[Show abstract][Hide abstract] ABSTRACT: BACKGROUND: Cannabis sativa (cannabis, marijuana) is a drug of abuse with well known psychoactive effects and therapeutic potential. A large number of cannabinoids chemically similar to Δ9-THC, the main active metabolite of marijuana, were synthesized in an attempt to exclude or minimize the psychotropic effects, maintaining the therapeutic potential. OBJECTIVES: The aim of this work was to review of the use of synthetic cannabinoids as emerging drugs of abuse, especially in the form of spice or herbal blends. METHODS: A bibliographic search was performed in PubMed employing the terms "synthetic cannabinoids", "spice", "legal highs", "herbal blends", "psychosis cannabis" and cross references. RESULTS: A number of synthetic cannabinoids can be found in Spice products, confirming that herbal incense emerged as new drugs of abuse. DISCUSSION: It is unclear whether the use of synthetic cannabinoids and Spice is a fad or will be established as common practice in our society. However, the phenomenon of designer drugs, especially synthetic cannabinoids, will remain a challenge to health authorities in the globalized world, requiring additional clinical and forensic research.
Revista de Psiquiatria Clínica 12/2011; 39(4):142-148. · 0.89 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Cannabis is the most commonly used illicit drug worldwide, with ~5 million daily users worldwide. Emerging evidence supports a number of associations between cannabis and psychosis/psychotic disorders, including schizophrenia. These associations-based on case-studies, surveys, epidemiological studies, and experimental studies indicate that cannabinoids can produce acute, transient effects; acute, persistent effects; and delayed, persistent effects that recapitulate the psychopathology and psychophysiology seen in schizophrenia. Acute exposure to both cannabis and synthetic cannabinoids (Spice/K2) can produce a full range of transient psychotomimetic symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to symptoms of schizophrenia. In individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Several factors appear to moderate these associations, including family history, genetic factors, history of childhood abuse, and the age at onset of cannabis use. Exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. Individuals with polymorphisms of COMT and AKT1 genes may be at increased risk for psychotic disorders in association with cannabinoids, as are individuals with a family history of psychotic disorders or a history of childhood trauma. The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence. At the present time, the evidence indicates that cannabis may be a component cause in the emergence of psychosis, and this warrants serious consideration from the point of view of public health policy.
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