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Está tarde Toño de Valdés y Enrique Burak hablaremos del cambio de Rafael Devers de Boston a San Francisco, Adams de lo que significa este movimiento en las grandes ligas. Se acerca el final de la finales de la NBA y todo sobre la enfermedad de Jason Kelce.

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

Audio FileGround Truths can also be found on Apple Podcasts, Spotify and YouTube.The UK is the world leader in human genomics, and laid the foundation for advancing medicine with the UK Biobank, Genomes England and now Our Future Health (w/ 5 million participants). Sir John Bell is a major force in driving and advising these and many other initiatives. After 22 years as the Regius Professor of Medicine at the University of Oxford he left in 2024 to be President of the Ellison Institute of Technology. Professor Bell has been duly recognized in the UK: knighted in 2015 and appointed Companion of Honor in 2023. In our conversation, you will get a sense for how EIT will be transformational for using A.I. and life science for promoting human health.Transcript with audio links Eric Topol (00:06):Hello, this is Eric Topol from Ground Truths. And I'm really delighted to welcome today, Sir John Bell who had an extraordinary career as a geneticist, immunologist, we'll talk about several initiatives he's been involved with during his long tenure at University of Oxford, recently became head of the Ellison Institute of Technology (EIT) in the UK. So welcome, John.Sir John Bell (00:30):Thanks, Eric. Thanks very much for having me.Eric Topol (00:34):Well, I think it's just extraordinary the contributions that you have made and continue to make to advance medicine, and I thought what we could do is get into that. I mean, what's interesting, you have had some notable migrations over your career, I think starting in Canada, at Stanford, then over as Rhodes Scholar in Oxford. And then you of course had a couple of decades in a very prestigious position, which as I understand was started in 1546 by King Henry VII, and served as the Regius Professor of Medicine at the University of Oxford. Do I have that right?Sir John Bell (01:11):It was actually Henry VIII, but you were close.Eric Topol (01:14):Henry VIII, that's great. Yeah. Okay, good. Well, that's a pretty notable professorship. And then of course in recent times you left to head up this pretty formidable new institute, which is something that's a big trend going on around the world, particularly in the US and we'll talk about. So maybe we can start with the new thing. Tell us more about the Ellison Institute of Technology (EIT), if you will.Sir John Bell (01:47):Yeah. So as you know, Larry Ellison has been one of the great tech entrepreneurs focused really on developing terrific databases over his career and through Oracle, which is the company that he founded. And Larry is really keen to try and give back something substantial to the world, which is based on science and technology. So he and I did quite a bit together over the Covid pandemic. He and I talked a lot about what we're doing and so on. He came to visit afterwards and he had, I think he decided that the right way to make his contributions would be to set up an institute that would be using the state-of-the-art science and technology with a lot of AI and machine learning, but also some of the other modern tools to address the major problems in healthcare, in food security, in green energy and climate change and in global governance.Sir John Bell (02:49):So anyway, he launched this about 18 months ago. He approached me to ask whether I would run it. He wanted to set it up outside Oxford, and he wanted to do something which is a bit different than others. And that is his view was that we needed to try and create solutions to these problems which are commercially viable and not all the solutions are going to be commercially viable, but where you can create those, you make them sustainable. So the idea is to make sure that we create solutions that people want to buy, and then if they buy them, you can create a sustainable solution to those issues. So we are actually a company, but we are addressing many of the same problems that the big foundations are addressing. And the big issues that you and I talk about in health, for example, are all on our list. So we're kind of optimistic as to where this will go and Larry's supporting the project and we're going to build out an institute here which will have about 5,000 people in it, and we'll be, I think a pretty exciting new addition to the science and technology ecosystem globally.Eric Topol (04:02):Well, I know the reverberations and the excitement is palpable and some of the colleagues I've spoken to, not just in England, but of course all over the world. So congratulations on that. It was a big move for you to leave the hardcore academics. And the other thing I wanted to ask you, John, is you had distinguished your career in immunology, in genetics, type 1 diabetes and other conditions, autoimmune conditions, and now you've really diversified, as you described with these different areas of emphasis at the new institute. Is that more fun to do it or do you have deputies that you can assign to things like climate change in other areas?Sir John Bell (04:50):Trust me, Eric, I'm not making any definitive decisions about areas I know nothing about, but part of this is about how do you set up leadership, run a team, get the right people in. And I have to say one of the really interesting things about the institute is we've been able to recruit some outstanding people across all those domains. And as you know, success is almost all dependent on people. So we're really pretty optimistic we're going to have a significant impact. And of course, we also want to take risks because not a lot of point in us doing stuff that everybody else is doing. So we're going to be doing some things that are pretty way out there and some of them will fail, so we are just going to get used to trying to make sure we get a few of them across the finish line. But the other thing is that, and you've experienced this too, you never get too old to learn. I mean, I'm sucking up stuff that I never thought I would ever learn about, which is fun actually, and really marvel.Eric Topol (05:55):It's fantastic. I mean, you've really broadened and it's great that you have the runway to get these people on board and I think you're having a big building that's under construction?Sir John Bell (06:07):Yeah, we've got the original building that Larry committed to is about 330,000 square feet of space. I mean, this is completely amazing, but we are of course to accommodate up to 5,000 people, we're going to need more than that. So we are looking at a much wider campus here that'll involve more than just that building. I think we'll end up with several million square feet of space by the time we're finished. So mean, it's a really big project, but we've already made progress in some domains to try and get projects and the beginnings of companies on the road to try and solve some of the big problems. So we're quite excited about it.Eric Topol (06:49):Now you, I assume it's pretty close to Oxford, and will you have some kind of inter interactions that are substantial?Sir John Bell (06:58):Yeah, so the university's been terrific about this actually, because of course most universities would say, well, why don't you do it inside the university and just give us the money and it'll all be fine. So of course Larry. Larry wasn't born yesterday, so I said, well, thank you very much, but I think we'll probably do this nearby. But the university also realized this is a really exciting opportunity for them and we've got a really good relationship with them. We've signed an agreement with them as to who will work where. We've agreed not to steal a lot of their staff. We're going to be bringing new people into the ecosystem. Some of the university people will spend some time with us and sometime in the university, so that will help. But we're also bringing quite a few new people into the setting. So the university has been really positive. And I think one of the things that's attractive to the university, and you'll be familiar with this problem in the UK, is that we're quite good. The discovery science here is pretty good.Sir John Bell (08:06):And we do startups now at scale. So Oxford does lots of little startup companies in the biotech space and all the rest of it, but we never scale any of these companies because there isn't the depth of capital for scaling capital to get these things scaled. And so, in a way what we're trying to do here at Ellison actually avoids that problem because Larry knows how to scale companies, and we've got the financial support now. If we have things that are really successful, we can build the full stack solution to some of these problems. So I think the university is really intrigued as to how we might do that. We're going to have to bring some people in that know how to do that and build billion dollar companies, but it's sufficiently attractive. We've already started to recruit some really outstanding people. So as a way to change the UK system broadly, it's actually quite a good disruptive influence on the way the thing works to try and fix some of the fundamental problems.Eric Topol (09:07):I love that model and the ability that you can go from small startups to really transformative companies have any impact. It fits in well with the overall objectives, I can see that. The thing that also is intriguing regarding this whole effort is that in parallel we've learned your influence. The UK is a genomics world leader without any question and no coincidence that that's been your area of emphasis in your career. So we've watched these three initiatives that I think you were involved in the UK Biobank, which has had more impact than any cohort ever assembled. Every day there's another paper using that data that's coming out. There's Genomes England, and then now Our Future Health, which a lot of people don't know about here, which is well into the 5 million people enrollment. Can you tell us about, this is now 15 years ago plus when these were started, and of course now with a new one that's the biggest ever. What was your thinking and involvement and how you built the UK to be a world leader in this space?Sir John Bell (10:26):So if you turn the clock back 20 years, or actually slightly more than 25 years ago, it was clear that genomics was going to have a play. And I think many of us believed that there was going to be a genetic element to most of the major common disease turn out to be true. But at the time, there were a few skeptics, but it seemed to us that there was going to be a genetic story that underpinned an awful lot of human disease and medicine. And we were fortunate because in Oxford as you know, one of my predecessors in the Regius job was Richard Doll, and he built up this fantastic epidemiology capability in Oxford around Richard Peto, Rory Collins, and those folks, and they really knew how to do large scale epidemiology. And one of the things that they'd observed, which is it turns out to be true with genetics as well, is a lot of the effects are relatively small, but they're still quite significant. So you do need large scale cohorts to understand what you're doing. And it was really Richard that pioneered the whole thinking behind that. So when we had another element in the formula, which was the ability to detect genetic variation and put that into the formula, it seemed to me that we could move into an era where you could set up, again, large cohorts, but build into the ability to have DNA, interrogate the DNA, and also ultimately interrogate things like proteomics and metabolomics, which were just in their infancy at that stage.Sir John Bell (12:04):Very early on I got together because I was at that stage at the Nuffield Chair of Medicine, and I got together, Rory and Richard and a couple of others, and we talked a little bit about what it would look like, and we agreed that a half a million people late to middle age, 45 and above would probably over time when you did the power calculations, give you a pretty good insight in most of the major diseases. And then it was really a question of collecting them and storing the samples. So in order to get it funded at the time I was on the council of the MRC and George Radda, who you may remember, was quite a distinguished NMR physiologist here. He was the chief executive of the MRC. So I approached him and I said, look, George, this would be a great thing for us to do in the UK because we have all the clinical records of these people going back for a decade, and will continue to do that.Sir John Bell (13:01):Of course, we immediately sent it out to a peer review committee in the MRC who completely trashed the idea and said, you got to be joking. So I thought, okay, that's how that lasted. And I did say to George, I said, that must mean this is a really good idea because if it had gone straight through peer review, you would've known you were toast. So anyway, I think we had one more swing at peer review and decided in the end that wasn't going to work. In the end, George to his credit, took it to MRC council and we pitched it and everybody thought, what a great idea, let's just get on and do it. And then the Wellcome came in. Mark Walport was at the Wellcome at the time, great guy, and did a really good job at bringing the Wellcome on board.Sir John Bell (13:45):And people forget the quantum of money we had to do this at the time was about 60 million pounds. I mean, it wasn't astonishly small. And then of course we had a couple of wise people who came in to give us advice, and the first thing they said, well, if you ever thought you were really going to be able to do genetics on 500,000 people, forget it. That'll never work. So I thought, okay, I'll just mark that one out. And then they said, and by the way, you shouldn't assume you can get any data from the health service because you'll never be able to collect clinical data on any of these people. So I said, yeah, yeah, okay, I get it. Just give us the money and let us get on. So anyway, it's quite an interesting story. It does show how conservative the community actually is for new ideas.Sir John Bell (14:39):Then I chaired the first science committee, and we decided about a year into it that we really needed the chief executive. So we got Rory Collins to lead it and done it. I sat on the board then for the next 10 years, but well look, it was a great success. And as you say, it is kind of the paradigm for now, large genetic epidemiology cohorts. So then, as you know, I advise government for many years, and David Cameron had just been elected as Prime Minister. This was in about 2010. And at the time I'd been tracking because we had quite a strong genomics program in the Wellcome Trust center, which I'd set up in the university, and we were really interested in the genetics of common disease. It became clear that the price of sequencing and Illumina was now the clear leader in the sequencing space.Sir John Bell (15:39):But it was also clear that Illumina was making significant advances in the price of sequencing because as you remember, the days when it cost $5,000 to do a genome. Anyway, it became clear that they actually had technology that gets you down to a much more sensible price, something like $500 a genome. So I approached David and I said, we are now pretty sure that for many of the rare diseases that you see in clinical practice, there is a genetic answer that can be detected if you sequenced a whole genome. So why don't we set something up in the NHS to provide what was essentially the beginnings of a clinical service to help the parents of kids with various disabilities work out what's going on, what's wrong with their children. And David had had a child with Ohtahara syndrome, which as you know is again, and so David was very, he said, oh God, I'll tell you the story about how awful it was for me and for my wife Samantha.Sir John Bell (16:41):And nobody could tell us anything about what was going on, and we weren't looking for a cure, but it would've really helped if somebody said, we know what it is, we know what the cause is, we'll chip away and maybe there will be something we can do, but at least you know the answer. So anyway, he gave us very strong support and said to the NHS, can you please get on and do it? Again massive resistance, Eric as you can imagine, all the clinical geneticists said, oh my God, what are they doing? It's complete disaster, dah, dah, dah. So anyway, we put on our tin hats and went out and got the thing going. And again, they did a really good job. They got to, their idea was to get a hundred thousand genomes done in a reasonable timeframe. I think five years we set ourselves and the technology advance, people often underestimate the parallel development of technology, which is always going on. And so, that really enabled us to get that done, and it still continues. They're doing a big neonatal program at the moment, which is really exciting. And then I was asked by Theresa May to build a life science strategy because the UK, we do this stuff not as big and broad as America, but for a small country we do life sciences pretty well.Eric Topol (18:02):That's an understatement, by the way. A big understatement.Sir John Bell (18:04):Anyway, so I wrote the strategies in 2017 for Theresa about what we would do as a nation to support life sciences. And it was interesting because I brought a group of pharma companies together to say, look, this is for you guys, so tell us what you want done. We had a series of meetings and what became clear is that they were really interested in where healthcare was going to end up in the next 20 years. And they said, you guys should try and get ahead of that wave. And so, we agreed that one of the domains that really hadn't been explored properly, it was the whole concept of prevention.Sir John Bell (18:45):Early diagnosis and prevention, which they were smart enough to realize that the kind of current paradigm of treating everybody in the last six months of life, you can make money doing that, there's no doubt, but it doesn't really fix the problem. And so, they said, look, we would love it if you created a cohort from the age of 18 that was big enough that we could actually track the trajectories of people with these diseases, identify them at a presymptomatic stage, intervene with preventative therapies, diagnose diseases earlier, and see if we could fundamentally change the whole approach to public health. So we anyway, went back and did the numbers because of course at much wider age group, a lot of people don't get at all sick, but we thought if we collected 5 million people, we would probably have enough. That's 10% of the UK adult population.Sir John Bell (19:37):So anyway, amazingly the government said, off you go. We then had Covid, which as you know, kept you and I busy for a few years before we could get back to it. But then we got at it, and we hired a great guy who had done a bit of this in the UAE, and he came across and we set up a population health recruitment structure, which was community-based. And we rapidly started to recruit people. So we've now got 2.9 million people registered, 2.3 million people consented, and we've got blood in the bank and all the necessary data including questionnaire data for 1.5 million people growing up. So we will get to 5 million and it's amazing.Eric Topol (20:29):It is. It really is, and I'm just blown away by the progress you've made. And what was interesting too, besides you all weren't complacent about, oh, we got this UK Biobank and you just kept forging ahead. And by the way, I really share this importance of finally what has been a fantasy of primary prevention, which never really achieved. It's always, oh, after a heart attack. But that's what I wrote about in the Super Agers book, and I'll get you a copy.Sir John Bell (21:02):No, I know you're a passionate believer in this and we need to do a lot of things. So we need to work out what's the trial protocol for primary prevention. We need to get the regulators on board. We've got to get them to understand that we need diagnostics that define risk, not disease, because that's going to be a key bit of what we're going to try and do. And we need to understand that for a lot of these diseases, you have to intervene quite early to flatten that morbidity curve.Eric Topol (21:32):Yeah, absolutely. What we've learned, for example, from the UK Biobank is not just, of course the genomics that you touched on, but the proteomics, the organ clocks and all these other layers of data. So that gets me to my next topic, which I know you're all over it, which is AI.Eric Topol (21:51):So when I did the NHS review back in 2018, 2019, the group of people which were amazing that I had to work with no doubt why the UK punches well beyond its weight. I had about 50 people, and they just said, you know what? Yeah, we are the world leaders in genomics. We want to be the world leader in AI. Now these days you only hear about US and China, which is ridiculous. And you have perhaps one of the, I would say most formidable groups there with Demis and Google DeepMind, it's just extraordinary. So all the things that the main foci of the Ellison Institute intersect with AI.Sir John Bell (22:36):They do. And we, we've got two underpinning platforms, well actually three underpinning platforms that go across all those domains. Larry was really keen that we became a real leader in AI. So he's funded that with a massive compute capacity. And remember, most universities these days have a hard time competing on compute because it's expensive.Eric Topol (22:57):Oh yeah.Sir John Bell (22:58):So that is a real advantage to us. He's also funded a great team. We've recruited some people from Demis's shop who are obviously outstanding, but also others from around Europe. So we really, we've recruited now about 15 really outstanding machine learning and AI people. And of course, we're now thinking about the other asset that the UK has got, and particularly in the healthcare space is data. So we do have some really unique data sets because those are the three bits of this that you need if you're going to make this work. So we're pretty excited about that as an underpinning bit of the whole Ellison Institute strategy is to fundamentally underpin it with very strong AI. Then the second platform is generative biology or synthetic biology, because this is a field which is sort of, I hesitate to say limped along, but it's lacked a real focus.Sir John Bell (23:59):But we've been able to recruit Jason Chin from the LMB in Cambridge, and he is one of the real dramatic innovators in that space. And we see there's a real opportunity now to synthesize large bits of DNA, introduce them into cells, microbes, use it for a whole variety of different purposes, try and transform plants at a level that people haven't done before. So with AI and synthetic biology, we think we can feed all the main domains above us, and that's another exciting concept to what we're trying to do. But your report on AI was a bit of a turning point for the UK because you did point out to us that we did have a massive opportunity if we got our skates, and we do have talent, but you can't just do it with talent these days, you need compute, and you need data. So we're trying to assemble those things. So we think we'll be a big addition to that globally, hopefully.Eric Topol (25:00):Yeah. Well that's another reason why I am so excited to talk to you and know more about this Ellison Institute just because it's unique. I mean, there are other institutes as like Chan Zuckerberg, the Arc Institute. This is kind of a worldwide trend that we're seeing where great philanthropy investments are being seen outside of government, but none have the computing resources that are being made available nor the ability to recruit the AI scientists that'll help drive this forward. Now, the last topic I want to get into with you today is one that is where you're really grounded in, and that's the immune response.Eric Topol (25:43):So it's pretty darn clear now that, well, in medicine we have nothing. We have the white cell neutrophil to lymphocyte ratio, what a joke. And then on the other hand, we can do T and B cell sequencing repertoires, and we can do all this stuff, autoantibody screens, and the list goes on and on. How are we ever going to make a big dent in health where we know the immune system is such a vital part of this without the ability to check one's immune status at any point in time in a comprehensive way? What are your thoughts about that?Sir John Bell (26:21):Yeah, so you seem to be reading my mind there. We need to recruit you over here because I mean, this is exactly, this is one of our big projects that we've got that we're leaning into, and that is that, and we all experienced in Covid the ins and outs of vaccines, what works, what doesn't work. But what very clear is that we don't really know anything about vaccines. We basically, you put something together and you hope the trial works, you've got no intermediate steps. So we're building a really substantial immunophenotyping capability that will start to interrogate the different arms of the immune response at a molecular level so that we can use a combination of human challenge models. So we've got a big human challenge model facility here, use human challenge models with pathogens and with associated vaccines to try and interrogate which bits of the immune response are responsible for protection or therapy of particular immunologically mediated diseases or infectious diseases.Sir John Bell (27:30):And a crucial bit to that. And one of the reasons people have tried this before, but first of all, the depth at which you can interrogate the immune system has changed a lot recently, you can get a lot more data. But secondly, this is again, where the AI becomes important because it isn't going to be a simple, oh, it's the T-cell, it's going to be, well, it's a bit of the T cells, but it's also a bit of the innate immune response and don't forget mate cells and don't forget a bit of this and that. So we think that if we can assemble the right data set from these structured environments, we can start to predict and anticipate which type of immune response you need to stimulate both for therapy and for protection against disease. And hopefully that will actually create a whole scientific foundation for vaccine development, but also other kinds of immune therapy and things like cancer and potentially autoimmune disease as well. So that's a big push for us. We're just busy. The lab isn't set up. We've got somebody to run the lab now. We've got the human challenge model set up with Andy Pollard and colleagues. So we're building that out. And within six months, I think we'll be starting to collect data. So I'm just kind of hoping we can get the immune system in a bit more structured, because you're absolutely right. It's a bit pin the tail on the donkey at the moment. You have no idea what's actually causing what.Eric Topol (29:02):Yeah. Well, I didn't know about your efforts there, and I applaud that because it seems to me the big miss, the hole and the whole story about how we're going to advanced human health and with the recent breakthroughs in lupus and these various autoimmune diseases by just targeting CD19 B cells and resetting like a Ctrl-Alt-Delete of their immune system.Sir John Bell (29:27):No, it's amazing. And you wouldn't have predicted a lot of this stuff. I think that means that we haven't really got under the skin of the mechanistic events here, and we need to do more to try and get there, but there's steady advance in this field. So I'm pretty optimistic we'll make some headway in this space over the course of the next few years. So we're really excited about that. It's an important piece of the puzzle.Eric Topol (29:53):Yeah. Well, I am really impressed that you got all the bases covered here, and what a really exhilarating chance to kind of peek at what you're doing there. And we're going to be following it. I know I'm going to be following it very closely because I know all the other things that you've been involved with in your colleagues, big impact stuff. You don't take the little swings here. The last thing, maybe to get your comment, we're in a state of profound disruption here where science is getting gutted by a madman and his henchmen, whatever you want to call it, which is really obviously a very serious state. I'm hoping this is a short term hit, but worried that this will have a long, perhaps profound. Any words of encouragement that we're going to get through this from the other side of the pond?Sir John Bell (30:52):Well, I think regardless of the tariffs, the scientific community are a global community. And I think we need to remember that because our mission is a global mission, and we need to lean into that together. First of all, America is such a powerhouse of everything that's been done scientifically in the human health domain. But not only that, but across all the other domains that we work in, we can't really make the kind of progress that we need to without America being part of the agenda. So first of all, a lot of sympathy for you and your colleagues. I know it must be massively destabilizing for you, not be confident that the things that work are there to help you. But I'm pretty confident that this will settle down. Most of the science is for, well, all the science is really for public good, and I think the public recognizes it and they'll notice if it's not being prosecuted in the way that it has to be. And the global science community cannot survive without you. So we're all leaning in behind you, and I hope it will settle. One of my worries is that these things take years to set up and literally hours or minutes to destroy. So we can't afford to take years to set them back up again. So we do need to be a bit careful about that, but I still have huge confidence in what you guys can achieve and we're all behind you.Eric Topol (32:37):Well, that's really helpful getting some words of wisdom from you there, John. So this has been terrific. Thanks so much for joining, getting your perspective on what you're doing, what's important is so essential. And we'll stay tuned for sure.Sir John Bell (32:59):And come and visit us at the EIT, Eric. We'd be glad to see you.*******************************Some of the topics that John and I discussed—immunology, A.I., genomics, and prevention—are emphasized in my new book SUPER AGERS. A quick update: It will have a new cover after making the New York Times Bestseller list and is currently ranked #25 for all books on Amazon. Thanks to so many of you for supporting the book!Here are a few recent podcasts:Dax Shepard: Dr. Mike Sanjay Gupta ***********************Thanks for reading and subscribing to Ground Truths.If you found this interesting please share it!That makes the work involved in putting these together especially worthwhile.All content on Ground Truths— newsletters, analyses, and podcasts—is free, open-access.Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don't hesitate to post comments and give me feedback. Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. Get full access to Ground Truths at erictopol.substack.com/subscribe

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

Acompáñanos en este programa en el que hablamos sobre el 100 aniversario de la Liga Mexicana de beisbol, sobre como van el standing y juegos en la LMB

En este episodio platicamos sobre el Draft de NFL, la rivalidad Diablos Tigres en los 100 años de la LMB y más.

En Italia los partidos regresan y en la Copa habrá un Derby entre Inter y Milán. Real Madrid recupera a Kylian Mbappe. Diablos Rojos del México se llevan la Guerra Civil de la LMB.

Iniciamos con la "Serie: 100 AÑOS DE LIGA MEXICANA DE BÉISBOL", en esta primera entrega abordamos las primeras catedrales del beisbol mexicano, así como algunos de los momentos que marcaron al béisbol de la LMB, en el Parque Franco Ingles, el Parque Delta y el Parque Deportivo del Seguro Social.Dime, te toco ir al Parque Deportivo del Seguro Social o al Parque Delta? Déjame tu opinión en la caja de comentarios

Friend, this topic is SO important I'm putting it back in front of you again. Here's the deal: Even people in strong, satisfying relationships can develop feelings of attraction for another person. It's part of the human experience. These feelings can be transient and meaningless... OR they could destroy your life, if you follow them.  Are crushes innocent, or on-ramps to an affair? Can you be "friends" with someone you have a crush on, without risking your relationship? What should you do when you're married, but have a crush on someone else? Oh, the questions! It happens: people in happy, healthy, committed relationships can still develop crushes on others. However, smart, self-aware people in committed relationships that they care about need to handle these maturely and with wisdom. That's what you'll learn how to do on today's show. We'll discuss:  The mechanics of a crush; how and why crushes develop The difference between a crush and a platonic friendship Why happy, committed married people can have crushes on others How crushes can turn into something more serious How to use self awareness, integrity, and honesty to protect your marriage How to use your crush experience in order to add energy and intimacy into your relationship Warning signs that your crush is developing into something else Why extramarital affairs are always a bad idea, and rarely end well How to stop having a crush on someone else How to avoid embarrassment and professional ruin if you have a crush on a coworker How to protect your relationship and stay true to your values even when you're having feelings for another. All this and more on today's episode of the Love, Happiness and Success Podcast. xoxo, Dr. Lisa Marie Bobby GrowingSelf.com Ps: As we discussed in this episode, part of your action plan needs to be leaning towards your partner in an authentic and emotionally intimate way, and that calls for excellent communication skills. To support you in this, please help yourself to my free two part communication skills training, "Communication That Connects." I made this for you!  ... LMB

El presidente saliente de los Olmecas de Tabasco, Gonzalo Medina González, resume su gestión al frente del equipo. ¿Se va satisfecho? ¿Cuáles fueron sus principales logros y sus momentos de crisis más significativos? Afirma que por logros, la franquicia vale 3 ó 4 veces más, que cuando lo asumió. Habla de las finanzas que heredará, incluidos 14 mdp en patrocinios firmados para 4 años. Ventila que a partir de octubre, participará como coordinador de festejos de los 100 años de la LMB.

En LMB siempre grabamos con escaladores con los que conectamos, y con Roberto esto fue muy fácil. Rápidamente nos dimos cuenta que Roberto trae un cotorreo elevado, sus ganas por escalar se desbordan, la pasión que le tiene a al escalada creemos que es inspiradora y probablemente su trabajo llegará muy lejos en los próximos años. Escucha a Roberto contarnos acerca de sus proyectos, zonas a desarrollar, motivación, personas con las que ha colaborados, marcas que lo apoyan y más. Este episodio viene cargado de bastantes saludos a personas que de alguna manera han inspirado o ayudado a LMB. Gracias!

Are Gen X Parents Ruining Retirement by Supporting Their Adult Children?In this episode, Dr. Preston Cherry delves into the critical issue of whether Gen X parents are jeopardizing their own retirement by financially supporting their adult children.By providing practical advice and discussing expert data, he equips parents with the tools to make informed decisions and set healthy financial boundaries.Want to learn more? Connect with us below! Dr. Preston D. Cherry on LinkedIn: https://www.linkedin.com/in/drprestoncherry/Dr. Preston D. Cherry's Website: https://www.drprestoncherry.com/Get your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website: https://concurrentfp.com

In this episode, Dr. Preston D. Cherry delves into the intricacies of moving your 401k after leaving your job, featuring expert insights from Dr. Philip Gibson, a seasoned wealth advisor and chief compliance officer at Concurrent Financial Planning.Together, they explore both direct and indirect transfers of employer-sponsored plans, providing clarity on the 60-day rule and the potential 20% tax hit if funds are not moved accordingly.Want to learn more? Connect with us below! Dr. Preston D. Cherry on LinkedInDr. Preston D. Cherry's WebsiteDr. Philip Gibson on LinkedInGet your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website: https://concurrentfp.com

Listen on your favorite podcast service: https://pods.to/wesoundcrazy Stream songs from the episode on our official We Sound Crazy playlists: https://lnkfi.re/8I8Drkfz This week, we're thrilled to have the multi-talented Avery*Sunshine as our special guest. With hits like “Call My Name” and “With You,” Avery has captivated audiences worldwide, earning critical acclaim and a loyal fan base. Her music, celebrated for its blend of soul, gospel, and R&B, has received praise from critics and peers alike, showcasing her extraordinary vocal talent and genuine artistry. And to top it off, she truly is a burst of sunshine! Join the We Sound Crazy crew for a truly great episode with the one and only, Avery*Sunshine. Don't wait, press play now! Hey, We Sound Crazy listeners! We're thrilled to share a special treat from the incredible Avery*Sunshine! To celebrate her recent episode on our podcast, Avery is offering an exclusive discount on her Lou*Mack Beauty beauty product line just for you! Use Code: SUNSHINEWEIRDOS for 25% OFF your entire purchase! Don't miss out on this chance to pamper yourself with Avery's luxurious beauty products. From radiant skincare to must-have cosmetics, LMB has everything you need to shine bright and feel fabulous! We Sound Crazy is your backstage pass to all things music and culture. Special thanks to our We Sound Crazy team! Director: Aaron Walton Camera Op: Tiffany Young, Aaron Walton Editing: Lamont Baldwin Producer: Michael "Roux" Johnson Assistant: Brittany Guydon PA: Bryan Bell, Aaron Walden Thank you to all of our listeners, as well as our partners at Visit Music City.   Special thanks to Avery*Sunshine! Subscribe to We Sound Crazy on Spotify, Apple Podcasts, and anywhere you get your favorite podcast.  Follow us on Twitter, Instagram, Facebook, YouTube, and TikTok! Follow We Sound Crazy on Social Media: ~ Facebook: https://wesoundcrazy.ffm.to/wscfacebook ~ Instagram: https://wesoundcrazy.ffm.to/wscinstagram ~ Twitter: https://wesoundcrazy.ffm.to/wsctwitter ~ TikTok: https://wesoundcrazy.ffm.to/wsctiktok ~ Email: https://ffm.link/wsc-signup Subscribe to We Sound Crazy on YouTube: https://wesoundcrazy.ffm.to/wscyoutube-subscribe Visit the official We Sound Crazy website: https://wesoundcrazy.ffm.to/officialwebsite #WeSoundCrazy #Avery*Sunshine Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode, Dr. Preston D. Cherry provides a comprehensive exploration into the world of luxury hotels, addressing the perennial question: Are luxury hotels worth it?  He delves into the critical alignment between personal finances and the value luxury accommodations bring to one's travel experience. Dr. Cherry offers clear and practical insights into the costs, benefits, and personal factors involved in choosing luxury accommodations.Want to learn more? Connect with us below! Dr. Preston D. Cherry on LinkedIn: https://www.linkedin.com/in/drprestoncherry/Dr. Preston D. Cherry's Website: https://www.drprestoncherry.com/Get your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website: https://concurrentfp.com

In this episode, Dr. Preston D. Cherry breaks down the true meaning of wealth, going beyond the numbers. He sheds light on how understanding and managing wealth can improve our quality of life by aligning financial and personal goals. Listen in for practical advice and a realistic view on how to use your financial resources to thrive in all areas of life.Want to learn more? Connect with us below! Dr. Preston D. Cherry on LinkedInDr. Preston D. Cherry's WebsiteGet your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website.

Join Dr. Preston D. Cherry and Dr. Renée Baker, as they dive deep into how aligning your life goals with smart financial planning can lead to true fulfillment. This episode is packed with valuable lessons on the importance of building strong relationships, being financially prepared, and keeping a growth mindset. Together, they inspire you to create a life where your dreams and finances thrive in perfect harmony.Want to learn more? Connect with us below! Dr. Renée Baker on LinkedIn.Dr. Renée Baker's WebsiteDr. Preston D. Cherry on LinkedIn Dr. Preston D. Cherry's Website Get your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website.

Got a bonus check that feels smaller than expected? Don't worry, you're not alone! In this episode, Dr. Preston Cherry explores why bonus checks often feel like they're taxed more heavily than regular paychecks and shares practical strategies to mitigate the tax impact.Want to learn more? Connect with us below!Dr. Preston D. Cherry on LinkedIn.Dr. Preston D. Cherry's Website.Get your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website.

Cristy es una escaladora llena de una energía contagiosa. Su habilidad para encadenar rutas duras es demasiado alta. La manera en la que nos describe sus mas recientes ascensos, viajes y estilo de vida, hacen de este episodio uno muy inspirador. Escucha a esta titana con cuerpo de acero en LMB. Seguramente te vas a motivar. --- Send in a voice message: https://podcasters.spotify.com/pod/show/la-mera-beta-podcast/message

Join Dr. Preston D. Cherry and Josh Brown, as they talk about the multifaceted relationship between wealth, spending habits, and time management. Through engaging anecdotes and practical advice, Dr. Cherry and Josh Brown encourage listeners to rethink their approach to wealth, time, and overall well-being.Want to learn more? Connect with us below! Josh Brown on LinkedIn.Dr. Preston D. Cherry on LinkedIn.Dr. Preston D. Cherry's Website.Get your free wealth assessment! Visit our website for more insights and personalized guidance. Click here to go to our website.

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

Join Dr. Preston D. Cherry and Danielle Miura, as they delve into the critical topic of long-term care conversations with loved ones. Plus, they break down the intricacies involved in navigating long-term care, from which topics to discuss to the financial implications of different care levels, such as in-home care and nursing homes. Want to learn more? Connect with us below! Danielle Miura on LinkedIn.Dr. Preston D. Cherry on LinkedIn.Dr. Preston D. Cherry's Website.Ready to explore these tax planning strategies for financial acceleration? Visit our website for more insights and personalized guidance. Click here to go to our website.

En el Deportres de hoy: Draft de NFL , acción en la postemporada de la NBA, todo el béisbol de LMB y de MLB , La Fecha 17 LIGA MX y tu participación y ¡mucho mas! www.deportres.com --- Support this podcast: https://podcasters.spotify.com/pod/show/deportres/support

Toros de Tijuana arranco con derrota su serie contra Charros de Jalisco en LMB. Además ayer se inauguró un estadio y se completó un ciclo en la jornada de martes

Diez juegos para hoy en LMB y todos los detalles están aqui en Círculo de Espera con los Toros de Tijuana enfrentando a Charros de Jalisco

Toros de Tijuana ganaron su serie de visita el domingo en un día en el que Trevor Bauer hizo historia en LMB

Recorded- April 17/18, 2024   Uploaded- April 20, 2024   We look at some new developments in Oakland and the development plan in the American Association. A conversation on new LMB rules and some happenings in the state of NJ. Included an interview with NY Boulders head scout Kevin Tuve.

Tijuana con la mejor asistencia en seris inaugural de LMB y de paso barrieron a Laguna. Sdemás le contaremos del visitante distinguido del jueves en el Estadio Chevron.

Ya sólo hay un invicto en LMB y le diremos de quien se trata con toda la actividad de la jornada de miércoles en la pelota mexicana de este lado de la frontera y del otro.

Hoy Toño de y Enrique nos hablaron de lo que se viene en los playoffs de la NBA además del posible récord que se pueda romper en el Draft de la NFL, además los Diablos arrancan con paso perfecto la temporada de la LMB.

Toda la información de las primeras jornadas de LMB y la fiesta que se viene mañana con los Toros de TIjuana en el Estadio Chevron

¿Cuántos jugadores nacidos en México aparecen en los rosters de los veinte equipos de LMB? ¿Qué equipos tienen a más nacidos en México y quiénes menos?

We workshop the LMB acronym to account for the Mexican League signing players of questionable character. We aren't just yanking Verdugo's chain, we are teaching you valuable vocabulary in multiple languages. We review your four options when you catch a home run ball during a game, starting with It Belongs To You. A little over a week in and our guys with slow starts are getting the bats in gear. We've got home runs bouncing off gloves and walls, we've got new nicknames (Turn and Burn O'Hearn!), and platelet infusions. Elly impresses off the field too, conducting his first press conference all in English. Wish wish Stephen Strasburg well on his retirement and as Nats fans we thank him for his service. Pottymouth turns our attention to Baseball United, the Dubai-based program that is attracting lots of attention and dollars from former MLB greats, and now Ronald Acuña Jr as well.  We remain suspicious. Shane and Spencer, just this Saturday, join the ranks of seriously injured pitchers and the MLBPA and MLB argue over the role of the pitch clock in all of this. Compton's MLB Youth Academy hosts the BFA Women's College Club Baseball Championships. Patti and Pottymouth got up early Saturday morning to make friends with Yankee fans for an important cause.  We participated in a live stream marathon “Pinstripes for a Cause” to help raise money for the World Parkinson Coalition. If you want to see us on coffee instead of craft beer, we start at 1:30 into the stream. Please consider adding your donation and add “Pinstripes for a Cause” or No Crying in Baseball to the notes.We say, “That's a Darwin test,” “One set of biceps was more productive than the other,” and “Is he pulling one of your six chains?” Fight the man, send your game balls to Meredith, get boosted, and find us on Twitter @ncibpodcast, on Facebook @nocryinginbball, Instagram @nocryinginbball and on the Interweb at nocryinginbball.com. Please take a moment to subscribe to the show, and leave us a review on Apple Podcasts or wherever you listen to NCiB. Become a supporter at Patreon to help us keep doing what we do. Say goodnight, Pottymouth.

LMB 62: Memeros en la escalada. ft. Climber.fresa Elgam.berro Los memes tienen un aporte cultural importante; el humor se emplea para expresar temas dentro de un nicho específico. En nuestra comunidad de escaladores, encontramos tanto aspectos positivos como negativos. Afortunadamente, estas cuentas de memes están aquí para resaltar situaciones de una manera diferente, utilizando la sátira, la astucia y la burla. Estos creadores de memes ya tienen un peso significativo dentro de la comunidad. Escucha a Climber.fresa y a Elga.mberro mientras comparten su trayectoria en la escalada y en el mundo de los memes relacionados con este deporte --- Send in a voice message: https://podcasters.spotify.com/pod/show/la-mera-beta-podcast/message

Are you hiding financial secrets from your partner? If you are, you're not alone. A new study finds that about 42% of couples admit to keeping secrets about money; that's almost half of all couples! This week, I sat down with Dr. Michael Thomas, Ph.D., AFC®, to discuss the often-overlooked issue of fiscal secrecy and its impact on relationships. A sneaky ice cream trip with the kids can sometimes become more than just a sweet treat, creating a pattern of behaviors detrimental to the relationship. Unveiling the reasons behind people's financial actions, this episode with Dr. Thomas offers a guide out of the shadows of monetary mistrust.Want to hear more from Dr. Michael Thomas? Dr. Michael Thomas on LinkedIn Dr. Michael Thomas on XDr. Michael Thomas on Instagram Dr. Michael Thomas's book on Black Financial Culture Ready to explore these tax planning strategies for financial acceleration? Visit our website for more insights and personalized guidance.Download your FREE guide: 10 Questions to Discover Your Money Mind, Aspirations & FreedomSubscribe to Life Money Balance® YouTube for content beyond the podcastDiscover a client relationship. Schedule a FREE, 20-minute Good Fit MeetingConnect with us across social media for more content - top right cornerFind your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Today, we're not just crunching numbers; we're delving into the neuroscience behind your spending habits, as Dr. Alex Melkumian helps illuminate the chemical reactions like cortisol and oxytocin that drive our financial behaviors. From identifying emotional triggers to understanding money scripts shaped by our past, this conversation is a deep dive into aligning the heart and mind for smarter financial decisions. And as always, we remind you that while we're here to educate and inspire, nothing beats tailored advice from a financial professional when it comes to your personal money matters.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

This week, we sit down with Don Graves, to have a discussion about retirement income planning. As we unravel the complexities of reverse mortgages, you'll discover the transformative potential these tools hold for your golden years. From debunking long-held myths to highlighting the modern applications of this misunderstood financial instrument, we dive into the heart of managing wealth when the traditional working years are behind you.This episode isn't just about presenting options; it's about equipping you with knowledge to make informed decisions in partnership with expert advisors, ensuring that your retirement planning is as robust and secure as possible.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Embark on a transformative journey with us as we explore the impact of positive psychology on financial resolutions, guided by the insightful expertise of Ashley Quamme. Discover how a shift in mindset, from mere goal-setting to embracing well-being and purpose, can turn your New Year's aspirations into reality. You'll learn the significance of writing down intentions for enhanced clarity and success, and why understanding the profound interplay between emotions and financial security is crucial for happiness. This episode promises to illuminate your path to financial well-being with the enlightening principles of positive psychology.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

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

Ever found yourself pondering whether to place your hard-earned cash into that one golden stock or to play it safe across the board? Join me, Dr. Preston Cherry, as we navigate the treacherous yet potentially lucrative waters of concentration risk in investment portfolios. Discover why betting big on a single sector, like tech, or diversifying your stakes among the vast sea of the S&P 500 can each steer your financial ship towards vastly different horizons.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Joining us on our latest episode is Charles H. Cherry Jr., my father, who brings a treasure trove of insights on how to gracefully glide into retirement. He and my mom have navigated the financial seas with a keen eye on their 401K and emergency funds, charting a course to a retirement filled with exploration, hobbies, and the luxury of time unbound by the nine-to-five. Through their story, we unearth the critical steps for financial security and the personal philosophies that have made their transition not just a mere change of pace, but an adventure in its own right.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Ever grappled with the discomfort that creeps in when checking your bank account? You're not alone. Pull up a chair as Dr. Preston Cherry, join forces with the remarkable Aja Evans to unravel the tangled web of emotions that underpin our financial behaviors. This meeting of minds on Life Money Balance goes beyond dollars and cents to address the psychological weight of money shame—a burden that knows no tax bracket. Prepare to have your eyes opened to the universal truths of financial emotions and the steps you can take to foster resilience and a healthier bank account.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Are you ready to finally feel confident about your financial future? Let's dive into one of the most critical cornerstones of secure retirement planning - the Secure Act 2.0. We're breaking it down into four key ways in which this act can revolutionize your retirement strategy, particularly if you're a Gen Xer. From securing higher contribution rates to employer-sponsored retirement plans and aligning money with life goals to leveraging the Internal Revenue Code for financial planning, we're giving you the tools to navigate your journey towards financial security.>>Download your FREE guide: 10 Questions to Discover Your Money Mind, >>Aspirations & Freedom>>Subscribe to Life Money Balance® YouTube for content beyond the podcast>>Discover a client relationship. Schedule a FREE, 20-minute Good Fit Meeting>>Connect with us across social media for more content - top right corner>>Find your story & learn about services that fit your journeyThank you for tuning in; we hope the information is educational and valuable. Remember to like and subscribe to the LMB® channel. We appreciate you. Listen to the disclaimer at the end of the show.#lifemoneybalance, #financialfreedom, #retirement, #aspiration, #wellbeing, #wealthbuiding, #wealth, #financialwellness, #compassion, #financialeducation

Hoy Enrique Burak, Pepe Segarra y Toño de Valdés nos hablaron de lo mejor de la semana 13 de la NFL además de los pronósticos de la semana 14. Pepe Segarra trajo a toda la pandilla de la mítica caricatura de “Don Gato”.

Hoy Toño de Valdés, Enrique Burak y Pepe Segarra nos hablaron de lo mejor de la semana 10 de la NFL además de los pronósticos de la semana 11 también lo mejor de la inducción al salón de la fama de la LMB, cómo se vivió la NBA en México y en el Baúl de Pepe nos llevamos una grata sorpresa.

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