Based on what we currently know about ageing, scientists believe that if we could engineer so-called “sluggish” cells, either to change their function or remove them from our genome completely, we could stop or even reverse the ageing process. A form of artificial “natural selection.”
But, unsurprisingly, it’s not that simple. As the body ages, certain cells slow down or lose function while others accelerate. We get grey hair because our cells stop producing pigment, but our risk of cancer is higher as we age due to the faster-than-normal growth.
By simulating what would happen if the sluggish cells were removed, mathematicians at the University of Arizona have found that not only would this artificial natural selection fail to slow down the ageing process, it could actually lead to cancer becoming more prolific.
"As you age, most of your cells are ratcheting down and losing function, and they stop growing, as well. But some of your cells are growing like crazy,” said Paul Nelson, lead author of the study published in the Proceedings of the National Academy of Sciences.
"What we show is that this forms a double bind - a catch-22. If you get rid of those poorly functioning, sluggish cells, then that allows cancer cells to proliferate, and if you get rid of, or slow down, those cancer cells, then that allows sluggish cells to accumulate. So you're stuck between allowing these sluggish cells to accumulate or allowing cancer cells to proliferate, and if you do one you can't do the other. You can't do them both at the same time.”
This goes some way to explaining why our bodies haven’t evolved to eradicate “ageing” as a form of disease. It also begins to unlock some of the reasons behind the mystery of why we age.
"People have looked at why ageing happens, from the perspective of 'why hasn't natural selection stopped ageing yet?' That's the question they ask, and implicitly in that is the idea that such a thing as non-ageing is possible, so why haven't we evolved it? We're saying it's not just a question of evolution not doing it; it can't be done by natural selection or by anything else," co-author Joanna Masel said.
"You might be able to slow down ageing but you can't stop it. We have a mathematical demonstration [that] you can fix one problem but you're stuck with the other one. Things will get worse over time, in one of these two ways or both: Either all of your cells will continue to get more sluggish, or you'll get cancer. And the basic reason is that things break. It doesn't matter how much you try and stop them from breaking, you can't."
Nelson's and Masel's work, Intercellular Competition and Inevitability of Multicellular Aging, was supported by the National Institutes of Health and the John Templeton Foundation.
The work supports, in some way, claims made by British neurobiologist and former chief executive of the British Medical Research Council, Professor Sir Colin Blakemore.
At a gerontology conference in 2014, Professor Sir Blakemore claimed that while we may be able to engineer it so humans live longer than they do now, 120 years might be a “real absolute limit” of our lifespan - even with medical and technological advances.
Yet, not everyone agrees. After editing the genes of the Caenorhabditis elegans - a worm commonly used to study ageing since it becomes the first animal to have its entire genome mapped - researchers from Buck Institute of Age Research, Novato, California found a way to boost its lift five-fold. If successful in humans, the technique could set the absolute list closer to 450 or 500.
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