Age† | Cohort‡ | Category | Results/outcomes | Exposure details |
Ref. |
---|---|---|---|---|---|
Fetus | |||||
17–22 GW | – | Growth | Reduced foot length and bodyweight | ≥0.4 J/day | [48] |
18–22 GW | – | Dopamine signaling | Decreased D2 mRNA in amygdala of males only | ≥0.4 J/day | [152] |
18–22 GW | – | Endorphin signaling | Decreased opioid peptide (PENK) and receptor (κ) in caudal putamen and thalamus, respectively; increased opioid receptor (µ) in the amygdala |
– | [74] |
Neonatal | |||||
Neonatal | OPPS | Neurobehavior | Increased tremors, exaggerated startles and diminished responsiveness to light | – | [46] |
Neonatal | MHPCD | Growth | Decreased body length | ≥1 J/day, first Trim |
[49] |
Neonatal | – | Growth Neurobehavior |
No effect on birthweight, length or gestational age No effect |
– – |
[54] |
Neonatal | VIPS | Growth | No effect on birthweight, preterm delivery or abruptio placentae | – | [35] |
Neonatal | – | Growth Behavior |
No effect on birthweight, length or gestational age More irritable, less responsive to calming, increased jitters and startles |
– – |
[52] |
Neonatal | NBDPS | Growth | No effect on birthweight, gestational age or preterm delivery | – | [40] |
1 mo | – | Behavior | Less irritable, more alert, more robust autonomic and motor systems, more autonomically stable and increased orientation |
≥2.86 J/day | [54] |
Toddler | |||||
8 mo | MHPCD | Growth | No effect | – | [49] |
9 mo | MHPCD | Mental/motor skills | Delayed mental development | ≥1 J/day, third Trim |
[26] |
1 y | OPPS | Mental/motor skills | No effect | – | [55] |
1 y | – | Mental/motor skills | Decreased motor scores, no effect on mental development | ≥0.5 J/day, first Trim |
[149] |
19 mo | MHPCD | Mental/motor skills | No effect | – | [26] |
2 y | OPPS | Mental/motor skills | No effect | – | [55] |
3 y | MHPCD | Intelligence Cognition |
No effect on overall IQ for entire cohort For African–Americans: decrease in short-term memory and verbal reasoning |
– ≥1 J/day, first/second Trim |
[57] |
3 y | MHPCD | Sleep and arousal | Lowered sleep efficiency, more nocturnal arousals and more awake time after sleep onset | – | [153] |
Childhood | |||||
4 y | – | Sustained attention | Increased number of omission errors | First Trim | [45] |
4 y | MHPCD | Motor skills | No effect on balance and coordination skills | – | [154] |
5–6 y | OPPS | Cognition and language |
No effect | – | [155] |
6 y | MHPCD | Growth | No effect | – | [156] |
6 y | OPPS | Memory Attention Behavior |
No effect Increased number of omission errors Described as more impulsive and hyperactive |
≥0.86 J/day | [58] |
6 y | MHPCD | Impulsivity Sustained attention |
Decrease in errors of omission Lower overall composite score |
Second Trim | [60] |
6 y | MHPCD | Intelligence Cognition |
Lower overall composite score Lower verbal reasoning, quantitative reasoning and short-term memory |
≥1 J/day, first/second Trim |
[59] |
9–12 y | OPPS | Reading and language | No effect in regards to reading or language | – | [68] |
9–12 y | OPPS | Intelligence Executive function |
No effect in terms of full scale IQ Impulse control and visual hypothesis aspects are negatively impacted |
– > 0.86 J/day |
[63] |
Adolescence | |||||
10 y | MHPCD | Behavior and emotion Behavior and emotion |
Fewer internalizing problems, although not correlated with teacher’s report Predicted lower scores in design memory and screening index |
≥0.4 J/day second Trim ≥0.89 J/day, first Trim |
[47] |
10 y | MHPCD | Learning and memory Sustained attention |
Predicted lower scores in design memory and screening index Increase in errors of commission |
≥0.89 J/day, first Trim ≥0.89 J/day, second Trim |
[47] |
10 y | MHPCD | Depression | Increased levels of depressive symptoms | >0.89 J/day, first/third Trim |
[64] |
12 y | – | Psychotic symptoms | No effect | – | [66] |
10–14 y | – | Volumetric MRI | No effect on cortical gray matter volume, white matter volume, cerebral spinal fluid or parenchymal volume |
– | [69] |
10 y 14 y |
MHPCD | Behavior and cognition Delinquent behaviors |
Negatively associated with depressive symptoms, IQ, learning and memory Increased delinquent behaviors |
≥0.89 J/day, first/second Trim ≥0.89 J/day |
[61] |
13–16 y | OPPS | Sustained attention | Decreased stability of attention over time | ≥0.86 J/day | [71] |
13–16 y | OPPS | Growth | No changes in weight, height or puberty symptoms | – | [157] |
13–16 y | OPPS | Visual memory | Lower scores in abstract designs and Peabody spelling | ≥0.86 J/day | [27] |
16 y | MHPCD | Fine motor coordination Visual–motor coordination |
Various light deficits in processing speed and interhemispheric motor coordination Slight increase in visual–motor coordination |
≥2 J/mo | [158] |
Young adult | |||||
18–22 y | OPPS | Response inhibition Response inhibition by fMRI Intelligence Working memory by fMRI |
Slightly more errors of commission Increased bilateral PFC activity, right premotor cortex activity; decreased activity in left cerebellum No effect Increased activity in left medial PFC, inferior frontal gyrus and left cerebellum; decreased activity in |
right brain regions – medial PFC, DLPFC and ventrolateral PFC
– – – – |
[72] [73] |
Prenatal Marijuana Exposure Studies in Humans
†Exposed offspring study age.
‡Specified conditions of prenatal exposure.
DLPFC: Dorsolateral prefrontal cortex; GW: Gestation week(s); J: Joint; MHPCD: Maternal Health Practices and Child Development
Project; mo: Month(s); NBDPS: National Birth Defects Prevention Study; OPPS: Ottawa Prenatal Prospective Study; PENK: Proenkephalin;
PFC: Prefrontal cortex; Trim: Trimester; VIPS: Vaginal Infections and Prematurity Study; y: Year(s).
This activity is intended for primary care clinicians, obstetricians, neurologists, psychiatrists, pediatricians, and other healthcare providers advising pregnant women regarding the effects of prenatal marijuana exposure and/or caring for their offspring.
The goal of this activity is to review the interaction of prenatal exposure to marijuana with endocannabinoid effects on neural development.
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Marijuana abuse during pregnancy and adolescence represents a major health problem owing to its potential consequences on neural development. Prenatally cannabis-exposed children display cognitive deficits, suggesting that maternal consumption has interfered with the proper maturation of the brain. Several pharmacological effects of THC, the active principle of Cannabis sativa preparations such as hashish and marijuana, are mimicked by the endogenous eCBs, 2-AG and AEA. On the other hand, pharmacological inhibition or genetic deletion of either FAAH or MAGL to elevate endogenous levels of AEA and 2-AG, respectively, does not reproduce the full spectrum of responses observed with THC. Interestingly, a recently developed dual FAAH/MAGL inhibitor (JZL195) induced THC-like drug discrimination responses, which were not observed with disruption of either FAAH or MAGL alone.[149] The observation that the THC-like additive effects of dual FAAH/MAGL blockade can be reversed by CB1R antagonists suggests that most, if not all, acute cognitive responses to THC are mediated through the CB1R.[150] Whether THC produces effect by partially activating CB1R or antagonizing the action of 2-AG and AEA at this receptor remains an open question.[151]
2-AG is the most abundant eCB in the brain. Basal 2-AG levels in the adult brain are approximately 200 times those of AEA,[83] while an approximately 1000-fold excess of tissue 2-AG concentrations over those of AEA exists in the fetal brain.[102] The relative contribution of the two arms of eCB signaling in regulating neurogenesis, axonal growth and guidance, and synaptogenesis during development is not well understood. The data from dual blockade of FAAH/MAGL indicate that AEA and 2-AG signaling pathways interact to regulate specific behavioral processes in vivo, including those relevant to drug abuse.[150] Hence, future studies employing novel pharmacological and genetic tools may help to dissect out specific eCB signaling pathways in regulating neural developmental processes.