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Aubrey de Grey

either not come into being in the first place, or they ought to have died and for whatever reason they haven’t. An example would be in the fat, in the abdominal cavity, which is important for bringing on diabetes. 

Number three is mutations in our chromosomes. This, of course, is very important in the cause of cancer, and, in my mind, that’s almost certainly the only thing that mutations in our chromosomes actually matter for.

Number four is mutations in a special part of the cell called the mitochondrion. It’s the only part of the cell that has its own DNA apart from the chromosomes, but that DNA matters as well, and mutations there don’t give us cancer but they do other stuff. 

Then number five is that, in our arteries and other tissues there are structural proteins that give them the shape and elasticity that they have, and these biomechanical, biophysical properties degrade with time, largely because of chemical reactions that cause extra chemical bonds between proteins that shouldn’t be there. These bonds build up and cause hardening of the arteries, for example.

Number six is, again, in the space between cells. But here it’s not changes to the structural proteins; it’s just the accumulation of aggregates of protein material that the body is incapable of breaking down. In other words, the accumulation of garbage. The best known example of this is the formation of a substance called amyloid, which is the material found in the brains of people with Alzheimer’s disease.

And then, finally, the seventh one is, again, the accumulation of garbage, but this time the accumulation of garbage inside cells. This is usually in a specific component of the cell called the lysosomes, although sometimes–especially in the brain–it is in other places in the cell. So these are the seven things that we need to fix.

David: And you have ideas for how to fix each one of them.

Aubrey: That’s right, although it would be wrong to call them all my ideas. For two of these things I have made very specific and very new and radical proposals for how we should go about this, which I think are pretty feasible, and are likely to be much more effective than anything else that’s on the table at the moment. But, for the others, all I’ve really done is read the right literature and talk to the right people, because all the ideas that I’ve brought in are ideas that other people have been working on already. In general, they have not been working on them within gerontology though. This is why I was the first person to come along and actually create this grand scheme, with all these components of a unified whole. I was able to do this because most gerontologists don’t know what’s going on in these areas well enough to know how close they are to being successful. 

It’s because biology is a very big field. So just as most biologists don’t know much gerontology, most gerontologists don’t much of other things. It’s much easier if you’re a theoretician like me and you don’t do experiments, because experiments, of course, are very time-consuming. Even writing the grant applications to get money for your students for the experiments is very time-consuming. So most gerontologists, like most biologists, don’t really have much time to read–and this is a major failure of biology in general, I have to say. The comparison with physics is very instructive here. 

In physics you don’t have this problem at all. In physics there are lots of people who do experiments, and there are also lots of people, like me, who are theoreticians–people like Stephen Hawking, just to name a famous example. They become experts in a much wider range of disciplines than you can if you’re spending all your time doing experiments. They have new ideas for new experiments to do, and new things to try that result from bringing concepts together from far apart. And there’s virtually nobody in biology doing that. There’s certainly nobody except me in gerontology doing that, and that’s a large part of why biology goes so slowly.  

David: So you think that’s the main reason why we haven’t made more progress in reversing the aging process, despite such remarkable achievements in molecular biology as the successful completion of the human genome project?

Aubrey: I think that’s a large part of it, yes. The human genome project, of course, was a bit over-hyped. The media made it out to be the most important thing since the wheel or whatever. But completing the human genome project certainly was a very good thing. It’s made a lot of experiments go much faster than they would have otherwise done. But yes, that’s a large part of the reason. It’s simply the absence of people bringing ideas together. To solve a very complicated problem you generally need a fairly complicated solution.

David: While we’re waiting for the SENS project to reach escape velocity, what do you think are currently the best ways to slow down, or reverse, the aging process and extend the human life span?

Aubrey: We basically don’t have anything. We certainly don’t have anything to reverse the aging process, and I’m not very optimistic about anything to actually even slow it down very much. Of course, if you’re the sort of person who has an unusually short life expectancy in the first place–either because you have dodgy genes of one sort or another, or because you just have a very bad diet, you smoke or whatever–then there are obviously lifestyle things that you can do that will make you live longer. But if we factor all them out, and we say What can you do over and above simply living and eating the way your mother told you to? then I take the view that there’s more or less nothing that can give you more than a couple of years. 

Some of my colleagues feel that caloric restriction might extend human life. As you probably know, if you feed mice or rats somewhat less than they would like you to then they live a bit longer, and some of my colleagues think this might also work in humans. I think it’ll work–but I think it’ll work much less well in humans than in most shorter-lived organisms. If you do this with rats and mice then you can probably get a thirty or forty percent extension of lifespan. So that’s a healthy amount. In a human lifespan that would be great. Even if you got twenty percent that would be very nice. But I think it’s very unlikely that we’ll get even as much as five percent. The reasons I think this are partly because of a whole bunch of data that exists that I feel my colleagues have actually really been sweeping under the carpet, and secondly because there’s very good evolutionary theoretical reasons to believe that longer-lived organisms will not have the genetic machinery to make them live proportionately as long in response to starvation as shorter-lived organisms would have. 

I have a paper that’s actually coming out tomorrow in a Swiss journal called Gerontology. It’s coming out online tomorrow and then in print version a week from then, which explains this in a lot of detail. It’s already caused quite some waves, and I expect it’ll cause quite a few more after it comes out.

David: Everyone that I interview is aware of how caloric restriction increases maximum lifespan, but few people are aware of the deprenyl studies that have been shown to extend maximum lifespan. Are you aware of these studies, and do you know if anyone has ever replicated them?

Aubrey: I’m surprised that people you’ve spoken to are unaware of these studies– they’re quite well-known.  Unfortunately, as you fear, they have not been readily reproducible, at least not in terms of magnitude.  A top Japanese gerontologist, Kenichi Kitani, has worked with deprenyl a lot over the past decade or more and you should look him up in PubMed if you want more detail.  The bottom line is that deprenyl is one of half a dozen substances, including growth hormone, DHEA, melatonin etc, that have occasionally been reported to extend maximum mouse lifespan but do not seem to do so reliably, or at least not by a significant extent.

David: What are some of the new anti-aging treatments that you foresee coming along in the near future?

Aubrey: A lot of my colleagues are working on things on the basis that calorie restriction may actually give us maybe fifteen or twenty years of extra life.

David: You mean working on ways to mimic caloric restriction?

Aubrey: That’s right–tricking the body into thinking it’s on calorie restriction when it’s not. I think that’s marvelous, because, you see, even though I’m pessimistic given what we know already about calorie restriction. I might be wrong in my interpretation of it, and it may be that we will actually get a lot more life extension from it, so I definitely think it ought to be tried, and these products may not be very far away. We have learned a great deal in the past five or ten years about the genetic basis for the life extension phenomena of calorie restriction in rodents. We ought to be able to use pretty realistic pharmacological and genetic tricks as  therapies to elicit the same sort of response in humans as they do in mice. These ideas, and the experiments to see whether this works, have been taken forward by a number of my senior colleagues. They managed to get all the venture capital that they need to support the work, so this will be tried fairly soon.

When it comes to the components of the actual SENS initiative some of the

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