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Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: follow-up study of 535 incident cases

  • Mikkel Arendt (a1), Raben Rosenberg (a1), Leslie Foldager (a1), Gurli Perto (a1) and Povl Munk-Jørgensen (a2)...
Abstract
Background

Few studies have examined samples of people with cannabis-induced psychotic symptoms.

Aims

To establish whether cannabis-induced psychotic disorders are followed by development of persistent psychotic conditions, and the timing of their onset.

Method

Data on patients treated for cannabis-induced psychotic symptoms between 1994 and 1999 were extracted from the Danish Psychiatric Central Register. Those previously treated for any psychotic symptoms were excluded. The remaining 535 patients were followed for at least 3 years. In a separate analysis, the sample was compared with people referred for schizophrenia-spectrum disorders for the first time, but who had no history of cannabis-induced psychosis.

Results

Schizophrenia-spectrum disorders were diagnosed in 44.5% of the sample. New psychotic episodes of any type were diagnosed in 77.2%. Male gender and young age were associated with increased risk. Development of schizophrenia-spectrum disorders was often delayed, and 47.1% of patients received a diagnosis more than a year after seeking treatment for a cannabis-induced psychosis. The patients developed schizophrenia at an earlier age than people in the comparison group (males, 24.6 v. 30.7 years, females, 28.9 v. 33.1 years).

Conclusions

Cannabis-induced psychotic disorders are of great clinical and prognostic importance.

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Copyright
Corresponding author
Mikkel Arendt, Centre for Basic Psychiatric Research, Aarhus University Hospital, Skovagervej 2, DK-8240 Risskov, Denmark. E-mail: mca@psykiatri.aaa.dk
Footnotes
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Declaration of interest

None.

Footnotes
References
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Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: follow-up study of 535 incident cases

  • Mikkel Arendt (a1), Raben Rosenberg (a1), Leslie Foldager (a1), Gurli Perto (a1) and Povl Munk-Jørgensen (a2)...
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eLetters

This could be due to lower DHEA...

James M. Howard, biologist
06 December 2005

It is my hypothesis that schizophrenia begins with interference of the actions of, or simply low, DHEA in utero. This produces reduced growth and development of the brain. This is the "early lesion." Later in life, the hormones cortisol and testosterone act to reduce the availability / action of DHEA. This often occurs around the time when DHEA begins to naturally decline, in the late teens or early twenties. These combine to reduce function and structure of the parts of the brain affected in schizophrenia; symptoms and anatomy show decline. Hence, schizophrenia is often associated with a stressful event, cortisol, follows puberty in both sexes, but affects males more, and occurs when DHEA declines. DHEA has been found to be low in schizophrenia.

DHEA utilizes androgen receptors. One study examining the "anti-androgenic effects" of cannabis found interference of androgens (dihydrotestosterone) with androgen receptors (Endocrinology 1980; 107: 848-50). I suggest cannbis use may adversely affect growth and development of the brain by interferring with the effects of DHEA via androgen receptors. This explanation may explain the findings of Arendt, et al.
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