A New Choice for Immortalists
By Michael R. Rose
Department of Ecology and Evolutionary Biology, University of California
Everyone whom I know to be registered for cryopreservation does so because they don’t want to die, for good and forever. That is to say, they are some type of immortalist. They may not be cyber-immortalists waiting to be uploaded to a successor to the present world-wide web. But basically they want the prospect, at least the possibility, of living forever. Like an agnostic contemplating the possibility that God does in fact exist, and a God in the business of providing accommodations comfortable or uncomfortable in the afterlife, immortalists are confronted with a menu of relatively stark, and often unappealing, alternatives, given that no one has yet brought a cryopreserved human, as body or head, back from the freezer alive.
I am not going to argue against cyber-immortality or cryo-immortality here. After all, the value of back-up plans is self-evident. Instead, what I am going to offer is an informal introduction to a third possibility. This possibility is one in which aging is stopped, and then repair and refurbishment are used to achieve immortality by the simple expedient of not dying in the first place.
Let me confess straightaway that if somebody had proposed this possibility to me just three years ago, I would have laughed at them outright. But I have spent the last two years reinterpreting my life’s work, at least my research since 1976, when Brian Charlesworth first started working me over to get me to do my doctoral thesis on the evolution of aging.
Here is one of the key points, really the central intuitive idea that the present article hinges on. Since Aristotle, virtually everyone who has worked on the biology of aging has conceived of it in terms of an underlying cumulative physiological process. The most famous, and indeed notorious, present-day proponent of this view is the inimitable Aubrey de Grey. Aubrey characterizes aging as a process of cumulative damage, chiefly at the cell and molecular levels. As such, notwithstanding his media reputation as a wild-eyed radical, Aubrey is thoroughly conventional. In this respect, he more or less agrees with the National Institute on Aging, of the NIH, and innumerable other cell and molecular biologists. While some of these cell-molecular aging researchers think that free-radical damage is the central cause of cumulative damage, others think that progressive dysregulation is more important. Classical-era biologists, from 2500 to 1600 years ago, thought that aging was due to a progressively worsening balance between the earth, water, fire, and air that were thought to make up the human body. In effect, classical thinking was that these four elements were combined to yield life in an unstable mixture, whereby aging involves the drying out and cooling of the body’s physiology. Modern-day cell biologists instead write about cumulative damage and/or dysregulation of pathways controlled by sirtuins, TOR, and the like. Regardless of details, all of these people agree with Aristotle’s original hypothesis that aging is a cumulative physiological process of some type.
But I don’t. Not anymore. And this break with the long Western academic tradition of aging theory is the key to the new choice I wish to offer here.
I should be clear that my present view is also not one generally held, at least not yet, even by most evolutionary biologists who work on aging. Like them, I spent more than thirty years thinking that William Hamilton’s declining forces of natural selection, which he published in 1966, showed that evolution by natural selection would allow cumulative processes of physiological deterioration to proceed unchecked, provided they killed off their victims at sufficiently late ages. And thus my very definition of aging, which I published in my 1991 book Evolutionary Biology of Aging, assumed that endogenous processes of physiological deterioration, whether due to damage or dysregulation, would proceed without remit until all members of a sheltered cohort given good conditions die.
My turning on the Road to Damascus started one day in 1992 when my good colleague Larry Mueller showed me two articles from the journal Science, articles from the laboratories of our colleagues Jim Curtsinger and Jim Carrey. The data in those articles were mind-blowing. They showed the complete cessation of the acceleration in age-specific death-rates that evolutionary biologists like Larry and myself regarded as the hallmark of aging. It looked as if aging came to a stop.
Both Larry Mueller and I were intensely skeptical about these results, and we voiced some of our skepticism in print, in correspondence that was published in Science together with our colleagues Joe Graves and Ted Nusbaum, as well as in other articles that involved Larry and Joe Graves only. But I was deeply troubled by these findings from the two Jim’s, and thought about them intermittently throughout the next two years.
By 1994, I was thinking that perhaps evolutionary biologists had misconceived the problem of the evolution of aging. Perhaps it was NOT natural selection just letting go, but something that specifically tracked Hamilton’s forces of natural selection.
This led me to convince Larry Mueller to do some explicit simulations of evolution, simulations in which we looked at what happened at very late ages, long after Hamilton’s forces of natural selection bottom out and stabilize. What the simulations generated were late-life plateaus in mortality, just as the Curtsinger and Carrey labs had found. We published this result in PNAS in 1996.
With this result in hand, we then checked how changes in Hamilton’s forces would change the age at which mortality plateaus occur, based on explicit simulations. These simulations showed that changing the last age of reproduction in a biological population, the parameter that Hugh Hefner is working on as I write, would tune the age at which mortality rates would plateau.
So Larry Mueller, my then graduate student Casandra Rauser, and many undergraduate students working in my laboratory tested populations that had been evolving in my laboratory for this predicted relationship between the last age of reproduction and the start of the plateau in mortality rates. Qualitatively, it worked. Shifting the last age of reproduction, which is when Hamilton’s force of natural selection acting on mortality itself plateaus, produces the qualitatively predictable shift in observed mortality plateaus in our fruit fly experiments. Not immediately, as a physiological effect, but eventually, over many generations, as a result of evolution occurring in my laboratory under controlled conditions.
Not only is the rate of aging, considered demographically, readily tuned by evolution, so is the age at which aging stops demographically readily tuned by evolution. And this is true not only of those aspects of aging that affect survival. It is also true of reproductive aging, the main theme of the doctoral research of Cassie Rauser in my laboratory. Reproductive aging is tuned by Hamilton’s other force of natural selection, the one that tunes age-specific fecundity.
Still for more than a decade I thought of aging as a physiological process, just one that comes to an end when the late-life plateaus in mortality and fecundity are reached. But I now think that this was the wrong conclusion to draw from our work.
Consider the following point. If aging is a physiological process, however multifarious, why should it come to a halt just when the organism is most debilitated? In the human case, demographic aging stops when the death rate is between 30 and 50 % per year, particularly among centenarians. These are very frail people, yet their aging abruptly stops. How is this supposed to make sense?
Instead, imagine an entirely different view. Suppose instead that aging only seems like a physiological process, but actually is no such thing. Suppose instead that aging is the age-dependent tuning of Darwinian adaptation, where the tuning is determined by the patterns of Hamilton’s forces of natural selection. Not a physiological process at all.
On this view, what seems like a physiological process is a scientific illusion, fully parallel to the illusion of the sun rising in the morning, crossing the sky, and setting in the evening. Because, of course, the sun does no such thing. Sunrise and sunset are optical illusions produced by the rotation of the Earth.
So why is this physiological illusion so convincing, and so reliable? It is convincing and obvious because the falls in Hamilton’s forces of natural selection are so predictable and so intense, at least in most animal species. Hamilton’s evolutionary forces are as strongly determinative of deterioration as any acute disease process. Only the illusory ‘physiological aging processes’ that they produce is extremely protracted in the human case.
If this view is correct, then those species in which Hamilton’s forces of natural selection do NOT fall should be free of aging. Even if they have the same basic cell biology as we do, and even if they are as subject to mechanical injury and oxidation as we are. This alternative view thus makes some strong predictions, predictions which are readily falsified by comparative data. IF, a big if, this theory is wrong.
And the comparative data show that such species DO indeed exist. For example, sea anemones that reproduce only by symmetrical fission are animal species that are thought to be free of aging, from experiments culturing them in aquaria. Similar results have been found among other fissile coelenterates, particularly in the work of Daniel Martinez. And Graham Bell has found results like these in flatworms that can also reproduce by splitting in two. So, not only can aging stop, sometimes it doesn’t even get started.
The problem for people is that when our aging normally stops, we are about a hundred years old, very fragile, and often demented. So who would want to sustain that state indefinitely?
But I kept on thinking about the cessation of aging. In the last two years I started thinking about some data that Cassie Rauser had collected on the cessation of reproductive aging in our fruit flies. She showed that the timing of this cessation, and the reproductive function of flies that have stopped reproductive aging, depended on their environment. These findings raised the possibility, in my mind, that we might be able to manipulate when mortality declines stop too, using environmental manipulation, in fruit flies or humans.
A few fruit fly experiments later, we are already seeing signs of such an opportunity: declining and stabilizing mortality too can be manipulated environmentally. This work is by Marta Santos and her team in my lab, and will be submitted for publication soon.
So, how to manipulate humans so as to stop our aging sooner, and in better condition? How to find a third option for immortalists, a less drastic choice before cryonic or cyber immortality?
As we explain in some detail in our book Does Aging Stop? (Mueller, Rauser, & Rose, 2011; Oxford University Press), shifting back to lifestyles that are physiologically comparable to those of hunter-gatherers provides a possibility of stopping aging at earlier ages, and in better shape. [For those who aren’t scientists, I have presented this possibility in some detail at the website Rob Patterson has built for me: 55theses.org.] This possibility is particularly available for those whose ancestors have never adapted to agriculture, such as the northern First Nations of Canada or the non-agricultural tribes of tropical rainforests. For them, Larry Mueller’s calculations suggest that they may be able to stop aging in middle-age in particularly good shape.
For the rest of us, the prospects are not quite as good, if we switch to hunter-gatherer lifestyles. But the possibility does present itself that we may be able to stop our aging phase, not our “aging process,” by an age like 70, and do so in much better condition than present-day 70 year-olds can sustain.
Then, as medicine becomes still better at rescuing us from the accidents of thromboses, malignancies, and car collisions, we could remain on this aging-arrested plateau indefinitely.
Something for you all to think about.
I am grateful to Max More for suggesting that I write this article, and to Joseph L. Graves Jr. and Marta Santos for their comments on an earlier draft.
Michael Rose went to the University of Sussex in 1976 for his doctoral studies on aging in Drosophila melanogaster. There he began his work on the evolution of aging and created Drosophila stocks with postponed aging. In 1991, his Evolutionary Biology of Aging appeared, offering a view of aging that was a complete departure from the views that had dominated the aging field since 1960. Evolution described the field of gerontology as now “after Rose”. In 1997, Rose was awarded the Busse Research Prize by the World Congress of Gerontology. In 2004, he published a technical summary of his work on the postponement of aging, Methuselah Flies, followed in 2005 by a popular book on the topic, The Long Tomorrow. In addition, Michael Rose has published general books on evolution: the wide-ranging Darwin’s Spectre, Evolutionary biology in the modern world, and the copiously illustrated Evolution and Ecology of the Organism (with L.D. Mueller). His most recent book, with L.D. Mueller and C.L. Rauser, is Does Aging Stop? (Oxford University Press).
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