Chronic exposure to nanomolar lysergic acid diethylamide extended lifespan in the roundworm Caenorhabditis elegans by up to 17.6% at the 25% survival point and reduced lipofuscin accumulation, an age-associated damage marker. The effect required serotonin receptor genes ser-1 and ser-5, and ser-4 and ser-7 mutants lived shorter. It persisted, with reduced magnitude, in tph-1 mutants that cannot synthesize serotonin. LSD also produced caloric-restriction-like traits: fewer offspring, smaller bodies, delayed vulval development, altered lipid stores and PHA-4 levels. Benefits vanished in eat-2 mutants and reversed under bacterial dilution.
This is animal evidence only, and it should not be read as a signal that psychedelics extend human life. Worm lifespan screens routinely produce hits that fail in mammals, and the effect size here is modest by C. elegans standards. The most informative detail is context dependence: LSD shortened lifespan when food was scarce, and no benefit appeared in eat-2 mutants. That suggests the compound interacts with nutritional state rather than acting as a clean pro-longevity switch, and a drug that harms under dietary restriction would be a serious caveat for any translation. The finding that feeding did not drop, yet CR-like phenotypes emerged, hints at serotonergic signaling mimicking a hunger cue, echoing older work linking serotonin and octopamine to worm longevity. Mouse lifespan studies, dose-response data, and pharmacokinetic comparison to human exposure are all missing. Incremental and mechanistically interesting, but a hypothesis generator, not an intervention.
