Every generation has tried to cheat death: from ancient Egyptians seeking eternal life to current scientists coming up with new medications and diets promising youth. However, so far, nothing has worked.
The main reasons we age:
- DNA damage
Every day our DNA gets damaged, from UV exposure, toxins we breathe in, even just normal metabolic processes happening inside our cells. Our body has many repair mechanisms to fix these things, but not all of them.
Over decades, these errors accumulate, with the damage effecting how our cells function. When this happens cells can malfunction, die or turn cancerous.
There’s also a specific type called oxidative damage – which is a byproduct of our cells producing energy. Whilst oxygen is essential for life, it also produces unstable molecules called free radicals that attack DNA. Antioxidants can neutralise them, which is why we hear about them all the time in healthy eating, however are not a complete solution.
- Inflammation
When a cell gets too damaged it has two options – it can die, or it can stop dividing but stay alive. This is called senescent cells, which are sometimes called zombie cells.
These zombie cells stay in your body and release inflammatory chemicals into the surrounding tissues – signalling nearby cells that something is wrong. In small amounts this is useful, as your immune system can deal with it, however as you age and senescent cells accumulate, the signal becomes constant background noise.
This is called inflammaging, a combination of inflammation and ageing. It is now thought to be a driver behind most age related diseases such as heart disease, cancer, Alzheimer’s, arthritis.
Your immune system is meant to clear out senescent cells, but as you age your immune system weakens too, leading the zombie cells to build up faster than they get cleared.
Scientists are trying to develop drugs that get clear out ‘zombie cells’ to delay these age related diseases.
- Telomeres
Every strand of our DNA has protective caps on the ends called telomeres (they’re often compared to plastic tips on the end of a shoelace). They stop our DNA from fraying and unravelling.
Every time a cell divides, it has to copy its DNA. However, the copying mechanism can’t quite reach the very end of the strand, so every time it divides the telomere gets slightly shorter.
Eventually it becomes too short, meaning if it divides any more, it will lose genetic information. So the cell either becomes senescent or dies.
This is called the Hayflick limit. The maximum number of times a cell can divided before its telomeres run out. Most human cells can divide around 50-70 times before hitting the limit.
However there’s an enzyme called telomerase that can rebuild telomeres. It’s very active in embryos, but in most adult cells, it’s switched off. Scientists are now researching whether reactivating telomerase could slow ageing, but the risk is it could also trigger cancer.
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