The Future of Longevity II | Part 1 | Panelist Questions

26 July 2021

Recently, Avi Roy, alongside Nathan Cheng & Laura Minquini, hosted the second Longevity Panel discussion, which assembled some of the brightest minds working on reversing aging, and enhancing health and life span.

As with the first event, this discussion was intended to illuminate how they are approaching longevity and to know if we are any closer in achieving it.

The talk was split into two sections: the first being open discussion guided by questions from the hosts. The talk was then opened up to the floor, allowing audience questions. Part 1 will provide the transcript from the first section of the Longevity Panel. Enjoy!

The hosts:

  1. Laura Minquini – the founder of MYKIGAI, a DTC longevity platform dedicated to the education, vetted curation and management tools for people to get on board with longevity as a lifestyle. Having spent most of her career in trend forecasting and branding design and fashion products she sees the potential of longevity becoming the next big consumer category empowering people to take their health in their own hands.
  2. Avi Roy – a biomedical scientist and entrepreneur based in Oxford. He advises and funds startups in the health and longevity space in North America, the EU, and India. He also work with governments to develop and refine policies that enable the longevity infrastructure.
  3. Nathan Cheng – the founder of the Longevity Marketcap Newsletter, a once a week roundup of the developments in the longevity biotech industry. He is also the founder of Longevity List — a website where you can find jobs, companies, and investors in the longevity biotech industry.

The panel:

George Church – George is the Robert Winthrop Professor of Genetics at Harvard Medical School, Professor of Health Sciences and Technology at Harvard and MIT, and a founding member of the Wyss Institute for Biologically Inspired Engineering.

Nir Barzilai – Nir is the director of the Institute for Aging Research at the Albert Einstein College of Medicine and the Director of the Paul F. Glenn Center for the Biology of Human Aging Research and of the National Institutes of Health’s Nathan Shock Centers of Excellence in the Basic Biology of Aging.

Jim Mellon – Jim is the co-founder and Chairman of Juvenescence, a company which aims to develop science-backed therapies that extend both healthspan and lifespan. Jim has also established the Mellon Longevity Science Programme at Oxford.

Jay Olshansky – Jay is currently a Professor in the School of Public Health at the University of Illinois at Chicago, Research Associate at the Center on Aging at the University of Chicago, and co-founder & Chief Scientist at Lapetus Solutions, Inc.

Alejandro Ocampo – Alejandro is Assistant Professor at the University of Lausanne. His research areas include epigenetics, stem cells, aging and mitochondrial diseases with the goal of clarifying disease mechanisms and developing novel therapeutic approaches to improve the quality of life of patients.

Kristen Fortney – Kristen is the CEO and co-founder of BIOAGE. A clinical-​stage biotechnology company on a mission to develop a broad pipeline of therapies that target aging in order to increase healthspan and address chronic diseases.

The questions:
(The timestamps relates to when the question in asked in the full video)

05:35 – How do you plan on reversing aging?

12:06 – How do we know that these therapies that are being developed in scientific labs or being brought to clinical trials, are actually having an effect on aging?

23:36 – This weekend Richard Branson went to space, while some of us saw a great feat of science and a 70 year old man accomplishing a lifelong dream, others saw a billionaire wasting money. Longevity also has this perception problem of being deemed another fancy of billionaires. Do you think it is important to change this and how do we do it?

35:19 – What are the two or three things that you fundamentally believe are inevitable in the future of longevity, aging, and health? And, what obstacles might prevent these things from happening?

Here’s what was said:

Avi Roy: How do you plan on reversing aging?

Kristen Fortney: Yeah, for sure. So I’ll dive right into that. So at BioAge, we think that really the low hanging fruit in aging is to copy what already works. There already are a lot of people who live to be a hundred plus in great cognitive health and great physical health.

What’s different about those people at the molecular level, that we can target with a drug. And so our whole approach at BioAge is to really follow large cohorts of people throughout their aging, because humans do age on the scale of decades from 50 to a hundred. And then map out using modern omex technologies and systems biology and AI, all the different pathways that predispose to exceptional longevity. And then target those with therapies.

And that’s true for the first three clinical bets we’ve made, as well as for additional ones we’ll make over time.

Avi Roy: Amazing. Anyone can take the next answer. So Nir, George, Jim, Alejandro.

Nir Barzilai: Sure I’ll strengthen Kristen’s approach because I’m doing centenarians study. Centenarians have longevity genes.

We’re doing an effort with Regeneron pharmaceutical to get 10,000 more centenarians in order to find all the longevity genes. There’s no one public longevity genes. They actually have several ways of getting to 100, but I think this is crucial for at least phase one, to start making improvements.

Now, of course, the centenarians have a limited capacity. They won’t live beyond 150 years, but at least we can make progress. Now, I also want to say, in my introduction, I’m also a founder of a company called Khobar. And it’s a public company. And what we have is the genome of the mitochondria.

You all know about the genome of our nucleus, but the mitochondria has a genome. And we discovered that the mitochondria produce lots of proteins that have a role in resiliency and aging, and we’re developing them into treatment. So this is just an example of another biotech that takes us to a certain approach and targets aging.

Laura Minquini: Jim, do you want to go ahead? 

Jim Mellon: Yeah, I’ll just say that to oversee I’m overwhelmed by the potency and capability of the scientists on this school, which are not. But the background of the founders is in drug development and we are taking the view that we’re not sure what’s going to work.

And I don’t think anyone really is sure what’s going to work, but we know something is going to work. And so we’ve got 20 projects, which is contrary to what most companies are doing with sniping our way towards success. We hope at least. But I absolutely agree with Kristen and Nir, I think they’re the same list, but alteration of the genes is going to be the factor that causes someone to live to 150. All the other stuff is probably going to be incremental. It won’t be revolutionary. But gene therapy ultimately will be the thing that will allow some people on this school to live to 150 and beyond. 

Laura Minquini: Thank you. George?

George: So as Nir agrees with Kristen about centenarians, I agree with Jim about the gene therapy. I think it is a great way of getting specific delivery to either systemically or to very specific parts of the body. It allows you to go directly from molecular biology hypothesis to a therapy, without doing a lot of stumbling around for drugs that are sufficiently sufficient specific.

So we’ve published a couple of combination gene therapies, each involving three different genes. One set was completely cell non autonomous, meaning it would spread out from the cells that were in. And that was a FGF21 and TGF-beta receptor and alpha Klotho. And then we did another one with David Sinclair’s lab working on the classic Yamanaka factors: Oct4, Klf4 and Sox2. But the key thing is that these have been shown in a variety of ways to actually do aging reversal. So it’s not particularly speculative nor particularly far off in the future. It really is a matter of just getting through the clinical trials which, we’ve done mouse and dog, and we’re looking forward to doing a human now.

Laura Minquini: Thank you, George. Alejandro?

Alejandro Ocampo: Thank you. Thank you. First of all, thank you for inviting me. This is an amazing panel and I’m super pleased to be part of it. Just to switch a little in a different direction for us, we strongly believe that aging is a epigenetic state. We believe that the aging is actually a reversible epigenetic state.

And therefore we think that the dysregulation of the beginning of that, of course, as we age, is probably one of the strongest drivers. So for us in order to target this, we are trying to develop, what I think my name is maybe known for – reprogramming, we are trying to develop a set-up that’s based on epigenetic reprogramming.

 So trying to reverse the epigenome back to a younger state. So this is a little the approach that we are taking. I would like to add, it’s true that the Yamanaka factors have the capacity to do this, but at the end, these genes that are already present in our genome. They are epigenetically silenced.

So for us, even epigenetic reprogramming of Yamanaka factors, endogenous, could be already awake. So we strongly think that epigenome is a main driver. And manipulating the epigenome and reprogramming back to a younger state, could reverse ageing.

Laura Minquini: Thank you, Alejandro. And last but not least, Jay?

Jay Olshansky: Sure. Thanks for inviting me.

My focus is on the logic and the rationale behind why all of these research scientists are working in an area that requires funding and exploring the value of this work for public health and for health span extension. I’m a little curious about the language about age reversal, cause I’ve heard it used several times here and I think the public may get the impression that we’re going to make us into younger versions of ourselves.

I’m 67. If my friends here are suggesting you’re going to turn me into a 20 year old version of myself, I would most welcome it, of course. But I don’t think that’s really what we’re talking about. So I would just urge caution about how we present this to the public. And then also in terms of lifespan itself, talking about 150 year old people, when the maximum lifespan we’ve observed is 122, even if we had a therapeutic intervention that could make us live to 150, we wouldn’t know that it worked for at least 30 to 40 years.

So I just want us to stick to science.

Laura Minquini: Thank you, Jay. That’s very interesting to have the public policy side of things here in that. We’re very glad that you were able to make it. Nathan, going back to the science, your question?

Nathan Cheng: What Jay mentioned is a good segue, right? So when we’re developing therapies that modulate aging perhaps slow it down, or whatever, I guess we should ask the panelists how do we know that these therapies that are being developed in scientific labs or being brought to clinical trials, are actually having an effect on aging?

Maybe we can start with Nir?

Nir Barzilai: Yes. Sure. The fact that Jay is 68 years old has to do a lot with the fact that at once one point we built sewers and we cleaned the water and we developed surgery and immunization. So we’re not going to one day wake up and say, “okay, this is 150 years.”

I think Jay alluded to other things. The major mission is, which is a frustrating mission is that you really need the FDA ,or the governments, or the world to understand that aging is preventable. And that there’s a lot of data to suggest that aging could be as the biology, that can be targeted.

It can be delayed. It can be stopped. It can really be reversed in certain situation, like in older people, if they have enough of senescent cells. And so the challenging is, to do a study that will open the gates so that pharmaceuticals will help the biotech, and there’ll be lots of studies out there.

So besides doing this study, the other thing that is missing, and it’s a kind of a catch 22, is those biomarkers for aging that Kristen can talk more about. We are just shy, and I think it’s going to be rapid now, but we’re just shy of having those biomarkers because after all, we don’t want to do a phase three study with billions of dollars to fail.

We need in several weeks or months to know if any tool that we have or any gero-therapeutics that we’ll have, will have this effect. So those are the two things on my mind, most of all.

Jay Olshansky: Good. Can I amplify this? What you’re talking about? So Nir is raising a critically important point here.

And that is, the first thing is to recognize something that a lot of folks still don’t recognize, which is the simple conclusion that aging itself is inherently modifiable, that has a profound conclusion in the world of aging science and aging biology and in public health. And let me just state that we don’t need to talk about adding 20, 30, 40, 50 years to life.

We don’t need to talk about immortality. All we need to talk about, is the delaying aging by one year. One year, in and of itself, would have a huge impact on quality of life, public health, and the economy. Just one year. And that’s all you need to argue here. And it’s now been documented in the literature what the economic value is of a single year of healthy life extension.

So, let’s just shoot for something that’s achievable and measurable.

George Church: So this is George. I agree with Jay that we need to have an impact of a year. But sometimes it’s hard to. You need a large cohort to show that it is a year of extension, but maybe less, a smaller cohort to show that you have reversal of a disease and to Nir’s point about convincing the public or the FDA about prevention, I think it’s a little bit easier to show that you have reversal of a disease. I agree with Jay that we don’t want to act like we’re 20 year olds or act like we’re going to be 20 year olds. But if we have reversal disease that fits much more into the standard logic of the FDA, but it can have with it, the prevention of all the other diseases as a side effect.

So rather than promising longevity or promising prevention, which is very hard to get FDA approval of treating an already healthy person, we can go with the flow and actually do reversal of a variety of diseases that have very little uncommon. Other than that, they have underlying epigenetic phenomenon that causes them to increase tremendously with age.

So we’re curing or reversing these diseases by a common mechanism. But all we have to do is extend someone’s life by a year that has one of these many common and deadly symptoms.

Kristen Fortney: Yeah, just to chime in there. I think that’s a really important point that aging and disease are two sides of the same coin, right?

You don’t have aging without disease. And for those of us that are in the clinic working on a true aging target or a true aging drug, it will have a significant impact on really multiple different age-related diseases, and that might be the first fast clinical path that’s practical.

But, to Nir’s point as well, right? Ideally you’d like to know in the course of your trial that not only is it just relevant to this one disease, but that you are ultimately affecting fundamental processes of aging. And to that end, I think that we all believe that biomarkers are going to be really important.

Something that really predicts your aging state, your lifespan, your future health span. I think the field has made tremendous strides just in the last decade, in terms of building really predictive markers from genomics data, like the methylome, the proteome the metabolome, and those are heavily used in research now.

And I hope to see them start to be used in the clinical setting as well.

Nir Barzilai: Can I add just… When you’re a clinician and when you go to medical school, the first thing they teach you is to do no harm. Okay. So that makes you conservative immediately.

And the second day they say there’s no always, and there’s no never in medicine. So you lose confidence. And I’m saying that just because those are the people who are making these decisions. So from their perspective, look what happens with a simple example of Metformin, a cheap generic safe drug that they’ve shown first of all, to prevent diabetes and people who don’t have diabetes.

The FDA is reluctant to approvement Metformin, for the prevention of diabetes. A study like a phase three trial that has occurred already. Not to talk about the fact that Metformin is shown to decrease cancer, Alzheimer’s, cardiovascular and mortality in clinical and association studies. So we have to think of it this way.

And by the way, everything you said is true, we have to do it in parallel. But if we really want people to focus about aging, if we want pharmaceutical to have this breath to say, we’re developing a appeal that everybody will take and you know what, they’ll take it for decades. If we want that, we need also to do the whole thing and not only diseases, which is a way to get money in order to get to aging. In my mind, mainly.

Laura Minquini: Jim, as an investor, how this is regulation or the way things affect investments and where the capital is allocated?

Jim Mellon: Okay, Laura. I think that the biomarkers is a very key parts of this, but obviously the FDA has to be persuaded that the biomarkers are an acceptable substitute for lengthy trials. And that’s going to be a big deal, if that happens. I think that the biomarkers are getting ever more sophisticated.

Biological clocks are getting ever more sophisticated and they’re going to be very accurate and potent I’m sure. In two or three years time. But we need to get the FDA and other regulatory agencies like the EMA to accept that they are good substitutes for lengthy trials, since human beings live relatively long lives.

The second thing is, I completely agree with Nir that Metformin is a very obviously… And Nir as Mr. Metformin in the world, I completely agree. And that is a no brainer in terms of its ability to do something in the field of aging. But I also think, and just to get back to my earlier point, that we’re in the dial-up phase of the internet at the moment. We really don’t know who the winner of the web browsers, the winner of the internet providers and all that sort of stuff is going to be. But we know that someone’s going to win.

Ultimately I agree. I also agree with Jay that one year would be a good start. But it’s really one year as a rounding error in terms of how long we live. Maybe we should go for 5 or 10 years as a sort of a objective to begin with. And we certainly don’t want to scare the horses by suggesting that everyone can live to 150 by some sort of pharmaceutical approach.

Cause that’s just not going to happen for a while. We do this thing in increments and then suddenly the increments become big jumps.

Avi Roy: Thanks, Jim. Alejandro, any comments before we move on to the next question about the biomarkers of aging or any other comments that any other speaker made?

Alejandro Ocampo: Yes. So I completely agree with most of the things that have been said. For us of course, if we think about epigenome as a main driver, of course we are very enthusiastic about DNA methylation production or any other clock that chemists are using based on the epigenome. I feel that the majority of the field does not agree on the value of these biomarker.

So I think maybe one of the first things we need is to agree on what biomarkers have good value to measure ageing. Because before that, it will be impossible to convince the FDA or investors that they should really allow us to run a trial. So I think again, methylation clocks for us are good. I think they are very accurate, but I think that there’s a large part of the field that does not believe they are good biomarkers.

I think sometimes because we confuse a good biomarker with a driver. I am saying that DNA methylation is good, but I’m not necessarily saying that DNA methylation drives aging. I think we can look at it and we can measure aging, but not necessarily say that these changes is what drives the process.

And then in a second line, I would like to add that blood for us, I completely agree with what Kristine and the team are doing, I think blood has a lot of value. Everything you can do in the blood from genomics to proteomics, to analyze cell populations, markers of senescence. So you will have a tremendous value there.

And of course, don’t forget, what people care about, how people behave, how they perform. Both functionally and also cognitive. And lastly, of course the incidents. So I would like just to group all together. But I think we need first to start agreeing on good biomarkers of aging.

Laura Minquini: Thank you, Alejandro. I just wanted to quickly say that Jay will have to step off the panel, but thank you again for being here and I’m mentioning public policy. Which is quite important.

For my next question, we’ve touched on public policy and regulation. So this weekend Richard Branson went to space and while some of us saw great feat of science on a 70 year old man accomplishing a lifelong dream, others saw a billionaire wasting money. Longevity also has this perception problem of by the media being deemed a fancy of billionaires. Do we think it’s important to change this and how do we do it, or how are your organisations doing it?

Nir Barzilai: Let me just say, first of all, I think scientifically didn’t go to space. But I would say that, that those who support this effort, and I have nothing against this effort, you should know that our mission is humanity’s not to go 50 miles if we want to go to Mars. Okay. We need to solve aging, first of all. Okay. So this is for me the connection. But it’s more than that. We’re not talking on me about aging. We’re talking about people who survive from cancer because they got chemicals and radiation that accelerated their aging.

They’re aging rapidly. They need help. People who have HIV die 10 years younger than their cohort. People who are debilitated, in wheelchairs. They have very bad health span and short lifespan. It’s not only about aging. There’s a lot of others who need help. And I think we have to frame it differently, so people don’t think that this is just a life extension this is something that’s important for humanity, whether to the poor unfortunate, or to those who want to go to space.

Jay Olshansky: Can I follow up one thing before I leave? So, just to reemphasize what Nir is saying here. This question comes up all the time. Whether or not we should be spending precious resources on reducing infectious disease mortality versus going after aging.

And I’ve heard it multiple times that this is all a waste of money, billionaires trying to extend their lives. That’s not what this is all about. This is a fundamental foundational public health effort like we saw something like this a little over 120 years ago with the foundation of public health, but with the introduction of antibiotics and vaccines. This is on the order of something like that. And what we’re talking about, and I think the language we should be using involves something simple, a simple metric that is referred to as a person year of healthy life. And think of a person year of healthy life as one of the most valuable commodities that exists on earth. And you talked to any of the billionaires of course, and they’ll trade their money in for healthy life any day of the week. And that’s what we’re talking about here. Is manufacturing through science, through technology, the most precious commodity that may exist which has health span extension. And you get more healthy life added with a one-year or two-year or three-year slowdown in the rate of aging, than you would get with a cure for cancer.

Think about that for a second. The impact has a cascading effect on multiple disease endpoints. And so the benefits are quite large, with small improvements in delayed aging. And I think that’s the logic and the rationale we should be using in general. And it’s the general response to the comment that this is just for billionaires. It’s not, it’s for everyone.

Laura Minquini: Thank you, Jay. And thank you for being here again. This is one of the reasons we have these conversations for people to understand this message. Anybody else wants to comment on this?

George Church: Yes, this is George. I was just going to say, along the lines of taking Jay’s in a slightly different direction, is that where my group is highly motivated to bring down the costs of technology so that it is accessible to everybody.

So we’ve brought down the cost of reading genomes by 20 million fold. The cost of some things, like vaccines drops precipitously once something goes extinct like smallpox. So aging, not just as not being elitist, it is possibly something that reduces costs of medicine in general. Because it might have a preventative mechanism that’s applicable to everyone.

In which case the fixed costs of the clinical trials is amortized over a much larger denominator of individuals. So it could be the opposite of elitists, if we play our cards. So I think that’s an important aspect. And what it’s also amplifies on what Nir said, is that this is not just one disease or about longevity. It really impacts almost every form of morbidity and mortality, including things like falling down and not getting up. So it really could have a huge impact on everyone and therefore be very inexpensive.

Kristen Fortney: I think the economic arguments, as you’ve outlined Jay and George, are incredibly compelling and that these therapies can ultimately help everybody. And I think its a misunderstanding that people are not identifying increase in life extension with health span extension, with freedom from disease.

But even in the very near term, I think it does resonate with people that studying agent can help us. Even in the way that we treat conventional diseases. Because remember, like we spend a fortune every year on treating cancers and research for cancerous, biotech for cancer and for Alzheimer’s disease. Diseases that happen to people that are old, that are in their eighties, that are not in their twenties. But that are still studied. Not usually in the context of aging. Like the most models for Alzheimer’s disease are in these genetic backgrounds that are very unlike how it happens naturally.

So I think there’s a message there too, that looking at disease through the lens of aging we’ll find important new causal targets in the near term. And then ultimately these mechanisms will also be helpful for prevention and for the population at large.

Nir Barzilai: It lets me also point… Andrew Scott was an economist in article that came in Nature Aging, that really looked at the economy of health span from many perspective because it’s not only the health cost. It’s what those guys are healthy doing.

They’re traveling, they’re buying things, they’re doing other things. And the bottom line is that we were underestimating those longevity dividends. If we look from GDP perspective, it can save 36.9% of GDP, if in the next 10 years we’ll extend health span by 2.6 years only. It’s 83.6 trillion dollars.

You should look at the figures in this paper and we have to really use it simply to explain to economies to people in the government that the longevity dividend here is huge. And then we can have money to do other things too.

Jim Mellon: I’ll just say, and thank you, Laura. I’ll just say that there has to be a price for innovation.

Some of us involved in the pharma development business, and, you have the greatest innovation in the United States, I think, drug prices ab initio have to be relatively high. Otherwise people won’t develop drugs. And that’s a straightforward proposition.

But the great news is that we live a long life, as I said earlier on, and the commercial exploitation period for drugs is only about 10 years. So very quickly, these drugs will be in wide dispersal across the populations in rich and poor countries alike. So I think that the initial inventors of these products have to make a profit, because the rate of failure is so high and the cost of innovation is so high. But very quickly, the price comes down to basically peanuts and it’s accessible to everyone. And I’ll give you a very brief example of that in earlier times.

Anti-ulcer drugs were developed in the 1980’s and they were very expensive drugs like Zantac or Tagamet or Omeprazole, they were really expensive drugs and people died of ulcers.

And today, you can go into Walgreens or Boots or wherever you are and buy them for almost nothing. And it will be the same with aging drugs. So this idea that it’s only for billionaires, it’s elitist, all this sort of stuff is absolutely nonsense because it will be accessible to everyone within 10 or 20 years.

Laura Minquini: Thank you. Alejandro, please go ahead.

Alejandro Ocampo: I would like to actually remind everyone that actually, when we speak about breakthroughs, I think, yes they will happen at some point, but I think first we need to make simple things to happen.

Now, I think in the aging field, if we compare the longevity with going to Mars, I think, first of all, you need to go to the moon, then we need to be able to fly a rocket. So I think even the early first steps have not been done. Like to me, to have even a trial for anti aging drugs needs to happen before we have a ultimate breakthrough where we can really reverse. And also to me, I want to be very cautious here. And to say that I think the first drugs that will be out there, would be drugs that you will take very frequently in a preventive way.

And then ultimately, at some point when we learn from all that you will have drugs that will reverse aging. But I think we need to go in step by step.

It’s true that now, why this time is different, is because the society and the world is feeling that aging is actually a real problem. In the past they just say it’s something natural and there is nothing you can do about it. So in the moment, the public has started to learn that it is something you can maybe do something about. And actually it’s important. Aging is becoming a real problem. Society, pension, retirement… It’s the climate change of the money, I hear people saying sometimes.

So I think, that personally, that societies interest is clearly accelerating. But I think still we are in the first steps of making this happen.

Laura Minquini: Thank you. Indeed, longevity and science is the promise for us to live longer with health, which most people would say yes, if they knew they had that choice.

And that’s why we want to hear from all of you directly explaining this to the audience and everybody who is curious about the field. With that said, I’m just going to quickly reset the room. And we are in our set on the future of longevity panel discussing the science of longevity with the most prominent scientists, innovators, and investors in the field.

And we have Nir Barzali, Alejandro Ocampo, Kristen Fortney, George Church and Jim Mellon. And co-hosting with me, Nathan Cheng and Avi Roy. And we are going to move into the Q&A part very soon. We’ll let you know, as soon as we start that up. Please remember to keep your questions short and not to make them about health recommendations.

Well that’s, it. I can’t remember it’s Avi or Nathan that has the next question. Please go ahead.

Avi Roy: I’ll just jump in. Jump straight up. This one will be a little bit exciting and hopefully audience, you will benefit from this. Nir, Alejandro, Kristen, you guys all have a vision of what the future looks like.

Jim, you were an investor. So you invest on that. What do you imagine that the world is going to be 10 or 20 years from now. I know that he even talks about that. George, you do that about technology. Nir, you will have been involved in clinical trials or are you now Kirsten? And of course Alejandro, as a scientist, you are definitely imagining what the future entails. So, the question is about two or three things that you fundamentally believe is inevitable in the future of longevity, aging, and health, and just pointing out about the next 10 years. And also, if you could talk about the obstacles that might prevent it from happening.

So anybody who wants to start with that. So two or three things that you fundamentally believe is inevitable in the future of longevity, aging, and health, and what are some of the obstacles?

Nir Barzilai: I sure can start. I want to quote Bill Gates, who said we are overestimating what we can achieve in two years and underestimating what we can achieve in a decade. I would take it and say, if I can predict the future, I’ll do it very expensively. So are there are four scenarios.

And by the way, I got those scenarios from this paper through school. There’s the Gulliver approach where Starbridge got older, but never died. But we don’t want that. We don’t want to extend lifespan without extending health span. Fortunately, we know that if we target aging, we do both.

So the next possibilities to do a Dorian gray scenario where Dorian gray, the mirror when he looked at the mirror age, but he stayed young. In other words, how or stayed in the same age, I should say. So how can we stop aging in people who are already old? I think this is something that’s achievable. We can start with simple drugs, like you all know, or exercise and stuff, and actually gain some years until George is doing the, the genetic therapy.

And then there is the Peter pan example, right? Where. Peter Pan doesn’t age. And I think that in the future, probably we’ll think about, we don’t have to stop aging when it happens. We have to stop aging before it happens. And maybe in in one monthly genetic epigenetic clearing will be all we need to stop it aging.

And of course there’s the Wolverine that that takes old and makes them young. I hope that we don’t need to do that, but in a certain way, the senolytics are doing that. They’re taking old people with a lot of senescence cells and we’ll make them much younger, at least functionally.

So I think that the vision is there. We have to work on it in parallel and we’ll get it at different times.

Kristen Fortney: What I believe is going to be true for human aging and true pretty soon is that we’re going to discover that really a lot of different things are going to work a lot of different mechanisms, a lot of different targets. Like I’m pretty bullish here. And I think the field is wide open and longevity science.

We have, I would say we’re still mapping out. What’s the most important for human aging, but we know, for example, like all the different things that can make a worm live longer, people have done these, genome-wide experiments.

And the answer is that hundreds of things can make a worm live longer and healthier. And while I expect the identity of those things to be different in humans, I expect the scale to be similar. There’s probably lots of different pathways you can intervene in, as Nir mentioned at the beginning, right, these centenarians seem to be living two to a hundred via different mechanisms. And probably those are going to be.

And in terms of what could get in the way of us making that discovery is just really not trying enough things. I think that we need to really do a lot of experiments in the clinic, in human populations, with safe and promising mechanisms.

Alejandro Ocampo: I can actually come in. So I actually believe in four things that will happen. The first three are actually interconnected. So I do believe that we will have drugs or therapies that will slow down or even reverse aging, that the regulatory agencies like FDA will approve aging as an indication, and that the investors will invest in developing anti-Asian drugs, that target aging organismal ageing.

I think the three of them need each other. I think scientists need to provide those drugs and those biomarkers regulatory agencies, when they believe in those, they will accept and allow you trials and investors will finally decide to invest.

So I think those three are actively interconnected. It’s like the chicken and egg.

And then the last one I want to mention is I do believe that there finally, the biomedical research field will realize that modeling age-associated diseases in young mice is useless. So I do believe that people will start using aged mice in order to model this sort of stuff.

Jim Mellon: Can I just say something, Avi, what is rather sad is that, is a lot of us on this call do multiple calls and there is a small cadre of people who will listen, but the big story has not yet got out there. And as a result, only of relatively small amounts of money, we think about $4.5bn has gone into the private sector of aging and a very small amount of the government research budgets around the world has got into aging, even though it’s probably the most critical scientific endeavor of anyone’s lifetime.

I think all of us need to find a way of getting our message out to a newer audience and also to an audience will bring much more money into the sector. Because if there’s not much more money, then we’re probably in five years time, could we be talking about more or less the same sort of stuff. So, I don’t know how that’s going to happen, but it’s very important that it does happen.

And Kristen, Nir, other people were older joining forces to try and make that happen, but it’s a difficult thing to happen. Meanwhile, cannabis attracts $100bn dollars of investment, psychedelics $20bn of investments, and Richard Branson going to space, I don’t know how much that costs, the wrong priorities are getting lots of money and we are not getting enough.

Avi Roy: Thank you, Jim. George, any insights?

George Church: Yeah I agree with Jim, that we need to have to expand the audience. A couple of ways to do that is one is to show results in a rapid way, and one way to do that is via veterinary. So a lot of people love their pets. And so one of the things we’re doing at rejuvenate bio is aiming our first wave at dogs, because the approval process is faster, the costs are lower and people can get can see where their own eyes, the impact of things that have been proven already in mice.

So that’s one approach. The other approach is that reaches, instead maybe a thousand people that this particular program will reach, you can reach tens of millions with television and movies and books, and magazines. So in in organizations like pgs.org that they have a conduit to a screenwriters and other writers.

So I think those are two things that could get a better set of priorities. I completely agree with them about that. And I agree with Kristen about how there are many ways to solve the problem, for example, in worms. But most of those ways are fairly small effects. And so we might want to combine them combinations are not always additive, sometimes they’re antithetical, and sometimes they’re synergistic, so that’ll take some finesse.

But I think we need to really probably have to get everything, all the pathways straight. So even though there’s many routes of making a small impact, there may be a slightly more difficult, but still something that could happen in the next couple of years because of the exponential technologies we have that we can get all the pathways right all at once. So I think that’s maybe the nuanced

Laura Minquini: Thank you, George. Longevity definitely needs somebody like an Oprah being an enthusiast, and I think we would see a very big jump in enthusiasm from the general public.

We would like to say a huge thank you to all of the panelists for giving us a portion of their busy schedules, and providing such an enlightening and thoroughly fascinating conversation. Our thanks also goes out to the hosts who cultivated such a fantastic discussion!

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