Study Unveils How Caffeine May Help Slow Ageing at the Cellular Level - Video

A new study from the Cellular Ageing and Senescence Laboratory at Queen Mary University of London's Centre for Molecular Cell Biology reveals that caffeine the world’s most widely consumed neuroactive compound may do more than keep us alert. Published in the journal Microbial Cell, the research uncovers how caffeine could help slow down the ageing process by acting on key cellular energy and stress response systems.

In this latest study, researchers used fission yeast, a single-celled organism with cellular processes strikingly similar to those of humans, to explore how caffeine affects ageing.

The new findings show that caffeine activates AMPK, a conserved system that functions as a cellular “fuel gauge.” “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 and senior author of the study. “And our results show that caffeine helps flip that switch.”

AMPK is also the target of metformin, a diabetes medication currently under investigation for its potential to extend human lifespan, much like rapamycin.

The researchers demonstrated that caffeine’s activation of AMPK influences how cells grow, repair DNA, and handle stress key factors in ageing and age-related diseases. “These findings help explain why caffeine might be beneficial for health and longevity,” said Dr John-Patrick Alao, the study’s lead author. “And they open up exciting possibilities for future research into how we might trigger these effects more directly with diet, lifestyle, or new medicines.”

So, your morning coffee may not just sharpen your mind it might also be giving your cells a subtle boost in the fight against ageing.

Reference: John-Patrick Alao, Juhi Kumar, Despina Stamataki, Charalampos Rallis. Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast. Microbial Cell, 12: 141-156 DOI: 10.15698/mic2025.06.852