Podcasts about Venki Ramakrishnan

Altern ist nicht angenehm. Aber keiner von uns kommt um diesen Prozess herum, der älter wird. Die Menschen streben mit viel Engagement und oft Geld an, diesem Prozess davon zu laufen. Geschafft hat es bislang noch keiner. Interessant, was ein Nobelpreisträger (Venki Ramakrishnan) dazu zu sagen hat. Einmal ganz nüchtern ...

First up on the podcast, Online News Editor Michael Greshko joins host Sarah Crespi to talk about stories set high above our heads. They discuss capturing fungal spores high in the stratosphere, the debate over signs of life on the exoplanet K2-18b, and a Chinese contender for world's oldest star catalog.   Next on the show, a look into long-standing questions on why and how our bodies respond to tickling. Producer Meagan Cantwell talks to Konstantina Kilteni, an assistant professor at the Donders Institute for Brain, Cognition and Behaviour and the Department of Neuroscience at the Karolinska Institute. They discuss how standardizing approaches to testing tickling in the lab could get us closer to answers.   Finally in this episode, the first in our book series on the science of death, with books host Angela Saini. Saini interviews Nobel Prize–winning biologist Venki Ramakrishnan about developments in longevity research and his book Why We Die: The New Science of Aging and the Quest for Immortality.   This week's episode was produced with help from Podigy.   About the Science Podcast Authors: Sarah Crespi, Angela Saini, Michael Greshko, Meagan Cantwell Learn more about your ad choices. Visit megaphone.fm/adchoices

First up on the podcast, Online News Editor Michael Greshko joins host Sarah Crespi to talk about stories set high above our heads. They discuss capturing fungal spores high in the stratosphere, the debate over signs of life on the exoplanet K2-18b, and a Chinese contender for world's oldest star catalog.   Next on the show, a look into long-standing questions on why and how our bodies respond to tickling. Producer Meagan Cantwell talks to Konstantina Kilteni, an assistant professor at the Donders Institute for Brain, Cognition and Behaviour and the Department of Neuroscience at the Karolinska Institute. They discuss how standardizing approaches to testing tickling in the lab could get us closer to answers.   Finally in this episode, the first in our book series on the science of death, with books host Angela Saini. Saini interviews Nobel Prize–winning biologist Venki Ramakrishnan about developments in longevity research and his book Why We Die: The New Science of Aging and the Quest for Immortality.   This week's episode was produced with help from Podigy.   About the Science Podcast Authors: Sarah Crespi, Angela Saini, Michael Greshko, Meagan Cantwell Learn more about your ad choices. Visit megaphone.fm/adchoices

 Scientists are using the secrets of biology to unlock living well past current human life spans. Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A member of the National Academy of Sciences, Venki runs a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. He joins host Krys Boyd to discuss the quest to live forever, if that's even ethical, and what it looks like to alter our physiology. His book is “Why We Die: The New Science of Aging and the Quest for Immortality.”  Learn about your ad choices: dovetail.prx.org/ad-choices

Transcript with time code:  https://cuttingedgehealth.com/wp-content/uploads/2025/02/Transcript-47-Dr-Venki-Ramakrishnan.pdf   In this episode, Jane interviews Nobel Prize winner Venki Ramakrishnan, a molecular biologist who offers a balanced perspective on the anti-aging field.   Ramakrishnan discusses various promising areas of anti-aging research, including caloric restriction drugs like rapamycin, senolytics to target senescent cells, and stem cell therapies. He emphasizes the importance of clinical trials and cautions against rushing into unproven treatments. The conversation covers lifestyle factors that can promote healthy aging, such as regular exercise, proper nutrition, and maintaining social connections.   Ramakrishnan shares personal insights, including his father's experience of maintaining an active lifestyle until age 99. He also touches on his own career journey and winning the Nobel Prize. Throughout the interview, he stresses the need for a scientific approach to anti-aging research while acknowledging the urgency felt by many to combat aging. The podcast provides a thoughtful exploration of the current state of anti-aging science, balancing excitement for potential breakthroughs with the need for rigorous scientific validation.   *****   Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A National Academy of Sciences member, Venki runs his research group at the MRC Laboratory of Molecular Biology in Cambridge, England. From 2015 to 2020, he served as president of the Royal Society, one of the world's oldest scientific organizations. He is the author of the frank scientific memoir Gene Machine: The Race to Decipher the Secrets of the Ribosome and Amazon bestselling book Why We Die: The New Science of Aging and the Quest for Immortality.   *****   Cutting Edge Health podcast website: https://cuttingedgehealth.com/   Cutting Edge Health Social and YouTube:   YouTube channel: youtube.com/@cuttingedgehealthpodcast   Instagram - https://instagram.com/cuttingedgehealthpodcast   Facebook - https://www.facebook.com/Cutting-Edge-Health-Podcast-with-Jane-Rogers-101036902255756   Please note that the information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Cutting Edge Health podcast, its employees, guests and affiliates assume no liability for the application of the information discussed.   Special thanks to Alan and Maria on the Cutting Edge Health team!    

Der menschliche Körper ist ein Wunderwerk, wie wir spätestens seit der Entdeckung des Doppelstrangs der DNA wissen. Die Gene bestimmen unser Leben und eben auch unser Altern. Das Altern aufzuhalten, das streben derzeit zahlreiche Startups an. Doch die Wahrscheinlichkeit, dass dies gelingt, ist sehr gering, wie Venki Ramakrishnan, 2009 Chemie-Nobelpreisträger in seinem Buch „Warum wir altern“ detailliert erklärt. Rezension von Johannes Kaiser

Der menschliche Körper ist ein Wunderwerk, wie wir spätestens seit der Entdeckung des Doppelstrangs der DNA wissen. Die Gene bestimmen unser Leben und eben auch unser Altern. Das Altern aufzuhalten, das streben derzeit zahlreiche Startups an. Doch die Wahrscheinlichkeit, dass dies gelingt, ist sehr gering, wie Venki Ramakrishnan, 2009 Chemie-Nobelpreisträger in seinem Buch „Warum wir altern“ detailliert erklärt. Rezension von Johannes Kaiser

"A shameless recycling of existing content to drive additional audience engagement on the cheap… or the single best, most valuable, and most insight-dense episode we put out in the entire year, depending on how you want to look at it." — Rob WiblinIt's that magical time of year once again — highlightapalooza! Stick around for one top bit from each episode, including:How to use the microphone on someone's mobile phone to figure out what password they're typing into their laptopWhy mercilessly driving the New World screwworm to extinction could be the most compassionate thing humanity has ever doneWhy evolutionary psychology doesn't support a cynical view of human nature but actually explains why so many of us are intensely sensitive to the harms we cause to othersHow superforecasters and domain experts seem to disagree so much about AI risk, but when you zoom in it's mostly a disagreement about timingWhy the sceptics are wrong and you will want to use robot nannies to take care of your kids — and also why despite having big worries about the development of AGI, Carl Shulman is strongly against efforts to pause AI research todayHow much of the gender pay gap is due to direct pay discrimination vs other factorsHow cleaner wrasse fish blow the mirror test out of the waterWhy effective altruism may be too big a tent to work wellHow we could best motivate pharma companies to test existing drugs to see if they help cure other diseases — something they currently have no reason to bother with…as well as 27 other top observations and arguments from the past year of the show.Check out the full transcript and episode links on the 80,000 Hours website.Remember that all of these clips come from the 20-minute highlight reels we make for every episode, which are released on our sister feed, 80k After Hours. So if you're struggling to keep up with our regularly scheduled entertainment, you can still get the best parts of our conversations there.It has been a hell of a year, and we can only imagine next year is going to be even weirder — but Luisa and Rob will be here to keep you company as Earth hurtles through the galaxy to a fate as yet unknown.Enjoy, and look forward to speaking with you in 2025!Chapters:Rob's intro (00:00:00)Randy Nesse on the origins of morality and the problem of simplistic selfish-gene thinking (00:02:11)Hugo Mercier on the evolutionary argument against humans being gullible (00:07:17)Meghan Barrett on the likelihood of insect sentience (00:11:26)Sébastien Moro on the mirror test triumph of cleaner wrasses (00:14:47)Sella Nevo on side-channel attacks (00:19:32)Zvi Mowshowitz on AI sleeper agents (00:22:59)Zach Weinersmith on why space settlement (probably) won't make us rich (00:29:11)Rachel Glennerster on pull mechanisms to incentivise repurposing of generic drugs (00:35:23)Emily Oster on the impact of kids on women's careers (00:40:29)Carl Shulman on robot nannies (00:45:19)Nathan Labenz on kids and artificial friends (00:50:12)Nathan Calvin on why it's not too early for AI policies (00:54:13)Rose Chan Loui on how control of OpenAI is independently incredibly valuable and requires compensation (00:58:08)Nick Joseph on why he's a big fan of the responsible scaling policy approach (01:03:11)Sihao Huang on how the US and UK might coordinate with China (01:06:09)Nathan Labenz on better transparency about predicted capabilities (01:10:18)Ezra Karger on what explains forecasters' disagreements about AI risks (01:15:22)Carl Shulman on why he doesn't support enforced pauses on AI research (01:18:58)Matt Clancy on the omnipresent frictions that might prevent explosive economic growth (01:25:24)Vitalik Buterin on defensive acceleration (01:29:43)Annie Jacobsen on the war games that suggest escalation is inevitable (01:34:59)Nate Silver on whether effective altruism is too big to succeed (01:38:42)Kevin Esvelt on why killing every screwworm would be the best thing humanity ever did (01:42:27)Lewis Bollard on how factory farming is philosophically indefensible (01:46:28)Bob Fischer on how to think about moral weights if you're not a hedonist (01:49:27)Elizabeth Cox on the empirical evidence of the impact of storytelling (01:57:43)Anil Seth on how our brain interprets reality (02:01:03)Eric Schwitzgebel on whether consciousness can be nested (02:04:53)Jonathan Birch on our overconfidence around disorders of consciousness (02:10:23)Peter Godfrey-Smith on uploads of ourselves (02:14:34)Laura Deming on surprising things that make mice live longer (02:21:17)Venki Ramakrishnan on freezing cells, organs, and bodies (02:24:46)Ken Goldberg on why low fault tolerance makes some skills extra hard to automate in robots (02:29:12)Sarah Eustis-Guthrie on the ups and downs of founding an organisation (02:34:04)Dean Spears on the cost effectiveness of kangaroo mother care (02:38:26)Cameron Meyer Shorb on vaccines for wild animals (02:42:53)Spencer Greenberg on personal principles (02:46:08)Producing and editing: Keiran HarrisAudio engineering: Ben Cordell, Milo McGuire, Simon Monsour, and Dominic ArmstrongVideo editing: Simon MonsourTranscriptions: Katy Moore

Wir feiern 35 Jahre Mauerfall, doch noch immer gibt es viel zu viele unerzählte Geschichten aus der deutsch-deutschen Vergangenheit. So wie die der Sexarbeiterin Uta aus Zwickau, die im Auftrag der Stasi auf Männer angesetzt wurde. Clemens Böckmann hat ihre Geschichte im Roman "Was du kriegen kannst" aufgeschrieben. Außerdem lassen wir uns von Chemie-Nobelpreisträger Venki Ramakrishnan ein Buch empfehlen, um die aktuelle Weltlage zu verdauen und suchen in der Buchbehandlung ein unterhaltsames Buch zum gegenseitigen Vorlesen.

“The invention of ways to increase human longevity is the world's second-oldest profession, or maybe even the first,” the biologist Leonard Hayflick once said. However, despite a lot of improvements over time, we still have to die. Is that actually necessary or is eternal life in reach? What are the reasons for ageing and dying and how can we prolong life? Are we going to freeze and resurrect or to be uploaded to a cloud as the Silicon Valley tech prophets believe? If not, how should society deal with death? And last but not least: if cells are like cities, what can our cities learn from cells? Enjoy the latest episode of Alter, was geht? and feel free to leave a review or comment! If you are interested in the book (strong recommendation!), you'll find it in your local book store: Venki Ramakrishnan (2024): Why we die. #longevity #oldage #antiaging #transhumanism (05:13) Understanding Aging: The Process and Its Implications (08:04) Analogies of Life: Cities and Cells (10:59) The Paradox of Aging and Reproduction (13:49) The Quest for Longevity: Limits and Possibilities (16:53) Fun Facts and Insights on Aging (19:35) Cryonics and Transhumanism: Myths and Realities (22:36) Societal Views on Death and Aging (23:49) Prolonging Healthspan vs Lifespan (24:35) Practical Advice for Healthy Aging

“The invention of ways to increase human longevity is the world's second-oldest profession, or maybe even the first,” the biologist Leonard Hayflick once said. However, despite a lot of improvements over time, we still have to die. Is that actually necessary or is eternal life in reach? What are the reasons for ageing and dying and how can we prolong life? Are we going to freeze and resurrect or to be uploaded to a cloud as the Silicon Valley tech prophets believe? If not, how should society deal with death? And last but not least: if cells are like cities, what can our cities learn from cells? Enjoy the latest episode of Alter, was geht? and feel free to leave a review or comment! If you are interested in the book (strong recommendation!), you'll find it in your local book store: Venki Ramakrishnan (2024): Why we die. #longevity #oldage #antiaging #transhumanism (05:13) Understanding Aging: The Process and Its Implications (08:04) Analogies of Life: Cities and Cells (10:59) The Paradox of Aging and Reproduction (13:49) The Quest for Longevity: Limits and Possibilities (16:53) Fun Facts and Insights on Aging (19:35) Cryonics and Transhumanism: Myths and Realities (22:36) Societal Views on Death and Aging (23:49) Prolonging Healthspan vs Lifespan (24:35) Practical Advice for Healthy Aging

"Die Suche nach Möglichkeiten, das Leben zu verlängern, ist der zweitälteste Beruf der Welt - vielleicht sogar der älteste", sagte der Biologe Leonard Hayflick. Es hat über die Zeit zwar schon enorme Fortschritte gegeben, aber bisher müssen wir weiterhin irgendwann sterben. Warum eigentlich? Was passiert im Körper, wenn wir altern? Und muss das so bleiben, oder werden wir bald in der digitalen Wolke, dem Äther oder dem Tiefkühler weiterleben können? Darüber spreche ich mit dem Nobelpreisträger Venki Ramakrishnan, der für sein neues Buch "Warum wir sterben" die neuesten Erkenntnisse der Wissenschaft für genau diese Frage aufbereitet hat. Es geht auch um die frappierenden Ähnlichkeiten von Städten und Zellen (Demokratien!) ebenso wie um die Gehirne von Verwandten, die man besser nicht essen sollte - auch wenn die Wissenschaft schonmal davon profitiert hat. Viel Spaß beim Zuhören und auf ein langes Leben! Das besagte Buch ist im Klett-Cotta-Verlag erschienen: Venki Ramakrishnan (2024): Warum wir sterben. Die neue Wissenschaft des Alterns und die Suche nach dem ewigen Leben. (03:30) Der Altersprozess (05:52) Städte und Zellen (08:47) Warum alle Neugeborenen jung sind (11:38) Lebensdauer: Möglichkeiten und Beschränkugnen (14:42) Fun Fact (17:23) Kryokonservierung und Transhumanismus (20:24) Gesellschaftlicher Umgang mit Alter und Tod (21:38) Längeres Leben oder längere Gesundheit? (26:02) Schluss #Alter #Longevity #Cryotech

"Die Suche nach Möglichkeiten, das Leben zu verlängern, ist der zweitälteste Beruf der Welt - vielleicht sogar der älteste", sagte der Biologe Leonard Hayflick. Es hat über die Zeit zwar schon enorme Fortschritte gegeben, aber bisher müssen wir weiterhin irgendwann sterben. Warum eigentlich? Was passiert im Körper, wenn wir altern? Und muss das so bleiben, oder werden wir bald in der digitalen Wolke, dem Äther oder dem Tiefkühler weiterleben können? Darüber spreche ich mit dem Nobelpreisträger Venki Ramakrishnan, der für sein neues Buch "Warum wir sterben" die neuesten Erkenntnisse der Wissenschaft für genau diese Frage aufbereitet hat. Es geht auch um die frappierenden Ähnlichkeiten von Städten und Zellen (Demokratien!) ebenso wie um die Gehirne von Verwandten, die man besser nicht essen sollte - auch wenn die Wissenschaft schonmal davon profitiert hat. Viel Spaß beim Zuhören und auf ein langes Leben! Das besagte Buch ist im Klett-Cotta-Verlag erschienen: Venki Ramakrishnan (2024): Warum wir sterben. Die neue Wissenschaft des Alterns und die Suche nach dem ewigen Leben. (03:30) Der Altersprozess (05:52) Städte und Zellen (08:47) Warum alle Neugeborenen jung sind (11:38) Lebensdauer: Möglichkeiten und Beschränkugnen (14:42) Fun Fact (17:23) Kryokonservierung und Transhumanismus (20:24) Gesellschaftlicher Umgang mit Alter und Tod (21:38) Längeres Leben oder längere Gesundheit? (26:02) Schluss #Alter #Longevity #Cryotech

Vanaf zo'n beetje de leeftijd van dertig jaar lijkt het onvermijdelijk: lichamelijke aftakeling. Valt dit verouderingsproces af te remmen of zelfs te stoppen? Deze wetenschappers proberen de sleutel tot de eeuwige jeugd te vinden. Als ze slagen, zal dat hele grote gevolgen hebben. Luister naar wetenschapsredacteur Maarten Keulemans. Lees hier het interview met Venki Ramakrishnan. Presentatie: Tonie MuddeMontage: Merle van der HorstEindredactie: Corinne van Duin, Julia van Alem en Lotte GrimbergenSee omnystudio.com/listener for privacy information.

Alle reden über Longevity - was wir alles tun und lassen müssen, um möglich lange und gesund zu leben. Die Literaturagenten gehen das tiefgründiger an. Wir wollen verstehen, "Warum wir sterben" und befragen dazu den Chemie-Nobelpreisträger Venki Ramakrishnan. In der Buchhandlung suchen wir für Hörerin Susanne einen Roman, mit dem es gelingt, auch im Alter lebendig frisch und neugierig zu bleiben. Außerdem geht es hoch hinaus mit gleich zwei Büchern über die Flugpionierin Amelia Earhart.

This is a selection of highlights from episode #202 of The 80,000 Hours Podcast. These aren't necessarily the most important, or even most entertaining parts of the interview — and if you enjoy this, we strongly recommend checking out the full episode:Venki Ramakrishnan on the cutting edge of anti-ageing scienceAnd if you're finding these highlights episodes valuable, please let us know by emailing podcast@80000hours.org.Highlights:Luisa's intro (00:00:00)Is death an inevitable consequence of evolution? (00:00:15)How much additional healthspan will the next 20 to 30 years of ageing research buy us? (00:03:10)The social impacts of radical life extension (00:05:46)Could increased longevity increase inequality? (00:10:06)Does injecting an old body with young blood slow ageing? (00:14:23)Freezing cells, organs, and bodies (00:18:35)Highlights put together by Simon Monsour, Milo McGuire, and Dominic Armstrong

Why We Die is a book about ageing and death, written by Nobel Prize-winning biologist and former president of the Royal Society, Venki Ramakrishnan.Venki is on the shortlist for the Royal Society Trivedi Science Book Prize. In the lead up to the winner's announcement, New Scientist books editor Alison Flood meets all six of the shortlisted authors.In this conversation, Venki explores humankind's unique ability to understand and contemplate our own mortality, why some animals live such short lives and others for hundreds of years, if ageing is simply an inevitable and evolutionary practical part of life and whether emerging technologies will make it possible for us to life forever - if that's really what we want.The winner of the Royal Society Trivedi Science Book Prize will be announced on the 24th October. You can view all of the shortlisted entries here:https://royalsociety.org/medals-and-prizes/science-book-prize/ To read about subjects like this and much more, visit https://www.newscientist.com/ Hosted on Acast. See acast.com/privacy for more information.

Aging and death happen to the best of us, but there are increasing efforts to do something about it. That effort requires that we have some reasonable understanding of why aging happens, and what processes are involved. You will be unsurprised to learn that it's complicated. Venki Ramakrishnan, who won the Nobel Prize for his work on the ribosome, investigates what we know about aging in his book Why We Die: The New Science of Aging and the Quest for Immortality. We talk about aging and death, and manage to get some thoughts in about ribosomes. Venki and many other great communicators will be speaking at New Scientist Live, which takes place at ExCeL London between 12 - 14 October 2024, and is also streamed live as well as on-demand.Support Mindscape on Patreon.Blog post with transcript: https://www.preposterousuniverse.com/podcast/2024/09/30/291-venki-ramakrishnan-on-the-biology-of-death-and-aging/Venkatraman (Venki) Ramakrishnan received his Ph.D. in physics from Ohio University. He is currently Group Leader at the MRC Laboratory of Molecular Biology, Cambridge, England, and is a Fellow of Trinity College. He previously served as President of the Royal Society of London. He shared the Nobel Prize in Chemistry for his work uncovering the structure of the ribosome.Lab web pageNobel citationGoogle scholar publicationsWikipediaAmazon author pageSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

"For every far-out idea that turns out to be true, there were probably hundreds that were simply crackpot ideas. In general, [science] advances building on the knowledge we have, and seeing what the next questions are, and then getting to the next stage and the next stage and so on. And occasionally there'll be revolutionary ideas which will really completely change your view of science. And it is possible that some revolutionary breakthrough in our understanding will come about and we might crack this problem, but there's no evidence for that. It doesn't mean that there isn't a lot of promising work going on. There are many legitimate areas which could lead to real improvements in health in old age. So I'm fairly balanced: I think there are promising areas, but there's a lot of work to be done to see which area is going to be promising, and what the risks are, and how to make them work." —Venki RamakrishnanIn today's episode, host Luisa Rodriguez speaks to Venki Ramakrishnan — molecular biologist and Nobel Prize winner — about his new book, Why We Die: The New Science of Aging and the Quest for Immortality.Links to learn more, highlights, and full transcript.They cover:What we can learn about extending human lifespan — if anything — from “immortal” aquatic animal species, cloned sheep, and the oldest people to have ever lived.Which areas of anti-ageing research seem most promising to Venki — including caloric restriction, removing senescent cells, cellular reprogramming, and Yamanaka factors — and which Venki thinks are overhyped.Why eliminating major age-related diseases might only extend average lifespan by 15 years.The social impacts of extending healthspan or lifespan in an ageing population — including the potential danger of massively increasing inequality if some people can access life-extension interventions while others can't.And plenty more.Chapters:Cold open (00:00:00)Luisa's intro (00:01:04)The interview begins (00:02:21)Reasons to explore why we age and die (00:02:35)Evolutionary pressures and animals that don't biologically age (00:06:55)Why does ageing cause us to die? (00:12:24)Is there a hard limit to the human lifespan? (00:17:11)Evolutionary tradeoffs between fitness and longevity (00:21:01)How ageing resets with every generation, and what we can learn from clones (00:23:48)Younger blood (00:31:20)Freezing cells, organs, and bodies (00:36:47)Are the goals of anti-ageing research even realistic? (00:43:44)Dementia (00:49:52)Senescence (01:01:58)Caloric restriction and metabolic pathways (01:11:45)Yamanaka factors (01:34:07)Cancer (01:47:44)Mitochondrial dysfunction (01:58:40)Population effects of extended lifespan (02:06:12)Could increased longevity increase inequality? (02:11:48)What's surprised Venki about this research (02:16:06)Luisa's outro (02:19:26)Producer: Keiran HarrisAudio engineering: Ben Cordell, Milo McGuire, Simon Monsour, and Dominic ArmstrongContent editing: Luisa Rodriguez, Katy Moore, and Keiran HarrisTranscriptions: Katy Moore

For millennia, humanity has obsessed about halting ageing and, ultimately, preventing death. Yet while advances in medicine and public-health have seen human life-expectancy more than double, our maximum lifespan stubbornly remains around 120 years.On the latest episode of Nature hits the books, Nobel laureate Venki Ramakrishnan joins us to discuss what scientists have learnt about the molecular processes underlying ageing, whether they can be prevented, and why the quest for longevity also needs to consider the health-related issues associated with old age.Why We Die: The New Science of Ageing and the Quest for Immortality Venki Ramakrishnan Hodder (2024)Music supplied by Airae/Epidemic Sound/Getty images. Hosted on Acast. See acast.com/privacy for more information.

Humans have always been obsessed with getting old, or rather staying young, and now science is beginning to catch up. Longevity has become a hot topic from university laboratories to Silicon Valley startups. In the second of a special Science Weekly three-part mini-series on ageing, Ian Sample talks to Venki Ramakrishnan, winner of the Nobel prize in chemistry and author of the book Why We Die. Venki outlines the most promising scientific advances in the field of longevity and discusses the more unusual ways that the wealthy are trying to extend their lives, from blood transfusions to cryonics. Help support our independent journalism at theguardian.com/sciencepod

What inspired Venki Ramakrishnan to transition from physics to molecular biology? How has Venki Ramakrishnan's groundbreaking research on ribosomes impacted the study? How does he envision the future of molecular biology? Venkatraman "Venki" Ramakrishnan is a leading molecular biologist whose groundbreaking work on ribosome structure has significantly advanced our understanding of protein synthesis. His discoveries earned him the 2009 Nobel Prize in Chemistry, making him one of the few Indians to receive this honour. Beyond his research, Venki has received numerous awards and held prestigious positions in the scientific community. Tune in for an insightful in-depth conversation by one of the most influential minds in molecular biology! Resource List - Gene Machine, Book by Venki Ramakrishnan - https://amzn.in/d/0eA1LySH Why We Die, Book by Venki Ramakrishnan - https://amzn.in/d/06JRkfCv Venki Ramamkrishnan's Profile on The Royal Society - https://royalsociety.org/people/venki-ramakrishnan-12139/#:~:text=He%20determined%20the%20atomic%20structure,in%20complexes%20with%20several%20antibiotics Venki Ramakrishnan's Profile on The LMC Website - https://www2.mrc-lmb.cam.ac.uk/group-leaders/n-to-s/venki-ramakrishnan/ Venki Ramakrishnan's Profile on The Academy of Achievement - https://achievement.org/achiever/venki-ramakrishnan-ph-d/ Venki Ramakrishnan on the Science of Aging - https://erictopol.substack.com/p/venki-ramakrishnan-the-new-science Compilation of Research Papers by Venki Ramakrishnan - https://scholar.google.co.in/citations?user=oTI5BjIAAAAJ&hl=en&oi=ao About SparX by Mukesh Bansal SparX is a podcast where we delve into cutting-edge scientific research, stories from impact-makers and tools for unlocking the secrets to human potential and growth. We believe that entrepreneurship, fitness and the science of productivity is at the forefront of the India Story; the country is at the cusp of greatness and at SparX, we wish to make these tools accessible for every generation of Indians to be able to make the most of the opportunities around us. In a new episode every Sunday, our host Mukesh Bansal (Founder Myntra and Cult.fit) will talk to guests from all walks of life and also break down everything he's learnt about the science of impact over the course of his 20-year long career. This is the India Century, and we're enthusiastic to start this journey with you. Follow us on our Instagram: / sparxbymukeshbansal Also check out our website: https://www.sparxbymukeshbansal.com You can also listen to SparX on all audio platforms! Fasion | Outbreak | Courtesy EpidemicSound.com Built to Last: Book by Jim Collins: https://amzn.in/d/06UJQDXy The HP Way, Book by David Packard: https://amzn.in/d/09M92m6N

Send us a Text Message.Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. He runs a lab at the MRC Laboratory of Molecular Biology in Cambridge, England. In this episode, Venki emphasizes the importance of enjoying the scientific process itself, not just aiming for major discoveries. He describes his creativity as a result of mulling over a problem and of talking with people. Venki also highlights the need for scientists to make daily judgment calls about their approach and the future of the project. And he encourages openness and collaboration, viewing the ability to seek help as a strength rather than a weakness.This episode was supported by Research Theory (researchtheory.org). For more information about Night Science, visit https://www.biomedcentral.com/collections/night-science .

Join Us for a Deep Dive with Nobel Laureate Venki Ramakrishnan!

The super-rich are trialling innumerable whacky theories to radically extend their lives, from not eating after 11pm to taking hundreds of supplements a day and even blood transfusions from their children. But what does the science tell us? Could some of these ideas actually prove effective? And why are we still so obsessed with the quest that is as old as mankind itself: immortality?This podcast was brought to you thanks to the support of readers of The Times and The Sunday Times. Subscribe today: http://thetimes.com/thestoryGuest: Dr. Venki Ramakrishnan, scientist at the MRC Laboratory of Molecular Biology at Cambridge and author of Why We Die: The New Science of Ageing and the Quest for Immortality.Host: Luke Jones.Clips: WIRED UK, Valuetainment Clips, Diary of a CEO, TalkTV. Find out more about our bonus series for Times subscribers: 'Inside the newsroom'Get in touch: thestory@thetimes.co.uk Hosted on Acast. See acast.com/privacy for more information.

ไลฟ์ #77: สรุปหนังสือ Why We Die: The Science of Aging and The Quest For Immortality ผู้เขียน Prof. Venki Ramakrishnan ได้รับรางวัลโนเบลในสาขาเคมี ในปี พ.ศ.2552 ร่วมกับ Thomas A Steitz และ Ada E. Yonath สำหรับการศึกษาโครงสร้างและหน้าที่ของไรโบโซม ซึ่งทำหน้าที่ในการอ่านข้อมูลทางพันธุกรรมเพื่อสร้างโปรตีนที่ถูกระบุ ไรโบโซมมีความซับซ้อนเชิงระดับโมเลกุลเพราะมีราวห้าแสนอะตอมที่ประกอบเป็นไรโบโซม ไลฟ์#76 ซึ่งตอนที่ 1 ของหนังสือเล่มนี้ เราสำรวจว่าวิวัฒนาการช่วยให้เข้าใจว่าทำไมความตายจึงเกิดขึ้น และวิวัฒนาการก็มีเป้าหมายที่จะ optimize fitness มากที่สุด จึงนำมาซึ่งความหลากหลายของอายุขัยในสิ่งมีชีวิตต่างสปีชีส์ นอกจากนั้นเรายังสำรวจด้วยว่าอายุขัยของสิ่งมีชีวิตโดยเฉพาะมนุษย์มันมีข้อจำกัดหรือไม่ แต่ก็ยังไม่ได้คำตอบว่าความแก่ชราเกิดขึ้นและนำไปสู่การตายได้อย่างไร ในตอนที่ 2 ของไลฟ์#77 เราจะมาสำรวจกันต่อใน บทที่ 3: Destroying the master control บทที่ 4: The problem with end บทที่ 5: Resetting the biological clock พบกันในไลฟ์#77 นะคะ ❤️ #หาคำตอบสุขภาพจากงานวิจัยไม่ใช่จากเรื่องเล่า#FatOutHealthspans

Venki Ramakrishnan is a Nobel Prize winning scientist, Former President of the Royal Society, a structural biologist at the University of Cambridge and author. Scientific and public interest into anti-aging has reached an all time high. With this has come a series of medical breakthroughs, as well as a detailed understanding of promising mechanisms that need to be targeted to slow down the aging process. However, there has also been a proliferation of misinformation, ineffective treatments and speculative claims, such as individuals suggesting that they may never die. To sort the fact from the fiction, we invited Venki on to share his thoughts on the current state of the anti-aging movement. 00:00 - Why enter the conversation? 03:15 - Is the desire to live forever a modern phenomena? 05:45 - Where does the state of the anti-aging field lay? 07:30 - Should we tackle specific diseases or aging? 12:20 - Should aging be classified as a disease? 14:10 - Is aging inevitable? 15:10 - What is the maximum age that we could live to? 17:45 - Would we live forever if we eradicated all disease? 19:30 - Metformin, NAD boosters, NMN, Rapamycin - effective or not? 27:20 - Are blood transfusions effective? 30:10 - What actually causes aging? 33:01 - What happens when we die? 34:30 - Hormesis, Exercise, Diet & Sleep 42:10 - Venki's opinion on the anti-aging community and death 45:10 - Philosophical ideas on death 47:10 - Connect with Venki 49:50 - What makes a life worth living Connect with Venki: Why We Die: https://www.amazon.co.uk/Why-We-Die-S... Profile: https://www2.mrc-lmb.cam.ac.uk/group-... Connect with us: youtube.com/freedompact Instagram.com/freedompact twitter.com/freedompactpod TikTok.com/personaldevelopment

In this podcast, Thomas Czech, Distinguished Professor at the University of Colorado, Boulder, with a lineage of remarkable contributions on RNA, ribozyme, and telomeres, discuss why RNA is so incredibly versatile.Video snippet from our conversation. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to the audio and external linksEric Topol (00:07):Well, hello, this is Eric Topol from Ground Truths, and it's really a delight for me to welcome Tom Cech who just wrote a book, the Catalyst, and who is a Nobel laureate for his work in RNA. And is at the University of Colorado Boulder as an extraordinary chemist and welcome Tom.Tom Cech (00:32):Eric, I'm really pleased to be here.The RNA GuyEric Topol (00:35):Well, I just thoroughly enjoyed your book, and I wanted to start out, if I could, with a quote, which gets us right off the story here, and let me just get to it here. You say, “the DNA guy would need to become an RNA guy. Though I didn't realize it at the time, jumping ship would turn out to be the most momentous decision in my life.” Can you elaborate a bit on that?Tom Cech (01:09):As a graduate student at Berkeley, I was studying DNA and chromosomes. I thought that DNA was king and really somewhat belittled the people in the lab next door who were working on RNA, I thought it was real sort of second fiddle material. Of course, when RNA is acting just as a message, which is an important function, a critical function in all life on earth, but still, it's a function that's subservient to DNA. It's just copying the message that's already written in the playbook of DNA. But little did I know that the wonders of RNA were going to excite me and really the whole world in unimaginable ways.Eric Topol (02:00):Well, they sure have, and you've lit up the world well before you had your Nobel Prize in 1989 was Sid Altman with ribozyme. And I think one of the things that struck me, which are so compelling in the book as I think people might know, it's divided in two sections. The first is much more on the biology, and the second is much more on the applications and how it's changing the world. We'll get into it particularly in medicine, but the interesting differentiation from DNA, which is the one trick pony, as you said, all it does is store stuff. And then the incredible versatility of RNA as you discovered as a catalyst, that challenging dogma, that proteins are supposed to be the only enzymes. And here you found RNA was one, but also so much more with respect to genome editing and what we're going to get into here. So I thought what we might get into is the fact that you kind of went into the scum of the pond with this organism, which by the way, you make a great case for the importance of basic science towards the end of the book. But can you tell us about how you, and then of course, many others got into the Tetrahymena thermophila, which I don't know that much about that organism.Tom Cech (03:34):Yeah, it's related to Tetrahymena is related to paramecium, which is probably more commonly known because it's an even larger single celled animal. And therefore, in an inexpensive grade school microscope, kids can look through and see these ciliated protozoa swimming around on a glass slide. But I first learned about them when I was a postdoc at MIT and I would drive down to Joe Gall's lab at Yale University where Liz Blackburn was a postdoc at the time, and they were all studying Tetrahymena. It has the remarkable feature that it has 10,000 identical copies of a particular gene and for a higher organism, one that has its DNA in the nucleus and does its protein synthesis in the cytoplasm. Typically, each gene's present in two copies, one from mom, one from dad. And if you're a biochemist, which I am having lots of stuff is a real advantage. So 10,000 copies of a particular gene pumping out RNA copies all the time was a huge experimental advantage. And that's what I started working on when I started my own lab at Boulder.Eric Topol (04:59):Well, and that's where, I guess the title of the book, the Catalyst ultimately, that grew into your discovery, right?Tom Cech (05:08):Well, at one level, yes, but I also think that the catalyst in a more general conversational sense means just facilitating life in this case. So RNA does much more than just serve as a biocatalyst or a message, and we'll get into that with genome editing and with telomerase as well.The Big Bang and 11 Nobel Prizes on RNA since 2000Eric Topol (05:32):Yes, and I should note that as you did early in the book, that there's been an 11 Nobel prize awardees since 2000 for RNA work. And in fact, we just had Venki who I know you know very well as our last podcast. And prior to that, Kati Karikó, Jennifer Doudna who worked in your lab, and the long list of people working RNA in the younger crowd like David Liu and Fyodor Urnov and just so many others, we need to have an RNA series because it's just exploding. And that one makes me take you back for a moment to 2007. And when I was reading the book, it came back to me about the Economist cover. You may recall almost exactly 17 years ago. It was called the Biology's Big Bang – Unravelling the secrets of RNA. And in that, there was a notable quote from that article. Let me just get to that. And it says, “it is probably no exaggeration to say that biology is now undergoing its neutron moment.”(06:52):This is 17 years ago. “For more than half a century the fundamental story of living things has been a tale of the interplay between genes, in the form of DNA, and proteins, which is genes encode and which do the donkey work of keeping living organisms living. The past couple of years, 17 years ago, however, has seen the rise and rise of a third type of molecule, called RNA.” Okay, so that was 2007. It's pretty extraordinary. And now of course we're talking about the century of biology. So can you kind of put these last 17 years in perspective and where we're headed?Tom Cech (07:34):Well, Eric, of course, this didn't all happen in one moment. It wasn't just one big bang. And the scientific community has been really entranced with the wonders of RNA since the 1960s when everyone was trying to figure out how messenger RNA stored the genetic code. But the general public has been really kept in the dark about this, I think. And as scientists, were partially to blame for not reaching out and sharing what we have found with them in a way that's more understandable. The DNA, the general public's very comfortable with, it's the stuff of our heredity. We know about genetic diseases, about tracing our ancestry, about solving crimes with DNA evidence. We even say things like it's in my DNA to mean that it's really fundamental to us. But I think that RNA has been sort of kept in the closet, and now with the mRNA vaccines against Covid-19, at least everyone's heard of RNA. And I think that that sort of allowed me to put my foot in the door and say, hey, if you were curious about the mRNA vaccines, I have some more stories for you that you might be really interested in.RNA vs RNAEric Topol (09:02):Yeah, well, we'll get to that. Maybe we should get to that now because it is so striking the RNA versus RNA chapter in your book, and basically the story of how this RNA virus SARS-CoV-2 led to a pandemic and it was fought largely through the first at scale mRNA nanoparticle vaccine package. Now, that takes us back to some seminal work of being able to find, giving an mRNA to a person without inciting massive amount of inflammation and the substitution of pseudouridine or uridine in order to do that. Does that really get rid of all the inflammation? Because obviously, as you know, there's been some negativism about mRNA vaccines for that and also for the potential of not having as much immune cell long term activation. Maybe you could speak to that.Tom Cech (10:03):Sure. So the discovery by Kati Karikó and Drew Weissman of the pseudouridine substitution certainly went a long way towards damping down the immune response, the inflammatory response that one naturally gets with an RNA injection. And the reason for that is that our bodies are tuned to be on the lookout for foreign RNA because so many viruses don't even mess with DNA at all. They just have a genome made of RNA. And so, RNA replicating itself is a danger sign. It means that our immune system should be on the lookout for this. And so, in the case of the vaccination, it's really very useful to dampen this down. A lot of people thought that this might make the mRNA vaccines strange or foreign or sort of a drug rather than a natural substance. But in fact, modified nucleotides, nucleotides being the building blocks of RNA, so these modified building blocks such as pseudoU, are in fact found in natural RNAs more in some than in others. And there are about 200 modified versions of the RNA building blocks found in cells. So it's really not an unusual modification or something that's all that foreign, but it was very useful for the vaccines. Now your other question Eric had to do with the, what was your other question, Eric?Eric Topol (11:51):No, when you use mRNA, which is such an extraordinary way to get the spike protein in a controlled way, exposed without the virus to people, and it saved millions of lives throughout the pandemic. But the other question is compared to other vaccine constructs, there's a question of does it give us long term protective immunity, particularly with T cells, both CD8 cytotoxic, maybe also CD4, as I know immunology is not your main area of interest, but that's been a rub that's been put out there, that it isn't just a weaning of immunity from the virus, but also perhaps that the vaccines themselves are not as good for that purpose. Any thoughts on that?Tom Cech (12:43):Well, so my main thought on that is that this is a property of the virus more than of the vaccine. And respiratory viruses are notoriously hard to get long-term immunity. I mean, look at the flu virus. We have to have annual flu shots. If this were like measles, which is a very different kind of virus, one flu shot would protect you against at least that strain of flu for the rest of your life. So I think the bad rap here is not the vaccine's fault nearly as much as it's the nature of respiratory viruses.RNA And Aging Eric Topol (13:27):No, that's extremely helpful. Now, let me switch to an area that's really fascinating, and you've worked quite a bit on the telomerase story because this is, as you know, being pursued quite a bit, has thought, not just because telomeres might indicate something about biologic aging, but maybe they could help us get to an anti-aging remedy or whatever you want to call it. I'm not sure if you call it a treatment, but tell us about this important enzyme, the role of the RNA building telomeres. And maybe you could also connect that with what a lot of people might not be familiar with, at least from years ago when they learned about it, the Hayflick limit.Tom Cech (14:22):Yes. Well, Liz Blackburn and Carol Greider got the Nobel Prize for the discovery of telomerase along with Jack Szostak who did important initial work on that system. And what it does is, is it uses an RNA as a template to extend the ends of human chromosomes, and this allows the cell to keep dividing without end. It gives the cell immortality. Now, when I say immortality, people get very excited, but I'm talking about immortality at the cellular level, not for the whole organism. And in the absence of a mechanism to build out the ends of our chromosomes, the telomeres being the end of the chromosome are incompletely replicated with each cell division. And so, they shrink over time, and when they get critically short, they signal the cell to stop dividing. This is what is called the Hayflick limit, first discovered by Leonard Hayflick in Philadelphia.(15:43):And he, through his careful observations on cells, growing human cells growing in Petri dishes, saw that they could divide about 50 times and then they wouldn't die. They would just enter a state called senescence. They would change shape, they would change their metabolism, but they would importantly quit dividing. And so, we now see this as a useful feature of human biology that this protects us from getting cancer because one of the hallmarks of cancer is immortality of the tumor cells. And so, if you're wishing for your telomeres to be long and your cells to keep dividing, you have to a little bit be careful what you wish for because this is one foot in the door for cancer formation.Eric Topol (16:45):Yeah, I mean, the point is that it seems like the body and the cell is smart to put these cells into the senescent state so they can't divide anymore. And one of the points you made in the book that I think is worth noting is that 90% of cancers have the telomerase, how do you say it?Tom Cech (17:07):Telomerase.Eric Topol (17:08):Yeah, reactivate.Tom Cech (17:09):Right.Eric Topol (17:10):That's not a good sign.Tom Cech (17:12):Right. And there are efforts to try to target telomerase enzyme for therapeutic purposes, although again, it's tricky because we do have stem cells in our bodies, which are the exception to the Hayflick limit rule. They do still have telomerase, they still have to keep dividing, maybe not as rapidly as a cancer cell, but they still keep dividing. And this is critical for the replenishment of certain worn out tissues in our such as skin cells, such as many of our blood cells, which may live only 30 days before they poop out. That's a scientific term for needing to be replenished, right?Eric Topol (18:07):Yeah. Well, that gets me to the everybody's, now I got the buzz about anti-aging, and whether it's senolytics to get rid of these senescent cells or whether it's to rejuvenate the stem cells that are exhausted or work on telomeres, all of these seem to connect with a potential or higher risk of cancer. I wonder what your thoughts are as we go forward using these various biologic constructs to be able to influence the whole organism, the whole human body aging process.Tom Cech (18:47):Yes. My view, and others may disagree is that aging is not an affliction. It's not a disease. It's not something that we should try to cure, but what we should work on is having a healthy life into our senior years. And perhaps you and I are two examples of people who are at that stage of our life. And what we would really like is to achieve, is to be able to be active and useful to society and to our families for a long period of time. So using the information about telomerase, for example, to help our stem cells stay healthy until we are, until we're ready to cash it in. And for that matter on the other side of the coin, to try to inhibit the telomerase in cancer because cancer, as we all know, is a disease of aging, right? There are young people who get cancer, but if you look at the statistics, it's really heavily weighted towards people who've been around a long time because mutations accumulate and other damage to cells that would normally protect against cancer accumulates. And so, we have to target both the degradation of our stem cells, but also the occurrence of cancer, particularly in the more senior population. And knowing more about RNA is really helpful in that regard.RNA DrugsEric Topol (20:29):Yeah. Well, one of the things that comes across throughout the book is versatility of RNA. In fact, you only I think, mentioned somewhere around 12 or 14 of these different RNAs that have a million different shapes, and there's so many other names of different types of RNAs. It's really quite extraordinary. But one of the big classes of RNAs has really hit it. In fact, this week there are two new interfering RNAs that are having extraordinary effects reported in the New England Journal on all the lipids, abnormal triglycerides and LDL cholesterol, APOC3. And can you talk to us about this interfering the small interfering RNAs and how they become, you've mentioned in the book over 400 RNAs are in the clinic now.Tom Cech (21:21):Yeah, so the 400 of course is beyond just the siRNAs, but these, again, a wonderful story about how fundamental science done just to understand how nature works without any particular expectation of a medical spinoff, often can have the most phenomenal and transformative effects on medicine. And this is one of those examples. It came from a roundworm, which is about the size of an eyelash, which a scientist named Sydney Brenner in England had suggested would be a great experimental organism because the entire animal has only about a thousand cells, and it's transparent so we can look at, see where the cells are, we can watch the worm develop. And what Andy Fire and Craig Mello found in this experimental worm was that double-stranded RNA, you think about DNA is being double-stranded and RNA as being single stranded. But in this case, it was an unusual case where the RNA was forming a double helix, and these little pieces of double helical RNA could turn off the expression of genes in the worm.(22:54):And that seemed remarkable and powerful. But as often happens in biology, at least for those of us who believe in evolution, what goes for the worm goes for the human as well. So a number of scientists quickly found that the same process was going on in the human body as a natural way of regulating the expression of our genes, which means how much of a particular gene product is actually going to be made in a particular cell. But not only was it a natural process, but you could introduce chemically synthesized double helical RNAs. There are only 23 base pairs, 23 units of RNA long, so they're pretty easy to chemically synthesize. And that once these are introduced into a human, the machinery that's already there grabs hold of them and can be used to turn off the expression of a disease causing RNA or the gene makes a messenger RNA, and then this double-stranded RNA can suppress its action. So this has become the main company that is known for doing this is Alnylam in Boston, Cambridge. And they have made quite a few successful products based on this technology.Eric Topol (24:33):Oh, absolutely. Not just for amyloidosis, but as I mentioned these, they even have a drug that's being tested now, as you know that you could take once or twice a year to manage your blood pressure. Wouldn't that be something instead of a pill every day? And then of course, all these others that are not just from Alnylam, but other companies I wasn't even familiar with for managing lipids, which is taking us well beyond statins and these, so-called PCSK9 monoclonal antibodies, so it's really blossoming. Now, the other group of RNA drugs are antisense drugs, and it seemed like they took forever to warm up, and then finally they hit. And can you distinguish the antisense versus the siRNA therapeutics?Tom Cech (25:21):Yes, in a real general sense, there's some similarity as well as some differences, but the antisense, what are called oligonucleotides, whoa, that's a big word, but oligo just means a few, right? And nucleotides is just the building blocks of nucleic acid. So you have a string of a few of these. And again, it's the power of RNA that it is so good at specifically base pairing only with matching sequences. So if you want to match with a G in a target messenger RNA, you put a C in the antisense because G pairs with C, if you want to put an A, if want to match with an A, you put a U in the antisense because A and U form a base pair U is the RNA equivalent of T and DNA, but they have the same coding capacity. So any school kid can write out on a notepad or on their laptop what the sequence would have to be of an antisense RNA to specifically pair with a particular mRNA.(26:43):And this has been, there's a company in your neck of the woods in the San Diego area. It started out with the name Isis that turned out to be the wrong Egyptian God to name your company after, so they're now known as Ionis. Hopefully that name will be around for a while. But they've been very successful in modifying these antisense RNAs or nucleic acids so that they are stable in the body long enough so that they can pair with and thereby inhibit the expression of particular target RNAs. So it has both similarities and differences from the siRNAs, but the common denominator is RNA is great stuff.RNA and Genome EditingEric Topol (27:39):Well, you have taken that to in catalyst, the catalyst, you've proven that without a doubt and you and so many other extraordinary scientists over the years, cumulatively. Now, another way to interfere with genes is editing. And of course, you have a whole chapter devoted to not just well CRISPR, but the whole genome editing field. And by the way, I should note that I forgot because I had read the Codebreaker and we recently spoke Jennifer Doudna and I, that she was in your lab as a postdoc and you made some wonderful comments about her. I don't know if you want to reflect about having Jennifer, did you know that she was going to do some great things in her career?Tom Cech (28:24):Oh, there was no question about it, Eric. She had been a star graduate student at Harvard, had published a series of breathtaking papers in magazines such as Science and Nature already as a graduate student. She won a Markey fellowship to come to Colorado. She chose a very ambitious project trying to determine the molecular structures of folded RNA molecules. We only had one example at the time, and that was the transfer RNA, which is involved in protein synthesis. And here she was trying these catalytic RNAs, which we had discovered, which were much larger than tRNA and was making great progress, which she finished off as an assistant professor at Yale. So what the general public may not know was that in scientific, in the scientific realm, she was already highly appreciated and much awarded before she even heard anything about CRISPR.Eric Topol (29:38):Right. No, it was a great line you have describing her, “she had an uncanny talent for designing just the right experiment to test any hypothesis, and she possessed more energy and drive than any scientist I'd ever met.” That's pretty powerful. Now getting into CRISPR, the one thing, it's amazing in just a decade to see basically the discovery of this natural system to then be approved by FDA for sickle cell disease and beta thalassemia. However, the way it exists today, it's very primitive. It's not actually fixing the gene that's responsible, it's doing a workaround plan. It's got double strand breaks in the DNA. And obviously there's better ways of editing, which are going to obviously involve RNA epigenetic editing, if you will as well. What is your sense about the future of genome editing?Tom Cech (30:36):Yeah, absolutely, Eric. It is primitive right now. These initial therapies are way too expensive as well to make them broadly applicable to the entire, even in a relatively wealthy country like the United States, we need to drive the cost down. We need to get them to work, we need to get the process of introducing them into the CRISPR machinery into the human body to be less tedious and less time consuming. But you've got to start somewhere. And considering that the Charpentier and Doudna Nobel Prize winning discovery was in 2012, which is only a dozen years ago, this is remarkable progress. More typically, it takes 30 years from a basic science discovery to get a medical product with about a 1% chance of it ever happening. And so, this is clearly a robust RNA driven machine. And so, I think the future is bright. We can talk about that some more, but I don't want to leave RNA out of this conversation, Eric. So what's cool about CRISPR is its incredible specificity. Think of the human genome as a million pages of text file on your computer, a million page PDF, and now CRISPR can find one sentence out of that million pages that matches, and that's because it's using RNA, again, the power of RNA to form AU and GC base pairs to locate just one site in our whole DNA, sit down there and direct this Cas9 enzyme to cut the DNA at that site and start the repair process that actually does the gene editing.Eric Topol (32:41):Yeah, it's pretty remarkable. And the fact that it can be so precise and it's going to get even more precise over time in terms of the repair efforts that are needed to get it back to an ideal state. Now, the other thing I wanted to get into with you a bit is on the ribosome, because that applies to antibiotics and as you call it, the mothership. And I love this metaphor that you had about the ribosome, and in the book, “the ribosome is your turntable, the mRNA is the vinyl LP record, and the protein is the music you hear when you lower the needle.” Tell us more about the ribosome and the role of antibiotics.Tom Cech (33:35):So do you think today's young people will understand that metaphor?Eric Topol (33:40):Oh, they probably will. They're making a comeback. These records are making a comeback.Tom Cech (33:44):Okay. Yes, so this is a good analogy in that the ribosome is so versatile it's able to play any music that you feed at the right messenger RNA to make the music being the protein. So you can have in the human body, we have tens of thousands of different messenger RNAs. Each one threads through the same ribosome and spills out the production of whatever protein matches that mRNA. And so that's pretty remarkable. And what Harry Noller at UC Santa Cruz and later the crystallographers Venki Ramakrishnan, Tom Steitz, Ada Yonath proved really through their studies was that this is an RNA machine. It was hard to figure that out because the ribosome has three RNAs and it has dozens of proteins as well. So for a long time people thought it must be one of those proteins that was the heart and soul of the record player, so to speak.RNA and Antibiotics(34:57):And it turned out that it was the RNA. And so, when therefore these scientists, including Venki who you just talked to, looked at where these antibiotics docked on the ribosome, they found that they were blocking the key functional parts of the RNA. So it was really, the antibiotics knew what they were doing long before we knew what they were doing. They were talking to and obstructing the action of the ribosomal RNA. Why is this a good thing for us? Because bacterial ribosomes are just enough different from human ribosomes that there are drugs that will dock to the bacterial ribosomal RNA, throw a monkey wrench into the machine, prevent it from working, but the human ribosomes go on pretty much unfazed.Eric Topol (36:00):Yeah, no, the backbone of our antibiotics relies on this. So I think people need to understand about the two subunits, the large and the small and this mothership, and you illuminate that so really well in the book. That also brings me to phage bacteria phage, and we haven't seen that really enter the clinic in a significant way, but there seems to be a great opportunity. What's your view about that?Tom Cech (36:30):This is an idea that goes way back because since bacteria have their own viruses which do not infect human cells, why not repurpose those into little therapeutic entities that could kill, for example, what would we want to kill? Well, maybe tuberculosis has been very resistant to drugs, right? There are drug resistant strains of TB, yes, of TB, tuberculosis, and especially in immunocompromised individuals, this bug runs rampant. And so, I don't know the status of that. It's been challenging, and this is the way that biomedicine works, is that for every 10 good ideas, and I would say phage therapy for bacterial disease is a good idea. For every 10 such ideas, one of them ends up being practical. And the other nine, maybe somebody else will come along and find a way to make it work, but it hasn't been a big breakthrough yet.RNA, Aptamers and ProteinsEric Topol (37:54):Yeah, no, it's really interesting. And we'll see. It may still be in store. What about aptamers? Tell us a little bit more about those, because they have been getting used a lot in sorting out the important plasma proteins as therapies. What are aptamers and what do you see as the future in that regard?Tom Cech (38:17):Right. Well, in fact, aptamers are a big deal in Boulder because Larry Gold in town was one of the discoverers has a company making aptamers to recognize proteins. Jack Szostak now at University of Chicago has played a big role. And also at your own institution, Jerry Joyce, your president is a big aptamer guy. And you can evolution, normally we think about it as happening out in the environment, but it turns out you can also make it work in the laboratory. You can make it work much faster in the laboratory because you can set up test tube experiments where molecules are being challenged to perform a particular task, like for example, binding to a protein to inactivate it. And if you make a large community of RNA molecules randomly, 99.999% of them aren't going to know how to do this. What are the odds? Very low.(39:30):But just by luck, there will be an occasional molecule of RNA that folds up into a shape that actually fits into the proteins active sighting throws a monkey wrench into the works. Okay, so now that's one in a billion. How are you going to find that guy? Well, this is where the polymerase chain reaction, the same one we use for the COVID-19 tests for infection comes into play. Because if you can now isolate this needle in a haystack and use PCR to amplify it and make a whole handful of it, now you've got a whole handful of molecules which are much better at binding this protein than the starting molecule. And now you can go through this cycle several times to enrich for these, maybe mutagen it a little bit more to give it a little more diversity. We all know diversity is good, so you put a little more diversity into the population and now you find some guy that's really good at recognizing some disease causing protein. So this is the, so-called aptamer story, and they have been used therapeutically with some success, but diagnostically certainly they are extremely useful. And it's another area where we've had success and the future could hold even more success.Eric Topol (41:06):I think what you're bringing up is so important because the ability to screen that tens of thousands of plasma proteins in a person and coming up with as Tony Wyss-Coray did with the organ clocks, and this is using the SomaLogic technology, and so much is going on now to get us not just the polygenic risk scores, but also these proteomic scores to compliment that at our orthogonal, if you will, to understand risk of people for diseases so we can prevent them, which is fulfilling a dream we've never actually achieved so far.Tom Cech (41:44):Eric, just for full disclosure, I'm on the scientific advisory board of SomaLogic in Boulder. I should disclose that.Eric Topol (41:50):Well, that was smart. They needed to have you, so thank you for mentioning that. Now, before I wrap up, well, another area that is a favorite of mine is citizen science. And you mentioned in the book a project because the million shapes of RNA and how it can fold with all hairpin terms turns and double stranded and whatever you name it, that there was this project eteRNA that was using citizen scientists to characterize and understand folding of RNA. Can you tell us about that?RNA Folding and Citizen ScienceTom Cech (42:27):So my friend Rhiju Das, who's a professor at Stanford University, sort of adopted what had been done with protein folding by one of his former mentors, David Baker in Seattle, and had repurposed this for RNA folding. So the idea is to come up with a goal, a target for the community. Can you design an RNA that will fold up to look like a four pointed cross or a five pointed star? And it turned out that, so they made it into a contest and they had tens of thousands of people playing these games and coming up with some remarkable solutions. But then they got a little bit more practical, said, okay, that was fun, but can we have the community design something like a mRNA for the SARS-CoV-2 spike protein to make maybe a more stable vaccine? And quite remarkably, the community of many of whom are just gamers who really don't know much about what RNA does, were able to find some solutions. They weren't enormous breakthroughs, but they got a several fold, several hundred percent increase in stability of the RNA by making it fold more tightly. So I just find it to be a fascinating approach to science. Somebody of my generation would never think of this, but I think for today's generation, it's great when citizens can become involved in research at that level.Eric Topol (44:19):Oh, I think it's extraordinary. And of course, there are other projects folded and others that have exemplified this ability for people with no background in science to contribute in a meaningful way, and they really enjoy, it's like solving a puzzle. The last point is kind of the beginning, the origin of life, and you make a pretty strong case, Tom, that it was RNA. You don't say it definitively, but maybe you can say it here.RNA and the Origin of LifeTom Cech (44:50):Well, Eric, the origin of life happening almost 4 billion years ago on our primitive planet is sort of a historical question. I mean, if you really want to know what happened then, well, we don't have any video surveillance of those moments. So scientists hate to ever say never, but it's hard to sort of believe how we would ever know for sure. So what Leslie Orgel at the Salk Institute next to you taught me when I was a starting assistant professor is even though we'll never know for sure, if we can recapitulate in the laboratory plausible events that could have happened, and if they make sense chemically and biologically, then that's pretty satisfying, even if we can never be absolutely sure. That's what a number of scientists have done in this field is to show that RNA is sort of a, that all the chemistry sort of points to RNA as being something that could have been made under prebiotic conditions and could have folded up into a way that could solve the greatest of all chicken and egg problems, which came first, the informational molecule to pass down to the next generation or the active molecule that could copy that information.(46:32):So now that we know that RNA has both of those abilities, maybe at the beginning there was just this RNA world RNA copying itself, and then proteins came along later, and then DNA probably much more recently as a useful but a little bit boring of genetic information, right?Eric Topol (46:59):Yeah. Well, that goes back to that cover of the Economist 17 years ago, the Big Bang, and you got me convinced that this is a pretty strong story and candidate. Now what a fun chance to discuss all this with you in an extraordinary book, Tom. Did I miss anything that you want to bring up?Tom Cech (47:21):Eric, I just wanted to say that I not only appreciate our conversation, but I also appreciate all you are doing to bring science to the non-scientist public. I think people like me who have taught a lot of freshmen in chemistry, general chemistry, sort of think that that's the level that we need to aim at. But I think that those kids have had science in high school year after year. We need to aim at the parents of those college freshmen who are intelligent, who are intellectually curious, but have not had science courses in a long time. And so, I'm really joining with you in trying to avoid jargon as much as possible. Use simple language, use analogies and metaphors, and try to share the excitement of what we're doing in the laboratory with the populace.Eric Topol (48:25):Well, you sure did that it was palpable. And I thought about it when I read the book about how lucky it would be to be a freshman at the University of Boulder and be having you as the professor. My goodness. Well, thank you so much. This has been so much fun, Tom, and I hope everybody's going to get out there and read the Catalyst to get all the things that we didn't even get a chance to dive into. But this has been great and look forward to future interactions with you.Tom Cech (48:53):Take care, Eric.*********************Thanks for listening or reading this edition of Ground Truths.Please share this podcast with your friends and network. That tells me you found it informative and makes the effort in doing these worthwhile.All Ground Truths newsletters and podcast are free. Voluntary 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 for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

Prof. Venki Ramakrishnan ได้รับรางวัลโนเบลในสาขาเคมี ในปี พ.ศ.2552 ร่วมกับ Thomas A Steitz และ Ada E. Yonath สำหรับการศึกษาโครงสร้างและหน้าที่ของไรโบโซม ซึ่งทำหน้าที่ในการอ่านข้อมูลทางพันธุกรรมเพื่อสร้างโปรตีนที่ถูกระบุ ไรโบโซมมีความซับซ้อนเชิงระดับโมเลกุลเพราะมีราวห้าแสนอะตอมที่ประกอบเป็นไรโบโซม Prof.Venki ดำรงตำแหน่งหัวหน้ากลุ่มวิจัยชีววิทยาโมเลกุลของสภาการวิจัยทางการแพทย์ในวิทยาเขตการแพทย์เคมบริดจ์ตั้งแต่ พ.ศ.2538 และเป็นสมาชิกของวิทยาลัยทรินิตี มหาวิทยาลัยเคมบริดจ์ และเคยดำรงตำแหน่งนายกราชสมาคม (Royal Society) ตั้งแต่ พ.ศ.2558 จนถึง พ.ศ.2563 พี่ปุ๋มสะสมหนังสือที่เกี่ยวข้องกับความชราไว้จำนวนมาก และก็ว่างเว้นจากการทำไลฟ์สรุปหนังสือดีมานานพอสมควร ที่ให้ความสนใจหนังสือเล่มนี้เพราะ 1. Venki Ramakrishnan ได้รับรางวัลโนเบลสาขาเคมี และระบุปัญหาสำคัญในระดับชีวโมเลกุลว่า ข้อมูลทางพันธุกรรมถูกอ่านเพื่อจะสร้างโปรตีนที่เฉพาะเจาะจง ตามคำสั่งได้อย่างไร 2. Venki มีความเชื่อพร้อมหลักฐานว่า Ribosome คือ organelle ภายในเซลล์ที่เป็นศูนย์กลางของ Molecular biology ที่เกี่ยวข้องกับความชรา ซึ่งแตกต่างจากนักวิทยาศาสตร์ความชราท่านอื่นที่ให้ความสำคัญกับ DNA หนังสือมีทั้งหมด 12 บท ก็จะทำไลฟ์แบ่งเป็นหลายตอนเลยค่ะ

#252It is not wise to stick cheese on your pizza with glue, even if Google tells you to do it. This is just one recommendation in a string of blunders made by Google's new AI search engine. It uses a large language model to summarise your searches, but clearly it's not always working as planned. Can (and will) the company fix it? No matter what language you speak, when you hear the word “bouba”, you probably imagine a round shape. And “kiki' will likely make you think of a sharp shape. This example of sound symbolism is thought to be a precursor to human language. But it may not be unique to humans – even chickens may make this association too, hinting at a deeper evolutionary role. Some physicists have long theorised that time is just an illusion that emerges from quantum properties of the universe. And there's even a new study that backs this idea up. If the maths is right, it could finally help us unite the worlds of big and small physics.We now know enough about the ageing process that scientists believe we can start to slow it down or even stop it altogether. Nobel Prize winning biologist Venki Ramakrishnan has written a new book, Why We Die, which explores the new science of ageing and longevity. Find out what he's learnt and what he thinks are the most promising areas of research.The clean energy revolution relies on rare earth metals for things like batteries and solar panels. But mining for them has its own environmental drawbacks. But seaweed may be able to help us with that. It turns out some species collect the minerals we need without damaging the environment. Will seaweed mining be the next big thing?Hosts Timothy Revell and Christie Taylor discuss with guests Matthew Sparkes, Chen Ly, Karmela Padavic-Callaghan and James Dinneen.To read more about these stories, visit newscientist.com.Links: https://www.newscientist.com/science-events/consciousness/ Hosted on Acast. See acast.com/privacy for more information.

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

The knowledge of death is so terrifying that we live most of our lives in denial of it. But, what if we could cheat disease and death and live many times our current lifespan? Nobel Prize winner Venki Ramakrishnan joins Tavis for a conversation about the new science of aging and the quest for immortality.

É possível evitar a velhice? Biólogo molecular Venki Ramakrishnan lançou livro em que destrincha processo de envelhecimento e busca por imortalidade.

É possível evitar a velhice? Biólogo molecular Venki Ramakrishnan lançou livro em que destrincha processo de envelhecimento e busca por imortalidade.

In Why We Die: The New Science of Ageing and the Quest for Immortality, Venki Ramakrishnan explores the current research on and prospects for human longevity.Ramakrishnan leads a group at the MRC Laboratory of Molecular Biology in Cambridge, England. For his research on the structure and function of ribosomes, he won the 2009 Nobel Prize in Chemistry. From 2015 to 2020, he served as president of the Royal Society. In his new book, Ramakrishnan explains the mechanisms of aging and their potential impacts on life expectancy, health span, and lifespan.Together with Martin Reeves, Chairman of the BCG Henderson Institute, Ramakrishnan discusses the likely social, economic, and ethical implications of increasing longevity as well as the specific efforts researchers are making to prolong healthy life—and how close they are to achieving a breakthrough. He shines a light on a set of technologies which could be every bit as impactful as artificial intelligence, which therefore also deserve our attention.Key topics discussed: 02:28 | Life expectancy vs. health span vs. maximum lifespan08:21 | Mechanisms of aging13:25 | Potential interventions for promoting longevity18:27 | How close are we to a longevity breakthrough?24:02 | Societal and ethical implications28:48 | The art of communicating complex ideaAdditional inspirations from Venki Ramakrishnan:The Most Promising Ways to Stop Ageing (New Scientist Interview, 2024)The Story of Deciphering the Ribosome (The Royal Society Talk, 2020)Gene Machine: The Race to Decipher the Secrets of the Ribosome (Basic Books, 2018)This podcast uses the following third-party services for analysis: Chartable - https://chartable.com/privacy

Just how much pesticides residue is on the produce you buy? Should you be concerned? Should you buy organic? Consumer Reports recently did an investigation into pesticides on fruits and vegetables and I begin this episode with some of the surprising results. https://www.consumerreports.org/health/food-contaminants/produce-without-pesticides-a5260230325/ Luck is just around the corner. It may be good luck or it may be bad luck but chance and luck have a huge impact on how things turn out for you. When you understand how luck and chance work in your life, you can do things to improve your good luck and minimize the bad. Joining me to explain how all this works is Mark Robert Rank, a professor at Washington University in St. Louis and author of the book The Random Factor: How Chance and Luck Profoundly Shape Our Lives and the World around Us (https://amzn.to/3W1mDb4). Every living thing will die one day. What's interesting is that some living things - for instance a butterfly - may live only a few days before it dies while a tortoise or whale might live hundreds of years. Why do something age quickly and others slowly. Can we somehow slow down human aging so we live longer than we do now? A lot is going on to understand the aging process and slow it down according to my guest Venki Ramakrishnan. He is a Nobel Prize-winning molecular biologist and author of the book Why We Die (https://amzn.to/49KII0z) Listen as he offers some fascinating insight into how aging works and we can slow down the inevitable. You've probably heard the advice to, “Stop and smell the roses.” While that's certainly a good idea, you may also want to stop and listen to the birds sing and chirp. Listen and I will explain how bird songs are good for your soul. https://www.treehugger.com/why-do-birds-sing-5179422 PLEASE SUPPORT OUR SPONSORS! Indeed is offering SYSK listeners a $75 Sponsored Job Credit to get your jobs more visibility at https://Indeed.com/SOMETHING We love the Think Fast, Talk Smart podcast! https://www.gsb.stanford.edu/business-podcasts/think-fast-talk-smart-podcast NerdWallet lets you compare top travel credit cards side-by-side to maximize your spending! Compare & find smarter credit cards, savings accounts, & more https://NerdWallet.com TurboTax Experts make all your moves count — filing with 100% accuracy and getting your max refund, guaranteed! See guarantee details at https://TurboTax.com/Guarantees Dell Technologies and Intel are pushing what technology can do, so great ideas can happen! Find out how to bring your ideas to life at https://Dell.com/WelcomeToNow eBay Motors has 122 million parts for your #1 ride-or-die, to make sure it stays running smoothly. Keep your ride alive at https://eBayMotors.com Learn more about your ad choices. Visit podcastchoices.com/adchoices

Richard C. Hoagland is the principal investigator and founder of The Enterprise Mission, as well as the vision and the voice of The Other Side of Midnight. In the first half, he discussed images from Odysseus, a recent unmanned American lunar mission. According to Hoagland, the new lunar mission's close-ups dramatically confirm his decades-old "ancient, artificial structures on the Moon model" that he first proposed at the National Press Club in March 1996. The Washington Post even published a "hit piece" 28 years ago on the press event. He suggested that the reason many private and non-US missions to the Moon have run into problems is because they are literally crashing into the glass dome, which he claims exists all over the Moon but is denser in certain regions.The dome, Hoagland continued, could be billions of years old and has been battered by a stream of interplanetary micrometeorites that, over eons, have left holes in it. In image #2 that he sent us, he explained that you can see the sun shining through the "incredible geometry of the glass dome" as the light bounces off of it, creating a refraction. He has concluded that a renegade group in and outside of NASA wants to reveal the truth about these structures on the Moon, and that the recent Odysseus mission functioned as a kind of Trojan horse for that goal. There are ruins throughout the solar system, he added, and it will be fascinating to eventually learn who placed them there and if they are related to our species.------------Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome and runs Ramakrishnan Lab. In the latter half, he discussed the science of mortality and aging, the giant strides being made in the field, and the possibility that we may someday be able to extend our lifespan. The oldest person that ever lived (that we have reliable records for) was a French woman named Jeanne Calment, who died at the age of 122 in 1997. Aging is the accumulation of chemical damage to our molecules and cells over time, he explained, and it starts gradually with small defects; these lead to medium-sized ones that manifest as the morbidities of old age, leading eventually to the system-wide failure that is death. Someone like Calment may have an extraordinary ability to fend off or repair the body's defects that come with aging. For instance, as we age, the risk of cancer goes up, he noted.Scientists are now asking if it's possible to extend our longevity past 120. Ramakrishnan believes we may have to alter our natural biology to achieve this, which could be a challenging proposition. He reported that larger species tend to live longer on average-- for instance, a blue whale or Greenland shark will live 400 years, and other whales live 200 to 300 years. He cited that stress can take a toll on a person, while the "trinity of health" is the combination of a good, moderate diet, exercise, and adequate sleep. Sleep deprivation, he pointed out, increases the risk of many diseases of aging, including cardiovascular problems, obesity, cancer, and Alzheimer's. This may be because during sleep the body performs various repair mechanisms. --- Send in a voice message: https://podcasters.spotify.com/pod/show/georgenoory/message

They're perhaps the oldest questions in the science: Why do we die? And could we find a way to live forever? But for decades, anti-aging research was a “backwater” of the scientific community, consider too fanciful and unrealistic. That is until the last few years. Modern advances in biology have taught us a lot about how we age and why we die—could that knowledge help us turn back the clock?In his new book, “Why We Die: The New Science of Ageing and the Quest for Immortality”, Nobel Prize-winning scientist Venki Ramakrishnan delves into the latest science of aging and investigates the nearly $30 billion dollar longevity industry to separate fact from fiction in our modern quest for immortality.

Scientists are using the secrets of biology to unlock living well past current human life spans. Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A member of the National Academy of Sciences, Venki runs a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. He joins host Krys Boyd to discuss the quest to live forever, if that's even ethical, and what it looks like to alter our physiology. His book is “Why We Die: The New Science of Aging and the Quest for Immortality.”

Why does death exist? Does getting older always mean getting wiser? Should we look to experience or youth for breakthroughs? In today's episode of the Reversing Climate Change podcast, Nori Cofounder Ross Kenyon is joined by Dr. Venki Ramakrishnan, a 2009 Nobel Laureate in chemistry and author of the new book, Why We Die: The New Science of Aging and the Quest for Immortality. Despite growing lifespans, it isn't clear that we have become less avaricious or kinder as a species, at least to the extent that may be desired. Would that change if we had radically longer lives? Is that even likely at this point? Venki challenges much of the discourse around anti-aging, immortality, trends made fun of in Silicon Valley like blood boys, consciousness uploads, and much else. And of course, they discuss if and how this will impact the world's attempts to grapple with climate change. Resources Why We Die: The New Science of Aging and the Quest for Immortality Connect with Nori ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Purchase Nori Carbon Removals⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Nori's website⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Nori on Twitter⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Check out our other podcast, ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Carbon Removal Newsroom⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Carbon Removal Memes on Twitter⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Carbon Removal Memes on Instagram --- Send in a voice message: https://podcasters.spotify.com/pod/show/reversingclimatechange/message Support this podcast: https://podcasters.spotify.com/pod/show/reversingclimatechange/support

The Nobel prize winning scientist Venki Ramakrishnan considers both why we might live longer and also the dilemmas this raises. In the last few years medical advance had led to treatments that really do offer the potential to tackle life threatening cancers and debilitating diseases such as Parkinson's and Alzheimer's. In discussion with Nuala McGovern, Venki also explores the questions such treatments raise. Initially they will be expensive, we already have a global society in which there is a direct link between life expectancy and affluence, will access to these treatments or lack of it, increase that disparity? And although your incurable disease may now be cured, what about the rest of your quality of life? Can the planet support an increasingly needy older and older generation? Does trying to live longer become a selfish act? Nobel prize-winning molecular biologist Venki Ramakrishnan heads a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. This is the first in a series of four programmes from the Oxford Literary Festival, Presented by Nuala McGovern and produced by Julian Siddle. Recorded in front of an audience at Worcester College Oxford.

Frustrated by the excessive hype around anti-ageing, molecular biologist Venki Ramakrishnan presents the facts in his new book Why We Die: The New Science of Ageing and the Quest for Immortality. With our fear of death fuelling a sense of urgency, "solid science" can often get lost in the hype, the Nobel Prize winner says. "The impression is the stuff is all going to happen tomorrow. It's just around the corner. And I'm very sceptical that that's true. I think it'll take a lot of effort and quite a bit of time," he tells Kathryn Ryan.

Today, we are living through a revolution in biology. Giant strides are being made in understanding why we age—and why some species live longer than others. Could we eventually cheat disease and death and live for a very long time, possibly many times our current lifespan? Venki Ramakrishnan, recipient of the Nobel Prize in Chemistry and former president of the Royal Society, takes us on a riveting journey to the frontiers of biology, asking whether we must be mortal. Covering the recent breakthroughs in scientific research, he examines the cutting edge of efforts to extend lifespan by altering our physiology. Venki's book, Why We Die: The New Science of Aging and the Quest for Immortality, is available now. Support the Show - Become a Patron! Help us grow and become a Patron today: https://www.patreon.com/smartpeoplepodcast Sponsors: Rocket Money - Cancel your unwanted subscriptions by going to RocketMoney.com/SMART Factor - use code smart50 to get 50% off at factormeals.com/smart50 Babbel - Get 55% off your Babbel subscription at babbel.com/spp Learn more about your ad choices. Visit megaphone.fm/adchoices

Nobel Prize-winning molecular biologist Venki Ramakrishnan walks us through the ongoing revolution in biology that could allow us to live for a very, very long time. • Venki's new book is "Why We Die: The New Science of Aging and the Quest for Immortality" • Subscribe to our newsletter • Download our app • Join our club (and use code DAILY for a special discount)

My guest today is Venki Ramakrishnan, a British-American structural biologist. He shared the 2009 Nobel Prize in Chemistry with Thomas Steitz and Ada Yonath for research on the structure and function of ribosomes. Since 1999, he has worked as a group leader at the Medical Research Council (MRC) Laboratory of Molecular Biology (LMB) on the Cambridge Biomedical Campus, UK and is a Fellow of Trinity College, Cambridge. The topic is his book Why We Die: The New Science of Aging and the Quest for Immortality. In this episode of Trend Following Radio we discuss: Evolutionary perspectives on lifespan and aging Mortality and its psychological implications Biological processes underlying aging and death Slowing down the aging process Aging research and investment by California billionaires Factors influencing human lifespan Scientific advancements in extending human lifespan and reversing aging Jump in! --- I'm MICHAEL COVEL, the host of TREND FOLLOWING RADIO, and I'm proud to have delivered 10+ million podcast listens since 2012. Investments, economics, psychology, politics, decision-making, human behavior, entrepreneurship and trend following are all passionately explored and debated on my show. To start? I'd like to give you a great piece of advice you can use in your life and trading journey… cut your losses! You will find much more about that philosophy here: https://www.trendfollowing.com/trend/ You can watch a free video here: https://www.trendfollowing.com/video/ Can't get enough of this episode? You can choose from my thousand plus episodes here: https://www.trendfollowing.com/podcast My social media platforms: Twitter: @covel Facebook: @trendfollowing LinkedIn: @covel Instagram: @mikecovel Hope you enjoy my never-ending podcast conversation!

My guest today is Venki Ramakrishnan, a British-American structural biologist. He shared the 2009 Nobel Prize in Chemistry with Thomas Steitz and Ada Yonath for research on the structure and function of ribosomes. Since 1999, he has worked as a group leader at the Medical Research Council (MRC) Laboratory of Molecular Biology (LMB) on the Cambridge Biomedical Campus, UK and is a Fellow of Trinity College, Cambridge. The topic is his book Why We Die: The New Science of Aging and the Quest for Immortality. In this episode of Trend Following Radio we discuss: Evolutionary perspectives on lifespan and aging Mortality and its psychological implications Biological processes underlying aging and death Slowing down the aging process Aging research and investment by California billionaires Factors influencing human lifespan Scientific advancements in extending human lifespan and reversing aging Jump in! --- I'm MICHAEL COVEL, the host of TREND FOLLOWING RADIO, and I'm proud to have delivered 10+ million podcast listens since 2012. Investments, economics, psychology, politics, decision-making, human behavior, entrepreneurship and trend following are all passionately explored and debated on my show. To start? I'd like to give you a great piece of advice you can use in your life and trading journey… cut your losses! You will find much more about that philosophy here: https://www.trendfollowing.com/trend/ You can watch a free video here: https://www.trendfollowing.com/video/ Can't get enough of this episode? You can choose from my thousand plus episodes here: https://www.trendfollowing.com/podcast My social media platforms: Twitter: @covel Facebook: @trendfollowing LinkedIn: @covel Instagram: @mikecovel Hope you enjoy my never-ending podcast conversation!

George Noory and Nobel Prize winning chemist Venki Ramakrishnan explore his research into the science of mortality and what causes people to die, and if there will be a way to change human physiology to improve our health and become immortal.See omnystudio.com/listener for privacy information.

The Nobel prize winning molecular biologist Venki Ramakrishnan explores how time affects our bodies, brains and emotions in his new book, Why We Die: The New Science of Ageing and the Quest for Immortality. As he explains the recent scientific breakthroughs to extend lifespan by altering our biology, he also considers the ethical questions such efforts raise. The neuroscientist Charan Ranganath asks a different question in his book, Why We Remember. Using case studies he unveils the principles behind how the brain retains information, and what and why we forget so much. He also looks at what happens to our memories as we age. In her new book, Nostalgia, the historian Agnes Arnold-Forster blends social history and psychology in a quest to understand this complex emotion. While it was thought of as an illness in the 17th century, it is now used as a widespread marketing tool impacting our choices from politics to food. But if nostalgia prompts us to glorify the past, Arnold-Foster asks how that impacts the present, and future.Producer: Katy Hickman

Could we one day cheat death? Are we hurtling towards a time when science will be so advanced that aging can be prevented or halted in its tracks? Nobel laureate Venki Ramakrishnan takes a skeptical view in a fascinating exploration of longevity research. In Why We Die: The New Science of Aging and the Quest for Immortality, the acclaimed scientist delves into the complexities of aging and the pursuit of extending healthy lifespan.A former president of the Royal Society in London, Ramakrishnan is a group leader at the Medical Research Council's Laboratory of Molecular Biology in Cambridge, England.  He shared the Nobel Prize in Chemistry in 2009 for his work uncovering the structure and function of tiny cellular particles called ribosomes and was knighted in 2012. In this interview with Peter Bowes, the molecular biologist provides a critical perspective on the dilemmas of aging research; questions the hype and financial interests linked to some aspects of longevity science; delves into the concept of compressed morbidity and its challenges, and explains his belief that dramatic life extension is not imminent. Read a transcript:  LLAMA podcast websitePhoto credit: Kate Joyce and Sante Fe Institute-Affiliation disclosure: This podcast receives a small commission when you use the code LLAMA for purchases from companies below which support our mission.   It helps to cover production costs and ensures that our interviews, sharing information about human longevity, remain free for all to listen. -▸ Movement & resistance training have long been associated with living a long, healthy life - along with a balanced diet and good sleep. Which is why we're delighted to be working with Hampton Fitness to provide a 15% discount on essential workout gear. Use code: llamapodcast15 at checkout-Fit, Healthy & Happy Podcast Welcome to the Fit, Healthy and Happy Podcast hosted by Josh and Kyle from Colossus...Listen on: Apple Podcasts SpotifyTime-line Mitopure (a highly pure form of Urolithin A) boosts the health of our mitochondria – the battery packs of our cells – and improves muscle strength. Time-line is offering LLAMA listeners a 10% discount on its range of products – Mitopure powders, softgels & skin creams. Use the code LLAMA at checkout- FlexBeam red light therapyRecharge Health is offering LLAMA listeners a discount on the purchase of FlexBeam, the wearable red light therapy device which targets key parts of the body to improve sleep, treat injuries and sooth aches and pains associated with aging. Discounts vary - see details of the current offer hereSupport the showThe Live Long and Master Aging (LLAMA) podcast, a HealthSpan Media LLC production, shares ideas but does not offer medical advice. If you have health concerns of any kind, or you are considering adopting a new diet or exercise regime, you should consult your doctor.

In this episode, Xavier Bonilla has a dialogue with Venki Ramakrishnan about his discovering and mapping the ribosome structure. They discuss his background in coming from India to study physics and then biology, layout of ribosome, DNA, RNA, mRNA, and proteins, what we have learned about the ribosome over the past 50+ years, x-ray crystallography, and his trip to the LMB. They also discuss his experience of seeing atomic subunits of ribosomes for the first time, winning the Nobel Prize, and the future of ribosome research. Venki Ramakrishnan is a biologist and group leader of the Medical Research Center (MRC) Laboratory of Molecular Biology and is a fellow of Trinity College, Cambridge. He was President of the Royal Society from 2015 to 2020. He was awarded the Nobel Prize in Chemistry in 2009 for his work on the sequence of the ribosome structure. He is also a member of the Order of Merit since 2012. He is the author of, Gene Machine: The Race to Decipher the Secrets of the Ribosome. Get full access to Converging Dialogues at convergingdialogues.substack.com/subscribe

Marta Shahbazi es una de las jóvenes investigadora españolas de mayor proyección internacional. Bióloga molecular de formación, trabaja actualmente sobre desarrollo y formación del embrión humano en el prestigioso laboratorio de Biologia Molecular de la Universidad de Cambridge, cuna de muchos premios Nobel. Pocos temas pueden ser más apasionantes como la investigación sobre el desarrollo del embrión humano en las primeras etapas de la vida, desde que somos simplemente una sola célula (fusión de un óvulo con un espermatozoide) hasta la formación en el utero materno del feto humano con todos sus órganos en desarrollo. Marta nos resume lo más significativo de sus trabajos sobre el conocimiento actual del desarrollo del embrión tanto en humanos como en ratones, sus principales líneas de investigación, y su experiencia de trabajar en uno de los Centros de Investigación más prestigiosos del mundo. 1:00 Formación. Doctorado CNIO Mirna Perez-Moreno. Post-Doc Magdalena Zernicka- Goetz. Cambridge. 4:00 Células madre embrionarias pluripotenciales. Los primeros días del embrión. 10:30 Implantación en utero. Pérdida de pluripotencialidad. Cavidad amniótica 15:30 Obtención de Embriones humanos para investigacion. Colección Carniege. 19:30 ¿Qué define al ser vivo? ¿Cuándo empieza la vida?. Reflexiones. 23:30 Cultivo in-vitro del embrión humano. Por qué el límite en el día 14 29:00 La caja negra del desarrollo. ¿Cómo estudiar el embrión implantado? 32:00 La reproducción humana es ineficiente. Pérdidas bioquímicas. Abortos espontaneos. 38:00 Mis momentos EUREKA 40:00 Reflexiones y consejos sobre la investigación. No todo el mundo vale. 46:00 Mis líneas de investigación. La Plasticidad embrionaria. 51:00 Diferencias investigación en España e Inglaterra: Importancia de Masa crítica internacional 59:00 Libro recomendado: “La máquina genética” de Venki Ramakrishnan. 1:00:01 Un país a visitar: Islandia Gracias al patrocinador de este podcast: Gofio La Piña https://gofio.shop/es/

In attesa dell'annuncio del premio Nobel per la medicina e la fisiologia 2021, abbiamo incontrato Venki Ramakrishnan

Professor Gautam Menon talks to host Pavan Srinath about the Nobel Prize, what they mean for scientists, and how they shape science.In episode 155 of The Pragati Podcast, Gautam and Pavan discuss the outsized role that the Nobel Prize plays in being an aspirational goal for young scientists, how they create role models, the work, and the people who win the awards, and the dynamics at play.Gautam I Menon (@MenonBioPhysics) is a Professor of Physics and Biology at Ashoka University. Prior to joining Ashoka, he was a Professor with the Theoretical Physics and Computational Biology groups at the Institute of Mathematical Sciences, Chennai, where he was the founding Dean of the Computational Biology group. He works on biophysical problems and the modeling of infectious diseases. He is an initiating member of the Indian Scientists' Response to COVID-19 (ISRC). Before working on biological problems, he worked in the broad fields of statistical physics and soft condensed matter physics.Visit tiny.cc/pragati155 for detailed episode notes and links to the Nobel winners and research who are discussed in the episode.For all queries and feedback, email us at pragatipod@gmail.com or reach out to host Pavan Srinath at @zeusisdead on Twitter: twitter.com/zeusisdeadFollow The Pragati Podcast on Instagram: instagram.com/pragatipod & Twitter: twitter.com/thinkpragati & Facebook: facebook.com/thinkpragatiThe Pragati Podcast is made possible thanks to the support of The Takshashila Institution and the Independent Public-Spirited Media Foundation (IPSMF).

In this podcast, Professor Sir Venki Ramakrishnan, President of the Royal Society, discusses the state of British science, science advice to government during coronavirus, and science issues of Brexit.

Nobel laureate Venki Ramakrishnan talks about of the importance of scientific thinking, medical research and breakthrough technologies to combat the current crisis and prepare better for future pandemicsSee omnystudio.com/listener for privacy information.

Venki Ramakrishnan is president of the UK’s Royal Society and he won the 2009 Nobel Prize in Chemistry for helping to unravel the secrets of ribosomes. The ribosome is the most important molecule you’ve never heard of - it’s the factory in our cells that produces everything in our bodies. New Scientist reporter Clare Wilson met him in the era just before lockdown to discuss why he made an early career pivot from studying physics to the life sciences, and what he thinks are the challenges facing science today in an era of denialism and fake news.

The Children’s Commissioner for England says that we need an urgent review of the care system. She is concerned that around 30,000 children in care are living miles away from friends and family, while others are living in unregulated and inadequate placements. Anne Longfield explains what she thinks needs to be done. Cancer treatment can have an impact on fertility, but a recent survey by the Teenage Cancer Trust suggests that nearly a third of young people did not have a discussion about their fertility before starting treatment. We speak to 18 year old, Ellie Waters who was diagnosed with a rare form of cancer aged 14, Dr Louise Soanes, a Teenage Cancer Trust Nurse Consultant for Adolescents and Young People and Professor Pamela Kearns, a Consultant Paediatric Oncologist. Elsie Widdowson was one of the British dietitians responsible for overseeing the government-mandated addition of vitamins to food and wartime rationing in Britain during World War II. Dr Venki Ramakrishnan the President of the Royal Society tells Jenni about her achievements. Many parents see location tracking apps as an easy way to keep tabs on their teenagers. We discuss the merits and drawbacks of on keeping tabs on your teenagers. Presenter: Jenni Murray Producer: Ruth Watts

The ribosome is the mother of all molecules without which nothing lives. This month, the Nobel Prize winner Venki Ramakrishnan in conversation with Vivienne Parry, tells the story of the race to uncover the structure of the ribosome - a fundamental discovery that resolves an ancient mystery of life itself and could lead to the development of better antibiotics to fight the most deadly diseases. Check out our website: www.rigb.org/ Twitter: twitter.com/Ri_Science YouTube: www.youtube.com/user/TheRoyalInstitution And Patreon: www.patreon.com/TheRoyalInstitution

Joint winner of the 2009 Nobel Prize for Chemistry, Venki Ramakrishnan’s work has gone past the whys and wherefores of DNA and on to the ribosome, the structure which helps decode our genetic make-up. In a live event at the Edinburgh International Book Festival 2019 the President of The Royal Society and Gene Machine author shares stories about his first uncertain experiments and making genuine scientific breakthroughs. An enlightening hour of conversation with Steve Brusatte.

Sir Venki Ramakrishnan is President of the Royal Society and was awarded the Nobel Prize in 2009 for his research into the ribosome – the mysterious ancient molecule that decodes DNA, what he terms ‘the mother of all molecules’. He’s what you might call a science all-rounder: he gained a PhD in Physics before turning to Biology, and his Nobel Prize was in Chemistry. Born in India, he moved to the US as a postgraduate student, and in 1999 came to Britain to work at the MRC Laboratory of Molecular Biology in Cambridge. Alongside science Venki Ramakrishnan has another passion – for music, and, in particular, chamber music, which grew out of the Indian classical music he heard as a child. His son Raman is the cellist with the Horszowski Trio and we hear their performance of music by Schubert, as well as a Brahms piano quartet and a Beethoven cello sonata, reflecting both Raman's and Venki’s deep engagement with that instrument. Venki's other great love is for the violin, and he chooses music by Mozart alongside Bach's Double Violin Concerto - which Venki himself played whilst learning the violin as a graduate student in the USA. He talks to Michael about the central role of music in his life, about how he would reform the Nobel Prizes in science, and why he swapped the mountains of Utah for the fens of East Anglia. Producer: Jane Greenwood A Loftus production for BBC Radio 3

Quería hablar de lo bonito que es escuchar a otros científicos hablar de su vida, pero se me ha ido un poco el tema. En realidad, os hablo de eso, de lo mucho que me impresionó una charla de Venki Ramakrishnan a la que fui hace unas semanas, pero también hablo de los techos de cristal, de los modelos para científicas y de la importancia de la salud mental en esto que hacemos. Todo sin olvidarme de algo fundamental: la marcha por la ciencia del sábado pasado! Gente: apoyad a los científicos, que la vida del científico es muy dura!Para cualquier duda o comentario, las formas de contactar conmigo son a través de Twitter @karmegd o por email a karmegd@gmail.com. Y no olvides pasarte por https://www.instagram.com/karmegd para ver las fotos que acompañan a este capítulo y por https://emilcarfm.singularshirts.com/ para comprar la camiseta del podcast. También esperamos tus comentarios en emilcar.fm/bacteriofagos y en nuestro grupo de Telegram https://t.me/Bacteriofagos, en el que discutimos muchos temas relacionados (o no) con la ciencia.

Quería hablar de lo bonito que es escuchar a otros científicos hablar de su vida, pero se me ha ido un poco el tema. En realidad, os hablo de eso, de lo mucho que me impresionó una charla de Venki Ramakrishnan a la que fui hace unas semanas, pero también hablo de los techos de cristal, de los modelos para científicas y de la importancia de la salud mental en esto que hacemos. Todo sin olvidarme de algo fundamental: la marcha por la ciencia del sábado pasado! Gente: apoyad a los científicos, que la vida del científico es muy dura!Para cualquier duda o comentario, las formas de contactar conmigo son a través de Twitter @karmegd o por email a karmegd@gmail.com. Y no olvides pasarte por https://www.instagram.com/karmegd para ver las fotos que acompañan a este capítulo y por https://emilcarfm.singularshirts.com/ para comprar la camiseta del podcast. También esperamos tus comentarios en emilcar.fm/bacteriofagos y en nuestro grupo de Telegram https://t.me/Bacteriofagos, en el que discutimos muchos temas relacionados (o no) con la ciencia.

Nobel Prize-winning structural biologist, Knight Bachelor, President of the Royal Society, brilliant structural biologist and enthralling author Venki Ramakrishnan tells the story of his race to discover the inner workings of biology's most important molecule - the ribosome, in this articulate, witty and surprisingly philosophical series of videos.

How can a Nobel Prize winning scientist feel like an outsider?

How can a Nobel Prize winning scientist feel like an outsider?

Dr. Venki Ramakrishnan, a molecular biologist, is president of the Royal Society in Great Britain, the same organization formerly headed by Sir Isaac Newton and Ernest Rutherford. He feels it is the duty and obligation of top scientists to explain, in understandable terms, their discoveries to the general population to extend understanding and knowledge. Dr. Ramakrishnan, in this Spectrum Podcast, explains ribosomes. They exist in every living cell to synthesize proteins. For his work in ribosomes, Dr. Ramakrishnan shared a Nobel Prize in Chemistry in 2009. In this podcast, he uses approachable metaphors to explain the functioning of these highly complex cell components. In recent years, Dr. Ramakrishnan has extended his work in ribosomes and has taken his discoveries to a higher level. He notes that malfunctioning ribosomes can be instrumental in causing certain diseases. However, harnessing and directing the functioning of ribosomes can bring about cures for some diseases and human maladies. For example, greater knowledge of ribosomes may lead to better antibiotics being developed against bacterial infections. Dr. Ramakrishnan also traces his career from his native India to getting a doctorate in physics from Ohio University. He then went on to have a postdoctoral position in biology with Dr. Peter Moore’s lab at Yale and he worked at several other American labs before transferring his talents to the Laboratory of Molecular Biology in Cambridge, England. Just recently, Dr. Ramakrishnan has released a book he authored titled: “Gene Machine: The Race to Decipher the Secrets of the Ribosome.” In the book, he talks about his discoveries and his path to uncover this critical component of living cells. In May, Dr. Ramakrishnan will receive an honorary doctorate from his alma mater Ohio University.

The 2019 Haldane Lecture was delivered by Sir Venki Ramakrishnan, President of the Royal Society, on February 7th at Wolfson College, Oxford. The lecture was introduced by College President Sir Tim Hitchens. The thousands of genes in our DNA are translated by ribosomes - ancient, enormous molecular machines that read the genetic code to make the thousands of proteins that carry out the functions of life. Although the ribosome was discovered in the 1950s, unravelling its million atom structure took over four decades. Venki Ramakrishnan will frame this in term of his career and show how science does not proceed in a series of logical steps but in fits and starts, with many characters and their egos, rivalries, competition and collaboration, blunders and dead ends. Sir Venki is a structural biologist who in 2009 received the Nobel Prize in Chemistry and was knighted in 2012. In 2015, he was elected as President of the Royal Society.

Venki Ramakrishnan in conversation with Priyamvada Natrajan. Nobel laureate Venki Ramakrishnan is a British-American structural biologist of Indian origin. He is also currently President of the Royal Society. His recent book, Gene Machine: The Race to Decipher the Secrets of the Ribosome is about the quest to understand the enormous ancient molecular machine, the ribosome, that decodes genetic information to build all life forms. But the book also is a frank description of what it was like for an outsider who found himself in a race to solve one of the most fundamental problems of biology. He will speak not only about the scientific voyage itself but also about the human side of science, including blunders, dead ends, changing careers, egos, competition and collaboration. The result is an insider look at how science actually works and what it felt like to be in the middle of it all. This episode is a live session from Day 2 of #ZEEJLF2019.

Nicola Davis sits down with Nobel prize-winning scientist Sir Venki Ramakrishnan to discuss the competition he faced in the race to discover the ribosome – AKA the gene machine. Is competition good for science, or would a collaborative approach be better?

Venki Ramakrishnan is a Nobel Prize-winning molecular biologist. He is most renowned for his research into the atomic structure of the ribosome - a complex molecule in the cell which translates DNA into chains of amino acids that build proteins, the essence of life. This work eventually secured Venki a Nobel Prize in 2009, which he shared with Ada Yonath and Thomas Steitz. Venki was born in Tamil Nadu, in the south of India. Both his parents were scientists, and both pursued postgraduate studies overseas when Venki was very young. He completed his schooling in India, and then moved to the United States. Life on an American campus in the early 1970s was, he recalls, a culture shock for a self-confessed nerdy young Indian. He completed a PhD in Physics in 1976, but then switched to biology which he felt was a more exciting discipline. His research into the ribosome began when he was working at Yale as a post-doctoral fellow in the late 1970s. He moved to the UK in 1999, joining the Laboratory of Molecular Biology in Cambridge as a group leader. He was knighted in 2012, and has served as President of the Royal Society since 2015, where he has argued that science should enjoy a central place in the curriculum and in our wider culture. Presenter: Lauren Laverne Producer: Sarah Taylor

Venki Ramakrishnan is a Nobel Prize-winning molecular biologist. He is most renowned for his research into the atomic structure of the ribosome - a complex molecule in the cell which translates DNA into chains of amino acids that build proteins, the essence of life. This work eventually secured Venki a Nobel Prize in 2009, which he shared with Ada Yonath and Thomas Steitz. Venki was born in Tamil Nadu, in the south of India. Both his parents were scientists, and both pursued postgraduate studies overseas when Venki was very young. He completed his schooling in India, and then moved to the United States. Life on an American campus in the early 1970s was, he recalls, a culture shock for a self-confessed nerdy young Indian. He completed a PhD in Physics in 1976, but then switched to biology which he felt was a more exciting discipline. His research into the ribosome began when he was working at Yale as a post-doctoral fellow in the late 1970s. He moved to the UK in 1999, joining the Laboratory of Molecular Biology in Cambridge as a group leader. He was knighted in 2012, and has served as President of the Royal Society since 2015, where he has argued that science should enjoy a central place in the curriculum and in our wider culture. Presenter: Lauren Laverne Producer: Sarah Taylor

VENKATRAMAN "VENKI" RAMAKRISHNAN is a Nobel Prize-winning biologist whose many scientific contributions include his work on the atomic structure of the ribosome. He is Group Leader and Former Deputy Director of the MRC Laboratory of Molecular Biology in Cambridge, and the current President of the Royal Society. The Conversation: https://www.edge.org/conversation/venki_ramakrishnan-soul-of-a-molecular-machine

All the information that's needed for life is written in our DNA. But how do we get from DNA code to biological reality? That's the job of the ribosomes - those clever molecular machines that are found in every living cell. And in 2008 Venki Ramakrishnan was awarded the Nobel Prize for determining their structure. Jim talks to Venki about the frantic race to crack the structure of the ribosome, probably the most important biological molecule after DNA; why he thinks the Nobel Prize is a terrible thing for science; and his new job as President of the Royal Society. Producer: Anna Buckley.

Kevin Fong talks to Venki Ramakrishnan, Professor of structural biology in Cambridge and joint-winner of the Nobel Prize in Chemistry in 2009. Celebrated for his work on the ribosome, the remarkable molecular machine at the heart of all cell biology, Ramakrishnan was knighted for services to Science in 2012 and later this year, will become the first Indian-born president of the Royal Society, the oldest and most prestigious scientific body in the world. And yet, as Kevin discovers, his education and early academic career was anything but predictable or conventional and included being rejected from both Indian and US Universities multiple times. Image: presenter Kevin Fong with Venki Ramakrishnan, BBC Copyright

In the first episode of MRC talks, we bring the stories covered in the summer 2014 issue of our quarterly Network magazine to life, by capturing scientific and personal insights from the scientists themselves. We talk to MRC scientists Lori Passmore (1min07), Venki Ramakrishnan (4min25) and Richard Henderson (8min33) about how they are developing and using electron microscopy to obtain structures of proteins at atomic resolution for the first time. MRC Senior Clinical Fellow Dr Richard Coward explains how his clinical work at Bristol Children’s Hospital is helping inform his laboratory research into kidney disease. And in our opinion piece, Dr Anne O’Garra tells us about how she is translating her knowledge of immunology and basic research in the lab into improving the diagnosis of tuberculosis.

Dr. Emilie Marcus talks with two of this year's Nobel Laureates, Dr. Elizabeth Blackburn and Dr. Venki Ramakrishnan about their groundbreaking research on telomeres (1:04) and the ribosome (14:29), respectively. Learn about the connection between two major molecular players in Alzheimer's disease (29:15).