Research+Supporting+Cannabis+Causing+Schizophrenia

= **Supporting Evidence**  = 

Cannabis is one of the most commonly used illicit drugs, in terms of both frequency of use and dosage (Casadio, Fernandea, Murray, & Forti, 2011). In 2009, The World Drug Report, published by the United Nations, estimated that the global number of people who used cannabis at least once in 2007 was between 143-190 million people (Casadio et al., 2011).

Cross-sectional surveys have found that rates of cannabis use are approximately twice as high among people with schizophrenia compared to people in the general population (van Os et al, 2002). Surveys of patients with psychotic illnesses from London England have found that between 20 and 40% report lifetime cannabis use (Duke et al, 2001). But, are these higher rates of cannabis use among people with schizophrenia a consequence or a cause of the condition?

It has been long accepted by research that cannabis use can lead to psychotic symptoms. However, from the 1990's forwards, research began to support that individuals suffering from schizophrenia are more likely to use cannabis compared to others. Also, it was proven that continued use of cannabis was associated with poor outcomes in those who already had existing psychotic symptoms. As well, past research has found that individuals who are predisposed to inherit schizophrenia seem to be at higher risk to the effects of cannabis.

**__Swedish Army Study__**
The first longitudinal study to test whether cannabis did cause psychosis was the Swedish Army Study in 1987. It involved 45,570 participants  who were followed up 15 years later. The study found that of those individuals who used cannabis by the time of the study began had double the risk of developing schizophrenia in the following 15 years (Casadio et al., 2011).  In a follow-up study to the Swedan conscript study,revealed that heavy cannabis users by the age of 18 years old were 6.7 times more likely than non-users to be diagnosed with schizophrenia 27 years later (Zammit et al, 2002).

These results although look significant, only reveal that 3% of heavy cannabis users developed schizophrenia from this sample. So, why isn't everyone who smokes cannabis developing psychosis? Low incidence can be attributed to several factors; the degree of cannabis exposure, genetic disposition, and environmental factors.

__**Cannabis Exposure**__
Individuals who develop psychosis from suspected cannabis use are more likely to have taken cannabis for longer periods of time and more frequently, and also are much more likely to use high potency cannabis "skunk", which has 3-4 times more THC than most cannabis (Casadio et al., 2011).

**Christchurch Health and Development Study** The Christchurch Health and Development Study (Fergussin et al, 2003) is a study that has followed its cohort over 20 years by examining the association between cannabis and psychotic symptoms at ages 18-21 years. Researchers found that those who met the criteria for cannabis dependence disorder at 18 years old had a 3.7 fold increase risk of psychotic symptoms compared to those without. Risk of psychotic symptoms at the age of 21 years was 2.3 times higher for those who had cannabis dependency disorder. After they controlled for many confounding variables; like anxiety disorders, childhood sexual or physical abuse, and psychotic symptoms at previous assessment, association remained significant at 21 years old.

In a recent study examining cannabis-induced psychosis and subsequent schizophrenia disorders in 535 cases (2005). Arendt, Rosenberg, Foldager, Perto, and Munk-Jorgensen (2005) found that of the sample of individuals who were treated with cannabis-psychotic symptoms, 44.5% of the individuals were diagnosed with schizophrenia-spectrum disorders. The researchers compared this experimental group to a control group of individuals who only with schizophrenia-spectrum disorders for the first time and no history of cannabis-induced psychosis. Arendt (2005) found that the development of schizophrenia disorders was often delayed and in 47.1% of people received a diagnosis more than a year after getting treatment for cannabis-induced psychosis. Patients also developed schizophrenia at an earlier age than the control group. This study shows that cannabis-induced psychosis is of real clinical significance and is something that needs to be researched further, but for the time being if you are experiencing psychosis due to your cannabis use you are at greater risk to develop schizophrenia.
 * <span style="color: #008000; font-family: Arial,Helvetica,sans-serif; font-size: 16px;">Schizophrenic-Spectrum Disorders **

<span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">A study conducted by the Netherlands Mental Health Survey and Incidence Study (NEMESIS) (van Os et al, 2002) examined the effect of cannabis use on self-reported psychotic symptoms among the general population. They used 4045 psychosis free people and 59 with psychotic disorders, over a 3 year period. Individuals using cannabis at baseline were almost 3 times more likely to develop psychotic symptoms at follow-up, even after adjusting for a range of clinically significant factors, ie. race, gender, ethnicity. Researchers also found that lifetime history of cannabis use at baseline, compared to at follow-up, was a stronger predictor of psychosis 3 years later. This means that the correlation between cannabis and psychosis is not just a result of short-term use of cannabis leading to acute psychosis.
 * <span style="color: #008000; font-family: Arial,Helvetica,sans-serif; font-size: 16px;">NEMESIS Study **

<span style="color: #008000; font-family: Arial,Helvetica,sans-serif; font-size: 120%;">__**Genetic Disposition**__
<span style="color: #008000; font-family: Arial,Helvetica,sans-serif; font-size: 16px;">**Genetic Evidence** <span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">Obviously not all patients who have schizophrenia use cannabis and not all cannabis users develop schizophrenia. Therefore we cannot say that cannabis use is a definite stand alone cause of schizophrenia, but there is a correlation. Cannabis is codependent on some other factors in order to have any causal influence on risk for developing psychosis. McGuire et al. (1995) found that the relatives of patients with acute psychosis who tested positive for cannabis use had 10 times higher morbid risk for schizophrenia than those who did not have relatives with schizophrenia. Similarly, Henquet et al. (2005) found that the 3.5 year risk of developing psychotic symptoms was 2.1% in young people who used cannabis in the absence of psychosis liability, but found that 51% of people who both used cannabis and psychosis liability. Psychosis liability was measured by a psychosis proneness scale shown to be sensitive to familial transmission of psychosis liability.

<span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">Another study that showed a direct link to genetic risk factors influencing the development of psychosis was conducted by Caspi et al. (2005). They showed that a functional polymorphism in catechol-O-methyltransferase (COMT) gene moderates the effect of adolescent cannabis use on risk for adult psychosis. Caspi et al. (2005) found that the individual homozygous for the COMT valine allele are most likely to show psychotic symptoms and to develop -spectrum disorder after adolescent cannabis use. <span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">Henquet et al. (2006) experimentally followed up Caspi's study by giving 300millagrams of THC/kg of body weight or a placebo to patients with psychotic disorders, relatives of patients with a psychotic disorder and control group. Henquet et al. (2006) found that those individuals with the homozygous Val genotype were more likely to develop THC-induced psychotic symptoms. These results were dependent on on prior evidence of psychometric psychosis liability (Henquet et al., 2006).

<span style="font-family: Arial,Helvetica,sans-serif;"> In a very recent study conducted by Van Winkel (2011), <span style="font-family: Arial,Helvetica,sans-serif; font-size: 120%;">examined whether genetic variation moderates the association between recent cannabis use and psychosis. Specifically the "interaction between cannabis use and 152 single-nucleotide polymorphisms in 42 genes in 740 unaffected siblings of 801 patients with psychosis" (Van Winkel, 2011, p. 4) was examined. Van Winkel (2011) found that AKT1, "a serine/threonine kinase and a focal point for signal-transduction pathways" (Van Winkel, 2011, p. 4), cannabinoids are able to activate the AKT1 pathway. Polymorphisms in the AKT1 gene could be involved in cannabis induced psychosis potentially though a mechanism of cannabinoid-regulated signaling of the dopamine receptor (Van Winkel, 2011).

<span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">Genetic evidence shows that if you are biologically predisposed to developing schizophrenia or psychosis symptoms and you are a cannabis user than your chances of developing schizophrenia dramatically increases. <span style="font-family: Arial,Helvetica,sans-serif; font-size: 16px;">

<span style="color: #008000; font-family: Arial,Helvetica,sans-serif; font-size: 120%;">**__Videos__**
**The Nature of Things: The Downside of High** [|http://www.cbc.ca/video/#/Shows/The_Nature_of_Things/1242300217/ID=1398511775] (30:15-32:40)