In aging C. elegans, whole-body zinc levels fall by roughly 90% between day 1 and day 13 of adulthood. Supplementing old animals with a low dose of zinc chloride (10 µM) restored zinc levels and improved healthspan, thermotolerance, and oxidative stress resistance — while higher doses proved toxic. Quantitative proteomics showed zinc's primary targets were ribosomal structural proteins, boosting protein synthesis without altering 45S pre-rRNA, suggesting zinc stabilises existing ribosomes rather than driving new biogenesis. Zinc also coordinately reversed age-associated declines in antioxidants, chaperones, proteasome activity, and energy metabolism, and suppressed both polyglutamine aggregation and amyloid-beta-induced paralysis.
This is animal-only evidence — C. elegans lifespan compresses into days and the worm lacks the metabolic complexity of mammals, so direct translation to human aging is speculative. That said, the finding adds mechanistic depth to a growing body of research linking zinc insufficiency — common in older adults — to accelerated biological aging. Human observational data already associate low serum zinc with frailty, cognitive decline, and increased all-cause mortality. What this preprint contributes is a plausible ribosomal mechanism: age-driven zinc depletion may undermine translational fidelity upstream of the proteostasis collapse seen in Alzheimer's and related diseases. The narrow therapeutic window (benefit at 10 µM, toxicity at higher doses) is a critical caution for anyone tempted to self-supplement aggressively. As a preprint not yet peer-reviewed, these findings require independent replication and mammalian validation before clinical implications can be drawn.