The Mortal Individual and the Immortal Species
To grunt and sweat under a weary life,
But that the dread of something after death,
The undiscovered country from whose bourn
No traveller returns, puzzles the will
And makes us rather bear those ills we have
Than fly to others that we know not of?
Thus conscience does make cowards of us all.
—Shakespeare, Hamlet, act 3, scene 1
How long would you like to live? Eighty? A hundred? Two hundred? How about five hundred years? Can you imagine what it would be like to live a thousand years? Me neither.
In surveys that ask such questions most people say that they would not want to carry on much past the current average life expectancy. It’s another example of the status quo bias, or our emotional preference for whatever we are accustomed to,1 and our personal life expectations are yoked to those of our generation’s life expectancy. According to a 2013 Pew Research Center poll of 2,012 American adults, for example, 60 percent said that they would not want to live past the age of ninety, while another 30 percent said they would prefer to cash out by age eighty. And these findings were consistent regardless of income, belief (or not) in an afterlife, and (in some cases) even anticipated medical advances. When it was proposed that “new medical treatments [could] slow the aging process and allow the average person to live decades longer, to at least 120 years old,” a slight majority (51 percent) said that they would not personally want such treatments, and that it would be “fundamentally unnatural” and “a bad thing for society.”2
The “it wouldn’t be natural” objection to radical life extension is gainsaid by a simple thought experiment. If you were given a death sentence of, say, tomorrow, would you want to live one more day in order to get your affairs in order and to tell everyone you love how you feel about them? Of course you would. How about one more week? Definitely. Another month? Absolutely. One more year? Well, there are more things I’ll bet you’d like to do, so sure you would. Another decade? That would give you time to travel and perhaps even take up a new career, so certainly. At some point I might find the time horizon in which you’d say “that’s enough,” but fast-forward to the day before that date and we’re back to the cycle of wishing for one more day, week, month, year, decade … Unless you are terminally ill and in such pain and misery that one more week or month would be manageable only through massive doses of morphine, at no point is a reasonably healthy and happy individual realistically likely to be willing to check out early just because “it wouldn’t be natural” to continue. As for society, let the nihilists and the cynics fall on their swords. I’ll take another sunrise and sunset, thank you.
The Pew findings bear this out. Respondents were more likely to favor life extension if they are younger, believe that future medical treatments would provide a higher quality of life, if they could still be productive by working longer, if they wouldn’t be a strain on our natural resources, if older people were not seen as a problem for society, and if living longer did not result in debilitating diseases and disabilities. What is natural is for healthy, happy, and productive people to desire to continue living and loving for as long as they remain healthy, happy, and productive. More and more, people are ignoring the aspiration reflected in the Who’s 1960s rock anthem My Generation: “I hope I die before I get old.” Although the band’s mercurial drummer Keith Moon died at the age of thirty-two from the then customary drug overdose, the Who’s aging front men Pete Townshend and Roger Daltrey are still touring half a century later.
WHY DO WE AGE AND DIE?
Toward the end of his life, reflecting on the “Topic of Cancer” (that would ultimately kill him) for his Vanity Fair column, Christopher Hitchens gave as good an answer as anyone to his self-directed rhetorical query:
To the dumb question “Why me?” the cosmos barely bothers to return the reply: Why not?3
This leads us to a deeper question: Why do we have to die at all? Why couldn’t God or Nature endow us with immortality?
The answer has to do with two facts of nature: (1) the Second Law of Thermodynamics, or the fact that there’s an arrow of time in our universe that leads to entropy and the running down of everything, and (2) the logic of evolution, or the fact that natural selection created mortal beings in order to preserve their immortal genes. In answering this question we must also distinguish between direct proximate causes and distant ultimate causes. Proximate causes are more immediate mechanical explanations for why things work the way they do, whereas ultimate causes tend toward deeper explanations for why things are a particular way. The proximate cause of why fruit tastes sweet, for example, is that taste receptors on the tongue detect the fructose molecules in ripe fruit and send neurochemical signals to the brain that register the sensation of “sweetness.” The ultimate explanation for why fruit tastes sweet in the first place involves our evolutionary past in which sweet foods such as ripe fruits were at once both rare and nutritious. Natural selection favored individuals for whom rare and nutritious foods were desired over those who had no such taste, and we are the descendants of those for whom fruits tasted sweet. Sex is subject to similar proximate-ultimate causal explanations. Proximately, sex feels good because the sex organs are rich in neurons that transduce touch into neurochemical signals that register in areas of the brain associated with pleasure, like the insula and anterior cingulate. Ultimately, sex feels good because it is evolution’s way of propagating the species and natural selection favored individuals for whom sex was enjoyable. Those for whom sex was unpleasant or neutral were outcompeted by those for whom it was pleasurable because the latter left behind more offspring than the former.
Proximate causes of death are readily apparent and subject to the availability heuristic, or the tendency to assign probabilities of potential outcomes based on examples that are immediately available to us, especially those that are vivid, unusual, or emotionally salient.4 Thus, our initial assessment of what is most likely to kill us—terrorist bombings, shark attacks, earthquakes, hurricanes, lightning strikes, police brutality, killer bees—is whatever happens to be on the evening news at the time we’re thinking about it.5 In fact, these are not the things most likely to kill us. According to the World Health Organization, the top ten killers are ischemic heart disease, stroke, COPD (chronic obstructive pulmonary disease), lower respiratory infection, trachea/bronchus/ lung cancers, HIV/AIDS, diarrheal diseases, diabetes, automobile accidents, and hypertensive heart disease.6 Other common risks far more likely to take you out before a terrorist or a shark will are cancer (liver, colorectal, breast, skin, prostate, cervical, pancreatic, etc.), poisoning, falls, drowning, fires, injury, drug overdose, and, if you live in the United States, guns—as many Americans die by gun homicides, suicides, and accidents each year as die in automobile accidents (33,636 and 33,804 respectively in 2013).7
The ultimate cause of death has long had a ready-made answer from theologians and religious believers, who contend that death is simply a transition from one stage to the next. This life is an interim theater from which we exit and receive our divine script for the next act. In the religious worldview, death needs no explanation other than “God wills it” as part of a deific design that will be disclosed once we get to the other side. This may be a satisfying account for some, but it doesn’t answer the question of why physical life must end, or shape-shift from biological to spiritual, even in a religious worldview. Since God is omnipotent and omnibenevolent, why couldn’t he just have created a heaven on earth and skipped the intermediate stage?
For scientists, the ultimate answer to why we age and die begins (and ends) with the Second Law of Thermodynamics, which guarantees that the cosmos is running down and in the long run must come to an end hundreds of billions of years from now. This results in entropy, and it applies to a closed system, which the entire universe is. So yes, ultimately, we—and the earth, the sun, and the universe itself, along with all life-forms therein—must come to an end. But Earth is an open system because of the energy generated by the sun. In principle, as long as there is a source of energy feeding into this open system, life could continue at least another four billion years, at which point the sun will expand outward and envelop the Earth. In the meantime, why can’t organisms live indefinitely?
Actually, some appear to do just that. Some organisms do not appear to age (or at least they exhibit negligible senescence), such as some tortoises and turtles, sturgeon, rougheye rockfish, and lobsters. Hydras may very well be biologically immortal. In 2016, scientists discovered a Greenland shark that may be the longest-lived vertebrate at 392 ± 120 years, for a range of 272 to 512 years.8 One specimen is computed to have been born in 1504, sixty years before Shakespeare’s birth! Even more extreme are tardigrades—water-born, eight-legged microanimals about half a millimeter long found nearly everywhere on Earth and capable of surviving temperature ranges from -458° to +300° F, atmospheric pressures six times greater than the deepest oceans, radiation levels hundreds of times higher than those that would kill humans, no food or water for decades, and even the vacuum of outer space. They are also capable of cryptobiosis, a state in which all metabolic processes cease but the organism does not die—a type of suspended animation that may last for thousands of years. If tardigrades can do it, why can’t humans? In fact, as we saw in the discussion of the identity problem in chapter 7, you are not the same “stuff” you were at birth because your atoms are recycled and replaced to the point where approximately every decade you are an entirely new person. Why can’t that material recycling go on indefinitely, or at least as long as there are atoms to recycle and the energy to drive the process?
To answer these questions we need a precise definition of aging. According to a 2007 paper in the journal Clinical Interventions in Aging that reviewed the vast literature on “The Aging Process and Potential Interventions to Extend Life Expectancy,” aging “is commonly defined as the accumulation of diverse deleterious changes occurring in cells and tissues with advancing age that are responsible for the increased risk of disease and death.” With hundreds of theories of aging on the offing, this plurality of ideas means that we are not close to a consolidation of solutions to slowing or halting the aging process, much less reversing it. Thus, the authors conclude, “the search for a single cause of aging has recently been replaced by the view of aging as an extremely complex, multifactorial process. Therefore, the different theories of aging should not be considered as mutually exclusive, but complementary of others in the explanation of some or all the features of the normal aging process.” As for remedies to aging, these scientists are not hopeful: “To date, no convincing evidence showing the administration of existing ‘anti-aging’ remedies can slow aging or increase longevity in humans is available.”9 Even if we found cures for all the leading proximate causes of death in old age (heart disease, stroke, cancer, etc.), the medical doctor and aging expert Leonard Hayflick has computed that it would add only about fifteen years to human life expectancy.10 Instead of thinking of aging as a disease for which we may one day find a cure, it is more accurate to describe it as the result of the deterioration of cells and their inability to continue dividing. Why do cells deteriorate and cease dividing?
We still do not know for certain, but the modern Methuselah quest began in 1951 with the Nobel laureate biologist Peter Medawar’s now epochal lecture titled “An Unsolved Problem of Biology,” in which he contrasted the “wearing out” theory of aging (physics) with the “innate senescence” theory of aging (biology). Medawar opted for the former, employing an analogy with test tubes in his lab in which the glass pipes don’t age gradually so much as they break suddenly. Applying his analogy to biology, Medawar turned to anecdotes from trappers who never seem to nab old and senile animals in their steel jaws, and anglers who never report catching senescent fish. In both cases the reason is that such organisms die from accident or predation before they reach old age. (They break before they chip and crack.) Plus, Medawar reasoned, natural selection operates on organisms in their prime reproductive age, so why would there be any reason for evolution to “select” against older members of a species? Without a genetic basis to senescence, aging and death must be the result of the entropy of wearing out. Thus, Medawar defined senescence “as that change of the bodily faculties and sensibilities and energies which accompanies ageing, and which renders the individual progressively more likely to die from accidental causes of random incidence.” By this definition, then, “all deaths are in some degree accidental. No death is wholly ‘natural’; no one dies merely of the burden of the years.”11
Not so, says Leonard Hayflick in a 2007 response article titled “Biological Aging Is No Longer an Unsolved Problem.” Hayflick’s solution to the problem involves identifying the “common denominator that underlies all modern theories of aging,” which is “change in molecular structure and, hence, function.” Hayflick’s ultimate explanation for aging and death is an “increasing loss of molecular fidelity or increasing molecular disorder,” which when you think about it is really just the physical entropy of cells. “The weight of the evidence indicates that genes do not drive the aging process but the general loss of molecular fidelity does.” Hayflick explains:
Unlike any disease, age changes (a) occur in every multicellular animal that reaches a fixed size at reproductive maturity, (b) occur across virtually all species barriers, (c) occur in all members of a species only after the age of reproductive maturation, (d) occur in all animals removed from the wild and protected by humans even when that species probably has not experienced aging for thousands or even millions of years, (e) occur in virtually all animate and inanimate matter, and (f) have the same universal molecular etiology, that is, thermodynamic instability.12
That sounds more like physics than biology.
More recently, in 2016 the physicist Peter Hoffman undertook a study of aging after he wrote a book called Life’s Ratchet, on molecular machinery in cells that prevents them from descending into total entropy. Hoffman was contacted by aging researchers who were curious to know more about how these cellular systems might be maintained indefinitely. They can’t, Hoffman explained, because ultimately entropy and the many assaults on cells that accumulate in the course of a lifetime, however long- (or short-) lived, would result in death. “Tinkering with constant risk is helpful, but only to a point. The constant risk is environmental (accidents, infectious disease), but more of the exponentially increasing risk is due to internal wear.” Thus, he concludes, “we need to be clear about one thing: We’ll never defeat the laws of physics.” Although Hoffman titled his article “Physics Makes Aging Inevitable, Not Biology,” it seems to me that it is both physics and biology that ultimately doom all living organisms. After all, biological systems can be reduced to physical processes, which are ultimately governed by the laws of physics, including the Second Law of Thermodynamics. So I fail to see the distinction between the physics and biology of aging as anything but arbitrary.
To that end, two of the most oft-cited causes of the physical and biological decay of cells are the free radical theory of aging and the related mitochondrial theory of aging. Mitochondrial respiration—the generation of energy by converting macronutrients into ATP (adenosine triphosphate) through the use of oxygen in the mitochondria of cells—leaves oxidative free radicals that damage DNA, proteins, and lipids because they have an unpaired electron that seeks to find another electron to pair with from neighboring molecules, thereby damaging them. Breaking these atomic bonds in molecules can cause cancer, as well as lead to the formation of arterial plaques that can result in heart disease and stroke. Antioxidants can help reduce damage from free radicals because they can lose an electron without themselves becoming a free radical, and this has led to endless antioxidant supplements ingested in the form of vitamins A, C, and E. Unfortunately for this otherwise coherent theory, according to a review article in the journal Free Radical Biological Medicine, “the current evidence is insufficient to conclude that antioxidant vitamin supplementation materially reduces oxidative damage in humans.”13
More promising as a causal explanation, albeit not yet for curative treatment, is the gene regulation theory of aging, which posits that senescence is the result of changes in gene expression as one grows older, although it is not clear whether the process of genes turning on causes aging itself or simply stops preventing it. It is obvious that one can breed for longevity in animal models, and that in humans one of the best predictors of how long one will live is the longevity of one’s biological parents. In other words, longevity runs in the genes. So research is now being conducted on genetic engineering and the use of stem cells, but aging is multicausal across many systems. Plus, broad-based gene manipulation may result in unintended consequences because of a genetic phenomenon called pleiotropy, or the production of two or more apparently unrelated phenotypic effects by a single gene (the phenotype is the physical expression of the genotype in interaction with the environment). The selection (or engineering) of one gene with the intention of producing one characteristic may result in the expression of additional unintended characteristics. A famous example is that of the selective breeding for domesticity in silver foxes (Vulpes vulpes) by the Russian geneticist Dmitri Belyaev. The normally humanphobic foxes were bred for friendliness toward people, defined by a series of criteria, from the animal allowing itself to be approached, to being hand-fed, to being petted, to actively seeking to establish human contact. In only thirty-five generations (remarkably short on an evolutionary time scale), the researchers were able to produce tail-wagging, hand-licking, pacific foxes. What they also fashioned were foxes with skulls, jaws, and teeth smaller than their wild ancestors, along with floppy ears, curly tails, and striking color patches on their fur, including a star-shaped pattern on the face similar to those found in many breeds of dogs.14
The biologist G. C. Williams was the first to link pleiotropy to the evolution of senescence in 1957 in a phenomenon he called antagonistic pleiotropy, arguing that traits beneficial to an organism early in its life may be detrimental later in life, such as women’s high ovarian steroid levels during peak reproductive age that can lead to breast cancer decades later, or high testosterone in young men that leads to prostate cancer in old age.15 So genetically engineering longevity, even if it could help push our maximum life-span beyond about 125 years (which it cannot), might result in unintended and possibly antagonistic pleiotropic effects as yet unknown.
The most promising research for breaking through the upper ceiling involves the telomere theory of aging, first proposed by the aforementioned Leonard Hayflick, famous for his discovery of the eponymous “Hayflick limit,” or the number of times that a normal human cell can divide before cell division stops.16 The reason has to do with telomeres, repeated nucleotide segments at the end of DNA molecules, some of which are lost every time a DNA molecule replicates. When none are left, the cell can no longer divide. There is an association between shortened telomeres and the onset of aging, and researchers have found that the enzyme telomerase impedes the shortening process, so perhaps telomerase might delay aging.17 The overused but instructive analogy is with the plastic ends of shoelaces that become worn until they break off and the lace material unravels. The good news is that there are immortal cells for which this does not happen. The bad news is that they are cancerous cells, so any “cure” for aging involving telomeres will have to avoid also producing cancer.18 There are some hopeful experiments in which skin cells exposed to an outside source of telomerase stop aging, and in some cases even appear to reverse senescence.19 Yet other research shows that telomeres cannot be the whole, or even significant, cause of aging, as not all cells that age show telomere shortening, and there are even examples of organisms whose telomeres grow longer with age but they nevertheless experience senescence.20 To whatever extent telomeres matter for longevity, it is encouraging to note that we may not have to wait for genetic engineering to do something about it, as a 2013 pilot study found that diet (plant-based) and exercise (cardiovascular at least thirty minutes a day, six days a week) increased subjects’ telomere length by 10 percent,21 although with a sample size of only thirty-five men we shouldn’t start counting our extra years just yet. Still, that’s encouraging, and a 2017 book titled The Telomere Effect by the Nobel laureate Elizabeth Blackburn documents how a number of lifestyle changes such as eating well, exercising regularly, and sleeping soundly can improve telomere integrity and possibly even longevity.22
If you want to go in whole hog on attenuating aging and delaying death, you might consider adopting Strategies of Engineered Negligible Senescence (SENS), the brainchild of an energetic biomedical gerontologist named Aubrey de Grey, editor of the journal Rejuvenation Research and author of the blindly optimistic Ending Aging.23 Aubrey is the tireless promoter of the belief that our generation will be the first to achieve immortality, or at least to live indefinitely, and he’s on record claiming that the first human to live a thousand years is alive today.24 An inheritance has enabled de Grey to build his SENS Research Foundation into a viable institute respectable enough to garner start-up money from Silicon Valley giants like Peter Thiel.25 If you’ve seen any television show or documentary film on aging, you’ve seen the inimitable Aubrey de Grey with his waist-length ponytail and Methuselah-like beard, expounding on life, the universe, and everything in a baritone British accent. I’ve met Aubrey and shared a beer or two with him (if there is a fountain of youth in de Grey’s world, it is a spring that bubbles beer) as he leaned in to bend my ear on the latest shields against the grim reaper’s scythe. In brief, if we want to understand aging in order to forestall death, de Grey says we must focus our research efforts on these seven types of cellular damage:
1. Chromosome mutations in nuclear DNA that lead to cancer.
2. Mitochondria mutations in the DNA that can disrupt cellular energy production and progressive cellular degeneration.
3. Intracellular junk (junk inside cells) that results from the breakdown of proteins and other molecules that can build up and lead to atherosclerosis and neurodegenerative diseases such as Alzheimer’s.
4. Extracellular junk (junk outside cells, or extracellular aggregates) such as the amyloid plaques entangling neurons in the brains of patients with Alzheimer’s.
5. Cellular loss at a rate higher than cellular replacement in youth that leads to general weakness of organs, such as loss of skeletal muscles and heart muscle, loss of neurons leading to Parkinson’s, and loss of immune cells that compromises the immune system.
6. Cellular senescence in which cells reach their Hayflick limit and can no longer divide.
7. Extracellular protein crosslinks between cells that cause tissues to lose elasticity and develop problems like arteriosclerosis.26
De Grey’s SENS Research Foundation has recommendations of what might be done about these assaults on our cells. Whether meeting these seven challenges would result in immortality, or living a thousand years, or even breaking the 125-year ceiling, however, is unknown because we are not even close to accomplishing any of them. Although a 2005 assessment of the program in MIT’s Technology Review concluded that “SENS does not compel the assent of many knowledgeable scientists; but neither is it demonstrably wrong,”27 a 2005 study of SENS in the molecular biology journal EMBO Reports (the voice of the European Molecular Biology Organization) concluded that none of the therapies recommended by de Grey to counter the SENS seven “has ever been shown to extend the lifespan of any organism, let alone humans.”28 Even de Grey’s own SENS Research Foundation admits: “If you want to reverse the damage of aging right now I’m afraid the simple answer is, you can’t.”29
Still, hope springs eternal, and as Scientific American reported in a 2016 article intriguingly titled “Is 100 the New 80?” there are some promising preliminary results on the antiaging properties of the diabetes drug metformin, which the FDA approved for clinical trials in 2015.30 Another 2016 article in Scientific American, boldly titled “Aging Is Reversible—at Least in Human Cells and Live Mice,” reports on a Salk Institute study in which four mouse genes were turned on that converted adult cells back into an embryonic-like state, thereby rejuvenating damaged muscle cells in a middle-aged mouse. The same was done with human cells (but not whole human bodies), suggesting that the epigenetic shift that leads to aging can be reversed by reprogramming specific genes.31 Unfortunately, some of the treated mice developed tumors and died within a week, so let’s not delude ourselves into believing radical life extension is around the corner.
This reality was well captured in a final pronouncement in Scientific American by S. Jay Olshansky, Leonard Hayflick, and Bruce A. Carnes, three of the world’s leading scientists in the field of aging: “no currently marketed intervention—none—has yet been proved to slow, stop or reverse human aging, and some can be downright dangerous.”32 They note that in addition to the unproven capacity of antioxidants to attenuate the deleterious effects of free radicals on cells, another popular antiaging nostrum called hormone replacement therapy may be effective for some short-term deficiencies such as loss of muscle mass and strength in older men and postmenopausal women, but the long-term negative side effects are still unknown and the slowing of the aging process unproven. Severe calorie restriction appears to work to decelerate aging and increase maximum life-span in a handful of species such as yeast, fruit flies, worms, rodents, and fish, but it is not clear it would work on humans even if you didn’t mind spending the rest of your life in a state of perpetual hunger. As one wag said, “You call that living?” I don’t. “Anyone purporting to offer an antiaging product today is either mistaken or lying,” Olshansky, Hayflick, and Carnes conclude. “It is an inescapable biological reality that once the engine of life switches on, the body inevitably sows the seeds of its own destruction.” Given these realities, we might as well eat, drink, and be merry … and have a beer. A 2016 study by the Mediterranean Neurological Institute in Italy concluded that imbibing a beer or two a day reduces the risk of heart disease by as much as 25 percent.33 Bottoms up.
Some of the radical life extension scientists and cryonics proponents I have met challenge me thus: Wouldn’t you like to live to be 200, 500, or 1000 years old? My reply: Sure, of course, but instead of such lofty goals that are very likely unattainable in my lifetime, if ever, I would be satisfied with living to be 90 without getting cancer, 100 without Alzheimer’s, 110 without senility, and 120 without being bedridden, immobile, and insentient. Let’s solve those problems first before we worry about what happens at age 200, 500, or 1000.
THE ULTIMATE REASON WE DIE
An ultimate explanation for why we grow old and die comes out of evolutionary theory and was well expressed by the physician Sherwin Nuland: “We die so that the world may continue to live. We have been given the miracle of life because trillions upon trillions of living things have prepared the way for us and then have died—in a sense, for us. We die, in turn, so that others may live.”34
The technical name for this declaration is the disposable soma theory of aging, soma being all the cells in the body except the germ cells, which are disposable after reproduction. It’s a Darwinian argument, first proposed by the evolutionary biologist Thomas Kirkwood in 1977.35 Once a body has passed prime reproductive age (in humans roughly age forty) there’s no reason to pour precious resources into it when they can be better invested in offspring. The evolutionary biologist Steven Austad tested the disposable soma theory of aging on two populations of opossums, one on an island with no predators and the other on the mainland with the usual assortment of predators and threats to life and limb. He found that the island opossums reproduced later and aged slower than the mainland opossums.36
What about in human populations? The anthropologist Richard Bribiescas recalls witnessing many young girls from the traditional hunter-gatherer Aché people of Paraguay age rapidly once they started having children. Why? Entropy. “The daily grind of activities necessary to care for a family surely contributes to their physical decline.” At his lab at Yale University, Bribiescas’s research group hypothesized “that women who have more children will exhibit physiological signs of accelerated aging,” and they tested this hypothesis on a group of rural postmenopausal Polish women who were part of a long-term study on women’s health by the University of Krakow. The researchers found that women with more children had significantly higher levels of oxidative stress compared to those who had fewer children, which is revealing because oxidative stress is one of the key physiological markers of genetic, cellular, and tissue damage associated with aging in all organisms. In the end there’s only so much you can do, Bribiescas concludes: “Place an individual into a perfect environment without hazards and with the perfect diet, cognitive stimulation, and every resource that one could identify to maximize life span and you will still eventually end up with a corpse.”37
Of course, in a species with an extended childhood like ours, parents are needed for many years after birth, and even grandparents can play a vital role in childcare and as repositories of knowledge and wisdom, so the decline is a gradual one lasting decades. But once your children’s children are of prime reproductive age, what use are you, really? This is why most organisms grow and flourish throughout childhood and into young adulthood and prime reproductive age, after which the deleterious effects of aging begin to accumulate. Whether the aging process happens by deterioration and the slowing of the maintenance of cells (passive aging) or through programmed cell death (active aging) is not fully understood and remains a theoretical debate among scientists who study the evolution of aging,38 but it is clear that any ultimate explanation for death must have at bottom an evolutionary framework undergirding it.39
The language I’ve employed here makes it sound as if there’s someone directing the evolutionary process, keeping track of investments and payoffs and allocating energy and resources for the good of the species. Not so. There is no intelligent agent running the show from on high, and no goal-directed process operating “for the good of the species” in the future. What Darwin demonstrated is that there is a bottom-up process called natural selection that results in apparent design. But the design is a functional by-product of an undirected process. Think about aging and death from the perspective of the genes instead of the body. Genes consist of self-replicating molecules housed inside a cell that contains machinery for energy consumption, maintenance and repair, and other features that keep these molecular structures intact long enough to reproduce. Once such molecular machinery is up and running, the replicating molecules become immortal as long as there is energy to feed the system and an ecosystem in which these processes can take place. Over time these replicating molecules outsurvive nonreplicating molecules by virtue of the very process of replication—those that don’t, fail to continue—thus the bodies in which the replicators are housed are survival machines. In this perspective, most famously proposed by the evolutionary biologist Richard Dawkins in his book The Selfish Gene, replicators are called genes and the survival machines are called organisms.40 A survival machine is the gene’s way of perpetuating itself into the future indefinitely. Genes that code for proteins that build survival machines that live long enough for them to reproduce win out over genes that do not. From there, selection forces grow weaker for maintaining the robustness of survival machines in old age, and so the life-span of an organism is a balance between the selection pressures that increase reproductive fitness and those that weaken it. The result is mortal bodies and immortal genes.41 This means that individuals are mortal but species are immortal, as long as they do not go extinct. In our case, the only way to guarantee that this does not happen is to become a multiplanetary species. We are in the process of doing just that.
THE IMMORTAL SPECIES
In 2016, Tesla and SpaceX CEO Elon Musk announced his program for establishing a permanent colony on Mars, starting with transporting one hundred people in eighty days to the red planet, and then repeating the process through reusable rockets until the colony becomes sustainable, perhaps as soon as a century from now. This would make our species multiplanetary, thereby ensuring our survival should something catastrophic happen on our home planet. “Without someone with a real ideological commitment,” Musk said in his stirring presentation accompanied by a video enactment, “it didn’t seem we were on any trajectory to become a spacefaring civilization.”42 From there it is only a matter of time to island hop from Mars to the moons of Jupiter and Saturn, and eventually work our way out to colonizing exoplanets around other stars. How does this make our species immortal?
There is no known mechanism—short of the end of the universe itself many billions of years from now43—to cause the extinction of all planetary and solar systems at once, so as long as our species inhabits multiple planets and moons we can continue indefinitely.44 In the far future, civilizations may become sufficiently advanced to colonize entire galaxies, genetically engineer new life-forms, terraform planets, and even trigger the birth of stars and new planetary solar systems through massive engineering projects.45 Civilizations this advanced would have so much knowledge and power as to be essentially omniscient and omnipotent. What would you call such a sentience? If you didn’t know the science and technology behind it you would call it God, which is why I have postulated that any sufficiently advanced extraterrestrial intelligence or far future human is indistinguishable from God.46
It would be too much to say that this form of species immortality satisfies our personal desire to live forever, but it is something well worth working toward, inasmuch as for all we know, we are the only sentient species in the cosmos, so it is incumbent upon us to survive and thrive so that the cosmos may continue to be self-aware. Moreover, given the distances and time scales involved, even if we are the only spacefaring species in the galaxy there is a good chance that each colonized planet will act like a new “founder” population from which a new species evolves, because as the great evolutionary biologist Ernst Mayr defined it, “a species is a group of actually or potentially interbreeding natural populations reproductively isolated from other such populations.”48 Different planets, solar systems, and galaxies will act as reproductive isolating mechanisms, and our genus Homo will return to a state it last saw tens to hundreds of thousands of years ago when multiple big-brained bipedal apes roamed the planet driven by hunger, lust, and wanderlust out of Africa, out of Asia and Europe, and out of Earth. Thus do we achieve immortality as a species by going to the stars.
Figure 11-1. Per Aspera Ad Astra
From Finland in the Nineteenth Century, published in 1894, illustrated by Finnish artists.47 Translation: To the stars through struggle. Sometimes rendered as I present it: To the stars through audacity, or per audacia ad astra.
Per audacia ad astra.49