IT HAPPENS to everyone who lives long enough, gradually at first and then suddenly. By the time we are in our 50s, most of us have at least one age-related health condition. By 85, almost all of us do, and typically several at once. Cancer, diabetes, cataracts, osteoarthritis, dementia. The list could go on and on.
None of which is surprising, at least to those of us old enough to have experience of ageing. What you may not be aware of, however, is that we now have a comprehensive understanding of ageing at the molecular and cellular level. Even more surprising is the growing consensus that ageing can be slowed or even reversed.
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鈥淭he belief that ageing is treatable is still there, there are optimists everywhere,鈥� says , director of the Max Planck Institute for Biology of Ageing in Cologne, Germany. 鈥淭he idea is very much that it鈥檚 going to be preventable.鈥�
Why we age has been debated for many years. There are two schools of thought. One is that it is the accidental but inexorable accumulation of damage to cells and biomolecules. The other is that ageing is biologically programmed, the evil twin of our development from embryo to adult.
Both hypotheses have evolution at their heart in the form of 鈥渞eproductive fitness鈥� 鈥� the ability to pass our genes on to our children. The damage-accumulation hypothesis argues that when we are young, it pays to invest in cellular repair processes to maximise that fitness. But after a certain age, that investment is no longer worth its cost, at which point repair processes falter and damage accumulates.
The programmed hypothesis counters that evolution has selected for a 鈥渟uicide鈥� programme that causes us to stop reproducing and drop dead, clearing the way for the carriers of our genes and maximising their reproductive fitness 鈥� which is, indirectly, ours.
In practical terms, why it happens hardly matters. The ageing process is the same regardless, and it contains multitudes. A lot of the damage happens to DNA, which accumulates mutations and becomes unstable. The ends of chromosomes erode and the pattern of chemical tags that can turn genes on and off, called epigenetic markers, changes in a way so predictable it can be used to estimate biological age.
The hallmarks of ageing
Plenty of other things fall apart, too. The intracellular waste-disposal system, known as autophagy, grinds to a halt; cells and tissues clog up with clumps of damaged protein and other detritus; the ability to sense sugars and other nutrients is blunted; mitochondria, the engines of our cells, become less efficient at producing energy; some cells become cancerous while others turn into zombies; stem cells stop dividing; low-level inflammation creeps throughout the body; and the gut microbiome becomes less healthy. All of these have been shown to contribute to age-related conditions.
The extent to which we now understand these processes is good news, because all these hallmarks have shown promise that they might be treatable. One of the criteria for the hallmarks is that each must be amenable to intervention, and all of them have passed that test 鈥� mostly in mice and rats, though some human trials have also been successful.
Already, there are promising signs that , reboot autophagy, , , clear out zombie cells and to full health.
This hardly constitutes a fountain of eternal youth, but it does explain the confidence that we can intervene in ageing. It may not lead to longer lives, but it will increase healthspan 鈥� that is, the number of healthy years before age-related conditions start piling up. And that is how we will think of ageing: as a health problem that can be treated, albeit never cured.
