THC alone disturbed time estimations, increased pulse rate, and induced strong psychological reactions, while up to 60 mg CBD alone produced no effects. Thirty to 60 mg CBD weakened or blocked time production impairment, psychological disturbances, and pulse rate acceleration produced by THC, when co-administered. CBD also decreased anxiety following THC, with subjects reporting more pleasurable effects. Severe AEs in Lennox-Gastaut patients receiving CBD treatment included increased ALT, AST, and GGT concentrations [65]. In a 2017, randomized, double-blind, placebo-controlled CBD trial on Dravet’s syndrome, 120 children received 20 mg/kg/day oral CBD or placebo for 14 weeks, in conjunction with their standard treatment (1 to 5 antiepileptic drugs) [71]. AEs occurred more frequently in the CBD than the placebo group, with somnolence (36% vs 10%) being the most common AE.
Associated Data
Cannabidiol (CBD) can change the way your body breaks down medicines you take. The bottom line is to talk with your health care provider about the CBD products you are taking and be completely honest about your dosing. Also, many of the CBD products aren’t necessarily pure, and the label does not always reflect the amount of the supplement contained or any contaminants, such as THC, that may be there. Because of the lack of regulation, some CBD products are marketed with misleading or false claims that may cause people to postpone doctor visits to get the right diagnosis and treatment. With the benefit of hindsight, we aimed to provide an update on CBD-related toxicity and AEs in humans.
Chronic CBD Studies in Humans
Most AEs were mild or moderate in severity; diarrhea and somnolence were the most common (30% and 24%, respectively). The data from the present systematic review agree with previous data on the safety of purified CBD. The most common adverse effects are mild and moderate, and serious adverse effects are rare and have been only reported in epilepsy studies, with concomitant use of CBD with antiepileptic drugs. Physicians must carry out the indication for the use of CBD through prescription, and its use must be monitored, especially at the beginning of the treatment.
- A total of 454 participants used oral CBD in the trials, and 303 participants were female (40.7%).
- This activity describes cannabinoid toxicity and highlights the role of the interprofessional team in its management.
- The most common AEs were diarrhea, nausea, vomiting, sedation, and somnolence.
- This neurotransmitter modulation may contribute to the central and peripheral effects observed in cannabinoid toxicity.
- Somnolence occurred more frequently in those receiving 20 mg/kg/day CBD than 10 mg/kg/day.
Respiratory effects
Twelve RCTs [10,11,12,13,14,15,16,17,18,19,20,21] involving 745 randomized subjects analyzed were included. A total of 454 participants used oral CBD in the trials, and 303 participants were female (40.7%). Daily CBD doses included fixed doses (300 mg/day to 800 mg/day) and doses adjusted by weight (from 20 mg/kg/day to 50 mg/kg/day). All RCTs evaluated the effects of CBD on clinical populations and most used CBD concomitant with other drugs (9/12). Three studies took place in Brazil, three in multiple countries, two in the United Kingdom, one in Australia, one in Canada, one in Germany, and one in the United States.
The term marijuana became popular in the 1930s; it was originally a slang word for the psychoactive part of cannabis smoked by Mexican soldiers. Hemp refers to the roots, stalk, and stems of the plant, which can be used to make rope and twine. A recent study with P-gp, Bcrp, and P-gp/Bcrp knockout mice, where is cannabidiol addictive 10 mg/kg was injected subcutaneously, showed that CBD is not a substrate of these transporters itself. This means that they do not reduce CBD transport to the brain.16 This phenomenon also occurs with paracetamol and haloperidol, which both inhibit P-gp, but are not actively transported substrates.
- CBD exposure during neuronal differentiation may sensitize immature cells to redox-active drug neurotoxicity.
- The toxic effects of cannabinoids are secondary to overstimulation of the endocannabinoid system by exogenous cannabinoids.
Neurological and neurospychiatric effects
However, it is very difficult to trigger a false positive with a detection concentration of 50 ng/mL. Passive smoke inhalation has been demonstrated to not reliably produce concentrations high enough to be detected in most urine drug screens. Serum concentrations may be quantified as a send out laboratory value, but this is not useful in the acute clinical setting. Serum concentrations of THC metabolites are useful for confirmatory testing and in legal situations and can be obtained through gas or liquid chromatography and mass spectrometry at a reference laboratory.
The term “marijuana” typically refers to the tobacco-like preparations of the leaves and flowers of the plant cannabis sativa. The active ingredient is believed to be tetrahydrocannabinol (THC), which is also responsible for intoxication. This activity reviews the pathophysiology, diagnosis, and management of marijuana toxicity and highlights the role of the interprofessional team in caring for affected patients. The toxic effects of cannabinoids are secondary to overstimulation of the endocannabinoid system by exogenous cannabinoids. This immoderate stimulation of the endocannabinoid system leads to the aforementioned erratic neurotransmitter modulation that can lead to toxicity.
