Friday, April 18, 2025

Cannabis and Psychosis in the 1980s - and since...

 



I thought I would commemorate one of the first papers I read on this issue when I became an acute care psychiatrist in 1988 (1).  It was my third year out of residency.  I started working on an acute care unit at St. Paul-Ramsey Medical Center in St. Paul, MN.  It was the highest acuity setting I have seen anywhere since then.  It was a combined unit that treated all forms of acute psychosis including affective psychoses and drug induced states.  There was also a forensic component so there was a lot of aggression and violence. There was no shortage of street drugs and even though it was 37 years ago – I have not seen more cases of hallucinogen and stimulant induced psychosis anywhere. I had the occasion to treat a patient who had a pocket full of PCP.  There were the more typical cases of alcohol and sedative withdrawal.  It was where I started to observe the connection between cannabis use and acute psychosis.

Like any compulsive psychiatrist fresh out of training – I was taught to study my patients’ conditions and find current literature. The very first paper I found was an observational study of Swedish army conscripts, their psychiatric conditions, cannabis use, and long-term psychiatric outcomes (1). It was also my introduction to registry studies that happen in Scandinavian countries.  Everyone in the population is on the same database so it is easy to follow them over time and look at outcomes.  In this case 45,470 draftees in the Swedish army were followed for 15 years.  Two questionnaires were administered at baseline – one to look at psychosocial determinants and risk factors for mental illness and the other for substance use history. The sample who refused to complete the substance use history were eliminated from the study. 

All the subjects were given an unspecified structured interview, psychological tests, and were seen by a psychologist.  Any subject with psychiatric symptoms were seen by a psychiatrist and any diagnosis determined was per the ICD-8 nomenclature.  The cohort was followed through a national registry of psychiatric care from 1969/1970 to 1983.  Psychiatric admissions and deaths were followed per the respective databases.   Cannabis consumption was documented as number of episodes of use with subjects using cannabis 50 or more times classified as heavy users. 

 Relative risks were calculated for estimated number of uses compared with a nonuse group and higher risk was noted at both the low and high ends. One lifetime use conferred a risk of 2.4 relative to no use.  For heavy lifetime use, the risk was 6 times greater than no use.  There was a dose dependent increase in cases of schizophrenia for the intermediate levels of use in between.

Of the other variables that were examined, several were noted to increase risk including psychiatric diagnosis at baseline, general childhood adversity, and school adjustment. 

In their discussion, the authors review possible explanations for the association with a schizophrenia diagnosis including cannabis use as causal, cannabis use as non-causal but psychiatric disorder causing cannabis use, and cannabis use as precipitating schizophrenia only in that subgroup of the population who are genetically and developmentally predisposed. They cite their own findings that show of the total number of schizophrenia cases – only 21/274 were in the high consumption group and only 49/274 had ever tried cannabis.  They conclude that cannabis was “an additional clue to the still elusive aetiology of schizophrenia.”  In their references, the authors have 12 case reports or series of cannabis induced psychosis dating back to 1972.

That was my introduction to the literature on cannabis, psychosis, and schizophrenia back in the late 1980s.  I had the good fortune to work with people who were admitted to my units for psychosis who were heavy cannabis users over the next 22 years.  I observed several patterns:

1:  Cannabis induced psychosis – this was probably the easiest to diagnose.  The patient is acutely intoxicated on cannabis and that resolves with detoxification.  The only further treatment that may be required is if the patient has a substance use disorder.

2:  Repeated episodes of psychosis that eventually do not resolve with detoxification -  these are generally heavy cannabis users and they typically have cannabis use disorder or uncontrolled use of cannabis. They have no pre-existing psychiatric diagnosis or family history of severe psychiatric disorders.  The most sensitive marker of heavy use was generally daily use but the specific method of use (blunts, spliffs, dabs) was also a sign.  These patients require treatment for psychosis for stabilization.  The duration of that treatment had to be individualized.

3:  Pre-existing psychiatric disorders exacerbated by use – recurrent episodes of psychosis in patients with a pre-existing diagnosis of schizophrenia, bipolar disorder, or depression with psychosis preceded by cannabis use is a very common problem.

As a clinician the practical approach to sorting out where cannabis fits into the scheme for psychosis and schizophrenia is a detailed evaluation and often getting to know the patient over time through repeated clinic visits or hospitalizations. The short-term goal is stabilizing them enough for hospital discharge with a plan to minimize or eliminate recurrent episodes.  If they can abstain from further cannabis use, gradual reduction and discontinuation of any medication required for stabilization is indicated. Educating the patient and their family about the psychotogenic potential of cannabis and referral for substance use treatment is also required.  That general outline is always dependent on other factors like severity of the episodes and patient preference.

One of the pieces left out of the debate on psychosis and cannabis use is the Naranjo scale.  This scale was developed in 1981 (2,3) to give the probability of an adverse event based on certain parameters. Just looking at the sequence of events I have described here – the relationship between cannabis and psychosis is probable to definite according to this scale.  The relationship to schizophrenia is less certain based on the fact it is a longitudinal diagnosis.

The treatment of cannabis induced disorders has been confounded by the widespread hype about cannabis in the American culture.  As an example – there are people who insist that you cannot develop uncontrolled consumption of cannabis, that it cannot cause psychosis, and that it is good for your mental health. There is scant evidence that any of those statements are true. After I changed to a strictly outpatient practice for the last 12 years, it was obvious that anxiety, depression, and insomnia were frequent problems related to cannabis use. At that time I was seeing a population with substance use problems.  The argument could be made that both major populations I treated over the course of my career had significant selection biases.  I would be the first to acknowledge that is true.  Those selection biases do not negate 35 years of very close observation often corroborated by many team members and collateral history. 

The issue of cannabis toxicity is highly politicized.  Like most things in the US, there are special interests set up to make a lot of money off cannabis and related compounds.  They have expected political and media influence. The idea that cannabis was a “medical” intervention was ultimately the rhetoric that led to legalization – even though there is negligible evidence that it is useful for any medical application.  I used to say that cannabis has been used by humans for over 6 centuries – what are the odds that there is an undiscovered miracle medical application?  I am willing to say that most people can probably smoke it and get high with the usual risks of any other intoxicants that includes accidents, injuries, and death.  The cannabis defenders will always say it is safer than alcohol. That is an argument based on low prevalence use.  As cannabis use picks up to the point where it is used as much as alcohol or more – the adverse outcomes including health outcomes will multiply.  I consider psychosis, exacerbations of pre-existing psychotic and other psychiatric disorders, addictions, lung disease, and cardiovascular disease to all be potential adverse outcomes.

Those are all the hard lessons I learned working with people who had these adverse effects over 35 years.  It all started for me with reference 1.

 

George Dawson, MD, DFAPA

 

References:

1:  Andréasson S, Engström A, Allebeck P, Rydberg U. Cannabis and schizophrenia a longitudinal study of Swedish conscripts. The Lancet. 1987 Dec 26;330(8574):1483-6. Full Text

2:  LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Adverse Drug Reaction Probability Scale (Naranjo) in Drug Induced Liver Injury. [Updated 2019 May 4]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK548069/

3:  Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, Janecek E, Domecq C, Greenblatt DJ. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981 Aug;30(2):239-45. doi: 10.1038/clpt.1981.154. PMID: 7249508.

Image Source:  English: CC 2.0 Attribution: please credit "Elsa Olofsson" and attribute a link to the original source of the image at: CBD Oracle.

Date   4 October 2020, 13:46:42

Source: https://www.flickr.com/photos/189516854@N06/50610714018/

Author:          elsaolofsson

 

Supplementary 1: There have been hundreds of references to cannabis induced psychosis in the literature since I first read this one.  I may take that on at some point - but I do not expect much modification to the initial results.  Human biology requires one to think probabilistically. Some people - even if they have the genetic constituents that make them vulnerable will not develop the condition being studied or they will develop it at a later time.  And of course without the vulnerability the probability of developing the condition is much lower to non-existent.  Those observations from genetics and biology can apply to the original study making the etiology of psychosis from cannabis less "elusive." 

Supplementary 2:  My go to interview questions for heavy cannabis use involved asking about daily use and type of use (how the smoke was delivered). Many of those questions were subsequently validated in a structured research interview for cannabis use.

Supplementary 3:  Naranjo scale for estimating the probability of an adverse drug event (see reference 2 for details).



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