Acute (short-term) effects of cannabis
The acute toxicity of cannabis and the cannabinoids is very low; no-one has ever died as a direct
and immediate consequence of recreational or medical use (DH QQ 219223). Official statistics
record two deaths involving cannabis (and no other drug) in 1993, two in 1994 and one in 1995
(HC WA 533, 21 January 1998); but these were due to inhalation of vomit. Animal studies have shown
a very large separation (by a factor of more than 10,000) between pharmacologically effective
and lethal doses.
One minor toxic side-effect of taking cannabis which merits attention is the short-term effect
on the heart and vascular system. This can lead to significant increases in heart rate and a lowering
of the blood pressure (Pertwee Q 299). For this reason patients with a history of angina or other
cardiovascular disease could be at risk and should probably be excluded from any clinical trials
of cannabis-based medicines.
The most familiar short-term effect of cannabis is to give a "high" — a state of euphoric intoxication.
This is, of course, precisely the effect sought by the recreational user, analogous to the effect
of alcohol and sought for similar reasons. We have been told, however, that people who use cannabis
for medical purposes regard it as an unwelcome side-effect (Hodges Q 97).
Intoxication with cannabis leads to a slight impairment of psychomotor and cognitive function,
which is important for those driving a vehicle, flying an aircraft or operating machinery (DH
Q 197). The Department of Health rate this as "the major concern from a public health perspective"
raised by recreational use (p 46), and Professor Hall considers it the most serious possible short-term
consequence of cannabis use, both for the user and for the public.
There is some disagreement about how long such impairments persist after taking cannabis: most
assume that they last for only a few hours (e.g. Kendall p 266); but Professor Heather Ashton
of the University of Newcastle-upon-Tyne, principal author of the BMA report, suggested that subtle
cognitive impairments could persist for 24 or even 48 hours or more (Q 72), whereas the DETR say
"probably .... 24 hours at most" (Press Notice 94/Transport, 11 February 1998). On the other hand
the impairment in driving skills does not appear to be severe, even immediately after taking cannabis,
when subjects are tested in a driving simulator. This may be because people intoxicated by cannabis
appear to compensate for their impairment by taking fewer risks and driving more slowly, whereas
alcohol tends to encourage people to take greater risks and drive more aggressively.
Analysis of blood samples from road traffic fatalities in 1996-97 (the results of the first 15
months of a three year DETR study—Press Notice 94/Transport, 11 February 1998) showed that 8 per
cent of the victims were positive for cannabis, including 10 per cent of the victims who were
driving. However, it is not clear what figures would have been obtained from a random sample of
road users not involved in accidents (DH Q 211); and some of those who tested positive may have
taken the cannabis as much as 30 days before, so that the effects would have worn off long since
(DH p 240). The interpretation of traffic accident data is further confounded by the fact that
22 per cent of the drivers found to be cannabispositive also had evidence of alcohol intake;
proportions of alcoholpositives among cannabispositive drivers as high as 75 per cent have been
reported in other countries in similar studies. Professor Hall considers cannabis's contribution
to danger on the roads to be very small; in his view the major effect of cannabis use on driving
may be in amplifying the impairments caused by alcohol (cp Keen Q 42). According to a survey of
1,333 regular cannabis users by the Independent Drug Monitoring Unit (IDMU) in 1994, users who
drove reported a level of accidents no higher than the general population; those with the highest
accident rates were more likely to be heavier poly-drug users.
It is difficult to see how cannabis intoxication could be monitored, if its use were permitted.
There could be no equivalent of the breathalyser for alcohol, since small amounts of cannabis
continue to be released from fat into the blood long after any short-term impairment has worn
off.
A single dose of cannabis for an inexperienced user, or an overdose for an habitual user, can
sometimes induce a variety of intensely unpleasant psychic effects including anxiety, panic, paranoia
and feelings of impending doom (BMA p 9, RCPsych p 282). These adverse reactions are sometimes
referred to as a "whitey" as the subject may become unusually pallid (Montgomery Q 577). These
effects usually persist for only a few hours.
In some instances cannabis use may lead to a longer-lasting toxic psychosis involving delusions
and hallucinations that can be misdiagnosed as schizophrenic illness (Strang Q 239, van der Laan
Q 512). This is transient and clears up within a few days on termination of drug use; but the
habitual user risks developing a more persistent psychosis, and potentially serious consequences
(such as action under the Mental Health Acts and complications resulting from the administration
of powerful neuroleptic drugs) may follow if an erroneous diagnosis of schizophrenia is made.
It is also well established that cannabis can exacerbate the symptoms of those already suffering
from schizophrenic illness (Q 239) and may worsen the course of the illness; but there is little
evidence that cannabis use can precipitate schizophrenia or other mental illness in those not
already predisposed to it (RCPsych p 283).
These relatively rare adverse psychological effects of cannabis are not considered to represent
a serious limitation on the potential medical use of the drug (Strang Q 244), save that patients
suffering from schizophrenic illness or other psychoses should be excluded. However they do constitute
an issue for public health. According to the Department of Health, cannabis contributes to the
extra cost of acute psychiatric services imposed by drug misuse, though this cannot be separately
costed (p 46; cp RCPsych p 282). The Royal College of Psychiatrists believe that the proportion
of users who experience acute adverse mental effects is "significant".
Chronic (long-term) toxicity
Cannabis can have untoward long-term effects on cognitive performance, i.e. the performance of
the brain, particularly in heavy users. These have been reviewed for us by the Royal College of
Psychiatrists and the Royal Society. While users may show little or no impairment in simple tests
of short-term memory, they show significant impairments in tasks that require more complex manipulation
of learned material (so-called "executive" brain functions) (Edwards Q 21). There is some evidence
that some impairment in complex cognitive function may persist even after cannabis use is discontinued[10];
but such residual deficits if present are small, and their presence controversial (van Amsterdam
Q 494, Hall Q 741). Dr Jan van Amsterdam of the Netherlands National Institute of Public Health
and the Environment, who has reviewed the literature on long-term cognitive effects of prolonged
heavy use and kindly came to Westminster to tell us his findings, pointed out the practical difficulties
of assessing possible residual effects (Q 487). These include the impossibility of obtaining predrug
baseline values (i.e. measures of the cognitive functioning of the subject before their first
use of cannabis), the difficulty of estimating the drug dose taken, the need for a lengthy "washout"
period after termination of use to allow for the slow elimination of residual cannabis from the
body, and the possibility of confusing long-term deficits with withdrawal effects. He felt that
many of the published reports on this subject had not taken adequate account of these problems.
The occurrence of an "amotivational syndrome" in long-term heavy cannabis users, with loss of
energy and the will to work, has been postulated. However it is now generally discounted (van
Amsterdam Q 503); it is thought to represent nothing more than ongoing intoxication in frequent
users of the drug (RCPsych p 283).
Animal experiments have shown that cannabinoids cause alterations in both male and female sexual
hormones; but there is no evidence that cannabis adversely affects human fertility, or that it
causes chromosomal or genetic damage (WHO report ch.7). The consumption of cannabis by pregnant
women may, however, lead to significantly shorter gestation and lower birth-weight babies in mothers
smoking cannabis six or more times a week (WHO report ch.8; DH p 47). These effects may be due
to the inhalation of carbon monoxide in cannabis smoke, which lowers the ability of the blood
to carry oxygen to the foetus, rather to any direct effect of cannabinoids. If so, they are comparable
with the effects of smoking tobacco.
The NHS National Teratology [i.e. foetal abnormality] Information Service advise, "There are a
few case reports of malformations following marijuana use in pregnancy. However, there is no conclusive
evidence to suggest either an increase in the overall malformation rate or any specific pattern
of malformations". Nevertheless, they warn: "We would not recommend the legalisation of cannabis
because of the potential fetotoxicity that may occur if it is used in pregnancy".
Extract from: House
of Lords Science & Technology Committee - Ninth Report
Cannabis: The Scientific and Medical Evidence (November 1998)
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