Interactions ofΔ 11-tetrahydrocannabinol with cannabinol and cannabidiol following oral administration in man. Assay of cannabinol and cannabidiol by mass fragmentographywith cannabinol and cannabidiol following oral administration in man. Assay of cannabinol and cannabidiol by mass fragmentography

Agurell, Stig; Carlsson, Stefan; Lindgren, Jan‐Erik; Ohlsson, A; Gillespie, H. K.; Hollister, Leo E.

doi:10.1007/bf02085029

Cited by 119 publications

(62 citation statements)

References 8 publications

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“…For instance, peak plasma concentrations following administration of CBD (600 mg) administration ranged from 17.0 ng/ml (Winton-Brown et al, 2011 ;Bhattacharyya et al, 2010, Borgwardt et al, 2008Fusar-Poli et al, 2009) to about 55 ng/ml (Englund et al, 2013). Although cannabis effects peaked 120 min after CBD administration in the current study, and 60 min earlier than peak CBD concentrations, there was no indication that CBD attenuated cannabis effects at any point during the 2-h cannabis time course (Figures 1 and 2); note, we did not assess whether CBD altered the metabolism of THC, as there is little to suggest that this occurs in humans (Hunt et al, 1981;Englund et al, 2013;Agurell et al, 1981;Karschner et al, 2011a, b). Future studies focusing on CBD and THC interactions might consider these considerable individual differences in plasma drug levels following the oral route of administration.…”

Section: Discussionmentioning

confidence: 60%

“…The broad and upper range of CBD doses were chosen to ensure pharmacological activity given its known poor oral bioavailability of o20% (Mechoulam et al, 2002). Timing of cannabis administration was designed to coincide with time-to-peak (T max ) plasma CBD concentrations estimated at 1-2 h (Agurell et al, 1981;Bhattacharyya et al, 2010;Winton-Brown et al, 2011;Englund et al, 2013).…”

Section: Study Drugsmentioning

confidence: 99%

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Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis

Haney

Malcolm

Babalonis

et al. 2015

Neuropsychopharmacol

172

180

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Cannabidiol (CBD), a constituent of cannabis with few psychoactive effects, has been reported in some studies to attenuate certain aspects of Δ 9 -tetrahydrocannabinol (THC) intoxication. However, most studies have tested only one dose of CBD in combination with one dose of oral THC, making it difficult to assess the nature of this interaction. Further, the effect of oral CBD on smoked cannabis administration is unknown. The objective of this multi-site, randomized, double-blind, within-subject laboratory study was to assess the influence of CBD (0, 200, 400, 800 mg, p.o.) pretreatment on the reinforcing, subjective, cognitive, and physiological effects of smoked cannabis (0.01 (inactive), 5.30-5.80% THC). Non-treatment-seeking, healthy cannabis smokers (n = 31; 17M, 14 F) completed eight outpatient sessions. CBD was administered 90 min prior to cannabis administration. The behavioral and cardiovascular effects of cannabis were measured at baseline and repeatedly throughout the session. A subset of participants (n = 8) completed an additional session to measure plasma CBD concentrations after administration of the highest CBD dose (800 mg). Under placebo CBD conditions, active cannabis (1) was self-administered by significantly more participants than placebo cannabis and (2) produced significant, time-dependent increases in ratings of 'High', 'Good Effect', ratings of the cannabis cigarette (eg, strength, liking), and heart rate relative to inactive cannabis. CBD, which alone produced no significant psychoactive or cardiovascular effects, did not significantly alter any of these outcomes. Cannabis self-administration, subjective effects, and cannabis ratings did not vary as a function of CBD dose relative to placebo capsules. These findings suggest that oral CBD does not reduce the reinforcing, physiological, or positive subjective effects of smoked cannabis.

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Section: Discussionmentioning

confidence: 60%

Section: Study Drugsmentioning

confidence: 99%

Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis

Haney

Malcolm

Babalonis

et al. 2015

Neuropsychopharmacol

172

180

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show abstract

“…Its therapeutic use, however, has some limiting factors. In addition to its low and variable oral bioavailability in humans [135], it causes bell-shaped dose-response curves and, judging from the studies with laboratory animals, possesses a narrow therapeutic dose range. A clear target of future research, therefore, is to try to develop compounds with similar safety and clinical profile but with larger effective dose ranges.…”

Section: Discussionmentioning

confidence: 99%

Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders

Campos

Moreira

Gomes

et al. 2012

Phil. Trans. R. Soc. B

343

228

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Cannabidiol (CBD) is a major phytocannabinoid present in the Cannabis sativa plant. It lacks the psychotomimetic and other psychotropic effects that the main plant compound D 9 -tetrahydrocannabinol (THC) being able, on the contrary, to antagonize these effects. This property, together with its safety profile, was an initial stimulus for the investigation of CBD pharmacological properties. It is now clear that CBD has therapeutic potential over a wide range of non-psychiatric and psychiatric disorders such as anxiety, depression and psychosis. Although the pharmacological effects of CBD in different biological systems have been extensively investigated by in vitro studies, the mechanisms responsible for its therapeutic potential are still not clear. Here, we review recent in vivo studies indicating that these mechanisms are not unitary but rather depend on the behavioural response being measured. Acute anxiolytic and antidepressant-like effects seem to rely mainly on facilitation of 5-HT1A-mediated neurotransmission in key brain areas related to defensive responses, including the dorsal periaqueductal grey, bed nucleus of the stria terminalis and medial prefrontal cortex. Other effects, such as anti-compulsive, increased extinction and impaired reconsolidation of aversive memories, and facilitation of adult hippocampal neurogenesis could depend on potentiation of anandamidemediated neurotransmission. Finally, activation of TRPV1 channels may help us to explain the antipsychotic effect and the bell-shaped dose-response curves commonly observed with CBD. Considering its safety profile and wide range of therapeutic potential, however, further studies are needed to investigate the involvement of other possible mechanisms (e.g. inhibition of adenosine uptake, inverse agonism at CB2 receptor, CB1 receptor antagonism, GPR55 antagonism, PPARg receptors agonism, intracellular (Ca 2þ ) increase, etc.), on CBD behavioural effects.

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“…On the other hand, CBD is not able to change delta9-THC blood level with co-administration of both compounds in rats 32 or humans volunteers. 33 Therefore, it has been suggested that CBD can antagonize delta9-THC effects pharmacodynamically. 34 Early evidence (1970's) on CBD pharmacological activity 1.…”

Section: Inactive Cannabinoid That Interact With Delta9-thc (1970's)mentioning

confidence: 99%

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Zuardi

2008

Rev. Bras. Psiquiatr.

340

297

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Interactions ofΔ 11-tetrahydrocannabinol with cannabinol and cannabidiol following oral administration in man. Assay of cannabinol and cannabidiol by mass fragmentographywith cannabinol and cannabidiol following oral administration in man. Assay of cannabinol and cannabidiol by mass fragmentography

Cited by 119 publications

References 8 publications

Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis

Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis

Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

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