Podcasts about altos labs

本集節目邀請到活躍於全球頂尖生物科技研究前沿的科學家陳沛均博士（Dr. Jin Chen），帶領聽眾探索生物醫學創新的前線！陳博士的職涯軌跡精彩而多元，他在史丹佛大學攻讀博士學位，於加州大學舊金山分校（UCSF）進行博士後研究，接著進入德州大學西南醫學中心（UTSW）擔任助理教授，近期踏入當前全球矚目的創新研究機構 Altos Labs。陳博士深入分享他在 Altos Labs 致力於「衰老與細胞再生」（aging and cell rejuvenation）的尖端研究，闡明這些基礎研究如何人類健康長壽帶來突破，更剖析從學術界跨入產業界的心路歷程與契機，並探討兩種研究環境在創新自由度、資源配置、團隊合作與研究推進速度上的關鍵差異。透過陳博士生動的經驗分享，探索他如何在職涯關鍵轉折點做出重要決策並面對挑戰，鼓勵年輕科學家擁抱 serendipity，勇敢追尋屬於自己的科學探索之旅！  

Don't miss the Make Money Easy Book Tour! https://lewishowes.com/moneyyouCheck out the full episode: greatness.lnk.to/1742"The epigenome resets completely and there's no sign of aging. It's kind of fascinating...I think that we might have a tuneup where we go and get rejuvenated." - Dr. Rhonda PatrickImagine a future where we could reset our biological clock, turning back aging at the cellular level. Dr. Rhonda Patrick takes us on a mind-blowing journey through cutting-edge longevity research, explaining how scientists have discovered ways to reprogram old cells into youthful ones with no signs of aging. She breaks down Nobel Prize-winning research on the Yamanaka factors—four special genes that can transform an 80-year-old skin cell into an embryonic stem cell, effectively erasing all signs of aging and allowing that cell to become any cell type in the body.The conversation ventures into the exciting field of partial cellular reprogramming, where scientists are finding ways to rejuvenate cells without completely changing their identity. Dr. Patrick shares insights about groundbreaking work at Altos Labs, where top scientists like Dr. Steve Horvath (pioneer of epigenetic clocks that measure biological age) are tackling the hurdles that stand between us and potential age reversal. With the exponential growth in synthetic biology and gene engineering, Patrick believes we could be just a couple of decades away from treatments that might reverse our biological age by ten years or more.Sign up for the Greatness newsletter: http://www.greatness.com/newsletter

BUFFALO, NY — February 26, 2025 — A new #research paper was #published in Aging (Aging-US) on January 27, 2025, in Volume 17, Issue 1, titled “Age-invariant genes: multi-tissue identification and characterization of murine reference genes.” Aging is a process driven by changes in gene activity, but researchers from Yale University School of Medicine and Altos Labs, led by first author John T. González and corresponding author Albert T. Higgins-Chen, have identified a set of genes that remain unchanged throughout the aging process. This discovery could improve the accuracy of aging research and provide insights into why some genes stay unchanged while others decline. “Reference genes have mostly been identified and validated in young organisms, and no systematic investigation has been done across the lifespan.” The study looked at gene activity in 17 different tissues in mice, from 1 month old to over 21 months old. Scientists used advanced bioinformatic analysis methods to analyze RNA sequencing data. They found nine genes that stayed the same across all tissues, as well as other genes that remained stable in specific tissues. These genes are usually shorter and have special DNA regions called CpG islands, which may help cells stay healthy and resist aging. Their stability throughout aging was confirmed by analyzing different datasets and using RT-qPCR. One of the most significant findings is that these stable genes are linked to essential cellular functions, such as mitochondrial activity and protein maintenance. This challenges the common belief that all aspects of aging involve gene dysregulation. Instead, the findings suggest that some cellular processes may naturally resist aging, leading the way for new research on longevity and potential anti-aging therapies. “Biological processes that change with age and those that resist age-related dysregulation are two sides of the same coin, and both will need to be investigated to fully understand aging.” Another key finding is that commonly used reference genes, such as GAPDH and ACTB, fluctuate with age, making them unreliable for aging studies. No single classical reference gene was found to be stable across all tissues. Researchers often use these reference genes as a control to measure gene activity, but if their expression changes over time, it can lead to inaccurate results. By identifying new, stable reference genes, this study provides scientists with better tools for studying aging-related diseases, regenerative medicine, and longevity science. Understanding how certain genes remain unchanged throughout life suggests that they may play a protective role in aging and could potentially be used to develop treatments that slow down age-related decline. While further research is needed, this discovery sets a new standard for measuring gene activity in aging studies and could have a significant impact on aging research and medicine. DOI - https://doi.org/10.18632/aging.206192 Corresponding author - Albert T. Higgins-Chen - a.higginschen@yale.edu 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 Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

https://www.sherylkline.com/blog/unlocking-bold-potential-with-connie-whiteIn this Fearless Female Leadership Interview, I had the pleasure of connecting with Connie White, Chief People Officer at Altos Labs, to discuss the art and science of unlocking bold potential. Connie's journey, insights, and passion for empowering others offer a roadmap for leaders and emerging professionals alike to tap into their own potential and that of their teams. We explored what it means to “unlock bold potential” and how that journey often starts with small, intentional actions. Connie's stories—from her formative years to her current leadership role—underscore the importance of staying curious, giving and receiving feedback, and taking bold, well-thought-out action.Key Takeaways~ The Value of Curiosity in Unlocking Potential (00:01:17)Connie emphasizes that curiosity is a powerful, often underappreciated factor in both personal and team development. As a leader, being curious about team members and their strengths helps create opportunities for growth. ~ Drawing Inspiration from Early Life Experiences (00:04:21)Connie reflects on how her disciplined upbringing instilled in her a sense of responsibility, resilience, and self-belief. She shared a story from her Little League days when she was asked to play catcher for the All-Stars, a role she hadn't previously trained for. ~ Building Trust Through Honest, Ongoing Feedback (00:12:22)Feedback can feel intimidating, but Connie describes it as a crucial element of professional growth. When leaders offer feedback with care and clear intention, it builds trust, reinforces bonds, and strengthens the team. ~ Taking Bold, Well-Thought-Out Action (00:22:55)Connie has learned that unlocking bold potential often requires making bold, thoughtful decisions. She encourages leaders to trust their intuition and act on it before overthinking leads to inaction.~ Communicate, Care, and Be Curious (00:35:36)To unlock potential on a larger scale, Connie champions the “three C's”: communicate, care, and be curious. Leaders should actively listen, show genuine care, and create space for open conversations that allow team members to express their aspirations and challenges. Connie's approach to leadership is deeply inspiring and highlights that bold potential isn't unlocked overnight. It's nurtured over time through consistent, thoughtful actions and a willingness to step out of comfort zones. Her insights offer valuable guidance for both established and emerging leaders on how to recognize and foster bold potential in themselves and others.If you're on a journey to unlock your bold potential or want to foster it within your team, I'd love to support you. Book a call with me to start the conversation. Let's make bold potential a reality, together.Cheering you on always,Sheryl

How Stress Is Speeding Up Your Aging – And How to Stop It “It's so much easier to prevent conditions and deterioration than to fix them once they've occurred. It's much harder to reverse than it is to prevent in the first place.” -Ryan Smith Summary: In this episode of the CEO Mastery Show, Amanda Holmes interviews Ryan Smith, CEO of a pioneering epigenetics company. The episode delves into Amanda's personal health journey, sparked by an epigenetics test that revealed rapid cellular aging due to stress. Ryan shares his path from studying biochemistry to leading a successful business in the epigenetics field. The conversation underscores the science of gene expression, DNA methylation, and the significant role of lifestyle choices on biological aging. Highlighting advancements in biohacking, they discuss promising research like the use of Yamanaka factors to reverse cellular aging, including notable experiments such as reversing blindness in mice, and the formation of high-investment initiatives like Altos Labs. The episode is rich with case studies, detailed explanations, and insights into the future of personalized health interventions aimed at extending lifespan and promoting health. Episode Highlights: 00:00 Episode Teaser 00:43 Podcast Intro: The CEO Mastery Show 01:11 Exploring Biohacking and Epigenetics 02:37 Ryan Smith's Journey into Epigenetics 04:39 Understanding Epigenetics and Its Impact 08:19 Personal Experiences with Epigenetic Testing 10:14 The Science Behind Epigenetic Clocks 20:40 Case Studies and Practical Applications 32:04 Future of Aging and Biohacking 33:42 Special Bonuses at Ultimate Sales Machine 33:57 Prioritizing Health and Wellness 34:25 The Wake-Up Call: Cellular Stress and Aging 34:41 Introduction to the CEO Mastery Show 35:09 Exploring Epigenetics with Ryan Smith 02:37 The Journey to Epigenetics Business 04:44 Understanding Epigenetics and Gene Expression 06:33 Real-Life Applications of Epigenetics 10:14 The Importance of Biological Age 13:54 Case Studies and Practical Insights 25:23 Precision and Validation in Epigenetic Testing 32:04 The Future of Aging and Biohacking 33:30 Conclusion and Final Thoughts ------------------------ Connect with Ryan: Instagram: https://www.instagram.com/trudiagnosticofficial/ LinkedIn: https://www.linkedin.com/in/ryan-smith-lexington-ky/ X: https://x.com/ryansmithepiage Connect with us: LinkedIn: https://www.Linkedin.com/company/chetholmesint Instagram: https://www.Instagram.com/UltimateSalesMachine⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Facebook: https://www.Facebook.com/UltimateSalesMachine⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Twitter: https://www.Twitter.com/ChetHolmes⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ------------------------ Listen to The CEO Mastery Show here: Apple Podcasts: https://podcasts.apple.com/us/podcast/the-ceo-mastery-show/id1589294044 Spotify: https://open.spotify.com/show/1LXkbAtWnCOxdiddkzteGx?si=05aaa25b4afe4c6d Don't forget to share your key takeaways from this episode and tag us on socials!

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. 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Subscribe to our channel: https://www.youtube.com/@optispan Related episodes: You Can Live Longer!: https://www.aspenideas.org/sessions/you-can-live-longer Estriol Shown to Increase Lifespan as Winner of Intervention Testing Program: https://youtu.be/1DQEuT0dtWk The Best Strategies for Living Longer RANKED: Longevity Tier List: https://youtu.be/41WUYgEkQeA Reversing Biological Age: Have we finally found the answer?: https://youtu.be/ivP3QTyQ2d4 In June 2024, the Aspen Ideas Festival held a three-day health-focused event in which speakers discussed new breakthroughs, policy developments, and possible futures in healthcare. "You Can Live Longer!" was a panel discussion during the festival that consisted of Altos Labs founder and chief scientist Rick Klausner, Cradle CEO and cofounder and venture capitalist Laura Deming, BioAge Labs CEO and cofounder Kristen Fortney, and NPR News Food and Health Correspondent Allison Aubrey discussing developments in the longevity field. In this episode, Matt and Nick react to the panel discussion and discuss the potential of epigenetic reprogramming for improving organ transplants and reversing organ aging, the limitations of current techniques, the relevance of aging models in disease research, and more. Producers: Tara Mei, Nicholas Arapis Video Editor: Jacob Keliikoa DISCLAIMER: The information provided on the Optispan podcast is intended solely for general educational purposes and is not meant to be, nor should it be construed as, personalized medical advice. No doctor-patient relationship is established by your use of this channel. The information and materials presented are for informational purposes only and are not a substitute for professional medical advice, diagnosis, or treatment. We strongly advise that you consult with a licensed healthcare professional for all matters concerning your health, especially before undertaking any changes based on content provided by this channel. The hosts and guests on this channel are not liable for any direct, indirect, or other damages or adverse effects that may arise from the application of the information discussed. Medical knowledge is constantly evolving; therefore, the information provided should be verified against current medical standards and practices. More places to find us: Twitter: https://twitter.com/optispanpodcast Twitter: https://twitter.com/optispan Twitter: https://twitter.com/mkaeberlein Linkedin: https://www.linkedin.com/company/optispan https://www.optispan.life/ Hi, I'm Matt Kaeberlein. I spent the first few decades of my career doing scientific research into the biology of aging, trying to understand the finer details of how humans age in order to facilitate translational interventions that promote healthspan and improve quality of life. Now I want to take some of that knowledge out of the lab and into the hands of people who can really use it. On this podcast I talk about all things aging and healthspan, from supplements and nutrition to the latest discoveries in longevity research. My goal is to lift the veil on the geroscience and longevity world and help you apply what we know to your own personal health trajectory. I care about quality science and will always be honest about what I don't know. I hope you'll find these episodes helpful!

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

Professor Venki Ramakrishnan, a Nobel laureate for his work on unraveling the structure of function of the ribosome, has written a new book WHY WE DIE which is outstanding. Among many posts and recognitions for his extraordinary work in molecular biology, Venki has been President of the Royal Society, knighted in 2012, and was made a Member of the Order of Merit in 2022. He is a group leader at the MRC Laboratory of Molecular Biology research institute in Cambridge, UK.A brief video snippet of our conversation below. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are available on Apple and Spotify.Transcript with links to audio and external linksEric Topol (00:06):Hello, this is Eric Topol with Ground Truths, and I have a really special guest today, Professor Venki Ramakrishnan from Cambridge who heads up the MRC Laboratory of Molecular Biology, and I think as you know a Nobel laureate for his seminal work on ribosomes. So thank you, welcome.Venki Ramakrishnan (00:29):Thank you. I just want to say that I'm not the head of the lab. I'm simply a staff member here.Eric Topol (00:38):Right. No, I don't want to give you more authority than you have, so that was certainly not implied. But today we're here to talk about this amazing book, Why We Die, which is a very provocative title and it mainly gets into the biology of aging, which Venki is especially well suited to be giving us a guided tour and his interpretations and views. And I read this book with fascination, Venki. I have three pages of typed notes from your book.The Compression of MorbidityEric Topol (01:13):And we could talk obviously for hours, but this is fascinating delving into this hot area, as you know, very hot area of aging. So I thought I'd start off more towards the end of the book where you kind of get philosophical into the ethics. And there this famous concept by James Fries of compression of morbidity that's been circulating for well over two decades. That's really the big question about all this aging effort. So maybe you could give us, do you think there is evidence for compression of morbidity so that you can just extend healthy aging and then you just fall off the cliff?Venki Ramakrishnan (02:00):I think that's the goal of most of the sort of what I call the saner end of the aging research community is to improve our health span. That is the number of years we have healthy lives, not so much to extend lifespan, which is how long we live. And the idea is that you take those years that we now spend in poor health or decrepitude and compress them down to just very short time, so you're healthy almost your entire life, and then suddenly go into a rapid decline and die. Now Fries who actually coined that term compression or morbidity compares this to the One-Hoss Shay after poem by Oliver Wendell Holmes from the 19th century, which is about this horse carriage that was designed so perfectly that all its parts wore out equally. And so, a farmer was riding along in this carriage one minute, and the next minute he found himself on the ground surrounded by a heap of dust, which was the entire carriage that had disintegrated.Venki Ramakrishnan (03:09):So the question I would ask is, if you are healthy and everything about you is healthy, why would you suddenly go into decline? And it's a fair question. And every advance we've made that has kept us healthier in one respect or another. For example, tackling diabetes or tackling heart disease has also extended our lifespan. So people are not living a bigger fraction of their lives healthily now, even though we're living longer. So the result is we're spending the same or even more number of years with one or more health problems in our old age. And you can see that in the explosion of nursing homes and care homes in almost all western countries. And as you know, they were big factors in Covid deaths. So I'm not sure it can be accomplished. I think that if we push forward with health, we're also going to extend our lifespan.Venki Ramakrishnan (04:17):Now the argument against that comes from studies of these, so-called super centenarians and semi super centenarians. These are people who live to be over 105 or 110. And Tom Perls who runs the New England study of centenarians has published findings which show that these supercentenarians live extraordinarily healthy lives for most of their life and undergo rapid decline and then die. So that's almost exactly what we would want. So they have somehow accomplished compression of morbidity. Now, I would say there are two problems with that. One is, I don't know about the data sample size. The number of people who live over 110 is very, very small. The other is they may be benefiting from their own unique genetics. So they may have a particular combination of genetics against a broad genetic background that's unique to each person. So I'm not sure it's a generally translatable thing, and it also may have to do with their particular life history and lifestyle. So I don't know how much of what we learned from these centenarians is going to be applicable to the population as a whole. And otherwise, I don't even know how this would be accomplished. Although some people feel there's a natural limit to our biology, which restricts our lifespan to about 115 or 120 years. Nobody has lived more than 122. And so, as we improve our health, we may come up against that natural limit. And so, you might get a compression of morbidity. I'm skeptical. I think it's an unsolved problem.Eric Topol (06:14):I think I'm with you about this, but there's a lot of conflation of the two concepts. One is to suppress age related diseases, and the other is to actually somehow modulate control the biologic aging process. And we lump it all together as you're getting at, which is one of the things I loved about your book is you really give a balanced view. You present the contrarians and the different perspectives, the perspective about people having age limits potentially much greater than 120, even though as you say, we haven't seen anyone live past 122 since 1997, so it's quite a long time. So this, I think, conflation of what we do today as far as things that will reduce heart disease or diabetes, that's age related diseases, that's very different than controlling the biologic aging process. Now getting into that, one of the things that's particularly alluring right now, my friend here in San Diego, Juan Carlos Belmonte, who went over from Salk, which surprised me to the Altos Labs, as you pointed on in the book.Venki Ramakrishnan (07:38):I'm not surprised. I mean, you have a huge salary and all the resources you want to carry out the same kind of research. I wouldn't blame any of these guys.Rejuvenating Animals With Yamanaka FactorsEric Topol (07:50):No, I understand. I understand. It's kind of like the LIV Golf tournament versus the PGA. It's pretty wild. At any rate, he's a good friend of mine, and I visited with him recently, and as you mentioned, he has over a hundred people working on this partial epigenetic reprogramming. And just so reviewing this for the uninitiated is giving the four Yamanaka transcription factors here to the whole animal or the mouse and rejuvenating old mice, essentially at least those with progeria. And then others have, as you point out in the book, done this with just old mice. So one of the things that strikes me about this, and in talking with him recently is it's going to be pretty hard to give these Yamanaka factors to a person, an intravenous infusion. So what are your thoughts about this rejuvenation of a whole person? What do you think?Venki Ramakrishnan (08:52):If I hadn't seen some of these papers would've been even more skeptical. But the data from, well, Belmonte's work was done initially on progeria mice. These are mice that age prematurely. And then people thought, well, they may not represent natural aging, and what you're doing is simply helping with some abnormal form of aging. But he and other groups have now done it with normal mice and observed similar effects. Now, I would say reprogramming is one way. It's a very exciting and powerful way to almost try to reverse aging because you're trying to take cells back developmentally. You're taking possibly fully differentiated cells back to stem cells and then helping regenerate tissue, which one of the problems as we age is we start losing stem cells. So we have stem cell depletion, so we can no longer replace our tissues as we do when we're younger. And I think anyone who knows who's had a scrape or been hurt in a fall or something knows this because if I fall and scrape my elbow and get a big bruise and my grandson falls, we repair our tissues at very, very different rates. It takes me days or weeks to recover, and my grandson's fine in two or three days. You can hardly see he had a scrape at all. So I think that's the thing that these guys want to do.Venki Ramakrishnan (10:48):And the problem is Yamanaka factors are cancer. Two of them are oncogenic factors, right? If you give Yamanaka factors to cells, you can take them all the way back to what are called pluripotent cells, which are the cells that are capable of forming any tissue in the body. So for example, a fertilized egg or an early embryo cells from the early embryo are pluripotent. They could form anything in the body. Now, if you do that to cells with Yamanaka factors, they often form teratomas, which are these unusual forms of cancer tumors. And so, I think there's a real risk. And so, what these guys say is, well, we'll give these factors transiently, so we'll only take the cells back a little ways and not all the way back to pluripotency. And that way if you start with skin cells, you'll get the progenitor stem cells for skin cells. And the problem with that is when you do it with a population, you're getting a distribution. Some of them will go back just a little, some of them may go back much more. And I don't know how to control all this. So I think it's very exciting research. And of course, if I were one of these guys, I would certainly want to carry on doing that research. But I don't think it's anywhere near ready for primetime in terms of giving it to human beings as a sort of anti-aging therapeutic.Aging and Cancer Shared HallmarksEric Topol (12:31):Yeah. Well, I couldn't agree more on that because this is a company that's raised billions of dollars to go into clinical trials. And the question that comes up here, which is a theme in the book and a theme with the aging process to try to artificially, if you will affect it, is this risk of cancer. And as we know, the hallmarks of aging overlap considerably with the hallmarks of cancer. And this is just one example, as you mentioned, where these transcription factors could result in generating cancer. But as you also point out in the book at many places, methylation changes, DNA, repair, and telomeres.Venki Ramakrishnan (13:21):And telomeres.Venki Ramakrishnan (13:24):All of those are related to cancer as well. And this was first pointed out to me by Titia de Lange, who's a world expert on telomeres at Rockefeller, and she was pointing out to me the intimate connection between cancer and aging and many mechanisms that have evolved to prevent cancer early in life tend to cause aging later in life, including a lot of DNA damage response, which sends cells into senescence and therefore causes aging. Buildup of senescence cells is a problem later in life with aging, but it has a role which is to prevent cancer early in life. And so, I think it's going to be the same problem with stem cell therapy. I think very targeted stem cell therapy, which is involved in replacing certain tissues, the kind of regenerative medicine that stem cells have been trying to address for a very long time, and only now we're beginning to see some of the successes of that. So it's been very slow, even when the goal and target is very specific and well-defined, and there you are using that stem cell to treat a pretty bad disease or some really serious problem. I think with aging, the idea that somebody might take this so they can live an extra 10 years, it's a much higher bar in terms of safety and long-term safety and efficacy. So I don't think that this is going to happen anytime soon, but it's not to say it'll never happen. There is some serious biology underlying it.Eric Topol (15:13):Right. Well, you just touched on this, but of course the other, there's several big areas that are being explored, and one of them is trying to deal with these senescent cells and trying to get rid of them from the body because they can secrete evil humors, if you will. And the problem with that, it seems that these senescent cells are sort of protective. They stop dividing, they're not going to become cancerous, although perhaps they could contribute to that in some way. So like you say, with telomeres and so many things that are trying to be manipulated here, there's this downside risk and it seems like this is what we're going to have to confront this. We have seen Venki with the CAR-T, the T-cell engineering, there's this small risk of engendering cancer while you're trying to deal with the immune system.SenolyticsVenki Ramakrishnan (16:07):Yeah, I think with senescent cells, the early in life senescent cells have an important role in biology. They're essentially signaling to the immune system that there's a site that's subject to viral infection or wounds or things like that. So it's a signal to send other kinds of cells there to come and repair the damage. Now, of course, that evolved to help us early in life. And also many senescent cells were a response to DNA damage. And that's again, a way for the body that if your DNA is damaged, you don't want that cell to be able to divide indefinitely because it could become cancerous. And so, you send it into senescence and get it out of harm's way. So early life, we were able to get rid of these senescent cells, we were able to come to the site and then clean up the damage and eventually destroy the senescent cells themselves.Venki Ramakrishnan (17:08):But as we get older, the response mechanisms also deteriorate with age. Our immune system deteriorates with age, all the natural signaling mechanisms deteriorate with age. And so, we get this buildup of senescent cells. And there people have asked, well, these senescent cells don't just sit there, they secrete inflammatory compounds, which originally was a feature, not a bug, but then it becomes a problem later in life. And so, people have found that if you target senescent cells in older animals, those animals improve their symptoms of aging improved dramatically or significantly anyway. And so, this has led to this whole field called senolytics, which is being able to specifically target senescent cells. Now there the problem is how would you design compounds that are highly specific for senescent cells and don't damage your other cells and don't have other long-term side effects? So again, I think it's a promising area, but a lot of work needs to be done to establish long-term safety and efficacy.Eric Topol (18:23):Right. No, in fact, just today in Nature, there's a feature on killing the zombie cells, and it discusses just what you're pointing out, which is it's not so easy to tag these specifically and target them, even though as you know, there's some early trials and things like diabetic macular edema. And we'll see how that plays out. Now, one of the things that comes up is the young blood story. So in the young blood, whether it's this parabiosis or however you want to get at it, and I guess it even applies to the young microbiome of a gut, but there's this consistent report that there's something special going on there. And of course the reciprocal relationship of giving the old blood to the young mice, whatever, but no one can find the factor, whether it's platelet factor 4, GDF11, or what are your thoughts about this young blood story?Venki Ramakrishnan (19:25):I think there's no question that the experiments work because they were reproduced and they were reproduced over quite a long period, and which is that when you connect an old mouse or rat with a young equivalent, then the old mouse or old rat benefits from the young blood from the younger animal. And conversely, the younger animal suffers from the blood from the older animal. And then people were wondering whether this is simply that the young animal has better detoxification and things like that, or whether it's actually the blood. And they gave it just as transfusion without connecting the animals and showed that it really was the blood. And so, this of course then leads to the question, well, what is it about young blood that's beneficial and what is it about old blood that is bad? But the problem is blood has hundreds of factors. And so, they have to look at which factors are significantly different, and they might be in such small quantities that you might not be able to detect those differences very easily.Venki Ramakrishnan (20:40):And then once you've detected differences, then you have to establish their mechanism of action. And first of all, you have to establish that the factor really is beneficial. Then you have to figure out how it works and what its potential side effects could be. And so again, this is a promising area where there's a lot of research, but it has not prevented people from jumping the gun. So in the United States, and I should say a lot of them in your state, California somehow seems to attract all these immortality types. Well, anyway, a lot of companies set up to take blood from young donors, extract the plasma and then give it to rich old recipients for a fee for a healthy fee. And I think the FDA actually shut down one of them on the grounds that they were not following approved procedure. And then they tried to start up under a different name. And then eventually, I don't know what happened, but at one point the CEO said something I thought was very amusing. He said, well, the problem with clinical trials is that they take too long. I'm afraid that's characteristic of some portion of this sort of anti-aging therapeutics community. There's a very mainstream rigorous side to it, but there's also at the other end of the spectrum, kind of the wild west where people just sell whatever they can. And I think this exploits people's fear of getting old and being disabled or things like that and then dying. And I think the fear seems to be stronger in California where people like their lives and don't want to age.Eric Topol (22:49):You may be right about that. I like your term in the book immortality merchants, and of course we'll get into a bit, I hope the chapter on the crackpots and prophets that you called it was great. But that quote, by the way, which was precious from, I think it was Ambrosia, the name of the company and the CEO, but there's another quote in the book I want to ask you about. Most scientists working on aging agree that dietary restriction can extend both healthy life and overall life in mice and also lead to reductions in cancer, diabetes, and overall mortality in humans. Is that true? Most scientists think that you can really change these age-related diseases.Caloric Restriction and Related PathwaysVenki Ramakrishnan (23:38):I think if you had to pick one area in which there's broad agreement, it is caloric restriction. But I wouldn't say the consensus is complete. And the reason I say that is that most of the comparisons are between animals that can eat as much as they want, called ad libitum diet and mice that are calorically restricted or same with other animals even yeast. You either compared with an extremely rich medium or in a calorically restricted medium. And this is not a great comparison. And people, there's one discrepancy, and that was in monkeys where an NIH study didn't find huge differences, whereas a Wisconsin study found rather dramatic differences between the control group and the calorically restricted group. And so, what was the difference? Well, the difference was that the NIH study, the controlled group didn't have a calorically restricted diet, but still had a pretty reasonable diet.Venki Ramakrishnan (24:50):It wasn't given a unhealthy rich diet of all you can eat. And then they tried to somehow reconcile their findings in a later study. But it leads to the question of whether what you can conclude is that a rich all you can eat diet, in other words, gorging on an all you can eat buffet is definitely bad for you. So that's why you could draw that conclusion rather than saying it's actually the caloric restriction. So I think people need to do a little more careful study. There was also a study on mice which took different strains of mice and showed that in some strains, caloric restriction actually shortened lifespan didn't increase lifespan. Now, much of the aging community says, ah, that's just one study. But nobody's actually shown whether there was anything wrong with that study or even tried to reproduce it. So I think that study still stands.Venki Ramakrishnan (25:51):So I think it's not completely clear, but the fact is that there's some calorie dependence that's widely been observed across species. So between the control group and the experimental group, whatever you may, however, you may define it as there's been some effective calories intake. And the other interesting thing is that one of the pathways affected by caloric restriction is the so-called TOR pathway and one of the inhibitors of the TOR pathways is rapamycin. And rapamycin in studies has also shown some of these beneficial effects against the symptoms of aging and in lifespan. Although rapamycin has the same issue as with many other remedies, it's an immunosuppressive drug and that means it makes you more prone to infection and wound healing and many other things. I believe one of them was there's a question of whether it affects your libido, but nevertheless, that has not prevented rapamycin clinics from opening up, did I say in California? So I do think that there's often serious science, which leads to sort of promising avenues. But then there are of course people who jump the gun and want to go ahead anyway because they figure by the time trials are done, they'll be dead and they'd rather try act now.Eric Topol (27:36):Right. And you make a good, I mean the rapamycin and mTOR pathway, you really developed that quite a bit in the book. It's really quite complex. I mean, this is a pleotropic intervention, whether it's a rapalogs or rapamycin, it's just not so simple at all.Venki Ramakrishnan (27:53):Right. It's not at all simple because the TOR pathway has so many consequences. It affects so many different processes in the cell from including my own field of protein synthesis. It's one of the things it does is shut down global protein synthesis, and that's one of the effects of inhibiting TOR. So, and it turns up autophagy, which is this recycling of defective proteins and entirely defective entire organelles. So I think the TOR pathway is like a hub in a very large network. And so, when you start playing with that, you're going to have multiple consequences.Eric Topol (28:37):Yeah, no. And another thing that you develop so well is about this garbage disposal waste disposal system, which is remarkably elaborate in the cell, whether it's the proteasome for the proteins and the autophagosome for the autophagy with the lysosomes and the mitochondria mitophagy. Do you want to comment about that? Because this is something I think a lot of people don't appreciate, that waste management in the cell is just, it's a big deal.Venki Ramakrishnan (29:10):So we always think of producing things in the cell as being important, making proteins and so on. But the fact is destroying proteins is equally important because sometimes you need proteins for a short time, then they've done their job and you need to get rid of them, or proteins become dysfunctional, they stop working, or even worse, they start clumping together and causing diseases for example you could think of Alzheimer's as a disease, which involves protein tangles. Of course, the relationship between the tangles and the disease is still being worked out, but it's a characteristic of Alzheimer's that you have these protein tangles and the cell has evolved very elaborate mechanisms to constantly turn over defective proteins. Well, for example, it senses when proteins are unfolded and essentially the chain has unraveled and is now sticking to all sorts of things and causing problems. So I think in all of these cases, the cells evolved very elaborate mechanisms to recycle defective products, to have proper turnover of proteins. And in fact, recycling of entire organelles like mitochondria, when they become defective, the whole mitochondria can be recycled. So these systems also break down with aging. And so, as we age, we have more of a tendency to accumulate unfolded proteins or to accumulate defective mitochondria. And it's one of the more serious problems with aging.Eric Topol (30:59):Yeah, there's quite a few of them. Unfortunately, quite a few problems. Each of them are being addressed. So there's many different shots on goal here. And as you also aptly point out, they're interconnected. So many of these things are not just standalone strategies. I do want to get your sense about another popular thing, especially here out in California, are the clocks, epigenetic clocks in particular. And these people are paying a few hundred dollars and getting their biologic age, which what is that? And they're also thinking that I can change my future by getting clocks. Some of these companies offer every few months to get a new clock. This is actually remarkable, and I wonder what your thoughts are about it.Venki Ramakrishnan (31:48):Well, again, this is an example of some serious biology and then people jumping the gun to use it. So the serious biology comes from the fact that we age at different rates individuals. So anyone who's been to a high school reunion knows this. You'll have classmates who are unrecognizable because they've aged so much and others who've hardly changed since you knew them in high school. So of course at my age, that's getting rarer and rarer. But anyway, but you know what I mean. So the thing is that, is there a way that we can ask on an individual level how much has that individual aged? And there are markers that people have identified, some of them are markers on our DNA, which you mentioned in California. Horvath is a very famous scientist who has a clock named after him actually, which has to do with methylation of our DNA and the patterns of methylation affect the pattern of gene expression.Venki Ramakrishnan (33:01):And that pattern changes as we age. And they've shown that those patterns are a better predictor of many of the factors of aging. For example, mortality or symptoms of aging. They're a better predictor of that than chronological age. And then of course there are blood markers, for example, levels of various blood enzymes or blood factors, and there are dozens of these factors. So there are many different tests of many different kinds of markers which look at aging. Now the problem is these all work on a population level and they also work on an individual level for time comparison. That is to say, if you want to ask is some intervention working? You could ask, how fast are these markers changing in this person without the intervention and how fast are they changing with the intervention? So for these kind of carefully controlled experiments, they work, but another case is, for example, glycosylation of proteins, especially proteins of your immune system.Venki Ramakrishnan (34:15):It turns out that adding sugar groups to your immune system changes with age and causes an immune system to misfire. And that's a symptom of aging. It's called inflammaging. So people have used different markers. Now the problem is these markers are not always consistent with each other because you may be perfectly fine in many respects, but by some particular marker you may be considered old just because they're comparing you to a population average. But how would you say one person said, look, we all lose height as we age, but that doesn't mean if you take a short person, you can consider them old. So it's a difference between an individual versus a population, and it's a difference between what happens to an individual by following that individual over time versus just taking an individual and comparing it to some population average. So that's one problem.Organ ClocksVenki Ramakrishnan (35:28):The other problem is that our aging is not homogeneous. So there's a recent paper from I believe Tony Wyss-Coray group, which talks about the age of different organs in the same person. And it turns out that our organs, and this is not just one paper, there are other papers as well. Our organs don't necessarily age at the same rate. So giving a single person, giving a person a single number saying, this is your biological age, it's not clear what that means. And I would say, alright, even if you do it, what are you going to do about it? What can you do about it knowing your biological, the so-called number of a biological age. So I'm not a big fan. I'm a big fan of using these markers as a tool in research to understand what interventions work because otherwise it would take too long. You'd have to wait 20 years to see some large scale symptoms. And certainly, if you want to look at mortality, you'd have to wait possibly even longer. But if you were to be able to follow track these interventions and see that these markers slowed down with intervention, then you could say, well, your interventions having an effect on something related to aging. So I would say these are very useful research tools, but they're not meant to be used at $500 a pop in your age.Venki Ramakrishnan (37:02):But of course that hasn't stopped lots of companies from doing it.Eric Topol (37:07):No, it's just amazing actually. And by the way, we interviewed Tony Wyss-Coray about the organ clock, the paper. I thought it really was quite a great contribution, again, on a research level.Venki Ramakrishnan (37:19):He's a very serious scientist. He actually spoke here at the LMB as well. He gave a very nice talk here.Is Aging A Disease?Eric Topol (37:26):He's the real deal. And I think that's going to help us to have that organ specific type of tracking is another edge here to understand the effects. Well, before we wrap up, I want to ask you a question that you asked in the book. Is aging a disease?Venki Ramakrishnan (37:49):That's again, a controversial subject. So the WHO, and I believe the FDA decided that aging was not a disease on the grounds that it's inevitable and ubiquitous. It happens to everybody and it's inevitable. So how could something that happens to everybody and inevitable be considered a disease? A disease is an abnormal situation. This is a normal situation, but the anti-aging researchers and especially the anti-aging therapeutics people don't like that because if it's not a disease, how can they run a clinical trial? So they want aging to be considered a disease. And their argument is that if you look at almost every condition of old age, every disease of old age like cancer, diabetes, heart disease, dementia, the biggest risk factor in all of these diseases is age. That's the strongest risk factor. And so, they say, well, actually, you could think of these diseases as secondary diseases, the primary disease being age, and then that results in these other diseases.Venki Ramakrishnan (39:07):I am a little skeptical of that idea. I tend to agree with the WHO and the FDA, but I can see both sides of the argument. And as you know, I've laid them both out. My view is that it should be possible to do trials that help with aging regardless of whether you consider aging a disease or not. But that will require the community to agree on what set of markers to use to characterize success. And that's people, for example, Tony Wyss-Coray has his proteome, blood proteome markers, Horvath has his DNA methylation clock. There are a whole bunch of these. And then there are people with glycation or glycosylation of various proteins as markers. These people need to all come together. Maybe we need to organize a nice conference for them in some place like Southern California or Hawaii or somewhere, put them together in a locked room for a week so that they can thrash out a common set of markers and at least agree on what experiments they need to do to even come to that agreement and then use that to evaluate anti-aging therapies. I think that would be a way forward.Eric Topol (40:35):Yeah, I think you're bringing up a really valuable point because at the moment, they're kind of competing with one another, whether it's the glycosylated proteins or the transcriptomics or the epigenetics. And we don't know whether these are additive or what they're really measuring.Venki Ramakrishnan (40:53):Some of them may be highly correlated, and that's okay, but I think they need to know that. And they also need to come up with some criteria of how do we define age in an individual. It's not one number, just like we have many things that characterize our health. Cholesterol is one, blood pressures another, various other lipids. They're all blood enzymes, liver enzymes. All these things are factors in defining our so-called biological health. So I don't think there's some single number that's going to say this is your age. Just like there isn't one single thing that says you're healthy, you're not healthy.DNA RepairEric Topol (41:38):Right, that's well put. Last topic on aging is on about DNA repair, which is an area that you know very well. And one of the quotes in your book, I think is important for people to take in. “Nevertheless, they will make an error once every million or so letters in a genome with a few billion letters. That means several thousand mistakes occur each time a cell divides. So the DNA repair enzyme, as you point out the sentinels of our genome, the better we repair, the better we age.” Can we fix the DNA repair problem?Venki Ramakrishnan (42:20):I think maybe, again, I'm not sure what the consequences would be and how much it would take. There's one curious fact, and that is that there was a paradox called Peto's paradox after the scientist who discovered it, which is why don't big animals get cancer much more frequently than say a mouse? In fact, a mouse gets cancer far more readily than an elephant does, and in reality, the elephant should actually get cancer more because it has many orders of magnitude more cells, and all it takes is for one cell to become cancerous for the animal to get cancer and die. So the chances that one cell would become cancer would be larger if there are many, many more cells. And it turns out that elephants have many copies of DNA repair proteins or DNA damage response proteins, not so much DNA repair, but the response to DNA damage and in particular, a protein called p53. And so, this leads to the question that if you had very good DNA repair or very good DNA damage response, would you then live longer or solve this problem? I'm not entirely sure because it may have other consequences because for example, you don't want to send cells into senescence too easily. So I think these things are all carefully balanced, evolutionarily, depending on what's optimized to optimize fitness for each species.Venki Ramakrishnan (44:13):For a mouse, the equation's different than for a large animal because a mouse can get eaten by predators and so on. So there, it doesn't pay for evolution to spend too much select for too much spending of resources in maintenance and repair, for larger animals the equation is different. So I just don't know enough about what the consequences would be.Eric Topol (44:40):No, it's really interesting to speculate because as you point out in the book, the elephant has 20 copies of p53, and we have two as humans. And the question is that protection from cancer is very intriguing, especially with the concerns that we've been talking about.Venki Ramakrishnan (44:57):And it was also true, I believe they did some analysis of genomics of these whales that live very long, and they found sorts of genes that are probably involved in DNA repair or DNA damage response.Eric Topol (45:14):Well, this is a masterful book. Congratulations, Venki. I thoroughly enjoyed it. It's very stimulating. I know a lot of the people that will listen or read the transcript will be grabbed by it.Crackpots and ProphetsVenki Ramakrishnan (45:28):I think what I've tried to do is give the general reader a real understanding of the biology of aging so that even a complete non-scientist can get an understanding of the processes, which in turn empowers them to take action to do the sort of things that will actually really help. And also it'll guard them against excessive hype, of which there's a lot in this business. And so, I think that was the goal, and to try and present a balanced view of the field. I'm merely trying to be a realist. I'm not being a pessimist about it, but I also think this excessively optimistic hype is actually bad for the field and bad for science and bad for the public as well.Eric Topol (46:16):Well, and you actually were very kind in the chapter you have on crackpots and prophets. You could have been even tougher on some of these guys. You were very relatively diplomatic and gentle, I thought, I don't know if you were holding back.Venki Ramakrishnan (46:28):I had two lawyers looked at it, so.Eric Topol (46:33):I believe it. And now one thing, apart from what we've been talking about because of your extraordinary contribution on the structural delineation of the ribosome back in the early 2000s and 2009 Nobel Prize. Now, the world of AI now with AlphaFold 3 and all these other large language models, would that have changed your efforts? Would that have accelerated things or is it not really?Venki Ramakrishnan (47:09):Well, it would've helped, but you would still need the experimental data to solve something like the ribosome, a large complex like the ribosome. And the other thing that would really change well has changed our world is the advent of cryo-electron microscopy of which Scripps is one of the leading places for it. And that has really changed it so that now nobody would bother to crystallize a ribosome and try to get an X-ray structure out of it. You would just throw it into an EM grid, collect your data and be off to the races. So new ribosome structures are being solved all the time at a fraction, a tiny fraction of the time it took to solve the first one.Eric Topol (48:02):Wow, that's fascinating. This has been a real joy for Venki to discuss your book and your work, and thanks so much for what you're doing to enlighten us and keep the balance. And it may not be as popular as the immortality merchants, but it's really important stuff.Venki Ramakrishnan (48:19):Yeah, no, I hope actually, I found that many of the public want to read about the biology of aging. They're curious. Humans have been curious ever since we knew about mortality, about why some species live so short lives and other species live such a long time and why we actually have to age and die. So there's natural curiosity and then it also empowers the public once they understand the basis of aging, to take action, to live healthy lives and do that. It's an empowering book rather than a recipe book.Venki Ramakrishnan (49:01):I think a lot of the public actually does appreciate that. And of course, scientists will like the sort of more balanced and tone.Eric Topol (49:13):Well, you do it so well. All throughout you have metaphors to help people really understand and the concepts, and I really applaud you for doing this. In fact, a couple of people who we both know, Max and John Brockman, apparently were influential for you to get to do it. So I think it's great that you took it on and all the power to you. So thank you, and I hope that we'll get a chance to visit further as we go forward.******************Headshot photo credits by Kate Joyce and Santa Fe InstituteThe 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 informativeVoluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff tor 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.A Poll on Anti-Aging Get full access to Ground Truths at erictopol.substack.com/subscribe

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

Age expert Dr. Morgan Levine explains why living to 100 is the wrong goal. Dr. Morgan Levine suggests that we should aim for living better, not just longer. In her book, “True Age,” Levine introduces the idea of healthspan, which is about staying healthy and enjoying life, rather than merely adding years to it. She explores the concept of “compression of morbidity,” a goal to squeeze most of our inevitable ailments into a short period before we die, mirroring the patterns seen in people who live to 100 or more. Levine also highlights a paradox: Women generally outlive men, but they also endure more age-related illnesses. Ultimately, she argues that the benefits of longevity science should be accessible to everyone, with the goal of health disparities rather than increasing them. Chapters: 0:00 The immortality obsession 0:30 The male-female survival paradox 1:34 Prolonging healthy life 2:07 Squeezing morbidity into fewer years 3:05 LIfe extension for all About Morgan Levine: Morgan Levine was previously a tenure-track Assistant Professor in the department of Pathology at Yale University where she ran the Laboratory for Aging in Living Systems. In 2022, she was recruited to join Altos Labs as a Founding Principal Investigator at the San Diego Institute of Science. She currently leads a research group at Altos Labs working at the intersection of bioinformatics, cellular biology, complex systems, and biostatistics with the overall goal of understanding the molecular trajectories aging cells, tissues, and organisms take through time. About Big Think | Smarter Faster™ ► Big Think Our mission is to make you smarter, faster. Watch interviews with the world's biggest thinkers on science, philosophy, business, and more. Get Smarter Faster, With Daily Episodes From The Worlds Biggest Thinkers. Follow Big Think Leave A 5 Star Review --- Send in a voice message: https://podcasters.spotify.com/pod/show/bigthink/message Learn more about your ad choices. Visit megaphone.fm/adchoices

Science can't stop aging, but it may be able to slow our epigenetic clocks. What if we could slow down the hands of our biological clocks? This question underpins much of the research of Morgan Levine, who leads a research team at the life science company Altos Labs. Levine investigates the fascinating intricacies of aging, recognizing that it doesn't happen at a uniform pace for everyone. Central to her exploration is the concept of epigenetics — the factors that influence gene activity without changing the DNA sequence. Levine focuses on DNA methylation, a significant epigenetic change that occurs with aging, and the development of models called "epigenetic clocks" that can be used to predict biological age. While she acknowledges that it might be possible to reverse aging at a cellular level, Levine clarifies that the ultimate goal is not to "cure" aging or death, but to delay disease onset and improve healthspan. Chapters: 0:00 Fast agers & slow agers 1:25 The hallmarks of aging 1:59 What is the epigenetic clock? 3:05 Can we ‘Benjamin Button' aging? 5:22 The holy grail for scientists Get Smarter Faster, With Daily Episodes From The Worlds Biggest Thinkers. Follow Big Think Share This Episode With A Friend Leave A 5 Star Review --- Send in a voice message: https://podcasters.spotify.com/pod/show/bigthink/message Learn more about your ad choices. Visit megaphone.fm/adchoices

Former Yale professor Morgan Levine shares 3 ways to change your diet to extend your life. Dr. Morgan Levine, author of "True Age," explains how the impact of diet on aging and longevity is determined by three factors: quantity, quality, and timing of food intake. First, caloric restriction, typically a 20% reduction in overall calorie intake, has been linked to increased lifespan in several animal models. However, the positive effects may stem from avoiding overeating rather than restriction per se. Second, a plant-based diet, with less animal products and refined sugars and more fruits, veggies, and whole foods, seems beneficial for aging and longevity. Third, fasting, or limiting eating to specific time windows, might mimic the benefits of caloric restriction by causing 'hormesis', mild stressors that boost resilience to aging-related changes. The optimal diet is likely individual, influenced by factors like genetics and age, and should be monitored through measures of biological age and personal well-being. Future research into aging biomarkers could further our understanding of diet's role in the aging process. Chapters: 0:00 Does diet affect aging? 0:35 #1 Caloric restriction 1:40 #2 What you eat 2:07 #3 When you eat: fasting 2:38 Hormesis: Building biological resilience 3:16 What is the optimal diet for you? ---------------------------------------------------------------------- About Morgan Levine: Morgan Levine was previously a tenure-track Assistant Professor in the department of Pathology at Yale University where she ran the Laboratory for Aging in Living Systems. In 2022, she was recruited to join Altos Labs as a Founding Principal Investigator at the San Diego Institute of Science. She currently leads a research group at Altos Labs working at the intersection of bioinformatics, cellular biology, complex systems, and biostatistics with the overall goal of understanding the molecular trajectories aging cells, tissues, and organisms take through time. Get Smarter Faster, With Daily Episodes From The Worlds Biggest Thinkers. Follow Big Think Share This Episode With A Friend Leave A 5 Star Review --- Send in a voice message: https://podcasters.spotify.com/pod/show/bigthink/message Learn more about your ad choices. Visit megaphone.fm/adchoices

La ciencia contra el envejecimiento, cada vez más sofisticada, promete alargarnos la vida y ya ha logrado avances significativos en ratones. El médico e investigador Manel Esteller ha pasado por ‘A vivir' después de visitar el famoso Altos Labs, el laboratorio que fundaron hace dos años algunos multimillonarios de Silicon Valley para alcanzar la inmortalidad y al que rodea un secretismo extremo.

La ciencia contra el envejecimiento, cada vez más sofisticada, promete alargarnos la vida y ya ha logrado avances significativos en ratones. El médico e investigador Manel Esteller ha pasado por ‘A vivir' después de visitar el famoso Altos Labs, el laboratorio que fundaron hace dos años algunos multimillonarios de Silicon Valley para alcanzar la inmortalidad y al que rodea un secretismo extremo.

WATCH THE VIDEO OF THIS PODCAST HERE: https://www.thetayf.com/pages/multimedia?wchannelid=c4ogwxwvtw&wmediaid=3ejofgyzqwEver wondered what it means to age in today's world? Join us as we explore this intriguing subject with our special guest, gerontology expert Dr. Ken Dychtwald. Ken unravels his latest research findings, shedding new light on society's shifting attitudes towards aging.We traverse new territory, revealing Robert Nelson's personal regimen with Altos Labs to prevent illness and extend longevity. Let's examine the colossal $3 billion investment in genomics and how advancements in this field could reshape our approach to diagnosing, treating, and preventing diseases.Lastly, we shift gears to blockchain technology, dissecting the blockchain trilemma and the risks associated with investing in this flourishing innovation. We also delve into the captivating world of Non-Fungible Tokens (NFTs), exploring how they're transforming the way we handle our digital and physical lives.Subscribe to podcast updates: https://form.jotform.com/223614751580152Ask Ric: https://www.thetayf.com/pages/ask-ricRic's Books: https://www.amazon.com/stores/Ric-Edelman/author/B000APYJPM-----Links from today's show:The New Age of Aging: https://agewave.com/ken-dychtwald-the-journal-on-active-aging/Global X Genomics and Biotechnology ETF (Symbol: GNOM): https://www.globalxetfs.com/funds/gnom/Age Wave (website): https://agewave.com/Age Wave (book): https://agewave.com/product/age-wave/Radical Curiosity: https://agewave.com/product/radical-curiosity/The Truth About Your Future: http://www.thetayf.com/TheTruthAYF (articles): https://www.thetayf.com/pages/exclusive-contentFollow Ric on social media:Facebook: https://www.facebook.com/RicEdelmanInstagram: https://www.instagram.com/ric_edelman/ LinkedIn: https://www.linkedin.com/in/ricedelman/X (formerly Twitter): https://twitter.com/ricedelman YouTube: https://www.youtube.com/@RicEdelmanBrought to you by:Global X ETFs: https://www.globalxetfs.com/Invesco QQQ: https://www.invesco.com/qqq-etf/en/home.htmlPrisidio: https://www.prisid.io/Schwab: https://www.schwab.com/Disclosure page: https://www.thetayf.com/pages/sponsorship-disclosure-fee-----

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

A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 14, entitled, “Human senescent fibroblasts trigger progressive lung fibrosis in mice.” Cell senescence has recently emerged as a potentially relevant pathogenic mechanism in fibrosing interstitial lung diseases (f-ILDs), particularly in idiopathic pulmonary fibrosis. In a new study, researchers Fernanda Hernandez-Gonzalez, Neus Prats, Valentina Ramponi, José Alberto López-Domínguez, Kathleen Meyer, Mònica Aguilera, María Isabel Muñoz Martín, Daniel Martínez, Alvar Agusti, Rosa Faner, Jacobo Sellarés, Federico Pietrocola, and Manuel Serrano from Hospital Clinic Barcelona, The Barcelona Institute of Science and Technology (BIST), Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), University of Barcelona, Karolinska Institute, Catalan Institution for Research and Advanced Studies (ICREA), and Altos Labs hypothesized that senescent human fibroblasts may suffice to trigger a progressive fibrogenic reaction in the lung. “Here we: (1) explored this hypothesis in vivo; (2) investigated the potential underlying biological mechanisms in vitro; and (3) studied the effects of one experimental senolytic compound (navitoclax) and two anti-fibrotic drugs currently used in the treatment of IPF in humans (nintedanib and pirfenidone), both in vivo and in vitro.” To address this, senescent human lung fibroblasts, or their secretome (SASP), were instilled into the lungs of immunodeficient mice. The researchers found that human senescent fibroblasts engraft in the lungs of immunodeficient mice and trigger progressive lung fibrosis associated to increasing levels of mouse senescent cells, whereas non-senescent fibroblasts do not trigger fibrosis. They also found that the SASP of human senescent fibroblasts is pro-senescence and pro-fibrotic both in vitro when added to mouse recipient cells and in vivo when delivered into the lungs of mice, whereas the conditioned medium (CM) from non-senescent fibroblasts lacks these activities. Finally, navitoclax, nintedanib and pirfenidone were found to ameliorate lung fibrosis induced by senescent human fibroblasts in mice, while only navitoclax displayed senolytic activity. “We conclude that human senescent fibroblasts, through their bioactive secretome, trigger a progressive fibrogenic reaction in the lungs of immunodeficient mice that includes the induction of paracrine senescence in the cells of the host, supporting the concept that senescent cells actively contribute to disease progression in patients with f-ILDs.” DOI - https://doi.org/10.18632/aging.204825 Corresponding authors - Manuel Serrano - mserrano@altoslabs.com, and Federico Pietrocola - federico.pietrocola@ki.se Keywords - aging, mouse model, cellular senescence, pulmonary fibrosis, antifibrotics, senolytic 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/ For media inquiries, please contact media@impactjournals.com.

We all know it, even if we try our best not to dwell on it: one day, we will age and eventually die. Or will we?Sara engages in a conversation with Sebastian Brunemeier to explore the potential reversal of aging and the prospect of avoiding death. Sebastian Brunemeier is a General Partner at Healthspan Capital, a venture fund focused on longevity biotech and regenerative medicine. He is also CEO of ImmuneAGE Bio, a drug discovery platform for immune system rejuvenation. He was previously co-founder and CIO at Cambrian Biopharma, one of the largest longbio companies, Founder and COO of Samsara Therapeutics, a clinical-stage autophagy drug discovery company in Oxford UK, and Principal at Apollo Health Ventures, the largest aging-focused venture fund with 200M under management. He was a Fulbright Scholar on telomere biology, holds a master's degree in molecular neuroscience and biotech business management from the University of Amsterdam, and was in the PhD program on the biochemistry of aging at Oxford as a Clarendon scholar before dropping out to launch Cambrian. He is an advisor to several companies including VitaDAO, the longevity DAO00:00 Introduction01:35 Understanding the connection between aging and mortality07:26 The pursuit of biological immortality11:24 Strategies for prolonging life15:45 Promising areas of research in the field of longevity24:10 Exploring autophagy during fasting26:03 Sebastian's personal longevity regimen28:05 Overrated and underrated aspects of longevity research32:29 Gender disparities in longevity studies35:17 Contributing to longevity research efforts37:28 Web3 and its intersection with biotech42:00 Should we truly extend human lifespan? Examining the downsides and longevity dividends48:39 The Vitalism movement54:00 Societal transformations in a world without aging01:02:03 The impact of an extended lifespan on birth rates

مهمان کادر ۱۹ پادکست آنکادر دکتر امین حقانی است. دکتر حقانی دامپزشک، دکترای تخصصی بیولوژی پیری و پژوهشگر از سال ۲۰۲۲ به عنوان محقق ارشد در آلتوس لبز یکی از بزرگترین استارتاپ‌های حوزه پیری در جهان مشغول به فعالیت می‌باشند.در این کادر دکتر حقانی به تحقیقات و پیشرفت‌ها در حوزه افزایش طول عمر انسان و کاهش روند پیری پرداختند.شبکه‌های اجتماعیInstagram: https://www.instagram.com/uncadr.podcast/Castbox : https://castbox.fm/channel/id4935315?utm_source=website&utm_medium=dlink&utm_campaign=web_share&utm_content=UnCadr%20%7C%20%D8%A2%D9%86%DA%A9%D8%A7%D8%AF%D8%B1-CastBox_FMSpotify: https://open.spotify.com/show/7G85ljGwWSmHOTV5ijBL7IApple podcast: https://podcasts.apple.com/us/podcast/uncadr-%D8%A2%D9%86%DA%A9%D8%A7%D8%AF%D8%B1/id1509976193Google podcast: https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5hY2FzdC5jb20vcHVibGljL3Nob3dzLzYyNzdhOWFjNmMwNThlMDAxMjRhMTI1OA?sa=X&ved=0CAMQ4aUDahcKEwiYxoitz7n4AhUAAAAAHQAAAAAQAQEverywhere else: https://yek.link/UNCADR Hosted on Acast. See acast.com/privacy for more information.

Die Sehnsucht nach einem langen und gesunden Leben vereint die meisten Menschen dieser Erde. Nachdem die Menschheit scheinbar Hunger, Krieg und Krankheiten besiegt hat, strebt sie laut Yuval Noah Harari nun nach Glück und Unsterblichkeit. Insbesondere Milliardäre haben dieses Thema für sich entdeckt und investieren sehr viel Geld in Wundermittel gegen den Tod. Das ewige Leben ist für sehr viele das Sehnsuchtsziel. In Episode 98 sprechen Timo und Michael über die womöglich nächste Stufe der Evolution - die beiden verraten wie weit wir noch von der Unsterblichkeit weg sind, welche Rolle ein mysteriöses Start-up aus Kalifornien dabei spielt und was eine Qualle mit all dem zu tun hat.

Preventing Cancer with a Vaccine w/ Stephen Johnston of Calviri   - BRT S04 EP17 (179) 4-23-2023   Things We Learned This Week Calviri is working on a Vaccine to PREVENT Cancer, currently largest animal clinical trial Inflammation - starting points of bad cells Cancer - bad cells replicate Could Prevent other diseases & extend longevity of people's lives - ex.- help w/ dementia Tumors make bad proteins Calviri vaccine works on RNA (proteins) kills tumor, & arms immune system       Guest: Stephen Johnston Founding CEO, Calviri Inc. LKIN: HERE https://calviri.com/    Bio: Chief Executive Officer & Chairman of the Board Stephen Albert Johnston is the inventor of the Calviri's central technologies. In addition to Calviri, he has been a founder of Eliance, Inc. (Macrogenics), Synbody Biotechnology and HealthTell, Inc. He is Director of the Arizona State University Biodesign Institute's Center for Innovations in Medicine and Professor in the School of Life Sciences. He has published almost 200 peer-reviewed papers and holds 45 patents. Prior to his appointment at ASU he was Professor and Director of the Center for Biomedical Inventions at UT-Southwestern Medical Center and Professor of Biology and Biomedical Engineering at Duke University. He is a member of the National Academy of Inventors. Dr. Johnston received his B.S. and Ph.D. degrees from the University of Wisconsin.    Calviri Inc. We are determined to offer humanity a better life, free from cancer. While our goal is hugely ambitious, we are intensely driven to rid the planet of worry from cancer. Calviri's mission is to provide affordable products worldwide that will end deaths from cancer. We are a fully integrated healthcare company developing a broad spectrum of vaccines and companion diagnostics that prevent and treat cancer for those either at risk or diagnosed. We focus on using frameshift neoantigens derived from errors in RNA processing to provide pioneering products against cancer. The company is a spin out of the Biodesign Institute, Arizona State University, located in Phoenix, AZ. We have the largest dog vaccine trial in the world underway at three premier veterinary universities. The five-year trial will assess the performance of a preventative cancer vaccine.    Notes:  Seg. 1   Calviri working to develop a vaccine to prevent cancer, not cure, but prevent. You would take the vaccine like any other vaccine. Currently testing a largest clinical trial of 800 dogs. They are in year 3 of a 5 year trial.  Dr. Johnston has been working on this for 15 years thus far.  There will be 2 phases, with Phase 1 being animal testing to create a dog vaccine. This is a $3 – 5 billion industry. Next year, Calviri wants to launch with FDA approval.  Phase 2 is Human clinical trials. These will be Therapeutic trials, working on treating cancer.  The Best Part of Calviri's research and vaccine is it could prevent other diseases also. In turn give more longevity of life for people, and maybe cure dementia. Inflammation is the starting point. Defined: localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection.  In a normal inflammatory response, immune cells produce chemicals that can kill a pathogen. These chemicals, known as reactive oxygen species, can also damage the DNA of normal cells, which increases the risk of mutations that could lead to cancer. Bad cells or zombie cells are put out. Bad stuff, don't die, cause inflammation to other cells Cancer is when bad cells replicate uncontrollably. Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldn't. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous (benign).  It can also cause bone dysfunction. Tumor is a normal cell, not part of a community like infection Body is made up of tissues and cells (community or tightly packed group of cells). All cells experience changes with aging. They become larger and are less able to divide and multiply. Among other changes, there is an increase in pigments and fatty substances inside the cell (lipids). Many cells lose their ability to function, or they begin to function abnormally.  A person's Immune system fixes the community of cells & wipes out ‘rogue' tumors.   Seg. 2  Stephen Johnston's background,  trained in science, and also an inventor with a degree in bio chemistry. Was working at UT Southwest Medical Center in Dallas, TX. Started working at ASU about 15 years ago to develop what would become the Calviri research. ASU supporting the Calviri patent.  Started Calviri Inc. circa 2018. It was a spun out patent & I.P. to Calviri, with an exclusive license to Calviri. ASU owns no equity which is unusual. Gets % of profits – did not invest Venture Capital or VC wants equity in any deal they invest in. They also do not want any Universities having ownership as it complicates a deal. Calviri Board has 6 members, with a few members also providing funding, this is an  uncommon setup. Calviri Stock in all common One of the board members is the former CEO of Humana  $2 Bill – Open Philanthropy is a philanthropic funder. Our mission is to help others as much as we can with the resources available to us. Our main funders are Cari Tuna and Dustin Moskovitz, a co-founder of Facebook and Asana. This organization is providing funding for health companies.  High risk – 2019 - $6 5 mil  Calviri 4/2023 Worldwide MKT – affordable   Seg. 3  Clinical trial phase, do hundreds of trials Common treatment for a person who has cancer, create a Personalized cancer vaccine with an estimated cost of $100k DNA sequencing is done, and that treatment is for that person only Calviri mission is to create an off the shelf & affordable product Stepping stone in medicine development, goes from therapeutic to prevention Moderna, one of the big phrama companies that made the Covid vaccine  MRNA Vaccine Survey blood w/ stage 1 or 3 cancer, search for commonalities Intel chip system being used in bio chemistry machines. Intel says its processors are behind efforts to find new breakthroughs in life sciences research and healthcare in a number of countries. It took 10 years of work to test blood DNA transcription produces a single-stranded RNA molecule that is complementary to one strand of DNA. In the first step, the information in DNA is transferred to a messenger RNA (mRNA) molecule by way of a process called transcription. Processing mistakes at the RNA level  Reduced to pieces to become  Proteins – tumor makes bad protein, which looks like a inflection Takes pieces of bad protein & make a vaccine, then Inject the vaccine & kill the tumor Teach your body, arm the immune system before foreign particle are created Pre-emptively give vaccine before there is any cancer cells     Seg. 4   The common theme of Calviri is simplicity. There are simple ways to do x.   Everyone said it's complicated to treat cancer. There are 200 types of cancer. Calviri is working to have a big impact, plus make their vaccine simple & affordable. They believe the logical solution is vaccines.   They have shown to prevent cancer in their trials with dogs.   Trial –   Find the common traits. As the expression goes: The light is better under lamppost.   Common research is done on DNA to learn about Cancer. A person with Cancer has their DNA mapped out and the treatment created is for them only.   The harder method is to look at RNA.   Found parts in tumor – foreign   1 preventive vaccine working with ‘common' traits in RNA, there are 40 component pieces of proteins. There hundreds (100s) of uncommon traits   Immune system has sensor cells Immune system response, it will identify foreign cells & destroy them   Auto ‘self' immune disease - attacks all cells Good cells – working too well, and attacking non bad cells    When we age, it is common for the immune system to break down. This make people more prone to cancer, or other diseases.   Anti-Aging is a topic getting attention and funding. Jeff Bezos has invested in Altos Labs. Altos is pursuing biological reprogramming technology, a way to rejuvenate cells in the lab that some scientists think could be extended to revitalize entire animal bodies, ultimately prolonging human life.       Thanks to Joan Kerber-Walker of Az Bio for the intro to Stan. AZ Bio & Life Sciences Innovation w/ Joan Koerber-Walker - BRT S04 EP10 (172) 3-5-2023   FULL Show w/ Joan of AZ Bio: Click HERE     AZ Tech Council Shows: HERE *Includes Best of AZ Tech Council show from 2/12/2023   Tech Topic: HERE Best of Tech: HERE    ‘Best Of' Topic: https://brt-show.libsyn.com/category/Best+of+BRT      Thanks for Listening. 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Joe Allen has become a mainstay on our War Room screens over the last few years, his understanding of how technology is negatively affecting our lives and his analysis of how we push back is second to none. The rise of AI, nano technology, genetic experimentation, biometric payment systems, digital ID and digital currencies are all new technologies that are creeping into our everyday lives. Who controls them? What is their purpose? Do we have a choice to opt out? How are governments planning on using these to control their citizens? Joe answers all of these questions as he takes us into a new reality that is marching towards artificial general intelligence. Joe Allen is the is Transhumanism editor at War Room: Pandemic. He is a fellow primate who wonders why we ever came down from the trees! Joe studied religion and science at the University of Tennessee and Boston University and writes about ethnic identity, transhuman hubris, and the eternal spiritual quest. His work has appeared in The Federalist, ColdType, The American Thinker, The National Pulse, This View of Life, The American Spectator, IBCSR: Science on Religion, Disinformation, and elsewhere. Follow Joe at.... Substack: https://joebot.substack.com/ GETTR: https://gettr.com/user/JOEBOTxyz Twitter: https://twitter.com/JOEBOTxyz?s=20 War Room: http://warroom.org/ Interview recorded 12.4.23 *Special thanks to Bosch Fawstin for recording our intro/outro on this podcast. Check out his art https://theboschfawstinstore.blogspot.com/ and follow him on GETTR https://gettr.com/user/BoschFawstin and Twitter https://twitter.com/TheBoschFawstin?s=20  To sign up for our weekly email, find our social media, podcasts, video, livestreaming platforms and more... https://heartsofoak.org/connect/ Please subscribe, like and share! Transcript [0:22] Joe Allen, thank you so much for joining us on Hearts of Oak today. Peter, very glad to be here. Thank you very much. Not all. I know many of our viewers will have seen you regularly on War Room as a transhuman editor. What does it take to be a transhuman editor? How did that end up? You've being in the War Room. Tell us about that. You know, well, transhumanist or transhuman, although I would say this, Peter, that I think transhuman editor might be most accurate now. Part of the gig obviously is a 24-7 screen time. So I think that my cyborg status is pretty much solidified at this point. You know, Steve reached out to me just a little over a year ago, just like two years ago, And I'd written an article about the transhumanist quest, to upload for the Federalist. And I'd been writing a series of articles about technology that dipped into transhumanism quite a bit. He got a hold of that article about transhumanists and their desire to upload their souls and liked it. And it was quite odd. I don't wanna get too long into the story, but a friend of mine who had tipped me off to the War Room some year or so prior to that. [1:49] He had tipped me off to the War Room. I watched it. I watched an interview with Steve on PBS. It was this long, uncut interview with Lester Holt. And I was like, man, I've got to get a hold of this guy, Steve Bannon. And, but the way it works, you don't just call up Steve Bannon. And no one I knew had his contact. So I just put it out of my mind. I roamed across the country during the pandemic, ended up in Montana. And that same friend about a year later tells me that Steve gave me a shout out on the war room. And I thought, what? And it wasn't two weeks or three weeks after that that I checked my Twitter DMs, which I never ever did at the time. It was a different handle. [2:34] And there was Cameron, the producer, asking if I would come on the show. And so, but it was already too late. Got back to him, went on the show. Steve asked me if I'd like to join the war room that day. And here I am. It's always interesting who connects you, to me. It was just Miller giving credit to who connected me with Steve. What Steve does with the War Room is phenomenal and he is a machine in terms of production, in terms of knowledge, in terms of what he pushes out. Yeah, love watching you on that. I think you're on Charlie Kirk recently as well, a few days ago. I mean, yeah, that's right.   Absolutely brilliant. But if we, you can, for the viewers, you can obviously find you at JoeBotXYZ on the GETTR and on Twitter. Obviously, he has his Substack account. All the links are in the description. And that's just JoeBot.Substack.com you can find there and sign up to his regular wisdom. But I probably, Joe, when I think of transhumanism. I think the most powerful men in the world, Sleepy Joe, Supreme Court judges, don't know who women are, Elon Musk. And I'm thinking maybe transhumanism would be an improvement. [3:57] You know, I wouldn't deny that. In many ways, I think that if the world was run by a Satanist cabal, at least they would have a plan. So yeah, it's interesting. Probably the most famous proponent of transhumanism, at least in elite circles, is Klaus Schwab. And I think people just, they really dismiss Schwab oftentimes because he tends to speak, and he and his co-author write in vacant corporate platitudes for the most part. But I do think that he's smart enough to know which way the wind's blowing. And the wind is definitely blowing in the direction of holding up technology as the highest power. And so really, I think his fourth industrial revolution in 2016 was in many ways a kind, of clarion call to the world that this is the way we are going. And some of it is him looking around the scene and evaluating it. Some of it is his own enthusiasm. He has this really strange, naïve enthusiasm for transhumanist technologies. [5:16] That represents a really, really important moment in Western history and perhaps world history because of the open declaration that technology will be the way forward, not political ideology, and in their view, certainly not religious ideology, but technology. [5:38] Well, let's maybe delve into the most relevant transhumanist technologies. You've got a number of things will be on people's radar, nanotechnology, you look at mRNA and that ability, your digital ID, I guess, world governments, institutions tracking us, monitoring us, you could chat, GBT has a lot of headlines recently. And when people talk about kind of most relevant transhumanist technology, how do you kind of start unpacking that? [6:12] It can get complicated, but to break it down as simply as possible, two categories have to be distinguished there, one being technocracy, ruled by expert, and in its more modern form, ruled by expert through science and technology. And then on the other end you have transhumanism itself, which is in some ways separate from that. They overlap a great deal, but it is ultimately two separate, these are two separate movements. That Patrick Wood put it best, I'll paraphrase him, as technocracy is to a society, transhumanism is to the individuals within that society. I think that really does encapsulate the overlap quite a bit. [7:05] So when you talk about something like digital identification or digital currencies, central bank digital currencies, these I would say fall more under the category of technocracy. It's more of a way of organizing a society. It's a social structure based on technological systems of control. And on the other side, you've got transhumanism. And this is much more of, I would say, a kind of spiritual quest on the part of the people who are involved. You could say that it is many decades old. You know, the term transhumanist coined by Julian Huxley, 1956, I've got an essay collection, New Bottles for New Wine, and the opening essay was a lecture in 1956 entitled Transhumanism. He isn't really talking about technology so much in this though. He's more talking about how science will transform human beings. [8:03] He's hinting at technology, but for the most part, he grounds it in science. And of course, technology by and large emerges from the scientific method and mathematical deduction. So it fits, but it really wasn't until the 80s or so that you started seeing a lot of people take on this term transhumanism as a description of using technology to transform the human being. FM 2030 I think was probably the first major figure, but then Max Moore, a philosopher, was probably the one who put the stamp on the term transhumanism in this realm. So relevant technologies. I think the most relevant, especially now, artificial intelligence, creating a digital brain. The belief being that artificial intelligence will have limitless memory. Artificial intelligence will be able to scrape over basically unlimited data, as much data as you can feed into it. [9:08] And of course, it's going to have better pattern recognition than human beings. It's going to be able to pick out patterns in that vast amount of data in a way that no human being would be able to. It's gonna be able to do it at really, really fast speeds, right? So human brain operates on neurochemical processes, artificial intelligence computers in general, that processing moves at the speed of light. So there's a religious idea behind it that artificial intelligence is becoming and will become a sort of God to human beings. How do you merge yourself with that God? How do you reap the benefits and blessings of that God? Descending from there, you've got robotics. Which requires artificial intelligence for sophisticated systems of control. [9:58] You also have brain-computer interfaces, so that could be anything from these screens that we're speaking through, and I think that is a valid interpretation, hence my transhuman editor label. And then you've got the non-invasive brain-computer interfaces, It's kind of skull caps that read the brain in increasingly great detail. They don't require implants. Some of them, they're planning to roll out, different corporations are planning to roll out sort of AirPod-like brain computer interfaces or small bands that fit on the back of your head used for anything from monitoring employees' mental states to controlling actual computer systems. Nita Farahany is probably the leading expert on the non-invasive brain computer interface, if your listeners would like to look into it. But then of course you have the implanted brain computer interface. You got three major corporations working on that. [11:01] Neuralink, which has yet to get FDA approval. You've got a hole cut out of your skull, chip put in, about 1,024 wires or more if they can get them into the brain, those read the brain, and then allow the human being to project thoughts into a computer system. At the moment, there's not really any input. They've been able to do muscular movements and other things, but for the most part right now, the technology is only output. And so any input would have to come in through the traditional method, visual audio. And then two other corporations though, that are right now implanting their brain computer interfaces in human brains. You've got Synchron out of Brooklyn. [11:49] And Synchron is instead of drilling a hole, you send a kind of stent, an electronic stent up the vein into the brain at the jugular. And it sits within the vein and is able to read the neurons around it. I don't know what their count is, probably something like six, seven, eight, less than 10 if I'm not mistaken. But they have implanted them and people who are locked in, who've had strokes, things like that, are basically being experimented on with the intention of Tom Oxley, their CEO, hopes that eventually that technology will be able to be used to throw your emotions to other people. Kind of hive mind-ish idea. And then you've got BlackRock Neurotech invested in by Peter Thiel, and they're based out of Utah. And again, a different sort of technology, the way it works, you get it under the skull on top of the brain. It's a micro electrode array patch that sits on top of the brain. [12:58] I think that they have around 36 patients that are currently implanted with that technology. And again, it allows them to operate robotic arms. It allows them to translate their thoughts into text on screen, things like that. Moving down from there you have the sort of biological, Neurological and biological [13:22] technologies so the the neurological technologies this kind of feeds into the brain-computer interface is just [13:30] transcranial stimulation whether it's magnetic or whether it's kind of a a sonogram of, sorry, What's the word I'm looking for? Using sound waves anyway, sorry, I blanked on the very common term. But you use the stimulation to do various things, change mood, change the ability to concentrate, those sorts of things. And then, of course, you have the implanted version of them. There's like 160,000 of those, and those range from everything from eliminating Parkinson's tremors to eliminating depression, oddly enough. [14:10] And then I think the most famous and the thing that really captures people's imagination, genetic engineering. Genetic engineering has been a thing for quite some time. The first real genetic engineering projects come out of Stanford in the 70s. But with the advent of CRISPR, basically a molecular complex found in E. coli, CRISPR-Cas9, that was really discovered, I would say, 2011. It was kind of a piecemeal discovery process. [14:42] But now CRISPR is used for all sorts of things. And the advantage of CRISPR is that it allows the geneticist to go in and spot edit the genome. So initially it was to cut out nucleotides in a faulty gene to shut the gene down. But now they're able to actually cut out and insert corrective nucleotides to change the gene, to correct the gene, to heal disease. And the goal going forward for a lot of people, not everyone by any means, but for a lot of people, the goal going forward is to use that to enhance human beings, to give us greater intelligence, to give us greater strength, and you know, whatever else may be desired. Beauty. Mood, temperament, all those sorts of things. So that hopefully gives your listeners a roadmap, artificial intelligence, robotics. [15:41] Brain-computer interfacing, neuro-enhancement, and genetic engineering. Two questions. One, obviously, one argument on this is this is just technological advancement. This is just humans bettering themselves. But then another part of that, when you mentioned some of those things, you realize that it is, much of it is very much about the person. It's not technology at arm's length, but actually people may not have control or the ability to decide yes or no that it will happen because it's on the person as opposed to a phone that you can pick up and set down if you can't actually pick it up and set down because it's part of you. But what are your, one, that this is just technological advancement, but then the flip other side that maybe humans will not be able to decide whether or not they're part of this. It's a thorny topic for a lot of reasons. One, a lot of transhumanists argue for a morphological freedom, right? So guys like Max Moore, guys like Zoltan Istvan, they talk about it in terms of freedom. It's the freedom to be able to alter one's body or use technologies in any way they see fit, even if it puts off the rest of us in normal human society. [17:03] Then you have the more kind of implicit totalitarianism that you see in the singularity prophecies, right? So Ray Kurzweil being the most famous, it's just the idea that these technologies have always increased in complexity and effectiveness at an exponential rate. Then that exponential curve will continue until it reaches basically vertical, basically infinite advancement. He calls this a singularity at which technology is completely out of human control and the technology is making all the decisions. And he predicts 2045 is the date we'll hit the singularity. [17:43] And so the implicit totalitarianism there is that not that these guys are creating technologies to control everyone, the idea there, and they never own up to it, but this is definitely there. The idea is that you're creating a technological system that is inescapable and a technological system that has ultimately the final say in whatever sort of state that human psychology or human society is in. And so, even if you don't believe in something like that, even if you don't believe something like that's possible, to the extent that ideology is driving the people making the technologies and is also kind of hypnotizing the public with this technophilia, you end up in a situation where whether the singularity comes or not, whether anything like that happens or not, you have a kind of techno-religion that sees, really the rise of artificial intelligence, nano robotics and genetic engineering as this sort of second coming or the realization of God. And I really do fear, Peter, that a lot of people are so enamoured by it that the effectiveness of the technology won't be as important as the social and psychological effects. Now moving over into the more totalitarian, like openly totalitarian end of it. [19:10] In the West, people really don't talk like that. Even Klaus Schwab, if you read his writing or really listen to what he's saying outside of the small snippets, and certainly if you listen to Yuval Noah Harari to any length, neither of them are talking about creating a digital dictatorship. Schwab sounds more like it than Harari. Harari, if you read Harari carefully or even just read him at all, or listen to him carefully or just listen to him at all. You hear him over and over again, warning that these technologies are a recipe for digital dictatorship, right? So this idea of hackable humans, yeah, he's very unsentimental and he's very hostile to religion. He mocks religion a lot, so it's very off-putting. But what he's talking about is the rise of the scientific paradigm in which human beings, don't have free will. It's a scientific paradigm that holds that our decision-making process is nothing more than the bubbling up of neurochemical processes, and that with sufficient surveillance technology, your phone being a big one. [20:19] Sufficient surveillance technology allows governments and corporations to monitor your behaviours and as he would put it, to know you better than you know yourself. Then they're able to manipulate the population en masse, and they're able to target individuals for direct psychological manipulation. And because of this belief that free will is an illusion, people won't even realize that they're being manipulated. They will think they're making their own decisions. Now where you do see a sort of overt application of this, you see it in China. China has you know, they're they're really it's unclear how advanced their artificial intelligence is, it's unclear how advanced their genetic engineering projects are but they have far fewer ethical constraints on, genetic engineering and they have, [21:15] basically, no real ethical constraints that I'm aware of on the development of artificial intelligence up to artificial general intelligence now, Really is officially speaking neither do we in the West? But for China, the real advance they have made in artificial intelligence is in surveillance technology. And so of course in any major city in China, you've got wall to wall surveillance sensors. And those are more and more starting to incorporate biometric sensors, biometric analysis of video footage or other biometric data, including genetic data. And so China, I think, represents kind of an overt expression of what we're talking about when transhumanism meets totalitarianism. And it's very chilling because more and more people at the World Economic Forum, including Klaus Schwab, seem very amenable to the Chinese model. And more and more, I think, people in America implicitly are embracing something like the the Chinese model. [22:21] Obviously one of the, just before we want to move on some of the individuals involved, but one of the headlines I think which you reposted was a zero hedge headline, 1st of April. The headline was unprecedented Chinese genetic experiment may lead to an army of radiation resistant super soldiers. They talk about Frankenstein like experiments with manipulation of human DNA. I guess the danger is that somewhere like China, you say it doesn't have restrictions, but also it doesn't have a sense of the individual, where in the West, the individual makes their choices and they can choose yes or no, where in China you don't have that ability. When you have stories like that out of China, it makes you wonder what else is happening, but in a country that doesn't have those controls and doesn't have those personal individualistic controls, then it's frightening where that can go, I guess. Yeah, I think that is a great example of two things. One, the sort of distracting over sensationalization of what's going on. It was an experiment. [23:31] It was an experiment on human embryos. Basically, they're fusing, they're injecting or stitching water bear genes into human genes, right? Of water bears and those tiny little microscopic creatures that I guess look like bears. They look more like some kind of monstrous doodle bug to me. But the idea then being that because water bears are resistant to radiation, these resulting humans would also be resistant to radiation. One of the things that I covered and looked into quite a bit was the creation of human monkey chimeras in China. [24:09] This was done in partnership with the Salk Institute in California, but the human monkey chimeras, basically a chimera is taking two different types of stem cells, right, two different species or multiple species stem cells and fusing them together to create a sort of hybrid creature. This has been done a lot in mice, but this was, these were human stem cells blended with, I believe it was macaque monkey stem cells and we're chimpanzee, whatever. And they let them grow until like 30 days, then offed them, right? Mass abortion basically. [24:51] And another great example, Ha-Xiang Hui, the Chinese geneticist, in I believe it was 2018 announced that he had created the world's first, at least known, CRISPR babies, a pair of twins whose father was HIV positive. So he went in and used CRISPR to alter their, it's a gene that is responsible for the enzymes on cellular membranes, a defensive enzyme that would give them immunity or at least resistance to HIV. He was of course imprisoned by the Chinese Communist Party after all of the global ethical outrage. Many would say and I think it's probably correct that the reason they imprisoned him is mainly because he bragged about it not because he did it. But, anyway, I think that in many ways the, in the same way that killer artificial intelligence is a is a diversion from the real dangers of just minimally powerful artificial intelligence or social control or surveillance. And in the same way that an implanted brain-computer interface kind of distracts attention away from the real human-machine symbiosis that occurs through our relationship with smartphones and other digital devices. In that same way, the focus on this idea of horrific mutants, [26:16] such as a human monkey chimera, or a part human, part water bear nuclear war super soldier, A, it's very unclear whether any of those creatures would ever develop into anything anyway, right? More than likely, they would just die as the genetic monsters that they are. But even if that was done, you're talking about a tiny minority of people We'll take another 10 to 20 years to really see what the realization of that means, What's more important? I think is something like the vast experiments done on the human population with mRNA injections, That alone is enough to give us pause. You know, it is terrified about half of us and [27:02] for very very good reason it has completely hypnotized seemingly the other half of us, which is also extremely alarming. But I really think that it's the extreme ends of these technologies It's very important to look at them because that tells you where they want it to go, but for the immediate, for right now for the present time. I think that the most important thing to look at is these these more mundane experiments being done on the whole on whole populations such as the mRNA injections such as as human smartphone symbiosis, and such as AIs like the chatbots, the chat GPT. Well, let's get into it. I want to talk about some of the individuals. I was saying actually what are the vision guiding these technologies, but the vision comes with the individuals. And of course, you've got Bezos with Amazon One, Sam Altman, who I actually hadn't come across until you put out the article about the biometric world ID. Someone like Jeff Bezos, us on the right on the conservative side, or we don't like. But then you've got Peter Thiel, you've got Elon Musk, and then there's confusion because they're pushed towards some of these technologies. So, I mean, give us a, you've touched on some of the figures, but maybe touch on some of those who are some of the key individuals pushing some of these technologies? [28:30] You know, since you mentioned them and none of them, none of the ones you've mentioned other than Peter Thiel are open transhumanist and even Peter Thiel now basically says transhumanism is a kind of a past, it's a fad that has passed. And in some sense he's correct because transhumanism was a very localized school of thought that whose ideas influenced a lot of people. And now you wouldn't call it transhumanism. You would call it the fourth industrial revolution, or you would call it the internet or you would call it bio-digital convergence, something like that. So just going across that spectrum and I'll just go from left to right. You would say, and I don't think that left and right really don't apply here because what you're talking about is an orientation towards a higher power technology and it really does cross the political spectrum. There's every reason for people on the right to want to use these technologies as there is for people on the left. So. Bill Gates, though, I think is at least most associated with kind of left-wing thinking, even if he's not really a leftist in any meaningful way. [29:36] He is probably, he's been the most resistant to publicly espousing transhumanist goals, right? He's more and more moving in that direction, especially with the release of the GPT technology. But, you know, for him, it's always this sort of latent thing. He's much more focused on the immediate so far as I can tell and he's also to me the most condemnable of all those individuals because of all the influence that he's wielded to [30:05] force these technologies on people in a technocratic fashion moving over to Jeff Bezos, you know, There are a lot of reasons that Jeff Bezos has gone under the radar because he is, He like gates. He's not been all that outspoken but just look at three different aspects of his career, four different aspects, sorry, four. Number one, the entire Amazon structure is technocracy personified, right? So a fulfillment center is a top-down control structure built off of algorithms and some advanced artificial intelligence that either employs robotics to do the work or it turns humans into kind of human algorithm symbiotes. So people literally sit around all day on their phones taking direction and they're monitored and artificial intelligence scrapes up that data to figure out how to make the system more efficient. It is without a doubt, the most effective digital super organism that exists on the planet, or at least among the maybe military grade super organisms are more powerful. Second, his entire infatuation with going out into outer space and... [31:22] At one point he was speaking at the National Cathedral. He talked about how maybe in one vision of the future, most people would live in outer space and Earth would remain as a sort of national park for them to visit on occasion, which is utterly inhuman and horrific to most normal people. But it just basically went without comment. A few people were like, oh my God, that sounds horrible. This billionaire is talking about putting us on space ghettos and keeping Earth for themselves. Well, I mean, that's our guy right there, right? And so the whole thing with Blue Origin with a penis-shaped rocket and the Amazon smile with a penis-shaped smile, I think it does in many ways represent the kind of masculine underpinning of transhumanism in the entire kind of technological endeavor. But also, he's invested in Altos Labs in conjunction with Yuri Milner. And Yuri Milner is much more openly transhumanist. He wrote a manifesto, I can't remember the name of it, talking about human life, giving away to Silicon Life. But Altos Labs is dedicated to human longevity through genetic engineering. Peter Thiel also involved in this. Obviously Bill Gates involved in this. Most of these, Larry Page and Sergey Brin at Google also involved in this. Very, very, very popular among the billionaires. [32:41] But as you mentioned, Amazon one. Here you're talking about really this kind of pop beast system, wherein Amazon customers, now Panera Bread customers, also Whole Foods customers using their palm biometrics in order to pay for things and identify themselves. I think that that is going to be a much more popular way of implementing what Christians would call a beast system because a lot of people fetishistically implant RFID chips for that purpose. That is really unnerving to a lot of people. Whereas if you take that away entirely and just have a biometric scan, it's much more amenable to the general population. I don't know what the numbers are yet for the customers, but I do know that it's many dozens of stores this is rolled out in so people are using it. Moving over to the right though, you've got Elon Musk who is everything but an open transhumanist, right? He he espouses all of the transhumanist values without ever using the term transhumanism It's very very common ploy, right? So everything from the idea that artificial intelligence will achieve this godlike state to, the only way that human beings will be able to survive in such an environment is to link our brains to it to friendly AIs through an invasive brain computer interface, which he's working on. [34:04] He's also working on artificial general intelligence with Tesla AI and one would imagine that, he has and will be using Twitter data for the same purpose, right? He didn't need to buy Twitter for that, just by the way. Twitter has always offered Firehose API for people who want to data mine Twitter. The only thing that really gives you is 24-7 fire hose access and also access to the DMs other than that a lot of people are training their a eyes on Twitter or have been, [34:36] interestingly musk has cut that off anyway, and then also you know musk and his obsession with going and living in space This is a recurring theme of transhumanist to get off of Earth and become the sort of multi planetary, species and The creation of the robot optimist would be another great example example, the rollout of autonomous vehicles is another great example. I mean, at that point you've got an infrastructure that controls you as much as you control it or maybe more. And so it's really interesting this way in which he's captured the hearts of the right, mainly because he's cool, he's funny, and he at the moment is so anti-PC or anti-woke that there is a certain alignment there. And I appreciate all he's done in that direction, but to me, his long-term vision of the future is more important than the short-term favors he might have to offer. And then moving to the farthest right, Peter Thiel, much more openly involved with these different transhumanist movements. [35:42] What is it called? The Methuselah Foundation, he's invested in heavily. A number of other sort of longevity start-ups he's invested in. He was very interested in Ambrosia, which was, was they've shut down operations now because of threats from the FDA. But Ambrosia is a process. They use the process of parabiosis. They would inject young people's blood into older people to give them more vitality. And of course, Peter Thiel founded Palantir. [36:13] Which even if they're not working on artificial general intelligence, their AI systems are among the most sophisticated in the world. And they're used to, uh, to really apply real world power through the military and through the security state in general. And so on and on, again, as I mentioned, Peter Thiel was an investor in, originally investor, an investor in Neuralink, now a major backer of BlackRock Neurotech brain computer interfaces. So, you know, across the spectrum, one last thing, actually, if I may, One last thing about Peter Thiel that's also really interesting. Of all those people I just mentioned, he is also explicitly religious in his outlook. And so Peter Thiel is oftentimes written about Christianity and the relationship it has with technology. And maybe the most important essay that I'm aware of personally is an essay that was published at First Things, Christian magazine, the title being Against Edenism. [37:21] And in that he argues there's no going back to Eden of Genesis, there's only going forward to the city of God in Revelation. And so Christians need to use these technologies to defend, to bolster and defend their civilizations, to create a sort of kingdom of God on Earth or some approximation of the city of God on earth, and city of heaven on earth. [37:50] To me, I think that it's a kind of gross perversion of what the Christian doctrine is. I mean, not that there's any single Christian doctrine. I know many of your religious listeners might take umbrage with that statement, but the sort of general orientation of Christianity is towards a higher spiritual realm and is at least disinterested in the outcomes of the physical body, this technological obsession is obsessed with physical outcomes. So Thiel is also interested in that way. Aside from funding all these kind of Christian Republican candidates, he also uses Christian mythology in order to push a kind of technocratic or transhumanist point of view. Can I pick some of the names? The whole chat-GBT thing. I know Peter Thiel and Elon Musk were involved in the beginning and then Microsoft came along and put in billions and seemed to have taken that partially as their own and then the whole letter from 1800 opposing, the move of AI in general. But I mean I'm Gen X so it did take my older son to show me the South Park episode about chatGBT and then I thought I have to get up to get up to speed. But I guess people just see that as [39:20] helping society, making your life easier. It doesn't seem too invasive. It's just [39:27] for lazy people, they can use that. And how does that kind of fit in? Because chat GPT has been very much in the media recently. ChatGPG set off a social atom bomb. It's just really insane. On the one side you have all these people who have embraced it. On the war room we've really focused on guys like Hans Monk at Epic Times who is very enthusiastic about it as being a way to break the left. And then of course Jordan Peterson. People really got mad at me, but he does sound like a real wiener when he's talking about it being smarter than you are. Are and oh Elon Musk is going to save us. Sorry for your Jordan Peterson fans but I find him to be very off-putting. Anyway, they talk about it as kind of this god-like entity in some sense. And then on the other side, which is really, really interesting, on the other side you've got guys like Eliezer Yudkowsky and Elon Musk and Yuval Harari and Max Tegmark. All of them, transhumanist basically, with the exception of maybe Harari. I know a lot of people would wonder why I would say that, but I don't see him as being a transhumanist in any meaningful way. Anyway, all of these transhumanists are saying that this represents a profound danger to human civilization. So why would they say that? It's a chatbot. It's nothing but a chatbot, right? [40:55] And the real reason, there's two major reasons, right? One, the unexpected capacities that GPT technology, has exhibited, the sort of general knowledge that it's able to put out on the basis of, you know, nothing more than a neural network, right? Like you're just talking about an artificial brain that exists in a virtual system, but because of its size and the scale of the data it was trained on, it surprised everyone. GPT-3 surprised everyone. GPT-3.5 or chat GPT really surprised everyone as they flooded the public with it and people started having these very, personal interactions with an artificial mind and that was really important before they put on the safety layers people oftentimes say oh AI is just woke, Initially it wasn't just woke before they started putting the safety layers on it. It was actually [42:03] unbiased hence the enthusiasm that people like Hans Monk and Jordan Peterson had for it and [42:09] GPT-4 has really stunned people because it's starting to edge towards general intelligence. And just, I've been speaking about it, but just for any listeners who aren't familiar, artificial narrow intelligence is an AI that can do one single task or one kind of narrow range of tasks, such as play chess or go or play video games or control a microchip production system or to spit out words like chat GPT, right? Artificial general intelligence is something more human-like in which you have multiple cognitive modules that thinks across all of these domains and oftentimes simultaneously. Doesn't exist yet, but GPT-4 represented a huge move in that direction. It was able to translate, for instance, vision into text and make reasonable conclusions about it. It was able to solve mazes, right? It's a language model, it was able to solve mazes. And maybe most importantly, it excelled on human testing. [43:18] So the two most impressive were the GRE verbal test, 99th percentile was its score. And then you've got the US Biology Olympiad, again, 99th percentile. And then you had the LSAT and the bar exam, law exams. And that was 90th percentile and 88th percentile, respectively. So [43:46] people saw this as this incredible potential. Where is it going to go next? That's the fear. Now I personally am quite stunned that people are so enamored by this and that they want to embrace it. I think the biggest danger that this technology poses is that people like Bill Gates, right? Because Microsoft backed OpenAI, They're incorporating all of these GPT technologies into their systems. And so Bill Gates is talking about using it for education. A lot of people are talking about using it for education, meaning that education will become more and more, more than it is now, e-learning, digital learning. And these students, the youngest generation is going to develop this human AI relationship that is going to stick with them for life. And transhumanists oftentimes talk about how in an ideal future, you would have your own kind of personal AI as a type of guardian angel that would teach you about the world and would learn you better than you know yourself, right? And give you the advice that you need to get through life. You're talking about the most powerful brainwashing technology ever created. [45:05] And, you know, aside from that, you've got all of these different jobs that are being obliterated, everything from copywriters to editors to lawyers and even doctors and nurses. So that is, again, you're talking about the digital mediation between humans and all these kind of critical services. Maybe most importantly, preachers, rabbis, imams, I assume, using these technologies, specifically chat GPT, to create their sermons or to read, you know, to maybe a more autonomous system, just a simpler system to read liturgy. This is already occurring in like small little points across the planet. It has not yet taken off. But I could definitely foresee a future, especially after all of these children have been brainwashed by this technology, in which as you and I get old and die, literally, we've got a robot standing over us, reading us our last rites, as our, you know, the contents of our consciousness are made manifest through some sort of digital zombie made from all of our data. I mean, it sounds sci-fi, but barring nuclear war or an EMP, something like that is going to happen in certain societies around the world. So the big danger I see are those more immediate dangers, the psychological danger and the sociological and economic dangers. But you've got guys like Eliezer Yudkowsky. [46:33] Who say that, Nick Bostrom is also a major figure, who says that this represents a move towards an artificial general intelligence that is not aligned to human values, and it's not necessarily aligned to human existence. And so if the next iteration in GPT-5, or the next iteration in GPT-6, or any of these other AI companies that are working in competition with them, or any of the militaries around the world who are developing other artificial intelligence systems, if any of these create a digital brain that is large enough and fast enough and astute enough, I guess is a way of putting it, then you end up in a situation where you might get a hard takeoff, right? An intelligence explosion, what Nick Bostrom calls a super intelligence. And if that super intelligence is not aligned to human values or does not regard human existence as being necessary or desirable then it could easily take control of [47:42] critical infrastructure it could take control of weapon systems It could take control of a biolab or a series of biolabs, Or it could take control of individuals within a society to use any of these critical systems in order to destroy some other people or all of humanity. That's the fear that Eliezer Yudkowsky is talking about and it's entirely based on all of these kind of emergent properties from a chatbot that should just be you know some sort of rote memorization sort of regurgitation of all this knowledge but instead is showing this flexibility. The fear is that chatbot or maybe it's a robotic system or maybe it's a military simulation system or maybe it's a military control system. It could be any type of AI But if it reaches a super intelligent state, The fear is from their side that it would obliterate some or all of humankind, again I think it's very very important to listen to just for this for the same reason that all the warnings about the atom bomb were were very, very important to listen to. But in some ways that distracts from the more immediate and certainly attainable goals of rolling out these AIs across the society and using them for social control, for indoctrination and for mass surveillance. [49:06] I just wanna, I'm looking at time, but just wanted to bring in one final post that you had put up. This is on your GETTR and this was a YouGov America. I just want to touch on just for a few minutes, because it's interesting to see what the public rise. It was interesting, actually, YouGov, asking the question, how concerned at all are you about the possibility that AI will not just have a negative effect, but will cause the end of the human race on Earth? So it was a very hyperbolic question. But on this, you had 19% very concerned, 27% somewhat. So you've got 46% are concerned, 13% not knowing. So it seemed very evenly split. Half the people who were asked either were concerned or didn't know what it was about or unconcerned and didn't know. That was not only the type of question asked, that was intriguing, but the response was also intriguing. What were your thoughts when you posted this? I think it was back on 5th of April or so when you posted this. Well, it's obviously is an expression of that open letter that was put out by the Future of Life Institute calling for a six-month moratorium [50:19] on any AI above the level of GPT-4. Then, of course, Eliezer Yudkowsky published the now famous, op-ed in Time Magazine saying that's not enough and that all large GPU clusters, all large AI training centres, data centres should be banned. And if intelligence is aware of a training center working on a massive AI system, a potentially super intelligent system, airstrike should be on the table even at the risk of nuclear war. So this has flooded the national consciousness here in America and I presume world consciousness across the globe. I've been very provincial of late, so you'd have to tell me. But I know that just regarding that poll, which is an American poll. [51:15] This is flooding people's consciousness. It's always been there, latent consciousness has always been there in science fiction, everything from the Terminator and things like HAL 9000, all these sorts of motifs have always been there. Now, it represents a distinct possibility in people's minds. But that 50-50 split that you're seeing there, roughly 50-50, half and half, what's interesting is that give or take 10, 15%, either direction, on a score of issues, that's what you see in the American psyche. So you saw during COVID, I would say roughly half of the population became, you know, COVIDians and wanted to mask up obsessively. The other half, even among those who complied, really weren't into it. And on the extreme end, which I would place myself, were fiercely opposed and furious about it. [52:14] Same thing, basically, basically enthusiasm for the Vax. I don't know of any hard statistics. Forgive me if I'm a little wrong, but basically you've got this split, a significant enough split that each side has some potential of taking over the federal government and applying their will on the other half. Well, another really interesting poll that was done by two researchers, led by two researchers from Harvard and I believe Cambridge, if I'm not mistaken, looking at the Americans, and they surveyed asking them, if your child would have a better chance of getting into a top 100 college, Would you be willing to one, edit the embryo's genes to give it higher intelligence, or to use a polygenic risk score, or the pre-implantation testing, genetic testing, to figure out whether or not the IQ was high enough. [53:14] To give your infant a better chance of having a high IQ. And so, about a third, and this is roughly the same roughly the same for uneducated or more educated, skewed towards more educated, skewed towards younger, about a third, almost 40% among educated said they would be willing to edit their embryos genome [53:38] in order to give a higher IQ, just under half, just under 50% for the polygenic risk score. And what that means is that you conceive the child in vitro, right? Right the test tube baby from the 1970s you conceive the child in vitro and then you freeze the embryo and what you really do is you you stimulate the ovaries to produce multiple eggs so you end up with around 10 to 15 eggs and you conceive all of these and then you freeze them after taking a sample of the cells you do a polygenic risk or you do genetic testing on all of them and I've described this as being somewhere between a basketball tournament and a spelling bee basically you, one that is deemed to be most likely to be smartest also tallest and certainly devoid of any major, deformities or genetic diseases that one gets picked that one gets implanted either in the mother or as it's become more popular a surrogate and [54:44] then you have this kind of slow rolling process of eugenics This is already being done. And one of the major companies is Genomic, what is it, I believe it's Genomic Prediction, if I have the name right. And that was a startup funded by our boy Sam Altman from OpenAI, and they offer a sophisticated polygenic risk score test that includes IQ. It doesn't include positive IQ scores, but what it can weed out is the lowest 2% in IQ, or the lowest 2% in height is one of the things they offer, right? And so you've got this sort of soft eugenics, what's called liberal eugenics by the scholar Nicholas Agar. But liberal eugenics is not state enforced, it's choice, it's freedom, right? I have the freedom to eugenicize my child and the next generation. So looking at those statistics, you see the significant portion of the population that has enthusiasm for it. And that tracks with a previous poll that was published, I believe, last year from Pew, which found that people, it was like roughly a third, if I'm not mistaken, roughly a third of people would be willing to use genetic engineering [56:06] to eliminate a disease. And some other, I believe it was also roughly a third, said that they would be willing to implant a digital device into their child's brain in order to give them increased intelligence. I'm a little fuzzy, it's been a minute since I've looked at that, but it's significant enough to push this forward. And you have the possibility of it, right? You have the technological possibility of it. Some of it just over the horizon, some of it right here. So going back to the idea, well, is AI going to kill us all? I think it's you know it represents the the people who are going to want to put a halt to AI and the people who are at least going to want to regulate it or to boycott any corporation working on it those are going to fall into that half that cares right that half is afraid the other half is going to be much more likely to either not care and dismiss it or perhaps be enthusiastic about it with a lot of overlap, but this is kind of I'm not much of a futurist look at any of my track records for girlfriends gambling or elections, but I [57:21] do think that what you do see is enough social momentum enough acceptance on the part of the population at large large that should these technologies actually be effective, you'll have a significant proportion who will want it. And even if they aren't entirely effective, even if it's just some sort of half-baked version of it, they will be willing to accept and adopt it. And so I don't see this going away at all. Again, barring nuclear war or an EMP, I just don't see it going away, there is a growing enthusiasm for the techno cult we call transhumanism and a growing acceptance of the kind of dictatorial social structure we call technocracy. And I sense that it is a fast-growing religion, and it will continue to impact those of us who want nothing to do with it. We have to learn to deal with it. We have to learn how to resist it effectively and and not just this year and next year, but across generations. [58:27] Yeah, no, absolutely. Joe, I appreciate you coming on. I've thoroughly enjoyed watching you on the War Room. I enjoyed meeting up with you at CPAC. And just for the viewers that they can find you, this will be going out Monday the 17th, the American Freedom Alliance Conference. I had the privilege of going to one back in June called Propaganda, and you'll be speaking at the World War III, the early years, 22nd to 23rd of April. So there are tickets available. You can go to the website, americanfreedomalliance.org and get a ticket. If you're over there on the West Coast, then I would really encourage the viewers or listeners to go and make it a trip because you'll thoroughly enjoy it from listening to Steve Bannon, Joe Allen, and everyone else in between. So Joe, thank you for your time today. Thank you very much, Peter. And just for your listeners, anyone who wants to go, promo code Joe, get a discount. So I would love to meet anyone who's over in that area. Come on down. But yeah, Peter, I really, really appreciate it. Thank you very much for having me on. It was absolute, it was fantastic meeting you in DC. Great time, hope to see you again.

Aubrey De Grey discusses the progress and potential of therapies related to his ideas on anti-aging medicine, including the four therapies that will be tested in a mouse rejuvenation trial. He also shares his thoughts on partnering with organizations and individuals in the field, integrating AI into his work, and the importance of structure in … Aubrey De Grey:longevity escape velocity, longevity, mouse rejuvenation, Altos Labs, Yamanaka factor #149 Read More »

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.

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.

Der tägliche Nachrichten-Podcast der deutschen Startup-Szene Heute u.A. mit diesen Themen: Robert Habeck trifft Berliner Startup-Szene Windeln.de meldet Insolvenz an Rechtsstreit um Gorillas-Marke IT-Sicherheitsmarkt wächst stark Europas Fintechs schöpfen Potenzial nicht aus CEOs sollen zu „Chief Energy Officers“ werden Elon Musk übernimmt Twitter Altos Labs will Alterungsprozess umkehren OpenAI finanziert Descript Quartalszahlen von Apple

If someone asks you how old you are, you'll probably answer with the number that reflects the birth date on your driver's license. But scientists are learning that chronological age is not the same as your biological age. Technology has given researchers the tools to measure countless metrics and cross-reference them to get a better picture of your true age. One of those researchers is Morgan Levine. This week, on Big Books and Bold Ideas, she spoke with host Kerri Miller about how your biological age can give you a glimpse into the future, but one that you have the power to alter. “Your biological age on any given day is not your destiny,” she writes in her new book, “True Age: Cutting-Edge Research to Help Turn Back the Clock.” Guest: Morgan Levine is a aging researcher, an adjunct professor of pathology at Yale and the founding investigator at Altos Labs, a biotech firm that aims to develop life extension therapies. Her new book is “True Age: Cutting-Edge Research to Help Turn Back the Clock.” To listen to the full conversation you can use the audio player above. Subscribe to the MPR News with Kerri Miller podcast on Apple Podcasts, Google Podcasts or RSS. Subscribe to the Thread newsletter for the latest book and author news and must-read recommendations. 

How long do you want to live? How healthy do you want to be in your later years? For many podcast listeners, healthspan is more important than lifespan, but it's difficult to figure out what–if anything⁠–can stack the deck in your favor. On this week's podcast, we'll meet PhD researcher and author, Morgan Levine, who is actively working to answer these questions.  Listen and learn:  Why exercise is probably the greatest anti-aging tool Metformin and rapamycin: do they work? Human age potential Heritability vs. epigenetics  Links Morgan Levine's Book ABOUT OUR GUEST Morgan Levine was an Assistant Professor in the department of Pathology at Yale University. She now works with Altos Labs, where she leads a research group on bioinformatics, cellular biology, and biostatistics. She is the author of, True Age: Cutting-Edge Research to Help Turn Back the Clock. Like the Show? Leave us a review Check out our YouTube channel Visit www.yogabody.com

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

‘In this world nothing can be said to be certain, except death and taxes.' While Benjamin Franklin's quote remains true for most, the same might not be said for some of the world's billionaires. And their efforts to extend life are under way too. Most recently, a Silicon Valley startup called Altos Labs signed up a dream team of scientists, including numerous Nobel laureates, with an aim to rejuvenate human cells. In this episode from February 2022, Ian Sample speaks to Prof Janet Lord about the science of ageing, extending our health as well as our lifespans, and how old we could actually go. Help support our independent journalism at theguardian.com/sciencepod

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

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

WE APPRECIATE OUR PARTNERS. CHECK THEM OUT!Skin Health & Healing: https://alituranaturals.com/shop/, use code DAVE20 for 20% off storewideDigestion & Immune Function: https://justthrivehealth.com, use code ASPREY to get 15% offBusiness Growth With SEO: https://www.stephanspencer.com, get a FREE consultationIN THIS EPISODE OF THE HUMAN UPGRADE™... …you'll learn how biological age, rather than chronological age, is the primary risk factor behind diseases like cancer, heart disease, diabetes, strokes, even Alzheimer's. Scientific discoveries show chronological aging may be written in the epigenome, those chemical tags attached to your DNA that control the way DNA operates.We're finding out more about both types of aging because of scientists like Morgan Levine, Ph.D., a leading voice in the field of aging and longevity science. She focuses her research on the science of biological aging, emphasizing health span over lifespan. “If you take the difference between someone's biological age and chronological age, it should predict the things we care about, the actual things we're trying to prevent—so death, disease,” she says. She's an assistant professor of pathology and the Director of the Laboratory for Aging in Living Systems at Yale University School of Medicine. Her team looks at using bioinformatics to quantify the aging process and test how lifestyle and pharmaceuticals alter the rate of aging. She's also a founding Principal Investigator at Altos Labs, a biotech company that focuses on cellular rejuvenation programming to restore cell health and resilience.Today, she's going to talk about the science of aging and longevity explored in her new book, “True Age: “Cutting-Edge Research to Help Turn Back the Clock.” Three main drivers—health behaviors, recent stressors and adversity, and genetics—determine your biological aging. She shares how to measure your own biological age and why you should track your aging regularly. This conversation gets into topics and makes them make sense for your own aging, like:Epigenetics & epigenetic clocksDNA methylation & telomeresCell lifespan Ageotypes (molecular assessment of aging)Phenotypic ageThe “Ceiling” effectThe “CALERIE” trialNutrition & aging (plants, fasting, ketosis)Fitness & aging (energy & brain health)Rest & relaxation (sleep & biological programming)Morgan gives great takeaways on how you can make lifestyle changes to maintain your youthfulness—both inside and out—with low-risk, data-driven biohacking. See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Listen to a blog summary of Dr. Blagosklonny's latest research perspective published in Oncoscience, entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” ___________________________ After the January 2022 launch of Altos Labs, a new anti-aging biotechnology company, Mikhail (Misha) Blagosklonny, M.D., Ph.D., joined this exciting public conversation with a recommendation. Dr. Blagosklonny is a prominent scientist in the fields of cancer and aging research. He is well-known for his experimental research articles and theoretical papers on the hyperfunction theory of aging and the pursuit of longevity with rapamycin. On April 22, 2022, his latest research perspective was published in Oncoscience, and entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” Full blog - https://aging-us.org/2022/05/dr-blagosklonnys-rapamycin-based-recommendation-for-altos-labs/ DOI - https://doi.org/10.18632/oncoscience.552 Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords - aging, longevity, lifespan, geroscience, rapalogs, gerostatics 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

BUFFALO, NY- May 11, 2022 – A new research perspective was published in Oncoscience journal by Mikhail Blagosklonny, M.D., Ph.D., entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” “Here I discuss how combining rapamycin with other modalities may let us live long enough to benefit from future discoveries in cellular reprogramming and what needs to be done at Altos Labs to make this happen.” Altos Labs—a new anti-aging biotechnology company funded by multiple billionaire investors, including Jeff Bezos and Yuri Milner—has reported a focus on reprogramming cells in order to reverse the trajectory of diseases, and thus, reverse aging. In his research perspective, Dr. Blagosklonny writes that potential life-extension with rapamycin may allow us to win time while awaiting future discoveries that will reverse aging. “Rapamycin treatment is rapidly becoming a mainstream anti-aging intervention.” However, Dr. Blagosklonny also writes that rapamycin alone is unlikely to extend lifespan sufficiently to benefit from Altos Labs' future discoveries in our lifetime. “If Altos Labs would allocate a small percentage of its funding to develop rapamycin based drug combinations, then additional decades of life extension may be available 3–5 years from now.” “The number of potential combinations with rapamycin is enormous.” Read Dr. Blagosklonny's research perspective: https://www.oncoscience.us/article/552/text/ Correspondence to: Mikhail V. Blagosklonny Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: aging, longevity, lifespan, geroscience, rapalogs, gerostatics Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny For media inquiries, please contact media@impactjournals.com. Oncoscience Journal Office 6666 East Quaker Str., Suite 1D Orchard Park, NY 14127 Phone: 1-800-922-0957, option 4 ###

Life extension often becomes a forgotten transhumanist area of research, but major investment is now happening in the field. Are billionaires putting their money down in an effort to attain eternal life? Topics: desert house completion, Jeff Bezos, Altos Labs, life extension, biological reprogramming, cell rejuvenation, billionaire investors, converging technologies, Greenland Shark, Batman movies, Sunset Boulevard, film noir

Vanilla Sky Electric Horse MuskThe Age of Transitions and Uncle LIVE 4-22-2022 AOT #351Life extension often becomes a forgotten transhumanist area of research, but the major investment is now happening in the field. Are billionaires putting their money down to attain eternal life?Topics: desert house completion, Jeff Bezos, Altos Labs, life extension, biological reprogramming, cell rejuvenation, billionaire investors, converging technologies, Greenland Shark, Batman movies, Sunset Boulevard, film noirUTP #261Uncle works on his electric horse idea, which he plans on pitching to Elon Musk someday soon. Topics include: Creative Accidents must call in, Middle Ages not a bad time to be alive, life extension, eternal life, religion, near-death experience, gas prices in Spain, Stanley Meyer's water-fueled car, electric vehicles, recreational vehicles, riding a horse, Elon Musk, Amish, live-streaming video gaming, vintage gamesOCHELLI LINKS:If You Appreciate what Ochelli.com Radio Does: https://ochelli.com/donate/Ochelli Effect - Uncle - Age of Transitions - T-shirts and MORE: https://theageoftransitions.com/category/support-the-podcasts/LIVE LISTENING OPTIONS:OCHELLI.COM https://ochelli.com/listen-live/ RADDIO https://raddio.net/324242-ochellicom/ ZENO https://zeno.fm/radio/ochelli-radio/ TUNEIN http://tun.in/sfxkx

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

Le PDG d'Amazon, Jeff Bezos, vient d'investir 3 milliards de dollars dans une start-up américaine dont le but est rien moins que de trouver la clé du rajeunissement humain. Il n'est d'ailleurs pas le seul à s'intéresser à cette entreprise.Une start-up californienneJeff Bezos a donc rejoint les rangs des gros investisseurs qui ont souhaité aider de leurs deniers une toute nouvelle entreprise. En effet, elle a vu le jour en janvier dernier.Son nom est Altos Labs. La société a élu domicile dans la Silicon Valley, en Californie. La société est également présente au Royaume-Uni et pourrait s'implanter ailleurs dans l'avenir.Altos Labs a sollicité le concours de scientifiques prestigieux, qu'elle attire en leur promettant des salaires fabuleux.Prolonger la vie humaineL'objectif d'Altos Labs est la reprogrammation cellulaire. De quoi s'agit-il ? C'est une méthode révolutionnaire, qui vise rien de moins que le rajeunissement humain. Elle consiste en quelque sorte à transformer des cellules différenciées, qui constituent divers organes du corps, en cellules pluripotentes.De telles cellules existent déjà : ce sont des cellules souches, capables de se différencier en n'importe quel type de cellule.Ces recherches sont considérées comme une avancée très prometteuse en matière de médecine régénérative, dont le but est de restaurer les organes et les tissus malades. Mais cette reprogrammation cellulaire pourrait avoir un but encore plus ambitieux : la prolongation de la vie humaine.Appliqué à l'organisme tout entier, ce rajeunissement des cellules pourrait contribuer à l'augmentation de l'espérance de vie.Dans un domaine aussi novateur, les investisseurs d'Altos n'attendent pas des résultats trop rapides. Mais ils espèrent que les travaux qui y seront menés ouvriront de nouvelles perspectives à la médecine.Ces techniques ont déjà été utilisées, avec un certain succès, pour prolonger la vie de souris de laboratoire. Ces expériences sur les animaux pourraient être poursuivies. Puis, dans un second temps, il sera peut-être possible d'envisager la reprogrammation de cellules humaines.Altos n'est pas la première entreprise à s'être intéressée à la reprogrammation cellulaire. Une autre société, Calico Labs, s'y consacre déjà depuis 2013, mais sans grands résultats pour l'instant. Voir Acast.com/privacy pour les informations sur la vie privée et l'opt-out.

En parlem amb Josep Corbella, periodista de La Vanguardia especialitzat en ciència i salut.

En parlem amb Josep Corbella, periodista de La Vanguardia especialitzat en ciència i salut.

Yuri Deigin is the founder and CEO of YouthBio Therapeutics which is a company that is working on Epigenetic reprogramming or using the Yamanka factors to achieve partial reprogramming. Epigenetic reprogramming has been in the news lately because of several companies being started in the space, with some notable ones being Altos Labs funded by Jeff Bezos and NewLimit founded by Brian Armstrong, CEO of Coinbase. If you're not familiar with this trending, hyped (rightly so this time - it is pretty amazing!) research on Epigenetic reprogramming and Yamanaka factors to turn cells back to a younger state, we dive into it in today's episode! As a last point to Yuri's introduction, because I'd be remiss if I didn't mention it, you may have heard of his name recently because he was in fact one of the first people to talk about the COVID lab leak theory and wrote extensively on it. This speaks to his scientific mindset and desire to uncover the truth. In today's episode, you will learn: - The Strong Epigenetic Theory of Aging, as coined by Yuri (He calls David Sinclair's theory The Weak Epigenetic Theory of Aging) - Epigenetic Reprogramming using Yamanaka factors to turn the cell into a younger state - What is it and what are the open questions in the field - What are the cancer risks associated with it - Why Yuri believes in Cryonics - Why Yuri got interested in uncovering the COVID-19 Lab Leak theory - Pharma in Russia If you are a premium subscriber, you can also read the summarized notes of these learnings in the show notes. All platforms / Episode Show Notes: https://livelongerworld.substack.com/p/ydeigin Find the previous podcast episodes & subscribe to be notified: https://www.livelongerworld.com/podcast Sign up for Premium Subscriber Summarized Show Notes on Key Points: https://www.livelongerworld.com/premium Support on Patreon: https://www.patreon.com/livelongerworld One-Time support: https://www.paypal.com/paypalme/livelongerworld YURI DEIGIN LINKS: Twitter: https://twitter.com/ydeigin LinkedIn: https://www.linkedin.com/in/yurideigin/ Medium: https://yurideigin.medium.com/ YouthBio Therapeutics: https://youthbiotx.com/ LIVE LONGER WORLD LINKS: Website: https://www.livelongerworld.com/ Twitter: https://twitter.com/livelongerworld Newsletter: https://livelongerworld.substack.com/ Instagram: https://www.instagram.com/longevityfuture/ Patreon: https://www.patreon.com/livelongerworld YouTube: https://www.youtube.com/c/LiveLongerWorld Premium Subscriber: https://www.livelongerworld.com/premium TIMESTAMPS: 00:00 "We're not crazy" 0:37 100% life extension & translation to humans 4:28 Aging is potentially an engineering problem 12:45 Strong Epigenetic Theory of Aging 19:26 Epigenetic Reprogramming 29:00 Risk of Cancer with Epigenetic reprogramming 33:00 Rejuvenation without cancer risk? 38:30 Why Cryonics Makes Sense 48:00 COVID Lab Leak Theory 53:45 Pharma in Russia 58:40 Optimism in Longevity 1:00:50 Aging is Universal. Let's Unite in this Fight Episode Show Notes: https://livelongerworld.substack.com/p/ydeigin Thanks for listening & if you enjoy the episode, let's spread the message on longevity. You can leave a review on Apple podcasts, subscribe and share the podcast. Aging is universal. Let's unite in this fight. Stay in good health - Aastha.

O podcast Health Innovation desta semana tem como tema os artifícios tecnológicos utilizados para buscar a vida eterna. Um grupo de empresários e pesquisadores se reuniu no Vale do Silício em prol da Altos Labs. A startup conta com investidores influentes como Jeff Bezos e Yuri Milner e tem como objetivo encontrar uma maneira de prolongar a vida. A partir do método de reprogramação biológica, os especialistas envolvidos no projeto desejam rejuvenescer células em laboratório. No episódio desta semana, Laura Murta, Camila Pepe e Jonas Sertório discutem os diferentes recursos utilizados para prolongar a vida humana. Esse podcast é um oferecimento da Sociedade Beneficente Israelita Brasileira Albert Einstein.

While Benjamin Franklin's famous quote about death and taxes remains true for most, the same might not be said for some of the world's billionaires. And their efforts to extend life are under way. Most recently, a Silicon Valley start-up called Altos Labs signed up a dream team of scientists, including numerous Nobel laureates, with an aim to rejuvenate human cells. Ian Sample speaks to Prof Janet Lord about the science of ageing, extending our health as well as our lifespans, and how old we could actually go. Help support our independent journalism at theguardian.com/sciencepod

Neste episódio do A Virada Talks, Gustavo Goldschmidt e Bruno Peroni falam sobre os destaques de janeiro de 2022: A compra da Activision Blizzard pela Microsoft, a Polêmica Envolvendo o Joe Rogan e o Neil Young e o Investimento do Jeff Bezos na Altos Labs, além do Giro de Mercado com os destaques do mês.

Wer ein neues Schlagwort in der HealthTech-Branche sucht, wird bei Longevity fündig. Kleine wie große Unternehmen suchen verstärkt nach Medikamenten, Therapien und digitalen Mitteln, um die Langlebigkeit von Menschen in überalterten Gesellschaften wie Europa oder Japan zu verbessern. Paradebeispiel ist Altos Labs - ein Silicon-Valley-Startup, das kürzlich mit mehr als drei Milliarden (!) Euro an den Start gegangen ist. Mit Maximon, gegründet von den Schweizer Unternehmern Tobias Reichmuth und Marc Bernegger, gibt es einen neuen Company Builder, der auf Longevity-Startups setzt. Im Podcast sprechen Tobias und Marc mit Jakob Steinschaden von Trending Topics über: - Gründung und Ziel von Maximon - die ersten Companies, die Maximon hervorgebracht hat - den Markt für Longevity - die Bedeutung von Altos Labs und Googles Schwester Calico für die Branche - Schnittstelle zwischen HealthTech, Longevity und der Krypto-Welt - Longevity als heikles Gesellschaftsthema Wenn dir der Podcast gefallen hat, gibt uns ein paar Sterne und/oder ein Follow auf den Podcast-Plattformen und abonniere unseren Podcast bei: - Spotify - Apple Podcast - Google Podcasts - Amazon Music - Anchor.fm und besuche unsere News-Portale - Trending Topics - Tech & Nature Danke fürs Zuhören!

Josefina Ríos y Sebastián Rivas conversaron con el ex director de Extranjería, Rodrigo Sandoval, sobre la situación migratoria en Tarapacá ante las manifestaciones ocurridas en Iquique. Además, junto a Paula Escobar analizaron la nueva idea loca de Silicon Valley para vivir eternamente.

0:00 Chamath's preferred cosplay 1:35 Reflecting on bad investment decisions and markup dynamics 15:20 Rising tensions between US and Russia over Ukraine, Putin's demands, NATO negotiations as the underreported key piece, Obama's savvy Russia dealings 39:16 Bill Ackman buys the Netflix dip, Tesla and Microsoft crush earnings, the Fed signals rate hikes 55:18 Altos Labs raises $3B in the largest Seed round ever, incredible Yamanaka factors breakthrough, dynamics of a richly capitalized bio-moonshot 1:04:08 The Stripe Mafia, Bolt CEO punches up, reflecting on old emails Follow the besties: https://twitter.com/chamath https://linktr.ee/calacanis https://twitter.com/DavidSacks https://twitter.com/friedberg Follow the pod: https://twitter.com/theallinpod https://linktr.ee/allinpodcast Intro Music Credit: https://rb.gy/tppkzl https://twitter.com/yung_spielburg Intro Video Credit: https://twitter.com/TheZachEffect Referenced in the show: https://www.bloomberg.com/opinion/articles/2013-05-30/bitcoin-the-perfect-schmuck-insurance https://twitter.com/DavidSacks/status/1480716684038049796 https://medium.com/@jason/do-the-work-skip-the-party-8f2864560195#724a--share-10-78 https://www.nytimes.com/2022/01/16/world/europe/russia-ukraine-invasion.html https://www.defense.gov/News/Transcripts/Transcript/Article/2910061/pentagon-press-secretary-john-kirby-holds-a-press-briefing https://www.theatlantic.com/magazine/archive/2016/04/the-obama-doctrine/471525 https://www.history.com/news/nato-article-5-meaning-history-world-war-2 https://www.latimes.com/opinion/op-ed/la-oe-shifrinson-russia-us-nato-deal--20160530-snap-story.html https://www.worldometers.info/gdp/gdp-by-country https://www.atlanticcouncil.org/blogs/natosource/obama-does-not-believe-invading-ukraine-or-saving-assad-makes-putin-a-player https://www.euractiv.com/section/global-europe/news/germany-agrees-to-axe-nord-stream-2-if-russia-invades-ukraine https://www.wsj.com/articles/william-ackman-takes-stake-in-netflix-11643236690 https://tesla-cdn.thron.com/static/WIIG2L_TSLA_Q4_2021_Update_O7MYNE.pdf?xseo=&response-content-disposition=inline%3Bfilename%3D%22tsla-q4-and-fy-2021-update.pdf%22 https://www.microsoft.com/en-us/Investor/earnings/FY-2022-Q2/press-release-webcast https://www.cnbc.com/2022/01/26/fed-decision-january-2022-.html https://www.tcv.com/tcv-insights/netflix-case-study https://www.cnbc.com/2021/11/16/peloton-files-to-sell-1-billion-in-stock-offering-shares-drop.html https://www.drugdiscoverytrends.com/biotech-altos-labs-emerges-with-3b-in-funding-to-focus-on-cellular-rejuvenation-programming https://www.biorxiv.org/content/10.1101/2022.01.20.477063v1.full.pdf https://twitter.com/theryanking/status/1485784823641755648 https://twitter.com/shaunmmaguire/status/1486082835974811650 https://twitter.com/Jason/status/1486113945790214146 https://twitter.com/shaunmmaguire/status/1486114773209006080 https://twitter.com/Jason/status/1486121975311339520 https://my.pitchbook.com/profile/107633-08/company/profile#deal-history/102358-00T

Na última quarta-feira (19), foi inaugurada no Vale do Silício a Altos Labs, companhia de tecnologia de reprogramação biológica, dedicada à pesquisa antienvelhecimento. Entre os investidores da startup que pretende “derrotar a morte” está o fundador da Amazon e da Blue Origin, Jeff Bezos. --- Support this podcast: https://anchor.fm/nativa-fm-campinas/support

With biotech in the dumps, we talk to Oppenheimer analyst Jared Holz about why the world has soured on the sector and what it means for the future of medicine. Then, STAT's Matthew Herper joins us to explain the latest big idea from biotech's big thinkers: a company called Altos Labs, which has raised $3 billion to do something or other. We also discuss the latest news in the life sciences, with a cameo from Shkreli and an update on Omicron.

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

A Altos Labs dedica-se ao desenvolvimento de uma tecnologia que permite a reprogramação biológica: uma forma de rejuvenescer as células em laboratório, que pode ser a chave para a imortalidade. Este trabalho tem por base uma descoberta revolucionária de reprogramação de células, que permite que as células sejam instruídas a voltar para um estado primitivo.Saiba mais sobre inovação e nova economia em supertoast.pt.

Este episodio (BS18) se grabó el viernes, 13 de septiembre de 2021 y con él comenzamos la 3ª temporada del programa. Tras volver de su estancia de investigación, Silvana se incorpora a la tertulia y nos comenta el primer artículo del episodio: se trata de un estudio en el que se muestra una correlación entre la microbiota de bebés prematuros y la incidencia de daño cerebral (la referencia es: Seki et al. (2021). Aberrant gut-microbiota-immune-brain axis development in premature neonates with brain damage. Cell Host Microbe.). En (bio)noticias comentamos 3 asuntos interesantes que nos trae Íker: la controversia por un artículo en el que se afirma que la tasa de hospitalización es mayor en pacientes Covid con la variante delta (la referencia es: Twohig et al. (2021). Hospital admission and emergency care attendance risk for SARS-CoV-2 delta (B.1.617.2) compared with alpha (B.1.1.7) variants of concern: a cohort study. Lancet Infect Dis.). Francis, nos da su opinión sobre el sesgo del tratamiento estadístico que los autores han utilizado para sacar conclusiones de los datos epidemiológicos. Otro asunto que nos trae Íker es el de los fichajes de grandes expertos en envejecimiento -entre ellos los españoles Manuel Serrano y Juan Carlos Izpisua- por la empresa Altos Labs, fundada y financiada por varios multimillonarios (Jeff Bezos entre ellos), cuyo objetivo es impulsar tecnologías para vivir más años con salud. Entre los responsables de esta empresa se encuentran también algunos de los fundadores de los premios Breakthrough, que se acaban de anunciar. Hemos aprovechado esta coincidencia para dedicar una buena parte de la sección a comentar los premiados de este año en el área de Ciencias de la Vida (con especial atención al premio a Katalin Karikó y Drew Weissman por desarrollar la tecnología de vacunas basadas en ARN, que ha permitido disponer de las vacunas Pfizer y Moderna contra la Covid19 en tiempo récord). También hemos aprovechado para comparar los premios Breakthrough con los Nobel y proponer a los oyentes que participen en nuestra quiniela para los Nobel de este año. Finalizamos la sección de (bio)noticias comentando los recientes fallecimientos de Edmond Fischer (Nobel de medicina en 1992) y del investigador español Dionisio Martín-Zanca. Silvana también nos anuncia el evento de divulgación científica “Desgranando Ciencia” (Granada). A continuación, Pepe nos comenta un artículo de señalización celular y cáncer, en el que se identifica la fosfatas de ciclo celular CDC25 como un nuevo sustrato de la quinasa DYRK2. Comentamos las implicaciones funcionales de este descubrimiento y entrevistamos al responsable del grupo investigador, Marco A. Calzado (IMIBIC, Córdoba) (la referencia del artículo es: Lara-Chica et al. (2021). A novel CDC25A/DYRK2 regulatory switch modulates cell cycle and survival. Cell Death Differ 1–13.). Esperamos que este episodio os resulte interesante y entretenido. ¡Bienvenidos!

✨Подкаст Далера «Читаем интернет»: https://anchor.fm/read-the-internet/episodes/ep-e16vrh9. Сайт Хобы: https://hobacast.ru.✨Темы выпуска:Трояны и бэкдоры в кнопочных мобильных телефонахhttps://habr.com/ru/post/575626/Китайская Xpeng Motors представила «первую в мире роботизированную лошадь, на которой можно ездить верхом»https://rozetked.me/news/18993-xpeng-motors-predstavila-roboloshad-na-ney-mozhno-ezditПро страх вечеринокhttps://m.facebook.com/#!/story.php?story_fbid=10158807393257499&id=528542498Проект Altos Labs. Как миллиардеры Кремниевой долины хотят жить вечноhttps://habr.com/ru/company/itsoft/blog/576928/***Вступайте в наш чат в Телеграме: https://t.me/hobacast.***Телеграм-каналhttps://t.me/hoba_channelБот для ваших сообщенийhttps://t.me/hobacast_botПочтаhobacast@gmail.comГруппа ВКhttps://vk.com/hobacast***Участники выпуска— Аня Линская, https://t.me/shel_sneg— Далер Алиёров, http://t.me/dalerblog— Адель Мубаракшин, https://t.me/exarg***Спасибо нашим патронам!— Александр Полоротов Датаголик— Karhorot— Konstantin Ulyanov— tahdisto— Денис Котов— enerdzaiser— Masha Kozhevnikova— Верните Аню— Sailor Moon— Бей, Адель— Anton Pimnev — Kujibki— Aleksandr Kudinov— Borodovich21— Marianna Kozhevnikova— Дмитрий Иванов— Alexander Lyan— Antonina Lyubenkova— Dima Girya— unclesocky— Vladislav Ryzhov— Борóвский Богдан— Михаил Шляйгер— Firdavs Murodov— Vlad Sazonov— Nadiia Maltseva— Aleksey Savin— Паша Пастернак

In questa puntata:- nuova sentenza USA: un'AI non può detenere brevetti- i tool automatizzati di selezione del personale fanno danni- negli USA i gig workers sono un terzo dell'occupazione totale- Bezos finanzia Altos Labs per sconfiggere l'invecchiamento con la riprogrammazione cellulare- il mondo finanzia i produttori di carne e le emissioni crescono- satelliti ed AI uniti per disegnare la mappa globale dei coralli- batterie a forma e dimensione di container per le navi elettrichewww.the-future-of.itIscrivetevi alla Newsletter.

Chaque semaine, De Quoi Je Me Mail ouvre le débat sur l'actu high-tech ! En compagnie de journalistes, mais aussi de personnalités spécialistes du numérique, nous analysons, décortiquons les grandes tendances du moment. Ce vendredi, nous commentons l'actu avec Nicolas Lellouche journaliste à 01net.com et Anthony Morel journaliste à BFM Business. Module 1 : Bientôt 7 ans de mises à jour sur nos smartphones ? DQJMM (1/2) - Bientôt 7 ans de mises à jour obligatoires pour les smartphones ? C'est ce que l'Allemagne demande à la Commission européenne. - Apple officialise sa keynote du 12 septembre. Ce qu'il faut attendre. - Le patron du projet Apple Car quitte Apple pour Ford. Nouvelle preuve que la voiture d'Apple est loin d'être assurée de voir le jour ? - Un record de recharge rapide battu cette semaine pour un smartphone, 25 minutes pour le Realme GT Master Edition selon les meusres de 01net. - La Silicon Valley en quête d'immortalité (Jeff Bezos et d'autres pontes de la tech ont investi dans Altos Labs, une startup qui veut vaincre la mort) - Amazon veut lancer ses propres télés Module 2 : Le prochain iPhone pourrait-il se connecter aux satellites ? DQJMM (2/2) François Sorel reçoit cette semaine Alexandre Tisserant CEO de Kineis, startup toulousaine spécialisée dans les objets connectés par satellite, avec le lancement en 2023 d'une vingtaine de mini satellites pour couvrir la planète entière. Alexandre Tisserant nous donne son avis sur cette rumeur étonnante d'un futur iPhone pouvant se connecter à des satellites dans des situations d'urgence. Est-ce techniquement possible ?

一个人的跳槽居然能带来打击苹果造车信心、波及股价的影响？ 美国当地时间 9 月 7 号，福特公司宣布，苹果电动汽车项目负责人道格菲尔德将离开苹果、加入福特，负责下一代汽车的云平台开发工作。时隔28年，道格菲尔德将带着他在苹果、特斯拉的多年经验，再次为他的老东家效力。 道格菲尔德是谁？一次跳槽为什么如此重要？通过这期轻解读来了解一下吧！我们也想问问你，如果选择一辆自己的电动车，你会更青睐科技公司还是传统车企的汽车呢？欢迎在评论区一起聊聊！ 本期还有关于曹操出行、小米、Altos Labs 和苹果的轻解读，欢迎收听！ #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

Head Line Mission Daily Report Sep 09, 2021 1. อัปเดตตัวเลขผู้ที่ได้รับการฉีดวัคซีน Covid-19 ในประเทศไทย 2. ราคาดัชนีตลาดหลักทรัพย์ / ราคาหุ้นต่างประเทศ / ราคาน้ำมันดิบ / ราคาทองคำ / ราคา Cryptocurrency 3. ศบค. แจง ทำไมจึงไม่นำผลตรวจ ATK มารวม 4. เปิดตัวรถฉีดวัคซีนเคลื่อนที่ใน กทม. 5. ไทม์ไลน์เลือกตั้ง กทม.ในเดือนพฤศจิกายน 6. Altos Labs กำลังพัฒนาเทคโนโลยียืดอายุ 7. ช่วงนี้มีหนังอะไรน่าดูบ้าง? 8. ฟิลิปปินส์ออกคำสั่งล็อกดาวน์ต่อ ก่อนถึงกำหนดเพียงไม่กี่ชั่วโมง 9. FAA สั่งระงับเที่ยวบินทัวร์อวกาศของบริษัทเวอร์จิน 10. In Time หนังน่าดูสะท้อนสังคม 11. กลุ่มตาลิบันประกาศจัดตั้งรัฐบาลชั่วคราวปกครองอัฟกานิสถาน 12. #ORISxMTTM ORIS ขอมอบ Exclusive Privilege ให้กับ MTTM Fanpage 13. สาธารณสุขชิลี อนุมัติใช้งานวัคซีนซิโนแวคกับเด็กอายุตั้งแต่ 6 ปีขึ้นไป 14. "หมอธีระวัฒน์" ยืนยัน "ฉีดวัคซีน" ให้เด็กได้ทุกช่วงอายุ แต่ต้อง "ชนิดเชื้อตาย" 15. จีนส่งพลังงานแบบไร้สายระดับกิโลวัตต์ไกล 20 เมตร ได้สำเร็จ 16. รวมศัพท์วัยรุ่น 2021 EP.1 เคยใช้คำไหนกันบ้าง 17. EIC เชิญชวนทุกท่านร่วมทำแบบสำรวจ กิน อยู่ อย่างไร? ในช่วง COVID 18. Xiaomi EV เตรียมผลิตรถยนต์ไฟฟ้าของตัวเอง

Head Line Mission Daily Report Sep 09, 2021 1. อัปเดตตัวเลขผู้ที่ได้รับการฉีดวัคซีน Covid-19 ในประเทศไทย 2. ราคาดัชนีตลาดหลักทรัพย์ / ราคาหุ้นต่างประเทศ / ราคาน้ำมันดิบ / ราคาทองคำ / ราคา Cryptocurrency 3. ศบค. แจง ทำไมจึงไม่นำผลตรวจ ATK มารวม 4. เปิดตัวรถฉีดวัคซีนเคลื่อนที่ใน กทม. 5. ไทม์ไลน์เลือกตั้ง กทม.ในเดือนพฤศจิกายน 6. Altos Labs กำลังพัฒนาเทคโนโลยียืดอายุ 7. ช่วงนี้มีหนังอะไรน่าดูบ้าง? 8. ฟิลิปปินส์ออกคำสั่งล็อกดาวน์ต่อ ก่อนถึงกำหนดเพียงไม่กี่ชั่วโมง 9. FAA สั่งระงับเที่ยวบินทัวร์อวกาศของบริษัทเวอร์จิน 10. In Time หนังน่าดูสะท้อนสังคม 11. กลุ่มตาลิบันประกาศจัดตั้งรัฐบาลชั่วคราวปกครองอัฟกานิสถาน 12. #ORISxMTTM ORIS ขอมอบ Exclusive Privilege ให้กับ MTTM Fanpage 13. สาธารณสุขชิลี อนุมัติใช้งานวัคซีนซิโนแวคกับเด็กอายุตั้งแต่ 6 ปีขึ้นไป 14. ""หมอธีระวัฒน์"" ยืนยัน ""ฉีดวัคซีน"" ให้เด็กได้ทุกช่วงอายุ แต่ต้อง ""ชนิดเชื้อตาย"" 15. จีนส่งพลังงานแบบไร้สายระดับกิโลวัตต์ไกล 20 เมตร ได้สำเร็จ 16. รวมศัพท์วัยรุ่น 2021 EP.1 เคยใช้คำไหนกันบ้าง 17. EIC เชิญชวนทุกท่านร่วมทำแบบสำรวจ กิน อยู่ อย่างไร? ในช่วง COVID 18. Xiaomi EV เตรียมผลิตรถยนต์ไฟฟ้าของตัวเอง

Head Line Mission Daily Report Sep 09, 2021 1. อัปเดตตัวเลขผู้ที่ได้รับการฉีดวัคซีน Covid-19 ในประเทศไทย 2. ราคาดัชนีตลาดหลักทรัพย์ / ราคาหุ้นต่างประเทศ / ราคาน้ำมันดิบ / ราคาทองคำ / ราคา Cryptocurrency 3. ศบค. แจง ทำไมจึงไม่นำผลตรวจ ATK มารวม 4. เปิดตัวรถฉีดวัคซีนเคลื่อนที่ใน กทม. 5. ไทม์ไลน์เลือกตั้ง กทม.ในเดือนพฤศจิกายน 6. Altos Labs กำลังพัฒนาเทคโนโลยียืดอายุ 7. ช่วงนี้มีหนังอะไรน่าดูบ้าง? 8. ฟิลิปปินส์ออกคำสั่งล็อกดาวน์ต่อ ก่อนถึงกำหนดเพียงไม่กี่ชั่วโมง 9. FAA สั่งระงับเที่ยวบินทัวร์อวกาศของบริษัทเวอร์จิน 10. In Time หนังน่าดูสะท้อนสังคม 11. กลุ่มตาลิบันประกาศจัดตั้งรัฐบาลชั่วคราวปกครองอัฟกานิสถาน 12. #ORISxMTTM ORIS ขอมอบ Exclusive Privilege ให้กับ MTTM Fanpage 13. สาธารณสุขชิลี อนุมัติใช้งานวัคซีนซิโนแวคกับเด็กอายุตั้งแต่ 6 ปีขึ้นไป 14. "หมอธีระวัฒน์" ยืนยัน "ฉีดวัคซีน" ให้เด็กได้ทุกช่วงอายุ แต่ต้อง "ชนิดเชื้อตาย" 15. จีนส่งพลังงานแบบไร้สายระดับกิโลวัตต์ไกล 20 เมตร ได้สำเร็จ 16. รวมศัพท์วัยรุ่น 2021 EP.1 เคยใช้คำไหนกันบ้าง 17. EIC เชิญชวนทุกท่านร่วมทำแบบสำรวจ กิน อยู่ อย่างไร? ในช่วง COVID 18. Xiaomi EV เตรียมผลิตรถยนต์ไฟฟ้าของตัวเอง

Terry Sawchuk, Founder & Chairman of Sawchuk Wealth. Meet Altos Labs, Silicon Valley's latest wild bet on living forever

As Jeff Bezos is backing an anti-aging company, Scott DeHuff talks about the hazards of extending our lifespans.

A new and somewhat shadowy Silicon Valley company dedicated to anti-aging research is getting major funding from the uber-wealthy.Altos Labs, a biological reprogramming tech company, is allegedly attracting big-name investors such as Amazon CEO Jeff Bezos and Russian-Israeli billionaire Yuri Milner...with the goal, to live forever...Should Billionaires live forever?http://www.troubledminds.org Support The Show! https://rokfin.com/creator/troubledminds https://teespring.com/stores/troubled-minds-store #aliens #conspiracy #paranormalRadio Schedule Mon-Tues-Wed-Thurs 7-9pst - https://fringe.fm/iTunes - https://apple.co/2zZ4hx6Spotify - https://spoti.fi/2UgyzqMStitcher - https://bit.ly/2UfAiMXTuneIn - https://bit.ly/2FZOErSTwitter - https://bit.ly/2CYB71Uhttps://youtu.be/ZiBnr_glUIwhttps://www.amazon.com/Stories-Fractured-Mind-Robert-Collection-ebook/dp/B07D1RVX7Yhttps://www.instagram.com/tamlbam/https://salsidoparanormal.podbean.com/----------------------------------------------------------------------------https://futurism.com/the-byte/altos-labs-wealthy-investorshttps://www.technologyreview.com/2021/09/04/1034364/altos-labs-silicon-valleys-jeff-bezos-milner-bet-living-forever/https://futurism.com/the-byte/11-year-old-physics-degree-immortalityhttps://www.thedailybeast.com/the-immortality-financiers-the-billionaires-who-want-to-live-foreverhttps://newsrescue.com/live-forever-lab-amazon-jeff-bezos-other-billionaires-give-unlimited-funding-to-new-age-reversal-lab-start-up/https://fortune.com/2013/04/04/5-billionaires-who-want-to-live-forever/https://archive.vn/feCumhttps://www.dailystar.co.uk/news/weird-news/new-blood-computer-brains-frozen-22695138https://archive.vn/dap6Phttps://www.newsweek.com/2015/03/13/silicon-valley-trying-make-humans-immortal-and-finding-some-success-311402.htmlhttps://www.theguardian.com/global/2019/jun/23/how-to-live-forever-meet-the-extreme-life-extensionists-immortal-sciencehttps://www.thedailystar.net/opinion/open-dialogue/news/economists-campaign-against-age-obsessed-billionaires-1778728https://metro.co.uk/2020/03/05/futurologist-claims-super-rich-will-live-forever-implanting-brains-robots-12352856/https://www.thejoint.com/arizona/phoenix/paradise-village-48004/blood-facials-blood-baths-and-looking-younghttps://romanticmetal.com/history/elizabeth-bathory-anna-darvulia/https://en.wikipedia.org/wiki/Elizabeth_B%C3%A1thory

ว่ากันว่าคนหนุ่มสาวฝันถึงความร่ำรวย และคนที่ร่ำรวยนั้นฝันถึงการเป็นหนุ่ม และการมีอายุที่ยืนยาว ซึ่งการรักษาโรคชราภาพ หรือการทำให้มนุษย์มีอายุที่ยืนยาวนั้น อาจเป็นธุรกิจที่มีมูลค่านับพันล้านเหรียญสหรัฐฯ Jeff Bezos มีความสนใจค่อนข้างยาวนานในการวิจัยเรื่องอายุยืน และก่อนหน้านี้เขาลงทุนในบริษัทต่อต้านวัยที่ชื่อว่า Unity Biotechnology ซึ่งการเดิมพันครั้งล่าสุดใน Altos Labs กำลังดำเนินตามเทคโนโลยีใหม่ทางชีววิทยา ซึ่งเป็นวิธีในการชุบตัวเซลล์ในห้องปฏิบัติการที่นักวิทยาศาสตร์บางคนคิดว่าสามารถขยายออกไปเพื่อฟื้นฟูร่างกายของสัตว์ทั้งหมดได้ ซึ่งท้ายที่สุดแล้วจะสามารถยืดอายุขัยของมนุษย์ เลือกฟังกันได้เลยนะครับ อย่าลืมกด Follow ติดตาม PodCast ช่อง Geek Forever's Podcast ของผมกันด้วยนะครับ ========================= ร่วมสนับสนุน ด.ดล Blog และ Geek Forever Podcast เพื่อให้เรามีกำลังในการผลิต Content ดี ๆ ให้กับท่าน https://www.tharadhol.com/become-a-supporter/ ——————————————– ติดตาม ด.ดล Blog ผ่าน Line OA เพียงคลิก : https://lin.ee/aMEkyNA ========================= ช่องทางติดตาม ด.ดล Blog เพิ่มเติมได้ที่ Fanpage : www.facebook.com/tharadhol.blog Blockdit : www.blockdit.com/tharadhol.blog Twitter : www.twitter.com/tharadhol Instragram : instragram.com/tharadhol TikTok : tiktok.com/@geek.forever Youtube : www.youtube.com/c/mrtharadhol Linkedin : www.linkedin.com/in/tharadhol Website : www.tharadhol.com