The health and psychological consequences of cannabis use

National Drug Strategy
Monograph Series No. 25

9. An overall appraisal of the health and psychological effects of

9.1 Summary 

The following is a summary of the major adverse health and
psychological effects of acute and chronic cannabis use, grouped
according to the degree of confidence in the view that the
relationship between cannabis use and the adverse effect is a causal

9.1.1 Acute effects 

The major acute psychological and health effects of cannabis
intoxication are:

        anxiety, dysphoria, panic and paranoia, especially in naive

        cognitive impairment, especially of attention and memory for the
        duration of intoxication; 

        psychomotor impairment, and probably an increased risk of
        accidental injury or death if an intoxicated person attempts to drive
        a motor vehicle or operate machinery; 

        an increased risk of experiencing psychotic symptoms among those
        who are vulnerable because of a personal or family history of
        psychosis; and

        an increased risk of low birth weight babies if cannabis is used
        during pregnancy.

9.1.2 Chronic effects

The major health and psychological effects of chronic cannabis use,
especially daily use over many years, remain uncertain. On the
available evidence, the major probable adverse effects appear to be:

        respiratory diseases associated with smoking as the method of
        administration, such as chronic bronchitis, and the occurrence of
        histopathological changes that are precursors to the development of

        development of a cannabis dependence syndrome, characterised by
        an inability to abstain from or to control cannabis use; and

        subtle forms of cognitive impairment, most particularly of
        attention and memory, which persist while the user remains chronically
        intoxicated, and may or may not be reversible after prolonged
        abstinence from cannabis.

The following are the major possible adverse effects of chronic, heavy
cannabis use which remain to be confirmed by controlled research:

        an increased risk of developing cancers of the aerodigestive
        tract, i.e. oral cavity, pharynx, and oesophagus;

        an increased risk of leukemia among offspring exposed in utero;

        a decline in occupational performance marked by underachievement
        in adults in occupations requiring high level cognitive skills, and
        impaired educational attainment in adolescents.

        birth defects occurring among children of women who used cannabis
        during their pregnancies.

9.1.3 High risk groups

A number of groups can be identified as being at increased risk of
experiencing some of these adverse effects. 


        Adolescents with a history of poor school performance may have
        their educational achievement further limited by the cognitive
        impairments produced by chronic intoxication with cannabis.

        Adolescents who initiate cannabis use in the early teens are at
        higher risk of progressing to heavy cannabis use and other illicit
        drug use, and to the development of dependence on cannabis.

Women of childbearing age

        Pregnant women who continue to smoke cannabis are probably at
        increased risk of giving birth to low birth weight babies, and perhaps
        of shortening their period of gestation.

        Women of childbearing age who continue to smoke cannabis at the
        time of conception or while pregnant possibly increase the risk of
        their children being born with birth defects. 

Persons with pre-existing diseases

Persons with a number of pre-existing diseases who smoke cannabis are
probably at an increased risk of precipitating or exacerbating
symptoms of their diseases. These include: 

        individuals with cardiovascular diseases, such as coronary artery
        disease, cerebrovascular disease and hypertension; 

        individuals with respiratory diseases, such as asthma,
        bronchitis, and emphysema; 

        individuals with schizophrenia, who are at increased risk of
        precipitating or of exacerbating schizophrenic symptoms; and

        individuals who are or have been dependent upon alcohol and other
        drugs, who are probably at an increased risk of developing dependence
        on cannabis.

9.1.4 A caveat

As has been stressed throughout this document, there is uncertainty
surrounding many of these summary statements about the adverse health
effects of acute, and especially chronic, cannabis use. To varying
degrees, these statements depend upon inferences from animal research,
laboratory studies, and clinical observations about the probable ill
effects. In some cases, the inferences depend upon arguments from what
is known about the adverse health effects of other drugs, such as
tobacco and alcohol. In very few cases are there sufficient studies
which provide the detailed evidence that epidemiologists would require
to make informed judgments about the health effects of cannabis; the
interpretation of what epidemiological evidence is available is
complicated by difficulties in quantifying degree of exposure to
cannabis, and in excluding alternative explanations (including other
drug use) of associations observed between cannabis use and adverse
health outcomes. These interpretative problems are especially obvious
in the case of many of the alleged psychological outcomes of cannabis
use in adolescence, since many of these putative "consequences" (e.g.
poor school performance, deviant behaviour) also antedate the use of
cannabis. Nevertheless, these statements provide the best available
basis for making societal decisions about what policies ought to be
adopted towards cannabis use.

9.2  Two special concerns

Two issues which have hitherto been ignored require brief discussion.
These are the possible health implications of: the storage of THC in
body tissue; and any increases in the average potency of cannabis
products (as indexed by THC content) that may have occurred in recent

9.2.1 Storage of THC    

There is good evidence that with repeated dosing of cannabis at
frequent intervals, THC can accumulate in fatty tissues in the human
body where it may remain for considerable periods of time (see above
pp34-35). Attitudes towards this fact are strongly coloured by the
perceiver's views about cannabis use: those who are opposed to its use
usually regard this as a cause for major concern; proponents of
cannabis use largely ignore it. There is no evidence to make a
confident judgment one way or the other. The storage of cannabinoids
would be serious cause for concern if THC were a highly toxic
substance which remained physiologically active while stored in body
fat. The evidence that THC is a highly toxic substance is weak,
although it does have a bewildering variety of biological effects
(Martin, 1986). Its degree of activity while stored has not been
investigated. One potential health implication of THC storage is that
the release of stored cannabinoids into blood may produce unexpected
symptoms of cannabis intoxication. The release of stored THC has been
suggested as an explanation of "flashback experiences" (e.g. Negrete,
1988; Thomas, 1993). Such experiences have been rarely reported by
cannabis users (e.g. Edwards, 1983), and even in these cases
interpretation of their significance is complicated by the fact that
those who have reported such experiences have typically used other
hallucinogenic drugs. Whatever the uncertainties about health
implications of THC storage, all potential users of cannabis should be
aware that it occurs.

9.2.2 Increases in the potency of cannabis 

Cohen (1986) has been credited (Mikuriya and Aldrich, 1988) with
initiating the recent claim that the existing medical literature on
the health effects of cannabis underestimates its adverse effects
because it was based upon research conducted on less potent forms of
marijuana (O.5 per cent to 1.0 per cent THC) than those that became
available in the USA in the past decade (3.5 per cent THC in
1985-1986). This claim has been repeated often in the popular and
scientific media, and supported by anecdotal evidence that samples
containing up to 40 per cent THC have been seized by the police. An
alleged "ten-fold" increase in potency has contributed to recent
concerns about the health effects of cannabis, because of the
assumption that increases in average potency necessarily mean
substantial increases in the health risks of cannabis use. In
Australia this concern has been recently raised by the discovery of
hydroponically cultivated clones of cannabis plants that produce high
levels of THC, and by reports of the importation of high THC producing
strains of cannabis from New Guinea. 

There are a number of points to be made about this issue. First, the
evidence for an increase in potency is not as clear as Cohen (1986)
claimed, or as it seems from the data reported by ElSohy and ElSohy
(1989). The inference that these data demonstrate that potency has
increased depends upon the assumption that the samples analysed are
representative of cannabis consumed. Mikuriya and Aldrich (1988), for
example, have contested this assumption. They cite the results of
chemical analyses conducted on cannabis samples in California during
the middle 1970s in which the average potency was well within the
ranges reported in samples seized by the US Drug Enforcement Agency in
the middle 1980s. They also argue that the analyses of the DEA samples
from the middle 1970s underestimated THC potency because the samples
were not properly stored, allowing their average THC content to be

Second, even if we allow that there probably has been a small increase
in the THC potency of cannabis products in the USA, there is at
present no evidence of a similar increase in Australia. There is good
evidence from police samples analysed in New Zealand over the past
decade that average potency has not increased there (Bedford, 1993).
Press reports of increased potency have often been misleading in that
they have been based upon individual samples of highly concentrated
cannabis extracts, such as hash oil, which have never had a major
share of the cannabis market.

Third, the use of average potency can be also be potentially
misleading, since the average ignores differences between cannabis
users in preferences for cannabis products of varying potency. There
probably has always been a market for more potent products among the
heavier, and hence, more THC-tolerant, cannabis users. Marijuana
probably remains the majority preference of cannabis users, although
this is an issue worthy of investigation.

Fourth, it is not obvious that more potent forms of cannabis
inevitably have more adverse effects on users' health than less potent
forms. Indeed, it is conceivable that increased potency may have
little or no adverse effect if users are able to titrate their dose to
achieve the desired state of intoxication, as some have argued they do
(e.g. Kleiman, 1992; Mikuyira and Aldrich, 1988). If users were able
to titrate their dose, the use of more potent cannabis products would
reduce the amount of cannabis material that was smoked, which would
marginally reduce the risks of developing respiratory diseases. 

Fifth, even if users do not titrate their dose of THC, (or if they do
so inefficiently), any increase in the average dose received would not
inevitably have an adverse impact on users' health. The effect would
depend upon the type of health effect in question, and the relative
experience of users. Higher average doses may produce an increase in
the risk of minor adverse psychological effects of acute use,
especially among naive users. This could be a desirable outcome if it
discouraged further experimentation with the drug. Among experienced
cannabis users, an increased average dose may increase the risks of
accidents among those who drive while intoxicated, especially if
combined with alcohol. Higher average doses may also increase the risk
of regular users developing dependence.

All considered then, it is far from established that the average THC
potency of cannabis products has substantially increased over recent
decades. If potency has increased, it is even less certain that the
average health risks of cannabis use have materially changed as a
consequence, since users may titrate their dose to achieve the desired
effects. Even if the users are inefficient in titrating their dose of
THC, it is far from certain that the probability of adverse health
effects will be thereby increased. Nevertheless, given these concerns
about THC potency, it would be preferable to conduct research on the
issue rather than to rely upon inferences about the likely effects of
increased cannabis potency. Studies of the ability of experienced
users to titrate their dose of THC would contribute to an evaluation
of this issue, as would the inclusion in sample surveys of questions
about the form and perceived potency of cannabis products used. 

9.3 A comparative appraisal of health risks: alcohol, tobacco and
cannabis use

The probable and possible adverse health and psychological effects of
cannabis need to be placed in comparative perspective to be fully
appreciated. A useful standard for such a comparison is what is known
about the health effects of alcohol and tobacco, two other widely used
psychoactive drugs. Cannabis shares with tobacco, smoking as the usual
route of administration, and resembles alcohol in being used for its
intoxicating and euphoriant effects.

Considerable care must be exercised in making such comparisons.
Firstly, the quantitative risks of tobacco and alcohol use are much
better known than the health risks of cannabis, since alcohol and
tobacco have been consumed by substantial proportions of the
population, and there have been 40 years of scientific studies of the
health consequences of their use. Cannabis, by contrast, has been much
less widely used, and for a shorter period, in Western society; it has
been primarily used by healthy young adults, and there have been few
studies of its adverse health effects. 

Secondly, the prevalence of use of alcohol and tobacco is much higher
than that of cannabis. For example, the proportions of the Australian
population who are at least weekly users of alcohol, tobacco and
cannabis are: 61 per cent, 29 per cent, (Department of Health, Housing
and Community Services, 1992), and 11 per cent (Donnelly and Hall,
1994) respectively. Any overall comparison of the health consequences
of the three drug types that was based upon existing patterns of use
would unfairly disadvantage alcohol and tobacco. Any attempt to adjust
for the differences in prevalence (e.g. by estimating the health
effects if the prevalence of cannabis use was the same as those for
alcohol and tobacco) would involve making controversial assumptions,
so no such attempt has been made.

The very different prevalence of use of alcohol, tobacco and cannabis,
and the fact that we know a great deal more about the adverse effects
of alcohol and tobacco use, precludes any quantitative comparison of
the current health consequences of these drugs. Nevertheless, a
qualitative comparison of the probable health risks of cannabis with
the known health risks of alcohol and tobacco serves the useful
purpose of reminding us of the risks we currently tolerate with our
favourite psychoactive drugs. 

In undertaking this qualitative comparison, we have avoided the
necessity to comprehensively review the vast literatures on the health
effects of alcohol and tobacco by using the following authorities as
the principal sources of evidence for our assertions about their
health risks: Anderson et al (1993); Holman et al's (1988) compendium
of the health effects of alcohol and tobacco; the Institute of
Medicine (1987); the International Agency for Research into Cancer
(1990); Roselle et al (1993); and the Royal College of Physicians

9.3.1 Acute effects

Alcohol. The major risks of acute cannabis use are similar to the
acute risks of alcohol intoxication in a number of respects. First,
both drugs produce psychomotor and cognitive impairment, especially of
memory and planning. The impairment produced by alcohol increases
risks of various kinds of accident, and the likelihood of engaging in
risky behaviour, such as dangerous driving, and unsafe sexual
practices. It remains to be determined whether cannabis intoxication
produces similar increases in accidental injury and death, although on
balance it probably does.

Second, there is good evidence that substantial doses of alcohol taken
during the first trimester of pregnancy can produce a foetal alcohol
syndrome. There is suggestive but far from conclusive evidence that
cannabis used during pregnancy may have similar adverse effects. 

Third, there is a major health risk of acute alcohol use that is not
shared with cannabis. In large doses alcohol can cause death by
asphyxiation, alcohol poisoning, cardiomyopathy and cardiac infarct.
There are no recorded cases of fatalities attributable to cannabis,
and the extrapolated lethal dose from animal studies cannot be
achieved by recreational users.

Tobacco. The major acute health risks that cannabis shares with
tobacco are the irritant effects of smoke upon the respiratory system,
and the stimulating effects of both THC and nicotine on the
cardiovascular system, both of which can be detrimental to persons
with cardiovascular disease.

9.3.2 Chronic effects

Alcohol. There are a number of risks of heavy chronic alcohol use,
some of which may be shared by chronic cannabis use. First, heavy use
of either drug increases the risk of developing a dependence syndrome
in which users experience difficulty in stopping or controlling their
use. There is strong evidence of such a syndrome in the case of
alcohol and reasonable evidence in the case of cannabis. A major
difference between the two is that it is uncertain whether a
withdrawal syndrome reliably occurs after dependent cannabis users
abruptly stop their cannabis use, whereas the abrupt cessation of
alcohol use in severely dependent drinkers produces a well defined
withdrawal syndrome which can be potentially fatal. 

Second, there is reasonable clinical evidence that the chronic heavy
use of alcohol can produce psychotic symptoms and psychoses in some
individuals. There is suggestive evidence that chronic heavy cannabis
use may produce a toxic psychosis, precipitate psychotic illnesses in
predisposed individuals, and exacerbate psychotic symptoms in
individuals with schizophrenia.

Third, there is good evidence that chronic heavy alcohol use can
indirectly cause brain injury - the Wernicke-Korsakov syndrome - with
symptoms of severe memory defect and an impaired ability to plan and
organise. With continued heavy drinking, and in the absence of vitamin
supplementation, this injury may produce severe irreversible cognitive
impairment. There is good reason for concluding that chronic cannabis
use does not produce cognitive impairment of comparable severity.
There is suggestive evidence that chronic cannabis use may produce
subtle defects in cognitive functioning, that may or may not be
reversible after abstinence. 

Fourth, there is reasonable evidence that chronic heavy alcohol use
produces impaired occupational performance in adults, and lowered
educational achievements in adolescents. There is suggestive evidence
that chronic heavy cannabis use produces similar, albeit more subtle
impairments in occupational and educational performance of adults. 

Fifth, there is good evidence that chronic, heavy alcohol use
increases the risk of premature mortality from accidents, suicide and
violence. There is no comparable evidence for chronic cannabis use,
although it is likely that dependent cannabis users who frequently
drive while intoxicated with cannabis increase their risk of
accidental injury or death.

Sixth, alcohol use has been accepted as a contributory cause of cancer
of the oropharangeal organs in men and women. There is suggestive
evidence that chronic cannabis smoking may also be a contributory
cause of cancers of the aerodigestive tract.

Tobacco. The major adverse health effects shared by chronic cannabis
and tobacco smokers are chronic respiratory diseases, such as chronic
bronchitis, and probably, cancers of the aerodigestive tract (i.e. the
mouth, tongue, throat, oesophagus, lungs). The increased risk of
cancer in the aerodigestive tract is a consequence of the shared route
of administration by smoking. It is possible that chronic cannabis
smoking also shares the cardiotoxic properties of tobacco smoking,
although this possibility remains to be investigated. 

It should be stressed that this section only describes the adverse
health effects of alcohol and tobacco for which there is some evidence
that chronic heavy cannabis use may also cause. It does not,
therefore, provide an exhaustive inventory of all the adverse health
effects of either chronic alcohol or tobacco use. Among the major
additional adverse health effects of chronic heavy alcohol use which
are not shared by cannabis are: liver cirrhosis, peripheral
neuropathy, and gastritis. 

9.4 Implications for harm reduction 

The simplest health advice to anyone who wishes to avoid the probable
acute and chronic adverse health effects of cannabis is to abstain
from using the drug. This advice is especially apt for persons with
any of the diseases (e.g. cardiovascular) or conditions (e.g.
pregnancy) which would make them more vulnerable to the adverse
effects of cannabis. 

Current cannabis users should be aware of the following risks of using
the drug. First, the risk of being involved in a motor vehicle
accident is likely to be increased when cannabis users drive while
intoxicated by cannabis. The combination of alcohol and cannabis
intoxication will substantially increase this risk. Second, the
chronic smoking of cannabis poses significant risks to the respiratory
system, apart from any specific effects of THC. Third, the respiratory
risks of cannabis smoking are amplified if deep inhalation and
breath-holding are used to maximise the absorption of THC in the
lungs. This technique greatly increases the delivery and retention of
particulate matter and tar. Fourth, daily or near daily use of
cannabis is to be avoided, as it has a high risk of producing


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