#027 Reversing Aging and the Future of Longevity. With Aubrey de Grey

00:00:00: Nobody wants to get sick and so they kind of pretend that aging is somehow special,

00:00:08: that it's somehow distinct from the so-called diseases of aging, which it isn't. There's no

00:00:14: biological difference between the so-called diseases of aging and aging itself. There's no

00:00:20: social thing as aging itself. Welcome to HealthWise, the health and longevity podcast brought to you

00:00:26: by Sunday Natural. I'm Nils Berens and in this podcast we explore what it truly means to be

00:00:31: healthy. Together we will dive into topics such as medicine, exercise, nutrition and emotional

00:00:38: well-being, always with a wise perspective on what generally benefits us. My guest today is

00:00:45: Orphe de Grey, a well-renowned biojewron-toll logist and a visionary in the field of longevity

00:00:51: research. He is best known for his groundbreaking approach as to reversing aging and his belief

00:00:57: that aging could soon be treatable. As the co-founder of the S.E.N.S. Research Foundation,

00:01:04: he dedicates his life to exploring how we can significantly extend human life and overcome

00:01:10: age-related diseases. And so I say a warm welcome to Orphe de Grey. Hi there, thank you for having me.

00:01:15: Dear Orphe, how does a perfect Sunday look like for you? Perfect Sunday. Perfect Sunday.

00:01:21: A perfect Sunday is a day when I am not traveling and I am just able to stare at the sky from my

00:01:28: hot tub at home. Okay, sounds very good. So when did you first realize that aging isn't necessary

00:01:34: inevitable? Well, the thing is I didn't really have a time when I realized that because nobody

00:01:43: ever told me that it wasn't treatable, that it was inevitable. You know, it had always been obvious

00:01:49: to me that the human body is a machine which accumulates damage like any other machine and

00:01:57: that this damage can be repaired. And if you do so, then you extend the functioning lifespan of

00:02:05: the machine, just like getting the rust off a car every so often before the doors fall off.

00:02:11: And the thing I didn't realize was that other people didn't think that way.

00:02:18: I only found out in my 30, well, around the age of 30 that most people viewed aging as this kind of

00:02:26: mystery that was kind of woven into the fabric of the universe and there was nothing we could do

00:02:33: about it. And that was a huge surprise to me because it was obviously not true and yet perfectly

00:02:40: intelligent, knowledgeable people seem to think it. That's really interesting. So how would you

00:02:46: explain your concept of reversing aging to someone who never heard of your work?

00:02:50: So the best, the simplest way to explain the way that I think we're going to bring aging under

00:02:57: medical control is to actually continue with this analogy that I just gave about remembering

00:03:04: that the human body is a machine. So if we look at cars or airplanes or whatever, then they have a

00:03:12: warranty period. There's an amount of time that they are guaranteed to last for. But we know that

00:03:18: some cars are working just as well as when they were built, even though they are 10 times older

00:03:24: than their warranty period, like more than 100 years old. And that's because if you use a machine,

00:03:31: it accumulates damage as a consequence of its normal operation, but the machine is set up to

00:03:37: tolerate a certain amount of that damage without any declining function. It's only when there's

00:03:42: more damage than that certain amount that you have a problem, that things start to not work so well.

00:03:47: So if you do preventative maintenance, if you just repair that damage and maintain and restore

00:03:56: the structure and composition of the machine to how it was when it was first constructed,

00:04:03: then it'll carry on working. The definition of a machine really is that its function is determined

00:04:09: by its structure. So if we come to the human body, you know, it's a really, really, really

00:04:13: complicated machine, but it's still a machine. And it accumulates damage as a consequence of its

00:04:19: normal operation. And if we can figure out a panel of treatments of medicines that can repair that

00:04:28: damage and restore the body at the molecular level and the cellular level to something like how it

00:04:34: was as a young adult, then that will stop us from going downhill, from getting sick as a result of

00:04:41: having been born a long time ago. That's the entire idea, really. And of course, the only reason it's

00:04:47: a sensible idea is because one can actually describe what it means in practice. One can describe

00:04:53: what changes occur to the structure and composition of the human body during adult life,

00:04:59: and therefore what one has to repair. And I was able to do that 25 years ago, almost,

00:05:06: pretty thoroughly because people have been studying aging for a long time. So we already knew

00:05:14: what changes occurred. The place where some innovation was needed was to develop ideas for

00:05:23: how we might repair some of that damage. There were some types of damage, like, for example,

00:05:27: cells dying and not being replaced by the division of other cells, that people already

00:05:33: understood, you know, you can use stem cell therapy to repair that kind of damage. But there

00:05:38: are other ones where I had to come up with whole new ways to repair the damage. Okay, excellent,

00:05:42: excellent. There are many skeptics when it comes to longevity research. How do you respond to the

00:05:47: biggest critics of your work? Well, there are not so many skeptics as they used to be. When I

00:05:54: started talking about all of this, first of all, I had to convince my colleagues in the academic

00:05:58: community, and this whole idea of damage repair was a big paradigm shift. Before then, people were

00:06:05: focused only on the possibility of slowing aging down, not of reversing it. And so that I had to

00:06:13: work quite hard to persuade my colleagues that this was a sensible way to think. That took maybe

00:06:17: 10 years. But in the mid-2000s, I guess, I started to come to the attention of the wider world and

00:06:24: started, you know, getting a lot of media attention and so on. And then, absolutely, there was a lot

00:06:30: of criticism from non-scientists, non-biologists, people who didn't really understand what I was

00:06:36: saying at all, but that didn't stop them from criticizing it. And of course, I was ready for

00:06:43: that. It wasn't in any way surprising. But it's just part of the job. If people don't know what

00:06:52: they're criticizing, but they criticize anyway, then you just have to be patient and explain to

00:06:56: them why they're wrong. You talk often about the seven deadly signs of aging. Could you briefly

00:07:01: explain what these are and why they are so crucial? Yeah, right. So as I was mentioning earlier, the

00:07:08: human body is a really, really complicated machine. And so the changes that happen in the body, the

00:07:15: things that are the underlying drivers of aging, these changes, there are lots and lots and lots

00:07:20: and lots of them. But it turned out to be useful to, if you like, classify these changes into a

00:07:29: manageable number of categories. And the reason that's useful is because it helps us to organize

00:07:37: the process of developing medicines that are going to be required to fix this thing.

00:07:42: So I mentioned loss of cells a minute ago. So this is like, obviously, the body is made of a

00:07:49: lot of cells, like 30 trillion cells or something like that. And cells come in different types.

00:07:58: Some of those cells just sit there and don't divide like brain cells, neurons. And that's kind of,

00:08:05: like, sometimes they die, but not very often. Some cells are very much more short lived, like the

00:08:13: cells in the blood, for example, most cells in the blood are very short lived. And they have to be

00:08:18: replaced regularly. So we have cells in our bone marrow that are stem cells that divide and

00:08:25: replenish the cells that the body is losing all the time, the same in the skin, the same in the

00:08:33: lining of the gut. But sometimes we lose those stem cells get depleted. We don't have so many of them

00:08:41: in old, old, old ages we did earlier. And the cells that are not replaced, the ones like neurons,

00:08:47: for example, they also get depleted. Because sometimes those cells die, and they're not replaced

00:08:53: at all. So of course, there's a problem there. Because eventually, after enough cells have died,

00:08:59: you're not going to have enough cells for the organing question to do the job.

00:09:03: So let's take Parkinson's disease, for example. That's a disease of, of course,

00:09:09: of neurodegeneration. And it's caused by cell loss. There's a particular type of cell in the

00:09:14: brain called a dopaminergic neuron, that we lose them rather rapidly compared to other brain cells.

00:09:20: And they're not replaced. But the thing is, we have a set an idea for how to fix that,

00:09:25: which is stem cell therapy. You can just inject stem cells into the right part of the brain.

00:09:30: And they will divide and transform to replace the cells that the body is not replacing on its own.

00:09:36: Okay, so we're not pretty good at that. And there are clinical trials going on

00:09:41: to do exactly what I just described. But then the question is, like, are there other cells in

00:09:48: the body that are also you need to replace? And of course, there are. But you can do the same kind

00:09:54: of thing, not exactly the same thing, but nearly the same thing. You can do stem cell therapy.

00:09:59: Different stem cell therapies for different cell, different organs have some differences.

00:10:05: But there are only differences of detail, which means that once you've got stem cell therapy

00:10:10: working reasonably well for one or two tissues, you can get the next one working on the one after

00:10:15: that much more quickly, much more easily, because you can reuse the knowledge, the expertise that

00:10:19: you gained in all the trial and error that you had to go into to get the first one working.

00:10:24: So that's why this classification is useful. So I had this, these seven deadly things, as you

00:10:29: rightly call them. These were categories of types of damage that accumulate in the body.

00:10:36: And they were for each one, there was this generic approach to doing the fixing. So for the cell,

00:10:42: last it was stem cell therapy for waste products that accumulate inside the cell. I had this idea

00:10:50: of using genes found in bacteria to break them down, things like that.

00:10:54: Okay, excellent, excellent. So when you look at the current technologies, which from your point

00:11:02: of view is the most promising, you said already stem cells, is this the most promising for you at

00:11:07: the moment? There's definitely no one thing that's the most promising. You can't really have that,

00:11:12: because we've got all these different types of damage, they need different approaches to fixing

00:11:17: them. So all of these things need to be developed and given to the same people at the same time.

00:11:22: There's no one that's the most important. However, what I will say, and it's very important when we

00:11:28: look at biomedical technologies to remember that

00:11:31: Aging is not something that we work on in isolation.

00:11:36: The most useful, many of the most useful technologies

00:11:41: that are going to be involved in treating aging

00:11:45: in this way and repairing the damage of aging

00:11:47: are ones that are equally useful across the whole of medicine,

00:11:52: not just aging.

00:11:53: So for example, CRISPR, which is this way

00:11:56: to modify the genome, that's useful for diseases of child

00:12:01: who just as it's useful for aging.

00:12:03: - Excellent, excellent.

00:12:06: So when you, we are at the moment here now on a conference

00:12:10: and we also have seen a lot of many new researchers here.

00:12:14: And when you look at some of these technologies

00:12:17: which are presented in terms of drug discovery

00:12:20: and things like that, are there anything

00:12:22: which you might see also extremely promising

00:12:26: for the future?

00:12:27: - Oh, definitely.

00:12:28: I mean, one of the big things that I always

00:12:31: emphasize when I give, well, I get interviews,

00:12:34: and also when I give talks is that 20 years ago

00:12:38: when I first started talking about the seven deadly things

00:12:41: and the way to fix them, I only had one approach

00:12:45: for each of the seven types of the categories of damage,

00:12:49: one possible way of going about fixing it.

00:12:52: And now for each of the seven, there are multiple approaches

00:12:55: that are out there.

00:12:56: So for example, cell loss, that we were talking about earlier,

00:13:00: we had stem cell therapy, but that's all we had.

00:13:02: Now we've got this thing called partial reprogramming,

00:13:05: which is a system for getting cells

00:13:08: that are already in the body to behave more like stem cells

00:13:13: than they normally would.

00:13:15: And to therefore be able to regenerate and replace

00:13:20: lost cells more effectively than they normally would

00:13:24: in an old person.

00:13:25: This is a very new idea.

00:13:26: It was only first started to be developed just a few years ago

00:13:31: as a result of work that was published first in like 2006,

00:13:36: which was after I had come up with the original scheme.

00:13:39: - I found it very interesting.

00:13:40: Yesterday there was a presentation

00:13:41: about the 12 hallmarks of aging,

00:13:44: and that at the end, most of the 11 hallmarks are caused

00:13:48: because of one hallmark, the dyspiosis.

00:13:52: Do you have an opinion about that?

00:13:53: - Yeah.

00:13:55: So all of the so-called hallmarks of aging

00:13:58: are linked to each other in one way or another.

00:14:01: So I mean, you could think of my seven deadly things,

00:14:04: as hallmarks before hallmarks were cool, right?

00:14:06: That was the original list of hallmarks.

00:14:10: And the more recent attempts to classify aspects

00:14:15: of aging into these hallmarks are actually,

00:14:18: I don't think they're quite as good as my one was,

00:14:21: largely because they are not built on the need

00:14:25: to have corresponding repair approaches.

00:14:30: They're more of just kind of a classification

00:14:32: for the sake of classifying.

00:14:34: But the thing is everything talks to everything else.

00:14:37: So there are other people who would say that cross-linking

00:14:41: is actually the hallmark that matters the most,

00:14:44: and it causes everything else.

00:14:46: But that's also a bit of an exaggeration.

00:14:48: Essentially, you can't have a hierarchy of these things.

00:14:52: Each of them has influences on the others,

00:14:54: but that goes in both directions.

00:14:57: - Okay, excellent.

00:14:59: So what would you say?

00:15:00: How realistic is it that we will see

00:15:02: a complete reversal of aging in the near future?

00:15:05: - Well, so of course, I've been thinking about time frames

00:15:07: since I started in this field.

00:15:09: At this point, I think we have a 50/50 chance

00:15:15: of getting to a pretty effective level of comprehensiveness

00:15:20: in developing these damage repair approaches

00:15:23: within the next 12 to 15 years.

00:15:25: So the second half of next decade.

00:15:27: - Yeah.

00:15:28: - And so that's a threshold that I call

00:15:31: longevity escape velocity, which is,

00:15:33: you know, the point where we haven't necessarily

00:15:37: completely fixed aging, but we've fixed enough of it

00:15:40: to be able to buy us maybe 20 years of additional life,

00:15:43: which will be enough time to figure out

00:15:46: how to make it even better and so on.

00:15:49: - What would you say are the biggest obstacles

00:15:52: when we need to overcome this achievement?

00:15:54: - The main obstacle is that still society

00:16:00: is terrified of getting its hopes up.

00:16:05: Almost everybody in humanity is absolutely terrified

00:16:10: of aging, so much so that their only way of coping with it

00:16:13: is to pretend that they're not terrified at all,

00:16:14: to make these stupid, you know, arguments

00:16:17: that aging is some kind of blessing in disguise or whatever.

00:16:21: And so aging is not taken seriously

00:16:23: as a medical condition the way it should be.

00:16:25: And that means that there's not nearly enough money

00:16:27: being spent trying to develop these things.

00:16:30: At the moment, I still have to spend most of my time

00:16:32: just raising a small amount of money to get work done.

00:16:36: - Okay, so in terms of the society,

00:16:39: what would you say is a view on stop aging?

00:16:43: Because I think a lot of people are thinking

00:16:45: that this is, aesthetically, not justifiable.

00:16:50: - So a lot of people say that it's ethically not justifiable,

00:16:55: or words to that effect.

00:16:56: But of course, do they really think that?

00:16:58: I don't think so.

00:16:59: Because, you know, nobody wants to get sick, right?

00:17:04: And that's all we're talking about.

00:17:06: We're just talking about stopping people

00:17:08: from getting sick.

00:17:10: It's as if, like, it's like saying that

00:17:13: it's terribly good to be trying as hard as you can

00:17:16: to do something just so long as one doesn't succeed.

00:17:21: It's ridiculous, right?

00:17:22: It's absurd.

00:17:22: Nobody wants to get sick.

00:17:24: And so they kind of pretend that aging is somehow special,

00:17:29: that it's somehow distinct

00:17:32: from the so-called diseases of aging, which it isn't.

00:17:36: There's no biological difference between

00:17:39: the so-called diseases of aging and aging itself.

00:17:43: There's no such thing as aging itself.

00:17:45: - Yeah.

00:17:46: What would you say, how likely it is that this

00:17:50: could become just a privilege of the, let's say, rich people?

00:17:54: - There's no way in the world that that would ever happen.

00:17:57: And it's very easy to explain why it couldn't happen.

00:18:00: The simple answer is, aging is extremely expensive

00:18:03: for society, extraordinarily expensive,

00:18:06: like the vast majority, 80%, 90% of the medical budget

00:18:10: of the Western world goes on the health problems

00:18:12: of late life.

00:18:13: If you can stop those health problems from happening,

00:18:15: you save a lot of money, right?

00:18:17: Now, of course, even if you have to spend some of that money

00:18:22: on the therapies, the preventative therapies

00:18:24: that stop people from getting sick when they get old, fine.

00:18:27: But you still, the therapies will pay for themselves

00:18:31: many, many times over really quickly,

00:18:33: which means that it would be economically suicidal

00:18:38: for any government not to make sure

00:18:40: that these treatments are available

00:18:43: independent of the ability to pay.

00:18:46: - longevity could have a significant impact

00:18:48: to the global population.

00:18:50: What is your view on that?

00:18:51: - This is probably the single most common criticism

00:19:00: of this kind of work.

00:19:03: They say, "Oh, well, we put all the people."

00:19:06: And of course, you could argue that today

00:19:08: we already have a problem of overpopulation,

00:19:11: and that's why we have like climate change

00:19:12: because there's so many people.

00:19:14: But this is not because of the number of people.

00:19:17: This is because of the amount of pollution that people make.

00:19:20: So everything that we're doing now

00:19:23: to develop other technologies like, you know,

00:19:25: carbon capture or, you know, bacteria that eat plastics

00:19:29: or artificial meat, things like that,

00:19:32: these are going to reduce the amount of pollution

00:19:36: that people make.

00:19:37: So we will actually have less of an overpopulation problem

00:19:40: as we go forward, even if we have more people.

00:19:43: We also remember that we will only have more people

00:19:46: very slowly, you know, even though we,

00:19:49: even if nobody dies at all, then we've still only got,

00:19:53: like people are only getting older at one year per year,

00:19:56: right?

00:19:56: And so, you know, there's no way that you possibly have

00:20:01: like 20 billion people on the planet

00:20:04: for 100 years at least.

00:20:07: And, you know, it's generally a bad idea

00:20:10: to make decisions today on the basis of what to do today,

00:20:13: on the basis of what you think the world

00:20:15: is going to be like 100 years from now.

00:20:17: We have no idea what the world's going to be like

00:20:19: 100 years from now.

00:20:20: I wish I could be more, you know, useful than that,

00:20:23: but I don't have any magical secrets.

00:20:25: The main thing that one can do is, first of all,

00:20:28: don't die in stupid ways when you're young,

00:20:33: like don't get into a car accident.

00:20:35: And secondly, do whatever you can

00:20:39: to speed up the research, right?

00:20:41: So that you have a better chance of benefiting

00:20:43: from that research, of things that don't yet exist.

00:20:47: So, you know, write me a large check if you can.

00:20:49: If you don't have a large bank balance,

00:20:52: you could interview me, for example,

00:20:54: or you could just be and get involved in advocacy.

00:20:58: Or if you're a scientist, get into an impactful area

00:21:02: of research that's relevant to this kind of work.

00:21:05: So what would you say, how does your work

00:21:07: and your knowledge of longevity

00:21:08: influence your own lifestyle?

00:21:10: Well, my lifestyle is, like,

00:21:16: it's really defined by my work.

00:21:21: You know, I spend a lot more time than I would like

00:21:24: travelling and, you know, travelling around the world,

00:21:27: giving lectures, going to conferences and so on.

00:21:31: Because I have to get the word out.

00:21:33: I have to get people to understand what's going on

00:21:35: and why it's important.

00:21:36: And finally, what is your biggest dream

00:21:38: for the future of humanity

00:21:40: if your visions of reverse aging becomes a reality?

00:21:44: What's my vision of humanity?

00:21:46: Well, honestly, you know,

00:21:49: it's a world in which there are lots of people

00:21:53: who were born a long time ago,

00:21:55: but there's no one biologically old, right?

00:21:57: And so basically everyone's healthy, right?

00:22:00: And that's a very nice world to be thinking about.

00:22:02: No one gets sick.

00:22:03: That would be nice.

00:22:05: Excellent. Thank you very much.

00:22:06: May I ask, do you take any supplements on a regular base?

00:22:12: No. Not at all.

00:22:13: That's right. Yeah. I mean, you know,

00:22:17: it's decidedly unclear whether supplements do you good or not.

00:22:22: I mean, but the point is,

00:22:24: they have different benefits for different people.

00:22:27: Everyone's different. Everyone's got different needs.

00:22:30: And I just seem to be well-built.

00:22:32: You know, I can eat and drink what I like and nothing happens.

00:22:34: And I don't even need to exercise.

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