Q&A with Eric and Brianna

In the final episode of season 3 we answer your biggest aging questions, from whether there is a single root cause of aging to why different organs fail in different ways. We also dig into what it would take to run human trials that prove real healthspan gains while staying honest about biomarkers, animal data, and online misinformation.

Eric Verdin, MD and Brianna Stubbs, PhD

Dr. Eric Verdin is President and CEO of the Buck Institute for Research on Aging and an internationally recognized physician-scientist whose research focuses on the molecular mechanisms of aging, metabolism, and the immune system. A native of Belgium, he earned his medical degree from the University of Liege and completed additional clinical and research training at Harvard Medical School. He has published more than 300 scientific papers, holds 18 patents, and is a member of several prestigious scientific organizations.

Dr. Brianna Stubbs is a Lead Translational Scientist at the Buck Institute and a world expert in exogenous ketone metabolism and its implications for performance, resilience, and healthy aging. She earned her PhD in metabolic physiology from the University of Oxford and is also a two-time world champion lightweight rower who competed on the British International Rowing Team.

Together, Drs. Verdin and Stubbs serve as co-hosts of Season 3 of the Live Better Longer podcast, bringing their expertise and passion for longevity science to conversations with leading researchers, clinicians, and innovators in the field of healthy aging.

Transcript

Welcome And Audience Q&A Setup

Eric Verdin 0:09

Hi, how are you, Brianna?

Brianna Stubbs 0:11

Doing well. Good to see you today.

Eric Verdin 0:12

Yes, we decided to do something a little different today, which is we get quite a few questions from our audiences and uh would love to be responsive to what all of you are wondering about the uh aging space is so the this is the first of uh what I hope will be many QA uh sessions uh between the two of us.

Brianna Stubbs 0:32

Yeah I have to say uh I got the list of questions and uh you know some of these questions if we knew the answers, then you and I would be out of work already. So some of them are some of them are pretty big questions, but I'm sure I'm sure we'll do our best to answer as many as we can and and um you know highlight where there's still a lot more work to be done, and and that's what you and I will be working on, I guess, the next few years here at the Buck. So um why don't you let me kick off here with one of these questions? So um why don't we start with perhaps perhaps the biggest one?

Is There One Cause Of Aging

Brianna Stubbs 1:00

With all of the different hallmarks and theories of aging, do you think that there is one single upstream cause of aging across all tissues? Or could different tissues age for fundamentally different reasons? And and that big old question is from Kyle.

Eric Verdin 1:14

That's a actually a a top question. Everyone loves um simple mechanism, one thing that explains everything. And in some cases, um, you know, it it has happened. Sometimes science provides an a model, a theory that just explains everything. Rarely though, uh and certainly not in the case of aging. Um I'll speak about two different aspects. One is um aging is pleomorphic, it is induced by a whole variety of mechanistic problems, what we call the hallmarks of aging. Um I do not believe there's a single cause of aging, and and therefore I do not believe there will be a single treatment against aging. So uh I hope I'm not bursting anybody's bubble. Uh you will hear some colleagues you know tout their theories as if it were explaining everything. And we've heard about this the epigenetic theory of aging, the stem cell theory of aging, uh oxidative stress theory of aging. I think I I do think about aging as a pleomorphic problem with multiple issues that we will have to solve over the long term.

Brianna Stubbs 2:26

So I heard um Nir Barzelai, I think it was, speak recently, and um it was it was he or someone other, you know, some other luminary in the space. And um, every time you go to an aging conference, there's that one slide with all of the hallmarks of aging placed in a circle, and everyone uses this slide. And they made the comment that it had to be a circle because nobody could be in the middle, because they're all interconnected, and it's not possible to pick one isolate one that isn't having some effects on the other. So um I think that idea of geroscience, which was of course, you know, founded and conceived by scientists who were here at the buck when it started 25 years ago, is that rather than just be one root cause, everything's interconnected, and rather than just have one treatment that will target one pathway that will, you know, fix aging, we're it by the very nature of the problem, it's all interlinked and modulating one pathway is gonna benefit others. So um, yeah, I think I agree with you that it would be nice if there was a magic bullet and maybe one pathway would emerge as the dominant one, but based on what we can see now, it's too intercollect, too interconnected, too complicated to be kind of so simply distilled.

Geroscience And The Big Unifying Idea

Eric Verdin 3:31

Exactly. I totally agree with this. There's one other aspect where there's a unification process that's happening, which I think is is important for the audience to know. And I'll make the analogy to what happened in the 1800s. There people were dying mostly from infectious diseases. You had cholera, you had uh bubonic plague, all of these horrible diseases, uh, pneumonia, people were essentially dying about 90% from infectious diseases. What happened in in 1850 to 1900 is the realization there were microbes. And these microbes provided a unification because many of these diseases were driven by distinct microbes, tuberculosis, vibrio cholera for cholera. And so there was uh something that came out of the work mostly of Pasteur, which was the germ theory of disease. And I think so that allowed people to really switch the way they were thinking of disease, first looking for an infectious agent, and then this led to penicillin, antibiotics, antivirals, and to essentially not the elimination, but disease of uh of infectious disease origin.

Brianna Stubbs 4:38

A big inflection point in how we thought about it and deal with it.

Eric Verdin 4:41

And and those diseases have mostly been eliminated, not completely, but in the control.

Brianna Stubbs 4:46

They don't they don't kill as many people as they used to.

Eric Verdin 4:48

No. And they're now we've replaced this by a whole series of other diseases that we are looking in the same way. Heart attacks, stroke, many forms of cancers, type 2 diabetes, and all of these diseases are driven by one single major factor, which is aging. And so we are, this is something called the geroscience hypothesis, comes out of the Buck Institute's work. And I think my prediction is that 100 years from now, we will look back at this period as saying this is the time when they realize all of these diseases that were treated as independent occurrences, what I call wacamole medicine, were actually driven by the aging process. So this is where I think the juroscience revolution is going to be taking place.

Why Different Organs Age Differently

Eric Verdin 5:32 Brianna Stubbs 5:32

Yeah, I'd kind of um love to take a time machine forward and look back at that now. Um I want to pull a bit more on this last second piece of this question, which is about different tissues aging for different reasons. That seems like there could be something there. You know, we know that there's say more uh protein misfolding, say, in the brain, um, and more, you know, different types of changes that happen in the aging immune system. So, you know, is there is there more you can say about without there being one ring to rule them all, as far as it goes with a hallmark that drives all of aging, are there processes that dominate in different tissues?

Eric Verdin 6:06

Absolutely. And I think we just talked about the idea that aging is a major risk factor for all of these diseases, but clearly not everybody is getting every one of these diseases. You see, one person will get a heart attack, another one will get uh COPD, another one will get macular degeneration. And the reason for this is uh is twofold. One is each organ has a series of frailty points. Obviously, if you're smoking, uh you're gonna be causing local problems in the lung, so you'll be more likely to have lung cancer. So the um so each organ has a unique set of frailty points that are influenced both by your genetics and if you're high cholesterol genetically, or if you're eating a pro diet or not exercising. So um, that being said, now we're at the stage where we can actually measure aging in specific organs. And I think that's going to be allowing to determine for each individual's what are your frailty points, what should be watching for in your case? And that in your case is determined sometimes by lifestyle factors, some other times by genetic factors.

Brianna Stubbs 7:13

I think you had um on this on this podcast series, we had a conversation with Tony Wiskori, and he's been developing organ-specific aging clocks based on blood measurements, right? Proteomic measurements that that um flag up which proteins might have come from and indicate damage or aging in specific organs. Is that does that relate to this kind of concept?

Eric Verdin 7:34

Absolutely. So the the the you've all heard about these biomarker, these clocks that allow you to measure aging. Um one big area of progress in the last couple of years, including from our our own institute, David Furman, has generated some new organ-specific clocks, uh, but also the work of Tony Whiskere and his company that he started called Viro. Um I believe there's uh uh Steve Horvat and others, uh Vadim Gladyshev, are all looking at the same aspect. So, how can how can we actually measure aging in individual organs? In each person, can we identify the really frailty points? And also, can we understand aging better? One of the things that came out of Tony's work that we discussed earlier is that when you look at individual organs and you try to determine which of these organs is more predictive of your demise, uh, there are two organs that emerge, the immune system and the central nervous system, which makes sense. They're both distributed organs. So it means we shouldn't most people try to preserve immune aging and um central nervous system

What Counts As Success In Trials

Eric Verdin 8:43

aging. That being said, so here's another question from one of our audience, from Giovanni. So, how should clinical trials measure success in slowing aging?

Brianna Stubbs 8:52

That's that's like the question that I wake up every morning thinking about and go to bed every night thinking about, um, because I think it's um one of the most important questions that those of us who work in clinical geroscience are thinking about right now. Um, you know, and I want the listeners to know that it's not just us thinking about it here at the buck a week or so ago. So, I mean, we were recording this in June, late May, I was um over in DC at an FDA um convention talking to regulators and industry experts about what it would look like, what would how would we know if a treatment or a drug slowed aging in humans? Because there is no regulatory pathway for that. As you mentioned, um, right now, aging is a risk factor for many diseases. The regulatory pathways are focused around getting approvals for a disease and not for the underlying aging biology. So this is this is a huge problem, but it's something that's being addressed currently. Um FDA are interested. Um the XPRIZE Health Span is is um putting in a big effort around communication and consensus building around um endpoints that focus on muscle function, um immune function, and cognitive health. And then also here at Buck and others across the US, we're participating in a program that RPRH is leading, RPRH is the government's health moonshot agency. So again, this is a big audacious, ambitious project, you know, trying to break new ground that hasn't hasn't hasn't been covered before. Um but the goal of this RPRH project is to get the FDA to agree to um an indication for non-disease aging, healthy aging. How would we know, you know, you're you're very well, Eric. You're you know, you're very well, you still ride your bike, you still do hot pilates, you're still, you know, functioning really, really well, but how would we know um you know when things are starting to go awry and could we intervene before you were not well to keep you to keep you functioning as well as you are now?

Eric Verdin 10:39

Actually, not so well today. Not so well today. My immune system is not working so well!

Intrinsic Capacity As A Human Endpoint

Eric Verdin 10:45 Brianna Stubbs 10:45

And so, really, like the central concept here, which I think that the listeners need to, you know, prick perk up their ears and listen about, because I hope that we'll more people will hear more about this in the future, is this concept that the WHO developed called intrinsic capacity. Um was developed in 2015, it's been around a little while. The WHO has enough organizational heft still to you know really um foreground this idea around the world. Um, intrinsic capacity is the sum of all of the capabilities available to you and me to live and enjoy our lives. So it has five sub-domains. Our physical function, can we move around, our cognitive function, can we think and remember, our psychological health? Um, have we got the motivation and the social connections that are you know enriching our lives? Um, our sensory function, can we hear, can we see and engage with our environment? And lastly, um our vitality, which is a little a little bit um less specific, but it kind of speaks to our inflammatory and immune status, our um muscle function, um, you know, muscle and nutritional status um and really underpins um those other kind of emergent properties. So APRH and the FDA and all of these, you know, all these bodies are starting to get together and um think about is intrinsic capacity something that we could measure as a main outcome in clinical studies? That means that the tests that we have to do in clinical studies, it won't just be a simple blood test, although um biospecimens will almost definitely be involved. We'll actually have to um use all of this new technology that we've got, maybe wearable devices, um, as well as um micro-sampling devices so that people can test at home to really pull out um much more granular detail about how people are functioning. So I think that um at this moment there's a regulatory interest in tailwind, there's a technology interest in tailwind with the wearables and our ability to analyze all of the data with AI and machine learning, um, as well as just, you know, enough groundwork been done in the field by yourself, all our colleagues at the buck, um, people who've been thinking about trial design for a while now, that potentially focusing on this retention of function, um, building an adult health curve. So we're all familiar with growth charts in pediatrics, you know, you know where you stand relative to others of at six months, at 12 months, at 18 months. Like, what if we had the same thing for everyone once they hit 40, say, um, and could follow people and say, well, you know, you're in the top 90th percentile for 50-year-olds, or actually, no, you know, you're in the bottom 20th percentile for 60-year-olds. Can we correct that? Could you then go to your doctor and they could give you some agent that's specifically targeted at geroscience to keep you aging better? So I hope that's where the future will go. It combines biomarkers with functional endpoints. Something I heard the FDA say a lot was they really care about how people feel, function, and survive. Um, and I was kind of encouraged by the idea of feel and function, because, you know, quite frankly, if you're 70 and, you know, you you have a slightly high blood pressure, it's probably not something that you experience that much in your day-to-day life. And you could take a drug, it would lower it. But it's not gonna make as much difference as if you take something that can means that you can go up the stairs without being winded or walk to the store that's half a mile away than you couldn't do that previously. So patients want to feel people want when they take a drug that targets aging, for them to feel better soon. And so focusing on function as well as bringing in all of these predicted biomarkers, I think is gonna be, you know, again, maybe something we look back on in 10, 15 years' time and wonder why we weren't doing it sooner.

Eric Verdin 14:04

Aaron Powell You can already feel this shift happening, and I think it's an incredibly important one because as you mentioned, uh what people care about is not having a low biological age.

Brianna Stubbs 14:16

Low CRP, who cares?

Eric Verdin 14:18

You know, what no people feel about they want to be able to sit on the ground with their grandchildren, they want to be able to be mobile, to to enjoy good food, so all of these things. And you know, we both you and I are working with the superage game, which is another manifestation of this uh, you know, can we measure aging functionally in people? You know, can you actually train to maintain your your mobility, your flexibility, and all this? So um I in some way I think some of the uh the X Prize competition is going to be driven by some of the same modules in in the long term, you know. So I think there's uh a lot of excitement in the field that we we're coming into the age of really tr trying to change aging in a way that matters to people.

The Problem With Aging Clocks

Brianna Stubbs 15:03

Yeah. And I think it's another thing that's in an interesting trend that's hard to navigate is that um with the increase in available data and our ability to process it, it feels like every other week there's some kind of new biomarker-based composite clock that predicts aging. And you know, some of the things that I think about here, and from time to time I'll review papers and looking at um, you know, what does it take to move something from an interesting result in a science paper to an actual biomarker that would be useful in a clinical trial? So I'm you know, think about what we we see a lot with the epigenetic-based clocks you can send off a blood sample. And and, you know, you've talked about this, and I know others have, that if you sent a blood sample to from a different arm separated by an hour, you might get something that's you know, five or ten or fifteen years different. And I recently was reviewing a paper that talked about the effects of stress and the effects of meals on epigenetic clocks. And so it's really um they're very useful and valuable, but if you need something to be stable enough to say, well, I I went on a, you know, I went on an exercise program and I took a before and after epigenetic age, is the difference that I'm seeing really due to that exercise program that I did, or is it some biological variation? So, you know, these um clocks and any anything we use to measure success, we need to make sure we know all understand all of the caveats before they're proposed to be ready. And there's a difference as well between being kind of broadly useful and a longitudinal cohort, like an observational, longitudinal cohort of, you know, like the UK Biobank, thousands and thousands of people, you can get enough signal in that because there's just so many people over so much time. But for you or me or individuals and small, small scale clinical trials, then there's an awful lot we need to think about before we pick, as powerful as a clock might be, a clock like that as an endpoint.

Speaker 1 16:50

Great point.

Mouse Longevity Drugs And Human Reality

Brianna Stubbs 16:51

Next question from the listeners, uh, that I think again ties nicely into what we were just talking about. So we've talked about what success would look like in clinical trials. We're we're not there yet, you know, with with having that framework, but we are doing a lot of work looking at interventions that extend lifespan in model organisms. We we we can pretty reliably make a worm or a mouse live longer in the lab. So um, we had a question from a listener that asked which interventions that are known to extend lifespan in model organisms will actually work in humans? So, again, a big question. What do you think about that?

Eric Verdin 17:21

Well, I think it's if I had a crystal ball, I would I would tell you right now that the problem is um is the following. So we, as you mentioned, we have a whole series of interventions that have been documented to increase lifespan and health span in animal models. The the probably the best known uh that is the closest related to humans would be a program run by the NIH called the ITP intervention testing program. So any scientist who works in the field can nominate drug candidates to the NIH to this program. And there's a two-page submission that you can you can send in, and if they decide, okay, there's enough preliminary evidence in other animal models, in the worm, in the fruit flies, then we'll test it in mice. And they do this across three different uh testing sites in the country.

Brianna Stubbs 18:10

It's another same intervention, that's the same.

Eric Verdin 18:12

Same intervention, three different sites, so you eliminate sort of variation in the you know the type of mice and so on. Um and then they test, they give the mice the compounds for the lifespan and they measure aging in males and females. So this they've gone through uh I think more than 70 different compounds. Out of those, I don't know the exact number, but it's close to 10 molecules have been shown to reproducibly increase lifespan across the three different cohorts. Interestingly, for reasons we don't clearly understand, there's a uh sexual dimorphism. That means so we see a lot more increased lifespan in males than we do see in females. Not understood. Across the board, which is across the board, which is interesting. We don't understand why that is. Um that being said, these molecules now, some of them the most well known is rapamycin. And uh, but there are others that are uh drugs that actually we have in the clinic. A carbose, it's a diabetes drug that prevents sugar absorption. Um there's uh so can we predict which one will actually work in humans? No. And this is where the biggest glut right now, and sort of a bottleneck in the in the aging field lies, is that we have so many interventions that could go into humans. Problems is um human trials are much more expensive. Although here at the Buck Institute, we are actively working at trying to, and under your your leadership, trying to make them cheaper, more effective, eventually decentralized. So I think there's a lot of area that that this work needs to be done, unfortunately. And we know from previous experiment experience in other animal model systems or other diseases that we can we can cure diabetes. We've done it a hundred times in in mice, and we still haven't done it in humans. So um, you know, out of these 10 drugs, how many of them are going to make it into the clinic? Um, I don't know. Uh I hope at least a couple. Right.

Brianna Stubbs 20:11

Um, on the flip side as well, there are some things that um don't show a lifespan effect in the ITP that are still um leading candidates for gyrotherapeutics in the clinic. Um, and I was actually just at the Age annual meeting and talking to Sarah Espinosa, who's down at Cedar Cyanai and um is one of the leading researchers running metformin trials with a geroscience kind of um, you know, focus on her research. And she was saying that she'd been kind of discouraged because the ITP had shown metformin didn't have a lifespan effect. But I was there looking at this poster with all of this data, and it's like, it's it's really doing something. It was metformin was one of the leading candidates for um a gerotherapeutic trial not that long ago. Um, and so you know, she and I kind of came to the conclusion that the ITP is one useful brick in the wall of data, but but it doesn't, you know, doesn't mean we should throw the baby out with the bathwater, insofar as if if something hasn't worked in the ITP, um, it doesn't mean that it's not going to work in the clinic also because of so many, you know, just unavoidable differences between mouse and human biology and and the difference between yes, doing an experiment in mice in a very controlled environment versus humans in this big messy world. So, you know, IT ITP I think is the gold standard, but it should always be interpreted relatively cautiously. And as you said, summarizing there at the end, until we have um scalable and a unified vision of what success looks like, then it's hard to you know make progress in this space. But we're getting there.

Eric Verdin 21:42

Totally agree. And I think you know, one key thing to realize about the ITP, it's looking mostly at uh lifespan. Yes. And so in and as you know, you know, we we're we're working on both health span and lifespan. So um and you could have a series of drugs that would actually really decrease morbidity. And and and not increase maximum high lifespan.

Healthspan Versus Mortality Endpoints

Brianna Stubbs 22:03

Something else came up a meeting I was at recently, and I'm interested in your take. So again, this FDA meeting, we're all talking about function, function health span being really, really important. One of the speakers um got on up and he said, Well, the thing is, you know, I hear you're all talking about function, but if I killed you tomorrow, it wouldn't matter, like, you know, whether or not you're gonna be functional. You know, so at the uh centrally, we still do care about lifespan. His central thesis was that mortality, mortality not lifespan per se, but mortality rate should be the thing that we look at. And I think that from other people that I speak to in the field, the feeling that is that mortality just means the trials have to be too big because especially in younger people, you have to follow people, you know, the cohort rate. You know, I can I can see why from a practical perspective mortality is not attractive. Where do you stand on, you know, well, at the end of the day, it matters, you know, the toes test, Jamie Jamie Justin says, you know, toes up, toes down. Like whether you're alive, whether you're dead, dead, that's what matters most. Where do you sit on that?

Eric Verdin 23:00

I sit on that from based on my personal experience talking to audiences, you know, and I I ask quite often the question, who wants to live to 120? This is like a long, long life. Um typically typical audience, I will have one out of a hundred people raise their hands. If I rephrase the question and say, who wants to live to 120 in the same shape as what you were would expect to be at 60, surrounded by your family with your job and all this, 99% of people, so everybody wants to live long, nobody wants to live sick. And I think in some way, you know, quite often the message that I'm giving is misunderstood as to being a health span message. No, it's just it's long life, but not at all costs. Trevor Burrus, Jr.

Brianna Stubbs 23:46

If they're not, they're not um mutually exclusive, right? They they they are codependent on one another. Yeah, no, I agree. It was it was an interesting, very provocative that the speaker was very provocative, I think deliberately because um because of the the other the other points that had been raised, but it made me kind of reevaluate my own my own thinking a bit. So um we'll move on to the next question.

Career Paths Into Aging Biotech

Brianna Stubbs 24:05

I I think that um hopefully listeners can tell that you and I are both really excited about all of the the growth in the field, the opportunities in the field. And so one of the questions um is about young scientists getting into the field. Um and our listener asked, how can young scientists who want to work in translational aging research or start biotech companies get their foot in the door? What path best prepares someone to develop therapies for targeting aging? And I think you and I both probably have some thoughts about this, but why don't why don't you kick us off?

Eric Verdin 24:33

Yeah, uh there is not such a thing as a path. And that's probably if looking at both of us, but maybe we can share our examples because we are in some way completely unorthodox ways to get into aging research. I I was trained as a physician, I did my whole research, uh, my career mostly in research. We discovered by chance uh a gene and a protein that were involved in the aging pathways, and this is how I got into aging. I just thought this is and you don't have a PhD. I don't have a PhD, no. I have I have an MD and a long postdoc. So that's a lifelong postdoc. Exactly. So this is uh um so for me, I I tell people, you know, it the the the biggest driver, you need some form of education, number one. We'll hear about what what you went through, which is completely separate from what I did, which is equally successful. So um you need passion, you need interest, you need some training at some level. So that would be the the key factor.

Brianna Stubbs 25:34

Before I say about my own journey, um that's a prompt for me to say um that um Dr. Newman, um, who's here at the Buck, one of our colleagues here at the Buck, as well as others at UConn, and I'm trying to think who which other institutes participate, but um the NIH recently funded a consortium called the Geroscience Education and Training Consortium GET, um, and they have been developing over the last two or three years an actual educational program for people who want to who have come from other areas of biomedical research but who want to learn about aging biology and aging research. So if anyone's a trainee and is listening to this, they should go away and look up the GET network, um, look at the educational opportunities that are coming online. I believe there'll be some online courses that are going to be offered through various institutions, and um that's the one the one um resource that I definitely remember, but I'm sure that they're developing other resources as well. Um, and that would be a really great place to start for someone whose PhD is related to aging, perhaps not purely in the aging field, or who wants to learn about aging to start a company. Um, but back to to where I came from, I guess. Um similar to you, wanted to impact people's health and wellness, studied um medical school over at Oxford University, halfway through my um medical training, got into research firstly as a participant, felt felt like it was kind of fun. It also gave me time to pursue my rowing, which was you know my side hustle as a professional athlete, and studying my PhD at Oxford. Um, following my PhD, actually moved over to the US to join a company. So I didn't do a traditional postdoc at all. I moved into a company. Um I felt like um getting experience in a startup. There is a couple of ways that you can get exposed to the types of skills that you're gonna need to start a company. You can either go and work in a really small company like I did, where you are one of ten people and you're really in the room when all of those hard decisions are being made, you get a lot more exposure. Um you can go and be in a pharmaceutical company and work through often they'll have formal training programs for people, recent graduates or PhD graduates, and there you'll have more structure. You maybe you'll um you'll get a higher, you know, different kind of exposure. And so that's that's two ways you could think about um ways to train post-um education. For me, I was was in the company, got a lot of exposure that way, and then ended up at at the buck um kind of by a happy accident because I was working on a on a research area that you were also working on as well.

Eric Verdin 27:55

It was not a happy accident. We've recruited you very actively.

Brianna Stubbs 27:58

Very actively. Okay, okay. Well, it was yeah, yeah, no, it was I it was it was great. I'm very happy to be here. Um so yeah, I think um being in a startup, going into pharmaceutical companies, um at the meeting I was just at, there was people who had done both, and you know, you'd I think one message that r resonates with me when I look at my career and this panel that I listened to also said is that they're that it's never too late to change. You can go and be in pharma for five years, learn a load, and then go and join a biotech, or you can um even go from being in a biotech back into a postdoc if you wanted to. So I think there's a lot of pressure on people to make a decision and make the right one instantly. And if, you know, you were gonna thinking you were gonna be a physician. I never thought that I would be here doing this. So I think if if people can take away one thing, it's um follow your passion, follow your interests, don't be afraid to try things because mostly there's not that many one-way doors that you can't, you know, change courses further on down the line.

Eric Verdin 28:51

That that being said, you know, we're we're both incredibly lucky to be in this job, in our respective jobs here at the Buck. And uh there is a bit of a dark cloud uh surrounding all of us in biomedical research at this time, but which I I hope uh will resolve in the near future, which is uh the the NIH and its role in in funding the whole the whole effort is a little bit uh is being challenged right now. So uh for those of you who are out there, you know, who've already gone through some training and looking for a job in in the future, I would say I try to stay optimistic because I think the work that we do is so important. The fund will come. They're just we're learning how to navigate a different system. And uh in the in the case here at the BAC, we've been able to attract significant funding from ARPA. So the work is actually, we had our biggest year last year. So I would say let's not uh you know, I try not to let the gloom and doom uh affect us. I think uh be creative, uh network, uh talk to us, talk to the people in the field. Um there's still a lot of very good jobs uh right now, and there will be more in the future. I'm really confident that if you're considering doing a career in biomedical research, of all the fields that you could go into, um uh aging research is the one to go into.

Brianna Stubbs 30:12

I agree. Okay, I think we have time for maybe one more question before we have to wrap up this session. Although I would say this has been this has been really fun. So if anyone has further questions, just send them in to us and we'll record another of these episodes sometime in the future.

Eric Verdin 30:25

I agree, love those.

How To Spot Reliable Health Advice

Brianna Stubbs 30:27

Been very fun. Um so to close us out, um, I know you've been thinking a lot, Eric, about um science communication. We had a question came in that is um, I think captures a lot of the sentiment nowadays. Um, in a world that is saturated with health influences, endless information sources, AI tools, and both credible and questionable experts, how should someone figure out what is actually reliable? And I think we all we all feel that in every element of our lives. So, how how have you been thinking about um building credibility, um weeding out less credible sources in in your own um internet basis?

Eric Verdin 31:03

Yes, I I'm I'm I'm both a practicing physician and scientist in the field, like like you are, but also I'm a consumer. So I'm I'm on Instagram and I get these uh reels, you know, touting this supplement, and and I must recognize from time to time I fall for it. I'll buy something and it comes into the mail, and realizing, why did I buy this? Uh so uh and that's attention, which I think is is both necessary and uh something to be aware of. So uh one aspect you mentioned that I'm passionate about uh communication, and and that really is linked to this whole question. Um we live in an environment where everybody can actually communicate. We used to have a very rigid structure by which information was being communicated and was almost implicitly trusted. Uh that has changed. Anybody who has a telephone and an Instagram account can become an influencer. If you're good enough, uh you can actually make a good living doing this. This did not exist 15 years ago.

Brianna Stubbs 32:07

There are people, you know, didn't exist probably like five years ago, you know, that you could be a kid and be like, Mom and dad, I want to be an influencer when I grow up. And like now, as you say, it's like a career.

Eric Verdin 32:15

It's a career. So um it it's not only bad, I think it is actually an incredible democratization of the ability to share information and so on. In our world, uh it can be problematic because uh there are, you know, there is real progress being made in aging research, but there's a lot of crackery. Uh snake oil is rampant. Um this used to be called Dr. Google. Uh right now I call it Instagram medicine. This is the idea that you're relying for making some medical decisions by someone who you know sits in his garage and sells you a pill that he's been making in his garage.

Brianna Stubbs 32:54

Or sits in his multimillion dollar mansion. Exactly, actually, in Bali in Bali, probably.

Eric Verdin 32:59

Uh so that being said, I think one of the problems is as physicians, as scientists, we've been reluctant to enter that debate. And I think uh we need to be much more because we haven't done this historically, and we we're all so passionate about our science, we forget to communicate it. And I think it is something critical for us to engage in. So you might have seen that uh I'm much more active on Instagram, on LinkedIn, we now have a Substack. The reason for this is not for my personal uh self-aggrandisement, it's more the idea that we need to bring our voice to the public. And the listener is asking, you know, how do you how do you decide who to listen to? I would say, listen to us. We don't have all the answers, but we're grounded in science. Um the Bach Institute is a recognized, you know, 26-year-old organization that's focused on science. 300 scientists working here. I mean, we're not the only ones, obviously, but uh if you're going to be uh getting some of your information, at least listen to us and then listen to others. We have not only my social account, me social media accounts, but also the buck itself. Um we have this podcast, we have a newsletter, there's many ways in which you can engage in this community and from there migrate into other people who are a recognized source of authority. And you know, be aware, be uh be questioning of everything you hear on the internet. You know, there's a lot of craziness right now. AI has just compounded this to some degree because you can now make fake videos. You can so we we're entering an era an era where because of AI, largely a lot of the information that you're going to be sub subjected to is going to be fake.

Brianna Stubbs 34:45

I do feel though that that change in the last year has maybe increased people's willingness to be skeptical. It's or it's at least made it like this huge um, you know, you look at something and you think every time I see something on the internet now, I ask myself, is this AI or not? And so I think that that building in that reflex and that skill of asking and then knowing how to, you know, look at the provenance of something being forced to the foreground a bit more by AI is is could be helpful for the whole space. But the problem is it's work. It's work to um assimilate, you know, cross-check against a few trusted sources, um, and you know, go do that digging and look and see. So I don't think that that's um in direct opposition to how that information is meant to be consumed. So I think how we make conclusions from information probably has to change as there's more information, uh higher risk that it's misinformation and not information. Um, we have to build good habits and skills around um you know building our own conclusions. Um it's funny because I think you consume social media to sort of switch your brain off. And I think maybe this is a call to action that you actually need to switch your brain back on when you're abusing these platforms before you make any life choices based on what you read there.

Eric Verdin 35:59

I agree. That's the place to be the most skeptical. And uh at the same time, I think it is here for to stay with us. Uh it is part of what I call the empowered patient, the idea that um all of us are becoming a participant to our medical decision. So versus having a doctor giving you orders, I think all of us I think will become much more active in the decisions that that lead to more this treatment or this this supplement. Um just um just be especially uh critical or suspicious of people who claim to have all of the answers. Because the bottom line is that uh science is um has one incredible virtue is that it makes mistakes and it recognizes them. So if you hear about something that just sounds too good to be true, that should be a reflex. Well, maybe there's not so good to be true. Someone is trying to sell me onto something. And we are, you know, I fall for this. It always amazes me from time to time I'll fall for something, and then I start digging around, you know, something just sounds too good to be true, a pimp claiming from a paper, and I'll go look in the paper. Yeah. And it's it's just it's mind-blowing how people will just distort what what they're reading for the purpose of making some notes.

Brianna Stubbs 37:17

That really scares me because I know that it as a site, you know, I'm I'm a PhD, I'm a research assistant professor. This is my job. And if it takes me to follow a link to PubMed, go into a paper, and then go, you know, into something you know, and actually make a conclusion based on all of those years of expertise, how is anyone else meant to, you know, to do that? So I think it's it's fair enough that people feel a little overwhelmed by by this, because I feel overwhelmed by that.

Eric Verdin 37:42

And I agree. And I'm I am amazed by the amount of sort of manipulation of existing paper paper that some people will go through. So again, this brings us back rather than trust these all these disparate sources that you do not know anything about, you know, as I mentioned, the guy or in his garage selling a supplement versus a place like the Buck Institute. I I I would argue that many people should migrate back to towards some of these uh trusted sources. Now, I have been told, well, your Buck are so conservative, that's not what I want to hear. I want to hear about someone who's gonna tell me I'm gonna live to 150. I said, Well, there you go. You can either live in that illusion that you're gonna live to 150, or you can say, well, aging is really complicated. The buck is studying it with 300 people, 70 million dollars a year, and they've come to the conclusion that the 150-year-old is probably not gonna happen soon. So decide who you want to trust. This is really um, you know, you can either dream or you can really look at the hard data.

Brianna Stubbs 38:48

Yeah, I totally agree. Um, I'm really proud to be a member of the community here at The Buck. Um, and I'd say to the listeners, all of the people that we bring on and we have conversations with, those are also people who we trust. And so I'd encourage all the listeners to look up our guests. Those are also great sources of information. And and you listeners, by consuming this podcast, by being part of our community, um, you're getting you're getting a better shot at getting trusted information and then learning who those trusted partners are. So thank you for being on this this journey with us.

Eric Verdin 39:15

Thank you all. I think it's great to have you as a as an active audience and just keep sending those questions. And we we love to read them and we love even better to answer them.

Brianna Stubbs 39:26

Thanks for sitting down today, Eric.

Eric Verdin 39:28

Thank you.

Closing Thanks And How To Support

Brianna Stubbs 39:31

Thank you so much for listening. Please subscribe, share, and give us a five-star review on Apple, Spotify, or wherever you get your podcasts.

Speaker 1 39:38

We're not getting any younger yet. It's produced by Vital Mind Media. The Buck Institute's very own Robin Snyder is the executive producer. Wellington Bowler is right next to us here directing the recordings. And the esteemed Sharif Ezzat weaves the show together for you.

Brianna Stubbs 39:55

If you're listening to this podcast, you know that there has never been a more exciting time in research on aging. Discoveries in the labs are moving into the clinic to help us all live better longer. The Buck Institute depends on the support of people like you to carry on our breakthrough research. Please visit us at BuckInstitute.org to learn more and to donate.com.

Speaker 40:27

Investment advisory services are provided by Ashton Thomas Private Wealth LLC and Ashton Thomas Securities LLC, SEC registered investment advisors. Securities are offered through Ashton Thomas Securities LLC, a registered broker dealer and member of Finros CIPIC.