Ageing causes grey hair and wrinkles, sore joints and memory loss. But what exactly is happening to our bodies as we age? Short answer: we really don’t know. The theories behind why we age are a bit like mirages, the closer we get the more they look like shimmering sand. But hopefully at least one of them turns out to be an oasis streaming from the fountain of youth.
As it stands now, there are two main theories of why we age. The first is that ageing is caused by degeneration of the maintenance and upkeep processes going on in our bodies – at the organ, tissue, cellular and DNA levels. We can divide this into three main (but interlinked) processes: oxidative damage; DNA repair problems; and telomere shortening. The second main theory of ageing is that all cells are pre-programmed to die at a certain point i.e. that each cell, organ and therefore person has a predetermined life span.
So let’s start with oxidative damage. Everything that happens in our bodies requires energy. This energy is made by organelles called mitochondria which are inside every cell. Chemical reactions occur inside mitochondria to transform the glucose and fatty acids we eat into useable energy. These reactions can inadvertently alter oxygen molecules and turn them into ‘reactive oxygen species’ also known as ‘free radicals’. These are normally mopped up by antioxidant molecules. But if for some reason the scales are tipped and there are more free radicals than antioxidants (e.g. due to environmental factors such as air pollution, or genetics such as a mutation in an antioxidant gene), the free radicals can start damaging the cell. They can cause damage to the cell membrane, the nuclear membrane and to DNA itself. This is called oxidative stress and is thought to contribute to ageing and many age-related diseases such as cancer, Parkinson’s, Alzheimer’s and heart failure.
DNA can be damaged by oxidative stress but it is also often damaged when cells reproduce. DNA must be copied each time a cell divides. There are 3 billion molecules in a full human DNA sequence, so mistakes are often made when the sequence is copied. The cell has an inbuilt system to identify and repair these mistakes. However if the repair system malfunctions, and these mistakes, or mutations, aren’t repaired, then the DNA may no longer work as a template to make RNA and proteins. Then the cell can’t make new proteins to replace old damaged ones and it can’t function properly.
The third potential ageing mechanism is telomere shortening. The DNA in all our cells is packaged into chromosomes which have sections of repeated nucleotides at each end. These sections are called telomeres. A small amount of DNA is lost from telomeres each time a cell divides. The telomeres are a bit like kamikaze pilots, they are essentially there to ‘take one for the team’ and make sure that important life sustaining DNA is not lost. When all the telomere sequence is lost, a cell can no longer divide. So new cells cannot be made to replace old and damaged cells. This inability to divide is called senescence.
Which brings me to the second major theory of ageing which is that senescence is in fact preprogrammed to occur and is not due to damage. The major evidence for this theory is that longevity is fairly consistent within species i.e. most cats live to be around 15-20, most humans live to be around 80-100. This implies that there must be a cellular ‘clock’ which knows when it is time for senescence to occur. And this clock ticks faster in cats than in humans.