Why Don’t Humans Live for More than 100 Years? | Physicist Geoffrey West | Big Think

You can determine, calculate many things about organisms, about their growth patterns, how they grow, how long they take to mature—and in particular one that concerns many of us, and that is: how long we live? What determines our longevity?

And, in fact, that’s what got me into this work originally; I became very intrigued in my fifties about the phenomenon of aging and of dying. I became more and more conscious that things had been changing in my life in terms of my body and my physiology. And that already I’d had friends die. So I became intrigued as to “what is that?”

And I also became intrigued very much as a physicist—not asking what is the mechanism, the systematics about aging and immortality, but the very question: “What determines 100 years for the lifespan of a human being? Why is it a hundred years, not a thousand years or a million years?” And also related to that: why is it that a mouse, which is made of pretty much the same stuff as we are (I mean we’re almost identical really in some kind of coarse-grained level looking at things), how come a mouse only lives two to three years?

So what is determining all this? And if you have this theory of networks underlying these scaling laws, manifesting themselves as scaling laws, you first ask: is there a scaling law for lifespan? This is work that had already been done by many people; it was to look at lifespan as a function of size, for a bunch of mammals in particular but organisms in general, just as we looked at how metabolic rate scales across these animals.

And what was discovered, what had been discovered was that lifespan also increases following these quarter power scaling laws—that it increased systematically. The one difference, by the way, and maybe I’ll say a few words about this in a moment, is that there’s much more scatter among the data for lifespan compared to things like metabolic rate.

So even though there is a kind of predictability—that is, you give me the size of a mammal, I will tell you on the average how long that mammal will live—there’s much more variance around that number than there is for saying, “you tell me the size of a mammal, I will tell you what its metabolic rate is and what the length of its aorta is, how many children it should have,” and so on, where there’s much less variance. The variance is much tighter. Lifespan has much more variance.

Now where does that number come from? So you have this theory that the scaling of metabolic rate and these many other quantities—and by the way, there’s probably 50 or 75 such measurable quantities—these are determined by the constraints of flows in networks such as the circulatory system.

So one of the things you immediately realize about those flows is that they are what we call “dissipative,” which simply means they involve wear and tear—just as, you know, outside in those streets outside this building there’s a lot of traffic going back and forth on the roads, and those roads wear out. They have to be repaired. The roadways have to be repaired, and the subways have to be repaired. They wear out from the traffic, so to speak.

And so it is the traffic through our multiple network systems that produces wear and tear. The most damaging wear and tear occurs at the terminal units, the terminal points of these networks because they’re the smallest tubes, like in our capillaries or within our cells, pushing fluid, pushing blood corpuscles or whatever it is, big molecules through them—has deleterious effects of various kinds.

That causes damage, and that damage is calculable because you have a theory. The theory is telling you what the flow rates and so on, and all the sizes are, and so on. So these are calculable. Now, so you can calculate the rate at which wear and tear is occurring, and you can also calculate something else that is going on, and that is: while it’s being damaged, there’s also repair going on.

And we do repair ourselves. But that repair is also determined by metabolism. That’s where the energy comes from to do repairs. So you can determine all these things and then you can postulate that the system will become nonviable, that is, it can no longer be sustained when a given fraction of un-repaired damages occur.

So the system eventually just cannot be sustained, and so that gives you a calculation of maximum lifespan. This is the, you know, if you were to do the best you possibly could, this is as long as you could possibly live for a given size of mammal. And if you do that, you can understand where, roughly speaking, this hundred years for a human being comes from.

But more importantly, or equally importantly, you can determine what the parameters are, the knobs that you could conceivably turn to change that lifespan. What could you do to make that go from 100 to 200, for example? And there are two pieces of that. One is you can decrease, of course, the wear and tear, or you can increase the repair.

Those are the two obvious things, and there are parameters that determine that. So if you think about the damage that is occurring from metabolism—so that means, okay, one way we could decrease damage is decrease the amount of food we take in. That would be one way. And indeed, by the way, the reason a large animal lives longer than a small one is because the metabolic rate per unit mass or per cell gets systematically smaller the bigger the animal, corresponding to these quarter power scaling laws.

So less damage is done at the cellular level the bigger the animal—in a systematic way. So the question is: how do you decrease that even further? One is you can eat less, and that’s called caloric restriction. So if you put yourself on a starvation diet, it may not be so pleasant in terms of your lifestyle, but this would predict that you live longer.

And there have been experiments done, on mice in particular and some on monkeys, most of which show an effect, and the effect is calculable in this theory. And many of the experiments done on that agree with the data that’s been taken—on mice. There have been some controversial experiments on monkeys which have not shown as big an effect. So this is still very much a work in progress.

But there’s another way you could also decrease your metabolism, and that’s a way that is very difficult for us but interestingly is very easy for almost all other organisms on the planet. And that’s to do with the fact that we are unique in that we are what’s called “homeotherms.”

Namely, we keep the same temperature. We discovered this extraordinary mechanism of keeping our body temperatures constant. That is fantastic because it dissociates us from the external temperature, the environmental temperature. Everything else is subject to the ambient temperature in their environment.

And here’s why it matters: It’s because metabolic rate is derived from chemical reactions, and chemical reactions depend exponentially on external temperature, on the temperature which they’re operating. That means a small change in temperature can have a huge effect.

So a small change in temperature, a small increase in temperature increases your metabolic rate exponentially. So that’s why if you look at insects in the cold—when they’re cold in the morning, they can barely move. They have to wait until the sun comes up to warm themselves, and then they can start flying around and moving around and so on.

That’s true of lizards and so on, essentially everything that’s around us. We are immune from that, and that’s been extraordinarily powerful for us and a tremendous advantage. Going back to lifespan, that means that if you could lower your body temperature you would decrease your metabolic rate and you would decrease therefore the damage, and you can live longer.

And that is indeed true of organisms, all other organisms. If you keep them at low temperatures, they live exponentially longer. They live much longer, so it’s a fantastic effect. It’s a huge effect.

And by the way, one tangential remark for that—and that is a critical one in our times—and that is to do with global warming. One of the things that I think is a bit mysterious to many people, in the kind of intelligent layperson, is that: why should one or two degrees change in the ambient temperature around us make any bloody difference to anything?

After all, where I live, the temperature often changes by 40 degrees from night to day. So we have these huge changes, yet the ambient, you know, just this little increase in the ambient, in the average temperature has such a big effect. The reason is that things like growth rates and death rates and everything to do with growing and therefore agriculture, but the whole ecosystem, the whole biosphere is exponentially sensitive to a change in temperature.

So one to two-degree change has an exponential effect, and some of that is, from our viewpoint, highly deleterious, and some may actually be advantageous. But I think this is an incredibly important point that—I’m afraid I’m a little bit critical here of my colleagues who work in global warming—they have not been very good at getting this across, especially obviously to politicians and especially, of course, the politicians in the United States.

But going back to the more parochial issue of lifespan, if we were to take drugs that could lower our body temperature (and this has actually been done for mice again), it increases concomitantly their lifespan. Decreasing their metabolic rate increases their lifespan. And that’s been seen, and it is in agreement with the theoretical predictions.