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Traditional marijuana, high-potency cannabis and synthetic cannabinoids: increasing risk for psychosis
Robin M. Murray, Harriet Quigley, Diego Quattrone, Amir Englund, Marta Di Forti
Institute of Psychiatry, Psychology and Neuroscience, King’s College, De Crespigny Park, London, SE5 8AF, UK
Epidemiological evidence demonstrates that cannabis use is associated with an increased risk of psychotic outcomes, and confirms a dose- response relationship between the level of use and the risk of later psychosis. High-potency cannabis and synthetic cannabinoids carry the greatest risk. Experimental administration of tetrahydrocannabinol, the active ingredient of cannabis, induces transient psychosis in normal subjects, but this effect can be ameliorated by co-administration of cannabidiol. This latter is a constituent of traditional hashish, but is largely absent from modern high-potency forms of cannabis. Argument continues over the extent to which genetic predisposition is correlated to, or interacts with, cannabis use, and what proportion of psychosis could be prevented by minimizing heavy use. As yet, there is not convincing evidence that cannabis use increases risk of other psychiatric disorders, but there are no such doubts concerning its detrimental effect on cogni- tive function. All of the negative aspects are magnified if use starts in early adolescence. Irrespective of whether use of cannabis is decriminal- ized or legalized, the evidence that it is a component cause of psychosis is now sufficient for public health messages outlining the risk, especially of regular use of high-potency cannabis and synthetic cannabinoids.
Key words: Cannabis, psychosis, marijuana, synthetic cannabinoids, cognitive function, brain structure, genetic predisposition, early adolescence
(World Psychiatry 2016;15:195–204)
The use of cannabis has been illegal in most countries since the 1930s, but this has not deterred use1. Currently, cannabis is used by around 180 million people globally2. The tensions produced by this unsatisfactory situation have resulted in much attention being paid to the legal status of cannabis.
Possession of the drug in small quantities has been decrimi- nalized officially in countries such as Portugal and the Nether- lands, and unofficially in many more. In 2013, Uruguay be- came the first nation to legalize the sale, cultivation and distribution of cannabis3. Four US states have also legalized recreational use, and another twenty-five US states as well as Canada permit so-called “medicinal marijuana”. While Uru- guay has strict rules concerning access, laws vary state by state in the US, with policy being increasingly driven by entrepre- neurs in search of profit, and law makers in search of taxes.
Given the above, it seems likely that consumption of canna- bis will increase rather than decrease. This makes it imperative to understand the possible adverse consequences of use, even if they only affect a minority of users. In this paper we start by reviewing cannabinoids and the endocannabinoid system. We then focus on cannabis use and risk of psychiatric disorder, particularly psychosis, before touching on the effects on cog- nition and brain structure.
CANNABINOIDS AND THE ENDOCANNABINOID SYSTEM
Cannabis contains over one hundred cannabinoids4, the most important of which are tetrahydrocannabinol (THC) and cannabidiol (CBD). These are produced in tiny crystal forma- tions around the flowering tops. Recreational cannabis has
been traditionally available as herb (marijuana, grass, weed) or resin (hashish, hash). In some countries such as the US it is smoked by itself, while in much of Europe it is smoked with tobacco. When smoked or inhaled, effects come on after a few minutes and last 2-3 hours; if eaten it can take 2 hours for the effects to be felt and they can last up to 8 hours.
Cannabinoids exert their effects primarily by interacting with the endocannabinoid system, which comprises endoge- nous ligands, their receptors, and the enzymes that synthesize and degrade them5.
There are two specific receptors: cannabinoid receptor type-1 (CB1) and cannabinoid receptor type-2 (CB2). The CB1 receptor is widespread throughout the brain, with high con- centrations in the neocortex, basal ganglia and hippocampus6. CB1 receptors are located pre-synaptically on the terminals of GABAergic and glutamatergic neurons, where they act homeo- statically to counteract the over- or under-activity of these sys- tems by modulating pre-synaptic neurotransmitter release7. The CB2 receptor, initially thought to be confined to immune cells and peripheral tissues8, has recently also been found in the cerebellum and brain stem.
The best known endogenous cannabinoid receptor ligands are N-arachidonoylethanolamide (anandamide, AEA) and 2- arachidonoylglycerol (2-AG). These are biosynthesized post- synaptically in an activity-dependent manner before being cleared by a reuptake mechanism and enzymatic hydrolysis.
THC is responsible for the euphoria and feelings of increased sociability and insightfulness, “the high” that users enjoy. It is a partial agonist at the CB1 receptor9. As the endo- cannabinoid system normally operates “on-demand” in an activity-dependent manner10, exogenous THC appears to overwhelm the endogenous system11-15, with resulting lower levels, for example, of AEA16.
World Psychiatry 15:3 - October 2016
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