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Aubrey de Grey

components are even further along than that. For example, there is a drug being produced by a company called Alteon in New York that actually breaks these extra chemical bonds that I was talking about that cause hardening of the arteries. And there’s another company in California that has been working on immunization against Alzheimer’s plaques to get rid of the garbage that accumulates between cells in the brain, by causing cells to actually internalize this stuff and break it down. 

Both of those drugs have been in clinical trials already. The Alzheimer’s one was aborted because the vaccine had bad side-effects, but they’re working really hard to produce better vaccines, and they will do so pretty quickly. The cross-link breaker one doesn’t even have any side-effects, so that’s going really well. But, in terms of life extension, the point is  we’re probably going to have to get all of these things–or at least most of them–working simultaneously in order to actually get a significant deferment of aging. So half of them working just won’t cut it.

David: Could you briefly explain what your strategies are for reversing each of the seven factors involved in aging?

Aubrey: Okay. I’ve mentioned two of them in the last answer. We’ve got these new drugs that break the chemical bonds that cause hardening to occur in structural proteins, and we’ve also got systems for stimulating the immune system against garbage outside cells. So the other one that everyone knows about is the ways to replace cells in tissues that don’t replace their own cells well enough, and that’s what stem cell therapy is mainly for. So stem cell therapy is being explored very heavily in, for example, type 1 diabetes, where you lose the ability to make insulin because you lose the islet cells in the pancreas. 

But it’s also being used for various age-related problems, in particular the one that’s got furthest is Parkinson’s disease, where people have been putting neural stem cells into the brain to differentiate into the particular type of neuron that’s lost in Parkinson’s disease. So there’s a long way to go with stem cell therapy of course. There are many things that we certainly can’t do yet with stem cell therapy, but that’s an area which can be approached incrementally. It’s an area which has got a lot of work going on, and little steps are discovered, little tricks, of how to treat and manipulate your cells in the laboratory so they get into a state where they will do the right thing after you put them into the body. There’s a lot of things like that going on. 

Then the one that’s sort of in an intermediate stage of development, I suppose, is the one about getting rid of cells that we’ve got too many of and we wish would just keel over. So there are various systems being developed to make such cells keel over, or else to put them into state where they’re not harmful after all. In the case of visceral fat–the fat of the abdominal cavity that seems to be largely responsible for diabetes–people have tried, in rats, just surgically removing the stuff, and that has had a marvelous effects on reversing diabetic complications in rats. 

There are also drug therapies being looked at that will make these cells transform into benevolent cells. Some people are looking at somewhat more high-tech approaches involving some sort of gene therapy that puts new genes into cells that kill those cells, and specifically only kills the cells that are in this bad state. Again, of course, this is a situation where the immune system can be activated to engulf and destroy cells that we want to get rid of. There are various ways of doing that, and most of these things are some way along in mice at this point.

The other three are all a lot further off, and we haven’t really got to the mouse stage even. We’re only the cell culture level. So one of them is, I mentioned, the mutations in the mitochondrion. It turns out that we’ve only got very little DNA in the mitochondrion–DNA that only encodes thirteen proteins, as opposed to tens of thousands of proteins encoded in the nucleus. It’s rather interesting that we have any genes in the mitochondrion, because the mitochondrion itself is a big complicated machine made of about a thousand different proteins. All the others, apart from these thirteen, are already encoded in the nucleus, and the proteins that they encode are constructed in the cell, outside the mitochondrion. Then they’re imported into the mitochondrion by a very special and really sophisticated system. 

So you’d think you could do the same with the other thirteen. Then you wouldn’t need mitochondrial DNA. It turns out that there are pretty good reasons why these things are encoded in the mitochondrial DNA, but these reasons are not complete show-stoppers. They have been show-stoppers for evolution, but we have different tools than evolution has, and so it’s looking very good now. There has been very important progress in that area recently that indicates that we ought to be able to put copies of these genes in to the nucleus, and that would solve the problem, because the nuclear DNA is enormously better protected and better maintained than the mitochondrial DNA. So if you had working copies of the mitochondrial DNA in the nucleus then it wouldn’t matter whether you had you had mitochondrial mutations any more. The proteins that had been constructed by the mitochondrion would be coming in from the outside, so it’d be okay.

David: The mitochondria are almost like organisms unto themselves, aren’t they?

Aubrey: Well, they used to be organisms. They were originally free-living bacteria, that’s right. But they are very much not organisms unto themselves anymore. They’re wholly integrated into their hosts now. 

All of the strategies that I’ve discussed so far are not my own ideas. The idea that I just explained, for example, was first discussed twenty years ago, and it was first discussed as a therapy more than fifteen years ago. People have been working on it for most of that time. One of their big breakthroughs will actually will be coming out in a paper in my journal Rejuvenation Research in the next issue in a month or so, with the results of a study that began in 1991. So we’ve been working on this for awhile, and I believe that we’ll crack it.

The other two that I haven’t dealt with are the ones where, basically, I have completely identified a new approach from scratch, that no one else has done before. The first one deals with the junk that accumulates inside cells. I have a really crazy idea here. I realized that this junk is energy-rich. If you go to a graveyard, for example–somewhere that’s enriched in human remains–you probably won’t find this stuff, because anything that energy-rich is not going to be sitting in the ground for very long if it’s worth eating. If you’re a bacterium, a microbe in the soil, you can eat this stuff and live off it. I didn’t come up with this principle myself by any means; this is the principle behind a field that’s been flourishing for fifty years called bioremediation, which is basically a part of the environmental decontamination industry. 

People are interested in getting rid of contaminants in the soil to build houses on the soil, for example, and this works. If you have any chemical in the soil that you want to get rid of that’s energy-rich, and it’s organic, then you can find bacteria that will break it down. Even explosives like TNT are no problem. You can find bacteria than can break down TNT, dioxins, and PCBs. It’s ridiculous, and it’s simply because evolution is very very clever. If you give evolution a reason to evolve the machinery to do something, it’ll do it eventually. 

So I reckon this ought to work for the junk that accumulates in our human bodies when we’re alive that we don’t know how to break down. There will be bacteria in the soil that do know how to break it down, and this idea has gone down very well. I’ve discussed it extensively over the past few years, and pilot studies have already been done to demonstrate that it really works, so this is likely to be developed fairly soon. But it is difficult to say how soon as there is only early data at this point. We don’t even have it actually working in cell cultures yet, so I would expect that it will be the best part of ten years before we see a serious improvement and it is functioning well in mice. Then, of course, it will be longer to get it working in humans.

The final one is mutations in chromosomes. I mentioned earlier that I think that the only mutations in our chromosomes that actually matter are those that cause cancer. Other mutations just don’t accumulate fast enough to do us any damage in anything like a normal life time.

So I came up with a really complicated, really ambitious therapy for cancer which I felt one needed in order to really avoid the fact that cancer is so insidious. Cancer is insidious because it has the advantage of natural selection. Cancers are a seething mass of genetic instability. They’re basically doing experiments all the time to try to work out how to evade all of the things that the body throws at them to kill them, and the things that the doctors throw at them to kill them for that matter. That’s why we’ve made so little progress over the past thirty years, since Nixon announced the war on cancer. Cancer is by far the hardest aspect of aging to fix.

So I came up

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