As a topic, psychosis is very taboo. It is never really talked about, let alone explored or investigated into by the general populace who, more often than not, erroneously think that it reflects a dissociative personality disorder, something that only affects approximately one percent of the populace (or between five and twenty percent of psychiatric in-patients). As a result, cannabis induced psychosis is not a well known topic area for most people, if known at all. In fact, in a recent survey carried out for the BBC, only 2% of youths understood that there were health risks associated with using the drug, whilst 79% of youths believed that cannabis was safe.
Psychotic symptoms, experienced in cases of schizophrenia, schizo-affective disorder and so on, can be best described as disconnections from reality, where an individual becomes withdrawn and deluded as to the state of the real world. Positive psychotic symptoms warp or over emphasise normal functions; for example, a patient may experience thought disorders whereby their thoughts and speech become disorganised and/or incoherent, exhibiting a loosening of associative abilities. Conversely, negative symptoms of psychosis diminish and reduce normal functioning; for example, a patient may experience avolition, whereby difficulties are found in achieving goals or targets, perhaps due to a lack of zest for life or a lack of social desires.
Psychosis is often used as a term for schizophrenia, a potentially elaborate disorder with many possible causes and treatments that affects roughly eleven in every thousand people. Most patients diagnosed with schizophrenia tend to fall into the category of undifferentiated schizophrenia, meaning that there is inadequate evidence to support the notion that the patient suffers from catatonic, disorganised or paranoid schizophrenia.
Catatonic schizophrenia is characterised by various motor disturbances bizarre, stationary poses maintained for many hours and waxy flexibility, in which the persons limbs can be moulded into new positions, which are then maintained [1]. People who suffer from this illness are often aware of the disorder and will willingly talk about the episodes they undergo. Disorganised schizophrenia is perhaps the most distressing strain of the disorder, exhibiting inappropriate emotion, disorganised thoughts and words. Finally, paranoid schizophrenia is best described as an inventive disorder. Patients will invent elaborate stories and fantasies that revolve around them and often go hand in hand with delusions of power, control and so on. The term paranoid is perhaps misleading, the common term meaning suspicious and hunted. Rather, patients are inventive and do not always possess a notion that they are being persecuted.
There are other psychotic disorders as well, such as the schizo-affective disorder, where patients exhibit both psychotic and affective (mood) disorders. There are also many other psychotic symptoms, too many to mention in fact. Briefly worth a mention, though, are delusions (falsely held beliefs, such as that one can fly) and hallucinations, (auditory, visual and so on), whereby the sufferor experiences sensation without stimulation similar to the effects of many hallucinogenic drugs. One such drug is Cannabis.
Cannabis as a drug is available in two forms: Marijuana and Hashish and is usually smoked, although it can also be eaten. Marijuana is best likened to tobacco, being made up of dried leaves whilst Hashish is a derivative of the resin produced by the plant. Cannabis itself is rich in chemicals unique to itself known as cannabinoids. These chemicals include cannabidiol, cannabinol and various strains of tetrahydrocannabinol, one of which (delta-9-tetrahydrocannabinol or THC) is thought to be primarily responsible for cannabis psychoactive properties. Cannabis also contains cannflavins and terpenoids, thought to be responsible for some of the more beneficial sides to the drug. THC itself is thought to affect appetite, sensation (auditory, visual and olfactory), concentration, relaxation levels and more.
Many animals, including humans, have two types of cannabinoid receptors, usually abbreviated and referred to as CB1 and CB2. It is the activation of these receptors that results in cannabis psychoactive effects. CB1 receptors are primarily found in the brain, specifically in the mesolimbic and mesocortical pathways, both believed to be important for the development of schizophrenia (Ameri, 1999) [2]; further to this, interaction between the CB1 receptors and the D2 dopamine receptors has been documented in rats and monkeys (Meschler et al, 2001) [3], suggesting a possible link in humans. CB2 receptors are primarily found in the immune system and are more responsible for the therapeutic effects of cannabis. Of the two receptors, THC appears to affect CB1 receptors more readily [4] and appears to be neuroprotective, mimicking the neurotransmitter anandamide which binds with said cannabinoid receptors in the brain. Interestingly, THC remains in the body for a long period after it was first administered, standing at 30% after a week.
Cannabis use can result in an increased awareness of sensation, an altered mindstate, inhibited motor control, relaxation, paranoia and so on by regulating dopamine levels within the brain (dopamine being a chemical responsible for, amongst other things, movement, cognition, motivation and perceived reward). Cannabis use can also seemingly result in psychotic disorders. Substance abuse itself can cause psychotic symptoms, but it can also seemingly cause psychotic episodes subsequently.
Chronic symptoms may occur following cannabis abuse, including the so called Amotivational Syndrome which details apathy, amnesia, loss of motivation and so on. These symptoms can unfortunately be permanent and there is an accumulating body of evidence to support the notion that smaller amounts of the drug over a period of time will do just as much damage as a large dose over a smaller period of time. Cannabis has also been linked to depression and anxiety [5] and more often than not disturbances of a psychotic nature within which cannabis is considered to have played a part are accompanied by an affective or mood disorder, most commonly a form of depression.
There is a growing body of evidence that suggests cannabis may be a causal factor in the development of psychosis [6]. However, it would be erroneous to say that cannabis is necessary or even sufficient for a psychosis to develop; many people develop psychotic disorders without ever consuming cannabis and many cannabis users lead psychosis free lives; correlation does not equal causation, as it were. A study (Fergusson et al, 2004) suggested that people who used cannabis daily increased their chances of psychotic symptoms by 1.6-1.8 times [7]; a study in 2002 based on research between 1970 to 1996 (Zammit et al) found that the risk of developing schizophrenia was increased (odds ratio = 1.9) [8] for cannabis users, with heavier users (use of cannabis more than 50 times prior to assessment) suffering an odds ratio of 6.7; the authors estimated that 13% of reported schizophrenia cases could have been avoided had cannabis use been nil. Further to this research, it was found that cannabis users were three times (300%) more likely to report psychotic symptoms three years after an initial appraisal [9], a significant result even considering the amount of compounding variables (the experiment was a naturalistic observation). Professor Robin Murray of the Maudsley Hospital (Kings College Psychiatry Unit), London, concluded that people were approximately 4.5 times more likely to be schizophrenic at 26 if they were regular cannabis users at the age of 15. Another researcher, one Professor John Henry, clinical toxicologist at Imperial College London, was quoted as claiming that research had shown that people with a certain genetic makeup were ten times more likely to suffer from schizophrenia should they use the drug at some point in their life. Earlier research claimed that the chance of being schizophrenic at a later date was 6 times as high in the group using cannabis than in the group not using it [10] [11]. Finally, another case study, Boydell (2003), concluded that the incidence of schizophrenia had doubled in thirty years in Camberwell, South East London (Boydell, 2003) [12], seemingly going hand in hand with the notion that cannabis is both stronger and more widespread than has been the case for decades.
Research indicates that early cannabis use puts users at greater risk of a psychotic illness later on in life, more so than more adult users [13]. Typically, people with a predisposition towards psychotic illnesses are affected far more profoundly than those without, although even those who are at little risk of developing a psychotic illness are still more at risk than had they not consumed cannabis [14]; it has been found that patients with previous cannabis abuse had significantly more rehospitalizations, tended to worse psychosocial functioning and were more hostile and generally disturbed [15].
Concerns over the safety of cannabis are not new. In 1997 it was suggested that cannabis use could emphasise tendencies towards psychotic and affective illnesses by W. Hall and N. Solowij [16]. Now there are suggestions that in a small number of cases Cannabis is capable of precipitating psychosis [17] in a characteristic manner [18] where there has been no history of psychological illness, personally or family. Then the suggestions that cannabis caused schizophrenia in certain cases especially in young people poorly able to cope with stress [19] started to flow.
Cannabis as a drug is now more concentrated than it was when research started and as such results obtained early on in research are now skewed. A review by the British Lung Association said that cannabis available now was approximately fifteen times more powerful than cannabis available three decades ago; in other words, less needs to be smoked to obtain the same effects.
There are problems, however, in determining whether these particular correlations are in fact links of causation. There are further difficulties in conducting research into the subject; patients may not confess to cannabis use for a variety of reasons, including fear of prosecution or fear of reaction or may not mention it, being under the assumption that it does not matter for one reason or another. Research into the field could be likened to structionalism, bearing many of the problems such as subjective bias; researchers essentially have to rely on reported symptoms and due to ethical reasons, experimentation on humans with a potentially harmful drug is out of the question.
Cannabis has, therefore, been linked to psychotic illnesses; however, correlation is not always causation and clearly more research is needed to detect any clear causal relationships between the two. So far, over thirty research projects have tackled the subject and as a result it is reasonably safe to say that there is a firm correlation between cannabis and psychosis.
[1] Carlson, Martin & Buskist, Psychology
[2] Rethink Organisation; Submission to the Advisory Council on the Misuse of Drugs, 2005
[3] Rethink Organisation; Submission to the Advisory Council on the Misuse of Drugs, 2005
[4] Heustis et al, 2001
[5] Andrew Johns, 2001, Psychiatric effects of cannabis, Br J Psychiatry, vol. 178, pp.116-122
[6] Rethink Organisation; Cannabis Overview 2005
[7] Rethink Organisation; Cannabis Overview 2005
[8] Rethink Organisation; Submission to the Advisory Council on the Misuse of Drugs, 2005
[9] Van Os et al, 2002
[10] Andréasson, S et al., LANCET, 1987, (ii), 1483-5
[11] Statistics Institute, Kings College London
[12] Rethink Organisation; Submission to the Advisory Council on the Misuse of Drugs, 2005
[13] Arsenault, L., Cannon, M., Poulton, R., Murray, R., Caspi, A., Moffit, T.E., 2002, Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study, British Medical Journal vol. 325, pp. 1212-1213
[14] Henquet C. et al, 2005, Prospective study of cannbis use, predisposition for psychosis, and psychotic symptoms in young people, British Meidcal Journal, vol 330, 1 Jan, pp 11-13
[15] Caspari D, Cannabis and Schizophrenia: Results of a follow-up Study Eur Arch Psychiatry Clin Neurosci 1999;249(1):45-9
[16] Hall W, Solowij N, Long-term Cannabis use and Mental Health 1997 British Journal of Psychiatry, August, 171:107-8
[17] Dr Brian Boettcher, Consultant Psychiatrist, Shelton Hospital
[18] Hall A, Degenhardt, Cannabis and Psychosis Australian National Drug and Alcohol Research Centre, Presented at The Inaugural International Cannabis and Psychosis Conference 1999 , Melbourne 16-17 February 1999
[19] van Amsterdam JG, van der Laan JW, Slangen JL, Cognitive and psychotic effects after cessation of chronic cannabis use Ned Tijdschr Geneeskd 1998 Mar 7;142(10):504-8
I was referring to Amsterdam, and that due to them not allowing tourists in the cafes, that the locals would be out selling it to the tourists instead, thereby increasing crime in their city.
