A reference work, not a recommendation to use: this profile describes mechanism and evidence and does not replace medical advice. The claims come from marketing and forums and are tested here, not endorsed. Manufacture, possession, trade or use may be prohibited; see “Legal status” for details.

Claims checked

  • Helps against anxiety and stress

    Mixed results

    Mood & stress · mixed: healthy (one study) and patients with anxiety disorders (two studies) · Human, randomised small studiesEvery study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

    Healthy people: in 57 men, only the middle of three doses reduced anxiety before a simulated speech (inverted U-shaped curve); the CBD was provided free of charge by STI-Pharm, several authors are co-inventors of a CBD patent [10]. Patients: in 24 people with social anxiety disorder, a single dose worked [9], but as an add-on to exposure therapy in 80 people with anxiety disorders it did not [11]. Studies over weeks in healthy people are lacking.

  • Helps against epilepsy

    Proven benefit

    Nervous system · Patients: Dravet and Lennox-Gastaut syndromes · Human, randomised manufacturer-fundedAccording to their funding or competing-interest statements, all studies behind this result were paid for, wholly or in part, by the maker of the product or compound, or list employees of the maker among their authors. Manufacturer-funded studies on average come out more favourably for the product.

    Two manufacturer-funded phase 3 RCTs: seizures per month 12.4 → 5.9 versus 14.9 → 14.1 under placebo [6]; drop seizures −43.9% versus −21.8% [7]. Authorization in the United States and the EU followed [8]. Not established for other epilepsies and over-the-counter products. Evidence for “manufacturer-funded”: both studies were paid for by GW Pharmaceuticals, the manufacturer, according to their funding statements [6][7].

  • Improves sleep

    Single unconfirmed finding

    Sleep · healthy · Human, randomised small studiesEvery study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

    Only one placebo-controlled crossover study with 27 healthy people over one night each: sleep architecture on polysomnography did not change [12]. Repeated intake and people with sleep disorders were not studied in it.

  • Helps with quitting cannabis

    Single unconfirmed finding

    Addiction & dependence · Patients: cannabis use disorder · Human, randomised small studiesEvery study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

    Phase 2a study with 82 participants: only the middle dose group clearly improved both endpoints (urinary THC metabolite lowered, +0.48 abstinent days per week, interval 0.15–0.82). The high group lowered the metabolite; for abstinent days the interval included zero (+0.27; −0.09 to 0.64); the lowest group was ineffective [14].

  • Works against psychoses

    Small benefit

    Mood & stress · Patients: schizophrenia · Human, randomised

    As add-on therapy over 6 weeks, 1.4 PANSS points fewer positive symptoms (88 participants) [13]; in a comparison study with amisulpride, similar improvement with fewer side effects [4].

small studies: Every study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

manufacturer-funded: According to their funding or competing-interest statements, all studies behind this result were paid for, wholly or in part, by the maker of the product or compound, or list employees of the maker among their authors. Manufacturer-funded studies on average come out more favourably for the product.

Mechanism of action

Evidence map: CBD (cannabidiol)

Each line stands for a published finding; line style and color show where it comes from. The filter hides weaker evidence levels. Sources: see references.

Unlike THC, cannabidiol hardly activates the cannabinoid receptors CB1 and CB2; in the laboratory, however, it inhibits the effect of CB1 and CB2 agonists with unexpectedly high potency [1]. In cell models it behaved as a noncompetitive negative allosteric modulator of CB1 and attenuated the signals of THC and 2-arachidonoylglycerol [2]. In addition, CBD in cell culture is an agonist with moderate affinity at the human 5-HT1A receptor [3]. In an RCT in acute schizophrenia, the anandamide level in serum rose under CBD, and the rise was related to clinical improvement; CBD moderately inhibits the breakdown of this endocannabinoid [4].

Pharmacokinetics in humans is incompletely studied: the half-life was between 1.4 and 10.9 hours (oral spray), 24 hours (intravenous), and 2 to 5 days with continuous intake, depending on the route; bioavailability with smoking was 31%, and for other routes it was not determined. High-fat meals and lipid formulations increased peak levels [5].

The benefit is established in two rare, severe epilepsies: in manufacturer-funded RCTs, the number of seizures in Dravet syndrome (120 children and young adults) [6] and of drop seizures in Lennox-Gastaut syndrome (171 participants) [7] fell more than under placebo; authorizations in the United States and the EU followed in 2018 and 2019 [8]. For anxiety, the data are thin: in 24 people with social anxiety disorder, a single dose reduced anxiety before a simulated speech [9], in 57 healthy men only the middle of three doses worked [10], and as an add-on to exposure therapy in 80 people with anxiety disorders, CBD achieved nothing [11]. CBD did not change the sleep of healthy people in a polysomnography study [12]. In schizophrenia it slightly reduced positive symptoms as add-on therapy [13], and in cannabis use disorder it reduced use in a phase 2a study [14].

Risks concern mainly the liver and interactions: in a study with 16 healthy people, 44% had elevated ALT values under high daily amounts, and 31% met the criteria of drug-induced liver injury [15]. In 13 children who additionally received clobazam, its active metabolite N-desmethylclobazam rose on average by 500%; the rise of clobazam itself was uncertain [16]. Over-the-counter products often contained different amounts of CBD than stated and sometimes THC [17]. EFSA still sees large data gaps on liver, hormone system, and reproduction and considers the safety for people under 25, pregnant and breastfeeding women, and people taking medication not established [18].

Targets

TargetTypeActionKey dataEvidence
Cannabinoid receptor 1 (CB1)ReceptorNegative modulatorNoncompetitive negative allosteric modulator; lowers efficacy and potency of THC and 2-AG (cell models) Laboratory[1][2]
Cannabinoid receptor 2 (CB2)ReceptorAntagonistInhibits CB2 agonists with high potency (laboratory, review) Laboratory[1]
Serotonin 1A receptor (5-HT1A)ReceptorAgonistAgonist with moderate affinity at the human receptor (cell culture, GTPγS, cAMP ↓) Laboratory[3]
Anandamide breakdown (fatty acid amide hydrolase, FAAH)EnzymeInhibitorModerate inhibition; serum anandamide ↑ under CBD in schizophrenia (RCT) Human, randomised[4]
Breakdown of clobazam (CYP-mediated)EnzymeInhibitorN-desmethylclobazam +500 ± 300% (95% CI 90–610%); clobazam +60 ± 80% (95% CI −2 to 91%, uncertain) after 4 weeks (children, n = 13) Human, non-randomised[16]

Effect profile

Which signaling systems the compound affects according to current data. ↑ enhanced, ↓ dampened, ≈ modulated, ○ no effect; dots = evidence level.

  • Dopamineno data
  • Noradrenalineno data
  • Serotonin↑ · Agonist at the 5-HT1A receptor in cell culture; relevance in humans not documented[3]
  • Acetylcholineno data
  • Glutamate · AMPAno data
  • Glutamate · NMDAno data
  • GABAno data
  • Histamineno data
  • Orexinno data
  • Adenosineno data
  • Opioidsno data
  • Melatoninno data
  • Neurotrophinsno data
  • Blood flowno data
  • Nitric oxideno data
  • Energy metabolismno data
  • Insulin · glucoseno data
  • Inflammation · oxidativeno data
  • Stress axisno data
  • Testosterone axisno data
  • Endocannabinoidsmodulated · Negative allosteric CB1 modulator in the laboratory; raised anandamide levels in humans[1][2][4]
  • Autophagy · senescenceno data
  • Immune systemno data
  • Lipid metabolismno data
  • Coagulation · fibrinolysisno data
  • Methylationno data

Routes of administration and bioavailability

How much of a compound reaches the blood or target tissue depends on the route into the body and on the dosage form. All routes of administration explained

  • Oral (swallowed) · Solution, oil, capsule

    not determined in humans

    Peak level after 0 to 4 hours; meals and lipid formulations raise peak levels; half-life with continuous intake 2 to 5 days [5].

    Human, non-randomised

  • Inhaled · Smoking

    31% (human)

    Faster peak levels than oral, half-life 31 hours in the cited study [5].

    Human, non-randomised

  • Buccal (inner cheek) · Oral spray (combined with THC in studies)

    Half-life 1.4 to 10.9 hours [5].

    Human, non-randomised

Human studies

  • Dravet syndrome (GWPCARE1)

    RCT, double-blind, placebo-controlled · Patients: Dravet syndrome, children and young adults · n = 120 · 14 weeks

    Measured: seizures per month

    Result: Median 12.4 → 5.9 versus 14.9 → 14.1 (difference −22.8 percentage points); more diarrhea, fatigue, liver value changes. Funded by GW Pharmaceuticals.[6]

    Human, randomised

  • Lennox-Gastaut syndrome (GWPCARE4)

    RCT, double-blind, placebo-controlled, phase 3 · Patients: Lennox-Gastaut syndrome, aged 2–55 · n = 171 · 14 weeks

    Measured: drop seizures per month

    Result: −43.9% versus −21.8%; discontinuation due to adverse events 14% versus 1%. Funded by GW Pharmaceuticals.[7]

    Human, randomised

  • Anxiety about public speaking

    RCT, double-blind, placebo-controlled, four groups · healthy (men) · n = 57 · single dose

    Measured: subjective anxiety, circulation

    Result: Only the middle dose lowered anxiety; low and high doses like placebo. CBD provided free of charge by STI-Pharm; several authors co-inventors of a CBD patent.[10]

    Human, randomised

  • CBD plus exposure therapy

    RCT, double-blind, placebo-controlled, three centers · Patients: social anxiety disorder, panic disorder with agoraphobia · n = 80 · 8 sessions, 6 months of follow-up

    Measured: Fear Questionnaire

    Result: No difference from placebo.[11]

    Human, randomised

  • Sleep in healthy people

    RCT, double-blind, placebo-controlled, crossover · healthy · n = 27 · two nights

    Measured: polysomnography, cognition in the morning

    Result: No change.[12]

    Human, randomised

  • Liver values in healthy people

    open phase 1 interaction study · healthy · n = 16 · about 3.5 weeks

    Measured: ALT

    Result: 44% above the normal range, 31% above five times; authors with ties to GW or Greenwich Biosciences.[15]

    Human, non-randomised

Risks and warnings

  • Liver injury

    In 16 healthy people under high daily amounts, ALT elevations in 44%, in 31% in the range of drug-induced liver injury, partly with hepatitis symptoms [15]. Liver value changes also in the epilepsy studies [6]; EFSA sees a hepatotoxic potential, especially together with other medications [18].

    Human, non-randomised

  • Interactions with medications

    The active clobazam metabolite N-desmethylclobazam rose on average by 500%; the rise of clobazam itself (+60%, 95% CI −2 to 91%, n = 13) was uncertain. Adverse effects improved after dose adjustment of clobazam [16]. According to EFSA, safety with concurrent medication use is not established [18].

    Human, non-randomised

  • Adverse effects in studies

    Diarrhea, vomiting, fatigue, fever, and somnolence more frequent than under placebo; more study dropouts [6][7].

    Human, randomised

  • Mislabeled products with THC

    Of 11 over-the-counter CBD oils, only 4 were correctly labeled, 6 contained THC; beverages contained on average only 60% of the stated CBD amount [17].

    Human, non-randomised

  • Pregnancy, adolescence, hormone system

    Animal studies show reproductive toxicity, effects on brain development after prenatal exposure, and changes in the thyroid and adrenal gland; CBD crosses the placenta. EFSA considers the safety for people under 25, pregnant and breastfeeding women not established [18].

    Animal study

Interactions

  • Clobazam: N-desmethylclobazam on average +500%; clobazam +60%, but uncertain with 95% CI −2 to 91% (13 children with epilepsy) [16].
  • THC: Attenuates THC signals at CB1 in cell models [2]; clinical relevance not tested in the cited sources.
  • Other medications: According to EFSA, greater liver risk in combination; safety not established [18].

Fact check: common claims

  • partly supported

    “CBD helps against anxiety”

    Single doses lowered speech anxiety in social anxiety disorder [9] and in healthy people only at a medium amount [10]; no benefit as a therapy add-on [11].

  • not supported

    “CBD oil helps with falling asleep”

    No change in sleep in healthy people [12].

  • refuted

    “CBD is completely harmless because it does not intoxicate”

    Liver value elevations up to drug-induced liver injury [15], interactions [16], and open safety questions according to EFSA [18].

  • refuted

    “CBD products contain no THC”

    THC was found in 6 of 11 examined oils [17].

  • partly supported

    “CBD works against epilepsy”

    Established and authorized for Dravet and Lennox-Gastaut syndromes [6][7][8]; not for other epilepsies and over-the-counter products.

Pharmacokinetics

Absorption
Peak level after 0–4 hours; higher with food and lipids; bioavailability determined only for smoking (31%) [5].
Half-life
1.4–10.9 hours (oral spray), 24 hours (intravenous), 31 hours (smoking), 2–5 days with continuous intake [5].
Metabolism
CYP-mediated interactions, including strongly raised levels of N-desmethylclobazam [16]; EFSA names accumulation in the body and transfer across the placenta [18].
Entry into the brain
Central effects (anandamide ↑, symptom changes in psychosis) shown in humans [4]; brain levels not measured in the cited sources.

Legal status

Germany
Authorized as a high-purity medicinal product (Epidyolex) through the 2019 EU authorization for seizures in Lennox-Gastaut and Dravet syndromes [8]. In foods, CBD is assessed in the EU as a novel food [18]; the marketing status of individual CBD products in Germany is not verified.
EU
Medicinal product: EMA authorization in 2019 for Lennox-Gastaut and Dravet syndromes from age 2 [8]. Food: novel food assessment by EFSA; safety for people under 25, pregnant and breastfeeding women, and people taking medication is not established according to EFSA [18].
USA
FDA approval in 2018 (Epidiolex) for the same epilepsies [8]; over-the-counter CBD products largely unregulated [17].

Related compounds

THC (Δ9-Tetrahydrocannabinol)same class (German only)

Open questions

  • Which mechanism explains the antiepileptic effect in humans?
  • Does CBD work against anxiety in healthy people over weeks, and why does a U-shaped dose-response curve appear?
  • At what amount and in whom does liver injury occur?
  • How good is oral bioavailability in humans?

References

  1. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153(2):199–215. doi:10.1038/sj.bjp.0707442 · PubMed
  2. Laprairie RB, Bagher AM, Kelly ME, Denovan-Wright EM. Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor. Br J Pharmacol. 2015;172(20):4790–805. doi:10.1111/bph.13250 · PubMed
  3. Russo EB, Burnett A, Hall B, Parker KK. Agonistic properties of cannabidiol at 5-HT1a receptors. Neurochem Res. 2005;30(8):1037–43. doi:10.1007/s11064-005-6978-1 · PubMed
  4. Leweke FM, Piomelli D, Pahlisch F, Muhl D, Gerth CW, Hoyer C, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry. 2012;2(3):e94. doi:10.1038/tp.2012.15 · PubMed
  5. Millar SA, Stone NL, Yates AS, O'Sullivan SE. A Systematic Review on the Pharmacokinetics of Cannabidiol in Humans. Front Pharmacol. 2018;9:1365. doi:10.3389/fphar.2018.01365 · PubMed
  6. Devinsky O, Cross JH, Laux L, Marsh E, Miller I, Nabbout R, et al. Trial of Cannabidiol for Drug-Resistant Seizures in the Dravet Syndrome. N Engl J Med. 2017;376(21):2011–2020. doi:10.1056/NEJMoa1611618 · PubMed
  7. Thiele EA, Marsh ED, French JA, Mazurkiewicz-Beldzinska M, Benbadis SR, Joshi C, et al. Cannabidiol in patients with seizures associated with Lennox-Gastaut syndrome (GWPCARE4): a randomised, double-blind, placebo-controlled phase 3 trial. Lancet. 2018;391(10125):1085–1096. doi:10.1016/S0140-6736(18)30136-3 · PubMed
  8. Nabbout R, Thiele EA. The role of cannabinoids in epilepsy treatment: a critical review of efficacy results from clinical trials. Epileptic Disord. 2020;22(S1):23–28. doi:10.1684/epd.2019.1124 · PubMed
  9. Bergamaschi MM, Queiroz RH, Chagas MH, de Oliveira DC, De Martinis BS, Kapczinski F, et al. Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. Neuropsychopharmacology. 2011;36(6):1219–26. doi:10.1038/npp.2011.6 · PubMed
  10. Linares IM, Zuardi AW, Pereira LC, Queiroz RH, Mechoulam R, Guimarães FS, et al. Cannabidiol presents an inverted U-shaped dose-response curve in a simulated public speaking test. Braz J Psychiatry. 2019;41(1):9–14. doi:10.1590/1516-4446-2017-0015 · PubMed
  11. Kwee CM, Baas JM, van der Flier FE, Groenink L, Duits P, Eikelenboom M, et al. Cannabidiol enhancement of exposure therapy in treatment refractory patients with social anxiety disorder and panic disorder with agoraphobia: A randomised controlled trial. Eur Neuropsychopharmacol. 2022;59:58–67. doi:10.1016/j.euroneuro.2022.04.003 · PubMed
  12. Linares IMP, Guimaraes FS, Eckeli A, Crippa ACS, Zuardi AW, Souza JDS, et al. No Acute Effects of Cannabidiol on the Sleep-Wake Cycle of Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled, Crossover Study. Front Pharmacol. 2018;9:315. doi:10.3389/fphar.2018.00315 · PubMed
  13. McGuire P, Robson P, Cubala WJ, Vasile D, Morrison PD, Barron R, et al. Cannabidiol (CBD) as an Adjunctive Therapy in Schizophrenia: A Multicenter Randomized Controlled Trial. Am J Psychiatry. 2018;175(3):225–231. doi:10.1176/appi.ajp.2017.17030325 · PubMed
  14. Freeman TP, Hindocha C, Baio G, Shaban NDC, Thomas EM, Astbury D, et al. Cannabidiol for the treatment of cannabis use disorder: a phase 2a, double-blind, placebo-controlled, randomised, adaptive Bayesian trial. Lancet Psychiatry. 2020;7(10):865–874. doi:10.1016/S2215-0366(20)30290-X · PubMed
  15. Watkins PB, Church RJ, Li J, Knappertz V. Cannabidiol and Abnormal Liver Chemistries in Healthy Adults: Results of a Phase I Clinical Trial. Clin Pharmacol Ther. 2021;109(5):1224–1231. doi:10.1002/cpt.2071 · PubMed
  16. Geffrey AL, Pollack SF, Bruno PL, Thiele EA. Drug-drug interaction between clobazam and cannabidiol in children with refractory epilepsy. Epilepsia. 2015;56(8):1246–51. doi:10.1111/epi.13060 · PubMed
  17. Miller OS, Elder EJ, Jones KJ, Gidal BE. Analysis of cannabidiol (CBD) and THC in nonprescription consumer products: Implications for patients and practitioners. Epilepsy Behav. 2022;127:108514. doi:10.1016/j.yebeh.2021.108514 · PubMed
  18. EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA); Turck D, Bohn T, Cámara M, Castenmiller J, De Henauw S, et al. Update of the statement on safety of cannabidiol as a novel food. EFSA J. 2026;24(2):e9862. doi:10.2903/j.efsa.2026.9862 · PubMed
How this profile was checked

Last reviewed: 2026-10-25. All sources with a DOI or PMID were resolved automatically via Crossref or doi.org and PubMed.

Translated from the German profile (version of 2026-10-25); translation checked on 2026-10-26.

Checked

  • All abstracts read via PubMed; DOIs and PMIDs resolved with tools/pruefe_profile.py.
  • At the abstract: high potency as an antagonist of CB1/CB2 agonists [1]; NAM in HEK293A and STHdh cells, residues 98 and 107 [2]; 5-HT1A agonist of moderate affinity [3]; anandamide ↑ and association with improvement, comparison with amisulpride [4]; 24 studies, t½ 1.4–10.9 h / 2–5 d / 24 h / 31 h, F 31% (smoking), Tmax 0–4 h [5]; n = 120, 12.4 → 5.9 vs. 14.9 → 14.1, −22.8 percentage points [6]; n = 171 (86/85), −43.9 vs. −21.8%, adverse events 86 vs. 69%, discontinuation 14 vs. 1% [7]; FDA 2018, EMA 2019, from age 2 [8]; n = 24 (12/12) [9]; n = 57 (15/15/12/15), only middle dose effective [10]; n = 80 (39/41), no difference [11]; n = 27 [12]; n = 88 (43/45), PANSS positive −1.4 (−2.5 to −0.2) [13]; n = 82, +0.48 days/week, lowest group ineffective [14]; n = 16, 44% or 31% [15]; n = 13, +60 ± 80%, +500 ± 300% [16]; 11 oils, 4 correct, 6 with THC, beverages 59.9% [17]; data gaps, liver toxicity, placental passage, safety for < 25 years, pregnant, breastfeeding, medication not established [18].
  • Interests: [6] and [7] funded by GW Pharmaceuticals; authors of [15] consultants to GW Research or employees of Greenwich Biosciences; [10] CBD provided by STI-Pharm, several authors inventors of a CBD patent, cooperation of the university with Prati-Donaduzzi; [14] Medical Research Council.
  • ClinicalTrials.gov: 616 entries for “cannabidiol” (October 24, 2026), none from the sponsor “Hudson Biotech”.
  • Cross-check October 24, 2026 (at the abstract): cannabis cessation only middle group with an interval excluding zero (+0.48; 0.15–0.82), high group for abstinent days −0.09 to 0.64 [14]; clobazam +60% with CI −2 to 91% as uncertain, documented only N-desmethylclobazam +500% (CI 90–610%) [16]; anxiety claim named as a mixture of healthy people [10] and patients [9][11], STI-Pharm supply and patent connection of [10] stated in the claim and in the study; sleep at “Single unconfirmed finding” (one night, n = 27) [12].
  • October 25, 2026, q010 (area nervous system): claim “Helps against epilepsy” from area “Regeneration & Heilung” to “Nervensystem”. Abstracts [6] and [7] reread: primary endpoints frequency of convulsive seizures (Dravet syndrome) and frequency of drop seizures (Lennox-Gastaut syndrome). Level and result unchanged.
  • Precision flags (m004; rules guideline October 26, 2026; participant numbers, direction, and funding checked on October 26, 2026 via PubMed efetch against abstract, conflict-of-interest statement, and affiliations): “Helps against anxiety and stress”: “kleine_studien” – [9] 24, [10] 57, [11] 80. “Helps against epilepsy”: “herstellerfinanziert” – [6] “Funded by GW Pharmaceuticals”, [7] “FUNDING: GW Pharmaceuticals.” ([8] review). “Improves sleep”: “kleine_studien” – [12] 27. “Helps with quitting cannabis”: “kleine_studien” – [14] 82 (48 and 34 in two stages).
  • October 26, 2026, cross-check of the precision flags (m004): evidence for the flags that were set additionally carried over into the rationale (“Evidence for …”, guideline “Präzisions-Flags”); numbers and statements rechecked via PubMed efetch (abstract, conflict-of-interest and funding statements, affiliations): “Epilepsy”: [6] “Funded by GW Pharmaceuticals”, [7] “FUNDING: GW Pharmaceuticals.”

Not verified

  • Binding values (Ki) of CBD at CB1, CB2, 5-HT1A, and GPR55 not checked against a primary source with figures.
  • Whether a CBD novel food authorization has already been granted in the EU was not checked (EFSA assessed synthetic CBD positively in 2026, the Commission's decision was not read).
  • Legal status of over-the-counter CBD products in Germany not checked.
  • Sponsor of the schizophrenia study [13] not checked in the full text (co-author P. Robson possibly GW Pharmaceuticals).
  • The frequently cited JAMA study on the labeling of CBD extracts sold online (Bonn-Miller 2017, PMID 29114823) has no abstract; numbers not checked and therefore not used.

No dosages, no sources of supply. This information does not replace medical advice.

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