Table 3.

A summary of preclinical and clinical trials that represent prenatal THC administration and the primary outcome that it had on inducing postnatal issues that can eventually lead to increased obesity risks later into the child’s adolescence, and even later in life. A majority of the obesity risk outcomes from the administration of THC were based on birth weight, but also levels of fetal stress during pregnancy. The limited information in certain sources resulted in some of the information that would have been contained within the table being omitted.

Species	Regimen	Sex (Child)	THC Dose	Route of Administration	Obesity Risk Outcomes	References
Rat	Chronic (15.5 straight days)	Male and female	3 mg/kg	Intraperitoneally	↓ fetal growth, ↓ expression of GLUT1, ↑ intrauterine growth restriction	[171]
Human	Chronic (multiple studies, no specific regimen)	Male and female	Self-report	Smoked	↑ overweight children, ↑ obesity risks	[172]
Human	Chronic (substance use through pregnancy)	Male and female	Self-report (exposure before or after knowledge)	Smoked	↓ birth weight, ↓ intracranial volume, ↓ white matter volume	[173]
Human	Chronic	Male and female	Self-report (during pregnancy, ever regular, lifetime)	Smoked	↓ birth weight, ↑ preterm birth, ↑ admission to NICU	[174]
Human	Chronic (8 straight days)	Cell culture	0.5–1.5 mg	Intratumorally	↓ levels of phosphorylated VEGFR-2, ↓ endothelial growth factor expression	[175]
Mice	Chronic (12 straight days)	Male and female	200 mg cigarettes	Smoked	↓ birth weight	[176]

Note: ↑ = Observed increase, ↓ = Observed decrease, GLUT1 = Glucose transporter type 1, NICU = Newborn intensive care unit, VEGFR-2 = Vascular endothelial growth factor receptor 2.