WEALTH

MICRO
» IT’S THE
BEGINNING OF THE
END OF THE
BEGINNING «
RICHARD A. MILLER
Yet it doesn’t have to be this way. Broad-acting
preventive medicines could dramatically
increase the period of life spent in good health
– our healthspan. This ray of hope reflects
progress in the science of aging, or geroscience.
We now possess reams of data about how
healthy lifestyles can lower risks of age-related
diseases. Geroscientists have also discovered
that altering certain genes can significantly
slow time’s toll in animals to enhance
longevity and health in later life.
Interventions that slow the rate of aging
are now a realistic prospect. They would
represent a “superefficient” way to attack the
diseases of aging, says Goldman, because they
would delay all of the diseases at once to
extend the period of healthy life. His 2013 study
showed that preventive interventions that only
modestly delay aging could achieve much
greater reductions in disability and per capita
medical costs than the reactive approach. For
example, according to research by Goldman, a
drug that increased life expectancy at age 51
by only 2.2 years in 2030 could, by 2060, boost
the number of healthy, non-disabled older
Americans by more than 11 million.
To be sure, anti-aging interventions would
likely increase the number of elderly people
eligible for government entitlement programs,
increasing the programs’ total costs. But
Goldman’s study showed these costs could be
readily offset by slightly raising eligibility ages
for the programs to reflect the fact that older
people would be healthier and living longer.
HOW TO DELAY AGING
Laboratory findings that suggest aging can be
slowed date to 1935, when scientists discovered
that putting rats on very-low-calorie diets
extends their lifespans by a third or more.
Later studies showed that such calorie
restriction, or CR, can delay aging in many
species. Importantly, it also makes animals
healthier in their extended later years.
For decades, CR remained little more
than a lab curiosity. Its dietary regimen was
demanding and there was no definite proof it
worked in humans; its mechanism of action
was too obscure to suggest drugs that would
mimic its benefits. This situation began to
change in the 1990s, however, when scientists
discovered gene mutations in worms, flies
and mice that extend healthy lifespan much
as CR does. Analyzing what these mutations
do within cells has suggested that there’s a
latent, anti-aging capacity in the body
engendered by networks of interacting genes.
These networks can be switched on by CR and
by mutations in specific genes, most notably
those that govern growth early in life. Probing
the networks’ molecular constituents has
suggested that certain drugs might tap them
to slow aging.
In 2003, the U.S. National Institute on Aging
launched a program to test such drugs’ effects
on lifespan in mice. Six years later, it yielded an
unprecedented success: rapamycin, a
medicine used to prevent rejection of
transplanted organs, robustly extended life
expectancy in elderly mice by about a third.
Subsequent studies have shown that the drug
also reduces cancer, neurodegeneration and
other ills while improving liver, heart, kidney
and muscle function in mice. Rapamycin’s side
effects, such as increased blood sugar, may
rule it out as a possible anti-aging drug. But
other candidates include acarbose, a drug for
lowering blood sugar in diabetics, and another
diabetes drug, Metformin, which mimics key
effects of CR while increasing both healthspan
and lifespan in mice.
Rigorously validated anti-aging drugs
would still take many years to develop. Among
other hurdles, scientists must find
“biomarkers” to measure the rate of aging so
that candidate drugs can be tested in relatively
short clinical trials. Still, “it’s the beginning of
the end of the beginning,” in humanity’s long
quest to delay aging, says Richard A. Miller,
professor of pathology at the University of
Michigan. And while the modestly slowed
aging that geroscientists now feel is achievable
wouldn’t repeal the Murphy’s law of aging, it
would profoundly reduce its penalties.
38 • Allianz