The Cellular Connection to Longevity: Telomeres, Aging and the Keys to Lifelong Health

By Elizabeth Blackburn, Ph.D. & Elissa Epel Ph.D, Conscious Lifestyle Magazine

What Are Telomeres and Why They Matter: The Keys to Longer Lifespan

Deep into the genetic heart of your cells—on your chromosomes—is where you’ll find 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 extraordinary discovery from our research labs and other research labs around the world is that the ends of our chromosomes can actually lengthen—and as a result of our telomeres, aging is a dynamic process that can be accelerated or slowed, and in some aspects, aging can even be reversed. Aging need not be, as thought for so long, a one-way slippery slope toward infirmity and decay. We all will get older, but how we age is very much dependent on our cellular health.

To an extent that has surprised us and the rest of the scientific community, telomeres do not simply carry out the commands issued by your genetic code. Your telomeres, it turns out, are listening to you. They absorb the instructions you give them. 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—reverse aging. 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. In short, one of the keys to a long healthspan is simply doing your part to foster healthy cell renewal, which can be done by learning how to lengthen telomeres.

Healthy Cell Renewal and Why You Need It: How Long Can Our Cells Last?

In 1961, before we knew about telomeres and aging, the biologist Leonard Hayflick discovered that normal human cells can divide a finite number of times before they die. Cells reproduce by making copies of themselves (called mitosis), and as the human cells sat in a thin, transparent layer in the flasks that filled Hayflick’s lab, they would, at first, copy themselves rapidly. As they multiplied, Hayflick needed more and more flasks to contain the growing cell cultures. The cells in this early stage multiplied so quickly that it was impossible to save all the cultures; otherwise, as Hayflick remembers, he and his assistant would have been “driven out of the laboratory and the research building by culture bottles.” Hayflick called this youthful phase of cell division “luxuriant growth.” After a while, though, the reproducing cells in Hayflick’s lab stopped in their tracks, as if they were getting tired. The longest-lasting cells managed about fifty cell divisions, although most divided far fewer times. Eventually these tired cells reached a stage he called senescence: They were still alive but they had all stopped dividing, permanently. This is called the Hayflick limit, the natural limit that human cells have for dividing, and the stop switch happens to be telomeres that have become critically short, This is the link between telomeres and aging.

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