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In the beginning, we’re nothing more than a single cell. Then we divide into 2 cells. Then 4. Eventually we become ourselves – a multicellular organism capable of understanding terms like multicellular organism.  

 

But even in adulthood, our cells never stop dividing and replicating. This has obvious advantages, like allowing our body to grow and repair. These functions came in handy after my last bad haircut. For now at least, my hair cells still grow back.  

 

DNA copying and telomere chopping

 

When a hair cell – or any normal human cell – divides, its DNA divides along with it. But as with everything in the human body, this process doesn’t exactly run like a Swiss watch. Every time a cell splits, in fact, a little chunk of replicated DNA gets lost. The chunk that gets lost is actually a chunk of telomere.

 

If DNA was a shoelace, telomeres are the doohickies on the ends that keep the laces from unraveling. They protect the DNA from mutations, copying errors, and damage. Every time DNA gets copied, however, telomeres get taken to the knife. Eventually they get sliced out of existence.

 

Cellular senescence, the telomeric brink, and heart disease

 

After about 60 divisions, our cells hit what’s known as the Hayflick limit, run out of telomere, and become inactive. But these inactive, or “senescent” cells, doesn’t just disappear. Instead they accumulate in our body, drive chronic inflammation, and increase our risk for degenerative disease. Not cool.

 

Because cells turn senescent when they run out of telomere, scientists speculate that the length of our telomeres sets an upper limit on human lifespan. They even have a sexy name for this limit: the “telomeric brink”. When we hit the telomeric brink – when our telomeres run out of length from all those cell divisions – our risk of death becomes imminent.

 

Even before the telomeric brink, though, short telomeres are linked to serious issues in the human body. For instance, two comprehensive meta-analyses (link, link) found an inverse relationship between telomere length and heart disease risk. In other words, the shorter your telomeres, the higher your risk for CVD. By one theory, this happens because short telomeres provide poor protection against oxidative damage, a driver of atherosclerosis.

 

Telomerase rebuilds telomeres

 

In another much-cited paper, researchers found that Ashkenazi centenarians bear a genetic mutation allowing them to maintain longer telomeres into their twilight years. The mutation increases the centenarians’ expression of a protein called telomerase in their cells. What does telomerase do, you ask? It rebuilds and lengthens telomeres.

 

Here’s the thing: telomerase is not usually active in our cells. And without it, our telomeres get shorter and shorter with the passage of time. Remember: every time our cells divide, we lose a little bit of telomere. Kind of sad.

 

But telomerase isn’t always dormant. In one observational study, researchers found that intensive meditation significantly boosted telomerase activity in a small group of retreat participants. In another pilot study, a group of men at risk for prostate cancer increased telomerase activity after merely making “lifestyle changes”.

 

Given the importance of telomerase and telomeres in the aging process, more research is surely on the way.

 

The dark side of long telomeres

 

Yet there’s a dark side to telomerase and it’s telomere-lengthening properties. This dark side can be summarized in a single word: cancer.

 

Remember how telomerase isn’t usually active in normal cells? Well it doesn’t work that way with cancer. Nope, telomerase is expressed in 85% of these malignant cells. Cancer loves telomerase. By preserving telomere length, telomerase makes cancer cells immortal.

 

Inhibiting telomerase is, in fact, a potentially promising cancer treatment. More research is needed though.

 

Even now though, there’s plenty of research linking long telomeres to cancer. In several large observational studies on humans, lung cancer, prostate cancer, and melanoma were all associated with long telomere length. Skin cancer is a strange one, however, because the risk of non-melanoma skin cancers actually decreases with long telomeres. It’s unclear why this is the case.

 

The bright side of short telomeres

 

We’ve already covered the pros and cons of long telomeres. Let’s turn now to the advantages of short ones.

 

Compared to most other mammals, we humans, you might be surprised to learn, have rather short telomeres. That’s right: quivering critters like squirrels and jack rabbits have longer telomeres and more telomerase activity than we do.

 

It all seems rather strange. Long telomeres are supposed to be the key to longevity. Why does a shrew have us beat in this category?

 

The leading theory, in fact, is that short telomeres and repressed telomerase are actually tumor-suppression mechanisms. This is true because cells that run out telomere can’t become immortal cancer cells. Here’s the evolutionary argument: since long-lived humans are more susceptible to cancer than short-lived squirrels, we require more tumor-suppression than they do. That’s what our short telomeres are for.

 

The telomere tradeoff

 

When it comes to telomere length, there’s clearly a tradeoff. Long telomeres protect against cell senescence and heart disease, yet short telomeres offer protection against cancer. Science is still trying to determine that Goldilocks, “just right”, telomere length for humans.

 

When you take cancer out of the picture, that length might be pretty long. Case in point: activating telomerase in genetically engineered, cancer-resistant mice, both delayed their rate of aging and improved their gut barrier function.

 

So if we can remove cancer from the human genome, telomerase activation could be a sweet anti-aging therapy. Until then, however, fooling with telomere length seems risky.

 

Thinking ahead…

 

We may start as one cell, but nowadays we’re more like 37.2 trillion. Every day, all throughout our body, trillions of cells are dividing, trillions of genes are copying, and trillions of telomeres are shortening. We’re all marching together towards the telomeric brink.

 

Yet the brink isn’t necessarily a bad thing. By handing us shorter telomeres, evolution may have made us more prone to oxidative damage, but it also protected us from cancer. It’s a tradeoff.

 

Perhaps in the future we’ll think our way out of this tradeoff. Perhaps we’ll engineer, as we did in mice, our resistance to cancer.

 

And when that day comes, bring on the telomerase.

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