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  • Cited by 3
Cambridge University Press
Online publication date:
November 2011
Print publication year:
Online ISBN:

Book description

The second edition of this critically acclaimed and award-winning text provides a comprehensive overview of the psychiatry and neuroscience of Cannabis sativa (marijuana). It outlines the very latest developments in our understanding of the human cannabinoid system, and links this knowledge to clinical and epidemiological facts about the impact of cannabis on mental health. Clinically focused chapters review not only the direct psychomimetic properties of cannabis, but also the impact consumption has on the courses of evolving or established mental illnesses such as schizophrenia. Effects of cannabis on mood are reviewed, as are its effects on cognition. This new edition has been extensively updated and expanded with ten new chapters to incorporate major new research findings. This book will be of interest to all members of the mental health team, as well as to neuroscientists, epidemiologists, public health specialists and those involved in drug and alcohol research.


‘The editors and publishers of this book have responded to a need for clear, research-based information on a topic of great current concern. They have done an excellent job.'

Source: American Journal of Psychiatry

‘The chapters are compact but filled with quality research and sophisticated, in-depth analysis. The authors do not oversimplify or overemphasize the evidence. We congratulate them on their accomplishment and recommend this book enthusiastically for all clinicians and researchers interested in substance related issues.'

Source: Journal of the American Medical Association

‘… provides an excellent and unparalleled overview of current evidence-based thinking about cannabis and psychotic disorders, and should be read by anyone involved in clinical practice or research with people who suffer serious mental illness and also use cannabis. And let's face it that is probably most of us.'

Source: Australian and New Zealand Journal of Psychiatry

'For colleagues in the mental health field, and in particular for those specializing in addictions, this text can serve as an up-to-date and comprehensive reference. Moreover, before moving ahead on marijuana-related legislation, any governor, lawmaker, or physician with 'medicinal' inclinations - as well as the general public - would be well-advised to become familiar with the contents of this book.'

Source: Journal of Clinical Psychiatry

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  • 8 - Cannabis and cognition: short- and long-term effects
    pp 91-102
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    This chapter reviews what is known about the interactions of cannabis with the cannabinoid system in the brain, and how the drug affects psychomotor, cognitive, perceptual and appetitive functions. In both animals and humans the cerebral cortex, particularly the frontal regions, contains high densities of CB1 receptors. The presynaptic localization of CB1 receptors suggests a role for cannabinoids in modulating the release of neurotransmitters from axon terminals. CB1 receptors are expressed at particularly high densities in the basal ganglia and cerebellum so it is not surprising that cannabinoids have complex effects on psychomotor function. Controlled clinical trials showed that tetrahydrocannabinol (THC) had significant beneficial effects in counteracting the loss of appetite and reduction in body weight in patients suffering from AIDS-related wasting syndrome. The interaction of the cannabinoid and opioid systems in CNS remains to be demonstrated convincingly in humans.
  • 9 - Does cannabis cause lasting brain damage?
    pp 103-113
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    Cannabidiol ameliorates cognitive and motor impairment in mice with bile duct ligation, a model of hepatic encephalopathy. Cannabidiol administration may thus represent an adjunct treatment dealing with the central nervous system symptoms secondary to liver disease, along with other drugs improving liver function. Cannabidiol is also an inhibitor of ID-1 gene expression in aggressive breast cancer cells. Cannabigerol inhibits keratinocyte proliferation in a concentration-dependent manner. It is a partial agonist at both the CB1 and CB2 cannabinoid receptors. The CB2 receptor is involved in the pathogenesis of experimental encephalopathy in mice, caused by thioacetamide-induced acute liver failure. This is an animal model for hepatic encephalopathy, a neuropsychiatric syndrome. Cannabinoid and endocannabinoid chemistry, biochemistry and pharmacology continue to be active fields of research. While advances in these areas have widened our understanding of numerous physiological processes and pathological states, there are as yet no new major cannabinoid therapeutic agents.
  • 10 - The association between cannabis use and depression: a review of the evidence
    pp 114-128
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    Cannabinoid receptors can be activated not only by cannabis-derived and synthetic agonists but also by endogenous cannabinoids produced in mammalian tissues and usually referred to as endocannabinoids. There are numerous data in the literature that provide strong support for the notion that the endocannabinoid system (ECS) plays a crucial role in the modulation of several other systems ranging from the central and autonomic nervous systems to the endocrine system, the gastrointestinal tract and the reproductive, immune and cardiovascular systems. The ECS has been reported to become upregulated in a wide range of disorders, such as multiple sclerosis, cancer, schizophrenia, post-traumatic stress disorders, certain types of pain, some intestinal and cardiovascular diseases, excitotoxicity and traumatic head injury. The ECS has prompted a number of important advances in the field of cannabinoid research. It is a key player in several physiological processes and pathological conditions in both central and peripheral tissues.
  • 11 - Cannabis, cannabinoids and bipolar disorder
    pp 129-136
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    The psychoactive ingredients of cannabis are the terpenophenolic cannabinoids. The main psychoactive cannabinoid is tetrahydrocannabinol (THC). In Canada, seized cannabis products are submitted for THC analysis for court purposes. Data on cannabis potency is generally obtained from the analysis of law enforcement seizures. In the Netherlands, data have been derived from cannabis products purchased in coffee shops since 1999. A study on the THC content of fresh illicit cannabis products seized on entry into the United Kingdom was conducted by the Laboratory of the Government Chemist (LGC). Cannabidiol, the main non-psychotropic constituent of cannabis, does not bind to the cannabinoid receptors, probably exerting its effects through novel cannabinoid receptors mediating non-CB1/CB2 receptor effects. In conclusion, it is clear that high-potency cannabis products are freely available on the international drug markets, and that cannabis products have at least a two-fold increased THC content compared with pre-2000 products.
  • 12 - Which cannabis users develop psychosis?
    pp 137-143
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    This chapter explores the policy implications of the evidence on cannabis and psychosis for mental health services, health education about the risks of cannabis use, and public policy toward recreational cannabis use. It is useful to compare the strength of the evidence on cannabis and psychosis with that of observational evidence on relationships between adverse health effects and other types of drug use. These comparisons facilitate more consistent, even-handed appraisals of the comparative strengths and weakness of evidence on the adverse effects of different drugs. Providing credible advice to young people on the mental health risks of cannabis use is complicated by the polarized views on the health risks of cannabis expressed in the larger cannabis policy debate. It seems likely that governments in most developed countries will continue to prohibit cannabis use by adults, regardless of whether they do so by imposing criminal or civil penalties for use.
  • 13 - Cannabinoids and the cerebellum: a potential role in the development of psychosis
    pp 144-159
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    The impact of prenatal cannabinoid exposure on brain development and interest in understanding its interference with normal adult neurological function has fostered the characterization of the endocannabinoid system (ECS) during nervous system development. Multiple lines of evidences show that the ECS regulates the functionality of neural progenitor cell populations during development and in adult neurogenic areas. CB1 receptors allow crosstalk with growth factor and neurotrophin signaling at different levels. The glutamatergic neuronal dysfunction hypothesis of schizophrenia suggests that malfunction of the developmental role of CB1 receptors in pyramidal neurogenesis may contribute to the pathogenesis of psychoses or schizophrenia symptoms. Recent findings have demonstrated that endocannabinoids and CB1 receptors are crucial regulators of neurogenic processes including neural progenitor cell proliferation and survival, neuronal specification, migration, synapse establishment and the correct connectivity of newly formed cells. The ECS may be considered as a novel regulatory signaling system of neurogenesis and nervous system maturation.
  • 14 - The neural basis for the acute effects of cannabis on learning and psychosis
    pp 160-168
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    This chapter surveys possible lasting consequences of cannabinoid exposure during crucial periods of pubertal and adolescent maturation reported from animal studies. Endocannabinoids and their cannabinoid receptors, CB1 and CB2, are present from the early stages of gestation and play a number of vital roles for the developing organism. Beside direct alterations in the endocannabinoid or other neurotransmitter systems, adolescent/pubertal cannabinoid exposure has been reported to affect cortical and limbic systems in particular. Global evidence indicates that cannabis use/abuse acts as a risk factor for the emergence of schizophrenia, especially among early-onset cannabis users. Similar indications were observed in animal studies, where chronic pubertal, but not adult, cannabinoid treatment resulted in lasting behavioral deficits, resembling at least some aspects of schizophrenia. Data from animal research point out clearly that the age at which an individual is exposed to cannabinoids has major impact on subsequent effects of this drug.
  • 15 - Does cannabis use cause schizophrenia? The epidemiological evidence
    pp 169-183
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    This chapter updates our knowledge of the short- and long-term effects of cannabis on cognition based on integrating evidence from the most recent literature on this topic. Numerous studies have examined the acute effects of cannabis on human cognition. Cannabis induces perceptual distortions and impairs memory and concentration during acute intoxication. Studies of long-term and heavy cannabis users have continued to investigate residual or persistent effects of cannabis on cognitive function. Verbal memory is consistently impaired in chronic cannabis users, with impaired performance on word list learning tasks. It might be expected that people with schizophrenia who are already cognitively impaired may be even more vulnerable to the adverse effects of cannabis on cognition. Cognitive functions, encompassing attentional, memory, executive and inhibitory processes are impaired during both acute intoxication period and following long-term use of cannabis.
  • 16 - Postmortem studies of the brain cannabinoid system in schizophrenia
    pp 184-192
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    A study of cannabinoid application in vitro showed that THC appears to accumulate primarily in neurons and that transformation to its metabolite, THC-COOH, depends on the presence of glia. The authors suggested that the adverse effects of cannabinoids on the brain may occur through a combination of pathways involving cannabinoid receptor activation, accumulation of cannabinoids and their metabolites and upregulation of neuroinflammatory cytokines. Findings of persistent alteration of brain function or cognitive impairment in human cannabis users support the notion that long-term cannabis use may result in morphological alterations of brain structures that subserve attention, learning, memory, executive functions and emotional processes. Since brain structural changes are evident in patients with schizophrenia, cannabis may exert greater adverse effects on brain morphology when the brain is already compromised. This chapter proposes that long-term heavy cannabis use leads to structural brain changes and associated deleterious functional sequelae that resemble aspects of schizophrenia.
  • 17 - The endocannabinoid system in schizophrenia
    pp 193-197
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    The association between cannabis and depression has received less attention than the links between cannabis use and psychosis. Some have suggested that cannabis use may be a contributory cause of suicidal behaviors. A number of studies have found association between cannabis use and suicide, but the quality of control for confounding variables has varied widely. There is increasing evidence that regular cannabis use and depression occur together more often than we might expect by chance. The association between cannabis use and depression may arise because the same factors that predispose people to use cannabis also increase their risk of depression. Cross-sectional and longitudinal studies have provided mixed evidence on the association between cannabis use and depression. There is a need for longitudinal and twin studies that assess the relationship between cannabis use, depression and confounding factors.
  • 18 - The acute effects of cannabinoids in patients with psychotic illness
    pp 198-209
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    To explore whether cannabis has a potential role in actually causing bipolar disorder, a general population cohort study design is informative. Cahill et al. reviewed the interactions between chronic cannabis use and cognitive compromise in bipolar disorder. In trying to understand the interaction between the cannabis and bipolar disorder, attention has been given to the endocannabinoid system. Ashton et al. have detailed the mechanisms of the endocannabinoid system that have been implicated in brain reward pathways, pain, sleep, mood and anxiety. The authors have acknowledged the difficulties with studying the cannabinoids, including issues with doses, mode of administration and tolerance. There is no doubt a great deal of comorbidity between bipolar disorder and cannabis use. There is also a growing body of evidence regarding the deleterious effects of cannabis use in patients with bipolar disorder.
  • 19 - Cannabis abuse and the course of schizophrenia
    pp 210-217
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    There has been much debate as to whether the association between cannabis and subclinical expression of psychosis is causal, or whether psychotic experiences may prompt cannabis use in individuals at genetic risk for psychosis as a means of self-medication. The Genetic Risk and Outcome in Psychosis (GROUP) study investigated the association between familial liability for psychosis and sensitivity to cannabis, using patient sibling and sibling-control pairs analyses. This study focused on gene-environment interactions relevant to psychotic disorders, and included patients with psychotic disorder, their siblings and community controls. Caspi and colleagues highlighted the importance of individual genetic vulnerability when they reported an interaction between cannabis use and variation in the gene that encodes catecholamine-O-methyl transferase (COMT). Given that different types of cannabis clearly affect mental health differentially, more research is needed to understand how genetic liability may increase sensitivity to, or preference for, the specific constituents of cannabis.
  • 20 - Understanding cannabis use in schizophrenia
    pp 218-224
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    The cerebellar peduncles are large axon bundles that interconnect the cerebellum with other areas of the nervous system. It is now well established that the cerebellum contains one of the highest densities of CB1 receptors in the mammalian brain. It appears that the primary mode of action of endocannabinoids in the cerebellum is self-regulation by Purkinje cells via retrograde signaling back to the presynaptic terminals that innervate them. In terms of behavioral outcomes, several studies have shown that cannabinoid administration in humans is associated with alterations in temporal processing and psychomotor performance, both of which are at least partly cerebellar-mediated. In addition to alterations in cerebellar-mediated behavioral outcomes, numerous studies have shown that patients with schizophrenia exhibit abnormalities in cerebellar structure and metabolism. To recapitulate, the current chapter has attempted to synthesize known literatures regarding the effect of cannabinoids on cerebellar function and the role of the cerebellum in schizophrenia.
  • 21 - Addressing cannabis use in people with psychosis
    pp 225-233
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    Studies that provide mechanistic evidence delineating how the enhancement of the risk of psychosis by cannabis may be mediated at the neural level in humans are important. The modulatory effects of tetrahydrocannabinol (THC) on medial temporal, anterior cingulate/medial prefrontal and striatal activation during verbal learning were observed in the absence of differential task performance between the drug conditions. This chapter summarizes the evidence from studies that have examined the acute neural effects of cannabis and its main psychoactive ingredients during cognitive tasks, as well as on resting state activity of the brain. The acute effects of cannabis on neural activity during cognitive processing paradigms apart from learning have been examined by few other studies. Studies are underway that aim to provide mechanistic insights into the genetic modulation of the acute symptomatic, cognitive and neural effects of cannabis in humans.


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