Cannabis for tic control: a systematic review and meta-analysis of its efficacy in Tourette syndrome management

Cannabis-based medicines are showing increasingly strong evidence for reducing tics in Tourette syndrome. In this systematic review and meta-analysis involving 306 adults, cannabinoid-based treatments significantly reduced tic severity on the Yale Global Tic Severity Scale and also significantly reduced premonitory urges—the uncomfortable sensations that often precede tics. The analysis found a mean YGTSS reduction of 13.29 points and a mean PUTS reduction of 4.09 points, providing quantitative evidence that cannabinoids can meaningfully improve two core features of Tourette syndrome.

“Background: Tourette syndrome (TS) involves motor and vocal tics, often with obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD). Cannabis-based medicines (CBMs) are a potential therapy due to their interaction with the endocannabinoid system, potentially reducing tics and associated symptoms. Compared to antipsychotics, CBMs may offer improved tolerability and fewer side effects. Although evidence is limited, emerging studies suggest their potential to improve quality of life in TS. This review was registered with PROSPERO (CRD420251088633).

Aim: To evaluate the effectiveness of CBMs in treating TS.

Methods: We systematically searched PubMed, Google Scholar, ScienceDirect, and the Cochrane Collaboration Database for cohort studies and randomized controlled trials (RCTs) up to July 2, 2025. Data extraction included study characteristics and efficacy outcomes measured by the Yale Global Tic Severity Scale (YGTSS) and Premonitory Urge for Tics Scale (PUTS). Meta-analysis using Review Manager 5.4 compared pre- and post-treatment scores using mean difference (MD) and 95% confidence intervals (CI).

Results: From 1,105 screened articles, eight studies met inclusion criteria for the review, and seven were included in the meta-analysis, involving 306 adult TS patients. CBMs significantly reduced YGTSS scores (MD = – 13.29, 95% CI [-21.67 to – 4.91], P = 0.002) and PUTS scores (MD = – 4.09, 95% CI [-7.24 to – 0.93], P = 0.01).

Conclusion: CBMs show promising potential in reducing tics and premonitory urges in TS. Larger, placebo-controlled trials are needed to confirm efficacy, ensure safety, and optimize dosing.”

https://pubmed.ncbi.nlm.nih.gov/42229830

“Cannabis-based medicines significantly reduced tic severity in Tourette syndrome.”

https://www.ibroneuroscience.org/article/S0306-4522(26)00367-2/abstract

Cannabinoids in Alzheimer’s disease: animal-human evidence and clinical pharmacology challenges

Cannabinoids are being studied in Alzheimer’s disease for effects that extend beyond symptom control to inflammation, oxidative stress, amyloid and tau pathology, and neuroprotection. This review brings together animal and human evidence showing that cannabinoid-based treatments can influence several biological processes involved in Alzheimer’s disease while also showing clinical potential for symptoms such as agitation, sleep disturbance, and behavioral changes. The authors highlight THC, CBD, and other cannabinoid strategies as promising therapeutic approaches, with the growing body of evidence supporting continued development of cannabinoid-based treatments for both neurological and behavioral aspects of Alzheimer’s disease.

“Cannabinoids have emerged as potential modulators of pathological processes in Alzheimer’s disease (AD), including neuroinflammation, synaptic dysfunction, and protein aggregation. Cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), the main phytocannabinoids from Cannabis sativa, interact with the endocannabinoid system and may influence neuronal and glial signaling pathways relevant to AD pathology.

This mini review summarizes evidence from transgenic animal models and clinical studies evaluating CBD, THC, and their combination in AD.

Preclinical studies show that CBD and THC reduce β-amyloid accumulation, attenuate tau phosphorylation, and regulate neuroinflammatory responses, often associated with improvements in learning and memory. Cognitive outcomes appear to depend on cannabinoid composition, with CBD or THC administered individually showing more consistent effects, while combined CBD + THC effects appear dose- and ratio-dependent.

Clinical evidence in AD patients remains limited and primarily reports improvements in neuropsychiatric symptoms, such as reductions in agitation, nighttime activity, and behavioral disturbances, whereas cognitive improvements are modest. Cannabinoid-based treatments are generally well tolerated, with mild sedation, somnolence, or disorientation as the most reported adverse effects.

Overall, current data support the biological plausibility of cannabinoids as modulators of neuroinflammatory and synaptic processes in AD. However, heterogeneity in formulations, dosing, and study design limits firm conclusions. Future research should focus on dose optimization, biomarker-guided clinical trials, and long-term safety assessments to better define their therapeutic potential in AD.”

https://pubmed.ncbi.nlm.nih.gov/42211879

“The ideal treatment for AD should be able to modulate the disease through multiple mechanisms rather than targeting a single dysregulated pathway.”

 “cannabinoids should be viewed as pleiotropic modulators of AD-relevant processes rather than as agents acting through a single unified mechanism.”

“cannabinoid-derived compounds with combined receptor-mediated and intrinsic antioxidant properties may represent promising therapeutic candidates.”

https://www.frontiersin.org/journals/behavioral-neuroscience/articles/10.3389/fnbeh.2026.1833021/full

Antitumor Activity of Cannabinoids and Their Interaction with Chemotherapy: A Systematic Review and Meta-Analysis of Preclinical Evidence

Cannabinoids are increasingly being studied for direct antitumor effects and for their ability to influence the response to conventional chemotherapy. This systematic review and meta-analysis of preclinical research found that cannabinoids significantly reduced tumor growth and cancer-cell viability across multiple models. The analysis also identified evidence that cannabinoids can enhance the effectiveness of several chemotherapy agents, supporting the possibility of useful combination strategies. The findings strengthen the case for cannabinoids as biologically active anticancer compounds with potential both as direct therapies and as adjuncts to standard treatment.

“Background: Cannabinoids are studied as anticancer agents, but their effects vary across tumors, compounds, and experimental settings, underscoring the need to define consistent patterns. Our objective was to map cannabinoid efficacy across cancer preclinical models and identify tumor settings with the greatest translational promise. 

Methods: The protocol was registered on PROSPERO (CRD42025543744); PubMed, Embase, and CENTRAL were searched on 4 April 2024 for in vitro and in vivo studies assessing cannabinoid antitumor effects alone or with chemotherapy versus vehicle or chemotherapy only. Random-effects models yielded pooled mean differences (MD) with 95% confidence intervals (CI). MDs of viable cells were calculated for in vitro assays and tumor volume (mm3) for in vivo studies. Reports of various compounds, cannabidiol (CBD), tetrahydrocannabinol (THC) or synthetic cannabinoids, were pooled. 

Results: We included 189 studies in the final analysis. In vitro, cannabinoids reduced cell viability modestly overall, with significant effects in glioblastoma (MD -18.77 [CI: -27.15; -10.39]) and a nonsignificant trend in breast cancer (MD -6.75 [CI: -13.90; 0.40]). For in vivo, monotherapy showed the most consistent efficacy in glioblastoma, significantly reducing tumor volume by MD -980.58 mm3; [CI: -1270.2; -690.88]. Addition to temozolomide produced a favorable but nonsignificant decrease of MD -220.65 mm3; [CI: -579.34; 138.03, vs. temozolomide]. In breast cancer, cannabinoids achieved smaller yet significant tumor reductions (MD -402.64 mm3); [CI: -671.84; -133.45]. Synthetic agents had the largest effect (MD -1295.19 mm3); [CI: -1664.33; -928.05] -CBD plus doxorubicin vs. doxorubicin). Lung cancer (MD -562.17 mm3); [CI: -693.99; -430.35] and prostate cancer (MD -1136.59 mm3); [95% CI: -1320.97; -952.21] also had a significant response, whereas colon, pancreatic, and hepatocellular carcinoma models showed inconsistent or null responses. 

Conclusions: Cannabinoids show promise as adjuncts in oncotherapy, particularly in glioblastoma and breast cancer, to enhance chemotherapy efficacy. These findings should be interpreted with caution given the high inter-study heterogeneity typical of preclinical research and should be considered hypothesis-generating, warranting further validation in standardized and clinically relevant models.”

https://pubmed.ncbi.nlm.nih.gov/42198443

“Cannabinoids have attracted growing attention in oncology as both supportive agents and potential direct antitumor therapies.”

“Beyond symptom management, preclinical studies over the past two decades have demonstrated that exogenous cannabinoids can influence key hallmarks of cancer, including proliferation, apoptosis, angiogenesis, and metastasis.”

“Notably, multiple studies indicate that cannabinoids can act synergistically with chemotherapy or radiotherapy, amplifying antitumor effects while potentially attenuating treatment-related toxicity. These interactions are clinically appealing, as they suggest a capacity to sensitize tumor cells to conventional agents and possibly enable dose reductions that limit systemic adverse effects.”

“Cannabinoids show emerging potential as adjuncts in oncological treatment, with relatively consistent signals observed particularly in glioblastoma and breast cancer models.”

https://www.mdpi.com/1424-8247/19/5/768

Computational Characterization of Nabilone-Induced Disruption of the CB2-HER2 Receptor Complex in HER2+ Breast Cancer

HER2-positive breast cancer is driven in part by abnormal signaling through the HER2 receptor, making disruption of that pathway an important therapeutic target. In this computational study, researchers found that nabilone, a synthetic cannabinoid, may disrupt the CB2-HER2 receptor complex and alter interactions involved in HER2-driven cancer signaling. The findings suggest a potential molecular mechanism through which cannabinoid-based compounds could interfere with breast cancer progression. This work adds another layer to the growing evidence linking cannabinoid receptor signaling with direct effects on HER2-positive breast cancer biology.

“Human epidermal growth factor receptor 2-positive (HER2+) breast cancer, accounting for 15% to 20% of cases, is often resistant to treatment.

Delta-9-tetrahydrocannabinol (THC) disrupts HER2-cannabinoid receptor (2CB2) receptor complexes and inhibits HER2 activation.

This study evaluates whether Nabilone, a synthetic cannabinoid, can similarly disrupt HER2-CB2 interactions.

A CB2-HER2 complex model was generated via protein-protein docking. Three 1-µs molecular dynamics simulations (CB2-HER2, CB2-HER2-THC, CB2-HER2-Nabilone) were performed using the Schrodinger Desmond with membrane embedding and solvent. Structural stability (root mean square deviation [RMSD] and root mean square fluctuation [RMSF]), binding free energy (molecular mechanics/generalized born surface area [MM/GBSA]), and intracellular/extracellular distances between receptors were analyzed. Intermolecular interactions were assessed using the MAPIYA server.

Nabilone induced comparable structural instability to THC, with increased RMSD and RMSF. The MM/GBSA analysis showed Nabilone increased the binding free energy between CB2 and HER2, indicating stronger disruption. Intracellular and extracellular distances between CB2 and HER2 increased, especially intracellularly, with Nabilone. Intermolecular interaction analysis revealed that Nabilone decreased the number of contacts, particularly hydrophobic interactions, between CB2 and HER2.

Our in silico model predicts that Nabilone may disrupt the HER2-CB2 complex, suggesting a hypothesis that it could serve as a potential therapeutic agent. These computational findings warrant urgent experimental validation.”

https://pubmed.ncbi.nlm.nih.gov/42164472

“Cannabinoids have produced antitumor responses in preclinical models of cancer, including HER2+ BC, via binding and activating cannabinoid receptors, CB1 and CB2, both G-protein coupled receptors (GPCRs).”

“Nabilone, a synthetic analog of THC, was Food and Drug Administration (FDA)-approved in 1985 as a relief treatment for chemotherapy-related side effects, such as vomiting and nausea.”

“Our results indicate that Nabilone effectively disrupts the oncogenic CB2-HER2 complex, weakening the heterodimer interface through a mechanism of structural instability similar to THC but with superior binding affinity to CB2. While these findings rely on in silico predictions, limited by simulation timescales and simplified membrane models, they highlight a distinct opportunity for repurposing Nabilone from symptom management to active cancer therapy. We conclude that these data provide a robust theoretical framework that justifies urgent experimental validation in living systems to confirm the therapeutic potential of disrupting CB2-HER2 signaling.”

https://journals.sagepub.com/doi/10.1177/11779322261449332

The association between prenatal exposure to cannabis with and without tobacco and early cognitive and language development in a sample of polysubstance-exposed children

Concerns about prenatal cannabis exposure often focus on possible effects on early brain and language development, but this large Danish cohort found no evidence of impaired cognitive or language development during the first three years of life. Children exposed prenatally to cannabis actually scored significantly higher on the Bayley-III Language scale than controls, while cognitive scores did not differ between children exposed to cannabis, tobacco, both substances, or neither. The findings suggest that prenatal cannabis exposure, alone or combined with tobacco, was not associated with disrupted early cognitive or language development in this high-risk, polysubstance-exposed population.

“Background: Prenatal cannabis exposure may have adverse effects on development which could be amplified by co-exposure with tobacco.

Objective: This study examined whether prenatal cannabis exposure was associated with disrupted language or cognitive development, and whether co-exposure to tobacco was associated with worse outcomes than to cannabis alone.

Methods: In this historical cohort study, we compared children from the Danish Family Outpatient Clinics who had prenatal exposure to cannabis (n = 106), tobacco (n = 138), cannabis and tobacco (n = 112), or no exposure to either drug (control group, n = 454) on the Bayley-III Language and Cognitive scales at 1-58 months of age (99.7% at ≤36 months). Roughly half were tested at multiple ages, yielding 1362 language assessments (49.2% tested ≥ twice) and 1549 cognitive assessments (53.6% tested ≥ twice). Most children had additional prenatal exposure to other drugs (49.8%), including the control group (63.9%). Scores were investigated in linear mixed models with factors Exposure Group, Age, and Exposure Group ∗ Age, and covariates alcohol exposure, other drug exposure, maternal medical diagnoses, and maternal education.

Results: Children with prenatal cannabis exposure scored significantly higher on the Language scale compared with controls (3.26 points; 95% CI = 0.26-6.26). There was a positive association between Language scores and age at assessment for children with cannabis and tobacco exposure (0.31 points/month; 95% CI = 0.11-0.51) but not the other groups. There were no significant effects of Exposure Group or Exposure Group × Age for the Bayley-III Cognitive scale.

Conclusion: Prenatal exposure to cannabis, alone or with tobacco, was not associated with disrupted cognitive or language development during the first three years of life in this sample of high-risk children.”

https://pubmed.ncbi.nlm.nih.gov/41990599

“Cannabis exposure was not associated with impaired cognitive or language development.”

“Using a sample of children with prenatal drug and alcohol exposure from the Danish FOCs, this study found that children with prenatal exposure to cannabis had higher scores on the Bayley-III Language scale compared with control children, and children with prenatal exposure to cannabis and tobacco had a greater increase in Bayley-III Language scores with age compared with all other groups. There were no differences on the Bayley-III Cognitive scale between children with prenatal exposure to cannabis, tobacco, both, or neither.

These results suggest that prenatal exposure to cannabis, alone or in combination with tobacco, is not associated with disrupted cognitive or language development during the first three years of life among polysubstance-exposed children. This could help to reduce the stigma experienced by women who use cannabis during pregnancy and potentially lower the barrier for seeking help in this group.”

https://www.sciencedirect.com/science/article/pii/S0378378226000745?via%3Dihub

Disrupted endocannabinoid signaling contributes to systemic inflammation in acute pancreatitis

Acute pancreatitis can trigger a powerful systemic inflammatory response that contributes to complications far beyond the pancreas itself. In this study, researchers found that disrupted endocannabinoid signaling was directly associated with heightened inflammation during acute pancreatitis, linking cannabinoid-related pathways to the progression of systemic immune dysfunction. The findings suggest that restoring or modulating endocannabinoid signaling may offer a new therapeutic strategy for limiting inflammation and reducing the broader damage caused by severe pancreatitis.

“Acute pancreatitis (AP) is an inflammatory disease that can lead to systemic complications in severe cases. The endocannabinoid system has emerged as a potential modulator of inflammation in AP.

We investigated the role of the endocannabinoid 2-arachidonoylglycerol (2-AG) and the cannabinoid receptors CB1 and CB2 during AP.

A severity-dependent decrease in circulating 2-AG was found both in patients and a murine AP model. Restoring 2-AG – by avoiding its degradation via monoacylglycerol lipase inhibitor or direct 2-AG administration – reduced local and systemic inflammation, modulated peritoneal macrophage polarization, and mitigated lung injury. Notably, endocannabinoid system effects were consistent across sexes.

Both cannabinoid receptors were involved in disease pathophysiology.

Genetic Cnr1 knockout and pharmacological CB2 blockade showed distinct and complementary roles of both receptors in regulating inflammation, immune infiltration, and pulmonary damage.

These findings highlight a protective role for 2-AG and highlight the endocannabinoid system – and cannabinoid receptors in particular – as a promising therapeutic target to modulate inflammation and reduce systemic complications in acute pancreatitis.”

https://pubmed.ncbi.nlm.nih.gov/42153289

“These findings raise the possibility that counteracting the inflammation-driven decline in endogenous 2-AG through pharmacological intervention may represent a promising therapeutic strategy for AP.”

“Our data clearly support a role for both CB1 and CB2 receptors in the pathophysiology of AP.”

“Overall, our study supports the ECS as promising therapeutic target to reduce inflammation and systemic complications in AP.”

https://pathsocjournals.onlinelibrary.wiley.com/doi/10.1002/path.70076

“The Diminished Availability of 2-AG in Aged Synaptic Terminals is Ameliorated by a Full-Spectrum Cannabis Extract with a High THC Content. This highlights the potential of high THC content extracts as therapeutic agents for restoring the decreased 2-AG levels observed in the aging brain.”

https://pubmed.ncbi.nlm.nih.gov/41880097

Medical Cannabis as an Opiate Alternative: A Prospective Observational Cohort Study

Medical cannabis is increasingly being studied as a way to reduce reliance on opioid medications in people with chronic pain. In this prospective observational cohort study, patients who used medical cannabis reported meaningful reductions in opioid use alongside improvements in pain and overall quality of life. The findings support the role of cannabis as a potential opioid-sparing treatment option, particularly for patients seeking alternatives to long-term opiate therapy.

“Opioid use for chronic pain has contributed to an epidemic of overdoses and deaths in the United States.

Some clinical studies suggest that medical cannabis may help alleviate pain and improve quality of life. However, cost can be a barrier to patients accessing medical cannabis.

This is the first prospective observational study evaluating medical cannabis as an alternative to opioids in a setting where cost was removed as a major barrier.

Methods: Twenty-nine patients were recruited from a university-based outpatient chronic pain clinic. Each patient underwent monthly pain assessments using the Numeric Pain Rating Scale (NRS). Daily opioid use, measured in morphine milligram equivalents (MMEs), was recorded and monitored over five months. Pain-related quality of life was assessed using the SF-36 Health Survey at baseline, and again at two and five months.

Results: Daily opioid use decreased from baseline to one month (from 46.8 MMEs to 16.2 MMEs, a 65% reduction), and this reduction was maintained through five months. The mean NRS score decreased by two points from baseline to one month (from 7.03 to 5.07; p < 0.0001), and this improvement was sustained at five months. The SF-36 Physical Functioning score increased from 15.3 at baseline to 21.4 at one month and was maintained at five months (p < 0.03 for both comparisons).

Conclusion: These results suggest that medical cannabis may be a useful adjunct therapy for reducing opioid use, relieving chronic pain, and improving health-related quality of life.”

https://pubmed.ncbi.nlm.nih.gov/42153072

“Opioids are associated with serious adverse events, including death, particularly at higher dosages or when used in combination with benzodiazepines.

In contrast, medical cannabis has not been associated with mortality from overdose. When used under appropriate medical supervision, medical cannabis may represent an effective adjunctive strategy for reducing opioid use among patients receiving long-term opioid therapy.

“Although cannabis has historically been characterized as a potential “gateway drug,” it may also serve as a harm-reduction tool for some patients seeking to reduce reliance on higher-risk opioid medications.”

https://www.cureus.com/articles/432327-medical-cannabis-as-an-opiate-alternative-a-prospective-observational-cohort-study#!

Feasibility, Safety and Preliminary Efficacy of 1:1 THC:CBD Cannabis Oil for Fibromyalgia Symptoms: Results From a Randomised, Double-Blind, Placebo-Controlled Pilot Trial

Fibromyalgia can cause persistent pain, fatigue, poor sleep, and reduced quality of life, often despite standard treatment. In this randomized, double-blind, placebo-controlled pilot trial, a 1:1 THC cannabis oil produced encouraging improvements in fibromyalgia symptoms, including pain and overall disease impact. The treatment was also feasible and generally well tolerated, supporting further interest in balanced THC formulations as a potential option for people with difficult-to-manage fibromyalgia

“Fibromyalgia is a chronic disorder characterised by widespread pain and other symptoms that substantially impact the quality of life.

This double-blind, randomised, placebo-controlled trial primarily assessed feasibility (procedures and intervention adherence) and safety/tolerability of a 1:1 delta-9-tetrahydrocannabinol:cannabidiol (THC:CBD) cannabis oil (10 mg/mL each) in 24 adults with fibromyalgia, with secondary, preliminary assessment of efficacy across symptom domains.

Participants completed a 4-week dose titration followed by 12 weeks of stable dosing. Of 77 prescreened individuals, 24 were randomised, yielding a screening-to-enrolment ratio of approximately 3:1 (31.2%). Recruitment reached 66.7% of the target (24/36); the shortfall was mainly due to geographic and legal barriers. Retention was 91.7% (22/24) and adherence was high, with all participants taking ≥ 90% of the prescribed doses.

The study medication was well tolerated in this small sample, with adverse events mostly mild and no serious events observed.

Secondary outcomes suggested medium to large between-group effects favouring cannabis for pain reduction, improved sleep quality, and reduced fibromyalgia impact (FIQR), but findings should be interpreted cautiously given the small sample.

Clinically meaningful FIQR improvement (predefined MCID 45.5%) occurred in 40% of the cannabis-treated participants versus 10% with placebo.

For pain, 70% of the cannabis group reported ≥ 30% reduction post-titration and at Week 12 (Placebo 20% and 40%, respectively). Fatigue and anxiety/depression showed no significant changes.

A randomised trial of 1:1 THC:CBD oil appears feasible with excellent retention and adherence, though recruitment barriers need addressing. Preliminary safety and efficacy signals warrant confirmation in larger, adequately powered trials.”

https://pubmed.ncbi.nlm.nih.gov/42142029

“In recent years, medicinal cannabis has emerged as a potential therapeutic option for fibromyalgia, with increasing patient interest in new treatment approaches [5]. Given fibromyalgia’s complexity and diverse manifestations, investigating multifaceted therapies such as medicinal cannabis is well justified.”

“Cannabis sativa L. is a plant with a long history of medicinal use, containing over 100 phytocannabinoids, including delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) [6]. These compounds interact with the endocannabinoid system, which plays a critical role in modulating pain, mood and sleep—key domains affected in fibromyalgia [7–9]. Consequently, cannabis is being investigated as a potential therapeutic agent for fibromyalgia, with several studies suggesting it may help reduce pain, improve sleep and enhance the quality of life, although findings to date remain mixed and optimal dosing strategies, including the THC:CBD ratio and routes of administration, still require further investigation.”

https://onlinelibrary.wiley.com/doi/10.1155/prm/7311235


Cannabis for Harm Reduction: Exploring Mental Health and Other Motivational Factors among Adults at Risk for Alcohol Use Disorder in Florida

Cannabis is increasingly being examined as a harm-reduction tool for people trying to reduce alcohol use and manage related mental-health symptoms. In this study of Florida adults at risk for alcohol use disorder, participants reported using cannabis for reasons including reducing alcohol consumption, managing anxiety and stress, improving sleep, and supporting overall well-being. The findings suggest that cannabis may serve as a self-directed substitute or complementary strategy for some people seeking to reduce alcohol-related harm, while also addressing symptoms that can contribute to continued drinking.

“Background: Prior research has suggested that cannabis may serve as a safer alternative to alcohol, this study examined “marijuana” (THC-dominant cannabis) and cannabidiol (CBD) use as strategies to reduce alcohol consumption among adults who report harmful levels of drinking.

Method: Online surveys were distributed to 451 Florida adults (≥18 years) who consumed ≥5 alcoholic drinks weekly and reported any lifetime cannabis use. Measures included comorbid health conditions, alcohol use severity (Alcohol Use Disorder Identification Test [AUDIT]), depressive symptoms (PHQ-8), anxiety (GAD-7), post-traumatic stress symptoms (primary care post-traumatic stress disorder [PC-PTSD]), childhood trauma (Adverse Childhood Experience Questionnaire [ACE-Q]), and readiness to change (Readiness to Change Questionnaire [RCQ-12]). Chi-square and ANOVA examined differences across alcohol use risk groups; logistic regression identified factors associated with marijuana and CBD use for alcohol reduction.

Results: High (AUDIT scores ≥16) were found in 61.4% of males and 40.9% of females. Higher alcohol use risk was significantly associated with younger age, higher PHQ-8 and GAD-7 scores, greater ACE-Q scores, PTSD positivity, more health conditions, and higher readiness to change (p < 0.001). Marijuana (37.9%) and CBD (32.2%) were the most frequently reported alcohol-reduction strategies; higher alcohol use severity was linked to greater perceived effectiveness. Factors associated with marijuana use for alcohol reduction included higher PTSD scores (OR = 1.76), more comorbid conditions (OR = 1.17), action-stage readiness to change (OR = 1.47), and higher AUDIT scores (OR = 1.83). Factors associated with CBD use for alcohol reduction included higher ACE-Q scores (OR = 1.14), more comorbid conditions (OR = 1.18), action-stage readiness (OR = 1.50), and higher AUDIT scores (OR = 1.95).

Conclusion: These findings identify key clinical and motivational correlates of cannabis use for alcohol harm reduction, informing future intervention development.

Plain language summary

“This study found that individuals with severe alcohol problems, especially those with trauma and mental health conditions, frequently use cannabis to reduce drinking. Many perceive these strategies as effective, particularly when traditional treatments are inadequate or inaccessible. Public health efforts should recognize this growing interest in cannabis-based harm reduction and address the unmet needs of individuals who wish to reduce alcohol consumption, exploring alternative, evidence-based strategies to improve outcomes for high-risk groups and reduce the broader burden of alcohol-related harm.”

https://www.tandfonline.com/doi/full/10.1080/10826084.2026.2670620

Phytocannabinoids as epigenetic regulators: bridging DNA methylation and redox homeostasis in glioblastoma

Glioblastoma is driven not only by genetic mutations, but also by epigenetic changes and oxidative stress that help tumor cells survive and resist treatment. This review examines how phytocannabinoids may influence both DNA methylation and redox balance in glioblastoma, potentially altering gene expression while disrupting cancer-cell defenses against oxidative damage. The evidence suggests that cannabinoids may act as epigenetic regulators as well as metabolic stressors, giving them multiple ways to interfere with glioblastoma progression and treatment resistance. The review highlights cannabinoid-based strategies as a promising direction for targeting the complex biology of this aggressive brain cancer.

“Glioblastoma, a primary brain tumor of the CNS, is the most malignant lesion among gliomas. It has a median survival time of about 12-15 months after diagnosis and limited treatment options.

That neoplastic processes result from changes in the cell’s redox potential and the overproduction of reactive oxygen species. As a consequence, the epigenetic marker, m5C of DNA, is oxidized with ROS to 5-hydroxymethylcytosine, but guanosine is damaged to 8-oxo-dG, a general probe of oxidative stress. If so, the m5C, as well as 8-oxo-dG content in DNA, are subject to dynamic changes induced by environmental and endogenous cellular factors. These markers can be used to evaluate new therapeutic agents, among others.

Currently, there are no effective drugs against human glioblastoma.

Cannabinoids, small, lipophilic molecular compounds, are increasingly being studied for their antitumor properties.

Using the precise nucleotide post-labelling method and thin-layer chromatographic analysis we monitored the effect of CBD, THC, and CFE, as well as their combination with temozolomide, on changes of global m5C and 8-oxo-dG contents.

These results show that cannabinoids alone or in combination with the current standard glioblastoma chemotherapeutic, TMZ, inhibit the progression of GBM and could be used for its clinical treatment. The mechanism of cannabinoids’ actions on glioblastoma cells is also proposed.”

https://pubmed.ncbi.nlm.nih.gov/42118523

“Recently, cannabinoids have gained attention for their anticancer properties. They are found, among others, in Cannabis sativa L.”

“This paper shows that CBD and THC induce hypermethylation and proposes a novel mechanism of action for cannabinoids in glioblastoma.”

https://link.springer.com/article/10.1007/s13353-026-01070-x