BiogerontologyOct 23, 2026

LSD may lengthen lifespan in a type of worm

Psychedelic Science Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Oct 24, 2026

Abstract

Chronic exposure to nanomolar LSD extends lifespan in Caenorhabditis elegans by up to 17.6% at the 25% survival timepoint.

LSD reduces age-associated lipofuscin accumulation in C. elegans.
The lifespan extension is linked to serotonergic signaling, as LSD did not extend lifespan in specific mutant strains lacking certain serotonin receptors.
LSD exhibited effects similar to caloric restriction, such as decreased reproductive output and smaller body size.
No reduction in food consumption was observed during adult feeding assays under the tested conditions.
The lifespan benefit from LSD was absent in eat-2 mutants and diminished under bacterial dilution, indicating nutritional context influences the response.
Transient exposure to LSD during early adulthood was sufficient to extend lifespan.

Simplified

Aging is modulated by conserved nutrient-sensing pathways that integrate metabolic cues to regulate growth, stress resilience, and lifespan. Caloric restriction (CR) extends longevity across species, motivating the search for compounds that engage related physiology. Lysergic acid diethylamide (LSD), a classic serotonergic psychedelic with emerging therapeutic applications, remains unexplored in the context of aging. Here we show that chronic exposure to nanomolar LSD extends lifespan in Caenorhabditis elegans by up to 17.6% at the 25% survival timepoint, and reduces age-associated lipofuscin accumulation. This response involves serotonergic GPCR signaling: LSD failed to extend lifespan in ser-1 and ser-5 mutants and shortened lifespan in ser-4 and ser-7 mutants, yet remained effective, although with reduced magnitude, in tph-1 animals deficient in serotonin synthesis, indicating that endogenous serotonin production is not strictly required. LSD also elicited phenotypes that overlap with CR, including reduced reproductive output, smaller body size, delayed vulval development, and time-dependent remodeling of lipid stores and PHA-4 levels, while adult food-consumption assays detected no reduction in feeding under the conditions tested. Notably, the lifespan benefit was absent in eat-2 mutants and was lost under bacterial dilution, where LSD instead shortened lifespan, indicating that nutritional context shapes the response. Transient exposure during early adulthood was sufficient to extend lifespan. Together, these findings identify LSD as a tool to investigate how serotonergic signaling interfaces with conserved longevity-related pathways.

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LSD may lengthen lifespan in a type of worm

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