A groundbreaking study by the Cellular Ageing and Senescence laboratory at Queen Mary University of London has revealed how caffeine activates a powerful cellular fuel sensor that bolsters resilience against stress and energy depletion.
Your morning cup of coffee may be doing far more than sharpening your focus—it might actually be helping your cells live longer. A groundbreaking study by the Cellular Ageing and Senescence laboratory at Queen Mary University of London has revealed how caffeine, the world’s most widely consumed psychoactive compound, activates a powerful cellular fuel sensor that bolsters resilience against stress and energy depletion.

Published in the journal Microbial Cell, the research unpacks how caffeine interacts with intricate molecular pathways to potentially delay the ageing process at a fundamental level. Long known for its health-linked perks—including a lower risk of age-related diseases—coffee’s influence on the microscopic machinery within our cells has remained largely elusive.
That is, until now.
The scientists turned to an unlikely but scientifically insightful ally: fission yeast. This single-celled organism shares many key cellular mechanisms with humans, making it a prime model for ageing research. The team previously discovered that caffeine influences a growth regulator called TOR (Target of Rapamycin), a master switch that has governed cellular energy balance for over half a billion years.
Your morning coffee flips an ancient longevity switch
But in a surprising twist, the researchers now reveal that caffeine’s anti-ageing power doesn’t come from TOR directly. Instead, it stimulates another ancient cellular player—AMPK (AMP-activated protein kinase), a biological fuel gauge that manages how cells respond when energy levels dip.
“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics and Fundamental Cell Biology at Queen Mary University of London, and the study’s senior author. “And our results show that caffeine helps flip that switch.”
Interestingly, AMPK is the same system targeted by metformin—a common diabetes drug under intense study for its potential to extend human lifespan—alongside the longevity-linked compound rapamycin.
Through meticulous experimentation with their yeast model, the researchers demonstrated that caffeine’s activation of AMPK orchestrates key cellular functions such as growth regulation, DNA repair, and stress adaptation—crucial processes that play a direct role in ageing and age-related disease.
“These findings help explain why caffeine might be beneficial for health and longevity,” said Dr John-Patrick Alao, the postdoctoral scientist who spearheaded the study. “And they open up exciting possibilities for future research into how we might trigger these effects more directly — with diet, lifestyle, or new medicines.”


