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THE LINK BETWEEN CANNABIS USE AND

SCHIZOPHRENIA
Cannabis use is a very controversial topic discussed nowadays, with more and more interest
manifested regarding its legalization, its economic importance and its partially unknown side
effects over the human body.
Schizophrenia has always been a very prominent mental illness, because of its disabling effects
on those who have it, its 1% prevalence and the high financial resources needed in treating it.
Therefore, it is natural for the link between these two controversial topics to be of main interest
as well.

Is there really a link?

Research up to date undoubtedly proves that there is a link between Cannabis use and
Schizophrenia. However, if the existence of this link is unquestionable, the nature of it is a long
way from being clarified.
In his article, which summarizes the advancement done in scientific research over the last decade
regarding this topic, Abhishek Ghosh explains that, nowadays, the association of cannabis and
Schizophrenia remains significant and that studies allude to the possibility of
gene-environment interaction: Cannabis and COMT gene functional polymorphism. (Ghosh,
Basu, 2015)

What kind of link is it?

Reviewing recent research that studies the relation between cannabis use and schizophrenia, one
may find different arguments and hypothesis which try to define this link. These could be
classified into 3 main groups, based on their interpretation. These 3 dimensions, however, are not
mutually-exclusive.
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The first group is the causal interpretation stating that Cannabis use causes Schizophrenia.
The second orientation is the one which claims that the existent link between Cannabis use and
Schizophrenia is due to common (genetic) etiology. Lastly, there are also those who argue that
there is a reverse causal relation, Schizophrenia being the one that causes Cannabis use,
because of its effect on the disturbing symptoms of this mental illness.

Does Cannabis use cause Schizophrenia?

Deepak DSouza summarizes very well what was known until 2009 about the influence cannabis
has over the onset of schizophrenia. Cannabinoids can produce a full range of transient
schizophrenia-like positive, negative, and cognitive symptoms in some healthy individuals. Also
() in individuals with an established psychotic disorder, cannabinoids can exacerbate
symptoms, trigger relapse, and have negative consequences on the course of the illness. () It is
likely that cannabis exposure is a component cause that interacts with other factors to cause
schizophrenia or a psychotic disorder, but is neither necessary nor sufficient to do so alone.
(D'Souza et al., 2009)
In 2011, Paola Casadio states that the research done on cannabis use in relation with
schizophrenia has largely been epidemiological in nature and has consistently found that
cannabis use is associated with schizophrenia outcomes later in life, even after controlling for
several confounding factors. While the majority of users can continue their use without adverse
effects, it is clear from studies of psychosis that some individuals are more vulnerable to its
effects than others. In addition, evidence from both epidemiological and animal studies indicates
that cannabis use during adolescence carries particular risk. (Casadio et al., 2011)
Ashley C Porals results in 2013 suggest that having an increased familial morbid risk for
schizophrenia may be the underlying basis for schizophrenia in cannabis users and not cannabis
use by itself. (Poral et al., 2013)
The same conclusion is drawn by Radhakrishnan in 2014: cannabinoids can produce acute,
transient effects; acute, persistent effects; and delayed, persistent effects that recapitulate the
psychopathology and psychophysiology seen in schizophrenia.() In individuals with an
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established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have
negative consequences on the course of the illness. Several factors appear to moderate these
associations, including family history, genetic factors, history of childhood abuse, and the age at
onset of cannabis use. (Radhakrishnan et al., 2014)
In 2015, Giordane reaches also pretty much the same conclusion: CA [Cannabis Abuse] has an
appreciable causal impact on future risk for schizophrenia. However, population-based estimates
of cannabisschizophrenia co-morbidity substantially overestimate their causal association.
Predictions of the cases of schizophrenia that might be prevented by reduced cannabis
consumption based on population associations are therefore likely to be considerably
overestimated. (Giordano et al., 2015)
Unlike DSouza, Casadio, Radhakrishnan and many others, who observed the actual effects of
cannabis use in relation to psychotic symptoms (and not schizophrenia), other voices found a
compelling argument to believe that cannabis use cannot cause schizophrenia. One of these
voices is Hickman, who, in 2009, wrote about the costs/benefits ratio, from the public health
point of view, between preventing schizophrenia and fighting cannabis use. His main conclusion
was that it doesnt seem to be worth it: The public health importance of preventing cannabis to
reduce schizophrenia or psychosis remains uncertain. (Hickman et al., 2009)
Trying to get to the bottom of this issue, from a neurobiological point of view, Amresh
Shrivastava conducted a study in 2015 whose conclusions were that The neurobiological
mechanisms associated with the development of psychosis and effects from cannabis use may be
similar but remain elusive.() epidemiologic evidence highlights potential causal links;
however, neurobiological evidence for causality remains weak. (Shrivastava et al., 2015)
The strongest argument against the viewing of cannabis use as the cause of schizophrenia is that
schizophrenias prevalence has remained at a stable 1% of the general population, even if
cannabis consumption has been and is, at present times, continuously increasing.
Another interesting way of seeing the presence or absence of this causality was the one taken by
Sarrazin in 2015, who compared schizophrenic patients that used to consume cannabis prior to
the onset of the mental illness to other patients that have never consumed it. Trying to see if there
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are any differences between the two, their results clearly argue against cannabis-associated
schizophrenia being a relevant distinct clinical entity of schizophrenia with specific features.
(Sarrazin et al., 2015)
Therefore, we can safely conclude that, the only close to certain relation of causality regarding
cannabis use and schizophrenia is the one between cannabis use and psychotic behaviors, which
can occur even in healthy individuals, but are not the cause of developing schizophrenia later on.
However, when already at risk of developing schizophrenia, due to other factors, cannabis use is
one of the triggers of schizophrenia.

Do Cannabis use and Schizophrenia share genetic etiology?

Some studies (Caspi et al., 2005, Power et al., 2014, Shrivastava et al., 2015) have subscribed to
the second orientation, which sees cannabis use and schizophrenia as two different effects of the
same genetic cause.
Caspis findings from 2005 provide evidence of a gene x environment interaction and suggest
that a role of some susceptibility genes is to influence vulnerability to environmental
pathogens.( Caspi et al., 2005), which means that the genetic predisposition to developing
schizophrenia may also be the cause of vulnerability towards cannabis use.
The most representative article of this orientation is the one published by Power in 2014, called
Genetic predisposition to schizophrenia associated with increased use of cannabis. By testing
2082 individuals, the authors show that there exists an association between a persons burden of
schizophrenia risk alleles and use of cannabis. This association was proven to be significant in
both cases, comparing users versus non-users, as well as quantity of use within users.
The conclusion reached by this study is that part of the association between schizophrenia and
cannabis is due to a shared genetic etiology. This form of geneenvironment correlation is an
important consideration when calculating the impact of environmental risk factors, including
cannabis use. (Power et al., 2014)

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Their results also suggest that individuals with an increased genetic predisposition to
schizophrenia are both more likely to use cannabis and to use it in greater quantities. This is not
to say that there is no causal relationship between use of cannabis and risk of schizophrenia, but
it does establish that at least part of the association may be due to causal relationship in the
opposite direction. (Power et al., 2014)

Does Schizophrenia cause Cannabis use?

Many schizophrenic patients are known to abuse substances such as alcohol, tobacco, cannabis
or other drugs, mostly in order to avoid the negative effects of their symptoms. Up to 42% of
schizophrenic patients also develop Cannabis Use Disorder, which may actually worsen disease
progression. (Fischer et al., 2014)
Some recent research (Schnell et al., 2013, Snchez-Torres et al., 2013, Cassidy et al., 2014,
Parshotam, Joubert, 2015) analyses the effects of cannabis use in schizophrenic patients.
Schnell finds that one of the main reasons why people with schizophrenia use cannabis is selfmedication or affect. (Schnell et al., 2013)
But are they right to do so? Although, as mentioned before, cannabis use has negative
consequences on people who are at risk of developing schizophrenia, it seems that, after the
onset of the disease, it also has some positive effects. Ana M. Sanchez-Torrez states that,
although acute and long-term use of cannabis causes impairment in cognitive performance in
healthy subjects, several studies have shown improved cognitive outcomes in patients with
schizophrenia spectrum disorders who use cannabis. (Snchez-Torres et al., 2013)
Their motives, except for the possible improved cognitive performance, are also affective and
motivational, having the purpose of avoiding unpleasant situations. This is shown by Clifford
Cassidy, who, by studying the motivation towards pleasant stimuli in relation to motivation for
avoiding unpleasant stimuli in schizophrenic patients, concludes that deficits in incentive
motivation may be an aspect of SSD [Schizophrenia Spectrum Disorder] which promotes
cannabis use in this population. (Cassidy et al., 2014)
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Also, by studying schizophrenic patients view on cannabis use, R. Parshotam states that most of
them believe that cannabis helps them to reduce tension, anxiety, to relax, to lift their mood, to
relieve their boredom, to feel more energetic and to sleep better. This is interesting because all of
these positive effects have the cost of adverse effects on the mental health of the patients. This
is a worrisome outcome, since those participants who feel that cannabis has more beneficial than
detrimental effects might not remain abstinent. (Parshotam, Joubert, 2015)
Another positive outcome of cannabis use in patients with schizophrenia is found by Bernard
Fischer in 2015 and is related to risk perception and risk-taking behaviors. It seems that patients
who are suffering from both schizophrenia and cannabis dependence have intermediate results
between those with only cannabis dependence or only schizophrenia on ratings of self-mastery,
sensation-seeking, and impulsivity. (Fischer et al., 2015)

Conclusion

There are many explanations for the high comorbidity between cannabis use and schizophrenia:
cannabis-related induction of psychosis, shared neurobiological alterations, a possible genetic
causality for the both or secondary development of addiction.
The reason why there is a prominent ongoing debate nowadays on this topic is the fact that all of
these interpretations of the link between cannabis use and schizophrenia are not mutuallyexclusive.

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References
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Cannabis use in young people: The risk for schizophrenia
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