In both rodent and cell culture models , CBD was found to exert a neuroprotective effect against adverse alcohol consequences on the hippocampus .
In rodent models , CBD was found to attenuate alcohol-induced hepatotoxicity , specifically , alcohol-induced steatosis .
Finally , findings from pre clinical rodent models also indicate that CBD attenuates cue-elicited and stress-elicited alcohol seeking , alcohol self-administration , withdrawal-induced convulsions , and impulsive discounting of delayed rewards .
In human studies , CBD was well tolerated and did not interact with the subjective effects of alcohol .
Collectively , given its favorable effects on alcohol-related harms and addiction phenotypes in pre clinical models , CBD appears to have promise as a c and i date AUD pharmacotherapy .
This is further bolstered by the absence of abuse liability and its general tolerability .
There is substantial interest in the therapeutic potential of cannabidiol ( CBD ) , a nonpsychoactive cannabinoid found in plants of the genus Cannabis .
The goal of the current systematic review was to characterize the existing literature on this topic and to evaluate the credibility of CBD as a c and i date pharmacotherapy for alcohol use disorder ( AUD ) .
Effect of Cannabidiol on Drop Seizures in the Lennox–Gastaut Syndrome
Background Cannabidiol has been used for treatment‐resistant seizures in patients with severe early‐onset epilepsy . We investigated the efficacy and safety of cannabidiol added to a regimen of conventional antiepileptic medication to treat drop seizures in patients with the Lennox – Gastaut syndrome , a severe developmental epileptic encephalopathy . Methods In this double‐blind , placebo‐controlled trial conducted at 30 clinical centers , we r and omly assigned patients with the Lennox – Gastaut syndrome ( age range , 2 to 55 years ) who had had two or more drop seizures per week during a 28‐day baseline period to receive cannabidiol oral solution at a dose of either 20 mg per kilogram of body weight ( 20‐mg cannabidiol group ) or 10 mg per kilogram ( 10‐mg cannabidiol group ) or matching placebo , administered in two equally divided doses daily for 14 weeks . The primary outcome was the percentage change from baseline in the frequency of drop seizures ( average per 28 days ) during the treatment period . Results A total of 225 patients were enrolled ; 76 patients were assigned to the 20‐mg cannabidiol group , 73 to the 10‐mg cannabidiol group , and 76 to the placebo group . During the 28‐day baseline period , the median number of drop seizures was 85 in all trial groups combined . The median percent reduction from baseline in drop‐seizure frequency during the treatment period was 41.9 % in the 20‐mg cannabidiol group , 37.2 % in the 10‐mg cannabidiol group , and 17.2 % in the placebo group ( P=0.005 for the 20‐mg cannabidiol group vs. placebo group , and P=0.002 for the 10‐mg cannabidiol group vs. placebo group ) . The most common adverse events among the patients in the cannabidiol groups were somnolence , decreased appetite , and diarrhea ; these events occurred more frequently in the higher‐dose group . Six patients in the 20‐mg cannabidiol group and 1 patient in the 10‐mg cannabidiol group discontinued the trial medication because of adverse events and were withdrawn from the trial . Fourteen patients who received cannabidiol ( 9 % ) had elevated liver aminotransferase concentrations . Conclusions Among children and adults with the Lennox – Gastaut syndrome , the addition of cannabidiol at a dose of 10 mg or 20 mg per kilogram per day to a conventional antiepileptic regimen result ed in greater reductions in the frequency of drop seizures than placebo . Adverse events with cannabidiol included elevated liver aminotransferase concentrations . ( Funded by GW Pharmaceuticals ; GWPCARE3 Clinical Trials.gov number , NCT02224560 .
In both rodent and cell culture models , CBD was found to exert a neuroprotective effect against adverse alcohol consequences on the hippocampus .
In rodent models , CBD was found to attenuate alcohol-induced hepatotoxicity , specifically , alcohol-induced steatosis .
Finally , findings from pre clinical rodent models also indicate that CBD attenuates cue-elicited and stress-elicited alcohol seeking , alcohol self-administration , withdrawal-induced convulsions , and impulsive discounting of delayed rewards .
In human studies , CBD was well tolerated and did not interact with the subjective effects of alcohol .
Collectively , given its favorable effects on alcohol-related harms and addiction phenotypes in pre clinical models , CBD appears to have promise as a c and i date AUD pharmacotherapy .
This is further bolstered by the absence of abuse liability and its general tolerability .
There is substantial interest in the therapeutic potential of cannabidiol ( CBD ) , a nonpsychoactive cannabinoid found in plants of the genus Cannabis .
The goal of the current systematic review was to characterize the existing literature on this topic and to evaluate the credibility of CBD as a c and i date pharmacotherapy for alcohol use disorder ( AUD ) .