What does the research say?
In a study of 88 people with schizophrenia, those who took CBD for 6 weeks in addition to their antipsychotic medicines had a small reduction in symptoms such as hearing or seeing things that are not really there or holding beliefs that are not true (positive symptoms), compared with those taking an inactive medicine (placebo). However, the difference in the total score for all symptoms, in thinking skills and in daily functioning was not statistically significant. In another study of 36 people, CBD improved neither symptoms nor thinking skills. In a 12-week study by the medicine's maker, in which 77 patients were randomly assigned to groups and whose results were published only in the study registry, symptoms also did not go down differently from placebo at two different doses; the study was stopped early by company decision.
In a study of 42 patients, CBD was compared with an antipsychotic called amisulpride. Both groups improved clearly, and there was no difference between them; however, it could not be shown statistically that CBD was as effective as this medicine, and the study was stopped early. In the CBD group, drug-related movement side effects, weight gain and a rise in a hormone (prolactin) were less common.
Two analyses published in 2026 reached different conclusions: one found no clear effect on psychosis severity, while the other reported a small but significant reduction in overall symptoms; no effect was seen on symptoms such as social withdrawal and lack of motivation (negative symptoms). A 2026 analysis that pooled all cannabinoid studies in mental disorders found no significant effect in psychotic disorders, and the Cochrane review (2014) also found the evidence insufficient to show that CBD reduces psychosis symptoms.
In a laboratory study of 30 patients with both schizophrenia and cannabis use disorder, participants were given high-dose CBD or placebo 3 hours before marijuana. CBD did not reduce the harmful effects of marijuana; on the contrary, after marijuana, memory was impaired more with CBD and symptoms such as unrealistic thoughts increased more. This result shows that the idea that "CBD cancels out the harm of marijuana" does not hold for these patients.
Smaller studies paint a similar picture. In a study with results available only in the study registry, in which 18 patients took CBD and placebo for 4 weeks each, there was no difference in symptoms. In a 31-person pilot study in which CBD-rich cannabis cigarettes were smoked instead of tobacco and participants knew which group they were in, no clear difference was seen either. Of two small studies that tested a single dose of CBD, one saw no benefit on an attention test; in the other (15 patients), the drop in symptoms was slightly larger on the CBD day, but this was a secondary measure of the study. A 4-week study of 31 patients in the early years of the illness focused mainly on brain measurements.
In a randomized study of 33 young people at high risk of psychosis, a single dose of CBD brought activity in brain regions linked to psychosis closer to that of healthy people. Years later, a short letter reported that in the same study, those taking 600 mg of CBD a day for 3 weeks had slightly lower symptom scores than those taking placebo; however, symptoms were not the study's pre-specified main question, and the study did not last long enough to look at progression to psychosis. A reduction in symptoms with CBD was reported in 6 patients with psychosis due to Parkinson's disease, but there was no comparison group.
The picture is different for THC-containing products. Controlled laboratory studies show that a single dose of THC clearly increases psychosis-like symptoms in healthy volunteers and temporarily worsens symptoms in people with schizophrenia; in a study of patients who used cannabis regularly, symptoms did not change within a few hours, but learning was impaired. In newer studies with healthy volunteers, adding CBD to cannabis did not reduce these effects. In observational studies, weekly or more frequent use, and especially high-THC use, goes hand in hand with a higher risk of psychosis; in Danish registries, this link is stronger in young men. Whether the cannabis-related risk of psychosis is even higher in people with ADHD has been studied very little: a systematic review published in 2026 found only 3 studies looking at this question and saw very little evidence of such an added risk; ADHD and cannabis use are each known risk factors for psychosis on their own. Among people who keep using cannabis after psychosis begins, relapses are more common; this difference is not seen in those who stop. These findings show an association, not proof of cause and effect on their own; still, expert groups recommend that people at particular risk stay away from cannabis.
Strength of evidence: ●●○○ Weak evidence. Finding: Mixed results. What does this mean?
Ongoing research on this topic
Trials testing CBD for this topic on ClinicalTrials.gov: 6 under way (2 recruiting). A trial being under way does not show that CBD works.
- NCT07434973: Phase 3, not yet recruiting, target 586 participants
- NCT07326124: Phase 3, not yet recruiting, target 250 participants
- NCT06778564: Phase 3, recruiting, target 250 participants
Registries in other countries also list 1 recruiting trial on this topic: other registries.
Possible side effects and drug interactions
High doses of CBD given in addition to an antipsychotic were generally well tolerated, and side effect rates were similar to placebo. In one study, sleepiness was more common in those taking CBD. In healthy volunteers, CBD increased the risk of diarrhea.
These studies did not look at drug interactions separately. CBD can slow the breakdown of some medicines in the body, so using it together with antipsychotics and other mental health medicines calls for caution. THC-containing products can increase the risk of psychosis.
Interactions with medicines used for this condition
Interactions reported for these medicines in peer-reviewed publications and official prescribing information. A medicine that is not listed can still interact with CBD; tell your doctor about every medicine you take.
| Medicine | Importance | Warning | Source |
|---|---|---|---|
| Other antipsychotics (haloperidol, etc.) (Norodol), Risperidone (Risperdal, Rileptid, Neoris), Olanzapine (Zyprexa, Oferta, Olfrex), Quetiapine (Seroquel, Ketilept, Cedrina), Aripiprazole (Abilify, Abizol, Aripa), Clozapine (Clonex, Leponex) | Information | Antipsychotics: No published study has measured antipsychotic blood levels with CBD. In schizophrenia studies, CBD (600–1000 mg a day) added for 6 weeks to the antipsychotic being taken was generally well tolerated; in one study, drowsiness was more common in those taking CBD. Drowsiness may increase when they are taken together; tell your doctor. | PMID 29241357, PMID 29619533, FDA Epidiolex label §7.4 (05/2026) |
| Clozapine (Clonex, Leponex) | Information | Clozapine: No study has looked at clozapine and CBD together. Clozapine is broken down mainly by CYP1A2, and also by CYP2D6 and CYP3A4; approved CBD raised the total amount in the blood of caffeine, which is broken down by CYP1A2, about 2-fold. The clozapine prescribing information recommends close monitoring of the patient, and lowering the clozapine dose if needed, when it is combined with weak or moderate CYP1A2 inhibitors such as caffeine and birth control pills. Do not start without talking to your psychiatrist. | PMID 33951339, FDA Epidiolex label §7.2 (05/2026), Clozapine prescribing information §2.7 and §7.1, dailymed.nlm.nih.gov |
To check interactions with the medicines you take: CBD drug interaction checker.
How was CBD used in studies?
In treatment studies, pure CBD was taken by mouth for 3–12 weeks, mostly at 600–1000 mg a day (300 mg in one study; study dose, not a personal recommendation); in single-dose laboratory studies, 300–1000 mg was given. These amounts are far above the doses in CBD oils on the market, and the results cannot be carried over to lower doses.
Study details (for health professionals)
Pure CBD has been tested only in addition to an antipsychotic or for short periods. One RCT saw a small reduction in positive symptoms (the difference in total score was not significant), and another saw no improvement at all; in the comparison with amisulpride, equivalence could not be shown statistically. In the maker's unpublished 12-week phase 2 study (77 patients randomized; results only in the registry), 300 and 1000 mg/day were no different from placebo on the PANSS total; the study was stopped early by company decision. Two meta-analyses in 2026 reached different conclusions; a 2026 meta-analysis covering all cannabinoids found no significant effect in psychotic disorders, and the Cochrane review (2014) found the evidence for CBD insufficient; Denmark's 2026 national guideline recommends not using cannabinoids for negative symptoms. Other small controlled studies also found no difference: an 18-person crossover study with results only in the registry (NCT02504151), an open-label pilot study with CBD-rich cannabis cigarettes (Köck 2021) and an attention test with a single dose (Hallak 2010); in a 15-patient single-dose study, the drop in symptoms was larger on the CBD day, but this was a secondary measure tested one-sided (O'Neill 2021). In 33 people at high risk of psychosis, the main outcome of the only placebo-controlled study was brain measurements; it was reported years later in a short letter that symptom scores were lower in the CBD group after 21 days of use (not a pre-registered outcome; Bhattacharyya 2018). In Parkinson's psychosis there is only an open-label series of 6 patients (Zuardi 2009). In people with schizophrenia who also have cannabis use disorder, 1000 mg CBD given before marijuana did not reduce but increased marijuana's memory-impairing and psychosis-increasing effects (30-person crossover RCT); in healthy volunteers, CBD added to cannabis also did not reduce THC's psychosis-like effects (Englund 2023, Lawn 2023); results of earlier small studies were mixed (Freeman 2019). The doses studied (mostly 600–1000 mg/day) are far above the doses of CBD oils on the market; do not stop an antipsychotic and switch to CBD. THC: treatment data are almost nonexistent (an uncontrolled series of 6 patients); experimental studies and their meta-analyses show that THC temporarily increases psychosis symptoms, and large observational studies show that frequent and high-THC use is associated with an increase in psychosis risk (association; causation is debated). October 2026 search (PubMed, Cochrane, ClinicalTrials.gov): 16 controlled studies of cannabinoids on this topic (11 with CBD in patients or people at high risk of psychosis, one of them with CBD-rich cannabis cigarettes; 3 with THC; 2 in healthy volunteers), 4 small uncontrolled series, 12 systematic reviews or meta-analyses (one Cochrane), 2 guidelines or consensus reports and 4 large observational studies were found; all are in the table below. Reviews repeating the same question, and volunteer studies already covered by the reviews in the table, were not listed one by one.
Evidence assessment: Weak (conflicting)
CBD alone
Pure CBD (mostly 600–1000 mg/day, added to an antipsychotic) produced a small reduction in positive symptoms in the largest study, but the difference in total symptom score was not significant (McGuire 2018); most other controlled studies saw no benefit (Boggs 2018, NCT04421456, NCT02504151, Hallak 2010). One meta-analysis found a small benefit on total symptoms (Di Francesco 2026), while two that looked at CBD and at all cannabinoids found no significant effect (Marchi 2026, Wilson 2026); the Cochrane review found the evidence insufficient. No effect was seen on symptoms of schizophrenia such as social withdrawal and lack of motivation (negative symptoms) (Di Francesco 2026); Denmark's national guideline recommends not using cannabinoids to treat these symptoms (Norlin Mølgaard 2026). In the only placebo-controlled study in 33 people at high risk of psychosis, those taking CBD for 3 weeks had slightly lower symptom scores, but this was not the pre-specified main outcome and was reported years later in a short letter (Bhattacharyya 2018); in Parkinson's psychosis there is only an uncontrolled series of 6 patients (Zuardi 2009). CBD taken before marijuana did not reduce marijuana's harm in people with schizophrenia (Chesney 2025), nor did it in healthy volunteers in newer studies (Englund 2023, Lawn 2023). The strength of evidence is weak; it does not replace standard treatment.
Products containing THC
In schizophrenia and psychosis, THC-containing products have been studied mainly for their possible harms. In controlled laboratory studies, a single dose of THC clearly increased psychosis-like symptoms in healthy volunteers (Hindley 2020; an umbrella review rated the certainty of this finding as high: Solmi 2023), temporarily worsened symptoms and memory problems in people with schizophrenia (D'Souza 2005), and increased suspiciousness in 6 people at high risk of psychosis (Vadhan 2017); in patients who used cannabis regularly, 15 mg dronabinol did not increase symptoms within a few hours but impaired learning (Brunette 2025). In observational studies, weekly or more frequent and high-THC use goes hand in hand with a higher risk of psychosis (Robinson 2023, Di Forti 2019); relapses are more common in those who keep using after psychosis begins (Schoeler 2016); among people with medical cannabis authorization, emergency visits and hospital admissions for psychosis are also slightly more common (Dubois 2024). These observational findings are associations; according to experts, there are signs supporting causation, but reverse causation and confounding factors cannot be fully ruled out (D'Souza 2022). Someone with a history of psychosis should not use THC-containing products. As a treatment, no benefit of THC has been shown: Denmark's national guideline recommends not using cannabinoids for negative symptoms, and there are no controlled treatment studies; the only data are an uncontrolled series of 6 patients (Schwarcz 2009).
Evidence: Insufficient (for treatment): there are no controlled studies of THC-containing products for treating schizophrenia or psychosis; there is only an uncontrolled series of 6 patients. The evidence of harm is much stronger: in controlled laboratory studies and their meta-analysis, THC temporarily increased psychosis symptoms (high certainty in an umbrella review); in large observational studies, frequent and high-THC use went hand in hand with a higher risk of psychosis (association; does not show cause and effect on its own)
Dose range in studies
300–1000 mg/day in treatment studies (mostly 600–1000 mg; median 800 mg/day in a meta-analysis), 3–12 weeks; 300–1000 mg in single-dose studies
Starting dose and titration
Leweke 2012: started at 200 mg/day and increased by 200 mg each day (research protocol)
These are doses researchers gave under medical supervision; they are not a recommended dose for you. "mg/kg/day" means milligrams per kilogram of body weight per day.
| Study | Participants | Product | Dose and titration | Duration | Result | Source |
|---|---|---|---|---|---|---|
| Leweke 2012 Double-blind RCT, active control (amisulpride) | 42 (39 mITT) Schizophrenia | Pure CBD | 800 mg/day (200 mg × 4) Started at 200 mg/day and increased by 200 mg each day | 4 weeks | Clear improvement in both groups, no difference between groups; equivalence could not be shown statistically (p=0.27); the study stopped early when funding ran out Side effects: Fewer extrapyramidal symptoms, less weight gain and less prolactin increase with CBD | PMID 22832859, doi:10.1038/tp.2012.15, NCT00628290, PMID 33995015, similar improvement in the CBD and amisulpride groups, no difference between groups, 2 authors are shareholders of the company curantis UG) |
| McGuire 2018 Multicenter, double-blind, placebo-controlled, exploratory RCT, add-on treatment | 88 (43/45) Schizophrenia | Pure CBD | 1000 mg/day not reported | 6 weeks | Small reduction in positive symptoms (PANSS positive difference −1.4; 95% CI −2.5 to −0.2); the difference in total PANSS score was not significant (−2.8; 95% CI −6.5 to 0.9; p = 0.13; registry results); difference in favor of CBD in the doctor's rating of overall improvement (CGI-I); differences in cognition and functioning not significant. The study's sponsor was the maker of the CBD medicine Side effects: Similar to placebo | PMID 29241357, doi:10.1176/appi.ajp.2017.17030325, NCT02006628, July 26, 2019, sponsor: the medicine's maker) |
| Boggs 2018 RCT, add-on treatment | 41 randomized (21/20); 36 analyzed (18/18) Chronic schizophrenia | Pure CBD | 600 mg/day not reported | 6 weeks | CBD gave no benefit in cognition (MCCB): only the placebo group improved over time (drug × time interaction p = 0.02). Symptoms (PANSS) decreased in both groups, with no difference between groups (p = 0.18) Side effects: Sedation more common with CBD | PMID 29619533, doi:10.1007/s00213-018-4885-9, NCT00588731, June 8, 2017) |
| NCT04421456 (maker's phase 2 study, registry results) Double-blind, placebo-controlled, 3-arm phase 2 RCT; 2-week single-blind placebo run-in period; stopped early by the sponsor's business decision; no peer-reviewed publication | 95 entered the run-in period; 77 randomized (300 mg 27, 1000 mg 24, placebo 26); 61 analyzed (23/19/19) Patients with schizophrenia not responding well enough to ongoing antipsychotic treatment (aged 18–55, PANSS 60–110) | Oral CBD solution (pharmaceutical-grade, pure CBD) | 300 or 1000 mg/day (added to an antipsychotic) | 12 weeks | No difference from placebo in PANSS total (least-squares difference 300 mg −1.75, p = 0.45; 1000 mg −1.96, p = 0.42); scores fell in all three groups Side effects: Serious side effects 300 mg 2/27, 1000 mg 2/24, placebo 1/26; no deaths | NCT04421456, 2023) |
| NCT02504151 (Yale crossover study, registry results) Double-blind, placebo-controlled crossover RCT (4 weeks of CBD or placebo, 2-week washout, 4 weeks of the other); no peer-reviewed publication | 18 randomized (8 starting with CBD, 10 starting with placebo); 16 people completed the first period Adults aged 18–65 with a primary psychotic disorder (schizophrenia or schizoaffective disorder); people with substance dependence were not included (USA) | Oral pure CBD | 800 mg/day not reported (in the registry) | 2 × 4 weeks (10 weeks with washout) | No difference between CBD and placebo in the primary outcomes: estimated mean difference in PANSS total −0.28 (95% CI −2.28 to 1.71; treatment × time interaction p = 0.08) and in overall illness severity (CGI-S) −0.03 (95% CI −0.12 to 0.07; interaction p = 0.48). In the registry, the p-values refer to the interaction of treatment and time, and the confidence intervals to the mean difference (two separate tests). In secondary outcomes, the mean differences for patients' self-rated functioning (−4.97; 95% CI −9.87 to −0.06) and quality of life (4.13; 95% CI 0.07 to 8.19) narrowly favored CBD, but the interaction tests were not significant (p = 0.49 and 0.99). An 18-person crossover study; results only in the registry, no peer-reviewed publication Side effects: Serious side effects (hospitalization) 2/8 in the group starting with CBD, 0/10 in the group starting with placebo; side effects were recorded by sequence group, not by treatment | NCT02504151, 2022) |
| van Boxel 2023 Double-blind, placebo-controlled RCT, add-on treatment; primary outcomes were brain measurements | 31 patients (abstract); 32 in the Di Francesco 2026 meta-analysis Clinically stable patients with psychotic disorder within the first 5 years of diagnosis (Netherlands) | Oral pure CBD (capsule) | 600 mg/day (added to an antipsychotic) not reported (in the abstract) | 4 weeks (28 days) | CBD changed connectivity in a resting brain network (the default mode network) differently from placebo (interaction p = 0.037); no difference in frontal brain metabolites or reward processing. The group comparison of symptom and cognition results is not in the abstract; full text could not be read (PANSS data were included in the Di Francesco 2026 meta-analysis) Side effects: not reported (in the abstract) | PMID 37207437, doi:10.1016/j.jpsychires.2023.05.019, NCT02932605 |
| Köck 2021 Randomized, open-label pilot study (control: regular cigarettes); participants and researchers knew the group | 31 randomized (16 CBD cigarettes / 15 regular cigarettes); 4 and 8 people dropped out during the treatment period Hospitalized adults with acute psychosis and nicotine dependence (including psychosis due to mood disorder; 52% also used cannabis; Switzerland) | CBD-rich cannabis cigarettes: 20% cannabis (10% CBD in the flower, less than 1% THC) and 80% tobacco; about 20 mg CBD per cigarette | ~20 mg CBD per cigarette; an average of ~10 cigarettes a day (~200 mg CBD/day, as calculated by Di Francesco 2026); in place of regular cigarettes None (participants set their own number of cigarettes) | 4 weeks of treatment, follow-up to week 25 | No significant difference between groups in any of the primary outcomes (PANSS, depression, violence, well-being under medication, antipsychotic dose); PANSS and depression scores decreased in both groups, and antipsychotic dose increased in the regular cigarette group. Blood CBD and THC levels were not related to symptoms. A small, unblinded pilot study with a high dropout rate Side effects: Generally well tolerated; 1 person stopped because of a mild headache. 1 patient in the CBD group died during follow-up; at autopsy, the cause of death was opiate poisoning | PMID 34803760, doi:10.3389/fpsyt.2021.736822, NCT04700930 |
| Hallak 2010 Double-blind, placebo-controlled single-dose study (three groups; groups matched by sex, education, age and symptom profile, randomization method not stated) | 28 (18 men), three groups Outpatients with schizophrenia, not in an acute episode, taking antipsychotics (Brazil) | Oral pure CBD | Single dose of 300 or 600 mg (or placebo) | Single dose (at least 1 month after a first drug-free session) | CBD gave no benefit on a selective attention test (Stroop): all three groups made fewer errors in the second session, but the 600 mg group made more errors than the placebo and 300 mg groups (group effect p = 0.014); no difference in skin conductance responses. Symptoms were not measured after the medicine. Funding partly from Brazilian public funds (CNPq, FAPESP); the CBD was donated by researcher R. Mechoulam of his university in Jerusalem; no company ties were declared in the article. 3 of the 9 authors later became inventors on CBD patents (fluorinated CBD compounds; international application WO/2014/108899) Side effects: not reported | PMID 20339735, doi:10.1590/s1516-44462010000100011 |
| O'Neill 2021 Double-blind, placebo-controlled crossover RCT (single dose, two days at least 1 week apart); primary outcome brain imaging | 15 patients completed both days (two scans in 13 patients); 19 healthy volunteers given no medicine for comparison Patients with psychosis taking antipsychotics (UK) | Oral pure CBD | Single dose of 600 mg | Single dose | During a memory task, CBD brought activity in brain regions linked to psychosis to a level between placebo and healthy volunteers (primary outcome). In symptoms, measured as a secondary outcome, the drop in PANSS total 4.5 hours after the dose was 9.5 points on the CBD day and 4.2 points on the placebo day (one-sided p = 0.016); the difference on the positive symptom subscale was not significant. A single-dose, very small study Side effects: not reported (in the abstract) | PMID 31994476, doi:10.1017/S0033291719003519, PMID 33860709, PMID 35775365, PMID 42552898 |
| Chesney 2025 Double-blind, placebo-controlled crossover laboratory RCT | 37 people took part in at least one experiment (3 only in low-dose pilot experiments); sensitivity analysis (ITT) 34; primary analysis (per-protocol) 30 Schizophrenia or schizoaffective disorder + cannabis use disorder | Oral CBD, followed 3 hours later by vaporized inhaled marijuana (THC 20–60 mg) | Single dose of 1000 mg 3 hours before marijuana | Single dose (two sessions) | CBD did not reduce but increased marijuana's harm: delayed verbal recall after CBD 3.5 vs 4.8 words (difference −1.3; p=0.001), positive psychotic symptoms +5.0 vs +2.9 (difference +2.2; p=0.01); blood THC levels did not change Side effects: 2 treatment-related side effects, both after CBD pretreatment: in 1 participant, a temporary paranoid delusion after marijuana (resolved on its own the next day; withdrawn from the study); in 1 participant, blood pressure rose to 224/78 mmHg after marijuana (resolved on its own by the end of the experiment) | PMID 40702165, doi:10.1038/s41386-025-02175-3, NCT04605393 |
| Bhattacharyya 2018 Double-blind, placebo-controlled parallel RCT; brain imaging after a single dose on the first day, followed by 21 days of daily dosing; the primary outcome in the registry was brain activity (fMRI), symptoms were not among the registered outcomes | 33 people at high risk of psychosis (16 CBD / 17 placebo; 15/16 in the imaging analysis); 19 healthy volunteers given no medicine for comparison Antipsychotic-naive young people and young adults at clinical high risk (CHR) of psychosis (London) | Oral pure CBD | 600 mg a day (single dose on the first day; 21 days in total) | Single dose and 21 days | Primary outcome: during learning, CBD brought activity in three brain regions linked to psychosis to a level between placebo and healthy people; no difference in task performance. Symptoms (published as a letter in 2024): after 21 days, the total score of at-risk symptoms (CAARMS; F = 7.17; p = 0.012), distress due to psychotic experiences (p = 0.039) and the PANSS total (p = 0.042) were lower in the CBD group than with placebo; the difference in positive at-risk symptoms was not significant (p = 0.14), it was significant in negative symptoms (p = 0.045), and there was no difference in anxiety (p = 0.86). Missing data were filled in with the last observation; with only those with complete data, the CAARMS difference was p = 0.033 and the PANSS difference borderline (p = 0.056). After 1 week of use, the difference between CBD and placebo in cortisol response on a stress test was not significant (Appiah-Kusi 2020). A very small and short study; progression to psychosis was not looked at Side effects: No difference between groups in treatment-emergent side effects; no one dropped out of the CBD group, 2 people dropped out of the placebo group (Bhattacharyya 2024) | PMID 30167644, doi:10.1001/jamapsychiatry.2018.2309, ISRCTN46322781, symptom results: Bhattacharyya 2024 (World Psychiatry, PMID 39279373, letter), PMID 31915861, 1-week dosing and stress test), PMID 31439831, PMID 32921794, PMID 34480630, PMID 39145348, PMID 37845827, PMID 41337954 |
| Zuardi 2006 Open-label case series (inpatient; 5 days placebo, 30 days CBD, then placebo and olanzapine); no control group | 3 Patients with treatment-resistant schizophrenia (Brazil) | Oral pure CBD (alone, without antipsychotics) | Starting at 40 mg/day, up to 1280 mg/day Started at 40 mg/day and increased to 1280 mg/day (research protocol) | 30 days of CBD | Mild improvement in one patient, no improvement in two; the authors concluded that CBD alone may not be effective in treatment-resistant schizophrenia. The conflict of interest statement and funding could not be read (full text not open access); 3 of the 7 authors later became inventors on CBD patents (fluorinated CBD compounds; international application WO/2014/108899) Side effects: Well tolerated; no side effects reported | PMID 16401651, doi:10.1177/0269881106060967 |
| Zuardi 2009 Open-label pilot study (no comparison group) | 6 Patients with Parkinson's disease and psychosis for at least 3 months (Brazil) | Oral pure CBD (added to usual treatment) | Flexible dose starting at 150 mg/day (doses reached not in the abstract) Started at 150 mg/day with flexible dose adjustment (research protocol) | 4 weeks | Psychosis symptoms (BPRS and Parkinson Psychosis Questionnaire) decreased significantly; movement symptoms did not worsen. Because there was no placebo group, it is not known how much of the improvement came from CBD; there are no controlled studies of CBD in Parkinson's psychosis. The conflict of interest statement and funding could not be read from the primary source (full text not open access); according to the table of a systematic review, the study was supported by Brazil's national and state science funds, and the table also lists the companies THC-Pharm (Germany) and STI-Pharm as supporters (Thanabalasingam 2021). 3 of the 8 authors later became inventors on CBD patents (fluorinated CBD compounds; international application WO/2014/108899) Side effects: No side effects seen | PMID 18801821, doi:10.1177/0269881108096519, PMID 34104218, PMC8161868, Table 2) |
| Schipper 2018 Case series (inpatient; no comparison group) | 7 Inpatients with psychotic disorder and treatment-resistant cannabis use disorder (Netherlands) | A low-THC, relatively CBD-rich medical cannabis variety (Bedrolite); instead of street cannabis | not reported (in the abstract) not reported (in the abstract) | not reported (in the abstract) | According to the authors, this low-THC medical cannabis was not effective in inpatients with psychosis and cannabis use disorder and does not look promising as a harm reduction method; detailed figures not in the abstract Side effects: not reported (in the abstract) | PMID 29039260, doi:10.1177/0269881117735684 |
| Englund 2023 Double-blind, crossover RCT (four sessions, randomized order) | 46 Healthy volunteers who use cannabis occasionally (UK) | Vaporized inhaled cannabis: 10 mg THC with 0, 10, 20 or 30 mg CBD (CBD:THC 0:1, 1:1, 2:1, 3:1) | 10 mg THC + 0–30 mg CBD per session | Single dose (4 sessions) | THC without CBD impaired delayed verbal recall (d = 0.50; p = 0.001) and increased positive psychotic symptoms (PANSS positive, d = 0.69; p < 0.001); these effects were not significantly reduced at any CBD dose. CBD did not change blood THC levels Side effects: not reported (in the abstract) | PMID 36380220, doi:10.1038/s41386-022-01478-z, NCT05170217 |
| Lawn 2023 Double-blind, placebo-controlled crossover RCT (three sessions) | 48 (24 adolescents, aged 16–17; 24 adults, aged 26–29) Healthy adolescents and adults using cannabis 0.5–3 days a week (London) | Vaporized inhaled cannabis: THC, THC + CBD or placebo | 8 mg THC or 8 mg THC + 24 mg CBD for 75 kg (adjusted by body weight) | Single dose (3 sessions) | Compared with placebo, both THC and THC + CBD increased psychosis-like symptoms (Psychotomimetic States Inventory difference 7.8; 95% CI 2.8–12.7 and 10.8; 95% CI 6.2–15.4) and impaired verbal memory; adding CBD did not reduce these effects. Adolescents and adults were affected similarly Side effects: not reported (in the abstract) | PMID 36750134, doi:10.1111/add.16154, NCT04851392 |
| D'Souza 2005 Double-blind, placebo-controlled, randomized 3-day laboratory study | 13 patients (results compared with healthy volunteers from another publication) Clinically stable patients with schizophrenia taking antipsychotics (USA) | Intravenous THC | 0, 2.5 and 5 mg (intravenous, single dose) | 3 test days (a single dose each day) | THC temporarily worsened learning and recall, and temporarily increased positive, negative and general schizophrenia symptoms, perceptual disturbances, involuntary movement side effects (akathisia, rigidity), attention problems, and prolactin and cortisol. Patients were more sensitive than healthy people to THC's memory effects; figures not in the abstract Side effects: No serious side effects in the short or long term | PMID 15780846, doi:10.1016/j.biopsych.2004.12.006 |
| Brunette 2025 Double-blind, double-dummy, placebo-controlled RCT (single-dose laboratory study, parallel groups); the primary outcome in the registry was imaging of the brain reward circuit (no difference between cannabis and placebo), symptoms and cognition were the paper's outcomes | 130 in total; randomized: schizophrenia + cannabis use disorder 34 (11 cannabis cigarette, 12 dronabinol, 11 placebo) and cannabis use disorder only 51; non-randomized comparison groups: schizophrenia only and healthy volunteers Adults with schizophrenia and cannabis use disorder (USA); for comparison, people with cannabis use disorder only | Oral dronabinol (synthetic THC) or a cannabis cigarette with 3.5% THC | 15 mg dronabinol or a cannabis cigarette with 3.5% THC (single dose) | Single dose | In people with schizophrenia + cannabis use disorder, neither the cannabis cigarette nor dronabinol changed positive or negative symptoms differently from placebo at 2 and 5 hours; dronabinol impaired verbal learning (B = −9.89; 95% CI −16.06 to −3.18; p = 0.004) and attention. As blood THC levels rose, negative symptoms also increased (0.40 points per 10 ng/ml; p = 0.001). Participants were regular users accustomed to THC Side effects: Serious side effects in the registry, in the schizophrenia + cannabis use disorder groups: cannabis 1/11, dronabinol 0/12, placebo 1/11 | PMID 38900958, doi:10.1093/schbul/sbae097, NCT01964404, 2025) |
| Vadhan 2017 Double-blind, placebo-controlled laboratory study (active and placebo cannabis sessions; dose order randomized) | 12 (6 at high risk of psychosis, 6 controls) Young people at clinical high risk (CHR) of psychosis who used cannabis weekly, and users not at risk (USA) | Smoked cannabis cigarette (5.5% THC; placebo 0%) | Half a cigarette (5.5% THC) | Single dose (two sessions) | In the high-risk group, active cannabis temporarily increased suspiciousness, anxiety, visual illusions, a sense of strangeness and inattention compared with placebo, and impaired working memory and impulse control (p < 0.05); these effects were not seen in users not at risk. Auditory or visual hallucination scores did not change. A very small preliminary study Side effects: not reported | PMID 28803095, doi:10.1016/j.psychres.2017.07.070, PMID 37287664 |
| Schwarcz 2009 Open-label case series (compassionate use; no comparison group) | 6 Patients with severe, treatment-resistant chronic schizophrenia who said they improved with marijuana (USA) | Oral dronabinol (synthetic THC) | not reported (in the abstract) not reported (in the abstract) | not reported (in the abstract) | Improvement was reported in 4 of the 6 patients, in core psychotic symptoms in 3 of them; no clinically significant side effects were reported. A series of selected patients without placebo; in controlled studies, THC temporarily worsened symptoms (D'Souza 2005) Side effects: No clinically significant side effects reported | PMID 19440079, doi:10.1097/JCP.0b013e3181a6bc3b |
| Marchi 2026 Meta-analysis (8 RCTs; 2 unpublished) | 288 Psychotic disorders | Pure CBD | Median 800 mg/day | 20 min – 12 weeks | No significant effect on psychosis severity (SMD −0.194; CI −0.444 – 0.056); quality of evidence low to very low Side effects: Similar to placebo | PMID 41948975, doi:10.1177/02698811261430501 |
| Di Francesco 2026 Meta-analysis (5 RCTs, add-on treatment) | 204 (103 CBD / 101 control; PANSS total analysis) Schizophrenia spectrum disorders | Pure CBD | Variable | 4–12 weeks | Small but significant reduction in PANSS total (mean difference, MD −1.91; 95% CI −3.73 to −0.10); no effect on negative symptoms. Of the five studies, one was open-label (CBD-rich cannabis cigarettes, compared with regular cigarettes) and one was the maker's unpublished study (NCT04421456). With the open-label study removed, the result was similar (MD −2.07; 95% CI −3.14 to −1.00); the authors rated the risk of bias as low only in McGuire 2018 Side effects: Similar dropout rates | PMID 42047775, doi:10.1007/s00406-026-02249-3 |
| McLoughlin 2014 (Cochrane) Cochrane systematic review (RCTs; up to August 12, 2013) | 8 RCTs, 530 participants (cannabinoid treatment: 1 RCT) People with schizophrenia or a similar illness (including cannabis users) | CBD (compared with amisulpride); other comparisons were psychological treatments and antipsychotics aimed at reducing cannabis use | Variable | No difference in short-term symptoms (BPRS, PANSS) between CBD and amisulpride; according to the authors, evidence is insufficient to show an antipsychotic effect of CBD. None of the treatments tried to reduce cannabis use (psychological treatments, antipsychotics) was better than another; the studies were few and the data poorly reported Side effects: No clear difference between treatments in the short term | PMID 25314586, doi:10.1002/14651858.CD004837.pub3, PMID 18646115 | |
| Wilson 2026 Systematic review and meta-analysis of RCTs (1980–May 13, 2025; GRADE) | 54 RCTs, 2,477 participants (all mental disorders; size of the psychotic disorder subset not in the abstract) People with mental disorders or substance use disorders (including psychotic disorders) | All types of cannabinoids (CBD, THC, THC and CBD together, etc.) | Variable | No significant effect of cannabinoids on symptoms was found in psychotic disorders (nor in anxiety, anorexia nervosa, PTSD or opioid use disorder). Across all studies, the likelihood of any side effect was higher in those taking cannabinoids (OR 1.75; 95% CI 1.25–2.46); no difference in serious side effects. Certainty of evidence low for most outcomes; high risk of bias in 44% of studies Side effects: Any side effect OR 1.75 (one extra side effect in every 7 people); no difference in serious side effects or study discontinuation | PMID 41856154, doi:10.1016/S2215-0366(26)00015-5, Correction: Lancet Psychiatry 2026, 13(8):e11, PMID 42302809, 2026, the axis of a figure and the study counts in the table were corrected, results unchanged) | |
| Freeman 2019 Systematic review (no meta-analysis) | 16 studies, 466 participants Human studies in which CBD and THC were given together or one after the other (mostly healthy volunteers) | CBD given together with or before THC (at different ratios and by different routes) | Variable | Results were mixed: in some studies CBD reduced THC's intense anxiety and psychosis-like effects, but this effect was not consistent across studies and measures; no dose-response relationship was seen. 10 of the 16 studies had a low risk of bias Side effects: Not assessed separately | PMID 31580839, doi:10.1016/j.neubiorev.2019.09.036 | |
| Hindley 2020 Systematic review and meta-analysis of crossover experimental studies (up to May 21, 2019) | THC: 15 studies (14 studies, 324 participants for positive symptoms); CBD with THC: 4 studies Healthy volunteers | Intravenous, oral or intranasal THC; CBD together with THC | Variable (single dose) | Single dose | Compared with placebo, a single dose of THC increased total psychiatric symptoms (standardized mean change 1.10; 95% CI 0.92–1.28), positive psychotic symptoms (0.91; 95% CI 0.68–1.14) and negative symptoms (0.78; 95% CI 0.59–0.97) with a large effect. Of the 4 studies looking at whether CBD changes the effect of THC, symptoms decreased in only 1; there is no consistent evidence Side effects: Not assessed separately | PMID 32197092, doi:10.1016/S2215-0366(20)30074-2 |
| Robinson 2023 Systematic review and dose-response meta-analysis of observational studies (2010–April 2021) | 10 studies (3 cohort, 7 case-control), 7,390 people Ages 12–65 | Cannabis (containing THC) | Frequency of use (yearly, monthly, weekly, daily) | The risk of psychosis increased significantly with weekly or more frequent use (weekly RR 1.35; 95% CI 1.19–1.52; daily RR 1.76; 95% CI 1.47–2.12); no significant increase with yearly or monthly use. Observational data Side effects: Not applicable (observational) | PMID 35321777, doi:10.1017/S0033291722000502 | |
| Suetani 2026 Systematic review (synthesis without meta-analysis, SWiM) | 3 studies People with ADHD who use cannabis (psychosis outcomes) | Cannabis use | Not applicable | Only 3 studies meeting the criteria were found in four databases (with different designs; one of moderate and two of good quality). Two suggested indirectly that cannabis use does not affect the risk of psychosis in people with ADHD, and one suggested that cannabis affects the risk of psychosis similarly in people with and without ADHD. According to the authors, there is very little evidence that the cannabis-related risk of psychosis is higher in people with ADHD, but the topic has been studied very little; ADHD and cannabis use are each known risk factors for psychosis on their own. Full text could not be read (the names of the included studies are not in the abstract) Side effects: Not applicable | PMID 41916924, doi:10.1177/10398562261439662 | |
| Solmi 2023 Umbrella review (meta-analyses of RCTs and observational studies; up to February 9, 2022) | 101 meta-analyses (50 observational, 51 RCT) General population and various patient groups | Cannabis, cannabinoids and cannabis-based medicines | Variable | In meta-analyses of observational studies, the association between cannabis use in adolescence and later psychosis (equivalent OR 1.71; 95% CI 1.47–2.00; no information on adjustment for confounders) was at the 'highly suggestive' (class II) level of evidence in the main analysis, and is given in the abstract as 'convincing' together with the sensitivity analyses; the association between cannabis use and relapse in people with psychosis remained in the weak–suggestive class. In RCTs, cannabis or THC increased positive psychotic symptoms (equivalent OR 5.21; 95% CI 3.36–8.01) and total psychiatric symptoms in the general population (GRADE: high). The authors recommend that people prone to or living with mental illness avoid cannabis Side effects: Nervous system and psychiatric side effects increased with cannabis-based medicines | PMID 37648266, doi:10.1136/bmj-2022-072348 | |
| Schoeler 2016 Systematic review and meta-analysis of observational studies (at least 6 months of follow-up) | 24 studies, 16,565 patients Patients with psychotic disorder | Cannabis (containing THC) | Continued use, stopping, or never using | At least 6 months of follow-up | In people who kept using cannabis after psychosis began, relapse was more common than in those who never used (d = 0.36; 95% CI 0.22–0.50) and those who stopped (d = 0.28; 95% CI 0.12–0.44); hospital stays were longer. The relapse rate of those who stopped was no different from that of those who never used (d = 0.02). Observational data Side effects: Not applicable (observational) | PMID 26777297, doi:10.1016/S2215-0366(15)00363-6 |
| Kraan 2016 Systematic review and meta-analysis of prospective studies (1996–August 2015) | 7 studies, 1,171 people People at ultra-high risk (UHR) of psychosis | Cannabis (containing THC) | Lifetime use; current misuse or dependence | Lifetime cannabis use was not significantly associated with progression to psychosis (OR 1.14; 95% CI 0.86–1.52); progression to psychosis was more common in those with current cannabis misuse or dependence (OR 1.75; 95% CI 1.14–2.71; 5 studies). Observational data Side effects: Not applicable (observational) | PMID 26568030, doi:10.1017/S0033291715002329 | |
| Javed 2026 Systematic review and meta-analysis of observational studies (up to January 1, 2025) | 13 studies, 7,515 patients People diagnosed with cannabis-induced psychosis | Cannabis (containing THC) | Not applicable | About one in five people with cannabis-induced psychosis (20%; 95% CI 15.8–29.5) later received a schizophrenia-spectrum diagnosis, and about one in twenty (5%; 95% CI 2.7–6.9) a bipolar disorder diagnosis. Observational data Side effects: Not applicable (observational) | PMID 41664079, doi:10.1186/s12888-025-07382-2 | |
| D'Souza 2022 (WFSBP) Consensus report (World Federation of Societies of Biological Psychiatry task force; literature review, not a systematic review) | Number of studies not in the abstract People who use cannabis and cannabinoids; patients with psychosis | Cannabis and cannabinoids | Not applicable | Different types of evidence show that cannabis increases the risk of psychosis, from transient psychotic states to chronic psychosis; the risk rises with higher doses and younger age at use. For some outcomes, part of the criteria for causation are met, but reverse causation and confounding factors cannot be ruled out with certainty; cannabis is neither necessary nor sufficient for psychosis, but one of many causes. In people with psychosis, cannabis worsens the course of the illness; delaying or preventing use is recommended, especially in those at risk Side effects: Not applicable | PMID 35315315, doi:10.1080/15622975.2022.2038797 | |
| Norlin Mølgaard 2026 (Danish guideline) National clinical guideline (expert consensus based on 2019–2024 systematic reviews and meta-analyses) | 21 recommendations Children, adolescents and adults with negative symptoms in psychotic disorders | Cannabinoids (assessed together with other medicines and psychosocial treatments) | Not applicable | It recommends not using cannabinoids to treat negative symptoms such as social withdrawal and lack of motivation (conditional approval for adding modafinil; cognitive behavioral therapy and cognitive remediation are recommended) Side effects: Not applicable | PMID 42482516, doi:10.1080/08039488.2026.2697960 | |
| Di Forti 2019 Multicenter case-control study (EU-GEI; 11 centers in Europe and Brazil, 2010–2015) | 901 patients with first-episode psychosis, 1,237 controls Ages 18–64 | Cannabis; low-potency (<10%) and high-potency (≥10%) types by THC content | Frequency of use and type of cannabis | Daily cannabis use increased the odds of psychotic disorder compared with never using (adjusted OR 3.2; 95% CI 2.2–4.1); OR 4.8 (95% CI 2.5–6.3) for daily use of high-THC cannabis. Assuming causation, 12.2% of new psychosis cases could have been prevented if high-THC cannabis were not available (30.3% in London, 50.3% in Amsterdam). Observational data Side effects: Not applicable (observational) | PMID 30902669, doi:10.1016/S2215-0366(19)30048-3 | |
| Hjorthøj 2023 Nationwide registry-based cohort (Denmark, 1972–2021) | 6,907,859 people; 45,327 new schizophrenia diagnoses Ages 16–49 | Cannabis (diagnosis of cannabis use disorder) | Not applicable | 129.5 million person-years | In people with cannabis use disorder, the risk of schizophrenia was adjusted HR 2.42 (95% CI 2.33–2.52) in men and 2.02 (95% CI 1.89–2.17) in women; IRR 3.84 in men aged 16–20. Assuming causation, about 15% of new schizophrenia cases in men and about 4% in women in 2021 were attributed to cannabis use disorder; this share increased over the years. Observational data Side effects: Not applicable (observational) | PMID 37140715, doi:10.1017/S0033291723000880, PMID 34287621, the share of schizophrenia cases rose from about 2% in 1995 to 6–8% after 2010) |
| Young-Wolff 2026 Retrospective cohort (Kaiser Permanente Northern California electronic health records, 2016–2023) | 463,396 adolescents Adolescents aged 13–17 screened at routine checkups and followed up to age 25 (USA) | Cannabis (use in the past year; reported in confidential screening) | Not applicable | Mean follow-up 3.7 years | Adolescents who used cannabis in the past year had a higher risk of a later psychotic disorder diagnosis (adjusted HR 2.19; 95% CI 1.97–2.42; 1.92; 95% CI 1.73–2.13 when previous mental illnesses were also taken into account). Observational data Side effects: Not applicable (observational) | PMID 41719031, doi:10.1001/jamahealthforum.2025.6839 |
| Dubois 2024 Retrospective, propensity score–matched cohort (Ontario cannabis clinics and administrative health data, 2014–2019) | 54,006 patients with medical cannabis authorization, 161,265 matched controls Adults authorized to use medical cannabis (Canada) | Medical cannabis (product type and THC/CBD ratio not in the abstract) | not reported (in the abstract) | The rate of emergency visits or hospital admissions for psychotic disorder was 3.00 per 1000 person-years in the cannabis group and 1.88 in controls; adjusted HR 1.38 (95% CI 1.19–1.60), and 1.63 (95% CI 1.40–1.91) in those without previous psychosis. Observational data Side effects: Not applicable (observational) | PMID 38330686, doi:10.1016/j.schres.2024.01.029 |
Reported side effects
- In healthy volunteers, CBD increased the risk of diarrhea (RR 5.85); a non-significant trend toward more abdominal pain and headache (Sawaira 2026, PMID 41789242)
- Psychiatric and nervous system side effects more common with THC-containing products (Filippini 2022, PMID 35510826); the likelihood of side effects increased with any cannabinoid (OR 1.75; Wilson 2026)
- Sedation (Boggs 2018)
- Single-dose THC: psychosis-like symptoms clearly increased in healthy volunteers (Hindley 2020); symptoms and memory temporarily worsened in people with schizophrenia (D'Souza 2005); dronabinol impaired learning and attention (Brunette 2025)
Who should be careful
- High doses cannot be compared with market doses: in low-dose (≤175 mg/day) studies, plasma levels were 5–100 times lower than with the 20 mg/kg Epidiolex dose (Warren 2026, PMID 42473010)
- Anyone taking long-term medicines should consult a doctor before starting; the studies on this page did not systematically assess interactions
- Do not stop an antipsychotic and switch to CBD; even if there is an effect, it is small and was tested only in addition to an antipsychotic
- THC can increase the risk of psychosis; someone with a history of psychosis should not use THC-containing products
- In people with schizophrenia and cannabis use disorder, CBD taken before marijuana did not reduce but increased marijuana's memory-impairing and psychotic effects (Chesney 2025); it should not be used on the idea that "CBD cancels out the harm of marijuana"
- Among people who keep using cannabis after psychosis begins, relapses and long hospital stays are more common; in those who stop, the relapse rate is close to that of people who never used it (Schoeler 2016, observational meta-analysis)
- In adults with medical cannabis authorization, emergency visits or hospital admissions for psychotic disorder are more common than in matched controls (HR 1.38; Dubois 2024, observational)
- In people diagnosed with schizophrenia, cannabis use was linked to suicide attempts (odds ratio 1.40) and, in follow-up studies, to the risk of death by suicide (hazard ratio 1.21); the link with attempts comes mostly from cross-sectional studies and fell just short of significance in follow-up studies; no significant link with suicidal thoughts was seen. This finding comes from a meta-analysis of 29 observational studies and does not show cause and effect (Mulligan 2025, PMID 40059733); it is important that a patient who uses cannabis can talk about it openly with their care team
- In people who use cannabis, psychosis began an average of 2.5 years earlier than in those who do not; the difference was not seen in samples in which psychosis began, on average, before age 20, and it grew as the average age at onset rose. This finding comes from an observational meta-analysis pooling 18,272 users and 52,801 non-users in 149 studies (Stevens 2026, PMID 42610992); it is an association and does not by itself prove that cannabis brings on psychosis earlier
Drug interactions
- The studies on this page did not systematically assess drug interactions; details are in the site's drug interactions section
- Adding 1000 mg/day CBD to antipsychotics was well tolerated; side effect rates were similar to placebo (McGuire 2017/2018)
Abbreviations: RCT, randomized controlled trial (a study in which participants are assigned to groups by chance); placebo, an inactive substance; SMD, OR and RR, effect measures used in analyses that pool studies; CYP, liver enzymes that break down medicines.
If you are considering CBD
- Do not stop or reduce your antipsychotic medicine on your own. CBD has only been tested in addition to these medicines or for short periods; even if it has an effect, it is small.
- If you are considering CBD, talk openly with your psychiatrist about it; deciding together is the safest way.
- Stay away from THC-containing products; check the label and certificate of analysis to see whether the product contains THC.
- Go over all the medicines you take with your doctor and pharmacist; checking for drug interactions is important.
- If you notice any change in your symptoms, or your loved ones do, tell your doctor without waiting.
Choose your age group, medicines and situation to prepare a short summary you can take to your doctor. Nothing you enter is sent anywhere.
Bottom line
Research on CBD in schizophrenia is intriguing, but the results are small and inconsistent. For now, CBD is not an option that can replace antipsychotic treatment. THC-containing cannabis, on the other hand, can increase psychosis symptoms; in observational studies, relapses are more common in people who keep using cannabis after a psychosis diagnosis, while in those who stop, rates look close to those of people who never used it. The most important step is to continue your treatment and share every question on your mind with your doctor.
Frequently asked questions
Does CBD oil work for schizophrenia?
For now, the evidence is weak and mixed. High-dose CBD given in addition to an antipsychotic produced a small reduction in symptoms in one study, and gave results no different from an inactive medicine (placebo) in another. Analyses that pooled the studies also reached different conclusions, and most other small studies saw no clear difference either.
Can CBD be used instead of an antipsychotic medicine?
No. CBD has only been tested in addition to an antipsychotic or for short periods, and it has not been shown to replace standard treatment. Do not stop or reduce your medicine on your own; plan every change together with your doctor.
Why are THC-containing products risky in schizophrenia?
THC can increase the risk of psychosis: in controlled studies, a single dose of THC temporarily increased psychosis symptoms both in healthy people and in people with schizophrenia; in observational studies, frequent and high-THC use goes hand in hand with a higher risk of psychosis, and continuing to use after psychosis begins goes hand in hand with more frequent relapses. Observational studies alone do not prove cause and effect, but the findings point in the same direction. For this reason, people with a history of psychosis are advised not to use THC-containing products. Because some CBD products can also contain THC, it is important to check the label and certificate of analysis.
Does CBD reduce the harm of marijuana in schizophrenia?
No, there is no result showing this. In a study of 30 people with schizophrenia who also used marijuana, high-dose CBD taken before marijuana did not reduce but increased marijuana's effects of impairing memory and increasing psychosis symptoms. In newer studies with healthy volunteers, CBD added to cannabis also did not reduce THC's psychosis-like effects. Marijuana use can worsen symptoms of schizophrenia; ask your doctor for support in quitting.
What doses were used in the studies?
In treatment studies, pure CBD was mostly used at 600–1000 mg a day (300 mg in one study); in single-dose laboratory studies, 300–1000 mg was given (study dose; not a personal recommendation). These amounts are far above the doses in CBD oils on the market, and the results cannot be carried over to lower doses.
Is CBD safe together with antipsychotics?
In studies where high-dose CBD was added to antipsychotics, side effect rates were similar to placebo. However, these studies did not look at drug interactions separately. Because CBD can slow the breakdown of some medicines in the body, the decision to use them together should be made with your psychiatrist.
In Turkey, can CBD oil be obtained with a prescription for schizophrenia?
In Turkey, cannabis-derived products are regulated by the Kenevirden Elde Edilen Ürünlere Dair Yönetmelik (Regulation on Products Derived from Hemp) dated January 31, 2026. These products, including CBD, can be sold only in pharmacies. Those classed as medicines and health products are dispensed with a prescription; the regulation does not state a prescription requirement for supplement products and cosmetics with a THC content of at most 0.3%. As of October 2026, there is no approved CBD medicine in Turkey. If you are thinking of using it, talk with your doctor first.
Has CBD been tested in young people at high risk of psychosis?
The only published placebo-controlled study on this included 33 people. Its main question was about brain measurements: a single dose of CBD brought activity in some brain regions linked to psychosis closer to that of healthy people. It was later reported in a short letter that in the same study, those taking CBD for 3 weeks had slightly lower symptom scores than those taking placebo; however, the study was very small, symptoms were not the pre-specified main outcome, and it did not last long enough to show progression to psychosis. Larger studies are under way or about to begin (October 2026). According to observational studies, progression to psychosis is more common among young people in this group who misuse or are dependent on cannabis.
References
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- D'Souza 2022 (WFSBP). Consensus report (World Federation of Societies of Biological Psychiatry task force; literature review, not a systematic review). PMID 35315315, doi:10.1080/15622975.2022.2038797
- Norlin Mølgaard 2026 (Danish guideline). National clinical guideline (expert consensus based on 2019–2024 systematic reviews and meta-analyses). PMID 42482516, doi:10.1080/08039488.2026.2697960
- Di Forti 2019. Multicenter case-control study (EU-GEI; 11 centers in Europe and Brazil, 2010–2015). PMID 30902669, doi:10.1016/S2215-0366(19)30048-3
- Hjorthøj 2023. Nationwide registry-based cohort (Denmark, 1972–2021). PMID 37140715, doi:10.1017/S0033291723000880, PMID 34287621, the share of schizophrenia cases rose from about 2% in 1995 to 6–8% after 2010)
- Young-Wolff 2026. Retrospective cohort (Kaiser Permanente Northern California electronic health records, 2016–2023). PMID 41719031, doi:10.1001/jamahealthforum.2025.6839
- Dubois 2024. Retrospective, propensity score–matched cohort (Ontario cannabis clinics and administrative health data, 2014–2019). PMID 38330686, doi:10.1016/j.schres.2024.01.029
Points that could not be verified from the full text
- Unpublished or ongoing studies (October 2026): a 29-patient placebo-controlled crossover CBD study in Cologne (NCT00309413) ended in 2008, no results; a comparison of CBD, olanzapine and placebo in Mannheim (NCT02088060) was stopped in 2024 when funding ran out, no results. CBD in early schizophrenia (NCT02926859, Germany), CBD in early psychosis (NCT04411225, USA), a comparison of CBD with risperidone in early psychosis patients who use cannabis (NCT04105231, Denmark), Oxford's CBD studies in early psychosis, treatment-resistant psychosis and people at high risk of psychosis (NCT06778564, NCT07326124, NCT07434973), CBD in young people at high risk of psychosis (CanARY; protocol PMID 34190422) and CBD in schizophrenia not responding to clozapine (Cancloz; ACTRN12622001112752) are ongoing or have not yet started
- Full texts that could not be read: McGuire 2018 (how many authors were employees of the manufacturer could not be determined), Boggs 2018, van Boxel 2023 (symptom results), D'Souza 2005, Wilson 2026 and Marchi 2026 (psychosis subanalyses; Wilson 2026's correction notice was read on October 29, 2026 and does not change the results), Dubois 2024 (product types), Suetani 2026 (which 3 studies were included), Zuardi 2006 and Zuardi 2009 (conflict of interest statement and funding; the publisher's page required bot verification, which was not passed; Zuardi 2009's funding was read only from the table of a systematic review); these rows were written from abstracts and ClinicalTrials.gov records. Supplementary information for the symptom results of the study in people at high risk of psychosis is on a separate website of the authors; it was not read.
Research history
Here we record what changed on this page, when and why, with dates. The newest change is at the top.
The last sentence of the page's short summary was rewritten in a calmer, more guiding tone: instead of "Talk to your doctor before you start.", it now says whom you can talk with, and about what, if you are considering CBD. The conclusion and the strength of evidence did not change.
Information from two large observational meta-analyses was added to the 'Who should be careful' section: the link between cannabis use in people diagnosed with schizophrenia and suicide attempts and, in follow-up studies, the risk of death by suicide (Mulligan 2025), and the onset of psychosis an average of 2.5 years earlier in people who use cannabis (Stevens 2026). Both show an association, not cause and effect; they were not added to the table as rows, and their sources are given within the items. The conclusion and the strength of evidence did not change.
The correction published in the journal for the Wilson 2026 meta-analysis was read: only the axis of one figure and the study counts in a table were corrected; the results on this page did not change.
Related studies: Wilson 2026, published April 2026 (PMID 41856154, doi:10.1016/S2215-0366(26)00015-5, Correction: Lancet Psychiatry 2026, 13(8):e11, PMID 42302809, 2026, the axis of a figure and the study counts in the table were corrected, results unchanged))
Older changes (7)
On October 28, 2026, sources found for this page during searches for other topics were processed. A systematic review looking at whether cannabis use further increases the risk of psychosis in people with ADHD (Suetani 2026; only 3 studies were found, and there is very little evidence of such an added risk) was added to the table and the text. Funding and company ties were re-examined for three older CBD studies from the Ribeirão Preto group in Brazil (Hallak 2010, Zuardi 2006, Zuardi 2009): Hallak 2010 was partly supported by public funds, the CBD was donated by a university researcher, and no company ties were declared in the article; the full texts of the other two studies could not be read, and for Zuardi 2009, the table of a systematic review lists public funds and two CBD manufacturers as supporters (the same information as the same row on the Parkinson's page); the CBD patents of three of the authors date from years after these studies. The conclusion and the strength of evidence did not change.
Related studies: Suetani 2026, published October 2026 (online March 31, 2026) (PMID 41916924, doi:10.1177/10398562261439662)
Display fix: internal working notes left over from the previous cleanup were removed; content and evidence did not change.
Display fix: leftover internal working file names were removed from the text; content and evidence did not change.
PubMed, Cochrane and ClinicalTrials.gov were systematically searched again in October 2026 (5,768 records in PubMed, 416 in ClinicalTrials.gov; together with an independent second check). Added: 6 controlled studies of CBD in patients and people at high risk of psychosis (one with results only in the registry); very small uncontrolled series with CBD in treatment-resistant schizophrenia and Parkinson's psychosis and with CBD-rich medical cannabis in psychosis with cannabis use disorder; 2 studies in healthy volunteers testing whether CBD added to cannabis reduces THC's effects; 3 studies testing the effect of THC against placebo in patients and people at high risk of psychosis, and a small series in which THC was tried as a treatment; the Cochrane review and 8 more systematic reviews; one national guideline and one expert consensus report; 4 large observational studies on cannabis use and psychosis risk (including medical cannabis users). Reviews repeating the same question and studies covered by the reviews in the table were not added separately. Corrected: it was added that the difference in total symptom score in the largest CBD study was not significant, that the study was exploratory and that it was run by the maker; the later-published symptom results of the study in people at high risk of psychosis were written up with their limitations; the number of people in two studies, the result details and side effects of one study, the product type and sensitivity analysis of one meta-analysis, registry numbers and table order were corrected; a strength of evidence was added to the THC conclusion (insufficient for treatment; experimental and observational data pointing to harm). The conclusion and the strength of the CBD evidence did not change.
Related studies: NCT02504151 (Yale crossover study, registry results), published September 6, 2022 (registry results) (NCT02504151, 2022)); van Boxel 2023, published July 2023 (PMID 37207437, doi:10.1016/j.jpsychires.2023.05.019, NCT02932605); Köck 2021, published November 4, 2021 (PMID 34803760, doi:10.3389/fpsyt.2021.736822, NCT04700930); Hallak 2010, published March 2010 (PMID 20339735, doi:10.1590/s1516-44462010000100011); O'Neill 2021, published March 2021 (PMID 31994476, doi:10.1017/S0033291719003519, PMID 33860709, PMID 35775365, PMID 42552898); Bhattacharyya 2018, published November 1, 2018 (PMID 30167644, doi:10.1001/jamapsychiatry.2018.2309, ISRCTN46322781, symptom results: Bhattacharyya 2024 (World Psychiatry, PMID 39279373, letter), PMID 31915861, 1-week dosing and stress test), PMID 31439831, PMID 32921794, PMID 34480630, PMID 39145348, PMID 37845827, PMID 41337954); Zuardi 2006, published September 2006 (PMID 16401651, doi:10.1177/0269881106060967); Zuardi 2009, published November 2009 (PMID 18801821, doi:10.1177/0269881108096519, PMID 34104218, PMC8161868, Table 2)); Schipper 2018, published March 2018 (PMID 29039260, doi:10.1177/0269881117735684); Englund 2023, published May 2023 (PMID 36380220, doi:10.1038/s41386-022-01478-z, NCT05170217); Lawn 2023, published July 2023 (PMID 36750134, doi:10.1111/add.16154, NCT04851392); D'Souza 2005, published March 15, 2005 (PMID 15780846, doi:10.1016/j.biopsych.2004.12.006); Brunette 2025, published March 14, 2025 (PMID 38900958, doi:10.1093/schbul/sbae097, NCT01964404, 2025)); Vadhan 2017, published November 2017 (PMID 28803095, doi:10.1016/j.psychres.2017.07.070, PMID 37287664); Schwarcz 2009, published June 2009 (PMID 19440079, doi:10.1097/JCP.0b013e3181a6bc3b); McLoughlin 2014 (Cochrane), published October 14, 2014 (PMID 25314586, doi:10.1002/14651858.CD004837.pub3, PMID 18646115); Wilson 2026, published April 2026 (PMID 41856154, doi:10.1016/S2215-0366(26)00015-5, Correction: Lancet Psychiatry 2026, 13(8):e11, PMID 42302809, 2026, the axis of a figure and the study counts in the table were corrected, results unchanged)); Freeman 2019, published December 2019 (PMID 31580839, doi:10.1016/j.neubiorev.2019.09.036); Hindley 2020, published April 2020 (PMID 32197092, doi:10.1016/S2215-0366(20)30074-2); Robinson 2023, published July 2023 (PMID 35321777, doi:10.1017/S0033291722000502); Solmi 2023, published August 30, 2023 (PMID 37648266, doi:10.1136/bmj-2022-072348); Schoeler 2016, published March 2016 (PMID 26777297, doi:10.1016/S2215-0366(15)00363-6); Kraan 2016, published March 2016 (PMID 26568030, doi:10.1017/S0033291715002329); Javed 2026, published February 9, 2026 (PMID 41664079, doi:10.1186/s12888-025-07382-2); D'Souza 2022 (WFSBP), published December 2022 (PMID 35315315, doi:10.1080/15622975.2022.2038797); Norlin Mølgaard 2026 (Danish guideline), published August 2026 (PMID 42482516, doi:10.1080/08039488.2026.2697960); Di Forti 2019, published May 2019 (PMID 30902669, doi:10.1016/S2215-0366(19)30048-3); Hjorthøj 2023, published November 2023 (PMID 37140715, doi:10.1017/S0033291723000880, PMID 34287621, the share of schizophrenia cases rose from about 2% in 1995 to 6–8% after 2010)); Young-Wolff 2026, published February 6, 2026 (PMID 41719031, doi:10.1001/jamahealthforum.2025.6839); Dubois 2024, published February 2024 (PMID 38330686, doi:10.1016/j.schres.2024.01.029)
The medicine maker's 12-week study, with results only in the study registry and no difference from placebo, was added; the number of people and outcome measure of a meta-analysis were corrected; the phrase 'well-designed studies' became 'controlled studies'. The conclusion and the strength of evidence did not change.
PubMed and ClinicalTrials.gov were searched for newly published and previously missed clinical studies. Study added: Chesney 2025. This information was added to the "Who should be careful" list: in people with schizophrenia and cannabis use disorder, CBD taken before marijuana did not reduce but increased marijuana's harm to memory and psychosis (Chesney 2025). The conclusion and the strength of evidence did not change.
Related studies: Chesney 2025, published November 2025 (PMID 40702165, doi:10.1038/s41386-025-02175-3, NCT04605393)
Page published. This first assessment reviewed 5 studies.