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It's not a very catchy name, is it?Yes, I know -- "Engineered Negligible Senescence" has ten syllables and is not the world's most memorable, or indeed self-explanatory, phrase. But it is a good name for our ultimate goal, honest -- as well as SENS being a catchy acronym. Here's an explanation. I'm afraid it starts with a rather long preamble, but trust me, it's worth it. First, let's be precise: our ultimate goal is the availability to the entire human race of technology that will restore them to whatever degree of youth they desire and keep them there for as long as they want. That's a bit stronger than simply "a cure for aging" -- it says that the cure should be available (at a price that they can afford, of course) to absolutely anyone who wants it. But then, what does "youth" mean? I don't think many 70-year-olds will want therapies that erase all the knowledge that they've gained in the second half of their life, for example, nor their taste for music that is eschewed by the younger generation. No -- what "youth" means for our purposes is physical robustness and vitality. That's where things get tricky. We know aging when we see it, but it is actually very hard indeed to measure .... until it's over. It isn't very hard to distinguish a dead person from a live one, but telling the difference (accurately, mind -- not just 70% of the time) between a person who's likely to live another 10 years and one who's likely to live another 20 is very much harder. We have one very approximate measure of how long someone's likely to live, namely how long they've lived already, and even though scientists have tried very hard they have so far failed to find an appreciably better one. But this isn't as hopeless as you might think. We can say, very clearly, that loss of physical robustness and vitality is what kills most of us (those that don't die of homicide and such like). It makes us less resistant to diseases like flu that we can fight off easily in our earlier years. It makes us more likely to break bones if we fall, and those breaks take longer to heal, so we have to stop exercising, so we get even more susceptible to diseases. It slows our reactions, so that when we slip on the stairs we can't catch ourselves, so we fall, etc. So actually, aging and death are more closely linked than they might be. People who are physically robust are not likely to die any time soon; people who are physically frail are more likely to die soon. There are two consequences of this. One is that the goal that a lot of biogerontologists (who should know better) advocate as the ultimate purpose of their work is totally impossible (even if it were desirable, which is unclear). That goal is often called "compression of morbidity", and what it means is a shortening of the average length of time that people spend in a frail state before they die. The idea is that we should not be trying to extend total lifespan, only healthy lifespan ("healthspan"). As you can see, the only way to do that is to limit access to medical care for things that people tend to die suddenly of, such as heart failure, so that fewer of us die of lingering diseases like cancer. And society, surprise surprise, seems dubious about that strategy -- or, indeed, any other strategy that shortens people's average total lifespan. The other consequence of the tight biological linkage between aging and death is that we can measure our ability to combat aging by observing our impact on death rates, and this is where I (finally!) get to explain the basis for the term "Engineered Negligible Senescence". Let's start at the end, with "senescence". This is a term that many biogerontologists have used for a very long time, and informally what they mean by it is the progressive loss of physical robustness that happens with time. But because of the linkage between aging and death, they have also been able to give "senescence" a formal, mathematical definition -- the progressive increase in an organism's likelihood to die soon. This is something that can be measured. It can't be measured on a single individual, because single individuals only die once and that single event doesn't give much information about how likely the person was to die at any prior time (or, indeed, at any later time if they hadn't died when they did). But if we look at a population of people (or other organisms, for that matter), we have a lot of information -- the age at death of each individual -- and we can use that to estimate the probability of death. In particular, we can use it to relate the probability of death to other characteristics of the individuals, such as their diet, their gender -- or their age. This is what gerontologists have done: they have defined the term "senescence" to mean a positive correlation between age and risk of death in the coming short time period (typically a year for humans). To see what this means in practical terms, think about radioactivity. We can talk about the half-life of a radioactive isotope, and indeed we can measure and state very very precisely what that half-life is. We do this by measuring the distribution of time of decay -- "death" -- of individual atoms in a sample of the isotope. And the point is, that half-life stays the same forever, even though atoms are decaying all the time. Each individual atom retains the exact same probability of decaying in the next hour (or second, or year -- it doesn't matter what unit of time you look at) as it had before, right up until the moment that it actually decays. In the language of biogerontology, radioactive atoms die but they don't senesce. People, on the other hand, do senesce, because the probability of a 70-year-old dying in the next year is higher than the probability of a 60-year-old dying in the next year. But hang on -- how do we know that radioactive atoms don't senesce? There are, after all, only a finite number of atoms in the sample that we measure the decay of -- a very large number, but still it's finite. So in fact, if they senesce just a tiny tiny bit over time -- that is, if their half-life gets shorter, very very slowly -- we wouldn't actually be able to tell that this was happening in the time that we took our measurements, because the acceleration in the rate of atoms decaying (relative, of course, to the number that had not decayed already, which is always decreasing) would be too tiny to be statistically detectable. With finite numbers of events, we are always only able to say things with confidence if we restrict ourselves to talking about possible ranges in which a rate might fall. So here, we can only say that there is a range of possible rates of senescence of the radioactive sample, and if there is a really tiny rate of senescence, that range would still include zero. This is not very interesting in radioactivity, because the number of atoms we look at is usually so huge that for practical purposes we can forget about the possibility of half-lifes getting shorter. But in gerontology it matters a lot, because the number of people (or animals) that we can look at the ages at death of is relatively small. This was recognised some time ago, especially by a very eminent and innovative gerontologist named Caleb Finch. He introduced the term "negligible senescence" to mean "senescence too slight to be statistically distinguishable from zero with the sample sizes at our disposal". That includes non-senescence, of course -- truly zero correlation between age and risk of death -- but the point was that it encapsulated the experimental and observational reality that if we found a genuinely non-senescing organism, we could never truly know that we had done so. (Indeed, most biogerontologists believe that some organisms, even some very primitive animals, are non-senescing, but they can't prove it, and Finch made this explicit.) Biogerontologists like the term "negligible senescence" for exactly this reason -- as scientists, they like to say what they know and no more. This of course means that they immediately understand the term "engineered negligible senescence" -- the biotechnological conversion of a population that shows senescence (humans, of course) into one that does not. So that's why I have chosen to use the term "engineered negligible senescence" (ENS) to describe what I want to help develop, and why my work is therefore best described as the development of strategies for ENS, or SENS. I'm a biogerontologist myself, after all -- and, never forget, I consider my fellow biogerontologists to be my most important audience, because they are so influential in determining what science is done, as I explain here. If every expert in the biology of aging agreed with me about the foreseeability of ENS, my job would be essentially done: public opinion would fall in behind the scientists (as it always does), the political weight would fall in behind public opinion (as it always does), and the research and development would proceed as fast as possible, with no financial obstacles whatsoever. So I like to use a term that my colleagues in biogerontology understand well and are comfortable with, even if it may be a bit of a mouthful. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||