Want to Live Forever? Lengthen Your Telomeres

Death may not be inevitable.

We are not machines whose parts get old and break. Our organs do not just get worn out and then give up. Our cells divide and die, leaving behind younger versions, so no cell in your body is as old as you.

Then how do we get old and why do we die?

Researchers in the last 50 years have shown that aging and natural death are the result of telomeres–the caps at the end of chromosomes–being chopped off with each replication. Once they have been completely chopped off, useful DNA is exposed, leading to the break down of the cell.

Living forever, therefore, is simply about finding ways to not only stop your telomeres from shortening but employing new–and perhaps controversial–methods to make them longer.

The Hayflick Limit: A Countdown to Death

A cell’s nucleus contains chromosomes, where DNA is packed closely and wrapped around proteins called histones, which determines how it is expressed. At the end of the chromosomes are telomeres, which help organize and protect the DNA. When DNA replicates, the DNA sequence is naturally shortened, as the enzymes responsible cannot reach all the way to the end, a problem known as “the end replication problem.” Therefore, vital information is at risk of being cut off with each cell division. 

To protect our DNA, nature has created a buffer of expendable DNA. These are telomeres. They serve no function other than to help organize and stop the end of DNA sequences from being chopped off. The problem, though, is that each replication whittles down the length of the telomeres, eventually exposing the useful DNA. When this happens, cells begin to break down.

Based on the above, the length of telomeres is correlated with age and a rough predictor of death. More specifically, babies are born with 8,000 to 13,000 base pairs in their telomeres, and each cell division removes 25-200 bases. Regardless of lifestyle, a person’s cells can only divide so many times, before a wall is it. This is the Hayflick Limit, named after Leonard Hayflick in 1961. He found that the typical human cell can only divide 40-60 times.

Lifestyle Choices Can Speed Up the Clock

Excessive drinking, large amounts of red meat, smoking, etc. have been shown to shorten telomeres, speeding up your biological clock. All of these can lead to oxidative stress, which is caused by free radicals. Free radicals are atoms, ions, or molecules–the majority of which are oxygen–with a missing electron in their outer shell, meaning they can easily bond with atoms they are not supposed to, causing damage. A healthy diet, on the other hand, is rich in antioxidants, which are stable atoms that can protect against that damage.

In particular, free radicals target telomeres, interfering in their normal functioning and shortening them prematurely. The results of this paper found that “Numerous studies have shown that oxidative stress is associated with accelerated telomere shortening and dysfunction.”

Telomerase and Cancer

Telomerase is an enzyme that naturally adds length to telomeres, but it is usually not active in most of the body’s cells. However, it is active in the germ cells (the sex cells). This makes sense as these cells need to be as young as possible. Otherwise, babies would be born with short telomeres, making them genetically older than they should be.

This is exactly what happened to Dolly, the sheep cloned in 1996. She was cloned from old cells, meaning she began to feel the decay of old age while still a baby. She was put down at the age of 6 due to a lung disease and severe arthritis.

Furthermore, scientists have found cancer cells have shortened telomeres and active telomerase. For cancer cells to multiply at a problematic rate, it makes sense that they must stabilize their telomeres.

Achieving Immortality, Hopefully

The obvious first step is to stop engaging in a lifestyle that speeds up the shortening of your telomeres. Next, try some experimental treatments and hope they don’t give you cancer.

Authors of a new study published in Biochemical and Biophysical Research Communications took blood samples from 3 people–114, 43, and 8 years old–and successfully added length to their telomeres. They did this by reprogramming their blood cells into mesenchymal stem cells, which are responsible for repairing structural tissue. The authors claim their results “indicate the potential to use reprogramming to reset both developmental state and cellular age in the ‘oldest of the old.'”

While this seems like a fountain of youth, a lot of work still needs to be done before being tried on a large scale. One fear in particular is the increased rates of cancer, as tinkering with telomeres has the potential to change the growth rate of the cells.

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