Products containing Δ9-THC are commonly referred to as cannabinoids, ranging from the more traditional forms (marijuana, hashish) to newer ones (for example, skunk), derived from selected botanical species, generally with the aim of obtaining mixtures with a higher concentration of active THC.
The problem of cannabis-induced disorders is a “hot” topic, both because our knowledge of the brain system that responds to cannabinoids is still incomplete and because there are no specific medications for cannabis-induced disorders. Furthermore, the importance attributed to cannabis-related disorders automatically becomes, at the political level, an argument either for or against the free circulation of these substances.
Let us try to provide an overview of what is known about disorders associated with cannabis use, beginning with the most serious one: psychosis. For the meaning of psychosis, please refer to the article dealing with the symptoms of psychosis and schizophrenia.
The category of “cannabis-induced” psychosis is a provisional one, and would more correctly be described as “cannabis-positive” psychosis, meaning psychosis associated with recent cannabis use, without this necessarily indicating a cause-and-effect relationship. Other studies refer to “cannabis-associated psychosis,” which also includes cases in which cannabis was used in the past but was no longer being used when the disorder became clinically evident.
When the term “psychosis” is used, it refers to the presence of certain symptoms, the most obvious of which are hallucinations and delusions. In “acute” forms, these symptoms are generally present. In more subtle and less explosive forms, there may instead be bizarre behavior, thought characterized by incomprehensible, vague, or unstable associations, a silly or apathetic mood accompanied by loss of the emotional meaning of external objects, and difficulty in social interactions.
Certainly, psychosis is not an expected effect of a single administration of cannabis. However, chronic users who develop acute psychosis are not rare (Kolansky and Moore; Altman and Evenson; Knight; Thomas), and psychotic symptoms are more frequent among cannabis users than among non-users (Degenhardt; Tien and Anthony; Verdoux, Ferdinand; Thomas; Fergusson; Stefanis).
Since cannabis is widespread among younger age groups—that is, the age groups in which the most common mental disorders may first emerge—the question is whether cannabis merely represents an occasional or triggering factor. The majority of people with cannabis-positive psychosis already had a psychiatric history or had indications of a predisposition to psychotic disorders (Ferdinand).
The presence of cannabis modifies the “classic” characteristics of known mental disorders without fundamentally changing them. For example, euphoric and excitatory phases occurring in the presence of marijuana have been described as “marijuana-filtered mania” (Harding & Knight), that is, a known psychiatric disorder that does not in itself require cannabis but is influenced by its presence.
In particular, excitatory (manic) phases associated with cannabis use more often involve impulsive violent behavior, unstable mood and intense, violent mood swings, disorganized behavior, and dissociative symptoms. These are “dream-like” states in which a person experiences a sense of estrangement from reality, as though living a dream from the outside, or fails to perceive in a unified way the meanings and emotions associated with experience (Thacore and Shukla; Chopra and Smith; Rottamburg).
Not all authors, however, have found differences from classical forms of psychosis (Imade and Ebie).
The substantial difference may become apparent later, in the course of the illness, which tends to be closer to that of an affective psychosis, with less affective flattening over time and a course that is more “dependent” on repeated cannabis use or sustained abstinence (Thacore and Shukla; Rottamburg).
The most typical form of cannabis-related psychosis therefore appears to remain linked to cannabis even after its onset, something that does not occur in spontaneous, chronic schizophrenic psychosis, which continues even in the absence of psychoactive substances.
In general, however, among psychotic patients, symptoms tend to improve when cannabis use stops and worsen when cannabis use resumes (Lintzeris; Van Os; Hide; Degenhardt; Basu). This applies both to psychiatric patients who use cannabis and to patients who experience psychotic episodes only when using cannabis (Mathers; Thacore; Keup).
However, at least in the case of bipolar psychosis, the fact that the disorder emerges only in the presence of drugs does not constitute a different illness. Rather, it represents a form with the same underlying mechanisms and consequences.
Excluding these forms that are simply “seasoned” or modified by cannabis, there remains the hypothesis of “cannabis-induced” psychosis as a new disease, that is, a psychosis arising in the absence of a known previous history of psychosis, without the possible contribution of other substances, and with a chronology in which cannabis use precedes the onset of psychosis (Palsson).
It has been established that the dose factor is important, in the sense that the probability of developing psychosis among cannabis users depends on the duration of use and is particularly related to periods in which higher doses are being used (Spencer; Bernhardson and Gunne). In practice, this would represent an intoxication effect.
This finding does not in itself tell us much, because the same observation could be explained simply by considering cannabis a triggering factor.
The crucial question, instead, is whether cannabis increases the incidence of psychosis in people who would not otherwise have developed it because of a predisposition, or at least in people with a predisposition who would not have developed psychosis in the absence of cannabis.
The suspicion arose from observations of American military personnel stationed in Europe in the 1960s and 1970s. During this period of the cultural explosion of marijuana use, there were many more cases of psychosis than would have been expected (Tennant & Groesbeck).
The diagnosis of schizophrenia used in the 1960s and 1970s was different, however, and the long-term course of these cases is not known. We can say that the frequency of acute psychosis was nevertheless higher than expected in that population.
The risk of developing psychotic symptoms while using cannabis is greater in the presence of a predisposition to psychosis (Henquet), although this does not mean that such predisposing factors must have manifested themselves previously as psychiatric symptoms (Ferdinand).
Thus, some people who develop cannabis-related psychosis had previously shown no obvious signs of mental illness, or at least no signs of the same type of disorder.
In 1987, an observational study was published involving 15 years of follow-up of a population of more than 45,000 Swedish subjects. Among other objectives, the study sought to establish a possible relationship between the risk of developing schizophrenia and cannabis use.
The study produced positive results: the risk in question was six times higher among those who had used cannabis (Andreasson et al., 1987; Zimmet).
The relationship appears to work in both directions. The strongest factor for predicting whether a person will develop cannabinoid-related psychosis is a family history of schizophrenia, suggesting that predisposition to schizophrenia and the effects of cannabis may interact (Allebeck, 1993).
The limitation of this knowledge is that the predisposition to schizophrenia depends on factors that are still only partly understood.
It is possible that, because of one of these factors, people predisposed to schizophrenia may also be more inclined to use cannabis, without cannabis itself necessarily having a facilitating effect.
In practice, many people with schizophrenia have a history of cannabis use without there necessarily being a causal relationship between cannabis and schizophrenia.
Naturally, given the nature of cannabis’s effects on the brain, the more plausible impression is that some relationship does exist, or at least that cannabis facilitates the onset of psychotic illness in people with some degree of predisposition that might otherwise have remained “latent.”
In the Swedish study, the risk was already increased in cases of occasional use.
Other studies of the same kind followed, but did not provide additional decisive evidence (Arseneault; Fergusson; Van Os; Kristensen).
Whether schizophrenia preceded by cannabis use is associated with a particularly strong familial burden remains uncertain.
One study found no differences between schizophrenic subjects with and without a history of cannabis use in terms of family history of schizophrenia (Boydell), whereas other studies found an association between a family history of schizophrenia and previous cannabis use, suggesting that cannabis-related psychosis may represent a mode of onset of schizophrenia rather than a distinct form of psychosis (Arendt).
Furthermore, it appears that a greater familial burden may also be associated with a greater tendency to abuse cannabis before the onset of the illness (McGuire). The same effect, however, may also be associated with a family history of mental disorders in general (Arendt).
On the other hand, there is no evidence that the increase in cannabis use—observed in Australia over the last 30 years—has been accompanied by an epidemic increase in the number of schizophrenia cases (Degenhardt).
Cannabis nevertheless appears to be a factor capable of triggering relapses and perhaps bringing forward the first psychotic episode (Hall; Di Maggio; Miettunen; Gonzalez-Pinto).
There is no definitive evidence, however, that cannabis increases the overall incidence of psychosis. Some authors suggest that the triggering effect is particularly likely during adolescence and young adulthood (Konings).
The less favorable course of these disorders is often directly related to repeated cannabis use, which produces relapses. If cannabis use is not resumed, “classic” medications appear to work equally well.
Treatment of psychosis associated with cannabis does not fundamentally differ from treatment of classical psychotic disorders.
Clozapine has produced the best results in terms of speed of action and reduction in the tendency to continue using cannabis. It is, however, a medication that requires particular monitoring and precautions.