Study Finds THC Amplifies CBD’s Role in Improving Schizophrenia Symptoms

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A new study published in the journal BMJ Mental Health reveals promising insights into the effects of cannabidiol (CBD) on key biomarkers associated with schizophrenia.

Conducted by researchers from Germany’s Central Institute of Mental Health, Goethe University Frankfurt, the University of Goettingen, and Australia’s University of Sydney, the randomized clinical trial explored how varying doses of CBD—both alone and in combination with delta-9-tetrahydrocannabinol (Δ9-THC)—impact endocannabinoid levels in healthy volunteers.

“The mental health benefits of cannabidiol (CBD) are promising but can be inconsistent, in part due to challenges in defining an individual’s effective dosage,” states the study’s abstract. “In schizophrenia, alterations in anandamide (AEA) concentrations, an endocannabinoid (eCB) agonist of the eCB system, reflect positively on treatment with CBD. Here, we expanded this assessment to include eCBs alongside AEA congeners, comparing phytocannabinoids and dosage in a clinical setting.”

For the study, researchers administered varying doses of CBD (600 mg or 800 mg), Δ9-THC (10 mg or 20 mg), and a combination of the two to 75 healthy volunteers. The participants’ endocannabinoid levels were measured at three intervals: baseline, 65 minutes, and 160 minutes post-administration.

“CBD-led increases in AEA (1.6-fold), OEA, and PEA (1.4-fold) were observed following a single 800 mg dosage (pcorr<0.05) but not 600 mg,” the study states. “Declining AEA was observed with Δ9-THC at 10 mg (-1.3-fold) and 20 mg (-1.4-fold) but was restored to baseline levels by 160 minutes. CBD+Δ9-THC yielded the highest increases in AEA (2.1-fold), OEA (1.9-fold), and PEA (1.8-fold) without reaching a maximal response.”

Based on these findings, the researchers conclude:

CBD-administered effects on AEA, OEA, and PEA are consistent with phase II trials reporting clinical improvement for acute schizophrenia (CBD≥800 mg). Including Δ9-THC appears to enhance the CBD-induced response toward AEA and its congeners. Our results warrant further investigation into the potential of these lipid-derived mediators as metabolic measures for CBD dose prescription and co-cannabinoid administration.

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