Feeding the nematode C. elegans live Lactococcus lactis JCM 5805 lifted maximum lifespan to 25 days, versus 21 days for controls and for worms given heat-killed bacteria; both live and dead cells raised mean lifespan. Live bacteria upregulated 74 cuticle genes, mostly collagens, without triggering host stress responses. Worms also accumulated L-citrulline and L-ornithine, products of the bacterial arginine deiminase (ADI) pathway, which worms cannot make themselves because they lack a functional urea cycle. Bacteria without ADI, and heat-killed cells, produced no citrulline.
This evidence comes entirely from worms, and nothing here tests a supplement or probiotic in people. The finding is mechanistically tidy: a living microbe supplies an enzyme the host lacks, and the resulting metabolites coincide with collagen maintenance. But the abstract shows correlation, not proof, that citrulline drives the lifespan gain; knocking out arcA in the bacterium and rescuing with citrulline would close that gap. Humans have a urea cycle and make citrulline endogenously, so the 'exploitation' logic may not transfer. Lactic acid bacteria have extended worm lifespan before, and such results have historically translated poorly to mammals. This is a preprint that has not been peer reviewed, so the lifespan figures and mechanism could shift. Treat it as an incremental, hypothesis-generating contribution to the microbiome-and-aging literature, not a reason to change what you eat or take.