PERSPECTIVES

Journal of Gerontology: BIOLOGICAL SCIENCES

2002, Vol. 57A, No. 8, B292B297

Copyright 2002 by The Gerontological Society of America

Position Statement on Human Aging

S. Jay Olshansky,1 Leonard Hayflick,2 and Bruce A. Carnes3
1School

of Public Health, University of Illinois at Chicago.

2University of California, San Francisco.
3University of Chicago/NORC, Illinois.

A large number of products are currently being sold by antiaging entrepreneurs who claim that it
is now possible to slow, stop, or reverse human aging. The business of what has become known
as antiaging medicine has grown in recent years in the United States and abroad into a multimillion-dollar industry. The products being sold have no scientifically demonstrated efficacy, in
some cases they may be harmful, and those selling them often misrepresent the science upon
which they are based. In the position statement that follows, 52 researchers in the field of aging
have collaborated to inform the public of the distinction between the pseudoscientific antiaging
industry, and the genuine science of aging that has progressed rapidly in recent years.

N the past century, a combination of successful public

health campaigns, changes in living environments, and
advances in medicine has led to a dramatic increase in human life expectancy. Long lives experienced by unprecedented numbers of people in developed countries are a triumph of human ingenuity. This remarkable achievement
has produced economic, political, and societal changes that
are both positive and negative. Although there is every reason to be optimistic that continuing progress in public
health and the biomedical sciences will contribute to even
longer and healthier lives in the future, a disturbing and potentially dangerous trend has also emerged in recent years.
There has been a resurgence and proliferation of health care
providers and entrepreneurs who are promoting antiaging
products and lifestyle changes that they claim will slow,
stop, or reverse the processes of aging. Even though in most
cases there is little or no scientific basis for these claims (1),
the public is spending vast sums of money on these products
and lifestyle changes, some of which may be harmful (2).
Scientists are unwittingly contributing to the proliferation of
these pseudoscientific antiaging products by failing to participate in the public dialogue about the genuine science of
aging research. The purpose of this document is to warn the
public against the use of ineffective and potentially harmful
antiaging interventions, and to provide a brief but authoritative consensus statement from 52 internationally recognized
scientists in the field of what we know and do not know
about intervening in human aging. What follows is a list of
issues related to aging that are prominent in both the lay and
scientific literature, and the consensus statements about
these issues that grew out of debates and discussions among
the 51 scientists associated with this article.

LIFE SPAN
Life span is defined as the observed age at death of an individual, whereas maximum life span is the highest documented age at death for a species. From time to time, we are
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told of a new highest documented age at death, as in the celebrated case of Madame Jeanne Calment of France, who
died at the age of 122 (3). Although such an extreme age at
death is exceedingly rare, the maximum life span of humans
has continued to increase because world records for longevity can move in only one directionhigher. However, despite this trend, it is almost certainly true that, at least since
recorded history, people could have lived as long as those
alive today if similar technologies, lifestyles, and population sizes had been present. It is not people that have
changed; it is the protected environments in which we live,
and the advances made in biomedical sciences and other human institutions, that have permitted more people to attain,
or more closely approach, their life-span potential (4). Although longevity records are entertaining, they have little
relevance to our own lives because genetic, environmental,
and lifestyle diversity (5) guarantees that an overwhelming
majority of the population will die long before attaining the
age of the longest-lived individual.
LIFE EXPECTANCY
Life expectancy in humans is the average number of
years of life remaining for people of a given age, assuming
everyone will experience, for the remainder of their lives,
the risk of death based on a current life table. For newborns
in the United States today, life expectancy is approximately
77 years (6). Rapid declines in infant, child, maternal, and
late-life mortality during the 20th century led to an unprecedented 30-year increase in human life expectancy at birth
from the 47 years that it was in developed countries in 1900.
Repeating this feat during the lifetimes of people alive today is unlikely. Most of the prior advances in life expectancy at birth reflect dramatic declines in mortality risks in
childhood and early adult life. Because the young can only
be saved once and because these risks are now so close to
zero, further improvements, even if they occurred, would
have little effect on life expectancy (79). Future gains in

POSITION STATEMENT ON HUMAN AGING

life expectancy will, therefore, require adding decades of

life to people who have already survived seven decades or
more. Even with precipitous declines in mortality at middle
and older ages from those present today, life expectancy at
birth is unlikely to exceed 90 years (males and females
combined) in the 21st century without scientific advances
that permit the modification of the fundamental processes of
aging (10). In fact, even eliminating all aging-related causes
of death currently written on the death certificates of the elderly population will not increase human life expectancy by
more than 15 years. In order for this limit to be exceeded,
the underlying processes of aging that increase vulnerability
to all common causes of death currently appearing on death
certificates will have to be modified.
IMMORTALITY
Eliminating all of the aging-related (11) causes of death
presently written on death certificates would still not make
humans immortal (12). Accidents, homicides, suicide, and
the biological processes of aging would continue to take their
toll. The prospect of humans living forever is as unlikely today as it has always been, and discussions of such an impossible scenario have no place in a scientific discourse.
GERIATRIC MEDICINE VERSUS AGING
Geriatric medicine is a critically important specialty in a
world where population aging is already a demographic reality in many countries and a future certainty in others. Past
and anticipated advances in geriatric medicine will continue
to save lives and help to manage the degenerative diseases
associated with growing older (13,14), but these interventions only influence the manifestations of agingnot aging
itself. The biomedical knowledge required to modify the
processes of aging that lead to age-associated pathologies
confronted by geriatricians does not currently exist. Until
we better understand the aging processes and discover how
to manipulate them, these intrinsic and currently immutable
forces will continue to lead to increasing losses in physiological capacity and death, even if age-associated diseases
could be totally eliminated (1520).
ANTIAGING MEDICINE
Advocates of what has become known as antiaging medicine claim that it is now possible to slow, stop, or reverse
aging through existing medical and scientific interventions
(2126). Claims of this kind have been made for thousands
of years (27), and they are as false today as they were in the
past (2831). Preventive measures make up an important
part of public health and geriatric medicine, and careful adherence to advice on nutrition, exercise, and smoking can
increase ones chances of living a long and healthy life,
even though lifestyle changes based on these precautions do
not affect the processes of aging (32,33). The more dramatic
claims made by those who advocate antiaging medicine in
the form of specific drugs, vitamin cocktails, or esoteric
hormone mixtures are, however, not supported by scientific
evidence, and it is difficult to avoid the conclusion that
these claims are intentionally false, misleading, or exaggerated for commercial reasons (34). The misleading marketing
and the public acceptance of antiaging medicine is not only

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a waste of health dollars; it has also made it far more difficult to inform the public about legitimate scientific research
on aging and disease (35). Medical interventions for agerelated diseases do result in an increase in life expectancy,
but none have been proven to modify the underlying processes of aging. The use of cosmetics, cosmetic surgery,
hair dyes, and similar means for covering up manifestations
of aging may be effective in masking age changes, but they
do not slow, stop, or reverse aging. At present, there is no
such thing as an antiaging intervention.
ANTIOXIDANTS
The scientifically respected free-radical theory of aging
(36) serves as a basis for the prominent role that antioxidants
have in the antiaging movement. The claim that ingesting
supplements containing antioxidants can influence aging is
often used to sell antiaging formulations. The logic used by
their proponents reflects a misunderstanding of how cells detect and repair the damage caused by free radicals and the important role that free radicals play in normal physiological
processes (e.g., the immune response and cell communication) (3739). Nevertheless, there is little doubt that ingesting
fruits and vegetables (which contain antioxidants) can reduce
the risk of having a number of age-associated diseases such
as cancer (40), heart disease (41,42), macular degeneration,
and cataracts (43,44). At present, there is relatively little evidence from human studies that supplements containing antioxidants lead to a reduction in either the risk of these conditions or the rate of aging, but there are a number of ongoing
randomized trials that address the possible role of supplements in a range of age-related conditions (4549), the results
of which will be reported in the coming years. In the meantime, possible adverse effects of single dose supplements,
such as beta-carotene (50), caution against their indiscriminate use. As such, antioxidant supplements may have some
health benefits for some people, but so far there is no scientific evidence to justify the claim that they have any effect on
human aging (51,52).
TELOMERES
Telomeres, the repeated sequence found at the ends of
chromosomes, shorten in many normal human cells with increased cell divisions. Statistically, older people have
shorter telomeres in their skin and blood cells than do
younger people (53,54). However, in the animal kingdom,
long-lived species often have shorter telomeres than do
short-lived species, indicating that telomere length probably
does not determine life span (5557). Solid scientific evidence has shown that telomere length plays a role in determining cellular life span in normal human fibroblasts and
some other normal cell types (58). However, increasing the
number of times a cell can divide may predispose cells to
tumor formation (59,60). Thus, although telomere shortening may play a role in limiting cellular life span, there is no
evidence that telomere shortening plays a role in the determination of human longevity.
HORMONES
A number of hormones, including growth hormone, testosterone, estrogen, and progesterone, have been shown in

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OLSHANSKY ET AL.

clinical trials to improve some of the physiological changes

associated with human aging (61,62). Under the careful supervision of physicians, some hormone supplements can be
beneficial to the health of some people. However, no hormone has been proven to slow, stop, or reverse aging. Instances of negative side effects associated with some of
these products have already been observed, and recent animal studies suggest that the use of growth hormone could
have a life-shortening effect (6365). Hormone supplements now being sold under the guise of antiaging medicine
should not be used by anyone unless they are prescribed for
approved medical uses.
CALORIC RESTRICTION
The widespread observation that caloric restriction will
increase longevity must be tempered with the recognition
that it has progressively less effect the later in life it is begun (66), as well as with the possibility that the control animals used in these studies feed more than wild animals,
predisposing them to an earlier death. Although caloric restriction might extend the longevity of humans because it
does so in many other animal species (6769), there is no
study in humans that has proven that it will work. A few
people have subjected themselves to a calorically restricted
diet, which, in order to be effective, must approach levels
that most people would find intolerable. The fact that so few
people have attempted caloric restriction since the phenomenon was discovered more than 60 years ago suggests that,
for most people, quality of life seems to be preferred to
quantity of life. The unknown mechanisms involved in the
reduced risk of disease associated with caloric restriction
are of great interest (70), and they deserve further study because they could lead to treatments with pharmacological
mimetics of caloric restriction that might postpone all agerelated diseases simultaneously (71).
DETERMINING BIOLOGICAL AGE
Scientists believe that random damage that occurs within
cells and among extracellular molecules is responsible for
many of the age-related changes that are observed in organisms (7274). In addition, for organisms that reproduce sexually, such as humans, each individual is genetically unique.
Therefore, the rate of aging also varies from individual to
individual (75). Despite intensive study, scientists have not
been able to discover reliable measures of the processes that
contribute to aging (76). For these reasons, any claim that a
persons biological or real age (77) can currently be measured, let alone modified, by any means must be regarded as
entertainment (78), not science.
ARE THERE GENES THAT GOVERN AGING P ROCESSES?
No genetic instructions are required to age animals, just
as no instructions on how to age inanimate machines are included in their blueprints (72,79). Molecular disorder occurs
and accumulates within cells and their products because the
energy required for maintenance and repair processes to
maintain functional integrity for an indefinite time is unnecessary after reproductive success. Survival beyond the reproductive years and, in some cases, raising progeny to independence, is not favored by evolution because limited

resources are better spent on strategies that enhance reproductive success to sexual maturity rather than longevity
(80). Although genes certainly influence longevity determination, the processes of aging are not genetically programmed. Overengineered systems and redundant physiological capacities are essential for surviving long enough to
reproduce in environments that are invariably hostile to life.
Because humans have learned how to reduce environmental
threats to life, the presence of redundant physiological capacity permits them and the domesticated animals they protect to survive beyond reproductive ages. Studies in lower
animals that have led to the view that genes are involved in
aging have demonstrated that significant declines in mortality rates and large increases in average and maximum life
span can be achieved experimentally (8184). However,
without exception, these genes have never produced a reversal or arrest of the inexorable increase in mortality rate that
is one important hallmark of aging. The apparent effects of
such genes on aging therefore appear to be inadvertent consequences of changes in other stages of life, such as growth
and development, rather than a modification of underlying
aging processes. Indeed, the evolutionary arguments presented herein suggest that a unitary programmed aging process is unlikely to even exist, and that such studies are more
accurately interpreted to have an impact on longevity determination, not the various biological processes that contribute to aging. From this perspective, longevity determination
is under genetic control only indirectly (15,85). Thus, aging
is a product of evolutionary neglect, not evolutionary intent
(8689).
CAN WE GROW YOUNGER?
Although it is possible to reduce the risk of aging-related
diseases and to mask the signs of aging, it is not possible for
individuals to grow younger. This would require reversing
the degradation of molecular integrity that is one of the hallmarks of aging in both animate and inanimate objects. Other
than performing the impossible feat of replacing all of the
cells, tissues, or organs in biological material as a means of
circumventing aging processes, growing younger is a phenomenon that is currently not possible.
GENETIC ENGINEERING
Following the publication of the human genome sequences, there have been assertions that this new knowledge
will reveal genes whose manipulation may permit us to intervene directly in the processes of aging. Although it is
likely that advances in molecular genetics will soon lead to
effective treatments for inherited and age-related diseases, it
is unlikely that scientists will be able to influence aging directly through genetic engineering (90,91) because, as already stated, there are no genes directly responsible for the
processes of aging. Centuries of selective breeding experience (e.g., agricultural, domesticated, and experimental
plants and animals) have revealed that genetic manipulations
designed to enhance one or only a few biological characteristics of an organism frequently have adverse consequences
for health and vigor. Therefore, there is a very real danger
that enhancing biological attributes associated with extended

POSITION STATEMENT ON HUMAN AGING

survival late in life might compromise biological properties

important to growth and development early in life.
REPLACING BODY PARTS
Suggestions have been made that the complete replacement of all body parts with more youthful components
could increase longevity. Although possible in theory, it is
highly improbable that this would ever become a practical
strategy to extend length of life. Advances in cloning and
embryonic stem cell technology may make the replacement
of tissues and organs possible (9297) and will likely have
an important positive impact on public health in the future
through the treatment of age-related diseases and disorders.
However, replacing and reprogramming the brain, which
defines who we are as individuals, is, in our view, more the
subject of science fiction than likely science fact.
LIFESTYLE MODIFICATION AND AGING
Optimum lifestyles, exercise, and diets along with other
proven methods for maintaining good health contribute to
increases in life expectancy by delaying or preventing the
occurrence of age-related diseases. However, there is no
scientific evidence to support the claim that these practices
increase longevity by modifying the processes of aging.
Since recorded history, individuals have been, and are
continuing to be, victimized by promises of extended youth
or increased longevity by using unproven methods that allegedly slow, stop, or reverse aging. Our language on this
matter must be unambiguous: there are no lifestyle changes,
surgical procedures, vitamins, antioxidants, hormones, or
techniques of genetic engineering available today that have
been demonstrated to influence the processes of aging
(98,99). We strongly urge the general public to avoid buying or using products or other interventions from anyone
claiming that they will slow, stop, or reverse aging. If people, on average, are going to live much longer than is currently possible, then it can only happen by adding decades
of life to people who are already likely to live for 70 years
or more. This manufactured survival time (100) will require modifications to all of the processes that contribute to
aginga technological feat that, although theoretically possible, has not yet been achieved. What medical science can
tell us is that because aging and death are not programmed
into our genes, health and fitness can be enhanced at any
age, primarily through the avoidance of behaviors (e.g.,
smoking, excessive alcohol consumption, excessive exposure to sun, and obesity) that accelerate the expression of
age-related diseases, and by the adoption of lifestyles (e.g.,
exercise and diet) that take advantage of a physiology that is
inherently modifiable (101).
CONCLUSION
We enthusiastically support research in genetic engineering, stem cells, geriatric medicine, and therapeutic pharmaceuticals, technologies that promise to revolutionize medicine as we know it. Most biogerontologists believe that our
rapidly expanding scientific knowledge holds the promise
that means may eventually be discovered to slow the rate of
aging. If successful, these interventions are likely to postpone age-related diseases and disorders and extend the pe-

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riod of healthy life. Although the degree to which such interventions might extend length of life is uncertain, we
believe this is the only way another quantum leap in life expectancy is even possible. Our concern is that when proponents of antiaging medicine claim that the fountain of youth
has already been discovered, it negatively affects the credibility of serious scientific research efforts on aging. Because
aging is the greatest risk factor for the leading causes of
death and other age-related pathologies, more attention
must be paid to the study of these universally underlying
processes. Successful efforts to slow the rate of aging would
certainly have dramatic health benefits for the population,
by far exceeding the anticipated changes in health and
length of life that would result from the complete elimination of heart disease, cancer, stroke, and other age-associated diseases and disorders.
Acknowledgments
Funding for this work was provided by grants from the National Institutes of Health/National Institute on Aging to Dr. Olshansky (Grant
AG13698-01) and Dr. Carnes (Grant AG00894-01). This article appeared
in Scientific American as No Truth to the Fountain of Youth (available
online at http://www.sciam.com/article.cfm?articleID0004F171-FE1E1CDF-B4A8809EC588EE). It is reprinted with permission of the authors,
who hold the copyright.
Endorsers (alphabetical order): Robert Arking, Allen Bailey, Andrzej
Bartke, Vladislav V. Bezrukov, Jacob Brody, Robert N. Butler, Alvaro Macieira-Coelho, L. Stephen Coles, David Danon, Aubrey D.N.J. de Grey,
Lloyd Demetrius, Astrid Fletcher, James F. Fries, David Gershon, Roger
Gosden, Carol W. Greider, S. Mitchell Harman, David Harrison, Christopher Heward, Henry R. Hirsch, Robin Holliday, Thomas E. Johnson, Tom
Kirkwood, ric Le Bourg, Leo S. Luckinbill, George M. Martin, Alec A.
Morley, Charles Nam, Sang Chul Park, Linda Partridge, Graham Pawelec,
Thomas T. Perls, Suresh Rattan, Robert Ricklefs, Leslie (Ladislas) Robert,
Richard G. Rogers, Henry Rothschild, Douglas L. Schmucker, Jerry W.
Shay, Monika Skalicky, Len Smith, Raj Sohal, Richard L. Sprott, Andrus
Viidik, Jan Vijg, Eugenia Wang, Andrew Weil, Georg Wick, Woodring
Wright.
Address correspondence to S. Jay Olshansky, PhD, School of Public
Health, University of Illinois at Chicago, 1603 West Taylor Street, Room
885, Chicago, IL 60612. E-mail: sjayo@uic.edu
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Received April 22, 2002

Accepted May 31, 2002
Decision Editor: James R. Smith, PhD