The evidence for metformin to modestly slow aging and extend life in mammals is very mixed, with study results falling all over the map. This is worth bearing in mind when reading any new paper claiming metformin to extend life in other species, as this is just one more item in a distribution of results that does not show clear, compelling, easily replicated evidence of life extension. So that said, here researchers are suggesting that metformin extends life via hormetic effects. Since they are proposing a mechanism, this should lead to ways to better test and replicate the claim without involving metformin itself:
Recently it has been suggested that metformin, the most commonly used antidiabetic drug, might also possess general health-promoting properties. Elucidating metformin's mode of action will vastly increase its application range and will contribute to healthy aging.
Via a quantitative proteomics approach using the model organism Caenorhabditis elegans, we gained molecular understanding of the physiological changes elicited by metformin exposure, including changes in branched-chain amino acid catabolism and cuticle maintenance.
We show that metformin extends lifespan through the process of mitohormesis and propose a signaling cascade in which metformin-induced production of reactive oxygen species increases overall life expectancy. We further address an important issue in aging research, wherein so far, the key molecular link that translates the reactive oxygen species signal into a prolongevity cue remained elusive. We show that this beneficial signal of the mitohormetic pathway is propagated by the peroxiredoxin PRDX-2. Because of its evolutionary conservation, peroxiredoxin signaling might underlie a general principle of prolongevity signaling.