2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/2iy5wruuedsh6.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/00yc7rcvua6a7.js","/_next/static/immutable/chunks/37ktb71aq3480.js","/_next/static/immutable/chunks/2d50b-7eu4558.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/2d6noqpp6ehas.js","/_next/static/immutable/chunks/1sx186c93bpzg.js","/_next/static/immutable/chunks/3dc-1n866s65i.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2w1bvggzb0ga8.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T8ff,Adolescents experience extensive neurocognitive development, with cannabis use potentially impacting developmental trajectories. Here, we comprehensively assess the influence of adolescent cannabis use onset on neurocognitive trajectories and consider how recent delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) may influence neurocognition. We use the large, diverse longitudinal Adolescent Brain Cognitive Development (ABCD) Study dataset, combining self-reported substance use with objective toxicological tests (hair, urine, breath, oral fluid). Longitudinal mixed methods of the full cohort (n = 11,036, ages 9-17; 47% Female/53% Male) investigate time-varying cannabis onset on neurocognitive performance. Primary model covariates include sociodemographics, family history of substance use disorder, prenatal substance exposure, early psychopathology, other substance use, and nesting for participant ID, study site, and family ID. Secondarily, in participants with repeat toxicological hair testing (n = 645; 38% Female/62% Male) at ages 12-16, we consider the influence of THC v. CBD v. Controls. Primary models included false discovery rate corrections (FDR-p < .05) while secondary models were interpreted at p < .01. Cannabis group interacted with age to show altered neurocognitive trajectories across domains (immediate recall and delayed memory, processing speed, inhibitory control, visuospatial processing, language, and working memory; βs = -0.11- -0.52). Secondary models indicated hair-identified THC exposure*age predicted worse episodic memory than in Controls (β = -0.60, p = .007), with no difference between CBD exposed and Controls. Data suggest those who use cannabis show likely pre-existing better cognitive performance during late childhood, with reduced improvement or flattened trajectories over time. These neurocognitive trajectories in youth (ages 9-17) who initiate cannabis use were demonstrated after accounting for within-person change and numerous known confounds and improving accuracy in identifying cannabis use through incorporating toxicological measures. Continued monitoring of this cohort will clarify cannabinoid-cognition relationships into young adulthood, including the impact of timing of cannabis use initiation.31:Ta3f,Abstract Adolescents experience extensive neurocognitive development, with cannabis use potentially impacting developmental trajectories. Here, we comprehensively assess the influence of adolescent cannabis use onset on neurocognitive trajectories and consider how recent delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) may influence neurocognition. We use the large, diverse longitudinal Adolescent Brain Cognitive Development (ABCD) Study dataset, combining self-reported substance use with objective toxicological tests (hair, urine, breath, oral fluid). Longitudinal mixed methods of the full cohort (n = 11,036, ages 9-17; 47% Female/53% Male) investigate time-varying cannabis onset on neurocognitive performance. Primary model covariates include sociodemographics, family history of substance use disorder, prenatal substance exposure, early psychopathology, other substance use, and nesting for participant ID, study site, and family ID. Secondarily, in participants with repeat toxicological hair testing (n = 645; 38% Female/62% Male) at ages 12-16, we consider the influence of THC v. CBD v. Controls. Primary models included false discovery rate corrections (FDR- p < .05) while secondary models were interpreted at p < .01. Cannabis group interacted with age to show altered neurocognitive trajectories across domains (immediate recall and delayed memory, processing speed, inhibitory control, visuospatial processing, language, and working memory; βs = -0.11- -0.52). Secondary models indicated hair-identified THC exposure*age predicted worse episodic memory than in Controls (β = -0.60, p = .007), with no difference between CBD exposed and Controls. Data suggest those who use cannabis show likely pre-existing better cognitive performance during late childhood, with reduced improvement or flattened trajectories over time. These neurocognitive trajectories in youth (ages 9-17) who initiate cannabis use were demonstrated after accounting for within-person change and numerous known confounds and improving accuracy in identifying cannabis use through incorporating toxicological measures. Continued monitoring of this cohort will clarify cannabinoid-cognition relationships into young adulthood, including the impact of timing of cannabis use initiation. 32:T975,To assess the efficacy of cannabis for the treatment of acute migraine. Preclinical and retrospective studies suggest cannabinoids may be effective in migraine treatment. However, there have been no randomized clinical trials examining the efficacy of cannabinoids for acute migraine. In this randomized, double-blind, placebo-controlled, crossover trial, adults with migraine treated up to four separate migraine attacks, one each with vaporized (1) 6% Δ9-tetrahydrocannabinol (THC) (THC-dominant), (2) 11% cannabidiol (CBD) (CBD-dominant), (3) 6% THC + 11% CBD, and (4) placebo cannabis flower in a randomized order. Washout period between treated migraine attacks was ≥1 week. The primary endpoint was pain relief, and secondary endpoints were pain freedom and most bothersome symptom freedom, all assessed at 2-h post-vaporization. Ninety-two participants were enrolled and randomized, and 247 migraine attacks were treated. THC + CBD was superior to placebo at achieving pain relief (67.2% vs. 46.6%, odds ratio [95% confidence interval] 2.85 [1.22, 6.65], p = 0.016), pain freedom (34.5% vs. 15.5%, 3.30 [1.24, 8.80], p = 0.017), and most bothersome symptom freedom (60.3% vs. 34.5%, 3.32 [1.45, 7.64], p = 0.005) at 2 h, as well as sustained pain freedom at 24 h and sustained most bothersome symptom freedom at 24 and 48 h. THC-dominant was superior to placebo for pain relief (68.9% vs. 46.6%, 3.14 [1.35, 7.30], p = 0.008) but not pain freedom or most bothersome symptom freedom at 2 h. CBD-dominant was not superior to placebo for pain relief, pain freedom, or most bothersome symptom freedom at 2 h. There were no serious adverse events. Acute migraine treatment with 6% THC + 11% CBD was superior to placebo at 2-h post-treatment with sustained benefits at 24 and 48 h. Many people with migraine self‐treat with cannabinoids or are interested in using cannabinoids to treat migraine. In this double‐blind study, people with migraine treated up to 4 migraine attacks, 1 attack was treated with each of 3 vaporized cannabis flower treatments (THC 6%, CBD 11%, and THC 6% + CBD 11%) or placebo cannabis flower without THC or CBD, within the first 4 h of migraine attack onset. Four puffs of cannabis flower containing THC 6% + CBD 11% was superior to placebo at treating migraine attacks, though the study did not examine the long‐term effects of frequent use.33:Tb9a,Abstract Objective To assess the efficacy of cannabis for the treatment of acute migraine. Background Preclinical and retrospective studies suggest cannabinoids may be effective in migraine treatment. However, there have been no randomized clinical trials examining the efficacy of cannabinoids for acute migraine. Methods In this randomized, double‐blind, placebo‐controlled, crossover trial, adults with migraine treated up to four separate migraine attacks, one each with vaporized (1) 6% Δ9‐tetrahydrocannabinol (THC) (THC‐dominant), (2) 11% cannabidiol (CBD) (CBD‐dominant), (3) 6% THC + 11% CBD, and (4) placebo cannabis flower in a randomized order. Washout period between treated migraine attacks was ≥1 week. The primary endpoint was pain relief, and secondary endpoints were pain freedom and most bothersome symptom freedom, all assessed at 2‐h post‐vaporization. Results Ninety‐two participants were enrolled and randomized, and 247 migraine attacks were treated. THC + CBD was superior to placebo at achieving pain relief (67.2% vs. 46.6%, odds ratio [95% confidence interval] 2.85 [1.22, 6.65], p = 0.016), pain freedom (34.5% vs. 15.5%, 3.30 [1.24, 8.80], p = 0.017), and most bothersome symptom freedom (60.3% vs. 34.5%, 3.32 [1.45, 7.64], p = 0.005) at 2 h, as well as sustained pain freedom at 24 h and sustained most bothersome symptom freedom at 24 and 48 h. THC‐dominant was superior to placebo for pain relief (68.9% vs. 46.6%, 3.14 [1.35, 7.30], p = 0.008) but not pain freedom or most bothersome symptom freedom at 2 h. CBD‐dominant was not superior to placebo for pain relief, pain freedom, or most bothersome symptom freedom at 2 h. There were no serious adverse events. Conclusion Acute migraine treatment with 6% THC + 11% CBD was superior to placebo at 2‐h post‐treatment with sustained benefits at 24 and 48 h. 34:T82f,Fibromyalgia is a common condition characterised by widespread chronic pain, associated with comorbid mental health disorders and reduced quality of life. Preclinical data suggest cannabis-based medicinal products (CBMPs) may have potential benefits in fibromyalgia, but there is a paucity of high-quality clinical evidence. This study aims to assess the change in patient-reported outcome measures (PROMs) and incidence of adverse events (AEs) in patients treated with CBMPs for fibromyalgia. This case series analysed data from the UK Medical Cannabis Registry (UKMCR). The primary outcome was change in PROMs [Fibromyalgia Symptom Severity, Fibromyalgia Widespread Pain Index, EQ-5D-5L, Generalised Anxiety Disorder-7, and Single-Item Sleep Quality Scale] from baseline to follow-up at 1, 3, 6, 12, and 18 months. Statistical significance was defined as p < 0.050. Four hundred ninety-seven patients were included. The mean age was 44.66 ± 12.02 years, 341 patients (68.61%) were female, and the majority of patients were unemployed (n = 268, 53.92%). There was an improvement in all PROMs (p < 0.010) from baseline to all follow-up periods. Higher CBD doses (> 25.00 mg/day) and previous cannabis use were associated with increased odds of improvement on fibromyalgia-specific scales (p < 0.050). 227 patients (45.67%) reported 2100 AEs (422.54%). Most AEs were mild-to-moderate (n = 1792, 85.33%). The most common AE was fatigue (n = 153, 30.78%). There was an association between treatment with CBMPs and improvements in pain, anxiety, sleep, and general quality of life. The high incidence of AEs in relation to other patient cohorts from the UKMCR may relate to the central sensitisation mechanism of fibromyalgia. Key Points • This study found that CBMPs were associated with short to medium-term improvements in pain, anxiety, sleep, and general quality-of-life in patients with fibromyalgia. • More randomised controlled trials are warranted to consolidate the literature, but this large analysis provides real-world data to inform their rollout.35:Tf51,Abstract Introduction Fibromyalgia is a common condition characterised by widespread chronic pain, associated with comorbid mental health disorders and reduced quality of life. Preclinical data suggest cannabis-based medicinal products (CBMPs) may have potential benefits in fibromyalgia, but there is a paucity of high-quality clinical evidence. This study aims to assess the change in patient-reported outcome measures (PROMs) and incidence of adverse events (AEs) in patients treated with CBMPs for fibromyalgia. Methods This case series analysed data from the UK Medical Cannabis Registry (UKMCR). The primary outcome was change in PROMs [Fibromyalgia Symptom Severity, Fibromyalgia Widespread Pain Index, EQ-5D-5L, Generalised Anxiety Disorder-7, and Single-Item Sleep Quality Scale] from baseline to follow-up at 1, 3, 6, 12, and 18 months. Statistical significance was defined as p < 0.050. Results Four hundred ninety-seven patients were included. The mean age was 44.66 ± 12.02 years, 341 patients (68.61%) were female, and the majority of patients were unemployed ( n = 268, 53.92%). There was an improvement in all PROMs ( p < 0.010) from baseline to all follow-up periods. Higher CBD doses (> 25.00 mg/day) and previous cannabis use were associated with increased odds of improvement on fibromyalgia-specific scales ( p < 0.050). 227 patients (45.67%) reported 2100 AEs (422.54%). Most AEs were mild-to-moderate ( n = 1792, 85.33%). The most common AE was fatigue ( n = 153, 30.78%). Conclusions There was an association between treatment with CBMPs and improvements in pain, anxiety, sleep, and general quality of life. The high incidence of AEs in relation to other patient cohorts from the UKMCR may relate to the central sensitisation mechanism of fibromyalgia.

Key Points • This study found that CBMPs were associated with short to medium-term improvements in pain, anxiety, sleep, and general quality-of-life in patients with fibromyalgia. • More randomised controlled trials are warranted to consolidate the literature, but this large analysis provides real-world data to inform their rollout.

36:Tdc8,Madhur Varadpande is a medical student at Imperial College London. Madhur Varadpande has no shareholdings in pharmaceutical companies.Simon Erridge is a resident doctor and Research Director at Curaleaf Clinic. Simon Erridge is a research fellow at Imperial College London. Simon Erridge has no shareholdings in pharmaceutical companies.Arushika Aggarwal is a medical student at Imperial College London. Arushika Aggarwal has no shareholdings in pharmaceutical companies.Evonne Clarke is the Patient Care Director at Curaleaf Clinic. Evonne Clarke has no shareholdings in pharmaceutical companies.Katy McLachlan is the Chief Pharmacist at Curaleaf Clinic. Katy McLachlan has no shareholdings in pharmaceutical companies.Ross Coomber is a consultant orthopaedic surgeon at St George’s Hospital, London, and Operations Director at Curaleaf Clinic. Ross Coomber has no shareholdings in pharmaceutical companies.Shelley Barnes is a consultant pain specialist at Curaleaf Clinic. Shelley Barnes has no shareholdings in pharmaceutical companies.Alia Darweish Medniuk is a consultant pain specialist at Curaleaf Clinic. Alia Darweish Medniuk has no shareholdings in pharmaceutical companies.Rahul Guru is a consultant pain specialist at Curaleaf Clinic. Rahul Guru has no shareholdings in pharmaceutical companies.Wendy Holden is a consultant rheumatologist and pain specialist at Curaleaf Clinic. Wendy Holden has no shareholdings in pharmaceutical companies.Mohammed Sajad is a consultant pain specialist at Curaleaf Clinic. Mohammed Sajad has no shareholdings in pharmaceutical companies.Robert Seale is a consultant pain specialist at Curaleaf Clinic. Robert Seale has no shareholdings in pharmaceutical companies.Azfer Usmani is a consultant pain specialist at Curaleaf Clinic. Azfer Usmani has no shareholdings in pharmaceutical companies.Sanjay Varma is a consultant pain specialist at Curaleaf Clinic. Sanjay Varma has no shareholdings in pharmaceutical companies.James Rucker is a consultant psychiatrist at Curaleaf Clinic. James Rucker is an honorary consultant psychiatrist at The South London & Maudsley NHS Foundation Trust, and an NIHR Clinician Scientist Fellow at the Centre for Affective Disorders at King’s College London. James Rucker is funded by a fellowship (CS-2017–17-007) from the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health. James Rucker leads the Psychedelic Trials Group at King’s College London. King’s College London receives grant funding from COMPASS Pathways PLC to undertake phase 1 and phase 2 trials with psilocybin. COMPASS Pathways PLC has paid for James Rucker to attend trial-related meetings and conferences to present the results of research using psilocybin. James Rucker has undertaken paid consultancy work for Beckley PsyTech and Clerkenwell Health. Payments for consultancy work are received and managed by King’s College London, and James Rucker does not benefit personally. James Rucker has no shareholdings in pharmaceutical companies.Michael Platt is a consultant in pain services at Curaleaf Clinic. Michael Platt has no shareholdings in pharmaceutical companies.Mikael Sodergren is a consultant hepatopancreatobiliary surgeon at Imperial College NHS Trust, London, a senior clinical lecturer at Imperial College London, and the chief medical officer of Curaleaf International. Mikael Sodergren has no shareholdings in pharmaceutical companies.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"delta-9-tetrahydrocannabinol: generic Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on delta-9-tetrahydrocannabinol (generic). Clinician-written summaries and actionable practice insights. 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At 50 mg, dronabinol was correctly identified as a cannabinoid, while 50 mg distillate was perceived as sedative/dissociative with moderate psychedelic similarity.","limitations":"- Extremely small sample (n=4), all white/non-Hispanic, three with graduate degrees — severely limits generalizability.\n- Set and setting were held constant; the contribution of pharmacology vs. expectancy cannot be fully disentangled.\n- No inferential statistics possible; results are purely descriptive.","practice_takeaway":"For clinicians running psychedelic trials, oral Δ9-THC (particularly 25 mg dronabinol) may warrant evaluation as an active comparator to improve blinding integrity — though this pilot is far too small to guide practice on its own. Be aware that high-dose oral THC under psychedelic-style session conditions can produce unexpectedly prolonged effects and nausea, especially at 50 mg."}},{"doi":"10.1002/mds.70449","pmid":"42563548","title":"Cannabis‐Based Oil for Pain and Other Non‐Motor Symptoms in Parkinson's Disease: A Randomized Controlled Trial","journal_title":"Movement Disorders","journal_issn":"0885-3185","published_at":"2026-08-07T00:00:00.000Z","url":"https://doi.org/10.1002/mds.70449","source_score":12,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-12T13:26:12.627Z","updated_at":"2026-08-12T13:26:12.627Z","tags":[{"paper_doi":"10.1002/mds.70449","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"condition","value":"Chronic Pain","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"condition","value":"Parkinson's Disease","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"generic","value":"cannabidiol","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"generic","value":"delta-9-tetrahydrocannabinol","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"modality","value":"Cannabinoid","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"sample_size","value":"n=101","value_numeric":101},{"paper_doi":"10.1002/mds.70449","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"warning","value":"Age group tagged as 'adult' by inference from PD population context; specific age range not provided in the abstract.","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"warning","value":"Sex of participants is not reported in the abstract; the sex tag was omitted.","value_numeric":null},{"paper_doi":"10.1002/mds.70449","tag_type":"warning","value":"The phase II designation suggests this trial was primarily designed for safety/feasibility; definitive efficacy conclusions require larger phase III studies.","value_numeric":null}],"summaries":{"what_studied":"This phase II RCT evaluated an oral Cannabis sativa extract (CBD 96 mg/ml + THC 2.1 mg/ml; final daily dose ~43.9 mg CBD / 0.96 mg THC) vs. placebo over 9 weeks in 101 PD patients with chronic pain, with the primary outcome being the PD-Pain Classification System (PD-PCS) score at final visit.","key_result":"No significant between-group difference in PD-PCS scores (P = 0.757) or any other non-motor scale; 87/101 participants completed the study and no serious adverse events were reported.","limitations":"- Small phase II sample (n=101) may be underpowered to detect modest effects.\n- Single formulation with a low THC dose (0.96 mg/day); results may not generalize to higher-dose or different cannabinoid ratios.\n- 9-week duration limits conclusions about longer-term use.","practice_takeaway":"This CBD/THC oral oil formulation did not relieve pain or other non-motor symptoms in PD compared to placebo, so it should not be recommended for this indication based on current evidence. Clinicians should continue prioritizing established NMS treatments while awaiting larger trials."}},{"doi":"10.3389/fpsyt.2026.1824748","pmid":null,"title":"Cannabis, psychosis, and violence: case reports and comprehensive evidence review","journal_title":"Frontiers in Psychiatry","journal_issn":"1664-0640","published_at":"2026-07-21T00:00:00.000Z","url":"https://doi.org/10.3389/fpsyt.2026.1824748","source_score":15,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":false,"crossref":true,"unpaywall":true},"created_at":"2026-07-29T13:31:19.309Z","updated_at":"2026-07-29T13:31:19.309Z","tags":[{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"category","value":"Psychiatry","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"condition","value":"Cannabis-Induced Psychosis","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"condition","value":"Cannabis Use Disorder","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"condition","value":"Psychotic Disorder","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"condition","value":"Schizophrenia","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"generic","value":"delta-9-tetrahydrocannabinol","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"modality","value":"Cannabis / THC","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"study_design","value":"Perspective / Narrative Review with Case Series","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"warning","value":"Funding was provided by Drug Free America Foundation, an advocacy organization with a stated anti-cannabis stance, which may introduce bias in framing and case selection.","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"warning","value":"Level of evidence is assigned as 5 (expert opinion/narrative review); the cited primary studies referenced within vary widely in design and quality.","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"warning","value":"Study design is a perspective/narrative review with media-identified case reports — not a systematic review or controlled study. Evidence on violence causality is correlational only; the authors explicitly acknowledge causality cannot be determined.","value_numeric":null},{"paper_doi":"10.3389/fpsyt.2026.1824748","tag_type":"warning","value":"The neurobiological mechanisms discussed (e.g., dendritic spine pruning) are largely based on animal models with limited direct human evidence, as noted by the authors.","value_numeric":null}],"summaries":{"what_studied":"This perspective paper reviews the association between cannabis use (especially high-potency THC products), psychosis, and violent behavior, combining media-identified case reports of cannabis-associated violence with a comprehensive narrative review of epidemiological, neurobiological, and clinical evidence.","key_result":"Cannabis-induced psychosis converts to schizophrenia in 34–47% of cases — the highest rate among all substance-induced psychoses. Adolescents (ages 12–19) using cannabis face an 11.2-fold increased risk of psychotic disorders, rising to 26.7-fold for severe outcomes. Daily use of high-potency cannabis (>10% THC) is associated with a 5-fold higher risk of psychotic disorder. Post-legalization in Canada, ED visits for cannabis-induced psychosis rose ~40%. Among recently discharged psychiatric patients, persistent cannabis users were 2.44 times more likely to be violent than non-users.","limitations":"- Case reports are drawn from mainstream media, not a systematic review of all violent events, introducing major selection bias with no denominator or controls.\n- Causality cannot be established from observational data; reverse causation and shared genetic/environmental confounders are not ruled out.\n- THC toxicology is inconsistently performed or legally withheld across U.S. jurisdictions, leading to significant under-ascertainment of cannabis involvement in violent deaths.","practice_takeaway":"Screen all patients — especially adolescents, young adults, and those with psychiatric disorders — for cannabis use and educate them about the elevated psychosis risk tied to high-potency products. Clinicians should provide long-term follow-up after any cannabis-induced psychosis episode given the high rate of conversion to schizophrenia, and consider second-generation antipsychotics plus behavioral interventions (motivational interviewing, CBT) to support cessation."}},{"doi":"10.1007/s00787-026-03126-z","pmid":"42400661","title":"Neurodevelopmental outcomes following prenatal cannabinoid exposure: a systematic review","journal_title":"European Child & Adolescent Psychiatry","journal_issn":"1018-8827","published_at":"2026-07-04T00:00:00.000Z","url":"https://doi.org/10.1007/s00787-026-03126-z","source_score":11,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-10T13:25:27.024Z","updated_at":"2026-07-10T13:25:27.024Z","tags":[{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"category","value":"Pediatrics","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"condition","value":"Attention-Deficit/Hyperactivity Disorder","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"condition","value":"Behavioural Dysregulation","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"condition","value":"Executive Dysfunction","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"condition","value":"Neurodevelopmental Disorders","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"condition","value":"Prenatal Cannabis Exposure","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"generic","value":"cannabidiol","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"generic","value":"delta-9-tetrahydrocannabinol","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"modality","value":"Cannabinoid","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"sample_size","value":"n=72","value_numeric":72},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"study_design","value":"Systematic Review","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"warning","value":"Findings on visuospatial development are based on only 6 studies — domain-level conclusions are particularly tentative.","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"warning","value":"Meta-analysis was planned but not performed due to heterogeneity; all synthesis is narrative, which limits precision of domain-level percentage estimates.","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"warning","value":"Sample size tag reflects number of included studies (n=72), not individual participants; individual study sizes ranged from <100 to several thousand mother-child pairs.","value_numeric":null},{"paper_doi":"10.1007/s00787-026-03126-z","tag_type":"warning","value":"The review includes both THC and CBD exposures under 'cannabinoids,' but most included studies focused on cannabis broadly rather than isolating specific cannabinoid components.","value_numeric":null}],"summaries":{"what_studied":"Systematic review of 72 observational studies (published 1985–2025) examining the association between prenatal cannabis exposure and neurodevelopmental outcomes in children from birth to 18 years, across domains including cognition, behaviour, attention/ADHD, language, motor development, executive function, and visuospatial development.","key_result":"Findings were domain-specific, not global. Behavioural dysregulation (73% of studies negative), executive dysfunction (70%), and attention/ADHD-related problems (69%) showed the most consistent adverse associations. In contrast, global cognition (84% no significant association), language (92%), and motor development (60%) were largely unaffected after confounder adjustment. Stronger associations were seen with heavier or persistent use beyond maternal awareness of pregnancy, suggesting possible dose-response and timing effects.","limitations":"- All studies were observational; causal inference cannot be established.\n- Exposure assessment varied widely—many relied on maternal self-report, risking recall bias and underreporting.\n- Substantial heterogeneity in outcome measures, confounder adjustment, and exposure definitions precluded meta-analysis; residual confounding (genetic, familial, psychiatric) cannot be excluded.","practice_takeaway":"Counsel pregnant patients that current evidence does not support global developmental harm from prenatal cannabis use, but consistent signals exist for behavioural regulation, attention, and executive function—domains with real downstream effects on academics and mental health. 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Hair-confirmed THC exposure predicted worse episodic memory trajectories vs. controls (β = −0.60, p = .007); CBD-exposed youth did not differ from controls. Notably, cannabis users showed slightly better cognitive performance at baseline (late childhood), suggesting pre-existing differences rather than acute impairment.","limitations":"The toxicology subsample (n=645) was predominantly male (62%) and smaller, limiting generalizability of secondary findings. The cohort only extends to age 17, so long-term effects into adulthood remain unclear. Causal inference is constrained because pre-existing cognitive differences preceded cannabis onset.","practice_takeaway":"Adolescents who initiate cannabis use show blunted neurocognitive growth across multiple domains over time — not just lower scores at a single point. Clinicians counseling teens about cannabis should emphasize that the key risk is slower cognitive development, and that this pattern holds even after controlling for family history, psychopathology, and other substance use."}},{"doi":"10.1001/jamainternmed.2025.8215","pmid":"41801216","title":"Cannabis and Mental Health","journal_title":"JAMA Internal Medicine","journal_issn":"2168-6106","published_at":"2026-03-09T00:00:00.000Z","url":"https://doi.org/10.1001/jamainternmed.2025.8215","source_score":846,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-07T22:49:09.189Z","updated_at":"2026-05-07T22:49:09.189Z","tags":[{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Anxiety Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Attention-Deficit/Hyperactivity Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Bipolar Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Cannabis Use Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Depression","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Posttraumatic Stress Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"condition","value":"Psychotic Disorder","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"generic","value":"cannabidiol","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"generic","value":"delta-9-tetrahydrocannabinol","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"modality","value":"Cannabinoid","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"modality","value":"Cannabis","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"warning","value":"No sample size is applicable as this is a review article, not a primary study.","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"warning","value":"The psychosis risk estimates (2- to 11-fold) span a very wide range, likely reflecting heterogeneous study designs and populations — clinicians should interpret these with caution.","value_numeric":null},{"paper_doi":"10.1001/jamainternmed.2025.8215","tag_type":"warning","value":"This is a narrative review published in JAMA Internal Medicine; it does not report a systematic search strategy or formal risk-of-bias assessment, so the synthesis of evidence may be selective.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the evidence for cannabis use — both THC-predominant products and cannabidiol (CBD) alone — in managing mental health conditions including PTSD, anxiety, depression, ADHD, bipolar disorder, and psychotic disorders, with attention to adverse effects and cannabis use disorder (CUD).","key_result":"Evidence is insufficient or low-certainty for most mental health benefits of cannabis. THC-predominant cannabis may not improve PTSD symptoms (low-certainty), and evidence is largely insufficient for anxiety, depression, and ADHD. CBD alone shows emerging low-certainty benefit for anxiety disorders. Serious harms include: worsening mania in bipolar disorder, increased psychotic symptoms, and CUD in ~3 in 10 past-year users (about half with moderate-to-severe disease). Adolescents and young adults face a 2- to 11-fold increased psychosis risk with high-THC products.","limitations":"Evidence base relies heavily on low-certainty or insufficient studies; long-term effects of THC-predominant cannabis on most mental health conditions remain poorly characterized; review does not detail systematic search methods or risk-of-bias assessments.","practice_takeaway":"Counsel patients — especially adolescents, young adults, and those with bipolar or psychotic disorders — that cannabis carries substantial mental health risks with little proven benefit; cannabis should be avoided in these high-risk groups. Routinely ask patients with mental health conditions about cannabis use, as it is common and likely a modifiable risk factor."}},{"doi":"10.1111/head.70025","pmid":"41469488","title":"Vaporized cannabis versus placebo for acute migraine: A randomized, double‐blind, placebo‐controlled crossover trial","journal_title":"Headache: The Journal of Head and Face Pain","journal_issn":"0017-8748","published_at":"2025-12-31T00:00:00.000Z","url":"https://doi.org/10.1111/head.70025","source_score":41,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2025-12-31","doi":"10.1111/head.70025","days":"14","issn":"0017-8748","rank":"5","field":"Clinical Medicine","score":"41","category":"Clinical Neurology","categories":["Clinical Neurology"],"_categories":["Clinical Neurology"]},"pubmed":{"doi":"10.1111/head.70025","title":"Vaporized cannabis versus placebo for acute migraine: A randomized, double-blind, placebo-controlled crossover trial.","journal":"Headache","methods":"","results":"Ninety-two participants were enrolled and randomized, and 247 migraine attacks were treated. THC + CBD was superior to placebo at achieving pain relief (67.2% vs. 46.6%, odds ratio [95% confidence interval] 2.85 [1.22, 6.65], p = 0.016), pain freedom (34.5% vs. 15.5%, 3.30 [1.24, 8.80], p = 0.017), and most bothersome symptom freedom (60.3% vs. 34.5%, 3.32 [1.45, 7.64], p = 0.005) at 2 h, as well as sustained pain freedom at 24 h and sustained most bothersome symptom freedom at 24 and 48 h. THC-dominant was superior to placebo for pain relief (68.9% vs. 46.6%, 3.14 [1.35, 7.30], p = 0.008) but not pain freedom or most bothersome symptom freedom at 2 h. CBD-dominant was not superior to placebo for pain relief, pain freedom, or most bothersome symptom freedom at 2 h. There were no serious adverse events.","abstract":"$32","keywords":["acute","cannabidiol","cannabinoids","cannabis","migraine","Δ9‐tetrahydrocannabinol"],"pubmed_id":"41469488","conclusions":"Acute migraine treatment with 6% THC + 11% CBD was superior to placebo at 2-h post-treatment with sustained benefits at 24 and 48 h.","publication_date":"2025-12-31T00:00:00"},"crossref":{"DOI":"10.1111/head.70025","URL":"https://doi.org/10.1111/head.70025","ISSN":["0017-8748","1526-4610"],"link":[{"URL":"https://headachejournal.onlinelibrary.wiley.com/doi/pdf/10.1111/head.70025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Vaporized cannabis versus placebo for acute migraine: A randomized, double‐blind, placebo‐controlled crossover trial"],"author":[{"given":"Nathaniel M.","family":"Schuster","sequence":"first","affiliation":[{"name":"Center for Pain Management, Department 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Adverse events were reported by 227/497 (45.67%) patients (2100 events; 85.33% mild–moderate), fatigue was most common (153, 30.78%); higher CBD dose (>25 mg/day) increased odds of improvement (SS OR 1.64 [1.04–2.61]; WPI OR 1.90 [1.19–3.03]) and current cannabis use did too (SS OR 2.32 [1.22–4.43]).","limitations":"Uncontrolled registry case series with subjective PROMs and baseline‑carried‑forward imputation; causality and placebo effects cannot be excluded. Selection bias is likely (68.61% prior cannabis use; private clinic cohort), limiting generalisability. AEs were not confirmed as treatment‑related and MCIDs for SS/WPI were not established.","practice_takeaway":"In this registry, CBMPs were associated with modest improvements in pain, anxiety, sleep, and quality of life up to 18 months, while nearly half reported AEs that were mostly mild–moderate. If considering CBMPs, monitor for fatigue and other AEs, and note that higher CBD doses (>25 mg/day) and prior cannabis use correlated with greater reported benefit in this cohort."}}],"initialOffset":8,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"generic","value":"delta-9-tetrahydrocannabinol"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Generics","href":"/hub/tag/generic"},{"name":"delta-9-tetrahydrocannabinol"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"generic","hub_tag_value":"delta-9-tetrahydrocannabinol"}}}]]

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