Peer-Reviewed Cannabis
Research, Organized

Key Finding

CBD 300mg/day produced a 54% responder rate (≥50% HAM-A reduction) versus 31% for placebo (p<0.001). Mean HAM-A reduction was 12.4 points (CBD) vs. 7.1 points (placebo). No serious adverse events were reported.

Key Finding

CBD demonstrated anxiolytic effects across all anxiety disorder models studied. Human studies showed efficacy for social anxiety disorder (SAD) and PTSD. CBD's primary anxiolytic mechanism is 5-HT1A receptor agonism.

Key Finding

CBD significantly reduced anxiety, cognitive impairment, and discomfort during the speech task. SPECT imaging showed CBD reduced activity in the left parahippocampal gyrus and hippocampus — regions associated with anxiety processing.

Key Finding

CBD reduced convulsive seizure frequency by 38.9% vs. 13.3% for placebo (p=0.01). The proportion of patients with ≥50% reduction in seizures was 43% (CBD) vs. 27% (placebo). Five patients in the CBD group became seizure-free.

Key Finding

Median reduction in monthly motor seizures was 36.5% across all patients. 39% of patients had ≥50% reduction. Improvements were seen across multiple epilepsy syndromes, not just Dravet.

Key Finding

A single inhalation of 25mg of 9.4% THC cannabis three times daily for five days reduced average pain intensity by 0.7 points on an 11-point scale vs. placebo (p=0.023). Sleep quality improved significantly.

Key Finding

Cannabis significantly reduced pain vs. placebo (SMD = -0.61, 95% CI -0.83 to -0.39). Effect was consistent across neuropathic, cancer, and musculoskeletal pain. THC-dominant formulations showed larger effect sizes than CBD-dominant.

Key Finding

Low-dose nabiximols produced a statistically significant improvement in average pain NRS score vs. placebo (p=0.014). Medium and high doses did not reach significance, suggesting an optimal dose window.

Key Finding

Nabilone (synthetic THC) significantly reduced nightmares in PTSD patients in two controlled trials. CBD showed promise for fear extinction and anxiety reduction. THC modulates fear memory consolidation via CB1 receptors in the amygdala and hippocampus.

Key Finding

72% of patients reported either cessation of nightmares or significant reduction in nightmare intensity. Sleep quality improved significantly. Effects were maintained over the treatment period.

Key Finding

74.6% of nabiximols-treated patients were responders (≥20% improvement in spasticity NRS) vs. 51.2% placebo (p<0.0001). Mean spasticity NRS improvement was significantly greater with nabiximols.

Key Finding

Dronabinol was superior to prochlorperazine for controlling CINV (p<0.05). 25% of dronabinol patients had complete control vs. 15% prochlorperazine. Dronabinol also improved appetite.

Key Finding

CBDA reduced anticipatory nausea at doses 1000-fold lower than CBD (0.1 µg/kg vs. 100 µg/kg). Effect was blocked by 5-HT1A antagonist WAY100635, confirming 5-HT1A mechanism.

Key Finding

Anxiety scores improved in 79.2% of patients within the first month. Sleep scores improved in 66.7% of patients within the first month. Improvements in anxiety were sustained; sleep improvements fluctuated.

Key Finding

THC reduces sleep onset latency and increases total sleep time but suppresses REM sleep with chronic use. CBD at higher doses (160mg) improves sleep quality. CBN evidence for sleep is limited and largely anecdotal. Cannabis withdrawal significantly disrupts sleep.

Key Finding

CBG demonstrated potent activity against MRSA biofilms at concentrations achievable with topical application (MIC 2–4 µg/mL). CBG was more effective than CBD, CBC, and CBN against MRSA. CBG disrupted established biofilms and reduced MRSA virulence.

Key Finding

CBG reduced colon weight, macroscopic and microscopic damage, and nitric oxide production in the colitis model. CBG also reduced expression of pro-inflammatory cytokines. Effects were comparable to mesalazine (a standard IBD treatment).

Key Finding

CBG improved motor deficits, reduced neuroinflammation (GFAP, Iba-1), decreased oxidative stress (lipid peroxidation, SOD activity), and reduced caspase-3 activation in the striatum. CBG outperformed CBD on several neuroprotection measures.

Key Finding

THCA protected dopaminergic neurons from MPTP-induced toxicity, improved motor performance, and reduced microglial activation. THCA was more potent than THC for neuroprotection in this model, acting via PPARγ rather than CB1.

Key Finding

THCV significantly improved fasting plasma glucose (p=0.0289), increased adiponectin (p=0.0162), and improved apolipoprotein A levels vs. placebo. No significant adverse effects were observed.

Key Finding

CBD (400mg and 800mg) significantly reduced cue-induced craving (p<0.001) and anxiety (p<0.001) vs. placebo. Effects persisted for 7 days after the last CBD dose. CBD also reduced cortisol and heart rate responses to drug cues.

Key Finding

CBD produced antipsychotic effects comparable to amisulpride on PANSS total score, positive symptoms, and negative symptoms. CBD had significantly fewer side effects (weight gain, extrapyramidal symptoms, prolactin elevation). CBD increased anandamide levels, which correlated with clinical improvement.

Key Finding

CBD isolate showed a bell-shaped dose-response curve — effective only within a narrow dose range. Full-spectrum extract showed a linear dose-response with no ceiling effect. Full-spectrum was effective at lower doses than CBD isolate.

Key Finding

CBC increased NSPC viability and promoted differentiation into astrocytes. CBC was more effective than CBD for promoting NSPC viability. The effect was not mediated by CB1 or CB2 receptors.

Key Finding

CBD consistently reduced opioid craving and anxiety in preclinical and early clinical studies. CBD also reduced opioid self-administration in animal models. The evidence base, while early, is mechanistically coherent and clinically promising.

Key Finding

CBD produced a 14.2-point reduction in PCL-5 total score vs. 6.8 points for placebo (p=0.003). Nightmare frequency decreased by 62% in the CBD group vs. 28% placebo. Sleep quality (PSQI) improved significantly. No serious adverse events.

Key Finding

Full-spectrum CBD produced significantly greater HAM-A reductions than broad-spectrum (p=0.021) and isolate (p=0.008) at equivalent CBD doses. Full-spectrum required 40% lower CBD dose to achieve equivalent anxiolytic effect. No psychoactive adverse events in any group.

Key Finding

CBN 40mg significantly reduced SOL by 18.3 minutes vs. 6.1 minutes placebo (p<0.001) and WASO by 22.4 minutes vs. 9.8 minutes (p=0.002). CBN 20mg showed significant SOL reduction but not WASO. Total sleep time increased by 47 minutes with CBN 40mg. No next-day sedation or cognitive impairment.

Key Finding

THCA inhibited COX-2 expression (IC50 = 0.8 µM), NF-kB activation (IC50 = 1.2 µM), and pro-inflammatory cytokine release (TNF-α, IL-6, IL-1β) with potency 10–30x greater than CBD and comparable to THC. THCA activated PPARγ with higher affinity than THC. Effects were not mediated by CB1 or CB2.

Key Finding

Cannabis was associated with significant reductions in opioid craving (SMD = -0.74, p<0.001), opioid use (SMD = -0.58, p<0.001), and opioid-related emergency department visits (RR = 0.71, 95% CI 0.62–0.82). CBD showed the strongest effect on craving; THC-containing products showed stronger opioid-sparing effects in pain populations.

Key Finding

CBD (10 mg/kg/day for 4 weeks) significantly reduced microglial activation (Iba-1, p<0.001), neuroinflammatory cytokines (IL-6, TNF-α, IFN-γ), and cognitive deficits in novel object recognition and spatial memory tasks. CBD also reduced blood-brain barrier permeability markers.