Healthspan, Lifespan, and the Biology of Aging

Steph: Hello, everyone, and welcome back to the A6CZ podcast. We've recently had a ton of new listeners come in, so I first just wanted to say hello and also welcome. If you're new to the show, I'm Steph, the host, and what we try to do here is cover the most important trends within technology alongside the people building it. And if you're just tuning in now, you've come at a great time. We've got some incredible guests and topics in the hopper, ranging from VR to hardware to how AI is reshaping everything from law to code. Plus, an upcoming episode with a very well-known founder that I don't think you'll want to miss.

Steph: But there is one episode that I'm particularly excited about, and it's about the state of the App Store. Look, Apple recently released that they've paid App Store developers over $320 billion. Yes, that's B for billion. And in this episode, we cover where things are, where they're going, but also how new founders can get involved. That includes a new age Beanie Baby app, a viral talking dog, an app from 2012 that finally broke the top 10, and a Chinese app that's been at number one for a majority of 2023. And let me tell you, that's not TikTok.

Steph: All right, I'll leave the teasers there, but make sure to subscribe so you don't miss out on those new episodes dropping very soon. Moving on to today's podcast, we're sharing an awesome episode from our sister podcast, BioEats World, on the biology of aging. I know there can be a lot of judgment surrounding the world of longevity, but it's hard to think of a more potentially impactful space on humanity. Living longer might mean having the time to write that book you've always wanted to, to found that company you've always wanted to build, or just spend more time with your loved ones. But also, imagine having another decade to contribute at your highest potential. Imagine what you could do. Imagine how that could reshape society.

Steph: And so naturally the question becomes, what if you knew what markers to look for in order to extend life? Well, in this episode, A16Z general partner Vijay Pandey and co-founder and CEO of BioAge, Kristen Fortney, discuss exactly that. As a listener of this episode, there were several aha moments for me, but here's one that really gripped me. Kristen asked Vijay the following question. What if you could cure all cancers tomorrow? What would that do to the average lifespan? Now, I'm not gonna give away the answer, but I want you to take a second and pause to think of your answer before listening to the rest of the episode. No, really, go pause the episode and have a think. What would curing all cancers do to the average lifespan?

Steph: All right, I hope you have your answer, and I also hope you enjoy this episode as much as I did. Look out for new episodes of the A16Z podcast coming this Tuesday.

Olivia Webb: Hello, and welcome to BioEats World, a podcast at the intersection of bio, healthcare, and tech. I'm Olivia Webb, the editorial lead for bio and health at A16Z. In today's episode, we talked with Kristen Fortney, the CEO and co-founder of BioAge Labs. You'll also hear from Vijay Pandey, general partner at A16Z Bio and Health. Together, we discussed how Kristen became interested in the biology of aging, how she started a company, the state of aging research today, and some more practical matters, like how long a hypothetical venture capitalists can expect to live. Let's get started.

Olivia Webb: So Kristen, welcome to BioEats World. Thank you for joining us.

Kristen Fortney: Thanks Vijay.

Olivia Webb: I thought we'd start off by talking a bit about your founder journey. The biology of aging and longevity is a pretty unique space and I think people would love to hear what got you here.

Kristen Fortney: That really dates back an incredibly long time. I've been really fascinated by science and science fiction and aging biology since I was a kid, really. You know, probably reading tons of science fiction as a kid.

Olivia Webb: Yep, yep, me too. I think that's important for a lot of founders that I talk to, actually. Actually, what was your favorite book as a kid?

Kristen Fortney: Oh, good question. I like a lot of Greg Egan stories, if you know him. They're really sort of like hard sci-fi.

Olivia Webb: I'm sorry, I don't. Oh, you don't? Oh, you should check him out. We can link it in the show notes. Yes, yes. Read lots of the classic stuff too. I still read tons of the stuff.

Olivia Webb: So that got you interested in science. I think many of us had similar backgrounds. So then what gets you on the path to doing it academically?

Kristen Fortney: I was always reading about aging biology. I was always very excited about that in particular because it seemed like it could have such tremendous potential for medicine, for healthcare, and it was still very new science. So I was always really reading from the outside. As an undergraduate, I actually went into math and physics first. but I was always kind of reading about aging biology on the side. And then for my PhD, I decided that I wanted to get into the field myself. So I did a PhD in bioinformatics, but focused on aging biology because that was sort of the quantitative skills that I knew applied to the problems that I cared about. And at the time, I analyzed large data sets to build biomarkers and to repurpose drugs. And really, I was brand new to modern biology, sort of really soaking all that up.

Olivia Webb: Yeah, especially you're coming from a physics background. Was that a bit of a shift?

Kristen Fortney: Oh, definitely. It's a huge shift, right? Came in with lots of unrealistic ideas, I think, about how easy it was. And then you meet all the hard realities of biology is actually really hard, right? And we still know so little. There's still so much to learn. And then I started to become more fluent in aging biology and aging science and decided for my postdoc, I really wanted to join an aging-focused lab. There are still very few of those. So can you put us in time when the postdoc was roughly?

Kristen Fortney: Yeah, this is 2012. And I came to an aging biology lab at Stanford. And what attracted me in particular was that they had samples from people who lived to be, like DNA samples, who lived to be over 100 or over 110. And that really excited me in particular because aging is so complicated, because aging is so difficult to intervene in. And I thought that if we can learn what, you know, these people who are already aging successfully, what's different about them, that could be a really great way to figure out new drug targets. Genetics has been really important in other areas of disease biology with PCSK9, et cetera, right? So I wanted to crack at those data.

Kristen Fortney: And, you know, over time, I'd been realizing that, like, what I really wanted to do was, like, develop therapies and, you know, impact lives, impact health, right? And realizing more and more that that's not, by and large, what happens within academia. I mean, not for most people in academia. And so it was at that point where you really, did you ever consider staying in academia? Potentially, but sort of got further and further from that. I had a particular thing I wanted to do, right? Like a particular project that seemed like it would be a great way to find drug targets that was not an academic project, right? And that was what really led to the founding of BioAge.

Kristen Fortney: And it really related to this idea. and that's kind of the idea that we're founded on, that there's going to be a lot that we can learn about how humans age by studying the 8 billion examples all around us, right? And we're going to learn a lot of pathways that can help people live healthier longer by, again, studying people who are already doing it. And that could unlock a lot of new biology, a lot of new target discovery, help us treat and delay disease.

Olivia Webb: Yeah, so it's roughly what time now? We're talking 2014? This is 2015. Late 2014, early 2015. So you decided to start a company. What was that like for you? Because the first time anyone starts a company, it's a very new thing. What was it like jumping in and how did you even just get started?

Kristen Fortney: Well, it's interesting, right? Because I did my PhD at the University of Toronto and that's Canada's largest research university. But there's not a whole lot of young startups founded by students, founded by postdocs. And I don't know that that would have been on my mental map I remained in Toronto. And then I came to the Bay Area for my postdoc. And Stanford and the Bay Area are very special environments. And you meet friends who are doing it. You realize that you can get to value creation for not too much money in the biotech world. And you learn more about how it's done. And you have friends who are founders and talk you through the process. The joke is that Stanford's an incubator with a football team. Yeah, exactly.

Kristen Fortney: So I think that was really critical, just meeting some people who'd been through the journey before and understanding that it could be done and the precise mechanics of how it was done. That's so important to have that help early on that opened that door.

Olivia Webb: Yeah, so you found the company and how does the company come together? I mean, you get a co-founder. And so Eric, when did you meet Eric? How does this actually come together?

Kristen Fortney: Yeah, my co-founder Eric has been my friend since high school. Oh wow, okay, I didn't realize that. So we were both reading our sci-fi novels. I think we first met on the math team. So it's been a very long relationship. That's fantastic. Yeah, and we both had actually shared an interest in aging biology. He'd gone down a career to get his MD, but we'd still always talk about aging biology, even collaborated on a paper together actually back when I was in grad school So it was very natural for us to do something together So I found the company you get some initial funding Yes And then you off to the races That great Maybe we could fast forward a bit How do you go from having the idea that aging biology could have an impact in disease to actually becoming a therapeutics company?

Kristen Fortney: The very first step for us was to establish that by looking at human biology, watching the process of aging unfold in the right human data sets, we could find compelling targets. As step one for us, the very first thing we did when we started the company, we located and found and negotiated with several very special biobanks that started collecting samples from people, humans, when they were healthy and middle-aged. And these samples were collected as long as 50 years ago. They had samples that were collected longitudinally throughout the lives of these people that were tied to health records with information on how long those people lived, the diseases they got as they aged, and also critically their health span. So how their muscles aged over time, how their brain aged over time. And this is what we really believed we needed, this kind of data to understand aging, because human aging doesn't happen overnight, or it doesn't happen in two weeks like it does in the worms, which we like to study in universities. Right, I mean, otherwise the company would have to be around for a couple hundred years to get some data. Right, exactly, exactly.

Kristen Fortney: So the idea was that we could do what is basically a 50-year experiment if we could get our hands on the right samples and analyze it in the right way using modern technologies like proteomics, metabolomics. And why would they even have this data? What were they thinking? That's a great question. It really differs by biobank. And sometimes it's really a case of they started the biobank for one purpose, and then after they've been collecting sample and data for two decades, well, now it's an aging study. Some of them are actually national-level biobanks. With Estonia or Norway, we work with those as well. And it's more of a longer-term collection process there.

Kristen Fortney: These biobanks have blood? Yes, usually it is serum and plasma. Because, you know, you're not going to get your hands on brain biopsies from healthy people. So you're more limited with the material there. Yeah, exactly. And the medical records, so you have some sense of how they're doing along the way. And the medical records. Yeah, that's really key.

Olivia Webb: Okay, and so let's say you got that. What do you do with that? Well, step one, so you have these really precious samples, 50 years old. They're incredibly rare. Like there's not a lot of biobanks like this out there. And then you want to know like what's in them, right? So you interrogate them with modern technologies like the proteome, like the metabolome. And the idea is really just to make a really big list of all the different molecules in there. And then you've got this huge data set of molecules by people, by time. And there's a lot of very interesting questions you can ask of the data. One of the ones, for example, that we're most interested in is like what molecular markers, whether it's a single marker or a pathway, but what things can we see when you're middle-aged that really predict the future of your aging, right? So what kind of pathways predict the difference between someone who goes on to live 90 plus in great health and their brain still works and their muscles are still highly functional versus someone who only makes it to 270 or so?

Kristen Fortney: And that's really the starting point for everything that we do at BioAge. We want to make a list of these molecular entities that are important for health span and lifespan and then drug them.

Olivia Webb: Yeah, and just that whole process is really interesting because, you know, probably around the time of the Human Genome Project, it seems like biology shifted from pipetting and one-off experiments to database lookups and statistics. And so you've got this enormous database with all this information, and now you can ask a series of questions. So I'm presuming you're asking what made these people that live longer live longer.

Kristen Fortney: Precisely. Yeah. And so what did you find? Well, to take my favorite example, because it's the one where we just had a clinical readout, right? So we just had a, I'll get to that in a minute, but we just had a clinical data announcement. But in one of our proteomics analyses, we discovered that there's a protein called apolin that circulates in your blood. And people, when they're middle-aged, if they have more apolin in their blood than other people their age, that's highly predictive for both living longer, having better muscle when they were older, and having better cognitive function when they were older. In a linear way, right? So the more apolin you had, that just seemed to correlate with better and better outcomes.

Kristen Fortney: And so that's how we initially got interested in this target. Interestingly, apolin was first described as what they call an exerkind. So it's actually something that your body produces more of on your own right after you exercise. Very nice. Yeah, so it's in the blood, impacts on the muscle. So we got very excited about this. So people knew about it as an exerkind, but didn't know about its connection to aging. Yeah, longevity. Exactly. That's right.

Olivia Webb: And so based on that, we tested out whether if we improved apolin signaling in older mice, if we could improve the function of their muscle. Let's back up a second because you were talking about human data all the way here. That's right. And now we're going to mice. Yeah, no, I would love there to be like a day when you actually don't need mice anymore, right? You can go directly from human data to the clinic. And, you know, for certain hypotheses, I think maybe we're getting more and more there. You have all this human data. That's right. Yeah, yeah. Well, so this is one of the ways that I think about it, right? So you've got this sort of lifetime signal where more apolin is good for you. And that's great. That means that if you get enhanced apolin signaling for decades, that's good for you. But the separate question, which we're going to be asking in the clinic, is if you're already sick and we improve your apolin signaling, can we see a dramatic effect quickly that actually impacts on a disease?

Olivia Webb: And that's a very different question. It's sort of taking a system that's disrupted and trying to fix it by tweaking this one variable and seeing if that alone suffices to fix the condition. So I do think, I still believe that the right preclinical experiments can be tremendously de-risking and value-creating as you move towards the clinic. Because, yeah, there are experiments that you would do with mice that we wouldn't do with people. And there'll be probably many areas of mouse biology that overlaps with human biology. Yeah, I'm sure we're going to miss things too, though, right? Like so much of what we do in aging biology is in invertebrates. A lot of it is in mice, and vertebrates, of course, are incredibly different from us. We are not flies or worms or yeast. But even mice in the lab, they die pretty much exclusively from cancer, right? That is not true for humans. It's cancer, cardiovascular disease, right? I think we need to develop better models. But at least for those things that are conserved, I think this is a great approach.

Kristen Fortney: Well, and you'll have specificity. Maybe you'll miss some sensitivity for the things that are not in both. Yeah, that's exactly how we think about it, right? We want to execute first on those targets with the most evidence that tick all the boxes. And yes, we might miss some that don't tick all the boxes, but because there are so many targets emerging, we can still have a big set we can move forward with with high confidence. And with confidence that it will work in humans. And that always seems to be such a big problem in biotech in that, you've heard my old joke, it's a great time to be a rich mouse. And so here you have some data that would suggest it would work in humans. Yeah, that's why we always like to start with human data, because you want to know that the pathway really matters there and compared to all the other pathways that are affecting the aging process, affecting the disease process.

Olivia Webb: Okay, so then you actually then put it in humans. Then we put it in humans. We put it into various mouse models of muscle aging and saw a positive impact in several different models from sarcopenia to stem cell function to muscle atrophy. And we actually focused on the atrophy aspect for the clinic because that's where we saw the biggest effect size in the shortest window of time, which is exactly what you want to see in the clinic.

Kristen Fortney: So the particular mouse experiment that motivated our clinical design was we took some very old mice and we put a cast on one of their arms. And after three weeks, you can remove the cast and weigh the muscle, and it's undergone substantial atrophy. In fact, they lose close to half the weight of their muscle. And we saw substantial protection for those mice that were on the drug. And in fact, there was no significant difference and the muscle decline. So a really enormous effect size. And that really motivated how we built the clinical trial.

Olivia Webb: Did you give the drug prior to putting the cast on the mice? Yes, we did. It was prior. Yeah, so it was exactly. So it was prior to the effect. Yeah, and when we did our clinical trial, we based it on the same kind of scenario. So it's what's called a bed rest trial. You know, sitting in bed is always bad for you. This is the part that I think most people would be shocked to hear. So 10 days of bed rest does what? 10 days of bed rest, yeah, you lose about 7% of your lean mass if you're past a certain age. And importantly, too, for a younger person to lose a similar amount of mass would take a couple of months of bed rest. So it's really dramatically accelerated by your age, but you do see substantial changes in the muscle. Usually these studies focus on the thigh. It's your biggest part, the most stationary part of you because people are sitting in bed still eating, still watching TV, but their legs are very stationy and their thighs are large. So you can look at the thigh muscle size, thigh muscle quality, thigh circumference. And we looked at all of those in the study and saw a significant difference, which we're really excited about as sort of the first proof of mechanism with a really clean story all the way from our human discovery platform through to some very nice in vivo mouse results and now to the clinic.

Kristen Fortney: And I guess you off to the races as a clinical stage company That right And next step would be phase two phase three trials Yep that right Yeah, up to next trials.

Olivia Webb: Okay, so I want to switch gears a little bit, and especially where we are in this story now, why is aging such an important factor in disease? Or to what extent is an important factor in disease? Like, why do you care about it?

Kristen Fortney: It's a tremendous risk factor, right? Like you can see, you can draw all these exponential curves of incidents and also death due to all the major diseases, Alzheimer's, heart disease, diabetes, the list goes on and on. So not a lot of 20-year Alzheimer's patients. Precisely, yeah, exactly. And at the same time, it's still understudied as a contributor. A lot of the times when people study these diseases, they study them in young animal models that they intervene in, so they kind of looked like the disease state, but that is so very different.

Olivia Webb: Well, this is a really interesting thing, that you have this colony of old mice. That's right. Yeah, yeah. And like, it just, you've got to wait for them to get older. They're like three years old? Yeah, that's right, that's right. We have 7,000 mice, and a young animal is so very different from an aged animal because an aged animal is in this really frail state, or it's predisposed to, like even if it's not already sick, right? It's just much more likely in the next span of time to get sick than a younger animal. And we believe that by targeting those differences, the differences between old and young, we can treat but also ultimately potentially delay age-related disease.

Olivia Webb: Yeah, and so this seems to be a lot of diseases, right? I mean, you said cancer, Alzheimer's. It sounds like what you're doing then is that you want to sort of understand the biology of aging, get into market with certain diseases, but then these drugs could be used just more broadly. That's right, that's right. And in some ways, you can think of this as following the statins playbook, right? Well, yeah, tell people about that. What's that playbook?

Kristen Fortney: So statins today are a drug that you can think of them, they're prescribed as though they were an aging drug, right? Like if you're over 40 and you have a couple of risk biomarkers, your doctor will give you a statin. They were actually first approved for an orphan disease, familial hypercholesterolemia, people who had genetically very high levels of cholesterol. And then they were found to be efficacious more broadly and the label was expanded over time to be ultimately everyone, right? And I think those of us in the aging space where we're working on small molecules, these are these easy levers that are going to add a few years of health span. So I feel like that we're going to have a handle on pretty soon. And I'd love to double click on health span versus lifespan. I was just talking about age, but why don't you explain the difference?

Olivia Webb: But yeah, the average lifespan in the US is around 80 or so. The average health span is around 60. So lifespan is how long you live and health span is how long you're healthy. And then you start to get diseases of aging and you spend a quarter of your life accumulating those. And we in the field talk about increasing the health span, which means really the portion of your life that you remain healthy and free of disease. And we believe this is doable because some of the research I mentioned earlier where when you give a drug to a mouse, it lives longer, it gets its diseases later, and actually spends a smaller proportion of its life being sick. And because also of the human examples these people who live to be over age 100 them their children it the same thing It increased health span or they also call it compressed morbidity And that's what we would all like to have.

Olivia Webb: Yeah, so in principle, even if the lifespan didn't increase, but the health span increased, that would still be a huge contribution. That would be huge, but honestly, they go together. But if you do delay the onset of disease, and if you do improve health, you're going to extend lives too. Yeah, one of the things that I always thought was really fascinating is that I was with a group of people and we're trying to think of like, what's the most audacious thing we could think about? Something so ridiculous we'd be embarrassed to tell people. And so I guess now I'm telling people. But I think, and so first it's like, oh, let's try, it would be great if we could cure cancer. And that'd be great, right? Or great if you cure Alzheimer's. But then like, okay, well, can we think of something more audacious? And the more audacious thing is like, cure all disease, right? Right. And that just sounds ridiculous, right? on many levels, but for diseases that are sort of exacerbated by aging, if you can slow aging, maybe you don't cure all disease, but maybe you greatly push back many, many diseases, and maybe even diseases that we haven't figured out or differentiated as different types of dementias or whatever. That's right. Yeah, I mean, that seems like the ultimate future of this because it always feels like doctors are doing a great job with heart disease. Now all these people are dying of Alzheimer's. Right. The next bottleneck, right? And really the underlying cause for all of these is aging.

Olivia Webb: There's actually a really good statistic related to this. People have said, what if you did cure all cancer? What would that do to average lifespan? It would add about three to four years, which is underwhelming. Actually, I didn't even realize that. That's it. That's all you get. Because again, most cancers are happening to older people. And just as you said, if it's not cancer, it's something else a couple years later. So it's really not making much of a dent at all. And in contrast, if we could, what we've discovered in mice translates to humans, and we can slow aging to the extent we've already done over and over again in animal species, that's adding 10 to 20 years of healthy life. So that's the promise, right? And we're still in the early days, but that's what I'm very excited about.

Olivia Webb: So this hypothetical Indian male might live to 110, maybe. Well, my feeling is that adding 10, like I don't think that we're really optimized at all for aging. Okay, so we're very different from worms, but I think there's a few things we can learn from worms. And one of them is that they've done this experiment where they've tried knocking every genome in the genome one at a time. And then how long does it live? How long does it live, right? And the answer is that actually there's a whole bunch of things you can do to a worm that make it live longer. You know, it's not that hard. And like a lot longer, like 10 times longer, right? That's a bit more hard. That one's harder. A bunch of things you can do have a fairly minor effect, but part of the lesson there is that there's a lot of different things that can work, right? There's nothing special. I don't think there's anything special about 80 years. I don't think we're really like maxed out there. And I do feel that we're going to get to the point fairly rapidly where we can add, say, 10 to 20 healthy years.

Olivia Webb: As we're running out of time, I want to end a little on a philosophical note and then pick your brain on a personal note. So on a philosophical note, when I think about organisms and evolution, I don't think it's just about evolving any one of us, but evolving the ecosystem. And maybe we're supposed to die. and if we didn't die at all that might not be so great for the ecosystem in a variety of ways do you ever think about this philosophically? I mean again it's like what's so special about 80 years right? that just happens to be the age at which we die now and the average life expectancy has changed substantially just in the last century so yeah that's a great point so what was it like 100 years ago? well it was I think in the mid 40s in large part due to childhood mortality But still, that's a big societal level shift, and we've borne it, right? Yeah, and Social Security being stuck at 65, I think the intention was that you wouldn't live that much past 65. Right. And so just even in that period, it's a pretty dramatic change. That's right. No, that's an important point, too, right? If we are extending healthy lifespans, that'll be extending the work span as well, right? So that's a great point, yeah, and productivity span. and possibly a different type of person, someone with the wisdom of a 60-year-old and the energy and body of a 30-year-old. That's right. Is that plausible? I think that's possible in the longer term. And I think that's one of the things that excites me about aging too. What if you had not just a couple decades to be in your prime, but double that time? Longer time horizons, better planning. There's good incentives there too. It's an exciting, exciting future. means I got a lot of work ahead of us.

Olivia Webb: Personal part, and if there's a team I can stay away from, but everyone always asks me, and so I'm curious to ask you, what supplements do you take? We should add this as a recurring feature. Actually, that's great. So I drink lots of coffee. Are you familiar with the retrospective analyses? Let's start with coffee. It's funny that people talk about it as though it's not healthy because the evidence is strongly in the opposite direction. And these are just retrospective analyses, right? But drinking more cups of coffee every day is very protective. So in many different retrospective analyses in large populations. When you say more, like more is better? More is better. Well, I think in these studies they went as high as like five cups a day. Because there have to be like. But that's not very many cups. Well, you have to have enough people in your population that are doing it to sort of actually know the answer. You're right. Five is not that much. Yeah, I routinely do seven to ten. Right. Measuring cups. Yeah, sure. Yeah, but yeah, more is more protective for cardiovascular mortality and for all-cause mortality. And that's like a really nice association, and coffee is delicious.

Olivia Webb: Okay, so that's already, you made a lot of people happy right there. Any other supplements you want to talk about? I don't do supplements yet. I do do intermittent fasting. Let's take each one in turn. So is there a reason why you don't do the supplements? Because you're a KOL in the space of aging, and other KOLs take a ton of stuff. That's fair. I mean, you know. So no metformin, no? So metformin and rapamycin are both on my list of things to try. You know, and I haven't started yet, but I will soon. Yeah, that's right. Yeah, maybe you're too young to worry about this. But then the intermittent fasting, so what do you believe about that? Well, I do the lazy version of that, right? Where a couple of days a week I have dinner. Yeah, I typically skip breakfast, but skipping lunch is kind of hard. Well, it'll be interesting to see what you end up doing when we'll do another podcast in a few years. As you age. As you age. Oh, yeah, one final question is that the biology of aging is a relatively new field. Yes. And longevity is a new area. One of the things that always strikes me, and another question people ask me is, how come everyone in the aging field are so young? Yeah, no, it's true. Partly because, maybe because it is a new field, right? So you need, it's a bit different from what's been done before. A lot of it, too, is people coming in from the science, right? And so they are younger. You don't have people coming in who are ex-BARMA experts in aging because there aren't any, right? So maybe I'll end with this. There's all these people in tech that are very excited about longevity and actually also interested in getting into life sciences and healthcare. What advice would you give them for transitioning?

Kristen Fortney: I think a really good way is just to go to conferences. I think it can be really helpful to wander around a poster session and really engage with scientists on their science. It's so important to figure out what you read in the literature is real and what is not real at all and what is very on firm ground or shaky ground. And you really can't tell that from the paper abstract. You get the real. Yeah, so learn to decode that language and what's trustworthy and what's not and what's promising but very far from translation. I think you have to learn how to read papers and you have to learn to just meet the people and engage with people. And if you go to conferences, people are very friendly. And I think they're always excited to have more people in the field. Definitely, yeah.

Olivia Webb: Thank you so much for being on BioEats World.

Kristen Fortney: Yeah, thanks, Vijay. Thank you for joining BioEats World.

Olivia Webb: BioEats World is hosted and produced by me, Olivia Webb, with