We finally know why we age - now to figure out how to stop it

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We finally know why we age - now to figure out how to stop it

Turns out it's our genes that age us and not wear and tear

Sarah Knapton

Humans do not age because of wear and tear but because biological processes – which once helped us – fail to shut off, new research suggests.
Scientists from University College London, Lancaster University and Queen Mary University of London believe that once-useful genetic programmes continue to “run on” pointlessly in later life causing age-related diseases.
For example when women breastfeed, calcium is taken from their bones to fortify their milk, but in later life the same process can fuel osteoporosis, arthritis and calcified blood vessels which leads to heart disease.Similarly men with high levels of testosterone, which is helpful for increasing sperm count in early life, are more at risk of prostate cancer in later life. So increased reproductive success has the downside of shortening lifespan.
“For decades scientists studying ageing have thought of ageing bodies as wearing out much like cars do, from a build-up of damage,” said Dr Alex Benedetto, a lead author on the study, formerly at UCL but now at Lancaster University.
“What’s exciting about this new work is that it shows something completely different. It turns out that we are not like cars – what kills us when we’re old is not random damage, but our own genes.“It seems that natural selection is short-sighted and ageing is the price we pay.”
The body physically deteriorates over time because of a process known as “senescence”  by which cells stop dividing and dying off, and instead enter a permanent state of inertia.Senescence is the main cause of disease and death worldwide and leads to dementia, cancer, cardiovascular disease and chronic obstructive pulmonary disease, but scientists have struggled to understand what causes it.To try and find out, the researchers focused on discovering the basic principles of ageing by studying simple animals such as Caenorhabditis elegans, a nematode worm which dies of old age after only two to three weeks.  
“Discovering the causes of ageing in these little creatures could provide the key to understanding human ageing, and where late-life diseases come from,” said Professor David Gems (UCL Institute of Healthy Ageing), corresponding author who led the team.  
“It is so important, because if you want to treat a disease you really need to understand what causes it. And senescence has really become the mother of all diseases, so understanding it is good news for all of us.”
In the new study, published in Current Biology, the scientists found that biological processes that make young worms better able to reproduce run-on pointlessly in older worms, causing disease.For example they found that the worms’ intestine consumes itself to create the yolk needed for its eggs, but in elderly worms, this process causes severe deterioration of the intestine and obesity and promotes tumours.
“Since genes we’ve found driving the destructive processes of ageing in worms are known to control lifespan in mammals, we think the findings are applicable to humans and mark a real paradigm shift in our understanding of ageing,” added first author Dr Marina Ezcurra, of UCL and Queen Mary.
The scientists conclude that when useful biological programmes run-on in later life, they can become disease-causing “quasi-programmes”.

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