Cheating Death: The Promise and the Future Impact of Trying to Live Forever

Cheating Death: The Promise and the Future Impact of Trying to Live Forever

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by Marvin Cetron, Owen Davies

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To live forever is one of man's oldest aspirations--and it might be become a reality. With advances in medicine and new gene research, human life span could extend into hundreds of years. But is this life extension a good thing? "Cheating Death" examines every side of the dilemma of aging and longevity--from improvements in diet and medicine to the grander promises of


To live forever is one of man's oldest aspirations--and it might be become a reality. With advances in medicine and new gene research, human life span could extend into hundreds of years. But is this life extension a good thing? "Cheating Death" examines every side of the dilemma of aging and longevity--from improvements in diet and medicine to the grander promises of science to the consequences of incredibly long life.

Editorial Reviews

Publishers Weekly - Publisher's Weekly
The dubious premise of this futuristic exercise is that baby boomers will achieve life spans of 110 to 120 years, and advances in aging research will "very likely" push death back to age 150 or 200. With dizzying speculation, the authors gauge the impact of life extension on Social Security, pension plans, work, the environment, medicine, hospices and home care for the elderly. Embedded in this crystal-ball gazing is advice on how to plan for one's postponed or delayed retirement (e.g., develop alternative sources of income, keep learning new skills, retire in stages). Nearly half the book consists of prognosticative lists of 124 trends in the coming "postmortal" world of artificial blood, plastic modular housing and memory-enhancing drugsa world where a fully funded U.N. will function effectively, while the industrialized nations distribute huge sums to jump-start the economies of poorer countries. Cetron, founder of Forecasting International, and Davies, former senior editor at Omni, whose previous collaborations include Probable Tomorrows, mine the techno-apocalyptic idiom of John Naisbitt or Alvin Toffler, but without the spirited vigor. (Feb.)

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Cheating Death

The Promise and the Future Impact of Trying to Live Forever

By Marvin Cetron, Owen Davies

St. Martin's Press

Copyright © 1998 Marvin Cetron and Owen Davies
All rights reserved.
ISBN: 978-1-4668-6090-2



All right, we admit it. Not even the most optimistic of scientists expect to live forever. The world will not soon be "postmortal" in the sense that science will abolish death. But our exaggeration is much smaller than you probably assume.

The most profound transformation in history, the most fundamental change that humanity ever will experience, is as near as next week. It may already have begun. From this decade onward, the years of our lives will not be threescore and ten, but far longer. The Baby Boom generation, and perhaps its parents, can expect to live healthy, active lives that stretch to between 110 and 120 years. It is even possible that some of us may never die, save by accident or choice. Medicine, government, economics, religion — no single facet of human existence will remain the same.


In the summer of 1995, several popular books told readers of a remarkable advance in the study of aging. A hormone called melatonin, they proclaimed, might have the power to hold time itself at bay. Mice receiving this natural, harmless substance survived to the human equivalent of 115 years. To the end of their very long lives, they retained all the health and vigor of youth. Just conceivably, people who used melatonin also might live far beyond their allotted span without ever growing old.

A furor greeted this announcement. Scientists debated the hormone's effects and squabbled about who deserved credit for the discovery of its age-fighting power. Doctors warned that melatonin might cause unknown harm. Skeptics denied that the results of experiments in mice could be applied to human beings. And in the United States, where melatonin is readily available, tens of thousands of ordinary people began to use this latest miracle drug. Some merely wanted a good night's sleep, for melatonin is a powerful sedative. Many others dreamed of taking a first step toward immortality.

Yet amid the hope and controversy, the true significance of this research was overlooked. What matters is not whether melatonin itself extends human life. It may well not. But discoveries related to melatonin have given scientists their first handle on aging. For decades, they struggled to figure out why we grow old. Now they can concentrate on developing a cure. And because the cause of aging has turned out to be relatively simple — a pinpoint failure in one biological system, rather than a general "wearing out" — a successful treatment should be much easier to find than, for example, the proverbial cure for cancer. Even if melatonin itself is not the final answer, it has become reasonable to believe that a practical remedy for aging is not far off.

This presents important problems. As individuals, we must plan for the forty years of added life that we suddenly can expect. As a nation, we must figure out how to support extra generations of healthy, vigorous, but chronologically ancient people who have no established role in society. As a world, we must find ways to share the benefits of aging research without undermining less flexible cultures or overcrowding our fragile planet. These and many other challenges could require answers in the next five years and almost surely will demand them in less than twenty.

In the pages that follow, we will seek to understand how the world must change when aging and death are no longer the ultimate facts of life.


As a technical problem, aging is one of the most complex and elusive phenomena that scientists have ever studied. As early as World War I, the Nobel Prize–winning physician Alexis Carrel observed that the wounds of older patients healed more slowly than those of the young. In the following years, he and his colleague P. Lecomte du Nouy discovered that some element in blood plasma caused the difference. Yet whether healing was promoted by a factor in the blood of the young or delayed by something in the blood of the old, they never were able to learn. It was the first of many such puzzles.

A few years later, Clive McCay of Cornell University found that putting rats on a diet that was nutritious but so low in calories that it could barely sustain life dramatically extended their survival. In one typical study, rats that ordinarily live for only 600 days survived to an average age of 1,100 days and some reached 1,800 days. Hundreds of scientists have confirmed this phenomenon in many different species. Mice, hamsters, and gerbils all live longer when calorie-restricted. Experiments with dogs and rhesus monkeys — much closer relatives of the human species — are not yet complete, but preliminary data suggest that calorie restriction will extend their lives as well.

These extreme diets confer other benefits as well. Mice and rats are prone to all the diseases that afflict aging men and women. However, when scientists cut their calorie intake by 30 to 50 percent, animals rarely become ill. Several years ago, scientists at Philadelphia's Institute for Cancer Research studied a kind of rat that always suffers from diseases of the heart, kidney, lung, and prostate, as well as several forms of cancer. When placed on a strict diet, only one animal in ten developed cancer. Just 2 percent suffered heart problems. None had kidney disease. Again, scientists have seen much the same reduction in disease in many different species.

In more than seventy years of careful work, no one has ever been able to explain how calorie restriction works its miracles. The trouble is that aging changes almost every aspect of the body's workings. Hormone levels, blood proteins, energy production, genetic activity — all these factors and many more vary with time, and there is no way to tell which might cause us to grow biologically "old" and which is merely an effect of aging. Scientists have proposed nearly fifty distinct theories to account for these observations. Experiments based on many of them have delayed the symptoms of aging, improved health, and extended the lives of laboratory animals.

Johann Björksten, a private researcher from Wisconsin, theorized that animals grew old because their proteins became damaged. He found that mice remained youthful when treated with enzymes that repaired the altered proteins.

Denham Harman, a biochemist at the University of Nebraska, suspected that aging stemmed from the effects of destructive chemicals known as free radicals. Drugs that combat free radicals also proved to slow aging.

Hematologist W. Donner Denkla, at the National Institutes of Health, believed that an unknown "death hormone" caused aging by shutting down energy production in the cell. To test this idea, he took aged rats and carefully removed their pituitary gland, the presumed source of the fatal hormone. Those animals too grew younger, lived longer, and rarely showed any sign of disease. "We never were able to identify the cause of death," Dr. Denkla once told us. "They appeared to be in perfect health right up to the end."

Other scientists have delayed aging in animals by reducing body temperature, by giving drugs to stabilize the cell membranes, by blocking the accumulation of waste products in the nerve cells, and by several other treatments. Each of these therapies was designed to test one theory of aging. None had any obvious connection with competing theories. Yet, in varying degrees, they all worked.

Although these results have puzzled biologists for decades, the explanation turns out to be simple. Almost all of these theories hold an element of truth, but each accounts for only a small part of the problem. Many of the changes wrought by time weaken the body and thereby promote further decay. Thus, preventing any of them slows the cumulative erosion that we know as growing old. However, all the early theories of aging — Björksten's protein damage, Harman's free radicals, and the rest — dealt with secondary factors. Hidden behind them, there lies a more fundamental source of aging.

This root cause has now been identified.


By the mid-1980s, Dr. Walter Pierpaoli had already built a productive research career. Trained in both immunology and endocrinology, he had studied the immune system for nearly two decades. Along the way he had founded his own research center, the Institute for Integrative Biomedical Research, in Ebmatingen, Switzerland. For five years or so, he had grown increasingly interested in the role of an obscure hormone called melatonin.

Though little known then outside a small research community, melatonin already had proved to be remarkably versatile. In childhood, melatonin floods our bloodstream. When our supply wanes, we enter puberty. This is more than coincidence. Melatonin actively restrains sexual maturation until our bodies are well enough developed to support reproduction. Melatonin levels also vary on a daily cycle, rising in the evening and falling toward morning. We sleep and wake at the prompting of this inner clock. Later in life, we produce less melatonin, and the cycle becomes irregular. As a result, the elderly seldom sleep as long or as well as the young. In the 1980s, Dr. Pierpaoli and other scientists found that melatonin also bolsters our defenses against disease. As we grow old, we become more susceptible to illness largely because we no longer produce enough melatonin to keep the immune system operating at peak efficiency. The more people learned about melatonin, the more central its role in our lives appeared to be.

As he pondered what he knew about this hormone, Pierpaoli found an intriguing connection beginning to form in his mind. Melatonin seemed uniquely involved with time. It controlled maturation. It regulated our daily cycle. It was needed for many of the functions that decline as we grow old. Might it somehow govern aging itself?

He tested this notion by giving mice doses of melatonin each night, when their natural supply was at its peak. The animals lived much longer than normal. It was his public announcement of this discovery, in a New York Times best-seller titled The Melatonin Miracle (Simon & Schuster, 1995), that triggered the current wave of interest in this hormone.

However, subsequent studies proved even more revealing. This continuing research, though mentioned in his book, has gone relatively unnoticed.

On the basis of his work with the immune system, Pierpaoli concluded that the daily rise and fall in melatonin levels was more important to the body than the absolute quantity of the hormone. Therefore he tested the effects of giving melatonin during the day, when it would not restore the nightly hormone peak of older animals. This time his mice grew old and died on their natural schedule.

This was important, because it ruled out all the traditional explanations for aging. For example, if free radicals caused us to grow old, then melatonin should be even more effective when given during the day, because that is when free radicals are most abundant. Instead, it had no noticeable effect. So while it is true that melatonin inhibits free radicals, that appears to be just a coincidence; the inhibition has little or nothing to do with aging. This experiment ruled out all the other previous theories of aging for similar reasons. Timing, more than dosage, was what counted.

He then turned to the gland that manufactures melatonin. Known as the pineal, it is a small structure, about the size and shape of a kidney bean, located deep within the brain. Since the late 1980s, Pierpaoli and his colleagues have been transplanting pineals between mice.

At first, they simply took the pineals of young mice and implanted them in old animals, leaving the recipient's own gland in place. The aged animals lived a bit longer than mice treated with melatonin.

In the next experiments, they removed the pineals from old mice and replaced them with glands from young animals. This is an enormously delicate, stressful operation, and one-fourth of the mice died in surgery. Yet the survivors enjoyed longer lives than even melatonin could provide, the human equivalent of 125 years. (This suggests that while melatonin is important in aging, it is not the only substance whose loss contributes to growing old. Some other pineal factor, yet unidentified, may also be involved.)

Most recently, the scientists have tried swapping pineal glands between young and old mice. When young mice receive an old pineal, they die roughly when the aged donor would have done. When old mice receive a young pineal, they survive up to the equivalent of 140 years, or double their natural span.

Even if melatonin itself turns out not to extend human lives, the lessons from this painstaking work are clear. Aging begins in the pineal, with a specific change that disrupts the daily cycle of melatonin and perhaps other hormones. Now that scientists know where to look, they can find that change and prevent it, fix it, or compensate for it. If practical human life extension has not arrived already, it lies only a few years off.

There is a good chance that longer lives will bring better health. Like the animals in other longevity experiments, Dr. Pierpaoli's mice appear forever young and healthy, then die without warning or obvious cause. When science extends our own lives, we may no longer have to fear cancer, heart disease, emphysema, or the other disorders that now strike us down as we age.

There is one more implication here as well. If we live forty years longer than nature allows, we have four more decades in which science can extend our lives still further. Before today's adults reach 115 or 120, new treatments may well push death back to age 150, 200, or even into the indefinite future. Dr. Pierpaoli, for one, believes he knows where to find the next major advance in life-extending therapy. Unlike pineal transplants, it will be practical for human use.

And while we believe that Dr. Pierpaoli's work with the pineal offers the most promising insights into aging yet achieved, our expectation of a longer life does not depend on his continued success. In the thoughtful book, Reversing Human Aging (William Morrow, 1996), Dr. Michael Fossel, professor of clinical medicine at Michigan State University, argues convincingly that genetic engineering soon will prolong our lives far beyond their natural span. One way or another, practical life extension is nearly here.

The world ten or twenty years from now may not be literally postmortal. Yet our deaths are not likely to arrive on schedule. They might not arrive at all.



In our first chapter, we told of the remarkable change that suddenly is overtaking an unprepared world. The ultimate limit placed on us, either by a wise and benevolent Deity or by a mechanistic and uncaring nature, is about to fall. In times past, "old" has been almost a synonym for "decrepit," and great age has led inevitably to death. A decade or so hence, neither of these historical facts is likely to be true. If we are sufficiently attentive, the advancing years may conceivably bring us a trace of wisdom. They will not carry the infirmities that always have followed a scant few decades of life. Well into what would have been our retirement years, we will retain the health and vigor of people chronologically much younger. Death will still be decades off, and further research may well put it forward into the unguessable future. We will not be literally immortal, for we will remain vulnerable to accident and disease. Yet even today, given what we can foresee of science, we need no longer live in the expectation of sickness and death. This is the ultimate liberation.

Like all great liberations, the postmortal revolution will uproot much of what has gone before. In this case, the change affects the single most important fact of existence. Psychology, government, social expectations — almost everything we believe and do is based on the understanding that we will grow old and die on nature's schedule. When this ancient truth changes, we can expect dislocations on an epic scale.

We will devote the rest of this book to examining what the postmortal revolution will mean to us, both as individuals and as an increasingly global society. If we anticipate more than a tiny fraction of the changes to come, we will be well satisfied. We have been bred for one environment, have spent all our lives in it, and have built its assumptions into our marrow. Like the first fish that hauled itself out onto dry land, none of us is well prepared to foresee the new life that awaits us.

Before making our attempt, we should spend a few pages mapping the territory to be covered. Mortality shapes us, if not more than we know, then at least more than we usually care to consider. Each point at which it touches us represents a locus at which the world is about to change.


Excerpted from Cheating Death by Marvin Cetron, Owen Davies. Copyright © 1998 Marvin Cetron and Owen Davies. Excerpted by permission of St. Martin's Press.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

Meet the Author

Marvin Cetron is founder and president of Forecasting International and has consulted to over half of the Fortune 500 companies in the U.S. and to various government agencies here and abroad. He lives in Virginia. With Owen Davies, he is the author of American Renaissance and Probably Tomorrows.

Marvin Cetron is founder and president of Forecasting International and has consulted to over half of the Fortune 500 companies in the U.S. and to various government agencies here and abroad. He lives in Virginia.
Owen Davies is Lecturer in History at the University of Hertfordshire.

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Cheating Death: The Promise and the Future Impact of Trying to Live Forever 5 out of 5 based on 0 ratings. 1 reviews.
Anonymous More than 1 year ago
You make me hard i say my sliding up between your ti.ts(strip res 2)