Cannabis and Psychosis: Are We any Closer to Understanding the Relationship?

Abstract

Purpose of Review This paper provides an update from the literature on understanding of the relationship between cannabis and schizophrenia. In particular, the paper focuses on the latest findings and remaining areas that require investigation. Recent Findings Three hypotheses have emerged as potential explanations for the association between cannabis and schizophrenia, namely cannabis can trigger schizophrenia, cannabis is used to mitigate symptoms of schizophrenia, and there are common factors which might account for the association. Biological and genetic factors dominate this field of research; this has been at the expense of exploring social and cultural contributory factors which influence cannabis and schizophrenia. Summary The evidence for cannabis acting as a causal factor for schizophrenia has so far not been established. Research needs to extend beyond males drawn from western countries if we are to advance knowledge and understanding of the link between cannabis use and schizophrenia.

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“…A consistent association between adolescent cannabis use and later risk of psychosis is also recognized, accounting for 8-14% of cases of schizophrenia. To what extent this is causal, and the magnitude of any effect remains a subject of debate (Hamilton and Monaghan, 2019), but is of sufficient concern, together with emerging evidence of similar but small effects in mania and suicide to support public health education efforts (Sideli et al). People with epilepsy, and in particular adults and children with early onset developmental epileptic encephalopathies and other severe drug resistant epilepsies, are already vulnerable to psychiatric and cognitive disorders (Mula and Cock, 2014).…”

Neuroprotection or Neurotoxicity of Illicit Drugs on Parkinson’s Disease

“…A major concern with phytocannabinoids use is the inherent risk of PD patients to develop psychosis and cognitive impairment. This aspect makes them more susceptible to psychomimetic substances agonists of CB1, such as ∆ 9 -THC or Nabilone [145,146]. In fact, it is well known that Nabilone may induce psychosis, even in patients without a psychiatric history [146].…”

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“…The return to baseline functioning as documented in these case reports is crucial in order to maintain the concept of CIPD. The difficulty in confidently diagnosing CIPD has been widely noted, as confirming absence of prior prodromal or psychotic symptoms and then also confirming return to baseline is quite difficult [31,52,53].…”