This study examined whether resveratrol's anti-aging effects differ by age in *C. elegans*, treating young worms (adult day 1–4) vs. middle-aged worms (adult day 8–11) for four consecutive days, with validation in human BJ fibroblast cells.
Resveratrol **extended lifespan, improved healthspan, and reduced ROS** in young worms, but **impaired these same outcomes** in middle-aged worms. The opposing effects were mediated by the daf-16/dod-6/sod-3 axis: dod-6 was up-regulated in young worms and down-regulated in middle-aged worms, and silencing daf-16, dod-6, or sod-3 abolished the age-dependent divergence. In human senescent (D-galactose-induced) BJ cells, resveratrol worsened β-galactosidase staining and pro-inflammatory cytokine expression.
- *C. elegans* and BJ fibroblast models may not fully translate to mammalian aging in vivo. - The study does not test resveratrol doses or duration beyond the 4-day window, limiting dose-response insight. - D-galactose-induced senescence in BJ cells is a chemical model that may not fully replicate physiological human cellular aging.
Resveratrol should not be assumed universally beneficial for aging — its effects appear to depend on the biological age of the organism at the time of treatment. Clinicians advising older patients on resveratrol supplementation should be aware that it may paradoxically accelerate aging-related cellular changes rather than prevent them.
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