Prenatal Cannabis Exposure Disrupts Brain Chemical Systems in Animal and Limited Human Studies

After screening 18,252 papers, only 16 animal and 4 human studies met criteria. Animal models revealed significant disruptions in neurotransmitter regulation, receptor function, and gene expression following prenatal cannabis exposure. Human studies suggested potential cognitive and behavioral risks for offspring. No studies directly addressed the monoamine system in the placenta, exposing a critical research gap.

Systematic review following PRISM guidelines with comprehensive database search. From 18,252 initial papers, rigorous screening yielded 16 animal studies and 4 human studies. Findings were synthesized to evaluate effects on neurotransmitter regulation, receptor function, and gene expression within the fetoplacental unit, framed through the Developmental Origins of Health and Disease (DOHaD) framework.

Cannabis use during pregnancy increased 170% between 2009 and 2016. The monoamine system (dopamine, serotonin, norepinephrine) is crucial for both placental function and fetal brain development. This review reveals that while animal evidence of disruption is strong, we lack the human studies needed to fully understand the risks.

The dramatic gap between animal evidence (showing clear neurotransmitter disruption) and human evidence (only 4 studies) highlights how little we know about prenatal cannabis effects on fundamental brain chemistry. As cannabis use during pregnancy rises, this knowledge gap becomes increasingly urgent.

Only 4 human studies met criteria, severely limiting clinical conclusions. Animal models use controlled cannabinoid exposure that may not reflect human use patterns. No studies examined monoamine effects specifically in placental tissue. Review cannot determine thresholds for harmful exposure.