Cannabigerol

CBG produced regressive hepatic histopathological changes, elevated oxidative stress markers (malondialdehyde, carbonylated proteins), disrupted white cell counts, and altered ALT activity in rats at chronic low doses (Polanska 2023). The geranyl moiety is proposed as the structural determinant. Human iPSC hepatocyte data (Gao 2024) ranked CBG as the least hepatotoxic cannabinoid tested, creating an unresolved contradiction. Until human hepatic safety data are available, individuals with pre-existing liver disease, elevated transaminases, or concurrent hepatotoxic medication use should exercise caution.

No published studies have evaluated CBG's effects on fertility, embryonic/fetal development, parturition, or lactation transfer. Given the complete absence of reproductive safety data and the chronic rat hepatotoxicity signals at low doses, use during pregnancy or breastfeeding cannot be recommended.

No clinical or preclinical studies have evaluated CBG safety or pharmacology in pediatric populations. The endocannabinoid system plays critical roles in neurodevelopment, and modulation by exogenous cannabinoids during development carries theoretical risks that cannot be assessed without data. CBG use in minors is not supported by evidence.

CYP3A4 substrates, CYP2C9 substrates, CYP2C19 substrates, Narrow therapeutic index drugs

No published CBG-specific CYP inhibition or induction studies exist. CBD, a structurally related non-psychoactive cannabinoid, is a known potent inhibitor of CYP2C19 and CYP3A4, contributing to clinically significant drug-drug interactions. Whether CBG shares this profile or possesses a distinct CYP interaction signature is unknown. Patients taking narrow-therapeutic-index medications metabolized by CYP3A4, CYP2C9, or CYP2C19 should be monitored until CBG-specific CYP data are available.