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World Health Organization
A Comparative Appraisal of the Health and Psychological Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
III. 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.
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.
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.
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).
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).
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.
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.
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