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The health and psychological consequences of cannabis use chapter 1

National Drug Strategy
Monograph Series No. 25

  1. Summary of report


    This review of the literature on the health and psychological effects
    of cannabis was undertaken at the initiative of the former Federal
    Justice Minister, Senator Michael Tate, who requested a review of
    knowledge relating to cannabis, to inform policy decisions. At Senator
    Tate's urging, a National Task Force on Cannabis was established on 25
    May 1992. The Task Force commissioned this review of the evidence on
    the health and psychological effects of cannabis use. A new and
    independent review was thought necessary because there has not been
    any major international review of the literature on the health and
    psychological effects of cannabis since 1981, when the Addiction
    Research Foundation and World Health Organization jointly reviewed the
    literature. The purpose of this review was to update the conclusions
    of earlier reviews in the light of research undertaken during the past

    Our approach to the literature

    Our review of the literature was not intended to be as comprehensive
    as the major review undertaken by the Addiction Research Foundation
    and the World Health Organization. The literature is too large, and
    the diversity of relevant disciplines represented in it beyond the
    expertise we had available for the task. Unavoidably, we have relied
    upon expert opinion in the areas that lie outside the authors'
    collective expertise which is primarily in areas of epidemiology,
    psychiatry, psychopharmacology, neurophysiology and neuropsychology.

    In order to minimise the effects of our lack of expertise in certain
    areas we have relied upon the consensus views expressed in the
    literature by experts in the relevant fields. When there has been
    controversy between the experts we have explicitly acknowledged areas
    of disagreement. We have checked our understanding and representation
    of these expert views by asking Australian and overseas researchers
    with expertise in the relevant fields to critically review what we
    have written.

    Our approach to assessing the health effects of cannabis

    The evaluation of the health hazards of any drug is difficult for a
    number of reasons. First, causal inferences about the effects of drugs
    on human health are difficult to make, especially when the interval
    between use and alleged ill effects is a long one. It takes time for
    adverse effects to develop and for research to identify such effects.

    Second, in making causal inferences there is a tension between the
    rigour and relevance of the evidence. The most rigorous evidence is
    provided by laboratory investigations using animals or in vitro
    preparations (e.g. cell preparations in a test tube) in which well
    controlled drug doses are related to precisely specified biological
    outcomes. The relevance of this evidence to human disease is
    uncertain, however, because many inferences have to be made in linking
    the occurrence of specific biological effects in laboratory animals to
    the likely effects of human use. Epidemiological studies of
    relationships between drug use and human disease are of greater
    relevance to the appraisal of the health risks of human drug use, but
    their relevance is purchased at the price of reduced rigour. Doses of
    illicit drugs over periods of years are difficult to quantify because
    of the varied dosages of blackmarket drugs and the stigma in admitting
    to illicit drug use. Interpretation is further complicated by
    correlations between cannabis use and alcohol, tobacco and other
    illicit drug use.

    Third, appraisals of the hazards of drug use are affected by the
    social approval of the drugs in question. The countercultural
    symbolism of cannabis use in the late 1960s has introduced an
    unavoidable sociopolitical dimension to the debate about the severity
    of its adverse health effects. Politically conservative opponents of
    cannabis use justify continued prohibition by citing evidence of the
    personal and social harms of cannabis use. When the evidence is
    uncertain they resolve uncertainty by assuming that the drug is unsafe
    until proven safe. Complementary behaviour is exhibited by proponents
    of cannabis use. Evidence of harm is discounted and uncertainties
    about the ill-effects of chronic cannabis use resolved by demanding
    better evidence, arguing that until such evidence is available
    individuals should be allowed to choose whether or not they use the

    Such evidential standards are rarely applied consistently. The
    politically conservative would reject a similar approach to the
    appraisal of the health hazards of industrial processes. Similarly,
    proponents of cannabis liberalisation rarely apply the principles used
    in their risk assessment of cannabis to the appraisal of the health
    effects of pharmaceutical drugs, industrial processes, and pesticides.
    To guard against such double evidential standards we will be as
    explicit as possible about the evidential standards we have used, and
    attempt to be as even-handed as we can in their application.

    Evidential desiderata

    The burden of proof concerns who bears the responsibility for making a
    case: those who make a claim of adverse health effects of cannabis, or
    those who doubt it. If the burden falls on those who claim that it is
    safe, uncertainty will be resolved by assuming that it is unsafe until
    proved otherwise; conversely, if the burden falls on those who claim
    that the drug is unsafe, then it will be assumed to be safe until
    proven otherwise.

    It is by no means agreed who bears the burden of proof in the debate
    about the health effects of cannabis use. Proponents of continued
    prohibition appeal to established practice, arguing that since the
    drug is illegal the burden of proof falls upon those who want to
    legalise it; opponents of existing policies argue that the burden of
    proof falls upon those who wish to use the criminal law to prevent
    adults from freely choosing to use a drug.

    We will vary the burden of proof depending upon the state of the
    evidence and argument. Once a prima facie case of harm has been made,
    positive evidence of safety is required rather than the simple absence
    of any evidence of ill effect. We will assume that a prima facie case
    has been made when there is either direct evidence that the drug has
    ill effects in humans or animals (e.g. from a case-control study), or
    there is a compelling argument that it could, e.g. since tobacco
    smoking causes lung cancer, and since cannabis and tobacco smoke are
    similar in their constituents, it is probable that heavy cannabis
    smoking also causes lung cancer.

    Standard of proof reflects the degree of confidence required in an
    inference that there is a causal connection between drug use and harm.
    In courts of law, the standard of proof demanded depends upon the
    seriousness of the offence at issue and the consequences of a verdict,
    with a higher standard of proof, "beyond reasonable doubt", being
    demanded in criminal cases, and the "balance of probabilities" being
    acceptable in civil cases. Scientists generally require something
    closer to the standard of "beyond reasonable doubt" than the balance
    of probabilities before they draw confident conclusions of harm.
    However, since there are few adverse health effects of cannabis use
    which meet this standard, we will indicate when the evidence permits
    an inference to be made on the balance of probabilities.

    The criteria for causal inference that we will use are standard ones.
    These are: (1) evidence that there is a relationship between cannabis
    use and a health outcome provided by one of the accepted types of
    research design (namely, case-control, cross-sectional, cohort, or
    experiment); (2) evidence provided by a statistical test or confidence
    interval that the relationship is unlikely to be due to chance; (3)
    good evidence that drug use precedes the adverse effect (e.g. from a
    cohort study); and (4) evidence either from experiment, or
    observational studies with statistical or other form of control, which
    makes it unlikely that the relationship is due to some other variable
    which is related to both cannabis use and the adverse health effect.

    In the trade-off between relevance and rigour, our preference will be
    for human evidence, both experimental and epidemiological, over animal
    and in vitro studies. In the absence of human evidence, in vitro and
    animal experiments will be regarded as raising a suspicion that drug
    use has an adverse effects on human health, with the degree of
    suspicion being in proportion to the number of such studies, the
    consistency of their results across different species and experimental
    preparations, and the degree of expert consensus on the
    trustworthiness of the inferences from effects in vitro and in vivo to
    adverse effects on human health under existing patterns of usage.

    Ideally, it would be desirable to quantify the magnitude of risk posed
    by cannabis use by estimating both the relative and attributable risks
    of specific health effects. However, since there is generally
    insufficient evidence to estimate these risks for many putative
    adverse effects of cannabis, the magnitude of a health risk posed by
    cannabis use will be qualitatively assessed by a comparison of its
    probable health effects with those of two other widely used
    recreational drugs, alcohol and tobacco. The motive for such a
    comparison is to minimise double standards in the appraisal of the
    health effects of cannabis use by providing some kind of common
    standard, however approximate, for making societal decisions about
    cannabis use.

    Cannabis the drug

    Cannabis is a generic name for a variety of preparations derived from
    the plant Cannabis sativa. A sticky resin which covers the flowering
    tops and upper leaves, most abundantly in the female plant, contains
    more than 60 cannabinoid substances. Laboratory research on animals
    and humans has demonstrated that the primary psychoactive constituent
    in cannabis is the cannabinoid, delta-9-tetrahydrocannabinol or THC.

    The cannabinoid receptor

    Cannabis resembles the opioid drugs in acting upon specific receptors
    in the brain. In this respect it differs from alcohol, cocaine and
    other illicit drugs which act by disrupting brain processes. The
    determination and characterisation of a specific cannabinoid receptor
    has made it possible to map its distribution in the brain, and to
    demonstrate that its well-known psychoactive effects are receptor
    mediated. Very recently an endogenous brain molecule has been
    discovered which binds to the cannabinoid receptor and mimics the
    action of cannabinoids. It has been called "anandamide", from the
    Sanskrit word for bliss. Its discovery promises to stimulate a great
    deal of research which will improve our understanding of the role
    played by a cannabinoid-like system of the brain, and elucidate the
    mechanism of action of cannabis.

    Forms of cannabis

    The concentration of THC varies between the three most common forms of
    cannabis: marijuana, hashish and hash oil. Marijuana is prepared from
    the dried flowering tops and leaves of the harvested plant. The
    potency of the marijuana depends upon the growing conditions, the
    genetic characteristics of the plant and the proportions of plant
    matter. The flowering tops and bracts are highest in THC
    concentration, with potency descending through the upper leaves, lower
    leaves, stems and seeds. The concentration of THC in a batch of
    marijuana containing mostly leaves and stems may range from 0.5-5 per
    cent, while the "sinsemilla" variety with "heads" may have THC
    concentrations of 7-14 per cent.

    Hashish or hash consists of dried cannabis resin and compressed
    flowers. The concentration of THC in hashish generally ranges from 2-8
    per cent, although it can be as high as 10-20 per cent. Hash oil is a
    highly potent and viscous substance obtained by extracting THC from
    hashish (or marijuana) with an organic solvent, concentrating the
    filtered extract, and in some cases subjecting it to further
    purification. The concentration of the THC in hash oil is generally
    between 15 per cent and 50 per cent.

    Routes of administration

    Almost all possible routes of administration have been used, but by
    far the most common method is smoking (inhaling). Marijuana is most
    often smoked as a hand-rolled "joint", the size of a cigarette or
    larger. Tobacco is often added to assist burning, and a filter is
    sometimes inserted. Hashish may also be mixed with tobacco and smoked
    as a joint, but it is probably more frequently smoked through a pipe,
    with or without tobacco. A water pipe known as a "bong" is a popular
    implement for all cannabis preparations because the water cools the
    hot smoke before it is inhaled and there is little loss of the drug
    through sidestream smoke. Hash oil is used sparingly because of its
    extremely high psychoactive potency; a few drops may be applied to a
    cigarette or a joint, to the mixture in the pipe, or the oil may be
    heated and the vapours inhaled. Whatever method is used, smokers
    inhale deeply and hold their breath for several seconds in order to
    ensure maximum absorption of THC by the lungs.

    Hashish may also be cooked or baked in foods and eaten. When ingested
    orally the onset of the psychoactive effects is delayed by about an
    hour. The "high" may be of lesser intensity but the duration of
    intoxication is longer by several hours. It is easier to titrate the
    dose and achieve the desired level of intoxication by smoking than by
    ingestion, since the effects from smoking are more immediate. Crude
    aqueous extracts of cannabis have been very rarely injected
    intravenously, but this route is unpopular since THC is insoluble in
    water, and hence, little or no drug is actually present in these
    extracts. Moreover, the injection of tiny undissolved particles may
    cause severe pain and inflammation at the site of injection, and a
    variety of toxic systemic effects.


    A typical joint contains between 0.5g and 1.0g of cannabis plant
    matter, which may vary in THC content between 5mg and 150mg (i.e.
    typically between 1 per cent and 15 per cent). The actual amount of
    THC delivered in the smoke has been estimated at 20-70 per cent, the
    rest being lost through combustion or sidestream smoke. The
    bioavailability of THC (the fraction of THC in the cigarette which
    reaches the bloodstream) from marijuana cigarettes in human subjects
    has been reported to range from 5-24 per cent. Given all of these
    variables, the actual dose of THC absorbed when cannabis is smoked is
    not easily quantified.

    In general, only a small amount of cannabis (e.g. 2-3mg of available
    THC) is required to produce a brief pleasurable high for the
    occasional user, and a single joint may be sufficient for two or three
    individuals. A heavy smoker may consume five or more joints per day,
    while heavy users in Jamaica, for example, may consume up to 420mg THC
    per day. In clinical trials designed to assess the therapeutic
    potential of THC, single doses have ranged up to 20mg in capsule form.
    In human experimental research, THC doses of 10mg, 20mg and 25mg have
    been administered as low, medium and high doses.

    Patterns of use

    Cannabis is the most widely used illicit drug in Australia, having
    been tried by a third of the adult population, and by the majority of
    young adults between the ages of 18 and 25. The most common route of
    administration is by smoking, and the most widely used form of the
    drug is marijuana. In the majority of cases cannabis use is
    "experimental", that is, most users use the drug on a small number of
    occasions, and either discontinue their use, or use intermittently and
    episodically after first trying it. Even among those who continue to
    use the drug over longer periods, the majority discontinue their use
    in their mid to late 20s.

    Only a small proportion of those who ever use cannabis use it on a
    daily basis over an extended period such as several years. Because of
    uncertainties about the dose received, there is no good information on
    the amount of THC ingested by such regular users. "Heavy" use is
    consequently defined approximately in terms of frequency of use rather
    than the estimated average dose of THC received. The daily or near
    daily use pattern over a period of years is the pattern that probably
    places cannabis users at greatest risk of experiencing long-term
    health and psychological consequences of use. Daily cannabis users are
    more likely to be male and less well educated; they are also more
    likely to regularly use alcohol and to have experimented with a
    variety of other illicit drugs, such as, amphetamines, hallucinogens,
    psychostimulants, sedatives and opioids.

    Metabolism of cannabinoids

    Different methods of ingesting cannabis give rise to differing
    pharmacokinetics, i.e. patterns of absorption, metabolism and
    excretion of the active agent. Upon inhalation, THC is absorbed from
    the lungs into the bloodstream within minutes. After oral
    administration absorption is much slower, taking one to three hours
    for THC to enter the bloodstream, and delaying the onset of
    psychoactive effects. When cannabis is smoked, the initial metabolism
    of THC takes place in the lungs, followed by more extensive metabolism
    by liver enzymes, with the transformation of THC to a number of
    metabolites. The most rapidly produced metabolite is 9-carboxy-THC,
    which is detectable in blood within minutes of smoking. Another major
    metabolite produced is 11-hydroxy-THC, which is approximately 20 per
    cent more potent than THC, and penetrates the blood-brain barrier more
    rapidly. It is present at very low concentrations in the blood after
    smoking, but at high concentrations after the oral route. THC and its
    hydroxylated metabolites account for most of the observed effects of
    the cannabinoids.

    Peak blood levels of THC are usually reached within 10 minutes of
    smoking, and decline rapidly thereafter to about 5-10 per cent of
    their initial level within the first hour. This initial rapid decline
    reflects both rapid conversion to its metabolites, as well as the
    distribution of unchanged THC to lipid-rich tissues, including perhaps
    the brain.

    THC and its metabolites are highly fat soluble and may remain for long
    periods in the fatty tissues of the body, from which they are slowly
    released back into the bloodstream. The terminal half-life of THC (the
    time required to clear half of the administered dose from the body) is
    significantly shorter for experienced or daily users (19-27 hours)
    than for inexperienced users (50-57 hours). Since tissue distribution
    is similar for both users and non-users, it is the immediate and
    subsequent metabolism that occurs more rapidly in experienced users.
    Given the slow clearance of THC, repeated administration results in
    the accumulation of THC and its metabolites in the body. Because of
    its slow release from fatty tissues back into the bloodstream, THC and
    its metabolites may be detectable in blood for several days, and
    traces may persist for several weeks. Several studies have examined
    measures of cannabinoids in fat, confirming that THC may be stored for
    at least 28 days.

    Detection of cannabinoids in body fluids

    Cannabinoid levels in the body depend on both the dose given and the
    smoking history of the individual, but are subject to a vast degree of
    individual variability. Plasma levels of THC in man may range between
    0-500ng/ml, depending on the potency of the cannabis ingested and the
    time since smoking. The detection of THC in blood above 10-15ng/ml
    provides evidence of recent consumption of the drug, although how
    recent is not possible to determine. A more precise estimate of time
    of consumption may be obtained from the ratio of THC to 9-carboxy-THC:
    similar concentrations of both in blood indicate very recent use (in
    the vicinity of 20-40 minutes) and a high probability of intoxication.
    When the levels of 9-carboxy-THC are substantially higher than those
    of THC itself, ingestion could be estimated to have occurred more than
    half an hour ago. It is very difficult to determine the time of
    administration from blood concentrations even if the smoking habits of
    the individual and the exact dose consumed were known. Therefore, the
    results of blood analyses are not easily interpreted and, at best,
    only confirm the "recent" use of cannabis.

    Intoxication and levels of cannabinoids

    Since there is evidence that cannabis intoxication adversely affects
    skills required to drive a motor vehicle (see below), it would be
    desirable to have a reliable measure of impairment due to cannabis
    intoxication that was comparable to the breath test of alcohol
    intoxication. However, there is no clear relationship between blood
    levels of THC or its metabolites and degree of either impairment or
    subjective intoxication. A general consensus of forensic toxicologists
    is that blood concentrations associated with impairment after smoking
    cannabis have not been sufficiently established to provide a basis for
    legal testimony in cases concerning driving a motor vehicle while
    under the influence of cannabis.

    Acute psychological and health effects

    The major reason for the widespread recreational use of cannabis is
    that it produces a "high", an altered state of consciousness which is
    characterised by mild euphoria, relaxation, and perceptual
    alterations, including time distortion and the intensification of
    ordinary sensory experiences, such as eating, watching films, and
    listening to music. When used in a social setting the high is often
    accompanied by infectious laughter, and talkativeness. Cognitive
    effects are also marked. They include impaired short-term memory, and
    a loosening of associations, which make it possible for the user to
    become lost in pleasant reverie and fantasy. Motor skills and reaction
    time are also impaired, so skilled activity of various kinds is
    frequently disrupted.

    Not all the acute psychological effects of cannabis are welcomed by
    users. The most common unpleasant psychological effects are anxiety,
    sometimes producing frank panic reactions, or a fear of going mad, and
    dysphoric or unpleasant depressive feelings. Psychotic symptoms such
    as delusions and hallucinations may be more rarely experienced at very
    high doses. These effects are most often reported by naive users who
    are unfamiliar with the drug's effects, and by patients who have been
    given oral THC for therapeutic purposes. More experienced users may
    occasionally report these effects after oral ingestion of cannabis,
    when the effects may be more pronounced and of longer duration than
    those usually experienced after smoking cannabis. These effects can
    usually be prevented by adequately informing users about the type of
    effects they may experience, and once developed can be readily managed
    by reassurance and support.

    The inhalation of marijuana smoke, or the ingestion of THC has a
    number of bodily effects. Among these the most dependable is an
    increase in heart rate of 20-50 per cent over baseline, which occurs
    within a few minutes to a quarter of an hour, and lasts for up to
    three hours. Changes in blood pressure also occur, which depend upon
    posture: blood pressure is increased while the person is sitting, and
    decreases while standing. In healthy young users these cardiovascular
    effects are unlikely to be of any clinical significance because
    tolerance develops to the effects of THC, and young, healthy hearts
    will only be mildly stressed.

    The acute toxicity of cannabis, and cannabinoids more generally, is
    very low. There are no confirmed cases of human deaths from cannabis
    poisoning in the world medical literature. This is unlikely to be due
    to a failure to detect such deaths, because animal studies indicate
    that the dose of THC required to produce 50 per cent mortality in
    rodents is extremely high by comparison with other commonly used
    pharmaceutical and recreational drugs. The lethal dose also increases
    as one moves up the phylogenetic tree, suggesting by extrapolation
    that the lethal dose in humans could not be achieved by either smoking
    or ingesting the drug.

    Psychomotor effects and driving

    The major potential health risk from the acute use of cannabis arises
    from its effects on psychomotor performance. Intoxication produces
    dose-related impairments in a wide range of cognitive and behavioural
    functions that are involved in skilled performances like driving an
    automobile or operating machinery. The negative effects of cannabis on
    the performance of psychomotor tasks is almost always related to dose.
    The effects are generally larger, more consistent and of increased
    persistence in difficult tasks which involve sustained attention. The
    acute effects of doses of cannabis which are subjectively equivalent
    to or higher than usual recreational doses on driving performance in
    laboratory simulators and over standardised driving courses, are
    similar to those of doses of alcohol that achieve blood alchol
    concentrations between 0.07 per cent and 0.10 per cent.

    While cannabis impairs performance in laboratory and simulated driving
    settings, it is difficult to relate the magnitude of these impairments
    to the risk of being involved in motor vehicle accidents. Studies of
    the effects of cannabis on on-road driving performance have found at
    most modest impairments. Cannabis intoxicated persons drive more
    slowly, and generally take fewer risks, than alcohol intoxicated
    drinkers, probably because they are more aware of their level of
    psychomotor impairment.

    There is no controlled epidemiological evidence that cannabis users
    are at increased risk of being involved in motor vehicle or other
    accidents. This is in contrast to the case of alcohol use and
    accidents, where case-control studies have shown that persons with
    blood alcohol levels indicative of intoxication are over-represented
    among accident victims. All that is available are studies of the
    prevalence of cannabinoids in the blood of motor vehicle and other
    accident victims, which have found that between 4 per cent and 37 per
    cent of such blood samples have contained cannabinoids, typically in
    association with blood alcohol levels indicative of intoxication.
    These studies are difficult to evaluate for a number of reasons.

    First, in the absence of information on the prevalence of cannabinoids
    in the blood of non-accident victims, we do not know whether persons
    with cannabinoids are over-represented among accident victims. Second,
    the presence of cannabinoids in blood indicates only recent use, not
    necessarily intoxication at the time of the accident. Third, there are
    also serious problems of causal attribution, since more than 75 per
    cent of drivers with cannabinoids in their blood also have blood
    levels indicative of alcohol intoxication.

    Attempts have been made to circumvent the first difficulty by using
    NIDA Household survey data (from the United States) to estimate what
    proportion of drivers might be expected to have cannabinoids in their
    blood and urine. These suggest that cannabis users are two to four
    times more likely to be represented among accident victims than
    non-cannabis users; cannabis users who also use alcohol, rather than
    cannabis only users, are even more likely to be over-represented among
    accident victims. Other indirect support for an increased risk of
    accidental death associated with cannabis use comes from surveys of
    self-reported accidents among adolescent drug users, and from
    epidemiological studies of the relationships between cannabis use and
    mortality, and health service utilisation.

    The known effects of interactions between cannabis and other drugs on
    psychomotor performance are what would be predicted from their
    separate effects. The drug most often used in combination with
    cannabis is alcohol. The separate effects of alcohol and cannabis on
    psychomotor impairment and driving performance are approximately

    The effects of chronic cannabis use

    Cellular effects and the immune system

    There is reasonably consistent evidence that some cannabinoids, most
    especially THC, can produce a variety of cellular changes, such as
    alterations to cell metabolism, and DNA synthesis, in vitro (i.e. in
    the test tube). There is stronger and more consistent evidence that
    cannabis smoke is mutagenic in vitro, and in vivo (i.e. in live
    animals), and hence, that it is potentially carcinogenic. If cannabis
    smoke is carcinogenic then it is probably for the same reasons that
    cigarette smoke is, rather than because it contains cannabinoids.
    Hence, if chronic cannabis smoking causes cancer, it is most likely to
    develop after long-term exposure at those sites which receive maximum
    exposure, namely, the lung and upper aerodigestive tract (see below).

    There is reasonably consistent evidence that cannabinoids impair both
    the cell-mediated and humoral immune systems in rodents. Humoral
    immune suppression is seen in decreased antibody formation responses
    to antigens, and decreased lymphocyte response to B-cell mitogens.
    Cell-mediated immune suppression is revealed by a reduction in
    lymphocyte response to T-cell mitogens. These changes have produced
    decreased resistance to infection by a bacteria and a virus. There is
    also evidence that the non-cannabinoid components of cannabis smoke
    impair the functioning of alveolar macrophages, the first line of the
    body's defence system in the lungs. The clinical relevance of these
    findings is uncertain, however. The doses required to produce these
    effects have generally been very high, and the problem of
    extrapolating to the effects of doses used by humans is complicated by
    the possibility that tolerance may also develop to such effects.

    The limited experimental and clinical evidence in humans is mixed,
    with a small number of studies suggesting adverse effects that have
    not been replicated by others. At present, there is no conclusive
    evidence that consumption of cannabinoids predisposes man to immune
    dysfunction, as measured by reduced numbers or impaired functioning of
    T-lymphocytes, B-lymphocytes or macrophages, or reduced immunoglobulin
    levels. There is suggestive evidence that THC impairs T-lymphocyte
    responses to mitogens and allogenic lymphocytes.

    The clinical and biological significance of these possible
    immunological impairments in chronic cannabis users is uncertain. To
    date there has been no epidemiological, or even anecdotal, evidence of
    increased rates of disease among chronic heavy cannabis users, such as
    was seen among young homosexual men in the early 1980s when the
    Acquired Immune Deficiency Syndrome was first recognised. There is one
    large prospective study of HIV-positive homosexual men which indicates
    that continued cannabis use did not increase the risk of progression
    to AIDS. Given the duration of large-scale cannabis use by young
    adults in Western societies, the absence of any epidemics of
    infectious disease makes it unlikely that cannabis smoking produces
    major impairments in the immune system.

    It is more difficult to exclude the possibility that chronic heavy
    cannabis use produces a minor impairment in immunity. Such an effect
    would be manifest in small increases in the rate of occurrence of
    common bacterial and viral illnesses among chronic users which could
    have escaped detection in the few studies that have attempted to
    address the issue. Such an increase could nonetheless be of public
    health significance because of the increased expenditure on health
    services, and the loss of productivity that it would cause among the
    young adults who are the heaviest users of cannabis.

    The possibility that cannabinoids may produce minor impairments in the
    immune system would also raise doubts about the therapeutic usefulness
    of cannabinoids in immunologically compromised patients, such as those
    undergoing cancer chemotherapy, or those with AIDS. AIDS patients may
    provide one of the best populations in which to detect any such
    effects. If it was ethical to conduct clinical trials of cannabinoids
    to improve appetite and well-being in AIDS patients, then studies of
    the impact of cannabis use on their compromised immune systems would
    provide one way of evaluating the seriousness of this concern.

    The cardiovascular system

    There is insufficient new evidence to change the conclusions reached
    by the Institute of Medicine in 1982, namely, that although the
    smoking of marijuana "causes changes to the heart and circulation that
    are characteristic of stress ... there is no evidence ... that it
    exerts a permanently deleterious effect on the normal cardiovascular
    system..." (p72). The situation may be less benign for patients with
    hypertension, cerebrovascular disease and coronary atherosclerosis, in
    which case there is evidence that marijuana poses a threat because it
    increases the work of the heart. The "magnitude and incidence" of the
    threat remains to be determined as the cohort of chronic cannabis
    users of the late 1960s enters the age of maximum risk for
    complications of atherosclerosis in the heart, brain and peripheral
    blood vessels. In the interim, because any such effects could be life
    threatening in patients with significant occlusion of the coronary
    arteries or other cerebrovascular disease, patients with
    cardiovascular disease should be advised not to consume cannabis, and
    perhaps not to use THC therapeutically.

    The respiratory system

    Chronic heavy cannabis smoking impairs the functioning of the large
    airways, and probably causes symptoms of chronic bronchitis such as
    coughing, sputum production, and wheezing. Given the adverse effects
    of tobacco smoke, which is qualitatively very similar in composition
    to cannabis smoke, it is likely that chronic cannabis use predisposes
    individuals to develop chronic bronchitis and respiratory cancer.
    There is reasonable evidence for an increased risk of chronic
    bronchitis, and evidence that chronic cannabis smoking may produce
    histopathological changes in lung tissues of the kind that precede the
    development of lung cancer.

    More recently, concern about the possibility of cancers being induced
    by chronic cannabis smoking has been heightened by case reports of
    cancers of the aerodigestive tract in young adults with a history of
    heavy cannabis use. Although these reports fall short of providing
    convincing evidence because many of the cases concurrently used
    alcohol and tobacco, they are clearly a major cause for concern, since
    such cancers are usually rare in adults under the age of 60, even
    among those who smoke tobacco and drink alcohol. The conduct of
    case-control studies of these cancers should be a high priority for
    research which aims to identify the possible adverse health effects of
    chronic cannabis use.

    Reproductive effects

    Chronic cannabis use probably disrupts the male and female
    reproductive systems in animals, reducing testosterone secretion, and
    sperm production, motility, and viability in males, and disrupting the
    ovulatory cycle in females. It is uncertain whether it is likely to
    have these effects in humans, given the inconsistency in the limited
    literature on human males, and the lack of research in the case of
    human females. There is also uncertainty about the clinical
    significance of these effects in normal healthy young adults. They may
    be of greater concern among young adolescents, and among males with
    fertility impaired for other reasons.

    Cannabis use during pregnancy probably impairs foetal development,
    leading to smaller birthweight, perhaps as a consequence of shorter
    gestation, and probably by the same mechanism as cigarette smoking,
    namely, foetal hypoxia. There is uncertainty about whether cannabis
    use during pregnancy produces a small increase in the risk of birth
    defects as a result of exposure of the foetus in utero. Prudence
    demands that until this issue is resolved, women should be advised not
    to use cannabis during pregnancy, or when attempting to conceive.

    There is not a great deal of evidence that cannabis use can produce
    chromosomal or genetic abnormalities in either parent which could be
    transmitted to offspring. Such animal and in vitro evidence as exists
    suggests that the mutagenic capacities of cannabis smoke are greater
    than those of THC, and are probably of greater relevance to the risk
    of users developing cancer than to the transmission of genetic defects
    to children.

    There is suggestive evidence that infants exposed in utero to cannabis
    may experience transient behavioural and developmental effects during
    the first few months after birth. There is a single study which
    suggests an increased risk of childhood leukemia occurring among the
    children born to women who used cannabis during their pregnancies. Its
    replication is of some urgency.

    Psychological effects of chronic cannabis use

    Adolescent development

    There is strong continuity of development from adolescence into early
    adult life in which many indicators of adverse development which have
    been attributed to cannabis use precede its use, and increase the
    likelihood of using cannabis. These include minor delinquency, poor
    educational performance, nonconformity, and poor adjustment. A
    predictable sequence of initiation into the use of illicit drugs was
    identified among American adolescents in the 1970s, in which the use
    of licit drugs preceded experimentation with cannabis, which preceded
    the use of hallucinogens and "pills", which in turn preceded the use
    of heroin and cocaine. Generally, the earlier the age of initiation
    into drug use, and the greater the involvement with any drug in the
    sequence, the greater the likelihood of progression to the next drug
    in the sequence.

    The causal significance of these findings, and especially the role of
    cannabis in the sequence of illicit drug use, remains controversial.
    The hypothesis that the sequence of use represents a direct
    pharmacological effect of cannabis use upon the use of later drugs in
    the sequence is the least compelling. A more plausible and better
    supported explanation is that it reflects a combination of two
    processes: the selective recruitment into cannabis use of
    nonconforming and deviant adolescents who have a propensity to use
    illicit drugs; and the socialisation of cannabis users within an
    illicit drug using subculture which increases the exposure,
    opportunity, and encouragement to use other illicit drugs.

    Although strong conclusions cannot be drawn, on the evidence from
    cross-sectional and longitudinal studies of cohorts of American
    adolescents in the 1970s and 1980s, there are suggestions that chronic
    heavy cannabis use can adversely affect adolescent development in a
    number of ways.

    There has been suggestive support for the hypothesis that heavy
    adolescent use of cannabis impairs educational performance. In
    cross-sectional surveys, cannabis use is related to an increased risk
    of failing to complete a high school education, and of job instability
    in young adulthood. These relationships in cross-sectional studies are
    exaggerated because those who are most likely to use cannabis have
    lower pre-existing academic aspirations and high school performance
    than those who do not use it. When pre-existing academic aptitude and
    interest are taken into account, the relationship between cannabis use
    and educational and occupational performance is much more modest. Even
    though modest, the suggestive adverse effects of cannabis and other
    drug use upon educational performance are important because they may
    cascade throughout young adult life, affecting choice of occupation,
    level of income, choice of mate, and quality of life of the user and
    his or her children.

    There is weaker but suggestive evidence that heavy cannabis use has
    adverse effects upon family formation, mental health, and involvement
    in drug-related (but not other types of) crime. In the case of each of
    these outcomes, the apparently strong associations revealed in
    cross-sectional data are much more modest in longitudinal studies,
    after statistically controlling for associations between cannabis use
    and other variables which predict these adverse outcomes.

    On balance, there are sufficient indications that cannabis use in
    adolescence probably adversely affects adolescent development to
    conclude that it is desirable to discourage adolescent cannabis use,
    and especially regular cannabis use.

    Adult adjustment

    The evidence that chronic heavy cannabis use produces an amotivational
    syndrome among adults is equivocal. The positive evidence largely
    consists of case histories, and observational reports. The small
    number of controlled field and laboratory studies have not found
    compelling evidence for such a syndrome, although their evidential
    value is limited by the small sample sizes and limited
    sociodemographic characteristics of the field studies, and by the
    short periods of drug use, and the youthful good health and minimal
    demands made of the volunteers observed in the laboratory studies. If
    there is such a syndrome, it is a relatively rare occurrence, even
    among heavy, chronic cannabis users.

    A dependence syndrome

    A cannabis dependence syndrome like that defined in DSM-III-R probably
    occurs in heavy, chronic users of cannabis. There is good experimental
    evidence that chronic heavy cannabis users can develop tolerance to
    its subjective and cardiovascular effects, and there is suggestive
    evidence that some users may experience a withdrawal syndrome on the
    abrupt cessation of cannabis use. There is clinical and
    epidemiological evidence that some heavy cannabis users experience
    problems in controlling their cannabis use, and continue to use the
    drug despite experiencing adverse personal consequences of use. There
    is limited evidence in favour of a cannabis dependence syndrome
    analogous to the alcohol dependence syndrome. If the estimates of the
    community prevalence of drug dependence provided by the Epidemiologic
    Catchment Area study are correct, then cannabis dependence is the most
    common form of dependence on illicit drugs.

    Recognition of the cannabis dependence syndrome has been delayed by a
    number of factors. First, heavy daily cannabis use has been relatively
    uncommon, and there have been few individuals who have requested
    assistance in stopping their cannabis use. Second, an overemphasis on
    evidence of tolerance and a withdrawal syndrome has hindered the
    recognition of the syndrome among individuals who have presented for
    treatment. Third, the occurrence of cannabis dependence has probably
    been overshadowed because it is most common among persons who are
    dependent on alcohol and opioids, forms of drug dependence which have
    understandably been given higher treatment priority.

    Given the widespread use of cannabis, and its continued reputation as
    a drug free of the risk of dependence, the clinical features of
    cannabis dependence deserve to be better defined. This would enable
    the prevalence of a dependence syndrome to be better estimated and
    individuals who are dependent on cannabis to be better recognised and
    treated. Treatment should probably be on the same principles as other
    forms of dependence, although this issue is also in need of research.

    Although cannabis dependence is likely to be a larger problem than
    previously thought, we should be wary of over-estimating its social
    and public health importance. Estimates of the risk of users becoming
    dependent suggest that it may be similar to that of alcohol, that it
    will be highest among the minority of daily cannabis users, and that
    even in this group the prevalence of drug-related problems may be
    relatively low by comparison with those of alcohol dependence. There
    is likely to be a high rate of remission of cannabis dependence
    without formal treatment. While acknowledging the existence of the
    syndrome, we should avoid exaggerating its prevalence and the severity
    of its adverse effects on individuals. Better research on the
    experiences of long-term cannabis users should provide more precise
    estimates of the risk.

    Cognitive effects

    The weight of the available evidence suggests that the long-term heavy
    use of cannabis does not produce any severe impairment of cognitive
    function. There is reasonable clinical and experimental evidence,
    however, that the long-term use of cannabis may produce more subtle
    cognitive impairment in the higher cognitive functions of memory,
    attention and organisation and integration of complex information.
    While subtle, these impairments may affect everyday functioning,
    particularly in adolescents with marginal educational aptitude, and
    among adults in occupations that require high levels of cognitive
    capacity. The evidence suggests that the longer the period that
    cannabis has been used, the more pronounced is the cognitive
    impairment. It remains to be seen whether the impairment can be
    reversed by an extended period of abstinence from cannabis.

    There is a need for research to identify the specific cognitive
    functions affected by long-term cannabis use, to identify the precise
    mechanisms that produce impairment and to relate them to biological
    mechanisms, including the cannabinoid receptors and the endogenous
    cannabinoid, anandamide. Such research also needs to investigate
    individual differences in susceptibility to such effects, and the
    impact of long-term cannabis use on adolescents and young adults.
    Appropriate treatment programs for long-term dependent cannabis users
    will also need to address the subtle cognitive impairments likely to
    be found in this population.

    Brain damage

    A suspicion that chronic heavy cannabis use may cause gross structural
    brain damage was provoked by a single poorly controlled study using an
    outmoded method of investigation, which reported that cannabis users
    had enlarged cerebral ventricles. This finding was widely and
    uncritically publicised. Since then a number of better controlled
    studies using more sophisticated methods of investigation have
    consistently failed to demonstrate evidence of structural change in
    the brains of heavy, long-term cannabis users. These negative results
    are consistent with the evidence that any cognitive effects of chronic
    cannabis use are subtle, and hence unlikely to be manifest as gross
    structural changes in the brain. They do not exclude the possibility
    that chronic, heavy cannabis use may cause ultrastructural changes at
    the receptor level.

    Psychotic disorders

    There is suggestive evidence that heavy cannabis use can produce an
    acute toxic psychosis in which confusion, amnesia, delusions,
    hallucinations, anxiety, agitation and hypomanic symptoms predominate.
    The evidence for an acute toxic cannabis psychosis comes from
    laboratory studies of the effects of THC on normal volunteers and
    clinical observations of psychotic symptoms in heavy cannabis users
    which seem to resemble those of other toxic psychoses, and which remit
    rapidly following abstinence.

    There is less support for the hypothesis that cannabis use can cause
    either an acute or a chronic functional psychosis which persists
    beyond the period of intoxication. Such a possibility is difficult to
    study because of the rarity of such psychoses, and the near
    impossibility of distinguishing them from schizophrenia and manic
    depressive psychoses occurring in individuals who also abuse cannabis.

    There is strongly suggestive evidence that chronic cannabis use may
    precipitate a latent psychosis in vulnerable individuals. This is only
    strongly suggestive because in the best study conducted to date, the
    use of cannabis was not documented at the time of diagnosis, there was
    a possibility that cannabis use was confounded by amphetamine use, and
    there are doubts about whether the study could reliably distinguish
    between schizophrenia and acute cannabis-induced, or other
    drug-induced, psychoses. Even if this relationship is causal, its
    public health significance should not be overstated: the estimated
    attributable risk of cannabis use is small (less than 10 per cent),
    and even this seems an overestimate, since the incidence of
    schizophrenia declined over the period when cannabis use increased
    among young adults.

    Therapeutic effects of cannabinoids

    There is reasonable evidence that THC is an effective anti-emetic
    agent for patients undergoing cancer chemotherapy, especially those
    whose nausea has proven resistant to the anti-emetic drugs that were
    widely used in the late 1970s and early 1980s, when most of the
    research was conducted. It is uncertain whether THC is as effective as
    newer anti-emetic drugs. Uncertainty also exists about the most
    optimal method of dosing and the advantages and disadvantages of
    different routes of administration. Nonetheless, there is probably
    sufficient evidence to justify THC being made available in synthetic
    form to cancer patients whose nausea has proven resistant to
    conventional treatment.

    There is also reasonable evidence for the potential efficacy of THC
    and marijuana in the treatment of glaucoma, especially in cases which
    have proved resistant to existing anti-glaucoma agents. Further
    research is required to establish the effectiveness and safety of
    long-term use, but this should not prevent its use under medical
    supervision in individuals with poorly controlled glaucoma.

    There is sufficient suggestive evidence of the potential usefulness of
    various cannabinoids as anti-spasmodic, and anti-convulsant agents to
    warrant further clinical research into their effectiveness. There are
    other potential therapeutic uses which require more basic
    pharmacological and experimental investigation, e.g. cannabinoids as
    possible analgesic and anti-asthma agents.

    There is a need for further research into the effectiveness of
    cannabis and its derivatives in assisting patients with
    HIV/AIDS-related conditions, and in particular, their value in
    counteracting weight loss associated with these conditions, improving
    mood and easing pain. Case reports have suggested that synthetic THC
    may be effective in reducing nausea and stimulating appetite in
    symptomatic AIDS patients. While there is a potential concern that
    possible effects of cannabinoids on the immune system may have more
    serious consequences for HIV positive individuals and AIDS patients, a
    recent study has failed to find a relationship between the use of
    cannabis, or any other psychoactive drugs, and the rate at which HIV
    positive people progress to clinical AIDS.

    Despite the basic and clinical research work which was undertaken in
    late 1970s and early 1980s, the cannabinoids have not been widely used
    therapeutically, nor has further investigation been conducted along
    the lines suggested by the Institute of Medicine in 1982. This seems
    attributable to the fact that, in the United States, where most
    cannabis research has been conducted, clinical research on
    cannabinoids has been discouraged by regulation and a lack of funding.
    The discouragement of clinical cannabis research, in turn, derives
    from the fact that THC, the most therapeutically effective
    cannabinoid, is the one that produces the psychoactive effects sought
    by recreational users. An unreasonable fear that the therapeutic use
    of THC would send "mixed messages" to youth has motivated the
    discouragement of research into the therapeutic effects of

    The recent discovery of a specific cannabinoid receptor and the
    endogenous cannabinoid-like substance anandamide may change this
    situation by encouraging more basic research on the biology of
    cannabinoids which may have therapeutic consequences. It may prove
    possible to separate the psychoactive and therapeutic effects of
    cannabis, fulfilling the ancient promise of "marijuana as medicine".

    Overall appraisal of the health and psychological risks of cannabis

    The following is a summary of the major adverse health and
    psychological effects of acute and chronic cannabis use, classified by
    the degree of confidence about the relationship between cannabis use
    and the adverse effect.

    Acute effects

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

    anxiety, dysphoria, panic and paranoia, especially in naive

    cognitive impairment, especially of attention and memory;

    psychomotor impairment, and possibly an increased risk of
    accident if an intoxicated person attempts to drive a motor vehicle;

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

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

    Chronic effects

    The major health and psychological effects of chronic heavy 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 may be 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 further 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; and

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

    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 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 dependent on alcohol and other drugs, who are
    probably at an increased risk of developing dependence on cannabis.

    Two special concerns

    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. The health
    significance of this fact is unclear. 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 and its
    degree of activity while stored has not been investigated. One
    potential health implication of THC storage is that stored
    cannabinoids could be released into blood, producing a "flashback",
    although this is likely to be a very rare event, if it occurs at all.
    Whatever the uncertainties about health implications of THC storage,
    all potential users of cannabis should be aware that it occurs.

    Increases in the potency of cannabis?

    It has been claimed 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 than
    became available in the USA in the past decade. This claim has been
    repeated and interpreted in an alarmist fashion in the popular media
    on the assumption that an increase in the THC potency of cannabis
    necessarily means a substantial increase in the health risks of
    cannabis use.

    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 not clear
    that the probability of all adverse health effects will be thereby
    increased. Given the existence of these concerns about THC potency, it
    would be preferable to conduct some 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.

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

    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. Although allowance has to be made
    for the very different prevalence of use of the two drugs, and for the
    fact that we know a great deal more about the adverse effects of
    alcohol and tobacco use, the comparison serves the useful purpose of
    reminding us of the risks we currently tolerate with our favourite
    psychoactive drugs.

    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
    the balance of probability it 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,
    whereas there are no recorded cases of fatalities attributable to

    Tobacco. The major acute health risks that cannabis share 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.

    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 for 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 at most suggestive
    evidence that chronic heavy cannabis use produces similar, albeit more
    subtle impairments in occupational and educational performance of

    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 (i.e. the mouth, tongue,
    throat, oesophagus, lungs).

    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. The
    increased risk of cancer in the respiratory 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.

    Implications for harm reduction

    Anyone who wishes to avoid the probable acute and chronic adverse
    health effects of cannabis should abstain from using the drug. This
    advice is especially pertinent 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 delive
    1. Summary of repo
    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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