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      Marijuana Use Among Young Adults (18–44 Years of Age) and Risk of Stroke : A Behavioral Risk Factor Surveillance System Survey Analysis

      1 , 2 , 3
      Stroke
      Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          Background and Purpose- Amidst legalization of therapeutic and recreational use of marijuana/cannabis in the United States, cerebrovascular effects of marijuana use remain largely unknown, especially among young adults. We aimed to examine the association between marijuana use (18-44 years) among young adults and stroke events. Methods- The study analyzed pooled data from the Behavioral Risk Factor Surveillance System (2016-2017)-a nationally representative cross-sectional survey collected by the Centers for Disease Control and Prevention. Weighted logistic regression models were used to examine an association of recent marijuana use (within the last 30 days) and stroke in young adults (18-44 years) adjusting for patient demographics, risk behavior, and relevant comorbidities. Results- Overall, 13.6% of participants (n=43 860; weighted 35.5 million; 49.9% men) reported using marijuana recently (in the last month), with 63.3% of them being men. Compared with nonusers, marijuana users were often younger (18-34 years; 73.8% versus 61%), non-Hispanic white or black, and with some college education. Marijuana users were often physically active (81.8% versus 77.5%), heavy drinkers (16.8% versus 4.9%), current combustible cigarette users (37.9% versus 15%) and had lower prevalence of hypertension, diabetes mellitus, and hyperlipidemia as compared with nonusers (P<0.01). Young adults with recent marijuana use showed 1.82× higher odds (adjusted odds ratio, 1.82 [95% CI, 1.08-3.10]) of stroke compared with nonusers, which further increased to 2.45× higher (adjusted odds ratio, 2.45 [95% CI, 1.31-4.60]) among frequent marijuana users (>10 days/month). Compared with nonusers, stroke odds were even higher among frequent marijuana users with concomitant combustible cigarette use (adjusted odds ratio, 3.12 [95% CI, 1.40-6.97]) and e-cigarette use (adjusted odds ratio, 2.63 [95% CI, 1.07-6.46]), respectively. Conclusions- There may be a significantly higher odds of stroke in young marijuana users (18-44 years) as compared with nonusers with even greater odds among frequent users (>10 days/month).

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          Recreational marijuana use and acute ischemic stroke: A population-based analysis of hospitalized patients in the United States

          Recreational marijuana use is considered to have few adverse effects. However, recent evidence has suggested that it precipitates cardiovascular and cerebrovascular events. Here, we investigated the relationship between marijuana use and hospitalization for acute ischemic stroke (AIS) using data from the largest inpatient database in the United States.
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            Tetrahydrocannabinol Induces Brain Mitochondrial Respiratory Chain Dysfunction and Increases Oxidative Stress: A Potential Mechanism Involved in Cannabis-Related Stroke

            Cannabis has potential therapeutic use but tetrahydrocannabinol (THC), its main psychoactive component, appears as a risk factor for ischemic stroke in young adults. We therefore evaluate the effects of THC on brain mitochondrial function and oxidative stress, key factors involved in stroke. Maximal oxidative capacities V max (complexes I, III, and IV activities), V succ (complexes II, III, and IV activities), V tmpd (complex IV activity), together with mitochondrial coupling (V max/V 0), were determined in control conditions and after exposure to THC in isolated mitochondria extracted from rat brain, using differential centrifugations. Oxidative stress was also assessed through hydrogen peroxide (H2O2) production, measured with Amplex Red. THC significantly decreased V max (−71%; P < 0.0001), V succ (−65%; P < 0.0001), and V tmpd (−3.5%; P < 0.001). Mitochondrial coupling (V max/V 0) was also significantly decreased after THC exposure (1.8±0.2 versus 6.3±0.7; P < 0.001). Furthermore, THC significantly enhanced H2O2 production by cerebral mitochondria (+171%; P < 0.05) and mitochondrial free radical leak was increased from 0.01±0.01 to 0.10±0.01% (P < 0.001). Thus, THC increases oxidative stress and induces cerebral mitochondrial dysfunction. This mechanism may be involved in young cannabis users who develop ischemic stroke since THC might increase patient's vulnerability to stroke.
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              The procoagulatory effects of delta-9-tetrahydrocannabinol in human platelets.

              Delta-9-tetrahydrocannabinol (THC) is increasingly used for the long-term treatment of nausea, vomiting, cachexia, and chronic pain. Recent reports, however, have indicated an increased risk of myocardial infarction and thromboangiitis obliterans after THC intake. Blood platelets have an essential role in the pathogenesis of these two diseases, but it is unclear whether platelets are potential target cells for cannabinoids. We investigated the effects of THC on human platelets and the expression of cannabinoid receptors on their cell membranes in this in vitro study. The effects of THC (final concentrations 10(-7) to 10(-5) M) on the expression of activated platelet fibrinogen receptor (glycoprotein IIb-IIIa) and P selectin were characterized by flow cytometry. Western blotting was performed with platelet membrane preparations to determine the surface expression of cannabinoid receptors on human platelets. THC increased the expression of glycoprotein IIb-IIIa and P selectin on human platelets in a concentration-dependent manner. The two known cannabinoid receptors (CB(1) and CB(2)) were both detected on the cell membrane of human platelets. Our functional results may suggest a receptor-dependent pathway of THC-induced platelet activation. However, further in vivo studies are warranted to evaluate the role of cannabinoid receptors in mediating the demonstrated procoagulatory effect of THC.
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                Author and article information

                Journal
                Stroke
                Stroke
                Ovid Technologies (Wolters Kluwer Health)
                0039-2499
                1524-4628
                October 31 2019
                November 11 2019
                Affiliations
                [1 ]From the Department of Health Administration and Policy, George Mason University, Fairfax, VA (T.P.)
                [2 ]Franconia Pediatrics Associates, Alexandria, VA (S.P.)
                [3 ]Division of Cardiology, Atlanta VA Medical Center, Decatur, GA (R.D.).
                Article
                10.1161/STROKEAHA.119.027828
                31707926
                e97c24be-1302-4c21-a35f-bdeebb1bd1ef
                © 2019
                History

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