- Mild stress strengthens the protein which builds the ‘powerhouse’ of our cells
- This happens because a ‘survival strategy’ kicks in in reaction to pressure
- But too much stress is bad, raising risk of heart attacks and other serious illness
A little bit of stress can slow down the effects of aging, reduce your risk of dementia and help you live longer, according to a new study.
Scientists found that when parts of DNA were put under mild pressure, the protein which builds them was strengthened.
Experts say this happens because a ‘survival strategy’ kicks in in reaction to stress.
However, too much pressure is bad, raising the risk of heart attacks and other serious illness.
Previous research has shown that chronic stress exposes your body to unhealthy, persistently elevated levels of stress hormones like adrenaline and cortisol.
It is also linked to changes in the way blood clots, which increases the risk of heart disease.
Research has found that mild stress can help prevent dementia but too much raises your risk of a heart attack (stock photo)
Senior study author Professor Richard Morimoto from Chicago’s Northwestern University, said: ‘This has not been seen before. People have always known that prolonged stress can be deleterious.
‘But we discovered that when you stress just a little, the mitochondrial stress signal is actually interpreted by the cell and animal as a survival strategy.
‘It makes the animals completely stress-resistant and doubles their lifespan. It’s like magic.’
Key findings
The team found putting mitochondria – the tiny bits of DNA known as the ‘powerhouse’ of cells – under stress in tapeworms strengthened the protein which builds them.
This, in turn, suppressed the damage that leads to a range of degenerative diseases including dementia, Huntington’s and Parkinson’s diseases and motor neurone disease.
The researchers hope that the results of their animal study can be replicated in humans.
‘Our findings offer us a strategy for looking at aging in humans and how we might prevent or stabilize against molecular decline as we age,’ said Professor Morimoto.
‘Our goal is not trying to find ways to make people live longer but rather to increase health at the cellular and molecular levels, so that a person’s span of good health matches their lifespan.’
The study was published in the journal Cell Reports.