长生不老不是不可能，科学依据在此，大家努力吧！
Buying time
Date July 15, 2013
Amy Klein
One of the most promising avenues of anti-aging research
comes from inside our own bodies: the telomere.
comes from inside our own bodies: the telomere.
Is ageing a process
that we simply have to accept as a fact of life?
that we simply have to accept as a fact of life?
A philosopher would say yes. Many doctors would also
agree: our cells eventually reach a point where they can no longer divide and
either die or reach senescence, or retirement phase. Scientists believe in the
Hayflick limit (named after molecular biologist Leonard Hayflick, who advanced
the idea of limited somatic cell division), which says no one can live past
about 120 years.
agree: our cells eventually reach a point where they can no longer divide and
either die or reach senescence, or retirement phase. Scientists believe in the
Hayflick limit (named after molecular biologist Leonard Hayflick, who advanced
the idea of limited somatic cell division), which says no one can live past
about 120 years.
De Grey believes a
person has already been born who will live to 1000.
person has already been born who will live to 1000.
These people might also say that ageing and dying are a
good thing; that the world is already overcrowded, that we already cannot
handle our ageing populations, that life must be finite to appreciate it, that
all good things must come to an end.
good thing; that the world is already overcrowded, that we already cannot
handle our ageing populations, that life must be finite to appreciate it, that
all good things must come to an end.
But an increasing number of people, including
gerontologists, biologists, engineers and futurists, believe ageing is a
disease, and one that can be cured. They believe ageing is not an immutable
process, an inevitable ''dying of the light'', to quote poet Dylan Thomas, but
one we can ''rage against'' through science, drugs and lifestyle changes.
gerontologists, biologists, engineers and futurists, believe ageing is a
disease, and one that can be cured. They believe ageing is not an immutable
process, an inevitable ''dying of the light'', to quote poet Dylan Thomas, but
one we can ''rage against'' through science, drugs and lifestyle changes.
Since 1900, the average life expectancy has risen from 47.3 years to 78 years in the US, which
is about a 60 per cent increase. It is not unlikely to believe that scientists
will be able to prolong healthy living rather than just ''life''.
Gerontologists and others in the field are not concerned with prolonging
end-of-life stages, when we are at our weakest, unhealthiest point (when
healthcare often steps in too late).
is about a 60 per cent increase. It is not unlikely to believe that scientists
will be able to prolong healthy living rather than just ''life''.
Gerontologists and others in the field are not concerned with prolonging
end-of-life stages, when we are at our weakest, unhealthiest point (when
healthcare often steps in too late).
Today's search is for a longer and healthier life. It's
about turning back our biological clocks to be younger for longer. They believe
in the ''longevity dividend''; that is, the economic benefits of extending
healthy lives, including savings on healthcare and entitlements, and an
increase in contributions to society.
about turning back our biological clocks to be younger for longer. They believe
in the ''longevity dividend''; that is, the economic benefits of extending
healthy lives, including savings on healthcare and entitlements, and an
increase in contributions to society.
Long and short of it: Telomeres, on the ends of
chromosomes preserve genetic information.
chromosomes preserve genetic information.
In today's popular scientific literature, many claim to
have cures for ageing or ways to retard ageing. Some believe a
kilojoule-restrictive diet can prolong lives. Oxford biogerontologist Aubrey de
Grey, a leader of the anti-ageing movement, believes we can rejuvenate the body
by repairing cellular and molecular damage. He believes that a person has
already been born who will live to 1000.
have cures for ageing or ways to retard ageing. Some believe a
kilojoule-restrictive diet can prolong lives. Oxford biogerontologist Aubrey de
Grey, a leader of the anti-ageing movement, believes we can rejuvenate the body
by repairing cellular and molecular damage. He believes that a person has
already been born who will live to 1000.
In his book Fantastic Voyage: Live Long Enough to Live
Forever, futurist Ray Kurzweil writes about the science behind radical life
extension, and investigates everything from diet and exercise to hormone and
gene therapy.
Forever, futurist Ray Kurzweil writes about the science behind radical life
extension, and investigates everything from diet and exercise to hormone and
gene therapy.
Some of these people are considered on the edge of
accepted science. Kurzweil, for example, takes more than 250 supplements a day,
while de Grey has arranged to have his head cryo-preserved after his death so
he can be revived. On the other hand, scientists in Scotland recently used a 3D
printer to replicate embryonic human stem cells. So who is to say what is
outrageous?
accepted science. Kurzweil, for example, takes more than 250 supplements a day,
while de Grey has arranged to have his head cryo-preserved after his death so
he can be revived. On the other hand, scientists in Scotland recently used a 3D
printer to replicate embryonic human stem cells. So who is to say what is
outrageous?
The cure within
One of the most promising avenues of anti-ageing research
comes from inside our own bodies: the telomere.
comes from inside our own bodies: the telomere.
Derived from the Greek nouns telos (end) and meros
(part), these ''end parts'' are at the tips of our chromosomes, serving as
protective caps for preserving genetic information; think of them as acting
like the plastic sheaths that prevent fraying at the ends of shoelaces. The
telomeres are disposable buffers blocking the ends of the chromosomes. Without
them, genomes would lose information after cell division. A cell's age can be
measured by the length of its telomeres.
(part), these ''end parts'' are at the tips of our chromosomes, serving as
protective caps for preserving genetic information; think of them as acting
like the plastic sheaths that prevent fraying at the ends of shoelaces. The
telomeres are disposable buffers blocking the ends of the chromosomes. Without
them, genomes would lose information after cell division. A cell's age can be
measured by the length of its telomeres.
Telomeres also protect a cell's chromosomes from fusing
with each other or rearranging (abnormalities that can lead to cancer). When
cells divide, telomeres shorten. When telomeres reach their shortest point,
cells stop dividing or die. These senescent cells, some believe, cause
age-related diseases, make us wrinkle, and weaken our immune and other systems.
with each other or rearranging (abnormalities that can lead to cancer). When
cells divide, telomeres shorten. When telomeres reach their shortest point,
cells stop dividing or die. These senescent cells, some believe, cause
age-related diseases, make us wrinkle, and weaken our immune and other systems.
In 2009, the Nobel prize in physiology or medicine was
awarded to Elizabeth Blackburn, Carol Greider and Jack Szostak for their 1984
discovery ''of how chromosomes are protected by telomeres and the enzyme
telomerase''. Telomerase is a protein that stabilises telomeres when they get
worn, or causes them to lengthen and aids cell division.
awarded to Elizabeth Blackburn, Carol Greider and Jack Szostak for their 1984
discovery ''of how chromosomes are protected by telomeres and the enzyme
telomerase''. Telomerase is a protein that stabilises telomeres when they get
worn, or causes them to lengthen and aids cell division.
Three months later, a genetics team at the Longevity
Genes Project, at the Institute for Ageing Research at the Albert Einstein
College of Medicine in New York, discovered a correlation between living to 100
and inheriting a mutant gene that makes their telomerase-making system extra
active and able to maintain telomere length more effectively. For the most
part, these people were spared age-related diseases such as cardiovascular
disease and diabetes, which cause the most deaths among elderly people.
Genes Project, at the Institute for Ageing Research at the Albert Einstein
College of Medicine in New York, discovered a correlation between living to 100
and inheriting a mutant gene that makes their telomerase-making system extra
active and able to maintain telomere length more effectively. For the most
part, these people were spared age-related diseases such as cardiovascular
disease and diabetes, which cause the most deaths among elderly people.
In March this year, University of Copenhagen researchers
mapped telomerase for the first time.
mapped telomerase for the first time.
The telomerase switch
''The key to immortality is turning the telomerase gene
from off to on,'' Dr Michael Fossel, Greta Blackburn and Dr Dave Woynarowski
write in The Immortality Edge: Realize the Secrets of Your Telomeres for a
Longer, Healthier Life (John Wiley & Sons, 2011).
from off to on,'' Dr Michael Fossel, Greta Blackburn and Dr Dave Woynarowski
write in The Immortality Edge: Realize the Secrets of Your Telomeres for a
Longer, Healthier Life (John Wiley & Sons, 2011).
Suppressing telomerase is already possible.
Anti-telomerase drugs have been found to stop some cancers growing, putting them
into senescence. The protein is present in almost 90 per cent of all cases, in
effect helping cancer grow unchecked. (Cancer cells and reproductive cells are
immortal - their telomeres do not shorten as the cell divides. This is why the
disease is fatal.
Anti-telomerase drugs have been found to stop some cancers growing, putting them
into senescence. The protein is present in almost 90 per cent of all cases, in
effect helping cancer grow unchecked. (Cancer cells and reproductive cells are
immortal - their telomeres do not shorten as the cell divides. This is why the
disease is fatal.
The Immortality Edge authors believe that in the next 20
years there will be a drug therapy that will turn on the telomerase gene in
healthy cells, thereby extending the telomere and reversing ageing. Aside from
TA-65, a controversial, expensive supplement that is claimed to lengthen
telomerase and costs up to $8000 a year, there have not been any solutions to
finding this ''on'' switch to produce the protein that would lengthen our
telomeres.
years there will be a drug therapy that will turn on the telomerase gene in
healthy cells, thereby extending the telomere and reversing ageing. Aside from
TA-65, a controversial, expensive supplement that is claimed to lengthen
telomerase and costs up to $8000 a year, there have not been any solutions to
finding this ''on'' switch to produce the protein that would lengthen our
telomeres.
Besides, genetic factors account for only 30 per cent of
what happens to us, according to the Human Genome Project. This means 70 per
cent is environmental. So even if our telomere length is genetic, there's a lot
we can do to protect our cells.
what happens to us, according to the Human Genome Project. This means 70 per
cent is environmental. So even if our telomere length is genetic, there's a lot
we can do to protect our cells.
Say no to stress
Is there anything we can do to preserve or lengthen our
telomeres? The short answer is yes, and some of us are already doing it. What
telomere researchers have discovered is that many of the practices we know are
healthy actually preserve telomeres, and other things we know are unhealthy
wear our cells down.
telomeres? The short answer is yes, and some of us are already doing it. What
telomere researchers have discovered is that many of the practices we know are
healthy actually preserve telomeres, and other things we know are unhealthy
wear our cells down.
Take stress, for example. We can see that it's bad for us
- stressed people often look older. Evidence shows it on a cellular level, too.
In Psychological and Metabolic Stress: A Recipe for Accelerated Cellular
Aging?, published in 2009 in the journal Hormones, Dr Elissa Appel of the
psychology department of the University of California, San Francisco, found
that stress coupled with overeating ''appears to be conducive to several cell
ageing mechanisms, mainly dampening telomerase and leading to telomere length
shortening and cell senescence''. She also found that chronic stress may lead
to ''immune cell senescence''; in other words, it will weaken our immune
system, causing us to age faster.
- stressed people often look older. Evidence shows it on a cellular level, too.
In Psychological and Metabolic Stress: A Recipe for Accelerated Cellular
Aging?, published in 2009 in the journal Hormones, Dr Elissa Appel of the
psychology department of the University of California, San Francisco, found
that stress coupled with overeating ''appears to be conducive to several cell
ageing mechanisms, mainly dampening telomerase and leading to telomere length
shortening and cell senescence''. She also found that chronic stress may lead
to ''immune cell senescence''; in other words, it will weaken our immune
system, causing us to age faster.
In studies that Appel did with Nobel laureate Blackburn,
they compared the mothers of children with chronic illness with mothers with
healthy children. The mothers of the children with chronic illness had shorter
telomeres and less telomerase. There was no genetic component, proving that our
telomeres are indeed affected by stress.
they compared the mothers of children with chronic illness with mothers with
healthy children. The mothers of the children with chronic illness had shorter
telomeres and less telomerase. There was no genetic component, proving that our
telomeres are indeed affected by stress.
The opposite is also true: alleviating stress strengthens
our cells. Appel and Blackburn were involved in Tonya Jacobs' 2010 study
published in Psychoneuroendocrinology, Intensive Meditation Training, Immune
Cell Telomerase Activity, and Psychological Mediators. The study compared a
group of people who meditated for three months to another similar group who had
not and found that telomerase activity was significantly greater in retreat
participants than in controls at the end of the retreat. They found that ''increases
in perceived control and decreases in negative affectivity contributed to an
increase in telomerase activity, with implications for telomere length and
immune cell longevity''.
our cells. Appel and Blackburn were involved in Tonya Jacobs' 2010 study
published in Psychoneuroendocrinology, Intensive Meditation Training, Immune
Cell Telomerase Activity, and Psychological Mediators. The study compared a
group of people who meditated for three months to another similar group who had
not and found that telomerase activity was significantly greater in retreat
participants than in controls at the end of the retreat. They found that ''increases
in perceived control and decreases in negative affectivity contributed to an
increase in telomerase activity, with implications for telomere length and
immune cell longevity''.
Blackburn, a professor in biology and physiology at the
department of biochemistry and biophysics at the University of California, San
Francisco, never thought she would be doing studies on meditation with
psychologists, but her research on telomeres has her working across disciplines
to see how her discovery affects all aspects of life.
department of biochemistry and biophysics at the University of California, San
Francisco, never thought she would be doing studies on meditation with
psychologists, but her research on telomeres has her working across disciplines
to see how her discovery affects all aspects of life.
… and yes to exercise
Telomere length has been linked to depression, anxiety,
obesity, cancer and heart disease, so it probably will come as no surprise to
find that exercise has a positive effect. In Physical Exercise Prevents Cellular
Senescence in Circulating Leukocytes and in the Vessel Wall, published in
Circulation (2009), Dr Christian Werner of the University of Hamburg and other
colleagues compared young and middle-aged sedentary and fit men who ran more
than 72 kilometres a week.
obesity, cancer and heart disease, so it probably will come as no surprise to
find that exercise has a positive effect. In Physical Exercise Prevents Cellular
Senescence in Circulating Leukocytes and in the Vessel Wall, published in
Circulation (2009), Dr Christian Werner of the University of Hamburg and other
colleagues compared young and middle-aged sedentary and fit men who ran more
than 72 kilometres a week.
They didn't find much difference in the telomeres when
comparing the sedentary and fit men in their 20s, which made sense, since the
younger men hadn't lived so long that their cells would divide enough to show
signs of ageing. But there was a significant difference in the telomere length
of the men in their 50s: the sedentary older men had 40 per cent shorter
telomeres than the fitter, older men. In fact, the telomeres of the older men
who were runners were only 10 per cent shorter than the younger men. In the
middle-aged runners, telomere loss was reduced by about 75 per cent.
comparing the sedentary and fit men in their 20s, which made sense, since the
younger men hadn't lived so long that their cells would divide enough to show
signs of ageing. But there was a significant difference in the telomere length
of the men in their 50s: the sedentary older men had 40 per cent shorter
telomeres than the fitter, older men. In fact, the telomeres of the older men
who were runners were only 10 per cent shorter than the younger men. In the
middle-aged runners, telomere loss was reduced by about 75 per cent.
When it comes to telomere length and diet, results are
mixed. While a 2008 study Dietary Patterns, Food Groups, and Telomere Length in
the Multi-Ethnic Study of Atherosclerosis, published in The American Journal of
Clinical Nutrition, found that the intake of whole grains, fruit and
vegetables, low-fat dairy, nuts or seeds, non-fried fish, coffee, refined
grains, fried foods, red meat, sugar-sweetened soft drinks had no effect on
telomeres. Eating processed meat, however, affected telomere length.
mixed. While a 2008 study Dietary Patterns, Food Groups, and Telomere Length in
the Multi-Ethnic Study of Atherosclerosis, published in The American Journal of
Clinical Nutrition, found that the intake of whole grains, fruit and
vegetables, low-fat dairy, nuts or seeds, non-fried fish, coffee, refined
grains, fried foods, red meat, sugar-sweetened soft drinks had no effect on
telomeres. Eating processed meat, however, affected telomere length.
But another study in the same journal two years later,
Associations Between Diet, Lifestyle Factors, and Telomere Length in Women,
found that fibre, waist size and saturated fats all affected telomere length in
older women. A 2012 study in Age found the Mediterranean diet reduced
senescence-associated stress in endothelial cells. In other words, general diet
recommendations for longevity correlate with longer telomeres. Drinking green
tea, following the Mediterranean diet and lowering sugar have all been shown to
protect our cells.
Associations Between Diet, Lifestyle Factors, and Telomere Length in Women,
found that fibre, waist size and saturated fats all affected telomere length in
older women. A 2012 study in Age found the Mediterranean diet reduced
senescence-associated stress in endothelial cells. In other words, general diet
recommendations for longevity correlate with longer telomeres. Drinking green
tea, following the Mediterranean diet and lowering sugar have all been shown to
protect our cells.
Will the secret to immortality be solved? Only time will
tell. But science will probably provide the answer on how to cure more diseases
and help us lengthen our healthy lives. Telomeres are just the first step.
tell. But science will probably provide the answer on how to cure more diseases
and help us lengthen our healthy lives. Telomeres are just the first step.
- Brain World
Amy Klein is the editor of Brain World magazine.
(sourced from http://www.theage.com.au/lifestyle/buying-time-20130712-2pudb.html)
