Science: Tell me about ... how we age

Charles Arthur
Sunday 18 January 1998 19:02 EST
Comments

Your support helps us to tell the story

From reproductive rights to climate change to Big Tech, The Independent is on the ground when the story is developing. Whether it's investigating the financials of Elon Musk's pro-Trump PAC or producing our latest documentary, 'The A Word', which shines a light on the American women fighting for reproductive rights, we know how important it is to parse out the facts from the messaging.

At such a critical moment in US history, we need reporters on the ground. Your donation allows us to keep sending journalists to speak to both sides of the story.

The Independent is trusted by Americans across the entire political spectrum. And unlike many other quality news outlets, we choose not to lock Americans out of our reporting and analysis with paywalls. We believe quality journalism should be available to everyone, paid for by those who can afford it.

Your support makes all the difference.

From the moment the human sperm mingles with the egg, the cells there can divide 100 times over. But eventually, even if we aren't hit by a bus or fall ill, everyone dies. Last Friday, a team of American scientists announced that they had found a way to make human cells in a test tube divide about another 20 times, the equivalent of living roughly one-fifth longer.

The way they did this was by investigating the telomere of the cells' DNA. The DNA inside our cell nuclei is arranged in 26 chromosomes, and each chromosome pair has a string of "base pairs" - the "letters" that make up DNA instructions - repeated over and over at their tail end. This is the telomere.

When a cell divides, the telomere shortens by roughly 65 base pairs. Eventually it shortens beyond a certain length. After this, the cell "refuses" to divide again. Instead it undergoes "programmed cell death", or apoptosis, which is the body's way of letting cells die quietly.

But you can make the telomere grow again, by applying an enzyme called telomerase. Our own bodies generate it to reset the length of the telomere in the cells which become our gametes (sperm or eggs). Thus there is a gene which makes telomerase too.

The American scientists found out how to switch on the telomerase gene in normal cells, the cells kept on dividing, and the telomere didn't shorten.

They described this as the "cellular fountain of eternal youth". But other scientists doubt it. Telomeres do not tell the whole story about ageing. There are many more reasons why we get old, and telomeres aren't involved in all of them.

Nobody is completely sure why we age, though there are plenty of theories. It may be linked to rapidity of cell reproduction - animals with fast metabolisms tend to live less long. It is not about size: tortoises can live hundreds of years, whereas a giraffe only lives about 40 years at best.

Genes play a significant part: some are very useful when we are young but a positive drawback when you're older - for example, castrated men live about 17 years longer than other men, but (for obvious reasons) that's not a trait they can pass on to children. Genes which help us reproduce, but make us die early, will always be favoured by evolution over those that make us live longer.

(And simple logic demolishes the idea that telomerase is the secret of eternal life. If it were, then evolution has had plenty of time to produce somebody whose telomere never shortens. That person would be immortal. No immortals are known. QED.)

A more favoured theory of ageing suggests that it occurs because of accumulated damage to the machinery of our cells - especially their powerhouses, the mitochondria - caused by exposure to natural toxins and the effects of generating energy in the cell. That fits best with everything we know so far.

l Further reading: "Why We Age" by Steven Austad (John Wiley & Sons, pounds 19.99).

The web site http://www3. hmc.edu/clewis/aging contains some useful discussions of competing theories.

Join our commenting forum

Join thought-provoking conversations, follow other Independent readers and see their replies

Comments

Thank you for registering

Please refresh the page or navigate to another page on the site to be automatically logged inPlease refresh your browser to be logged in