Cracking the Aging Code: The New Science of Growing Old—and What It Means for Staying Young

By Josh Mitteldorf and Dorion Sagan

A revolutionary examination of why we age, what it means for our health, and how we just might be able to fight it.

In Cracking the Aging Code, theoretical biologist Josh Mitteldorf and award-winning writer and ecological philosopher Dorion Sagan reveal that evolution and aging are even more complex and breathtaking than we originally thought. Using meticulous multidisciplinary science, as well as reviewing the history of our understanding about evolution, this book makes the case that aging is not something that “just happens,” nor is it the result of wear and tear or a genetic inevitability. Rather, aging has a fascinating evolutionary purpose: to stabilize populations and ecosystems, which are ever-threatened by cyclic swings that can lead to extinction.

When a population grows too fast it can put itself at risk of a wholesale wipeout. Aging has evolved to help us adjust our growth in a sustainable fashion as well as prevent an ecological crisis from starvation, predation, pollution, or infection.

This dynamic new understanding of aging is provocative, entertaining, and pioneering, and will challenge the way we understand aging, death, and just what makes us human.

• Language: English
• Publisher: Open Road Integrated Media
• Release date: Jun 14, 2016
• ISBN: 9781250061720

Book preview

PREFACE

What This Book Is About

---

What Is Aging?

Scientists sometimes use the word senescence. The common meaning is a deterioration in many body functions that comes with age. Sometimes we will use the demographer’s definition: an increased risk of death with passing time.

It is a common belief that aging is inevitable and universal. Not on your life!

---

During the twentieth century, medical technology took enormous strides toward the conquest of infectious disease and recovery from trauma. With hygiene and sanitation, then antibiotics in the 1930s and an ever-expanding arsenal of vaccines, many plagues of the past have been vanquished: polio, syphilis, whooping cough, diphtheria, and cholera were once feared as a death sentence, and now they are footnotes in the mortality statistics. The diseases that remain are all associated with aging; diabetes, arthritis, and osteoporosis are growing, and the Big Three killers are cardiovascular disease, cancer, and Alzheimer’s. Tens of billions of dollars have been spent on medical research over several decades trying to conquer these diseases with the same approach that succeeded so well for infectious disease.

That approach has been to work with the body, to stimulate the body’s growth and inborn strength, to buttress its natural defenses. Even the reductionist tradition of Western, allopathic medicine has been influenced by the philosophy of natural medicine, working with the body instead of attempting to overpower it with technology or drugs. But what the doctors do not yet realize is that they are working with a suicidal patient.

Suicide Genes

Man overboard!

You run to the railing and throw him a lifeline. If only you can get the buoy within his reach, you might pull him back to safety …

Good toss! The life preserver is right in front of him, but he is not taking it. Is he just too weak? Has he lost the will to live? You call to him. Go away, he answers. Leave me alone! And now your understanding of his situation is changed.

He didn’t fall off the boat—he flung himself into the sea. To save a man from drowning is one thing; to dissuade him from suicide will require a different approach. In the immediacy of the crisis, you might take advantage of his exhaustion, jump in the water, overpower him, and carry him forcibly to safety. But next week, he might make another attempt. To help this man, you will have to get to know him, learn what is important to him, understand why he wants to kill himself, and convince him to choose life.

*   *   *

Doctors today are trying to help a body that does not want to be helped. Efforts to restore the body’s natural balance won’t work, because as we age, the body’s natural metabolism is bent on self-destruction. Attempts to bolster the body’s natural defenses are doomed to failure because the natural defenses are slowly being shut down with age.

Progress can be made against the Big Three diseases, and aging itself can be abated, but a different approach is required. We must be willing not just to assist the body but to coax, cajole, and even fight with it when appropriate. We must learn more about hormones and the signaling language that regulates metabolism. We must whisper the word youth in the body’s own native language of biochemistry, a language as yet still somewhat foreign to us. But this is the language in which the entire life plan is spelled out, from development in the womb to aging and death.

Selfish Genes

The central idea of this book is that aging is built into our bodies. Aging doesn’t just happen but is regulated and controlled by our genes. Our self-destruction is scheduled as much as is our development in childhood or our sexual development at puberty. Growth, puberty, and aging all unfold on a schedule programmed into the regulatory segments of our DNA.

But to an evolutionist, these things are not the same at all. A strong body helps us to survive and preserve ourselves. Sexual development is necessary for reproduction. These things are good for us, good for the prospects of our genes. They help our genes to be passed along, to prevail, and to spread in succeeding generations. This fits well with the idea of natural selection, the fundamental premise of Darwinian evolution. It is easy to understand how genes for growth and sexual development evolved. They are selfish genes, because they help the body, their vehicle, and so they help themselves.

But aging is about weakening and dying. It cannot be good for the body. Genes may cause aging, but aging cannot promote the prospects of those genes; quite the contrary, aging ends the careers of the very genes that cause it. This does not make sense from the prevailing evolutionary perspective. Why would selfish genes kill their bodies? But in fact multiple lines of evidence suggest that is exactly what they are doing. As we get older, our genes turn against us, killing healthy nerve cells and muscle cells, permitting the thymus gland to wither away, which undermines our immune system. We consider this self-destruction normal, but in fact, it doesn’t apply to all species. There are a few animals and many plants that do not age. And although selfish gene theory cannot explain why our bodies do this, another theory—the Demographic Theory described in chapter 8—does. The self-destruction we take for granted is in fact under evolutionary control. These evolutionary suicidal tendencies, while they do not make us as individuals live long and prosper, turn out to have a vital evolutionary function.

These suicide genes are the opposite of selfish genes. In the course of evolution, genes for aging must have fought an uphill battle against natural selection. How could aging have evolved?

This is a question that has been asked over and over since Darwin first skirted the issue 150 years ago. In fact, there was no mention at all of life span or aging in the first edition of On the Origin of Species (1859). Skeptics confronted him with the great range of life spans in nature. Why have life spans not evolved ever longer? Isn’t that what we should expect from your theory? Darwin’s answer in later editions was uncharacteristically vague and unconvincing. Although many volumes and thousands of articles have been written on the subject ever since, there are really only three kinds of answers.

Three Evolutionary Stories About Aging

Answer number one is that there really is no aging in nature. Animals in the wild do not live long enough to die of old age, because they die of other things first. It’s a highly competitive world out there, red in tooth and claw.* Organisms are ever at risk from predators, accidents, and starvation. We are aware of aging when we look at domesticated animals protected from their natural enemies, and of course civilization has afforded humans a safety that is completely uncharacteristic of our evolutionary history. Aging is an artifact of protected environments, and in the natural world where evolution runs its course, aging doesn’t exist—so there is nothing to explain.

Answer number two is that natural selection encounters trade-offs and makes compromises. The body is doing its best to repair itself and forestall damage, but there are other priorities that keep it from doing a perfect job. In youth, the body allows itself to gradually accumulate damage, even though this eventually will prove fatal, because neglecting the infrastructure frees up resources for survival and reproduction.

Answer number three is that even though aging is bad for the individual, it is important for the community. Aging creates opportunities for the young and thus it promotes population turnover for adaptive change. Another communal benefit of aging is the stabilization of populations. Aging levels the death rate so individuals don’t all die at once, as in famines and epidemics.

Answer number one (aging is an artifact of protected environments) has been thoroughly discredited by population studies of animals in the wild. It has been established that, indeed, animals in nature live long enough for aging to matter. Answer number two (trade-offs and compromises) depends crucially on the assumption that the body can only do a good job of one thing at a time. Although this seems to be true in particular cases, there is no reason to think that a strengthening in one area must always come at the expense of a weakening in another, and indeed there are abundant counterexamples. There is a lot of genetic and experimental evidence in favor of answer number three (communal benefit), but deeply entrenched evolutionary theory has created a strong prejudice against it.

This prejudice is a deep vein in our culture of individual competition. In economics, it is the myth of free markets. Socially, it is the conceit that status is a reward for talent and hard work. In health, it is the belief that nature knows best. And in the academic study of evolution, the prejudice is echoed as an assumption that natural selection takes place only between individuals, never between teams or groups or communities. As these pages unfold, I hope to show you that these are prejudices, not science, and that the evolutionary prejudice is related historically to discredited economic and social ideas.

Aging Genes

Breeding animals is an ancient art. Dogs were domesticated long before recorded history. But in the 1980s, the breeder’s art took a big step closer to being a quantitative science as techniques were developed to analyze small differences in DNA, to see exactly what genes were being bred. Tom Johnson, working at UC–Irvine, was onto the advantages of studying aging in the lab worm Caenorhabditis elegans. These worms are happy growing on a petri dish, they live just a couple of weeks, and their aging is remarkably flexible in response to feeding, temperature, and genes.

Johnson studied worms with a mutation in a gene that rendered it inoperative, as if it wasn’t there. After he discovered that worms with the defective gene lived half again as long as normal worms, he dubbed the gene AGE-1. No one had ever imagined that a single gene could have such an effect on life span. In fact, the best experts in evolution had theorized that everything ought to wear out at once, so that no single gene could have any noticeable effect. Johnson’s discovery was the more remarkable because longer life required nothing new but rather the deletion of an existing gene. This implied that the effect of the AGE-1 gene was to cut the worm’s life short. What was it doing in the genome? How did it get there? And why did natural selection put up with it?

Johnson had a ready explanation. He believed (and still believes, I believe) in the conventional explanation for evolution of aging, answer number two in the section above (trade-offs and compromises). The worms without AGE-1 laid only a quarter as many eggs as other worms. It was easy to see how they had been losers in Darwin’s struggle. In fact, Johnson’s finding looked like a dramatic confirmation of the theory that aging was a side effect of genes for greater fertility, greater individual fitness. Aging had not evolved directly, selected for its own sake, but as a cost of greater fertility, so the paradox was avoided.

But a few years later, this story unraveled, and what had been confirmation of theory number two became a direct contradiction. Johnson discovered that his mutant worms actually had two genes that were different. In addition to AGE-1, there was another, unrelated gene defect (FER-15) on a separate chromosome. By crossbreeding, he was able to separate the two. Worms with the FER-15 mutation had impaired fertility without extended life spans. Worms with the AGE-1 mutation had extended life spans with unimpaired fertility. This was a full-fledged Darwinian paradox: the AGE-1 gene found in nature was the one that gave the worm a short life span. It was the defective gene that caused the worm to live longer. AGE-1 looked not like a selfish gene but an aging gene. It was just the kind of gene that natural selection ought to eliminate handily. How had this gene survived, and what was it doing in the worm genome?

*   *   *

AGE-1 was only the first case of an aging gene in worms. There are now hundreds of genes known that lengthen life span when they are deleted. In other words, these genes, when present, have the effect of shortening life span. Some of them tend to improve fertility; some don’t. Some have other beneficial side effects, but about half the known life-shortening genes offer nothing in return, or at least nothing that has yet been identified. This is direct evidence in favor of answer number three, the answer that defies conventional evolutionary theory.

Aging genes have been discovered in other lab animals as well as worms. The other popular species for aging scientists to study have been yeast cells, fruit flies, and mice. These four species come from very different branches of the evolutionary tree. Nonetheless, they share common ancestors, going back hundreds of millions of years ago to the first eukaryotes (complex cells with nuclei and certain other organelles). You and I and the mouse and the worm and the fly and the yeast cell are all eukaryotes, and there are some genes—including deleterious ones—that we share. Why? Why has nature conserved life-shortening, killer genes?

The answer must reflect the unity of life. There are certain core functions of the cell that arose in the distant past and have been conserved through aeons of evolution. We all transcribe our genes into proteins using the same genetic code, we all burn sugar for energy using the Krebs cycle, and we all reproduce sexually using a style of cell combination and division known as meiosis. We all age and die.

It is remarkable that aging is one of these core life functions that almost all eukaryotes share. There are genes that modulate aging in yeast cells that are close cousins of aging genes in worms, in flies, and in mammals, including you and me. Despite the fact that aging is a disaster for the individual, evolution seems to have guarded and preserved the genes for aging as though they were the crown jewels. This is a dead giveaway that aging must have an essential biological function.

Patrician Genes

There is a natural analogy between population cycles in ecology and the economic cycles of boom and bust that appear in the brand of capitalism embraced by America and the West.

In the wake of the 1929 economic collapse, the Roosevelt administration was able to pass a broad program of government oversight and regulation of business practices. There followed forty years of unprecedented growth and the rise of an American middle class, the first time in history that any economic system had supported a majority of its citizens in comfort and security. But in 1980 began the Reagan backlash, deregulation, and the return of unbridled economic competition. Capitalism became predatory, the middle class began to shrink, business cycles deepened, and a growing rift now separates a wealthy elite from the struggling majority. There have been three major stock market crashes in the thirty years since deregulation, each followed by painful unemployment and economic stagnation.

Without regulation, competition becomes destructive. The idea that stability and a broad prosperity can emerge from pure competition is thoroughly discredited in practice, but it is a useful myth for the 1 percent who profit mightily when there are no rules and no regulators. If they told the truth about their motives, the rapacious corporate giants could never sell deregulation to an enlightened democracy. So they promote the dogma of a free market, not because they believe in this or any ideology but because it supports the freedom of the largest and the strongest to pillage everyone else.

Historically, an important part of the argument for the benignity of free markets comes from the analogy with evolution. (Just look at the marvels nature hath wrought using only the chisel of bare-knuckled competition!) This is social Darwinism, the doctrine that the rich and successful not only contribute more to society than you and I but that they have better genes to boot. It is a perversion of Darwin’s ideas, but from the very beginning, his sound biological theory has been linked to an elitist social ideology. During the early years of the twentieth century, social Darwinism played a crucial role in shaping the version of evolutionary theory that emerged and predominates to this day.

People are rich and powerful because their parents were rich and powerful—nothing remotely fair or just about it. But social Darwinism promotes the fiction that there is a natural order in the predominance of an elite hereditary class. Like the invisible hand of Adam Smith a century earlier, Darwin’s struggle for existence has been caricatured to support the myth that pure, unrestrained competition can be magically transmuted into a harmonious society. The truth is that tooth and claw competition doesn’t work in economics, and it doesn’t work in ecology. Competition is vital, but it must be regulated, or it poses a fatal risk of instability for the whole system.

Darwin himself was of the British aristocracy, and he had some trouble acknowledging the huge evolutionary significance of cooperation. Yet in his later work The Descent of Man, Darwin spoke explicitly of a group that could have an evolutionary advantage distinct from the sum of its individuals.

By the mid-twentieth century, the existence of cooperation was denied utterly by the mainstream of evolutionary theory. We live now in an age of hyperindividualism, and it is no accident that, in our culture, the dominant version of Darwin’s theory is based on pure selfishness.

Where This Book Is Headed

Aging is the very antithesis of what Darwin called fitness—the competitive vigor and reproductive potential of organisms. If aging is governed by genes that cause us to become frail, to lose our fertility, and to die, then how did those genes prevail in evolutionary competition? How could aging have evolved?

That is a central question in this book. The answer is that natural selection is not just the life and death of individuals but also the rise and collapse of local populations and of entire ecosystems. Evolution is about cooperation as well as selfishness, and aging has evolved as part of the dues owed by an individual for participating in a stable ecosystem. Evolution and ecology have inscribed a death sentence in our genes. We literally pay with our lives to protect ecosystems, as increased death rate via aging prevents the sort of wild overgrowth that presages wholesale population collapse.

Aging appears to be caused by an explicit genetic program. One consequence of this is that medical science will have to approach the diseases of old age with a different attitude. We can’t use natural medicine. We can’t help the body to heal, because the body isn’t trying to heal—it’s trying to destroy itself. Instead, we must decode the signals that trigger self-destruction and replace them artificially with the signals of youthful vitality.

Another consequence is that the selfish gene version of evolutionary theory is not the whole story. Mothers teach their children to take care of themselves. What mother wants her child to be indifferent to the welfare of others? Mother Nature, like all mothers, has counseled her children against excessive selfishness. She wants them to take care of themselves to be sure, but because she wants them to get along in the world, she has tempered selfishness with altruism.

This seems to be an intuitive truth, easy to grasp for anyone who does not have an advanced degree in evolutionary biology (and to their credit, not a few professional evolutionists have figured out that the selfish gene version they learned in school was a tortured picture of reality).

Ripe for Scientific Revolution

The science of aging is a very active field, expanding in scope, with new labs, new techniques, and an influx of creative young talent. The field is not at all moribund, but it is flailing. At meetings and in journal articles, the puzzling mismatch between experimental results and theoretical expectations is everywhere apparent. Some researchers try to paper it over, and their explanations come out as incoherent or obviously flawed. But most are presenting the data with an honest admission, appending such comments as:

We don’t understand why this happens.

There is some kind of dysregulation here, a failure of the body to do the right thing.

It’s strange that the damage the body suffers seems completely avoidable, and yet …

What they are seeing—or refusing to see—is the body destroying itself on a schedule.

Evolutionary theorists have tried to understand aging within the framework of the theory as they learned it. They have done a workmanlike job of extending and modifying the theory as each new result comes in, carving out exceptions and elaborations on the basic themes. But specialists in the field tend toward myopia, and few have stepped back to look at the big picture, to see the signs that the basic principles of the theory no longer match the basic observations.

The essential problem is that the theory has been built from the bottom up, taking the individual animal and its individual success to be primary. (Darwin did not make this error; it came into the field only later, in the twentieth century.) Neglected are all the ways in which a community functions as a collective, with logic that cannot be understood simply as the sum of individuals. The limited perspective of the selfish gene is very much the standard today. Evolutionary scientists are quite aware that their paradigm is based on individuals to the exclusion of communal adaptation, and they have their reasons for this strong bias in favor of the individual over the group. Such reasons include an overreaction to an earlier excess in the opposite direction, when naturalists spoke too glibly about the good of the species. But although the biomathematicians’ skepticism of group selection was understandable, it is clear now that they are wrong. I* am in the minority, but I am not alone in saying this. Many smart people, including Nobel laureates and experts on the edge of the field, have recognized that evolutionary science today is missing something basic. Perhaps you have sensed this already; if not, I think that you will come to see it in the chapters that follow.

Why Should It Matter If Evolutionary Competition Is Individual or Communal? And What Does All This Have to Do with Aging?

Having a fixed life span—dying on a schedule—is bad for the individual, but it has advantages for the community. To understand what aging is and how it came to be, it is necessary to adopt a communal perspective for evolution. Aging is a paradox if your paradigm is confined to selfish genes, but it is possible to understand aging if you imagine natural selection in a broader context, with cooperative groups competing in a classical Darwinian struggle. The fashion in evolutionary theory these last fifty years has been to think exclusively in terms of individual competition, to disallow group competition. This has been the root of the scientific community’s failure to understand aging.

I have said all this in scientific forums and on the pages of biology journals, and now I am going over the heads of the experts to appeal to your good sense. For eighteen years, I have been watching the response of the academic community to ideas about communal evolution, including my own ideas. It has been both deeply gratifying and intensely frustrating for me—gratifying because the scientific world is moving in the right direction, frustrating because the movement is so slow. There is still a great deal of unthinking bias against group selection. Lab scientists still report their results in terms of the failed theories.

A few years ago, I was visiting my mother (now ninety-three years old and sharp as a tack) when I complained about the conservatism of the scientific community. I had wanted to initiate a scientific dialogue, and I was frustrated. Take your case to the people, she said. Write a book. That project proceeded in fits and starts for two years. Then I hit the jackpot and found an ally in Dorion Sagan. He quickly understood my ideas about aging and was able to help me both put them in the context of broader evidence-based evolutionary theory and make them more accessible. This book is our first collaboration.

PROLOGUE

Your Inner Stalker

· DORION SAGAN ·

The void, the concept of nothingness, is terrifying to most people on the planet. And I get anxiety attacks myself. I know the fear of that void. You have to learn to die before you die. You give up, surrender to the void, to nothingness.

—HARRY DEAN STANTON

When noir writer Jim Thompson titled his 1952 crime novel, The Killer Inside Me, he was referring to the unhinged mind of a small-town Texas cop, not the automatic behavior of cells. And yet we very well could have used his title on our book, for it turns out, you too are prey to an inner assassin. Unlike Thompson’s cliché-spewing deputy sheriff, your killer has its sights set on itself.

The book you hold in your hands makes a case for something as astounding as it is unexpected: that our aging—which kills us if we don’t die first by accident, war, or disease—is genetic. What is aging? Aging, or senescence, cannot merely be defined as the process of getting older. Time goes by for a rock, but it may not perceptibly change in thousands of years. To be more precise, we should define senescence—aging—not just as the passing of time but as an increased chance of dying with the passage of time. Thus, for example, my near namesake (my astronomer father might have been thinking about Orion, the constellation, closer to my spelling), Dorian, in Oscar Wilde’s gothic classic The Picture of Dorian Gray, temporarily escapes the senescence that normally affects all of us after reaching adulthood. (See the Mortality Table and a more in-depth definition of aging here.) Dorian keeps his youth while a portrait of him, kept in a closet, ages instead. A nice arrangement—or a diabolical deal. After a failed relationship in which his actress fiancée kills herself with cyanide, Dorian becomes an unhappy hedonist, kills the painter of his portrait, bribes someone to dispose of the body, and finally, at his wit’s end, stabs the now-hideous painting. At this point, the painting recovers its original form while Dorian ages eighteen years in minutes, his corpse identified only from his rings. Such is senescence, with a vengeance. And although it is fictional, such an aging-in-a-hurry lifestyle, although rare, seems to mark some bird species, such as the albatross. Senescence, as you’ll see, is not a one-size-fits-all sentence of death by deterioration. It can be fast, slow, or—surprisingly—not at all. (See chapter 2.) These are the kind of raw, on-the-ground facts that mathematically hypertrophied but evidentially undernourished neo-Darwinism has had trouble making sense of. Until now.

I say that advisedly—very advisedly—because to say that suggests that my coauthor, Josh Mitteldorf, is a neo-Darwinist—a designation he stringently rejects.

Nonetheless, he shares with the best (and perhaps worst) of the neo-Darwinists a familiarity with, an attraction to, the development and analysis of mathematical equations and models that abstract the elements of biology in sometimes illuminating, even predictive ways. I am more philosophically inclined but have sometimes had the advantage, I would say, of being able to see the forest for not being distracted by the trees. Josh and I agree on this: it is, you might say, the underestimated advantage of the words out of the mouth of the not-yet-socialized babe; a kind of emperor-who-wore-no-clothes phenomenon. Like the child in Hans Christian Andersen’s tale who stated the obvious—that the emperor whose gown everybody was pretending to admire was in fact without one—my glimpses of a scientific field were always from the outside. I did not get lost in the details because I did not know them, and I was not crushed by the inertia of grad school mantras I’d never heard. When, in first trying to popularize the idea of my biologist mother, Lynn Margulis, that evolution proceeds largely by symbiosis, I used the term group selection—to refer to the process of certain interspecies alliances and well-orchestrated societies outliving their less unified competition—she said, You can’t say that.

Why? I wanted to know.

You just can’t; the phrase isn’t allowed.

In this book, you’ll see why this was—and still largely is—the case. It is a core of Josh’s fascinating new biophysical worldview, which has rather huge stakes for us humans, so long duped by the promisers of extended life and the religious counterpart, life after death. Josh himself, trained in astrophysics, comes to the field of biology, and specifically how organisms age, from the outside. But here he is in good company; the influential innovators of modern neo-Darwinism, from the right-wing Ronald Fisher to left-wing J. B. S. Haldane, came from the hard sciences, from physics, mathematics, and statistics. This was in fact part of the point: to put soft biology on a rock-hard foundation, even if that meant, ultimately, the sacrifice of common-sense assumptions upon the altar of mathematical workability and disciplinary prestige. When Richard Dawkins calls William D. Hamilton his intellectual hero, he is paying homage not to the equations that attempted to demonstrate that aging is an evolutionary inevitability but to the curious, creative, but mathematically checked imagination that would devise such a thing.

Of interest to socialists and communists no less than capitalists and fascists, life does indeed seem to be a social phenomenon. Not just social but, as the accumulating evidence for symbiogenesis—the production of new life-forms from the melding of separately evolved organisms—suggests, hypersocial. The surface of this planet has been crowded for billions of years. And it is in this context of crowds, the benefit of their organization compared to the dangers of their rampant growth, that aging, according to Josh, must be understood.

Aging, in the view laid out here—which you can think of as a kind of giant case study of humanity’s once-naïve view of the process—is not what you thought it was. This book does not contain your grandfather’s view of aging. It does not contain the view of aging implied by my grandfather’s advice, Whatever you do, don’t make the same mistake I made. About thirty years ago, I started getting old.

"Don’t make the same mistake": clearly a joke, ironically underscoring that there is nothing we can do, wittingly or unwittingly, about an inexorable process. But according to the theory laid out here, my grandfather’s assumption is dead wrong. Aging is no mistake. Rather, it is something that nature—however unconsciously—does on purpose. On the new view presented for the first time to a popular audience here, senescence does not come about through mere external exigency or as a result of the inevitable tendency for usable energy to be lost to the environment (entropy). Rather, as you will see, aging, or senescence, seems to be the result of multiple genetic systems all but conspiring to kill us from within. There are many signs that aging is genetic. The clearest proof is our ability to easily make organisms live longer. Fruit flies can be bred to live eight times as long. Starved rodents live 40 percent longer. Nematodes—tiny, fast-breeding roundworms, a favorite species for lab studies—insulated from the mere smell of food live significantly longer. The same is true of fruit flies. In other lab experiments with worms and yeast cells, geneticists have been able to increase life span just by disabling certain genes, which some have dubbed gerontogenes. Josh refers to them more simply as aging or suicide genes.

Suicide genes present more than a little puzzle within the strict selfish gene paradigm. The realization that aging destroys organisms that have the tools to live longer—much longer—flies in the face of one of the most deeply held tenets of modern biology: that genes and individuals have evolved to maximize their own maintenance and reproduction. And yet there is now smoking-gun evidence that nature has been killing off her own for a good long time. Why? We know that Mother Nature is not always nice, but how could she—how could she do such a thing?

Josh shows us. Although aging certainly does not preserve individuals like you or me, it protects and invigorates communities, which, come to think of it, are integral parts of our species’ survival. In evolutionary history, whole populations—not unlike certain economies and empires vulnerable in their dotage, too big not to fail—have routinely been completely wiped out. Suddenly running out of resources, their individuals starved to death. Or they became soft targets for predators that whittled their populations down beyond the point of renewal. Or they became sitting ducks for rapidly reproducing bacteria or viruses.

This population’s-eye perspective has a checkered history. In its earlier phase, it was roundly ridiculed and in some cases appropriately criticized for careless rhetoric and naïve mathematics. But Josh, an innovator in biological computer modeling with a Ph.D. in theoretical physics, is no mathematical naïf. Evolutionary science is in the midst of a transition from a perspective based on pure competition to a broader schema in which