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Telomeres: Major Discovery Reveals the

Secret to Dramatically Slowing Aging

”Originally published in Dr. Robert Rowen's Second Opinion
Newsletter, June 200
Dr. Robert Rowen
!hat does the 200" Nobel #ri$e in %edicine ha&e to do with you and
%e' ( lot) *his particular pri$e concerned a %a+or disco&ery about
how you and , grow old. !hat's %ore, it gi&es us real insight in how
we can re&erse the aging process with ine-pensi&e supple%ents and
an easy treat%ent you can do at ho%e.
On October ., 200", three (%ericans won the pri$e /or a disco&ery
they %ade in the "00s. !hat was the disco&ery' *he telo%ere. *he
telo%ere is the 1tail1 o/ each chro%oso%e in your cells. 2or decades,
scientists thought that this section was +ust +un3 4non/unctional5 DN(.
6ut recent disco&eries ha&e /ound +ust the opposite. *his seg%ent o/
your DN( is critical /or healthy cell di&ision and /unction. (nd /or
healthy, youth/ul li&ing.
DN( pro&ides the te%plate /or all your proteins and en$y%es. 6ut,
the telo%ere does not code /or these. ,t acts %ore li3e the cap to your
shoelace. !ithout the cap, your shoelace would unra&el and beco%e
useless. *he telo%ere is li3e the handle o/ the chro%osone where the
DN( transcribing en$y%es attach. *hese en$y%es acti&ate gene
/unction. *hat leads to %a3ing proteins and en$y%es.
6ut, with the telo%ere, there's a proble%. 7ach ti%e your cell di&ides,
the telo%ere shortens. 7&entually, it shortens so %uch that the
chro%oso%e can't /unction. !hen this happens, the DN( coil can
/igurati&ely 1unra&el.1 ,t beco%es useless. *elo%ere length is
absolutely critical /or how your chro%oso%es beha&e 8 and how
%any ti%es the cell can di&ide. *he shorter the telo%ere, the less
gene acti&ity you ha&e.
!hen you were young your telo%eres were long. (s you age, and
your cells di&ide, all your telo%eres shorten, e-cept /or reproducti&e
cells. ,/ they shortened, we would be born 9uite old a/ter +ust a /ew
( special en$y%e called telo%erase can restore telo%eres.
*elo%erase is /ully /unctional in reproducti&e cells. Ste% cells also
ha&e signi/icant a%ounts o/ telo%erase. *hat's because they are
responsible /or replacing cells and need to di&ide /re9uently.
:owe&er, e&en their telo%erase acti&ity wanes with age. Ste% cells
get old as well.
;ost o/ your cells co%e into the world with a preset nu%ber o/
di&isions 4around <05. (s your telo%eres shorten, your cells lose their
ability to generate the en$y%es and proteins o/ youth. !hen your
telo%eres get too short, your cell beco%es senescent. *hat %eans it
no longer di&ides. ,t's old and /eeble. ,n other words, telo%ere
shortening is a %a+or 3ey to the aging process)
:ealthy telo%ere /unction 3eeps you at a healthy distance /ro%
cancer. *his is the yin and yang o/ aging. !e are not %eant to li&e
/ore&er. =ells nor%ally are not %eant to di&ide /ore&er. =ancer cells
are the e-ception. *hey ha&e /igured out a way to acti&ate telo%erase
so that they can di&ide inde/initely. ,/ we could /igure out a way to do
that with our healthy cells, it would 3eep us %ore youth/ul, while at
the sa%e ti%e, it would ward o// cancer. *he process beco%es
1unhealthy1 when, due to /actors ,'&e discussed in these pages 4such
as to-ins, stress, and bad nutrition5, your cells brea3 /ree o/ >od?
designed controls.
!ouldn't it be great i/ we could slow your telo%ere shortening
process, or acti&ate telo%erase' *he latter would lengthen your
telo%eres. !ell, there is a way.
:igher le&els o/ ho%ocysteine see% to inacti&ate telo%erase. @ou
can lower ho%ocysteine with &ita%ins 62, 6< and /olic acid. ,/ these
don't lower your ho%ocysteine, consider other %ethylating
supple%ents li3e S(;e, ;S; and betaine. *hey %ight do the +ob /or
your particular bioche%istry. #lease consult your integrati&e physician
about this.
Other supple%ents ,'&e discussed and reco%%ended in these pages
can enhance telo%erase acti&ity. >reen tea is %y /a&orite be&erage.
,t supports longer telo%eres. *hose who drin3 the e9ui&alent o/ three
cups per day ha&e telo%eres, on a&erage, /i&e years longer 4younger5
than those drin3ing only a 9uarter cup per day. @ou 3now how %uch ,
ra&e about green tea. , drin3 it al%ost e&ery day.
Aita%in D is another o/ %y reco%%ended nutrients. ,t, too, can
lengthen telo%eres. Scientists e-a%ined a group o/ wo%en aged B?
0", with an a&erage age o/ C".C. !o%en with the highest le&els o/
&ita%in D had telo%eres /i&e years longer than wo%en in the lowest
concentrations. (nd, this was a twin?based study helping to re%o&e
any genetic pre?bias to the study.
6ut there %ight be so%ething /ar %ore power/ul than any supple%ent
out there /or %odulating telo%erase acti&ity. ,t's so%ething ,'&e told
you about %any ti%es in the past. ,t's %y belo&ed o-idation therapy)
:ow and why %ight o-idation therapy induce longer telo%eres' ,t has
to do with the en$y%e SOD.
SOD 4supero-ide dis%utase5 is an antio-idant en$y%e. ,t's absolutely
critical /or protecting cells /ro% routine co%bustion o/ o-ygen, carbon,
and hydrogen. O$one sti%ulates SOD. *his protects and pro%otes
greater telo%erase acti&ity. ,n 2002, a >er%an study showed that
higher le&els o/ e-tracellular SOD slowed telo%ere shortening.
6ut that's not all. O-idation therapy also increases the nitric o-ide
4NO5 in your endothelial cells. *hese are the cells that line your
arteries. NO 3eeps your arteries dilated. (nd higher NO le&els
increase telo%erase acti&ity. ;y o$one %entor and researcher, Aelio
6occi, wrote that o$one therapy %ay acti&ate your own critical ste%
cells. :e said it induces NO synthesis. *his can pro%ote regeneration
o/ tissues su//ering /ro% a lac3 o/ o-ygen.
,'&e ta3en o-idation therapy inter%ittently throughout the years. ;y
lab and blood pressure nu%bers belie %y chronological age.
4:owe&er, , credit %y Di&ing 2oods Diet the %ost.5
!ith this in/or%ation, ,'% now ta3ing o$one on a regular basis 4at
least once a wee35, by rectal insu/lation. , could do it by ,A, but ,'&e
chosen the /or%er. Rectal insu//lation is so%ething you can do at
ho%e as well. O$one 1%odulates1 your bioche%ical processes. *hat
%eans it helps your body per/or% at its ideal le&el. Drugs don't
%odulate. *hey /orce things, which can result in terrible to-ic e//ects.
Donge&ity Resources in =anada 4B00?.CE?EE"B5 %a3es o$one water
puri/iers. 6y si%ply attaching a catheter to the o$one line, you can
direct the gas into your lower intestine rather than a /las3 o/ water.
Rectal o$one is not as potent as blood o$one therapy. 6ut, scientists
repeatedly ha&e shown its e//ecti&eness on circulation, i%%une
acti&ity, and anti?in/ection. 7&en gi&en rectally, ,'% sure its e//ects will
result in greater SOD production, su//icient to trigger %ore telo%erase
acti&ity. @ou can read %ore about using o$one at ho%e on %y
@ou also can cheaply assist telo%erase acti&ity with the /ollowing
supple%entsF *a3e @es 72(), /our to si- capsules daily in di&ided
doses. *hen ta3e seleniu% 4200?C00 %cg daily5, 3eep your
ho%ocysteine below 0 4with the a/ore%entioned supple%ents5, and
adhere to a %ostly Di&ing 2oods diet 4which is rich in SOD5. =onsider
green tea capsules 4one daily5. (nd %a3e sure your &ita%in D le&el is
in the upper 9uarter o/ your lab's re/erence range. @ou can order @es
72(), green tea capsules, and &ita%in D /ro% (d&anced
6ionutritionals 4B00?0"?EE".5.
,/ you are interested in ha&ing your white blood cell telo%eres
e&aluated, Spectracell Daboratories has a con&enient test. #lease call
B00?220?.220 to ha&e a test 3it %ailed to you and your blood drawn
in your own ho%e. No doctor's appoint%ent necessary.
, +ust did the test. ,t's &ery easy. (nd ,'% delighted to report that %y
anti?aging li/estyle wor3s. ;y telo%eres are the length o/ the a&erage
E. year old G and ,'% <0) No wonder , can al%ost 3eep up with %y
2B?year?old daughters on an arduous 0 %ile cross?country s3i trail.
Re/F =irculation Research. 2000HB0F.C0H 6r. J. Nut. 200 January
40E545H (% J. =lin Nutr. 2000, No&e%berHB<4.5H O$one, ( New
Drug, Springer 200..
Dr. Rowen is a #hi 6eta Iappa graduate o/ Johns :op3ins Jni&ersity
and the Jni&ersity o/ =ali/ornia at San 2rancisco. :e has been board
certi/ied and recerti/ied by the (%erican 6oards o/ 2a%ily #ractice
and 7%ergency ;edicine. :e is currently certi/ied by the (%erican
6oard o/ =linical ;etal *o-icology. :e also ser&ed on the (las3a
State ;edical 6oard.
Dr. Rowen is 3nown as 1*he 2ather o/ ;edical 2reedo%1 /or
pioneering the nation's /irst statutory protection /or alternati&e
%edicine in ""0.
Dr. Rowen also edits Second Opinion, an alternati&e %edicine
newsletter. :e /ocuses on big brea3throughs that really wor3, o/ten
years be/ore they're co&ered anywhere else. *o subscribe, &isit the
Second Opinion newsletter web site or call B00?0"?ECC.. ,/ you are
interested in a personal phone consultation with Dr. Rowen, please
call his ad%inistrati&e o//ice in =ali/ornia at 000?.0B?00B0 40F00 a.%.
8 EF00 p.%. #S*, ;on?*hurs.5 /or a schedule and rates.
Telomeres and Telomerase in Antiaging
S*7#:7N :OD* ;D, Distinguished #ro/essor o/ ;edicine 47%erite5,
Scienti/ic (d&isor, Natural =linician DD= and
*he 6asics
*elo%eres are DN( caps on linear chro%oso%es that /unction to
pre&ent aberration or loss genetic in/or%ation during cell di&ision.
*hese Kprotecti&e regions” o/ DN( shorten with repeated cell di&ision
in so%atic cells. *he en$y%e telo%erase 4a re&erse transcriptase5
acts to e-tend telo%eres and reduce their attrition.
Shortened telo%eres %ay reach a point where they cannot support
nor%al di&ision o/ chro%oso%es, resulting in cell senescence
4replicati&e arrest5 and abnor%al chro%oso%al /unction. *hese
changes can result in altered or loss o/ nor%al /unctions o/ genes,
cancer propagation, i%%une dys/unction, aging o/ tissues and the
e%ergence o/ chronic disease.
,/ telo%ere shortening correlates with age and telo%erase can sustain
or lengthen telo%ere, then si%ple logic dictates that inter&entions to
%odulate the telo%ereLtelo%erase Kduo” present a pro%ising and
no&el strategy /or anti?aging or disease pre&ention or treat%ent.
!hile ta%pering with telo%eres and telo%erase enchant %any
scientists and clinicians, %atters are not 9uite as si%ple as so%e
indi&iduals %ay ha&e hitherto supposed.
Obser&ations on *elo%ere *a%pering
*elo%ere length and telo%erase e-pression appear to be lin3ed in
%any, but not all studied species o/ li/e. !hile telo%eres shorten with
age, so%e people start with longer telo%eres than others. Shortened
telo%eres tend to Kpush” a cell towards senescence prior to apoptosis
4cell death5.
*elo%erase acti&ity %ay lengthen telo%eres, but this en$y%e is /ound
to be e-pressed pre/erentially in cancer, certain ger% cells and ste%
cells 4i%%ortal cells5. *his lea&es an unanswered 9uestion Kwill direct
telo%erase induction lead to cancer'” !e 3now relati&ely little about
selecti&e telo%erase enhancers, *his selecti&e approach /or telo%ere support is an
i%portant target /or phar%aceutical or nutraceutical de&elop%ent as
the potential longe&ity pro%oting properties o/ telo%ere support
Shortened telo%eres e-ert a Ktelo%ere position e//ect” which alters
genetic e-pressions at the cellular le&el. ,n this circu%stance, DN(
repair genes do not e-ert opti%u% /unction and those genes that
pro%ote cellular aging %ay e%erge. *he aging cell with its shortened
telo%ere, see%s to lead to a circu%stance that /acilitates or /a&ors
%ista3es. :owe&er, one %ust pause and thin3 about the induction o/
cellular senescence with age as a potential de/ense %echanis%
against the occurrence o/ age?related cancer. Senescence and
apoptosis ser&e both aging and disease pre&ention options. *he gene
that regulates telo%erase e-pression is Ksilenced” in healthy cells.
KSwitching on” or Kswitching o//” this gene, to a &ariable degree, in
possible by genetic %anipulations and the ad%inistration o/ certain
*elo%ere loss or co%pro%ise is not consistently shown to be
telo%erase dependent and it %ay not always show a linear
relationship with ad&ancing years. 2or e-a%ple, loss o/ telo%ere
length is accelerated in childhood 4up to the age o/ 20 years5 and
%anage%ent in the elderly 4greater than <. years5. !hile telo%erase
is not e-pressed in %ost so%atic cells, so%e cells 4e-panding
i%%unocytes, ger% cells and cancer cells5 e-press high le&els o/
telo%erase. Does telo%erae shortening in laboratory tests o/ white
blood cells 4*?ly%phocytes5 %irror telo%ere shortening in other cell
*elo%eres loss is associated with sedentary li/estyles, o-idati&e
stress, cancer, insulin resistance and chronic in/la%%atory diseaseM
to na%e a /ew disorders, but so%e degree o/ Kchic3en and egg”
argu%ents pre&ail. *o add to the conundru%, laboratory studies o/
ger%inal centers, that produce 6 cells 4ly%phocytes5, show that
telo%ese length that can increase, in spite o/ intense cell replication.
2urther%ore, so%e studies i%ply that telo%ere loss %ay not always
e-hibit a clear correlation with certain cells history o/ replicati&e
acti&ity. *hese /actors, and other concerns, %ay 9uestion the
sensiti&ity and speci/icity o/ so%e %easures o/ telo%ere length as a
reliable %easure%ent o/ physiological age.
*he telo%ereLtelo%erase literature is replete with pro%ises o/ the
potential bene/it o/ targeted therapeutic inter&entions. !hile no
phar%aceutical is appro&ed /or telo%ere %odulation, natural
approaches are e%erging with the use o/ speci/ic dietary
supple%ents 4e.g. (stragalus e-tracts5. !hile this long ter% sa/ety or
e//icacy o/ nutraceutical inter&entions /or telo%ere support re%ain
un3nown, the desirability o/ telo%ere retention or lengthening
strategies are so appealing that the use o/ sa/e and si%ple strategies
to achie&e this outco%e see%s to be a reasonable inter&ention.
=linical *elo%ere Support
#rocesses that %ay increase loss o/ net telo%ere length or rebuilding
o/ a shortened telo%ere 4*able 5. Se&eral /actors act to shorten
telo%ere length and so%e are a%enable to corrections are shown in
*able .
*able .
2(=*OR =O;;7N*
>ender *end to be longer in wo%en
(ge =hildren ha&e longer telo%eres
(ge o/ parents Older parents %ay de&iate shorter telo%eres to their
o//spring 4e.g. Dolly the sheep5
Sedentary li/estylesN 7-ercise tends to cause retained telo%ere
=hronic ,n/la%%ationN =lear e&idence e.g. rheu%atoid disease
O-idati&e StressN 7%erging studies on antio-idants /or retention o/
;enopause and (ndropauseN #redictable loss o/ telo%ere length with
%ilestones o/ aging. :or%one dependency o/ telo%ere length
*elo%eraseN (cti&ity can be induced
,nsulin resistanceN 7%erging association with telo%ere shortening.
;etabolic Syndro%e O and *ype 2 Diabetes are clearly a disorder o/
pre%ature aging.
*able. 2actors that alter telo%ere length. *he asteris3 4N5 denotes
so%ewhat a%enable to inter&ention
A Telomere Support Protocol
Research data and clinical outco%e obser&ations per%it the
reco%%endation o/ a clinical protocol /or telo%ere support 4*able 2.5.
*he e-istence o/ other Knatural protocols” /or telo%ere lengthening
4e.g. the #atton #rotocol, %ay be superseded
by a %ore co%prehensi&e approach to telo%ere support and age
%anage%ent. *his proposed protocol /or the natural clinician is best
su%%ari$ed in line ite% state%entsF
P Di/estyle =hange ;any positi&e li/estyle changes %ay inhibit
telo%ere shortening. *hese include opti%u% nutrition, weight control,
stress reduction, withdrawal o/ substances o/ abuse 4si%ple sugar,
tobacco, alcohol, unnecessary prescription or o&er the counter or
illicit drugs5 and the restoration o/ nor%al sleep patterns.4*able .5
P Dietary Supple%ents ( nu%ber o/ nutraceutical are associated with
supporting telo%ere structure and /unction including, speci/icallyF
e-tracts o/ >ing3o biloba, (stragalus, =hinese >inger root, &ita%in D,
/olic acid 4and perhaps Aita%in 625, nicotina%ide and o%ega E /atty
acids 4*able 2.5. Studies i%ply that ta3ing %ulti&ita%in and or
antio-idant use %ay be associated with enhanced telo%ere length or
inter/erence with telo%ere shortening. 7le&ated le&els o/ blood
ho%ocysteine should be addressed 42olic acid, Aita%in 62 etc.5.
NTRA!"T#!A$ "%#D"N!"&'AS"&()R
(stragalosides 4cycloastragenol5 or the speci/ic %olecule *(?<. are
proposed as telo%eres. ( clinical trial that showed i%pro&e%ents in
i%%une /unction, eyesight, se-ual /unction and s3in color
characteristics. 4Re&iewed at *( accessed 2ebruary <,
)mega * (atty Acids ,n a group o/ patients with coronary heart
disease there was a in&erse relationship between blood le&els o/
%arine o%ega E /atty acids and telo%ere shortening o&er a /i&e?year
inter&al. 4Rai%in 2, et al, J(;(, E0E, 2.0?2.0, 2005
*he rate o/ telo%ere shortening is %odulated by o-idati&e stress
4certain in &itro5 4Saret$3i >, Aon Qglinic3i, *, (nn N@ (cad Sci, ".",
2C?", 20025. 6reast cancer ris3 %ay be a//ected by telo%ere length in
wo%en with low inta3e o/ antio-idants or antio-idant supple%ents
4 Shen J et al, ,nt. J. =ancer, 2C, <E0?CE, 200"5
%itamin D ,igher %itamin D concentrate in seru% are associated
with longer telo%ere length 4Richards J6 et al, (%. J. =lin. Nutr., B<,
., C20?C2., 20005
(olate-'./ (olate status alters telo%ere length in a non?linear
%anner probably by its e//ects on the integrity o/ DN( and epigenetic
in/luences 4=attaneo #D, et al, J Nutr., E", 0, 20E?20B, 200"5
#las%a ho%ocysteine ele&ation due to /olate and &ita%in 62
de/iciency is associated with decreased telo%ere length in older
%ales 46ull =2 et al, Re+u&enation R. Sep. 2B, 200"5
Nicotinamide Nicotina%ide e-tends the li/espan o/ hu%an /ibroblasts
as a presu%ed conse9uence o/ reduce %itochondrial production o/
reacti&e o-ygen species 4Iang :* et al, (ging =ell, ., C2E?E<, 200<5
Multivitamins 7pide%iological e&idence associates %ulti&ita%in use
with longer telo%ere length 4Ou, R et al, (% J =lin Nutr. B", <, B.0?
<E, 200"5
!hinese 0inger Root 7&idence is e%erging that ginger root %ay
support telo%erase lengthening and ha&e other bene/icial actions.
Alpha&tocopherol De%onstrated to inhibit telo%ere shortening and
retain telo%erase acti&ity in %icro&ascular endothelial cells in the
brain. 4*ana3a @ et al, J. =ell 6ioche%, 02, E, <B"?00E, 20005
N&acetylcysteine N?acetylcysteine bloc3s the nuclear e-port o/ h
*7R* into cell cytoplas% and sdelays replicati&e senescence o/
endothelial cells that are attracted by reacti&e o-ygen species
4:aendeler J, et al =linc. Res, "C, 0<B?00., 200C5
Statins *reat%ent with statins increases ly%phocyte telo%ere length
46rouillette S! et al, Dancet, E", 00?C, 20005 Statins inter/ere with
redo- balance o/ endothelial cells 4:aendeler J et al, =lin Res, "C,
0<B?00., 200C5 and 4Spyridopolens ,, et al circulation, 0, EE<?
EC2, 200C5
0ing1o 2ilo2a 7-tracts o/ >ing3o biloba e-tracts ha&e been show to
delay the onset o/ cellular senescence by acti&ating #E3L(3t
signaling pathways that aug%ent telo%erase acti&ity 4Ou D et al, D O
et al, J =ardio&asc. #har%acol, C?",?., 20005.
*able 2. (n e%erging e&idence base /or nutraceuticals that support
the structure and /unction o/ telo%eres.
Dietary supple%entation is not a substitute /or speci/ic dietary
guidelines in the 9uest /or telo%ere support. ,n brie/, the anti?aging,
telo%ere supporting diet should in&ol&eF
P Reductions in si%ple carbohydrate inta3e with increase in dietary
/iber inta3e 4to counter insulin resistance5.
P Nutrient dense /ood selections that are low in calories. =alorie
restriction enhances %a-i%u% and a&erage li/espan and this process
%ay be enhanced by the use o/ calorie restriction %ionetic
P :igh antio-idant load in a diet rich in /ruit and &egetables.
;ulti&ita%ins ta3en in greens, berries, /ruit and &egetable %i-es are a
pre/erred /or% o/ general nutritional support. #hytonutrients are
&ita%in co?/actors and pro&ide an antio-idant /ood.
P 7nrich sources o/ o%ega E /atty acids in acti&e /or%s e.g. cold
water, /ish, sal%on etc.
P Decreased sources o/ saturated /at, hydrogenated oils and trans?
/atty acids.
P (&erage balance protein inta3e with rotation a%ong %eat, dairy,
&egetable and /ish protein sources 4not greater than g%L3g o/ body
weight per day, unless otherwise indicated5.
P ,nter%ittent short periods o/ /asting and %ethods /or body
deto-i/ication 4dietary and otherwise5 %ay support telo%ere structure
and /unction.
P Disease ;anage%ent ( clear association e-ists between co%%on
diseases 4cancer and degenerati&e diseases5 and shortening o/
telo%ere length e.g. cardio&ascular disease 4altherosclerosis5,
hypertension, insulin resistance 4;etabolic Syndro%e O5, diabetes
%ellitus and diseases associated with cogniti&e decline 4de%entia5.
;eticulous %anage%ent o/ co?%orbid conditions is obligatory.
;etabolic Syndro%e O and diabetes are classic disorders o/
pre%ature aging.
P ?;iscellaneous 2actors 7&ery atte%pt should be %ade to tac3le the
/ollowing issues with appropriate %edical inter&entionsF. (tte%pts to
eli%inate coronary heart disease and atherosclerosis ris3 /actors
%ust be applied e.g. reduce DDD 4target S"0 %gTU, reduce o-idi$ed
and dense particle si$e DDD, increase :DD. =ontrol blood glucose
4i%portant in both established and pre?diabetes or ;etabolic
Syndro%e O5, control blood pressure, 3eep blood ho%ocysteine in
chec3, reduced chronic in/la%%ation 4%onitor =?Reacti&e #rotein,
%aintain :S?=R#S.
,nstitute an e-ercise progra% is obligatory, lin3ed to le&els o/ aerobic
/itness 4pro/essional trainers reco%%ended5. =ontrol o/ weight with
holistic inter&entions o/ diet, e-ercise, beha&ior %odi/ication and
supple%ent ad+uncts are %andatory. ,nter&entions that support ste%
cell /unctions, increase nitric o-ide signaling, i%pro&e %itochondrial
/unction, deto-i/y the body and opti%i$e hor%onal controls 4e.g. bio?
identical hor%one therapy5 %ay be &aluable ad+uncti&e approaches to
telo%ere support.
,n %y educational colu%ns on natural therapeutics, , ha&e /ocused on
three &ery i%portant issues in anti?aging or regenerati&e %edicine.
*hese areas include ste% cell support, the use o/ calorie restriction
%i%etics and support /or telo%ere structure and /unction 4*he (nti?
(ging *rilogy5. , belie&e that these three areas o/ longe&ity %edicine
interdigitate in a %anner that creates the %ost i%portant and
pro%ising /rontier /or Kturning bac3 the cloc3” in the /ield o/ aging
%edicine. *his article is abstracted /ro% Dr3 ,olt4s new 2oo1
entitled the Anti&Aging Trilogy 5www3hiom3org6

Docated at the tips o/ each o/ our C< chro%oso%es, telo%eres help
protect DN( and are particularly i%portant during cell di&ision.
*elo%eres ha&e recei&ed a lot o/ notoriety due to their relationship
with aging. *hese protecti&e structures shorten with each cell
di&ision, e-posing DN( to potential danger. ,n ti%e, telo%eres get too
short to shield DN(. *hatWs when cells stop wor3ing, /unction poorly
or, e&en worse, de&elop disease.
*hereWs a lot o/ research being conducted on ways to preser&e
telo%eres. ;uch o/ this wor3 /ocuses on telo%erase, an en$y%e that
helps rebuild telo%eres a/ter cell di&ision. So%e researchers propose
that boosting telo%erase %ay be a way to preser&e telo%ere /unction
and increase longe&ity and health. :owe&er, thereWs another side to
the coinF *oo %uch telo%erase acti&ity %ay be associated with
cancer /or%ation, because it allows cells to replicate uncontrollably.
6ut other studies debun3 this lin3.
!hat researchers are suggesting o&erall is that healthy telo%ere
/unction, li3e so %any other co%ple- syste%s in the body, re9uires a
care/ul balance. 2urther%ore, itWs beco%ing clear that telo%ere
/unction is in/luenced by nu%erous en&iron%ental and li/estyle /actors
and that shortened telo%eres can lead to a nu%ber o/ chronic,
degenerati&e diseases. Ob&iously, %ore research is needed, but data
suggests that preser&ing telo%ere health can play a role in
%aintaining long?ter% &itality.
Ris3y 6usiness
*elo%eres can be pre%aturely shortened by %any /actors.
7n&iron%ental to-ins, stress, s%o3ing and an unhealthy diet play a
part. Shortened telo%eres ha&e been lin3ed to cancer, heart disease,
in/la%%ation, insulin resistance, osteoarthritis, obesity and de%entia.
,tWs not entirely clear whether shortened telo%eres are causing these
conditions. Still, thereWs ob&iously a relationship. ( study conducted at
the Jni&ersity o/ Jtah /ound that people with shorter telo%eres ha&e
a shorter li/e e-pectancy. ,n particular, they see%ed to be susceptible
to heart disease and in/ections. ( %ore co%prehensi&e study
conducted in Den%ar3 showed that reduced length increases the
chance o/ pre%ature death by 2. percent.
*a3ing (ction
#reser&ing telo%eres is not a %agic health bullet. ,/ we eat poorly,
s%o3e, drin3 hea&ily and neglect e-ercise, thereWs no a%ount o/
telo%ere support that will guarantee protection.
On the other hand, i/ we de&elop a healthy li/estyle and control 3nown
disease %ar3ers, li3e blood pressure and chronic in/la%%ation,
supporting telo%ere length can co%ple%ent these e//orts.
(s always, the starting point is diet and e-ercise. 7at plenty o/ /ruits
and &egetables, drin3 lots o/ /iltered water, and choose lean proteins
and healthy /ats. (dopt a sustainable e-ercise progra%F bris3, E0?
%inute wal3s pro&ide e-cellent cardio&ascular support.
DonWt /orget stress reduction. *here are a nu%ber o/ studies lin3ing
stress to shortened telo%eres. (gain, weWre not sure whether this is
cause or e//ect, but it hardly %atters. 7e 1now that stress releases
the hormone cortisol and can cause chronic in8lammation along
with other degenerative e88ects3 )n the other hand9 a study 8rom
researchers in !ali8ornia 8ound that positive 8eelings9 such as
those produced 2y meditation9 seem to activate telomerase3
They also 8ound that people who sustained :good 8eelings; had
healthier telomeres3
,n other words, we should adopt acti&ities that 9uiet the %ind and
help center us. ;editation, yoga, *ai =hi, wal3ing in nature or
swi%%ing a /ew laps in the pool can all be bene/icial.
,%portant Supple%ents
*here are a wide &ariety o/ herbs and nutrients that ha&e been lin3ed
to healthy telo%eres. (stragalus has been used /or centuries in
traditional %edicines. Recent research has shown that (stragalus
boosts i%%une /unction. (t present, at least two phar%aceutical
co%panies are /ocusing on this herbWs potential to preser&e
Aita%ins also see% to play a role. Se&eral &ita%ins, speci/ically
&ita%in D, appear to boost telo%ere length. (ntio-idants, which can
be /ound in &ita%ins and other sources, are also i%portant. O-idati&e
stress is lin3ed with shortened telo%eresH ar%ing the body against
this pro?in/la%%atory process is always bene/icial3
Dong touted /or its ability to boost heart and cogniti&e /unction,
o%ega?E /atty acids ha&e also been lin3ed with telo%ere length. ,n
one study, lower o%ega?E le&els in the bloodstrea% were associated
with accelerated telo%ere shortening.
(s noted, en&iron%ental to-ins such as hea&y %etals %ay play a
signi/icant role, as well as being har%/ul to health in other ways.
*here are a couple o/ supple%ent /or%ulas , reco%%end to help the
body re%o&e these pollutants. ( co%prehensi&e, botanical
deto-i/ication /or%ula containing &ita%ins, %inerals, astragalus,
ging3o, antio-idants and other botanicals helps rid the body o/ to-ins
and %ay preser&e telo%ere health.
, also reco%%end %odi/ied citrus pectin 4;=#5, which has long been
used to re%o&e hea&y %etals and other to-ins. ,n addition, ;=#
helps reduce le&els o/ an in/la%%atory protein o/ten associated with
cardio&ascular disease and cancer.
*his is by no %eans the /inal word on telo%eres. New research will
/urther illu%inate these 3ey structures, helping to guide our e//orts to
preser&e long?ter% health. ;eanwhile, a si%ple co%%on?sense
approach that includes a healthy diet, e-ercise, stress reduction and
/ocused supple%entation can go a long way toward preser&ing
telo%eres and pro%oting health and longe&ity.
Turning on #mmortality: The De2ate )ver
Telomerase Activation
6y !illia% (ndrews, #hD and ;ichael !est, #hD
*urning on ,%%ortalityF *he Debate O&er *elo%erase (cti&ation
*he role o/ telo%erase in allowing the i%%ortal growth o/
reproducti&e cells is well established in the scienti/ic literature.
,n the laboratory dish, the introduction o/ telo%erase into cultured
hu%an cells trans/or%s otherwise aging %ortal cells into i%%ortal
cells without trans/or%ing the% into cancer cells. On the heels o/ this
disco&ery, s%all %olecule acti&ators o/ telo%erase are being
de&eloped /or use in treating cellular aging and at least one nutritional
supple%ent is being %ar3eted /or the treat%ent o/ aging.
Do these co%pounds really wor3 and are they sa/e' *hat is the
9uestion that was posed to two leaders in the /ield3
(rguing in /a&or o/ the %ar3eting o/ telo%erase acti&ators /or
nutritional use is !illia% :. (ndrews, #hD, president X =7O, Sierra
Sciences, who pre&iously was director o/ %olecular biology at >eron
=orporation where the telo%erase genes were /irst isolated.
*a3ing the opposing position is ;ichael D. !est, #hD, who was the
/ounder o/ >eron =orporation, and is currently the =7O o/ 6io*i%e,
,nc, which /ocuses on the ste% cell biology and the resetting o/ cell
li/e span by cellular reprogra%%ing.
Jntil %ore hu%an data are co%piled, the Di/e 7-tension 2oundationY
does not ha&e a position, one way or another, on the use o/ this
particular telo%ere?e-tending therapy. *he in/or%ation /or this article
is written by two highly respected scientists. So%e %e%bers %ay /ind
this %aterial technically challenging to co%prehend.
Dr. (ndrews !rites in 2a&or o/ M
*here is now co%pelling e&idence that the length o/ a personWs li/e
span is dictated by the li%ited nu%ber o/ ti%es a hu%an cell can
di&ide. *hough the i%%ortal reproducti&e cell can di&ide a li%itless
nu%ber o/ ti%es, once the hu%an reproducti&e cell, in the de&eloping
e%bryo, turns into a de&elop%ental cell the cloc3 starts tic3ing and
the cellWs /ate is doo%ed to a li%ited 0.?00 nu%ber o/ cell di&isions
4the :ay/lic3 Di%it5. Once that li%it has been reached, the cell and all
o/ its progeny co%pletely lose the ability to di&ide and then enter a
phase called senescence.
*he tic3ing cloc3 in this case is /ound at the tips o/ the cellWs
chro%oso%es in a region called the telo%ere. ,t is belie&ed that
telo%eres %ay ha&e e&ol&ed to pre&ent the unli%ited growth o/ cells
by li%iting their li/e span. *elo%eres are %ade up o/ subunits 4or
bases5 o/ DN( called (, =, >, and *. ,n the telo%ere, these bases are
arranged in si- base repeat units o/ **(>>>. !hen a hu%an is /irst
concei&ed, the length o/ the telo%eres a&erages about .,000 bases
4up to 2,.00 **(>>> repeat units5 as %easured by a process called
ter%inal restriction /rag%ent length analysis. *he length then begins
to decrease at a rate o/ about 00 bases per cell di&ision. 6y the ti%e
a person is born, the a&erage telo%ere length has already dwindled
to about 0,000 bases and then throughout the rest o/ a personWs
li/eti%e the a&erage length o/ the telo%eres gradually decreases to
about .,000 bases at which ti%e the personWs cells lose the ability to
di&ide. *hese cells are then senescent, and the person su//ers and
dies o/ old age.
Dr. (ndrews !rites in 2a&or o/ M
*elo%eresF a region o/ highly repetiti&e DN( at the end o/ a linear
chro%oso%e that /unctions as a disposable bu//er.
Aery recently, re%edies ha&e been de&eloped that could possibly
alle&iate, abolish, or re&erse this Kup to now” ine&itable /ate by
acti&ating an en$y%e called telo%erase, which %ay help %aintain
telo%ere length. One such re%edy, a nutraceutical called *(?<., is
already co%%ercially a&ailable and se&eral people ha&e already
signed up to bene/it /ro% its potential to e-tend health span and li/e
span. Jn/ortunately, this re%edy also carries with it a potential /or
pro%oting cancer. (nd so, we are brought bac3 to the age?old
9uestion, KDo you gi&e a ris3y cure to a dying person, or do you
si%ply let the person die because the cure is too ris3y'” 7&ery one o/
us is su//ering /ro% this disease, but %ost o/ us are in only the &ery
early stages and ha&e the lu-ury not to %a3e this choice so hurriedly.
:owe&er, %any o/ the people in the later stages o/ aging /eel that
they donWt ha&e this lu-ury and choosing to ta3e *(?<. %ay be what
they /eel to be their only recourse to Ksa&ing” their li&es. Should these
people be depri&ed' Should they be allowed to intentionally increase
their ris3 o/ cancer to potentially enhance and prolong their health
span and li/e span' !e should let people who are concerned about
their age?related deterioration, whether or not in the later stages o/
aging, decide /or the%sel&es.
*(?<. is presently the only potential cure /or telo%ere shortening and
there wonWt be another one /or a long ti%e co%ing. *hough the data
are not o&erwhel%ing enough yet to con&ince scientists that *(?<. is,
in /act, e-tending health span and li/e span, they do show a lot o/
pro%ise and are supported on %any theoretical grounds. Di3ewise, as
stated abo&e, there are also a lot o/ theoretical grounds /or *(?<.
increasing the chances that the person will be a//licted with cancer.
(bout B.?".T o/ all cancers e-press telo%erase acti&ity 4but
telo%erase acti&ity doesnZt pro&e solely the e-istence o/ a cancer5.
;any research labs are wor3ing &ery hard to de&elop inhibitors o/
telo%erase acti&ity to cure cancer. So, one %ight thin3 that we %ust
be out o/ our %inds to now want to intentionally turn telo%erase
acti&ity on. 6ut, the data show that telo%erase is, in /act, not the
cause o/ cancer. ,nstead, cancers turn on telo%erase e-pression only
to e-tend their li/e spanH +ust li3e we want to turn on telo%erase
e-pression in our non?cancer cells to e-tend their li/e span. So, weW&e
learned a lesson /ro% cancer cells on how to e-tend cellular li/e span.
6ut, true cancer cells already ha&e telo%erase acti&ity. >i&ing
so%eone a telo%erase inducer isnWt going to %a3e an i%%ortal
cancer %ore i%%ortal. So, itWs not actually the true cancers we are
concerned about. *he cancers that are really at issue here are the
pre?i%%ortal cancersH that is, the cells that ha&e lost growth control
but that donWt e-press telo%erase acti&ity or so%e other i%%ortal
pathway 4such as the (D* [alternati&e lengthening o/ telo%eres\
2ortunately, *(?<. is a transient inducer o/ telo%erase acti&ity.
=essation o/ ta3ing *(?<. will shut down the e-pression o/
telo%erase acti&ity in cells, including the pre?i%%ortal cancer cells,
thus pro&iding opportunities to still treat the pre?i%%ortal cancer cells.
*hough, on one hand, the ris3 o/ cancer has still been ele&ated
because o/ the e-tended telo%ere lengths, there are also strong
reasons to belie&e that the longer telo%eres ha&e also signi/icantly
reduced the cancer ris3sH especially in the people su//ering /ro% later
stages o/ aging. *hat is, short telo%eres %ay actually be one o/ the
%a+or causes o/ cancer. !hen telo%eres are short, they ha&e a
higher propensity to induce chro%oso%e rearrange%ents. *his can
lead to aberrant e-pression o/ oncogenes and aberrant repression o/
tu%or suppressor genes. ,n addition, our i%%une cells show
decreased abilities to target and destroy cancer cells when telo%eres
are short. Ieeping telo%eres long should there/ore decrease the
incidence o/ cancer and help our i%%une syste%s to /ight cancer. ,tWs
hard to 3now i/ the Kpros” outweigh the Kcons” when considering the
cancer issues. *he lac3 o/ a good ani%al %odel that ages by
telo%ere shortening %a3es these issues al%ost untestable. So, at
this ti%e we can only speculate.
,n the %eanti%e, people are aging, and people are dying o/ old age.
;any cancer sur&i&ors will tell you that cancer is a /ate worse than
death. ;any elderly people will tell you that su//ering old age is a /ate
worse than death. *here is little doubt that the potential /or increased
ris3 o/ cancer due to *(?<. is real. 6ut the potential /or increased ris3
o/ su//ering /ro% old age due to not ta3ing *(?<. is %ore real.
Dr. !est !rites (gainstM
Recent ad&ances in %olecular and cell biology ha&e allowed
spectacular progress in our understanding o/ the %olecular
%achinery o/ hu%an aging. !ith this new in/or%ation co%e insights
into how that cloc3wor3 can be %odi/ied to slow or e&en re&erse
&arious /acets o/ hu%an aging. *he disco&ery o/ the telo%erase gene
as a central regulator o/ replicati&e i%%ortality and the K3ey” that
winds and sets the length o/ telo%eres 4and hence cell replicati&e li/e
span5 in hu%an cells has led to great opti%is% about the prospects o/
turning on the gene in the body to e-tend telo%eres and potentially
hu%an li/e span.
;any scientists belie&e that the reason telo%erase, and hence
cellular i%%ortality, is repressed in the %a+ority o/ cells in the body
while being le/t on in the reproducti&e cells is that this allows the
hu%an species to continue inde/initely, while repressing the unli%ited
growth o/ cells in the process o/ cancer /or%ation. *his conclusion is
based in part on the obser&ation that appro-i%ately "0T o/ hu%an
%alignant tu%ors show the abnor%al e-pression o/ telo%erase
co%pared with nor%al tissues.
The events initiated 2y telomere shortening
;iguel >odinho 2erreira in&estigates
*elo%eres, regions o/ DN( at the tips o/ chro%oso%es that protect
against the loss or garbling o/ &ital genetic in/or%ation. *elo%eres
per/or% this protecti&e /unction through sel/?sacri/ice, gi&ing up bits o/
the%sel&es each ti%e the cell di&ides, beco%ing shorter and shorter
until they are too s%all to do their +ob. *his /inal loss o/ /unction has
been lin3ed to the deterioration and death o/ cells that occurs as we
grow older and %ay underlie the in/ir%ities o/ old age.
(n en$y%e called telo%erase pre&ents telo%ere shortening by
adding bac3 seg%ents to telo%ere ends. 6ut while this en$y%e plays
a /unda%ental role in single?celled organis%s that di&ide inde/initely,
it is absent /ro% %ost types o/ hu%an cells. *hat %ay not be such a
bad thing. ,n "0 percent o/ cancers analy$ed to date, telo%erase is
acti&e, suggesting that the en$y%e helps cancer cells di&ide
uncontrollably, a 3ey /actor in %alignancy.
Since establishing his *elo%ere and >eno%ic Stability Daboratory at
the >ulben3ian Science ,nstitute 4,nstituto >ulben3ian de =i]ncia5 in
200<, >odinho 2erreira has concentrated on understanding the
%olecular %echanis%s that underlie telo%ere protection. K,W&e been
trying to /igure out how cells cap chro%oso%e endsGthe
%echanis%s by which they pre&ent short or da%aged telo%eres,”
>odinho 2erreira e-plains. #re&iously, he studied /ission yeast, a
single?celled organis% whose chro%oso%es are re%ar3ably si%ilar
to those o/ hu%ans. Now he wants to e-pand his studies to a
%ulticellular organis%, the $ebra/ish, which, li3e hu%ans and /ission
yeast, has telo%eres that shorten with age.
*wo %ain $ebra/ish pro+ects are ta3ing shape in his lab. ,n one, his
group is using a $ebra/ish %odel o/ %elano%a to /ind out whether the
cancer can be controlled by inhibiting telo%erase and, i/ so, e-actly
when tu%ors are %ost susceptible to antitelo%erase treat%ent.
,n the other line o/ wor3, >odinho 2erreiraWs lab is in&estigating
whether telo%ere shortening a//ects only the cell in which it occurs or
i/ that cell also signals neighboring cells with the %essage, K:ey,
none o/ us is getting any younger, you 3now)”
K*he idea is that there %ay be ^sentinel organsW that send signals to
the rest o/ the body so that aging is a coordinated e&ent in the whole
organis%,” >odinho 2erreira e-plains.
Telomerase Therapies in our (uture
*elo%ere biology has the potential to e-tend hu%an li/e span, to
dra%atically lower rates o/ the great re%aining 3iller diseasesF heart
disease, stro3e, and (l$hei%erWs. (ll three diseases increase
e-ponentially with age, and their toll will be slashed as we we learn
how to address the bodyWs aging cloc3s.
@ou would thin3 that the 200" Nobel #ri$e %ight ha&e done %ore to
raise the pro/ile o/ research in telo%ere biology, but the /ield re%ains
a speciali$ed bac3water o/ %edical research, and /ew biologists
4/ewer doctors5 ta3e it seriously as a panacea /or the diseases o/ old
age. ,/ the National ,nstitute o/ :ealth has %oney to put into heart
disease and cancer and (l$hei%erWs and #ar3insonWs diseases, there
is no better place to in&est than in telo%ere biology. Research on
these diseases co%%ands %ulti?billion dollar budgets, because they
are considered K%edicine”, /unded by N,:, while telo%ere biology is
considered Kscience” and is /unded by NS2. *he total NS2 budget /or
all cell biology is only _2E %illion, and the portion de&oted to
telo%ere biology is a /ew %illion. *he pri&ate sector is doing a little
better 8 there are se&eral co%panies selling herbs that sti%ulate our
own bodies to liberate telo%erase. 6ut this is short?sighted &enture
capital, and what we need is /ocused research with a ten?year &ision.
*here is good reason to thin3 that telo%ere length is a pri%ary aging
cloc3 in the hu%an body. *he body 3nows per/ectly well how to
lengthen telo%eres, but chooses not to. (ll we ha&e to do is to signal
the body to acti&ate the telo%erase genes that are already present in
e&ery cell. O/ course, there is no guarantee that this will wor3, but
co%pared to the sluggish rate o/ progress on indi&idual diseases, itWs
a pretty good bet, and the target is rather si%ple. ,;:O, itWs worth a
crash research e//ort.
Ob+ections raised against telo%erase research
. K(ging is ine&itable because #hysics tell us that nothing can last
/ore&er.” *his state%ent re/ers to the Second Daw o/
*her%odyna%ics, which says that closed syste%s, e&ol&ing in
isolation, %ust beco%e %ore disordered o&er ti%e. 6ut li&ing
syste%s are open, ta3ing in /ree energy in the /or% o/ /ood or
sunlight, du%ping their entropy out into the en&iron%ent. *here is no
reason that such syste%s cannot %aintain the%sel&es inde/initely.
,ndeed, growth and %aturation would not be possible i/ this law o/
physics applied to open ther%odyna%ic syste%s. Since the "th
=entury when the laws o/ ther%odyna%ics were /or%ulated, it has
been understood that aging cannot be e-plained /ro% physics, and
there/ore co%%ands an e-planation /ro% e&olution.
2. K7&olution has been wor3ing to %a-i%i$e ani%al li/e spans in order
to increase /itness. ,t is unli3ely that any si%ple ad+ust%ent to
physiology that hu%ans can disco&er will do better than e&olution has
done o&er %illions o/ years.” ,n /act, e&olution has not wor3ed to
%a-i%i$e li/e span, but only to %a3e it su//icient to assure ti%e /or
reproduction. (ging is a /or% o/ progra%%ed death, on a /le-ible but
/inite schedule. ,t is /i-ed in our genes. *here are %echanis%s o/
aging that ha&e been progra%%ed into li&ing things since the /irst
eu3aryotic cells. *elo%ere attrition has been used to ti%e the li/e
cycle and /or% a basis /or progra%%ed death /or at least a billion
years. ;any species o/ proto$oans do not e-press telo%erase during
%itosis 4but only during con+ugation5, so their telo%eres shorten with
each reproduction, leading to a li%it o/ a /ew hundred reproductions
per cell line. *his %echanis% is the precursor to telo%eric aging that
e-ists to the present day in hu%ans and %any other higher ani%als.
E. K7-pressing telo%erase will increase the ris3 o/ cancer.” *here is a
great deal o/ theoretical concern in this direction, which , thin3 is
entirely %isguided. ,t is true that cancer cells e-press telo%erase. ,t
is not true that e-pressing telo%erase causes a cell to beco%e
cancerous. *his relationship is clearly e-plained by two seasoned
e-perts 4Shay and !right 205
,n early studies, the only way o/ increasing telo%erase acti&ity in lab
ani%als was to add e-tra genes /or telo%erase. *echnology in the
early 2000s did not per%it a gene to be added at a targeted location,
but only inserted rando%ly into a chro%oso%e. *a%pering with the
structure o/ DN( in this way is 3nown to increase cancer ris3 no
%atter what gene is added or subtracted. ,n three o/ these early
studies, cancer rates in %ice were increased [, 2, E\.
*here are no lab studies to %y 3nowledge in which acti&ating the
nati&e telo%erase has increased the ris3 o/ cancer. *he %odern &iew
is that Kwhile telo%erase does not dri&e the oncogenic process, it is
per%issi&e and re9uired /or the sustain growth o/ %ost ad&anced
cancers.” Recent perspecti&es /ro% both :ar&ard lab o/ de #inho
and the Spanish lab o/ 6lasco /ocus on the potential /or telo%erase to
decrease cancer ris3, and these were the &ery people who produced
the three studies suggesting caution a decade earlier.
(nd there are %any studies showing that 4a5 telo%erase e-pression
does not increase cancer ris3 in lab ani%als, and 4b5 short telo%eres
are a &ery strong cancer ris3. , belie&e that telo%erase acti&ators will
greatly reduce the cancer rate, /irst by eli%inating cells that are pro?
in/la%%atory and potentially carcinogenic because their telo%eres
ha&e beco%e short, and second by re+u&enating the i%%une syste%,
which is our pri%ary de/ense against cancer. , published an article on
this sub+ect last year.
!hy we %ight e-pect big li/e e-pectancy gains /ro% e-tending
*his is the a//ir%ati&e 9uestion, thenF what %a3es %e thin3 that
telo%ere e-tension will ha&e such a power/ul e//ect on di&erse
aspects o/ aging biology'
(5 *elo%ere attrition is an ancient %echanis% o/ aging.
#rotists were the /irst eu3aryotic cells, and they appeared on earth a
billion years ago 4they were a leap up in co%ple-ity /ro% bacteria,
which had been around E billion years be/ore5. ,n protists, DN( is
linear and hence there are telo%eres and a need /or telo%erase.
Since protists reproduce by si%ple cell di&ision, you would not e-pect
that the cells would Kage” or e&en that the concept o/ aging could
ha&e any %eaning /or their li/e cycle. 6ut a protist cell lineage can
age, and indeed so%e do. *his is the oldest 3nown %echanis% o/
aging, and it is i%ple%ented through withholding telo%erase3
#ara%ecia are an e-a%ple. !hen para%ecia reproduce, their cells
si%ply /ission, the DN( replicates, and telo%erase is e-pressed.
:ence, telo%eres get shorter with each cell di&ision. #ara%ecia can
con+ugate, which is a pri%iti&e /or% o/ se-ual gene e-change. *wo
para%eciu% cells %erge, %ingle their DN(, and then separate. ,t is
only in the con+ugation process that telo%erase is e-pressed.
*here/ore, any cell lineage that does not con+ugate will die out a/ter a
/ew hundred generations. *his pre&ents cell colonies /ro% beco%ing
too ho%ogeneous. *hus aging is a billion years old, and so%e o/ the
genetic %echanis%s o/ aging ha&e been conser&ed and passed on
through all the trans/or%ations o/ %ulticellular li/e 4!illia% R =lar3
has written two accessible boo3s [, 2\ on this topic.5
65 *elo%eres shorten with age in hu%ans.
*his has been 3nown /or twenty years.
=5 #eople with shorter telo%eres ha&e a %uch higher ris3 o/
*his was established by Richard =awthon 4200E5 in a paper which
too3 the /ield by surprise. Researchers be/ore then had assu%ed on
erroneous theoretical grounds that telo%ere attrition, which was
3nown to occur, could not ha&e anything to do with hu%an aging. ,t
was assu%ed that the nu%ber o/ cell replications, though li%ited,
%ust be su//icient to last through the longest li/eti%e that hu%ans
nor%ally e-perience. (/ter all, i/ aging were as si%ple as telo%ere
attrition, then the body could sol&e the proble% %erely by e-pressing
telo%erase. *his would enhance indi&idual /itness. !hy would not
e&olution ha&e /ound such a si%ple e-pedient' 4*he answer, o/
course, is that natural selection /a&ors aging, /or the sa3e o/ the
de%ographic stability 8 an e&olutionary /orce not recogni$ed by %ost
e&olutionary biologists.5 ,n =awthonWs study, the top ` o/ <0?year?
olds in ter%s o/ telo%ere length had hal/ the o&erall %ortality ris3 as
the botto% `. =awthon had access to a uni9ue database o/ 20?year?
old blood sa%ples, and to %y 3nowledge his study has not been
replicated or re/uted these years.

D5 #eople with short telo%eres ha&e a higher ris3 o/ diseases,
especially =AD, a/ter ad+usting /or age. *he association with
cardio&ascular disease has been consistent, not +ust in =awthonWs
original study, but also se&eral other studies [Re/ Re/ Re/\. *here are
also associations with de%entia [Re/, Re/\ and with diabetes [Re/,
75 (ni%als with short telo%eres also ha&e a higher ris3 o/ %ortality,
a/ter ad+usting /or age.
*his has been established in se&eral bird species [Re/ Re/ Re/\, and
in baboons. ,n 200E, it was already 3nown that long?li&ed species
tend to lose telo%ere length %ore slowly, and short?li&ed species lose
telo%eres %ore rapidly.
25 ,n li%ited studies with %ice, telo%erase enhancers ha&e led to
re+u&enation. 4;ice are e-pected to be a %uch less e//ecti&e target
/or this strategy than hu%ans, because to all appearances, aging in
hu%ans relies on telo%ere attrition %uch %ore so than in %ice.5
*he /irst e-peri%ent o/ this type was done in 200B. ,n the Spanish
lab o/ ;aria 6lasco, *o%as?Doba engineered %ice that were both
cancer?resistant and contained an e-tra telo%erase gene, e-pressed
in so%e tissues where, e&en in %ice, it would not nor%ally be /ound.
=ancer?/ree %ice with the e-tra telo%erase li&ed BT longer than
cancer?/ree %ice with only the nor%al gene /or telo%erase.
6ut soon it was disco&ered that all the e-peri%ental precautions
around cancer %ay not ha&e been necessary. *he sa%e lab
6ernardes de Jesus 4205 reported that they could increase health
span in %ice with the co%%ercial product called *(?<. 4widely
ru%ored to be cycloastragenol5 with no increase in the incidence o/
cancer. =ycloastragenol is a wea3 telo%erase acti&ator co%pared to
%an?%ade che%icals disco&ered at Sierra Sciences, and e&en
co%pared to so%e other herbal e-tracts. Ne&ertheless, the 6lasco
lab was able to show that the shortest telo%eres in the %ice were
elongated, and that %ar3ers o/ health including insulin sensiti&ity
were i%pro&ed by short?ter% treat%ent with *(?<..
6lascoWs lab then wor3ed with a %ore potent 4though %ore
dangerous5 %ethod o/ telo%erase inductionF in/ection with a
retro&irus engineered to introduce telo%erase into the nuclear DN( o/
the in/ected cell. K*reat%ent o/ ? and 2?year old %ice with an adeno
associated &irus 4((A5 o/ wide tropis% e-pressing %ouse *7R* had
re%ar3able bene/icial e//ects on health and /itness, including insulin
sensiti&ity, osteoporosis, neuro%uscular coordination and se&eral
%olecular bio%ar3ers o/ aging.” 46ernardes de Jesus, Aera et al.
2025 *he %ice li&ed ET longer when ((A treat%ent began at age
2 years, and 2CT longer when treat%ent began at year. *here was
no increase in cancer incidence.
*he %ost dra%atic e-a%ple o/ re+u&enation is /ro% the :ar&ard
laboratory o/ Robert de #inho. Nor%ally, %ice 4unli3e people5
e-press telo%erase /reely through their li/eti%es. *hese scientists
engineered a %ouse without the nor%al 4always on5 gene /or
telo%erase, but instead had a telo%erase gene that could be turned
on and o// at will by use o/ a che%ical signal that the e-peri%enters
could /eed to the %ice. (s these %ice grew older, they de&eloped
%ultiple, se&ere sy%pto%s o/ degeneration in the testes, spleen,
intestine, ner&ous syste% and elsewhere. (ll these sy%pto%s were
not +ust halted but re&ersed when telo%erase was turned on late in
the ani%alsW li&es. *he e//ect on the ner&ous syste% is particularly
interesting because ner&e cells last a li/eti%e and do not depend on
continual regeneration /ro% ste% cells, the way blood and intestinal
and s3in cells do. Ne&ertheless, these %ice with telo%erase turned
o// su//ered sensory de/iciencies and i%paired learning that was
re&ersed when the e-peri%enters ad%inistered the che%ical signal to
turn telo%erase bac3 on3
A Stan8ord-0eron research group wor1ed with :s1in; grown 8rom human cells in a
la2 setting. *hey /ound they were able to restore youth/ul elasticity,
so/tness and te-ture to the cultured Ks3in” by in/ecting the cells with
an engineered retro&irus that inserted the gene /or telo%erase.
>5 ,n addition to its /unction in lengthening telo%eres, telo%erase
also acts as a 3ind o/ growth hor%one.
*his /act was suspected as early as the ""0s, and con/ir%ed
de/initi&ely in a Stan/ord e-peri%ent [Re/, Re/, Re/, Re/\. ,n this
e-peri%ent, %ice were engineered with Kdenatured” telo%erase that
lac3ed the RN( te%plate /or creating telo%eres. Still, the telo%erase
was shown to induce hair growth. *elo%erase has been shown to
a//ect a hor%onal signaling pathway called !nt. Other /unctions /or
telo%erase are re&iewed by =ong and Shay 4200B5.
:5 ,n one hu%an case, huge doses o/ herbal telo%erase
acti&ators has led to re+u&enation.
, a% recently in touch with a physicist /ro% Iansas who has been
ta3ing super?high doses o/ telo%erase?acti&ating herbs and
supple%ents /or si- years and clai%s to loo3 and /eel younger, with
i%pro&ed athletic per/or%ance. :e %ay be an interesting case study.
Ji% >reen has co%%ented on this blog site.
*he 6otto% Dine
,n %y opinion, telo%erase acti&ation is a /ield that
o//ers the %ost potential /or hu%an li/e e-tension in
the ne-t /ew years. *his research is languishing /or
lac3 o/ /unds, and /or lac3 o/ attention.
Josh ;itteldor/
(ging ;atters