Intimations of Immortality

This is a progress report. It's about immortality. I went out looking for signs, any signs, of progress in the work of making us immortal. What's happening in immortality research today? Are we getting any more immortal, or can we become immortal, or, failing immortality, can we live a lot longer, or, failing that, can we live a little longer, and does anyone know why we age in the first place? And how come, with all this top-of-the-line equipment of ours, these adaptable bodies and big, wily brains, we have to check out somewhere on the near side of 100 years?

I found out a lot, some of it trivial but interesting, some of it discouraging, some of it really promising. But the first thing you should know, the first thing I found out, is that immortality in the here and now isn't in the cards. The second law of the universe is that all physical systems run down, even the (continued on page 140)Immortality(continued from page 134) universe itself. The black holes are going to swallow up the universe someday, and anyone hanging around for the show is going to be swallowed up, too, and that's the end of that.

But immediately you say, "Dummy, no one's talking about billions and billions of years, we're talking about maybe thousands and thousands of years, functional immortality; and, speaking of thousands and thousands of years, what about the incredible track record of the bristle-cone pines?" Well, it's true the bris-tlecone pines have been around for 4000 years and they're still going strong, but it's not true that they're old. That's just a story the Sierra Club puts out. You can count the rings as long as you like, the bristlecone pines are only a few hundred years old at a time. They make a new ring of cells every year and then a little more heartwood dies. That's not immortality, that's a family tree. Roots, so to speak, with only an outer Alex Haley band of pine left alive to tell us, standing sturdy on the mountainside.

So no immortality in the classic sense. But. But we might, if all goes well, if science and medicine do their stuff, get to live out our allotted span of 100 years in reasonably good health. And that within the next 21 years, no later than the millennium, by the magical year 2000, when the calendars turn. And later on, we might get to live 200 years or 350 years or 1000 years or even 20,000 years. That's not immortality, by a long shot, but you and I both know we'd take it if we could. Even if it meant 5000 years of childhood, God forbid, and 5000 years of youth and middle age and then 10,000 years of old age, as it almost certainly would. If we didn't want that second 10,000 years, we'd just down the hemlock, right? Skip the last act, just like Hemingway. But that first sweet 10,000--fantastic.

I had to cover a lot of ground to find out what's going on. There's no one place, except maybe the CIA, where they're working on immortality. There's no National Institute of Immortality, though there's a National Institute on Aging, fairly new. There are people all over the place working to keep us alive a little longer, and that's phase one of this report. There are people all over the place working on aging itself, on keeping us young, and that's phase two. And there are a few people working on figuring out our DNA. If they can figure out how our DNA works, they might someday be able to reprogram it; and if they can reprogram it, they might be able to reprogram it for longer life span, the 200 or 350 or 1000 or 20,000 years I mentioned. And that's phase three.

One more cavil before I start phasing. I didn't go exploring among religions, new or old. Everyone who's ever been near a church or a synagogue or a temple knows that story. The more recent claims--Elisabeth Kübler-Ross's evidence of life after death in the visions of the temporarily dead, for example--strike me as suspect, to say the least. The heart stops, consciousness dims, but the brain's still clicking on, making up those incredible stories. What else is a poor brain to do? Give me someone who's been dead for at least a week--heart-dead, brain-dead, no artificial life supports--and let her come back with her stories, and maybe then I'll believe. No, I went looking in science, where the action is. If you want to trust in spiritual immortality, you're welcome to. I'm interested in the here and now.

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Let's start with the basics, phase one, keeping us alive a little longer. That means medicine and maybe bionics. Medicine's been extending our lives for about the past 200 years. Before that, the average life expectancy was around 40 years. By 1900, in the United States, life expectancy at birth had climbed to 46.3 years for men and 48.3 years for women. Today it's in the 70s. The early gains came from improving public health--vaccination, sanitation, safer childbirth. Then the conquest of childhood diseases added more years and antibiotics added still more. These days, the increments come harder. A cure for all the forms of cancer, doctors estimate, would add an average of two years to our lives. Great for cancer victims, but not exactly the Irish Sweepstakes. Medicine's close to bumping up against the life-span barrier. In 1964, the Rand Corporation reported expert predictions that by the turn of the century we'd see a 50 percent increase in average life expectancy, but that's almost certainly too high. We might average 95 or 98 years, though, most of them healthy middle years instead of old age. I'd buy 35 extra years to kick around in. So would you.

There's still a lot of fixing up that medicine is learning to do. I'd like to report that bionics is a big item, but despite The Bionic Woman and The Six Million Dollar Man, it isn't. It's so back-ward that those two space-age super-people still make bionics researchers mad. Have a look.

At the Liberty Mutual Insurance Company Research Center in Hopkinton, Massachusetts, Dr. Carlo J. De Luca and his associates show me a white rabbit with electrodes implanted on the severed nerve that transmits motor signals to one of its legs. The animal hops, but one leg is affected; we see a nerve signal on an oscilloscope. Dr. De Luca sets the rabbit on a table and tips it. The rabbit tries to balance itself and the nerve fires and the signal jumps on the screen. "The Six Million Dollar Man infuriated me. It raised false expectations," De Luca says. "I couldn't watch it. I never did." He has sorted out the nerve signals, the one for up, the one for down. If he can figure how to make an implant that won't rot the nerve, he might be able to develop a motorized limb controlled directly from the brain, like Steve Austin's arm and leg.

But that's a long way off. For now, the insurance company manufactures something called the Boston Arm, a prosthesis for above-the-elbow amputees with a servomotor in its elbow and batteries and a printed circuit in its forearm that is controlled by muscle signals. It has a hollow plastic upper arm that contains electrodes on its inner surface that touch the skin, picking up control signals from the amputee's muscles. Flex your biceps, what's left of it, and the artificial forearm goes up. Flex your triceps and the forearm goes down. There are only about 40 Boston Arms in use, and the amputees who own them are glad to get them after making do with World War Two-vintage harness-and-cable arms, but they're ten years behind NASA-level technology, and Steve Austin wouldn't have given them the time of day.

"The problem with this bionics business on television," says Robert Mann, professor of biomedical engineering at MIT, "is that it overdramatizes the possibilities and makes them appear so commonplace. The lay citizenry assumes that all it takes is putting resources to bear. That's a gross oversimplification. The problem's really bimodal. The hardware could be greatly improved if the economics were better. Twenty million people requiring rehabilitation and almost as many problems. It's just not big business. The people who make prostheses are metal benders and plastic molders, not electronics men.

"But the fascinating and, in the long run, more important problem is relating the machine to the human. The interface. Creating a symbiosis between the human and the machine, so that the human will command the machine in a way he finds compatible and comfortable. (continued on page 208)Immortality(continued from page 140) There's where I was bugged by The Six Million Dollar Man. The lay view is that science and technology can do anything they set their minds to. The fact is that the really exquisite, marvelous mechanism is the human. Intriguing, complex, not understood. We know very little about how to connect a machine to a human. The hardware can be done. The interfacing cannot be done. Not yet."

But some exotic work on bionic vision is under way at the University of Utah. Researchers implant a grid of 64 platinum electrodes against the visual center of the cerebral cortex at the back of a blind volunteer's brain. They attach the feed from the implant to a computer and fire the electrodes one by one. The volunteer senses points of light in his mental visual field and charts on a pad the location of the flashes in his visual space. The chart reveals distortions. Electrodes 1 and 16 appear side by side; electrodes 30 and 32, which ought to be next door, appear at the bottom and the top of the field. The computer adjusts for the discrepancies and the volunteer learns to read Braille at 30 letters per minute, faster than he can read by hand. Someday a miniature camera might be implanted in the socket of his eye and he might see patterns with the same coarse discrimination as the flashing scoreboards at football stadiums.

At Utah and elsewhere, researchers continue to develop artificial hearts. They've kept calves alive for seven months on prototypes, but the power source is outside. The hearts need a cool, portable, reliable power supply, and that's still being tested. Fidelity Electronics of Chicago, the largest American distributor of prostheses and bionics, sells a myoelectric hand that, like the Boston Arm, reads muscle signals to open and close a plastic hand or a triad of metal hooks. Fidelity has a switch a stroke victim can wear in his shoe to fire a dragging leg to lift when he walks. And a sip-and-puff control for quadriplegics, a straw attached to a control center that allows the paralyzed to adjust their beds, make telephone calls, turn on lights and TVs. Fidelity's tooling up to install a hot-cold, hard-soft touch-feedback system in its myoelectric hand. And that's about it for bionics, though university and VA laboratories are hard at work.

If not bionics, what about transplants? We've been hoping for success in that department since the first successful kidney transplants in the late Fifties. Nothing ought to lengthen life more certainly than brand-new or slightly used organs.

The transplant record improves. At Stanford, Dr. Norman Shumway counted 69 of his heart-transplant patients alive at the beginning of 1979, one of them on his third heart, the best record in the world. Kidney transplants have become almost routine. Livers have been transplanted, and lungs, and heart and lung together, though only experimentally. Rejection is still the stone wall. The host rejects the graft or the graft rejects the host. Tissues have types just as blood does, but many more of them. The closer the tissues are matched, the less chance of ultimate rejection, which is why the first successful kidney transplants were performed on identical twins. Kidney transplants today get their organs from their immediate families, matches close enough that there are some 20,000 still alive around the world. But Mom and Sis and your kid brother aren't allowed to donate their hearts, though someone in Pennsylvania once offered to donate his heart to ailing ex-President Eisenhower. Dr. Shumway's Stanford group monitors its heart patients with catheters and biopsies, doses them carefully with immunosuppressive drugs, floods them with antibiotics at the least sign of infection, gets them up and makes them jog. Heart transplants come out of Stanford these days at the rate of 20 a year. You might want to file that fact away for reference.

A Playboy researcher discovered what looked like the ultimate transplant in a story in Der Spiegel, West Germany's answer to Time. I tracked its developer down in Cleveland, Ohio, close to home. Suppose your body were dying but your brain were OK. Suppose you could get a new body. Suppose someone could transplant your head. You'd take it, right? This is an old medical-school joke. The joke goes on: Would you take it if they couldn't reconnect the spinal cord and you couldn't move the new body but would still be alive and quadriplegic? Would you take it if they could keep your brain alive but cut off from the outside world, a brain in a jar? Most medical students shudder at that point in the joke and say, Christ, no, who'd want to be a brain in a jar? Some take the head on the pillow with the bright, searching eyes.

Dr. Robert J. White is a distinguished Ohio neurosurgeon, professor of neuro-surgery at Case Western Reserve and a former Mayo Clinic man, and he has perfected most of the technology necessary for a head transplant. He calls the procedure a cephalic transplant, points out that it's really a body transplant, since the identity of the survivor would come from the head, and emphasizes that it isn't high on his list of priorities. He has transplanted the heads of rats and monkeys and kept them alive for three or four days. The monkeys were trained to respond to tests with facial signals, and after their transplantations, they did, indicating that they were aware and functioning. While working on the cephalic transplant, Dr. White and his team have developed skills useful in brain surgery. But he can't reconnect the spinal cord, which means the grafted bodies serve only as immobile power packs--organic equivalents of artificial life-support systems like artificial kidneys and heart-lung machines and respirators. And since it's only rats and monkeys, he hasn't yet had to worry about graft-host rejection. He hasn't kept his experimental animals alive that long. If he did, they'd start rejecting just as heart transplants do.

When medicine masters the rejection process, a cephalic transplant will be a possibility to consider if all else fails. You'd be what White calls a "head on a pillow," but he notes that he has patients in that predicament right now. You could have a man's body or a woman's body or whatever turned you on, except you wouldn't feel it below the neck. White and I speculated on the ethics of hooking up the head of a dying Einstein to the brain-dead torso of a strapping young motorcyclist and the conversation turned philosophic. The chimerical monkeys, set in little chairs and serving the worthy purpose of improving neurosurgery, have been seen to grin. A year, White says (discounting the problem of rejection), would give him the technology to do as much for humans.

Since we're still talking about phase one, about patching people up and keeping them alive a few years longer, let's look at predictions of medical progress. At the beginning of 1977, Medical World News published the results of a Delphi poll conducted for it by a Baltimore think tank. The Delphi poll method was developed by the Rand Corporation, which is why it wears such an oracular name. It predicts future developments by asking questions of a panel of specialists eminent in whatever field is under study. M.W.N.'s specialists were eminent in medicine. Their predictions are encouraging and, taken together, they explain Rand's prediction of a 50 percent increase in life span. This is the cream of the crop, listed with the year of probable achievement:

And repeated again and again in the estimates of these experts: treatment, prevention or cure of most forms of cancer by the year 2000. That's the best we're going to get in phase one. That's 100 years of youth and middle age. That's a wrap.

Which brings us to murkier waters, phase two, the ugly business of aging. Doctors can cure our diseases and transplant our organs, but aging still goes on. It goes on throughout the body at a more or less uniform rate. Skin loses its elasticity, connective tissue toughens, muscles weaken, the lungs move less air and the heart pumps less blood. One of the difficulties with heart transplants is that strong young hearts put excessive pressure on weak old blood vessels. The kidneys last a lifetime if they aren't diseased, and so does the liver, but the hormone system slowly goes haywire and the immune system retreats, recruiting disease. The balance tips between the various systems of the body, and no amount of patching will fix it up, and eventually we depart--right around the 100-year mark, maximum, though a few of us live to see our second century, if we can still see. It's been 100 years for 100,000 years now, and before that, it was less. Aging's the turn of the screw, the kick of the gun, and no one has yet figured out how to slow it down, much less reverse it.

Not for want of trying. There have been almost as many theories of aging, and remedies for aging, as there have been researchers in the field. Some of those theories and remedies have been misguided, some of them have been out-rightly fraudulent, some of them have been merely oversimple and none of them have worked. The company cafeteria and the health-food store sell yogurt because of the autointoxication theory of an aging Russian Nobel laureate named Elie Metchnikoff. Metchnikoff believed we age because harmful bacteria in our intestines poisons our bodies. As a remedy, he proposed a diet of cooked food and sour milk: yogurt. A London surgeon took Metchnikoff's theory one step further. He cut away great sections of his patients' intestines. "Abdominal spring cleaning," one of his followers called it. A French physiologist touted testicular extracts from guinea pigs to rejuvenate his clients. A Russian surgeon transplanted monkey testicles. An American con man from Kansas named John Romulus Brinkley got rich transplanting the testicles of billy goats. A Viennese advised vasectomy to seal in the youthful hormones. Others injected novocaine or scrapings of cells from unborn lambs. In Europe, they still do. John F. Kennedy worked at staying young with lamb cells. Wheat germ, vitamin E, the sardine diet are recent additions to the list.

To see how far the science of aging--gerontology--has been from finding simple, reasonable answers to the questions of why and how we age, you have to hear some of the theories. I talked with researchers all over the East Coast, and I began to think aging must be beyond human comprehension. Bear with me while I summarize, because there's a ray of hope at the other end.

One theory I didn't hear was wear and tear. Wear and tear's the obvious theory, and for a long time it was the only theory (forgetting yogurt and animal glands), but it has been thoroughly discredited. It argues, basically, that the body's a machine, and machines wear out, therefore, so does the body. But the body isn't a machine; it can repair itself, and does, though repair systems break down as we grow older.

Another theory, still popular in some circles, is aging due to the accumulation of metabolic by-products. They accumulate in the body's cells and the cells can't work as well. The evidence is there, metabolic by-products do accumulate in cells--trace-metal ions, "age pigments," chemical cross-linkages. But the rate of cross-linkage is the same for all animals, and some animals live longer than others. The degree of cross-linkage in the cells of a three-year-old mouse is the same as the degree of cross-linkage in the cells of a three-year-old child, but the mouse at three is old, the child at three just getting started.

Another theory is error accumulation. When our cells divide, as many of them do, they transcribe the genetic information stored on their DNA. Sometimes they make errors, and then the errors get passed on and multiply. Enough errors, goes the theory, and the whole system gets out of whack. But young cells repair their genetic material more efficiently than older cells, so something behind error accumulation governs aging.

Some researchers have argued that we're programed for aging. They've proposed the existence of a "death clock" in the hypothalamus, the master hormone-control center buried deep in the brain. They think the clock causes the hypothalamus to lose its sensitivity to information feedback from the body, throwing the hormone system out of balance and causing us to age. The death-clock theory goes against everything that scientists know about evolution. Evolution selects positive, not negative characteristics. It picks out the characteristics that keep us going, not the ones that knock us off, and there's no evidence that aging is a positive characteristic for which evolution would select. The old argument that aging is designed to make room for the young by killing off the old doesn't make sense: If no one aged, the entire population would be young.

Those aren't the only theories, but the common denominator in all the ones I heard is that they don't explain why we age and they don't explain why, despite our best efforts, we live a maximum of only 100 years.

Except one. At the end of two weeks of interviewing, after a month of reading the literature, when I was ready to give up, I almost accidentally bumped into a man in Baltimore who has figured out life span. He doesn't know what specifically causes aging, but he knows what aging is and why we have it, and he thinks he knows a little of what we might do about it. Maybe most important of all, his theory puts all the other theories based on reliable experiment in a sensible context. The only trouble is, most of the other researchers with whom I talked hadn't heard of him yet.

Dr. Richard G. Cutler, a biophysicist, became interested in gerontology when he noticed its mass of conflicting theories and sensed the possibility of a simple explanation. He conducted research in aging at the Brookhaven National Laboratory. Today, at 43, he is on the staff of the Gerontology Research Center of the National Institute on Aging in Baltimore.

Instead of studying individual bodily systems, as most researchers do, Dr. Cutler stepped back to look at life span in a larger context. That context was evolution, and the choice turned out to be inspired, because it was in evolution that he found the elusive answer. He noticed, first of all, that mammals are structurally very similar. They have the same kinds of organs, the same kinds of bones, the same kinds of tissue. In terms of DNA, they have the same kinds of structural genes. The chimpanzee shares more than 98 percent of its structural genes with its closest relative, man. On the structural level, man and the chimpanzee are almost identical.

But man and the chimpanzee are dramatically different in life span. Man's maximum life-span potential--Cutler abbreviates the phrase to M.L.P.--is about 100 years. The chimpanzee's M.L.P. is about 50 years. And there are equally dramatic differences in M.L.P. among all the species of mammals, which are structurally so much alike. One common laboratory mouse has an M.L.P. of three to four years. Another common laboratory mouse, almost identical, has an M.L.P. of eight years. Cutler found those differences intriguing.

"If you compare different mammalian species," he explains, "you find that they have different life spans. It's hard to convince some people of that. They say, 'Are you sure? Wouldn't a lion live just as long as man if you took equally good care of it?' But, no, no matter how well you take care of a lion, or a deer, or a mouse, it still ages faster than man. Moreover, the life spans are different, the rate of aging is different, but the process of aging is the same. The same problems pop up, the same kinds of physical decline. So man, for example, appears to age at a slower rate across the board than the chimpanzee. The chimp ages about twice as fast as man. He loses his immune function twice as fast, he loses his eyesight twice as fast, and his hearing, his cognitive ability, and so on."

Which dispenses, Cutler points out, with any simple theory of wear and tear. If you want a car to last twice as long, you build it better from the frame up. Stronger materials, better parts, more careful machining and assembly. A better structure. If aging were only wear and tear, man would have better structures than other mammals. He doesn't. "Life span," Cutler concludes, "isn't a matter of better design."

If not better design, then what? Cutler's startling insight, for which he marshals considerable evidence, is that life span evolved. It evolved to fill up the time each species had available to live, if that makes sense--in a minute, I'll let Cutler explain it--and aging is a byproduct of that evolution.

All living species have had the same amount of evolutionary time. That's a basic fact of evolution. Then why, asks Cutler, didn't they all evolve 100-year M.L.P.s?

Because they couldn't use them. "If you go out into the wild and try to find an old mouse," Cutler says, "you won't find it. Old fish, old deer--you don't find them, either. In their natural environments, animals are always killed off before they show any signs of senescence. A one-year-old bird has the same probability of being killed as a half-year-old bird, even though there aren't as many one-year-old birds around. The probability remains constant. Take a bird with a short life span in the wild and put it in a laboratory and see how long it really can live and you'll find that it doesn't live much longer. It starts to age about the time that it would have been killed off. So do animals. The longer-lived animal is able to live longer in the wild because its environmental hazards are lower." Which suggests, Cutler concludes, that "animals evolve a life span that is the maximum for their environmental niche, for its hazards."

"If you look at man," Cutler explains, "you don't have to go very far back to find that the mean life span used to run around 30 to 40 years. There was always the man who'd squeak out to 90, but the mean life span was much lower, and above the mean, the survival curve was exponential, just like the bird's. And when does man really begin to undergo senescence? At 35 or 40. We evolved with genes to keep us alive until about 35 or 40, when we'd normally have been killed off. But then we suddenly lowered our environmental hazards drastically, within the past 200 years. And so we see this aging. Aging is completely unnatural. Nature doesn't like aging, it's not good, there's nothing good about it."

Picture it this way: Nature's primary strategy for lengthening life span has been to lengthen childhood and youth. The chimpanzee is immature for seven years, man for 14. The chimpanzee is young from seven to 25, man from 14 to 35 or 40. After that, the system begins to break down, because after that, the hazards of life--disease and predators--begin to wipe out the chimps and the men and women who survive. By 50 for the chimp, by 100 for man, the mortality is almost 100 percent.

If longer life evolved, then it must have been an advantage, or evolution wouldn't have selected for it. What was the advantage? "The first primate appeared about 65,000,000 years ago," Cutler notes. "It had a life span of about seven or eight years. It was a small, shrewlike organism. From there, primate life span steadily increased. We've never found an example of where it went down. And this increase has always been accompanied by an increase in brain size.

"Well, there's an advantage to having a larger brain. The mammals may be unique in exploiting the advantages of learned behavior over instinctive behavior. Learned behavior gives more adaptability. But to take advantage of learned behavior, you have to have time to learn. And you have to have time to teach. So suppose you had two mutations: a greater ability to learn, meaning a larger brain, and a little more longevity. Those two mutations would evolve. They'd be mutually beneficial."

And that's Cutler's hypothesis: that brain size and M.L.P. evolved together to give the larger brain time to learn and time to teach its offspring. One of his most impressive tables shows the estimated M.L.P. of man's extinct relatives and immediate ancestors, the hominids. Ramapithecus, which appeared on earth about 14,000,000 years ago, had a predicted M.L.P. of 42 years, though it probably averaged less than 20. Homo habilis, which appeared about 1,500,000 years ago, had a predicted M.L.P. of 61 years. Homo erectus, which appeared about 700,000 years ago, had an M.L.P., based on evidence of tooth wear, of at least 60 years; Cutler predicts it to have been about 69 to 78 years. Neanderthal man, 45,000 years ago, had an M.L.P. of 93 years. Our own M.L.P. Cutler puts at between 95 and 100 years. The brain size of these hominids goes up accordingly: Ramapithecus, 300 cubic centimeters: Homo habilis, 660 c.c.s; Homoerectus, 860 c.c.s; Neanderthal man, about the same as modern man, 1460 c.c.s. Brain size evolved, and life span with it, as far as it could go, given the natural hazards. And there it stopped, because dead men don't reproduce their kind.

Equally important--the promising part of Cutler's theory--is that the evolution of life span was fast, amazingly fast as evolution is measured. Between 1,500,000 years ago and 100,000 years ago, the hominid brain more than doubled in size, and life span also increased remarkably along with it. Which means that not many genes can be involved. Evolution proceeds across the long run by mutation, by random changes in the genes. "We know," says Cutler, "that the rate of mutation in living creatures is constant and fairly slow. New genes don't appear very often. If you compare the evolution of life span with the rate of mutation, you find that there can't have been very many mutations involved in lengthening life span. I calculated that only a very few, maybe 100 to 300 mutations, accompanied the evolution of about every 14 years of human M.L.P. Which is a drop in the bucket compared with how many genes there really are." Biologists estimate that man's DNA comprises at least 100,000 genes, and possibly 1,000,000 or more. By Cutler's calculation, no more than 100 of them may be involved in setting man's life span.

"The general conclusion in studying the evolution of species," Cutler points out, "is that the structural genes are identical. There's not much difference from one species to the next within the mammals. What's different is the other broad category of genes, the regulatory genes, the genes that turn the structural genes on and off. Apparently, the genes for aging are regulatory genes."

The regulatory genes turn man on for 40 years and then shut him down. Here Cutler begins to elaborate a theory of aging. His example is the two species of laboratory mice with different life spans, three to four versus eight years. "They're virtually identical in every other way. But we find that the DNA in the longer-lived species keeps on repairing itself. The longer-lived mouse has a more efficient repair process. Not different, just more efficient. In 1974, Ronald W. Hart and Richard Setlow at the Oak Ridge National Laboratory determined the DNA repair capacity for a number of mammalian species, from the mouse up to man. They found a beautiful correlation: The longer-lived the species was, the more repair it had. Same system, just a matter of degree. Turning something on a little more intensely. It doesn't have to be a whole new set of genes. That's why it could evolve so quickly."

Go back, then, to phase one, to the Delphi poll, to the prediction of enzyme-replacement therapy by 1990. Regulatory genes convey their messages to structural genes to produce important enzymes. If science can dope out which enzymes are implicated in aging and can synthesize them and replace them, it might have devised a way to keep us young. Unfortunately for you and me, there's probably a catch: To benefit from enzyme-replacement therapy, people will probably have to start it young, before aging begins.

But whether we're a youngish 100 or an ancient 100, we're likely to continue dying at 100 or earlier until the genes themselves can be modified. Cutler's cheering news is that not many genes will need to be modified and that the evidence from evolution is that modification works. "No inherent biological limitation for the further increase in longevity in any mammalian species is evident," he has written. "If positive selective pressure exists to evolve a longer life span, it should occur. The same is true for man."

Since man has lowered his environmental hazards and opened a larger niche for himself, evolution may already be pushing up his M.L.P. But the process is slow and Cutler doesn't think we're likely to wait around for it. He believes we'll try to accomplish it ourselves. "These changes might be achieved," he writes, "by inducing the enzymes involved to higher levels by analogue stimulants, by direct enzyme-addition therapy or by genetic engineering." Well, stimulating the enzymes is obvious, and we've talked about enzyme-replacement therapy. What about phase three, genetic engineering? What about redesigning man himself?

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It's promising, but it's primitive, and it's in trouble these days, and nature may have fixed things so it won't work.

A little basic information: We've been doing genetic engineering for the past 10,000 years, but not on man. We took wild plants and wild animals and bred them into domestic plants and domestic animals, and that was genetic engineering eons before anyone ever heard of DNA. We never did it with people, because it would have taken hundreds of years and no one was willing to sit still that long. We do it today in a helpful, voluntary way with genetic counseling, warning some people that their offspring have an increased risk of genetic disease. Man is still literally a wild animal, and genetically highly diverse. That's why the supposedly inferior poor aren't going to breed the supposedly superior rich out of existence and pollute the race. The poor have as much genetic potential as the rich. More, since God made more of them.

Identifying the function of human genes is the work of the new science of molecular biology. The work's barely begun. Molecular biology became a promising science only 26 years ago, when James D. Watson and Francis Crick discovered the structure of DNA, the large biopoly-meric molecule that is the basic unit of genetic information for every species on earth. We reproduce by transmitting DNA. DNA guides the manufacture of all the body's proteins and regulates their functions. It's life's master control system, the secret of life. Scientists assembled for a biology conference a few years ago were asked to define life. All the old textbook answers came out--"Life is matter that reproduces," and so on. The molecular biologists cooked up the plainest and coldest and bluntest and most precise answer of all. "Life," they said, "is the expression of the surface properties of the biopolymers."

A polymer is a large molecule built up of repeating, linked small molecules. The DNA molecule takes the shape of a double helix, two exterior backbones of sugar phosphate coiled around each other with a right-hand twist. Bridged between the two backbones like the steps of a spiral staircase are small repeating molecules of four chemicals. Their names are usually abbreviated to A and T, G and C. T combines with A, G combines with C by locking their surfaces together. The four chemicals are the genetic alphabet; the sequence in which they are laid down in DNA spells out the genetic message, and with it, DNA reads out a program for the living form it is coded to produce.

I saw a sequence written with colored chalk on the blackboard of one of the laboratories I visited, and I asked a scientist about it. "That's a gene from a bacterium," he said casually. "We just figured it out." The more complicated the life form, the longer its DNA. Man's DNA is fiercely complex, a molecular strand six feet long and 1/250,000,000th of an inch wide coiled up inside almost all the body's cells. No one has yet figured it out.

"We want to know the structure of the genes in our body," Dr. Walter Gilbert, a molecular biologist at the Harvard Biological Laboratories, told me. "That's the question that people are just now beginning to try to attack. In a bacterium, which we understand very well by now, there are genes and each one does something. But there are tremendous areas of human DNA that don't seem to be doing anything. We've got ten times more DNA than we seem to need. There's something else going on that we don't understand. In fact, there's real mystery about what's going on in our bodies in detail, both the structure of the genes and how they're controlled. It's only in the past three years that people have begun to get interesting genes out in a form that they can examine. That's the leading edge of biological research, but it hasn't produced any answers yet."

The new and controversial technique called recombinant DNA makes it likely that it will, given enough time. In the recombinant-DNA technique, the biologist isolates a small piece of DNA that he wants to study by cutting it out of the long DNA strand with enzymes. Next, with other enzymes, he glues it to a small piece of bacterial DNA called a plasmid. Then he reinserts the plasmid into the bacterium. If the bacterium can live with the strange DNA in its midst, it proceeds to make copies while it's making copies of its own DNA--while it's dividing and reproducing. In a sense, recombinant DNA is a kind of microscope. It allows the biologist to enlarge a tiny fragment of DNA by duplication until he has a volume of identical copies large enough to work with. Then he can play around with the test tube full of copies until he figures out what that particular piece of DNA does.

Recombinant-DNA research has raised fears of doomsday diseases, of man-made Andromeda strains destroying the world. The city of Cambridge, Massachusetts, hearing of such research starting up at Harvard and MIT, declared a recombinant-DNA moratorium a couple of years ago--until a committee of citizens it appointed decided that the work wasn't dangerous to the city's safety and health. But biologists themselves still quarrel acrimoniously over the safety issue. They assembled in California in 1974 and voluntarily imposed restrictive guidelines on themselves. One of the extreme cases, which someone had actually proposed in attempt, involved inserting a piece of DNA from a virus known to cause cancer in monkeys and suspected of causing cancer in man into a laboratory strain of the common human intestinal bacteria E. coli. Someone raised the possibility that such a chimera, if it escaped from the laboratory, might introduce a virulent new kind of cancer into the world.

The biologists agreed not to do any cancer-virus insertions. They agreed to (continued on page 226)Immortality(continued from page 220) categorize their research into four stages of potential risk and to proceed through the stages only in increasingly isolated laboratories. Stage-four research would require a laboratory at least as well sealed as the one NASA built for its first look at the rocks that the astronauts brought back from the moon, rocks NASA feared might harbor extraterrestrial microbes. The biologists also agreed to try to design a special research strain of E. coli so fragile that it couldn't live outside the laboratory. They're using it today.

The debate over the possible dangers of recombinant DNA continues. It serves to alert the rest of the world to a truth that molecular biologists have already discerned: that biological research today is as pregnant with possibilities for the good and ill of mankind as research in nuclear fission was in the late Thirties. A recombinant-DNA strain of bacteria that manufactures insulin has already been designed. If new discoveries take place at the same rate at which they've taken place in the past, it may be possible within the next two decades to change the genetic structure of some plants. Wheat, for example, might be fitted with the nitrogen-fixing system of legumes, allowing it to grow without artificial fertilizer in average soil.

But redesigning bacteria is one thing: redesigning human DNA--comping up a life span of 20,000 years--is entirely another. Dr. Gilbert again: "We understand the level of control very well in bacteria. We don't know beans about it in human beings. We assume the control operates on the DNA, but we don't know what to point to, or how to do anything, or how it's being done. Abysmal ignorance. The higher cell is a thousandfold more complicated than the bacteria, and we've understood the bacteria only in the past decade. It won't take 1000 years, but it will take some reasonable-fraction of time."

No functional immortality tomorrow. There's another strategy. It will be much easier to make copies of living men and women than to design new ones. The technology of individual copy making is called cloning. Successful cloning of a higher organism was first reported in 1966 by Oxford University zoologist Dr. J. B. Gurdon. Dr. Gurdon cloned seven frogs. To make each clone, he extracted the nucleus--the part of the cell that contains its DNA--from the intestinal cell of a frog and implanted it in an enucleated frog egg. The eggs developed into tadpoles and the tadpoles into frogs. Gurdon's clones were perfect copies of the frog from whose intestinal cells they had come. In effect, they were identical twins one generation removed.

Cloning has progressed to the stage of promising work with mice and rabbits. In the near future, it will probably be used to improve the quality of domestic animals. Cloning could populate America's farms and ranches with identical copies of prize bulls, cows, pigs, chickens and sheep, producing a quantum jump in the quality of American livestock.

Human cloning should be feasible within the next 50 years. It will be an important medical treatment for genetic disease. Parents who are symptomless carriers of such disease might choose to clone their children rather than risk producing diseased offspring.

Cloning may have other advantages. Identical twins apparently communicate with each other more quickly and completely than the rest of us do. A genius might choose to have himself cloned and teach his clonal offspring, who might then surpass him. What appears certain is that when human cloning becomes possible, some parents will choose to reproduce that way. "My, doesn't he look just like his daddy?" will then be a statement of fact. A clone's M.L.P. would still be 100 years, however: The "immortality" cloning would confer would be sequential, not accumulative.

There's a catch to all this business of figuring out human DNA and redesigning it, a nasty catch that Nobel laureate Watson and several of his colleagues recently proposed. DNA may not allow itself to be redesigned. It took over the role of preserving information in the first place, back in the soup of the primordial seas at the beginning of life, because it was the most efficient preserver of information of any of the molecules brawling there. In those ancient days, it wasn't protected by a surrounding bubble of cell, it was naked to its enemies, and its enemies were all the billions of other combinations of elements and molecules that wanted to break it down and use its components to keep themselves "alive." It's had several billion years to perfect its defenses. It may be proof against any kind of attack scientists can devise. One recalls the quandary of the scientists who tried to develop new diseases for bacteriological warfare: They ended up with plague and encephalitis and anthrax. Nature had already done the job better than they knew how to do.

But if DNA lets us in, and if man gets around to redesigning himself, it's going to be tedious. He can't redesign every one of the body's billions of cells. He'll have to redesign an egg or a sperm or both, and mate them, and then wait until the recombinant child is born, and then wait at least 20 years to make sure it isn't a monster. And he can't redesign too many genes at once, or he won't know which one went wrong. If Cutler's calculation of the small number of genes responsible for human life span is correct, then engineering for longer life spans might be one of the first recombinations attempted. Men with longer life spans would have time to learn more and could apply what they learned to more elaborate redesign.

No one knows how much increased life span those future generations are likely to get. The body changes with chronological age in ways that aren't affected by its rate of aging. Muscles get stringier regardless. Waste products accumulate regardless. The ultimate human life span might be 350 years or it might be 1000 years or it might even be the fabled 20,000. It won't be forever; that's still the prerogative and the curse of the gods.

But you know us. We'll give it a shot. J. Robert Oppenheimer, the physicist who hated the title the world correctly gave him, Father of the Atomic Bomb, made the point about us near the end of his painful 62 years of life. "It is a profound and necessary truth," he said, "that the deep things in science are not found because they are useful; they are found because it was possible to find them." If it's possible to find a way to redesign mankind, to improve the model, to give it a little more time, to cheat death, mankind will.

"If you want to trust in spiritual immortality, you're welcome to. I'm interested in the here and now."

"Suppose your body were dying and someone could transplant your head. You'd take it, right?"