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Antworten auf den Artikel von Prof. Henry und Dr. Oldfield (British Medical Journal)
- British Medical Journal vergleicht Cannabis mit Tabak
[CLN#109, 09.05.2003]
John A Henry, William L G Oldfield, and Onn Min Kon
BMJ 2003; 326: 942-943
Rapid responses published:
- [Read Rapid response] A valid point but several speculative claims
- Andrew Parfitt, SG 15 (2 May 2003)
- [Read Rapid response] Comparing cannabis with tobacco: the arithmetic does not add up
- Leslie L Iversen (3 May 2003)
- [Read Rapid response] Cannabis and Lung Health
- Mitchell S. Earleywine, University of Southern California, Los Angeles, CA, USA 90089-1061 (3 May 2003)
- [Read Rapid response] Editorial Bias
- Thomas J O'Connell MD, none (4 May 2003)
- [Read Rapid response] Can cannabis and tobacco be compared? Apples and oranges!
- Andrew Byrne (5 May 2003)
- [Read Rapid response] Evidence based responses to cannabis
- Alex D Wodak (5 May 2003)
- [Read Rapid response] CHRONIC CANNBIS USE AND CYCLICAL VOMITING SYNDROME
- James H. Allen. (5 May 2003)
- [Read Rapid response] Cannabis: A 'lesser evil' for lung cancer risk?
- Zubair Kabir (5 May 2003)
- [Read Rapid response] Effects of Cannabis on Educational Performance
- Mary D. Brett (6 May 2003)
- [Read Rapid response] THE DETRIMENTAL EFFECTS OF CANNABIS
- Roy Robertson (7 May 2003)
- [Read Rapid response] Cannabis in the real world
- C. Heather Ashton (7 May 2003)
- [Read Rapid response] Biased, scaremongering
- Mark Pawelek (7 May 2003)
- [Read Rapid response] Comparing cannabis with tobacco
- Gary D Williams (7 May 2003)
- [Read Rapid response] Reefer madness revisited - why?
- Rod MacQueen (7 May 2003)
- [Read Rapid response] Competing Interests
- Bernie K Masters (10 May 2003)
- [Read Rapid response] Competing Interests and Stereotypes about Cannabis
- Mitch Earleywine, Los Angeles, CA USA 90089-1061 (11 May 2003)
- [Read Rapid response] Numerous misunderstandings in this editorial
- Clive D Bates (12 May 2003)
- [Read Rapid response] A Science Based Evaluation of Cannabis and Cancer
- Robert Melamede (23 May 2003)
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Andrew Parfitt, Consultant A and E Lister Hospital Stevenage, SG 15
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Sir, I read with interest the editorial by Henry et al. I should like to address the fact that cannabis use is as they say associated with an increased incidence of mental illness however the casual relationship remains to be proven and to follow on in the same sentence to state 'to examine its potential to 'cause' other illnesses is imprecise and may be read that we have excepted the evidence that cannabis does indeed cause mental illness. No such casual evidence exists. The paper by BAchs et al relating to acute cardiovascular fatalities following cannabis use is far again from conclusiveand the authours themselves were cautious to stress the , and I quote , possible nature of the association. Again the text of the Henry paper reads 'attributed' clearly there is a difference again between cause and association. In addition one must remember that many users of cannaboids are staunch antismokers and instead prefer to cook so called 'hash cakes'I wonder how many of the schoolchildren who admitted taking cannabis had done this in preference to smoking. Indeed if users are eating rather than smoking then the putative causal relationship is many times less likely. Competing interests: None declared |
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Leslie L Iversen, Visiting Professor of Pharmacology Dept Pharmacology, Univ of Oxford, OX1 3QT
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A recent editorial suggested that in the future as many as 30,000 deaths a year in Britain may be caused by smoking cannabis(1). But this conclusion was not based on any new scientific evidence and the arithmetic appears to be based on a series of questionable assumptions. Cannabis smoke does contain many of the same poisonous substances that are found in tobacco smoke and cannabis smokers deposit more tar in their lungs than cigarette smokers because they inhale more deeply and tend to hold their breath(2). But to expose the lungs to the same amount of tar as an average 15 - 20 a day cigarette smoker, cannabis users would have to smoke 4-5 times a day every day of the week. In fact surveys of young cannabis users in Britain suggest that very few fall into this category ¨C a large majority are occasional ¡°weekend¡± users, and even among more frequent users few fall into the high use category of 4-5 times a day(3). It is obviously impossible to get accurate statistics on the numbers of daily cannabis users, but the figure of 3.2 million in Britain cited by the authors of the editorial is far too high. It is also difficult to get accurate scientific data on the effects of regular cannabis use on the lungs because many users mix cannabis resin with tobacco. But studies of cannabis-only smokers in California showed that they do tend to develop signs of chronic bronchitis ¨C but there is no evidence that this progresses to more severe lung diseases such as emphysema or lung cancer(4). An important factor is that unlike cigarette smokers most cannabis smokers tend to quit when they reach their 30¡¯s. Long term surveys of cigarette smokers showed that those who quit before the age of 35 had only a very slightly increased risk of lung cancer(5). The risk of developing lung cancer depends far more on the duration of smoking than on the number of cigarettes consumed. Thus smoking 40 cigarettes a day as opposed to 20 doubles the risk of lung cancer, but smoking for 30 years as opposed to 15 years increases the risk by 20-fold. If the risks of cannabis smoking equate to those of tobacco and the majority of users give up before the age of 35 they may run little additional medical risk. The BMJ authors also suggested that the more potent forms of cannabis that are sometimes available nowadays somehow carry an increased medical risk ¨C but one could argue exactly the opposite. THC, the active chemical ingredient in herbal cannabis, is not known to be harmful to the lungs ¨C indeed there is some scientific evidence that it may possess anti -cancer properties(6). It is also known that users when exposed to more potent forms of cannabis adjust their smoking behaviour to inhale less frequently and less deeply, while obtaining the same amount of THC (2,7). The users of potent forms of herbal cannabis may thus benefit from a reduced exposure to potentially harmful tar. Finally, the BMJ authors added some gratuitous additional warnings about the dangerous effects of cannabis on the heart. It is true that cannabis tends to stimulate the heart and it could potentially be harmful to people who have a pre-existing heart disease, but the published scientific data has not shown this to be a serious medical problem. The two publications cited are based on very small samples and circumstantial data. In Britain virtually no cases of drug-related death due to cannabis have been reported in recent years ¨C despite our strict national system for reporting substance abuse-related deaths. While cannabis cannot be considered to be completely harmless and it does cause adverse effects on the lungs ¨C the sort of scientific/medical scaremongering indulged in by the authors of this editorial is completely unscientific and fails to advance the public health debate about cannabis. Their arithmetic simply does not add up. Instead they help to bring science into further disrepute, and make it less likely that young people will listen seriously to any health message concerned with drugs. Professor Les Iversen PhD FRS Department of Pharmacology University of Oxford References 1. Henry JA, Oldfield WLG, Min Kon O. Comparing cannabis with tobacco. BMJ 2003; 326: 942-943 2. Wu TC, Tashkin DP, Rose JE, Djahed B. Influence of marijuana potency and amount of cigarette consumed on marijuana smoking pattern. J.Psychoactive Drugs 1988; 20: 43-46 3. Iversen LL ¡°The Science of Marijuana¡± 2000, pp215-220; Oxford University Press, New York 4. Tashkin DP, Baldwin GC, Sarafian T, Dubinett S, Roth MD. Respiratory and immunological consequences of marijuana smoking. J Clin Pharmacol 2002; 42 Suppl 11:71-81S 5. Doll RR, Peto K, Wheatley K, Gray R, Stherland I. Mortality in relation to smoking: 40 years¡¯ observations on male British doctors. BMJ 1994; 309: 901-910 6. Guzm¨¢n N, S¨¢nchez C,Galve-Roperh I. J.Mol.Med.2001; 78: 613-625 7. Matthias P, Tashkin DP, Marques-Magallanes JA, Wilkins JN, Simmons S. Effects of varying marijuana potency on deposition of tar and ¦¤9-THCin the lung during smoking. Pharmacol.Biochem.Behav. 1997; 58: 1145-50 Competing interests: None declared |
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Mitchell S. Earleywine, Associate Professor Department of Psychology, University of Southern California, Los Angeles, CA, USA 90089-1061
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Henry, Oldfield, and Kon sounded the alarm about potential lung problems in cannabis smokers. 1 As these authors mention despite their concerns, large studies still show little lung damage in those who smoke cannabis and not tobacco2. Nevertheless, new information may allay the fears of some readers worried about the plant’s pulmonary effects. First, the reported increase in cannabis potency does not translate into greater risk for pulmonary problems. Though many authors argue that estimates from the 1970s of .5% THC are clearly inaccurate, most believe current data suggesting that THC concentrations average near 5% and can reach as high as 20%. The stronger cannabis, however, yields less tar per unit of THC than weaker cannabis, and leads to less deposition of tar into the lungs of smokers 3. Because problem users are often reluctant to abstain from cannabis completely, health care professionals might suggest ways to increase the safety of the drug. The common habit of holding smoke in the lungs for extended periods provides greater exposure to noxious materials. This practice should be actively discouraged. At least 3 studies show that longer breathhold durations have little meaningful impact on intoxication 4. In addition, vaporizing cannabis rather than smoking it can create the same subjective effects with no exposure to many toxins.5 Vaporizers have become readily available and relatively inexpensive. These machines have the potential to eliminate pulmonary problems associated with cannabis use. Smoking small amounts of potent cannabis through a vaporizer and refraining from holding smoke in the lungs presents little risk of lung troubles. Mitchell Earleywine, associate professor of clinical science Department of Psychology, University of Southern California, Los Angeles, CA, USA 90089-1061 earleyw@usc.edu 1. Henry, J. A., Oldfield, W. L. G., Kon, O. M. Comparing cannabis with tobacco, BMJ 2003; 326:942-943. 2. Polen, M. R. Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med 1993; 158: 596-601. 3. Matthias, P., Tashkin, D. P., Marques-Magallanes, J.A., Wilkins, J. N. & Simmons, M.S. Effects of varying marijuana potency on deposition of tar and delta9-THC in the lung during smoking. Pharmacol Biochem Behav 1993; 58: 1145-1150. 4. Azorlosa, J. L., Greenwald, M. K., Stitzer, M. L. Marijuana smoking: effects of varying puff volume and breathhold duration. J Pharmacol Exp Ther 1995; 272: 560-569. 5. McPartland, J.M., Pruitt, P.,L. Medical marijuana and its use by the immuno-compromised. Altern Ther Health Med 1997; 3:39-45. Competing interests: None declared |
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Thomas J O'Connell MD, none Northern California 94401, none
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The brief editorial, “Comparing Cannabis with Tobacco” by Henry, Oldfield and Kon (British Medical Journal, May 3) is so full of gross inaccuracies, unsupported assumptions and unjustified speculation that, were it not for the fact that it decries chronic use of cannabis, it’s unlikely a reputable journal would publish it. For starters, there is considerable evidence that cannabis provides significant relief of a wide variety of troublesome symptoms; given fierce US prohibition policy (as reflected in United Nations treaties), data supporting that contention has been understandably difficult to gather and publish. Beyond that, the editorial clearly infers that the only way cannabs is used is by smoking in the manner the authors describe at some length. Actually, that manner of smoking, while still too popular, was fokelore based on erroneous assumptions; it has been repudiated in responsible articles for years. There are actually many ways cannabis can be ingested other than smoking; perhaps the best is vaporization, a technique endorsed by knowledgeable clinicians because it preserves the rapid cerebral feedback that allows a user to avoid unwanted intoxication and also largely eliminates the harms of smoking.1 This brief response permits only passing reference to work I am now engaged in-- thanks to the passage of a medical cannabis initiative in California (Proposition 215). That law, passed in 1996, has effectively allowed certain chronic users to ‘come in from the cold ‘ as it were. Systematic interviews of several hundred reveal them to be a very specific population which is surprisingly uniform in the way they became chronic users, their lifetime use of other psychotropic agents (including alcohol and tobacco), and also in their belief that sustained moderate use of cannabis has afforded them considerable benefit over years and-- in many cases-- decades Seen in that context, the editorial is a throwback to “Reefer Madness,” the mid-Thirties American propaganda campaign which eventually led to creation of a huge criminal market for one the most versatile and useful plants ever cultivated. It’s unlikely that the editorial will deter that market significantly, but it certainly contributes to the confusion precluding adoption of an intelligent drug policy; one based on factual evidence rather than empty dogma. 1) D. Gieringer, "Cannabis Vaporization: A Promising Strategy for Smoke Harm Reduction," Journal of Cannabis Therapeutics Vol. 1#3-4: 153-70 (2001) Competing interests: Member of several organizations advocating drug policy reform. |
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Andrew Byrne, Dependency Physician 75 Redfern St, Redfern, NSW, 2016, Australia
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'Comparing cannabis with tobacco'. Henry JA, Oldfield WLG, Kon OM. BMJ (2003) 326: 942-943 I would commend these authors on using the correct scientific term cannabis, unlike some colleagues who seem to prefer terms allegedly introduced by governments rather than scientists. That said, this is one of the most un-scientific BMJ articles I have read. Despite their being opposites in most respects, Henry and co-authors try to compare cannabis and tobacco. While both are common psychoactive drugs, cannabis is a relaxant, tobacco a partial-stimulant. One is highly addicting, the other is not. One has been prescribed by physicians down the ages and continues to be recommended in certain clinical circumstances by doctors of good repute. Hence a 'comparison' is an intriguing concept unless clearly stated objectives are being examined (eg. dependency, mortality, side effects, beneficial effects, etc). . Cannabis has an extremely low mortality while tobacco's toll is legion. Nearly 20,000 Australians die from tobacco related disease each year with few if any cannabis reported deaths. When examining any drug, one looks for costs and benefits but these authors have only looked for 'costs' and, for cannabis, then they can only point to 'associations'. Even if cannabis actually caused some cases of mental disease (and it does induce dependency in a small proportion of heavy users), the drug may also alleviate some conditions such as anxiety, insomnia, depression, anorexia or chronic pains. These authors state that it might be seen as 'scaremongering' to speculate on the basis of cannabis being of equal toxicity as tobacco ... yet they go ahead and do just that: "the corresponding figure for deaths among 3.2 million cannabis smokers would be 30,000" [annually in the UK]. Can these authors be serious when no group of suspected cases is yet to be reported after the drug has been used for thousands of years in western society? If they are interested in speculation, why don't they look at alcohol consumption in cannabis smokers? Quite apart from their tenuous position in trying to point to cardiovascular complications which may occur with smoking cannabis, they make numerous questionable and unreferenced statements in their paper including the howler about cannabis strength increasing over the years (by 10 to 20 times!). Even if this were true, it would mean less by-products for the same amount of drug and thus possibly safer smoking. Also, cannabis can be taken orally with no effect on the lungs at all, but these authors do not canvass that issue, nor other harm reduction steps. Without references, they also quote "Nederweed" ('the variety smoked in the Netherlands') which they claim has an *average* of 10-11% tetrahydrocannabinol. This is obviously unhelpful since Holland, like other countries, has a variety of cannabis and resins available on the market, including cannabis cookies. These authors make much of the increase in cannabis use and the reductions in tobacco consumption in recent years. However, they are not open enough to discuss the legal status of the drugs. If these authors are honestly concerned about harms from cannabis then it is hard to understand why they would ignore the spectacular failing of current prohibitions in addressing these harms. The results of long term cannabis decriminalization (eg. South Australia, Holland) are equally ignored by these 'scaremongers' (to use their own term). comments by Andrew Byrne .. Competing interests: None declared |
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Alex D Wodak, Director, Alcohol and Drug Service St. Vincent's Hospital, Victoria Street, Darlinghurst, NSW, 2010, Australia
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Dear Sir, Oldfield and Kon observe, quite correctly, that cannabis consumption is rising while tobacco consumption is declining in the United Kingdom. This is true in many other countries and has been the case now for several decades. These developments are no accident. In numerous countries, achieving a decline in tobacco consumption required a steadfast committment to policy based on research evidence concerning which prevention measures work and which do not. The critical public health achievment of tobacco control has been won despite the immense power of the tobacco industry. In contrast, vast resources have been allocated to law enforcement efforts to reduce cannabis smoking with very little benefit identifiable and much in the way of unintended adverse consequences. Surely if there is a lesson to be learnt from this, it is that those who are concerned to reduce the prevalence of cannabis smoking should support the same measures that worked so well for tobacco. Tobacco control has been achieved within the framework of a taxed and regulated drug. There is virtually no support among tobacco control experts for the re-introduction of tobacco prohibition. A sustained decline in cannabis consumption will only be achievable when the drug is taxed and regulated like tobacco and policy is based on evidence. The retention of cannabis prohibition despite the lack of success and the high financial and social cost of this policy, has required a 'talking up' of the toxic effects of cannabis. Cannabis is not by any means innocuous. But the health and other adverse consequences of cannabis are dwarfed by those of alcohol and tobacco. This point was made by several reputable authors in a recent WHO review that was dropped following political pressure. One of the many costs of cannabis prohibition is the publication in reputable medical journals of highly questionable commentary on the relattive toxicity of cannabis. Yours sincerely, Dr Alex Wodak, Director, Alcohol and Drug Service St. Vincent's Hospital, Darlinghurst, NSW 2010 Australia Competing interests: None declared |
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James H. Allen., Visiting Medical Officer Mt.Barker Hospital.Wellington rd.Mt.Barker.South Australia.5255.
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South Australia has had liberal cannabis laws for many years[1].Within our area of the Adelaide Hills it has become apparent that much of what might have previously been described as "psychogenic vomiting" or Cyclical Vomiting syndrome is, in fact, a cannabis related illness.[2] This disorder is characterised by: {a}A history of several years of cannabis abuse prior to the onset of hyperemesis in susceptible individuals. {b}The hyperemesis will follow a cyclical pattern every few weeks or months,often for many years, against a background of regular cannabis abuse. {c}Cessation of cannabis leads to cessation of the hyperemesis in the presence of a negative urine drug screen. {d}Cannabis resumption will herald a return of the hyperemesis many weeks or months later. {e}The patient will compulsively bathe .i.e,will take multiple hot showers or baths during the acute phase of the illness in an attempt to quell the hyperemesis. REFERENCES: [1]South Australia:Controlled Substances Act.1984. [2]Allen J.H. "Cannabinoid Hyperemesis or Marijuana Morning Sickness" ClinMed.Netprints/200111000141. BMJ/Stanford University Highwire Press. Competing interests: None declared |
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Zubair Kabir, Research Fellow CResT Directorate, St. James's Hospital, Dublin 8.
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Sir, I read with interest the editorial of Henry et al (1). Tobacco smoking is the greatest evil in lung cancer risk across 90% of all lung cancer cases. However, evidence suggested that cannabis use is not far behind. Recent trends in lung cancer mortality in the United States showed that there is an apparent ‘birth cohort’ effect in lung cancer risk after 1950 (2). The authors’ have speculated that this observation may be attributed to cannabis smoking, in addition to changing tobacco-smoking habits across the populations. Interestingly, one of the cannabinoids (delta 9-tetrahydrocannabinol) has shown to have an apparent beneficial effect on lung adenocarcinoma in animal models (3). By contrast, there is accumulating evidence of histopathologic and molecular changes in lung tissue of smokers, suggesting cannabis could increase lung cancer risk in humans (4). Is this a paradoxical observation? In addition, cannabis smoke contains many of the same carcinogens found in cigarettes, as pointed out by Henry et al (1). Until the cause-effect relation of cannabis on human health, including lung cancer, is clear, is it ‘scientific’ or rather ‘premature’ to contemplate on cannabis cessation programmes in line with tobacco smoking programmes? References 1. Henry JA, Oldfield WLG, Kon OM. BMJ 2003: 326: 942-3. 2. Jemal A, Chu KC, Tarone RE. Recent trends in lung cancer mortality in the United States. J Natl Cancer Inst 2001; 93: 277-83. 3. Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA. Antineoplastic activity of cannabinoids. J Natl Cancer Inst 1975; 55: 597- 602. 4. Barsky SH, Roth MD, Kleerup EC, Simmons M, Tashkin DP. Histopathologic and molecular alternations in bronchial epithelium in habitual smokers of marijuana, cocaine and/or tobacco. J Natl Cancer Inst 1998; 90: 1198-205. Competing interests: ZK is a Research Fellow in Lung Cancer Epidemiology at the University of Dublin (Trinity College). |
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Mary D. Brett, Head Of Health Education Dr Challoner's Grammar School HP6 5HA
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Apart from the damaging effects of cannabis on the lungs and mental health addressed by Professor Henry et al in their editorial, I would like to draw attention to the harmful consequences to young occasional, even monthly, users. Because of the long-term storage of the drug in the fatty cell membranes of the brain, the chemical transmission system is impaired. Concentration, learning and memory are all badly affected. The educational performance of pupils deteriorates, their grades fall and many miss out on their chosen university places. Our vulnerable children need to be warned of the possibility of lost educational opportunities and subsequent employment, this is not scare- mongering, it is common sense. References: 1 Chait LD, Pierri J, Effects of Smoked Marijuana on Human Performance: A Critical Review. Marijuana/Cannabinoids: Neurobiology and Neurophysiology. Murphy L, Bartke A,(eds)387-423, Boca Raton, CRC Press 1992. 2 Schwartz RH et al, Short-term memory impairment in Cannabis- dependent Adolescents Am. J. Dis. Child.143:1214-1219,1989. 3 Lynskey M, Hall W, The Effects of Adolescent Cannabis Use on Educational Attainment: A Review. Addiction 95 1621-1630. 2000. 4 Solowij N, Cannabis and Cognitive Functioning, Cambridge University Press, 1998. 5 Lundqvist TT, Cognitive Dysfunctions in Chronic Cannabis Users Observed During Treatment - An Integrative Approach, Almqvist and Wiksell International, Stockholm, 1995. Competing interests: None declared |
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Roy Robertson, GP principal Muirhouse Medical Group, 1 Muirhouse Avenue, Edinburgh, EH4 4PL
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Professor Henry and others quite rightly draw attention to the damaging effects of cannabis and the potential problems likely to emerge from its increasing use.(1) There are many aspects to this debate, not least the inevitability of the progress to further use, although other countries have shown this to peak in young people and to deteriorate subsequently. It is also, like most addiction problems, complicated by there being many different side effects, some more serious than others. Like alcohol, cannabis is likely to cause acute physical and psychological as well as long-term damage. Research therefore is urgently required in all these areas. Our own recent study showed, we think, importantly, the relationship between dose and at least some complications.(2) It makes intuitive sense that, like other drugs of intoxication, the harmful effects of cannabis are likely to be dose-related. The public health message, therefore, becomes like that of illegal drugs, not geared towards total abstinence so much as minimising the damage and diverting habitual users from the most serious complications. Cannabis used in small quantities, that is, less than 2 or 3 grammes per day, presents quite a different prospect from more heavy use and truly recreational (intermittent, infrequent and non-dependent type use) must present less of a poor prognosis than dependent type use. Patients with dependent type use, similarly to opiate and alcohol use of this sort, are more likely to be unemployed, maringalised and in the poorer part of the population and it is frequently our experience that self-medication with cannabis is a control mechanism for another wise unrewarding lifestyle. Rather than becoming absorbed with the mechanisms for control or the morality of use of the drug, the Health Service requires an urgent response to another healthcare imperative, that of providing services for the acute effects and the chronic damage caused by another largely ignored (by the Health Service) addictive drug. Yours sincerely Dr Roy Robertson References (1)Henry, J. A., Oldfield, W., L., G., Min Kon, O. Comparing cannabis with tobacco. The British Medical Journal 2003; 326: 942. (2)Robertson, J. R., Miller, P., Anderson, R. Cannabis Use in the Community. The British Journal of General Practice 1996; 46: 671-674. Competing interests: None declared |
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C. Heather Ashton, Emeritus Professor Dep't Psychiatry, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, UK
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I have contact (through North East Council for Addictions - NECA) with cannabis users in the North East. The fact is that many young people (including 1% of schoolchildren) do actually smoke at least 5 (up to 15) spliffs daily and/or inhale from "buckets". Thus they obtain high concentrations of cannabis smoke containing all the constituents of tobacco smoke (except nicotine) including carbon monoxide, bronchial irritants, and carcinogens. Smoking may start as young as 8 years and more and more smokers are continuing for longer - into their 40s and 50s. These kids do not use hash cakes or cookies as suggested by Leslie Iverson. Figures for numbers involved not available, but NECA Counsellors see such users daily. These young people also smoke tobacco and the effects of cannabis and tobacco smoke on the lungs are additive. Unlike tobacco (nicotine) cannabinoids also have adverse psychiatric effects. A large amount of evidence shows that young and adolescent users are especially vulnerable to these effects. Those starting to use cannabis while in their early teens are more likely to suffer intellectual and emotional impairment, escalate to weekly or daily use, to become dependent, to progress to other illicit drugs, to become anxious, depressed and suicidal and to be involved in deliquency and crime than those starting later. References: Fergusson DM, Horwood LJ, Swain-Campbell N. Cannabis and psychosocial adjustment in adolescence and young adulthood.Addiction 2002; 97: 1123-35. Copeland J, Swift W, Rees V. Clinical profile of participants in a brief intervention program for cannabis use disorders. Journal of Substance Abuse Treatment 2001; 20: 45-52. British Lung Foundation. The impact of cannabis smoking on respiratory health. A smoking gun? 2002. Rey JM, Sawyer MG, Raphael B, Patton GC, Lynskey M. Mental health of teenagers who use cannabis. Results of an Australian Survey. British Journal of Psychiatry 2002; 180: 216-21. Swift W, Hall Wa, Copeland J. One year follow-up of cannabis dependence among long-term users in Sydney, Australia. Drug and Alcohol Dependence 2000; 59: 309-18. Swift W, Hall W, Teeson M. Cannabis use and dependence among Australian adults: results from the national survey of mental health and wellbeing. Addiction; 2001; 96: 737-48. Competing interests: None declared |
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Mark Pawelek, I am not a doctor Currently home. DA17 6NL
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To the editorial board Dear Sir, I was surprised at some of the things said in the recent BMJ editorial. "Can you compare cannabis with tobacco?" In future, when someone editorialises on such a contentious issue, could you please ask them to declare their political allegiance. In particular do Dr Henry and Dr Oldfield support the current practice of criminalising cannabis smokers? Should cannabis smokers be locked up in prison? This is an issue they ignore but it is the major public policy used to discourage cannabis use. In fact, the editorial states that "At present, there is no battle against cannabis and no clear public health message." Are they unaware that unauthorised possession of cannabis is a criminal offence? Does a 'War on Drugs' not 'battle' against cannabis? Cannabis and Tobacco can't be compared in this way. In a ranking of addictivity of 6 drugs both Henningfield (NIDA) and Benowitz (UCSF) ranked Nicotine as the most addictive and marijuana as the least addictive (comparing Nicotine, Heroin, Cocaine, Alcohol, Caffeine and Marijuana). [Hilts, P.J. The New York Times 2-Aug-94, C3] The writer states that "there are indications that smoked cannabis may cause similar effects to smoking tobacco, with many of them appearing at a younger age" But cannabis smokers
While tobacco smokers:
It is impossible for me to understand how the writers arrive at their 'comparison', given that one of them is a consultant, specialist registrar at a Department of Respiratory Medicine. I'm all in favour of improving research into the harmful effects of smoking and of discouraging the smoking of anything but scaremongering and/or criminalisation are not the way to do it. Competing interests: None declared |
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Gary D Williams, Mycologist and Harm Reduction Advocate V2B 3L4
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Ms. Brett, If concern for our children's future is indeed your primary motive, should you not include the harm done to our children who must now somehow try to succeed in life now with the ball and chain of a criminal record with them.. "Them" is our children. The "outcast" status that a criminal record bestows on our brothers, mothers and fathers, and of course our children, and it's effect on their future needs no study to determine how destructive it is on their lives. It is severe. And this is obvious. There is no controversy here. It is common sense. I snipped your references because you referenced nothing. You gave an opinion.....your own opinion. You stated that cannabis "impairs" the chemical transmission system. You also inserted the word "badly". Which study used those value judgements?. Interfering with the bodies own chemistry or natural functions is how drugs work. All drugs. Aspirin and caffeine for example. This interference is not inherently a bad thing, as you seem to be suggesting. No, it's time that reality rather than blind hysteria is brought to the subject of drugs. For example; have you ever been given a shot of morphine in the hospital? Did you know that heroin is in fact nothing more than morphine that has been slightly altered so as to pass the blood:brain barrier more quickly, providing a faster onset of the morphine? . Yes... morphine. The heroin, once past the blood brain barrier reverts back to morphine and from that point on, the high is indistinguishable from morphine because it is morphine. My point is that the demonization of heroin has succeeded in turning a useful drug into something that no one of their right mind would ever want to do. Well unfortunately, millions of people, and perhaps you, although convinced that heroin will kill them and is immediately addictive, etc, have in fact, for all intents and purposes, already done it. That is the power of misinformation Ms. Brett. Thousands of people in jail for doing a substance that doctors are giving to patients, in the hospitals, by the bathtubs full, daily. If you want to help our children, please rethink your stance on drugs. Driving the users of the seriously harmful drugs like the stimulants, (methamphetamine and cocaine) into back-alleys only exacerbates the problem. Drugs will not go away using laws. Countries that summarily execute drug-dealers or users have not stopped it. Drugs, whether you like it or not, are here to stay. All that can be done is to reduce the damage done. Common sense. Sincerely,
Competing interests: None declared |
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Rod MacQueen, Clinical Director, A&OD, Mid Western Area Health Service; VMO, Lyndon Detox Unit Clinical Services Building, Bloomfield Hospital, Orange 2800 Australia
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Editor, The editorial by Henry et al on cannabis is quite simply the most unbalanced and inappropriate piece of writing on this subject I have seen for some time. It puts together questionable assumptions, wooly science and urban myths (such as the "potency" of modern cannabis) which conflict with the vast majority of reputable current literature. One must ask what the authors reasons were for this article - it could hardly have been to educate the profession. And, as Wodak notes, such scare tactics are not likely to do much good - entrenching hardline prohibitionist policy will, based upon 50 years of evidence (rather than rhetoric), only increase the damage from cannabis, most of which stems from its prohibition, not the drug itself. Ashton raises the issue of 8 year old smokers without, apparently, asking how these kids come to have the drug, where their parents or teachers are, and whether these kids may have problems apart from cannabis use which may impact upon their health and wellbeing. Easier to blame the drug, perhaps but that gets us.......where? More prohibition, more money spent on a counterproductive war on drugs, and thus not on schools, welfare, equity, justice. Even if cannabis where the cause of these kids problems, do the current policies and practices prevent these problems (clearly, no) or worsen them (probably, yes). Canada, The Netherlands and many other jurisdictions have broken away from the mesmerised trance that chanting pro-prohibition mantras induces in many otherwise thoughtful people and institutions. Time for Britain, and Australia, to do likewise. Competing interests: None declared |
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Bernie K Masters, Member of parliament Western Australia 6280
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Just as I willingly acknowledge that my anti-smoking passion is driven by 17 years of addiction to tobacco which was overcome in 1983, should not respondents declare whether they are or were cannabis users? Competing interests: Please see my response |
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Mitch Earleywine, Associate Professor University of Southern California, Los Angeles, CA USA 90089-1061
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Masters raises an interesting question: Should scientists involved in the cannabis debate reveal if they have ever used the drug? He mentions his own anti-smoking work and his recovery from nicotine addiction as a parallel. The stigma associated with nicotine is not the same as that associated with cannabis, which may weaken the analogy dramatically. Readers often view those who break a nicotine habit with some admiration for a job well done. They often view those who cannot break the habit as unfortunate victims of the tobacco industry. Cannabis users lack this luxury because of prejudice. Cannabis remains illegal. American public service announcements suggest that cannabis users might kill their siblings in traffic accidents, engage in ill-advised sexual encounters, and support terrorism. Stereotypes about cannabis users include notions that they will soon turn to hard drugs, that they lack motivation, and that they might have cognitive impairments. Despite extensive data to the contrary, these stereotypes persist. Why believe the hard work and reasoned logic of someone with impaired cognitive abilities? Stereotypes about abstainers also exist. Readers may view them as drug warriors. Some may see them as eager to publish Type I errors suggesting cannabis-induced harm. Some accuse them of being quick to exaggerate small effects in an effort to vilify the plant. Many cannabis debates begin with data but soon degenerate into ad hominem arguments about personal habits. We cannot resolve problems this way. It’s easier to dismiss someone as a pothead or tea-totaller than it is to listen to nuanced research. But we can do it. Good peer review and extensive discussion of detailed presentations of data, especially in forums like this one, will definitely help. Let science prevail over stereotypes. The cannabis debate must be judged on the merits of the arguments rather than the actions of the arguers. Competing interests: None declared |
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Clive D Bates, Personal capacity London N16 5UF
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There are serious problems and misunderstandings with this editorial. I would like to list several: 1. Most of the mortality risk associated with tobacco use arises from sustained use over several decades, and the risks increase sharply as lifetime exposure accumulates. The importance of lifetime exposure was underlined in a major study of tobacco smokers in 2000 which found that: "People who stop smoking, even well into middle age, avoid most of their subsequent risk of lung cancer, and stopping before middle age avoids more than 90% of the risk attributable to tobacco." [1]. A similar pattern should be expected for CHD and COPD - the two other major tobacco-related fatal diseases. To the extent there is data on use of cannabis, it suggests that most users (so far) quit using it in their 30s. In the OPCS Psychiatric Morbidity Survey carried out in 1993, some 14% of adults aged 16-24 were users, but the figure dropped to 2% among those aged 35-44, and was less than 0.5% in people aged over 45. There may be cohort effects operating here, and it is possible that today's young people will have longer cannabis careers, but at present what this seems to indicate is that few people have accumulated 20 or more years of continuous use. The very high risks due to tobacco use ultimately arise from its addictiveness, which causes many tobacco smokers to continue to smoke well after they would choose to stop. Over 70% of current users say they would like to stop, and over 80% regret ever starting: a sure indicator of addiction sustaining long term and heavy use. As cannabis has very different dependency characteristics (it is much less addictive) then its pattern of use is different most users smoke less and quit earlier. 2. Completely incompatible characterisations of the user population are used in the editorial. The figure of 13 million tobacco users is determined by those answering ‘yes’ to the question 'do you smoke nowadays'. In practice over 80% of these are daily users and the average consumption is just over 15 cigarettes per day per smoker. Tobacco / nicotine is an intensive drug-using syndrome for most of its users. In contrast, the Home Office figure of 3.2 million users quoted for cannabis is 'use in the last 12 months'. The figure for use in the last month (not quoted in the editorial) is 2,062,000. The Home Office does not assess how many use cannabis daily, but it will be very substantially less. Again the reason is grounded in addictiveness - the lower dependency-forming characteristics of cannabis allow for more occasional use than cigarette smoking, which generally consolidates into a powerful addiction needing constant attention by the user. 3. The point that THC concentrations have increased by a factor of ten over the last twenty years is dubious as a point of fact, but more importantly, it is completely misinterpreted. Put bluntly, a ten-fold increase in THC concentration does not mean that modern users are ten times as stoned as in the past. Users of both cannabis and nicotine control their drug exposure by varying how much smoke they inhale and retain. Higher concentrations of THC may therefore lead to LOWER smoke inhalation for a given drug exposure. This is well understood for tobacco (and the reason why 'light' cigarettes are such a fraud) but not well studied for cannabis - however it is unlikely that users do not control their intake or they would be ten times as stoned as they were 20 years ago. Ironically, the concern raised in the editorial about different puff volumes for cannabis (based on 1987 data, by the way) may actually have been alleviated by the asserted increase in THC concentration in the drugs now in use leading to lower smoke exposure as users control their dose by taking fewer and lighter puffs. 4. The derivation of the figure of 30,000 deaths is so facile it shouldn’t really have been written down. At this stage, there is only limited evidence linking cannabis use to the big tobacco-related killers - cancer, CHD and COPD. While these links should be expected, the magnitude of the risk to the user (simply assumed to be equivalent to tobacco in the derivation of the 30,000 figure) will depend on a variety of factors, in particular the lifetime exposure and patterns of use - and these are very different indeed. Very few of the 120,000 smoking-related deaths occur in people under 40, yet hardly any of the users of cannabis are over 40 – so who are the 30,000 dying? Given that the smoking careers differ so much, and the usage patterns are so different, the estimate of 30,000 deaths is ridiculous. Qualifying the calculation by saying it may be ‘a fraction’ of that adds nothing if we don’t know whether the fraction in question is one half or one-thousandth. It does leave the media-sensitive headline number in place and puts the figure into the public domain as the only estimate. It is sure to be used by those with agendas other than forming rational evidence-based insights into public health issues. 5. The case has not made that cannabis is a 'major public health hazard' as asserted in the editorial. It is certainly not harmless and the authors suggest several harmful effects. But there is a continuum between 'harmless' and 'major public health hazard' and simply showing there are dangers is insufficient to place a phenomenon like cannabis on that continuum. Most credible reviews to date have tended to suggest limited public health impacts. For example, the Advisory Council on Misuse of Drugs [2], concluded in March 2002 after a thorough review of the evidence... "The high use of cannabis is not associated with major health problems for the individual or society." There is always a need to challenge such assessments, but any challenge has to be credible. 6. To say there is no battle against cannabis when it is a criminal offence (even after reclassification) to use it, grow it or sell it is absurd. I agree that more could be done to promote understanding of the harm it causes and I hope the findings about the link between cannabis schizophrenia, which appear to settle the question over the direction of causation, are filtering through to users. However, one reason why health promotion efforts sometimes fail is the lack of credibility of the arguments presented to users. The casually fabricated mortality figure and 'war-on-drugs' rhetoric of the editorial are wholly counter-productive in that regard. (Incidentally, the illegal status of cannabis is a barrier to wider and better understanding of its risks because it denies opportunities for mandatory labelling and inserts in the packaging.) Finally, the finding that cannabis is not harmless is not new and adds little to the important and highly-charged debate about its legal status, which is really about societal management of personal risk and relationship between the state and the individual. Understanding of addictiveness and its impact on personal choice and patterns of consumption are crucial in positioning different drugs, and entirely absent from the analysis presented in the editorial. Sadly, editorials like this play well in a particularly rabid section of the popular media, which has no interest in a thoughtful societal response to all drugs based on harm-reduction, respect for civil liberties and cost effectiveness. Rather than fanning the flames of tabloid ignorance, the BMJ is usually a beacon of rational and measured debate on these vital issues. I fear the editorial guard may have been down on this one. Clive Bates I don't think it is a competing interest, but in the interest of clarity I would like to disclose that I was Director of Action on Smoking and Health (UK) until March 2003. I am writing in a personal capacity. [1] Peto R et al. Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies. BMJ 2000; 321: 323-329. [2] Advisory Council on the Misuse of Drugs. The classification of cannabis under the Misuse of Drugs Act 1971, (UK Government) Home Office, March 2002 (5.1). Competing interests: None declared |
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Robert Melamede, UCCS 80933-7150
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While there can be little doubt that smoking anything is likely to be detrimental to the health of one’s respiratory system, scientific data does not support the extension of the biological consequences resulting from tobacco smoke to marijuana smoke(1). Two complementary pieces of information support the position that the effects of the two, tobacco and marijuana, are different. The irritant properties of all smoke will naturally tend to promote a pro- inflammatory immune response with the corresponding production of potentially carcinogenic free radicals. However, cannabis promotes immune deviation to an anti-inflammatory Th2 response via immune-system specific CB2 receptors(2). Thus, the natural pharmacological properties of marijuana’s cannabinoids, that are not present in tobacco smoke, would minimize potential irritant initiated carcinogenesis. In contrast, the nicotine present in tobacco smoke, but lacking in cannabis smoke, specifically activates nicotine receptors in respiratory pathways that in turn protect these cells from apoptosis normally promoted by genotoxic agents found in smoke(3). Thus, the pharmacological activities of tobacco smoke would tend to amplify its carcinogenic potential by inhibiting the death of genetically damaged cells. Together these observations support the epidemiological study of the Kaiser Foundation that did not find cannabis smoking to be associated with cancer incidence(4). Additionally, the demonstrated cancer killing activities of cannabinoids has been ignored. Cannabinoids have been shown to kill some leukemia and lymphoma(5), breast and prostate (6), pheochromocytoma(7), glioma(8) and skin cancer(9) cells in cell culture and in animals. 1. Henry JA, Oldfield WL, Kon OM. Comparing cannabis with tobacco. BMJ. 2003;326:942-943. 2. Yuan M, Kiertscher SM, Cheng Q, Zoumalan R, Tashkin DP, Roth MD. Delta 9-Tetrahydrocannabinol regulates Th1/Th2 cytokine balance in activated human T cells. J Neuroimmunol. 2002;133:124-131. 3. West KA, Brognard J, Clark AS, Linnoila IR, Yang X, Swain SM, Harris C, Belinsky S, Dennis PA. Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells. J Clin Invest. 2003;111:81-90. 4. Sidney S, Beck JE, Tekawa IS, Quesenberry CP, Friedman GD. Marijuana use and mortality. Am J Public Health. 1997;87:585- 590. 5. McKallip RJ, Lombard C, Fisher M, Martin BR, Ryu S, Grant S, Nagarkatti PS, Nagarkatti M. Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood. 2002;100:627-634. 6. Melck D, De Petrocellis L, Orlando P, Bisogno T, Laezza C, Bifulco M, Di Marzo V. Suppression of nerve growth factor Trk receptors and prolactin receptors by endocannabinoids leads to inhibition of human breast and prostate cancer cell proliferation. Endocrinology. 2000;141:118-126. 7. Sarker KP, Obara S, Nakata M, Kitajima I, Maruyama I. Anandamide induces apoptosis of PC-12 cells: involvement of superoxide and caspase-3. FEBS Lett. 2000;472:39-44. 8. Sanchez C, Galve-Roperh I, Canova C, Brachet P, Guzman M. Delta9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Lett. 1998;436:6-10. 9. Casanova ML, Blazquez C, Martinez-Palacio J, Villanueva C, Fernandez-Acenero MJ, Huffman JW, Jorcano JL, Guzman M. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest. 2003;111:43-50. Competing interests: None declared |
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