Chapter Five The Spurious Arguments for Prohibition
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Drug Abuse
Chapter Five The Spurious Arguments for Prohibition
There is a terrible, demoralizing fascination in the possibility that gigantic lies and monstrous falsehoods can eventually be established as unquestioned facts, that man may be free to change his own past at will, and that the difference between truth and falsehood may cease to be objective and become a mere matter of power and cleverness, of pressure and infinite repetition.
Hannah Arendt (165)
The terrorist mythology of those who support the repression of cannabis is a mosaic of motley formulae that are presented as self-evident scientific truths, but in fact collapse under the most casual scrutiny. It is probably quite impossible to keep up with these people's unlimited inventiveness and the impressive speed with which they fabricate a new 'scientific' argument as soon as the previous one has been demolished. A glance at the pack of unfounded accusations that have been produced purely and simply in order retrospectively to legitimise and perpetuate the persecution of cannabis and cannabis users leads to the inevitable conclusion that the scaremongering practised by the crusaders for repression and prohibition essentially consists in no more than the trite repetition of a handful of untruths and groundless assertions. These are that:
1) Cannabis `is addictive'
2) Cannabis `is the first step towards heroin'
3) Cannabis `causes brain damage'
4) Cannabis `leads to chromosome damage'
5) Cannabis `weakens the body's defences'
6) Cannabis `reduces testosterone'
7) Cannabis `leads to hashish psychosis'
8) Cannabis `causes aggression'
9) Cannabis `causes dangerous driving'
The completion of the internationally acclaimed scientific studies conducted for years on chronic cannabis users in Jamaica, Costa Rica, and Greece dealt a harsh blow to the imaginative crusaders for repression, though their myth-making continued unabated.(166)
The fact that the supporters of prohibition remain undaunted and inflexible before the findings of a stream of scientific investigations that demolish their anecdotal, unrealistic claims simply shows either that they have an inexhaustible supply of fantasies and obsessions governed by phobomania or that 'anti-drug' soteriology is unfortunately still a thriving business that can guarantee its shareholders a social `career'. And more in some cases.
Even though they are repeatedly contradicted by past experience and present scientific research, the advocates of prohibition persist in regurgitating the flagrant untruth that cannabis leads to drug addiction; which means, first and foremost, physical dependence, always assuming that such terms still mean anything at all. (167)
The use of cannabis does not lead to physical dependence; cessation of use is not followed by withdrawal symptoms, and consequently `THC is not a drug.' (168) In 1953, L. J. Thompson and R. C. Proctor summed up the attitude of the great majority of the medical profession in their firm assurance that `the use of cannabis does not give rise to biological or physiological dependence and discontinuance of the drug does not result in withdrawal Symptoms.'(169) And in 1976, Stephen Szara of the United States' NIDA categorically stated that `the question of physical dependence. . . has been answered with a flat no. No physical dependence, of the type seen in opiates, has been seen in man and this is true even today." (170)
That cannabis is not addictive is also proven by the fact that there is no mention of how to treat `cannabis addiction' in the textbooks on the treatment and cure of addiction which are used in US universities and medical schools and are approved by the medical profession all over the world. (171)
In this respect, the results of the research conducted on regular users of cannabis and tobacco by the Canadian Government's Commission of Inquiry into the Non-Medical Use of Drugs are particularly eloquent. When asked whether they would rather give up cannabis or tobacco if they had to choose, they all replied that they would prefer to give up tobacco. But when they were asked to do so, by the end of the first day they all opted to give up cannabis after all, being unable to cope with the terrible withdrawal symptoms. A comparative study of cannabis and alcohol produced similar results.(172)
However, the medical literature does contain some accounts of cases of tolerance and mild withdrawal symptoms in individuals taking large doses of synthetic A9-THC under laboratory conditions (a daily dose of 210 mg of synthetic Q9-THC, which is equivalent to 20-40 joints of natural marihuana). (173)
The American Psychiatric Association, however, preferred to ignore these essential differences; to spotlight the observations relating to the experimental administration of large doses of A9-THC under totally different circumstances from the everyday situation in which cannabis is generally used; and to devise the diagnostic category of `cannabis dependence' which it included in its Guide to Diagnostic Criteria DSM-III. (174)
To spare my readers a tiring peregrination through many volumes of scientific literature that flatly contradict this figment, let me present the conclusions of some Greek scientists who have looked into the matter. I must stress that, despite what they concede in theory, not one of them has ever made a public stand even for the decriminalisation of cannabis, much less for its legalisation.
In contrast to opiates, prolonged use of hashish presents no physical syndrome of chronic poisoning'.
(Yannis Ayoutandis, Professor of Forensic Medicine)
Tolerance and physical dependence apparently do not arise from the use of cannabis, hashish or marihuana.
(Dionyssios Varonos, Professor of Pharmacology)
The organism apparently does not become habituated [to hashish], for the dose does not have to be increased. Nor is physical dependence observed, as with addictive drugs that is to say no withdrawal symptoms are observed.
(Yorgos Logaras, Professor of Pharmacology)
Long-term consumption of cannabinoids has not been correlated with the development of physical dependence.
(Marios Marselos, Professor of Pharmacology)
Cannabis does not cause biological dependence.
(Kostas Stefanis, Professor of Psychiatry)
[Hashish] does not cause habituation, it does not develop physical dependence.
(Andreas Davaroukas and Yannis Souretis, Surgeons General) (175)
2. Cannabis `is the first step towards heroin'
The only supporting evidence for this particular joke put about by the supporters of repression is the fact that so many of them have told it. The numerous reports produced by national scientific bodies and government commissions in various countries, (176) not to mention all the relevant investigations, whose gravity has never been doubted by the scientific community, unequivocally contradict the discredited and groundless `escalation theory'.
As early as 1952, surveys amongst heroin addicts in Chicago found that only 11 % of them had a history of marihuana use. At the same time two large-scale surveys in New York City concluded that "marihuana use was not a causal element in the aetiology of heroin use. "(177)
After a follow-up study of an in-depth investigation, Zinberg and Weil concluded that their results provided `absolutely no evidence that cannabis users progress to hard drugs' and that the herb users were actually less inclined to use other drugs, including alcohol.(178)
The British pharmacologist W. Patton explicitly confirms that `cannabis and heroin-taking have nothing to do with each other. In that case the incidence of cannabis-taking among known heroin-addicts should be the same as that of the general population.'(179)
Lester Grinspoon, Professor of Psychiatry at Harvard Medical School and internationally acclaimed expert on marihuana and its medical uses, categorically states that `there is nothing to indicate that the use of marihuana is one of the causal factors behind this heavier use of more dangerous substances." (180)
Jerome Jaffe, Professor of Psychiatry, Nixon's and Ford's adviser on drugs, and nicknamed the `drug pope' in the USA, explains that the belief that cannabis use leads to heroin is erroneous.' (181)
And it is not only scientists who unequivocally confirm that cannabis is not the first step towards the use of addictive substances. When they are not soliloquising in front of an unsuspecting public, but delivering a report to specialists or informed politicians, even the preachers of prohibition are forced to concede the truth of the matter.
Not only is cannabis use not `the first step towards heroin', it is already being tested with encouraging results, and may eventually prove useful in efforts to release people from dependence on such toxic substances as alcohol and heroin.' (182)
3. Cannabis `causes brain damage'
The third favourite claim of those who have their money on the banning of cannabis is the deliberately invented and sustained fiction that use of cannabis causes "various kinds of organic damage, particularly atrophy of the brain".
It is a claim that was first made after A. Campbell and his associates published an article in The Lancet in November 1971, maintaining that "the brains of 10 heavy marihuana smokers showed evidence of cerebral atrophy as demonstrated by air encephalography."(183) An impressive amount of pseudo-scientific hot air was subsequently produced on the basis of Campbell's article, despite the fact that it was harshly criticised and dismissed by the international scientific community as being of no significance whatsoever.' (184)
Professor Lester Grinspoon stringently criticised Cambell's article and showed that it was totally unreliable. He wrote, inter alia:
The deficiencies of the Campbell study are crippling. All 10 subjects were psychiatric patients, and no comparison was made with psychiatric patients who did not use cannabis. At least 1 and maybe 2 were epileptics, several had suffered head injuries, I was mentally retarded, and as many as 5 had been schizophrenic. All had taken LSD, most had used amphetamines, and a few were heavy users of opiates, barbiturates, and tranquillizers. The possible role of alcohol, which is known to be neurotoxic, was not considered. The peculiarity of this sample and the absence of controls make Campbell's results valueless. It would be useful to have controlled prospective studies on cannabis brain damage, but there is little reason to expect that any connection will be discovered. In a controlled retrospective study of chronic cannabis users in Greece, for example, echoencephalography revealed no evidence of cerebral atrophy.(185)
Professor Jerome Jaffe's critique was equally dismissive, and he emphatically asserted that studies had been conducted that were very well controlled with regard to methodology, and not one had found evidence of cerebral atrophy, nor any kind of permanent brain damage.(186)Not only was there not the slightest indication of cerebral atrophy, but many large-scale surveys of American students have found no evidence whatsoever that regular users of cannabis are less academically successful than non-users.(187)
4. Cannabis `leads to chromosome damage'
On the same level of seriousness is the prohibition brigade's assertion that cannabis use "has adverse effects on chromosomes". This one came to life in 1972 after Stenchever and Allen published a `study' reporting chromosome breaks in white blood cells caused by the effects of marihuana.'(188)
These findings were completely contradicted by the three long-term studies conducted in Jamaica, Costa Rica, and Greece, and Stenchever and Allen's work was conclusively discredited by all the systematic investigations carried out thereafter in order to investigate their claims.
Professor S. Matsuyama affirms that "a comparison of the frequency of [chromosome] breaks before and after marihuana smoking (for 72 days) revealed no significant difference... No structural abnormalities other than simple chromatid and isochromatid breaks and fragments were seen either before or after the experimental periods."(189) In summary, the available cytogenetic data provide no definitive evidence of chromosome damage as a result of marihuana use. (190)
Professor Jerome Jaffe has established that no contemporary study, whether of human beings or of animals, has shown chromosome changes connected with the use of cannabis.'(191)
And Professor Lester Grinspoon confirms that all the "recent prospective studies on both animals and human beings have shown no chromosome differences between cannabis users and controls."( l92)
5. Cannabis `weakens the body's defences'
The assertion that cannabis use affects the immune system was made by Gabriel Nahas in an article in 1974.(193)It was absolutely refuted by all subsequent investigations, most notably the study conducted by White et al. in 1975 and the investigative study carried out by J. Silverstein and Lessin of Los Angeles University, who proved that "chronic marihuana use does not produce a gross cellular immune defect that can be detected by skin testing."(194) This was also confirmed by the Jamaican, Costa Rican, and Greek studies mentioned earlier, and many other studies. (195)
On this basis, the US Department of Health and its National Institute on Drug Addiction concluded that no proof has yet been produced that marihuana users are more susceptible to illnesses such as viral infections and cancer, which are connected with reduced T-cell production. (196)
6. Cannabis `reduces testosterone'
The assertion that cannabis reduces the level of testosterone in users' blood was put forward by Kolodny in 1974. In an article in the New England Journal of Medicine he stated that marihuana use `decreases plasma testosterone and plasma luteinizing hormone levels in healthy young men.' (197)
The paper did not specify the users' testosterone levels prior to their use of cannabis, and it was thus impossible to make a comparison and draw conclusions. So the report itself cast doubt on its own credibility right from the start.(198)
A few months later the same journal published a study by Mendelson, who had examined 27 young men, who had been smoking cannabis for an average of 5.6 years. They refrained from smoking for two weeks and then used marihuana for a period .of 21 days (12 of them smoked 1-5 joints a day and the rest 1-8 joints a day). The comparison of testosterone levels before, during, and after this period showed that there were no significant differences: their testosterone level remained stable. "High-dosage marihuana intake was not associated with suppression of testosterone levels." (199)
In 1976, Kolodny's claim was refuted by the study carried out in Costa Rica by Coggins et al., who compared the testosterone levels of 38 individuals who had smoked an average of 9.6 joints a day for 17 years and 38 non-users. No difference was found either between the two groups or between the heavy and light users.(200)
In 1977, in the US Department of Health's sixth annual report to Congress, the National Institute on Drug Abuse evaluated all the studies produced hitherto and concluded that the biological significance of the changes in testosterone levels was doubtful: the results might have been significant in the case of individuals already presenting reduced fertility or endocrinal dysfunction, but they were of no significance in normal subjects. Furthermore, studies had recently shown that regular consumers of alcohol could present reduced testosterone levels, which made it difficult to distinguish between the effects of cannabis and of alcohol, since people frequently use both substances. (201)
7. Cannabis `leads to hashish psychosis'
The assertion that the use of cannabis produces `hashish psychosis' was made in 1957 by the Moroccan psychiatrist A. Benabud and dismissed as groundless when many careful studies proved that he was referring not to real permanent psychosis but to toxic reactions due to enormous doses of hashish (20-30 pipes a day) in association with the extremely overcrowded living conditions of the poorer people in underdeveloped countries.(202)
Benabud's hypothesis was also dismissed in the reports of the scientific commissions appointed by the US and Canadian governments,(203)in the long-term studies of chronic hashish users conducted in Jamaica, Costa Rica, and Greece under the aegis of the World Health Organisation,(204) and by virtually all the scientists who have investigated it.
As Giancarlo Arnao points out, many of these scientists (such as Fort, Grinspoon, Murphy, et al.) have concluded that the use of cannabis not only does not lead to psychosis but, on the contrary, probably helps to rectify certain pathological mental conditions and to alleviate the most obvious symptoms in certain individuals.(205)
8. Cannabis `causes aggression'
The notion that "the use of cannabis causes violent and aggressive behavioural manifestations" is really not worth commenting on, for it is obviously addressed to the ignorant, either by the very naive, who may justifiably say whatever they please, or by people who are well aware of the truth and are deliberately distorting it to serve political and economic ends.
In complete contrast to licit alcohol, which (given that 50% of the murders and 25% of the suicides committed in the United States every year - an annual average of 11,700 cases - and 50% of the traffic accidents all over the world take place under its influence) demonstrably increases its consumers' destructive aggression, the use of illicit cannabis not only does not promote violence or aggression, but on the contrary suppresses or drastically reduces it. This is why, quite rightly, most laboratory experiments have found that during the process of toxification aggression is reduced. The evidence generally indicates that cannabis does not lead to violence, but that alcohol-induced drunkenness very frequently promotes and reinforces violent behaviour.(206)
9. Cannabis `causes dangerous driving'
Despite the allegations of those who support the banning of cannabis, it does not in fact pose an appreciable threat to road safetycertainly much less than alcohol.
In 1969, Crancer et al. compared the effects of marihuana and alcohol on people undergoing a simulated driving test, and found that those who had consumed alcohol made many more errors than those who had taken cannabis (whose error-rate was very slightly higher than that of the control group). They also found that cannabis users tended to drive more slowly than the other groups.
Impairment in simulated driving performance does not seem to be a function of increased marihuana dosage or inexperience with the drug... None of the subjects showed a significant change in performance. Four additional subjects who had never smoked marihuana before were pretested to obtain control scores, then given marihuana to smoke until they were subjectively `high' with an associated increase in pulse rate... All subjects showed either no change or negligible improvement in their scores. (207)
Weil et al. studied the effects of cannabis use on both experienced and inexperienced consumers and concluded that the driving ability of the experienced users was affected slightly less than that of the inexperienced users.(208)
Kielholz conducted a similar investigation on behalf of the Canadian Government Commission, administering 24-32 mg of synthetic Δ9-THC to the research subjects.(209) He found that the subjects' response to constantly changing situations was inadequate.(210)
Hansteen, Miller, Lonero, Reid, and Jones, also on behalf of the Canadian Government Commission, investigated the effects of cannabis, alcohol, and a combination of the two in driving situations very similar to real ones.(211)
COMPARISON BETWEEN CANNABIS AND ALCOHOL The volunteers were divided into three groups. Group 1 received a moderate dose of cannabis equivalent to 1.4 mg of Δ9-THC. Group 2 received a large dose of cannabis equivalent to 5.9 mg ofΔ9-THC. And group 3 received a large dose of alcohol, giving a blood alcohol level of 0.07% .(212) The control group consisted of people who had consumed neither alcohol nor cannabis. When the effects of the substances had begun to make themselves felt, the volunteers underwent a driving test along a specified route and at a specified speed, with the following results.
a) Number of errors: Group 3 made 32% more errors than the control group. Group 2 made 27% more. And there was no difference between Group 1 and the control group.
b) Speed: Group 3 drove faster than the control group. Group 2 drove slightly slower, and group 1 considerably slower.
c) Lack of co-ordination: Group 3 scored 2.7, group 2 scored 2.2, group 1 scored 1.9, and the control group scored 1.7.
COMPARISON BETWEEN CANNABIS, ALCOHOL, AND CANNABIS AND ALCOHOL TOGETHER The volunteers were divided into five groups. Group 1 was given a large dose of cannabis equivalent to 6.8 mg of I9-THC. Group 2 received a moderate dose of cannabis equivalent to 1.6 mg of 09-THC. Group 3 received a large dose of alcohol, giving a blood alcohol level of 0.07%. Group 4 received a moderate dose of alcohol, giving a blood alcohol level of 0.03%. And group 5 received a moderate dose of alcohol together with a moderate dose of cannabis. When the effects of intoxication were felt, the groups underwent a driving test along a specified route and at a specified speed, with the following results.
a) Number of errors on a simple route: Group 3:130, Group 5:105, Group 4:95, Group 1:90, Group 2:85 (control group: 75).
b) Number of errors on a complicated route: Group 5:205, Group 3:195, Group 1: 185, Group 2:160, Group 4:150 (control group: 160).
c) Reaction time: Reaction time was longer for Groups 3, 4, and 5. It remained the same for Groups 1 and 2 and the control group. When the tests were repeated three hours later, there was no difference between the volunteers and the control group.(213)
Investigating the subject on behalf of the US government, Dott studied the behaviour of volunteers undergoing driving tests after taking 11.2-22.5 mg of synthetic Δ9-THC by mouth. He found that they were all reluctant to get involved in a slightly dangerous situation (e.g. overtaking), and that their reaction time was increased. Light and Keiper repeated the experiment on volunteers who were given alcohol (blood alcohol level of 0.089%) and found that their behaviour was more aggressive and their reaction time also longer.
After examining the results of these two experiments, Dott affirmed that, though the attention of people under the influence of marihuana is reduced, they are able to rectify the effect of this if necessary. In contrast, people under the influence of alcohol are powerless to rectify its effects. Therefore, he concluded, from the point of view of road safety, intoxication with alcohol is more dangerous than intoxication with marihuana.(214)
In 1972, the Canadian Government Commission analysed the results of the studies conducted in the United States and Canada together with the conclusions of investigations conducted by scientific groups on its behalf, and concluded that there was no evidence that marihuana had a negative effect on either alertness or reaction time. The use of cannabis could, it seemed, reduce driving ability, but the effects were closely linked to the individual's experience of driving while high. Obviously, driving while intoxicated was dangerous and should be avoided, but there was no proof that the use of cannabisincreased the dangers of driving. The risk of driving a car or an aeroplane while under the influence of any substance could not be stressed too highly, yet cannabis gave no cause for alarm. The Commission pointed out that the Canadian Penal Code laid down specific sanctions for dangerous driving, and that, in the Commission's opinion, was sufficient.(215)
Also in 1972, the US National Commission on marihuana and Drug Abuse concluded in its report that although marihuana could not be considered completely harmless, experimental and occasional use of it posed minimal risk to public health. It was an offence to operate a vehicle or dangerous machinery while under the influence of either marihuana or alcohol. Being under the influence of marihuana was not an extenuating factor in the commission of a criminal act: anyone causing personal or material damage while under the influence of marihuana was held to be fully responsible.(216)
165 H. Arendt, The Origins of Totalitarianism (1951), p.333.
166 There were no noticeable differences between the findings of the three investigations: V. Rubin and L. Commitas (1975), P. Satz, J. Fletcher, and L. Sutker (1977), C. Stefanis, J. Boulougouris, and A. Liakos (1976).
167 See Chapter 1, section 9, `Tolerance and dependence'.
168 R. Julien, A Primer of Drug Action (1992), p.270.
169 L. Thompson and R. Proctor (1953), pp.520-3.
170 S. Szara, in Braude and Szara, eds, Pharmacology of Marihuana (1976), p.29.
172 Commission of Inquiry into the Non-Medical Use of Drugs, Interim Report (1970), 124.
173 See Chapter 1, section 9, `Tolerance and dependence'.
174 American Psychiatric Association (1980).
175 Y. Ayoutandis (1973), D. Varonos (1987), Y. Logaras (1971), M. Marselos (1986), p.212, C. Stefanis (1990), A. Davaroukas and Y. Souretis (1981), p.66.
176 The most important of which are mentioned in Chapter 4: `Official Reports'.
177 L. Grinspoon, Marihuana Reconsidered (1977), p.243.
178 N. Zinberg and A. Weil (1970), p.119, 122.
179 W. Patton (1968), pp.200-12.
180 L. Grinspoon, Marihuana Reconsidered (1977), p.251.
181 J. Jaffe, R. Peterson, and R. Hodgson, Addictions (1980), p.77.
182 E. Birch (1889); L. Thompson and L. Proctor (1953); T. Mikuriya (1970); J. Scher (1971).
183 A Campbell et al. (1971), p.1224.
184 Commission of Inquiry into Non-Medical Use of Drugs: Interim Report (1970); US DHEW (1971).
185 L. Grinspoon, Marihuana Reconsidered (1977), p.387.
186 J. Jaffe, R. Peterson, and R. Hodgson, Addictions (1980), p.76;
187 J. Jaffe, R. Peterson, and R. Hodgson, Addictions (1980), p.74.
188 M. Stenchever and M. Allen (1972), p.821.
189 S Matsuyama et al, `Chromosome Studies Before and After Supervised Marihuana Smoking', in Braude and Szara, eds, Pharmacology of Marihuana (1976), pp.726-7.
190 S. Matsuyama, 'Cytogenic studies of Marijuana', in Marihuana and Health Hazards (1975).
191 J. Jaffe, R. Peterson, R. Hodgson, Addictions (1980), p.75.
192 L. Grinspoon, Marihuana Reconsidered (1977), p.390.
195 B Petersen, J. Graham, L. Lemberger, and B. Dalton, 'Studies of the immune response in chronic marihuana smokers', Pharmacologist, 16 (1974), 259.
196 US Department of Health, Marihuana and Health, Annual Report to the US Congress (1977 and 1980).
197 R. Kolodny et al. (1974), New England Journal of Medicine, 290 (1974), 872-4.
199 J. Mendelson et al. (1974), `Plasma testosterone level before, during and after chronic marihuana smoking', New England Journal of Medicine 291 (1974), p.1051
200 W. Coggins, E. Swenson, and W. Dawson, in NYAS, Chronic Cannabis Use (1977), p.160.
201 US Department of Health, Marihuana and Health, Annual Report to the US Congress (1977), p.18.
202 G. Arnao, Erba Proibita (1978), p.104.
203 Commission of Inquiry into Non-Medical Use of Drugs: Interim Report (1970), p.71.
205 G. Arnao, Erba Proibita (1978), p.105.
209 Thirty per cent of which was absorbed, i.e. 8-10 mg. A normal joint of natural marihuana contains 500 mg of marihuana with a content of 1 % THC; i.e. it contains 5 mg of THC, of which the smoker's body absorbs 30%, i.e. approximately 2 mg. Consequently, in order to absorb 8-10 mg of THC, one has to smoke 4-5 joints.
210 US Department of Health (1973), p.139.
211 US Department of Health (1973), p.139.
212 A blood alcohol level of 0.07% equates to 320 gr. (two glasses) of 12° wine or 96 gr. of 40° whisky. In most Western countries it is an offence to drive with a blood alcohol level of more than 0.08%.
213 All the data pertaining to the driving tests are taken from G. Arnao, Erba Proibita (1978).
216 US National Commission on Marihuana and Drug Abuse (1972)
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