CNR1 and fetal growth restriction: On the contrary, our previously published study demonstrated that gestational exposure to Δ9-THC results in symmetrical IUGR, which is often associated with early gestation insults.11,59 With respect to why hypertrophic hearts at birth were not observed in our model, it has been demonstrated that in fetal cardiomyocytes, CB1R and CB2R agonists impede cardiomyocyte growth/hypertrophy.28 Given 10% of maternal Δ9-THC results in fetal circulation,29,30 this suggests that Δ9-THC, via activation of CB1R in the heart, could have a direct effect on cardiac growth.