Aging
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June 2017
Why You Can’t Help But Act Your Age
The surprising relationship between mindset and getting old.
By Anil Ananthaswamy
In 1979, psychologist Ellen Langer and her students carefully
refurbished an old monastery in Peterborough, New Hampshire, to
resemble a place that would have existed two decades earlier. They
invited a group of elderly men in their late 70s and early 80s to spend
a week with them and live as they did in 1959, “a time when an IBM
computer filled a whole room and panty hose had just been introduced to
U.S. women,” Langer wrote. Her idea was to return the men, at least in
their minds, to a time when they were younger and healthier—and to see
if it had physiological consequences.
Every day Langer and her students met with the men to discuss “current”
events. They talked about the first United States satellite launch,
Fidel Castro entering Havana after his march across Cuba, and the
Baltimore Colts winning the NFL championship game. They discussed
“current” books: Ian Fleming’s Goldfinger and Leon Uris’ Exodus. They
watched Ed Sullivan and Jack Benny and Jackie Gleason on a
black-and-white TV, listened to Nat King Cole on the radio, and saw
Marilyn Monroe in Some Like It Hot. Everything was transporting the men
back to 1959.
When Langer studied the men after a week of such sensory and mindful
immersion in the past, she found that their memory, vision, hearing,
and even physical strength had improved. She compared the traits to
those of a control group of men, who had also spent a week in a
retreat. The control group, however, had been told the experiment was
about reminiscing. They were not told to live as if it were 1959. The
first group, in a very objective sense, seemed younger. The team took
photographs of the men before and after the experiment, and people who
knew nothing about the study said the men looked younger in the
after-pictures, says Langer, who today is a professor of psychology at
Harvard University.
breaker 1 IN THE YEAR 1959A psychology experiment that took seniors
back to a time when they were young—1959, to be exact, evoked by the
images above—revealed that living as they did in 1959 improved their
memory, vision, and hearing.
Clockwise: Robert Riger / Getty Images; Wikipedia; Wikipedia; Luis
Korda/ Wikipedia; Wikipedia; Wikipedia
Langer’s experiment was a tantalizing demonstration that our
chronological age based on our birthdate is a misleading indicator of
aging. Langer, of course, was tackling the role of the mind in how old
we feel and act. Since her study, others have taken a more objective
look at the aging body. The goal is to determine an individual’s
“biological age,” a term that aims to capture the body’s physiological
development and decline with time, and predict, with reasonable
accuracy, the risks of disease and death. As scientists have worked to
pinpoint a person’s biological age, they have learned that organs and
tissues often age differently, making it difficult to reduce biological
age to a single number. They have also made a discovery that echoes
Langer’s work. How old we feel—our subjective age—can influence how we
age. Where age is concerned, the pages torn off a calendar do not tell
the whole story.
While we intuitively know what it means to grow old, precise
definitions of aging haven’t been easy to come by. In 1956, British
gerontologist and author Alex Comfort (later famous for writing The Joy
of Sex) memorably defined senescence as “a decrease in viability and an
increase in vulnerability.” Any given individual, he wrote, would die
from “randomly distributed causes.” Evolutionary biologists think of
aging as something that reduces our ability to survive and reproduce
because of “internal physiological deterioration.” Such deterioration,
in turn, can be understood in terms of cellular functions: The older
the cells in an organ, the more likely they are to stop dividing and
die, or develop mutations that lead to cancer. This leads us to the
idea that our bodies may have a true biological age.
The road to determining that age, though, has not been a straight one.
One approach is to look for so-called biomarkers of aging, something
that’s changing in the body and can be used as a predictor of the
likelihood of being struck by age-related diseases or of how much
longer one has left to live. An obvious set of biomarkers could be
attributes like blood pressure or body weight. Both tend to go up as
the body ages. But they are unreliable. Blood pressure can be affected
by medication and body weight depends on lifestyle and diet, and there
are people who certainly don’t gain weight as they age.
Where age is concerned, the pages torn off calendar do not tell the
whole story.
In the 1990s, one promising biomarker stood out: stretches of DNA
called telomeres. They appear at the ends of chromosomes, serving as
caps that protect the chromosomes from fraying. Telomeres have often
been likened to the plastic tips that similarly protect shoelaces. It
turns out that telomeres themselves get shorter and shorter each time a
cell divides. And when the telomere shortens beyond a point, the cell
dies. There’s a strong relationship between telomere length and health
and diseases, such as cancer and atherosclerosis.
But despite a range of studies trying to find such a link, it’s been
hard to make the case for telomeres as accurate biomarkers of aging. In
2013, Anne Newman, director of the Center for Aging and Population
Health at the University of Pittsburgh, and her student Jason Sanders
reviewed the existing literature on telomeres and concluded that “if
telomere length is a biomarker of human aging, it is a weak biomarker
with poor predictive accuracy.”
“Twenty years ago, people had high hopes that telomere length could
actually explain aging, as in biological aging. There was a hope that
it would be the root cause of aging,” says Steve Horvath, a geneticist
and biostatistician at the University of California, Los Angeles. “Now
we know that that’s simply not the case. In the last 10 to 15 years,
people realized that there must be other mechanisms that play an
important role in aging.”
Attention shifted to how fast stem cells are being depleted in the
body, or the efficacy of mitochondria (the organelles inside our cells
that produce the energy needed for cells to function). Horvath scoured
the data for reliable markers, looking at, for example, levels of gene
expression for any strong correlations to aging. He found none.
But that didn’t mean there weren’t reliable biomarkers. There was one
set of data Horvath had been studiously avoiding. This had to do with
DNA methylation, a process cells use to switch off genes. Methylation
mainly involves the addition of a so-called methyl group to cytosine,
one of the four main bases that make up strands of DNA. Because DNA
methylation does not alter the core genetic sequence, but rather
modifies gene expression externally, the process is called epigenetics.
breaker 2 EPIGENETIC CLOCKUCLA geneticist Steve Horvath (above)
identified methylation levels on the human genome that serve as
remarkable signs of biological aging. “I had never seen anything like
it,” he says. “It’s a cliché, but it really was a smoking gun.”
Courtesy of Steve Horvath
Horvath didn’t think that epigenetics would have anything to do with
aging. “I had data sitting there and I would not really touch them,
because I thought there was no meaning in it anyway,” he says.
But some time in 2009, Horvath gave in and analyzed a dataset of
methylation levels at 27,000 locations on the human genome—an analysis
“you can do in an hour,” he says. Nothing in his 10 years of analyzing
genomic datasets had prepared him for the results. “I had never seen
anything like it,” he says. “It’s a cliché, but it really was a smoking
gun.”
Because their minds were taken back to a time when they were
younger, their bodies went back too.
After a few more years of “labor intensive” work, Horvath identified
353 special sites on the human genome that were present in cells in
every tissue and organ. Horvath developed an algorithm that used the
methylation levels at these 353 sites—regardless of the cell type—to
establish an epigenetic clock. His algorithm took into account that in
some of these 353 sites, the methylation levels decreased with age,
while in others they increased.
In 2013, Horvath published the results of his analysis of 8,000 samples
taken from 51 types of healthy tissue and cells, and the conclusions
were striking. When he calculated a single number for the biological
age of the person based on the weighted average of the methylation
levels at the 353 sites, he found that this number correlated well with
the chronological age of the person (it was off by less than 3.6 years
in 50 percent of the people—a far better correlation than has been
obtained for any other biomarker). He also discovered that for
middle-aged people and older, the epigenetic clock starts slowing down
or speeding up—providing a way of telling whether someone is aging
faster or slower than the calendar suggests.
Despite the correlation, Horvath says that biological age, rather than
being for the whole body, is better applied to specific tissues and
organs, whether it’s bone, blood, heart, lungs, muscles, or even the
brain. The difference between the biological age and chronological age
can be negative, zero, or positive. A negative deviation means that the
tissue or organ is younger than expected; a zero indicates that the
tissue is aging normally; and a positive deviation means the tissue or
organ is older. Data show that different tissues can age at different
rates.
In general, diseases speed up the epigenetic clock, and this is
particularly striking in patients with Down’s syndrome or in those
infected with HIV. In both cases, the tissues tend to age faster than
normal. For instance, the blood and brain tissue in those infected with
HIV show accelerated aging. Obesity causes the liver to age faster. And
studies of people who died of Alzheimer’s disease show that the
prefrontal cortex undergoes accelerated aging. Horvath also analyzed
6,000 samples of cancerous tissue and found that the epigenetic clock
was ticking much faster in such cases, showing that the tissue had aged
significantly more than the chronological age.
Despite this wealth of data, there is a gaping hole in our
understanding of this striking correlation between methylation markers
and biological age. “The biggest weakness of the epigenetic clock is
that we just don’t understand the precise molecular mechanism behind
it,” says Horvath. His speculation—and he stresses it’s just
speculation—is that the epigenetic clock is related to what he calls
the “epigenetic maintenance system,” molecular and enzymatic processes
that maintain the epigenome and protect it from damage. “I feel that
these markers are a footprint of that mechanism,” says Horvath. But
“why is it so accurate? What pathway relates to it? That’s the biggest
challenge right now,” he adds.
Even without understanding exactly how and why it works, the epigenetic
clock gives researchers a tool to test the efficacy of anti-aging
interventions that can potentially slow aging. “It’d be very exciting
to develop a therapy that allows us to reset the epigenetic clock,”
says Horvath.
While Horvath is thinking about hormonal treatments, Langer’s work with
elderly men at the monastery in New Hampshire suggests that we can use
the power of our mind to influence the body. Langer didn’t publish her
results in a scientific journal in 1979. At the time, she didn’t have
the resources to do a thorough study for the leading journals. “When
you run a retreat over the course of five days, it’s very hard to
control for everything,” Langer says. “Also, I didn’t have the funds to
have, for instance, a vacationing control group. I could have published
it in a second-rate journal, but I didn’t see any point to that. I
wanted to get the information out there and I wrote it first in a book
for Oxford University Press, so it was reviewed.”
Also, her argument that mind and body are one was potentially a little
too path-breaking for the journals. “I think they were unlikely to buy
the theoretical part of it,” she says. “The findings, improving vision
and hearing in an elderly population, were so unusual that they were
not going to rush to publish and stick their necks out.” Since then,
Langer has pursued the mind-body connection and its effects on
physiology and aging in rigorous studies that have been published in
numerous scientific journals and books.
Traditionally, the mind-body problem refers to the difficulty of
explaining how our ostensibly non-material mental states can affect the
material body (clearly seen in the placebo effect). To Langer, the mind
and body are one. “Wherever you put the mind you are necessarily
putting the body,” she says.
So Langer began asking if subjective mental states could influence
something as objective as the levels of blood sugar in patients with
Type 2 diabetes. The 46 subjects in her study, all suffering from Type
2 diabetes, were asked to play computer games for 90 minutes. On their
desk was a clock. They were asked to switch games every 15 minutes. The
twist in the study was that for one-third of the subjects, the clock
was ticking slower than real time, for one-third it was going faster,
and for the last third, the clock was keeping real time.
Most of us are slaves to our chronological age.
“The question we were asking was would blood sugar level follow real or
perceived time,” says Langer. “And the answer is perceived time.” This
was a striking illustration of psychological processes—in this case the
subjective perception of time—influencing metabolic processes in the
body that control the level of blood sugar.
Although Langer did not explore a connection between the mind and
epigenetic changes, other studies suggest such a link. In 2013, Richard
Davidson of the University of Wisconsin at Madison and his colleagues
reported that even one day of mindfulness meditation can impact the
expression of genes. In their study, 19 experienced meditators were
studied before and after a full day of intensive meditation. For
control, the researchers similarly studied a group of 21 people who
engaged in a full day of leisure. At the end of the day, the meditators
showed lowered levels of activity of inflammatory genes—exactly the
kind of effect seen when one takes anti-inflammatory drugs. The study
also showed lowered activity of genes that are involved in
epigenetically controlling expressions of other genes. The state of
one’s mind, it seems, can have an epigenetic effect.
Such studies taken together provide clues as to why the week-long
retreat in New Hampshire reversed some of the age-related attributes in
elderly men. Because their minds were taken back to a time when they
were younger, their bodies too went back to that earlier time, bringing
about some of the physiological changes that resulted in improved
hearing or grip strength.
But it’s important to point out that biological aging is an inexorable
process—and there comes a time when no amount of thinking positive
thoughts can halt aging. If body and mind are one and the same—as
Langer suggests—then an aging body and aging mind go hand-in-hand,
limiting our ability to influence physiological decline with
psychological deftness.
Still, Langer thinks that how we age has a lot to do with our
perceptions of what aging means—often reinforced by culture and
society. “Whether it’s about aging or anything else, if you are
surrounded by people who have certain expectations for you, you tend to
meet those expectations, positive or negative,” says Langer.
Related Articles
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we age.
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MARCH 2017 What Good Is Grandma?
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human biology.
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Most of us are slaves to our chronological age, behaving, as the saying
goes, age-appropriately. For example, young people often take steps to
recover from a minor injury, whereas someone in their 80s may accept
the pain that comes with the injury and be less proactive in addressing
the problem. “Many people, because of societal expectations, all too
often say, ‘Well, what do you expect, as you get older you fall apart,’
” says Langer. “So, they don’t do the things to make themselves better,
and it becomes a self-fulfilling prophecy.”
It’s this perception of one’s age, or subjective age, that interests
Antonio Terracciano, a psychologist and gerontologist at Florida State
University College of Medicine. Horvath’s work shows that biological
age is correlated with diseases. Can one say the same thing about
subjective age?
People’s perception of their own age can differ markedly from person to
person. People between the ages of 40 and 80, for example, tend to
think they are younger. People who are 60 may say that they feel like
they are 50 or 55, or sometimes even 45. Rarely will they say they feel
older. However, people in their 20s often perceive their age to be the
same as their chronological age, and may say they feel somewhat older.
Terracciano and colleagues have found that subjective age correlates
with certain physiological markers of aging, such as grip strength,
walking speed, lung capacity, and even the levels of C-reactive protein
in the blood, an indication of inflammation in the body. The younger
you feel you are, the better are these indicators of age and health:
You walk faster, have better grip strength and lung capacity, and less
inflammation.
Subjective age affects cognition and is an indicator of the likelihood
of developing dementia. Terracciano and colleagues looked at data
collected from 5,748 people aged 65 or older. The subjects’ cognitive
abilities were evaluated to establish a baseline and they were then
followed for a period of up to four years. The subjects were also asked
about how old they felt at each instance. The researchers found that
those who had a higher subjective age to start with were more likely to
develop cognitive impairments and even dementia.
These correlation studies have limitations, however. For example, it’s
possible that physically active people, who have better walking speed
and lung capacity, and lower levels of C-reactive protein in their
blood, naturally feel younger. How can one establish that our
subjective age influences physiology and not the other way around?
That’s exactly what Yannick Stephan of the University of Grenoble in
France and colleagues tried to find out. They recruited 49 adults, aged
between 52 and 91, and divided them into an experimental and control
group. Both groups were first asked their subjective age—how old they
felt as opposed to their chronological age—and tested for grip strength
to establish a baseline. The experimental group was told they had done
better than 80 percent of people their age. The control group received
no feedback. After this experimental manipulation, both groups were
tested again for grip strength and asked about how old they felt. The
experimental group reported feeling, on average, younger than their
baseline subjective age. No such change was seen in the control group.
Also, the experimental group showed an increase in grip strength, while
the grip strength of the control decreased somewhat.
These correlations do not necessarily mean that feeling young causes
better health. Terracciano’s next step is to correlate subjective age
with quantitative biological markers of age. While no study has yet
been done to find associations between the newly developed epigenetic
markers and subjective age, Terracciano is keen to see if there are
strong correlations.
Still, the message seems to be that our chronological age really is
just a number. “If people think that because they are getting older
they cannot do things, or cut their social ties, or incorporate this
negative view which limits their life, that can be really detrimental,”
says Terracciano. “Fighting those negative attitudes, challenging
yourself, keeping an open mind, being engaged socially, can absolutely
have a positive impact.”
* Anil Ananthaswamy is an award-winning journalist and author. His
first book, The Edge of Physics, was named Book of the Year in 2010
by PhysicsWorld. His second book, The Man Who Wasn’t There, was
nominated for the PEN/E. O. Wilson Literary Science Writing Award.
@AnilAnanth
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Aging is produced with financial support from the Glenn Foundation.
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