Cannabis e Schizofrenia.

appunti del dott. Claudio Italiano

Gli studi appresso riportati vogliono rispondere al quesito che un nostro gentile navigatore ci pone, se cioè sia possibile e provato scientificamente, che l'abuso del fumo di canna possa slatentizzare la schizofrenia. Alcuni autori sembrano confermare questa ipotesi, che cioè abusando droghe, in soggetti già predisposti geneticamente, l'abuso della droga possa slatentizzare una psicosi latente. I passi salienti degli abstracts sono stati riportati in rosso.

CannabisCannabis abuse and risk for psychosis in a prodromal sample.

Kristensen K, Cadenhead KS.
Department of Psychiatry, 0810, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0810, USA.

The goal of the present study was to examine the rate of cannabis use among participants in the Cognitive Assessment and Risk Evaluation (CARE) Program, a longitudinal program for individuals who are "at risk" for developing a psychotic disorder. Cannabis abuse was assessed in 48 individuals identified as at risk for psychosis based on subsyndromal psychotic symptoms and/or family history. At 1 year follow-up, 6 of the 48 (12.5%) at risk subjects had made the transition to psychosis. Of the 32 subjects who had no use or minimal cannabis use, one subject (3.1) converted to psychosis. Of the 16 subjects who met criteria for cannabis abuse/dependence, five (31.3%) converted to psychosis. The results show a significant association between cannabis abuse and conversion to psychosis in this sample. Nicotine use was also found to be significantly associated with later conversion. The significant associations between cannabis and nicotine abuse and conversion to psychosis in individuals at risk for schizophrenia suggest that early identification and intervention programs should screen for and provide education about the deleterious effects of these substances.


Cannabis use and psychotic disorders: an update.

Hall W, Degenhardt L, Teesson M.
Office of Public Policy and Ethics, Institute for Molecular Bioscience University of Queensland Australia.

This paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidence from prospective epidemiological studies. These are that: (1) cannabis use causes a psychotic disorder that would not have occurred in the absence of cannabis use; (2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and (3) that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence of recent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countries have found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis of schizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptoms and they have persisted after adjustment for potentially confounding variables. The absence of any change in the incidence of schizophrenia during the three decades in which cannabis use in Australia has increased makes it unlikely that cannabis use can produce psychoses that would not have occurred in its absence. It seems more likely that cannabis use can precipitate schizophrenia in vulnerable individuals. There is also reasonable evidence for the third hypothesis that cannabis use exacerbates psychosis.

Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia.

Arendt M, Mortensen PB, Rosenberg R, Pedersen CB, Waltoft BL.
Centre for Psychiatric Research, Aarhus University Hospital, Skovagervej 2, Risskov, 8240 Risskov, Denmark.


Cannabis-induced psychosis is considered a distinct clinical entity in the existing psychiatric diagnostic systems. However, the validity of the diagnosis is uncertain. OBJECTIVES: To establish rate ratios of developing cannabis-induced psychosis associated with predisposition to psychosis and other psychiatric disorders in a first-degree relative and to compare them with the corresponding rate ratios for developing schizophrenia spectrum disorders. DESIGN: A population-based cohort was retrieved from the Danish Psychiatric Central Register and linked with the Danish Civil Registration System. History of treatment of psychiatric disorder in family members was used as an indicator of predisposition to psychiatric disorder. Rate ratios of cannabis-induced psychosis and schizophrenia associated with predisposition to psychiatric disorders were compared using competing risk analyses. SETTING: Nationwide population-based sample of all individuals born in Denmark between January 1,1955, and July 1, 1990 (N = 2,276,309). Patients During the 21.9 million person-years of follow-up between 1994 and 2005, 609 individuals received treatment of a cannabis-induced psychosis and 6476 received treatment of a schizophrenia spectrum disorder. RESULTS: In general, the rate ratios of developing cannabis-induced psychosis and schizophrenia spectrum disorder associated with predisposition to schizophrenia spectrum disorder, other psychoses, and other psychiatric disorders in first-degree relatives were of similar magnitude. However, children with a mother with schizophrenia were at a 5-fold increased risk of developing schizophrenia and a 2.5-fold increased risk of developing cannabis-induced psychosis. The risk of a schizophrenia spectrum disorder following a cannabis-induced psychosis and the timing of onset were unrelated to familial predisposition.


Predisposition to both psychiatric disorders in general and psychotic disorders specifically contributes equally to the risk of later treatment because of schizophrenia and cannabis-induced psychoses. Cannabis-induced psychosis could be an early sign of schizophrenia rather than a distinct clinical entity.


oppure cfr indice di psichiatria