Closure for the marijuana thread.

[cooltuba]

Decent, Jas. It'll take me a while to reply, but I'm going to read each and every study you quoted. If they're non-plausible studies (studies employing synthetic THC in large doses), I'm disreguarding their findings.

Peace,

Tim

[cooltuba]

[quote name='jasJis' date='Dec 18 2004, 08:13 AM'] This first point is easy to establish. Your own reference to the Netherlands fully supports my position. The experience with Alaska’s decriminalization supports it as well. As you noted, legalization in Alaska and the Netherlands resulted in an increase in the use of marijuana. Period. Legalization of marijuana did nothing to decrease the use of harder drugs. Period. Legal pot does not decrease the use of pot, nor cause a decrease in other illegal drug use.
[/quote]
I was starting to respond to your first rebuttal, quoted above, but I ran across this study by the WHO (world health organization, you've heard of them, no?):

On the face of it there is a reasonable cause for concern about the public health significance of cannabis use in many developed societies. First there is a high prevalence of cannabis use in such societies, especially among adolescent sand young adults. Second, cannabis is an intoxicant like alcohol that is usually smoked like tobacco so there is a reasonable presumption that it shares at least some of the adverse health effects of these two drugs, both of which have a substantial public health impact.

There are a number of obstacles to providing a confident appraisal of the personal and public health significance of cannabis use. The first set of issues concerns difficulties in making causal inferences about the connections between cannabis use and the adverse health and psychological consequences which have been attributed to it. The second set of issues concerns the quantification of the seriousness of the risks of cannabis use for users and for the broader community.

A third set of issues concerns the difficulties in making comparative appraisals of risk. Since no human activity is ever risk free, the appraisal of the health risks of cannabis presupposes a comparison of its risks with those of other relevant activities. The most obvious comparison is with the risks of using the other major recreational drugs in Western societies namely, alcohol, and tobacco. We have also included some comparisons with opiates which, serves the useful purpose of calibrating the health risks of cannabis against those of a drug which is widely regarded as a major public concern even though it is not widely used.

Our purpose in making these comparisons is not to promote one drug over another but rather to minimise the double standards that have operated in appraising the health effects of cannabis by persons on both sides of the debate about its legal status. On the one hand, there has been a disproportionately greater concern about the use of cannabis than alcohol on the part of many older persons who are opposed to cannabis use. On the other hand, younger cannabis users have denied the existence any adverse health effects of cannabis despite the fact that it intoxicates like alcohol and is smoked like tobacco. A further reason for the comparison is that many of our inferences about the probable adverse health effects of cannabis use depend upon analogies between the health effects of alcohol, cannabis and tobacco.

A factor which complicates the comparative assessment is the way in which the drug is taken. In present-day developed societies, the main route of administration of cannabis and of tobacco is by smoking, that is, inhaling the smoke of a smouldering preparation containing the drug. In pharmaceutical use, opiates are administered orally or by injection, while nonmedical use is primarily by injection, snorting, or smoking. Alcohol is consumed orally, although in combination with a wide variety of other substances. The route of administration of a drug can change over time in a given society: for instance, in North America tobacco was primarily chewed or sniffed in the late 19th century, and there is evidence there of some shifting at present from injecting to smoking heroin. In this analysis, we have focused on predominant routes of administration in developed societies, but it should be recognised that a shift in route of administration can substantially change the size and profile of adverse effects. In particular, the most serious adverse health problems of cannabis and tobacco are associated with smoking as the mode of administration.

The approach we have adopted in addressing each of these issues is as follows. First, we have identified the most probable causal relationships between cannabis use and specific health effects. In doing so we have used standard criteria for assessing the strength of evidence for a causal relationships, although we have had to relax the degree of confidence required so that some provisional conclusions could be drawn.

Second, in so far as it is possible we have attempted to quantify the severity of personal and public health risk for each adverse health effect that can be reasonably attributed to cannabis. We have attempted to estimate the probable relative risk, and the prevalence of the relevant pattern of use.

Third, we have compared these estimates with the best estimates of the mortality and morbidity burden of alcohol, opiates and tobacco. This has been done initially in a qualitative way by indicating whether or not particular adverse health effects that may reasonably be attributed to cannabis have also been attributed to alcohol, nicotine, and opiates. This is followed by a discussion of the probable quantitative risks of cannabis by comparison with those of alcohol and nicotine, and some direct comparative evidence on consequences reported by users of the three drugs.

In making these comparisons we have relied on epidemiological evidence on the health and psychological consequences of cannabis use which is largely based on studies conducted in the English-speaking countries, and most particularly the United States. Unfortunately, countries with a long tradition of heavy cannabis use are not well represented in the research literature. The preponderance of American research on the health effects of cannabis use reflects societal concern about the emergence over the past several decades of widespread cannabis use among adolescents and young adults in the USA; concern that has been translated into funding for epidemiological studies of the health and psychological consequences of cannabis use. The conduct of research on cannabis use in developing countries should be a priority, especially in the countries that have a long history of traditional use, including very heavy use among some subpopulations. These subpopulations are the ones most likely to show any adverse health and psychological effects of chronic heavy use.

Our comparisons of health effects are also largely confined to the effects on the health of users. We have said little about the effects of cannabis use on the health and well being of other persons who do not use cannabis. Such indirect health effects have not been well studied for most drugs, with the limited exceptions of motor vehicle accidents, and violence for alcohol, and passive smoking for tobacco. They perhaps deserve more attention that they have hitherto received but in the absence of the necessary research we are unable to address them in this review.

THE PROBABLE HEALTH EFFECTS OF CANNABIS USE

Acute Psychological and Health Consequences

The acute toxicity of cannabis is very low. There are no confirmed cases of human deaths from cannabis poisoning in the world medical literature. Animal studies indicate that the dose of THC required to produce 50% 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 increases as one moves up the phylogenetic tree, suggesting by extrapolation that the lethal dose in humans could not be very easily achieved by smoking or ingesting the drug (Grinspoon and Bakalar, 1993; Rosencrantz, 1983).

Dysphoric effects

The most common unpleasant acute psychological effects of cannabis use are anxiety, sometimes producing unpleasant depressive feelings (Tart, 1970; Weil, 1970). 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 receiving a much larger than intended dose of THC. These effects can usually be prevented by adequate preparation of users about the type of effects they may experience, or they can be managed by reassurance and support (Weil, 1970).

Motor vehicle accidents

The major potential health risks from the acute use of cannabis arise from its effects on cognitive and psychomotor performance. Intoxication produces dose-related impairments in a wide range of cognitive and behavioural functions that are relevant to a skilled performance like driving an automobile or operating machinery. These include: slowed reaction time and information processing, impaired perceptual-motor coordination and motor performance, impaired short term memory, signal detection, tracking behaviour and slowed time perception. (Chait and Pierri, 1992).

The negative effects of cannabis on the performance of psychomotor tasks is almost always related to dose (Chait and Pierri, 1992). The effects are generally larger, more consistent and persistent in different tasks which involve sustained attention. The acute effects of "recreational" doses of cannabis on driving performance in laboratory simulators and over standardised driving courses are similar to those of doses of alcohol that achieve BACs between 0.07% and 0.10% (Hansteen, Miller, Lonero, Reid and Jones, 1976; Peck et al, 1986; Smiley, 1986).

While cannabis impairs performance in laboratory and simulated driving settings, it is difficult to relate the magnitude of these impairments to an increased risk of being involved in motor vehicle accidents. Students of the effects of cannabis on on-road driving performance have found at most modest impairments (e.g. Sutton, 1983). Cannabis intoxicated persons drive more slowly perhaps because they are more aware of their level of psychomotor impairment than alcohol intoxicated drinkers who generally drive at faster speeds (Smiley, 1986).

No controlled epidemiological studies have established that cannabis users are at increased risk of motor vehicle accidents. A prospective Swedish study of mortality over 15 years among military conscripts found an increased risk of premature mortality among men who had smoked cannabis 50 or more times by age 18. Violent deaths were the major contributor to this excess, of which 26% were motor vehicle and 7% other accidents (e.g. drownings and falls). The increased risk disappeared, however, after multivariate statistical adjustment for confounding variables such as alcohol and other drug use (Andreasson and Allebeck, 1990).

Uncertainty about the role of cannabis in motor vehicle accidents is likely to remain since case-control studies are difficult to conduct and interpret (see chapter by Smiley this volume). Blood levels of cannabinoids do not indicate whether a driver or pedestrian was intoxicated with cannabis at the time of an accident, and many drivers with cannabinoids in their blood were also intoxicated with alcohol at the time of the accident (Smiley, 1986). Factors other than psychomotor performance also contribute to the danger of drug use when driving. Foremost among these is the user's preparedness to take risks when intoxicated, which the available evidence suggests is reduced by cannabis intoxication by contrast with alcohol intoxication which consistently increases risk-taking (Smiley, 1986)

The Health Effects of Chronic Cannabis Use

The Immune System

There is reasonably consistent evidence that THC can produce cellular changes such as alterations in cell metabolism, and DNA synthesis, in vitro (Bloch, 1983). There is even stronger evidence that cannabis smoke is mutagenic in vitro, and in vitro, and hence, that it is potentially carcinogenic for the same reasons as tobacco smoke (Leuchtenberger, 1983).

There is reasonably consistent evidence that cannabinoids impair both the cell-mediated and humoral immune systems in rodents (Munson and Fehr, 1983). These changes have decreased resistance to infection by bacteria and viruses. There is also evidence that the noncannabinoid components of cannabis smoke impair the functioning of alveolar macrophages, the first line of the body's defence system in the lungs (Munson and Fehr, 1983). The relevance of these findings to human health is uncertain: the doses required to produce these effects are often very high, and the problem of extrapolating from the effects of these doses to those used by humans is complicated by the possibility that tolerance develops to the effects on the immune system (Hollister, 1992).

Moreover, the limited experimental and clinical evidence on immune effects in humans is mixed, with a small number of early studies that have suggested adverse effects not being replicated by later ones (Munson and Fehr, 1983; Hollister, 1992). At present, there is no conclusive evidence that consumption of cannabinoids predisposes humans to immune dysfunction, as measured by reduced numbers or impaired functioning of T-lymphocytes, B-lymphocytes or macrophages, or reduced immunoglobulin levels.

The clinical and biological significance of these possible immunological impairments in chronic cannabis uses is uncertain. To date there has been no epidemiological evidence of increased rates of disease among chronic heavy cannabis users. 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 (Kaslow et al, 1989). 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 minor impairments in immunity. Such effects would produce small increases in the rate of occurrence of common bacterial and viral illnesses among chronic users which would be of public health significance because of the increased expenditure on health services, and the increased loss of productivity that this would entail among the young adults who are the heaviest users of cannabis. A recent epidemiological study by Polen at al (1993) which compared health service utilisation by nonsmokers and daily cannabis only smokers has provided the first suggestive evidence of an increased rate of presentation for respiratory conditions among cannabis smokers. This remains suggestive, however, because infectious and noninfectious respiratory conditions were not distinguished.

The Cardiovascular System

The conclusion reached by the Institute of medicine in 1982 still stands: the smoking of marijuana "causes changes to the heart and circulation that are characteristics of stress ...[but] there is no evidence ... that it exerts a permanently deleterious effect on the normal cardiovascular system ..." (p 72). The cardiovascular effects of cannabis may be less benign in patients with hypertension, cerebrovascular disease and coronary atherosclerosis for whom marijuana poses a threat by increasing the work of the heart (Aronow and Cassidy, 1974, 1975).

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, and wheezing (Bloom et al, 1987; Huber et al, 1988; Tashkin et al, 1988a, 1990). Given the documented adverse effects of tobacco smoke which is qualitatively very similar in composition to cannabis smoke (Tashkin, 1993; Wu et al, 1988). There is as yet little direct evidence that the latter occurs (Huber et al, 1988) although there is evidence that chronic cannabis smoking may produce histopathological changes in lung tissues of the kind that precede the development of lung cancer (Fligiel et al, 1988).

More recently, concern about respiratory cancers has been heightened by a series of case reports of cancers of the aerodigestive tract in young adults with a history of heavy cannabis use (e.g. Caplan and Brigham, 1989; Donald, 1991; Taylor, 1988). Although these reports fall short of providing convincing evidence because they were uncontrolled and many of the cases concurrently used alcohol and tobacco, they are clearly cause for concern since such cancers are rare in adults under the age of 60, even among those who smoke tobacco and drink alcohol (Tashkin, 1993). Smoking cannabis may also pose an acute risk to individuals with respiratory diseases such as asthma. Evidence linking tobacco smoke to asthma and asthmatic symptoms is increasing.

The potential adverse effects of cannabis on the respiratory system are specific to smoking as the route of administration, and could not result from oral ingestion.

Reproductive Effects

Chronic cannabis use probably disrupts the male and female reproductive systems in animals, reducing the secretion of testosterone, and sperm production, motility, and viability in males, and disrupting the ovulatory cycle in females (Bloch, 1983; Institute of Medicine, 1982). It is uncertain whether it is these effects in humans, given the inconsistency in the limited literature on human males (Mendelson and Mello, 1984), and the lack of research in the case of human females (Hollister, 1986). 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 whose fertility has been impaired for other reasons.

Cannabis smoking during pregnancy probably impairs foetal development Gibson et al, 1983; Hatch and Bracken, 1986; Tennes et al, 1985; Zuckerman et al, 1989, leading to a reduction in birthweight (Abel, 1985). This may be a consequence of a shorter gestation period, and probably occurs 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. There is some animal evidence of such effects although these studies have usually involved very high doses by the oral route (Abel, 1985). The limited studies in humans have generally but not consistently produced null results (Gibson et al, 1983; Hatch and Bracken, 1986; Hingson et al, 1982; Zuckerman et al, 1989).

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 (Bloch, 1983; Hollister, 1986).

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 (e.g. Fried 1985, 1989). There are several case-control studies which suggest that there is an increased risk of certain childhood cancers (namely, astrocytomas and leukemia) among children born to women who reported that they had used cannabis during their pregnancies (Kuitjen et al, 1990; Robison et al, 1989).

Possible Health Effects of Contaminants in Cannabis

Because cannabis is an illegal drug its cultivation, harvesting and distribution are not subject to quality control mechanisms to ensure the reliability and safety of the product used by consumers. It is well recognised in developing countries, such as Kenya, that illicit alcohol production can result in the contamination with toxic by-products or adulterants that can kill or seriously affect the health of users. The same may be true of illicit drugs such as opiates, cocaine and amphetamine in developed societies. There is no evidence of comparable health effects for cannabis although there were concerns expressed about the possible health effects of the use of cannabis contaminated by herbicides (such as paraquat) that were used to control illicit cannabis cultivation in the US in the 1970s. These concerns proved unfounded (Hollister, 1986). There have also been concerns about the microbial contamination of cannabis leaf but there has been little evidence (other than a small number of case histories) that this has adversely affected the health of cannabis users (Hollister, 1986).

Psychological Effects of Chronic Cannabis Use

Adult Motivation

One of the major concerns about the psychological effects of chronic heavy cannabis use has been that it impairs adult motivation. The evidence for an "amotivational syndrome" among adults consists largely of case histories and observational reports (e.g. Kolansky and Moore, 1971; Millman and Sbriglio, 1986). The small number of controlled field and laboratory studies have not found compelling evidence for such a syndrome (Dornbush, 1974; Negrete, 1983; Hollister, 1986). The evidential value of the field studies is limited by their small sample sizes, and the limited sociodemographic characteristics of their samples, while the evidential value of the laboratory studies is limited by the short periods of drug use, the youthful good health of the volunteers, and minimal demands made on volunteers in the laboratory (Cohen, 1982). Some regular cannabis users report a loss of ambition and impaired school and occupational performance as adverse effects of their use (e.g. Hendin et al, 1987) and that some ex-cannabis users give impaired occupational performance as a reason for stopping (Jones, 1984). Nonetheless, it is doubtful that cannabis use produces a well defined amotivational syndrome. It may be more parsimonious to regard the symptoms of impaired motivation as symptoms of chronic cannabis intoxication rather than inventing a new psychiatric syndrome.

Adolescent Development

In the United States in the 1970s and 1980s, cannabis use appears to have increased the risk of discontinuing a high school education, and of experiencing job instability in young adulthood (Newcombe and Bentler, 1988). The apparent strength of these relationships in cross-sectional studies (e.g. Kandel, 1984) has been exaggerated because those adolescents who are most likely to use cannabis have lower academic aspirations and poorer high school performance prior to using cannabis than their peers who do not (Newcombe and Bentler, 1988). It remains possible that factors other than the marijuana use account for apparent causal relations. To the extent they may exist, these adverse effects of cannabis and other drug use upon development over and above the effect of pre-existing nonconformity may cascade throughout young adult life, affecting choice of occupation, level of income, choice of mate, and the quality of life of the user and his or her children.

A major finding of research into the adult consequences of adolescent cannabis use has been the strong evidence of a regular sequence of initiation into the use of illicit drugs among American adolescents in the 1970s in which cannabis use preceded involvement with "harder" drugs such as stimulants and opioids (Kandel et al, 1984; Donovan and Jessor, 1983; Yamaguchi and Kandel, 1984 a, b). The causal significance of this sequence of initiation into drug use remains controversial. The hypothesis that it represents a direct effect of cannabis use upon the use of the later drugs in the sequence is the least compelling. There is better support for two other hypotheses which are not mutually exclusive: that there is a selective recruitment into cannabis use of nonconforming adolescents who have a propensity to use other illicit drugs; and that once recruited to cannabis use, the social interaction with other drug using peers, and exposure to other drugs when purchasing cannabis on the black-market, increases the opportunity to use other illicit drugs (Baumrind, 1983; Goode, 1974; Kandel, 1988).

A Dependence Syndrome

A cannabis dependence syndrome as defined in DSM-IV (American Psychiatric Association, 1994) can occur 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. There is also suggestive evidence that some users may experience a withdrawal syndrome on the abrupt cessation of cannabis use, although one that is much milder and less marked than that experienced when withdrawing from alcohol or opiates (Compton, Dewey and Martin, 1990; Jones and Benowitz, 1976). DSM-IV notes that "symptoms of possible cannabis withdrawal (e.g. irritable or anxious mood accompanied by physical changes such tremor, perspiration, nausea and sleep disturbances) have been described in association with the use of very high doses, but their clinical significance is uncertain." (American Psychiatric Association, 1994:215).

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 (Jones, 1984; Roffman et al, 1988; Weller et al, 1984). There is limited clinical evidence for a cannabis dependence syndrome analogous to the alcohol dependence (Kosten et al, 1987). Epidemiological surveys of the prevalence of drug dependence in the general population (e.g. Anthony and Helzer, 1991) show that cannabis dependence, as defined in the diagnostic manuals, is among the most common forms of drug dependence in Western societies by virtue of its high prevalence of use. On the other hand, relatively few users seek treatment for cannabis dependence (American Psychiatric Association, 1994: 220-221).

Cognitive Effects

The weight of the available evidence suggests that even the long term heavy use of cannabis does not produce any severe or grossly debilitating impairment of cognitive function (Carter et al, 1980; Fehr and Kalant, 1983b, Rubin and Comitas, 1975; Wert and Raulin, 1986). If it did research to date should have detected it. There is some 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 the integration of complex information (Page et al, 1988; Solowij et al, 1991, 1992, 1993 and see chapter by Solowij in this volume). While subtle, these impairments may affect everyday functioning, particularly among individuals 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 (Solowij et al, 1992, 1993). It remains to be seen whether the impairment can be reversed by an extended period of abstinence from cannabis.

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 (Campbell et al, 1971). 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 (e.g. Co et al, 1977; Kuehnle et al, 1977). 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.

Serious Psychiatric Disorder

There is suggestive evidence that large doses of THC can produce an acute psychosis in which confusion, amnesia, delusions, hallucinations, anxiety, agitation and hypomanic symptoms predominate. The evidence comes from laboratory studies of the effects of THC on normal volunteers and clinical observations of psychotic symptoms in heavy cannabis users which remit rapidly following abstinence (Bernardson and Gunne, 1972; Chopra and Smith, 1974; Edwards, 1976).

There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are 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 use cannabis (Ghodse, 1986).

There is strongly suggestive evidence from a prospective study that heavy cannabis use may precipitate schizophrenia in vulnerable individuals (Andreasson et al, 1987; Schneier and Siris, 1987; Thornicroft, 1990). This relationship is still only strongly suggestive because in the only prospective study conducted to date (Andreasson et al, 1987) 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, or other drug-induced, psychoses (Negrete, 1989; Thornicroft, 1990).

There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are 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 use cannabis (Ghodse, 1986). There is better evidence that cannabis use can adversely affect the course of schizophrenia in affected individuals who continue to use it (Cleghorn et al, 1991; Jablensky et al, 1991; Martinez-Arevalo et al, 1994).

A QUALITATIVE COMPARISON OF THE HEALTH RISKS OF ALCOHOL, CANNABIS, NICOTINE AND OPIATE USE


A useful way of assessing the health risk posed by cannabis use is a comparative qualitative appraisal of its risks with those of other widely used recreational of its risks with those of other widely used recreational drugs such as alcohol and tobacco (ARF/WHO, 1981). The motive for such comparisons is to use a common standard when making societal decisions about the control and regulation of cannabis use. Like tobacco, cannabis is most commonly smoked, and like alcohol, cannabis is commonly used for its intoxicating and euphoriant effects in developed societies (although it may be used for more utilitarian reasons, such as, making heavy physical work tolerable, in some developing countries). The opiates provide a useful illicit drug class against which to calibrate the adverse effects of cannabis since this class of drugs has a fearsome although not always deserved reputation as a major risk to the health of young adults. Nonmedical use of opiates is initially primarily for euphoria or for relief of pain.

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 warrant 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).

In the absence of an authoritative current review of the health effects of the opioids as a class of drugs, it was necessary to look to several sources to identify the health effects of opioids. General pharmacological texts, and other reviews, were used to describe the pharmacological effects of the opioids (e.g., Belkin and Gold, 1991; Jacobs and Fehr, 1987; Duggan and North, 1983). In addition, information on the chronic health effects and social consequences of illicit opiates (injectable and non-injectable) and of methadone was taken from reports of several longitudinal studies of opioid users (e.g. Vaillant, 1973; O'Donnell, 1969; Maddux and Desmond, 1981; Simpson, Joe, Lehman and Sells, 1986; Joe and Simpson, 1987; 1990). These cohort studies typically involve populations in contact with drug treatment services rather than representative samples of users.

Acute Effects

Alcohol

The major risks of acute cannabis use show some parallels with the acute risks of alcohol intoxication. 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. It may also increase the likelihood of engaging in risky behaviour such as dangerous driving, and unsafe sexual practices. While cannabis intoxication increases the risks of casualties in hazardous situations, it remains to be determined to what extent it increases the likelihood of engaging in risky behaviour.

Alcohol and cannabis intoxication appear to differ in their relation to intentional rather than accidental casualties. Alcohol intoxication is strongly associated with aggressive and violent behaviour. The relationship is complex, and the nature and extent of drinking's causal effect remains controversial at the level of the individual drinker (Pernanen, 1991; Martin, 1993; Pohorecky, Brick and Milgram, 1993). But there is good causal evidence that changes in the level of alcohol consumption affect the incidence of violent crime, at least in some populations (Room, 1983; Lenke, 1990; Cook and Moore, 1993). There is also increasing evidence to indicate that alcohol may play a role in suicide (Edwards et al., forthcoming). There is little to suggest that causal relationship of cannabis use to aggression or violence, at least in present-day developed societies.

Second, there is good evidence that substantial doses of alcohol taken during pregnancy can produce a foetal alcohol syndrome. There is suggestive but far from conclusive evidence that cannabis can also adversely affect the development of the foetus when used during pregnancy. A clear equivalent for cannabis of the foetal alcohol syndrome has not been established.

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 overdose fatalities attributed to cannabis, and the estimated lethal dose for humans extrapolated from animal studies is so high that it 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 and respiratory diseases. For both drugs, the respiratory effects do not apply to ingestion that is not by inhalation.

Opioids

Some of the opioids share with alcohol and cannabis an acute intoxicating effect, although the sedative effect is more pronounced. Acute administration of heroin causes euphoria in many users, although other opioids such as methadone do not have this effect in tolerant individuals. The extent of euphoria is also affected by route of administration. As is found with cannabis, some naive users report unpleasant feelings with opiate use, specifically nausea and dysphoria. All opioids are CNS depressants and as such can reduce level of consciousness and cause sleep.

The literature on the effects of opiates on driving and other exacting skills is not well developed. A maintenance dose in a tolerant user may produce little psychomotor or cognitive impairment. A heroin user who has reached a stage of "nodding" is in no condition to drive a car, but will probably have little inclination to do so. As with cannabis, there is little direct epidemiological evidence of opiate-induced casualties. One study showed that the driving-related skills of persons maintained on stable doses of methadone were not impaired when assessed on a laboratory task that is sensitive to the effects of alcohol (Chesher, Lemon, Gomal and Murphy, 1989).

While there is no risk of overdose associated with cannabis, use of illicit opioids carries a real risk of overdose. High doses of most opioids can lead to suppression of breathing rate and blood pressure and cause respiratory arrest. The risk of overdose is worsened by use in combination with alcohol or other drugs, and is thought to be worsened by variations in the potency of opiates obtained illegally.

Opioids, like cannabis, cause some suppression of hormone levels. These decreased hormonal levels, however, do not necessarily result in infertility in men or women using opioids\do for extended periods (Belkin and Gold, 1991; Duggan and North, 1983; Martin and Martin, 1980). Like alcohol, tobacco and cannabis, the opiates have been associated with miscarriage, foetal death and low birth-weight. There is no clear relationship with an identifiable syndrome of foetal defects from opioids that parallels foetal alcohol syndrome. Although poor nutrition and pre-natal care clearly contribute to the risk of adverse outcomes in pregnant women addicted to street drugs, even methadone maintenance has been found to result in higher rates of pregnancy problems. Methadone and other orally administered opioids have been shown to cause foetal death and low birthweight in laboratory animals (Martin and Martin, 1980; Caviston, 1987; Woody and O'Brien, 1991).

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 withdrawal symptoms are either absent or mild 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, either during acute intoxication or during the process of withdrawal in dependent drinkers. There is some clinical evidence that chronic heavy cannabis use may produce a toxic psychosis. One prospective epidemiological study suggests that heavy cannabis use may precipitate schizophrenia in predisposed individuals,. that is, those with a personal or a family history of psychiatric disorder. There is better evidence that continued cannabis use may worsen the course of 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 in the absence of countervailing cultural beliefs chronic heavy alcohol use generally impairs occupational performance in adults and 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 would 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 clinical evidence that chronic cannabis smoking may also be a contributory cause of cancers of the aerodigestive tract. There is also some epidemiological evidence that alcohol use moderately increases the risk of cancer of the breast in women and of the colon in both sexes.

Seventh, alcohol use is a major cause of liver cirrhosis, accounting for upward of 80% of cases in non-tropical countries with substantial alcohol consumption levels. Heavy drinking is also implicated in gastritis, high blood pressure, stroke, cardiac arrhythmias, cardiomyopathy, pancreatitis, and polyneuropathy. On the other hand, regular drinking of small amounts of alcohol appears to reduce the risk of coronary heart disease, particularly in older individuals with positive risk factors such as tobacco smoking or a fatty diet. No equivalent protective effects have been found for cannabis although there is some evidence for the therapeutic usefulness of some cannabinoids (Hall et al, 1994).

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. These respiratory risks could be avoided by a change to the oral route of administration which would also reduce but not eliminate the cardiovascular risk since THC affects the cardiovascular system when taken orally.

Tobacco smoking is associated with a wide variety of other chronic health conditions for which cannabis smoking has not so far been implicated. These include cancer of the cervix, stomach, bladder and kidney, coronary heart disease, peripheral vascular disease, and stroke, as well as cataracts and osteoporosis.

Opioids

The specific health effects of opioid use largely depend on the route of administration. The use of injectable opiates carries risks not common to alcohol, tobacco or cannabis, especially when associated with illegally obtained injectables and shared needles. Injecting heroin or morphine can lead to trauma, inflammation and infection at the site of administration. Liver damage in opiate addicts may be caused by viral hepatitis contracted through needle sharing or from chronic alcohol abuse. Serious infection such as endocarditis is also possible. Local tissue and organ damage may also result from the adulterants in injection drugs obtained on the street (Belkin and Gold, 1991). Intravenous drug use is a major concern for the transmission of communicable diseases such as viral hepatitis and AIDS.

Chronic use of non-injected opioids appears to carry little risk of adverse health effects other than a modest effect on endocrine activity, some suppression of the immune system which has similar implications to the immune suppression associated with cannabis use, and chronic constipation.

While it is unclear that a withdrawal syndrome exists for cannabis, physical dependence on opiates has been recognised for centuries. Opiate withdrawal is associated with considerable discomfort but is rarely life-threatening. The withdrawal syndrome is generally less dangerous than rapid withdrawal from sedatives-hypnotics or from alcohol, although it may be life-threatening in neonates. Despite the low risk, avoidance of withdrawal appears to be a powerful motive for continued use of opiates among very heavy users.

Chronic opioid users may experience instability of mood, anorexia, lethargy and depression which are related to acute drug effects. Opioids have not been linked to chronic psychiatric disorders, but street addicts have a shortened life expectancy and more frequently experience social and emotional problems. This is in part due to their exposure to infection, violence and poor living conditions rather than their drug use.

COMPARING THE MAGNITUDE OF RISKS

The standard ways of measuring the magnitude of health risks are relative risk and population attributable risk. The relative risk of cannabis use, for example, is the increase in the odds of experiencing an adverse health outcome among those who use cannabis compared to those who do not. The population attributable risk represents the proportion of cases with an adverse outcome which is attributable to cannabis use. Relative risk is of most relevance to individuals attempting to estimate the increase in their risk of experiencing an adverse outcome if they use a drug. Attributable risk is of most relevance to a societal appraisal of the harms of drug use.

The personal and public health importance of the two measures of risk magnitude depends upon the prevalence of drug use and the base rate of the adverse outcome. An exposure with a low relative risk may have a low personal significance but a large public health impact if a large proportion of the population is exposed (e.g. cigarette smoking and heart disease). Conversely, an exposure with a high relative risk may have little public health importance because very few people are exposed to it but major personal health implications for those who are exposed. Consequently, an appraisal of the personal and public health importance of cannabis and other illicit drug use must take account not only of the relative risk of harm but also the prevalence of use and the base rate of the adverse effect.

The Relative Risks of Adverse Health Effects of Cannabis Use

Many of the quantitative risks of cannabis use can only be guessed at in the absence of studies of the dose-response relationship between cannabis use and the various adverse health effects. The following are guesstimates of the risks of cannabis use for the most probable adverse health effects. When in doubt we have adopted the strategy of assuming as a worst case that the relative risks of cannabis use are comparable to the relevant risks of alcohol or tobacco.

Motor Vehicle Accidents

If we assume that driving while intoxicated with cannabis produces a comparable increase in the risk of accidents to that produced by driving while intoxicated with alcohol (say with a blood alcohol level of 0.05% to 0.10%), then a RR in the range of 2 to 4 would be reasonable. The fact that alcohol and cannabis are often used in combination complicates the task of estimating the relative risk of cannabis use alone to motor vehicle accidents.

Respiratory Diseases

If we assume that a daily cannabis user who smokes 5 or more joints per day faces a comparable risk of respiratory disease to that of a 20 a day tobacco smoker, then the RR of developing chronic bronchitis would be 5 or greater for those who had ever smoked cannabis, and substantially higher among those who also used tobacco and those had been daily smokers over many years (Holman et al, 1988). The increased risk of respiratory disease is, of course, specific to use of cannabis by smoking.

Respiratory Tract Cancers

If we make the same worst case assumptions about daily cannabis smoking then the relative risks of various cancers of the respiratory tract would be of the order of: 4 for oral cancer, 6 for pharyngeal cancers, 4 for oesophageal cancer, and 7 for lung cancer (Holman et al, 1988). Again these risks could be substantial higher among cannabis smokers who also smoke tobacco, but would be minimal for non-smoking cannabis use.

Low Birthweight Babies

Making a worst case assumption in the absence of good data, a woman who smokes cannabis during pregnancy approximately doubles her chance of giving birth to a low birthweight baby (Holman et al, 1988).

Schizophrenia

This is one of the few health consequences for which there is quantitative estimate of relative risk. If we use the estimated RR from the study by Andreasson et al (1987) after adjustment for confounding variables, then an adolescent who had smoked cannabis 50 or more times by age 18 would have approximately a 2 to 3 times higher risk of developing schizophrenia than an adolescent who had not been a cannabis smoker.

Dependence

Since cannabis use is a necessary condition of developing dependence, it is not appropriate to estimate a relative risk. The best way of quantifying the risk of dependence is to estimate the proportion of those who have ever used cannabis, or who have had a history of daily use, who become dependent on the drug. The best estimates of these percentages are based primarily upon US data from the late 1970s and early 1980s. These are that 10% to 20% of those who have ever used, and 33% to 50% of those who have had a history of daily use, will become dependent on cannabis (see Hall et al, 1994). Comparable percentages for tobacco and opiates would be higher than these.

Summary

From the perspective of the individual cannabis user, the major health risks of cannabis use are, with one exception, most likely to be experienced by those who smoke the drug daily over a period of years. These are in order of decreasing risk: developing a cannabis dependence syndrome, developing chronic bronchitis, and being involved in a motor vehicle accident if driving while intoxicated. In all these cases, the risk will be increased if cannabis is combined with either alcohol or tobacco or both. The risk most likely to be experienced by the occasional user is an increased risk of a motor vehicle accident if used when driving a car, especially if cannabis is combined with alcohol.

Public Health Significance

Motor Vehicle Accidents

An assessment of the public health significance of motor vehicle accidents caused by cannabis is made difficult by the strong association between cannabis and alcohol use. The epidemiological studies indicate that in its own right, cannabis makes at most a very small contribution to motor vehicle accidents, and so on the whole it may seem be a minor road safety problem by comparison with alcohol. Its major public health significance for road safety may be in amplifying the adverse effects of alcohol in those of drivers who combine alcohol and cannabis intoxication.

Respiratory Diseases

The public health significance of respiratory diseases caused by cannabis smoking is probably greater than that for respiratory cancers. This is so for two reasons. First, respiratory cancers require a greater length of exposure to cigarette smoke (15 to 20 years) than is required to develop chronic bronchitis. Second, there are very few cannabis users who use the drug for more than 5 years. The exposure period for chronic bronchitis may be shorter still among those cannabis smokers who also smoke tobacco since there is good evidence that concurrent tobacco and cannabis smoking have additive adverse effects on the respiratory system. The contribution of cannabis to respiratory diseases is more a matter of morbidity than mortality.

Respiratory Tract Cancers

Even if we make the worst case assumption that the risks of cancer are comparable among daily tobacco and cannabis smokers then cannabis smoking will make at most a small contribution to the occurrence of these cancers, at least on the basis of current patterns of use in developed societies. This is because only a minority of those who ever use cannabis become daily users, and a much smaller proportion of these daily users persist in smoking cannabis beyond their middle twenties by comparison with the proportions of tobacco smokers who do so. Among this minority concurrent cannabis and tobacco use may amplify the adverse respiratory effects.

Low Birthweight Babies

Again making a worst case assumption, cannabis smoking during pregnancy may double the risks of a woman giving birth to a low birthweight baby. The public health significance is likely to be much lower than that of tobacco smoking during pregnancy because the prevalence of cannabis use is likely to be much lower. Although foetal exposure to cannabis smoke may be relatively low, the risks of a low birthweight baby will be even higher among those women who also smoke tobacco, as do most of those smoking cannabis during pregnancy.

Schizophrenia

As argued in detail elsewhere (Hall et al, 1994), there is uncertainty about whether the association observed between cannabis use and schizophrenia is a token of a causal relationship. But even if it is, its public health significance should not be overstated. Schizophrenia affects approximately 1% of the adult population, and on the data of Andreasson et al, cannabis use would account for less than 10% of cases of schizophrenia. Even this low figure seems unlikely, however, since the incidence of schizophrenia has probably declined during the period when cannabis use among adolescents and young adults has increased (Der et al, 1991).

Dependence

Cannabis dependence is potentially a larger public health problem than any of the other potentially adverse health effects of cannabis. On the ECA estimates, approximately 4% of the adult US population met diagnostic criteria for cannabis abuse or dependence, as against 14% who met diagnostic criteria for alcohol abuse and dependence. This is a nontrivial proportion of the population, although its consequences are somewhat ameliorated because there is probably a high rate of remission of symptoms in the absence of treatment.

Summary

Overall, most of these risks are small to moderate in size. In aggregate they are unlikely to produce public health problems comparable in scale to those currently produced by alcohol and tobacco. This is largely because on current patterns of use in developed societies the proportion of the population that uses cannabis heavily over a period of years is much smaller than the proportions that use alcohol or tobacco in a comparable way (Hall, 1995).

We should beware of becoming too complacent about this situation. The comparison based upon existing patterns of use cannot be used to predict what would happen if there was a major change in the prevalence of cannabis use, as some may argue would happen if existing criminal penalties were removed or replaced with civil penalties. But even if there were more users, it is unlikely that the proportion of cannabis users who become very heavy users would ever be as high in industrial societies as it often for stimulants such as tobacco or cocaine, since heavy use of a stimulant fits more easily into the rhythms of daily life in such societies.

In principle, it would seem a simple matter to estimate what the health risks of cannabis use would be if its prevalence was the same as that of alcohol and tobacco. Although conceptually a simple matter, a number of assumptions have to be made. The most questionable assumption is that the public health consequences of an increased prevalence of cannabis use would simply be the product of the current patterns of use multiplied by the ratio of the new to old users. Such a calculation assumes that the risks are the same regardless of the characteristics of the user, or the legal regime under which the drug is used.

The first assumption may be unreasonable. It may be, for example, that cannabis is used by a different population when its prevalence of use is low than when it was high. This phenomenon has been reported with alcohol, for example, with different patterns of alcohol consumption and problems in "dry" and "wet" cultures. If adult use were legalised, it might also be easier to reduce some of these health risks. For example, with greater availability it may be possible to reduce the major respiratory risks of cannabis smoking, either by encouraging cannabis users to ingest rather than to smoke the drug, or by increasing the THC content and reducing the tar content of marijuana, for those who continue to smoke. It would also be easier if cannabis use were legal to give users advice on other ways of reducing their risks of using the drug. Estimating the net effects of such harm reduction efforts is difficult, however, because it would also be likely that decriminalising cannabis for adult use would lead to an increased use by adolescents, and the health effects of this would be difficult to predict.

For these reasons we have not attempted to provide estimates of the health risks of cannabis if its prevalence of use were to approach those of alcohol and tobacco. All that can be said with any confidence is that if the prevalence of cannabis use increased to the levels of cigarette smoking and alcohol use, its public health impact would increase. It is impossible to say by how much with any precision. However, on even the most worst case scenario, it is unlikely that the public health effect of cannabis use would approach those of alcohol or tobacco use. Unlike alcohol, cannabis does not produce cirrhosis for example. Moreover, in developed societies cannabis appears to play little role in injuries caused by violence, as does alcohol, although recently concern has been expressed in some developing countries that cannabis may be used to fortify criminal offenders. Unlike tobacco, all the evidence suggests that the proportion of cannabis smokers who become daily smokers is substantially less than the proportion of tobacco smokers who do so.

Some Direct Comparative Evidence on Consequences:

What Users Report

To a limited extent, epidemiological data are available on the consequences of drug use that users attribute to their drug use. Since this data has not been collated and reviewed, we summarise some of it here. As we shall discuss, the data should be interpreted with caution. And it should be recognised that the range of consequences considered here reaches far beyond the bounds of the clinically significant physical and mental illnesses which are our focus elsewhere in this review.

In a large sample of U.S. men aged 20 - 30, interviewed in 1974 (Table 1), a higher proportion of tobacco smokers rated the effects of their use as bad, and more drinkers of alcohol gave a bad than a good rating. Good ratings outweighed bad for marijuana users. In a survey of Ontario adults in 1994 (Table 1), current users aged 18 to 34 gave a similarly negative weighting to tobacco, but gave alcohol a relatively more favourable weighting. Again, marijuana users were the most likely to give a favourable rating.

In another Ontario survey in 1992, current users were asked whether their use of a drug had a harmful effect on different aspects of their life in the past 12 months. Table 2 shows the results for users of alcohol, tobacco and marijuana, and also for heavier or more frequent users of each drug: drinkers who drank five or more drinks on an occasion at least once a month, marijuana users who smoked at least once a month, and tobacco smokers who smoked at least 11 cigarettes a day. Tobacco smokers were more likely than marijuana or alcohol users to report harm to their physical health, to their finances, and to their friendships or social life, among both lighter and heavier users. The small number of regular marijuana users seemed more likely than heavier drinkers to report harm to their home life or marriage and to their finances. On other comparisons, the proportions reporting harm for each drug were fairly similar.

In the 1991 U.S. National Household Survey on Drug Abuse, large samples of current tobacco, alcohol and marijuana users were asked comparable questions about 11 consequences of use. Marijuana users were a little more likely to report consequences (15.5% reporting any of the 11 consequences) than alcohol users (11.4%) or cigarette smokers (11.2%). If these rates are extrapolated to the whole population, including nonusers, then 1.9% of the population reported consequences of marijuana use, 7.2% reported consequences of drinking, and 3.4% reported consequences of cigarette smoking. Marijuana users reported noticeably higher rates on four items: "became depressed or lost interest in things", "found it difficult to think clearly", "got less work done than usual at school or on the job", and "felt suspicious and mistrustful of people". Responses to the last two items may be particularly influenced by marijuana's illegal status. Drinkers reported higher rates of "arguments and fights with family or friends" and "found it difficult to think clearly". Cigarette smokers reported higher rates of "felt very nervous and anxious" and "had health problems" (USDHHS, 1993, Table 9.2).

Great caution must be used in interpreting the results of such comparisons. In the first place, the base of users is different for each drug. Those using a widely-used drug are likely to differ on salient characteristics from those using a more rarely used drug. Second, the reported consequence may not be seen by the respondents themselves as adverse. For instance, if the purpose of use in intoxication, it may not be seen as a problems that the respondent "found it difficult to think clearly". Third, responses are likely to be influenced by cultural beliefs about causal connections. The high proportion of young adult smokers reported smoking has harmed their health may reflect acceptance of conventional wisdom as much s personal experience. Fourth and most important, the connection between drug use and adverse consequences will be influenced by a variety of factors applying differentially to different drugs. In particular, a drug's illegal status can itself create adverse consequences for the user, not only directly, through arrest, but also indirectly, for instance in the form of "harm to home life" from the adverse reactions by others to the drug use that involves a risk of arrest.

Keeping these caveats in mind, it is clear that a minority of marijuana users do report harm from their smoking, and some would be likely to do so even if cannabis were legalised. In an era where the health consequences of tobacco smoking are well recognised, tobacco smokers seem to be more likely than users of either cannabis or alcohol to regard their use as doing more harm than good in their lives, and the good is seen as outweighing the bad more often by cannabis smokers than by drinkers or tobacco smokers. In the present circumstances of North America, cannabis smokers are least as likely as alcohol drinkers to report adverse consequences of their use. But the higher rate for alcohol of "arguments and fights with family or friends" reminds us of the special potential alcohol consumption has to have harmful effects on others. Given current patterns of use, when r

[IcePrincessKRS]

[quote name='cooltuba' date='Dec 18 2004, 04:58 AM'] Umm...no, it doesn't point to the [i]use[/i] of drugs as contrary to the moral law. When a pronoun is used twice in a sentance, the antecedent (the noun a pronoun refers to) does not change. Sorry.

Tim [/quote]
So in your opinoin what practices that are contrary to the moral law DOES that paragraph refer to? The first two sentances condemn using drugs except on "theraputic grounds," the third states that production and distribution are morally wrong. I understand the final sentance to refer to both parts, production is evil since it encourages people to use drugs which is contrary to the moral law.

[quote]CCC 2291 The use of drugs inflicts very grave damage on human health and life. Their use, except on strictly therapeutic grounds, is a grave offense. Clandestine production of and trafficking in drugs are scandalous practices. They constitute direct co-operation in evil, since they encourage people to practices gravely contrary to the moral law.[/quote]

[jasJis]

[quote name='cooltuba' date='Dec 18 2004, 11:34 AM'] CONCLUSIONS

There are health risks of cannabis use, most particularly when it is used daily over a period of years or decades. Considerable uncertainty remains about whether these effects are attributable to cannabis use alone, and about what the quantitative relationship is between frequency, quantity and duration of cannabis use and the risk of experiencing these effects. Using analo [/quote]
That long post and this is the only conclusion?

The article does not deny, in fact, it affirms that there is real harm is smoking pot. It does not deny, infact, it again affirms there are psychoactive changes caused by THC.

What justification is there to promote the increased use of pot?

[cooltuba]

[quote name='IcePrincessKRS' date='Dec 18 2004, 12:19 PM'] So in your opinoin what practices that are contrary to the moral law DOES that paragraph refer to? The first two sentances condemn using drugs except on "theraputic grounds," the third states that production and distribution are morally wrong. I understand the final sentance to refer to both parts, production is evil since it encourages people to use drugs which is contrary to the moral law.

[/quote]
I think that both instances of "they" in that sentance refer to the production and distribution of drugs. Using the rules of the English language, both instances of "they" have to refer to the same antecedant, unless the CCC is using incorrect English.

What about mine and Winchester's comment that 2291 would also prohibit the use of alcohol except for theraputic purposes?

Peace,

Tim

[cooltuba]

[quote name='jasJis' date='Dec 18 2004, 12:38 PM'] That long post and this is the only conclusion?

The article does not deny, in fact, it affirms that there is real harm is smoking pot. It does not deny, infact, it again affirms there are psychoactive changes caused by THC.

What justification is there to promote the increased use of pot? [/quote]
That article affirms the health risks of marijuana when used daily over a period of years or decades.

While there would be increased use, there wouldn't nessesarily be increased daily use.

Talk to the WHO about the length of their study, I just posted it for your convience.

The conclusion of the study was quite worth the length in my opinion. Alcohol and tobacco are more harmful than marijuana. Pretty cut-and-dried if you ask me.

The study even included many of the non-plausible studies that I'm not too fond of, and they still concluded that marijuana is less harmful to humans than alcohol and tobacco.

I never said that marijuana wasn't harmful, just that it's not as harmful as many would have us believe, and that many of the mis-conceptions are untrue (the gateway effect, permanent short term memory loss, etc.).

I'm tired. It's nap time.

Peace,

Tim

[IcePrincessKRS]

[quote name='cooltuba' date='Dec 18 2004, 05:40 PM'] I think that both instances of "they" in that sentance refer to the production and distribution of drugs.  Using the rules of the English language, both instances of "they" have to refer to the same antecedant, unless the CCC is using incorrect English.

What about mine and Winchester's comment that 2291 would also prohibit the use of alcohol except for theraputic purposes? [/quote]
I understand that, I never disagreed and said "they" meant anything different, I was trying to define what "practices gravely contrary to the moral law" means. I think the CCC is saying, essentially, "production and distribution constitute direct co-operation in evil, since production and distribution encourage people to practices (namely using drugs) gravely contrary to the moral law." Since both instances of "they" refer to "production and distribution" it doesn't make sense that "practices" also means "production and distribution." Besides, how could it be a sin to produce the stuff but not a sin to use it (without grave reason for theraputic purposes)?

The CCC addresses alcohol seperately from drugs, so perhaps as Winchester said the wording is poor, but I don't think alcohol falls under 2291.

Edited December 18, 2004 by IcePrincessKRS

[jasJis]

[quote name='cooltuba' date='Dec 18 2004, 04:51 PM'] That article affirms the health risks of marijuana when used daily over a period of years or decades.

While there would be increased use, there wouldn't nessesarily be increased daily use.

Talk to the WHO about the length of their study, I just posted it for your convience.

The conclusion of the study was quite worth the length in my opinion. Alcohol and tobacco are more harmful than marijuana. Pretty cut-and-dried if you ask me.

The study even included many of the non-plausible studies that I'm not too fond of, and they still concluded that marijuana is less harmful to humans than alcohol and tobacco.

I never said that marijuana wasn't harmful, just that it's not as harmful as many would have us believe, and that many of the mis-conceptions are untrue (the gateway effect, permanent short term memory loss, etc.).

I'm tired. It's nap time.

Peace,

Tim [/quote]
cooltuba,
You aren't blind.

What is the difference in the rate of usage between pot and alcohol? Alcohol is used more because it's legal.
What did the Netherlands and Alaska find out when it was legalized or decriminalized? Usage went up. Of course daily usage goes up. THC is stored in the fat cell of the human body and it's presence is culmulative. No matter what your complaints are about some studies, no studies have concluded that THC is harmless or clearly identified what the longterm physiological effects are in order to prove it as harmless.
More people die from the flu every year than from LSD. Should we legalize LSD? Alcohol has been ingrained in our cultures for thousands of years as a Significant activity enjoined by the majority of the population. Considering it's inebriating harmful effects that we now fully understand, why can't we learn a lesson and not add to societie's proplems?

You have not answered my question: "Why should any society encourage increased usage of a chemical (THC) that is known to have certain harmful effects and we don't know what other long-term harmful effects may be?"