The effect of cannabidiol, alone and in combination with ethanol, on human performance

Belgrave, B. E.; Bird, Kevin D.; Chesher, G. B.; Jackson, David M.; Lübbe, Kristina; Starmer, G. A.; Teo, R. K. C.

doi:10.1007/bf00496070

Cited by 49 publications

(40 citation statements)

References 15 publications

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“…Our results are consistent with previous experimental and epidemiological studies that have reported additive effects of alcohol and marijuana on driving performance and crash risk (Dubois et al 2015; Bates & Blakely 1999; Sewell et al 2009; Doty et al 1992; Belgrave et al 1979; Drummer et al 2004; Chesher 1986) and possibly synergistic (Brault et al 2004; Biecheler et al 2008; Sutton 1983; Perez-Reyes et al 1988) effects. For instance, a recent case–control study found that, relative to drivers using neither alcohol nor marijuana, drivers who tested positive for both alcohol (BAC ≤ 0.08 g/dL) and marijuana had up to 128% increased odds of committing an unsafe driver action compared to 16% for those using marijuana alone and 117% for those using alcohol (BAC ≤ 0.08 g/dL) alone (Dubois et al 2015).…”

Section: Discussionsupporting

confidence: 92%

Interaction of marijuana and alcohol on fatal motor vehicle crash risk: a case–control study

Chihuri

Chen

2017

Inj. Epidemiol.

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BackgroundConcurrent use of marijuana and alcohol in drivers is of increasing concern but its role in crash causation has not been well understood.Methods Using a case–control design, we assessed the individual and joint effects of marijuana and alcohol use on fatal crash risk. Cases (n = 1944) were drivers fatally injured in motor vehicle crashes in the United States at specific times in 2006, 2007 and 2008. Controls (n = 7719) were drivers who participated in the 2007 National Roadside Survey of Alcohol and Drug Use by Drivers.ResultsOverall, cases were significantly more likely than controls to test positive for marijuana (12.2% vs. 5.9%, p < 0.0001), alcohol (57.8% vs. 7.7%, p < 0.0001) and both marijuana and alcohol (8.9% vs. 0.8%, p < 0.0001). Compared to drivers testing negative for alcohol and marijuana, the adjusted odds ratios of fatal crash involvement were 16.33 [95% confidence interval (CI): 14.23, 18.75] for those testing positive for alcohol and negative for marijuana, 1.54 (95% CI: 1.16, 2.03) for those testing positive for marijuana and negative for alcohol, and 25.09 (95% CI: 17.97, 35.03) for those testing positive for both alcohol and marijuana.ConclusionsAlcohol use and marijuana use are each associated with significantly increased risks of fatal crash involvement. When alcohol and marijuana are used together, there exists a positive synergistic effect on fatal crash risk on the additive scale.

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Section: Discussionsupporting

confidence: 92%

Interaction of marijuana and alcohol on fatal motor vehicle crash risk: a case–control study

Chihuri

Chen

2017

Inj. Epidemiol.

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“…Unfortunately, relatively little is known about the neurocognitive consequences of simultaneous use, and previous findings in adults have been conflicting. Some have found no additive acute motor or cognitive effects of combined cannabidiol (CBD) or THC and alcohol use (Belgrave et al, 1979b;Liguori et al, 2002), while others have found cumulative acute effects of THC or CBD and alcohol in perceptual and motor function (Belgrave et al, 1979a;Chait & Perry, 1993;Consroe et al, 1979). Additionally, simultaneous use of CBD and ethanol actually decreased blood alcohol levels (Consroe et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

Effects of alcohol and combined marijuana and alcohol use during adolescence on hippocampal volume and asymmetry

Medina

Schweinsburg

Cohen-Zion

et al. 2007

Neurotoxicology and Teratology

238

191

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Background-Converging lines of evidence suggest that the hippocampus may be particularly vulnerable to deleterious effects of alcohol and marijuana use, especially during adolescence. The goal of this study was to examine hippocampal volume and asymmetry in adolescent users of alcohol and marijuana.Methods-Participants were adolescent (aged 15-18) alcohol (ALC) users (n=16), marijuana and alcohol (MJ+ALC) users (n=26), and demographically similar controls (n=21). Extensive exclusionary criteria included prenatal toxic exposure, left handedness, and psychiatric and neurologic disorders. Substance use, cognitive, and anatomical measures were collected after at least 2 days of abstinence from all substances.Results-Adolescent ALC users demonstrated a significantly different pattern of hippocampal asymmetry (p<.05) and reduced left hippocampal volume (p<.05) compared to MJ+ALC users and non-using controls. Increased alcohol abuse/dependence severity was associated with increased right > left (R>L) asymmetry and smaller left hippocampal volumes while marijuana abuse/dependence was associated with increased L>R asymmetry and larger left hippocampal volumes. Although MJ +ALC users did not differ from controls in asymmetry, functional relationships with verbal learning were found only among controls, among whom greater right than left hippocampal volume was associated with superior performance (p<.05).Conclusions-Aberrations in hippocampal asymmetry and left hippocampal volumes were found for adolescent heavy drinkers. Further, the functional relationship between hippocampal asymmetry and verbal learning was abnormal among adolescent substance users compared to healthy controls. These findings suggest differential effects of alcohol and combined marijuana and alcohol use on hippocampal morphometry and the relationship between hippocampal asymmetry and verbal learning performance among adolescents.

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“…Although the CB 2 cannabinoid receptor partially mediates the antiinflammatory effects of THC (3), CBD does not bind well to the known cannabinoid receptors (4); this low affinity results in the inability of CBD to produce the subjective ''high'' and cognitive effects that are characteristic of marijuana and THC (5,6). To date, the mechanism by which CBD decreases inflammation is unknown, although micromolar concentrations of CBD have been shown to inhibit lipoxygenase activity (7).…”

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confidence: 99%

Inhibition of an equilibrative nucleoside transporter by cannabidiol: A mechanism of cannabinoid immunosuppression

Carrier

Auchampach

Hillard

2006

Proc. Natl. Acad. Sci. U.S.A.

416

317

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The plant-derived cannabinoids ⌬ 9 -tetrahydrocannabinol (THC) and cannabidiol (CBD) both have immunosuppressive effects; although some effects of THC are mediated by the CB2 receptor, CB2 binds CBD weakly. In examining the effects of THC and CBD on microglial proliferation, we found that these compounds potently inhibit [ 3 H]thymidine incorporation into a murine microglial cell line with no effect on cell cycle. Because adenosine agonists have antiinflammatory effects, and because uptake of adenosine is a primary mechanism of terminating adenosine signaling, we tested the hypothesis that CBD is immunosuppressive because it enhances endogenous adenosine signaling. In vivo treatment with a low dose of CBD decreases TNF␣ production in lipopolysaccharide-treated mice; this effect is reversed with an A2A adenosine receptor antagonist and abolished in A2A receptor knockout mice. These studies demonstrate that CBD has the ability to enhance adenosine signaling through inhibition of uptake and provide a non-cannabinoid receptor mechanism by which CBD can decrease inflammation.adenosine ͉ lipopolysaccharide ͉ tetrahydrocannabinol ͉ thymidine ͉ tumor necrosis factor-␣ T he marijuana-derived cannabinoids ⌬ 9 -tetrahydrocannabinol (THC) and cannabidiol (CBD) each have immunosuppressive effects (1) and are currently in clinical trials for treatment of multiple sclerosis (2). Although the CB 2 cannabinoid receptor partially mediates the antiinflammatory effects of THC (3), CBD does not bind well to the known cannabinoid receptors (4); this low affinity results in the inability of CBD to produce the subjective ''high'' and cognitive effects that are characteristic of marijuana and THC (5, 6). To date, the mechanism by which CBD decreases inflammation is unknown, although micromolar concentrations of CBD have been shown to inhibit lipoxygenase activity (7).In addition to multiple sclerosis, CBD has shown promise in several rodent models of inflammation. Oral treatment with CBD decreases edema and hyperalgesia in a rat paw model of carrageenan-induced inflammation (8). A single dose of CBD also decreases serum TNF␣ production in lipopolysaccharide (LPS)-treated mice (9). CBD improves arthritis symptoms and joint pathology in murine collagen-induced arthritis while inhibiting IFN-␥ production and lymph node cell proliferation, as measured by [ 3 H]thymidine incorporation (9). Treatment with THC also decreases proliferation of lymph node cells as well as splenocytes (10).Given the potential of THC and CBD to decrease proliferation in immune cells, we initially examined the effects of several natural and synthetic cannabinoids on microglial cell proliferation by using [ 3 H]thymidine incorporation. Microglia are the resident immune cells of the brain, and their proliferation has been linked to a number of neurodegenerative diseases (11). However, CBD and THC decreased [ 3 H]thymidine incorporation into EOC-20 microglial cells with no effect on cell cycle. Further experiments demonstrate that this decrease in [ 3 H]thymidine incor...

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The effect of cannabidiol, alone and in combination with ethanol, on human performance

Cited by 49 publications

References 15 publications

Interaction of marijuana and alcohol on fatal motor vehicle crash risk: a case–control study

Interaction of marijuana and alcohol on fatal motor vehicle crash risk: a case–control study

Effects of alcohol and combined marijuana and alcohol use during adolescence on hippocampal volume and asymmetry

Inhibition of an equilibrative nucleoside transporter by cannabidiol: A mechanism of cannabinoid immunosuppression

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