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December 30, 2004
Schizophrenia and cannabis
Read more... Schizophrenia Research Journal Articles
New Perspectives in the Studies on Endocannabinoid and Cannabis: Cannabinoid Receptors and Schizophrenia
Hiroshi Ujike and Yukitaka Morita
J Pharmacol Sci 96, 376 – 381 (2004)
This article reviews the evidence of cannabis (marijuana) with respect to psychosis and schizophrenia. The authors pose adding another element to the model of schizophrenia that includes cannabinoid receptors. These receptors (referred to as CB-1 receptors) are increased in the brains of many people with schizophrenia. Recently, there was an attempt at using a medication designed to target these receptors that did not show a benefit over a placebo (Click here for my review). However, there is evidence that cannabis can cause similar cognitive (thinking) deficits in someone acutely intoxicated from THC (the active ingredient in marijuana).
Additionally, many people experience some degree of psychosis/hallucination while under the influence of THC. Some have described a more persistent “cannabinoid psychosis” in ultra-high level users. In people with schizophrenia, positive symptoms are typically worsened by the use of cannabis, even if the person is regularly taking antipsychotic medications. Some studies have also argued that the use of cannabis in a high risk population may precipitate the development of schizophrenia. In other words, people with a genetic predisposition may receive the trigger to develop schizophrenia from using marijuana heavily, though this is not fully proven yet.
Cannabinoid receptors are found in both the brain and the body’s periphery. When they are in the brain they are referred to as CB-1 and in the rest of the body they are called CB2. Why has the human body got receptors for use with THC? It is because there are endogenous (produced by our own body) molecules that have evolved to fit in these receptors .The most studied is called anandamide and it is a fatty-acid derivative. When rodents have been given synthesized anandamide, they behaved just as if they were given marijuana. In one study of the fluid around the brain and spinal cord (CSF) of people with schizophrenia, it was found that there was a 2-fold increase in the amount of anandamide compared to healthy controls. This level did not change even with the administration of antipsychotic medications. In people with schizophrenia, there is an increase in the CB-1 receptors located in the caudate and putamen (areas of the brain associated with the dysfunctions found in schizophrenia.) It is thought that this increase in receptors may have to do with negative symptoms and with some of the cognitive (thinking) disturbances found in schizophrenia.
There are many genetic variations of the CB-1 receptor. It is possible that having a particular genotype (genetic variation) of the receptor may put someone at greater risk of cannabinoid psychosis. Some have described this type of condition as “amotivational syndrome” because of the profound negative symptom quality to it. One particular genotype has been most clearly linked to people with disorganized type of schizophrenia; a type more characterized by inability to maintain activities of daily living than with positive/psychotic symptoms. This variation has also been seen in people with the amotivational syndrome due to marijuana but not with psychosis due to amphetamine (speed, etc.) or other drug use. However, this genetic variation is merely an association and not yet determined to actually be a testable risk factor for schizophrenia. The role of cannabinoids will be the subject of much further research over the upcoming years.
For more information on Marijuana/cannabis and schizophrenia risk, see: http://www.schizophrenia.com/hypo.html#street
Posted by Megan at December 30, 2004 12:03 AM
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