YouSaid · the spoken record

Kristen Fortney

lines on the record: 56
first: 2023-02-03
most recent: 2023-02-03
sittings or episodes: 1
sources: podcast

Every line below is reproduced as it was said and linked to the record it came from. Nothing here is summarised or generated. Directory · Search · Corrections

“A really good way is just to go to conferences. You know, I think it can be really helpful to wander around a poster session and really engage with scientists on their science. So important to figure out what you read in the literature is real and what is not real at all and what is like, you know, very on firm ground or shaking ground. And you really can't tell that from the paper abstract, you know, right? The real, yeah, so learn to decode that language and what's trustworthy and what's not and what's promising and what's not and what's Of exciting, 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“So I may well end with this. So there's all these people in tech that are very excited about longevity and actually also interested in getting into life sciences and healthcare. Like what advice would you give them for transitioning?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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. Like you don't have people coming in who are like X-Parma experts in aging because there are 10, right?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, I typically skip breakfast, but not skipping lunch is kind of hard. Well, it'll be interesting to see what you end up doing when we'll do another podcast. Oh, 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?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Right. Measuring cup 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 cuff is delicious. So yeah. Okay.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“So, I mean, it's funny that people talk about it as though it's not healthy because the evidence event is strongly in the opposite direction. And these are just retrospective analyses, right? But drinking more cups of coffee every day is very protective in many different retrospective analyses in large populations.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“It's an exciting, exciting future. It means I got a lot of work ahead of us. A personal part, and this, if this is 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?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“I think that's possible in the longer term. And I think that's one of the things that excites me about aging too, right? Like, you know, what if you had not just a couple decades to be in your prime, but like double that time, right? Longer time horizons, better planning. Like there's good incentives there too.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“I mean, again, it's like, what's so special about 80 years, right? Like, it just happens to be the age at which we die now. And, you know, the average life expectancy has changed substantially just in the last century, right? So”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“In like a lot longer, like 10 times longer As we're running out of time, I want to end a little on a philosophical note and then on a 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 like 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?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“110, maybe. Well, my feeling is that adding 10, like I don't think that we're really optimized at all for aging. And 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 genote 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. And then a lot longer, like 10 times longer, right? That's a bit more hard. That was harder. Okay, okay. 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 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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 or it's something else a couple years later, right? 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 an 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“The next bottleneck, right? And really the underlying cause for all of these is aging 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?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, one of the things that I always thought was really fascinating is that I was with a group of people and we were trying to think of like what's the most audacious thing we could think about something so ridiculous would be embarrassed to tell people and so I guess now I'm telling people but I think and so first is like oh let's try it would be great if we could cure cancer that'd be great right or great if you could 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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, right? And that's, 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, right, these people who live to be over age 100, them, their children, it's the same thing. It's increased health span or they also call it like compressed morbidity. Yes. And that's what we would all like to have.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Right, my general hunch about the field is that, you know, like at BioWage and everybody else working on small molecules, these are sort of 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, basically, and I read a convoy published that, I think, a couple years ago, and I think there's a couple of companies working now to bring that to the clinics. It's an easy thing to test. It's a very easy thing to test. Yeah. This is sort of more the bad factor hypothesis, right? Actually, there's just some bad stuff in there. And if there's just less of it, then that's going to be beneficial. It's at least something that we'll know the answer to, I think, in a couple years.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“You're going to have to bring science into this, aren't you? And so you'd find the factors either the presence of the negative factors or the absence of the positive factors and add the positive and try to remove the negative.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, parabiosis is the very Frankenstein sounding experiment where showing that if you surgically attach a young mouse to an old mouse, that ends up being a good thing for the old mouse. So blood circulates from the young to the old animal and back again. It's also terrible for the young animal. But the idea that that suggests is that there are either good factors in young blood or bad factors in old blood or some combination that can impact aging in multiple different systems, which is exciting.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Well, think of it in this way, right? Like senescence, for example, can be thought of as an adaptive process, like senescence is when a cell can no longer copy itself, make more of itself. And it becomes a very sick cell. And there's evidence in aging biology that actually eliminating senescent cells is really good for you. And it's actually even specifically thought to be an anti-tumor mechanism. So you're starting to accumulate these DNA damage and you don't want that proliferating, right? But then if you go and take one of these cells and rewind the clock and tell it everything's normal now, go and multiply. That's a theoretical concern, I think, but I'm actually pretty excited about the prospects there longer term.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, so we're still in fairly early days. It looks promising from some of the short term studies. We still have to definitively establish that it does increase animal lifespan. That's still it's worth pointing out too, right? There can be risks as well associated with winding back the clock in these cells. If you do it too much, you might get something that looks like cancer.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Well, people still argue about what that means. And, you know, as your cells get older, there's a whole bunch of different things that go wrong with them, right? Your gene expression profiles drift. They accumulate gunk in them. They can go.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“That's But it's interesting to put this in the context of companies or institutes that are going straight after longevity. What do you think that's going to look like? It almost feels like it's trying to make a tunnel by going from two ends. You can go from the specific indications and broaden them, or you could go after longevity more broadly. I mean, maybe it's worth talking, especially for the audience, something like the Amanaka factors.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, we've seen that start to happen already with some other drugs, right? Like a great example is perhaps metformin. So metformin is one of these first line diabetes therapies. It's been used by millions of people over decades. And people did a retrospective analysis some time ago now and showed that diabetics on metformin were living longer and getting less cancer than diabetic and other medicines or even then control people. Some caveats retrospective analysis, but really very exciting finding. And today it's actually fairly standard to get Metformin off-label. You probably know people who are doing that. That's true for REPAMYCIN as well. And I mean, that said, that said, we as a field, I think, still need to, we don't know if it's going to make them live 10 years longer. That takes a long time to measure. But the field is coming up with better biomarkers. And honestly, we still need real clinical trials of some of these.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“So fingers crossed, some of these drugs get across the finish line, across the finish line in their first indications, these indications start to get broadened a bit. And when do you think we start making this transition, or how does this transition work from, oh, I have this drug for muscle atrophy to now we have waste to dress longevity”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“What's that playbook? 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 targets that have this amazing potential, it's all about getting that first approval and then like widening to really get to all the patients as rapidly as you can. With statins that took 20 years to go from that first approval to the sort of broad use and hopefully we can do better. Hopefully we as a field can learn to do better. But there is that potential and it's been done before. It's not like a new way to develop drugs.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yes. Right. Yeah, and so this seems to be a lot of diseases, right? I mean, it's you said cancer, Alzheimer's. What sounds like what you're doing then is that you want to sort of understand biology of aging, get into market with certain diseases, but then these drugs could be used just more broadly.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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. Yeah.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Precisely, yeah, exactly. And at the same time, it's still understudied as a contributor, right? Like 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“It's a tremendous factor, risk factor, right? Like you can see, you can draw all these exponential curves of incidence and also death due to all the major diseases, Alzheimer's, heart disease, diabetes. The list goes on and on.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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?”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yes, he 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 bedrest trial, you know, sitting in bed is always bad for you.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“We put it into various mouse models of a 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. So the particular mouse experiment that motivated our clinical design as we took some very old mice and we put a cast in 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 in the muscle decline. So a really enormous effect size. And that really motivated how we built the clinical trial.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Always 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”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“With confidence that it will work in humans. And that always seems to be such a big problem in biotech in that, you know, you've heard my old joke, like it's a great time to be a rich mouse. And so here you have some data that was suggested would work in humans.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, I'm sure we're going to miss things too, though, right? Like so much of what we do in aging biology is invertebrates. A lot of it is in mice. And invertevertebrates, 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 and 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“That's right. Yeah, yeah. Well, so this is one of the ways that I think about it, right? Like, so you've got this sort of lifetime signal where more appelin is good for you. And that's great. That means that if you get enhanced appelin signaling for decades, that's good for you. But the separate question, which we're going to be asking in the clinic, is like, if you're already sick and we improve your aplin signaling, can we see a dramatic effect quickly that actually impacts on a disease? 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 preclinical experiments can be tremendously de-risking and value creating as you move towards the clinic.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“No, I would love to 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 for certain hypotheses, I think maybe we're getting more and more there.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“As an exercise. Yeah, longevity, exactly. That's right. Longevity and muscle function. Yeah. And so based on that, we tested out whether if we improved aplon signaling in older mice, if we could improve the function of their muscle.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Well, to take my favorite example because it's the one where we just had a clinical readout, right? So we just had, 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 apilin 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 apline you had, that just seemed to correlate with better and better outcomes. And so that's how we initially got interested in this target. Interestingly, Apelin was first described as what they call an exarkine. So it's actually something that your body produces more of on your own right after you exercise. Yeah, circulates in the blood, impacts on the muscle. So we got very excited about this. That's kind of step one.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, and just that whole process is really interesting because probably around the time of 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 access a series of questions. So presumably you're asking what made these people that live longer.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Well, step one so you have these really precious samples at 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 what's in them, right? So you interrogate them with modern technologies, like the proteome, like the metabolum. 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 70 or so. And that's really the starting point for everything that we do.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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, they're like, well, now it's an aging study. Some of them are actually national level biobanks, like with Estonia or Norway. We work with those as well. And it's more of a longer-term collection process there.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“you Right, exactly, exactly. Yeah. 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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. 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 like 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, you know, or doesn't happen in two weeks like it does in the worms, which we'd like to study in universities. I mean, otherwise.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, my co founder, Eric, has been my friend since high school. Okay, no, 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, yeah. And he, you know, we both had actually shared an interest in aging biology. He'd gone down on 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Yeah, exactly right. 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, like that's so important to have that help early on, that opened that door.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“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, right? And then I came to the Bay Area for my postdoc in Stanford. 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.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source
“Potentially, but like 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. And it really related to this idea, and then 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. And that was really the founding idea of bioage.”
2023-02-03 · a16z Podcast · Healthspan, Lifespan, and the Biology of Aging · IDENTIFIED FROM THE TRANSCRIPT · source