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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