Psychosis Risk
Study register · detail RCT (between-subjects, experimentell) · Psychosis Risk · 2013

Cannabidiol inhibits THC-elicited paranoid symptoms and hippocampal-dependent memory impairment

Clear benefit GRADE Moderate 462 citations
Samplen = 48 Pat.
DurationSingle dose, 210 min…
ControlOral placebo, 210 min before intravenous…
EndpointPANSS positive
Blindingdoppelblind
DesignRCT (between-subjects, experimentell)
Cannabinoidkombination
Max. dose601.5 mg
Routeoral
Key finding

CBD 600 mg significantly inhibited THC-induced paranoia and hippocampus-dependent memory impairment compared with placebo.

Summary

n=48 healthy subjects (CBD n=22, placebo n=26), oral CBD 600 mg vs. placebo before intravenous THC (1,5 mg). Clinically significant positive psychotic symptoms (PANSS ≥3 point increase) less frequent in the CBD group: OR=0,22 (χ²=4,74, p<0,05). Paranoia (SSPS) lower in the CBD group (t=2,28, p<0,05). Episodic memory (HVLT-R): -0,4% CBD vs. -10,6% placebo (t=2,39, p<0,05). Demonstrates a protective effect of CBD against THC-induced psychosis risk symptoms.

P
PopulationHealthy adults, n=48 (CBD group n=22, placebo group n=26)
I
InterventionOral CBD 600 mg, 210 min before intravenous THC 1,5 mg
C
ControlOral placebo, 210 min before intravenous THC 1,5 mg
O
OutcomeLower clinically significant positive psychosis symptoms in the CBD group (OR=0,22, p<0,05); lower paranoia (SSPS, t=2,28, p<0,05); better episodic memory performance (HVLT-R: -0,4% vs. -10,6%, t=2,39, p<0,05)
Confidence in the evidence
Moderate

The third of four GRADE levels, the effect estimate is probably reliable.

Downgraded for
Imprecision
Quality profile
Sample size
Blinding Double-blind
Effect size Clear benefit
Citations / year
Authors
Englund A, Morrison P D, Nottage J et al.
DOI 10.1177/0269881112460109
Design: RCT (between-subjects, experimentell)
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Abstract
Community-based studies suggest that cannabis products that are high in Δ⁹-tetrahydrocannabinol (THC) but low in cannabidiol (CBD) are particularly hazardous for mental health. Laboratory-based studies are ideal for clarifying this issue because THC and CBD can be administered in pure form, under controlled conditions. In a between-subjects design, we tested the hypothesis that pre-treatment with CBD inhibited THC-elicited psychosis and cognitive impairment. Healthy participants were randomised to receive oral CBD 600 mg (n=22) or placebo (n=26), 210 min ahead of intravenous (IV) THC (1.5 mg). Post-THC, there were lower PANSS positive scores in the CBD group, but this did not reach statistical significance. However, clinically significant positive psychotic symptoms (defined a priori as increases ≥ 3 points) were less likely in the CBD group compared with the placebo group, odds ratio (OR)=0.22 (χ²=4.74, p<0.05). In agreement, post-THC paranoia, as rated with the State Social Paranoia Scale (SSPS), was less in the CBD group compared with the placebo group (t=2.28, p<0.05). Episodic memory, indexed by scores on the Hopkins Verbal Learning Task-revised (HVLT-R), was poorer, relative to baseline, in the placebo pre-treated group (-10.6 ± 18.9%) compared with the CBD group (-0.4% ± 9.7 %) (t=2.39, p<0.05). These findings support the idea that high-THC/low-CBD cannabis products are associated with increased risks for mental health.

The impediment to action advances action. — Marcus Aurelius