BiologyofAgingarticle
Just need a question answered after reading an article. Questions are —–″There are obvious biological limits to life span. Despite being spared from a multitude of lethal agents (e.g., Tuberculosis) that were present a century ago, we find ourselves up against other factors that can end our lives. With people striving to find the proverbial “fountain of youth”, what evidence does scientific research show are two possible ways to delay death and extend maximum lifespan? Why and how do scientists believe these two biological paths help slow down aging?
ffiwffiwwmw’fln&ffi$ffigffi
ffi The
KffiEffi
Why, after being so exquisitely
assembled, do we fall apart
so predictably? Why do we
outlive dogs, only to be
outlived by turtles? Could we catch up with them? Living to 200
is not a realistic goal for this generation, but a clearer picture
of how we grow old is already
within our reach.
F ONLY GOD HAD FOUND A
more reliable messenger. Back around
the beginning of time, according to east
African legend, he dispatched a scaveng-
ing bird knov,n as the halawaka to give us
the instructions for endless self-renewal.
The secret was simple. Whenever age or
infirmity started creeping up on us, we
were to shed our skins like tattered shirts.
We would emerge with our youth and
our health intact. Unfortunately the ha-
lawaka got hungry during his journey,
and happened upon a snake who was
eating a freshly killed wildebeest. In the
bartering that ensued, the bird got a sat-
isfying meal, the snake learned to molt
and humankind lost its shot at immortal-
ity. People have been growing old and
dytrg ever since.
The mystery of aging runs almost as
deep as the mystery of life. During the
past century, life expectancy has nearly
doubled in developed countries, thanks
to improvements in nutrition, sanitation
PHOTOGRAPHS BY CHRISTOPHER GRIFFITH12 NEwswEEr{ sPEcrAL rssuE
;tr;i!,irl]i
I
_t
ffim$mmswwiiiffiffiffiffiBffi
and medical science. Yet the potential life
span of a human being has not changed
significantly since the halawaka met the
snake. By age 50 every one ofus, no mat-
ter how fit,
Until recently, all we could do rn’as
guess. But as the developed v’orld’s
population grows grayer, scientists are
bearing down on the dynamics of aging,
and they’re amassing crucial insights.
Much of the new understanding has
come from the study of rvorms, flies,
mice and monkeys-species rvhose life
cycles can be manipulated and observ-ed
in a laboratory. Hou’exactly the findings
apply to people is still a matter of conjec-
ture. Could calorie restriction extend our
lives by half? It would take generations
to find out for sure. But the big questions
of why we age-and which parts of the
experience we can change-are already
coming into focus.
The starkest way to see hon’ time
changes us (aside from hauling out an old
photo album) is to compare death rates
for people of different ages. In Europe
and North America the annual rate
among tS-year-olds is roughly .05 per-
cent, or one death for er.ery 2,000 kids.
Fifty-year-olds are far less likely to ride
their skateboards down banisters, yet they
die at 30 times that rate (1.5 percent annu-
ally). The yearly death rate among 105-
year-olds is 50 percent, 1,000 times that
of the adolescents. The rise in mortality is
due mainly to heart disease, cancer and
stroke-diseases that anyone over 50 is
right to worry about. But here’s the rub.
Eradicating these scourges would add
only 15 years to U.S. life expectancy (half
the gain we achieved during the 20th cen-
tury), for unlike children spared of small-
pox, octogenarians without cancer soon
die of something else. As the biologist
Leonard Hal.flick observes, u-hat ulti-
mately does us in is not disease per se, but
our declining abiliry to resist it.
Biologists once regarded senescence as
nature’s way of pushing one generation
aside to make way for the next. But under
natural conditions, virtually no creature
lives long enough to experience decrepi-
tude. Our own ancestors $pically starved,
froze or got eaten long before they reached
16 NEws\r/EEK sPEcIAL Issu!l
old age. As a result, the genes that leave us
r’.ulnerable to chronic illness in later life
rarely had adverse consequences. As long
as they didn’t hinder reproduction, natural
selection had no occasion to rveed them
out. Natural selection may even fauor a
gene that causes cancer late in life if it
makes 1,oung adults more fertile.
But rvhy should “later life” mean 50 in-
stead of 150? Try thinking of the body as a
vehicle, designed by a group of genes t
o
transport them through time. You might
expect durable bodies to have an inherent
advantage. But if a mouse is sure to be-
come a cat’s dinner within five years, a
body that could last twice that long is a
waste of resources. A S-year-old mouse
that can produce eight litters annually
will leave twice the legacy of a 1O-year-old
mouse that delivers only four each year.
Under those conditions, mice will evolve
to live roughly five years. A sudden disap-
pearance of cats may improve their odds
of completing that life cycle, but it won’t
change their basic genetic makeup.
That is the predicament we face. Our
bodies are nicely adapted to the harsh con-
ditions our Stone Age ancestors faced, but
often poorly adapted to the cushy ones
u’e’ve created. There is no question that
In childhood the body is wonderfully resilient,
and sound sleep supports the growth of tissues
and bones. During the teenage years, hormonal
changes trigger the development of sexual organs.
Boys add muscle mass. Even the muscles in their
voice box lengthen, causingvoices to deepen.
In girls, fat is redistributed to hips and breasts.
-:.. br-rrer br- exercising, eating
–.,’.. ir\oiding cigarettes and stay-
-.,-r- and mentallv acti\r. But can
-::. “lh e \l)ect to extend our maxi-
:c:pansi
: i:,’-:.hers have already accomplished
-:-:: in lab experiments. In the
:> :iudied so far, the slrrest \vay to
. … litb span has been to cut back on
:s riav bach. In studies dating
– – r the 1930s, researchers have found
.recies as r,’ariecl as rats, monkeys
:raker’s yeast age more slo\\{y if
‘n- gir-en 30 to 60 percent fetver calo-
iiran they rn’ould normallv consume.
No one has attempted such a trial among
humans, but some researchers have al-
readv embraced the regimen themselves.
Dr. Rov Walford, a 77-,vear-old patholo-
gist at the University of California, Los
Angeles, has surived for years on 1,200
calories a da.v and expects to be doing the
same u’hen he’s 120. That may be opti-
mistic, but he loohs as splT as any 60-
year-old in the photo he posts on the
Web, and the anirnal studies suggest at
least a partial explanation. Besides delay-
ing death, caloric restriction seems to
preserve bone mass, skin thickness, brain
function and immune function, u’hile
providing superior resistance to heat,
toxic chemicals ancl traumatic injury’.
Ho’rv could something so pen’erse be so
good for you? Scientists once theorized
that caloric restriction extended life b,v de-
la,ving development, or by reducing bodv
fat, or bi- slou’ing metabolic rate. None of
these explanations surr.ir,-ed scrutinv, but
stuclies have identified several likely
mechanisms. 1’he first involves oxidation.
As mitochondria (the power plants in our
cells) release the energv in fr-rod, they gen-
erate corrosive, unpaired electrons knorm
as free radicals. B)’ reacting n’ith nearbv
fats, proteins and nucleic acids, these tinv
terrorists foster eventhing from cataracts
to vascular disease. It appears that caloric
restriction not only slorvs the production
of free radicals but helps the bod,v colrnter
them more efiicientl,v.
Food restriction may also shield tissues
from the damaging effects of glucose, the
sugar that enters our bloodstreams u’hen
Another possible approach is to ma-
nipulate hormones. No one has shorvn
conclusivelV that anSr of these substances
can alter life span, but there are plenty of
tantalizing hints. Consider human
gro\\.th hormone, a pituitary protein that
helps drive our ph-ysical development.
Enthusiasts tout the prescription-only
svnthetic version as an antidote to all as-
pects of aging, but mounting evidence
suggests that it could make the clock tick
faster. The first indication came in the
mid-1980s, u.hen phvsiologist Andrzej
Barthe outfitted lab mice u.ith human or
bovine genes for growth hormone. These
mightv mice grerv to br.ice the size of
normal ones, but they aged earl,v and died
young. Bartke, nou. based at Southern
In manyways, the 20s are the prime oflife. We’re
blessedwith an efficient metabolism, strong loones
and good f lexi loility. As early as the 3 0 s, however,
metabolism begins to slow and women’s hormone
levels staftto dip. Bones mav startto lose densitv
in peoplewho don’t exercise orwho don’t get the
vitamin D required for calcium absorption.
NEwsw!rEK sPECIAL IssTTE 1l
ffiwffiwswww.s,&ffiffim#
Illinois Universilv, witnessed something
very different in 1996, when he began
studying a strain of rodents called Ames
dwarf mice. Due to a congenital lack of
growth hormone, these creatures reach
only a third the size of normal mice. But
they live 5O to 6o percent longer.
As it happens, the mini-mice aren’t the
only ones carrying this auspicious gene.
The island of Krk, a Croatian outpost in
the eastern Adriatic, is home to a group of
people who harbor essentially the same
mutation. The “little people of Krk” reach
an adult height ofjust four feet five inch-
es. But like the mini-mice, they’re excep-
tionally long-lived. Bartke’s mouse stud-
ies suggest that besides stifling growth
hormone, the gene that causes this stunt-
ing may also improve sensitivity to-you
guessed it-insulin. If so, the mini-mice,
the Croatian dwarles and the half-
starved rats and monkeys have more than
their longevity in common. No one is
suggesting that we stunt people’s growth
in the hope of extending their lives. But if
you’ve been pestering your doctor for a
vial of growth hormone, you may want to
reconsider.
Growth hormone is just one of several
that decline as we age. The sex hormones
Around 40, people often staft noticing gray hairs,
mild memory lapses and difficulty focusing their
eyes on small t1pe. Around 5 1, most women will
experience menopause. Estrogen levels plummet,
making the skin thinner and bones less dense.
Men suffer more heart disease than women at
this age. Metabolismslows downinboth sexes.
estrogen and testosterone follow the
same pattern, and replacing them can re-
iuvenate skin, bone and muscle. But like
growth hormone, these tonics can have
costs as well as benefits. They evolved not
to make us more durable but to make us
more fertile. As the British biologist
Roger Gosden observed in his 1996 book,
“Cheating Time,” “sex hormones are re-
quired for fertility and for making biolog-
ical gender distinctions, but they do not
prolong life. On the contrary a price mav
have to be paid for living as a sexual be-
ing.” Anyone suffering from breast or
prostate cancer would surely agree.
In most of the species biologists have
studied, fertility and longevity have a see-
saw relationship, each rising as the other
declines. Bodies designed for ma-rimum
fertility have fewer resources for self-
repair, some perishing as soon as they re-
produce (thinh of spawning salmon). By
contrast, those with ertraordinary life
spans are tlpically slow to bear offspring.
Do these rules apply to people? The evi-
dence is sketchy but provocative. In a
1998 study, researchers at the Universig’
of Manchester analyzed genealogical
records of 32,ooo British aristocrats born
during the 1,135-year period between 740
and 1875 (long before modern contracep-
tives). Among men and women who
made it to 60, the least fertile u’ere the
most likely to sundve beyond that age. A
u’hopping 50 percent of the rvomen u’ho
reached 81 u.ere childless.
Eunuchs seem to enjoy (if that’s the All of this research holds a fairly obvi- M’, R{CHELDAVIS ffim$mwemw+1′:&gffiweffi
o H KA3-TFS
&HXTltr{!TS 6€h s$*$siFi&& K*8″tEffi: ” @ Influenzah B pandemicFtt”s ‘ Or.,.: , , 1, 500
1,000
5oo
Oi $mart choices can reduce health risks. CIGARETTE CONSUMPTION
fuXFffi.$:::YLM
5,OOO . — , 1,000 YEem &$du and ‘0ld 0ld’ system weakens and we become more susceptible
to cancer and other ills. Stren$th declines, but Throughout life, the body retains its ability
to add mass to existing muscles.
life expectancy has risen dramatically, ryI 80 99
All deaths , Those turning 5o today can 20 NEwswEEK sPECIAL ISSUtI o I) ctttre rlffiqk[Tffil:#,;il’ne-have 1900
s#”d
Pneunonia
Tuberculosis
Diarrhea,/enteriti s
Heart disease
Stroke
$lWrr.s 1998 -G–cancer ffiz:.0 locate what ails u
ry
wg*l”*sffi*g&
ffi1974-79 x1989-94
White males I9sI White lem
$T&Yt$* #SEES8: Wb’re notjust living ffi 1910 B 2000 ilfl:xiimffi4- flJfff;m*’- M agnet’it re sonance im aging Acciclents S +.t
*€E&ttrtffiffiSffi$r MATERNALDEATHS tntuffioos ? {ir!n
tlilu$ sss
#i.*,i?H1,””. m Private 70
S*lg&&, $e$S**: Our srveet r33?% €*Y*F$*ffiEdKYH: We’re ffisffi;-
PEOPLFT 20 TO 74 SS T?t€ ffi*&S: Although we’re dliving more, \ LH ICLE M I LES \,IOTOR-VEHICI,I.: PEoPLE ovER 65 ffi 1900 I 2000 YV OI!CN K u.’ffioz
c01
&l**1t#{&t* *EWs#$: slqnocketed, but the DEATH VS. DOIJ,ARS 750
500 25tl
2,000
l,OOO
o It 6# lOO OOO PFOF] F
SOUFCESCDI,IH,USJAtCONOI”IaFESEAFaFSEH!,iE,ilATONALSAFFIiCO!NCIL!5CEN5!SE!F[A!CENtEFSFOFtvt:DCAtEA 60 ‘ tr*S!{frrufi PRS’ tr*S!{frrufi PRS$&f;$$; Newtreat- have improved our chances of C \.\CER-SI R\I\ \I, RqTES
M ul.. g7
ffi 81
ffi Prostate
ffi r< 5l
ffi ffi 19 53
ffi *# TT€I -$SS: Black males
Black fema.les
Exerrise can reduce serious health problems
N-U\VS\\rEEK SPECIT\t ISSUE 21 ill begin a slow decline in Until recently, all we could do rn’as -:.. br-rrer br- exercising, eating ffiwffiwswww.s,&ffiffim# made it to 60, the least fertile u’ere the Another possible approach is to ma- ffiwffiwswww.s,&ffiffim# made it to 60, the least fertile u’ere the Until recently, all we could do rn’as -:.. br-rrer br- exercising, eating ffiwffiwswww.s,&ffiffim# made it to 60, the least fertile u’ere the Turnitin Report Formatting Title Page Citation Outline
u’ord) a similar advantage in longevity.
During the 1940s and 5Os, anatomist
James Hamilton studied a group of men-
tally handicapped men lr.ho had been cas-
trated at a state institution in Kansas. Life
expectancy $,?s just 56 in this institution,
but the neutered men lived to an average
age of 69-a 23 percent advantage-and
not one of them went bald. No one l
ous lesson. Life itself is lethal. and the
things that make it sweet make it more
lethal. Chances are that by starving and
castrating ourselves, we really could se-
cure some extra vears. But most of us
would gladly trade a lonely decade of
stubborn sun’ival for a richer middle age.
Our bodies are designed to last only so
long. But with care and maintenance,
they’ll live out their u’arranties in style.
In tg0o,justsur-
vivingchildhood
was a challenge.
Nearly 13 percent
ofchildren died
before their lst
birdrdav. Now
more than 99
pelcentlivepast
the age ofl.
Sewers. clean
drinkingwater
and food
refrigeration
combined with
antibiotics and
vaccines to
reduce deaths
from infectious
diseases.
%& &:t $€c$*$
1920 40 6a
1900 zo 40 60 80 96
We’ve lained glround in some areas but
continue to struggle with others. Below,
here’s how our lifestyles have changed.
4,ooo Per person
3.000
2,OO0
o
uYep&ssxgl
Old age begins o{ficially al65,when robust
health is still possible. Eventually the immune
the losses can be minimized through exercise.
from 47 years in 1900 to 77 years in 1998.
Here’s a look at the progress we’ve made
and the problems that remain.
lnfant mortality
PER I,OOO LIVE BIRTHS
100 -‘ ‘
PER TOO,OOO POPUL{TroN
2.OOO.. ..-.
I expect to live longer than 50-
I year-olds in the early 1900s.
r-**””i.1.;:!,@-“-*-“-*”J
$*lmffi C&*}$H*r In 19o0 acute illnesses
like pneumonia and TB causecl most
deaths. Now our longer life spans increase
rhe lil
Wrr.:
Ws.:
ffis.o
Wo.z
–
rrroKe S;.,
Respiratory diseas”. SF 5.2 techn’iqwes can help docs
-.65 ryffi l
#sffiffit
ffi ffi |
wi*t ffizt!
Colon Prostate I
longer, we’re living better, too.
DIS \BILITY R-TTES
\ge 50-64 {ge 60 7+
oim”utnffi2s oim.uttyW3zwalUng”ffis watking’ffili*-*”
and other advanrcd scanning
Improved obstetrics
drastically reduced the
risk that women will
die from pregnancy-
related prtrblerns.
PER IOO,OOO BIRTHS
1SeSi7
‘!,***
1i:l::,1,*lllatic #ffi
BENEFTTS |SJS 98
lnsutance
co\refage
tooth continues to grow.
slvEE t’UNER CONSUMI/TION,
POUNDS PER CAPITA*
CALOFIi SVr’EFENEFS LSUGAi, HONEX COFN SyFUPj
more likell’to imbibe.
PF]RCEN’I’AGE OF ADUI,TS
\1’HO CONSUX{EALCOHOL
wr{o ARE oBEsE*
saGtv features have hclped cut down on tie
ratc olaccident-related cleaths.
TB*A,VELEDPERYEAR DEATHRATD
In billions Per 1O0 million milcs
J.000 20
IN THE WORK FORCE
#o
we
Health spencling has
associated decline in death
rates has been minimal.
$1,000 billicn .
fff
1e35 s5 75 9572 84 96,PEF
\4EDCADSEF”ESGALLIFPOLLSAOYDEAIOIII]I]’NAL’ENTIffFOHHEALTHSTAISTC5NATONALBUFEAUCFE’ONOIr”FISIAFCI
CFAIH’!IFIANPO!!ELL iiJE!FCHAI!DTEX tsf .] L] PASI’FF
0*
1948
ments ancl detection techniques
f;$; Newtreat-
ments ancl detection techniques
surviving cancer for fir’e years.
Colon
Breast
ffiFffi
Rreast
Colon
Colon
Social Securitv
an
organ function and sensory acuity. And
though some will enjoy another half cen-
tury of robust health, our odds of living
past 120 are virtually zero. Why, after be-
ing so exquisitely assembled, do we fall
apart so predictabll,? Why do we outlive
dogs, only to be outlived by turtlesl And
what are our prospects for catching up
with them?
guess. But as the developed v’orld’s
population grows grayer, scientists are
bearing down on the dynamics of aging,
and they’re amassing crucial insights.
Much of the new understanding has
come from the study of rvorms, flies,
mice and monkeys-species rvhose life
cycles can be manipulated and observ-ed
in a laboratory. Hou’exactly the findings
apply to people is still a matter of conjec-
ture. Could calorie restriction extend our
lives by half? It would take generations
to find out for sure. But the big questions
of why we age-and which parts of the
experience we can change-are already
coming into focus.
The starkest way to see hon’ time
changes us (aside from hauling out an old
photo album) is to compare death rates
for people of different ages. In Europe
and North America the annual rate
among tS-year-olds is roughly .05 per-
cent, or one death for er.ery 2,000 kids.
Fifty-year-olds are far less likely to ride
their skateboards down banisters, yet they
die at 30 times that rate (1.5 percent annu-
ally). The yearly death rate among 105-
year-olds is 50 percent, 1,000 times that
of the adolescents. The rise in mortality is
due mainly to heart disease, cancer and
stroke-diseases that anyone over 50 is
right to worry about. But here’s the rub.
Eradicating these scourges would add
only 15 years to U.S. life expectancy (half
the gain we achieved during the 20th cen-
tury), for unlike children spared of small-
pox, octogenarians without cancer soon
die of something else. As the biologist
Leonard Hal.flick observes, u-hat ulti-
mately does us in is not disease per se, but
our declining abiliry to resist it.
Biologists once regarded senescence as
nature’s way of pushing one generation
aside to make way for the next. But under
natural conditions, virtually no creature
lives long enough to experience decrepi-
tude. Our own ancestors $pically starved,
froze or got eaten long before they reached
16 NEws\r/EEK sPEcIAL Issu!l
old age. As a result, the genes that leave us
r’.ulnerable to chronic illness in later life
rarely had adverse consequences. As long
as they didn’t hinder reproduction, natural
selection had no occasion to rveed them
out. Natural selection may even fauor a
gene that causes cancer late in life if it
makes 1,oung adults more fertile.
But rvhy should “later life” mean 50 in-
stead of 150? Try thinking of the body as a
vehicle, designed by a group of genes to
transport them through time. You might
expect durable bodies to have an inherent
advantage. But if a mouse is sure to be-
come a cat’s dinner within five years, a
body that could last twice that long is a
waste of resources. A S-year-old mouse
that can produce eight litters annually
will leave twice the legacy of a 1O-year-old
mouse that delivers only four each year.
Under those conditions, mice will evolve
to live roughly five years. A sudden disap-
pearance of cats may improve their odds
of completing that life cycle, but it won’t
change their basic genetic makeup.
That is the predicament we face. Our
bodies are nicely adapted to the harsh con-
ditions our Stone Age ancestors faced, but
often poorly adapted to the cushy ones
u’e’ve created. There is no question that
In childhood the body is wonderfully resilient,
and sound sleep supports the growth of tissues
and bones. During the teenage years, hormonal
changes trigger the development of sexual organs.
Boys add muscle mass. Even the muscles in their
voice box lengthen, causingvoices to deepen.
In girls, fat is redistributed to hips and breasts.
–.,’.. ir\oiding cigarettes and stay-
-.,-r- and mentallv acti\r. But can
-::. “lh e \l)ect to extend our maxi-
:c:pansi
: i:,’-:.hers have already accomplished
-:-:: in lab experiments. In the
:> :iudied so far, the slrrest \vay to
. … litb span has been to cut back on
:s riav bach. In studies dating
– – r the 1930s, researchers have found
.recies as r,’ariecl as rats, monkeys
:raker’s yeast age more slo\\{y if
‘n- gir-en 30 to 60 percent fetver calo-
iiran they rn’ould normallv consume.
No one has attempted such a trial among
humans, but some researchers have al-
readv embraced the regimen themselves.
Dr. Rov Walford, a 77-,vear-old patholo-
gist at the University of California, Los
Angeles, has surived for years on 1,200
calories a da.v and expects to be doing the
same u’hen he’s 120. That may be opti-
mistic, but he loohs as splT as any 60-
year-old in the photo he posts on the
Web, and the anirnal studies suggest at
least a partial explanation. Besides delay-
ing death, caloric restriction seems to
preserve bone mass, skin thickness, brain
function and immune function, u’hile
providing superior resistance to heat,
toxic chemicals ancl traumatic injury’.
Ho’rv could something so pen’erse be so
good for you? Scientists once theorized
that caloric restriction extended life b,v de-
la,ving development, or by reducing bodv
fat, or bi- slou’ing metabolic rate. None of
these explanations surr.ir,-ed scrutinv, but
stuclies have identified several likely
mechanisms. 1’he first involves oxidation.
As mitochondria (the power plants in our
cells) release the energv in fr-rod, they gen-
erate corrosive, unpaired electrons knorm
as free radicals. B)’ reacting n’ith nearbv
fats, proteins and nucleic acids, these tinv
terrorists foster eventhing from cataracts
to vascular disease. It appears that caloric
restriction not only slorvs the production
of free radicals but helps the bod,v colrnter
them more efiicientl,v.
Food restriction may also shield tissues
from the damaging effects of glucose, the
sugar that enters our bloodstreams u’hen
$’e eat carbohvdrates. Idealll-, our bodies
respond to any rise in blood glucose by
releasing insulin, u’hich shuttles the
sugar into fat and muscle cells for stor-
age. But age or obesity can make our cells
resistant to insulin. Ancl u,hen glucose
molecules linger in the bloodstream, therr
link up u’itl”r collagen and other proteins
to rvreak havoc on nerves, organs and
blood vessels. When rats or monheys are
allou’ed to eat at rvill, their cells become
less sensitive to insulin over time, just as
ours do. But according to Dr. Marh Lane
of the National Institute on Aging, older
animals on calorie-restrictecl diets exhibit
the high insulin sensitivitl’, low blood
glucose and robust health of l.oungsters.
No one knou’s r,r,’hether people’s bodies
u’ill respond the same n’ari But the find-
ing suggests that life extension could
prove as simple, or rather as complicated,
as preseniing the insulin response.
Another possible approach is to ma-
nipulate hormones. No one has shorvn
conclusivelV that anSr of these substances
can alter life span, but there are plenty of
tantalizing hints. Consider human
gro\\.th hormone, a pituitary protein that
helps drive our ph-ysical development.
Enthusiasts tout the prescription-only
svnthetic version as an antidote to all as-
pects of aging, but mounting evidence
suggests that it could make the clock tick
faster. The first indication came in the
mid-1980s, u.hen phvsiologist Andrzej
Barthe outfitted lab mice u.ith human or
bovine genes for growth hormone. These
mightv mice grerv to br.ice the size of
normal ones, but they aged earl,v and died
young. Bartke, nou. based at Southern
In manyways, the 20s are the prime oflife. We’re
blessedwith an efficient metabolism, strong loones
and good f lexi loility. As early as the 3 0 s, however,
metabolism begins to slow and women’s hormone
levels staftto dip. Bones mav startto lose densitv
in peoplewho don’t exercise orwho don’t get the
vitamin D required for calcium absorption.
NEwsw!rEK sPECIAL IssTTE 1l
Illinois Universilv, witnessed something
very different in 1996, when he began
studying a strain of rodents called Ames
dwarf mice. Due to a congenital lack of
growth hormone, these creatures reach
only a third the size of normal mice. But
they live 5O to 6o percent longer.
As it happens, the mini-mice aren’t the
only ones carrying this auspicious gene.
The island of Krk, a Croatian outpost in
the eastern Adriatic, is home to a group of
people who harbor essentially the same
mutation. The “little people of Krk” reach
an adult height ofjust four feet five inch-
es. But like the mini-mice, they’re excep-
tionally long-lived. Bartke’s mouse stud-
ies suggest that besides stifling growth
hormone, the gene that causes this stunt-
ing may also improve sensitivity to-you
guessed it-insulin. If so, the mini-mice,
the Croatian dwarles and the half-
starved rats and monkeys have more than
their longevity in common. No one is
suggesting that we stunt people’s growth
in the hope of extending their lives. But if
you’ve been pestering your doctor for a
vial of growth hormone, you may want to
reconsider.
Growth hormone is just one of several
that decline as we age. The sex hormones
Around 40, people often staft noticing gray hairs,
mild memory lapses and difficulty focusing their
eyes on small t1pe. Around 5 1, most women will
experience menopause. Estrogen levels plummet,
making the skin thinner and bones less dense.
Men suffer more heart disease than women at
this age. Metabolismslows downinboth sexes.
estrogen and testosterone follow the
same pattern, and replacing them can re-
iuvenate skin, bone and muscle. But like
growth hormone, these tonics can have
costs as well as benefits. They evolved not
to make us more durable but to make us
more fertile. As the British biologist
Roger Gosden observed in his 1996 book,
“Cheating Time,” “sex hormones are re-
quired for fertility and for making biolog-
ical gender distinctions, but they do not
prolong life. On the contrary a price mav
have to be paid for living as a sexual be-
ing.” Anyone suffering from breast or
prostate cancer would surely agree.
In most of the species biologists have
studied, fertility and longevity have a see-
saw relationship, each rising as the other
declines. Bodies designed for ma-rimum
fertility have fewer resources for self-
repair, some perishing as soon as they re-
produce (thinh of spawning salmon). By
contrast, those with ertraordinary life
spans are tlpically slow to bear offspring.
Do these rules apply to people? The evi-
dence is sketchy but provocative. In a
1998 study, researchers at the Universig’
of Manchester analyzed genealogical
records of 32,ooo British aristocrats born
during the 1,135-year period between 740
and 1875 (long before modern contracep-
tives). Among men and women who
most likely to sundve beyond that age. A
u’hopping 50 percent of the rvomen u’ho
reached 81 u.ere childless.
Eunuchs seem to enjoy (if that’s the
u’ord) a similar advantage in longevity.
During the 1940s and 5Os, anatomist
James Hamilton studied a group of men-
tally handicapped men lr.ho had been cas-
trated at a state institution in Kansas. Life
expectancy $,?s just 56 in this institution,
but the neutered men lived to an average
age of 69-a 23 percent advantage-and
not one of them went bald. No one l
nipulate hormones. No one has shorvn
conclusivelV that anSr of these substances
can alter life span, but there are plenty of
tantalizing hints. Consider human
gro\\.th hormone, a pituitary protein that
helps drive our ph-ysical development.
Enthusiasts tout the prescription-only
svnthetic version as an antidote to all as-
pects of aging, but mounting evidence
suggests that it could make the clock tick
faster. The first indication came in the
mid-1980s, u.hen phvsiologist Andrzej
Barthe outfitted lab mice u.ith human or
bovine genes for growth hormone. These
mightv mice grerv to br.ice the size of
normal ones, but they aged earl,v and died
young. Bartke, nou. based at Southern
In manyways, the 20s are the prime oflife. We’re
blessedwith an efficient metabolism, strong loones
and good f lexi loility. As early as the 3 0 s, however,
metabolism begins to slow and women’s hormone
levels staftto dip. Bones mav startto lose densitv
in peoplewho don’t exercise orwho don’t get the
vitamin D required for calcium absorption.
NEwsw!rEK sPECIAL IssTTE 1l
Illinois Universilv, witnessed something
very different in 1996, when he began
studying a strain of rodents called Ames
dwarf mice. Due to a congenital lack of
growth hormone, these creatures reach
only a third the size of normal mice. But
they live 5O to 6o percent longer.
As it happens, the mini-mice aren’t the
only ones carrying this auspicious gene.
The island of Krk, a Croatian outpost in
the eastern Adriatic, is home to a group of
people who harbor essentially the same
mutation. The “little people of Krk” reach
an adult height ofjust four feet five inch-
es. But like the mini-mice, they’re excep-
tionally long-lived. Bartke’s mouse stud-
ies suggest that besides stifling growth
hormone, the gene that causes this stunt-
ing may also improve sensitivity to-you
guessed it-insulin. If so, the mini-mice,
the Croatian dwarles and the half-
starved rats and monkeys have more than
their longevity in common. No one is
suggesting that we stunt people’s growth
in the hope of extending their lives. But if
you’ve been pestering your doctor for a
vial of growth hormone, you may want to
reconsider.
Growth hormone is just one of several
that decline as we age. The sex hormones
Around 40, people often staft noticing gray hairs,
mild memory lapses and difficulty focusing their
eyes on small t1pe. Around 5 1, most women will
experience menopause. Estrogen levels plummet,
making the skin thinner and bones less dense.
Men suffer more heart disease than women at
this age. Metabolismslows downinboth sexes.
estrogen and testosterone follow the
same pattern, and replacing them can re-
iuvenate skin, bone and muscle. But like
growth hormone, these tonics can have
costs as well as benefits. They evolved not
to make us more durable but to make us
more fertile. As the British biologist
Roger Gosden observed in his 1996 book,
“Cheating Time,” “sex hormones are re-
quired for fertility and for making biolog-
ical gender distinctions, but they do not
prolong life. On the contrary a price mav
have to be paid for living as a sexual be-
ing.” Anyone suffering from breast or
prostate cancer would surely agree.
In most of the species biologists have
studied, fertility and longevity have a see-
saw relationship, each rising as the other
declines. Bodies designed for ma-rimum
fertility have fewer resources for self-
repair, some perishing as soon as they re-
produce (thinh of spawning salmon). By
contrast, those with ertraordinary life
spans are tlpically slow to bear offspring.
Do these rules apply to people? The evi-
dence is sketchy but provocative. In a
1998 study, researchers at the Universig’
of Manchester analyzed genealogical
records of 32,ooo British aristocrats born
during the 1,135-year period between 740
and 1875 (long before modern contracep-
tives). Among men and women who
most likely to sundve beyond that age. A
u’hopping 50 percent of the rvomen u’ho
reached 81 u.ere childless.
Eunuchs seem to enjoy (if that’s the
u’ord) a similar advantage in longevity.
During the 1940s and 5Os, anatomist
James Hamilton studied a group of men-
tally handicapped men lr.ho had been cas-
trated at a state institution in Kansas. Life
expectancy $,?s just 56 in this institution,
but the neutered men lived to an average
age of 69-a 23 percent advantage-and
not one of them went bald. No one l
guess. But as the developed v’orld’s
population grows grayer, scientists are
bearing down on the dynamics of aging,
and they’re amassing crucial insights.
Much of the new understanding has
come from the study of rvorms, flies,
mice and monkeys-species rvhose life
cycles can be manipulated and observ-ed
in a laboratory. Hou’exactly the findings
apply to people is still a matter of conjec-
ture. Could calorie restriction extend our
lives by half? It would take generations
to find out for sure. But the big questions
of why we age-and which parts of the
experience we can change-are already
coming into focus.
The starkest way to see hon’ time
changes us (aside from hauling out an old
photo album) is to compare death rates
for people of different ages. In Europe
and North America the annual rate
among tS-year-olds is roughly .05 per-
cent, or one death for er.ery 2,000 kids.
Fifty-year-olds are far less likely to ride
their skateboards down banisters, yet they
die at 30 times that rate (1.5 percent annu-
ally). The yearly death rate among 105-
year-olds is 50 percent, 1,000 times that
of the adolescents. The rise in mortality is
due mainly to heart disease, cancer and
stroke-diseases that anyone over 50 is
right to worry about. But here’s the rub.
Eradicating these scourges would add
only 15 years to U.S. life expectancy (half
the gain we achieved during the 20th cen-
tury), for unlike children spared of small-
pox, octogenarians without cancer soon
die of something else. As the biologist
Leonard Hal.flick observes, u-hat ulti-
mately does us in is not disease per se, but
our declining abiliry to resist it.
Biologists once regarded senescence as
nature’s way of pushing one generation
aside to make way for the next. But under
natural conditions, virtually no creature
lives long enough to experience decrepi-
tude. Our own ancestors $pically starved,
froze or got eaten long before they reached
16 NEws\r/EEK sPEcIAL Issu!l
old age. As a result, the genes that leave us
r’.ulnerable to chronic illness in later life
rarely had adverse consequences. As long
as they didn’t hinder reproduction, natural
selection had no occasion to rveed them
out. Natural selection may even fauor a
gene that causes cancer late in life if it
makes 1,oung adults more fertile.
But rvhy should “later life” mean 50 in-
stead of 150? Try thinking of the body as a
vehicle, designed by a group of genes to
transport them through time. You might
expect durable bodies to have an inherent
advantage. But if a mouse is sure to be-
come a cat’s dinner within five years, a
body that could last twice that long is a
waste of resources. A S-year-old mouse
that can produce eight litters annually
will leave twice the legacy of a 1O-year-old
mouse that delivers only four each year.
Under those conditions, mice will evolve
to live roughly five years. A sudden disap-
pearance of cats may improve their odds
of completing that life cycle, but it won’t
change their basic genetic makeup.
That is the predicament we face. Our
bodies are nicely adapted to the harsh con-
ditions our Stone Age ancestors faced, but
often poorly adapted to the cushy ones
u’e’ve created. There is no question that
In childhood the body is wonderfully resilient,
and sound sleep supports the growth of tissues
and bones. During the teenage years, hormonal
changes trigger the development of sexual organs.
Boys add muscle mass. Even the muscles in their
voice box lengthen, causingvoices to deepen.
In girls, fat is redistributed to hips and breasts.
–.,’.. ir\oiding cigarettes and stay-
-.,-r- and mentallv acti\r. But can
-::. “lh e \l)ect to extend our maxi-
:c:pansi
: i:,’-:.hers have already accomplished
-:-:: in lab experiments. In the
:> :iudied so far, the slrrest \vay to
. … litb span has been to cut back on
:s riav bach. In studies dating
– – r the 1930s, researchers have found
.recies as r,’ariecl as rats, monkeys
:raker’s yeast age more slo\\{y if
‘n- gir-en 30 to 60 percent fetver calo-
iiran they rn’ould normallv consume.
No one has attempted such a trial among
humans, but some researchers have al-
readv embraced the regimen themselves.
Dr. Rov Walford, a 77-,vear-old patholo-
gist at the University of California, Los
Angeles, has surived for years on 1,200
calories a da.v and expects to be doing the
same u’hen he’s 120. That may be opti-
mistic, but he loohs as splT as any 60-
year-old in the photo he posts on the
Web, and the anirnal studies suggest at
least a partial explanation. Besides delay-
ing death, caloric restriction seems to
preserve bone mass, skin thickness, brain
function and immune function, u’hile
providing superior resistance to heat,
toxic chemicals ancl traumatic injury’.
Ho’rv could something so pen’erse be so
good for you? Scientists once theorized
that caloric restriction extended life b,v de-
la,ving development, or by reducing bodv
fat, or bi- slou’ing metabolic rate. None of
these explanations surr.ir,-ed scrutinv, but
stuclies have identified several likely
mechanisms. 1’he first involves oxidation.
As mitochondria (the power plants in our
cells) release the energv in fr-rod, they gen-
erate corrosive, unpaired electrons knorm
as free radicals. B)’ reacting n’ith nearbv
fats, proteins and nucleic acids, these tinv
terrorists foster eventhing from cataracts
to vascular disease. It appears that caloric
restriction not only slorvs the production
of free radicals but helps the bod,v colrnter
them more efiicientl,v.
Food restriction may also shield tissues
from the damaging effects of glucose, the
sugar that enters our bloodstreams u’hen
$’e eat carbohvdrates. Idealll-, our bodies
respond to any rise in blood glucose by
releasing insulin, u’hich shuttles the
sugar into fat and muscle cells for stor-
age. But age or obesity can make our cells
resistant to insulin. Ancl u,hen glucose
molecules linger in the bloodstream, therr
link up u’itl”r collagen and other proteins
to rvreak havoc on nerves, organs and
blood vessels. When rats or monheys are
allou’ed to eat at rvill, their cells become
less sensitive to insulin over time, just as
ours do. But according to Dr. Marh Lane
of the National Institute on Aging, older
animals on calorie-restrictecl diets exhibit
the high insulin sensitivitl’, low blood
glucose and robust health of l.oungsters.
No one knou’s r,r,’hether people’s bodies
u’ill respond the same n’ari But the find-
ing suggests that life extension could
prove as simple, or rather as complicated,
as preseniing the insulin response.
Another possible approach is to ma-
nipulate hormones. No one has shorvn
conclusivelV that anSr of these substances
can alter life span, but there are plenty of
tantalizing hints. Consider human
gro\\.th hormone, a pituitary protein that
helps drive our ph-ysical development.
Enthusiasts tout the prescription-only
svnthetic version as an antidote to all as-
pects of aging, but mounting evidence
suggests that it could make the clock tick
faster. The first indication came in the
mid-1980s, u.hen phvsiologist Andrzej
Barthe outfitted lab mice u.ith human or
bovine genes for growth hormone. These
mightv mice grerv to br.ice the size of
normal ones, but they aged earl,v and died
young. Bartke, nou. based at Southern
In manyways, the 20s are the prime oflife. We’re
blessedwith an efficient metabolism, strong loones
and good f lexi loility. As early as the 3 0 s, however,
metabolism begins to slow and women’s hormone
levels staftto dip. Bones mav startto lose densitv
in peoplewho don’t exercise orwho don’t get the
vitamin D required for calcium absorption.
NEwsw!rEK sPECIAL IssTTE 1l
Illinois Universilv, witnessed something
very different in 1996, when he began
studying a strain of rodents called Ames
dwarf mice. Due to a congenital lack of
growth hormone, these creatures reach
only a third the size of normal mice. But
they live 5O to 6o percent longer.
As it happens, the mini-mice aren’t the
only ones carrying this auspicious gene.
The island of Krk, a Croatian outpost in
the eastern Adriatic, is home to a group of
people who harbor essentially the same
mutation. The “little people of Krk” reach
an adult height ofjust four feet five inch-
es. But like the mini-mice, they’re excep-
tionally long-lived. Bartke’s mouse stud-
ies suggest that besides stifling growth
hormone, the gene that causes this stunt-
ing may also improve sensitivity to-you
guessed it-insulin. If so, the mini-mice,
the Croatian dwarles and the half-
starved rats and monkeys have more than
their longevity in common. No one is
suggesting that we stunt people’s growth
in the hope of extending their lives. But if
you’ve been pestering your doctor for a
vial of growth hormone, you may want to
reconsider.
Growth hormone is just one of several
that decline as we age. The sex hormones
Around 40, people often staft noticing gray hairs,
mild memory lapses and difficulty focusing their
eyes on small t1pe. Around 5 1, most women will
experience menopause. Estrogen levels plummet,
making the skin thinner and bones less dense.
Men suffer more heart disease than women at
this age. Metabolismslows downinboth sexes.
estrogen and testosterone follow the
same pattern, and replacing them can re-
iuvenate skin, bone and muscle. But like
growth hormone, these tonics can have
costs as well as benefits. They evolved not
to make us more durable but to make us
more fertile. As the British biologist
Roger Gosden observed in his 1996 book,
“Cheating Time,” “sex hormones are re-
quired for fertility and for making biolog-
ical gender distinctions, but they do not
prolong life. On the contrary a price mav
have to be paid for living as a sexual be-
ing.” Anyone suffering from breast or
prostate cancer would surely agree.
In most of the species biologists have
studied, fertility and longevity have a see-
saw relationship, each rising as the other
declines. Bodies designed for ma-rimum
fertility have fewer resources for self-
repair, some perishing as soon as they re-
produce (thinh of spawning salmon). By
contrast, those with ertraordinary life
spans are tlpically slow to bear offspring.
Do these rules apply to people? The evi-
dence is sketchy but provocative. In a
1998 study, researchers at the Universig’
of Manchester analyzed genealogical
records of 32,ooo British aristocrats born
during the 1,135-year period between 740
and 1875 (long before modern contracep-
tives). Among men and women who
most likely to sundve beyond that age. A
u’hopping 50 percent of the rvomen u’ho
reached 81 u.ere childless.
Eunuchs seem to enjoy (if that’s the
u’ord) a similar advantage in longevity.
During the 1940s and 5Os, anatomist
James Hamilton studied a group of men-
tally handicapped men lr.ho had been cas-
trated at a state institution in Kansas. Life
expectancy $,?s just 56 in this institution,
but the neutered men lived to an average
age of 69-a 23 percent advantage-and
not one of them went bald. No one lOrder an Essay Now & Get These Features For Free:
