TAKE two nocturnal marsupials. Perched in a tree, they look almost
indistinguishable. They behave in similar ways, have similar social lives and
even share a fondness for tree sap and spiders. So how come the Australian sugar
glider lives almost twice as long as its cousin the Leadbeater’s possum?
Live fast, die young seems to be the first rule of ageing. So perhaps the
fountain of youth is to be found in the sugar glider’s physiology. Perhaps it
burns calories more slowly than the possum. In fact, the opposite is true. But
Steven Austad of the University of Idaho thinks he can explain the sugar
glider’s longevity. Austad is a pioneer in testing evolutionary theories of
ageing and believes the answer lies in a six-centimetre flap of skin stretched
between the animal’s front and hind legs—its sailing membrane.
Fountain of youth
Austad is part of the growing band of researchers who are challenging the
traditional view that ageing is simply a matter of cells wearing out with use
like old washing machines. They are looking to ecology and evolution to explain
why the life spans of animals vary so dramatically between species. At the core
of their thinking is the idea that living things can resist the ravages of time.
They can evolve mechanisms to slow down the rate of cellular damage that leads
ultimately to death. But this happens only after a creature has evolved survival
strategies that reduce its chances of accidental death.
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In the early decades of this century, a German physiologist called Max Rubner
was the first to study the connection between how quickly animals burn
calories—their metabolic rates—and how long they live. He used the
metabolic rate and maximum life span of cows, horses, dogs, cats and guinea pigs
to work out the number of calories each burns in a lifetime. Then he divided
this by the body mass of adult animals to give a crude estimate of how much
energy a fixed mass of tissue from different species uses in a lifetime. The
figures for the different species were remarkably similar. Austad, who has
repeated Rubner’s calculation using more up-to-date information about longevity,
found that a gram of guinea pig uses 260 calories in a lifetime compared with
280 calories per gram of horse.
It almost seems as if nature has allotted each gram of animal—be it in
a rodent or a horse—the capacity to use a set amount of energy over a
lifetime. The faster the cells utilise that energy, the logic goes, the sooner
the animal dies. “If animals were cars, we might say that they all start with
some amount of fuel,” says Austad, explaining the conventional view. “If they
use it rapidly, they die early, as mice do. If they use it slowly, they may live
as long as turtles.” Most biogerontologists believe this explains why smaller
animals tend to have shorter lives, because their greater ratio of surface area
to volume means they have to burn fuel quickly to maintain their body
temperature.
The obvious implication of this “rate of living” theory of ageing is that
burning fuel eventually damages cells. “After all, metabolism is nothing more
than a cold, controlled fire,” says Austad. “And fires—even controlled
fires—can be damaging.” Instead of soot and flame, cellular fires produce
metabolic wastes, some of which are destructive. Energetic particles known as
free radicals, for example, constantly bombard other molecules, including DNA.
Other metabolic by-products may eventually gum up the cellular machinery. The
rate at which a cell burns fuel to power the chemical reactions that sustain
life determines how quickly harmful metabolic wastes pile up—and how soon
cellular wear and tear reaches a critical threshold, triggering physical decline
and death. Or so the theory goes.
Indeed, cool the chamber in which fruit flies are kept and you will slow down
their metabolic rates and extend their lives. Of course, this doesn’t work with
warm-blooded animals such as mammals, because they simply increase their
metabolism to keep their body temperature constant in a cold environment. But
when researchers found that by restricting how much food a rat eats they could
extend its life span dramatically—by up to 75 per cent in some
studies—they assumed that this too must have something to do with a
reduction in metabolic rate.
Then, in 1985, Roger McCarter from the University of Texas, San Antonio, and
his colleagues showed that caloric restriction does not extend life spans by
slowing metabolism. McCarter’s team found that after a brief decline, the
metabolism of half-starved rodents actually jumps back to normal levels, or even
slightly higher. Animals that are forced to survive on fewer calories are
“capable of using their energy in a less damaging fashion”, says Austad.
Together with Edward Masoro, a member of McCarter’s team, he has suggested that
the delays in ageing and death could be the consequence of an evolutionary
adaptation that allows animals to redirect energy into body maintenance and
repair during lean years, instead of investing in the production of offspring
that would be unlikely to survive.
Accidental death
The notion that life span is explained by metabolic rate alone is further
undermined by findings from animals not typically used in the labs of molecular
biologists. Birds, for example, have considerably higher metabolic rates than
similar-sized mammals, but can live more than twice as long. Marsupials live
shorter lives than placental mammals of the same size, despite having much
slower metabolic rates. And then there are the sugar gliders and Leadbeater’s
possums. Such findings are all grist to the mill for Austad and the other
researchers who believe that ecology and evolution can explain why some species
are fated to die young, while others are designed to resist the ravages of
time.
The idea was first proposed half a century ago by Nobel prizewinner and
evolutionary theorist Peter Medawar. He pointed out that even the best designed
organism faces the possibility of death by accident or predation, and suggested
that the rate at which an animal ages depends on the level of this so-called
extrinsic mortality. “If a predator is likely to kill you in the next few weeks
or months,” says Austad, “it makes little sense to waste resources on a
long-lasting, effective immune system or an array of free-radical defences.” Of
course, he doesn’t mean that conscious decisions are being made. Instead, when
extrinsic mortality is high, natural selection will favour the genes of
individuals that front-load their reproductive life—seeking parenthood as
early as possible and pouring resources into baby-making instead of devoting
time and calories to maintaining their own bodies, which are likely to succumb
soon to an accident or predation.
In other words, variation in cellular repair mechanisms, not merely the
passive accumulation of cellular damage, underlies the differences in life span
between species. “Even though some processes inherent to life are fundamentally
damaging, given the proper ecological circumstances, natural selection would
have designed defences and repair abilities to combat that destruction,” says
Austad. This happens, for example, when a species evolves a feature that helps
it to evade predators—a protective shell, for example, or wings. Once such
traits have reduced the risk of extrinsic mortality, natural selection can begin
to reshape body designs to delay cellular ageing, so maximising an animal’s
reproductive life.
According to Austad, smaller mammals grow old more quickly not because they
are living “faster”, metabolically speaking, but because the improbability of
their escaping predators for more than a few years has left natural selection
with precious little fodder for building bodies that can stand the test of time.
Larger animals enjoy lower predation rates, on average, and are better able to
tolerate other environmental risk factors such as extreme temperatures and
nutritional stress.
If environmental risks really affect the rate of ageing then you would expect
flying mammals such as bats to live much longer than other mammals of similar
size. In 1991, while he was at Harvard University, Austad teamed up with
anthropologist Kathleen Fischer to test this prediction. They found that bat
life spans are several times as long as one would expect for mammals of their
size. Mouse-sized bats can survive 30 years or more—at least six times the
life span of a mouse. And this isn’t true only of hibernating bat species:
tropical bats that are active all year round also live longer than other mammals
of equivalent size. “Bats have fewer environmental hazards because of their gift
of flight,” says Austad. “They can better escape predators or local food
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Next, Fischer and Austad looked at gliding mammals and again found that they
aged more slowly than expected. The results were not as pronounced as in bats,
but most gliders still survived longer than their non-flying counterparts. North
American flying squirrels, for example, survive almost twice as long as the
similarly sized chipmunk. Austad and biologist Donna Holmes, have since
christened this the “fly now, die later” effect.
Shells and spines
After working on the theory for over a decade, Austad can cite a litany of
other examples. There are the thick-shelled ocean bottom clams called quahogs,
which can survive for more than 200 years—the longest-lived animals known.
Indeed, clams in general are survivors, averaging as much as 14 years, while
related molluscs that lack shells rarely live to see their fifth year.
Mammals sporting defensive spines also live longer than their less well
defended counterparts. The egg-laying short-nosed echidna, for example, can
survive over 50 years, and porcupines, the longest-lived rodent, can notch up 20
years. “All the spined mammals are exceptionally long-lived,” says Austad.
Austad reasoned that if increased life spans really do go hand in hand with
reduced risk of accidental death, you should be able to catch this happening.
What’s more, this logic should apply within species as well as between them. If
one isolated population of animals finds itself with no predators, it should
start to age more slowly than a population that is threatened by predation.
Austad has found that this is the case with the Virgina opossums of Sapelo
Island, five miles off the coast of Georgia, which have lived without predators
for almost 4000 years. They survive up to 50 per cent longer than mainland
possums, which rarely live past their second year.
What’s more, the island possums do seem to remain youthful for longer, with
many females producing a second litter, while the mainland possums usually
become infertile after their first and only reproductive season. Austad also
measured the deterioration of their ligament tissues—a recognised physical
measure of ageing—and found that it was nearly twice as fast in mainland
possums as in their island counterparts.
But how do animals such as the Sapelo Island possums resist ageing?
Researchers are only just starting to look at the cellular defences and repair
mechanisms that keep animals youthful. One chemical known to be involved is
superoxide dismutase, an antioxidant enzyme that mops up free radicals.
Longer-lived species tend to have higher levels of this enzyme, for any given
metabolic rate.
And just this year, a team led by Pankaj Kapahi at the University of
Manchester found that cells in long-lived species are more resistant to chemical
stress. Using cultured fibroblast cells from a variety of species, from rodents
to humans, they measured their survival when stressed by exposure to chemicals.
For a given metabolic rate, cell survival rates were highest in those animals
that lived longest.
Birds seem to have evolved another cellular defence against ageing. Avian
metabolisms are considerably less “leaky”, producing fewer free radicals than
mammalian metabolisms, despite the fact that birds have faster metabolic rates
for their size. Exactly how this works, however, is unclear. In theory, another
way to resist ageing would be to produce more DNA repair enzymes. These simply
identify damaged bits of genetic code and replace the nucleic acids. The
replacements are random and therefore imperfect, but they are less damaging than
broken DNA.
Our Pleistocene ancestors reduced their risk of predation by evolving
language to share survival strategies with one another. Perhaps this explains
why—despite our lack of wings—we enjoy a maximum life span four
times that predicted by our size and metabolic rate. Modern medicine has
undoubtedly increased average life expectancy, mainly by slashing infant
mortality. But centenarians, it seems, should thank our evolutionary legacy
rather than medical technology alone for their longevity.
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Further reading:
Positive correlation between mammalian life span and cellular resistance to stress
by Pankaj Kapahi, Free Radical Biology and Medicine, vol 26, p 495 (1999) -
Why we age
by Steven Austad, (John Wiley & Sons, New York, 1997) -
The evolution of the antiaging action of dietary restriction: a hypothesis
by Edward Masoro and Steven Austad, Journal of Gerontology A, vol 51, p B387 (1996) -
Fly now, die later
by Donna Holmes and Steven Austad, Journal of Mammalogy, vol 75(1), p 224 (1994)
