Cannabis -
(Wiki)
“Cannabis is
not risk free. We have known for years that using cannabis
makes the symptoms of schizophrenia far worse in people who
already have the illness. There is a rapidly growing body
of evidence showing that cannabis can trigger schizophrenia
in people already at risk – and probably even in people who
should only be low risk.” -- Matt Prior, Rethink
Organisation
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withdrawn and deluded as to the state of the real world.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