Live a Lot Longer After decades of fumbling in the dark, researchers are fitting together the puzzle of how we age--and how we may be able to...
By David Stipp

(FORTUNE Magazine) – Chin up, fellow boomers, aging has its compensations. Our fingernails are growing slower, so we don't need to clip them as often. Our sweat glands are waning, so we have less body odor to worry about.

There's probably more, but I forget. Oh, well, the debit side is more interesting anyway. It starts around age 25, when the ability to detect odors begins to go. Lung power and brain size peak about then and head south. General shrinkage sets in around 35, after which height diminishes and inexorable muscle degeneration begins. After 40 the skin begins losing its memory: Pinch the back of your hand hard at 45, and it smooths out in two seconds; by 65 it generally takes 20 seconds. After 50 our tissues start drying out, one reason weight usually drops after 55. Erotic daydreams, closely linked to sexual activity, dwindle and typically fade out around 65. The nose and ears elongate.

All this suggests why gerontology, the study of aging, is the true dismal science--not so much because the subject is a downer but because it encompasses the most bewildering hodgepodge of data in all of medicine. Our biological clocks tick at wildly different rates, a variability that has defeated gerontologists' quest for reliable "biomarkers" of aging. So even if there were a drug that slowed aging, there would be no practical way to prove it works--establishing that people who took it live longer would take decades. That's a major reason the drug industry has left the anti-aging business to quacks.

In fact, gerontology has long been a stagnant backwater tainted by snake oil, where baffled researchers grow old fishing up miscellany and piecing it into rickety hypotheses that sink soon after they're floated. By one count, more than 300 theories of aging have gone down with hardly a trace. Many scientists believe the aging process is sheer anarchy loosed upon the body, too complex to analyze, hence not worth the effort.

But quite unexpectedly, a range of new findings is snapping into focus the prospect of a radically new science of aging--one that points toward the possibility of lengthening human life span by the relatively simple manipulation of a small number of genes. If the new science pans out, almost everything will change, especially the meaning of "old." The population might soar. We would have to extend our working lives lest our nest eggs get used up too soon. Millions of parents might live on as their children reached ripe old ages--the two generations would jointly explore a vast temporal frontier opened at the far end of the human life span.

If you put together recent findings and stand back, you can already descry the engine of these changes: the first robust, big-picture theory on aging supported by a great diversity of data. Its core idea is that a wide array of creatures, from fruit flies to British aristocrats, possess a kind of life-span rheostat embedded in their genes. This genetic rheostat probably evolved so that animals, including humans, could adjust to their circumstances by applying the body's inner resources either to reproducing fast or to guarding their cells against the ravages of time. Certain stimuli, such as caloric restriction, can twirl the rheostat to cell-maintaining "hibernation mode"--it pays to hunker down and put reproduction on hold when food is scarce.

Importantly, several recent studies--including ones on centenarians and on a clan of fearless opossums on an island off the Georgia coast--suggest that a small number of genes, perhaps fewer than ten, governs the rheostat in mammals. If true, that's the best news of all: Therapeutically tweaking fewer than a dozen genes seems a tractable problem, unlike trying to address bodywide anarchy.

Now the hunt is on for the rheostat genes, whose discovery would pave the way for anti-aging drugs. The quest's implications dwarf those of any other line of medical research, notes David Harrison, who studies long-lived mice at Jackson Laboratory in Bar Harbor, Me. Since aging is by far the biggest risk factor for almost every major disease in the developed world, drugs that brake it would curb a myriad of scourges at one fell swoop. When the Reaper finally got us, he'd be hopping mad--we'd have cheated him both by living longer and by spending a larger proportion of our lives in good health.

All this hinges on big ifs. Some gerontologists, prominently the University of Washington's George M. Martin, argue that time's toll involves thousands of genes--he dismisses talk of anti-aging therapies coming anytime soon as "simplificationist" dreaming.

Therapies to extend our lives to 150 aren't bubbling up in the lab yet, contrary to recent effusions of pop gerontology in the media. But "the gloom is gone" in gerontology, declares Steven Austad, a University of Idaho zoologist who studies aging. If he and other guarded optimists are right, the field is about where bacteriology was in the 1870s, when a flurry of discoveries linking germs to diseases paved the way for the antibiotic revolution--and this century's huge upswing in life expectancy.

New talent and money are flowing in. When biologist Gary Ruvkun realized a few years ago that his work had major implications for gerontology, he initially was nonplussed. "I thought, 'Oh, God, now I'm in aging research--your IQ halves every year you're in it,'" says Ruvkun, who studies genetics in tiny worms called nematodes at Boston's Massachusetts General Hospital. Now the National Institute on Aging and a foundation set up by Larry Ellison, Oracle's billionaire CEO, have awarded him grants to study genes that make some nematodes live three times longer than normal. "This field looks like it's going somewhere quickly," Ruvkun says.

More than a dozen gene mutations have been discovered over the past decade that dramatically extend the life spans of certain animals, including worms, flies, and mice--a sign there's more genetic rhyme and reason to aging than previously thought. Buttressing that view are studies on the Olympic athletes of aging, human centenarians, whose numbers have risen enough in recent years to reveal that extreme longevity runs in families, suggesting a strong genetic influence on aging. Other studies are probing genes that are activated in slow-aging animals on low-calorie diets--caloric restriction, the only well-established life extender, can keep a mouse lively for a span roughly equal to 150 human years.

Researchers have inserted genes in fruit flies that extend their lives, on average, by about 50%. Clues abound about where to look for life-span-rheostat genes in higher animals. Some of the genes appear to retard growth. Thus scientists have scoured the world for undersized mice and scanned the medical literature for cases of "leprechaunism" caused by rare human mutations. Toy dogs like Chihuahuas are getting a close look too.

Perhaps the hottest leads are the ones coming from worms. Ruvkun showed in 1997 that a life-extending gene in nematodes bears a striking resemblance to a human gene involved in regulating blood sugar--a finding that fits with the idea of life-span rheostats geared to the availability of food. It also suggests that the "hibernation response" is one of evolution's most ancient inventions. Genes underlying it may have been conserved, as biologists say, through the eons, hence may be widely shared across species. If so, says University of Michigan gerontologist Richard A. Miller, a leading proponent of the rheostat idea, then life-extending genes "may well be hidden in our fields, orchards, kennels, and perhaps even among our colleagues."

Like most big ideas, the rheostat one isn't all that novel in some respects. The notion of a tradeoff between reproducing and long life was around long before the era of exhausted working couples. One indicator of that is the tendency of long-lived animals, such as humans, to start reproducing later and have fewer offspring than short-lived creatures, such as rabbits. Some animals, like salmon, age at light speed after reproductive bursts. This pattern makes sense in light of a gloomy Darwinian theorem: Our genes are designed by evolution to keep us going strong only until we reproduce. Soon after the peak reproductive years, genes that protect us from aging start losing their beneficent force. Then things get random, and our bodies wear out as insults such as "free radicals," the notorious chemical cousins of oxygen that can clobber DNA and other cellular molecules, take their toll.

This theorem, one of few ideas about aging with staying power, was detailed in 1952 by immunologist Peter Brian Medawar. The logic: Consider two gene mutations that might have arisen separately in a couple of our Stone Age forerunners. One promotes agility during youth; the other retards muscle deterioration after 40. Say the bearers of these two genetic gifts, at age 10, find themselves facing a saber-toothed tiger. The one with the agility gene might leap clear, enabling him to live long enough to pass on his gene, which likely would be spread by his progeny and become a standard fixture in the genome. The one with the other mutation probably wouldn't get to pass it along--aging gracefully didn't matter during the time evolution was sculpting our genomes, when disease, accidents, and predators limited life span to about 30.

The ominously named "disposable soma" hypothesis, championed by British researcher Thomas B.L. Kirkwood, added a twist to Medawar's theory: It brought to the forefront the "cost" of making babies. Kirkwood posits that the more energy we invest in reproduction, the less we can expend on metabolic systems that slow aging. One such system includes antioxidant enzymes that mop up the free radicals our cells churn out as they burn sugar to produce energy. People who grow fast and reach puberty early, enabling speedy reproduction, may be genetically geared to put fewer inner resources into making antioxidants, hence age faster, than those who aren't built for reproductive speed. Our selfish genes are willing to make such tradeoffs since they effectively regard our bodies as disposable egg cartons, no longer necessary once the genes have sprung forth to the next generation of throwaway bodies, or "somas."

This theory got a big boost in 1984 when Michael Rose, a researcher at the University of California at Irvine, reported a simple experiment: By selectively breeding normal fruit flies that tended to reproduce unusually late in life, he generated flies of increasing longevity--in effect, he forced the insects to trade early fertility for slower aging. Eventually he got ones that lived nearly twice as long as their ancestors.

Last year Kirkwood reported a similar finding in humans, based on genealogical records on British aristocrats born between 740 and 1875. The study shows that among women who reached at least age 60, those who had many children early in life tended to die younger than those who had fewer kids, relatively late. A similar pattern was found among the men.

Given all this, you'd think the mystery of aging had a tidy solution: After we pass our reproductive primes, our genes simply step back and let us get trashed by free radicals and other random damage. But some things don't fit. One is emerging data that conflict with the Danish twin study, which many gerontologists look to like a lighthouse in the murk. Published in 1993, it's regarded as having established that environmental factors, not genes, are what predominantly influence longevity--just as you'd expect if genes' life-preserving power wanes a few years after puberty.

Twins make good subjects for determining this issue--if genes dominate, then identical twins, who are genetic duplicates, should have about the same life spans. But after examining data on twins born in Denmark between 1870 and 1888, researchers estimated that genes account for only about 30% of longevity. That implies environmental factors are the primary influence.

The twin data also imply that only about one in 400 centenarians has a centenarian sibling. That would make sense if the effect of environment dominates, because by age 100, the influence of the twins' shared genes on aging is overwhelmed by life's wear and tear. Thus centenarian siblings should be as rare as a brother and sister who separately win millions in the state lottery.

But new studies on centenarians are turning up more hyper-old siblings than the Danish findings predict. Catherine McCaig, a 103-year-old subject in the New England Centenarian Study at Harvard Medical School, is a member of one of these surprising "sibships." She lives in Marshfield, Mass., near her 94-year-old sister Winifred Whynot and, until recently, their brother Nat, who died at 94. A truly astonishing sibship found by the Harvard team included four siblings who lived past 100 and a 97-year-old sister; the siblings also had seven centenarian cousins. The odds of such cases occurring by chance, rather than by inherited genes, are vanishingly small, notes Thomas Perls, the study's director.

Perls argues that the Danish twins may have yielded misleading results because only a few of them reached their 80s and none lived past 90. Thus they couldn't reveal the effects of longevity-enabling genes that are manifested in centenarians--just as studying the running speeds of wild horses wouldn't necessarily reveal how thoroughbreds can inherit the wind.

Another sign of longevity genes' existence is the fact that there is no centenarian lifestyle--researchers studying the hyper-old have repeatedly failed to find commonalities in diet or exercise, or any other environmental factor, that could explain their longevity. Some centenarians say they've eaten very little red meat through their lives, while others ate it every day, notes Perls. One of his subjects had a daily breakfast of three eggs and bacon for many years. France's Jeanne Calment, who died in 1997 at 122 and set the record for longevity, was a smoker.

None of which, Perls hastens to add, means we can all pig out and light up with impunity (see box). Rather, it suggests that those of us destined to become centenarians possess special genes that make our tissues resistant to a wide array of insults.

There is one striking pattern among centenarians: They tend to have upbeat personalities. When I recently visited McCaig, the Massachusetts centenarian, she regaled me for over two hours with jolly stories, such as all the fun she'd had in the hospital making new friends after breaking her hip two years ago. When a reporter asked Calment at 115 how she saw her future, she replied with characteristic drollery: "Short, very short." Intriguingly, this lightness of being is a matter of temperament, which, because of other studies, scientists believe is determined largely by genes.

But even if great genes are key to extreme longevity, there might be too many of them to pin down as starting points to develop anti-aging drugs for the masses. Fortunately, Austad's weird old possums beg to differ.

Austad, a sinewy 52-year-old who worked as a Hollywood animal trainer before getting his Ph.D. in zoology, is the only gerontologist to have tangled with a lion while wearing a skirt and wig on an episode of the TV series The Bionic Woman. "The lion knocked me half goofy," says Austad, who was impersonating the show's heroine being attacked by the king of beasts. "Then it tried to mate with me. Everyone on the set was roaring by the time they got it off me." Austad's foot also appeared in the same episode--it was shown getting stepped on by an elephant.

Austad became fascinated by the mystery of aging as a youth, when he watched his dog Spot pass from puppyhood to senility in 12 years. His curiosity was further piqued when he later learned how wildly variable life spans are. Tortoises can seem young at 150, and in a sense, they're immortal--they keep growing without physiological decline until disease, starvation, or people get them. Mice die around 2, yet bats, which resemble winged mice, can live into their 30s. Humans can live to at least 122, while the longevity record for the famously long-lived elephant is a mere 81.

It gradually dawned on Austad that the rate of aging is like tooth size--a highly plastic trait that evolution through the ages has readily dialed up or down to optimize fitness in different species. Rose's selective breeding of long-lived flies suggested an even more alluring idea: This plasticity exists within a species and can swiftly be brought into play by Darwinian forces favoring longevity. Rose, after all, didn't create mutant superflies--he simply coaxed into view a capacity for radical longevity that was hidden in normal flies' genes. Shortly after Rose's report, Austad set out to find similar life-span plasticity in higher animals.

He didn't have enough money and time to breed Methusaleh mammals in the lab--mimicking Rose's method with relatively long-lived animals might take decades. So he looked for a case in which nature had performed the experiment in the wild. He focused on opossums for two reasons: They age very fast, seldom living past two years, so cases of unusual longevity would be detectable fairly quickly. And he knew that since opossums were everywhere in the southeast U.S., he could probably find an isolated group on one of the region's many coastal islands.

It was a clever Darwinian ploy. Scientists believe the main reason animals such as turtles, bats, and humans are long-lived is that they possess strong defenses against predators--armor, flight, and smarts, respectively. That lets them reproduce over an extended period, which, in turn, has exerted evolutionary pressure to live longer--if we aged as fast as good old Spot, we'd miss out on a lot of the mating opportunities afforded by our imperviousness. In contrast, prey animals like mice and opossums have faced different evolutionary pressure: Since predators ensure they don't last long, it pays for them to make all the offspring they can ASAP and, in keeping with disposable-soma theory, let their cells wear out quickly.

But if such animals somehow landed on a predator-free island, Austad reasoned, evolution would push them toward greater longevity. After a long search, he found just the place: Sapelo Island, Ga. A small, largely deserted barrier island that geological records indicate separated from the mainland about 4,000 years ago, it's possum heaven. Austad found his subjects so oblivious to predators that they let him walk up to them in broad daylight and strap on radio collars. After monitoring the animals off and on for several years, he reported compelling evidence of life-span plasticity: the Sapelo Island opossums live, on average, about 25% longer than their mainland relatives. And they tend to have unusually small litters, as if they have traded fertility for longevity.

Austad's findings, detailed in his 1997 book Why We Age, generated little excitement in gerontology. His request for a grant to further study the island opossums was rejected. But to a few leading-edge thinkers, the report had a provocative implication: Aging may be a unitary process governed by a handful of key genes. One of those thinkers was Michigan's Miller, a pioneer in research on how the immune system ages.

Miller is known for penning pithy rebuttals to the idea that genes don't matter much in aging. What especially impressed him about Austad's opossums was the speed at which their life expectancy had risen--their 4,000 years of island adaptation is an eye blink in evolutionary time.

Consider a dog analogy, he says. "The evolution of a big dog to a small one doesn't require mutation in the gene for leg size, the gene for kidney size, the gene for nose size, and so on." Otherwise, breeding, say, the first Chihuahua would have required a myriad of small-body mutations to have arisen simultaneously in one of the toy dog's larger forerunners--an event about as likely as typing chimps composing Hamlet. Instead, says Miller, small dogs evolved via a "twist of a genetic rheostat for size-of-things in the dog body." Similarly, evolution's invisible hand couldn't have swiftly slowed a myriad of unlinked age-related processes in the opossums. Instead, it probably twisted a rate-of-aging "pacemaker" regulated by a small set of genes.

The discovery in the late 1980s that worms' life spans can be doubled by a mutation in a single gene suggests that such pacemakers can be shockingly simple. Our pacemakers, if they exist, are likely to be more complex. Still, the extraordinary case of the Massachusetts family with five siblings near or over 100 suggests that inheriting no more than ten special genes may confer extreme longevity, says Perls, the Harvard centenarian researcher. It's simple probability: Because siblings get a different mix of genes from each parent, it's highly unlikely that the five siblings, and their seven centenarian cousins, would have drawn the same set of longevity-enabling genes if there were many more than ten involved.

But which genes twist the rheostat?

For answers, scientists are looking to one of gerontology's most tantalizing areas of research: life extension by caloric restriction, or CR. The phenomenon was first demonstrated in the 1930s, when one Clive McCay found that cutting rats' usual dietary calories by about a third extended their average life spans by up to 75%. It has been replicated in many species, most remarkably with Freddy, the longest-lived mouse on record. A resident of Harrison's lab in Maine, Freddy was nearly 5 when he died in 1987--lab mice normally live about two years.

As yet there's no proof that caloric restriction slows human aging, though a number of people are trying it. Many of them can be found on the Internet, endlessly chatting about food.

CR clearly isn't for the masses, but studies on it suggest what an anti-aging drug should do. "People used to think [CR] simply prevents cancer in lab animals," says Arlan Richardson, a CR expert at the University of Texas Health Science Center at San Antonio. "But now we think it actually affects the aging process. Probably 90% of the things that change with age are slowed down."

Indeed, CR's multitudinous benefits have proved almost as complex as the aging process itself, thwarting efforts to single out key metabolic changes that drive its life-extending effect. But the confusing welter began to fall into a coherent pattern after the calamitous shutdown of an air conditioner in Richardson's lab.

For a study on CR's effects, Richardson had set up a colony of mice in a hospital laboratory, including a group on restricted diets and a control group fed at will. One hot summer day, workers at a nearby construction project accidentally cut off electricity to the hospital wing housing the mice. When one of Richardson's colleagues arrived four hours later, many of the rodents had overheated and expired.

But something strange had happened: Some 80% of the well-fed control group were dead, compared with less than 25% of the CR mice. It was a classic case of serendipity. Richardson was interested in whether CR activates genes that make "heat-shock proteins," cellular guardian angels that help protect tissues from damage caused by heat and other kinds of stress. But he hadn't yet tested the idea. In effect, the construction workers had carried out an experiment that gave it strong support. In 1993, Richardson, with some trepidation about publicizing the accident, reported its results in a scientific journal.

The report helped trigger a flurry of studies on longevity and resistance to various insults, such as toxins, radiation, and heat. Over the next few years, a team led by Thomas Johnson, a University of Colorado researcher who studies life-extending mutations in nematodes, showed that long-living worms could survive a variety of stresses that kill normal ones.

Suddenly puzzle pieces were falling into place. Worm mutations that confer long life and stress resistance are known to help trigger a kind of suspended animation in nematodes called the dauer state. It begins when the nematodes sense, via chemical signals, that they're hemmed in by fellow worms--a cue that food is about to be in short supply. To Richardson and other researchers, the dauer state in worms looks a lot like what happens to mice on CR. In both cases, it appears that aging is slowed by revving up the "stress response," a complex system that includes genes for heat-shock proteins and antioxidant enzymes. The similarity also suggests why evolution seems to have favored life-span rheostats in many species: They've all had to cope with periodic food shortages, necessitating a mechanism that can retard aging when famine looms.

Johnson believes a vibrant stress response is crucial for healthy, long life in animals from worms to people. Indeed, centenarians may be born with stress-response genes permanently set on yellow alert--a possibility that's under intense scrutiny. San Antonio's Richardson is studying mice that have been genetically tweaked to boost certain stress-response genes activated by CR--if their lives are significantly extended, you can bet that stress genes will become hot, hot, hot.

The stress response, however, may well be just part of an array of "downstream" systems that rheostat master genes switch on to slow aging in higher animals. Three years ago, a little-known physiologist in Carbondale, Ill., named Andrzej Bartke blind-sided gerontologists with a breakthrough: The discovery of the first such mammalian master gene.

Bartke, a professor at Southern Illinois University, had been studying the effects of growth hormone. That's an urgent topic in the Corn Belt, for the hormone is given to cows to boost milk production. His team's experimental subjects were a race of giant mice implanted with extra growth-hormone genes. "When the animals are young, they look like supermouse, big and slick," he says. "But we noticed that they begin to get old and gray much sooner" than normal mice and live only about half as long. "So we thought, 'If more growth hormone means short life, maybe less of it means long life.'"

It was a radical idea. Bartke knew of a diminutive mutant mouse lacking growth hormone, called the Ames dwarf, but it was widely believed to show just the opposite tendency--supposedly it lived only a few months. Moreover, faddish physicians in places like Southern California routinely dispense growth hormone to older patients as an anti-aging elixir--it's claimed to help beef up muscles. But Bartke had worked with the dwarf mice, which are about the size of man's thumb, and knew the rumors of their early demise were greatly exaggerated. He also knew that within various species, including rats, horses, and humans, small body size is linked to longevity--tall men, for instance, appear more likely to get prostate cancer and other life-shortening diseases.

The pattern is most striking in dogs--giant breeds like Irish wolfhounds live only about six years, while toy breeds like Chihuahuas make it past ten. Fascinated by this pattern, Austad and other scientists theorized that when a life-span rheostat is set for slowed aging, it retards development early in life, when body size is being hormonally shaped.

Bartke's work added weight to the theory--and plausibility to the notion of life-span rheostats. In 1996 he reported that the dwarf mice live, on average, some 50% longer than their normal litter mates, and they seemed geared for famine--they won't reproduce without hormone shots, and they get so pudgy some researchers call them "butterball mice."

A rush of findings soon buttressed Bartke's discovery. Kevin Flurkey, a researcher with Harrison's group at Maine's Jackson Laboratory, showed that another strain of pudgy dwarf mice were similarly long lived. California Institute of Technology researchers identified a gene mutation in fruit flies, dubbed methusaleh, that revs their stress genes, fattens them up, and lengthens their average life spans by 35%. Ruvkun, the worm specialist in Boston, showed that a fattening, life-extending mutation in nematodes alters a gene that bears a striking resemblance to a human gene that's involved both in regulating blood sugar and growth.

The human gene, for the "insulin receptor," may be part of our rheostat circuitry. But fiddling with it is dangerous. When it's mutated in people, it appears to cause either morbid obesity or leprechaunism, a fatal syndrome in which growth is arrested at birth. Still, Ruvkun felt such cases could shed light on how the rheostat works: "I called around and asked endocrinologists whether they'd ever seen leprechauns that don't die soon after birth," he says. They hadn't.

That's not surprising. Mutating rheostat genes is like shorting out wires in an electric clock--it might run slower, but it's more likely to go haywire. Thus many researchers believe the best hope of pinpointing mammalian rheostat genes is to find a breed of metabolically normal, long-lived mice and study how they differ genetically from short-lived strains.

Soon after Bartke's report was published, Austad set out to do just that. Following the logic of his opossum study, he mounted an expedition to two remote Pacific islands, where he found a race of undersized mice. It's too early to say whether they possess anti-aging genes. But when crossed with purebred lab mice, they give birth to offspring that show a striking resemblance to long-lived British aristocrats--they reproduce later in life than most mice.

Meanwhile, Maine's Harrison crossed four strains of lab mice to produce the "Ancients," a breed that shows signs of slowed aging. Now he and Michigan's Miller are racing to pinpoint longevity-associated genes in such mice.

If the scientists succeed and the genes they find turn out to be analogues of ones that underlie longevity in worms, flies, and mice on CR, future historians will probably record the advance as the first time scientists lifted the cover off the life-span rheostat and peered at its wiring. And if the genes also resemble ones that researchers are racing to find in centenarians, gerontology may soon get its first Nobel prize.

It's hard to say how soon this grand scientific convergence could occur. Various researchers interviewed for this story hint that it's closer than anyone imagined only a year ago. "We are so much on the edge of major discoveries in this field," says Perls, who declines to elaborate on his latest centenarian findings until they're published in a scientific journal.

Translating the convergence into anti-aging medicines would doubtless take many years, and testing their efficacy wouldn't be easy. But perhaps it wouldn't take decades--it would be a matter of bioengineering, not magic, as with the bottled hogwash now sold to retard aging. Boston's Ruvkun adds that the rheostat quest appears to be leading to a handful of brain-produced hormones that govern the hibernation response. Though hormone therapy is notoriously tricky, he says, "if life span is hormonally regulated, it shouldn't be very hard to change it. I find that almost frightening. I think society would have a hard time coping with a rapid increase in life span."

True--to pay for all our extra years, we'd probably have to push early retirement out to age 80 or so. But who wants to spend 50 years playing golf, anyway?

NEXT INSTALLMENT: How much will our life spans increase, and will our "health spans" keep pace?