The health and psychological consequences of cannabis use
9. An overall appraisal of the health and psychological effects of cannabis 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 one. 9.1.1 Acute effects The major acute psychological and health effects of cannabis intoxication are: anxiety, dysphoria, panic and paranoia, especially in naive users; 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 malignancy; 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; and 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 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 decades. 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 degraded. 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 (1987). 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 dependence. References Anderson P., Cremona, A., Paton, A., Turner, C. and Wallace, P. (1993) The risk of alcohol. Addiction, 88, 1493-1508. Bedford, K. (1993) THC levels in New Zealand cannabis and cannabis products. 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Holman, C.D., Armstrong, B. et al (1988) The Quantification of Drug-Caused Morbidity and Mortality in Australia. Prepared for the Commonwealth Department of Community Services and Health. Canberra: Australian Government Publishing Service. Institute of Medicine (1987) Causes and Consequences of Alcohol Problems: An Agenda for Research. Washington DC: National Academy Press. International Agency on Cancer (1990) Cancer: Causes, Occurrence and Control. (Ed) L. Tomatis. Lyon: International Agency on Cancer. Kleiman, M.A.R. (1992) Against Excess: Drug Policy for Results. New York, Basic Books. Martin, B.R. (1986) The cellular effects of cannabinoids. Pharmacological Reviews, 38, 45-74. Mikuriya, T. and Aldrich, M.R. (1988) Cannabis 1988, old drug, new dangers: the potency question. Journal of Psychoactive Drugs, 20, 47-55. Negrete, J (1988) What's happened to the cannabis debate? British Journal of Addiction, 83, 359-372. Roselle, G., Mendenhall, C.L. and Grossman, C.J. (1993) Effects of alcohol on immunity and cancer. In R. Yirmiya and A.N. Taylor (eds) Alcohol, Immunity, and Cancer. Baton Rouge: CRC Press. Royal College of Physicians (1987) A Great and Growing Evil: The medical consequences of alcohol abuse. London: Tavistock. Thomas, H. (1993) Psychiatric symptoms in cannabis users. British Journal of Psychiatry, 163, 141-149.
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