A POSITION PAPER BY LEADING HEALTH SCIENTISTS ON THE ANTIAGING SCAMS
products are big business--a multibillion-dollar industry. But the marketing of these products often misrepresents the science.
Rather than let their silence imply compliance, 51 of the top researchers in the field of aging research collaborated to create
a position paper that sets out the current state of the science. A shorter, more pointed essay, called "No Truth to the Fountain
of Youth," by three of the position paper's signers, S. Jay Olshansky, Leonard Hayflick and Bruce A. Carnes, is in Scientific
American's June 2002 issue; the position paper itself is here. --The Editors Scientific American, June 2002.
POSITION STATEMENT OF 51 TOP SCIENTISTS ON FAD ANTIAGING PRODUCTS
In the past century a combination of successful public health campaigns,
changes in living environments and advances in medicine have 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 , the public is spending vast sums of money on these products and lifestyle changes,
some of which may be harmful . 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 51 internationally recognized scientists in the field about 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, along with the consensus statements about these issues that grew out of debates and
discussions among the 51 scientists associated with this paper.
Life span is defined as the observed age at death of an individual; maximum
lifespan is the highest documented age at death for a species. From time to time we are 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 . 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 direction: higher. Despite this trend, however, 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  Longevity records are entertaining, but they have little relevance to our own lives because genetic,
environmental and lifestyle diversity  guarantees that an overwhelming majority of the population will die long before
attaining the age of the longest-lived individual.
Life expectancy in humans is the average number of years of life remaining
for people of a given age, assuming that everyone will experience, for the remainder of their lives, the risk of death based
on a current life table. For newborns in the U.S. today, life expectancy is about 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 be saved only once and because these risks are now so close
to zero, further improvements, even if they occurred, would have little effect on life expectancy [7-9]. Future gains in 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 . In fact, even eliminating all aging-related causes of death currently written
on the death certificates of the elderly will not increase human life expectancy by more than 15 years. To exceed this limit,
the underlying processes of aging that increase vulnerability to all the common causes of death will have to be modified.
Eliminating all the aging-related  causes of death presently written
on death certificates would still not make humans immortal . 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 in
which 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 aging--not 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 [15-20].
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 [21-26]. Claims of this
kind have been made for thousands of years , and they are as false today as they were in the past [28-31]. 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 one’s 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 . The misleading marketing and the public acceptance of antiaging medicine is not only 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 . Medical interventions for age-related diseases do result in an increase in life expectancy, but none have
been proved 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.
The scientifically respected free-radical theory of aging  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 (such as the immune response and cell communication) [37-39]. Nevertheless, there is
little doubt that ingesting fruits and vegetables (which contain antioxidants) can reduce the risk of having various age-associated
diseases, such as cancer , 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 [45-49], 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 , 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, 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]. In the animal kingdom, though, long-lived species often have shorter telomeres
than do short-lived species, indicating that telomere length probably does not determine life span [55-57]. 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 . Increasing the number of times a cell can divide, however, 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.
A number of hormones, including growth hormone, testosterone, estrogen
and progesterone, have been shown in 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.
No hormone, however, has been proved 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 [63-65]. 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.
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 , 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
[67-69], there is no study in humans that has proved 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 over quantity of life. The unknown mechanisms involved in the reduced
risk of disease associated with caloric restriction are of great interest  and deserve further study because they could
lead to treatments with pharmacological mimetics of caloric restriction that might postpone all age-related diseases simultaneously.
Determining Biological Age
Scientists believe that random damage that occurs within cells and among
extracellular molecules are responsible for many of the age-related changes that are observed in organisms [72-74]. In addition,
for organisms that reproduce sexually, including humans, each individual is genetically unique. As such, the rate of aging
also varies from individual to individual . Despite intensive study, scientists have not been able to discover reliable
measures of the processes that contribute to aging . For these reasons, any claim that a person’s biological or
"real age"  can currently be measured, let alone modified, by any means must be regarded as entertainment, not science.
Are There Genes That Govern Aging Processes?
No genetic instructions are required to age animals, just as no instructions
on how to age inanimate machines are included in their blueprints [79-80]. 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 . 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 we protect to survive beyond the 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 [82-85]. Without exception, however, 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 above suggest that
a unitary programmed aging process is unlikely to even exist and that such studies are more accurately interpreted to have
an effect on longevity determination, not the various biological processes that contribute to aging. From this perspective,
longevity determination is under genetic control only indirectly [86,87]. Thus, aging is a product of evolutionary neglect,
not evolutionary intent [88-91].
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.
After 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
[92,93]. because, as stated above, there are no genes directly responsible for the processes of aging. Centuries of selective
breeding experience (in agricultural, domesticated and experimental plants and animals) has 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. As such, there is a very real danger that enhancing biological attributes associated with extended 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. Though 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 [94-99] and will likely have an important positive impact on public health
in the future through the treatment of age-related diseases and disorders. But replacing and reprogramming the brain that
defines who we are as individuals is, in our view, more the subject of science fiction than science fact.
Lifestyle Modification and Aging
Optimum lifestyles, including exercise and a balanced diet 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. There is no scientific evidence, however, 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
[100,101]. 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"  will require modifications to all of the processes that contribute to aging--a technological feat that,
though 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
(such as smoking, excessive alcohol consumption, excessive exposure to sun, and obesity) that accelerate the expression of
age-related diseases and by the adoption of behaviors (such as exercise and a healthy diet) that take advantage of a physiology
that is inherently modifiable .
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 period 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 universal underlying processes. Successful
efforts to slow the rate of aging would 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.
Authors and Endorsers
Dr. Olshansky is Senior Research Scientist and Professor at the School
of Public Health, University of Illinois
at Chicago. Dr. Hayflick is Professor of Anatomy at the University
of California at San Francisco. Dr. Carnes is Assistant Professor of Geriatric Medicine at the University
of Oklahoma. Drs. Olshansky and Carnes are also coauthors of The Quest for Immortality (Norton, 2001), a book-length antidote to anti-aging hype.
The Position Statement on Human Aging has been endorsed by 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,
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, Ladislas (Leslie) 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 and Woodring Wright. Drs. Olshansky and Carnes received funding for this work from the National Institute on Aging.
The position paper was previously published in Scientific American Magazine and the Journal of Gerontology: Biological Sciences.
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This article was posted on August 27, 2004.
THE ABOVE ARTICLE CAN BE FOUND IN THE JUNE ISSUE 2002 OF SCIENTIFIC
AMERICAN AND ON THEIR WEBSITE sciam.com--for a price.
PATHOLOGY OF AGING Michelle Magid What
is Biological aging? Ex. At 20, a top athlete is #1 in the world at his sport. At 35, he is #150. What happened?
Ans. He underwent BIOLOGICAL AGING.
Biological aging is not the same as disease. What is the cause of Biological
aging? Ans. Unknown
As aging proceeds, the ability to ADAPT becomes impaired. If we could eliminate
all premature deaths, we would all still die at about 85. MAXIMUM LIFESPAN IS NOT CHANGED BECAUSE WE WILL ALL UNDERGO
This graph shows a sudden drop off at the end of the plot in the protected animals'
mortality rate. Thus, protection helps prevent early age death, but life expectancy is not altered b/c of biological
Trends: Life expectancy in the US has increased for children under 2, increased for people age 30-40,
but has barely increased for people of about age 75. Why??? We have combated birth complications leading to death
of babies, and we can treat illnesses leading to death of middle-aged adults, but we CANNOT GET RID OF BIOLOGICAL AGING.
organ functions and abilities decrease with age. Ex. At age 25, we have 6% bone mineral. At age 70, we have 5% bone
mineral. Thus, as we get older, we are naturally more likely to get osteoporosis. Ex. An aged mouse will not be able
to adapt to increased cold stress. Its heart will slow down; it won't shiver as much etc? Thus it will get sick and
die. A younger mouse will be able to ADAPT better to stressful environments. Ex. As we age, our vascular system doesn't
adapt as well. Ex-our blood pressure rises, as we get older. Ex. As we age, we cannot ADAPT to increased blood sugar
(our blood sugar concentrations will show increase in a cortisone glucose tolerance test.) Ex. Females are born with 733,000
oocytes. At about age 15, they have 389,300 oocytes. At age 45, they only have 10,900 oocytes. Although some of
the oocytes are lost in the menstrual cycle, most of the loss of oocytes is due to Biological Aging in the Ovary.
IS BIOLOGICAL AGING DUE TO ENVIRONMENTAL STRESS (ex. Radiation)? Two mice strains were examined. The strain with
more chromosomal abnormalities had a shorter lifespan. It was thought that more environmental stress= more chromosomal
damage=more biological aging= decreased lifespan. This theory hasn't held up. If this theory were true, pilots, who
are exposed to radiation, should have decreased lifespan, but they don't.
THEORY: IS BIOLOGICAL AGING DUE TO LIPOFUSCIN
ACCUMILATION? Lipofuscin increases with age. Caused by lipid peroxidation (by free radicals for ex.). The accumulation
of lipofuscin= Biological aging. Lipofuscin build-up is a good indicator of free radical oxidation damage being done
to cells. Cells get rid of free radicals via various mechanisms. If the radicals aren't destroyed, they will slowly
cause cell damage. This may be a factor in Biological aging.
THERE IS A STRONG GENETIC COMPONENT TO BIOLOGICAL
AGING> Ex. Non-identical twins have a much larger difference in lifespan than identical twins. Regular siblings
have a larger difference in lifespan than non-identical twins. A genetic component may be DNA repair mechanisms.
If you increase the amount of DNA repair enzymes, you will increase your lifespan.
HAYFLICK PHENOMENON- normal fibroblasts
will grow and divide in a cell culture, BUT at some point, the cells will stop growing (ex at about fifty doublings) regardless
of nutrients etc? This is a normal process. (Side note: if you transform the cell with radiation or something, the cell becomes
immortal and will NOT stop growing after 50 doublings. Cell is actually cancerous. This is not a normal process) Is
Biological aging merely due to the cessation of cells dividing? Ans: Probably not. Aging takes its greatest toll
on cells that DON'T divide (terminally differentiated cells) such as brain cells. Aging is not as relevant with continuously
dividing cells such as fibroblasts and Gastric mucous cells. However, there IS a correlation between lifespan and population
doublings in vitro. Hmmmm?.
DISEASES: Progeria and Werners- Children age very quickly. They are bald and wrinkled by
age 12. The fibroblasts of these sick children have a fibroblast doubling of about 5, not 50. Again, there is a correlation
between lifespan and population doublings of dividing cells.
There is also something about chromosome 1 that has to
do with biological aging. We are not sure what it is, but it adds evidence that there is a genetic component to Biological
There is a progressive shortening of chromosomes with each chromosomal replication. You reach a point
where the shortening of chromosomes infringes upon the CODING SEQUENCES in the gene. Thus, the loss of coding sequences
may lead to or cause biological aging. TELOMERASE prevents the shortening of chromosomes with replication. Coincidentally,
there is a lot of telomerase in cancer cells. Perhaps increased telomerase in a person hinders biological aging, but
may also cause cancer.
If we could eliminate all premature deaths, we would all still die at about 85. MAXIMUM
LIFESPAN IS NOT CHANGED BECAUSE WE WILL ALL UNDERGO BIOLOGICAL AGING.
SECOND YEAR CURRICULUM
This is part of a collection
of articles found at http://www.geocities.com/Athens/Styx/3148/secondyear.html
BY COMMENTS JK:Aging has many causes.I first seriously studied this topic in 1984, when on a visit to my mother in law’s,
I spent visited the University of Colorado and purchased there a textbook on aging.From my reading of it, I produced typed notes.Periodically, I returned
to this topic.
Aging is a product of a
variety of causes.At the most basic level it is the product of chemical reactions
that occur randomly, at a low frequency, and for which there are imperfect biological mechanism to reduce their frequency,
their effect, or to undo their effect.There are certain reactive chemicals produced
as bi-products of reactions (super oxides, acids, bases, and various oxidizing and reducing agents).These chemical agents affect the structure of DNA and RNA, they change the structure of proteins, an frequently
they change the special shape of these compounds, not by reacting with them and attaching thereto, but merely by braking certain
weak bonds, such as hydrogen bonds and the sulfur-to-sulfur bond on one of the amino acids.The result of these changes is a reduction in functions.This gradual
reduction in functions because of these changes produce the visible and functional changes observed in the aging process.Blood vessels and skin lose their elasticity, bone become brittle, muscles contract
with less force, blood cells survive less days, the number of sells in senescence increase, and so on.