Today the HKRB is delighted to run a special interview with none other than Aubrey de Grey, the internationally renowned author and scientist whose work is among the most controversial and exciting in the entire field of the sciences. The HKRB interview series interviews the most exciting authors in the world about their new work. Follow it on Facebook.
de Grey researches the ways in which regenerative medicine and technology can prevent and reverse the ageing process. With his project SENS (Strategies for Engineered Negligible Senescence) de Grey not only works on scientific techniques to rejuvenate the human body and stop the ageing process, but he also explores the ideological issues of technology that could transform our entire conception of ageing, lifespan and linearity.
Later this year he has an interview book coming out with Douglas Lain, the novelist and publisher of Zero Books. This HKRB interview gives a taster of what is to come in this project. Read a little more about it here. Interview by Douglas Lain.
Douglas Lain: Let’s start then by defining our terms and figuring out the full scope of the project that your foundation SENS is working on. That’s “Strategies for Engineering Negligible Senescence.” That’s what SENS stands for.What is aging? This is what you’re fighting. What is aging and how do you and others who are working on achieving negligible senescence define that term and how does the scientific community think about aging, perhaps in contrast to how you think about it?
Aubrey de Grey: Aging is a really simple phenomena. A lot of people in the broader world presume that aging is still a mystery, that nobody understands really what’s going on. But that’s bullshit. The actual fact is that people who study the biology of aging feel that they have a pretty good understanding of what’s actually going on. Sure we could always get a better understanding, there are details that are still unclear, but at the end of the day the fundamentals are really well understood.
The aging of a human being, or any living organism, is actually really similar, really very similar, to the aging of an inanimate object like a car or an airplane. It’s simply the accumulation of damage as a side effect of the machine’s normal operation. So, in exactly the same way that a car will progressively accumulate rust and eventually the doors will fall off, similarly the human body accumulates… well, the equivalent of rust, various types of molecular and cellular damage, and eventually that damage accumulates to a level of abundance that is more than what the body is set up to tolerate. And that’s when the overall function of the body starts to decline.
That’s all that aging is. It’s a really simple phenomenon. That’s not controversial at all, you ask any gerontologist, any person who studies the biology of aging, what aging is, then they may use slightly different words, but essentially they’ll say what I just said. Then the question is, what will we do about it? And certainly there are many different approaches that people have taken to that.
I believe the approach that the SENS Research Foundation is taking, which is essentially a comprehensive damage-repair approach, is the most promising. But, some people have been working hard for a long time on the idea of simply slowing down the rate at which the body creates that damage in the first place. And that’s another alternative. No question. It’s another alternative. As things stand it looks to me very much as though that alternative is never going to work. It’s not. It’s far less practical than the damage-repair approach. But, we shall see.
DL: Maybe the people who are working on slowing down the damage that the body does to itself have a slightly different conception of what aging is. They tend to talk about changing the genes, almost like we have a clock that ticks through our lives, and then at a certain point the alarm goes off. Am I misunderstanding this? Is there a slight difference here in the perspective on aging?
AdG: Yes you are misunderstanding. There is really no difference in perspective. Everyone understands that ultimately the reason why an older body works less well than a younger body is because the older body is carrying around more damage. The damage has come to exist as a result of the body’s normal operation. The things that body has to do to keep us alive. There is really no controversy about that.The only real controversy is with regards to what is plausible in terms of dealing that damage, in terms of making that damage go away, or slowing down the accumulation of that damage. So, the language that is often used, especially when gerontologists talk to the general public and journalists, may be a little misleading sometimes. Some of my colleagues, for example, let me pick out Cynthia Kenyon who is a good friend and an excellent scientist, but she sometimes is prone to use language that journalists misunderstand as in some way implying that aging is the consequence of some kind of program. She doesn’t really mean that, she is just talking about the modulation, the ability of the body to modulate the rate of aging in response to certain pressures. And she’ll often, of course, speak about her own work which is in very short-lived organisms. But, ultimately there is not a fundamental difference between her view and my view of what aging actually is.
DL: Have previous attempts to overcome aging… there’s a long history of people working to defeat aging, going back to really pre-scientific times. Have previous attempts to overcome this process had a different conception of aging?
AdG: That’s a great question. I really don’t think they have. I think that even if you go back to Roger Bacon in the 1200s or whatever, you’ve still got an understanding that aging is a medical problem that should be amenable to medical intervention. And certainly if we go back to, for example, the ’50s when the free-radical theory of aging was first put forward, that was the first really bona fide molecular theory of how aging actually goes on. And there, it was totally clear. Everyone understood, even back then, that the process of aging consists of the accumulation of damage.
DL: To me it seems like there are two different issues once you come to accept that aging is just this process where the body damages itself as it goes through its daily practices and that the damage is going to build up over time, and that when you start to think about intervening, the first thought that comes to mind is maybe not too realistic. It’s about overcoming death. The other though is about extending our good health.
I can imagine that if there really was a program, there isn’t, but if there was a program in the body somehow that just was set so that we all die at seventy-six years of age, that your kind of intervention, what you’re talking about, would still be really worth investing in because even if you didn’t extend life you would be improving people’s health dramatically by undoing that damage.
AdG: Well you’re right. Yeah.
There is an awful lot of talk around gerontologists about the idea of what they often call the compression of morbidity. In other words, essentially extending the healthy lifespan without similarly extending total lifespan. Therefore reducing the gap between the two, the amount of time that people spend at the end of life being unhealthy. That sounds terribly seductive and, of course, it’s very politically correct and that’s probably why so many of my colleagues have spent so much time highlighting their ideas that this might in principle be possible, but in practice it’s not possible at all. Pretty much all of my colleagues accept perfectly well, that actually the only way we’re ever going to extend lifespan is by extending healthspan, by extending healthy lifespan. That ultimately, being frail, being in a bad state of health, is always going to be risky. It’s always going to be a state in which your likely future lifespan is short. Your likelihood of dying soon is high. Therefore, the only way we’re ever going to get any kind of serious extension of lifespan is as a side effect of postponing ill health in the first place, in other words by extending healthy lifespan.
DL: And your organization is working on many things that will extend a healthy lifespan and that I would think people would be very excited about even if they’re not truly interested in longevity. I saw a video presentation on your site about heart disease and macro-phages and undoing the damage done by oxidized cholesterol. I would think that you wouldn’t have to be a gerontologist interested in longevity research but could just be a heart specialist and be very interested in what you’re working on.So, how solid is the science behind that speculation and do you anticipate that this project might be able to contribute to breakthrough therapies before you get everything else in line to truly extend the lifespan?
AdG: You very cogently highlight the issue here – the relationship between the diseases of old age on the one hand and aging itself on the other hand. Essentially what you’re really doing is highlighting the fact that there is no such thing as aging itself. In other words, that all of the aspects of the ill health of old age are intertwined. There is no real profit, no real merit, in trying to dissect them or to bifurcate that set of problems into things that are diseases on the one hand and things that are not diseases on the other hand. It’s just… it’s pointless. It makes no sense, and it’s counterproductive because it makes people over-optimistic about some aspects of aging and unduly pessimistic about others.
In particular, if we look at, for example, the case that you mentioned of the role of oxidized cholesterol in driving heart disease then we can say, okay, yeah, heart disease is the number-one killer in the Western world and therefore if we could develop ways to enhance the robustness of white blood cells so they would be able to continue to process cholesterol without being poisoned by oxidized cholesterol the way they are today, then great! We might be able to more or less entirely prevent heart disease. But what would that mean in terms of the extension of healthy lifespan? Not a lot.
It turns out that, because of the exponential nature of the relationship between age and the risk of these diseases, we would only actually extend healthy lifespan by a few years, three or four years, before all the other things kicked in – cancer and Alzheimer’s and so on – that were also increasing exponentially with age. We’ve got to hit the entire spectrum.
Douglas Lain is a novelist whose books include Billy Moon (Tor Books) and After the Saucers Landed (Nightshade Books), which was recently nominated for the Phillip K. Dick Prize. He is also the publisher of Zero Books and the host of the weekly Zero Books podcast.
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