Caffeine may slow the ageing process at a cellular level by activating a key energy-sensing system in cells, researchers have found.
The stimulant works by triggering AMPK, a cellular fuel gauge that helps cells respond when energy levels drop. This pathway is evolutionarily conserved in both humans and simpler organisms and plays a role in regulating cell growth, DNA repair and stress responses.
The findings come from scientists at Queen Mary University of London, who studied fission yeast – single-celled organisms that share many features with human cells.
A few years ago, the same research team showed that caffeine extends cell lifespan by influencing TOR (Target of Rapamycin), a growth regulator that controls when cells grow based on nutrient availability.
The TOR pathway is found across many species and has been conserved for over 500 million years.
However, the latest study, from the Cellular Ageing and Senescence laboratory at Queen Mary’s Centre for Molecular Cell Biology, shows that caffeine does not act on TOR directly.
Instead, it activates AMPK – the same target as metformin, a diabetes drug also being investigated for its potential role in extending human lifespan.
Dr Charalampos Rallis is reader in genetics, genomics and fundamental cell biology and senior author of the study.
Rallis said: “When your cells are low on energy, AMPK kicks in to help them cope,” said“And our results show that caffeine helps flip that switch.”
Using yeast models, the researchers demonstrated that caffeine’s impact on AMPK affects several key processes involved in ageing and disease, including cell growth, DNA repair and the ability to manage stress.
Dr John-Patrick Alao, the postdoctoral scientist who led the study, said: “These findings help explain why caffeine might be beneficial for health and longevity.
“And they open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines.”