MYTHBUSTERS: SEPARATING FACT FROM FICTION IN THE ACMD AND THE MEDIA
When Professor David Nutt was sacked by the Home Secretary for arguing against government policy on drug classification, he stated that his proposals were based on scientific evidence. Professor Andy Parrott goes mythbusting.
It has been highly publicised across the national media – but how ‘scientific’ was Professor David Nutt’s proposal to downgrade cannabis and Ecstasy/MDMA ?
Nutt was sacked by the Home Secretary last November as chair of the UK Advisory Council on the Misuse of Drugs, or ACMD, for arguing against government policy on drug classification. He defended himself by saying that his proposal to downgrade cannabis and ecstasy reflected scientific evidence. In this article, I list published statements made by Nutt about cannabis and Ecstasy/MDMA; after each statement are comments and quotations from scientific papers written by academic researchers in this field.
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1. Nutt (2009): “Cannabis use does not lead to major health problems”.
The smoke from cannabis contains a similar cocktail of damaging chemicals to the smoke from tobacco. Hence it is linked with a similar range of medical disorders: cancers of the respiratory tract, heart disease, and premature death.
In a detailed review of its adverse health effects, two australian researchers, Hall and Degenhardt (2009) recently wrote: “Epidemiological, clinical, and laboratory studies have established an association between cannabis use and adverse outcomes. We focus on adverse health effects of greatest potential public health interest – those most likely to occur and to affect a large number of cannabis users. The most probable adverse effects include a dependence syndrome, increased risk of motor vehicle crashes, impaired respiratory function, cardiovascular disease, and adverse effects of regular use on adolescent psychosocial development and mental health”.
In an earlier review on health consequences of cannabis/marijuana, Khalsa et al (2002) similarly noted: “The use of marijuana is not without significant health hazards. Marijuana is associated with effects on almost every organ system in the body, ranging from the central nervous system to the cardiovascular, endocrine, respiratory/pulmonary, and immune systems... in addition to marijuana abuse/dependence, marijuana use is associated in some studies with impairment of cognitive function in the young and old, foetal and developmental consequences, cardiovascular effects (heart rate and blood pressure changes), respiratory/pulmonary complications such as chronic cough and emphysema, impaired immune function leading to vulnerability to and increased infections, and the risk of developing head, neck, and/or lung cancer”.
There is also MRI evidence for localised brain damage, to the hippocampus and amygdala, in heavy regular cannabis users (Yucel et al, 2008).
2. Nutt (2009): “Cannabis wouldn’t have killed anyone because it doesn’t kill”.
Just as with cigarette smoking, cannabis can kill smokers through heart and respiratory disorders. There are differences between people who smoke for nicotine and those who smoke for cannabinoids/THC – for instance, tobacco smokers generally consume more cigarettes per day, whereas cannabis smokers tend to inhale unfiltered smoke for longer inhalation periods.
Many cannabis smokers also smoke tobacco. Aldington et al (2008) compared lung-cancer risks from smoking cannabis vs tobacco, and reported: “The risk of lung cancer increased 8% for each joint-year of cannabis smoking, after adjustment for confounding variables including cigarette smoking; and 7% for each pack-year of cigarette smoking, after adjustment for confounding variables including cannabis smoking”.
Cannabis can also impair driving ability, and is linked with increased car accidents. Mura et al (2006): “The risk of road crash after a recent use of cannabis is increased by more than 2.4 in all studies”.
Finally, cannabis is associated with a number of acute deaths, mostly in polydrug combinations – although in some acute fatalities, cannabis was the only drug detected (Schifano, 2007).
3. Nutt et al (2007): “For drugs which have only recently become popular eg, Ecstasy or MDMA, the longer-term health and social consequences can only be estimated from animal toxicology at present”.
I was particularly surprised to read this statement. I have been publishing about the adverse effects of ecstasy/MDMA in humans for many years, and there are many other research groups. So I undertook a PubMed search using the key words “MDMA and human”. The computer search listed about 1,400 published papers.
4. Nutt et al (2007) rated ecstasy/MDMA as less pleasurable than cocaine or nicotine.
Nutt noted that the most powerful drugs were the most pleasurable and the most damaging. But MDMA was given one of the lowest pleasure scores for any drug. By doing this, they also gave MDMA a surprisingly low harm score.
Nutt must be one of the few people to think that ecstasy is less pleasurable than smoking a cigarette. Recreational Ecstasy/MDMA users often report pronounced euphoria (Cohen, 1998).
MDMA is a powerful stimulant drug (Green et al, 2003; Parrott et al, 2008) but its use can lead to a wide range of psychobiological problems, including depression, irritability, aggression, memory loss, reduced problem solving/reasoning skills, impaired psychomotor/driving skills, reduced social intelligence, weight loss, poor sleep, sexual dysfunctioning, reduced immunocompetence, occupational stress, interpersonal difficulties and other problems (Brookhuis et al, 2004; Curran et al, 2004; Parrott, 2001, 2006, 2008; Topp et al, 1999; Reay et al, 2006; Zakzanis and Campbell, 2006).
MDMA-related deficits in young people have been shown after an average consumption of three tablets lifetime (Schilt et al, 2007).
5. Nutt et al (2007) gave maximum ‘Injection Potential’ scores to cocaine and heroin (3.0), whereas MDMA was rated at 0.0.
The empirical literature shows that some experienced Ecstasy users do inject MDMA. In a survey of 329 regular Ecstasy users, 54 reported injecting Ecstasy for the increased rush (Topp et al, 1999). They also noted that MDMA injections were more intense, the come-down more severe, and its dependency potential was higher.
So MDMA can be injected (Parrott, 2009) but, as with other illicit drugs, injections are linked to extensive polydrug use and multiple drug-related problems.
6. Nutt et al (2007): MDMA was rated as 18th out of 20 drugs on the Lancet list for drug-related harm.
This low harm score reflects many of the erroneous statements on MDMA made in the Lancet article (see points 3-5).
With amended scores for “intensity of pleasure” and “injection potential”, MDMA rises from 18th to 9th on the overall harm list. Several other harm scores in Nutt et al (2007) were also surprisingly low, since recreational Ecstasy/MDMA is linked to numerous psychobiological deficits (see previous references).
With revised scores based on empirical literature, MDMA becomes the 5th most harmful drug on the Lancet scale (Parrott, 2009).
7. Nutt (2006): “In contrast to alcohol, ecstasy is less toxic in overdose as it does not cause respiratory depression”.
MDMA is a stimulant drug which increases heart rate and breathing. Respiratory depression is found with sedative drugs such as alcohol. For a professor in the field of pharmacology to suggest that respiratory depression is a potential cause of death with a stimulant drug such as MDMA, is difficult to understand.
MDMA can cause death – but through very different mechanisms (Schifano et al, 2003).
8. Nutt (2006): Ecstasy was less harmful than alcohol, since it was not addictive, did not cause car driving deaths, was not linked with aggression, nor lead to cirrhosis or heart damage, and was safer in overdose.
None of these statements is consistent with the empirical literature. Like all recreational CNS stimulants, MDMA displays addictive properties. Ecstasy dependence has a two-factor structure, with compulsive use and escalating use (Topp et al, 1997). Chronic tolerance and dosage escalation are noted by 85% of regular users (Parrott, 2005). Recreational Ecstasy can also impair car driving (Brookhuis et al, 2004); lead to mid-week aggression (Curran et al, 2004), damage the heart, liver, kidney and brain (Parrott, 2007).
Gesi et al (2002) noted that “Persons abusing ecstasy typically suffer cardiac symptoms, such as tachycardia, hypertension, and arrhythmia”.
MDMA also has hepatotoxic properties, causing apoptosis or programmed-cell-death in cultured liver cells (Montiel-Duarte et al, 2002), while liver failure can occur in young recreational Ecstasy users (references in Parrott, 2007).
9. Nutt (2009): “Equasy, the equine addiction syndrome”.
Nutt stated that horse riding was more dangerous than taking Ecstasy. Natural pleasures are real and enduring. People who ride horses, cycle, canoe, sail, windsurf, climb mountains or play rugby have genuine natural pleasures which can benefit health and wellbeing. Sadly, some normal recreational activities can be linked with occasional accidents or death [note: some deaths in horse riders might be traffic accidents caused by poor driving]. But most participants experience a natural boost in pleasure, which can continue for decades. Furthermore, these natural activities can increase physical health and promote general wellbeing. This contrasts with psychoactive drug users and their many problems, which generally worsen with continued usage (Parrott, 2008).
It is strange that Nutt does not seem to recognise the difference between natural healthy pleasures such as horse riding, and drug-induced short-cuts to pleasure which paradoxically tend to heighten distress.
In conclusion, Nutt has published statements about cannabis and Ecstasy/MDMA – many of which do not reflect the scientific evidence.
Professor Andy C Parrott works at the Department of Psychology, Swansea University. He has published extensively on the psychobiological effects of recreational drugs such as Ecstasy/MDMA. He has also organised international MDMA conferences and edited the published proceedings. He is the first author of a leading European textbook in this field: Understanding Drugs and Behaviour. The Ecstasy/MDMA papers from his research group have been given the British Association for Psychopharmacology journal award, on two occasions.
REFERENCES:
Aldington S, Harwood M, Cox B, Weatherall M, Beckert L, Hansell A, Pritchard A, Robinson G, Beasley R; Cannabis and Respiratory Disease Research Group.(2008). Cannabis use and risk of lung cancer: a case-control study. Eur Respir Jour 31: 280-286.
Brookhuis KA, de Waard D, Samyn N.(2004) Effects of MDMA (ecstasy), and multiple drugs use on (simulated) driving performance and traffic safety. Psychopharmacology 173: 440-445.
Cohen RS (1998). The Love Drug: Marching to the Beat of Ecstasy.
Curran VH, Rees H, Hoare T, Hoshi R, Bond A (2004). Empathy and aggression: two faces of ecstasy? A study of interpretative cognitive bias and mood change in ecstasy users. Psychopharmacology 173: 425–433.
Gesi M, Soldani P, Lenzi P, Ferrucci M, Giusiani A, Fornai F, Paparelli A(2002). Ecstasy during loud noise exposure induces dramatic ultrastructural changes in the heart. Pharmacol Toxicol.91: 29-33.
Green AR, Mechan AO, Elliott JM, O’Shea E, Colado MI (2003). The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, “ecstasy”). Pharmacol Revs 55: 463-508.
Hall W, Degenhardt L (2008). Adverse health effects of non-medical cannabis use. Lancet 374: 1383-1391.
Khalsa JH, Genser S, Francis H, Martin B (2002). Clinical consequences of marijuana. J Clin Pharmacol 42 (11 Suppl): 7S-10S.
Montiel-Duarte C, Varela-Rey M, Oses-Prieto JA, Lopez-Zabalza MJ, Beitia G, Cenarruzabeitia E, Iraburu MJ. (2002). 3,4-Methylenedioxymethamphetamine ("Ecstasy") induces apoptosis of cultured rat liver cells. Biochim Biophys Acta 1588: 26-32.
Mura P, Brunet B, Favreau F, Hauet T (2006). Cannabis and road crashes: a survey of recent French studies. Ann Pharm
Nutt DJ (2006). A tale of two E’s. J Psychopharmacol 20: 315-317
Nutt DM, King LA, Saulsbury W, Blakemore C (2007). Development of a rationale scale to assess the harm of drugs of potential misuse. Lancet 369: 1047-1053.
Nutt DJ (2009). Estimating drug harms: a risky business? Eve Sackville lecture. Centre for Crime and Justice Studies, Briefing 10: 1-13. King’s College London.
Parrott AC (2005). Chronic tolerance to recreational MDMA (3,4-methylenedioxymethamphetamine) or Ecstasy. Jour Psychopharmacol 19: 71-83.
Parrott AC (2006). MDMA in humans: Factors which affect the neuropsychobiological profiles of recreational ecstasy users, the integrative role of bioenergetic stress. Jour Psychopharmacol 20: 147-163.
Parrott AC (2007). Ecstasy versus alcohol: Tolstoy and the variations in unhappiness. Jour Psychopharmacol 21:3-6.
Parrott AC, Morinan A, Moss M, Scholey A (2004). Understanding Drugs and Behaviour. Wiley,
Reay JL, Hamilton C, Kennedy DO,
(2007). Cognition in novice ecstasy users with minimal exposure to other drugs: a prospective cohort study. Arch Gen Psychiat 64: 728-736.
Topp L, Hando J, Dillon P, Roche A, Solowij N (1999). Ecstasy use in
Yücel M, Solowij N, Respondek C, Whittle S, Fornito A, Pantelis C, Lubman DI (2008). Regional brain abnormalities associated with long-term heavy cannabis use. Arch Gen Psychiatry 65: 694-701.
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Thank you Prof. Parrot for your words of wisdom on the meanderings of Prof. Nutt.
The UK Government were within their rights to fire someone of such gross incompetance. Nutt by name..Nutt by nature.A true friend to the drug liberal agenda.
As an experienced addiction counsellor I can reassure Prof.Nutt drugs not only cause mental illness but death by various means. Not all overdoes.
As a counselor I would strongly advise the Professor to take time out and look closer to home.
We are all lucky to have people of Prof.Parrot's calibre to advise and inform. Thank you for taking the time.
Posted by: Grainne kenny | January 06, 2010 at 04:05 PM
Very well said! It is so refreshing to see the established orthodoxy on cannabis and Ecstasy challenged by an academic working in the field.
Posted by: Frugal Dougal | January 07, 2010 at 12:14 AM
Under Nutt "science" was never the ACMD's strong point, nor has it ever been independent, controlled as it has been by the psycho-pharmaceutical industries.
Seven members form a quorum, which makes four members a majority, allowing the numerous members of the vested interest tail to wag the government policy dog.
How can any Advisory Council on drug harm, drug usage and addiction recovery ever be scientific when it allows its brief to omit licensed substances such as alcohol and prescription drugs like the benzos and the huge range of addictive pharmaceutical substances, all of which together form a vastly greater proportion of the problem addictive substances supply industry than just the illegal drugs the ACMD deals with.
As a psychiatrist and a pharmacist, Nutt now wants to take over the booze market. But who for? Who is his much vaunted "backer"?
The ACMD should be comprised of truly independent addiction prevention and avoidance specialists and those who DEMONSTRATE the ability to CONSISTENTLY recover users from addiction. i.e those centres which can recover at least two- thirds of their clients from addiction, and by logical definition, recovery must mean returning an addict to the natural relaxed state of abstinence into which 99% of the population is born.
To try and maintain maximum psycho-pharmaceutical influence Nutt is now forming his own "advisory" body to comment on the harm caused by drugs (but not the psycho-pharmaceuticals of course!).
But that is something which has been examined by such so-called scientists for decades with no real improvement, because the more important investigation should be into solutions.
Alan Johnson got off to a good start. Let's hope he can continue by widening the scope of the ACMD and by focusing on moving Britain in the direction of a drug-free country and by appointing a membership comprised of those who have proven records of addiction avoidance and genuine recovery rates.
Kenneth Eckersley,
C.E.O. Addiction Recovery Training Services.
Posted by: Kenneth Eckersley | January 08, 2010 at 01:08 AM
I think the harms allegedly caused by cannabis must be separated from those caused by the act of smoking, whether with or without tobacco - at least for the point of clarity to allow users to establish which method of ingestion would be preferable. Certainly there are many forms of vapourisers that substantially reduce toxic stream and of course cannabis can be readily prepared in foodstuffs entirely eliminating the smoke risk.
A far as lethal consumption of cannabis goes - I think that is such a remote possibility that it ought to be discounted. We are talking about relative risks here (something David Nutt was keen to emphasise), and very small risks, particularly those which affect only the user cannot be used to formulate public policy.
It is worth remembering that the law reasonably distinguishes between (mis)use which is harmful and where such use has a social impact (the latter being the object of the Misuse of Drugs Act regulations to minimalise). For every report showing harmful effects of cannabis there seems to be at least as much written about how it is beneficial to the body, not least for the so-called medical users. I think that before demonising a controlled drug like this, and bear in mind that quiet users of the drug are prone to get their doors booted in in the early hours and their lives turned upside down, that we compare these health issues to the known harms of alcohol and tobacco. These of course are drugs and are tolerated in society - it seems that drug choice is legally limited to these known lethal drugs alongside numerous so-called legal highs sold problematically as not for human consumption. There appears to be no legal basis for insisting that the controlled drugs that Nutt discussed in terms of their relative harms ought to be any more demonised than alcohol or tobacco - it is the un-level playing field of biased drug law administration that gives rise to much of the misunderstandings about drugs and the subsequent harm.
By the way, I watched a short film by the motoring journalist Quentin Wilson which involved testing a driver with and without cannabis for the key driving safety issues - this demonstrated that this user drove better under the influence of the drug than without it. I think it depends on the experience of the user.
I am incredulous at the statistics cited for intravenous ecstasy use - I have known a fair few people around that scene when it was popular and I have never heard of anyone injecting it - even so, such conduct is borne from the moronic mindset worsened by prohibition.
The part of the article that I have most difficulty with is the value judgment about natural and unnatural leisure activities. This is true dogma and would surely alienate the very audience that the author seeks to ultimately connect with. Drug taking is I guess naturalised into the human condition, certainly cannabis and various psychedelics (psilocybin, DMT and mescaline containing plants) have been used for thousands of years across civilisations. Pleasure and drug taking does have a social utility value that is not lost on our licensed trade.
Finally, the insinuations made by Grainne Kenny are beneath contempt. Even the Sun newspaper had to apologise for slurring David Nutt's family and the parroting the Nutt by name and by nature joke seems rather weak way of causing offence.
Kenneth Eckersley making a critical comment about David Nutt's science credentials with the ACMD is laughable - I'd like to post your CV next to his, if you would like to forwards it to me I will arrange that.
See drugequality.org
Posted by: Darryl Bickler | January 08, 2010 at 03:15 PM
Professor Parrott, even if you do not agree with Professor Nutt's conclusions about cannabis (note that I use the proper term for the plant and NOT the slang Mexican term, marijuana), the least you can do is show him some professional courtesy as a professional in his own right and refer to him as PROFESSOR NUTT and not Nutt as you so rudely call him.
If the only way you can get your point across is by showing disrespect then you are showing that your argument isn't very strong.
By the way most of the "research" you have quoted has already been debunked...especially the part where you say that cannabis causes head and neck cancer (see research carried out by Dr Thaskin in the US).
Cannabis also DOESN'T cause lung cancer, in actual fact it has been shown to shrink tumours in rats, it also shrinks skin cancers too. It also helps with ADHD, autism, MS, muscular dystrophy..I could go on.
I don't suppose this will make its way onto your site as you have to vet every post so only the ones that agree with you appear but at least you would have read it. If you wish to reply to me via my email address then please feel free, but I don't suppose you will will you?
Posted by: Jo Urquhart | January 08, 2010 at 11:49 PM
I reply solely to Jo Urquhart's first inaccuracy. It is the editorial style of most quality business publications to refer to a person in full at the start of an article, thereafter only by surname. All Addiction Today articles comply with this business style. No exception was made for this particular article.
Deirdre Boyd
Editor
Posted by: Deirdre Boyd | January 09, 2010 at 10:50 AM
nice to see a scientist using science to prove a point and not quoting from a list
Posted by: big boss | January 11, 2010 at 04:48 AM
Cannabis use therapeutically or recreationally can be administered in a variety of ways: GW Pharmaceuticals of the UK have developed and patented a sublingual (under the tongue) spray of tincture of the whole cannabis plant. Canisol, a cannabis based eye drop for glaucoma was developed and is available to patients in Jamaica. Vaporizers (a method of inhalation in which the plant material is heated to the point of releasing vapor but is not hot enough to cause combustion) are currently being developed on several continents for patients who find great benefit from an inhaled administration. These vaporizers will allow patients to inhale the therapeutic properties of cannabis without the tar or other dangerous substance released when cannabis is burned and the smoke inhaled. Cannabis can also be cooked and eaten, therefore eliminating any possible risk caused by smoke.
Chronic cannabis usage was first studied in 1894 and published as the Indian Hemp Drugs Report by the British government. This was a three-year study that interviewed hundreds of Indian and Western doctors about therapeutic cannabis use. The conclusion was that cannabis had negligible adverse effects on health, even in chronic application. Similar conclusions were reached by The LaGuardia Report of 1944 (NYC), which was the first study to employ clinical and scientific methods of research. Three important systematic epidemiological studies undertaken in the 1970's exhaustively examined medical issues in chronic cannabis use. Ganja in Jamaica: A Medical Anthropological Study of Chronic Marijuana Use (Rubin and Comitas 1975) with 60 patients; a Greek study, Hashish: Studies of Long-term Use (Stefanis, Dornbush and Fink 1977) with 60 patients; and Cannabis in Costa Rica: A Study of Chronic Marijuana Use (Carter 1980) with 41 patients - all reached the same health conclusions as stated in the IOM report of 1999.
New studies of the 21st century also report minimal negative long-term effects of cannabis use. In May of 2001, four of the seven surviving U.S. legal medical marijuana patients (supplied with medical cannabis by the federal government through the FDA's Investigational New Drug program) were examined intensively for three days, at St. Patrick's Hospital in Missoula, MT (known as the Missoula Chronic Use Study). The complete study is available at www.medicalcannabis.com. These patients had used cannabis for 25 years, 27 years, 26 years and 11 years. Monthly consumption was 8 or 9 cured ounces with one patient receiving 11 cured ounces every three weeks. The study concluded that with very minor pulmonary negative changes (within that expected for age) each patient was in very good health and took no additional medications. Although the U.S. government provided these patients their medicine, they never cared enough to study what it did to them. We did and now we know it has been vital to their health and the quality of their lives.
The difference between what Parrott calls “natural healthy pleasures” and “drug-induced pleasures” is embarrassingly unscientific, as it is obvious to anyone that drugs are natural (that’s even more obvious when regarding a plant as cannabis, which grows naturally all over planet earth). More convincing would be to call unnatural the denying of the use of such drugs to humankind, when we have enjoyed their use during thousands of years without major problems until the prohibitionist experiment was implemented.
Posted by: daniel campos | January 12, 2010 at 12:05 AM
Not only has modern science refuted the notion that marijuana is neurotoxic, recent scientific discoveries have indicated that cannabinoids are, in fact, neuroprotective, particularly against alcohol-induced brain damage. In a recent preclinical study -- the irony of which is obvious to anyone who reads it -- researchers at the US National Institutes of Mental Health (NIMH) reported that the administration of the non-psychoactive cannabinoid cannabidiol (CBD) reduced ethanol-induced cell death in the brain by up to 60 percent. "This study provides the first demonstration of CBD as an in vivoneuroprotectant ... in preventing binge ethanol-induced brain injury," the study's authors wrote in the May 2005 issue of the Journal of Pharmacology and Experimental Therapeutics. Alcohol poisoning is linked to hundreds of preventable deaths everyday around the world.
NIMH scientists in 1998 first touted the ability of natural cannabinoids to stave off the brain-damaging effects of stroke and acute head trauma. Similar findings were then replicated by investigators in the Netherlands and Italy and, most recently, by a Japanese research in 2005.
Of all cancers, few are as aggressive and deadly as glioma. Glioma tumors quickly invade healthy brain tissue and are typically unresponsive to surgery and standard medical treatments. One agent they do respond to is cannabis.
Writing in the August 2005 issue of the Journal of Neurooncology, investigators at the California Pacific Medical Center Research Institute reported that the administration of THC on human glioblastoma multiforme cell lines decreased the proliferation of malignant cells and induced apoptosis (programmed cell death) more rapidly than did the administration of the synthetic cannabis receptor agonist, WIN-55,212-2. Researchers also noted that THC selectively targeted malignant cells while ignoring healthy ones in a more profound manner than the synthetic alternative. Patients diagnosed with glioblastoma multiforme typically die within three months without therapy.
Previous research conducted in Italy has also demonstrated the capacity of CBD to inhibit the growth of glioma cells both in vitro (e.g., a petri dish) and in animals in a dose dependent manner. As a result, a Spanish research team is currently investigating whether the intracranial administration of cannabinoids can prolong the lives of patients diagnosed with inoperable brain cancer.
Most recently, a scientific analysis in the October issue of the journalMini-Reviews in Medicinal Chemistry noted that, in addition to THC and CBD's brain cancer-fighting ability, studies have also shown cannabinoids to halt the progression of lung carcinoma, leukemia, skin carcinoma, colectoral cancer, prostate cancer and breast cancer.
Emerging evidence also indicates that cannabinoids may play a role in slowing the progression of certain neurodegenerative diseases, such as Multiple Sclerosis, Parkinson's disease, Alzheimer's, and Amyotrophic Lateral Sclerosis (a.k.a. Lou Gehrig's Disease). Recent animal studies have shown cannabinoids to delay disease progression and inhibit neurodegeneration in mouse models of ALS, Parkinson's, and MS. As a result, the Journal of Neurological Sciences recently pronounced, "There is accumulating evidence ... to support the hypothesis that the cannabinoid system can limit the neurodegenerative processes that drive progressive disease," and patient trials investigating whether the use of oral THC and cannabis extracts may slow the progression of MS are now underway in the United Kingdom.
what about claims of cannabis' damaging effect of cognition? A review of the scientific literature indicates that rumors regarding the "stoner stupid" stereotype are unfounded. According to clinical trial data published this past spring in the American Journal of Addictions, cannabis use -- including heavy, long-term use of the drug -- has, at most, only a negligible impact on cognition and memory. Researchers at Harvard Medical School performed magnetic resonance imaging on the brains of 22 long-term cannabis users (reporting a mean of 20,100 lifetime episodes of smoking) and 26 controls (subjects with no history of cannabis use). Imaging displayed "no significant differences" between heavy cannabis smokers compared to controls, the study found.
Previous trials tell a similar tale. An October 2004 study published in the journal Psychological Medicine examining the potential long-term residual effects of cannabis on cognition in monozygotic male twins reported "an absence of marked long-term residual effects of marijuana use on cognitive abilities." A 2003 meta-analysis published in theJournal of the International Neuropsychological Society also "failed to reveal a substantial, systematic effect of long-term, regular cannabis consumption on the neurocognitive functioning of users who were not acutely intoxicated," and a 2002 clinical trial published in the Canadian Medical Association Journal determined, "Marijuana does not have a long-term negative impact on global intelligence."
Finally, a 2001 study published in the journal Archives of General Psychiatry found that long-term cannabis smokers who abstained from the drug for one week "showed virtually no significant differences from control subjects (those who had smoked marijuana less than 50 times in their lives) on a battery of 10 neuropsychological tests." Investigators further added, "Former heavy users, who had consumed little or no cannabis in the three months before testing, [also] showed no significant differences from control subjects on any of these tests on any of the testing days."
I am sure, Professor Parrot, that you are a honest man that just didn't know about the existence of all these studies, and that’s why you wrote such a misleading article. But now you know that cannabis is less harmful than alcohol. Please, do the decent thing and write an apology.
References:
Comparison of cannabidiol, antioxidants and diuretics in reversing binge ethanol-induced neurotoxicity. Journal of Pharmacology and Experimental Therapeutics. 2005
Cannabidiol prevents cerebral infarction. Stroke. 2005
Post-ischemic treatment with cannabidiol prevents electroencephalographic flattening, hyperlocomotion and neuronal injury in gerbils. Neuroscience Letters. 2003
Neuroprotection by Delta9-tetrahydrocannabinol, the main active compound in marijuana, against ouabain-induced in vivo excitotoxicity. Journal of Neuroscience. 2001
Cannabidiol and Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proceedings of the National Academy of Sciences. 1998
Cannabinoids selectively inhibit proliferation and induce cell death of cultured human glioblastoma multiforme cells. Journal of Neurooncology. 2005
Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry. 2005
Anti-tumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines.Journal of Pharmacology and Experimental Therapeutics. 2003
Cannabinoids and neuroprotection in CNS inflammatory disease. Journal of the Neurological Sciences. 2005.
Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders. 2004
Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain. 2003
Lack of hippocampal volume change in long-term heavy cannabis users. American Journal of Addictions. 2005
Neuropsychological consequences of regular marijuana use: a twin study. Psychological Medicine. 2004
Non-acute (residual) neurocognitive effects of cannabis use: A meta-analytic study. Journal of the International Neuropsychological Society. 2003
Current and former marijuana use: preliminary findings of a longitudinal study of effects on IQ in young adults. Canadian Medical Association Journal. 2002
Neuropsychological Performance in Long-term Cannabis Users. Archives of General Psychiatry. 2001
Posted by: Sergio Montes | January 12, 2010 at 02:57 AM
Professor Parrott's informed critique of some of Professor Nutt's generalisations was instructive. Politicians should take note: first that scientists are not omniscient and nor does the current fashion for 'evidence based' policy make them so; second that many of the so-called experts on their committees are not experts at all and the advice they propound is often less evidence based than opinion; third committee members have been less capable of challenging their 'leader's' interpretation than genuinely expert scientists excluded from the process - as the complete absence of minority reports from the ACMD indicates. That in it self should have been a warning light.
Kathy Gyngell
Chair - Prisons and Addictions
Centre for Policy Studies
Posted by: Kathy Gyngell | January 12, 2010 at 10:37 AM
There's a danger on both sides this debate of picking evidence that fits a preconceived narrative, rather than doing a more thorough review of the evidence and coming to a balanced conclusion - a literature or thematic review, or meta analysis. Thus those interested in over-emphasising drug risks, or playing them down, can misrepresent the total body of research.
Professor - You make a number of observations/critiques here and whilst some are reasonable, many appear confusing or misleading.
To consider your points:
1 - this is a quote from a lecture not a published journal piece, and is quoted out of context. It doesn't reflect the body of Nutt's work on cannabis. The lit reviews he oversaw for the ACMD (built of detailed work commissioned by the WHO and DoH) clearly reflect the risks and harms of cannabis and state so explicitly, albeit with an attempt to rank them relative to other drugs, and also reflecting the ambiguities in the findings. This is specifically made clear in the rest of the lecture. I note you have never critiqued the ACMD cannabis reports themselves (which strike me as authoritative, balanced, and thorough) - instead picking on odd phrases from Nutt, seemingly because you take issue with the recommendations that the ACMD made re classification, or him personally. Neither is especially scientific.
2. Again - this is out of context. The next sentence in the lecture specifically positions it in terms of overdose mortality risk, which for cannabis is effectively zero. You state there is a lung health risk (true - although again some, eg Tashkin, take a different view to those you cite), but not that it can be consumed without smoking in ways that reduce the lung harm risk to zero. The driving risk is similarly not a toxic risk - which is what Nutt is talking about at this point of the lecture - relative to other drugs. It goes without saying that any drug that impairs competence can lead to accidental deaths - this is an issue that Nutt and the ACMD have identified and discussed on numerous occasions and to suggest otherwise is misleading.
3 - I don't understand the point you are making here. Nutt is clearly referring to the 'long term' consequences, i.e. over a longer using time span than the quality research on ecstasy currently covers (its mainstream use only beginning in the late 1980s, and research a period after that ). The number of papers has no bearing on this specific point, which anyway is a cautionary one, not an attempt to play down harms. He saying there may be risks we don't know about yet. Which is an obvious truism.
4. This was a paper on which Nutt was one of 4 co-authors, and the pleasure rankings for drugs were determined by a group of 30 other drug specialists - not Nutt himself. Additionally the 'pleasure' component was included as a factor of addictiveness. Clearly nicotine and cocaine are far more associated with addiction/dependence than ecstasy. And finally the pleasure/ addiction component was only one of a series of variables being evaluated to establish the final harm scores - so you can't then suggest that this was the sole reason for ecstasy's 'low harm score', which was in fact the result of it scoring low on all or most of the criteria. The Nutt et al Lancet paper is available online here for clarification: http://bit.ly/yN5FP
I don't think you make a good case to contradict the point either. The references for ecstasy related problems have no specific bearing on the pleasure scores under discussion.
5. Some problem injectors will inject anything they get their hands on, but just because it has been observed does not mean to suggest this has significant bearing on the overwhelming majority of ecstasy use, which is oral consumption. The vague suggestion that 15% of ecstasy users inject (from a single ref) isn't credible - I not clear if this is what you are suggesting. Go to a nightclub or party and see how many ecstasy injectors there are - it will be zero. There is simply no reason to inject it.
6. The scores in the Lancet paper are averaged from the group asked to make them - not a single individual like yourself. You don't provide any detail for how you have revised these scores or what empirical literature the revisions are based on. How scientific is that?
7. Respiratory depression is the cause of the large majority of overdose drug deaths. The fact that ecstasy is a stimulant and therefore does not present this risk is precisely the point Nutt is making - there is no confusion on his part; Ecstasy deaths are not 'overdoses' in the classic sense, but acute toxic/allergic reactions, or behaviour/environment related (overheating/hydration related). There are a range of estimates of ecstasy mortality figures.
8. This is not a quote from the paper, which is rather more nuanced. It is available here should anyone care to read it: http://bit.ly/8O8o6k - As it happens I don't think it is a very good paper (I would agree that road traffic accidents should not be at zero for example), but the list of harms and refs you then produce (again somewhat selectively) confuses the fact that ecstasy risks are being described in Nutt’s paper as relatively less than comparable harms for alcohol. You do not make comparisons to contradict this re alcohol harms which is what his paper was about.
9. The concept of 'natural pleasures' or 'normal' activities are your personal subjective/moral judgments and have no bearing on the science of relative risks/ harms.
I don't think Nutt's or the ACMD's work is beyond question and it should rightly be scrutinised and critiqued. I have done so myself ( http://bit.ly/7NiOEw ).
You have done some pioneering and important research on ecstasy harms but unlike that journal published work, with this piece I don't think you have contributed anything useful; It feels selective and subjective, rather personal and rather angry. You accuse Nutt of myth-making and low scientific standards (itself rather ad-hom and unnecessary) but you fail to meet reasonable standards yourself. Why not publish a proper critique in a peer reviewed journal - the Lancet perhaps?.
I await a your response to the HTA paper: http://www.hta.ac.uk/execsumm/summ1306.shtml
"The harmful health effects of recreational ecstasy: a systematic review of observational evidence"
Which, over 400 pages, considered over 4000 papers (including many of yours), and is the most detailed and exhaustive ecstasy review yet undertaken, or the ACMD ecstasy review paper that it informed.
OR the ACMD's 3 cannabis review papers and the WHO/DoH literature reviews that informed them.
Posted by: Steve Rolles | January 12, 2010 at 01:07 PM
I guess that Kathy Gyngell cannot wait for the end of this "current fashion for 'evidence based' policy".
Too much light there Kathy?
Posted by: Neil Anderson | January 12, 2010 at 07:28 PM
Its interesting to see so many people getting hot under the collar about Cannabis.I have been treating people for the effects of cannabis for many years and I hate it as a drug,principly becaues of the damage to young people whos brains are still developing, but I also know that the it pales to insignificance when compared with the wreckage that alcohol leaves behind.I dont hear a great shout about making alcohol illegal. Why not ? -because the majority dont have a problem with it. Surely we need to concentrate on helping those who suffer, not sabre rattling, leave that to the political bods. If we are looking for something to shout about I would contest that the NTA are more dangerous to the health of addicts than cannabis.
Posted by: David Smallwood | October 13, 2010 at 02:51 PM