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One current, predominant, scientific view of human aging is that the DNA of our cells becomes progressively damaged, causing cells to become irreversibly aged and dysfunctional.
Telomeres throughout the body shorten as we age, and this underlying mechanism contributes to most diseases of aging. Telomeres explain how we run out of the abilty to replenish tissue (called replicative senescence).
You’re born with a particular set of genes, but the way you live can influence how your genes express themselves.
As the obesity researcher George Bray has said, “Genes load the gun, and environment pulls the trigger.”
telomeres (tee-lo-meres), repeating segments of noncoding DNA that live at the ends of your chromosomes. Telomeres, which shorten with each cell division, help determine how fast your cells age and when they die, depending on how quickly they wear down.
The way you live can, in effect, tell your telomeres to speed up the process of cellular aging. But it can also do the opposite. The foods you eat, your response to emotional challenges, the amount of exercise you get, whether you were exposed to childhood stress, and even the level of trust and safety in your neighborhood—all of these factors and more appear to influence your telomeres and can prevent premature aging at the cellular level.
Cells reproduce by making copies of themselves (called mitosis),
Eventually these tired cells reached a stage he called senescence: They were still alive but they had all stopped dividing, permanently.
From a linguistic perspective, the word senescent has a shared history with the word senile. In a way, that’s what these cells are—they’re senile. In one way it is definitely good that cells stop dividing. If they just keep on multiplying, cancer can ensue. But these senile cells are not harmless—they are bewildered and weary. They get their signals confused, and they don’t send the right messages to other cells. They can’t do their jobs as well as they used to. They sicken. The time of luxuriant growth is over, at least for them. And this has profound health consequences for you. When too
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Many healthy human cells can divide repeatedly, so long as their telomeres (and other crucial building blocks of cells like proteins) remain functional. After that, the cells become senescent. Eventually, senescence can even happen to our amazing stem cells. This limit on cells dividing is one reason that there seems to be a natural winding down of the human healthspan as we age into our seventies and eighties,
There are around three hundred thousand centenarians worldwide, and their numbers are rapidly increasing.
Based on trends, it is thought that over one-third of children born in the United Kingdom now will live to one hundred years.
Some of us respond to difficult situations by feeling highly threatened—and this response is linked to shorter telomeres. We can reframe our view of situations in a more positive way.
Several mind-body techniques, including meditation and Qigong, have been shown to reduce stress and to increase telomerase, the enzyme that replenishes telomeres.
Exercise that promotes cardiovascular fitness is gre...
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Telomeres hate processed meats like hot dogs, but fresh, whole foods are good for them.
Neighborhoods that are low in social cohesion—meaning that people don’t know and trust one another—are bad for telomeres.
Children who are exposed to several adverse life events have shorter telomeres.
Telomeres can build up as well as shorten.
Even if you are currently on a fast track to premature cellular aging, you can switch lanes.
telomerase, an enzyme in our cells that helps keep the protective sheaths around our chromosome ends in good shape.
By cultivating your telomeres, you can optimize your chances of living a life that is not just longer but better.
One study has found that people who tend to focus their minds more on what they are currently doing have longer telomeres than people whose minds tend to wander more.5 Other studies find that taking a class that offers training in mindfulness or meditation is linked to improved telomere maintenance.
Mental focus is a skill that you can cultivate. All it takes is practice.
telomerase (pronounced tell-OMM-er-ase)
When cells can no longer renew themselves, the body tissues they supply will start to age and function poorly.
Cells in our tissues originate from stem cells, which have the amazing ability to become many different types of specialized cells.
If you go jogging
and tear your calf muscle, some of your muscle stem cells will divide, each stem cell creating two new cells. One of those cells replaces the original stem cell and remains comfortably in its niche; the other can become a muscle cell and help replenish the damaged tissue. Having a good supply of stem cells that are able to renew themselves is key to staying healthy and to recovering from sickness and injury.
An old cell’s DNA can’t communicate well with the other parts of the cell, and the cell can’t keep house well. The old cell gets crowded inside, with—among other things—clumps of malfunctioning proteins and brown globs of “junk” known as lipofuscin, which can cause macular degeneration in the eyes and some neurological diseases.
With age, these fibroblasts secrete less collagen and elastin, which makes the outer layer of visible skin look old and loose. This effect translates upward through the skin layers to create a more aged outer appearance. Aged skin becomes thinner, as it loses fat pads and hyaluronic acid (which acts as a natural moisturizer for skin and joints).
The UV rays from sun exposure can damage telomeres.6 Petra Boukamp, a telomere skin researcher from the German Cancer Research Center in Heidelberg, and her colleagues have compared skin from a sun-exposed site—the neck—to a sun-protected site—the buttocks. The outer cells on the neck showed some telomere attrition from the sun, whereas the protected buttock cells showed almost no telomere attrition with aging! Skin cells, when protected from the sun, can withstand aging for a long time.
The observation that inflammation increases with age and is a cause of the diseases of aging is so important that scientists have a name for it: inflamm-aging. This is a persistent, low-grade inflammation that can accumulate with age. There are many reasons why this occurs, such as proteins becoming damaged. One other common cause of inflamm-aging involves telomere damage.
A shortened telomere can sit inside an aging cell for months, signaling and signaling for help but not allowing the cell to take action to resolve the damage. This unremitting but futile signaling can have devastating consequences. Because now that cell becomes like the rotten apple in the barrel. It starts affecting all the tissues around it. The SASP process involves chemicals like proinflammatory cytokines that, over time, travel through the body, leading to system-wide chronic inflammation. Judith Campisi of the Buck Institute of Aging discovered SASP, and she has shown that these cells
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If you want to slow inflamm-aging, if you want to stay in the healthspan for as long as possible, you’ve got to prevent chronic inflammation.
Just being in the bottom third of the population’s blood telomere length means you are 40 percent more likely to develop cardiovascular disease in the future.
short blood cell telomeres can also trigger inflammation, which sets the stage for cardiovascular disease. Inflammatory cells stick to the sides of the arteries and trap cholesterol to form plaques or make existing plaques unstable. If a plaque ruptures, a blood clot can form over the plaque, blocking the artery. And if this artery is a coronary artery, it chokes off the heart’s blood supply and causes a heart attack.
Lacking robust telomere maintenance, lung stem cells and blood vessels of the lungs become senescent. They cannot keep the lung tissues replenished and supplied with their needs.
In one study of otherwise healthy seventy-year-olds, shorter telomeres predicted general cognitive decline years later.
The hippocampus, for example, is a part of the brain that helps form, organize, and store memories; it also helps link those memories to your emotions and your senses.
The hippocampus is made up of cells that need to regenerate—and if you want to have good memory function, it’s essential for your body to be able to replenish the hippocampus’s cells.
One study found if you have this gene variant and also have short telomeres, your risk of dying earlier is nine times greater than if you have the same gene variant but your telomeres are long.
People who long to be a chronologically younger age (say, a man in his fifties who wishes he could be thirty again) tend to be unhappier and more dissatisfied with their lives.
If you think of aging in a positive way, odds are that you’ll live seven and a half years longer than someone who doesn’t,
In the Kaiser Permanente Research Program on Genes, Environment, and Health study of one hundred thousand people’s salivary telomere length, telomeres on average grew shorter and shorter as people progressed from their twenties, hitting rock bottom at around age seventy-five.1 In an interesting coda, telomere length appears to stay the same or even go up as people live past seventy-five.
Many large studies have shown that people with shorter telomeres are more likely to have a chronic disease, such as diabetes, cardiovascular disease, lung diseases, impaired immune function, and certain types of cancers, or to develop one of these diseases over time.
Telomerase creates new telomeres patterned on its own biochemical sequence.
Telomerase is the enzyme responsible for restoring the DNA lost during cell divisions. Telomerase makes and replenishes telomeres.
Telomerase can slow, prevent, or even reverse the shortening of telomeres that comes with cell division. Telomeres can, in a sense, be renewed by telomerase.
After these discoveries, both the scientific world and the global media buzzed with hopeful speculation. What if we could increase our supply of telomerase? Could we be like Tetrahymena, with cells that renew forever? (This may have been the first recorded instance of humans fervently wishing to be more like pond scum.)
