of the younger folks in healthcare as to how to pull that off? Because you were able to do it and it's not easy.Rachael Bedard (39:39):My main advice when people ask me about this, especially to students and to residents who are often the people who are asking is to write when you can or pursue your humanities interests, your critical interests, whatever it is that you're doing. Do it when you can, but trust that your career is long and that you have a lot of time. Because the thing that I would say is I didn't start publishing until I was in fellowship and before that I was busy because I was learning to become a doctor. And I think it's really important that my concern about being a doctor who's a hybrid, which so many of us are now. A doctor or something else is you really do want to be a good doctor. And becoming a good doctor is really hard. And it's okay if the thing that is preoccupying you for the first 10 years of your training is becoming a great clinician. I think that's a really, really important thing to do. And so, for my first 10 years for med school and residency and chief residency and fellowship, I would write privately on the side a fair amount, but not try to publish it, not polish that work, not be thinking in sort of a careerist way about how I was going to become a doctor writer because I was becoming a doctor. And that was really preoccupying.(41:08):And then later on, I both sort of had more time and mental space to work on writing. But also, I had the maturity, I think, of being a person who was comfortable in my clinical identity to have real ideas and insights about medicine that felt different and unique to me as opposed to, I barely understand what's going on around me and I'm trying to pull it together. And that's how I would've been if I had done it more, I think when I was younger. Some people are real prodigies and can do it right out the gate, but I wasn't like that.Eric Topol (41:42):No, no, I think that's really sound advice because that's kind of the whole foundation for everything else. Is there a book in the works or will there be one someday?Rachael Bedard (41:53):There may be one someday. There is not one now. I think about it all the time. And that same advice applies, which is I believe in being a late bloomer and taking your time and figuring out what it is you really want to do.Eric Topol (42:10):Yeah. Well, that's great. Have I missed anything? And obviously we only can get to know you in what, 40 minutes to some extent, but have I not touched on something that you want to bring up?Rachael Bedard (42:23):No, I don't think so. Thank you for this conversation. It's been lovely.Eric Topol (42:28):No, I really enjoyed it. I'll be following your career. It's extraordinary already and you've got decades ahead to make an impact and obviously thinking of all these patients that you look after and have in the past, it's just extraordinary. So what a joy to talk with you, Rachael, and I hope we'll have a chance to do that again in the times ahead.Rachael Bedard (42:51):Me as well. Thank you so much for inviting me.**********************************************Thank you for listening, reading or watching!The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informative!Voluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly help fund our education and summer internship programs.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

What is biological vs chronological age?

Health Longevity Secrets

Play Episode Listen Later Oct 29, 2024 31:52 Transcription Available

How young are we really, on a cellular level? This week we are joined by Chris Mirabile, a brain tumor survivor and the visionary CEO of Novos, shares his journey of significantly reducing his biological age. In full disclosure, I am a scientific advisor to NOVOS but I only affiliate with those companies that I believe in. Chris discusses the difference between chronological and biological age and learn how advanced epigenetic tests can offer insights into your health and longevity. We go through the evolution of epigenetic clocks, from Steve Horvath's groundbreaking research to the sophisticated tools we have today. These third-generation clocks provide the most accurate assessments, incorporating factors like gait speed and quality of life metrics, and Chris also reveals an exciting initiative from Novos offering a free biological age test based on survey data.We explore the progression of biological aging research, discussing how these assessments can measure the pace of aging and predict morbidity and mortality risks. Chris elaborates on second-generation clocks like PhenoAge and GrimAge and introduces the Dunedin Pace Clock, which highlights the impact of lifestyle on aging. Look forward to potential fourth-generation clocks that aim to integrate multiple biological markers for even more comprehensive health predictions. Our conversation emphasizes the power of lifestyle changes and personalized interventions in slowing the aging process, underscoring that aging is influenced more by lifestyle and environment than by genetics.Empower yourself with the knowledge that aging is an elastic process. Chris shares practical advice for adopting healthier habits and mindsets to improve your life quality and longevity. He emphasizes the importance of a positive mindset and affordable lifestyle changes over expensive treatments. Don't miss out on these insights to maximize your potential for anti-aging and lead a healthier, longer life.These sponsors support this podcast: Siphox Health, at-home health testing for all (15% off with this link):https://pathlongevity.com/Prolon, maker of the Fasting Mimicking Diet (20% off with this link):https://prolonlife.com/Lufkin Download a free sample chapter of Lies I Taught In Medical School here:https://www.robertlufkinmd.com/lies/ *** CONNECT WITH DR ROB ON SOCIAL MEDIA ***Web: https://robertlufkinmd.com/X: https://x.com/robertlufkinmdYoutube: https://www.youtube.com/robertLufkinmdInstagram: https://www.instagram.com/robertlufkinmd/LinkedIn: https://www.linkedin.com/in/robertlufkinmd/Facebook: https://www.facebook.com/robertlufkinmd Threads: https://www.threads.net/@robertlufkinmd...

Longevity Secrets

Health Longevity Secrets

Play Episode Listen Later Oct 15, 2024 44:20 Transcription Available

This week we uncover the secret to a longer, healthier life as we sit down with Dr Buck Joffrey, a former neurosurgery and otolaryngology resident turned cosmetic surgeon and serial entrepreneur. Buck's journey from the operating room to the forefront of longevity science was ignited by a personal health scare and fueled by the pioneering work of David Sinclair. Join us as Buck shares his transformative story, emphasizing the profound impact of lifestyle changes like diet, exercise, and sleep on extending our lifespans, and even hints at the tantalizing possibility of age reversal.Explore the groundbreaking science of epigenetics and its crucial role in the aging process. We dissect how chemical modifications such as DNA methylation can alter gene expression and affect our biological clocks. With insights from researchers like Steve Horvath, we delve into how epigenetic clocks can predict biological age and mortality risk. Discover the potential of reversing epigenetic age through lifestyle choices, proper nutrition, and medications like rapamycin. Buck also underscores the vital need to manage inflammation and metabolic syndrome to mitigate age-related diseases.This episode also delves into holistic health optimization, covering the interplay between nutrition, exercise, and sleep. We discuss the alarming decline in testosterone levels in men and its implications for metabolic health and longevity. The conversation navigates the delicate balance between optimizing for longevity versus performance, shedding light on the Goldilocks effect of exercise. To top it off, we emphasize the importance of educating the public on these critical insights, ensuring that more people have access to life-extending knowledge.https://www.sapiopodcast.com/These sponsors support this podcast: Siphox Health, at-home health testing for all (15% off with this link):https://pathlongevity.com/Prolon, maker of the Fasting Mimicking Diet (20% off with this link):https://prolonlife.com/Lufkin Download a free sample chapter of Lies I Taught In Medical School here:https://www.robertlufkinmd.com/lies/ *** CONNECT WITH DR ROB ON SOCIAL MEDIA ***Web: https://robertlufkinmd.com/X: https://x.com/robertlufkinmdYoutube: https://www.youtube.com/robertLufkinmdInstagram: https://www.instagram.com/robertlufkinmd/LinkedIn: https://www.linkedin.com/in/robertlufkinmd/Facebook: https://www.facebook.com/robertlufkinmd Threads: https://www.threads.net/@robertlufkinmd...

discover dna explore threads buck goldilocks david sinclair prolon fasting mimicking diet longevity secrets buck joffrey steve horvath

Steve Horvath: Our Epigenetic Age Clocks

Play Episode Listen Later Aug 23, 2024 41:25

Steve Horvath made the seminal discovery of the—Horvath Clock— an epigenetic clock based on DNA methylation, which is now being used extensively in medical research and offered commercially for individuals (←we talk about that!). He was on the faculty at UCLA from 2000-2022 as a Professor of Human Genetics and Biostatistics, and now works on anti-aging research at Altos Labs.A perspective on the importance of epigenetic clocks this week's Nature”This insight is crucial for deriving reliable biological markers of ageing in tissues or blood. Such a feat has been accomplished through the ingenious identification of epigenetic clocks in our genome. But these insights are even more important for revealing targets that enable intervention in the ageing process.”A video snippet on vegetable intake and epigenetic clocks. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to Audio and External LinksEric Topol (00:06):Hello, it's Eric Topol with Ground Truths, and I've got a terrific guest with me today, Steve Horvath. He's a geneticist, a statistician, a mathematician. He's got a lot of background that has led to what is a landmark finding in biomedicine, the Horvath clock. So Steve, welcome.Steve Horvath (00:30):Thank you for having me.Eric Topol (00:33):Well, it's really fascinating. I followed your work for well over a decade since you introduced the pan-tissue clock in 2013, and it's fascinating to go back a bit on that finding, which initially, I guess was in saliva a couple of years prior, and then you found it everywhere you looked, wherever cells had a nucleus and tissues. And what gave you the sense that these markers of methylation on the DNA would give us some clues about the aging process? How did you even come about to make this discovery?SerendipitySteve Horvath (01:17):It was an accidental discovery because before the methylation clock, I had worked very hard on a gene expression clock, a transcriptomic biomarker. I mean, I was at the height of my energy levels. I worked really on weekends, really eight hour days during the week. But all the weekends I had collected a large set of gene expression data and I dredged the data. And for two years and I couldn't get anywhere, there was nothing I could do. But nowadays, of course, you see various publications where people built transcriptomic clocks. But back in the day when we had these arrays, I just couldn't see a signal. And then at some point I got roped into a study of homosexuality where my collaborator at UCLA wanted to see whether there's an epigenetic correlate of sexual orientation in saliva. And so yeah, being a biostatistician, I said, sure, I analyzed the data and I couldn't find any signal for homosexuality.(02:48):But then I just looked for an aging signal in the same, and really within an hour of analyzing the data, I knew that I have to completely drop gene expression. I need to go after methylation. And the signal is so profound, and as you said initially we looked at saliva samples and we thought, isn't it curious? You spit in a cup and you can measure someone's age. And we were of course, hoping that this could become a valuable readout of biologic age, but it took, of course, many years to realize that potential. Nowadays, there's several companies that offer a saliva based methylation clock test. But yeah, many years passed, and it was important to fill in the details and to build the case that methylation clocks are predictive of things we care about time to death or time to various forms of morbidity. So it took many, many years to analyze large cohort studies and to accumulate the evidence that it actually works.Eric Topol (04:16):Yeah, I mean, it was pretty amazing back almost a decade ago when I would see, we would take tissue or blood sample and look at your clock and it would say, age of the person is 75 years. And then we look at the actual age of the person who is 75 years to say, wait a minute, how can this be? So I mean, the plausibility of this discovery, if you look back, I mean you say, well, this is just kind of the rust of the pipes, or how do you process that the methylation is such a marker potentially of a person's biologic age? Of course, we're going to get into how it could be a way to intervene to change the aging process. But would it be fair to say that its epigenetic clocks are not the same as biologic aging or how do you put all that together?Epigenetic Age vs Biologic AgeSteve Horvath (05:21):Yes, for sure. An epigenetic age estimate is certainly not the same as a biologic age estimate. And the reason why I say it is because biologic age is really determined by so many things and by so many organs. And as I mentioned initially, we had a clock for saliva later for blood and so on. And so, if you only have an epigenetic readout of a certain cell type, it's really too limited to assess the whole organismal state. And arguably you would want to measure also proteomics, readouts and many other data modalities. So I typically avoid the terminology biologic age, because to begin with, we don't have a definition of it. Decades of discussions, nobody really has a precise definition of it.Second Generation Epigenetic ClocksEric Topol (06:35):Well, from the first generation Horvath clock then became this newer second generation, GrimAge, PhenoAge, the DunedinPACE of aging. How has that helped to advance the field? Because as you touched on, they're measuring different things and what is it meant by kind of a second generation clock?Steve Horvath (07:03):Yeah, so a second generation clock truly aims to predict mortality or morbidity risk. As opposed to simply chronologic age or what is known as calendar age. And fortunately, there's no doubt that the second generation clocks can do that. I often finish a talk on GrimAge by telling the audience that I give them a money back guarantee, that it will be predictive of mortality in their cohort study. I'm 100% certain that it works if you analyze a hundred people or so. The question is more whether an individual could benefit from such a test. And there are now many providers of various epigenetic clock tests. These biomarkers have different names, but they're quite pricey. A couple of hundred dollars are needed to get such a measurement. And the question is, is it helpful for the individual should you get such a test? And I would say we are not quite there yet for a variety of reasons. The main reason being we don't have good interventions against accelerated epigenetic age. So because when you think about it, why does a doctor order a test for you? For example, cholesterol levels. Well, because they have a drug against elevated cholesterol levels, the statin. And at the moment, we don't have validated interventions against accelerated epigenetic age. So that's kind of missing.Eric Topol (09:13):Yeah, we're going to get to that because obviously a lot of things are in the pipeline there, but are you saying then that these people that are getting these consumer tests, that they're getting a test that really wasn't validated at an individual level, so it predicts their mortality that it may be good at a cohort or population level, but maybe it's not so helpful, accurate, or would you say it is accurate? I mean, GrimAge is a good name because since it says when you're going to die. How do you make the differentiation between the individual level or beyond?Steve Horvath (09:59):Yeah, I think it's good to compare to other biomarkers. So take glucose levels, hemoglobin A1C, nobody doubts that these levels predict mortality risk when you study couples a hundred people. But how accurate is such a test for an individual? Clearly there is substantial noise associated with a prediction. Two people could have exactly the same hemoglobin A1C levels, but live very different lifespans. And the same holds for epigenetic clocks. They do predict how long you live. In theory, one could arrive at an estimate of age and death. There's a complicated mathematical formula that allows you to do that, but there would be a substantial error bar associated with it, an order of magnitude plus minus five years. And so, for the individual, such an estimate is not that important because the error bar is substantial. But I want to add that these second generation clocks, they do predict mortality risk. There's no question.Maximal LifespanEric Topol (11:35):Well, as you know, the longevity space is now very crowded with all sorts of clubs, and it's like a circus out there. And some of these things are being promoted that really don't have the basis or have a false sense to consumers who want to live forever and be healthy forever. But maybe these markers are not really helping guide them so much. Now, you recently published you and your group a fascinating paper, so getting away from the individual for a second, but now at the species level and in Science Advances, and we'll put this diagram with the podcast, but you looked at 348 mammal species for the maximal lifespan with DNA methylation. And it was amazing to see the display from the desert hamster all the way to the humpback whale with somewhere along the way, the humans. So you could predict maximal lifespan pretty well, right?Steve Horvath (12:43):Yes. So I collected this very large dataset over seven years, and one of the reasons was to understand the mystery of maximum lifespan. The bowhead whale can live over 211 years, whereas certain mice only three or four years. And my question was, can methylation teach us something about maximum lifespan? And the answer is a resounding, yes. The methylation profiles very much predict the maximum lifespan of a species. And maybe to use a metaphor to explain the patterns. So one can visualize methylation around the DNA molecule, like a landscape. You want that certain regions exhibit high levels of methylation. These regions must be really shut down and other parts of the DNA as opposed to exhibit very low methylation, for example, a transcriptional start sites. And long lived species have a very hilly landscapes, high hills of methylation and steep valleys of low methylation. Where shorter lived species have flatter landscapes. So that was one of the insights of that study. The other perhaps paradoxical insight was that the locations in our DNA that gain methylation with chronologic age, these regions often differ from regions that determine the maximum lifespan of our species. So that's a bit perhaps paradoxical and counterintuitive, but it just shows that the DNA encodes our species characteristics at different locations from our mortality risk.The Other ClocksEric Topol (15:13):Right. No, and I mean it's fascinating. I can imagine how it could take seven years to pull all that data together. It's amazing. Now, one of the issues of course, is if you're trying to gauge the biologic age, which we already established is somewhat different than epigenetic age or a clock, there are many different ways to do that. And you mentioned transcriptome clocks, which are not as well perhaps developed. Obviously, none of these others are developed like the Horvath clock and newer generation clocks, but there's immuno aging clocks like iAge, there's proteomic clocks, there's organ clocks with high-throughput proteomics, thousands of proteins. Do you see these as complimentary, like orthogonal where they each add to the story? Or do you really see the methylation as distinct?Steve Horvath (16:20):Well, I think ideally you measure all of the above to really get a very granular understanding of different facets of aging. And however, scientists always like to find deep connections between different readouts. For example, it would be wonderful if we could use proteomics instead of methylation, or my group has worked on the opposite. So we can actually estimate protein levels in the plasma based on methylation for about 10% of all plasma proteins, you can estimate their levels based on methylation. So yeah, people who are interested in these deeper programs that ideally link everything, some sort of aging program that underlies these different manifestations of aging, they will want to reduce everything. But until we have a deeper understanding, I think let's air on the side of measuring too much.Eric Topol (17:45):Well, what's interesting, as you mentioned, I didn't realize you could basically impute the protein story from the methylation, but one of the issues is if you want to do 11,000 plasma proteins, it could cost a thousand dollars. But if you want to do a bisulfite methylation, you might do that for very inexpensively. So there's a practical part of this too, and the immune characterization is even more expensive and difficult from a practical standpoint. So we go back to that initial work that you did and how you got into an area that is practical, inexpensive compared to some of the alternatives. But as you say, they may have features that are also helpful. Now, this is now the craze, this epigenetic clocks, and I want to mention you probably didn't see it because it's not a journal that you would look at, but just yesterday, July 29th, there were 12 papers published in JAMA Network Open.Modulating Your Epigenetic Clock(18:51):Everything from how loss of loved ones changes your epigenetic clock to PTSD, to vegan diets, to inequities. I mean, just incredible. So it is the rage now. It's taken the biomedical community some years to catch up to where you were. And one of the things of course that we know that from your prior work that is an intervention that helps give a less accelerated epigenetic clock is exercise. And in fact, that was highlighted in our Lancet essay in the first week August issue. But can you comment on that and anything else that we know like plant diets and anything that favorably influence our DNA methylation pattern?Steve Horvath (19:52):Yes. So interestingly, vegetable intake really has a strong effect on GrimAge and many other epigenetic clocks. And maybe this is obvious to the listener, everybody knows that vegetable intake is healthy. However, it's very surprising to me as a scientist to contemplate how is it that vegetable intake affects the methylation levels of your blood? How does it affect the hematopoietic stem cells? I just don't understand the mechanism behind it, and however, the effect is very strong. So we studied postmenopausal women in the women's health initiative, and for these women, we had blood measures of carotenoid levels. So this is an objective measure of vegetable intake, and the correlations were substantial. So that's one intervention I'm quite certain about. Other intervention that have a strong effect relate to metabolic syndrome, anything that relates to type 2 diabetes such as obesity, high glucose levels, that part of the biology very much affects our epigenetic clocks. So disturbed metabolism has a strong effect.Eric Topol (21:37):Has these findings changed your diet or made you exercise more or anything like that?Steve Horvath (21:44):. So I eat a lot of frozen vegetables. My freezer as full frozen vegetables.Eric Topol (21:56):That's great. Well, there's a lot of uses today as we touched on in the Lancet piece as we're waiting for more benchmarking and more work on this. But for example, we have a shortage of donor organs, and there are people who might be of calendar age advanced, but their epigenetic clock might put them at a much younger age. Is that ready for use in the transplant world as one application?Steve Horvath (22:37):I haven't seen that yet. I've seen several studies that have explored that idea. The idea is rather obvious, but I haven't seen it implemented in practicum.Eric Topol (22:53):Another one is that we don't, as you've seen from some of these studies on organ clocks, our organs age at different paces and some people are accelerated heart agers or brain agers. If you had access to tissue to get methylation, would you see the same thing or this is of course of interest because we're trying to understand high risk individuals for age related diseases, whether it's dementia or heart disease or cancer. So is the second generation clocks like PhenoAge just good enough, or would you think that the organ clocks would give you some added insight?Steve Horvath (23:47):Yeah, I would say this is literally the frontier of research. Several groups attempt to use blood methylation or saliva or skin or fat adipose as surrogates for various other organs. And I've seen very encouraging results. So I do think this idea makes scientific sense, and which comes back to one of the miracles of methylation that this is even possible because if you had written a grant 10 years ago where you said, I will measure blood methylation to assess cognitive functioning, for example, you wouldn't have received any score, not in no funding, but however, interestingly, blood methylation does relate to cognitive functioning and many other organ functions. And so, the proof of concepts have been established. Blood methylation relates to fatty liver disease, kidney disease, lung disease. It has all been done in epidemiological studies. However, the question is how much could a blood methylation measurement help an individual? Should I measure my blood methylation to learn about my liver? And I would say we are not there yet because arguably there are wonderful plasma biomarkers to assess organ functions. And in certain ways, one needs to provide evidence that a methylation measurement is superior or compliments plasma based biomarker. And that's a hard hurdle to take.Eric Topol (26:02):Right. I imagine someday it may become the norm of assessing people's risk, but as you say, we're not there yet because it's a tough bar to meet, for sure. Now, you were a Professor from year 2000 at UCLA in multiple departments in genetics and biostats, and then in more recent times you joined the Cambridge unit of Altos, which is one of the companies that has gotten the most attention for its diverse efforts towards modulating, rejuvenating the aging process. So you and many top scientists around the world were recruited to Altos. I know some here at the San Diego campus. Was this thinking that it could help accelerate the whole idea of modulating aging in a favorably way or where do you see that the biotech world can play a role?Can We Change the Pace of Aging?Steve Horvath (27:15):Yes. I mean, speaking for myself, I was getting tired of writing scientific papers and not affecting clinical care. I felt I needed to help identify or validate rejuvenating interventions because of the great promise, and this is perhaps best done in the setting of a biotech that is focused on translation. And that's why I joined. I'm moving away from biomarker development towards finding interventions that move the needle and ideally rejuvenate multiple organs and cell types at the same time.Eric Topol (28:09):Right. Now, there's lots of ideas of how we could do that from senolytics that would get rid of specific senescent cells that are bad actors to epigenetic reprogramming or chemical reprogramming or so many anti-inflammatory, like the recent paper of IL-11 that I'm sure you saw in Nature just a couple of weeks ago and many, many other ways to get there. What are you thinking? Is this going to be possible? Obviously, there's lots of naysayers. Is it going to be possible body wide or only for specific ways? For example, maybe we could bring back the thymus from its involution or we could stop ovarian failure in women so that their loss of advantage is delayed many years. Or do you think we're going to get to body wide anti-aging?Steve Horvath (29:13):Yeah, I think of it as divide and conquer. So ultimately I do believe that we can rejuvenate most cell types and tissues. The question is how do you roll out this program? Do you look for this one silver bullet that does it? For example, this idea of interrupted reprogramming based on Yamanaka factor combinations that looks of course very promising and rodent models. But then such silver bullet treatments could be risky for patient keyword malignant transformation, cancer risk, and it could be far safer to focus on one organ system or one tissue. For example, David Sinclair's company Life Biosciences looks at optic nerve regeneration for a reason. It could be safer. And so yeah, I'm very happy that companies explore different strategies. Certain companies focus on one condition, fatty liver disease or NASH. Other companies focus on immune system restoration. But I think many people think of one condition as really a first step to establish safety and efficacy, and then hopefully they could translate it to other body systems and organ systems.Eric Topol (31:02):But is it fair to say you're optimistic that we will be able to change the aging pace in people?Steve Horvath (31:10):Yes, I think yes. I'm very optimistic and there are several reasons for this optimism. The first is that dramatic results can be achieved in mice and rats. So we and others have published studies that show that you can reduce the epigenetic age by 30% or so and you can extend the lifespan, and you cited this very exciting paper by Stuart Cook on IL-11 inhibition that just came out in Nature. So I keep seeing these kinds of headlines, and then I want to think that one of these will actually work for humans. So the second thing that makes me optimistic is really this combination of artificial intelligence and biomedical research. Then going forward, robotics. So I can see several ways of accelerating biomedical research. So I'm quite optimistic.The Role of A.I.Eric Topol (32:24):Maybe go a little deeper on the AI potential to help here. How does AI come into play?Steve Horvath (32:33):So AI can help in so many different ways. The first topic is biomarker development. I of course spent 10 years on a certain statistical model for building biomarkers, which is known as penalized regression. It works well, but AI allows the community to build imaging based biomarkers. So for example, based on MRI images, but also cells growing in a dish, we can say this treatment aged the cells growing in the dish or rejuvenated them. So that's one topic, biomarker discovery. The second is, of course, to design small molecules, keyword, these protein design where it has greatly accelerated drug discovery. And there are several companies working in this space, and again, there's wonderful case studies that look very convincing to me. And the third aspect of AI is another obvious one. AI can read many papers. I mean, you could be a 50-year-old professor who has read papers their entire life, but an AI can really read far better and summarize insights better.Eric Topol (34:27):Yeah, the complimentary in terms of the reasoning of that information. So absolutely right now, one of the problems we have here is that aging is not seen as a disease. Of course, we can remember when obesity was not considered a disease and then there was a drug and everything changed. But here we don't have a classification it's a disease. It's considered a natural process that is highly variable in people. But the question is, we can't do studies that are going to wait 20, 30 years to find out if we promoted health span and lifespan. And so, we have to rely on these clocks. So how do you see this playing out? Do you think that we might see a regulatory approval on a surrogate proxy, like an advanced Horvath clock, or do you think that's not going to cut it, that you're going to have to show more to get a anti-aging treatment across the regulatory threshold?Steve Horvath (35:42):Yeah, that's a very good question. So I believe that the biomarker community has already assembled enough evidence to offer a battery of tests that could be used as surrogate endpoints of interventional study. And we could discuss the components of this battery. But I would say we already have biomarkers beyond just methylation. One could have the readouts of walking speed or muscle function, many readouts, and they could be aggregated into an index to summarize the biologic age, perhaps, of the individual. So that already exists. At the same time, this field is undergoing explosive growth. You mentioned every day new papers come out in the relatively small field of epigenetic clocks. There's so many papers that it's hard to keep track, but I embrace it. I think it's wonderful because clocks get ever more powerful.(37:11):So yeah, I would say there should be different versions. Ideally, a regulatory agency would make an executive decision and say, for the next three years, use the following five biomarkers. Then a few years later, as the science advances, they could come up with an updated version, but even a 90% solution would very much accelerate progress in the whole field of rejuvenating interventions. So I would very much embrace a top down decision on which biomarkers should be made, because the bottom up approach, by the way, simply doesn't work. The minute you put three professors in the room to come up with a decision, which biomarker is best, there will be three different opinions. We need impartial arbiter that makes a decision.GLP-1 Drugs and Aging Eric Topol (38:23):Now, the drug class that's come on the scene, of course it was in incubating for decades for diabetes, but now obesity and so of the obesity related. But now we're seeing the GLP-1 drugs that are showing potential effects in Parkinson's and Alzheimer's and cardiovascular disease, and even in obesity related cancers. And I mean across the board. And you mentioned metabolic derangement as one of the things that accelerate aging. Do you think these class of drugs that has greatly passed our expectations already and it's being tested of course, with even more potent drugs or triple receptors and pills and whatnot, will that be a candidate as one of the anti-aging interventions in the future?Steve Horvath (39:19):Yeah, for sure. A couple of months ago, I participated in a conference and one of the speakers showed unpublished results from a study, and they looked good to me. I mean, they registered on epigenetic clocks. This is all unpublished, but it made perfect sense to me because I mentioned the clocks do relate to metabolic health. So I was quite pleased that they registered that intervention.Eric Topol (39:56):It's fascinating because we could all be taking GLP-1 drugs someday, not for obesity or not for sleep apnea, but for things that are more far reaching. I didn't know about that unpublished result. That's fascinating.Steve Horvath (40:15):Yeah, I have a joke, which is I wish I was chubby because I would be using these drugs, but I'm relatively slender, so I don't have any good reason to take them.Eric Topol (40:28):That says a lot. I don't know anybody who knows more about this process than you and is very candid and frank about it. So Steve, this has been terrific to have your insights, the body of work that you should be so proud of that extends over many years and many great years and more contributions to come undoubtedly. So thank you for joining us today, and we will follow this continued evolution of our ability, not just to track the aging process, but also to modulate. So thanks very much.Steve Horvath (41:06):Thank you. I really like your podcast Ground Truths, it's very informative. So thank you for this.********************************************************We're appreciative of your reading and subscribing to Ground Truths. All content of these newsletter/analyses and podcasts are free, with no advertisements.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Please share this post, especially if you found it interesting or informative.If you do elect to be a paid subscriber, all proceeds are donated to Scripps Research and such support has already been extremely helpful for our summer internship programs and other educational activities. Comments and questions from paid subscribers are welcome. Get full access to Ground Truths at erictopol.substack.com/subscribe

Co-analysis of Methylation Platforms for Signatures of Biological Aging in the Domestic Dog

covid-19 university dogs cancer web buffalo pinterest domestic platforms biological doi signatures differing chronological methylation california los angeles altos labs steve horvath altmetric

Play Episode Listen Later Jul 23, 2024 3:20

BUFFALO, NY- July 23, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Co-analysis of methylation platforms for signatures of biological aging in the domestic dog reveals previously unexplored confounding factors.” Chronological age reveals the number of years an individual has lived since birth. By contrast, biological age varies between individuals of the same chronological age at a rate reflective of physiological decline. Differing rates of physiological decline are related to longevity and result from genetics, environment, behavior, and disease. The creation of methylation biological age predictors is a long-standing challenge in aging research due to the lack of individual pre-mortem longevity data. In this new study, researchers Aitor Serres Armero, Reuben M. Buckley, Lajoyce Mboning, Gabriella J. Spatola, Steve Horvath, Matteo Pellegrini, and Elaine A. Ostrander from the National Human Genome Research Institute, the University of California Los Angeles, and Altos Labs ask whether dogs experience changes in their epigenetic age at a rate predicted by breed longevity. “The consistent differences in longevity between domestic dog breeds enable the construction of biological age estimators which can, in turn, be contrasted with methylation measurements to elucidate mechanisms of biological aging.” The researchers drew on three flagship methylation studies using distinct measurement platforms and tissues to assess the feasibility of creating biological age methylation clocks in the dog. They expanded epigenetic clock building strategies to accommodate phylogenetic relationships between individuals, thus controlling for the use of breed standard metrics. The team observed that biological age methylation clocks are affected by population stratification and require heavy parameterization to achieve effective predictions. “Finally, we observe that methylation-related markers reflecting biological age signals are rare and do not colocalize between datasets.” DOI - https://doi.org/10.18632/aging.206012 Corresponding author - Elaine A. Ostrander - eostrand@mail.nih.gov Video short - https://www.youtube.com/watch?v=Rr2gA8bpJwk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206012 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biological age, methylation, dog, lifespan, penalized regression About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Depression, Antidepressants, Epigenetic Age Acceleration, and Mortality in Postmenopausal Women

Play Episode Listen Later Jun 10, 2024 4:12

BUFFALO, NY- June 10, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Relationships of depression and antidepressant use with epigenetic age acceleration and all-cause mortality among postmenopausal women.” In this new study, researchers May A. Beydoun, Hind A. Beydoun, Jason Ashe, Michael F. Georgescu, Steve Horvath, Ake Lu, Anthony S. Zannas, Aladdin H. Shadyab, Su Yon Jung, Sylvia Wassertheil-Smoller, Ramon Casanova, Alan B. Zonderman, and Robert L. Brunner from the National Institute on Aging, U.S. Department of Veterans Affairs (Washington, DC), University of Texas Health Science Center at Houston, University of California Los Angeles, University of North Carolina at Chapel Hill, University of California San Diego, Albert Einstein College of Medicine, Wake Forest University School of Medicine, and University of Nevada Reno investigated relations of depressive symptoms, antidepressant use, and epigenetic age acceleration with all-cause mortality risk among postmenopausal women. “Frequently under-recognized depression is a major contributor to the Global Burden of Diseases [1, 2] while being the most prevalent mental illness among geriatric populations [2].” Data were analyzed from ≤1,900 participants in the Women's Health Initiative study testing four-way decomposition models. After a median 20.4y follow-up, 1,161 deaths occurred. Approximately 11% had elevated depressive symptoms (EDS+), 7% were taking antidepressant medication at baseline (ANTIDEP+), while 16.5% fell into either category (EDS_ANTIDEP+). Baseline ANTIDEP+, longitudinal transition into ANTIDEP+ and accelerated epigenetic aging directly predicted increased mortality risk. GrimAge DNA methylation age acceleration (AgeAccelGrim) partially mediated total effects of baseline ANTIDEP+ and EDS_ANTIDEP+ on all-cause mortality risk in socio-demographic factors-adjusted models (Pure Indirect Effect >0, P < 0.05; Total Effect >0, P < 0.05). Thus, higher AgeAccelGrim partially explained the relationship between antidepressant use and increased all-cause mortality risk, though only prior to controlling for lifestyle and health-related factors. “Antidepressant use and epigenetic age acceleration independently predicted increased all-cause mortality risk. Further studies are needed in varying populations.” DOI - https://doi.org/10.18632/aging.205868 Corresponding author - May A. Beydoun - baydounm@mail.nih.gov Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205868 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, depressive symptoms, epigenetic age acceleration, mortality About Aging-US Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer's disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan. Please visit our website at https://www.Aging-US.com and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Aging Contributes to 2024 Systems Aging Gordon Research Conference

france japan ucla crossfit longevity genetics epigenetics nad lifespan biomarkers biohackers centenarians german american methylation altos labs steve horvath

Play Episode Listen Later May 20, 2024 2:57

BUFFALO, NY- May 20, 2024 – Aging is a contributor at the 2024 Systems Aging Gordon Research Conference (GRC) on “Systems Modeling, Aging Biomarkers, and Longevity Interventions” — taking place from June 2–7, 2024, in Castelldefels, Barcelona, Spain. “The conference will present recent advances in systemic rejuvenation, multi-omics approaches, applications of machine learning/artificial intelligence, and approaches for enhancing the chance of successfully translating basic research results to the clinic.” – GRC.org Additionally, many Aging authors have been invited to speak and lead discussions at the 2024 Systems Aging GRC. Among them are distinguished members of Aging's Editorial Board, including Steve Horvath, David Sinclair, Vera Gorbunova, Vadim Gladyshev, Guido Kroemer, and Anne Brunet. “The program will include speakers from diverse fields who are united in their pursuit of pioneering longevity and rejuvenating interventions. The 2024 Systems Aging GRC also aims to present advanced approaches for identifying comprehensive interventions that alleviate age-related pathology.” – GRC.org About Aging: Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer's disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). Please visit our website at https://www.Aging-US.com and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

618: Methylation, Epigenetics & Longevity with Steve Horvath

The Lucas Rockwood Show

Play Episode Listen Later May 1, 2024 45:41

Kane Tanaka of Japan died in 2022 at the age of 119. Lucile Randon of France died in 2023 at 118. Jiroemon Kimura of Japan died in 2023 at 116, the oldest male ever. What did these people have in common? Were they biohackers? Did they do CrossFit? Did they take NAD supplements or run marathons? Nope. Like almost all centenarians they lived exceptionally long lives most-likely due to genetics, combined with a moderately healthy or even average healthy lifestyle. Despite the overwhelming abundance of evidence that we're all going die sooner rather than later, the quest for longevity never stops. My guest on this week's podcast has developed a unique way to measure biological age and his work is playing a key role in longevity research and biohacker communities. Listen and learn: The overlooked role of epigenetics in your health and lifespan Biohackers, science fiction, and the reality of living a long time How methylation patterns can be predictive of lifespan The significance of GrimAge for reducing early mortality Links Steve on X ABOUT OUR GUEST Steve Horvath is a German-American researcher, geneticist, and biostatistician. He is a professor at UCLA and the principal investigator at Altos Labs, specializing in epigenetic biomarkers of aging, genomics, and comparative biology. Like the Show? Leave us a review Check out our YouTube channel

Coleen Murphy: The Science of Aging and Longevity

Play Episode Listen Later Mar 3, 2024 44:30

“A few years ago, I might have chuckled at the naiveté of this question, but now it's not so crazy to think that we will be able to take some sort of medicine to extend our healthy lifespans in the foreseeable future.”—Coleen MurphyTranscript with external linksEric Topol (00:06):Hello, this is Eric Topol from Ground Truths, and I'm just so delighted to have with me Professor Coleen Murphy, who has written this exceptional book, How We Age: The Science of Longevity. It is a phenomenal book and I'm very eager to discuss it with you, Coleen.Coleen Murphy (00:25):Thanks for having me on.Eric Topol (00:27):Oh yeah. Well, just so everyone who doesn't know Professor Murphy, she's at Princeton. She's the Richard Fisher Preceptor in Integrative Genomics, the Lewis-Sigler Institute for Integrative Genomics at Princeton, and director of the Paul Glenn Laboratories for Aging Research. Well, obviously you've been in this field for decades now, even though you're still very young. The classic paper that I can go back to would be in Nature 2003 with the DAF-16 and doubling the lifespan of C. elegans or better known as a roundworm. Would that be the first major entry you had?Coleen Murphy (01:17):Yeah, that was my postdoctoral work with Cynthia Kenyon.Eric Topol (01:20):Right, and you haven't stopped since you've been on a tear and you've put together a book which has a hundred pages of references in a small font. I don't know what the total number is, but it must be a thousand or something.Coleen Murphy (01:35):Actually, it's just under a thousand. That's right.Eric Topol (01:37):That's a good guess.Coleen Murphy (01:38):Good guess. Yeah.Eric Topol (01:39):So, because I too have a great interest in this area, I found just the resource that you've put together as extraordinary in terms of the science and all the work you've put together. What I was hoping to do today is to kind of take us through some of the real exciting pathways because there's a sentence in your book, which I thought was really kind of nailed it, and it actually is aligned with my sense. Obviously don't have the expertise by any means that you do here but it says, “A few years ago, I might have chuckled at the naivety of this question, but now it's not so crazy to think that we will be able to take some sort of medicine to extend our healthy lifespans in the foreseeable future.” That's a pretty strong statement for a person who's deep into the science. First I thought we'd explore healthy aging health span versus lifespan. Can you differentiate that as to your expectations?Coleen Murphy (02:54):So, I think most people would agree that they don't want to live necessary super long. What they really want to do is live a healthy life as long as they can. I think that a lot of people also have this fear that when we talk about extending lifespan, that we're ignoring that part. And I do want to assure everyone that the people in the researchers in the aging field are very much aware of this issue and have, especially in the past decade, I think put a real emphasis on this idea of quality of life and health span. What's reassuring is actually that many of the mechanisms that extend lifespan in all these model organisms also extend health span as well and so I don't think we're going to, they're not diametrically opposed, like we'll get to a healthier quality of life, I think in these efforts to extend lifespan as well.Eric Topol (03:50):Yeah, I think that's important that you're bringing that up, which is there's this overlap, like a Venn diagram where things that do help with longevity should help with health span, and we don't necessarily have to follow as you call them the immoralists, as far as living to 190 or whatever year. Now, one of the pathways that's been of course a big one for years and studied in multiple species has been caloric restriction. I wonder if you could talk to that and obviously there's now mimetics that could simulate that so you wouldn't have to go through some major dietary starvation, if you will. What are your thoughts on that pathway?Coleen Murphy (04:41):Yeah, actually I'm really glad you brought up mimetics because often the conversation starts and ends with you should eat less. I think that is a really hard thing for a lot of people to do. So just for the background, so dietary restriction or caloric restriction, the idea is that you would have to take in up to 30% less than your normal intake in order to start seeing results. When we've done this with laboratory animals of all kinds, this works from yeast all the way up through mice, actually primates, in fact, it does extend lifespan and in most metrics of health span the quality of life, it does improve that as well. On the other hand, I think psychologically it's really tough to not eat enough and I think that's a part that we kind of blindly ignore when we talk about this pathway.Coleen Murphy (05:30):And of course, if we gave any of those animals the choice of whether they want to start eating more, they would. So, it's like that's not the experiment we ever hear about. And so, the idea for studying this pathway isn't just to say, okay, this works and now we know how it works, but as you pointed out, mimetics, so can we target the molecules in the pathway so that we can help people achieve the benefits of caloric restriction without necessarily having to do the kind of awful part of restriction? I think that's really cool, and especially it might be very good for people who are undergoing certain, have certain diseases or have certain impairments that it might make it difficult ever to do dietary restrictions, so I think that's a really great thing that the field is kind of getting towards now.Eric Topol (06:15):And I think in fact, just today, it's every day there's something published now. Just today there was a University of Southern California study, a randomized study report comparing plant-based fasting-mimicking diet versus controlled diet, and showed that many metabolic features were improved quite substantially and projected that if you stayed on that diet, you'd gain two and a half years of healthy aging or that you would have, that's a bit of an extrapolation, but quite a bit of benefit. Now, what candidates would simulate caloric restriction? I mean, what kind of molecules would help us do that? And by the way, in the book you mentioned that the price to pay is that the brain slows down with caloric restrictions.Coleen Murphy (07:10):There's at least one study that shows that.Coleen Murphy (07:13):Yeah, so it's good to keep in mind. One of the big things that is being looked at as rapamycin, looking at that TOR pathway. So that's being explored as one of these really good mimetics. And of course, you have things that are analogs of that, so rapalogs, and so people are trying to develop drugs that mimic that, do the same kind of thing without probably some of the side effects that you might see with rapamycin. Metformin is another one, although it's interesting when you talk to people about metformin who work on it, it's argued about what is exactly the target of metformin. There's thought maybe also acts in the TOR pathway could affect complex one of mitochondria. Some of the things we know that they work, and we don't necessarily know how they work. And then of course there's new drugs all the time where people are trying to develop to other target, other molecules. So, we'll see, but I think that the idea of mimetics is actually really good, and that part of the field is moving forward pretty quickly. This diet that you did just mention, it is really encouraging that they don't have to take a drug if you don't want to. If you eat the right kind of diet, it could be very beneficial.Eric Topol (08:20):Yeah, no, it was interesting. I was looking at the methods in that USC paper and they sent them a box of stuff that they would eat for three cycles, multiple weeks per cycle. It was a very interesting report, we'll link to that. Before we leave the caloric restriction and these mTOR pathway, you noted in the book that there some ongoing trials like PEARL, I looked that up and they finished the trial, but they haven't reported it and it's not that large. And then there's the FAME trial with metformin. I guess we'll get a readout on these trials in the not-too-distant future. Right?Coleen Murphy (08:57):Yeah, that's the hope that especially with the Metformin trial, which I think is going to be really large the FAME trial, that just to give the listeners a little background, one of the efforts in the field is not just to show that something works, but also to convince the FDA that aging could be a pharmaceutical, a disease that we might want to have interventions for. And to do that, we need to figure out the right way to do it. We can't do 30-year studies of safety and things to make sure that something's good, but maybe there are reasonable biomarkers that would tell us whether people are going to live a long time. And so, if we can use some of those things or targeting age-related diseases where we can get a faster readout as well. Those are reasonable things that companies could do that would help us to really confirm or maybe rule out some of these pharmaceuticals as effective interventions. I think that would be really great for consumers to know, is this thing really going to do good or not? And we just don't have that right now in the field. We have a lot of people saying something will work and it might and the studies in the lab, but when we get to humans, we really need more clinical studies to really tell us that things are going to be effective.Eric Topol (10:12):Right, I'm going to get to that in a bit too because I think you're bringing up a critical topic since there's an explosion of biopharma companies in this space, billions of dollars that have been put up for in capital and the question is what's going to be the ground rules to get these potential candidate drugs to final commercial approval. But before I leave, caloric restriction and insulin signaling and the homolog and the human to what your discovery of DAF-16, FOXO and all this, I just want you to comment, it wasn't necessarily developed in the book, but as you know, the GLP-1 drugs have become just the biggest drug class in medical history, and they do have some effects here that are very interesting. They are being tested as in Alzheimer's disease. Do you see that this is a candidate too that might promote healthy aging?Coleen Murphy (11:12):Yeah, I'm so glad you brought that up because my book, I finished writing it right before all this stuff came out, and it's looking really very compelling. People are on these drugs, they lose a ton of weight, but their blood biomarkers really become very good and on top of just the changes in weight and those kinds of effects. Let me just say, I think the biggest thing, the biggest risk actually for aging people right now are cardiovascular problems, cardiovascular disease, and these drugs, no doubt, it's going to basically make a huge dent in that. I'm absolutely sure of that. What I also find really interesting with those drugs is that the users report that they have fewer cravings for other things. So, this is not being looked at to treat alcoholism and drug addiction, other things, so it really opens up a whole new world of things that are bad for us that maybe we could avoid this with these peptides. It's almost staggering. I really think this going to be a huge, and as far as an aging drug, if you reduce your weight, you improve all your cardiovascular function, you don't feel like drinking all the time, all these things might be really great and I do think that people will live longer.Eric Topol (12:32):Yeah, no, it does have that look and you just have to wonder if as these will go on to oral drugs with triple receptors and very potent, maybe even avoiding peptides in the future too, that this could wind up being something that's exceedingly common to take for reasons far removed from the initial indication of type two diabetes and more recently of course, obesity. Now the next topic I wanted to get into with you were senolytics, these agents that basically are thought to reverse aging or slow aging. And again, since everything's coming out in a daily basis, there was a trial in diabetes macular edema where giving senolytic after people had failed their usual VEGF treatment was highly successful. So, we're starting to see, at least in the eye results. I wonder if you could describe how you conceive this field of senolytics?Coleen Murphy (13:41):Actually, I think they've made great progress in the past couple of years because there were some initial failures, like some of the things for osteoarthritis that went through I think phase two, but I think that one of the great things about the longevity biotech field is that they're starting to identify not just longevity, these age-related disorders that they could actually use. And so, it's kind of doubly beneficial. It tells us that the drugs actually do something and so maybe it'll be used for something else in the future and you get through, you can test safety, but also helping people actually have a very real problem that's acute that they really need to take care of. And so that's really exciting. Then in addition to the example you just mentioned, I was at a conference last summer where it was being explored whether some of these senolytics could be helpful for middle aged survivors of childhood cancers who do show various health effects from having gone through chemotherapies at a young age. So that's really exciting. Could you help people who are not aging, but they actually are showing having problems that we kind of associate with aging. And senolytics were at least the first thing I'd heard about that are actually being used for that, so there may be other approaches that help as well, but I think that's really great.Eric Topol (15:05):Well, and just to be clear the senolytics, I guess could be categorized at least one function might be to help clear dead cells. These senescent cells are bad actors and either they're taken out or they're somehow neutralized in their impact of secreting evil humors, if you will. Are there other forms of senolytics besides that way of dealing with these senescent cells?Coleen Murphy (15:33):I know that some people are exploring senomorphs, so things that make those cells just arrest but I do want to mention, of course, we lost a great Judith Campisi recently, and she was the one who discovered and described the senescent associated secretory phenotype, and she did amazing work in that field really opening that up. So, this idea that bad cells aren't just bad because they don't function, but they're actually toxic to other cells.Coleen Murphy (16:04):That's important for listeners to know. Yeah, so I don't know. I think that one of the things I'm excited about in the aging field is that it doesn't seem like there's one magic bullet. A lot of researchers will spend their time working on that one thing so if you only talk to that one person, you might get that impression, but there's a whole host of things that for bad or good, that things go wrong when we age, but those all end up being maybe targets that could help us live longer or at least in a healthier way. And so, we've already talked about a couple of them, but readers will see as we learn more, there might be more ways to help cells survive or to help us replace ourselves, for example.Eric Topol (16:45):I mean, I think what you're bringing up here is central because there's all these different, as I can see it, shots on goal that of course could be even used as combinations, no less senolytic interventions so we're getting closer as we started this conversation to fulfilling what you, I think is in store in the years ahead, which is extraordinary. Along with the senolytics, I wonder if you could just talk a little bit about these autophagy enhancers as a class of agents, maybe first explaining autophagy and then is this a realistic goal that we should be taking autophagy enhancers, or is this something that's too generalized that might have onward mTOR effects?Coleen Murphy (17:39):Well, it's interesting. Autophagy, so just for the listeners, autophagy literally means self-eating. So this is a pathway whereby proteins basically get degraded within the cell and those parts get recycled. And the idea is that if you have a cell or protein that's damaged in some way, or it can be renewed if you induce autophagy. I think I could be wrong here, but my sense is that the cancer field is really excited about autophagy enhancers. And so, I think that's probably where we'll see the biggest breakthroughs but along the way, of course we'll know because we'll know if they're safe and if there's other off-target effects. I think that that's largely being driven by the cancer field and the longevity field is kind of a little bit behind that, so we'll learn from them. It seems like a really exciting approach as well.Eric Topol (18:34):Yeah, it does. And then as you know, the idea of giving young blood, young plasma, which there already are places that do this, that it can help people who are cognitively impaired and have basically immediate effects, and sometimes at least with some durability. It's very anecdotal, but this idea, we don't know what's in the young blood or young plasma to some extent. How do you process that?Coleen Murphy (19:10):Okay. Well, so what we do know, and this is really work that a lot of people like Saul Villeda and Tony Wyss-Coray have done where they really have, they've taken that blood or plasma and then found the parts in the plasma that actually do specific jobs. And so, we actually are starting to learn a lot about that and that's exciting because of course, we don't really want to give people young blood. What we really would like to do is find out is there a particular factor in the blood? And there seems to be many that could be beneficial. And so, we really are getting close. We as a field, and specifically like the research I just mentioned and that's exciting because you can imagine, for example, if there's one factor that's in blood, that's in young blood, that's very helpful, manufacturing, a lot of that particular thing.Coleen Murphy (20:01):The other exciting thing, again, this is Saul Villeda's lab that found that exercise mice. So even if they're the same age mice, if one of them is exercised, it makes factors that actually from the liver of the mouse upon exercise, that then gets secreted and then affect, improve cognitive function as well. So it seems like even within the blood, there's multiple different ways to get blood factors that are beneficial, whether they're from young blood or from exercise blood. And so, there's a lot of things we don't yet know, but I do think that field is moving very fast and they're identifying a lot of things. In fact, so I'm the director of Simons Collaboration Plasticity in the Aging Brain, and on that website we're developing basically a page that can tell you what are the factors and what has it been shown to be associated with, because we're very interested in slowing normal cognitive aging and blood factors seem to be one of the really powerful ways that might be available to us very soon to be able to improve that.Eric Topol (21:03):Yeah, no, I'm glad you mentioned that, Coleen. I think the point that you made regarding exercise, I certainly was struck by that because in the book, because we've known about this association with exercise and cognition, and this I think is certainly one potential link. An area that is also fascinating is epigenetics, so a colleague of mine here in the Mesa, Juan Carlos Belmonte, who was at Salk and left to go to Altos, one of these many companies that are trying to change the world in health span and lifespan. Anyway, he had published back several years ago.Coleen Murphy (21:53):Yeah, 2016.Eric Topol (21:54):Yeah, CRISPR basically modulation of the epigenome through editing and showed a number of through specific pathways, a number of pretty remarkable effects. I wonder if you could comment about epigenetics, and then I also want to get into this fascinating topic of transgenerational inheritance, which may be tied of course to that. So, what about this pathway? Is there something to it?Coleen Murphy (22:29):Well, absolutely. I just think we need to learn a lot more about it. So just for the listener, so epigenetics, we think about genetics that's basically based on DNA and chromosomes. And so, when we think about epigenetics, that could be either, we could be talking about modulation of the histone marks on the chromosomes that allow the genes to be expressed or be silenced. And then on the DNA itself, there are methylation marks. And so, people have used, of course, Steve developed a, sorry, I'm sorry. Steve Horvath developed a very nice, he was first to develop a DNA methylation clock. So this idea that you could, and that was really interesting because he based it on, he used this machine learning method to narrow down to the 353 marks that were actually predictive or correlated with age, but we don't understand how it biologically what that manifests in. I think that's not well understood. At the chromatin level, there's a lot of work on the specific histone marks that may change, for example, how genes are transcribed and so understanding that better will maybe help us understand what those changes. There's things called epigenetic drift, so genes stop being carefully regulated with age, and then how can we make that maintain better with age? It's one of the goals of the field in addition to basically understanding what's going on at the epigenetic level.Eric Topol (24:01):So now of course, could we alter that? Oh, it is fascinating as you say, that you could have the Horvath clock to so accurately predict a person's biological age. And by the way, just a few days ago, there was a review by all these clock aging folks in nature medicine about the lack of standards. There's so many clocks to basically determine biological age versus chronological age. Before we get into the transgenerational inheritance, what is your sense? Obviously, these are getting marketed now, and this field is got ahead of its skis, if you will, but what about these biologic age markers?Coleen Murphy (25:02):Yeah, I'm glad to hear that. I haven't seen that review. I should look it up. It's good to know that the players in the field are addressing those points. So just for the listeners, so these DNA methylation clocks so when Steve Horvath developed the first one, it was based on the controls from a very large number of cancer controls for other reasons, so he used a huge amount of information. It really depended on the, he was trying to develop a clock that was independent of which tissue, but it turned out there's more and more clocks that are tissue specific and really organism specific, species specific. It really depends on what you're looking at to make these, and whether you're looking at chronological age or trying to predict biological age. I think it's a little frustrating because what you'd really like to know as a consumer, if you send off for one of these clock kits, is it right?Coleen Murphy (25:57):What's the margin of error? If I took it every week, would I get the same number? And so, I think my sense is that people take it until they get a low number then, but you'd really like to know if they work, because if you want to take it, do a control and they start, get your clock number and then start taking some intervention and ask whether it works, right? Yeah. So, I think because the players in the field recognize these issues, they're going to straighten it out, but I think one part that drives a little bit of the problem is that we don't understand what that DNA methylation mark change translates into biologically. If we understood that better, I think we'd have a better feeling about it. Anne Brunet and Tony Wyss-Coray maybe a year and a half ago, they had a nice paper where two years ago where they looked at, they use a different type of clock, a transcriptional clock, and that worked really well. So they were looking at transcriptional clock in the subventricular zone, and they were able to actually see changes not just with age, but also when there was an intervention. I can't remember if they look at dietary restriction and then maybe an exercise in the mice. And so that's important for us to know how well those clocks work.Coleen Murphy (27:13):I think it'll get there. It'll get there.Eric Topol (27:15):You don't want to pay a few hundred dollars and then be told that you're 10 years older biologically than your chronologic age, especially if it's wrong. Right?Coleen Murphy (27:25):Yes. It'll get there. I think it may not be quite there yet.Eric Topol (27:30):And by the way, while we're on that, the organ clocks paper, in fact, just a recent weeks, I did interview Tony Wyss-Coray from Stanford, and we talked about what I consider really a seminal paper because using plasma proteins, they're able to basically clock each organ. And that seems like a promising approach, which could also help prove the case that you're changing something favorably with one of these various intervention classes or categories. Do you think that's true?Coleen Murphy (28:05):That feels more real directly looking at the proteins then.Eric Topol (28:08):Yeah, exactly. I thought that was really exciting work, and I'm actually going to visit with Tony in a few weeks to discuss it further. So excited about it.Coleen Murphy (28:18):That's great. He's doing great work, so it'll be a fascinating conversation.Eric Topol (28:21):Yeah, well this is also fascinating. Now, transgenerational inheritance is a very controversial topic in humans, which it is not so much in every other species. Can you explain why that is?Coleen Murphy (28:38):Well, there's a lot of, I would say emotional baggage attached here, right? Because that's what people are talking about, like transgenerational trauma. There's no doubt that traumatic experiences in childhood actually do seem to change the genome and change have very real biological effects. And that's been shown. So that's within the first generation. It's also no doubt that in other organisms, like in plants like DNA methylation, that's exactly how they regulate things, and that's multiple generations. So that's kind of the norm. And so, the question for humans is whether something like this, like a traumatic experience or starvation or thing, has an effect, not just on the person who's experiencing it, but also on their progeny, even on their grand progeny. And so, it's tough, right? Because the data that are out there are from pretty terrible experiences like the Dutch hunger winter. And so, there's a limited set of data, and some of those data look good, and some of them look weaker. Yeah, I think that we still need to figure out what's going on there, and if it's real, it'd be interesting to know. Are there ways, for example, with these epigenetic modulators, are there ways that you could help people be healthier by erasing some of those marks of trauma, generational trauma?Eric Topol (30:03):Yeah. So, I mean, the theory as you're getting to would be you could change the epigenome, whether it's through chromatin, acetylation, methylation, somehow through these experiences and it would be going through down through multiple generations. The reason I know it's controversial is when I reviewed Sid Mukherjee's book, the Gene, he had put in that it was real in humans, and the attack dogs came out all over the place. Now, we've covered a lot of these pathways. One that we haven't yet touched on is the gut microbiome, and the idea here, of course, it could be somewhat linked to the caloric restriction story, but it seems to be independent of that as well. That is there, our immunity is very much influenced by our gut microbiome. There's the gut brain axis and all sorts of interactions going on there, but what about the idea of using probiotics and particular bacterial species as a introducing the people as an idea in the future to promote health span?Coleen Murphy (31:18):Yeah, it's a great idea. So, I just want to back up and say the microbiome, the reason it's so fraught is because for a long time, people had confused correlation and causation. So, they would see that a person who has X disease has a difference in the microbiome from people who don't have that disease. And so, the question was always, do they have that disease because of a difference in the microbiome or the disease influence in the microbiome? And of course, even things that's eating different food. For example, if a child with autism doesn't want to eat certain range of food, it's going to have an effect on the microbiome. That does not mean the microbiome cause their autism. And so that's something where, and the same thing with Alzheimer's disease patients. I think that's often the source of some of this confusion. I think people wish that they could cure a lot of diseases by taking a probiotic.Coleen Murphy (32:09):On the other hand, now there's actually some really compelling data. Dario Valenzano's lab did a really nice experiment in killifish, which is my second favorite aging model research organism. So killifish, turquoise killifish, only live a few months. And so, you can do aging studies really quickly and what Dario's group did was they took the microbiome at middle aged fish, they wiped out their microbiome with antibiotics, and they added back either young or same age, and they saw a really nice extension of lifespan with the young microbiome. So that suggests, in that case where everything else is the same, it really does have a nice effect. John Cryan's group in Ireland did something similar with mice, and they showed that there was a beneficial effect on cognitive function in older mice. So those are two examples of studies where it really does seem like there is an effect, so it could be beneficial. And then there's of course things like microbiome transfer for people who are in the hospital who have had other things, because your microbiome also helps you prevent other diseases. Those being there, if you wipe out all of your microbiome, you can actually get infected with other things. It's actually a protective barrier. There's a lot of benefits, I think in order to, we don't know a ton about how to control it. We know there are these, it's gross, but fecal microbiome transplantation.Eric Topol (33:42):FMT. Yeah, yeah.Coleen Murphy (33:44):Exactly. And so, I think that is kind of the extreme, but it can be done. I think in appropriate cases it could be a very good strategy.Eric Topol (33:53):It's interesting. There was a study about resilience of the immune system, which showed that women have a significant advantage in that they have just the right balance of not having a hyper inflammatory reaction to whether it's a pathogen or other stimulus. And they also have, of course, an immunocompetent system to respond, so unlike men overall, that although the problem of course with more prone to autoimmunity because of having two x chromosomes and exist or whatever other factors. But also, there's a balance that there's an advantage, in the immune system as a target for health span and lifespan, a lot of things that we've talked about have some interaction with the immune system. Is there anything direct that we can do to promote a healthier immune system and avoid immunosenescence and inflammaging or immuno aging or whatever you want to call it?Coleen Murphy (35:04):Sure, I will admit that immunology is a field that I want to learn more about, but I do not know enough about it to give a really great answer. I think it's one of the things I kind of shied away from when I wrote the book that if I were to rewrite it, I would add a whole new section on it. I think that's a really booming field, this interaction between immunology and aging. Obviously, there's immune aging, but what does that really mean?Coleen Murphy (35:28):I feel like I can't give you a really intelligent answer about that. Even though I'd like to, and I don't know how much of it's because there's just sort of this general idea that the immune system stops functioning well, but I do feel like the immune system is actually so mysterious. I have a peanut allergy, for example. We don't even really, I mean, we can prime ourselves against that now. We can give kids little bits of peanuts, but all the things that I feel like immunology is the one that's probably taking off the most, and we'll probably in a decade know way more about it than we do now, but I can't give you a very smart answer right now.Eric Topol (36:09):Yeah, no, I do think it's really provocative and the fact that if you have these exhausting T cells that are basically your backup system of your immune system, if they're not working, that's not good. And maybe they can be revved up without being problematic. We'll see.Coleen Murphy (36:27):And I guess the real question is do we need to do something independent or is that folded into everything else? If you were giving someone a drug that seemed very good systemically or some of these blood factors, would you have to do something special just for the immune system or is that something that would also be effective? I feel like that would be good to know.Eric Topol (36:44):Now the other area that I want to bring up, which is a little more futuristic is genome editing. So recently when I spoke to David Liu, he mentioned, well, actually it was Jennifer Doudna who first put it out there, but we discussed the idea of changing the people like me who are APOE4 carriers to APOE2, which is associated with longer life and all these other good things. Why don't we just edit ourselves to do that? Is that a prospect that you think ever could be actualized?Coleen Murphy (37:20):Well, I was just at a talk by Britt Adamson just moments ago, and that field is moving really fast, right? All the work that David Liu has done, and it's really exciting, this idea that you can now cure sickle cell anemia.Coleen Murphy (37:35):Fascinating. And I think Jennifer Doudna rightly proposed early on that what we should really be hitting first are like blood. Blood's really good because it's not hitting the germline. It's really something where we can help people at that stage. I was thinking about that while Britt was talking, what are the things we'd really want to address with CRISPR? I'm not sure how high up in the list aging related factors would be compared to a lot of childhood diseases, things that are really debilitating, but certainly is true since when we're looking at APOE4. I think that's the one exception because that is so strongly correlated with healthy lifespan and Alzheimer's and things, so we really want to do something about that. The question is how would we do that? That's not a blood factor. I think we'd have to think hard about that, but it is on the list of looming on the horizon.Eric Topol (38:35):I wouldn't be surprised if someday, and David, of course thought it's realistic, but it's not, obviously in the short term. Well, this has been enthralling to go through all these possibilities. I guess when you put it all together, there's just so many ways that we might be able to, and one of the things that you also pointed out in your book, which something that should not be forgotten, is the fact that all these things could even worsen the inequities that we face today. That is you have any one of these click, if not multiple, it isn't like they're going to be available to all. And the problem we have now, especially in this country without universal health and access issues, could be markedly exacerbated as we're seeing with the GLP-1 drugs too, by the way.Coleen Murphy (39:27):Absolutely.Eric Topol (39:28):So, I just want to give you a chance to reinforce what you wrote in the book, because I think this is where a lot of times science leads and doesn't realize the practical implications of who would benefit.Coleen Murphy (39:42):Yeah, I think actually for aging research often, even when I first started doing this work back in 2000, the first thing people would ask me if they're below a certain age was, don't you think that's terrible? Make the rich people just live the longest? And they're not wrong about that. I think what it can, we should raise awareness about the fact that even these things that we consider simple, like doing caloric restriction or getting exercise, even those things are not that straightforward if you're working two jobs or if you don't have access to excellent foods in your neighborhood, right? Fruits and vegetables. If we really want to not just extend longevity but raise life expectancy, then we should be doing a lot more that's for improving the quality of life of many people. And so there is that idea. On the other hand, I do want to point out that as we discover more and more of these things, like metformin is off patent, it's like it's really old. And so, it's more of these things get discovered and more broadly used. I do think that that may be a case where we could end up having more people might have access to things more easily. So that's my hope.Coleen Murphy (40:57):I don't want to discourage anyone from developing a longevity dry. I think eventually that could help a lot of people if it's not too absurdly expensive.Eric Topol (41:04):Yeah, no, I certainly agree. And one last footnote is that we did a study called The Wellderly here, about 1,400 people over age 85 who'd never been sick, so our goal here wasn't lifespan. It was to understand if there was genomics, which we did whole genome sequencing of this group. We didn't find much like the study that you cited in the book by the Calico group. And so just to give hope that people, if they don't have what they think are family genetics of short life or short health span, that may not be as much to that as a lot of people think. Any final thoughts about that point? Because it's one that's out there and data goes in different directions.Coleen Murphy (41:55):Yeah. The Calico study you mentioned, I think that's the one where they found that your health or lifespan mostly went with almost like your in-laws, which actually points again to your socioeconomic group probably you marry people, most people marry people are in a similar socioeconomic group. That's probably what that mostly had to do with. I do think if I'm going to say one thing because a lot of these drugs are on the horizon, they're not yet available, or there's nothing I can hang onto for an FDA approved drug to extend that. I do think the one thing that I would encourage people to do even more than the dietary restriction stuff, it is exercise because that's just generally beneficial in so many different ways. And so, if we can get people doing a little more exercise, I think that would be the one thing that probably could help a lot of people.Eric Topol (42:40):Well, I'm glad we are winding up with that because I think the data from lifestyle, which is exercise as you're pointing out, as well as nutrition and sleep.Coleen Murphy (42:54):All the boring things we already thought, right.Eric Topol (42:55):That we know about, but we don't necessarily put in our daily lives. There's a lot there. There's no question that studies, I think, really have reinforced that even recent one. Well, what a pleasure to talk to you about this and do this tour of the various exciting prospects. I hope I haven't missed anything. I know we can't go over all the pathways, and obviously there've been some bust in the past, which we don't need to review like the famous Resveratrol Sirtuin story, which you addressed in the book. I do want to encourage people that this book is extraordinary. Your work that you put into it had to be consumptive for I don't know how many years of work.Coleen Murphy (43:37):There was many years of work. My editor, we sat down to lunch right after it finished. She was like, so what are you going to work on for your next book?Eric Topol (43:50):Well, it's a scholarly approach to a very important field. If you can influence the aging process, you influence every part of our body function. The impact here is profound, and the contribution that you've made in your science as well as in your writing here is just so terrific. So thank you, Coleen. Thanks so much for joining us today.Coleen Murphy (44:17):Thank you so much. It's been a pleasure.Thanks for listening and/or reading this edition of Ground Truths, aimed at bringing you cutting-edge biomedical advances via analyses and podcasts.All content is free. Voluntary paid subscriptions go to support Scripps Research and have funded our summer intern program. Get full access to Ground Truths at erictopol.substack.com/subscribe

university science nature blood dna ireland fame southern california stanford alzheimer's disease dutch fda usc longevity fruits mesa fascinating tor crispr glp voluntary venn altos horvath calico metformin autophagy mtor jennifer doudna salk eric topol aging research apoe4 fmt vegf aging brain scripps research david liu john cryan steve horvath cynthia kenyon professor murphy tony wyss coray

Aging's Top 10 Papers in 2023 (Crossref Data)

data dna martinez papers rna doi daniel levy janssens escherichia matthew arnold steve horvath c57bl

Play Episode Listen Later Feb 15, 2024 7:59

Crossref is a non-profit organization that logs and updates citations for scientific publications. Each month, Crossref identifies a list of the most popular Aging (Aging-US) papers based on the number of times a DOI is successfully resolved. Below are Crossref's Top 10 Aging DOIs in 2023. 10: Old-age-induced obesity reversed by a methionine-deficient diet or oral administration of recombinant methioninase-producing Escherichia coli in C57BL/6 mice DOI: https://doi.org/10.18632/aging.204783 Authors: Yutaro Kubota, Qinghong Han, Jose Reynoso, Yusuke Aoki, Noriyuki Masaki, Koya Obara, Kazuyuki Hamada, Michael Bouvet, Takuya Tsunoda, and Robert M. Hoffman 9: Metformin use history and genome-wide DNA methylation profile: potential molecular mechanism for aging and longevity DOI: https://doi.org/10.18632/aging.204498 Authors: Pedro S. Marra, Takehiko Yamanashi, Kaitlyn J. Crutchley, Nadia E. Wahba, Zoe-Ella M. Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Masaaki Iwata, Hyunkeun Ryan Cho, and Gen Shinozaki 8: Age prediction from human blood plasma using proteomic and small RNA data: a comparative analysis DOI: https://doi.org/10.18632/aging.204787 Authors: Jérôme Salignon, Omid R. Faridani, Tasso Miliotis, Georges E. Janssens, Ping Chen, Bader Zarrouki, Rickard Sandberg, Pia Davidsson, and Christian G. Riedel 7: Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic DOI: https://doi.org/10.18632/aging.204616 Authors: Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip 6: Potential reversal of biological age in women following an 8-week methylation-supportive diet and lifestyle program: a case series DOI: https://doi.org/10.18632/aging.204602 Authors: Kara N. Fitzgerald, Tish Campbell, Suzanne Makarem, and Romilly Hodges 5: Leukocyte telomere length, T cell composition and DNA methylation age DOI: https://doi.org/10.18632/aging.101293 Authors: Brian H. Chen, Cara L. Carty, Masayuki Kimura, Jeremy D. Kark, Wei Chen, Shengxu Li, Tao Zhang, Charles Kooperberg, Daniel Levy, Themistocles Assimes, Devin Absher, Steve Horvath, Alexander P. Reiner, and Abraham Aviv 4: DNA methylation GrimAge strongly predicts lifespan and healthspan DOI: https://doi.org/10.18632/aging.101684 Authors: Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, and Steve Horvath 3: Deep biomarkers of aging and longevity: from research to applications DOI: https://doi.org/10.18632/aging.102475 Authors: Alex Zhavoronkov, Ricky Li, Candice Ma, and Polina Mamoshina 2: An epigenetic biomarker of aging for lifespan and healthspan DOI: https://doi.org/10.18632/aging.101414 Authors: Morgan E. Levine, Ake T. Lu, Austin Quach, Brian H. Chen, Themistocles L. Assimes, Stefania Bandinelli, Lifang Hou, Andrea A. Baccarelli, James D. Stewart, Yun Li, Eric A. Whitsel, James G Wilson, Alex P Reiner, Abraham Aviv, Kurt Lohman, Yongmei Liu, Luigi Ferrucci, and Steve Horvath 1: Chemically induced reprogramming to reverse cellular aging DOI: https://doi.org/10.18632/aging.204896 Authors: Jae-Hyun Yang, Christopher A. Petty, Thomas Dixon-McDougall, Maria Vina Lopez, Alexander Tyshkovskiy, Sun Maybury-Lewis, Xiao Tian, Nabilah Ibrahim, Zhili Chen, Patrick T. Griffin, Matthew Arnold, Jien Li, Oswaldo A. Martinez, Alexander Behn, Ryan Rogers-Hammond, Suzanne Angeli, Vadim N. Gladyshev, and David A. Sinclair Aging is an open-access, traditional, peer-reviewed journal that has published high-impact papers in all fields of aging research since 2009. All papers are available to readers (at no cost and free of subscription barriers) in bi-monthly issues at Aging-US.com. For media inquiries, please contact media@impactjournals.com.

200. YNGRE: metformin, hormese, gener, epigenetikk og anti-aldersbrytere med Hanne S. Finstad

Biohacking Girls Podcast

Play Episode Listen Later Feb 12, 2024 66:19

Hva er den ledende årsaken til at vi dør, er det aldring eller er det sykdom?I denne podcasten snakker vi med biokjemiker med en doktorgrad i Omega 3 fettsyrer og forfatter Hanne S. Finstad. Hanne er aktuell med boken "Yngre" der hun inviterer oss inn på sitt selvstudie og foryngeslesreise. Hanne blir i følge flere biologiske alderstester 5 år yngre i løpet av dette året. Du får høre detaljerte beskrivelser om hennes protokoller og utprøving som består av mat, faste, trening, hormetisk stress, medisiner og tilskudd. Det er tydelig at hun er inspirert av store forskere på feltet som bl.a Dr David Sinclair og Steve Horvath. Hør hva som funket for Hanne og hennes reise som startet i 2020, og hva som ble utfordrende. Et godt utgangspunkt for å starte en antialdringsreise er å ta utgangspunkt i deg selv, kjenne etter hvordan du har det og hvilken alder du føler du bærer.Å utsette aldringstegn betyr å utsette sykdom. Å minimere risiko for sykdom og død.Å utsette aldring kan også spare samfunnet for penger og medisinering. I episoden vil du blant annet høre og lære om:hva kronologisk og biologisk alder erhva epigenetiske klokker målerhva epigenetisk og immunologisk epigenetisk alder erhva Telomer alder erforskjellen på gener og epigenetikkhvordan mat og fasterutinene gjorde henne yngrehvilken mat Hanne spiste og hva hun sluttet medalkohol, sukker og traumerHva slags trening hun gjordehvordan dyr og natur kan redusere stress og være foryngendesøvn, hvile og aldringhvordan Hanne føler seg nå etter hun er blitt yngrehva skjedde med vekten, og hvorfor genet Pon 3 kan hindre vekttapHannes nivå ligger på samme nivå som milliardæren Bryan Johnsonhvordan et sosialt nettverk påvirker aldringom rødt kjøtt med aminosyrene fremskynder aldringtilskuddene hun tok og hvordan de virker (NMN - resveratrol og metformin) + rapamycin11 anti-aldersbrytere (AMPK - autofagi - zombieceller - glykering (AGE)- IGF 1 -inflammasjon - mTOR -oksidering - sirtuiner - telomerer)nye prøver og veien viderejobben i "Forskerfabrikken" der hun inspirere barn og unge med motivasjon som også bidrar til bedre helseLink til Dunedin Pace her: https://www.epivity.noBoken "Yngre": https://kagge.no/produkt/sakprosa/dokumentar/yngre/Hanne S. Finstad finner du her: @5aryngre FLERE EPISODER:Antialdring:196. ANTIALDRING: biologisk alder, telomerene, sykdom, håp og mortalitetBiohacking Girls - Din podcast for optimal helse · 22 January 2024Spermidine:165. SPERMIDINE: med Leslie Kenny (English)Biohacking Girls - Din podcast for optimal helse · 14 September 2023Longevity:190. LONGEVITY: med Dr.Jason Sonners (re-run)Biohacking Girls - Din podcast for optimal helse · 28 December 2023

longevity omega hva hannes pon gener hanne metformin david sinclair mtor nmn ampk yngre steve horvath jason sonners

Tony Wyss-Coray: The Science of Aging

entrepreneur advice dna fish fda richardson purdue university intriguing composed fountain of youth weldon your dna steve horvath

Play Episode Listen Later Dec 26, 2023 32:03

The science to advance our understanding of the aging process—and to potentially slow it down—has made important strides. One of the leading scientists responsible for this work is Professor Tony Wyss-Coray, whose work has particularly focused on brain aging but has implications for all organs. I believe his December 2023 Nature paper on blood proteins that can track aging for 11 of our organs is one of the most important aging reports yet.Here is the audio and transcript of our conversation, recorded 20 December 2023, with a few relevant external links.This is the last Ground Truths post for 2023 and I hope you'll find it informative. I look forward to sharing many more exciting, cutting-edge biomedical advances with you in 2024!00:10.38Eric TopolHello this is Eric Topol and for this edition of Ground Truths. I'm so delighted to have with me Professor Tony Wyss-Coray of Stanford, a Distinguished Professor at Stanford and who directs the Knight Initiative for Brain Resilience. So welcome Tony.00:30.19Tony Wyss-CorayThank you, thank you for having me, Eric.00:32.84Eric TopolWell, I've been following your career and your work for decades I have to say and what you just published a couple weeks ago in Nature. The cover paper about internal organ clocks. It blew me away. I mean it's a built on a foundation of extraordinary work. I thought we could start with that because to me that's really a breakthrough in that when we think of aging and how to gauge a person aging with things like the Horvath clock of methylation markers or telomeres or —not at all specific to any part of the body, just overall, l but you published an extraordinary work about plasma proteins for 11 organs that predicted the outcomes things like heart failure and Alzheimer's so maybe you could tell us about this. Seems to be a big deal to me.01:28.41Tony Wyss-CorayThank you so much I'm honored. Really, you know I think if you work on this stuff, especially for several years it feels sort of obvious to do it? But I think you know it is in a way. It is. Pretty simple. So what we argued is that the thousands of proteins that you know are present in our blood. They must originate from somewhere now a lot of proteins are you know, produced by cells throughout the body. But some proteins are very specifically produced. For example, only in the brain or only in the liver or only in the heart because they have specialized functions and we have you know being taking advantage of that in clinical medicine where you measure. Often you know one of these proteins to sort of diagnose pathology in a tissue, but we took this It's just a level further and said, well, let's just find out of thousands of proteins that we can measure assign them to specific organs and tissues. And then see whether they change with age and many of them turn out to change. We found you know about 1500 proteins or so in the study that we did although that number can grow dramatically if we you know keep.03:01.11Tony Wyss-CorayImproving our technologies or techniques to measure them and many of them come from the brain or from other tissues and because they change with age. They tell us something about the aging of that organ. And as others have shown in the field including Steve Horvath is that that prediction of the age if it doesn't really match exactly your actual age contains information about the state the physiological state or the risk to develop. Organ-specific disease.03:37.75Eric TopolRight. And you found that about 1 in 5 people had evidence of accelerated aging of 1 organ which of course is really starting to nail down ability to detect aging you know to localize it and um. What strikes me Tony is that now because we're seeing at the cusp of advancing in the science of aging a field that you have done so much to propel forward and one of the issues has been well, how are we going to prove it. We can't wait for 20 years to show that. Whatever intervention led to promotion of healthy aging. But when you have a marker like this of organ specificity, it seems like the chances of being able to show that intervention makes a difference is enhanced would you say so?04:29.28Tony Wyss-CorayYeah, absolutely I think that's one of the most exciting aspects of this that we can now start looking at interventions whether they are you know a specific intervention that tries to target the aging process, or you know just that. Let's say a cholesterol lowering drug or blood pressure lowering drug does that have a beneficial effect on the heart. For example, on the kidney or you can also start thinking of lifestyle interventions where they actually have an effect right? If you started exercising you collect your blood before and then a year after you have an exercise regimen does that actually change the age that we can measure with these different clocks.05:22.55Eric TopolRight? Well I mean it's really a striking advance and by a marker of aging so that gets me to your other work. You've done well over 10 years which is that you could identify that given young blood. First of course in mice and then later verified in people could improve cognitive function in older whether it's experimental models or in people. So what are your thoughts about that is that if that's something you've been ruminating on for many years and I'm sure there are places around the world that are trying to do this sort of thing. What do you think of that potential?06:11.40Tony Wyss-CorayYeah, so there really this recent observation or study really came out of you know that finding that young blood can change the age of different organs and you know we. We were not the first to show this. We showed it for the brain but Tom Rando who studied muscle stem cell aging showed this you know a few years earlier in the muscle and we worked with Tom to explore this for the brain, but it shows sort of that this you know the composition of the blood. It is really not just reflecting the age of organs and tissues. But it actually also affects them. It directs them in a way and so you can speculate that you know if you had an organ that shows accelerated aging. Because some of the factors end up in the blood. They might actually induce aging in other tissues and so promote the aging process and people in the field have also shown that this is true for specific cells. We call them senescence cells. So these are a specific type of cell that seem to somehow stop dividing and assume the state that releases inflammatory factors these cells too. They seem to almost infect the neighborhood where they live in with an age promoting sort of.07:41.95Tony Wyss-CorayThe secretome , as we call it, so they release factors that seem to promote aging locally but potentially across the organism and interfering in that could potentially have rejuvenating effects and so that brings us back to this observation that.08:01.23Tony Wyss-CorayYoung blood could potentially rejuvenate organs We know old blood can accelerate it at least in mice. So could we neutralize the age promoting factors in people and could we deliver sort of the rejuvenating factors. Now what's been frustrating for me is that it has been incredibly challenging to identify the key factors.08:33.30Tony Wyss-CorayI think we became to realize as a field that there is not 1 factor. There's not 1 magic factor that will keep us young or keep our organs young but rather different cells and different organs in our body seem to respond in different ways actually to this young blood. Can show this with molecular tools. We can show that every cell actually responds. So if you take a mouse an old mouse and you give it young blood every cell in that mouse shows a transcription of the response to the young blood.09:10.80Tony Wyss-CoraySome of them may regenerate mitochondria and others activate other pathways. We see that stem cells respond particularly well the stem cells of the Immune system hematopoietic stem cells um while other cells show less of a response. And that to me suggests that they respond to different factors in the young blood and that you know they have very specific um receptors Probably that recognize some of these beneficial factors and then respond in a specific way. So that's what we need to.09:33.16Eric TopolRight.09:48.63Tony Wyss-CorayFigure out I think as a field to translate this really to the clinic is what are the key factors and will it be possible to make a cocktail that sort of mimics Nature's you know elixir10:06.13Tony Wyss-CorayI Said this before it's almost like the fountain of youth is within us, but it just dries out as we get older and if we could figure out what are the key factors that that make up this fountain. We could potentially you know either, as a treatment, deliver it again or reactivate that found and so that the body produces these factors again.10:34.73Eric TopolWell, you know that's something that years ago I was very skeptical about and because of your work and others in the field. I've come a long way thinking that we're on the cusp of really identifying ways to truly promote healthy aging. And so this is a really you know extraordinary time in our lives I wonder you of course mentioned 2 critical paths that have been identified the senescent cells—removing them— or the infusion of young plasma. Would you say it's too simplistic to reduce this to decreasing inflammation or is that really the theme here, or is it much more involved than that.11:28.48Tony Wyss-CorayI think inflammation has a big part in that but you know inflammation is such a broad term and such an ill-defined term that um yeah I can say yes to your question.11:44.45Tony Wyss-CorayAnd I'm probably not going to be wrong. Um, but if we really want to know which molecular pathways in the inflammatory cascade are key to this detrimental process that seems to accelerate aging. Um, I think we have to work a bit harder and really so define what we're saying you can't just have thousands of proteins or genes that have something to do with immune and inflammatory process. It's called inflammation.12:21.25Tony Wyss-CorayThen? yes, everything is inflammation. But I think we have to be more precise. Otherwise, you can't really target it. Having said that you know if we use sort of the conventional tools that biologists use these pathway analyses if we give young plasma. To an aged organism then the top pathway or one of the top pathways in almost every cell is inflammation, suggesting that we reduce the inflammatory process. But again, it's in a very broad sense and I want to know more? what? what. What we're finding? In fact, you know 1 of our first observations when Saul Villeda was in my lab and the first parabiosis study to look at factors that might promote brain aging. Yeah, he identified beta-two-microglobulin and eotaxin is a chemokine that is involved in a lot of you know, sort of inflammatory responses and has actually recently more recently again been implicated by Michelle Monje here at Stanford. To be a mediator of you know the chemobrain as people call it at least in animal models and we showed that it's part of the age plasma that causes sort of, an acute impairment of cognitive function in mice.13:46.90Tony Wyss-CoraySo that would be an example of a bad factor and that is part of an inflammatory cascade but we want to know what exactly is it. Um, we tried a small molecule that targets the receptor One of the main receptors for this chemokine. But unfortunately that compound had some side effects on the liver and we've never got to really test. The question is this you know potentially Important. It's one of the challenges you know for drug development.14:20.82Tony Wyss-CorayYou often don't get to test your questions because the drug has side effects that don't allow you to do that.14:26.14Eric TopolWell, speaking of drugs out there this past week there was a very provocative paper from Daniel Drucker University of Toronto on the GLP-1 effects on brain inflammation and interestingly with. You may have seen it but with mice that were either knocked out of GLP-1 for their blood cells or their brain. It was clear that inflammation reduction with these drugs and they tested several different GLP-1s, all worked through the brain. Which is really fascinating and I wonder of course these drugs are now you know they craze for anti-obesity. But do you see something like that this this peptide agonist as a potential way to achieve some of the effects that you've been. Working on for a long time.15:25.40Tony Wyss-CorayYeah I think this is extremely fascinating. Um I mean these drugs. Um, we don't understand them exactly what they're doing as you know for many drugs.15:31.24Eric TopolRight? right? right.15:37.13Tony Wyss-CorayBut it's really amazing the effects that you see and you know I'm very hopeful. There's a large phase 3 trial in Alzheimer's disease ongoing. The phase 2 looked very positive very promising so you know it. It is really possible that.15:49.65Eric TopolUm, yeah.15:56.49Tony Wyss-CorayUm, that there that there are key pathways that are responsible for you know cognitive decline and a cognitive impairment and inflammation is ah is a key aspect of that again inflammation in a broad term. We need to define it but it could be that it goes through. You know, um through these glib receptors and um and that ah might be ah, some regulator of a broader process but you know we see for example with aging just with normal aging you get um activation of.16:35.96Tony Wyss-CorayInflammatory pathways in the brain vasculature and young plasma reduces these changes acutely and maybe this is you know all part just dampening that inflammation gives you some additional brain power, if you will, for lack of a better word. That much of you know at least the early stages of cognitive impairment that lead to Alzheimer's disease.17:12.10Tony Wyss-CorayRelatively transient and are more like a fog like we say you know the chemofog the chemobrain or brain fog but that you know with Covid that you also commented very prominently that. That suggests that it's not a structural damage early on but that that it might be some soluble factors that would go a long way if you could just suppress them.17:35.83Eric TopolRight? right? Well, It's really fascinating to see and I'm glad you mentioned the Phase 3 trial in Alzheimer's for this one class because I think that's expected in 2025 to read out and that'll be really important. I Wanted to ask you because now there's many shots on goal to change the natural arc of aging at all these companies like Altos and Unity and Calico and I mean there's so many of them I can't even keep track. Um, they're all taking different strategies. I Have to think because they need to have their own intellectual property. What do you see as the alluring ways that we're going to be able to modulate this process.18:25.65Tony Wyss-CorayThat's a very tough question. I think it's hard to predict I would say you know like always in in biology. First of all, as you know what we discussed earlier. It could be that. Ah, drug that tries to test the pathway like you know one that Unity tried has side effects and you know you can't actually test your hypothesis. But I think one of the key sort of aspects of the aging process is really that it's both global across the organism but it's also very localized and so it's possible that targeting the aging process will first show benefits. In individual tissues if we target you know the aging process in 1 particular tissue that might show the first benefits. But then again it could be that if there is sort of a key inflammatory driver that to some extent responsible for overall aging of the organism and you manage to target that and slow it or block it. You may have an organism-wide effect. But I think we have to be we have to be realistic that.19:51.88Eric TopolUm, yeah.19:56.99Tony Wyss-CorayYou know this is going to be an incremental process I think.20:00.92Eric TopolSo is there anything that you've seen that has grabbed you as having tremendous potential that is new or is it really you know the things that I've already been percolating that that we know about.20:17.41Tony Wyss-CorayYeah I mean just to the GLP-1 study I've been actually ah a bit involved in that. Um I find this really fascinating. Um, yeah.20:23.98Eric TopolUm, yeah, yeah, well that I spoke.20:29.81Tony Wyss-CorayI Mean not in that study that got published but in sort of more on the cognitive side.20:33.78Eric TopolWhere I right? I Thought that was especially welcome news because the drugs we have now for Alzheimer's seem to have you know some pretty serious side effects and somewhat low efficacy relative to the to the risk rssessment. So, this would be a drug that we know now as people have taken for years that I do want to get back to you with you on the durability. So if you give young blood to an old person who has let's say mild Cognitive impairment. Will you see a durable impact or is it just a very short lived one.21:13.76Tony Wyss-CorayI think some of the effects will be durable and I'm saying that because of an experiment that James White and Vadim Gladyshev did they use this parabiosis model where you suture a young and an old mouse together.21:32.10Tony Wyss-CorayLeft these mice together for two months I mean or three months and then they separated them and let them live and looked at how long does an old mouse live that was paired with a young mouse for a few months. Compared to an old mouse that was paired with another old mouse and they saw that there is clear extension of lifespan if the mouse was exposed to young blood. Now this is in the context of you know, 2 major surgeries first suturing them together and then taking them apart. But I always note that when I present this experiment but I also say at the same time that this is the problem that a lot of older people have right when they have a surgery they don't recover from it as well. And it's often the beginning of cognitive decline if you ask families. You know when did it start? Oh they had heart surgery or they fell and had you know had a hip surgery or something like that or a major infection. That is often the trigger where it's almost like you know the organism is hanging in there and it's still functioning and then there's an injury and it collapses. Um and so you know what's remarkable with the rejuvenating intervention with.23:02.11Tony Wyss-CorayWith parabiosis is that it seems to overcome this to a very significant event and they also showed you know with many other tools including with the Horvath clock that tissues are actually getting younger through this process.23:20.51Tony Wyss-CorayWe have also found that you know stem cells are rejuvenated for a long period of time if you treat with young plasma infusions in mice and so I'm hopeful that some of the effects are going to be long-lasting. But. You know, practically you would probably still treat people on a regular basis like we do with all drugs. But maybe you would do an infusion every 3 months or every six months and you know we're still trying with um.23:52.20Eric TopolPray.23:57.00Tony Wyss-CorayA company that I so that that I started Alkahest to you know, convince people to do a Phase 3clinical trial and see how far we can push this.24:09.38Eric TopolWell, it'd be really interesting to see you get that done then going back to the senescent cells which is another leading prospect. It seems to be more difficult to get these cells out of the body. We know they're bad actors but it isn't like we can you know. Ah, very selectively remove them. But what are your thoughts about that approach.24:35.76Tony Wyss-CorayI mean I'm always really puzzled and amazed at the effects that people show with you know, senescence cell removal in in animal models.24:46.20Eric TopolRight.24:49.57Tony Wyss-CorayThere is something really almost magical there that you remove these few cells and you know the body is doing much better. Um, So I think you know we should. We should keep trying very hard to translate this to humans. But it's possible that again there are they're very likely different types of senescence cells and different tissues I mean in the brain you know there are no rapidly dividing cells. So. It's not the classic. You know arrest of cell cycle.25:24.11Tony Wyss-CorayBut it's probably more like an astrocyte type of cell that might mimic a senescent state. But I think it will be. It will be. You know very much organ specific. And may require very specific interactions or drug targets.25:44.83Eric TopolAh, right? right? Well then gets us back to kind of where we started before you're what I consider a landmark paper. Um, it would be difficult. To be able to go to a regulatory body like the FDA and say we show that this is affecting the aging process and we show in you know 3 organs 5 organs whatever the 11 organs you could track we are reversing the aging process. I mean you have that now as an extraordinary finding. Do you think that will help accelerate the field by having not having to have a whole-body aging story with an epigenetic clock but rather you know much more pinpointing. Organs that can be helped that they can be promoting healthy aging. It seems to me this is where not only advancing the theories of how to do it but the proof that you have done it. It seems like this is what. You know why I consider such an extraordinary finding.26:59.90Tony Wyss-CorayI totally agree with you but I'm a bit biased I think you know this is what we need I mean this was always a criticism to me and you know we're very good friends with Steve Horvath andMorgan Levine who you know came up with these remarkable aging clocks. But my my question was always how can you get information about the whole body aging. By looking at changes in blood cells or cheek cells. Um, that cannot contain information about how your pancreas ages or your heart ages at the high resolution. It will correlate. Admittedly, but it will not give you tissue-specific information most likely. So you know going more directly at molecules that are derived from cells across the organism is of course going to be much more informative. Um, we've just started to do this. You know it's a concept. Um, we are super excited about you know, looking now at large datasets like the UK biobank. We just get access. Through a collaboration to 50,000 individuals where we have 1500 protein measurements with a different proteomic platform and it seems most of the findings replicate.28:47.45Tony Wyss-CorayYou know, very strong risk for people who have older brains to develop the men in the future. Um, and you know we still see these extreme organ ages that I find very puzzling.29:00.89Eric TopolYeah, it's really striking and the fact that you could replicate the best biomarker for the brain.—Plasma pTau-181— through these proteins is exceptional. How much did machine learning AI help you? And deciphering this large data set of proteins was it really critical or was it just a small part.29:26.23Tony Wyss-CorayAh, oh it's certainly I mean this is I think you know the terminology are not so clear and I have to admit you know I'm not a computer scientist by any stretch. But I think this is classic machine learning using statistical elements of learning as you know. We use linear modeling. Um, but I think it will become more sophisticated. Um, and I think ai will help us to bring this. To a much higher level by but by basically learning from the relationship between proteins directly and then compare that in healthy people versus control similar to what Christina Theodoris recently did for gene expression. Ah, the single cell level. Um I think we will see that and we're trying this and I'm sure others are trying this too at the protein level but the current the current study uses really more traditional machine learning models. Um that you know are sophisticated but it's not.30:42.33Tony Wyss-CorayYou know I'm not sure we call this artificial intelligence.30:44.85Eric TopolSure. Well I think as you say it can build on that and you know putting in more models to more data sets and where the future goes. You'll get even more precision output as you know know, Tony.30:51.58Tony Wyss-CorayUm, yeah. Absolutely.31:02.44Eric TopolThis This has been a real joy. I have to say congratulations to you and your team for such exceptional work. This has been a multi-decade run, you know one layer of after another of building on the science of aging particularly the brain aging I've learned so much from you and your team.31:07.28Tony Wyss-CorayThank you.31:21.81Eric TopolI have to say the paper you just published you and your group got me excited I mean I really thought of all the things I've seen on aging this was the one that really opens it up for you know all the other possible ways to claim you're making a difference. You've got a metric that's emerging and so kudos to you and I know this is got to be of course that you probably just say oh, it's just 1 more thing we've been doing but I am so duly impressed.31:52.30Tony Wyss-CorayThank you so much. Thank you for the nice word means a lot.31:58.94Eric TopolWell keep up the great stuff because we're all, we're all depending on you so that we can have a better arc of our healthy aging process and we'll keep in touch. If you can just stay on it!32:10.30Tony Wyss-CorayThank you! Thanks so much.Thank you for listening, reading, subscribing to and sharing Ground Truths!Happy new year,Eric Get full access to Ground Truths at erictopol.substack.com/subscribe

Tom Weldon - A Fountain of Youth

Angel Invest Boston

Play Episode Listen Later Dec 20, 2023 45:47

Aging Fit Substack: Learn More Repeat life science entrepreneur Tom Weldon is now taking on aging. He is commercializing a compound to extend health span developed at a prominent institution. Composed of substances generally considered as safe by the FDA, the formula has shown impressive results in mice and, to date, in one human, Tom himself. Intriguing chat with a dynamic founder. Sponsored by Purdue University entrepreneurship and Peter Fasse, patent attorney at Fish and Richardson. Highlights: Sal Daher Introduces Tom Weldon What Problem Rejuvant Addresses "... Then the first time the combination is not additive, take it out. That's a process that would probably take a year or two, but it ensures that you'll have an optimal result. Or, you can buy Rejuvant, because we did all that work already..." "... if you decide that you'd like to try Rejuvant and you go on subscription, we give you a free DNA methylation test at time zero and then we give you another one after six months, which is included in the cost ... They're different and they have different algorithms. All of them except two that I'm aware of, one of which is what we provide, requires your current chronologic age as an input..." "... It was actually discovered by Steve Horvath and he developed the first biologic clock ... Your DNA is damaged every second that you're alive. Prior to puberty, your body does an exceptional job of repairing all of that. However, after that, it starts to decline..." "... Is there any evidence that repair is actually at work? How do we know that it's not just removing the methyl molecule from the DNA, and you have damaged the DNA that's just not methylated?..." "... How long have you been on Rejuvant?..." How Tom Became an Entrepreneur "... This company had this trajectory and now it's just gone Chapter 7 recently. That is the tough side of these life science technology companies because the technology moves so fast..." "... very difficult space. What I have seen in the medical device space, these 510k pathway devices where there is an existing predicate device, and then you can design something which is, no worse and perhaps much better than the predicate device..." Advice to the Audience Topics: biotech, discovering entrepreneurship, founding story

Longevity Summit Dublin: four new mini-interviews

London Futurists

Play Episode Listen Later Sep 6, 2023 44:28

This episode, like the previous one, consists of a number of short interviews recorded at the Longevity Summit Dublin between 17th and 20th August, featuring a variety of different speakers from the Summit.In this episode, we'll hear first from Matt Kaeberlein, the CEO of a company called Optispan, following a 20 year period at the University of Washington studying the biological mechanisms of aging and potential interventions to improve healthspan. Among other topics, Matt talks to us about the Dog Aging Project, the Million-Molecule Project, and whether longevity science is at the beginning of the end or the end of the beginning.Our second speaker is João Pedro de Magalhães who is the Chair of Molecular Biogerontology at the University of Birmingham, where he leads the genomics of aging and rejuvenation lab. João Pedro talks to us about the motivation to study and manipulate the processes of aging, and his work to improve the low-temperature cryopreservation of human organs. You may be surprised at how many deaths are caused by the present lack of such cryopreservation methods.Third is Steve Horvath, who has just retired from his position as a professor at the University of California, Los Angeles, and is now a Principal Investigator at Altos Labs in Cambridge. Steve is known for developing biomarkers of aging known as epigenetic clocks. He describes three generations of these clocks, implications of mammalian species with surprisingly long lifespans, and possible breakthroughs involving treatments such as senolytics, partial epigenetic reprogramming, and altering metabolic pathways.The episode rounds off with an interview with Tom Lawry, Managing Director for Second Century Tech, who refers to himself as a recovering Microsoft executive. We discuss his recent bestselling book "Hacking Healthcare", what's actually happening with the application of Artificial Intelligence to healthcare (automation and augmentation), the pace of change regarding generative AI, and whether radiologists ought to fear losing their jobs any time soon to deep learning systems.Selected follow-ups:https://longevitysummitdublin.com/speakers/https://optispanlife.com/https://orabiomedical.com/https://rejuvenomicslab.com/https://oxfordcryotech.com/https://horvath.genetics.ucla.edu/https://altoslabs.com/team/principal-investigators-san-diego/steven-horvath/https://www.tomlawry.com/https://www.taylorfrancis.com/books/mono/10.4324/9781003286103/hacking-healthcare-tom-lawryMusic: Spike Protein, by Koi Discovery, available under CC0 1.0 Public Domain Declaration

Predict, Measure and Take Action on Your Biological Clock l How to Slow Down the Aging Process with Hannah Went of TruDiagnostic Epigenetic Testing

Biohacker Babes Podcast

Play Episode Listen Later Aug 21, 2023 69:10

We're thrilled to bring you this conversation with Hannah Went all about aging, biological clocks and epigenetics! She brings incredible insight into the options for testing your biological age, thoughts on telomere testing, the biggest drivers of aging, and what we can learn from the Dunedin pace of aging test. Tune in if you're interested in extending your healthspan! Hannah Went has a lifelong passion for longevity and breakthrough, disruptive technologies that drive radical improvement to the human condition. She attended the University of Kentucky and graduated with a degree in Biology. During that time, she had multiple research internships studying cell signaling and cell biology. After graduation, she worked for the International Peptide Society as their Director of Research and Content. Through work in the integrative medicine industry, Hannah saw an opportunity for methylation based age diagnostics and started TruDiagnostics in 2020. TruDiagnostic is a company focusing on methylation array-based diagnostics for life extension and preventive healthcare serving functional medicine providers. TruDiagnostic has a commitment to research with over 30 approved clinical trials investigating the epigenetic methylation changes of longevity and health interventions. Since TruDiagnostic's inception, they have created one of the largest private epigenetic health databases in the world with over 15,000 patients tested to date. Hannah has since created Everything Epigenetics where she shares insights on how DNA regulation has an impact on your health.SHOW NOTES:0:51 Welcome to the show!1:45 Pop Quiz of the Day3:48 Non-Alcoholic Alternatives4:33 Kava & Kratom4:59 The emotional benefits of alcohol7:18 STUDY: Alcohol & Amygdala8:04 Hannah Went's Bio9:38 Welcome Hannah!10:38 How do Epigenetics affect Healthspan15:30 Steve Horvath & Biological Age17:24 Dr. Morgan Levine & 2nd Generation Clocks18:58 Is Telomere testing still valuable?22:04 Senolytics for Senescent Cells25:07 NEW STUDY: Predicting Age in Women28:30 Measuring Spermidine levels28:25 Epigenetic vs Blood/Serum Testing30:33 Spermidine, NMN, NR & Rapamycin33:55 Caloric Restriction & Dunedin PACE35:20 *Magnesium Breakthrough*37:30 The nuances of fasting/feeding39:28 Stress, thoughts & mindset on Aging40:20 3rd Generation Clock: Dunedin PACE44:35 The “Rejuvenation Olympics”45:50 Pregnancy, Illness & Surgeries47:01 How else can we slow the aging process?48:28 Effect of green space on aging50:04 How detrimental is alcohol?55:24 Sleep deprivation & age57:24 Transgenerational Epigenetic Inheritance59:52 Are we all doomed?1:02:35 How can we be more pro-active?1:03:22 Lab Grown Meat1:07:21 Her final piece of advice1:07:55 Where to find more of her!1:08:19 Thanks for tuning in!RESOURCES:Website: Everything EpigeneticsWebsite: TruDiagnosticIG: Everything Epigenetics Email: hannah@everythingepigenetics.comMagnesium Breakthrough - code: BIOHACKERBABES10Support this podcast at — https://redcircle.com/biohacker-babes-podcast/donationsAdvertising Inquiries: https://redcircle.com/brands

Supply Chain Cyber Risk Management with Steve Horvath

Innovation in Compliance with Tom Fox

Play Episode Listen Later Jun 27, 2023 25:52

Imagine a world where your organization is constantly at the risk of a cyber-attack, yet no solution seems fully secure. In this episode of Innovation In Compliance, host Tom Fox and guest Steve Horvath explore the complex landscape of supply chain cyber risk management. They explore the high-profile breaches of Home Depot and Target, as well as the critical importance of frameworks like the NIST Cybersecurity Framework. Steve delves into the challenges faced by organizations, the need for effective risk management strategies, and the evolving landscape of cybersecurity in public and private sectors. Steve Horvath is a seasoned cybersecurity expert who has spent nearly two decades at Telos, a prominent cybersecurity firm focused on protecting government and industry networks. Since joining Telos in 2006, Steve has been instrumental in developing cybersecurity strategies and services for various elements of the U.S. federal government, including the intelligence community and the Department of Defense. Today, he leads the way in driving compliance and risk management initiatives with a focus on innovative solutions like Xacta. You'll hear Tom and Steve discuss: Telos' platform, Xacta, began as a web-based application focused on facilitating the rigorous compliance activities of federal standards, and has since evolved into a sophisticated platform for managing cybersecurity risks. Cybersecurity risk is unique and highly challenging, and unlike other forms of risk, it doesn't lend itself to transference. Insurance policies won't save an organization from a devastating cyber attack. Many organizations, particularly public ones, need to shift their mentality from accepting some level of risk to striving for robust cybersecurity operations that minimize risk as much as possible. Education at the board level about the threats and implications of cybersecurity is a crucial yet often overlooked factor. The conversation around this is gaining traction, with initiatives such as the SEC's rule about having a board member with a cybersecurity background. The Home Depot and Target hacks brought widespread attention to cybersecurity risks, highlighting the need for organizations to be proactive in managing threats and vulnerabilities. The NIST Cybersecurity Framework provides a practical and easily understood framework for organizations to assess and improve their cybersecurity posture. It enables effective communication between security operators and the board, fostering a common language and understanding. Supply chain cybersecurity is a critical concern, particularly for software and IT hardware sourcing. Having a software bill of materials and understanding the ingredients within the software helps organizations assess their exposure and potential vulnerabilities. Network attack services refer to understanding an organization's attack surface and identifying potential points of ingress or exfiltration of data. Mitigating risks, such as phishing attacks, requires robust security education programs for users. Creating an actionable cyber intelligence strategy involves having the right stakeholders and roles within the organization, selecting a suitable framework (such as NIST or ISO standards), and ensuring continuous validation and improvement of cybersecurity measures. KEY QUOTE: “You really have to do exceptional cybersecurity operations, and the best way to influence cybersecurity operations… is having some teeth behind a set of conditions and compliance requirements that guide you toward making the best decision…" - Steve Horvath Resources: Steve Horvath on LinkedIn | Twitter Telos | Telos Corporation on Twitter

education network defense target insurance sec cybersecurity supply supply chains home depot iso mitigating nist telos tom fox cyber risk management nist cybersecurity framework steve horvath

DNAmFitAge: Biological Age Indicator Incorporating Physical Fitness

power entrepreneur discovering scientists ucla genetics epigenetics ryan smith dhea steve horvath

Play Episode Listen Later Jun 7, 2023 3:50

A new research paper was published in Aging (Aging-US) Volume 15, Issue 10, entitled, “DNAmFitAge: biological age indicator incorporating physical fitness.” Physical fitness is a well-known correlate of health and the aging process and DNA methylation (DNAm) data can capture aging via epigenetic clocks. However, current epigenetic clocks did not yet use measures of mobility, strength, lung, or endurance fitness in their construction. In this new study, researchers develop blood-based DNAm biomarkers for fitness parameters including gait speed (walking speed), maximum handgrip strength, forced expiratory volume in one second (FEV1), and maximal oxygen uptake (VO2max) which have modest correlation with fitness parameters in five large-scale validation datasets (average r between 0.16–0.48). “These parameters were chosen because handgrip strength and VO2max provide insight into the two main categories of fitness: strength and endurance [23], and gait speed and FEV1 provide insight into fitness-related organ function: mobility and lung function [8, 24].” The researchers then used these DNAm fitness parameter biomarkers with DNAmGrimAge, a DNAm mortality risk estimate, to construct DNAmFitAge, a new biological age indicator that incorporates physical fitness. DNAmFitAge was associated with low-intermediate physical activity levels across validation datasets (p = 6.4E-13), and younger/fitter DNAmFitAge corresponds to stronger DNAm fitness parameters in both males and females. DNAmFitAge was lower (p = 0.046) and DNAmVO2max is higher (p = 0.023) in male body builders compared to controls. Physically fit people had a younger DNAmFitAge and experienced better age-related outcomes: lower mortality risk (p = 7.2E-51), coronary heart disease risk (p = 2.6E-8), and increased disease-free status (p = 1.1E-7). These new DNAm biomarkers provide researchers a new method to incorporate physical fitness into epigenetic clocks. “Our newly constructed DNAm biomarkers and DNAmFitAge provide researchers and physicians a new method to incorporate physical fitness into epigenetic clocks and emphasizes the effect lifestyle has on the aging methylome.” DOI - https://doi.org/10.18632/aging.204538 Corresponding authors - Kristen M. McGreevy - kristenmae@ucla.edu, Zsolt Radak - radak.zsolt@tf.hu, and Steve Horvath - shorvath@mednet.ucla.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204538 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetics, physical fitness, biological age, DNA methylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

covid-19 dna soundcloud pinterest physically incorporating biological doi indicator physical fitness vo2max 2e 4e 6e 1e fev1 steve horvath altmetric

Human Skeletal Muscle Epigenetic Clock Explained with Dr. Sarah Voisin

Everything Epigenetics

Play Episode Listen Later Apr 26, 2023 35:55 Transcription Available

Maintaining muscle mass is crucial for healthy aging, as it is closely linked to overall physical function and quality of life. As we age, our bodies naturally experience a decline in muscle mass and strength, known as sarcopenia. This loss of muscle mass can lead to a range of negative health outcomes, including decreased mobility, increased risk of falls and fractures, and decreased metabolic rate. Additionally, loss of muscle mass can contribute to chronic conditions such as obesity, diabetes, and cardiovascular disease. By developing an epigenetic clock for skeletal muscle, Dr. Voisin and her colleagues have identified specific methylation patterns that are associated with muscle aging. This research not only sheds light on the biological mechanisms behind sarcopenia, but may also provide new targets for interventions aimed at preserving muscle mass and function in older adults.In this week's Everything Epigenetics podcast, Dr. Sarah Voisin and I focus on her 2020 paper which describes her development of a human muscle-specific epigenetic clock that predicts age with better accuracy than the pan-tissue clock. Yes - you heard that right… better accuracy than Dr. Steve Horvath's 2013 clock. Dr. Voisin and I also chat about the importance of skeletal muscle and how this relates to epigenetics and aging, the power of machine learning, and how identifying which methylation positions change as we age may give us insight into the underlying reason as to WHY we age rather than just HOW. She is now focused on creating an atas of epigenetics for all human tissues at the cellular level by combining 75,000 DNA methylation profiles across 18 tissues. In this episode of Everything Epigenetics, you'll learn about: How Dr. Voisin got her start in statistics and biology The importance of skeletal muscle tissue and how this relates to Epigenetics and AgingWhen to start exercising and moving your bodyThe importance of weight lifting How often we should be moving our body Why Dr. Voisin decided to develop this type of Epigenetic ClockThe limitations of the Horvath 2013 Clock as it relates to skeletal muscle The complications of data miningThe importance of collaboration and data sharing How Dr. Voisin created her muscle-specific Epigenetic Clock The power of machine learningHow the muscle clock outperforms Dr. Steve Horvath's 2013 pan-tissue ClockDr. Voisin's epigenetic wide association studies (EWAS) she performedDifferentiated methylated positions (DMPs) in this studyDifferentiated methylation regions (DMRs) in this studyThe utility/application of the skeletal muscle Epigenetic ClockDr. Voisin's next big project (I'm so excited about her next project!!!) MEAT (muscle epigenetic age test)Where to find Dr. Voisin:Email: sarah.voisin@vu.edu.au Twitter: https://www.vu.edu.au/research/sarah-voisinGitHub account:https://github.com/sarah-voisinSupport the showThank you for joining us at the Everything Epigenetics Podcast and remember you have control over your Epigenetics, so tune in next time to learn more about how.

dna maintaining meat clock epigenetics horvath epigenetic voisin bodythe skeletal muscle dmps steve horvath ewas

Discovering the Potential of Epigenetics with Entrepreneur Scientist Ryan Smith

The Power of Genetics

Play Episode Listen Later Feb 23, 2023 32:06

In this episode of the Power of Genetics podcast, Ryan Smith shares his journey as an entrepreneur and scientist in the fields of epigenetics and diagnostics. He discusses the importance of maintaining scientific integrity and finding something you're passionate about in order to truly succeed in any field. Ryan shares his insights on the potential of epigenetics in predicting a variety of outcomes related to age and chronic diseases. He highlights the importance of tracking outcomes and using data to prove the efficacy of treatments, which can be challenging in a field that is constantly evolving and subject to regulatory issues. Throughout the conversation, Ryan emphasizes the importance of finding a niche and staying focused on one's goals, no matter how difficult or unconventional they may seem. He shares his personal experience of successfully building a compounding pharmacy business before ultimately leaving to pursue his work in epigenetics and diagnostics. Topics discussed in this episode: Ryan Smith's journey as an entrepreneur scientist. The importance of maintaining scientific integrity and being passionate about your work. The potential of epigenetics in predicting a variety of outcomes. The need for larger and better data sets to create more accurate algorithms. The need for a focus on preventative medicine and managing age as a primary risk factor. The definition of epigenetics and how it differs from genetics. The ability to measure gene expression and how it impacts health. The significance of epigenetics in reading insights from lifestyle, diet, and nutrition. The challenges in measuring epigenetic data, including the need for cell type-specific and time point-specific data. The first ever interventional trial on epigenetic age marks, led by Steve Horvath and Greg Fay from UCLA. The Trim Trial and its aim to drive down the ages of patients using metformin, growth hormone, and DHEA.

DNA Methylation GrimAge Version 2

Play Episode Listen Later Dec 21, 2022 3:44

A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 23, entitled, “DNA methylation GrimAge version 2.” Researchers Ake T. Lu, Alexandra M. Binder, Joshua Zhang, Qi Yan, Alex P. Reiner, Simon R. Cox, Janie Corley, Sarah E. Harris, Pei-Lun Kuo, Ann Z. Moore, Stefania Bandinelli, James D. Stewart, Cuicui Wang, Elissa J. Hamlat, Elissa S. Epel, Joel D. Schwartz, Eric A. Whitsel, Adolfo Correa, Luigi Ferrucci, Riccardo E. Marioni, and Steve Horvath from the University of California Los Angeles, Altos Labs, University of Hawaii at Manoa, Fred Hutchinson Cancer Research Center, University of Edinburgh, National Institute on Aging, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Harvard T.H. Chan School of Public Health, University of California – San Francisco, and the University of Mississippi Medical Center previously described a DNA methylation (DNAm) based biomarker of human mortality risk DNAm GrimAge. In their current study, the researchers describe version 2 of GrimAge (trained on individuals aged between 40 and 92) which leverages two new DNAm based estimators of (log transformed) plasma proteins: high sensitivity C-reactive protein (logCRP) and hemoglobin A1C (logA1C). “To arrive at version 2 of GrimAge, we developed two additional DNAm based surrogates for plasma proteins that are widely used in the clinic (DNAm logCRP and DNAm logA1C).” The team evaluated GrimAge2 in 13,399 blood samples across nine study cohorts. After adjustment for age and sex, GrimAge2 outperforms GrimAge in predicting mortality across multiple racial/ethnic groups (meta P=3.6×10-167 versus P=2.6×10-144) and in terms of associations with age related conditions such as coronary heart disease, lung function measurement FEV1 (correlation= -0.31, P=1.1×10-136), computed tomography based measurements of fatty liver disease. The researchers presented evidence that GrimAge version 2 also applies to younger individuals and to saliva samples where it tracks markers of metabolic syndrome. DNAm logCRP is positively correlated with morbidity count (P=1.3×10-54). DNAm logA1C is highly associated with type 2 diabetes (P=5.8×10-155). DNAm PAI-1 outperforms the other age-adjusted DNAm biomarkers including GrimAge2 in correlating with triglyceride (cor=0.34, P=9.6×10-267) and visceral fat (cor=0.41, P=4.7×10-41). Overall, the team demonstrated that GrimAge version 2 is an attractive epigenetic biomarker of human mortality and morbidity risk. “GrimAge2 will not replace existing clinical biomarkers. Rather, GrimAge2 complements existing clinical biomarkers when evaluating an individual's aging rate.” DOI: https://doi.org/10.18632/aging.204434 Corresponding Author: Steve Horvath - shorvath@mednet.ucla.edu About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

The Gary Null Show - 11.22.22

The Gary Null Show

Play Episode Listen Later Nov 23, 2022 60:17

Videos: Heather Mac Donald On How The Delusion of Diversity Destroys Our Common Humanity(11:02) This intense AI anger is exactly what experts warned of, w Elon Musk. (15:50) The FTX corruption is even worse than we thought | Redacted with Clayton Morris (13:00) Almonds can help you cut calories University of South Australia, November 20, 2022 Weight loss is never an easy nut to crack, but a handful of almonds could keep extra kilos at bay according to new research from the University of South Australia. Examining how almonds can affect appetite, researchers found that a snack of 30-50 grams of almonds could help people cut back on the number of kilojoules they consume each day. Published in the European Journal of Nutrition, the study found that people who consumed almonds – as opposed to an energy-equivalent carbohydrate snack – lowered their energy intake by 300 kilojoules (most of which came from junk food) at the subsequent meal. “Our research examined the hormones that regulate appetite, and how nuts – specifically almonds – might contribute to appetite control. We found that people who ate almonds experienced changes in their appetite-regulating hormones, and that these may have contributed to reduced food intake (by 300kJ).” The study found that people who ate almonds had 47 per cent lower C-peptide responses (which can improve insulin sensitivity and reduce the risk of developing diabetes and cardiovascular disease); and higher levels of glucose-dependent insulinotropic polypeptide (18 per cent higher), glucagon (39 per cent higher), and pancreatic polypeptide responses (44 per cent higher). Glucagon sends satiety signals to the brain, while pancreatic polypeptide slows digestion which may reduce food intake, both encouraging weight loss. “Almonds are high in protein, fibre, and unsaturated fatty acids, which may contribute to their satiating properties and help explain why fewer kilojoules were consumed.” The findings of this study show that eating almonds produce small changes to people's energy intake, Dr Carter says this may have clinical effects in the long term. Probiotics help maintain a healthy microbiome when taken with antibiotics Texas Christian University, November 18 2022. A systematic review published in the Journal of Medical Microbiology helps answer the question concerning whether probiotics should be taken along with antibiotics to support gut health. Although probiotics decrease the adverse gastrointestinal effects caused by antibiotics, their ability to preserve intestinal microbial composition that is negatively impacted by antibiotic therapy is not well understood. “Like in a human community, we need people that have different professions because we don't all know how to do every single job,” she explained. “And so, the same happens with bacteria. We need lots of different gut bacteria that know how to do different things.” While it is well known that antibiotics destroy some beneficial intestinal microorganisms, some healthcare professionals have expressed a concern that administering probiotics to antibiotic-treated patients could further alter the established gut microbe balance. The review included 29 studies published during a 7-year period. The authors concluded that consuming probiotics with antibiotics can prevent or reduce some changes caused by antibiotics to the microbiome. “When participants take antibiotics, we see several consistent changes in some bacterial species,” Dr Marroquin observed. “But when treatment was combined with probiotics, the majority of those changes were less pronounced and some changes were completely prevented.” New study shows repeated stress accelerates aging of the eye University of California, Irvine, November 21, 2022 New research from the University of California, Irvine, suggests aging is an important component of retinal ganglion cell death in glaucoma, and that novel pathways can be targeted when designing new treatments for glaucoma patients. The study was published today in Aging Cell. Along with her colleagues, Dorota Skowronska‐Krawczyk, Ph.D., at the UCI School of Medicine, describes the transcriptional and epigenetic changes happening in aging retina. The team shows how stress, such as intraocular pressure (IOP) elevation in the eye, causes retinal tissue to undergo epigenetic and transcriptional changes similar to natural aging. And, how in young retinal tissue, repetitive stress induces features of accelerated aging including the accelerated epigenetic age. Aging is a universal process that affects all cells in an organism. In the eye, it is a major risk factor for a group of neuropathies called glaucoma. Because of the increase in aging populations worldwide, current estimates show that the number of people with glaucoma (aged 40-80) will increase to over 110 million in 2040. In humans, IOP has a circadian rhythm. In healthy individuals, it oscillates typically in the 12-21 mmHg range and tends to be highest in approximately two thirds of individuals during the nocturnal period. Due to IOP fluctuations, a single IOP measurement is often insufficient to characterize the real pathology and risk of disease progression in glaucoma patients. Long-term IOP fluctuation has been reported to be a strong predictor for glaucoma progression. This new study suggests that the cumulative impact of the fluctuations of IOP is directly responsible for the aging of the tissue. Researchers now have a new tool to estimate the impact of stress and treatment on the aging status of retinal tissue, which has made these new discoveries possible. In collaboration with the Clock Foundation and Steve Horvath, Ph.D., from Altos Labs, who pioneered the development of epigenetic clocks that can measure age based on methylation changes in the DNA of tissues, it was possible for researchers to show that repetitive, mild IOP elevation can accelerate epigenetic age of the tissues. What do people experience at the border between life and death? University of London & New York University, November 20, 2022 A new study on near-death experiences featured 567 men and women whose hearts stopped while hospitalized in the United States and the United Kingdom. Out of 28 survivors of cardiac arrest interviewed as part of the study, 11 recalled memories suggesting consciousness while undergoing CPR. Additional cardiac arrest survivors provided self-reports about what they experienced while their hearts stopped. Reports included perceiving separating from their bodies and meaningful examinations of their lives. Researchers discovered spikes of brain activity up to an hour into CPR. Dr. Parnia, who served as lead investigator of the study, explained that he and the other researchers undertook this research in an attempt to scientifically explore something that health professionals have discussed anecdotally for decades: The similar stories people revived by cardiopulmonary resuscitation (CPR) often tell about the time when their hearts stopped. “For decades now, millions of people who've gone through this have reported having lucid heightened consciousness, even though from the perspective of their doctors they were not conscious and they were in death,” Dr. Parnia told MNT. The study centered around 567 men and women who received CPR after their hearts stopped beating while at one of 25 participating hospitals in the United States and the United Kingdom. When health practitioners began CPR on a patient whose heart stopped, researchers rushed to the scene, bringing along a portable electroencephalogram, or EEG, to monitor electrical activity in different parts of the brain, and near-infrared spectroscopy (NIRS) to measure oxygen saturation of superficial brain cortex regions. Taking care not to get in the way of health practitioners performing CPR, researchers also clamped a tablet computer above the patient's head. The tablet was connected to Bluetooth headphones which were placed on the patient's ears. Of 567 subjects, 213 or about 38% experienced sustained return of spontaneous circulation, meaning their pulse was restored for 20 minutes or longer. Only 53, or fewer than 10% of the participants, lived to be discharged from the hospital. Of those 53, 25 were unable to be interviewed by researchers due to poor health. The remaining 28 participants were interviewed 2 to 4 weeks after cardiac arrest depending on their recovery. Of the 28 participants interviewed, 11 — or 39% — reported having memories during cardiac arrest. Two of the 28 participants could hear the medical staff working while receiving CPR. One participant recalled seeing the medical staff working and could feel someone rubbing his chest. Using the near-death scale, six participants had transcendent experiences. Three participants reported dream-like experiences, which included a singing fisherman. Six of the 28 participants interviewed remembered the experience of dying. These recollections included one person who heard a deceased grandmother telling her to return to her body. “We characterize the testimonies that people had and were able to identify that there is a unique recalled experience of death that is different to other experiences that people may have in the hospital or elsewhere,” Dr. Parnia said, “and that these are not hallucinations, they are not illusions, they are not delusions, they are real experiences that emerge when you die.” Fifty-three participants had interpretable EEG data. Researchers discovered spikes of brain activity, including so-called gamma, delta, theta, alpha, and beta waves emerging up to 60 minutes into CPR. Some of these brain waves normally occur when people are conscious and performing functions like memory retrieval and thinking. According to the researchers, this is the first time such biomarkers of consciousness have been identified during CPR for cardiac arrest. “We found the brain electrical markers of heightened […] lucid consciousness, the same markers as you get in people who are having memory retrievals who are having […] high order cognitive processes, except that this was occurring when the brain had shut down. Research suggests agmatine can boost brain health and uplift your mood naturally Yonsei University College of Medicine (S Korea), October 28, 2022. Athletes and bodybuilders are always eager to learn more about new products that can help enhance their workouts by promoting strength and stamina. Agmatine, a natural compound, is often used by health enthusiasts as a pre-workout supplement. According to research, agmatine can also potentially be used to boost brain health and improve mood. In one scientific review, researchers suggest that the compound can help prevent neurodegenerative diseases and assist in the recovery of brain injury patients. Agmatine or 4-aminobutyl-guanidine is produced in your body from arginine, an amino acid found in foods like chickpeas, lentils, pork and poultry. When used as a pre-workout supplement, experts recommend not taking it with protein since dietary protein can slow the absorption of agmatine. This then diminishes its benefits. Agmatine is often listed on supplement labels as agmatine sulfate. Dosages range between 250 mg to 1,000 mg per scoop, with intake recommendations between one to two grams per day. Agmatine has antioxidant and anti-inflammatory effects and can scavenge harmful free radicals that cause oxidative damage to your organs and tissues. Some people believe agmatine can help enhance workouts by increasing levels of beneficial nitric oxide. This then dilates blood vessels and promotes healthy circulation. Data also suggests that agmatine may help activate the release of pain-killing, mood-lifting endorphins, which can boost motivation and mood. This suggests taking agmatine can help make you feel more inclined to exercise. The compound may also help block aged glycation end products. Your body produces these potentially carcinogenic compounds after you eat charcoal-broiled or well-done meats. Agmatine may also help down-regulate matrix metalloproteinases (MMPs), which are tissue-degrading enzymes that can facilitate the spread of malignant tumors. Studies show that agmatine works against the glutamate receptors that affect pain perception. Data from preliminary studies have supported agmatine's ability to reduce pain and strengthen the pain-killing effects of prescription opioids. Experts hope that agmatine can be used to help reduce the amount of medications needed and decrease the possibility of addiction to opioids. Supplementation with agmatine may help activate serotonin, the “feel good” chemical in your body while also decreasing levels of cortisol, the “stress” hormone that builds up when you are under duress. In a review published in the European Journal of Neuropsychopharmacology, scientists suggest that agmatine has antidepressant effects. According to a 2018 study published in the journal Human and Experimental Toxicology, agmatine can help protect brain cells from oxidative stress and inflammation caused by laboratory-induced Parkinson's. Prenatal phthalate exposure can significantly impact infant behavior and cognition, says study University of Illinois Urbana-Champaign, November 16, 2022 Prenatal exposure to phthalates, a set of chemicals commonly found in plastics and personal care products, has been shown to significantly impact aspects of behavior and cognition in infants, according to a team of researchers at the University of Illinois Urbana-Champaign. “Phthalates are widespread, and several well-known studies have reported that 100% of pregnant individuals had detectable levels of phthalates in their bodies,” said developmental neurotoxicologist Jenna Sprowles, a former postdoctoral research associate at the Beckman Institute for Advanced Science and Technology. Children's toys, cosmetics, and constructional materials are all potential sources of phthalate exposure, as are other materials made from polyvinyl chloride. When individuals who are pregnant are exposed to phthalates, the chemical compound crosses the placental barrier to interact directly with the fetus. Phthalates can also be transferred to a newborn through breast milk. Their study, reported in the journal Neurotoxicology and Teratology, investigated the neurobehavioral impacts of prenatal phthalate exposure in infants aged 4.5 and 7.5 months. Since many existing studies focus on individuals in early and middle childhood, providing attention to this age group is especially important. “Phthalates are endocrine-disrupting chemicals, meaning they interact with and alter how hormones typically act in the body. Hormones play crucial roles in brain development, so when the activities of hormones are altered by chemicals like phthalates, adverse functional effects are possible,” Sprowles said. “While we do know that different phthalates can affect different hormone systems, we don't yet know exactly how particular phthalates exert their specific effects.” The researchers found that the impact of prenatal phthalate exposure was specific to each phthalate's particular properties. For example, higher prenatal concentrations of a phthalate called MEP, which is commonly found in personal care products, were associated with lower ASQ scores (indicating below-average development) in certain domains. Their results align with existing studies, some of which have been carried out in animal models, which indicate that both prenatal and neonatal exposure to phthalates alters neural structure and function, resulting in impaired cognition and altered behavior.

Longevity & Aging Series (EP 3): Dr. Steve Horvath - Epigenetic Clocks

covid-19 professor soundcloud ucla pinterest longevity publications clocks principal investigators epigenetic biostatistics special collections human genetics altos labs steve horvath

Play Episode Listen Later Aug 23, 2022 23:55

In the third episode of the Longevity & Aging Series, Dr. Steve Horvath, Professor of Human Genetics and Biostatistics at UCLA, and Principal Investigator at Altos Labs, discusses the evolution of aging research and epigenetic clocks with host Brian Chen. Special Collection on Steve Horvath's Publications in Aging - https://www.aging-us.com/special-collections-archive/steve-horvath Author contact - Steve Horvath - shorvath@mednet.ucla.edu Longevity & Aging Series - https://www.aging-us.com/longevity Transcript - https://aging-us.net/2022/08/23/longevity-aging-series-ep-3-dr-steve-horvath-epigenetic-clocks/ About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com or connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Longevity & Aging Series (EP 2): Dr. Steve Horvath's Special Collection in Aging

covid-19 university california professor llc soundcloud pinterest longevity principal investigators biostatistics special collections human genetics altos labs steve horvath

Play Episode Listen Later Aug 4, 2022 72:44

In the second installment of the Longevity & Aging Series, Dr. Steve Horvath, a world-renowned researcher, geneticist, biostatistician, Professor of Human Genetics and Biostatistics at the University of California, and Principal Investigator at Altos Labs, revisits 29 papers he co-authored that were published by Aging (Aging-US) and featured as a special collection of his research. Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath Author contact - Steve Horvath - shorvath@mednet.ucla.edu About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com or connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Multi-region Methylation Principal Component Based Clock in the Context of Alzheimer's

dogs humans clocks epigenetic steve horvath

Play Episode Listen Later Aug 1, 2022 4:39

A new research paper was published in Aging (abbreviated as "Aging (Albany NY)" by Medline/PubMed and as "Aging-US" by Web of Science) on the cover of Volume 14, Issue 14, entitled, “Aging the brain: multi-region methylation principal component based clock in the context of Alzheimer's disease.” Alzheimer's disease (AD) risk increases exponentially with age and is associated with multiple molecular hallmarks of aging, one of which is epigenetic alterations. Epigenetic age predictors based on 5' cytosine methylation (DNAm), or epigenetic clocks, have previously suggested that epigenetic age acceleration may occur in AD brain tissue. “Epigenetic clocks are promising tools for the quantification of biological aging, yet we hypothesize that investigation of brain aging in AD will be assisted by the development of brain-specific epigenetic clocks.” In this new study, researchers Kyra L. Thrush, David A. Bennett, Christopher Gaiteri, Steve Horvath, Christopher H. van Dyck, Albert T. Higgins-Chen, and Morgan E. Levine, from Yale University, Rush University Medical Center, University of California Los Angeles, VA Connecticut Healthcare System, and Altos Labs, hypothesized that a brain age methylation-based predictor could be developed with meaningful disease associations and broad multi-brain-region utility. “To test this, we used DNAm capture to generate a PC-based epigenetic predictor of brain aging which we show to: (1) strongly reflect AD neuropathology and cognitive decline, and (2) track age across multiple brain regions.” The team generated a novel age predictor, termed PCBrainAge, that was trained solely in cortical samples. This predictor utilizes a combination of principal components analysis and regularized regression, which reduces technical noise and greatly improves test-retest reliability. “To characterize the scope of PCBrainAge's utility, we generated DNAm data from multiple brain regions in a sample from the Religious Orders Study and Rush Memory and Aging Project.” PCBrainAge captures meaningful heterogeneity of aging: Its acceleration demonstrates stronger associations with clinical AD dementia, pathologic AD, and APOE ε4 carrier status compared to extant epigenetic age predictors. It further does so across multiple cortical and subcortical regions. “Overall, PCBrainAge's increased reliability and specificity makes it a particularly promising tool for investigating heterogeneity in brain aging, as well as epigenetic alterations underlying AD risk and resilience.” DOI: https://doi.org/10.18632/aging.204196 Corresponding Author: Albert T. Higgins-Chen - Email: a.higginschen@yale.edu Keywords: epigenetic clocks, unsupervised machine learning, brain, Alzheimer's disease, age acceleration Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204196 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Epigenetic clocks for humans and dogs

PNAS Science Sessions

Play Episode Listen Later Jul 18, 2022 13:16

Steve Horvath and Elaine Ostrander explain the usefulness of epigenetic clocks in humans and dogs.

Announcement: Aging (Aging-US) and FOXO Present: The Longevity & Aging Series

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Play Episode Listen Later Jun 22, 2022 3:32

Aging (Aging-US) and FOXO Technologies have teamed up to present a special collaboration on aging research with a new monthly video series: the Longevity & Aging Series. This series of video interviews invites Aging researchers to speak with researcher and host Dr. Brian Chen. Dr. Chen is an adjunct faculty member at the Herbert Wertheim School of Public Health and Human Longevity Science at the University of California San Diego. He is also the Chief Science Officer of FOXO Technologies. The Longevity & Aging Series offers a platform for Aging authors to discuss their aging research in a long-form video format. Once a month, Dr. Chen will invite distinguished authors to present their research studies and results published in Aging (Aging-US). Upcoming author interviews include Drs. Alex Zhavoronkov, Frank Pun, Steve Horvath, Andrew DiNardo, Cristian Coarfa, Carly Bobak, and Amit Sharma. The goal of this collaboration between Aging (Aging-US) and FOXO Technologies is to foster the rapid dissemination of research, encourage thought leadership and jumpstart new breakthrough studies in the field of aging. The series will be available to watch on our YouTube and LabTube channels, and will also be available for listeners on Spotify, SoundCloud or wherever high-quality podcasts are downloaded. In addition, Longevity & Aging Series discussions will be posted on Aging-US.com, Aging-US.net and ImpactJournals.com, and promoted across our family of social media channels. Watch the first episode of the Longevity & Aging Series, featuring Drs. Alex Zhavoronkov and Frank Pun as they discuss their recently published research paper, entitled, “Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine.” “This is an exciting partnership between FOXO and Aging,” Dr. Chen said. “Remarkable breakthroughs are emerging every day in aging and healthy longevity. I hope this series helps to promote all the exciting work that is being done to a broader audience.” AVAILABLE NOW: Episode One with Drs. Alex Zhavoronkov and Frank Pun: https://www.youtube.com/watch?v=Td8tK5SX0kA About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Follow Aging on social media: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus LinkedIn – https://www.linkedin.com/company/aging/ Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

Announcement: Sponsoring Systems Aging Gordon Research Conference

Play Episode Listen Later May 25, 2022 3:43

BUFFALO, NY- May 24, 2022 – Aging (Aging-US) is sponsoring the Systems Aging Gordon Research Conference, “Systemic Processes, Omics Approaches and Biomarkers in Aging,” from May 29 to June 3, 2022, at the Grand Summit Hotel at Sunday River in Newry, Maine, USA. This year, the Chair and Vice Chair of the conference are Aging Editorial Board members Vadim N. Gladyshev, Professor of Medicine at Harvard Medical School and Director of Redox Medicine at Brigham and Women's Hospital, and Steve Horvath, Professor of Human Genetics and Biostatistics at the University of California, Los Angeles. Dr. Gladyshev is known for his characterization of the human selenoproteome. He was also elected as a member of the U. S. National Academy of Sciences in 2021. Dr. Horvath is a world-renowned researcher, geneticist and biostatistician. Recently, Aging devoted a research collection to Dr. Horvath's profound contributions in epigenetics and DNA methylation research. Read Aging's Special Collection on Steve Horvath Publications: https://www.aging-us.com/special-collections-archive/steve-horvath. Both Drs. Gladyshev and Horvath will be speaking and leading discussions at this meeting. In addition, a number of prestigious researchers from renowned institutions will be presenting at this conference. Presenters who are also members of Aging's Editorial Board include Cynthia Kenyon, Manuel Serrano, Alex Zhavoronkov, and Vera Gorbunova. Over the course of the six-day Systems Aging Gordon Research Conference, presentations will cover many topics, including delaying aging, aging clocks, clinical biomarkers, advances in systemic rejuvenation, comparative and multi-omics approaches, applications of machine learning and artificial intelligence, the current understanding of the molecular basis of aging, and longevity interventions in model organisms. The organizers of the conference hope this meeting will facilitate deep discussions and the free exchange of ideas between not only established researchers but also junior scientists. “The 2022 Systems Aging GRC will set the stage for subsequent meetings and future development of this field, with the idea to ultimately help delay and reverse aging and age-related pathology.” (Source: 2022 Systems Aging GRC) About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Follow Aging on social media: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus LinkedIn – https://www.linkedin.com/company/aging/ Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

#072 Morgan Levine, PhD, on PhenoAge and the Epigenetics of Age Acceleration — can we change the pace?

THE ONE'S CHANGING THE WORLD -PODCAST

Play Episode Listen Later Apr 12, 2022 89:17 Very Popular

Morgan Levine, Ph.D., developed the phenotypic aging clock called PhenoAge and is a Founding Principal Investigator at Altos Labs, a biotech company that seeks to understand the mechanisms that drive the aging process and age-related diseases with the hope of identifying possible interventions. Additionally, Dr. Levine is an assistant professor of pathology at the Yale University School of Medicine, where her research focuses on the science of biological aging. Dr. Levine completed a postdoctoral fellowship with previous guest Dr. Steve Horvath, a pioneer in the field of epigenetic clocks. In this episode, Dr. Levine and I discuss: 00:01:19 - What is aging and why does it matter to scientists? 00:04:45 - Hallmarks of aging 00:08:59 - The advantage of epigenetic clocks in research 00:19:05 - Epigenetic age acceleration 00:36:40 - Are epigenetic changes in aging a cause or consequence? 00:42:15 - Reversing epigenetic age with interrupted reprogramming techniques 00:49:27 - Therapeutic plasma exchange in aging and pro-aging factors in blood 00:56:01 - Lifestyle factors that accelerate epigenetic age 01:03:23 - Reliability of consumer epigenetic aging tests 01:06:12 - Construct validity of epigenetic clocks 01:12:06 - Thoughts on most exciting research in aging field 01:13:44 - Dr. Levine's lifestyle habits Get the show notes: foundmyfitness.com/episodes/morgan-levine Looking for more? Join over 300,000 people and get the latest distilled information on sleep, depression, and fasting straight to your inbox weekly: https://www.foundmyfitness.com/newsletter Try thirty days of our FoundMyFitness premium member to get access to exclusive episodes, emails, a live Q+A with Rhonda and more: https://www.foundmyfitness.com/trial

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BREAKTHROUGH IN AGE REVERSAL WITH YOUNGBLOOD PLASMA - DR HAROLD KATCHER - CTO NUGENICS RESEARCH

Play Episode Listen Later Apr 11, 2022 31:50

#nugencis #nugenicsresearch #humanlongevity #agereversal #blissatomic Dr. Harold has been a pioneer in the field of cancer research, in the development of modern aspects of gene hunting and sequencing. He carries expertise in bioinformatics, chronobiology, and biotechnology and is currently working in the capacity of Chief Technical Officer at Nugenics Research Pvt Ltd. exploring in anti-aging modalities. They recently released a paper online on #biorxiv regarding their breakthrough research on Human Age Reversal using Young Blood #plasma, the paper's authors include recognized Longevity academician Steve Horvath. The paper also caught the attention of #davidsinclair the leading researcher/voice in the field of Human Longevity. Dr Katcher spoke about how & why he moved from cancer research to Human Longevity, his research & results of 54% age reversal in Rats, his partner #akshaysanghavi, the future road map/timelines on how & when this might be commercially available. https://www.linkedin.com/in/harold-katcher-340aa78 https://www.biorxiv.org/content/10.1101/2020.05.07.082917v1 https://blissatomic.blogspot.com/ Watch our highest viewed videos: 1-India;s 1st Quantum Computer- https://youtu.be/ldKFbHb8nvQDR R VIJAYARAGHAVAN - PROF & PRINCIPAL INVESTIGATOR AT TIFR 2-Breakthrough in Age Reversal- -https://youtu.be/214jry8z3d4DR HAROLD KATCHER - CTO NUGENICS RESEARCH 3-Head of Artificial Intelligence-JIO - https://youtu.be/q2yR14rkmZQShailesh Kumar 4-STARTUP FROM INDIA AIMING FOR LEVEL 5 AUTONOMY - SANJEEV SHARMA CEO SWAAYATT ROBOTS -https://youtu.be/Wg7SqmIsSew 5-TRANSHUMANISM & THE FUTURE OF MANKIND - NATASHA VITA-MORE: HUMANITY PLUS -https://youtu.be/OUIJawwR4PY 6-MAN BEHIND GOOGLE QUANTUM SUPREMACY - JOHN MARTINIS -https://youtu.be/Y6ZaeNlVRsE 7-1000 KM RANGE ELECTRIC VEHICLES WITH ALUMINUM AIR FUEL BATTERIES - AKSHAY SINGHAL -https://youtu.be/cUp68Zt6yTI 8-Garima Bharadwaj Chief Strategist IoT & AI at Enlite Research -https://youtu.be/efu3zIhRxEY 9-BANKING 4.0 - BRETT KING FUTURIST, BESTSELLING AUTHOR & FOUNDER MOVEN -https://youtu.be/2bxHAai0UG0 10-E-VTOL & HYPERLOOP- FUTURE OF INDIA"S MOBILITY- SATYANARAYANA CHAKRAVARTHY -https://youtu.be/ZiK0EAelFYY 11-NON-INVASIVE BRAIN COMPUTER INTERFACE - KRISHNAN THYAGARAJAN -https://youtu.be/fFsGkyW3xc4 12-SATELLITES THE NEW MULTI-BILLION DOLLAR SPACE RACE - MAHESH MURTHY -https://youtu.be/UarOYOLUMGk Connect & Follow us at: https://in.linkedin.com/in/eddieavil https://in.linkedin.com/company/change-transform-india https://www.facebook.com/changetransformindia/ https://twitter.com/intothechange https://www.instagram.com/changetransformindia/ Listen to the Audio Podcast at: https://anchor.fm/transform-impossible https://podcasts.apple.com/us/podcast/change-i-m-possibleid1497201007?uo=4 https://open.spotify.com/show/56IZXdzH7M0OZUIZDb5mUZ https://www.breaker.audio/change-i-m-possible https://www.google.com/podcasts?feed=aHR0cHM6Ly9hbmNob3IuZm0vcy8xMjg4YzRmMC9wb2RjYXN0L3Jzcw Kindly Subscribe to CHANGE- I M POSSIBLE - youtube channel www.youtube.com/ctipodcast

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Announcement: Special Collection of Dr. Steve Horvath Publications in Aging

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Play Episode Listen Later Mar 31, 2022 5:09

Listen to a blog summary of the announcement for a special collection of Steve Horvath research papers published by Aging (Aging-US). ____________________ Epigenetics is the study of gene expression and the changes that occur which do not involve alterations in the DNA sequence. These changes can occur as a result of environmental influences, including exposure to chemicals, diet and stress. Epigenetic modifications can be passed down through generations and play an important role in disease development. An exciting area of epigenetics research is its role in the aging process. Studies have shown that epigenetic modifications can affect aging and the onset of age-related diseases. Recently, researchers also discovered that epigenetic modifications may be used to measure biological age and aging rate. Steve Horvath, Ph.D., ScD is a world-renowned researcher, geneticist, biostatistician, and Professor of Human Genetics and Biostatistics at the University of California, Los Angeles. His research areas of study include aging, cancer, cardiovascular disease, HIV, Huntington's disease, and neurodegenerative diseases. Today, he is well-known for his contributions in epigenetics research. In 2013, Dr. Horvath developed the first multi-tissue DNA methylation-based epigenetic biomarker of aging, known as the Horvath aging clock. Dr. Horvath earned numerous awards for his groundbreaking research, including the Allen Distinguished Investigator award, the Open Philanthropy Project award and the Schober Award. In 2018, 2019, 2020, and 2021, the Clarivate Web of Science Group named him as one of the world's most influential scientific researchers. Full blog - https://aging-us.net/2022/03/special-collection-of-steve-horvath-publications-in-aging/ Steve Horvath Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath Contact information - Steve Horvath - shorvath@mednet.ucla.edu Keywords - aging, aging research, epigenetics, epigenetic clock, longevity, healthspan, lifespan, lifestyle, research, research papers About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Beyond the Portfolio: Steve Horvath

The Investing Podcast

Play Episode Listen Later Mar 25, 2022 44:17

Steve Horvath is a former senior tech fellow at Lockheed Martin. Steve graduated from Georgia Tech with an engineering degree and spent his whole career with Lockheed. In this interview, Steve offers insight into why he stayed at Lockheed, what led to his success at the company, some leaders that he admired during that time, and his financial advice to younger listeners.

#138 Why We Will Live Past 200 years with Sergey Young

The Doctor's Kitchen Podcast

Play Episode Listen Later Feb 23, 2022 64:14

I am fascinated with the science of longevity and I think this is probably the most disruptive area of science and technology that will have huge implications for not only health but also drastically impact culture, society and the planet.We've spoken to longevity researchers in the field, but today I wanted to open up the conversation to the drivers of this research area.Sergey Young is a longevity investor and visionary with a mission to extend the healthy lifespans of one billion people. To do that, Sergey founded the Longevity Vision Fund to accelerate life extension technological breakthroughs and to make longevity affordable and accessible to all. Sergey is on the Board of Directors of the American Federation of Aging Research (AFAR) and is the Development Sponsor of the AGE REVERSAL XPRIZE, a global competition designed to cure aging.His recent book, The Science and Technology of Growing Young is a Wall Street Journal and USA Today bestseller. Sergey works closely with and is invested in the research and companies of people like Dr. David Sinclair who's been on the podcast, Dr. George Church, and Dr. Steve Horvath.Given the advancement of science and technology in the field of life sciences, it is Sergey's belief that those who are very healthy in 15 year's time, will live to 150+ years old.We talk about the key areas that will disrupt healthcare in the next 5 to 10 years including:Gene TherapyLongevity Drug discovery and developmentRegenerative medicineAnd we glimpse into the future and talk about the inevitability of Radical longevity extensionThe IOB - internet of bodiesUsing AGI to power medicineAnd the unsettling topic of transhumanismToday's episode will take a bit of open mindedness, but I think one thing is for sure, the direction of travel is certainly increasing health and lifespan. For that reason, we need to start having these unnerving conversations.Stick around to halfway through because I ask about Sergey's daily routine of exercise, supplements, longevity habits and diet, and if you're an avid listener to the podcast you'll be pleased to know that pretty much everything that I talk about with Sergey and his longevity activities align with what we talk about here on this podcast!The podcast recipe of the week is my “Sulforaphane Saute” a recipe packed with anti-inflammatory ingredients including broccoli, edamame and a delicious sesame dressing thatyou can find on the app here: https://apple.co/3G0zC0Z.We would love to get your feedback on the subject matter of these episodes - please do let me know on our social media pages (Instagram, Facebook & Twitter) what you think, and give us a 5* rating on your podcast player if you enjoyed today's episode. See acast.com/privacy for privacy and opt-out information.

director science technology young board wall street journal radical usa today sergey american federation david sinclair growing young george church sergey young steve horvath longevity vision fund age reversal xprize

DNA Methylation-based Measures of Biological Age

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Play Episode Listen Later Jan 4, 2022 14:18

Aging-US published "DNA methylation-based measures of biological age: meta-analysis predicting time to death" in 2016, which reported that estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. These authors previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, they expanded their original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, they examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality, independent of chronological age, even after adjusting for additional risk factors. The authors said, "DNA methylation-based biomarkers, often referred to as ‘epigenetic age' or ‘epigenetic clock', are robust estimators of chronological age of an individual." Full Press Release - https://www.aging-us.com/news_room/dna-methylation-based-measures-of-biological-age Full Text - https://www.aging-us.com/article/101020/text/ Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu Keywords: all-cause mortality, lifespan, epigenetics, epigenetic clock, DNA+methylation, mortality About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com or connect with us on: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Epigenetic Age of the Pre-frontal Cortex

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Play Episode Listen Later Jan 4, 2022 4:51

Aging-US published "Epigenetic age of the pre-frontal cortex is associated with neuritic plaques, amyloid load, and Alzheimer's disease related cognitive functioning" in 2015, which reported that there is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. Here the authors use n=700 dorsolateral prefrontal cortex samples from Caucasian subjects of the Religious Order Study and the Rush Memory and Aging Project to examine the association between epigenetic age and Alzheimer's disease related cognitive decline, and AD related neuropathological markers. The neuropathological markers may mediate the association between epigenetic age and cognitive decline. Genetic complex trait analysis revealed that epigenetic age acceleration is heritable and has significant genetic correlations with diffuse plaques and possibly working memory. Overall, these results suggest that the epigenetic clock may lend itself as a molecular biomarker of brain age. Dr. Steve Horvath said, "Cognitive aging is on a continuum from normality, to mild cognitive impairment (MCI), to dementia." Complete Press Release - https://www.aging-us.com/news_room/epigenetic-age-of-the-pre-frontal-cortex Full Text - https://www.aging-us.com/article/100864/text/ Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu Keywords: epigenetics, neuritic plaques, amyloids, cognitive functioning, memory, Alzheimer's disease, epigenetic clock, DNA methylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com or connect with us on: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

EP 136 - Dr. Kara Fitzgerald

The Empowering Neurologist Podcast

Play Episode Listen Later Nov 1, 2021 56:11

Can aging be reversed? This is certainly a question that's been asked for a long time. And if it is indeed achievable, how would it be measured? Over the years, a variety of theories of aging have been proposed. The various theories have paved the way for testing of one sort or another to allow the development of an age assessment tool. These have included studies to look at genomic instability, the length of telomeres, evaluations of how mitochondria are functioning, markers of cellular senescence, and even measurements of the competence of stem cells. But perhaps the most widely accepted candidate these days is a measurement of what are called “epigenetic alterations.” Basically, this is an assessment of the degree of binding of our DNA to specific chemicals called methyl groups, and not just the binding of these methyl groups, but the specific pattern by which they attach themselves to our DNA. This technology was developed by UCLA professor Dr. Steve Horvath and involves identification of 323 points on human DNA (among tens of thousands) where these methyl groups attach. Assessment of biological age using this technique has been called an epigenetic clock, a methylation clock, or nowadays, the Horvath clock. This is perhaps the most objective technology for considering age and aging. Early on in his research as this aging clock was beginning to make its way into our understanding, Dr. Horvath made it quite clear that the clock was basically inviolate, meaning that we could not influence it, for better or worse. Recently however, the notion that the Horvath clock was not subject to our manipulation has been challenged, and this is extremely good news. Dr. Kara Fitzgerald has just published what I consider to be a landmark paper. She studied 43 healthy adult males between the ages of 50 and 72 and put them on an eight-week treatment program with special attention to things like diet, sleep, exercise, and relaxation guidance along with supplemental probiotics and other phytonutrients. The subjects had an evaluation of their epigenetic age at the beginning of the study and at its conclusion. Remarkably, the intervention program was associated with a dramatic 3.23 years decrease in the epigenetic age in comparison to controls as measured by the Horvath technology. The implications of this research are profound. Using the most widely accepted state-of-the-art measurement of aging, a specific lifestyle intervention program has led to age reversal. Today on The Empowering Neurologist we talk with Dr. Kara Fitzgerald about her exciting research, how the study was designed, and most importantly, what are the implications of this work. ==== Kara Fitzgerald, ND, received her doctor of naturopathic medicine degree from the National University of Natural Medicine in Portland, Oregon. She completed the first Counsel on Naturopathic Medicine-accredited post-doctorate position in nutritional biochemistry and laboratory science at Metametrix Clinical Laboratory (now Genova Diagnostics) under the direction of Richard Lord, PhD. Her residency was completed at Progressive Medical Center, a large, integrative medical practice in Atlanta, Georgia. Dr. Fitzgerald is the lead author and editor of Case Studies in Integrative and Functional Medicine and is a contributing author to Laboratory Evaluations for Integrative and Functional Medicine and the Institute for Functional Medicine (IFM)'s Textbook for Functional Medicine. With the Helfgott Research Institute, Dr. Fitzgerald is actively engaged in clinical research on the DNA methylome using a diet and lifestyle intervention developed in her practice. The first publication from the study focuses on reversal of biological aging and was published 04-12-2021 in the journal Aging. A consumer book and application-based program with DNA methylation assessment are scheduled for release 01-2022. Dr. Fitzgerald is on the faculty at IFM, is an IFM Certified Practitioner and lectures globally on functional medicine. She runs a Functional Medicine Clinic Immersion program for professionals, and maintains a podcast series, New Frontiers in Functional Medicine and an active blog on her website, www.drkarafitzgerald.com. Her clinical practice is in Sandy Hook, Connecticut. www.drkarafitzgerald.com

S5E29｜重金押注抗衰老公司，硅谷真的可以做出长生不老药吗？

What's Next｜科技早知道

Play Episode Listen Later Oct 20, 2021 53:42

2021 年 9 月 4 日，《麻省理工科技评论》发布报道，称亚马逊创始人 Jeff Bezos 和硅谷著名投资人 Yuri Milner 在近期投资了专注于抗衰方向的生物科技公司 Altos Labs，一家今年四月才成立的抗衰老公司，科学家团队包括 2012 年诺贝尔生理学或医学奖的获得者山中伸弥；截至今年六月，该公司已经吸引了至少 2.7 亿美元的投资。这并非硅谷富豪们第一次入局抗衰领域。 2018 年， Jeff Bezos 和 PayPal 联合创始人 Peter Thiel 共同投资抗衰领域独角兽 Unity Biotechnology；而更早之前，还有谷歌创始人 Larry Page 宣布 10 亿美元投资生物科技公司 Calico，目前 Calico 已经被整合至谷歌母公司 Alphabet Inc。我们似乎可以清晰地看见，在颠覆互联网、物流制造、航空航天等领域之后，硅谷大佬们的下一个目标，正是通过生物工程技术突破人类目前的寿命上限，将长生不老的选择权紧紧握在手里。本期节目，我们邀请到了同样在抗衰领域被视为明星公司的硅谷新贵 Gordian 的首席科学家 Martin Borch Jensen。他和主播 Diane 一起探讨了硅谷的投资者们都是出于什么原因投资 Altos Labs 等生物科技公司，值得关注技术路径有哪些，投资人应该如何看待生物科技领域的超长投资周期和技术挑战，头部公司可以通过什么途径实现商业回报。 #加入我们# 声动活泼正在招聘「内容研究员」、「业务拓展和合作管理总监/经理」、「声音设计师」、「播客制作实习生」、「内容营销负责人」及「节目制作人」，查看详细讯息请在公号「声动活泼」回复暗号：入场券。简历接收邮箱

Paul Hynek: Medically Verified Age Reversal Is Happening Now

SuperAge: Live Better

Play Episode Listen Later Mar 31, 2021 45:04

Paul was in the first medically verifiable trial making people younger. How does it work? Why is this important? Is it even the right thing to do? Why is he doing it again?Is it possible for us to prevent the breakdown of our physical bodies? What is standing in our way from increasing our lifespan? Do we owe it to future generations to take radical steps to live longer?The TRIIM (Thymus Regeneration, Immunorestoration, and Insulin Mitigation) trial is literally making people younger. This trial has proven that we can regrow the thymus with human growth hormones and the help of metformin. Why is this important? Our thymus is the master gland of immunity. As we age, so does our thymus which leads to the collapse of our immune system and increases our risk of death. Being able to regrow the thymus means that we can add years to our lifespan, like Paul Hynek did. Paul Hynek is the son of J. Allen Hynek, American astronomer and UFO researcher, and professor at Pepperdine. Paul's personal lifespan was increased by 4 years after participating in the groundbreaking TRIIM trial. This was the first time in history that someone was tested by Steve Horvath's epigenetic clock test and actually tested younger than they previously had. Paul shares with us the revolutionary results that the TRIIM trial had, what this means for the future of humanity, and what it means to be a transhumanist. This trial is now accessible to the public through Intervene Immune. You can learn more about the TRIIM trial and Intervene Immune at http://interveneimmune.com/interveneimmune.com/“If people 100 years ago had said, “You know what? Lifespan of 40-50 years thats enough. We don’t need to do anything more”, you and I wouldn’t be here now. So, we owe it to future generations to do what we can to extend healthy life span.”“Why wait for things to go wrong to restore them? Get ahead of all of these diseases and increase lifespan.”“We’re not talking about 30 extra years in a wheelchair. We’re talking about extra time of robust health.”Listen to the SuperAge podcast wherever you get your pods.

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Für immer jung: Machen Forscher einen Menschheitstraum wahr?

Die Story

Play Episode Listen Later Mar 3, 2021 43:16

Der Wissenschaftler Steve Horvath hat eine bahnbrechende Entdeckung gemacht: Die sogenannte "Horvathsche Lebensuhr", die in jeder Körperzelle tickt.

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Episode 85 - Building a Future and Making a Difference

ASA Podcast

Play Episode Listen Later Mar 3, 2021 23:49

Episode 85 – Building a Future and Making a DifferenceJohn Glosek grew up in Pennsylvania loving golf and muscle cars. He built his first engine at 16 and worked in a machine shop, honing his automotive skills in high school. After earning degrees in business management and automotive technology, he followed his passion and now works for Steve Horvath as the Service Manager at Jeno’s Auto Service, Inc. in Littleton, Colorado. John is a thirty-something and one of the next generation of leaders in the automotive service industry. Listen in as John discusses:· How he found his love for anything automotive in a small town with lots of muscle cars and mentors.· His pride in being an ASE-Certified professional.· John’s insights into what he sees as the biggest challenges for himself and our industry.· What shop owners need to do to find and keep top technicians in the business.· Working with different generations in the shop.· How he grows entry-level technicians into Master Techs.· Keeping up with changing technology and how training needs to change.· The industry shift to electrical diagnosis and what’s on the horizon.· Maintaining his work/life balance.· The Hands of the Carpenter Charity everyone at Jeno’s supports.· How he’s preparing for what’s next and how ASA has helped his career.

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Für immer jung: Machen Forscher einen Menschheitstraum wahr?

Die Story

Play Episode Listen Later Mar 3, 2021 43:16

Der Wissenschaftler Steve Horvath hat eine bahnbrechende Entdeckung gemacht: Die sogenannte "Horvathsche Lebensuhr", die in jeder Körperzelle tickt.

patients immer einen machen jung immunsystem forscher entdeckung nebenwirkungen wahr zwillinge steve horvath altersforschung lebensuhr

Telos Corporation: The Evolution of Cybersecurity

State of Identity

Play Episode Listen Later Feb 11, 2021 30:56

Host Cameron D’Ambrosi chats with Steve Horvath, VP of Strategy and Cloud at Telos Corporation. Tune in to learn how the NIST Cybersecurity Framework is applicable across public and private sectors and what mobile technologies have blurred the corporate lines. Horvath gives a candid view into the lessons he's learned in handling systems and compliance issues for federal IT professionals, and the benefits of automated vs. manual compliance in accommodating new cybersecurity regulations.

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Dr. Steve Horvath on epigenetic aging to predict healthspan: the DNA PhenoAge and GrimAge clocks

Podcast Notes Playlist: Latest Episodes

Play Episode Listen Later Jan 6, 2021 93:59

Found My Fitness - Rhonda Patrick Podcast Notes Key Takeaways The Horvath Aging Clock is collected through DNA sample and currently the most accurate estimate of chronological ageThe epigenetic clock is under genetic control – evidence strongly suggests the epigenetic clock is a continuous readout that links prenatal tissue directly to disease and healthspan in older ageSome people inherit DNA which allows their epigenetic clock to progress slowerEarly studies show DNA GrimAge is a good predictor of time to heart disease and chronic disease before clinical markers appearCompared to the epigenetic clock, telomere length is a weak predictor of agingIn healthy people, even a “perfect” lifestyle won’t make a big dent in epigenetic ageThe weakness of the epigenetic clocks is that we don’t understand the specific regulators of these clocks Read the full notes @ podcastnotes.orgConsistent patterns of age-based alterations in DNA methylation can be harnessed to estimate age, serving as a sort of "clock," the premise of which is truly remarkable: Predict a person's age (or even lifespan), based on chemical modifications to their DNA that reflect the biological life history of the organism. Dr. Steve Horvath has analyzed large data sets of DNA methylation profiles to derive an algorithm that accurately predicts a person's chronological age across multiple cells, tissues, and organs, and even mammalian species. He built on this algorithm to develop second-generation clocks that could predict time-to-death among people of the same chronological age, as well as lifespan and healthspan. In this episode, Dr. Steven Horvath describes epigenetic clocks and their role in predicting – and possibly slowing – aging. Get this show's notes, timeline, and transcript: https://www.foundmyfitness.com/episodes/steve-horvath Dr. Horvath's faculty bio page: https://ph.ucla.edu/faculty/horvath Dr. Horvath's Wikipedia page: https://en.wikipedia.org/wiki/Steve_Horvath Dr. Rhonda Patrick's 3-minute video crash course in epigenetics: https://www.foundmyfitness.com/episodes/epigenetic-clock The FoundMyFitness overview article of epigenetic clocks: https://www.foundmyfitness.com/topics/epigenetic-clocks

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Dr. Steve Horvath on epigenetic aging to predict healthspan: the DNA PhenoAge and GrimAge clocks

dna wikipedia consistent longevity predict clocks horvath healthspan epigenetic rhonda patrick found my fitness steve horvath

Play Episode Listen Later Dec 22, 2020 93:59

Consistent patterns of age-based alterations in DNA methylation can be harnessed to estimate age, serving as a sort of "clock," the premise of which is truly remarkable: Predict a person's age (or even lifespan), based on chemical modifications to their DNA that reflect the biological life history of the organism. Dr. Steve Horvath has analyzed large data sets of DNA methylation profiles to derive an algorithm that accurately predicts a person's chronological age across multiple cells, tissues, and organs, and even mammalian species. He built on this algorithm to develop second-generation clocks that could predict time-to-death among people of the same chronological age, as well as lifespan and healthspan. In this episode, Dr. Steven Horvath describes epigenetic clocks and their role in predicting – and possibly slowing – aging. Get this show's notes, timeline, and transcript: https://www.foundmyfitness.com/episodes/steve-horvath Dr. Horvath's faculty bio page: https://ph.ucla.edu/faculty/horvath Dr. Horvath's Wikipedia page: https://en.wikipedia.org/wiki/Steve_Horvath Dr. Rhonda Patrick's 3-minute video crash course in epigenetics: https://www.foundmyfitness.com/episodes/epigenetic-clock The FoundMyFitness overview article of epigenetic clocks: https://www.foundmyfitness.com/topics/epigenetic-clocks

#062 Dr. Steve Horvath on epigenetic aging to predict healthspan: the DNA PhenoAge and GrimAge clocks

phd dna ucla longevity predict clocks healthspan epigenetic found my fitness public health dr steve horvath

Play Episode Listen Later Dec 22, 2020 93:59

Steve Horvath Steve Horvath, PhD, is a professor of human genetics and biostatistics at UCLA's Fielding School of Public Health Dr. Steve Horvath has analyzed large data sets of DNA methylation profiles to derive an algorithm that accurately predicts a person's chronological age across multiple cells, tissues, and organs, and even mammalian species. He built on this algorithm to develop second-generation clocks that could predict time-to-death among people of the same chronological age, as well as lifespan and healthspan. If you're interested in learning more, you can read the full show notes here: https://www.foundmyfitness.com/episodes/steve-horvath Join over 300,000 people and get the latest distilled information on aging straight to your inbox weekly: https://www.foundmyfitness.com/newsletter Become a FoundMyFitness premium member to get access to exclusive episodes, emails, live Q+A's with Rhonda and more: https://www.foundmyfitness.com/crowdsponsor

Episode 232 – the Holidays edition

This Week in FCPA

Play Episode Listen Later Dec 11, 2020 29:26

As TrumpLand continues to live in fantasy and denial, going 1-55 in lawsuits while over 3000 American die daily from Covid-19; Tom and Jay are back to look at some of the top compliance articles and stories which caught their eye this week. The Vitol FCPA enforcement action. Tom takes a deep dive on the FCPA Compliance and Ethics Blog. Part 1, Part 2, Part 3, Part 4. Mike Volkov has a 3-part series on Corruption Crime and Compliance. Is the SEC whistleblower program too opaque? Harry Cassin considers in the FCPA Blog. AML reform and a new whistleblower law. Matt Kelly considers in Radical Compliance. Tom and Matt go into the weeds in the latest episode of Compliance into the Weeds. Is the SEC discouraging whistleblowers under Dodd-Frank. Mengui Sun explores in the WSJ Risk and Compliance Journal. Where did the Cheesecake Factory go wrong? Sara Kropft in the Grand Jury Target. 5 Compliance Triumphs from 2020? Kyle Brausser in Compliance Week. (sub req’d) GDPR compliance challenges in 2021. Steve Horvath in CCI. China-US audit showdown? Michael Rapoport reviews in The Dig. A new month is here and a new guest on The Compliance Life. Kim Yapchai, Chief Counsel - Environmental, Social & Governance at Tenneco Inc. In this week’s second episode, we take up the in-house roles In Kim held on her road towards the CCO chair. Check out the series here. My podcast with Mikhail Reider-Gordon on Wirecard was so popular we spun it out into its own series, The Wirecard Saga. Check out the latest episode, Dirty Deeds Down Under. On 31 Days to a More Effective Compliance Program, we consider Training and Communications. Monday, Sharing to 360-degrees of communication Tuesday- Speical Guest Vin DiCianni on Compliance and the clash of cultures.Wednesday- Using 360 Degree of Compliance to Tell a Story; Thursday- Using Communications to Drive a Speak Up Culture; Friday- Using communications to foster your compliance brand. Note 31 Days to a More Effective Compliance Program now has its own iTunes channel. If you want to binge out and listen to only these episodes, click here. Check out the a replay of London Stock Exchange event which featured Tom, Neta Meidav, CEO, Vault Platform and Maxine Gee, Chief Risk Officer - UK Capital Markets LSE on why culture drives compliance. You can view and listen to it here. Join K2 Integrity for two great events in December. On Dec. 14, they host a webinar on “Proliferation Financing: Risks, Threats, and Mitigation.” The webinar will explore critical issues around understanding and combatting the financing of WMD proliferation. https://bit.ly/2VujK1O. On December 17, DOLFIN and K2 Integrity’s financial crimes compliance experts will host their latest “Ask an Expert FINQuiry” webinar. Expect answers to questions on topics such as: the latest developments in AML/CFT, sanctions, fraud, anti-bribery and corruption, and export controls; financial integrity risks related to the global pandemic; and regionally focused financial crime risks. https://bit.ly/39zzhFP Tom Fox is the Compliance Evangelist and can be reached at tfox@tfoxlaw.com. Jay Rosen is Mr. Monitor and can be reached at jrosen@affiliatedmonitors.com. Learn more about your ad choices. Visit megaphone.fm/adchoices

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Episode 138: How fast are you aging? Reveal your biological age through epigenetics with Dr Keith Booher

Pushing The Limits

Play Episode Listen Later Feb 13, 2020 51:15

Molecular Biologist Dr. Keith Booher talks about the Horvath epigenetic clock and the why and how behind finding out your biological age. Keith Booher received his PhD from the University of California, Irvine in 2011 where he conducted research in the field of cancer cell metabolism. He then began work at Zymo Research Corporation developing methods and assays for the investigation of epigenetics. Along with colleagues, he contributed to a high impact study evaluating methods for DNA methylation validation in 2016. Keith continues to study epigenetics in his current position as Application Scientist at The myDNAge company or Epimorphy, LLC, in Southern California where his research is focused on healthy aging and longevity. In his free time, you can find Keith either on the dance floor, at the local library, or spending time with his family. "The world population is aging, especially in the West and the industrialized countries of Asia. In fact, the percentage of the population over the age of 65 is expected to more than double by the year 2050. An aging population presents many societal challenges as advanced age is the number one contributor to chronic ailments such as heart disease, cancer, neurological disorders, and more. It is imperative that meaningful and effective anti-aging interventions are identified and deployed in order to ease the transition from a younger to a gradually older population. Epigenetics involves the modification of gene expression without changing the underlying DNA sequence. Importantly, many recent scientific studies demonstrate the connection between epigenetics, especially DNA methylation, and aging. To date, analyzing changing DNA methylation patterns at key genes is the most accurate way to quantify the aging process. Understanding the connection between epigenetics and the aging process allows us to gain deeper insight into the mechanisms that cause aging, with the ultimate hope of devising interventions that will potentially lead to better health and longevity. Dr. Booher highlights the use cases for this new type of testing and it's used for those individuals or teams wanting to understand what protocols, training regimes, food plans, supplement regimes etc impact their own aging and how you can maybe even turn back the clock ticking on us all. Get yourself tested and find out your biological age at: https://www.mydnage.com/ Use the code 'LISA15" to get a 15% discount on the cost of the test Watch Dr. Keith's Ted Talk https://www.youtube.com/watch?v=PeT1RcwsDMc We would like to thank our sponsors for this show: www.vielight.com Makers of Photobiomodulation devices that stimulate the brains mitocondria, the power houses of your brains energy, through infrared light to optimise your brain function. To get 10% off your order use the code: TAMATI at www.vielight.com For more information on Lisa Tamati's programs, books and documentaries please visit www.lisatamati.com For Lisa's online run training coaching go to https://www.lisatamati.com/page/runningpage/ Join hundreds of athletes from all over the world and all levels smashing their running goals while staying healthy in mind and body. Lisa's Epigenetics Testing Program https://www.lisatamati.com/page/epigenetics/ Get The User Manual For Your Specific Genes Which foods should you eat, and which ones should you avoid? When, and how often should you be eating? What type of exercise does your body respond best to, and when is it best to exercise? Discover the social interactions that will energize you and uncover your natural gifts and talents. These are just some of the questions you'll uncover the answers to in the Lisa Tamati Epigenetics Testing Program along with many others. There's a good reason why epigenetics is being hailed as the "future of personalized health", as it unlocks the user manual you'll wish you'd been born with! No more guesswork. The program, developed by an international team of independent doctors, researchers, and technology programmers for over 15 years, uses a powerful epigenetics analysis platform informed by 100% evidenced-based medical research. The platform uses over 500 algorithms and 10,000 data points per user, to analyze body measurement and lifestyle stress data, that can all be captured from the comfort of your own home For Lisa's Mental Toughness online course visit: https://www.lisatamati.com/page/mindsetuniversity/ Develop mental strength, emotional resilience, leadership skills and a never quit mentality - Helping you to reach your full potential and break free of those limiting beliefs. For Lisa's free weekly Podcast "Pushing the Limits" subscribe on iTunes or your favorite podcast app or visit the website https://www.lisatamati.com/page/podcast/ Transcript of the Podcast: Speaker 1: (00:01) Welcome to pushing the limits, the show that helps you reach your full potential with your host, Lisa Tamati, brought to you by Lisatamati.com welcome to pushing the limits. Speaker 2: (00:12) Let's see everyone. Thanks for joining me again today. I have a scientist to guest on the show, Dr. Keith Booher. Now, Dr. Keith is a molecular biologist and he works for a company called mydnage.com. Now this is a company that uses Dr. Steve Horvath's epigenetic clock. This tells us our biological age. So we have a very interesting conversation around the difference between your biological age your, your chronological age, and also the method of telling how old you are based on your DNA. So we're looking at DNA methylation as opposed to some of the other processes that look at biological aging from other factors. And we get to into a deep dive about looking at your biological age. Now this is really interesting from a perspective from coaching, from I'm trying to draw a line in the sand to see where you are now. Speaker 2: (01:08) And I can see this having benefits. We are looking at it for our mastermind program where we're thinking about having this as our baseline to start from where we can actually see what your biological age is at one point in time when you start. And then using that as we go through our program to see how you come out at the other end. And hopefully you would have lost a number of years off your life as far as your biological ages going. So this was a very interesting deep dive into this topic. So I hope you enjoy the show. And just before we go over to Dr Keith just like to remind you that I have my book relentless coming out in just a couple of weeks time or four weeks time and it's on the 11th of March and launches, it's available for preorder now you can jump on my website, hit the shop button and preorder it. Speaker 2: (01:57) And at moment you'll get access to my mindset Academy mindsetu for free. If you join or buy the book in the preorder stage, you'll also get a discount. It'll normally be retailing for $35. You'll get it for $29 plus you get access to mindset, you a value of $275. So really good idea to go on and jump and now and get it. And that helps me get the book rolling, get it out into the world. It's been a two year long process. So really excited to see that baby launch. As always, reach out to me if you've got any questions on this episode or on any of the other episodes that we've recorded. And I really appreciate your help with ratings and reviews on iTunes that really helps the show get exposure and of course sharing it with your friends and family if you got value out of it. So thanks and now over to Dr. Keith Booher from mydnage.com. Speaker 3: (02:49) Well, hello everyone. Lisa Tamati speaking and here I'm pushing the limits. I thank you once again for joining me today. I have a wonderful guest, Dr. Keith Booher who is a biochemist. Is that correct case? Speaker 4: (03:02) Yes, that's correctly. So thank you for having me. Speaker 3: (03:04) Yeah, it's wonderful to have you. So Keith is going to talk to us today about the biological clock. He works for a company called mydnage which does testing of the biological age as opposed to your chronological age. And this is a very interesting area we in our company through it continued existing without athletes and clients. So this is something that I'm very interested in finding out more about in cases coined the agreed to come on the show and talk to us about it. So. Okay. Can you give us a little bit of background about who you are and where you come from and, and the work that you're doing? Speaker 4: (03:46) Yes, certainly. So, so my name is Keith Booher. I'm a scientist. I worked for the company epi Morphe that offers the mydnage test. This isn't a epigenetic, a base test to quantify aging or biological age. And my background I got a PhD in biological chemistry. I'm from the university of California, Irvine here in Southern California right now. They've worked and where the company's headquartered. I then joined a research companies. I'm a research, Oh, also in California when I started doing epigenetics research in an industrial setting and then transitioned to a, working with the epi Murphy and offering the mydnage test. Speaker 3: (04:28) Wonderful. So can you tell us a little bit, well, for the listener, what is epigenetics and the area of study of epigenetics and what is on those a biological clock? Speaker 4: (04:39) Yeah, so I think, so the scientific, no definition of epi genetics, so it's a biological term. So simply refers to any changes in gene expression that occur without altering the primary DNA sequence. So what that sort of means in lay context is any, any instance where our genetics interacts with the environment. So sort of nature versus nurture a concept. So what epigenetics then does at the molecular level is to help control gene expression or to help turn genes on or off, or how strongly genes are expressed in the cell. I think an analogy that I've heard before, which is it's not perfect, but I think gives you the idea would be that our genes, our genetics, it'd be the hardware with which we operate. And epigenetics would be the software or instructions that tells that hardware what to do. Speaker 3: (05:33) Wow. Okay. So, so in other words, our environment, what we eat they, the, the, the, the toxins in our environment. Eric's the size, whether we do any or not, all of these things will have an effect on how our genes express themselves. So we've gone as sort of DNA code, which we can't really change. Yeah. What genes are turned on and off can be affected by environment. That, correct. Speaker 4: (05:58) Yeah, that's absolutely correct. So there's lots of studies looking at how epigenetics change in response to environment. So this, you know, in the past decade, decade and a half, there's been a lot of progress made by the scientific community. So we know that you know, people that go on a controlled exercise regimen you know, when they start versus a, when they stop after six months and compared to control group. So there are genetic changes that, that occur in a skeletal muscle. So we know that people have also looked at adipose or the fat tissue and also seeing epigenetic changes in response to certain exercise programs. We also know that smokers have a different epigenetic, I'm marks highly correlative with smoking. Mmm. That these epigenetic marks behind people in certain occupations where they're exposed to a lot of environmental pollutants such as coal miners, a certain factory workers also have pronounced epigenetic changes compared to those that aren't occupied in such fields. Speaker 4: (07:04) I think another, sorry, maybe another example just to really, it would be easy to understand is if you look at twins. So twins are genetically identical individuals. However, through the course of their lives. So we know what, you know, when they're young, we can take it classmates in grade school with some twins. I mean, you couldn't tell them apart. Right. But if we think of older twins, you know, throw the course of their lives, you know, they maybe move to different places there obviously the families that they no start you know, they have different sort of traditions, different diets perhaps they like to eat, you know, brought in from their own partners and all these different influences impact their epigenetics. Right? So these still genetically identical individuals but the epigenetics change based on their environment and their lifestyle and when they're older, they actually don't resemble each other as much as they did when they were. Yeah, sure. Speaker 3: (07:59) That's really good example of, of, of the, the power of epigenetics isn't it? I saw a photo of a pair of twins that I think were on the Oprah Winfrey show years ago. And two ladies, one very, very overweight one, one not and the identical twins. It's a really, it's an easy way to understand how much your environment fix your epigenetics of fakes your and how you end up. So in other words, we can't just blame mum and dad and our ancestors for what we've got. We have some responsibility for how we tune out. Is that right? Speaker 4: (08:37) Yeah, that's right. And I think it's it's actually allows us to take control and you know, kind of dictate where we want to be so we can, we're not destined for some, you know, fate just based on our, our genetics. We, we can actually influence what those genetics do. Speaker 3: (08:55) Yeah. So is this so I'm, I, I've read a lot of Dr. Bruce Lipton's work and books. And you know, I have found this whole area really, really fascinating and it's pretty new, isn't it? In the scientific world, like we're talking what the last 30, 40 years or Mmm. Oh, that, that scientists have really understood that the, it's not just your DNA that makes you who you are. Is it pretty new field? Speaker 4: (09:22) Yes and no. So I think we're all familiar with the Charles Darwin and in his theories on evolution. He's one of the preeminent scientists, the modern world. Actually before Darwin, there's a French, a scientist and philosopher, a Lamarck who, you know, he actually predicted that the, you know, wow. What are our, our parents or the mother and father the type of lifestyle they live. Okay. Their environment will impact. Mmm. The children. So it's actually a heritable trait passed on just based on, so he said that if you were, if your parents, did you follow with a blacksmith, you know, all the hard work that makes them strong will then be passed onto to his children. Mmm. And like a giraffe that you know, needs to a stretch to reach the the leaves from on the tallest branches of the tree will, you'll get a longer neck and then that'll be passed down for the next generation. Speaker 4: (10:17) And this is, this is a way that, okay. Drafts have evolved. Mmm. Once Darwin's theories came out and were tested you know, Mendell then proved how genes, I kind of demonstrated how James can, can, can behave. A lot of the marks, theories were just you know, kind of put in the, the dustbin of history and he was sort of left off, you know, these were, these were sort of thought as ridiculous principles, but a sure enough, as you, as you just mentioned, Lisa, in the past several decades, actually, the Mark's original theories have been proven to be a, have a lot of Yeah. He was before his time. And we know this to be true. I mean, the, the biology is clear that and then we're learning more about it all the time. And even in I think 2014 as these studies were coming out more and more showing the power epigenetics you know, a portrait of what Mark was on the cover of nature magazine and they kind of featured and, you know, paid homage to his, his original theories. Speaker 3: (11:15) Wow. What a shame. He wasn't around to say that a bit. That would have been the kinds of a lot of things. So in other words, so when we're talking evolution here or intergenerational . I, I read some way that, for example, when a mother smokes and the baby's in the, in the womb, that that can affect the baby's DNA and then it can affect also who children's DNA. Is that correct? The intergenerational nature, or is that a Zeta? It's not, is it epigenetics or is that more genetic changes? Speaker 4: (11:54) Oh, well, so any genetic change that's altered in a, what we call the germline. Oh, you know, the the male gametes are the chemo sites. That's certainly genetically heritable changes that occur in our you know, the scan for example, know if we know examples that give rise to cancer or something don't. So those wouldn't be heritable. Right. So like if something like skin cancer epigenetics, then, so, so for it to be heritable, it has to occur in the germline so that that would be the same for genetics or, right. Yeah. So we, so certainly genetic change is hard. I mean, that's, that's very clear. Epigenetic is it seems to also be true. There's lots of circumstantial evidence. It's very difficult to do these studies in humans for obvious reasons. Hmm. Other studies and other types of model organisms, the biologists often used to study different phenomenon indicates that indeed epigenetic inheritance inheritance is, is a observed phenomenon. I think it's very strong evidence in plants. I mean, these, these, these traits are, I mean, they persist for it. Dozens of generations in mammals, you know, maybe more temporal. So two to three or even four generations, but not not, not that stable, but it appears that they are here. Speaker 3: (13:16) Wow. Okay. So so we can affect our whole, yeah, the intergenerational aspect of it is quite interesting, but if we, if we just back up a little bit now and go into the dr Steve Horvath's work in the Horvath clock and I believe that is the basis of the work that has his work is the basis of, of the testing that you do. Can you explain what dr Horvath discovered and what that means for biological age and what, you know, how, how, how we can use it perhaps? Speaker 4: (13:50) Yeah. So this biological aging or epigenetic aging clock. So dr Horvath I think is the worldwide leader in this research. So he originally published a study in 2013. There was actually another study that came out actually a little before his that did something very similar. So I should mention too, it, he's, dr Horvath is a professor at UCLA. Oh. Petitioning biologists, computational biologists. So what both these research groups did, so her about that UCLA and then another group led by Hannah at a UC San Diego. So both in Southern California. So what they did was they looked at the epigenetic, a data for thousands of individuals and the applied some complex statistical mathematical algorithms. And what they found was that there were patterns of a change, epigenetic change that occurs with age. And so by of tapping into these different patterns, they could develop a model that would predict [inaudible] predict age based on epigenetic information. So, so that's where the clock came from. So basically, depending on what your epi genetics show, you can then assign a biological age Speaker 3: (15:05) Without any information. On the individual yourself. If you can take just a drop of blood, you can actually say with, with pretty, hi Jackness call it 98, the single thing. How well would that individual is based on the work from dr Hova? So most people fall into this, this Linea Patton that would say, well, this person has these markers on the DNA before that person is the Savage, is that how it works? Speaker 4: (15:42) That's correct. That's correct. So I think there's one. So it's not, it's not just that you want to predict an age, but it's actually a signing up biological age. Yes. So I think that's a key kind of thing to keep in mind. So no, we talked about the twins earlier, you know, a few moments ago and we can see that some based on, you know, one was overweight and the other was more fit based on their lifestyle choices. So the did the choices that we make in our lives. So whether we exercise or eat a healthy diet other things, Mmm. Influencer epigenetics, which can turn in turn influence our aging. So we can actually have and accelerated aging compared to an average person or actually a slower rate of aging compared to someone else. So the Horvath clock measures that, that biology based on the epigenetics. So, you know, you may be 10 years younger biologically than your chronological age, which would be indicative of, you know, good health or good cause I've stopped choices you've made. Speaker 3: (16:45) Do you see big swings in the like, you know, 10 years or is it mostly that most people are in the, you know, within a year or two off via at their actual chronological age. Speaker 4: (16:56) So most people will be within a year or two. That's, that's Mmm, that's what you know, Horvath and others have shown. And that's what we see in our data. However you do see outliers. And I think every time we see a case where someone is okay, we do see 10 or, or greater years difference. Wow. It, it seems to be associated with, I mean, it almost in every case, there's some reason why. So some known this person may be suffering from a genetic disease or I think one thing common in, and you know, people we've looked at is, Oh, they've been treated with chemotherapy. So these are very powerful drugs that you know, obviously to, to treat cancer, but I have very strong side effects. I mean, this is very well known. These, you know, some are just not tolerated well at all. And we know these, these type of people have actually accelerated aging, very rapid aging compared to an average person. Mmm. Speaker 3: (17:53) Do you see the other way like, people who have lived a, you know, extremely good, healthy lifestyle with good food, good exercise not too much stress you know, 18 or more years younger than there a chronological edge. Speaker 4: (18:08) So I don't think just for lifestyle choices, I don't think we've seen a huge effect in that regard. But there we have seen some strong effect. I think for certain people are doing certain targeted interventions, it's a little more and just trying to eat more vegetables or run a little further. These are taking drugs. So I think Metformin Speaker 3: (18:32) hmmm Speaker 4: (18:33) There's one that's looked at very seriously for some of these anti-aging effects and we do see a pretty consistent, strong effect towards a slower aging. Yeah. Speaker 3: (18:44) [Inaudible] Is a, is an interesting one because it doesn't let up think though negatively the, the mitochondria. And, but, but it was a little bit confusing when I looked into just some surface level research on Metformin thinking, gosh, this sounds interesting. I want to have that. It, it produces more longevity, but it can damage the mitochondria. How would that work? Because your mitochondria, your rap part of this whole metabolic pertussis, I mean, it's probably too deeper questions to ask you, you know, but do you know why? Speaker 4: (19:20) Well, that's, that's a very good question, huh? The short answer is no one knows why. So, so yeah, there's sort of a antagonistic effects on or seemingly that would, that would associated with adverse health outcomes. But the data showed, we know it has been prescribed for type two diabetics years and has very good outcomes. And it seems to be off target prescribed for other melodies as well. You know, that the side effects are, are small. I mean, that's just based on you know, lots of people taking the drug. It seems that small side effects and clearly the benefits in most cases outweigh the whatever side effects may occur. Mmm. As to the reason why, I mean, it may be that the positive affects to regulate glucose metabolism, insulin, Speaker 3: (20:16) Yup. Speaker 4: (20:18) Maybe more important than the damage it causes or we have you know, just backup systems to deal with mitochondrial damage or stress that we don't have as robust. I mean, just as you know, living human beings that we don't have for when our glucose metabolism goes awry. Speaker 3: (20:35) So you know, that would be especially the case for, you know, people with diabetes or prediabetes. It has the same effect then on the healthy, you know the healthy person who doesn't have insulin resistance or any glucose Speaker 4: (20:49) Problems. So, yeah. So we get this, I get this question a lot. I would be very careful about just taking any drugs, you know, getting home from certain websites for example, I would, I would consult a physician for that. Yeah. Yeah. Cause I know your listeners are probably very interested on what types of things they can do to, to help them. Speaker 3: (21:15) Nobody don't go out there and do anything solid, not advocating this. We definitely won't. But, but it's interesting to look at the data. I know that there was a study done just a couple of years ago, I think by dr Horvath where they were able to reverse the, the epigenetics Speaker 4: (21:33) Clock Speaker 3: (21:34) In a small clinical study by giving people growth hormone and to diabetic medications, I believe. One. Mmm. And they took two and a half years off the year. Speaker 4: (21:49) Mmm. Speaker 3: (21:49) I'll say biological Speaker 4: (21:51) Age. Speaker 3: (21:53) That's, that's pretty exciting to actually be able to reverse. I mean, I know this was a small clinical trial and, and certainly not a big one. And obviously it's a very difficult area to do big blocks studies end, but a w would suggest that we're going to be able to in future reverse the aging process, which is super exciting rather than just slowing it down. Speaker 4: (22:17) Yeah. So this was the study you mentioned was a, that was a big one. So there's a lot of I don't know a lot, but there's a, there's a decent amount of studies you know, the Horvath and others have been involved in showing on ways to slow the rate of aging. But I was at a, a, a conference actually I gave a presentation along with the, dr Horvath was a keynote speaker and there was another, a surgeon Jim Watson. No. And Jim Watson said, you know, we think that we will be able to reverse actually reverse the clock. And Horvath was, this was January, 2018. He was pretty, he pushed back pretty hard on that idea. He said, you know, there's, there's nothing we found that can actually reverse aging clock. I, there's nothing in the data that shows that, you know, Jim Watson, he's a, he's a prominent Sergeant, you know, he works with patients and you know, from his medical person, he's like, well, I respectfully disagree. Yeah. And if you look at the authors on the paper, you mentioned Steve Horvath, but actually Jim Watson is, I think he's a senior author on that. Mmm. They ended up collaborating after this, you know, and [inaudible] looking into ideas from the medical side and then from, you know, dr horvath, you know, using this, these, these epigenetic aging clocks. And sure enough just as you mentioned, the study showed it was small, but it showed clearly that the aging was reversed to these individuals Speaker 3: (23:39) In a, in a very short space of time too, which is exciting to think what would happen if these interventions were, you know, extrapolated over a longer period of time. Mmm. Speaker 4: (23:52) Yeah. That's, that's right. I, you know, if you look at the, the intervention in that case, it was a drug cocktail. It was a two, two hormones, DTA I think human growth Speaker 3: (24:05) Yeah. Speaker 4: (24:06) And then I met foreman again was a drug they use to kind of help regulate some of the hormonal side effects of those drugs. And it was this three drug cocktail. Mmm. The the original goal of that study was to help reverse some of the immune decline. It had been well documented. We know our immune system starts to decline and as we grow older and the famous of course this organ that it functions in immune, you know, healthy immune function tends to get weaker and shrink. And so that's what the, the study was originally designed to just boost thymus function in the immune system. And okay. The authors showed clearly with, yeah, with, with clinical measurements, famous enemy and functions were restored and it was then shown, that's when Horvath came in and looked at the the epigenetics to show that actually reversed in these people who had responded well to the treatment. So Speaker 3: (25:04) Yeah, that's a short time frame as you mentioned. Yeah. Yeah. Very exciting. There's hope for us who are aging that we bought. So hurry up. You guys get started in so with the, the Magii and H test which people, you know, the public can go and get the SKUs. So if you wanting to actually, after listening to this episode want to go and just what your biological ages, I'll give you the address. It's just my, my DNA h.com. So DNA G a.com and you can order a test the and have the stun, which I, I'm, I'm finding fascinating from a coaching perspective and from an athlete's perspective to be able to draw a line in the sand and say, well, this is where we started from. And then we, you know, instigate L a epigenetic program for example, and our training regimes and nutrition and so on. Speaker 3: (26:00) And then perhaps in six to 12 months time retest to see what the I need a fake was. So I'm, I'm excited to be able to hopefully incorporate this into some of our, of our programs. And one of the reasons I reached out you today when we, let me go to the, look at the the testing that you do. So you're looking at the DNA methylation, is that right? Mmm. Can you explain what the United w what exactly that you're looking there with the, when you're looking at the methylation marks on DNA? Speaker 4: (26:36) Yeah, yeah, that's right. So we're looking at DNA methylation. So know anyone who wants to use our test, I might, do you need Speaker 3: (26:44) To test? Speaker 4: (26:45) We would send them a kit. Mmm. We would it comes with you know, slow land so we can take a blood drop. Mmm. That's put into a, you know, a special preservation stage or buffer solution. Speaker 3: (26:57) [Inaudible] Speaker 4: (26:57) Your preserve the integrity of the sample and then it can just be mailed back at room temperature. So it doesn't need to be frozen or cold or anything. I think also send a urine sample as well. So it's, it's, it's up to the it's each individual if they feel comfortable with, Mmm. That's sent back to us from the blood or urine sample. We will extract the DNA and then perform some fancy chemistry to quantify DNA methylation levels at a panel of genes that are known to be highly associated or highly informative of aging. Speaker 3: (27:32) Huh. Speaker 4: (27:33) Based on those values, we can then plug it into a mathematical model to predict the biological age. And again, this is, this is based off of a, you know, Horvath and others of the based on original publications. We sort of make it a economic one available too. And Speaker 3: (27:54) Sorry, Carry on. Speaker 4: (27:58) So we can make that that technology, which would otherwise not be accessible to non scientists. The general public, we can make it accessible to them. So they can, they can get their own biological age assessment. Speaker 3: (28:10) Yeah. It's really, really exciting. So, so you're looking at around 2000 different James. Mmm how do you, how do you express it? He was signs on there. They had assigned basically there was damage here. So you're looking at damage, Marcus. Speaker 4: (28:30) It's not, it's not famous markers per se. So specifically it's, it's DNA methylation. So a methyl group is a, you know, if you think from your organic chemistry, this is the most the oxidized form of carbon. A ch three is added to DNA and basis known as cytosines any basis on the cytosines. And when it's added biologically, what's going on at the molecular level is it's influencing gene expression. So helping genes turn on or off, on or off. Mmm. And these levels change over the course of our lives and it's this change that can then be related to, to, to the Speaker 3: (29:12) Marcus. Okay. I get that. Yeah. So does it take into consideration things like inflammation or cardiovascular health or kidney and liver function or metabolic metabolic state as well? Or is that readable from the DNA? Speaker 4: (29:32) Not with, not with the mighty age test. So if there's something specific like that, again, I'm in consultation with a physician. If you're worried about your Speaker 5: (29:41) Kidney health, metabolic health, Mmm. Then, right. You know, there's more specific tests to directly look at. Right, right. I think as a pan health indicator it gives you some information. Right. Cause I know that there is you know, other companies that do biological age tests that are based not on the Horvath clock, but on, I'm looking at these are the tops of biomarkers, like your inflammation, inflammation, they've always been your, your cardiovascular health. And I was trying to understand what is the difference in the, in the approach, you know, in the approaches and which one is, Mmm. Well going to give us some more exact calculation if you like. Do you know of the other ones and the difference between, well I mean, so there's, there's a lot, you know, people have been using like in a doctor's office, just a grip, the grip test, your vape. Speaker 5: (30:39) How will you walk? Yeah. The way you walk. But you know, there's a really broad era for those, for people you know, between the ages of teen until some point in your, your older years. Mmm. It's just not very, not very good. It's very precise, very precise. There's other molecular tests. Even if you look at DNA methylation or epigenetic tests, they may focus on a single gene or just a few genes having a, a more focused, you lose a lot of robustness so they can be more susceptible to small changes or small, Mmm. Environmental insults that may actually not have a big impact. So by incorporating thousands of sites into the tests, which, or my teenage test does, it's more robust to small changes. So overall picture. Yeah, that would be it. You know, cause when I heard about things like grip strength and stuff, I was like, well, if I got into the gym a lot, obviously I'm going to have a lot more grip strength. Speaker 5: (31:39) It doesn't necessarily, I'm biologically younger. Right, right. Yeah. Basically you say, I have a normal or we're better than average. Right. Or it's not good. Right? I mean that's, you get kind of a yes or no kind of a yes, yes. But it's not, it's difficult to say, you know, you know, you're looking at the also your body type, you know, like, and with your, you're a muscular person or you're a someone who is more of a flexible person, you know, there's, there's just too much. Okay. Wavering in the air. I mean things like inflammation markers of course. Can you look at the state of your health but perhaps notch the actual, you know, whether it's having damage, you mean you can have inflammation markers because you've got a cold as well, which would be skew the data satisfied. and a bad week. Speaker 5: (32:35) Yeah. And this wouldn't happen with the, with us taste. So how w I know you've done a Ted talk that I listened to that was very interesting thing and wants to look that up. We can put that in the show notes as well. We've got an aging world population and we have huge problems all around the world without, but their health care system. I think we probably can all agree with that. We're heading into times where chronic disease is going to be costing economically, governments in, in, in, you know, a lot of suffering around the world and a lot of resources. Mmm. So increasing health span is, is a very important piece of being able to lower the costs involved with chronic disease. Would you see that as being one of the areas where this this theory or science is really, really key and an important from a, from an economic standpoint as well as from the personal suffering standpoint? Speaker 5: (33:39) Right. Yeah, absolutely. Yeah. Right, right. I think the potential to benefit society is really there's a, there's a lot a DNA aging test, epigenetic aging tests can, can provide. So it is clearly the best tool, two, assess, aging accurate and precise way. Mmm. And so by using this tool, I mean, whether it's, you know, our company and our researchers doing, you know, in their own labs are their own ways. Mmm. Those interventions which will have the greatest benefit can be more rapidly identified and no, very okay track to be very cheap. I'm an actress. So this, I think this is, you know, beyond just individual testing, which I think is important. And, you know, very interesting people empower themselves by getting some information here, but broader for the broader impact it can have on society. It can be really profound. Yeah. And I know you've, you've done a little bit of work with you mentioned the, in your, in your talk you know, looking at things like sporting H, you know, like how if kids are really in the right age group or people who don't have documents working out how old they are. Speaker 5: (34:56) When they coming into countries perhaps as, as refugees without, without any paperwork and things like that. There's a, there's a, there's a whole lot of areas that this could be utilized and couldn't it. Yeah, absolutely. Yeah. So the the youth age testing I think that's, there's sort of a, the, the, the consequences are not as, as grave as like, you know, that aging population in Europe, you know, to some extent, North America and Asia. But but I, it just goes to show the potential applications for something like that. And I actually just learned that, you know, I did some work with [inaudible] law enforcement in Germany a couple of years ago for some for forensics application of using this aging. You can sort of the gauge person of interest in different law enforcement investigations. And in part thanks that work actually I just found out that lie in Germany changed December Oh about 2019. Speaker 5: (36:01) Sort of allow this scientific approach, you too well know wow. To work out someone's is being adopted in a lot of different areas. And I mean, Oh yeah. And, and for me I think in working in the, in the health as a health professional and, and training people and so on, it's just going to give us another, I'm wiping the Nantucket toolkit to get people motivated and moving and having a benchmark is really important I think for us to, well, this is where we started from and hopefully through different health interventions, we can see other results. Is there any way that we can, is there any of those things that are quantified, like what, what people are, you know, that are doing your tests perhaps and then doing different interventions, obviously not as a clinical study, but are you gathering any of the data of the interventions that people are undertaking to change the biological age? Speaker 5: (37:01) Let's see. What has it effect? So I mean, we have to be sort of careful about this, right? So that, I mean, the personal information of ours customers is yes. Obviously I can only do so much, right? I mean we're not, we're not trying to but so what I can say, we work with clinics, certain clinics doctors. So the doctors are incorporating this test into part of their medical practice and whether they're advising certain, you know, dietary interventions or different exercise programs or they can use this for their medical practically, I mentioned Metformin earlier. We are working with the group by testing this. So that's something that we, yeah, we can say has had a, yeah, a two. The rate of aging in these, in the samples, the subjects that we've examined. Mmm, yeah. Mmm. Yeah. Yeah. So that's got an interesting future too. I mean, what, what are you think, so are there any interventions which have been proven besides a Metformin and growth hormone? Mmm. To actually slow down the aging or to pervasive stop the aging process? Mmm, well that have been proven to be beneficial as it, you know, like lifestyle interventions. So yes, yes, there are. So, but I, I needed qualify that. So this has been clearly shown to occur in laboratory animals, so model research organisms and a lot of these, Speaker 4: (38:34) These pathways a Speaker 4: (38:35) Evolutionarily shared all the way from, you know, simple East to or complex organisms like fruit flies and more recently into mammals like mice lab, mice rats or even nonhuman primates. So there's clearly potential. Mmm. You know some of these interventions are related to altering metabolic pathways, insulin response. Mmm. Mmm. I think one that's gained a lot of interest in you know, the broader news media is this compound resveratrol. Yes. Resveratrol found in a grapes in higher concentrations, in certain nuts. I'm certain it's been shown to activate certain pathways related to protecting our DNA or protecting our genes and genomes and also influencing that metabolism in certain ways. So in laboratory animals, there's clear evidence to show that aging can be slow to reverse. In humans it's not as clear. So again, it's more difficult to do these types of studies. Speaker 4: (39:39) Okay. Ethical and logistical reasons. Yeah. But the Metformin is a hot candidate drug especially because it is well tolerated. So, so this may be something that can be easily prescribed. And individuals we mentioned the study that came out last last fall where the the growth hormone and Metformin combination reverse the aging in this was in a small court of men from the ages of 52 late sixties, I think. Years of age. Mmm. In terms of those are for reversing the aging clock. There's also evidence showing that the clock can be slowed from simple lifestyle changes. So if you think about diet, so it appears that, you know eating more plants plant based foods, so fruits and vegetables. So right carotinoids levels in the blood. You know, indicators of the. Speaker 4: (40:37) Okay. Metabolism are associated with slower rates of aging. Interestingly, a fish, actually, those who consume more fish, it seems to have the greatest impact on a slowing the rate of aging. Well, okay. That's interesting, huh? Yeah. Even greater than the vegetarian diets. That's what the data indicates at this time, at least. Right. Also you know, we can look at things that accelerate the aging clock. Mmm. So certain corn oil certain insulin levels a triglyceride levels you know, elevated or, or, or levels that are out of whack or associated with an accelerated aging. So these are indicators of a poor diet. Yup. I think one that's a, everyone's sort of interested to hear or happy to hear is that actually moderate alcohol consumption. It's associated with a slower Speaker 3: (41:34) Rate of eating. So, so we have an all glass of red wine with berry in it, Speaker 4: (41:40) I think. I think so. Yeah. Yeah. But this has been a also shown to have beneficial effects on heart health. So it's interesting to see that the studies our agreement, you know, coming back, coming at it from different angles, but, you know, finding beneficial health, mental health. Speaker 3: (41:55) So the, the things that we sort of intuitively know that exercise lots of fruit and veggies and you know, that type of thing. It can definitely slow down the aging clock. It's an exercise aspect of it as Sierra, any sort of data or omit, it's how much and what types of exercise or anything like that. Speaker 4: (42:22) So not that I'm aware of. So not that I'm aware of. But that's, but that's interesting. What you say is, you know, people hear this and they say, okay, great, eat more vegetables. You know, I already knew that. Right. But it's interesting the study, but I think you can see, right. So, okay, yes, vegetables are associated with slow rates of aging. So increase that. So it gives, we can show that in the data, but but what's really interesting about the clock of the state, but if you want, if there was one thing you could pick to slow your rate of aging, actually it's fish, right? So it's, it's a it kinda shows you you know, we can kind of rank these. So what's the most important thing? So, you know, vegetables are important, but actually according to the data fishes is even more important. Mmm. And you knew, and also people that die. While I've been doing vegetables, I've been actively trying to do better in, and so I've already incorporated that, but, well, what else is there that that might be, it might be missing. Oh, so a olive oil seems to be also beneficial. A dietary component. It can be incorporated absolute rate of aging. So, so what the clock does is it's able to quantify these and really pinpoint with some precision what, Speaker 3: (43:33) Yeah, yeah. Rather than just one out a feeling as and what we've, you know, at the top, some studies have seen what about ketones and the key she turned on us. Any, any data there on MCT oils or ketone esters or anything like that? Speaker 4: (43:52) Again, I'm not familiar with those studies. We haven't conducted any and we're not working with anyone specifically looking at this sort of thing that I'm aware of some. Again, you know, a lot of institutes and clinics are incorporating different things. We don't necessarily know what they're doing. I mean, it could be very well be that, you know, some of these changes are being prescribed or administered in certain way. I simply don't know the answer to that. Speaker 3: (44:16) Yeah, yeah, yeah. No, fair enough. So this is, you know, to actually get the data to get some concrete data is actually really, really helpful. And strengthening the arguments for reaching the goals and cutting out the, the donuts and the, the the biscuits in the sugar and so on. And, and the more data we have behind that, the beta what I had dr Andrew go Andrews on, on the podcast. We all would go, I'm looking at telling me and like something and NTA aging. Is there any sort of crossover between those sort of areas, like in the anti aging sciences in do you look at it telling me length is or anything like that in these biological tests or are they completely different area of science? Speaker 4: (45:11) It is different. It is different. So Tila mirrors have been I think before Horvath and Hanham's studies a few years ago came out showing the power of epigenetic aging assessments tumors were probably the most popular, well, I color test to look at this since then. You know, clearly that these DNA methylation clocks are by far the most accurate, most precise and robust to measure biological aging. Horvath and others tried to kind of assess how this interaction between Tealium or Lang and you know, epigenetic change and they found that they're not measuring the same thing. So they in the biology is they're looking at different things. And you know, I, I think for, you know, telomeres, you know, I just, in my opinion, I, I think they've been Sur surpassed by the power of the, you know, yeah. Speaker 4: (46:07) Inherent robustness of looking at epigenetics to assess aging. I think, you know, concrete example of this is so the telomere length, so the longer the telomeres, sort of the slower aging or more youthful, that's, that's the basic idea. And as those shrink, it indicates increased age or advanced age. That's, that's the basic idea. We find that this, you know, completely breaks down. When you look at something like cancer where a hallmark is the ability to increase the length of telomeres to kind of okay. You know, maintain the integrity of cancer cells or tumor size. And if you knew, if you look at it from that perspective, they would look biologically young. If you look at the same type. Okay. Tissue cancer tissue according to the epigenetic clock. I mean, these show very accelerated aging. So it's, it's clear indication of it for health. The telomere tests wouldn't be able to show that at all. You were so good. Sorry. Okay. Speaker 3: (46:59) Thats Really you know, emerging area of science that that's, I'm going to be interesting in the next few years to watch. Mmm. Keith, thank you so much for your time today. Is it, I, I think we've, we've, we've covered quite a lot of ground. Do you think there's anything we've missed out that, that people should hear about? In regards to doing, you know, like doing mydnage test can you actually, because we're sitting in New Zealand and obviously a lot of my lessons are in Zealand and Australia. Can you do the test from that far away when you're going to be seeding it in the post? Speaker 4: (47:33) Yes. So the test, so I think we're just trying to get the but just logistics, business-wise, just the paperwork in order too. We've gotten a lot of demand in Australia, New Zealand, you know, it should be a broadly. Yeah. Currently we're only offering and North America, Mmm. In Europe. Mmm. Canada, U S and . But we're trying to get to a New Zealand, Austria. That should be soon. So any listeners in New Zealand or thereabouts, that should be available very soon. Technically there's no issue. So the once the kids arrive the blood or urine sample can be mixed with the preservative solution. This is preservation. Yeah. Shipped back to our labs in California at room temperature with no problems. Speaker 3: (48:22) Nice. So we should be through that. Still already the tastes, even though you haven't got the laboratories and stuff down here, we came can already, you know, through that and seen it. But look, thank you so much for your time today. I think this is a really interesting area of science. And I'm encouraged people to think about doing these tastes because, you know, I will give you a line in the same tree to motivate you. I think a lot of 'em, you know motivation is a big key to being successful in your, in demons to be better and stronger and be there and plaster and normalize going to good things and tuning the, we're slowing down the clock with tuning back even. So having tastes like this that are available to the public, the weekly is exciting. You know, I think it gives us another thing that we can do that we can then use to help better our lives, you know, as we, as we move forward. Speaker 4: (49:20) Yeah. That's the mission of you know, making this test available to the broader, the broader public, Speaker 3: (49:25) The more things that are available direct to the public, the there or my opinion, it's not dangerous and you know, but being a bit of a biohacker, obviously I have a bit of a, a boss towards having your own power and making your own decisions. But I think this one is a, you know, it's a no brainer. It costs so obviously, but apart from that, if you you want to try this out I'll have the links in the show notes and case thank you so much for your time today. I wish you well with all your studies and with loved side contact and yeah, very, very interesting conversation today. Speaker 4: (50:03) Oh my pleasure. Lisa. It was great to, to speak with you. Thank you very much. Speaker 2: (50:07) If your brain is not functioning at its best in checkout, what the team at vielight.com Do now being like producers, photo biomodulation devices, your brain function, the pin's largely on the health of the energy sources of the brain cells. In other words, the mitochondria and research has shown that your brain with near infrared light revitalizes mitochondria. I use these devices daily for both my own optimal brain function and also for other age-related decline issues and also for my mom's brain rehabilitation after her aneurism and stroke. So check out what the team do vielight.com. That's V I E L I G H T .com. And use the code "TAMATI" and checkout to get 10% of any of their devices. Speaker 1: (50:58) That's it this week for pushing the limits. Be sure to write, review, and share with your friends and head over and visit Lisa and her team at Lisatamati.com.

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Precision Approach to Aging

Precisione: The Healthcast

Play Episode Listen Later Jan 4, 2020 32:32

Dr. Tom Stubbs, PhD Tom graduated from Oxford University with a 1st in biochemistry and went on to Cambridge University to study the epigenetics of ageing. Tom built the first ageing model in mice, and worked closely with Prof. Steve Horvath of UCLA. He saw the potential for epigenetics and AI to open a new frontier in health sciences, quantifying wellbeing and ageing as never before. Tom founded Chronomics in 2017 to bring epigenetics out of the lab and into people's hands for proactive and preventive health management. What you will learn from this episode: How the best way to determine our biological age is. What epigenetics is all about. How epigenetic testing is different from telomere testing. How we can slow down our age acceleration. How environmental triggers or toxins like smoking can make us age faster and what we can do about it to try to reverse that process. How to learn more about our guest: https://www.chronomics.com https://www.linkedin.com/in/dr-tom-stubbs-982b3071/?originalSubdomain=uk https://www.facebook.com/chronomics/ https://www.instagram.com/chronomics/?hl=en Please enjoy, share, rate and review our podcast and help us bring the message about precision health care to the world!

ai prof ucla oxford university precision cambridge university originalsubdomain steve horvath chronomics

Nerd Alert #4: Biological Age Reversed w/ This Protocol

High Intensity Health with Mike Mutzel, MS

Play Episode Listen Later Dec 6, 2019 20:13

Next time you hear someone say, “We’re all getting older together!” around a birthday, remind them that’s not entirely true. Links to show notes/research: http://bit.ly/388zyg0 This episode is brought to you by our very own, MYOXCIENCE Nutrition, tools to support your sleep, blood sugar health and more. https://myoxcience.com/ Use code HIH to save 17% OFF. About Today's Show: New testing, aka the myDNAge test, reveals our “epigenetic aging clock” that’s been characterized by Dr. Steve Horvath. This test analyses methylation patterns on more than 2,000 gene regions. So, while we’re all aging at the same chronological time, our biological age is variable based upon our diets and lifestyles. In fact, Dr. Horvath recently published data showing how low-dose growth hormone DHEA combined with berberine can actually slow down biological aging. Here’s the video review and link to the study: We discuss more about: -Age-associated inflammation or “inflammaging” (chronic, low-grade inflammation) as the reason why you age -How this protocol enlarges the thymus gland, which has been shown to shrink with age -DHEA and metformin as tools to slow down age-related changes in glucose metabolism Personally, I’ve been a huge fan of both DHEA and berberine (which functions similarly to metformin) for a long time.

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#049 Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & More

phd dna theory alzheimer's disease genetics harvard medical school sinclair nad informational david sinclair resveratrol paul f nicotinamide sirtuins found my fitness david a sinclair steve horvath

Play Episode Listen Later Nov 6, 2019 82:02

David A. Sinclair David A. Sinclair, PhD, is a professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biological Mechanisms of Aging. He is the co-founder of the journal Aging, where he serves as co-chief editor. Dr. Sinclair's work focuses on understanding the mechanisms that drive human aging and identifying ways to slow or reverse aging's effects. In particular, he has examined the role of sirtuins in disease and aging, with special emphasis on how sirtuin activity is modulated by compounds produced by the body as well as those consumed in the diet, such as resveratrol. His work has implications for human metabolism, mitochondrial and neurological health, and cancer. In this episode, you'll discover: 00:17:59 - How caloric restriction, fasting, and exercise increase levels of a molecule called NAD+ and how this activates sirtuins, a family of genes involved in longevity. 00:21:47 - How NAD+ levels and sirtuin activities decrease with age, and how animal studies suggest that raising cellular NAD+ levels can trick the body into thinking it is younger. 00:23:03 - How resveratrol enhances the binding of sirtuins to NAD+ thus making sirtuins more easily activated for a longer period. 00:27:36 - We also discuss Steve Horvath's epigenetic aging clock, which measures DNA methylation groups, and how they may play a role in widespread gene regulation, including sirtuin genes, and how NAD+ may participate in resetting the clock. 00:31:54 - How the signal that resets the epigenetic clock in mice involves the Yamanaka factors -- a group of four transcription factors that can reprogram an adult cell to become a pluripotent stem cell that can form any cell type. 00:46:48 - How resveratrol is a xenohormetic compound and is produced when grape plants are stressed either in response to fungus or lack of water. 00:55:35 - How a phase 2 clinical trial involving people with Alzheimer's disease showed resveratrol improved cognitive function, improved cerebrospinal fluid amyloid beta levels, lowered markers of activated microglia, and more. 00:58:03 - How both nicotinamide riboside and nicotinamide mononucleotide have been shown to improve cognitive function and brain pathology in mice that have been engineered to get a disease similar to Alzheimer's disease. 01:06:19 - How older mice that were given nicotinamide mononucleotide experienced delayed aging in the liver, muscle, immune cells, eyes, and bones, but those that took a lower dose had improved mitochondrial function and enhanced physical performance. 01:01:22 - How there may be challenges in translating animal studies on nicotinamide riboside and nicotinamide mononucleotide to humans particularly due to the need to determine the dose required to promote health benefits. And so much more! If you're interested in learning more, you can read the full show notes here: https://www.foundmyfitness.com/episodes/david-sinclair Join over 300,000 people and get the latest distilled information straight to your inbox weekly: https://www.foundmyfitness.com/newsletter Become a FoundMyFitness premium member to get access to exclusive episodes, emails, live Q+A's with Rhonda and more: https://www.foundmyfitness.com/crowdsponsor

Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & More

Podcast Notes Playlist: Fitness

Play Episode Listen Later Nov 6, 2019 82:02

Podcast Notes Key Takeaways Sirtuins are a class of proteins that protect organisms from deterioration and disease by regulating gene expression (turning genes on/off)Sirtuins need NAD+ to function properlyAs we get older, our NAD+ levels dropBy the time you’re 50, your NAD levels are about half what they were when you were 20“You could argue NAD+ is the most important molecule in the body, maybe with the exception of ATP. But without either of them, you’re dead in about 30 seconds.” – David SinclairNR and NMN are NAD+ precursors you can supplement with – both have been shown to raise NAD+ levelsYou can also raise NAD+ levels with fasting and exercise If sirtuins are the car, and NAD+ is the fuel, resveratrol is the accelerator pedalResveratrol also seems to improve cardiovascular health as well as stimulate autophagy pathwaysThe primary cause of aging is a loss of epigenetic information (the pattern to which genes are turned on/off)Read the full notes @ podcastnotes.orgDavid A. Sinclair, PhD, is a professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biological Mechanisms of Aging. He is the co-founder of the journal Aging, where he serves as co-chief editor. Dr. Sinclair's work focuses on understanding the mechanisms that drive human aging and identifying ways to slow or reverse aging's effects. In particular, he has examined the role of sirtuins in disease and aging, with special emphasis on how sirtuin activity is modulated by compounds produced by the body as well as those consumed in the diet, such as resveratrol. His work has implications for human metabolism, mitochondrial and neurological health, and cancer. In this episode, we discuss... 00:17:59 - How caloric restriction, fasting, and exercise increase levels of a molecule called NAD+ and how this activates sirtuins, a family of genes involved in longevity. 00:21:47 - How NAD+ levels and sirtuin activities decrease with age, and how animal studies suggest that raising cellular NAD+ levels can trick the body into thinking it is younger. 00:23:03 - How resveratrol enhances the binding of sirtuins to NAD+ thus making sirtuins more easily activated for a longer period. 00:27:36 - We also discuss Steve Horvath's epigenetic aging clock, which measures DNA methylation groups, and how they may play a role in widespread gene regulation, including sirtuin genes, and how NAD+ may participate in resetting the clock. 00:31:54 - How the signal that resets the epigenetic clock in mice involves the Yamanaka factors -- a group of four transcription factors that can reprogram an adult cell to become a pluripotent stem cell that can form any cell type. 00:46:48 - How resveratrol is a xenohormetic compound and is produced when grape plants are stressed either in response to fungus or lack of water. 00:55:35 - How a phase 2 clinical trial involving people with Alzheimer's disease showed resveratrol improved cognitive function, improved cerebrospinal fluid amyloid beta levels, lowered markers of activated microglia, and more. 00:58:03 - How both nicotinamide riboside and nicotinamide mononucleotide have been shown to improve cognitive function and brain pathology in mice that have been engineered to get a disease similar to Alzheimer's disease. 01:06:19 - How older mice that were given nicotinamide mononucleotide experienced delayed aging in the liver, muscle, immune cells, eyes, and bones, but those that took a lower dose had improved mitochondrial function and enhanced physical performance. 01:01:22 - How there may be challenges in translating animal studies on nicotinamide riboside and nicotinamide mononucleotide to humans particularly due to the need to determine the dose required to promote health benefits. And so much more! Click here to get this episode's show notes and transcript Watch this episode's highlights on the FMF Clips channel Get early access with the premium members early access podcast feed, monthly Q&A sessions, an exclusive bi-weekly science digest email, and more! Click here to get started. Submit your raw genetic data to get the latest version of the genetic report at foundmyfitness.com/genetics.

phd dna theory alzheimer's disease genetics harvard medical school sinclair atp nad informational david sinclair resveratrol nmn paul f nicotinamide sirtuins steve horvath

Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & More

phd dna theory alzheimer's disease genetics harvard medical school sinclair nad informational david sinclair resveratrol paul f nicotinamide sirtuins david a sinclair steve horvath

Play Episode Listen Later Nov 6, 2019 82:02

David A. Sinclair, PhD, is a professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biological Mechanisms of Aging. He is the co-founder of the journal Aging, where he serves as co-chief editor. Dr. Sinclair's work focuses on understanding the mechanisms that drive human aging and identifying ways to slow or reverse aging's effects. In particular, he has examined the role of sirtuins in disease and aging, with special emphasis on how sirtuin activity is modulated by compounds produced by the body as well as those consumed in the diet, such as resveratrol. His work has implications for human metabolism, mitochondrial and neurological health, and cancer. In this episode, we discuss... 00:17:59 - How caloric restriction, fasting, and exercise increase levels of a molecule called NAD+ and how this activates sirtuins, a family of genes involved in longevity. 00:21:47 - How NAD+ levels and sirtuin activities decrease with age, and how animal studies suggest that raising cellular NAD+ levels can trick the body into thinking it is younger. 00:23:03 - How resveratrol enhances the binding of sirtuins to NAD+ thus making sirtuins more easily activated for a longer period. 00:27:36 - We also discuss Steve Horvath's epigenetic aging clock, which measures DNA methylation groups, and how they may play a role in widespread gene regulation, including sirtuin genes, and how NAD+ may participate in resetting the clock. 00:31:54 - How the signal that resets the epigenetic clock in mice involves the Yamanaka factors -- a group of four transcription factors that can reprogram an adult cell to become a pluripotent stem cell that can form any cell type. 00:46:48 - How resveratrol is a xenohormetic compound and is produced when grape plants are stressed either in response to fungus or lack of water. 00:55:35 - How a phase 2 clinical trial involving people with Alzheimer's disease showed resveratrol improved cognitive function, improved cerebrospinal fluid amyloid beta levels, lowered markers of activated microglia, and more. 00:58:03 - How both nicotinamide riboside and nicotinamide mononucleotide have been shown to improve cognitive function and brain pathology in mice that have been engineered to get a disease similar to Alzheimer's disease. 01:06:19 - How older mice that were given nicotinamide mononucleotide experienced delayed aging in the liver, muscle, immune cells, eyes, and bones, but those that took a lower dose had improved mitochondrial function and enhanced physical performance. 01:01:22 - How there may be challenges in translating animal studies on nicotinamide riboside and nicotinamide mononucleotide to humans particularly due to the need to determine the dose required to promote health benefits. And so much more! Click here to get this episode's show notes and transcript Watch this episode's highlights on the FMF Clips channel Get early access with the premium members early access podcast feed, monthly Q&A sessions, an exclusive bi-weekly science digest email, and more! Click here to get started. Submit your raw genetic data to get the latest version of the genetic report at foundmyfitness.com/genetics.

The DataBETA project, and Aging Interventions: Dr Josh Mitteldorf

Move the human story forward! ™ ideaXme

Play Episode Listen Later Oct 21, 2019 45:29

Ira Pastor, ideaXme longevity and aging ambassador and founder of Bioquark, interviews evolutionary biologist, researcher, and author, Dr. Josh Mitteldorf. Ira Pastor Comments: On the last couple of shows we’ve been spending a lot of time on the different hierarchical levels of the aging processes, talking about the genome, the microbiome, tissue engineering, systems biology, and many other topics, and we’ve been speaking to a broad range of thought leaders in these various fields. As the study of aging and longevity as areas of biotherapeutic interventions has become more popular in recent years, an extensive catalogue has grown, and continues to grow, with everyone’s key aging hallmark, or damage target of interest, piling on the mix. This lengthy list, many of which we’ve touched on during the show, currently includes, but is not limited to, the following: inflammation, oxidation, heat shock, microbial burden, xeno-toxin accumulation, somatic mutations to the genome, epigenetic modifications, stem cell exhaustion, senescence cell accumulation, damaged mitochondria, telomere variability, ECM cross-linking, nutrient sensing dysfunction, intra / extra-cellular aggregates / junk accumulation, and so on. While this list, no doubt, contains a wide variety of fascinating topics connected to health and aging, and areas for potential intervention that may improve outcomes in various disease states associated with aging, we still have not yet touched on a unified picture of why we age in the first place. In addition, we have not yet touched on many of the paradoxes that get swept under the rug that challenge a lot of the ingrained doctrine in longevity biomedical research. These paradoxes include: Why do some extremely damaged organisms live long healthy lives? Why do some pristine organisms drop dead in the prime of life? Why are all of these aging hallmarks, or forms of damage, that I have listed above, not only found in elderly, decrepit, disease ridden individuals, but also happen to be all found (some to a much greater degree proportionately) in the earliest stages of life in developing embryos and fetuses? We still have an incomplete big picture of aging and that’s no good if we want to truly intervene in it. That’s why I’m so happy that joining us today to take us deeper into this topic, and expose us to some truly fascinating ideas and theory, is Dr. Josh Mitteldorf. After earning a PhD in astrophysics at University of Pennsylvania and spending a decade or so in that field, as well as in the areas of optical design and energy conservation, Dr. Mitteldorf made a move and transitioned into the field of evolutionary biology and currently studies evolutionary theory of aging using various computer simulations. He has spent a lot of time over the years looking to correct what he feels is a fundamental error in the foundations of evolutionary theory where he feels that evolutionary biologists had focused too much on the "selfish gene theory" (the gene-centered view of evolution that purely holds that adaptive evolution occurs through the differential survival of competing genes), and not enough on the ecological context surrounding those organisms and their genes, which he feels has everything to do with why we age and, by extension, what we have to do to stay healthy as we get older. Over the years he has lectured extensively at universities including Harvard, MIT, Berkeley, Bryn Mawr, LaSalle and Temple. He’s the author of two books on the topic including Cracking the Aging Code: The New Science of Growing Old - And What It Means for Staying Young and Aging is a Group-Selected Adaptation: Theory, Evidence, and Medical Implications. He also is responsible for the “Aging Maters / Playing the Game for a Longer Life” blog, which is truly an encyclopedic resource for all things happening in the longevity biotech space. He is also creator of the Data-BETA project, a project conducted in cooperation with the UCLA laboratory of Steve Horvath, to study the synergy of various different supplements and drug interventions, designed to find the rare combinations that work together to produce a big anti-aging benefit. On this show we will hear from Dr. Mitteldorf: About his background and what it is like to be astrophysicist in the world of evolutionary biology and aging. His aging theories. The Data-BETA Project. His other passions including meditation, yoga, music, environmentalism, and campaigning for a smoke-free / tobacco-free world. For the full text with links please visit www.radioideaxme.com. ideaXme is a global podcast, creator series and mentor programme. Mission: Move the human story forward!™ ideaXme Ltd.

Wie man das Altern aufhält

Der Benecke | radioeins

Play Episode Listen Later Oct 12, 2019 6:22

Es klingt ein wenig nach der Rückkehr in den Garten Eden oder vielleicht auch wie der Eintritt ins Zeitalter der Vampire: Altersforscher haben eine kleine Gruppe von Menschen um 18 Monate verjüngt. Einem der bereits ergrauten Herren sprießen jetzt wieder dunkle Haare. Doch woran erkennt man, dass sich die Lebensuhr tatsächlich rückwärts dreht? Ein Autor der Studie, Steve Horvath, hat auch ein Verfahren entwickelt, mit dem sich das biologische Alter von Menschen erfassen lässt. Dr. Mark Benecke ist unser Spezialist für das Leben nach dem Tod. Ob ihm durch die Anti-Aging Studie die Arbeitslosigkeit droht, das erzählt er uns selbst.

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Roundtable Discussion on Telomere | Dr. Steve Horvath from the UCLA Fielding School of Public Health

dna ucla roundtable roundtable discussion ori fielding horvath telomere school of public health epigenome steve horvath

Play Episode Listen Later Aug 26, 2019 30:16

Roundtable discussion involving Dr. Yunsung Lee, Dr. Anil P.S. Ori, Dr. Ake T. Lu, and Dr. Steve Horvath talking about the connections between Dr. Horvath's two papers submitted to the Journal Aging-US “Epigenome-wide association study of leukocyte telomere length” and “DNA methylation-based estimator of telomere length” "Epigenome-wide association study of leukocyte telomere length" Full text - https://www.aging-us.com/article/102230/text Press release - https://www.aging-us.com/news_room/epigenome-wide-association-study-of-leukocyte-telomere-length "DNA methylation-based estimator of telomere length" - Full text - https://www.aging-us.com/article/102173/text Press release - https://www.aging-us.com/news_room/dna-methylation-based-estimator-of-telomere-length

#90: Mapping Autophagy with Dr. Jeffrey Bland

15-Minute Matrix

Play Episode Listen Later Aug 9, 2019 17:18

In today’s episode Dr. Jeffrey Bland shares his wisdom on the factors that impact cellular repair and renewal, a process known as autophagy. Autophagy is an indicator of long-term health and optimal function and in turn, has many determinants, from the modifiable lifestyle factors to key biomarkers. Tune-in to hone your cellular biochemistry! August 9, 2019 > Click here to download the completed Matrix from this week’s episode > You can learn more about Dr. Bland’s work and PLMI here > Dr. Bland’s brilliant book ‘The Disease Delusion’ is a must read! Still curious? The references that Dr. Bland noted include: > Dr. Valter Longo > Dr. Satchidananda Panda > Steve Horvath Get 15-Minute Matrix podcast notifications delivered to your inbox!

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#059 - Are You Biologically Older or Younger Than Your Chronological Age? - Ken Raj, PhD

humanOS Radio

Play Episode Listen Later May 28, 2019 33:08

We tend to think of age in terms of the number of years we have been alive - meaning our chronological age. But the year that you were born is not necessarily an accurate measure of your health or your life expectancy. We are coming to realize that a better predictor is your biological age - and that can be quite different from your chronological age. So how do you learn your biological age? And what can you do with this information? In this episode of humanOS Radio, Dan speaks with Ken Raj. Ken is a Senior Scientific Group Leader at Public Health London, and has worked extensively with Dr. Steve Horvath of UCLA in developing and interpreting genomic biomarkers of aging. They are best known for developing the “epigenetic clock,” a tool that predicts life expectancy by examining age-related changes to DNA methylation, then using that information to calculate biological age in relation to chronological age. The epigenetic clock is able to predict life expectancy with remarkable accuracy, with a margin of error of plus or minus three years. In this podcast, we discuss: -How the epigenetic clock uses DNA methylation to compare biological to chronological age. -Whether DNA methylation changes are the “drivers” or the “passengers” of biological aging, and how direct a role they play in the aging process. -Whether or not epigenetic changes can be passed down from generation to generation. -Whether or not someone with a biological age greater than their chronological age is more likely to develop certain pathologies. -On the other hand, whether having a younger biological age than chronological age means greater health and a longer life. -What diet and lifestyle factors have been researched to show an impact on epigenetic aging. -Whether or not epigenetic drugs have the ability to modify this clock and slow aging. -The potential for extracting the exact mechanisms through which things like exercise and certain dietary interventions slow down epigenetic aging. -If the epigenetic clock can be used for earlier diagnosis of such age-related conditions as cancer, diabetes and neurodegenerative diseases, leading to better outcomes. To learn more, check out the blog!

dna ucla older younger chronological biologically steve horvath

#66: Mapping Epigenetic Methylation with Dr. Kara Fitzgerald

15-Minute Matrix

Play Episode Listen Later Feb 28, 2019 16:35

Dr. Kara Fitzgerald speaks my language in this week’s podcast! She reports that our methylation “toolkit” should incorporate diet, food-based nutrients, sleep, stress reduction, detoxification, exercise and more. Tune-in to better understand how methylation is both mediated by epigenetic factors and how it acts as a mediator itself. Confused? I promise you won’t be after listening. March 1, 2019 > Click here to download the completed Matrix from this week’s episode > Get your hands on Dr. Fitzgerald’s ‘Methylation, Diet & Lifestyle’ book here > To access her Methylation Adaptogen Handout, head to her website > Information regarding the Epigenetic Clock, from Steve Horvath at UCLA can be found here > You might also enjoy Tom Malterre’s episode of the podcast mapping sulforaphane (episode #10) > And if you don’t have my 3 Tiers to Epigenetic and Nutrition Mastery, download that now! Get 15-Minute Matrix podcast notifications delivered to your inbox!

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Meeple Maniacs Radiocast #121 - Jogatina BG News e Meeple Hazard com Moisés da Moby Studio

Play Episode Listen Later Aug 22, 2018 75:18

Estréia do novo Meeple Maniacs Radiocast com participação especial de André Zabu do Jogatina BG trazendo um novo bloco de notícias. E o entrevistado no Meeple Hazard será nosso convidado Moisés Pacheco, co-designer do jogo Grasse, que está em financiamento coletivo. https://www.catarse.me/grasse Jogatina BG: https://www.facebook.com/jogatinabg/ Este programa é um oferecimento de nossos assinantes.Seja um colaborador mensal do canal em https://www.catarse.me/meeplemaniacs E da Loja Lúdica. Nossa loja parceira https://www.lojaludica.com.br JOGOS QUE VIRAM MESA Pantone - https://boardgamegeek.com/boardgame/248584/pantone-game RailRoad Ink - https://www.cmon.com/product/railroad-ink/railroad-ink Hail Hydra - https://boardgamegeek.com/boardgame/256877/hail-hydra MEEPLE NEWS COM ANDRÉ ZABU DO JBG NEWS Notícia 1 - A editora Steamforged anunciou a versão de boardgame do jogo exclusivo de Playstation 4: Horizon Zero Dawn - o jogo eletrônico foi produzido pela Guerrilla e é um dos títulos mais legais para você jogar no console da sony :hearts:. Sobre o boardgame, não há mais informações sobre preço e data de lançamento: http://steamforged.com/sfg-news-blog/hzdtbg Notícia 2 - Christian T. Petersen, fundador da editora Fantasy Flight Games (1995) e idealizador da franquia Twilight Imperium, deixará o cargo de CEO da Asmodee North America no final do ano fiscal de 2018. Após a saída dele a Asmodee North America terá 2 seguimento com 2 gerências: Asmodee North America Publishing que será liderado por Steve Horvath e Asmodee North America Distribution que será liderado por Andre Kieren. Muito se especula sobre a saída dele do cargo de CEO, ainda mais com relação a recente venda das ações do Grupo Asmodee para o grupo Eurazeo. http://bit.ly/2O8O78j Notícia 3 - No ano que vem vai rolar a campanha via kickStarter da versão de boardgame de Bloodborne pela editora CMON. Essa informação foi revelada pelo twitter do designer Eric M. Lang https://twitter.com/eric_lang/status/1025889793731784704 Notícia 4 - A Horrible Games anunciou para a Essen a 2ª expansão para Potion Explosion que irá trazer a opção de jogar com um 6º jogador, além de 2 novas poções (the Generosity Confection e the Concentrate of Selfishness!), 1 novo dispensador de ingredientes e 1 novo modo de jogo para 5-6 jogadores http://bit.ly/2vv0CEx Notícia 5 - A editora brasileira Geeks N' Orcs em parceria com o ilustrador/quadrinistra Vitor Cafaggi anunciaram para o mês de setembro a campanha de financiamento coletivo de um jogo baseado nas Histórias de Quadrinho de Valente lançadas aqui no Brasil pela editora Panini https://www.google.com.br/search?q=cao+valente+Vitor+Cafaggi&tbm=isch&tbo=u&source=univ&sa=X&ved=2ahUKEwiVg8T74fzcAhVBIZAKHZkqCGgQsAR6BAgDEAE&biw=1229&bih=613 " Valente – O Amor em Jogo é um jogo de construção de narrativa baseado nas histórias criadas por mim, Vitor Cafaggi, sobre este jovem e garboso cãozinho, o Valente. Através da aleatoriedade das cartas e usando sua própria habilidade, raciocínio e experiência, os jogadores vão montar tirinhas contando a história e as desventuras amorosas do Valente. Os jogadores têm o desafio de guiar o nosso herói para a escolha certa. " https://pt.wikipedia.org/wiki/Valente_(quadrinhos) Notícia 6 - Saiu mais informações sobre do que se trata o Discover: Lands Unknown da editora Fantasy Flight Games. Assim como KeyForge: Call of the Archons, esse título vai seguir o formato apresentado pela editora no selo Unique Games - que tem a proposta de trazer experiências únicas em cada unidade vendida do jogo - e foi desenvolvido por Corey Konieczka, e se trata um jogo de exploração e sobrevivência que atende de 1 a 4 jogadores, com seu lançamento previsto para o final desse ano https://www.fantasyflightgames.com/en/news/2018/8/13/discover-lands-unknown/ Notícia 7 - A Kronos Games em parceira com a GaleForce Nine anunciaram o jogo Covil dos Dragões (em Inglês: Vault of Dragons) para o mercado brasileiro. Esse título é uma reimplementação do jogo Sons of Anarchy: Men of Mayhem para o universo de D&D - visto que a G9F perdeu a licença do série de TV. A informação foi revelada na live no canal do Meeple Maniacs na última terça-feira. https://boardgamegeek.com/boardgame/255332/vault-dragons Notícia 8 - A franquia Dune - dos livros de Frank Herbert - terá diversos produtos na linha de jogos, miniaturas e RPG pela Gale Force Nine. http://bit.ly/2Mgr1QW https://www.google.com.br/search?q=DUNE&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiT9rXK4vzcAhXFEpAKHVXeAMMQ_AUICigB&biw=1229&bih=613 Notícia 9 - A empresa Games Workshop quer transformar as suas propriedades intelectuais, em especial a franquia Warhammer, em filmes ou séries de TV. Essas informações foram divulgada no Relatório Anual da empresa para investidores e acionistas, emitido em 31/07/2018, confira aqui: https://www.google.com.br/search?q=WARHAMMER&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjBuJvm4vzcAhVCxpAKHTVlC2sQ_AUICigB&biw=1229&bih=613 Notícia 10 - O jogo The Towers of Akhanos (As Torres de Arkhanos) de Daniel Alves e Eurico Cunha terá campanha de Financiamento Coletivo via kickstarter pela editora Creative Games Studio LLC ainda esse ano: http://bit.ly/2OGdHSm MEEPLE HAZARD MOISÉS PACHECO DE SOUZA - O MOITA CO-DESIGNER DO JOGO GRASSE

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Meeple Maniacs Radiocast #121 - Jogatina BG News e Meeple Hazard com Moisés da Moby Studio

Play Episode Listen Later Aug 22, 2018 75:18

Meeple Maniacs Radiocast #121 - Jogatina BG News e Meeple Hazard com Moisés da Moby Studio

Play Episode Listen Later Aug 22, 2018 75:18

Meeple Maniacs Radiocast #121 - Jogatina BG News e Meeple Hazard com Moisés da Moby Studio