Goat testicle transplants. Elixirs of jade. Inhaling the breath of
virgins. Injecting crushed dog gonads. Drinking radioactive waters.
These are just a few of the ways people have sought to lengthen
their lives and renew their vitality. The oldest narrative to come
down to us through the millennia -- the Gilgamesh saga, from ancient
Sumeria -- describes a quest for immortality and perpetual youth.
Enkidu, bosom buddy of the semi-divine King Gilgamesh, is killed for
mocking the gods. The heartbroken king seeks the advice of Utnapishtim
and his wife, the only two mortals to whom the gods have granted
eternal life. Utnapishtim directs Gilgamesh to a certain waterweed
that will restore his youth. Gilgamesh finds it but falls asleep, and
a snake eats the weed. In the end, Gilgamesh realizes that the only
immortality human beings can aspire to is making names for themselves
as builders of cities.
This is, to say the least, unsatisfactory. As Woody Allen once put
it, "I donít want to achieve immortality through my work. I
want to achieve it through not dying." Modern biomedical
researchers, in the quest for the equivalent of Gilgameshís
waterweed, have made great progress in unraveling the mystery of
aging. Physical immortality may not be in the immediate offing, but
the day may come when death is radically postponed, if not fully
The barriers to this goal are not just biological but political.
Believe it or not, some of our most influential contemporary
intellectuals are opposed to the idea of long, healthy lives.
"The finitude of human life is a blessing for every individual,
whether he knows it or not," wrote Leon Kass, the presidentís
favorite bioethicist, in the May 2001 issue of First Things.
Francis Fukuyama warns in his new book Our Posthuman Future
that young geezers will "refuse to get out of the way; not just
of their children, but their grandchildren and great
And then thereís Daniel Callahan, co-founder of the Hastings
Center, the nationís leading bioethics think tank. "There is no
known social good coming from the conquest of death," he declared
at a March 2000 conference on aging and life extension. He added,
"The worst possible way to resolve this issue is to leave it up
to individual choice."
On the scientific front, though, thereís good reason for
optimism. "The prospects of dramatically increasing human
longevity are excellent," declares Steven Austad, a biologist at
the University of Idaho. "Donít expect them tomorrow, but there
will be major advances within the next 50 years." Austad, author
of the 1997 book Why We Age: What Science Is Discovering About the
Bodyís Journey Through Life, expects 20- to 40-year jumps in
longevity to occur later in this century.
"We see ourselves on the cusp of the second longevity
revolution," agrees Jay Olshansky, a demographer at the
University of Chicago and the author of The Quest for Immortality
(2001). "Scientists are on the verge of discovering major secrets
of aging." The first longevity revolution occurred in the early
20th century, as infant mortality declined and infectious diseases
were conquered; as a result, more young people now enjoy the
opportunity to become old. The next longevity revolution, by contrast,
will actually postpone old age.
Of the two researchers, Olshansky can be considered the pessimist.
He bet Austad $500 million that there will no 150-year-old person
alive and in fairly good shape in 2150. The bet was set up as a trust
fund endowed by $150 from each scientist. Given the math behind
compound interest, the winnerís heirs will get the $500 million
payout on January 1, 2150.
Love and Death
Woody Allen might appreciate the science of longevity as well as
the results. Sex and death, it turns out, are inextricably
intertwined. "It doesnít pay to have a body that will last
forever," notes Austad. "Evolution only cares about
reproduction." Every body harbors a line of immortal cells: the
germ cells that produce eggs and sperm. Germ cells migrate from body
to body down the millennia, disposing of their worn-out carriers as
they move on. Once your ovaries or testes are done with you, they
couldnít care less whether you live.
Here, then, is the definitive an-swer to the eternal question:
Which came first, the chicken or the egg? The egg did. A chicken is
merely an eggís way of making more eggs.
In the case of human beings, evolution has selected for a set of
genes that keep our bodies in pretty good shape long enough to mature
sexually, produce progeny, and raise those progeny to sexual maturity.
Time elapsed: about 40 years. The evolutionary insight here is that if
a body invests a lot of energy in repairing itself, it will reduce the
amount it can devote to reproduction. That may be good for individual
bodies, but your germ cells have no interest in keeping you forever
The UCLA biologist Michael Rose firmly established the evolutionary
connection between sex and death by breeding fruit flies. Rose
selected only those flies that reproduced late in life and bred them
with one another. The longer it took the insects to reproduce, the
longer they lived. Rose now has flies that live 130 days instead of
the usual 40.
The connection was further bolstered this January by Cynthia
Kenyon, a biologist at the University of California at San Francisco.
Kenyon reported that she could double the life spans of nematode worms
by removing their germline stem cells -- the cells that produce eggs
and sperm. Then thereís Lawrence Donehowerís recent research at
Baylor Medical College. Donehower has found that the genes that are
helpful in guaranteeing a robust youth are harmful in the long run.
The tumor-suppressing p53 gene keeps us from developing cancers in
early life, but at the cost of stimulating our immune systems to
destroy over time the reserve of rapidly dividing stem cells that
replenish our tissues. As our stem cells are killed off, our tissues
deteriorate. The result of this "antagonistic pleiotropy" is
Another example of antagonistic pleiotropy was discovered by the
biologist Leonard Hayflick in 1961. Hayflick, now at U.C.ĖSan
Francisco, found that human cells in vitro would divide only 50 to 80
times, then stop. For a while, some researchers thought this "Hayflick
limit" might be the key to aging. What it appears to be is an
evolved mechanism to prevent cancer. Cancer is the uncontrolled
proliferation of cells, and as cells divide they often accumulate
errors that predispose them toward becoming cancerous. If there is a
limit on the number of times a cell can divide, such a limit prevents
cells from eventually mutating into cancer cells.
How do cells know when to stop? Through telomeres, caps composed of
repetitive DNA sequences at the ends of chromosomes. These function
somewhat like the aglets on the ends of shoelaces that keep them from
unraveling. Through a peculiarity in DNA replication, each time a cell
divides, its daughter cells lose a tiny bit of their telomeres. Once
the telomeres are gone, the cell stops dividing and becomes senescent.
Two types of cells do not suffer this problem. One is the germ
cells that are the progenitors of sperm and eggs. Their telomeres are
restored by an enzyme called telomerase, making them essentially
immortal. The other group is cancer cells. They can divide without
limit, which is what makes them so deadly.
Significant aging is a relatively new phenomenon. Over evolutionary
history, once creatures began to falter in any way, they were eaten or
dropped dead of disease -- eaten by bacteria, as it were -- so they
never had a chance to get old. "As soon as an animal in the wild
starts to slow down even a little bit, itís eliminated from the
population very quickly," says Simon Melov, a researcher at the
Buck Institute, a nonprofit organization devoted to aging research.
"Aging is not a natural state for us either," he adds.
"The evidence we have indicates that 10,000 to 20,000 years ago,
most people didnít live much past 30." Today, the only
creatures that actually experience aging are human beings and the
animals they protect, such as pets and livestock.
The Roots of Aging
But what is aging, anyway? We all know it when we see it, but
itís very hard to tease aging itself from the various diseases that
accompany it. Michael Straight, a former editor of The New Republic,
was asked when he was 80 what it felt like to be an old man. Straight
replied, "I feel like a young man whoís got something very bad
wrong with him." In the language of gerontology, there are no
good biomarkers for aging.
Even today, many things besides aging kill people -- primarily,
diseases and accidents. Then again, as we age we become increasingly
vulnerable to the shocks and diseases that can kill us. In modern
societies, disease plays a relatively small role in killing off
younger people: If all the causes of death in the United States before
age 50 were eliminated, average life expectancy would increase by only
three and a half years. Meanwhile, Jay Olshansky has estimated that if
all deaths from heart disease, cancer, and stroke were eliminated
entirely the average life expectancy in the United States would
increase to between 90 and 95. In the 19th century the insurance
actuary Benjamin Gompertz pointed out that as people age, their chance
of dying doubles every eight years or so. Thus, a 35-year-old is twice
as likely to die at age 43 and four times as likely to die at age 51.
Is there an upper limit on human lifespans? Researchers reported in
the April 29 Science that life expectancy has been increasing
at about two and a half years per decade for the last 160 years.
Demographers like Olshansky, they note, have been consistently wrong
in predicting an upper limit to human life expectancy. In 1928, for
example, the demographer Louis Dublin predicted that average life
expectancy in the United States would never exceed 64.75 years. Today
it is 76.7.
At this rate of improvement, the authors of the Science
report conclude, "record [average] life expectancy will reach
about 100 in six decades." Still, as far as we know, the maximum
human life span is the 122 years achieved by the cigarette-smoking
French woman Jeanne Calment, who died in 1997.
Aging is accompanied by lots of simultaneous changes -- graying
hair, thinning bones, weakening muscles, failing immune systems. So
far, researchers have not figured out whether those changes are aging
itself or just symptoms of some more general process of decay.
Scientists are now in wide agreement that aging can largely be
traced to the damage done to our cells by free radicals. A free
radical is an atom or molecule that has at least one unpaired
electron, causing it to be very chemically reactive. Lots of free
radicals are created in cells as they produce energy. Free radicals
disrupt a cellís DNA and protein synthesis and repair mechanisms.
The Berkeley biologist Bruce Ames has calculated that oxygen radicals
damage the DNA inside each cell some 10,000 times per day.
Each time a cell replicates, it copies all of the billions of DNA
base pairs that comprise its genome. Cells are very crowded and
chemically energetic places, so miscopying sometimes occurs.
Fortunately, evolution has devised molecular machines that can rapidly
read and then correct most of the copying mistakes, keeping the cells
to a fantastically accurate rate of one error per billion nucleotide
replications. However, each time the repair mechanisms miss a mistake,
it becomes encoded in the DNA -- and the next time duplication occurs,
the miscopied DNA is treated as correct. As a result, errors
accumulate over time. Miscopied genes lead to the production of
distorted proteins, which are inefficient when they work at all. The
accumulated molecular damage causes a 0.5 percent decline per year in
overall physical capacity after age 30.
Increasingly, researchers are focusing their attention on the
damage free radicals cause in the tiny energy-producing organelles
called mitochondria. Like any other power plant, mitochondria produce
not just energy but also wastes and pollution, including copious free
radicals. As good as mitochondria are at mopping these up, some of
them nevertheless get loose and damage the tiny DNA genomes at the
heart of the mitochondria. Free radicals create a cellular death
spiral by mutating mitochondrial DNA, which in turn degrades their
energy production and increases the production of free radicals,
refueling the cycle.
Other research points to another process linking free radicals to
aging. Apparently, we are literally cooking ourselves to death. In
cooking, sugars and proteins stick together to form tasty brown crusts
like those on French toast. Our own metabolisms are a form of
low-temperature cooking that causes sticky sugars such as glucose to
cross-link with proteins to create advanced glycation end products (AGEs).
AGEs are biological junk that accumulates in cells, interfering with
their functions over time. For example, AGEs reduce the elasticity and
flexibility of the collagen in our ligaments. They are also linked to
diabetes and to cardiovascular disease.
In a related process, our cellsí recycling centers, called
lysosomes, become clogged with cross-linked proteins and other
cellular rubbish. This cellular gunk is called lipofuscin. Lipofuscin-filled
lysosomes slowly crowd and hinder other cellular functions.
Another process involving free radicals is inflammation.
Inflammation occurs when our immune system cells drench invaders such
as bacteria and viruses with free radicals to rip them apart. The
problem is that sometimes the inflammatory attacks donít ratchet
down when the threat is gone, and our immune cells keep pumping out
free radicals. Chronic inflammation has been linked to many diseases
associated with aging, including arthritis, atherosclerosis, diabetes,
Alzheimerís, and cancer.
The free radical theory of aging is backed by more than seven
decades of research on calorie restriction. In 1935 Clive McCay, a
professor of nutrition at Cornell, noted that if laboratory rats are
fed only about two-thirds of the food they would freely choose to eat,
their life spans increase by 40 percent to 50 percent. This result has
been confirmed many times since then. Researchers think that
semi-starvation may make metabolic processes more efficient, producing
fewer free radicals and also perhaps boosting cellsí DNA repair
systems, since the hungry organism may have to live longer in order to
Besides free radicals and telomere shortening, re-searchers have
long noted that as our bodies age the levels of several key hormones
begin to decline -- testosterone for men, estrogen in women, DHEA and
growth hormone for everyone. Boosting the levels of these hormones has
become the stock in trade for the growing business of longevity
So what are your chances of living forever? First the bad news. As
U.C.ĖSan Franciscoís Leonard Hayflick recently told The
Washington Post, "There is no intervention that has been
proven to slow, stop, or reverse aging. Period."
Now the good news: Despite that, researchers are making a lot of
Probably the most promising immediate thing you can do to increase
your chances of seeing your great-grandchildren is to stop eating so
much. Calorie restriction is the only known technique for increasing
the life spans of many different organisms. The foremost advocate of
this approach is probably the UCLA biologist Roy Walford, whose Web
site offers menus for those who want to pursue longer life by dieting
themselves nearly to death. Calorie restriction may not make your life
longer, but it will certainly make it feel that way.
Barbara Hansen, a diabetes researcher at the University of
Maryland, has spent 20 years investigating the effects of calorie
restriction on rhesus monkeys. The experiment has not run long enough
to determine if the ultimate life spans of the calorie-restricted
monkeys will be increased. But on several related issues, her findings
are unequivocal: When she compares old calorie-restricted monkeys to
old monkeys that eat what they want, the calorie-restricted ones do
not have heart disease, diabetes, or hypertension, and their
cholesterol is lower. Theyíre healthier.
There is no question that maintaining a reasonable weight prevents
the onset of many illnesses associated with aging. But what if you
find the notion of living without foie gras and pepperoni pizza
unbearable? Is there hope for you?
There may be. Hansen hopes that by starving monkeys she can pave
the way to a pill providing all the health benefits of calorie
restriction while allowing you to inhale all the ice cream and beer
you want. She has identified a compound that affects the PPAR-Delta
receptor, which improves the bodyís response to insulin and glucose,
mimicking the benefits of calorie restriction. It is now in early
testing by Glaxo.
Calorie restriction research could also help us discover agingís
elusive biomarkers. With the sequencing of the human genome and the
advent of chip gene technologies, researchers can monitor the
simultaneous actions of thousands of genes in tissues. The aim is to
characterize the differences between the gene activity in tissues from
old people and the gene activity in tissues from young people.
Already, chip tests have found that the gene expression of tissues
taken from old, calorie-restricted mice is similar to that found in
Among other benefits, finding such biomarkers would be a major
advance in testing interventions for their effectiveness in slowing
aging. Right now, the only way to see whether a proposed longevity
treatment works is to wait for people to die.
Cloning for Longevity
If calorie restriction isnít your cup of tea, regenerative
medicine is the next best bet for near-term success. The most
promising path to regenerative medicine is the controversial process
known as therapeutic cloning. If you need a new heart or liver, it
might be possible to grow a new perfect transplant using your own
cells. The process would involve transferring the nucleus of one of
your skin cells to an enucleated human egg, which would then grow in a
petri dish to the blastocyst stage. Stem cells would be harvested from
the blastocyst and transformed into the desired tissues for
Stem cells have been found in adult tissues, in umbilical cord
blood from newborns, and in embryos. All have shown some promise.
William Haseltine, the CEO of Human Genome Sciences, recently
predicted in The Washington Post that it will one day be
possible to "reseed the body with our own cells that are made
more potent and younger, so we can repopulate the body." But stem
cell transplants are at least 10 years away -- or even longer, if Leon
Kass and his allies succeed in banning therapeutic cloning. Since the
chorus calling for a ban includes President Bush, the prospects for
research in this area are not as bright as they ought to be.
Another problem: Regenerative medicine does not stop or slow aging.
It just fixes the problems and diseases that accompany aging.
In a sense, itís just a better form of conventional medicine.
Continually trading in your old, worn-out organs for new ones is
certainly better than the alternative, but it would be ever so much
more pleasant if you could just stay young forever.
The true fountain of youth will involve stopping those pesky free
radicals that are wrecking your DNA and cooking your tissues to death.
The most popular anti-aging regimen, practiced by millions of
Americans, is to pop anti-oxidant vitamin and mineral pills. There is
no firm scientific evidence that gobbling down such supplements
actually increases life spans. Simon Melov of the Buck Institute for
Aging Research notes that the effects of anti-oxidant pills are fairly
weak, since most of the nutrients donít get inside the cells where
the free radical damage is occurring. Jay Olshansky dismisses megadose
vitamin supplements as "a way to make expensive urine."
On the other hand, Olshansky admits that some people can benefit
from vitamin supplements. Epidemiological studies show that vitamin E
supplements might help 12 percent of the population. The problem is,
each individual has no way of knowing now whether he or she is part of
that 12 percent. Nevertheless, many of us cover our bets by taking
A recent study conducted by Bruce Amesí team at Berkeley found
that lethargic old rats are perked up by l-carnitine and alpha lipoic
acid. Their mitochondrial function improves, they become more active,
and their memories get better. A company called Juvenon, founded by
Ames and others, is testing the supplements in people with the goal of
finding an effective human dose.
Meanwhile, Thomas Perls of Harvard is hunting for longevity genes.
Perls noticed a decade ago that people who live to be 100 are often in
remarkably good shape. Today, he runs the New England Centenarian
Project, whose participants must be 100 years old and have siblings
who lived to be over 90. By looking at DNA taken from some 600
participants so far, Perls has found that a region on chromosome four
appears to help its carriers become healthy geezers.
Perls and his colleagues have formed a company called Centagenetix
to narrow the search for the longevity gene. Once itís identified,
Centagenetix will try to produce a Methuselah pill that mimics the
activity of the proteins made by the
The M.I.T. biologist Leonard Guarente recently showed that nematode
worms with more than one copy of a gene called SIR2 live 50 percent
longer than normal worms. This may explain why calorie restriction
increases life span, because SIR2 slows down gene activity when a cell
is being starved. Guarente and Cynthia Kenyon have already identified
genes and enzymatic pathways that increase the life spans of
invertebrate species. They believe that these same mechanisms will be
found in people, giving them targets at which to aim anti-aging drugs.
Guarente and Kenyon have created a company called Elixir, which will
try to develop such pharmaceuticals.
Eurkarion, a privately held biotech start-up in Massachusetts, is
working with the Buck Instituteís Melov to test its novel
small-molecule anti-oxidant compounds. Melov has genetically
engineered mice that donít produce superoxide dismutase, the
oxygen-scavenging enzyme that protects mitochondria from free
Such mice typically die within a week after birth. They suffer from
enlarged hearts, damaged livers, and a spongiform brain ailment that
looks very much like mad cow disease. But when these mice are injected
with compounds that mimic the effects of superoxide dismutase and
catalase (a compound that transforms hydrogen peroxide into water),
they live four times longer. Eukarion is currently testing one of its
compounds as a topical application to heal skin damaged by radiation
treatments. It plans to test further compounds as treatments for
degenerative neurological diseases in human beings.
As for the gunk built up in our cells, researchers are testing some
compounds that break apart AGEs, enabling cells to get rid of them. In
preliminary testing, a compound called Pimagedine has improved cardiac
function in rats, dogs, and primates. It is also being tested for
efficacy in treating kidney failure associated with diabetes. Another
anti-AGEing compound, ATL-711, has shown some promise as a treatment
to reverse age-related and diabetes-related cardiovascular diseases
and restore function to the cardiovascular system.
What about lengthening telomeres? Remember, our immortal germ cells
activate the gene that produces the enzyme telomerase, which restores
the ends of their telomeres whenever they divide. Cancer cells also
stimulate production of the enzyme. The Geron Corporation is
conducting research into how to use telomerase to fight cancer. The
idea is that if you can turn off telomerase in the cancer cells they
will stop dividing and commit cellular suicide, called apoptosis.
Some researchers have suggested that it might be possible to make
normal cells immortal by getting them to produce telomerase, which
could prevent the shortening of their protective telomeres. It seems
logical that if telomere shortening causes cells to become senescent,
lengthening them should rejuvenate them and the tissues in which they
reside. Still, according to Barbara Hansen, there is little evidence
that telomere shortening causes senescence on the organism level.
Hormone replacement therapy is second only to vitamin supplements
in popularity among those seeking the fountain of youth. The aim here
is to restore the hormones that decline with age to their youthful
levels. The most popular hormones involved are DHEA, human growth
hormone, melatonin, testosterone, and estrogen.
The notion that hormones could restore youth has a long and
disreputable history. In the late 19th century the noted French
physiologist Charles Edouard Brown-Sequard injected himself and his
patients with extracts from the testicles of young dogs and guinea
pigs, then declared that the treatments had restored his physical
vigor and mental acuity. In the early 20th century the American John
Brinkley claimed to restore menís vitality by transplanting goat
testicles into them. He performed over 16,000 transplants before he
died, though his medical license was revoked after some of his
customers claimed a new compulsion "to chew sprouts."
More recently, hormone replacement therapies took off after the
endocrinologist Daniel Rudman reported in 1990 that a dozen older men
he had injected with growth hormone three times a week had more muscle
mass, less fat, tauter skin, and lower cholesterol levels. Subsequent
studies have shown that these quality-of-life benefits are real but
slight. In fact, regular exercise is more effective in obtaining most
of the gains achieved from injecting growth hormone.
Furthermore, there is no evidence that growth hormone treatments
increase longevity. Indeed, mice that overproduce growth hormone die
sooner than normal mice, and fruit flies that underproduce growth
hormone live longer than normal flies. In addition, some researchers
suspect that supplementary growth hormone may increase the risk of
HEA is the most abundant steroid in the body, yet nobody knows much
about what it does. It is clear that DHEA levels peak in a personís
early 20s and decline as he or she ages. Interestingly, feeding DHEA
to mice, which produce very small quantities of this hormone
naturally, increases their life spans by 40 percent. In Why We Age,
Steve Austad notes that in the few scientifically valid human trials
involving DHEA supplementation, the hormone produced "some
improvement in immune response, muscle strength, and sleep patterns
among the elderly." Still, not much is known about the effects of
the long-term use of this hormone, so most researchers advise caution.
Much has also been made of the so-called "melatonin
miracle." But rigorous testing of melatoninís effects on human
beings has not been done yet. Mice that are fed melatonin live 5
percent longer but are at a greater risk of developing tumors. Again,
most researchers advise caution.
So far, estrogen replacement therapy is the most effective hormone
treatment. Epidemiological evidence suggests that supplemental
estrogen after menopause helps prevent osteoporosis. But recent
research has undercut claims that estrogen therapy reduces the risk of
heart disease and dementia. Using estrogen does slightly increase the
risk of ovarian cancer and promotes the growth of existing breast
tumors. Estrogen may delay the onset of certain diseases that become
more common as women grow older, but there is no evidence that it
increases usersí life spans.
Testosterone levels generally drop in men as they age. Research on
testosterone has lagged behind estrogen research, perhaps because of
the unsavory treatments of the past and perhaps because of steroid
abuse among athletes. There are some indications that testosterone
replacement can provide benefits to older men, including increasing
muscle tone, overcoming erectile dysfunction, and improving their
overall sense of well-being. On the other hand, it might promote the
growth of any pre-existing prostate tumors. There are other unwelcome
side effects, including increased hairiness and acne. And there is no
evidence that testosterone supplementation will increase longevity.
The Genetic Imperative
Looking further down the road, once the genes that promote disease
(Alzheimerís, diabetes, cardiovascular problems) and those that
promote longevity are identified, it will become possible for parents
to select favorable genes for their progeny. Already, more than 1,000
healthy children have been born after their parents used
pre-implantation genetic diagnosis to select among eight-cell embryos
to find the ones that were free of disease genes. In the future,
parents might also select embryos that bear longevity-promoting genes
and implant those. Further in the future, parents will be able to add
genes that improve their progenyís immune systems, mental acuity,
and athletic abilities by installing artificial chromosomes.
The Cambridge gerontologist Aubrey de Grey wants to genetically
engineer mitochondrial genes into the nuclei of cells, where they
would be better protected from the ravages of free radicals. He
believes that once those genes are better protected they will not be
so quickly mutated into the free radical death spiral. Once the
vicious circle of mitochondrial mutations producing ever more free
radicals is broken, longer life should result, he argues.
Even further in the future, another method to improve how human
cells protect themselves from the ravages of free radicals might be
possible. Some animals, such as birds, have more effective
anti-oxidant protective mechanisms. Using them as a model, we might
tweak our own genes. This could be the moral equivalent of replacing
human anti-oxidant genes with similar but more effective genes from
An even more visionary approach has been suggested by Robert
Bradbury, whose startup Robiobotics is investigating the possibility
of repairing whole genomes by using bacteria to ferry artificial
chromosomes into human cells. The genetically engineered bacteria
would infect billions of a patientís cells and deliver artificial
chromosomes carrying a suite of hundreds of genes specifically aimed
at repairing the damage done by free radicals. Some genes on the
artificial chromosomes might be replacements for damaged genes; others
would be designed to enhance cellular DNA repair. Skeptics point out
that our immune systems would likely do in Robioboticsí designer
bacteria, but Bradbury suggests that the problem might be dealt with
by using a transitory immunosuppressive therapy that would give the
genetically engineered bacteria an opportunity to reach their desired
But this focus on biological interventions may be wrongheaded.
After all, some argue, we donít fly because we sprouted wings, so
neither will we live longer because weíve fiddled with our genomes.
Why not make machines that hunt down harmful disease organisms and
repair damaged cells? That is the ambitious aim of nanomedicine.
Nanotechnology is the science and technology of building devices
using single atoms and molecules. A nanometer is a billionth of a
meter, a length that is just over the diameter of many atoms.
Conceptually, nanotechnology and biotechnology are not all that
distinct. In the words of Rita Colwell, the director of the National
Science Foundation, "Life is nanotechnology that works."
Proponents of medical nanotechnology -- such as Ralph Merkle, a
former research scientist at Xeroxís Palo Alto Research Center and
now a fellow at the Texas nanotech company Zyvex -- outline an
ambitious vision. "Nanotechnology will let us build fleets of
computer-controlled molecular tools much smaller than a human cell and
with the accuracy and precision of drug molecules," Merkle
declared in the Winter 1999 issue of the Anti-Aging Medical News.
He added, "These machines could remove obstructions in the
circulatory system, kill cancer cells or take over the function of
subcellular organelles." Robert Freitas, author of the 1999 book Nanomedicine,
foresees a day when oxygen-carrying red blood cells could be
supplemented by artificial respirocytes made of carbon that would be
200 times more efficient.
If that isnít wild enough, Freitas recently unveiled a scheme
that would replace your entire circulatory system with a sapphire
vasculoid weighing two kilograms. No heart, no blood -- just a system
of nanotech machines that would ferry oxygen, carbon dioxide,
nutrients, and immune protective machines throughout your body, all
encased in nearly unbreakable sapphire that would line your
old-fashioned veins and arteries. Since 80 percent of what kills most
people can be traced to the circulatory system -- heart attacks,
strokes, wounding, metastasizing cancer -- such a vasculoid would
dramatically increase oneís life span. Freitas thinks the first
models will be available in 40 years.
"With nanotechnology we could someday be rebuilding our own
bodies, regenerating organs, slowing down aging," a bullish
Samuel Stupp, professor of materials science and medicine at
Northwestern University, predicted at a National Science Foundation
conference earlier this year.
Pharmaceutical manufacturers are already building new drugs -- atom
by atom, essentially -- to treat diseases. Merkle believes that it
will be another 20 to 30 years before the visionary technologies he
foresees will be available. In the medical arena, nanotechnology and
biotechnology may well be destined to meld together.
Nanotechnology also plays a role in what some consider the second
best alternative to living forever: cryonics. Cryonicists freeze
people in liquid nitrogen with the idea that future technologies will
be sufficiently advanced that the patients can be thawed out, revived,
and cured of whatever ailments, including old age, afflicted them
before they entered the deep freeze.
One problem facing cryonics enthusiasts is that no animal larger
than a microscopic human embryo or a tiny tardigrade -- an insect that
measures only a couple hundred microns across -- has yet been frozen
and successfully revived. Freezing causes water in cells to expand,
which disrupts them. But some researchers have developed a
preservation technique called vitrification, essentially glassifying
cells. This approach, it is claimed, causes far less disruption to
cellular organization and destruction of cell walls. Scores of people
have chosen to have either their full bodies or just their heads
When it comes time to revive patients, the plan goes, nanotech
machines will race through the patientsí bodies, repairing the
damage they have suffered from disease and freezing. Will it work? Who
knows? Cryonicists put it this way: "The clinical trials are in
progress. Come back in a century and weíll give you a reliable
answer." Cryonicists divide the world into two groups, those who
are experimenting with cryonics by being frozen vs. those who just die
and are buried. Which would you rather be in, they ask: the control
group or the experimental group?
The defining political conflict of the 21st century will be the
battle over life and death. On one side stand the partisans of
mortality, who counsel humanity to quietly accept our morbid fate and
go gentle into that good night. On the other is the party of life, who
rage against the dying of the light and yearn to extend the enjoyment
of healthy life to as many as possible for as long as possible.
The most moderate critics of longevity simply worry that
immortality would cause massive overpopulation. Worry not, says
demographer Olshansky. If everyone on the planet were made immortal
tomorrow, while maintaining the current projected trends in human
fertility, world population would rise to around 13 billion by 2100.
That, he notes, is the same number that alarmists like Paul Ehrlich
used to predict for the middle of this century. Olshansky thinks that
100 years will give human society plenty of time to adjust to longer,
Death to Radical Mortalists!
Then there are the more radical mortalists, such as Fukuyama,
Callahan, and Kass. Writing in the aforementioned issue of First
Things, Leon Kass asserts that "to argue that human life
would be better without death is, I submit, to argue that human life
would be better being something other than human." Without the
sound of timeís winged chariot rushing at our backs, Kass claims,
humanity would become frivolous, frittering away eternity with
meaningless pastimes. Apparently, if we live longer, weíll just
watch more Baywatch reruns and revisit Disney World.
For Kass, the sting of death makes for stronger friendships,
greater loves, more ardent learning, and nobler deeds. But the fact of
human mortality has also led people to commit all manner of villainy,
cowardice, and crime. If one man nobly sacrifices his life to save his
family and friends from invaders, it is because those invaders have
themselves overcome their fear of death to seek glory, goods, and
dominion. Gilgamesh wanted to avoid the oblivion of eternity, so he
built a city, fought wars, and sought glory so that his name would
ring down the ages.
Meanwhile, the names of all those thousands crushed under his
tyranny -- those who labored to build the walls and temples of his
city -- are lost for all time. The certainty of death may cause us to
aspire, but not necessarily to the fulfillment offered by the gentler
Kass also points to the "undesired consequences of medical
success in sustaining life, as more and more people are kept alive by
artificial means in greatly debilitated and degraded conditions."
Here he is engaged in what might be called Struldbruggism, after an
episode in Gulliverís Travels. Gulliver visits the land of
the Luggnuggians, among whom are occasionally born immortals called
Struldbruggs. This is no blessing, since the immortals still grow
older, weaker, and sicker.
But the goal of research on aging is not to turn us into a race of
miserable Struldbruggs. As Olshansky puts it, "We donít want to
make ourselves older longer, we want to make ourselves younger
longer." Characteristically, Kass ignores the real goals of
anti-aging research, misleading readers with a gruesome scenario in
hopes of frightening them into embracing his pro-death dogma.
Future generations will look back at the beginning of the 21st
century and marvel that intelligent people actually tried to stop
biomedical progress just to protect their cramped and limited vision
of human nature. But the chances that the Kassians will actually hold
back longevity seem small. "Itís too alluring," says
Olshansky. "Itís been the dream of humanity forever. How can we
not?" Austad agrees. "People want this so badly, itís
going to happen no matter what the government does," he predicts.
"The government can help or it can hinder this research, but it
"A dramatic increase in lifespan is inevitable," Aubrey
de Grey said in the British Sunday Times two years ago.
"We understand aging at the molecular level sufficiently to not
just imagine interventions to retard aging, but enough that we can
describe them. Itís an engineering project now, not a scientific
one. We just donít know how long it will take."
To which I say: Hurry up! The 22nd century looks too interesting to
Ronald Bailey is Reasonís science correspondent.