Lysergic Acid Diethylamide extends lifespan in Caenorhabditis elegans

Lysergic acid diethylamide (LSD) extends lifespan and reduces age-related lipofuscin accumulation in the roundworm Caenorhabditis elegans, suggesting delayed aging. LSD produces effects similar to caloric restriction, such as reduced reproduction and smaller body size, without decreasing food intake. LSD also alters lipid stores and other cellular markers linked to nutrient-sensing pathways. These findings indicate that LSD engages evolutionarily conserved longevity pathways and may serve as a tool for studying serotonergic regulation of aging.

Study at a glance

Abstract

Aging is modulated by nutrient-sensing pathways that integrate metabolic and hormonal cues to regulate growth, stress resilience, and lifespan. Caloric restriction (CR), a well-established intervention, extends longevity in diverse species through modulation of conserved nutrient-sensing pathways, including TOR signaling. Lysergic acid diethylamide (LSD), a classic serotonergic psychedelic with emerging therapeutic applications, remains largely unexplored in the context of aging. Here, we show that LSD treatment significantly extends lifespan in Caenorhabditis elegans and reduces age-associated lipofuscin accumulation, suggesting delayed age-associated decline. LSD induces several phenotypes that overlap with those observed in some caloric restriction paradigms, including reduced reproductive output, decreased body size, and the absence of an additive effect in lifespan assay performed in dietary restriction model, without apparent decreasing in food intake. In addition, LSD treatment modulates lipid stores and other cellular readouts associated with nutrient-sensing physiology. Together, these findings suggest that LSD engages evolutionarily conserved pathways linked to longevity and identify this compound as a tool to investigate serotonergic control of aging biology.