Vulnerability hypothesis

Those who support the vulnerability position conceptualize cannabis use as a risk factor - so something that may indeed be casually related to the outcome of experiencing psychosis but at the same time, may not be the sole or primary casual factor.

Mental illness is often explained by the stress diathesis model. This model understands behaviours and illnesses and in this case, psychosis-related illnesses, as being a product of the interaction between a vulnerable hereditary predisposition, with precipitating events or "stressors" in the environment. There are many recent studies which support this hypothesis and essentially see cannabis use as a factor or stressor that may interact with an underlying susceptibility

It has been purposed for example, that cannabis use precipitates schizophrenia in individuals who have a vulnerability to the illness due to a family history of schizophrenia . McGuire et al found that individuals who were heavy cannabis users and developed psychosis were 10 times more likely to have a family history of schizophrenia than individuals with psychosis who were not cannabis users (1995). So here the outcome of developing schizophrenia is the work of a stressor (the cannabis) acting on the genetic "diathesis" to develop schizophrenia.

 More recently a few studies of note have suggested an association between a genetic polymorphism of the CB1 receptor and schizophrenia. This implies that variation in ones genes may present vulnerability to psychosis-related disorders (Leroy et al 2001; Ujike et al 2002)

A few years later Caspi et al. (2005) took this genetic approach and assessed the catechol-O-methyltransferase (COMT) gene. Their rationale for this is that COMT is involved in the metabolism of dopamine in the prefrontal cortex and dopaminergic deregulation is thought to play a role in the pathogenesis of schizophrenia. The authors concluded that the link between cannabis and psychosis was moderated by a COMT gene polymorphism. That is, cannabis users in their teen years who carried the COMPT valine allele were the most likely to develop psychotic symptoms. On the other hand, teens with two copies of the methionine allele did not present this risk even when using cannabis.  This study presented some strong evidence for the stress diathesis model of cannabis and psychosis.

 However in 2005, Phillips et al. refuted genetic explanation of cannabis-psychosis link and similarly two years later Zammit et al. conducted a large case-control study and failed to replicate this result. More work has to be carried out in this area in order to gain more insight regarding this issue of particular genes being the possible mediator between cannabis use and psychosis.

Nevertheless, the evidence still remains strong for the claim that a pre-existing vulnerability to psychosis is a very important factor that influences the link between cannabis use and psychosis. In fact, some studies have shown that once childhood psychotic symptoms are controlled for, cannabis use no longer predicted the development and diagnoses of schizophreniform disorder and other psychosis-related illnesses (Arseneault et al., 2002). Accordingly, readers must consider this point in order to correctly interpret results in studies linking cannabis to psychosis. 

There is also strong evidence to support the claim that cannabis use exacerbates the symptoms of schizophrenia and other psychosis-related illnesses (though paradoxically it can also temporarily relieve symptoms see vulnerability hypothesis section). This is supported both by retrospective and prospective studies which control for confounding variables as well as biological facts which link the dopamine neurotransmitter system with psychotic disorders (Adams & Martin, 1996). Crudely put, psychosis, from a biological/neurological perspective, involves disturbances in the dopamine system. Drugs given to individuals to reduce psychotic symptoms reduce dopamine levels in the brain while other drugs, such as cannabis increase dopamine levels in the brain. More specifically cannabinoids, such as tetrahydrocannabinol (THC) increases dopamine release in the brain.  This relates to the often cited dopamine hypothesis of schizophrenia   and while the jury is still out regarding the precise role of dopamine in the illness, it is quite clear that is does somehow factor into the manifestation of psychotic symptoms.

Given the extensive evidence it is relatively safe to say that cannabis use is not a necessary cause for psychosis as the statistics have failed to show that all adults with psychosis related illnesses used cannabis as a young person and nor is it a sufficient cause- as the majority of adolescent users did not develop psychosis in adulthood. The most likely explanation is that cannabis is a component cause, among other possible causes which ultimately forms part of the causal constellation that leads to psychosis.

This complex, interactive explanation reflects our limited understanding of schizophrenia (and other psychosis-related illnesses) itself. There is evidence that both genetic and environmental factors are implicated but the exact origin is still relatively murky.  For the present time, it is helpful to see cannabis as a modifiable risk factor both in individuals who are vulnerable to develop psychosis and in the time of the onset of psychosis. The practical implication of this information is that young people who are indentified as being "at-risk" for developing psychosis should avoid cannabis at all costs. This is not to say that avoiding cannabis will prevent a psychotic episode from occurring all together (many studies estimate that there would be an 8 % reduction in diagnoses of schizophrenia if cannabis was 100% abstained from) but it would certainly help improve prognosis. Furthermore, if young people at risk for developing psychosis avoided cannabis they may delay the onset or in the best case scenario, they may prevent it from occurring all together. Future work should focus not only on the link between cannabis and psychosis from an etiological perspective but also from a public education perspective. The more the general public knows about these issues, the better and more knowledgeable they will be equipped to help and treat young people suffering with psychosis.