Cannabidiol

Cannabidiol (CBD)

1. Identity: Botanical Source, Chemistry, and Forms

1.1 Botanical and Chemical Identity

Cannabidiol (CBD) is a non-psychoactive cannabinoid of Cannabis sativa that exhibits several pharmacological effects, including anti-inflammatory and antioxidant properties. It is designated chemically as 2-[(1R,6R)-3-Methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-1,3-benzenediol, with the empirical formula C₂₁H₃₀O₂ and a molecular weight of 314.46. CBD is a white to pale yellow crystalline solid that is insoluble in water and soluble in organic solvents.

Cannabidiol is one of the over 140 identified phytocannabinoids in the Cannabis sativa plant, first isolated in 1940 by Adams et al. through its ester bis-3,5-dinitrobenzoate from marijuana red oil. In 1963, Israeli scientist Dr. Raphael Mechoulam achieved a landmark breakthrough by identifying CBD's stereochemistry and exact chemical structure. It is a major constituent of the Cannabis plant, representing up to 40% in its extracts.

Cannabis produces CBD through the same metabolic pathway as THC, until the next-to-last step, where CBDA synthase performs catalysis instead of THCA synthase. Compared with THC, CBD has a very low affinity for CB1 and CB2 receptors, which results in this substance being non-psychoactive.

The molecule can be obtained via extraction from the plant or through a biosynthetic route. CBD can be extracted from various Cannabis plant species including Cannabis sativa, indica, and ruderalis.

1.2 Common Preparations and Forms

Commercial CBD products exist in several distinct categories that differ in the extent to which other plant constituents are retained alongside the CBD molecule itself.

• Full-spectrum extracts retain CBD alongside minor cannabinoids, terpenes, and other phytochemicals naturally present in the plant. Non-psychoactive hemp, as defined by U.S. federal law, is any part of the cannabis plant containing a Δ9-tetrahydrocannabinol concentration of no more than 0.3% on a dry-weight basis.
• Broad-spectrum extracts are processed to remove detectable THC while retaining other cannabinoids and terpenes.
• CBD isolate: Isolate is pure CBD with virtually all other compounds removed. Isolate CBD products do not offer the same entourage effect that full- or broad-spectrum CBD products can. It is nearly chemically pure cannabidiol (generally at least about 98–99% cannabidiol) in the form of a powder rather than liquid oil.
• Oil/Tincture: This form is typically used in over-the-counter applications and is frequently known as CBD "tincture," typically marketed with an eye dropper for application under the tongue.
• Pharmaceutical oral solution (Epidiolex®): The Food and Drug Administration has approved cannabidiol oral solution (Epidiolex, GW Pharmaceuticals) for the treatment of two rare pediatric seizure disorders.
• Nabiximols (Sativex®): Nabiximols (brand name Sativex), an oromucosal spray made of a complex botanical mixture containing cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and additional cannabinoid and non-cannabinoid constituents from Cannabis sativa plants, was approved by Health Canada in 2005.

Residual solvent or its byproducts, including carcinogenic polycyclic aromatic hydrocarbons, are contaminants identified in CBD products that likely result from insufficient removal of the solvent extractor. Because CBD is extracted from a plant, it is also susceptible to unintentional contamination that may occur with plant-based products, including the introduction of pesticides, heavy metals, and microorganisms.

2. Traditional and Historical Use

2.1 Pre-Isolation Historical Use of Cannabis

It is important to distinguish between the traditional use of Cannabis sativa as a plant preparation and the specific compound cannabidiol. CBD as an isolated molecule was unknown prior to 1940; historical uses were of whole-plant cannabis preparations that would have contained CBD among other cannabinoids. The following records accordingly describe the broader traditional use of cannabis, within which CBD was an uncharacterized constituent.

Cannabis sativa has long been a versatile crop for fiber extraction (industrial hemp), traditional Chinese medicine (hemp seeds), and recreational drugs (marijuana). Historically, Cannabis use encompassed various productive and religious purposes. Originally, Cannabis was primarily cultivated to obtain seeds and fiber. Approximately 3,000 years ago, "The Book of Songs" provided a detailed record of the entire process involved in hemp clothing production, likely making it the earliest written record.

The earliest documentation of the medical use of cannabis dates back to 2800 BC in China, where Emperor Shen Neng, considered the father of Chinese medicine, prescribed cannabis tea to treat gout, rheumatism, malaria, and poor memory. Egyptians documented the use of topical cannabis for inflammation around 1500 BC. Assyrians also documented the medicinal use of cannabis on clay tablets.

Under names such as Vijaya, cannabis has been used for thousands of years in Ayurvedic medicine to reduce pain, nausea, and anxiety, improve appetite and sleep, relax muscles, and produce a feeling of euphoria. The god Shiva supposedly favored cannabis, which had a religious role as an agent for mystic inspiration.

In 1839, medical researcher William Brooke O'Shaughnessy published the first study on the hemp plant's potential therapeutic properties.

2.2 Isolation and Early Scientific History

Cannabidiol was studied in 1940 from Minnesota wild hemp and Egyptian Cannabis indica resin. In 1963, Israeli scientist Dr. Raphael Mechoulam achieved a landmark breakthrough by identifying CBD's stereochemistry and exact chemical structure. A year later, he and his team isolated and characterized tetrahydrocannabinol (THC), the compound responsible for cannabis' psychoactive effects. Cannabis faced global prohibition in the twentieth century because of the psychoactive properties of Δ9-tetrahydrocannabinol; however, recently, the perspective has changed with the recognition of additional therapeutic values, particularly the pharmacological potential of cannabidiol.

3. Key Constituents of Cannabis and Active Compounds in Cannabidiol

Cannabis sativa and Cannabis indica contain myriad chemicals, including more than 500 identified cannabinoids and terpenes. Within this phytochemical matrix, cannabidiol is the most extensively studied non-psychoactive constituent.

CBD itself is a single defined molecular entity, but the preparations in which it is delivered may contain additional bioactive compounds. Isolate CBD products do not offer the same entourage effect that full- or broad-spectrum CBD products can. The precise pharmacological significance of the "entourage effect" in humans remains an active area of research and is not yet firmly established in clinical evidence.

4. Mechanisms of Action

Cannabidiol exerts complex, multifaceted effects on the central nervous system, and its full mechanisms of action remain incompletely understood. Several established and proposed molecular targets have been identified.

4.1 Endocannabinoid System Interactions

While CBD has low affinity for classical cannabinoid receptors CB1 and CB2, it functions as a negative allosteric modulator of CB1 receptors, altering receptor conformation and attenuating CB1-mediated signaling without directly activating the receptor. CBD also indirectly influences the endocannabinoid system by inhibiting FAAH (fatty acid amide hydrolase), thereby increasing endogenous levels of anandamide.

Research indicates that CBD can elevate levels of anandamide within tissues through two potential mechanisms: one involves restricting the transport process facilitated by fatty acid binding proteins, while the other centers on inhibiting the action of fatty acid amide hydrolase, an enzyme responsible for anandamide breakdown. Human clinical studies have demonstrated CBD's capability to increase anandamide plasma concentrations.

4.2 Serotonin System Interactions

Evidence has shown that CBD interacts with 5-HT receptors, in particular with 5-HT1AR and 5-HT2AR. CBD has shown potential as an anxiolytic through its partial agonism of the 5-HT1A receptor and its negative allosteric modulation of CB1 receptors, which may help mitigate the anxiogenic effects of tetrahydrocannabinol (THC). In vitro studies suggest this interaction with the 5-HT1A receptor may require higher concentrations than typically achieved in vivo.

4.3 Ion Channels and Other Non-Cannabinoid Targets

CBD also interacts with non-endocannabinoid receptors including G protein-coupled receptors (GPR3, GPR6, GPR12, and GPR55), transient receptor potential channels (TRPM8, TRPA1, TRPV1, and TRPV2), serotonin receptors, mu- and delta-opioid receptors, peroxisome proliferator-activated receptor gamma, and glycine receptors.

CBD partially activates GPR55, which modulates neurotransmission and may contribute to anticonvulsant effects. Acute anxiolytic effects of CBD at low and intermediate doses are believed to be caused by integration with 5-HT1A receptor activation, and higher CBD doses are thought to involve TRPV1 receptor antagonism.

The mechanisms of action for CBD are complex, varied, and still only partially understood. The exact mechanism by which cannabidiol contained in Epidiolex creates anticonvulsant effects is not known. Clinical data suggests that cannabidiol does not create anticonvulsant effects through interaction with cannabinoid receptors.

5. Scientific Evidence by Area of Use

5.1 Epilepsy — Strongest Clinical Evidence

The strongest and most rigorously established body of clinical evidence for CBD concerns drug-resistant epilepsy, culminating in regulatory approval in both the United States and Europe.

The FDA approved cannabidiol oral solution (Epidiolex, GW Pharmaceuticals) for the treatment of two rare pediatric seizure disorders. The approval — the first for a marijuana-derived pharmaceutical product — applied to Lennox-Gastaut syndrome and Dravet syndrome in patients 2 years of age and older.

The FDA Peripheral and Central Nervous System Drugs Advisory Committee's positive recommendation was based on three randomized, double-blind, placebo-controlled clinical trials. These trials showed a 50% reduction of drop seizure frequency in 40%–44% of patients with Lennox-Gastaut syndrome, and a 39% decrease in convulsive seizure frequency for trial participants with Dravet syndrome. A total of 516 patients with one of the two seizure disorders participated in the clinical trials.

In a Phase III trial reported in the New England Journal of Medicine, two doses of cannabidiol were compared with placebo for patients with LGS. There was a 41.9% reduction in drop seizures in patients prescribed a 20 mg/kg/day cannabidiol regimen, a 37.2% reduction in those on a 10 mg/kg/day cannabidiol regimen, and a 17.2% reduction in the group given placebo.

A new drug application for Epidiolex was accepted for review by the FDA in December 2017 and the drug was approved in June 2018 to treat rare childhood-onset epilepsies. The European Medicines Agency (EMA) granted orphan drug designation to Epidiolex for the treatment of LGS, Dravet syndrome, West syndrome, and tuberous sclerosis complex (TSC) in March 2017.

Epidiolex is FDA-approved for seizures associated with Lennox-Gastaut syndrome, Dravet syndrome, and tuberous sclerosis complex.

A systematic review and meta-analysis of 152 RCTs involving 12,123 participants across medical cannabinoid types found that CBD has a significant therapeutic effect for epilepsy (SMD −0.5 [CI −0.62, −0.38], high grade of evidence) and for Parkinsonism (−0.41 [CI −0.75, −0.08], moderate grade).

A 2024 systematic review of CBD in drug-refractory epilepsy in children and young adults reported that included studies reported positive outcomes, with CBD leading to a reduction in seizure frequency ranging from 50% to complete seizure freedom. Adverse effects were mostly mild and reversible, including drowsiness, diarrhea, and loss of appetite.

An earlier systematic review of CBD dosing covering 35 studies across 13 medical contexts found that CBD was reported as well tolerated, and epilepsy was the most frequently studied medical condition, with all 11 studies demonstrating positive effects of CBD on reducing seizure frequency or severity (average 15 mg/kg/d within randomized controlled trials).

5.2 Anxiety — Preliminary to Moderate Evidence

Evidence for CBD in anxiety disorders is growing but remains limited by small sample sizes, short durations, and heterogeneous methodologies.

Studies reviewed in a 2024 systematic review of randomized controlled trials varied widely in terms of the types of anxiety disorders and CBD dosages examined, leading to results that were often contradictory. Despite these conflicting outcomes, the data suggest that CBD may reduce anxiety with minimal adverse effects when compared to a placebo.

Further RCTs with improved methodologies, encompassing a broad range of doses and continuous CBD administration across specific anxiety disorders, are needed.

An open-label Phase 2 clinical trial (NCT02548559) at McLean Hospital/Harvard Medical School treated 14 outpatients with moderate-to-severe anxiety using a full-spectrum, high-CBD sublingual solution (9.97 mg/mL CBD, 0.23 mg/mL Δ9-tetrahydrocannabinol) for four weeks. Findings suggest significant improvement on primary outcomes measuring anxiety and secondary outcomes assessing mood, sleep, quality of life, and cognition, specifically executive function, following treatment. However, as an open-label study without a placebo control arm in this phase, results must be interpreted with caution.

A follow-up open-label pilot study used 0.5 mL of sublingual solution containing approximately 30 mg/mL CBD twice daily (BID), for a target daily dose of 30 mg CBD, over 6 weeks, which demonstrated very large effect sizes for anxiety reduction.

A systematic review covering a broad range of CBD uses found 23 studies reported a significant improvement in primary outcomes (e.g., psychotic symptoms, anxiety, seizures), with doses ranging between less than 1 and 50 mg/kg/d. Notably, the review also identified no signal of positive activity of CBD in small randomized controlled trials assessing diabetes, Crohn's disease, ocular hypertension, fatty liver disease, or chronic pain.

5.3 Sleep Disorders — Preliminary Evidence

There is insufficient evidence concerning CBD's efficacy from randomized controlled clinical trials for sleep, leading to unclear dosage and therapeutic guidelines for sleep benefits.

A 2024 randomized, placebo-controlled pilot trial explored the efficacy of 150 mg of CBD (n = 15) compared with placebo (n = 15) as a sleep aid in primary insomnia. Using a double-blind randomized dosing phase, participants consumed the assigned treatment sublingually 60 minutes before bed nightly. The small sample size limits the generalizability of these findings.

A separate double-blind, placebo-controlled, randomized crossover trial enrolled 125 individuals with insomnia who received an oral administration of CBD (300 mg) and terpenes for at least 4 days per week over 4 weeks. The study medication was devoid of Δ9-tetrahydrocannabinol.

5.4 Psychosis and Schizophrenia — Preliminary Evidence

Psychotic disorders such as schizophrenia are heterogeneous and often debilitating conditions. The introduction of dopamine D2 receptor antagonists in the 1950s revolutionized treatment, and they remain the mainstay of the treatment arsenal for psychosis. However, traditional antipsychotics are associated with a number of side effects and a significant proportion of patients do not achieve adequate remission of symptoms. There is therefore a need for novel interventions, particularly those with a non-D2 antagonist mechanism of action.

Recent preclinical research suggests that CBD's multifaceted mechanisms of action in the brain, involving multiple molecular targets, underlie its neuroprotective, anti-inflammatory, anxiolytic, and antipsychotic effects. While current drugs for psychosis typically target the dopaminergic neurotransmitter system, it appears increasingly likely that CBD may directly or indirectly affect multiple distinct modes of neural signalling, including both glutamate and dopamine.

A randomized, double-blind, parallel-arm trial of 39 patients with acute exacerbation of schizophrenia symptoms treated over 4 weeks found a significant reduction in positive symptoms as measured by the Positive and Negative Syndrome Scale (PANSS) in the CBD group. Further evidence regarding the antipsychotic efficacy of cannabidiol has emerged from independent clinical trials, though results have not always been consistent. The overall evidence base for CBD in psychosis remains small and preliminary.

5.5 Pain — Weak-to-Preliminary Clinical Evidence

Cannabidiol has demonstrated analgesic and non-psychoactive properties. A 2024 systematic review updated and gathered the clinical and preclinical evidence on CBD in pain treatment. This review was performed following PRISMA guidelines; from an initial sample of more than 500 articles, a total of 40 studies were selected. Inclusion criteria required CBD in pain treatment without THC in monotherapy, including both clinical and preclinical trials.

However, there was no signal of positive activity of CBD in small randomized controlled trials assessing chronic pain. The large-scale meta-analysis of medical cannabinoids found that the highest-grade evidence for pain benefits applied to other cannabinoids (dronabinol, nabiximols) rather than to CBD alone. Clinical evidence for CBD monotherapy in pain therefore remains at a preliminary stage.

5.6 Neurological and Neuroprotective Effects — Preclinical and Limited Clinical Evidence

A comprehensive review brought together recent findings on the endocannabinoid and neurotransmitter systems, as well as anti-inflammatory pathways underlying CBD's modes of action, with synthesized efficacy and safety assessments for a range of neurological illnesses, covering human trials, in vitro studies, and animal models.

Preliminary studies suggest that CBD could not impair or worsen motor functions and may be an effective, safe, and well-tolerated treatment of psychosis in Parkinson's disease. A meta-analysis found moderate-grade evidence for CBD's benefit in Parkinsonism (SMD −0.41 [CI −0.75, −0.08]).

Anti-inflammatory and neuroprotective properties of CBD have been proposed in preclinical work. In vitro, CBD significantly attenuated LPS-induced neuroinflammation in BV2 microglia by reducing pro-inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6). These findings are, however, primarily preclinical and do not establish clinical efficacy.

6. Body Systems and Health Areas Associated with Cannabidiol

The discovery of CB1 and CB2 receptors, the targets of cannabinoids in the human body, and the endocannabinoid system (ECS), has revealed the relationship between cannabinoids and human health in maintaining homeostasis and influencing various functions such as sleep, appetite, pain perception, inflammation, memory, mood, and reproduction.

Based on published research, the body systems most studied in relation to CBD include:

• Central nervous system: Anticonvulsant effects (established in RCTs), putative anxiolytic, antipsychotic, and neuroprotective effects (preliminary to moderate evidence).
• Immune/inflammatory system: Anti-inflammatory activity via cytokine modulation demonstrated in preclinical models; not yet confirmed in high-quality clinical trials.
• Sleep regulation: Under investigation in RCTs; clinical evidence remains preliminary.
• Endocannabinoid system: CBD indirectly influences the endocannabinoid system by inhibiting FAAH, thereby increasing endogenous levels of anandamide.
• Hepatic system: CBD is metabolized by the liver and has documented interactions with liver enzymes — both therapeutically relevant and as a safety consideration (see Section 8).
• Gastrointestinal system: No signal of positive activity of CBD was found in small RCTs assessing Crohn's disease.

7. Dosage Forms and Dosages Reported in Clinical Studies

CBD has a wide active dosing range of less than 1 to 50 mg/kg/d within a variety of medical conditions including epilepsy, anxiety, and graft-versus-host disease. Studies that used higher doses tended to have better therapeutic outcomes compared to lower doses overall. There is a strong existing need for dose-ranging clinical studies in which plasma concentrations can provide a better indication of the therapeutic range of cannabidiol.

Specific dosages reported across major clinical studies include:

• Epilepsy (Lennox-Gastaut syndrome, RCT): 10 mg/kg/day and 20 mg/kg/day cannabidiol oral solution compared with placebo, with reductions in drop seizures of 37.2% and 41.9%, respectively.
• Epilepsy (overall RCT average): An average of 15 mg/kg/d within randomized controlled trials.
• Anxiety (open-label clinical trial): Full-spectrum, high-CBD sublingual solution at 9.97 mg/mL CBD (0.23 mg/mL THC), 1 mL three times daily, for 4 weeks.
• Anxiety (open-label pilot study): 0.5 mL of sublingual solution containing approximately 30 mg/mL CBD twice daily (BID), for a target daily dose of 30 mg CBD.
• Insomnia (pilot RCT): 150 mg of CBD nightly.
• Insomnia (crossover RCT): 300 mg CBD orally per dosing occasion, with terpenes, for at least 4 days per week over 4 weeks.
• Mild-to-moderate adverse effects reported at doses under 10 mg/kg/day: Oral CBD trials conducted for a period of 3 months found mild side effects such as reduced appetite, weight gain/loss, and tiredness when prescribed at doses less than 10 mg/kg/day.

8. Safety, Adverse Effects, and Drug Interactions

8.1 General Tolerability

CBD is a non-intoxicating major constituent of the Cannabis sativa plant with a generally favorable safety and tolerability profile. Side effects are generally mild and infrequent, such as sleepiness, diarrhea, or increased temperature.

Most studies investigated CBD efficacy and safety in neurological conditions, such as treatment-resistant epilepsies, although a growing number of studies are focusing on specific psychopathological conditions, such as substance use disorders, chronic psychosis, and anxiety. Most studies report mild or moderate severity of adverse events. The most common adverse events are diarrhea, somnolence, sedation, and upper respiratory disturbances.

8.2 Dose-Related Adverse Effects

Somnolence, sedation, the elevation of liver transaminase levels, skin rash, and respiratory disturbances were the most commonly reported serious adverse events in a systematic review of clinical CBD toxicity. These effects appear to be related to drug-drug interactions, especially with valproate in the case of increased liver transaminase levels, and with clobazam in the case of sedation and somnolence.

Higher doses (10–20 mg/kg/d) were associated with a higher rate of serious adverse events, including elevated liver transaminase and respiratory infections.

No significant serious adverse events were found in studies conducted on healthy subjects or patients with Parkinson's disease, Huntington's disease, type 2 diabetes, Crohn's disorder, and social anxiety disorders, even considering the concomitant medications.

8.3 Hepatotoxicity

Epidiolex can cause transaminase elevations. Concomitant use of valproate and higher doses of Epidiolex increases the risk of transaminase elevations. Human CBD studies for epilepsy and psychiatric disorders reported CBD-induced drug-drug interactions, hepatic abnormalities, diarrhea, fatigue, vomiting, and somnolence.

8.4 Drug–Drug Interactions

Drug interactions are an important issue to be carefully considered when prescribing CBD. CBD is often added to a regimen of other medications, especially other anti-epileptics, and the potential for drug-drug interactions could lead to serious health consequences. In vitro and in vivo data suggest that CBD interacts with pharmaceuticals, specifically drugs metabolized by the liver.

Common adverse drug events include transaminase elevations, sedation, sleep disturbances, infection, and anemia. Given CBD effects on common biological targets implicated in drug metabolism (e.g., CYP3A4/2C19) and excretion (e.g., P-glycoprotein), the potential for drug-drug interactions with commonly co-administered drugs is significant.

8.5 Chemical Stability Considerations

In strongly basic media and the presence of air, CBD is oxidized to cannabinodiol and a quinone. Under acidic conditions it cyclizes to a multitude of products including THC-9 and iso-THC, which also occurs during pyrolysis and during smoking. In the typical operating temperature range of e-cigarettes (250–400°C), 25–52% of CBD is transformed into other chemical substances including Δ9-THC, Δ8-THC, cannabinol, and cannabichromene as predominant pyrolysates.

8.6 Product Quality and Contamination

Residual solvent or its byproducts, including carcinogenic polycyclic aromatic hydrocarbons, are contaminants identified in CBD products that likely result from insufficient removal of the solvent extractor. Because CBD is extracted from a plant, it is also susceptible to unintentional contamination, including the introduction of pesticides, heavy metals, and microorganisms.

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