A Review Found Adolescent Cannabis Use Causes Lasting Cognitive Changes Through Epigenetic and Synaptic Mechanisms

Cannabis use during adolescence causes lasting aberrations in synaptic development, often secondary to epigenetic changes. High-potency and synthetic cannabis, heavy/frequent use, and early initiation compound the risks. Genetic vulnerability and environmental factors also contribute. Preclinical studies show cannabinoid exposure during developmental windows durably changes dendritic structure, synaptic function, and endocannabinoid-mediated circuits.

Narrative review of preclinical and clinical evidence on adolescent cannabis use and lasting cognitive/psychiatric consequences, focusing on synaptic and epigenetic mechanisms.

This review connects the epidemiological findings (cannabis harms developing brains) to specific biological mechanisms (epigenetics, synapse remodeling), providing the mechanistic foundation for why adolescent use is uniquely risky compared to adult use.

The shift toward cannabis legalization has coincided with increasing potency and new product formats. The mechanistic evidence reviewed here suggests these trends amplify the risk for adolescents, whose developing brains are most vulnerable to lasting disruption.

Narrative review without systematic methodology. Much mechanistic evidence is from animal models. Human epigenetic studies are limited. Dose-response relationships in humans are poorly characterized. Difficult to separate cannabis effects from confounding factors in human studies.