Will new drug driving law reduce minimise harm?

By Nicholas Lay

Earlier this month the government chose to ignore the recommendations of its own Advisory Council on the Misuse of Drugs (ACMD) regarding the legal status of the herbal stimulant khat, proposing instead that it be banned. Hot on the heels of this decision, the government has once again ignored evidence-based guidance, this time when drawing up its recently announced new drug driving laws. At the behest of the government, a panel of experts produced a report carefully calculating the threshold amounts of illegal and prescription drugs which would produce impairment comparable with the drink driving limit. It was published in March of this year. Despite the scientific rigour of the report (or because of it?), the government has chosen to disregard the thresholds advised for illegal drugs, instead opting for a ‘zero tolerance’ approach where the question of whether the driver is impaired is discounted.

Under these new laws, roadside tests and/or blood samples will see drivers prosecuted for drug driving if they are found to have any detectable amount of any one of eight specified illegal drugs (includingcannabisMDMA and cocaine) in their system, regardless of whether it is biologically possible that this amount is causing impairment. While the reduction of drug driving is of course a noble aim, and the law is in need of clarification in this area, this zero tolerance approach once again raises questions concerning the government’s attitude to evidence and reason. Then there is the issue of the policy itself, as it is debatable as to whether any benefits will outweigh the harms.

While the government has proposed that any trace of these eight illegal drugs that is enough to rule out passive consumption will warrant prosecution, it will adopt the limits recommended by the expert panel for eight controlled prescription drugs (including morphine, methadone and variousbenzodiazepines, such as diazepam). This inconsistency gives the impression that the effect of banned drugs on driving is a categorically darker threat than the effects of prescription drugs or alcohol. Of course in reality, someone just under the drink-drive limit, or indeed someone who is tired or has a headache will be more impaired than someone who took cannabis the day before. The official press release  lists the eight illegal drugs, but leaves the prescription drugs embedded in its report, perhaps suggesting the ‘zero tolerance’ rhetoric in relation to certain infamous illegal drugs is the factor of most importance in terms of posturing to the media.

The same can be said for the specific addition by the government of the hallucinogen LSD (acid) on the list of eight drugs. LSD was not even recommended for inclusion in the law in the experts’ report. Discouraging people from driving on LSD is a good thing, but its insertion into these laws appears to be unnecessary, even ridiculous. As the lead expert on the report, Dr Kim Wolff, points out; to date LSD has “not been detected in drivers apprehended for drug driving or involvement in road traffic collisions in this country”. Indeed, if LSD needs to be strictly controlled when it comes to drug driving, why did the government not include psilocybin (the main active ingredient in magic mushrooms) or the legal hallucinogen salvia, both of which have similarly dramatic effects, and are more popular and easier to obtain? Without any conceivable scientific justification, it seems likely that LSD was included solely because of its notoriety in comparison to the others, a gesture to the press.

The civil liberties implications of this law are serious. For good reasons, drug use itself is not illegal (actual crimes include possession and supply) so this law is worrying in the way it resembles a back door approach to the criminalisation of people for having drugs in their system. This new level of powers has the potential to cause harm without preventing greater harms. A young, sober driver pulled over by the police for a broken taillight could have no cannabis in their vehicle or on their person, but may have trace amounts in their system. Even if they have not been stoned for a day or two, they might be prosecuted, despite posing no driving-related threat to either themselves or other road users. On top of the yearlong ban, they will face all of the harms consistent with a drug conviction. These include a criminal record, a potential fine or even jail time, difficulty getting or keeping a job or a place at university and travel restrictions abroad, particularly to the United States.

The current, contrasting drink drive limit supports this theory of back door criminalisation. Under the current law, drink drive limits are in place which punish people for driving whilst impaired, rather than for their drug use itself. The expert panel presented thresholds based on extending this system, yet the government has deemed such a method to be inappropriate. Hypocritical is the only way to describe this action. If driving with illegal drugs in your system cannot be tolerated in the slightest, the same should apply to alcohol. After all, it causes far more injuries and deaths on the roads.

Quite simply, these new laws give the impression of an attempt by the government to appear tough on drugs and to crack down on drug users, rather than to merely curb drug driving, the actual issue at hand. The benefits of a law designed to deter drug driving and save lives could still be achieved without causing the unnecessary harms discussed above. Putting appropriate laws in place, i.e. the ones outlined in the government-commissioned report produced by a panel of experts, would do this. The government should be consistent with its laws rather than posturing as tough. Most importantly of all, it should take heed of the scientific evidence available to it. That way, everyone wins.

Uruguay is set to legalise cannabis. Should we celebrate?

Assuming this law will pass though the country’s Senate, Uruguay is set to become the first country to legalise cannabis. Might this reduce the level of harm cannabis causes there to individuals and society?

To get closer to an answer, it is essential to move beyond the binary of legal and illegal, and to think more about the controls and regulations in place. Legality can look very different depending on the details of how a product is controlled. Compare an uncontrolled ‘legal high’, a legal and aggressively marketed drug like alcohol and a legal drug like paracetamol. The obsession with legal vs. illegal disguises the complexities and subtleties of how policy can produce positive or negative outcomes. Markets for legal drugs can be dangerously unregulated just as illegal markets are. It is clear that neither legalisation nor prohibition are themselves solutions to drug harm.

The good news is that the government of Uruguay are not so naive to believe that drug harms can be tacked simply through the legalisation or prohibition of drugs. They have been consulting in depth with many international experts to develop detailed plans to reduce the harms of cannabis. They are even setting up a unit which will evaluate and monitor evidence in how the law is performing so it can continue to be optimised. We will need to wait to see how these plans are implemented, but at this very early stage, Uruguay are making all the right signals that they intend their policy to work to reduce harm, not just to signify a particular posture on drug use. This looks like truly evidence-led policymaking.

Uruguay have had a policy of depenalisation for a while, where cannabis is prohibited, but possession of small quantities for personal use is tolerated. So their public and politicians know that the sky does not fall in when cannabis users go unpunished. That knowledge is not quite so widely accepted here, but international evidence shows that the wide variation and many local readjustments in ‘toughness’ of cannabis policy have no clear connection to how popular the drug is. And if use rises somewhat in Uruguay, is that itself a disaster if the overall burden of harm can be reduced? If we consider the harms of scuba-diving, is it better for this to be a popular and licensed activity with some risks or an illicit and dangerous habit of fewer people? We will have to look beyond the raw figure of cannabis prevalence to evaluate this law. Drops in crime and the use of more dangerous drugs are other vital measures of success.

Those who are close-minded to options beyond criminalisation frequently point to alcohol and cigarettes, which despite their legality causes more harm than any other drugs. As stated above, they are right, in the sense that legality itself is no magic bullet. But Uruguay intends to have a state monopoly over the production and sale of cannabis. Whilst kids’ sporting heroes are sponsored by booze companies here, all promotion of cannabis in Uruguay will be illegal, no companies will be seeking to maximise their sales. For our government, where a man who earns money from Big Tobacco has a job in the heart of the system, it proved a step too far to regulate tobacco packets so that they are not designed to appeal to new users. In Uruguay, to buy cannabis a user will have to be over 18, will need to register, and will buy the drug from pharmacies, unless they want to grow a personal supply themselves. Scrutiny of this state monopoly will still be essential to ensure that policy is never skewed by any vested interests that conflict with harm minimisation.

Alcohol provides a useful comparison in other ways. Illegal alcohol often contains a high amount of methanol, which blinds and kills drinkers. Legal alcohol has quality control. Like alcohol, the chemistry of cannabis affects the risks. Cannabis in this country has changed, 24 hour lighting in growhouses have produced a product with less or no CBD in it, which now dominates the market. CBD is a chemical which offers some protection from both the more unpleasant and more harmful effects that THC in cannabis can have. Uruguay has a great opportunity to offer their cannabis users access to a better, less harmful product. It is worth noting that illegal alcohol still exists and kills; a regulated market can only aim to outcompete and minimise the illegal market. Legalisation should slash the harms drug crime and illegal markets do to society, but will not eliminate them. Uruguay must follow the evidence of outcomes to find the optimum between over-regulation (for example a very weak product), which will push users back to unregulated illicit sources, and under-regulation, which I would argue is what we have for tobacco and alcohol, where opportunities to reduce harm, such as plain packaging, are rejected.

This article has focussed on the ways politicians can influence drug harm, but the Uruguayan proposals show understanding that top-down State action is not enough, and users’ decisions determine outcomes too. They propose education that equips citizens to make these judgements over their drug use, and healthcare and support for people needing help with cannabis problems. 

Cannabis is not harmless, for example it can worsen the mental health of some heavy users, especially the young. But the mental health impact of prison, unemployment and illegal drug gangs is considerable, legalisation reduces this burden of criminalisation. When deciding a drug's legal status, the question of whether it is harmful is less important than the question of how the legal status might reduce or increase those harms.

The world must watch what happens in Uruguay closely. If their approach works, this evidence should provoke reform elsewhere.

Khat - the claims vs. the evidence

Proponents of a ban on khat, however well-intentioned, are using a range of arguments which do not stand up well against the facts, or survive the application of reason.

Argument 1: the drug chemistry justifies a ban

The Claim;-

Khat is a natural form of mephedrone (or amphetamine/speed) which is banned, therefore it is logical that khat must be banned too. Khat is like cocaine, khat is like ecstasy....


Mark Lancaster MP – “The main component, cathinone, is found in meow meow” ...“I was shocked to learn that cathinone and cathine, are members of the same group of drugs as methadone(sic) ... Cathinone and cathine are illegal as is mephedrone yet contradicting all common sense, khat containing these same substances is legal. How can we continue to promote this hypocritical message?”

The Reality;-

Mark is muddled over his molecules. Cathinone isn’t mephedrone, although they are indeed related. However that tells us very little that is useful about its risks of khat leaves, which are lower than the risks of either cathinone in a pure form, or mephedrone. Whilst mephedrone is a powder that can be easily binged on, or even injected to produce an instant rush, cathinone is found in low concentrations in khat leaves, and released slowly by chewing over the course of an hour or so. Fatal overdose with khat is impossible, with mephedrone overdose is rare, with alcohol it’s common. Extracted cathinone is already illegal. Pure caffeine (not illegal) is pretty harmful, but that says little about the dangers of coffee.

Media guidance;-

Comparisons with other drugs such as amphetamine, caffeine, mephedrone etc, are of limited validity and should be used with care.

Argument 2: the drug effects justify a ban

The Claim;-

Khat is extremely dangerous and potently intoxicating, with various noxious effects on physical and mental health, so a ban is needed.

Mark Lancaster MP,
Baroness Warsi... “It can trigger paranoia and hallucinations. It is carcinogenic”. 

The Reality;-
The ACMD review found; “In summary, the evidence shows that khat has no direct causal link to adverse medical effects, other than a small number of reports of an association between khat use and significant liver toxicity.”

This is corroborated by DrugScience's review. Having said that, khat, like any drug, and indeed like anything, can cause harm if used inappropriately. As with alcohol or fast food, it is usual to make a distinction between problematic excessive use and ordinary use. This distinction is abandoned by the critics of khat.

Khat is not a hallucinogen like LSD, nor does it alter consciousness in the way that cannabis or alcohol are. It is a stimulant, and after a moderate amount of it, there is no evidence that a user would be incapacitated to think or even drive (although it’s best never to combine drugs with driving). As an aside, there is NO connection between the degree of intoxication a drug causes and its dangers, so implications that a drug are mind-bending and therefore need banning are usually rooted in morality rather than science. Cigarettes cause no intoxication and kill up to half of their persistent users. LSD is one of the most mind-altering drugs, but poses comparatively minimal risks to physical health.

It is likely that khat could play a role in mental health crises in which hallucinations, paranoia and aggression may occur. For example, if someone with a history of trauma from war in Somalia has a breakdown and chews khat without sleeping for days, they may suffer psychosis. Once again, alcohol is associated with mental health issues like this, but few call hallucinations an effect of wine. Hallucination should not be mistaken for an effect that khat causes in normal use.

There is no conclusive evidence that khat is carcinogenic. If khat does prove to cause a risk of cancer so slight that it hasn’t been picked up in some studies asking this very question, this does not make it uniquely dangerous. You can go through the alphabet (Alcohol, Bacon, Coal...) listing objects linked to cancer to some degree. The important factor is the level of risk. Tobacco poses a huge cancer risk to khat users.

Media guidance;-

Care should be taken to distinguish claims and facts about the effects of khat. Claims of its dangers should not go unchallenged, and could be set against the evidence reviewed by the ACMD.

Argument 3: the will, the cri de coeur, of the affected communities justifies a ban

The Claim;-

Communities affected want a ban, it’s racist not to ban it, banning it is a caring, kind act towards the user communities. 


Political proponents,

Abukar Awale (self-proclaimed Somali representative)  

The Reality;-

It is true that significant numbers of the Somali community express support for a ban, enough to rally small crowds that have protested in Downing Street. However, one cannot claim to have a democratic mandate by looking only at those who vigorously support the plan. Opinions on khat are diverse. In the UK, there are other communities aside from the Somali community (Ethiopian, Yemeni communities) in which regular khat use is also very common, but who seem to suffer hardly any of the harms that khat allegedly causes in the Somali community.  The opinions of these communities are never mentioned. For various cultural and religious reasons, people are less willing to shout about their right to use khat than they are to shout about how evil it is.

Opposition to khat is driven by a small handful of highly motivated individuals such as Awale Akubar, equipped with emotive anecdotes about the devastation khat causes. The ACMD’s review examined the diversity of views and found that the idea that khat is a food, not a drug, and that it has beneficial properties, also has very considerable support in the user communities. If policy is to be justified by anecdotal evidence without concern for establishing the facts, we would like an explanation why the first type of anecdotal belief is considered more valid than the second. Is it any more rational to impose a blanket ban because of anecdotes of harm than to impose universal provision of khat on the NHS because of anecdotes of health benefits?

When such conflicting personal perspectives exist, the need to examine the peer-reviewed scientific evidence is all the more vital. This is not to say that anecdotes about khat are useless, or to say that those who hate khat should pipe down until they have doctorates in drug science. As the ACMD’s review points out, anecdotal evidence is indispensable in guiding research to the right questions. Avoiding khat and warning against its use based on personal opinion is entirely legitimate. However it is another question whether the government should step in to coercively enforce anti-khat values on other adults without objective evidence of exceptional harms.

Psychologists know that collecting reliable evidence of people’s opinions is much harder than it appears. It has been suggested for example that evidence from surveys of considerable support for the proposition that khat should be banned is complicated by the possibility that the question is understood as shorthand for “Do you think khat use is a good or bad thing?” or “would you prefer if khat didn’t exist?” It is also likely that, similar to other drugs, big chunks of the Somali community and the public overestimate the deterrent effect of drug bans and underestimate the unintended consequences, genuinely believing that it is in the government’s power to make problematic drug use go away with the stroke of a pen. 

One can imagine a very different result if the question was phrased differently, for example “do you think that people who chew khat should be arrested?” A more sophisticated survey, capable of better separating people’s personal liking /disliking of khat from the practical question of effective policy responses might ask participants to choose between 3 options for the government;-

 1) Do nothing

 2) Control khat under the Misuse of Drugs act so that criminal sanctions are attached to its possession (with description of potential costs and benefits)

 3) Implement ACMD’s recommendations in full, review in 7 years (with description of potential costs and benefits)

The Misuse of Drugs Act 1971 is designed to classify and control drugs on the objective basis of their harm. Experts have shown that khat is not harmful enough to qualify for the Misuse of Drugs Act so if Theresa May wants a khat ban on a moral basis, she should put before Parliament for their consideration a new Act which does so transparently, rather than misusing the Misuse of Drugs Act. 

Media Guidance;-

It is essential to include Somali people’s opinions when reporting on this issue but no single individual, however forthright, can claim to speak for the Somali community, and this should be made clear. Opinions on drug use based in subjective values or religion are of course important, but a distinction needs to be maintained between such moral claims against khat, which cannot be measured as true or false, and objective claims against it, which need to be evaluated against the evidence.

Argument 4: international prohibition, even in the Netherlands, justifies a ban

The Claim;-

Look internationally, even the Netherlands, home of wacky drug liberalism, have banned khat! We’ve become ‘out of step’.


Mark Lancaster MP

Home Office

Sections of press.

The Reality;-

The Netherlands currently have a fragile centre-right government, in which anti-Islam politicians have gained prominence. They are not a bunch of stoned hippie lefties. When they banned khat, they also did so in spite of evidence collected by scientific advisors (Trimbos). 

The Dutch scientific advisers of course made a similar assessment as the ACMD have, as the facts are the facts. Co-author Clary van der Veen said, "We made very different recommendations based on our study. The large group of social users is not a problem. You may need to inform them better and point out the long-term effect, just like with smoking and drinking,"  "In countries where khat has been banned, the integration of Somalis is not faring better," she said. 

By following the example of the Netherlands we are following a policy of denial of the evidence.

As we are seeing here, calls to ban khat were mixed up with anti-immigrant sentiment and plain racism. Khat was the excuse for the then Immigration Minister Gerd Leers (now resigned in disgrace) to say that 10% of Somali men were "lethargic and refuse to co-operate with the government or take responsibility for themselves or their families". The 10% figure for problematic khat use appears to be a novel invention, but the image of the lazy, black man who breeds without looking after his offspring and doesn't heed white authority figures is certainly not novel. It barely needs stating that ACMD found no evidence to support a causal link between khat use and social problems like these. They found that for an unemployed person, excessive khat use could indeed be a barrier to getting employment, but cited research for the Home Office by Patel et.al. (2005) that found that a smaller proportion of unemployed Somali men use khat than employed Somali men. The ACMD pointed out that "the majority of users moderate their consumption to fit in with work patterns".

The Dutch Government also cited antisocial behaviour such as littering as a justification to ban khat. The ACMD points out that such problems have already been effectively tackled in the UK through "community-level action working in partnership with police and local authorities".

Whilst the evidence clearly challenges the notion that khat is to blame, in a straightforward way for family breakdown, unemployment etc, there IS irrefutable evidence that criminal records for drug offences cause family breakdown, unemployment and the rest.

The ACMD looked at the international situation, and noted that the bans internationally either were imposed without a scientific assessment, or in the face of the scientific evidence. Where bans have been imposed, the problems of the Somali diaspora have not vanished. Neither has khat. But the price has risen sharply.

In the UK, it is clear that perceptions around khat are highly influenced by anti-immigration (or more plainly racist) sentiment. On the 4th July 2013, the ‘best rated’ comment on the story that a ‘Defiant’ Home Secretary was outlawing khat was simply "ban the drug and deport the users".

Media Guidance;-

The Misuse of Drugs Act 1971 is designed to classify drugs on the basis of their harmfulness.

Argument 5: terrorist links justify a ban

The Claim;-

Khat is “linked to al-Qaeda”, or the trade funds al-Shabaab, or the khat cafes breed radicalisation, so we need a ban. 


Awale Akubar,

Daily Mail, Sun


It is notable that Abukar Awale, the self-proclaimed Lead Campaigner for a khat ban, appeared to admit to a journalist that he likes to feed fears about terrorism as that is the key which forces political action.

"This is the tool for me," Awale said. "I will put this on the table and say, 'Now you must act'. And they will act. When this country hears terrorism, they will act."

Awale deserves a well-paid job as a phenomenally talented political lobbyist. Baroness Warsi cited him in the Conservatives first calls to ban khat in 2008, this year he told the Mail on Sunday that Lee Rigby’s murder was linked to khat.

After the ACMD had reviewed the evidence for the link between khat and terrorism, the chair of the ACMD called this a ‘nasty little rumour’. Whilst Somali use of khat is often integrated into the local Muslim tradition, so that it is used in celebrations and to fuel nights of Koranic study, most Muslim authorities from other traditions internationally consider khat-use to be at best undesirable and at worst forbidden. In fact, radicals spreading a fundamentalist interpretation of Islam into East Africa have been a major force behind the prohibition of khat there.

There is no reason to believe that khat cafes are linked to radicalisation, and the narrative is indicative of a general suspicion of Muslims, or indeed any people who are not white British. The Sun’s article making these lurid claims has the following comments below it;- ‘scouseviking’ says “Maybe if U turn Osborne put VAT on it, the Somalians  might all want to protest then you can round em all up and ship em home.....simples” 

Once drugs are illegal, the trade goes underground, becomes massively more profitable, and the illegal trade in heroin certainly has been a major source of funds for the Taliban and other fanatics. The sheer injustice of a ban like this targeted on an already marginalised population within a country that celebrates the legal use and abuse of our own socially lubricating drug, alcohol, would, if anything, foster the alienation and ostracision which radicalisers feed upon. 

Perhaps Theresa May has in the back of her mind a hope of some favourable headlines in certain tabloids that gave her a hard time over her struggles with Abu Hamza and Abu Qatada. But it is very ironic that a khat ban seems to appeal to the very same anti-immigration demographic as a way of taking a tough stance regarding Muslims in the UK, since Abu Hamza would likely have been very much in favour of Sharia law banning khat in the UK. Since May can’t justify banning khat on public health grounds, she’d be better off taking a Sharia-like approach and banning it on grounds of morality!

There's more than one way to skin a cat

A version of this post was published by The Guardian

Now this is embarrassing. I'm expected to have something to say about Theresa May's intention to ban the plant-drug khat, but due to a texting error by a new intern, I'd been preparing my thoughts on the Tory plan to ban cats, a plan which I now learn may not exist. Fortunately for her, I find that many of the same arguments apply, so I'm not quite back at square one.

The proponents of a ban on cats khat may be well intentioned, but rely on a mixture of exaggerated, selective, anecdotal, prejudiced and most frequently erroneous and illogical arguments. Cats are Khat is indeed associated with harm, which can be very serious at times, but it is unwise to generalise from the most extreme cases, or assume that cats are khat is solely to blame for complex problems of owners users.

Advocates for a ban are sometimes prone to demonise cats khat and, cynically or credulously, to fuel unfounded fears against owners users.Historically, cat owners were persecuted as witches. Khat users find themselves linked spuriously to terrorists, the ultimate folk-devils of our era.

Despite all the rhetoric, when detailed studies are made that explore the actual empirical evidence, suspicions about the dangers of cats khatare revealed time after time to have little basis in reality. A balanced assessment also exposes the prejudices of those campaigning for a ban on cats khat. Theresa May, who wants to disregard expert advisers and label as criminals any people who possess cats khat, has disregarded the evidence before, personally undermining her own government's promise to reduce the far greater harms caused by dogs alcohol.

By nearly every possible objective measure, dogs cause alcohol causes far greater danger to health, life and society at large than cats khat, or indeed any other pet drug. People rightly worry about the harm caused to society when people are irresponsible with dogs alcohol: the thousands of hospital admissions; the mess and intimidation we encounter on our city streets. However, insight and experience show that these harms to society can best be minimised through education, co-operation and maybe regulation, not by criminalisation and ostracism. Bans offer an opportunity for governments to posture and express their toughness to the electorate, but our legislative agenda should be driven not by the naive assumption that simple bans solve complex problems, but by evidence of what might actually best serve the interests of the public.

Those wanting a ban on cats khat might do well to consider the historical precedent. Driven by tabloid hysteria, the UK government introduced The Dangerous Dogs Act 1991, banning four breeds of dog. Since then, hospitalisations for dog bites have more than quadrupled , with experts highlighting the absurdity of criminalising possession of particular types of dog instead of addressing issues of owner behaviour and responsibility . Driven by a moral agenda, alcohol was banned in the US in the 1920s, successfully handing the trade to organised crime networks. While prohibition probably reduced consumption, overall harm rose as the people most harmed by alcohol were denied the help they needed and were instead branded criminals. Now in the UK, the freedom of individuals to lawfully own a dog drink is respected, and we recognise even that pets alcohol might have some social value too.

Those who don't like going near dogs alcohol, who think that dog owners drinkers are wasting good money on dog food alcohol and valuable family time going on walkies to the pub have a valid opinion, but we don't think their values should be imposed on others through the criminal justice system. The same is true of cats khat: no one should mistake their inalienable right to find cats khat disgusting with a right to interfere with the personal choices and pleasures of others.

The risks associated with dogs and cats alcohol and khat are not something we should take lightly, but bans are an excuse to do nothing productive to address a problem, which the government has been doing very well already. Twice they have asked the Advisory Council on the Misuse of Drugs (ACMD) to review the harms of khat, (they are obliged to get expert advice before they ban it), and twice the ACMD has said that a ban would be inappropriate and disproportionate, while making a series of considered recommendations for awareness-raising and community engagement, access to treatment services and improving health standards of khat cafes. While the government has no problems collecting millions in tax on khat imports, it seems reluctant to consider any investment in looking after khat users, except if they are in prison cells.

All right, I think we've chewed over the khat/cat analogy long enough, but there is a serious point to be made here. I got into a little trouble for comparing the risks of death and serious injury from horse-riding and ecstasy, so I should be sure to say that whilst horse-riding really is comparably risky to the class A drug, in terms of acute harm, I expect that khat use is more often seriously problematic than cat-ownership. However, we should be comfortable with the idea of comparing the risks of drug use with other risks we might face: cooking, trampolining, sunbathing or pet ownership. Our drug laws are purportedly there to protect individuals and society from harm – they are not meant to be there to uphold any specific moral values and punish deviance from them. If politicians wish to argue for drug prohibitions on a moral basis, because they think it is obnoxious and dissolute to sit around getting high from leaves or intoxicated by drink, that's fine, let them make the case, and see whether parliament or the electorate have an interest in policing people's personal habits. What they must not be allowed to do is to push a moral agenda against an already marginalised group through laws intended to regulate drugs on the basis of evidence of their harmfulness.

Let’s get the War on Drugs out of our hospitals and laboratories

There are politicians in every major party who hold sensible attitudes to drugs, and a few of them even have the integrity to air these attitudes in public, rather than just acknowledging them in private, or when they have left office. Unfortunately, while they serve in government and have a chance to tinker with the creaking old banger of our drug policy, they only ever pick up the hammer or wrench to toughen and tighten the rules. They never reach for the oil or the fuel that might ease the rusted up axles and make our policy actually work.

Beneath the rust, our drug policy does have the mechanisms in place to operate (whether an entirely different mechanism might work better is quite another question). There are twin engines under the bonnet, the familiar Misuse of Drugs Act (MDA 1971), which details how different drugs are controlled to prevent ‘misuse’, and the lesser known Misuse of Drugs Regulations (MDR 2001), which details how different drugs are controlled to allow legitimate use for research and medicine. If our drug policy ‘worked’, we’d see the harms associated with drugs driven down through MDA 1971, and the benefits associated with medical advances and scientific progress driven forward by MDR 2001. Sadly, these engines seem to have seized up.

Today, with Les King and David Nichols I’m publishing a paper in Nature Reviews Neuroscience which with your support will kick-start a debate on one of the principal failings of our drug policy, one that could be mended tomorrow if politicians knew that most voters want their drug policy to work, rather than to sit there symbolising something about the tough values of its engineers. I am highlighting the fact that here and internationally, the Regulations on using controlled drugs in research are so illogical and obstructive that they amount to the greatest act of censorship on scientists since Galileo was tried before the Inquisition, and texts advocating the sun being the centre of the universe were banned.

The Regulations classify drugs into several ‘Schedules’, with different degrees of control. Schedule 2 for example contains drugs with significant dangers, but also medical uses, like morphine. They are regulated to allow legitimate use in hospitals and laboratories whilst minimising the risk of the drugs getting into the wrong hands. Schedule 1 is for the most tightly controlled of all, it contains drugs that, at the time of writing the laws, were deemed not to have any proper medical value. Therefore, in theory, those drugs could be stringently restricted with no compromise to future human welfare. With political motivations often trumping evidence, into the bottomless pit of Schedule 1 went LSDmagic mushroomscannabis, and ecstasy, each of which actually have considerable therapeutic potential. More recently, our government has tipped into this black hole barrowloads of totally un-researched new chemicals (e.g. cannabinoids, cathinones, arlycyclohexamines) because they are chemically related to banned drugs. All these drugs are caught in purgatory, stuck in a paradox; without an established medical use they can’t be freely researched, but without this research, any medical potential they may have will never be uncovered.

Drugs get sucked into the black hole of Schedule 1 all too easily, but no evidence of medical value seems enough to get them out. We need to resist the scary fairy-tale that removing drugs such as cannabis from Schedule 1, or reforming the Regulations, will open a Pandora’s box. There’s much more reason to believe that we’ll unleash a Neuroscientific Enlightenment, making new discoveries about the brain and consciousness, developing new treatments for debilitating disorders like PTSD, depression and chronic pain, and giving a boost to our economy along the way.

LSD was used as a therapeutic tool, and research thrived before UN Conventions and domestic laws controlled it as if it were akin to smallpox. The controls on Schedule 1 drugs like LSD, magic mushrooms and MDMA are purported to counter the threat of diversion, yet far more harmful drugs including heroin, (categorised as Schedule 2), are safely researched and used therapeutically in UK hospitals under more proportionate controls. Research on Schedule 1 drugs is technically still permitted under licence, and indeed some goes ahead, allowing the authorities to deny that scientific progress is being stifled, yet the figures tell their own story. Since this censorship began, there have been just one or two studies published on the therapeutic potential of LSD in human subjects, compared to the hundreds of studies before. With Schedule 1 licences costing thousands of pounds, and with endless bureaucratic obstacles, it is remarkable that any research on these drugs is done at all.

I’m not calling for scientists and doctors to be let off from the rules on drugs that apply to other citizens. I’m calling for the regulations on controlled drugs to be proportionate to the risks they pose. One simple gesture that could be introduced tomorrow would be to introduce minimum quantity thresholds below which a lower tier of regulations apply. It’s hard to argue that a 50mg reference sample of MDMA in a locked cabinet,- less than a single dose- poses a greater threat to public health than the cleaning products and medications in our bathroom cupboards. Another progressive change would be to make Schedule 1 licences free, which would be cost-effective considering how the economic powerhouse of biosciences in the UK would be invigorated. Moreover, it is essential that new compounds, with no known dangers and unknown therapeutic potential, are not lost into the black hole of Schedule 1.

I hope for regulations that support scientists and the biosciences industry to uncover new knowledge and treatments, rather than holding them back. If you agree, why not write to your MP?

Cocaine: the perfect heart attack drug?

By George Gifford

A recent paper, presented at the American Heart Association's Scientific Sessions 2012, suggests that using cocaine as little as once a month can lead to stiffening and narrowing of blood vessels (atherosclerosis) and thicker heart muscle walls (hypertrophic cardiomyopathy). The results of study have broken new ground: firstly because the cocaine users in the study did not use massive amounts of the drug; secondly because the cocaine users in this study were not dead, most other studies suggesting that cocaine may cause stiffening of blood vessels being post mortem. 

Being about drugs and death, this study was quickly picked up by newspapers, using the soundbite, ‘Cocaine- the perfect heart attack drug’. Now, the negative effects of cocaine on the cardiovascular system have actually been explored for some time and are not surprising given cocaine’s well known acute effects of blood pressure and heart rate, and the substantial amount of case reports of cocaine induced heart attacks. Very relevantly, there have also been some larger studies (epidemiological studies) linking regular cocaine use to an increased likelihood of having a heart attack. The point here is that there is already a body of evidence linking cocaine use to heart attacks and associated damage to the cardiovascular system.

This is important because the study in question only involved 20 cocaine using participants, meaning without past research, it would make a weak case for the relationship between cocaine use and the increased likelihood of having a heart attack. With this in mind, you can take the Daily Mail’s headline ‘Cocaine is ‘the perfect heart attack drug’- even if you use it a few times a year’, with some scepticism. All of the participants used the drug at least once a month and there were only 20 of them meaning, as it stands, it really applies to regular (at least monthly) users. 

This is not to say that cocaine does not have a specific underlying action that causes damaging changes to the heart and blood vessels as the study suggests, quite the opposite. This study provides an answer to the question of why cocaine may cause heart attacks in those otherwise not at risk. The problem is that how the study has been reported (and drug science is often reported) sensationalises the drug harms without really providing any useful information.

For example, it would be common sense to mention that cocaine use would be more dangerous if you were doing something that also causes atherosclerosis, namely smoking (if you need convincing, here is a study of 91 case reports of cocaine induced heart attacks- 87% of which were cigarette smokers). Additionally, some people have a genetic predisposition to thickening of heart muscle, which is actually one of the most common genetic heart conditions out there, and can often go undetected (until people have sudden heart attacks). The main advice here is that anyone with a family history of sudden heart attacks (especially in younger relatives) may be at particular danger from further thickening of the muscle in the heart. 

It would have been helpful if papers mentioned that taking cocaine if you have high blood pressure or pre-existing heart problems could be particularly harmful or at the very least linked readers to some kind of cocaine harm reduction information. In absence of this, the impression we get is that the writers of such articles take it upon themselves to portray drugs in as harmful a light as possible, to convince people to never use the drug ever. Whilst this may deter people who have never used the drug, drug users can be those who are fully aware of the risks, but don’t see them as that personally relevant. 

With this in mind, here are the take home points of what the study suggests, and how they could relate to you: 

•    Thickening of the heart’s walls and stiffening of blood vessels is likely with regular (even just monthly) use of cocaine.
•    If you are already doing something that can cause athesclerosis (e.g. smoking), regular cocaine use could add to this, making it riskier.
•    If there is a history of sudden cardiac deaths in the family, cocaine may be particularly harmful to you.

The Dustbin of Schedule 1: How Schedule 1 control may stifle medical advances

The Back-story
Months ago, the Advisory Council on the Misuse of Drugs (ACMD) were asked by the government to gather the evidence on the harms of methoxetamine (MXE, ‘mexxy’), a new drug related to ketamine (a ketamine ‘analogue’), and recommend to the Home Secretary what should be done about it. The ACMD did this, produced a report, the conclusions of which the government has accepted. As a result, an Amendment Order to the Misuse of Drugs Act 1971 has been drawn up, adding methoxetamine into the Class B and Schedule 1 categories of the Act. In an attempt to prevent legal high manufacturers looking for a new ketamine analogue to sell, the government will also follow the ACMD’s advice to place countless other ketamine analogues into Class B and Schedule 1.

This Amendment Order, making methoxetamine and a range of ketamine analogues Class B Schedule 1 drugs is of real concern to the ISCD. As will be outlined, Schedule 1 regulation, a dustbin category for controlling drugs with no medical use, may prevent medical advances that could help relieve depression and pain. 

More harm than good?

There are a number of problems with this approach, not least that ketamine is by far and away the major drug of this class causing problems, with use massively greater than that of methoxetamine which users tend to dislike. Methoxetamine was made the first ever subject of a Temporary Class Drug Order in March 2012. Since then its use appears to have dwindled and although there have been cases of extreme intoxication requiring hospital assessment and treatment the ACMD did not find evidence to date of lasting harm or deaths directly caused by it. A recent report by the All-Party Parliamentary Group on Drug Policy Reform interestingly suggested that making TCDOs a model for a more permanent form of control rather than proceeding with full bans could work to reduce harms without criminalising users.

Reducing the impacts of ketamine use is a priority because of the known problems of bladder pathology, addiction, depression and cognitive impairment. However the banning of a range of analogues causes concern because it is unlikely to be an effective way to minimise the harms of these ketamine-type drugs but will also inevitably significantly impair research, particularly into finding medicines that work in the brain, a field that is currently in crisis.

For ketamine analogues, in addition to their potential as new anaesthetics (tiletamine, an analogue already in use as an animal anaesthetic, is exempt from the ban) there is growing interest in their potential as treatments of depression. The finding that ketamine can rapidly ease depression is widely considered the most significant advance in the last 50 years for tackling treatment-resistant depression and suicidal thinking. However, ketamine itself has significant side-effects, so the ketamine analogues are being considered as even more useful drugs for this indication.

Moreover the growing use of long-term ketamine for chronic pain syndromes, and the emergence of high-dose approaches raises the concern of bladder damage as a side-effect in these patients so safer alternatives would be welcome. Medicine progresses by finding better alternatives to existing drugs, a point well demonstrated by ketamine itself. Ketamine was discovered by scientists looking for a safer analogue of phencyclidine (PCP, ‘angel dust’), which was tried as an anaesthetic. PCP worked, but was pretty useless because patients emerging from anaesthesia experienced a long delirium. So analogues were systematically tested until ketamine was discovered, which produced the same benefits but fewer problems. 

Now, decades later, the side-effects of ketamine are driving fresh interest in finding better drugs that work in a similar way. Some hopeful signs are appearing already, with successful trials of one new drug with ketamine’s antidepressant effects (one that has a structure that would not be covered by the new ban). Ketamine derivatives based on tenocyclidine have been studied as anti-organophosphate poisoning agents and in the treatment of cancer, and others are potential treatments of sepsis. Also, the psychoactive effects of ketamine provide a useful model of psychosis for research, but one that might be improved by the testing of analogues.

Although putting analogues in Schedule 1 still theoretically allows them to be researched, the current situation regarding Schedule 1 licenses is such that this research will be severely hampered. The holding of Schedule 1 drugs is subject to a specific Home Office license that now costs about £5000 to obtain and then incurs significant time and other costs in relation to inspection . It also takes up to a year to get one. Currently we know of only 4 hospitals in the UK with one; neither Hammersmith Hospital or University College Hospital, two of the leading clinical research centres in the UK hold one. In contrast NHS hospital and university departments that conduct biomedical research which requires controlled drugs in Schedules 2-5 are exempt from the need to purchase a license to hold these. These hurdles induced by Schedule 1 status, though surmountable, effectively stifle research.

Many university pharmacology depts. do not have Schedule 1 licenses so would not be able to work with these compounds. One compound covered by the proposed ban, eticylidine, has been a useful radioligand for studying NMDA receptors and is being considered as a starter molecule for PET tracers. Moreover we know that forensic chemistry experts working in this field of legal highs have found Scheduling of other drug classes, particularly the cathinones and cannabis agonists severely hampers their ability to work in this area due to restrictions of supply and increased costs.

History tells us that pharmaceutical companies are very averse to funding work on compounds that would be subject to controls. This aversion also applies to close analogues of currently controlled drugs since there is no guarantee that these too would not be controlled under analogue legislation, such as that being proposed. 

Conclusion - we cannot continue depositing drugs into the dustbin of Schedule 1
Control, particularly at Schedule 1 level, stifles and may kill research in a field. It is imperative we do our best avoid this outcome with drugs like ketamine that act at the NMDA receptor as these are so promising therapeutically. This is particularly important as there is no reason to think that this legislation will have any impact on ketamine use and harms. Indeed it may paradoxically increase harms if safer analogues are not discovered and so ketamine use – both clinical and illicit - continues.

Time for a second opinion? Where we are going wrong on ‘Legal Highs’

There are parallels between the responsibilities GPs and MPs hold; Doctors in prescribing drugs to maintain our health, politicians in proscribing (banning) drugs to protect public health. When doctors write us a new prescription, they do so in the knowledge that prescriptions have side effects. But we trust them to make an evidenced judgement, that the benefits of what they prescribe should outweigh the risks of the treatment. 

We should expect equivalent balance when politicians write us a new bit of legislation. We should be able to trust that they understand the potential ‘side-effects’ their legislation may have, and have weighed them against the benefits to public health that the ‘treatment’ offers. Unfortunately, some of our politicians seem less concerned by evidence than doctors. In their current efforts to treat a spreading rash of ‘legal highs’, our government is prescribing some seriously bad medicine, as will be explained in this extended blogpost.

“Towards a Safer Drug Policy”

The proliferation of New Psychoactive Substances, often called ‘legal highs’, is rightly seen as a threat to public health. Enforcing the prohibition of familiar recreational drugs has proved far from a walk in the park, but when labs can churn out new drugs which mimic illicit ones but can be sold freely, what is a government to do? In the last few years, the government has repeatedly made Amendments to the Misuse of Drugs Act in an attempt to keep up. They banned GBL, (the solvent which the body converts into the sedative GHB), mephedrone and various similar drugs (which have effects similar to MDMA or speed), and more than 140 synthetic cannabinoids (which have cannabis-like effects). They have also introduced ‘generic’ bans; outlawing as-yet-unmade drugs matching complicated descriptions of molecular architectures, because they might be exploited in future. For example, structures related to mephedrone were outlawed.

To return to the analogy between policymaking and medical treatment, has there been any improvement from the regime that has been tried? Today, GBL is still popular and still allegedly sourced online, drug dealers are doing a roaring trade in mephedrone, although it is now as adulterated as other illicit drugs, and a new legal generation of synthetic cannabinoids has seamlessly displaced those that were banned. Like severing the Hydra’s heads, the government’s strategy seems only to have stimulated the proliferation of new legal drugs. New psychoactive substances currently appear at a rate of one every six days. The market for psychoactives has never offered more choice. The All-Party Parliamentary Group on Drug Policy Reform today publish their detailed report into the situation, “Towards a Safer Drug Policy; Challenges and Opportunities arising from ‘legal highs". They collected evidence from a wide range of witnesses involved in drug science, policy and law, from the ISCD to the Association of Chief Police Officers. The consensus amongs witnesses that the current approach is doomed is striking. Their analysis and recommendations are deserving of serious attention.

When a treatment doesn’t work, we don’t necessarily blame the doctor, but we expect them to look at the facts and consider an alternative course of therapy, according to the tenets of evidence-based medicine. This is an urgent issue, with the government currently lining up the next batch of bans in a Statutory Instrument, a type of legislation that does not undergo scrutiny in Parliament. This new legislation, The Misuse of Drugs Act 1971 Amendment Order 2013, is cause for serious concern about the status of evidence in drug policy. The rest of this blog examines the Amendment in more detail, showing reasons to expect that it will do more harm than good.

The Misuse of Drugs Act 1971 Amendment Order 2013

The new Amendment Order to the Misuse of Drugs Act 1971 bans yet more chemicals, making them Class B. These include O-desmethyltramadol, (a dangerous opioid), methoxetamine (related to ketamine, but stronger), and yet more synthetic cannabinoids that have been developed since the last ban in 2009. Generic definitions have been used in an attempt to prevent more ketamine analogues getting sold, banning molecular structures considered too close to ketamine, and similarly, generic definitions have been used to close off several new avenues for making new legal synthetic cannabinoids. 

In evidence-based medicine, when a doctor makes a prescription they ask themselves questions like;-

1. Is there evidence that this course of treatment is effective (better than nothing)?
2. Are there any unpleasant side–effects?
3. Are there safer or more effective alternatives?

Let’s put the Amendment Order to these same tests to find out how evidence-based it looks. 

1) Is there evidence that this piece of legislation could be effective?

It sounds obvious enough, but to answer this question we need to know what ‘effective’ looks like. What outcome do we want to see from the Amendment Order? Politicians sometimes justify drug bans as “sending a message”, but it is vital to stress that the Misuse of Drugs Act is not for sending messages about drugs (it would be nice if we sent messages through education rather than criminalisation). The stated objective of the Amendment Order is simply to “control substances considered "dangerous or otherwise harmful" … as a public health and protection measure”. This is clearly stated in the Explanatory Memorandum.

By this measure, the Amendment Order is a flop. So far, successive Amendments have failed to control the availability and use of New Psychoactive Substances. The Home Office and Police are “flat-footed” according to the Association of Police Chief Officers spokesperson. If the purpose is truly to protect public health, such legislation cannot be considered effective even if it works in stopping people using particular named chemicals, if it merely encourages the proliferation of new chemicals the risks of which we know even less about.

The control of new synthetic cannabinoids in the Amendment Order is particularly noteworthy for being a guaranteed embarrassing failure because, astonishingly, since the generic definitions in the Amendment Order were drafted to make legal cannabinoids a thing of the past, at least 12 brand new synthetic cannabinoids have been identified which circumvent these definitions. Dr Les King, one of the most knowledgeable drug chemists around and an ex-member of both the government’s ACMD and the ISCD has reported this situation exclusively on the ISCD website. The upshot of this is that before the Amendment Order has even become law, it is redundant.

Conclusion;- there is no evidence of effectiveness for the new Amendment Order to the Misuse of Drugs Act 1971 .

2) Are there any unpleasant side–effects?

All medical treatments have a risk of side-effects, and in evidence-based medicine, side-effects make a treatment unacceptable if they outweigh the benefits of treatment. The technical word for harmful side-effects of treatment is iatrogenesis. Here, by analogy, we’re asking if the Amendment Order is an ‘iatrogenic’ law.

The Amendment Order will make methoxetamine a Class B drug, and to prevent another ketamine analogue being sold to replace it, a generic definition has been written controlling any future drugs closely related to ketamine. This move could have serious and lasting side-effects because our current drug control regulations mean that these family-members of ketamine will become very difficult to research. Ketamine is a valuable pharmaceutical drug, with uses in anaesthesia, pain control and treatment-resistant depression, but with side-effects including bladder damage from long-term use. There is every reason to hope that amongst its relatively unexplored analogue family may be drugs with similar or improved properties but less adverse effects. These may never come to light if they are banned before being made.

A more immediately obvious harmful side-effect of the Amendment Order is one that applies to our drug law more generally, that arrest and up to five years in prison, (the maximum sentence for Class B drugs) does harm to people’s lives more surely than most drugs. Methoxetamine for example was banned on the evidence of a few fairly nasty medical crises, all of which however resolved over time, unlike criminal records.

The damage criminalisation does to young people is acknowledged by the government’s drugs advisors, but in the Home Office’s ‘Policy Equality Statement’ in the Explanatory Memorandum, the belief is expressed that the damage risked by criminalisation is “outweighed by the need for Government intervention to protect young people from harmful drug use in light of the assessment that they have made it clear that the belief that these substances are “legal and therefore safe” is the main driver for trying them”. If, as discussed, banning new drugs is ineffective in curtailing the availability of legal drugs, then the cost of criminalisation cannot be an acceptable side-effect. Also, research led by ISCD member Dr John Ramsey shows that consumers actually have little knowledge or control as to whether they are breaking the law or not. So-called ‘legal highs’ are so poorly regulated that people who purchase a product disingenuously labelled as an ‘incense blend’ will have no way of knowing if it is laced with genuinely legal cannabinoids or one of the ones that have been outlawed. Neither will the police, as made clear by Tim Hollis of the Association of Chief Police Officers, who opposes the unenforcable strategy of “adding inexorably to the list of illicit substances”. In any case, ISCD member Dr Fiona Measham gave evidence to the All-Party Parliamentary Group's inquiry to the effect that legal status has a minimal impact on most clubgoers' decisions to use legal highs. To genuinely reduce harms, it would seem more urgent to tackle the dangerous belief that legal drugs are safer than illicit ones.

Conclusion;- Potential side-effects of the Amendment Order are worrying. To outweigh these costs, the legislation would have to offer marked benefits.

3) Are there safer or more effective alternatives?

Everyone is concerned about the harms that new psychoactive substances can cause. It is intolerable that, whilst people argue over whether drugs like cannabis should be legal and regulated, decriminalised or prohibited, much more dangerous substances are virtually unregulated and available legally to anyone.

In this context, the new report by the All-Party Parliamentary Group on Drug Policy Reform is timely. They make many recommendations for better prevention and treatment for the use of new drugs, rather than relying on the justice system to take care of public health concerns. They also want to see discussion of the ultimate causes of the proliferation of products mimicking the effects of illicit drugs. If the possession of small quantities of illicit drugs was decriminalised, would there be such an appetite for untested legal alternatives? The report recommends serious consideration of the regulated approach being instituted in New Zealand, where the onus is on the supplier of a new drug to demonstrate a low risk of harm. The New Zealand model also explicitly demands that “the harms of any form of regulation should not be greater than the harms of the substance being regulated”. It will be some time until we can say with any certainty that this model works well, but it has the advantage of having been developed through a rational evaluation of the challenging situation. As ISCD members Dr Tim Williams and Prof. Val Curran told the All-Party Parliamentary Group's inquiry, when drug users see that the system for drug control is conceived rationally, they will begin to trust it.

Conclusion;- We can’t hope to ‘solve’ the problems new drugs cause. Drugs harm and some people will always use them. But by taking an evidence-based approach, we can do so much to reduce unnecessary harm caused by drugs and by drug legislation.

Cannabis and IQ

By George Gifford

A recent paper by Ole Rogenberg has challenged previous findings that adolescent cannabis use may lower IQ. The research in question by Meier et al. (2012) found that those who started smoking cannabis weekly before age 18, and carried on regularly use into adulthood, showed an average 8 point drop in IQ. This study involved a sample of 1,037, who were followed from birth to age 38, with five intermittent interviews ascertaining drug use, and IQ tests at ages 13 and 38.

New criticism of this work comes in the form of a simulation statistical model suggesting that the results in Meier et al. (2012) could be confounded by the variable of poverty, those with lower socioeconomic status being more likely to smoke cannabis from a younger age and do less well in school. In reply to this researchers from Meier et al. (2012) have stated that when they restrict their data to only including those from middle-class homes their results are the same, suggesting that Rogenberg’s claims are not represented in their data. Despite this, critics such as Rogenberg still maintain that Meier et al. (2012) does not account for potentially confounding factors and their results do not suggest the neurotoxicity of cannabis as claimed. Put simply, Meier et al. (2012) think their results show a biological effect of cannabis on young brains and Rogenberg (2012) does not.

This controversy here is somewhat reminiscent of the controversy surrounding studies which have found differences in IQ between groups with different racial origin. Most importantly, whilst some researchers have previously chosen to interpret results on a biological basis, IQ has often been shown to be affected by some very un-biological and quite subtle factors. For example, one study by Day and Anthony (2006) found that black Americans only underperformed white Americans in IQ tests when they were told the tests were measures of their performance, rather than a set of puzzles the researchers wanted their opinions on. This supports the ‘stereotype threat’ explanation of racial IQ differences, which suggests that anxiety about confirming negative stereotypes in such situations can affect performance.

We could perhaps apply ‘stereotype threat’ to cannabis users, most of whom we could presume would be well aware of negative stereotype of the underachieving stoner. This could relate to how cannabis using participants engaged with education, from their happiness and motivation in school, to how they were treated by parents and teachers. This means that regardless of how Meier et al (2012) controlled for education by accounting for years spent at school and university, education may still be the mechanism in which cannabis affected the cohort’s IQ scores.

Such alternative explanations for the differences in IQ scores do not prove that smoking cannabis does not have an effect on developing brains. It does however highlight that we have an incomplete understanding as to how this would work, and no definite answer as to why cannabis affected later IQ in Meier et al (2012).

This point is thankfully not lost on researchers, but may not be apparent to many of those on either side of the cannabis debate.

Drugs Live: the facts behind the programme

Last week we presented the first results of our new study on MDMA - ecstasy - and brain function over two live Channel 4 programmes. We hope you saw it! It was generally very well received as being a bold attempt to show the neuroscience behind a popular drug that might have therapeutic potential. It also introduced scientific concepts such as fMRI, double-blind trials and placebo control to a general audience.

There have been a few criticisms of the programme, some fair, some less so. One tweeter highlighted the absence of statistical significance on the graphics. We sympathise with this request, and had included them (and error bars) on the graphs we provided, but for clarity Channel 4 took them off (because explaining statistical significance is difficult to a general audience). However we can say that all the reported findings for subjective psychological effects were at a significance level of p<0.001.

It has also been claimed that our study was not as original as claimed, and was merely a TV gimmick that trivialised and potentially glamourised MDMA use

We refute this unfounded assertion. The claim was that our research is not important because there are 60 or more papers using brain imaging to explore the effects of MDMA. That claim is misleading because our study was very different. Of course there has indeed been a history of research on this drug, and as with all scientific endeavour we were building on the findings of others. It would be great to have a TV programme just to consider the breadth of existing evidence in detail. However, the research we presented in Drugs Live was novel.

We conducted an experiment where we scanned each participant’s brain twice, once after they had been given a dose of pure MDMA, and once when they had been given a placebo. The experiment was ‘blinded’, meaning that neither the researchers nor the participants knew which was being given on each occasion. All but a handful of the other 60 or so studies, however important they may be, did not involve an experiment looking at the brains of people after they had been given MDMA. They were brain scanning studies, but they did not give anyone MDMA or scan anyone whilst they were undergoing the effects of the drug. Mostly they compared the brains of long-term ecstasy users with the brains of non-users, to see if there were differences.

These studies are useful for finding out some things about the chronic effects of the drug, but they have some limitations that our experiment avoids. With our study, we can be more certain that the results we see are caused by MDMA, because we gave the MDMA under controlled conditions. In most of the other studies, it is hard to tell which differences are caused by MDMA use, and which are caused by other drugs that the users also take, elements of the clubbing lifestyle, or other things mixed in with their ecstasy. Some of the brain differences found might be connected to the reasons why that individual used lots of MDMA in the first place, rather than being a result of their MDMA use.

So how was our Channel 4 funded study unique? We had 25 participants which makes it the largest experimental brain imaging study of acute MDMA ever conducted. It also was much more comprehensive than the very few comparable studies, with many distinctive features, each of which explored specific aspects of the neuroscience of MDMA including psychological measures exploring its effects on the following tasks:
• Pro-social psychological processes
• self-referential memory encoding
• a trust task (investment)
• personal memory recall - both positive and negative memories
• emotional memory and cognitions (tested on day 3)

In addition, we conducted studies on the effects of MDMA using MRI measures of brain activity that to our knowledge have never before been reported for MDMA:
• arterial spin labelling measures of brain blood flow
• functional connectivity - particularly in the default mode network

We also measured fMRI activity during the psychological tasks.

Although Drugs Live was based on preliminary results from our study, we couldn't possibly present all aspects of the research in the programme. However all will, in time, be published in peer-reviewed scientific journals. We predict 5-6 major papers reporting findings from this single study.

The main purpose of the programme was to increase public understanding of brain research techniques and methods, and of how initially scientists go about assessing the potential properties of MDMA which might make it an aid in psychological therapies. We also wanted to convey harm reduction advice to recreational users of the drug. We wanted to promote scientific research, NOT the use of MDMA and are confident that this aim was achieved.

Hypothesising an alternative: Applying the scientific process to drug policy

As you may know, earlier this month I gave evidence to the Home Affairs Select Committee’s (HASC) current inquiry into drugs. We had a wide-ranging discussion across many aspects of alcohol and drug harms particularly in relation to the value of drug law reform and decriminalisation. (You can watch the session, including the interesting evidence of the subsequent witnesses online). I strongly believe that we should focus on public health approaches to the drug problem, and decriminalise the possession of drugs for personal use, for the following simple reason;- If users are addicted then they are ill, and criminal sanctions are an inappropriate way to deal with an illness. If they are not addicted then criminalisation will almost always lead to greater harms to the user than the effects of the drug. For example, it can severely limit career options in public service and prevent travel to some countries particularly the USA.

However, it was clear from questions from several of the HASC committee that they are very frightened that reducing or removing the criminal penalties for drug possession will lead to greater use – and then greater harms overall.  This is a reasonable hypothesis. Forming hypotheses represents the first step in thinking scientifically. Next, we should test the hypothesis against the available evidence.

I think that the following evidence allows us to reject this hypothesis:

  1. There is good evidence that decriminalisation does not radically increase drug use and can reduce some measures of harm, as shown by a balanced review of the first ten years of the Portugal experience of decriminalisation. The collapse of society predicted by some did not occur; they had slight increases in drug use followed by slighter falls, which compares favourably with the trends in the neighbouring countries and the rest of the EU over the same period. More importantly, young people growing up under this system used fewer drugs, and harms and deaths from heroin went down as a result of a treatment-centred attitude replacing a punishment-centred approach. Remarkably, young people who have grown up in the Netherlands, where cannabis use is decriminalised, are less likely to be users of the drug than young people in Britain, the US and many other countries which criminalise young users. Perhaps the cachet of illegality here promotes some use.
  2. An increase in the availability of some drugs may actually lead to a reduction in the use of other more harmful drugs, so reducing net harms to society. We saw a noteworthy example of this in the past few years with the advent of the stimulant mephedrone. As this became popular, cocaine users seem to have switched to mephedrone and cocaine deaths fell by almost a quarter. Mephedrone gives a strong high and has potential to harm and kill, but seems much less likely to kill than cocaine. By switching, cocaine users reduced their risk of dying. It appears that the mephedrone phase caused the first significant impact on the steady rise of cocaine deaths we had seen in 20 years. It seems to have been a major – if unplanned and temporary – public health success. Relatively fewer young people progress to problematic drug use in the Netherlands than in most comparable Western countries. There is evidence that the legalisation of medical cannabis in some states of the USA has been associated with a considerable reduction in fatal road traffic accidents, comparable with the benefits of laws requiring seatbelts. This, the authors of the study show, is mostly due to the large drop in the number of fatal crashes involving alcohol as people appear to substitute cannabis for drinking.
  3. Regulating access to drugs such as cannabis as in the Dutch model reduces the need for users to go to dealers. So it minimises their exposure to people whose main goal is to get their clients onto the most addictive substances such as heroin and crack. Indeed this was the main reason why the Dutch initiated the coffee shop model in the first place and it has been successful; by separating the markets of cannabis and heroin they have among the lowest rates of heroin use in young people in Europe. The Netherlands is now in the process of restricting tourists' access, on a city by city basis, to coffeeshops, making them primarily for Dutch residents. As drug tourism was never the aim of the coffeeshop policy, this change is not without logic, however, given that there is already a mature market for cannabis that may now be pushed into the illicit market with a correlating effect on street disorder and crime, as has already been seen in Maastricht.
  4. Approaches to dealing with addicted users which swap punishment for healthcare have been successful. In 1994, despite strong resistance from the UN, Switzerland began a program which allowed long-term treatment-resistant addicts to take clean pharmaceutical heroin under medical supervision. This has been criticized for maintaining rather than ending addictions, but it has stabilised chaotic lives, allowing users to be socially reintegrated, getting homes and sometimes jobs, and as well as removing the health harms associated with polluted, inconsistent street drugs. Addicts in this treatment get fitter, they virtually never overdose, and very few die. Unlike those in other regimes, most stay in treatment, allowing some to progress later to abstinence. It isn’t just the addicts who benefit; crime fell enormously once users could access heroin from the State rather than profiteering dealers. The State, and taxpayers don’t lose out in this arrangement, the expensive program more than pays for itself in healthcare and law enforcement savings.
  5. Approaches which explicitly reject an evidence-based public health approach, but instead focus on incarceration and criminalisation of addicts, continue to utterly fail, at enormous financial and human cost. The Global Commission on Drugs Policy have just published a new evidence-rich report, well worth reading, which focuses on the effect of different approaches to drug users on the HIV/AIDS pandemic. The spread of disease cannot be considered a wholly natural, biological phenomenon, it is also social, economic and very political. Political choices determine whether a huge majority or a small minority of new HIV infections are caused by injecting drug use. In Russia, where organisations trying to help heroin addicts look after their health have been persecuted, a million people are HIV positive, over 80% of them through their drug habit. In comparison, here in the UK, Margaret Thatcher, the only PM we’ve had with a science degree, heeded her scientific advisors, brushed off moralising critics, and instituted a needle-exchange programme. Since then, UK policy has at least accepted the need for harm-reduction alongside punishment, and less than 2% of new HIV infections in 2010 were caused by injecting drugs. In the US, where incarceration rates are high, but harm-reduction measures (like distributing clean hypodermics) is politically taboo, unfunded or even illegal, HIV spreads in prisons where syringes carrying heroin and HIV are passed around. Whilst use of prescription heroin in a clean needle rarely harms anyone besides the user, these preventable HIV infections across the world in injecting drug users cause infections in their sexual partners and continually infuse HIV into wider society.
  6. Treating addicts with more humanity doesn’t make drug use look more appealing. The idea that less punitive approaches would encourage drug use is again a reasonable hypothesis, but science demands that hypotheses are tested against the evidence. The Swiss evidence shows that rather than making heroin more popular, numbers of people becoming addicts have steadily fallen. It has been suggested that whilst heroin use can appear rebellious where the focus is on punishment (think of Pete Doherty photographed with an entourage of police, or sashaying in and out of court), in Switzerland, young people think of addicts as simply ill, which deters use. It is no surprise that Switzerland’s policy has won broad democratic support and has inspired similarly successful projects in other European countries, including small trials here in the UK. It’s also no surprise that much of the world remains strongly opposed to this approach despite such strong evidence that it works.

Moreover criminalisation produces many perverse consequences that actually increase the harms of drugs and costs to society. Criminal networks coalesce around drug supply; America in the era of alcohol prohibition was the heyday of organised crime.  The lack of quality control in illegal drug markets leads to wholly unnecessary harms like deadly outbreaks of anthrax in heroin injectors. Dealers with concerns only for their profits adulterate and mis-describe drugs, for example selling the much more potent and riskier drug PMMA as the less risky ecstasy. Badly enacted prohibition also severely limits research so denies the possible therapeutic benefits of drugs such as MDMA for treating PTSD and psilocybin for treating depression and the anxiety of cancer.

It is now time to begin to introduce a more rational evidence-based approach to drug policy to minimise harms. We must consider all drugs, including alcohol, as part of the problem to be tackled. I hope that the Select Committee will recommend a more progressive approach than the current one of interdiction and punishment which has, and will continue to fail.


Smoke without fire? Scaremongering by the British Lung Foundation over cannabis vs tobacco

The BLF is an admirable charity that promotes lung health and supports those affected by lung disease. Unfortunately, last week they produced a press release promoting unfounded claims about the harms of cannabis to the lungs. These claims were uncritically parroted from this press release as ‘news’ by the BBCChannel 4Skythe IndependentTelegraphMetroEvening Standardthe Huffington Post and more. The BLF, who wish to promote awareness of “the serious, even fatal impact [cannabis] can have on the lungs”, managed to hit the headlines with a survey about public attitudes to cannabis commissioned alongside their new report reviewing existing evidence. Surveys, with their (often unsupported) appearance of objectivity, are a popular way for groups, commercial or otherwise, to win press attention. It has worked for them before - the Daily Mail has a ten-year old article archived online reporting a virtually identical story of BLF “research” apparently showing that the dangers of cannabis are underestimated, and worse than tobacco. Then, as now, the BLF received news coverage as if they had made a breakthrough just through publishing a survey and a report of evidence. Confusingly, whilst this is the BLF's second special report on cannabis, they have never dedicated a special report to tobacco, which causes the vast majority of lung cancer deaths and many other lung conditions.

This time around, the BBC, whose science coverage usually deserves praise, rehashed the first lines of the BLF’s press release, writing “88% [of the public] incorrectly thought tobacco cigarettes were more harmful than cannabis ones - when the risk of lung cancer is actually 20 times higher”. In this sentence, as in almost every news article I have seen on the subject, almost 9 in 10 of the public are condescended to as being mistaken, but where is the evidence for this assertion that tobacco is so much kinder to the lungs than cannabis? Could the public perhaps be wiser about drug harms than the BLF and the media? I had a closer look at the BLF’s report to check their evidence. The BLF’s report itself references a great deal of scientific evidence, but it seems to be an attempt to collect evidence that supports their predetermined opinion that cannabis harms the lungs, rather than exploring the evidence to find out what the balance of findings really suggests. When the evidence they found was mixed, they came to firm conclusions that the most alarming interpretation of the most alarming evidence was true.

This is most striking in the case of the lung cancer claim that tops the press release: that a cannabis joint is 20 times as carcinogenic as a cigarette. This is an old chestnut, listed amongst Wikipedia’s list of popular drug myths. But that didn’t stop Kenneth Gibson of the Scottish National Party lodging a motion (look for S4M-03197) in the Scottish Parliament last week on 8th June endorsing the BLF’s claims and recommendations. This claim about the 20-fold cancer risk is prominent in the introductory ‘background’ information section of the BLF’s report. Here it assures the reader that the evidence explored in the report (section 3.2) shows this. But the report contradicts itself: Section 3.2 on cancer actually very reasonably says that “studies in human populations have yielded conflicting evidence on the subject: some suggest there is a link between smoking cannabis and lung cancer while others don’t [3 references]. It’s worth noting that these studies are of limited value as they looked at relatively small numbers of people and didn’t take into consideration the quantity of cannabis smoked or the effects of smoking a mixture of tobacco and cannabis. In addition, some previous evidence suggests that THC may have anti-carcinogenic effects”. Having explained, with directions to three references, that the evidence is mixed and inconclusive, the report’s writer(s) disappointingly then give a long and overgenerous account of one of the three papers referenced, a 2008 study by Aldington et.al. (a thorough scientific rebuttal of which can be found here). They then dubiously interpret the study as suggesting that a joint is as carcinogenic as 20 cigarettes. Christopher Snowdon has written a blog poston just why this interpretation is wrong. Do the BLF at least give other evidence an airing? After considering Aldington’s paper, a much smaller account is given of another of their references, which says cannabis increases lung cancer risk 2.4 times, and they do not write anything about their third reference, which found no link to lung cancer. This last study, by Hashibe et. al., looked at more people’s cannabis use over a longer time, and so has a claim to be the most valid.

Why did the BLF reference three studies then largely ignore the findings of two? We cannot doubt the BLF’s worthy intentions to help us all look after our lungs, and indeed there are harm-reduction messages that should be heard about cannabis smoke, specifically that if you must use the drug despite the risks, rolling with tobacco may increase risk of harms, and that using a cannabis vaporiser instead of smoking it may decrease harms. The BLF’s lack of care with the evidence, and the media’s lack of care in fact-checking, could have the opposite effect from their good intentions. Public confidence in science as a means of getting to the truth can only be harmed when the BBC reports “experts” mistakenly declaring that what 88% of us apparently think about cannabis is wrong. What’s more, if the BLF’s misguided information is believed, people could actually be put at greater risk of lung cancer, for example by cutting down on the cannabis in their joints and padding them out with more tobacco, or by making parents relatively more relaxed about finding out that their teenagers smoking cigarettes every day than finding out that they smoke the occasional joint.

What can be done? The ISCD contacted the BBC on the 6th of June, but as yet the BBC have not replied or removed the inaccuracies although they have now included an alternative opinion on the subject from Peter Reynolds of Clear. The Metro, on the other hand, can be thoroughly commended for their prompt and prominent publication of critical responses to their article fromme and other readers. We will pursue further corrections, firstly by contacting editors directly, and if that fails, through the PCC. I will update readers of this blog on any progress. The ISCD's aim is for ordinary people, without scientific expertise, to be able to find reliable information about the effects and risks of drugs. With thousands of voices clamouring to be heard, each offering conflicting views, it’s a huge challenge. As I write, the BLF’s claim about cannabis cigarettes being more carcinogenic than tobacco ones has already found its way onto Wikipedia’s information about cannabis harms, so Wikipedia currently reports, on different pages, the same claim as an evidenced fact and as a popular myth. Though I trust it won’t be there long, this shows how easily misinformation can gain the stamp of truth. The ISCD website, www.drugscience.org.uk, should help individuals who are looking for evidence-based information. Our drugs information page on cannabis provides scientifically evidenced information on the drug and its effects and harms. For information on the specific connection between cannabis and cancer, see Cancer Research UK’s balanced information. We gave the BLF the opportunity to address the inaccuracies and inconsistencies of their report which they declined, thus missing an important opportunity to address the very real harms of smoking. Public health organisations are to be commended for trying to help the general public make better choices.  Unfortunately in this case, the choice made was to confuse rather than inform.

Does drinking alcohol during pregnancy lower child IQ?

By George Gifford

A recent study by Lewis et al, 2012, suggests that moderate alcohol intake during pregnancy can affect later IQ scores. This study is particularly striking as it suggests changes in IQ in children with pregnant mothers involved drank very small amounts, between 1-6 units a week. Additionally, there has been a real lack of conclusive evidence in this area, many studies suffering methodological flaws, making this new study particularly interesting.

Media coverage of this study was both very sensible and horrendously bad. For example, the Sun’s headline, ‘any wine and kid’s a plonker’, is grossly inaccurate and offensive to the very real effects that alcohol can have on a child’s development. In addition, there was a very defensive article in the Daily Mail, which saw the study as an affront to pregnant women, very much missing the point that science is objective.

On top of this, some articles only really half reported the study, stating simply that it found that women who drank 1-6 units of alcohol a week caused an average point drop of 1.8 IQ points in their children. Although this is sort of reported in the study, without the full picture it is misleading as it suggests some sort of predictable calculation for the amount of alcohol a pregnant woman can drink and how many IQ points their child will lose.

When looking at the specifics of the study we get a very different impression from this. Researchers identified genes involved in the breakdown of alcohol in mothers and children and found that those with genes making them better at breaking down alcohol had, on average, slightly higher IQ scores than those who did not. This effect was only found amongst the pregnant women who drank alcohol and not those who abstained, suggesting alcohol to be what caused the difference in IQ scores.

To summarise: the study showed higher genetically based efficacy in breaking down alcohol protected prenatal children from the effects of alcohol on their later intelligence.

Now the 1.8 drop actually refers to the effects of alcohol intake on IQ scores for each individual alcohol-breakdown-related gene (allele). In particular researchers focused on 4 alcohol breakdown genes in the child and 1 in the mother (all important because they code for enzymes which break down alcohol molecules- alcohol dehydrogenases).What is complicated about these genes is that some code for alcohol breakdown enzymes in the stomach, so for pregnant drinkers this means breaking down alcohol before it reaches the blood and baby, and some code for enzymes produced by the liver, which means breakdown when the alcohol is in the blood circulation. Further complicating this, some genes may play more active roles at different points in the pregnancy, genes may interact with each other, and there could be many more genes which affect the breakdown of alcohol in the mothers or prenatal baby.

The point we can take from this is that genetic differences in how well mothers and foetuses break down alcohol make alcohol’s impact of prenatal development unpredictable. This is why it is nearly impossible to know how much alcohol would be safe to drink during pregnancy, and why some guidelines suggests women should drink no alcohol at all. Certainly, you should not think that the statistic of 1.8 IQ points for every 1-6 units of alcohol per week would apply to all, not least because there is likely a big difference between drinking 1 or 6 units of alcohol a week (especially if you drank 6 units in one session- binge drinking may be particularly bad), but also because an acceptable amount for one woman and baby could be significantly damaging to another.

It can be said however, that the changes in IQ in the study were small enough for some to see as insignificant (around 3 IQ points from those judged most genetically vulnerable and those judged the least genetically vulnerable). Even looking at a more extreme experiment where children dropped 7 IQ points with mothers who drank 2 drinks per day, all the children involved were functioning in the average range of intelligence (though please don’t have 2 drinks a day if you are pregnant). Given that it is not unlikely that anyone reading this was exposed to a little bit of wine in the womb, it would be wrong to stigmatise pregnant women who had the occasional small glass of wine.

Despite being minimal however, these changes in the study in question were matched with moderate amounts of alcohol. The overall picture we get from this is that alcohol’s effect on the developing foetus cannot be seen in terms of a threshold, rather it can be seen as simply, the more alcohol you drink when pregnant-the more the child will be impaired. We know that very heavy drinking produces severe damage to the foetus particularly in terms of brain development.

With all this in mind, we can see that the National Institute of Clinical Excellence (NICE) guidelines for drinking when pregnant are really very sensible, suggesting that pregnant women ideally should not drink alcohol in the first three months, and if they do drink after this, to drink only 1-2 units once or twice a week.

Main points of this article:

  •  The study used certain genes that effect how well pregnant mothers and foetuses break down alcohol to explore the risk of alcohol to the foetus. As there are quite a few of these genes, this differs greatly from person to person, making alcohol’s effects on the foetus unpredictable.

  • The study suggests that small amounts of alcohol can have some detectable effect on developing foetuses in terms of a small reduction in IQ.

  • The NICE guidelines for drinking when pregnant are very sensible.

Popular intoxicants – how do alcohol and cannabis compare?

I am often asked the question “if cannabis was as freely available as alcohol would more use it and would its harms increase?.  Of course the answer is yes to both. However as about half of young people use cannabis, the increase from removing criminal sanctions would be relatively modest unless it was actively marketed as is alcohol. Certainly the Dutch coffee shop model of regulated but not legalised cannabis access appears not to have increased use since young people in the Netherlands have some of the lowest rates of cannabis use in Europe.

Perhaps the more interesting question is in this circumstance would be what would the net effect on population harms be?  Would liberalising access to cannabis reduce alcohol use to an extent that might reduce the sum total of harms?  This issue is touched on in my new paper in the Journal of Psychopharmacology [Weissenborn and Nutt 2011, Popular intoxicants: what lessons can be learned from the last 40 years of alcohol and cannabis regulation? (PMID:21926420)].  The key points of this paper are briefly outlined below.

A good measure of harm is the costs to the NHS. Hospital admissions for cannabis number less than 1000 per year whereas alcohol now accounts for 1000x as many – over a million last year of which 13,000 were aged under 18yrs.  The role of cannabis in causation of schizophrenia is still controversial – the ACMD in their 3rd cannabis review estimated that to stop one case of schizophrenia one would have to stop 5000 young men or 7000 young women from ever smoking cannabis. Some studies are now suggesting cannabis may help patients with schizophrenia. In contrast, that alcohol causes liver disease is as incontrovertable as is its contribution to the massively accelerating death rates from liver disease in the UK. The frightening contribution that alcohol use makes to domestic violence, child abuse and road traffic accidents were some of the reasons why alcohol scored as the most harmful drug to UK society today in the ISCD scale of drug harms, published in the Lancet last year.

Until the last government induced them to think otherwise by making cannabis a target, the police have always taken the view that cannabis users were much less prone to violence than those intoxicated with alcohol.  Indeed the police were strong supporters of the ACMD recommendation to downgrade cannabis to Class C in 2004. It seems likely that the recent rise in alcohol intake in the UK may have been in part due to the pressure of anti-cannabis policing leading to young people switching their preferred intoxicant to alcohol.

Estimating the true relative harms of alcohol and cannabis is not easy as there are no societies today where the two drugs are equally available. However where neither are legal – as in some Islamic states – alcohol appears to cause more dependence than cannabis, even in Morocco a traditional cannabis growing country.

Taken together we estimate that alcohol is at least twice as harmful to users than cannabis and 5 times more harmful to society. The obvious conclusion is that the current legislation criminalising cannabis users is illogical as well as inhumane and may be causing much more harm than it does good. Time for a rational intervention Mr Cameron?

The full paper can be found in the Journal of Psychopharmacology http://jop.sagepub.com/content/early/2011/09/03/0269881111414751

Evidence based policy? Why banning mephedrone may not have reduced harms to users

A guest post by Dr Les King.

The control of mephedrone and related compounds under the Misuse of Drugs Act in April 2010 was largely prompted by the media attention given to numerous alleged mephedrone fatalities. Subsequent toxicology examinations showed that most of those deaths were not caused by mephedrone, a finding now underscored by the latest statistics (REF 1) from the Office for National Statistics (ONS). In 2010, in England and Wales, there were just 6 deaths where mephedrone was mentioned on the death certificate. By comparison, there were 144 fatalities where cocaine was mentioned. The significance of this comparison can be understood when it is recognised that cocaine is a drug which was often substituted by mephedrone. The number of deaths alone does not tell us much about the intrinsic toxicity of a substance. However, the ratio of the number of deaths to suitable proxy measures of prevalence does provide a useful index (REF 2). The British Crime Survey (Drug Misuse Declared) (REF 3) provides one such denominator. For 2010/2011, it was reported that in England and Wales, 4.4% of 16 to 24 year olds used mephedrone in the last year. This was the same as the number using cocaine, a figure only increased to 4.7% if crack cocaine is also included. If we choose instead to look at last year use by 16 to 59 year olds, the respective proportions were: mephedrone = 1.4% and cocaine = 2.1%. Caution may be needed in interpreting the small number of mephedrone deaths in 2010, and it is possible that some cases were missed because not all toxicology laboratories were able to identify this new substance. The mortality statistics also suffer from other confounding issues, as discussed by Bird (REF 4), but it would seem that regardless of which age group we consider, and bearing in mind the uncertainties, the fatal toxicity of mephedrone is low by any standard, and may be less than 10% of that of cocaine. This confirms the concerns raised by Bird (REF 5); an unintended consequence of banning mephedrone would be a lost opportunity to save the lives of many who would succumb to cocaine poisoning.


1. Deaths related to drug poisoning in England and Wales, 2010. Office for National Statistics, 23 August 2011
2. L.A.King and J.M.Corkery, 2010, An index of fatal toxicity for drugs of misuse, Hum. Psychopharmacol. Clin. Exptl., 25, 162-166
3. Drug Misuse Declared: Findings from the 2010/11 British Crime Survey, England and Wales, Home Office, 28 July 2011
4. S.Bird, 2011, Drugs deaths in England and Wales - a wake-up call to the Registrar General, http://www.straightstatistics.org/article/drugs-deaths-england-and-wales-wake-call-registrar-general
5. S.Bird, 2010, Banned drug may have saved lives, not cost them, http://www.straightstatistics.org/article/banned-drug-may-have-saved-lives-not-cost-them

Curiouser and curiouser: Could ecstasy actually heal brains as well as minds?

For 30 years we have had a systematic attack on the safety of ecstasy [MDMA]. This has been fueled by a desire by governments, lobbyists and some scientists to justify the illegal status of this drug which in the UK is at the very highest level – Class A. This puts it alongside drugs such as crack cocaine and heroin which by all scientific assessments are much more harmful [Nutt King and Phillips 2010].

Much of the so called scientific evidence that has been used to justify MDMA as being harmful is flawed, some just simply wrong as they used the wrong drug [Ricaurte et al 2002] and most findings are exaggerated. For example, a well reported recent study that claimed to provide proof that MDMA impaired memory in fact found a minimal effect in only one memory measure that was of no clinical significance. This was taken as proof that MDMA damaged the brain despite the fact that on some other measures of brain function, the MDMA-using group performed better than the controls [Schilt et al 2007].

It appears there is an assumption that MDMA will damage human brains because in studies in some animal species [rats and monkeys] it can lead to damage to the serotonin nerve cells. These effects are most pronounced at high doses and are not seen when human equivalent doses are used [Fantegrossi et al 2004]. But still the concern is there, at least in the mind of the Home Sec Jaqui Smith when she announced that MDMA would remain Class A against the recommendations of the ACMD. She said that as long as there were “public concerns” about the risks of ecstasy on the brain she would not be moved, even though these concerns were largely manufactured by the media and magnified by bad science on ecstasy [Forsyth 2001].

However you might feel that as all drugs may be harmful then ecstasy could surely only be harmful also?  Well maybe not. We should remember that MDMA was developed as a therapeutic tool for psychotherapy and its successful role here was severely curtailed when the drug was made illegal. Thirty years on, MDMA has only recently been reintroduced into clinical trials with great success in one study in resistant PTSD [Mithoefer et al 2010].

But what about the rats – does it still cause brain damage there? A new paper shows an intriguing effect and one, which many will find paradoxical: MDMA improved recovery from brain injury rather than worsening it [Edut et al 2011]. This paper has not apparently received any media attention so far which I why I felt compelled to do what I could to make it more widely known.

However the results are not so paradoxical if one remembers that the potential utility of such stimulant drugs to aid recovery from brain trauma was first reported over 30 years ago for amfetamine [see Gladstone and Black 2000]. I have made efforts to get stimulant drugs tested in clinical trials for the brain injured in the UK but always their controlled status makes using them difficult. Doctors are frightened, ethics committees worried, special licenses are required and are expensive and patients and relatives concerned (if it's classified then it must be surely be dangerous?). For these reasons, we need to work to minimise the damage that legal controls on drugs have to impede research. The recent banning of mephedrone and naphyrone is likely to significantly limit new drug discovery in the area of antidepressants and anti-addiction agents [Nutt 2010, Nutt 2011].

Lets hope that this intriguing new finding of the potential therapeutic benefit of MDMA as a brain repair agent is taken up by the medical and scientific communities working in the fields of stroke and brain trauma. Some encouragement from the media could help this process.


Edut S, Rubovitch V, Schreiber S, Pick CG (2011) The intriguing effects of ecstasy (MDMA) on cognitive function in mice subjected to a minimal traumatic brain injury (mTBI)  Psychopharmacology 214, Number 4214, 877-889, DOI: 10.1007/s00213-010-2098-y

Fantegrossi WE, Woolverton WL, Kilbourn M et al. (2004) Behavioral and neurochemical consequences of long-term intravenous self-administration of MDMA and its enantiomers by rhesus monkeys. Neuropsychopharmacology 29(7): 1270–81.

Forsyth A Distorted? a quantitative exploration of drug fatality reports in the popular press International Journal of Drug Policy 12 (2001) 435–453

Gladstone DJ, Black SE. Enhancing recovery after stroke with noradrenergic pharmacotherapy: a new frontier? Can J Neurol Sci. 2000 May;27(2):97-105

Mithoefer et al (2010) The safety and efficacy of _3,4-methylenedioxymethamphetamineassisted psychotherapy in subjects with chronic, treatment-resistant posttraumatic stress disorder: the first randomized controlled pilot study. Journal of Psychopharmacology. July 2010.

Nutt 2010

You say precaution, I say perversion: eight harms deriving from the precautionary principle


The ACMD and naphyrone – another example of evidence-free policy making?

Nutt 2011 Perverse effects of the precautionary principle: how banning mephedrone has unexpected implications for pharmaceutical discovery Therapeutic Advances in Psychopharmacology Editorial – in press

Nutt DJKing LA Phillips LD (2010) Drug harms in the UK: a multicriteria decision analysisLancet 376: 155866

Ricaurte GA, Yuan J, Hatzidimitriou G et al. (2002) Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA (“ecstasy”). Science 297: 2260–3. Retraction printed in: Science (2003) 301: 1479.

Schilt T, Maartje ML de Win, Koeter M et al. (2007) Cognition in novice ecstasy users with minimal exposure to other drugs. Archives of General Psychiatry 64: 728–36.

Blair's other war

I write this from Mexico, where the ‘War on Drugs’ and clashing drug cartels have claimed thousands of lives. The billions of dollars worth of aid being pumped in countries in South America, Afghanistan and elsewhere have resulted in, at best, the ‘balloon effect’, where production is pushed down in one area only to pop up in another. In the fifty years since the 1961 UN Single Convention on Narcotic Drugs, the ‘War on Drugs’ has morphed from a figurative battle to a literal one. The fog of war has driven politicians to go beyond the bounds of law in their lust for battle: the Single Convention allows for the medical and scientific use of controlled drugs and yet, many countries interpret it as prohibiting all use of all Schedule I drugs, hindering potentially life changing research.

Domestic law has also been trampled upon in the rush to act tough on drugs. The UK’s 1971 Misuse of Drugs Act [MDAct] was designed to remove decision-making about drugs from the party politics of parliament to minimise the risk that short term party interests might lead to bad laws.  The MDAct classified drugs in three levels – A B C – based on their relative harms of drugs, which were decided upon by an expert group, the ACMD [Advisory Council on the Misuse of Drugs]. This worked well for the first 30 years and even Margaret Thatcher accepted its recommendations on needle-exchange to limit HIV spread.  Though this went against her political philosophy, she accepted that it was logical to be guided by experts and was rewarded by the UK leading the world in terms of slowing the rate of HIV spread from intravenous drug use.

In the last decade under Tony Blair’s government, things began to change. It decided it knew better than experts and hunted for evidence to support its policy decisions rather than the other way round.  In late 2004, Blair decided to wage a different type of war – this time on drugs. For unknown reasons – at least not explained in his autobiography – he decided to ignore the MDAct (i.e. break the law)  and make decisions on drugs without consulting the experts on ACMD. He convened a special meeting of senior police, military and customs officials, from which the war was initiated.

The first salvo was aimed at magic mushrooms. These were legal at the timebut the government decided that they had to be hard on head-shops selling freeze-dried preparations so they made them a Class A drug without consulting the ACMD.  The well known adage“the first casualty of war is the truth” certainly applied to the mushroom decision as by no metric are mushrooms as harmful as the real Class A drugs such as crack cocaine and heroin.

The mushrooms were an easy battle to win and perhaps this rewarding feeling of success fueled the next campaign against cannabis. In 2004, all preparations of cannabis had been made Class C (they had been either Class A or Class B previously). This downgrading was made after an extensive review of the evidence by the ACMD, yet was viciously opposed by parts of the media and many politicians.  From that date a concerted war was waged against cannabis users justified by statements that cannabis, particularly the new variant skunk, was more harmful than its Class C status would indicate.

Gordon Brown continued the war when he took over as Prime Minister. Within weeks of coming to power, he made the absurd claim that “skunk was lethal” when in reality cannabis, in contrast to alcohol and controlled drugs, has never killed anyone by direct toxicity/poisoning.  He oversawa new Home Office war policy of increasing convictions for cannabis users in an attempt to deter use. This doubled the number of people convicted for cannabis possession from 88,000 in 2004/5 to 158,000 in 2007/8.  Police with sniffer dogs became a common site on London tube stations where young men were searched and prosecuted if cannabis was found.  That this behaviour almost certainly breached their human rights was ignored; rights have a lesser place when at war. Predictably an even greater injustice was seen by the ethnic bias in convictions with Asian and Afro-Caribbean men being significantly overrepresented.

Worse, the war extended to those using cannabis for medicinal purposes such a people with multiple sclerosis or spasticity. Police would conduct dawn raids on possible users, smashing down their front doors just in case they might leap from their wheelchairs and abseil out the window! Why? Because violence is what wars allow, if not demand.

The war on medicinal cannabis became more aggressive in 2005 when the Law Lords seriously aggravated the situation of those using cannabis for medicinal purposes. They colluded with the government by changing the law to disallow the centuries old “Defense of Necessity” for medicinal cannabis use. This common law allows users to plead that their use of a drug was simply and solely to ameliorate a medical condition for which other treatments had not worked.  The Law Lords decided that since the government had decreed that cannabis was sufficiently harmful to be a Class B drug, patients should be deterred from using it by removing this defense. A truly cruel and inhumane piece of legislation that brings shame on those who enacted it and great distress to those prosecuted because of it.  However it was predictable as the corruption of the law is a recognized element of war.

The final battle before my sacking was on MDMA (ecstasy). This had been classified alongside cocaine and heroin as a Class A drug ever since it was made illegal. This was patently absurd from any evidence-based perspective but the government had actively resisted any attempts to review the evidence on which ecstasy was classified until ordered to do so by a Select Committee report. When the ACMD with the help of a NICE health technology assessment unit reported that its harms had been overestimated and were commensurate with a Class B status, the government refused to reclassify.

My response to both the cannabis and ecstasy decisions was to point out how they undermined the scientific integrity of the MDAct and, by allowing longer than appropriate prison sentences, were bound to lead to injustice. Moreover, I believed that these decisions could increase the harms from legal drugs particularly alcohol; by scaring people from ecstasy and cannabis they might be increasing use of alcohol, a more harmful drug.  By fighting battles on mushrooms, cannabis and ecstasy the government was deflecting attention away from the rising tide of deaths from alcohol.

Military wars are evaluated through public enquiries - surely it is time to seek the truth about the war on drugs and make good the damage done to drug users, their families and the scientific process caused by this unhappy example of political lust for wars.


Unnecessary adulterants: Confusion over mephedrone legislation

In this guest post, Dr Les King and Rudi Fortson Q.C.  highlight how the last government’s meddling in legislation regarding cathinones, including mephedrone, at this time last year has generated confusion for forensic scientists and legal practitioners regarding the precise placing of some cathinones within Class B.  It is a problem that is only now being addressed.

Instead of accepting the generic definitions of cathinones drafted by members of the ACMD that would cover all the various types of cathinones, the Home Office took the unusual step of changing the legislation to specifically mention mephedrone to ‘send a message’ to the public, presumably in response to the (unfounded) hysteria over mephedrone use by young people.  In taking this course, one variant of methylmethcathinone (mephedrone) was listed in one sub-paragraph of Part 2 of Schedule 2 to the MDA, while other variants of methylmethcathinone were listed in another sub-paragraph, thereby generating confusion.  Logically, all variants of that substance ought to have been classified as a single group.     To understandhow this came about requires a little more understanding of the chemistry of cathinones.

Dr King explains: The crux of the problem is peculiarly technical, but rests on the existence of mephedrone isomers. While mephedrone is 4-methylmethcathinone , both 2- and 3-methylmethcathinonecan also exist. To distinguish those different isomers is a challenging task for a laboratory, and certainly cannot be done by the routine methods used in drug analysis. That is where well-crafted generic control is so useful: all three isomers can be controlled without ever mentioning them by name in the Act or needing to be analytically-specific about which one has been found in a questioned sample.

That advantage was lost following Home Office tinkering. Eventually, following many discussions between the forensic science community and the CPS, a legally acceptable work-around was concocted. Yet that legal fudge could only be a temporary measure, which is why the Government has announced that the original clauses in the Modification Order of 2010 will now be replaced with what should have been there in the first place. This is a clear case of government acting without a clear understanding of the issues. Instead of supposedly protecting the public from harm with the controlling of mephedrone, the previous government unnecessarily weakened legislation for political gain.

However, whilst recognising the advantages of generic descriptions from a technical point of view, Rudi Fortson has expressed a note of caution.  For him, the law should not only be precise but it should also be clear and capable of being understood by lawyers and non-lawyers alike.  There is a risk that various substances, readily identifiable by their popular name (such as “mephedrone”), will be lost in the language of chemistry, making it difficult for non-chemists to identify, when reading the MDA, which drugs are controlled and which are not.


Addiction: a life long illness not lifestyle choice

Addiction is a major health problem that costs as much as all other mental illnesses combined (about £40 billion per year) and about as much as cancer and cardiovascular disorders also.

At its core addiction is a state of altered brain function that leads to fundamental changes in behaviour that are manifest by repeated use of alcohol or other drugs or engaging in activities such as gambling.  These are usually resisted, albeit unsuccessfully, by the addict.  The key features of addiction is therefore a state of habitual behaviour such as drug taking or gambling that is initially enjoyable but which eventually becomes self-sustaining or habitual. The urge to engage in the behaviour becomes so powerful that it interferes with normal life often to the point of overtaking work, personal relationships and family activities. At this point the person can be said to be addicted: the addict’s every thought and action is directed to their addiction and everything else suffers. 

If the addictive behaviour is not possible e.g. because they don’t have enough money then feelings of intense distress emerge. These can lead to dangerously impulsive and sometimes aggressive actions.  In the case of drug/alcohol addiction the situation is compounded by the occurrence of withdrawal reactions which cause further distress and motivate desperate attempts to find more of the addictive agent. This urge to get the drug may be so overpowering that addicts will commit seemingly random crimes to get the resources to buy more drug. It has been estimated that about 70% of all acquisitive crime is associated with drug and alcohol use.

Addiction is driven by a complex set of internal and external factors.  The external factors are well understood:  the more access to the desired drug or behaviour e.g. gambling the more addiction there is. 

The internal factors are less clear. Although most addiction is to alcohol and other drugs, addiction to gambling and other behaviours such as sex or shopping can occur. These tell us that the brain can develop hard-to-control urges independent of changing its chemistry with drugs.  All addictions share a common thread in that they are initially pleasurable activities, often extremely enjoyable. This results in these behaviours hijacking the brain’s normal pleasure systems so that naturally enjoyable activities such as family life, work, exercise become devalued and the more excessive addiction behaviours take over. 

However, not everyone who engages in drug use or gambling becomes addicted to them so clearly other factors are important. These are not yet understood but are now being actively studied. Some people may be particularly sensitive to the pleasurable effects of alcohol, drugs or gambling, perhaps because of coming from deprived backgrounds. In others, addiction may occur because of an inability to adopt coping strategies.  Others may have an underlying predisposition to develop compulsive behaviour patterns. Some unfortunate people may have several of these vulnerability factors and there are also genetic predispositions to some of them.

Also a significant amount of drug use is for self-medication, examples includecannabis for insomnia, alcohol to reduce anxiety, opioids for pain control etc. This therapeutic use can escalate into addiction in some people though by no means all. Not all drugs which are used for recreational purposes are addictive. LSD and magic mushrooms seem not addictive at all, and some have a low risk of addiction (MDMA/ecstasy; cannabis). The most addictive drugs are nicotine, heroin and crack cocaine plus metamfetamine (crystal meth) although this is not much used in the UK.

Just because some people – including leading politicians – have used drugs but stopped before they became addicted does not mean that anyone can stop that easily.  Starting to use drugs may be a lifestyle choice but once addiction sets in, choosing to stop is very much more difficult if not impossible.

We are beginning to understand how addictions start in the brain. The pleasurable or rewarding effects of addictions are mediated in the brain through the release of chemicals such as dopamine [by cocaine, amphetamines, nicotine] or endorphins [heroin] or both [alcohol].  The pleasures are then laid down as deep-seated memories, probably through changes in other neurotransmitters such as glutamate and GABA that make memories. These memories link the location, persons and experiences of the addiction with the emotional effects. These memories are often the most powerfully positive ones the person may ever experience, which explains why addicts put so much effort into getting them again.  When the memories re-occur, which is common when people are still using drugs or gambling, as well as when in recovery/abstinence, they are experienced as cravings.  These can be so strong and urgent that they lead to relapse.

A great deal of research has been conducted into the role of dopamine in addiction and we now know that the number of dopamine receptors seems to predispose to excessive pleasure responses from stimulant use. This excessive response is thought to initially occur in the reward centre of the brain – [the nucleus accumbens] – but then move into other areas where habits are laid down.  This shift from voluntary (choice use) to involuntary (habit-use) explains a common complaint of addicts that they don’t want to continue with their addictions, and even that they don’t enjoy them anymore, but cant stop themselves.  In this sense addiction can be seen as a loss-of-control over what starts out as a voluntary behavior.  Thus addiction is not, as some like to suggest, simply a “lifestyle” choice. It is a serious, often lethal, disease caused by an enduring (probably permanent) change in brain function.

We know that personality traits especially impulsivity, predict excess stimulant use and in animals this can be shown to correlate with low dopamine and high opioid receptor levels.  Similarly in humans low dopamine and high opioid receptor levels in brain predict drug use and craving.  These observations give new approaches to treatment, both psychological interventions such as behavioural control, and anti-impulse drugs such as those used for ADHD e.g. atomoxetine and modafinil, are being tested. 

For some addictions, especially heroin, the risk to the addict (life expectancy less than that from many cancers) and to society (from crime and infections), is so high that the prescription of substitute opioid drugs or even heroin itself saves lives and reduces crime. These substitute drugs are methadone and buprenorphine [Subutex]. As well as reducing crime and social costs by removing the need for addicts to commit offences to feed their habit, they also protect from accidental overdose and reduce risk of infections such as HIV and hepatitis.  Similar substitute pharmacological approaches exist for other addictions e.g. gammahydroxybutyrate (Alcover) and baclofen for alcohol addiction, and varenicline (Champix) for nicotine dependence.

Another major reason for relapse in addiction is stress. This may work through increasing dopamine release in brain so priming this addiction pathway or by interactions with other neurotransmitters such as the peptide substance P. As antagonists of these neurotransmitters are now available they are being tested in human addictions and may offer an alternative to substitution treatments.

Further reading

Nutt DJKing LA Phillips LD (2010) Drug harms in the UK: a multicriteria decision analysisLancet 376: 1558-66

Nutt DJ Lingford-Hughes A (2008) Addiction the clinical interface Brit J Pharmacology 1-9

Nutt DJ, Law FD (2008) Pharmacological and Psychological aspects of drug abuse. New Oxford Textbook of Psychiatry 2nd edition

Robbins TR, Everitt B,  Nutt DJ (2010) The Neurobiology of Addiction – New Vistas.   OUP

Teaching the tricks of the liquor trade

A guest blog from Paul Myles

Alcohol is a major public health problem and one that is growing in young people mostly from the increase in binge drinking. There are several reasons for the increase in drinking in this age group particularly the availability of low priced strong ciders lagers and breezers but advertising plays a significant role as well.

The recent BMA publication ‘Under the Influence’ [British Medical Association 2009] clearly shows that the drinks industry cynically targets very young people, revealing the techniques that they employ, of which many parents are unaware.  These include targeted email campaigns with embedded film clips advertising alcohol, Facebook links and mobile phone text messaging.

How can we combat this sophisticated and cynical approach? One approach is to tell young people directly of the dangers of alcohol. However it seems that direct scare tactics about the outcome of alcohol use or any other substance that can be misused has been ineffective and may even be counterproductive (Drugscope 2010) (Coggans et al 1991).

Another way is to develop a teaching module for school students that reveals the subtle ways in which positive messages about alcohol are communicated. This how now been done and piloted in East Sussex with great success.

The teaching module shows the students how the drinks industry makes its own voluntary codes and them blatantly ignores them. It shows how the Portman Group [that has responsibility for alcohol education] whilst appearing to be concerned about alcohol harm is actually dominated by the drinks industry. Also it is revealed that the public health message in the UKis left to the drinks industry. The myths surrounding alcohol are discussed and then the students are asked to make up their own mind about the issues. Profit motives of the drinks industry, the tax income and political agendas are exposed and compared with the cost to society, mortality and shortening of life caused by alcohol use.

The rationale for the module is to enable students to critically evaluate the way that young people are targeted to buy alcohol. The lessons examine the mechanics behind the commercial enterprise of alcohol sales. The students analyse the management/mismanagement of the substance misuse issue.

This approach does what the advertisers do, get this message out to as many people as possible, to show the public how they are being hoodwinked by the drinks industry. It is hoped that the British public will realise that they are being duped and react accordingly by contacting their MP and local authorities.

The Independent Scientific Committee on Drugs (ISCD) is now working to see how this might roll out the programme to many more schools.


This comprehensive package includes a 2 lesson module for students, a teacher training session and a presentation to parents and interested members of the community developed by Paul Myles from his MSc research at Sussex University. The module contains multi media and is designed to address a wide spectrum of learning abilities. The lesson plans were developed by researcher Paul Myles supported by East Sussex County Council.

British Medical Association 2009. Under The Influence:The damaging effect of alcohol marketing on young people. BMA Science and Education Department and the Board of Science. BMA Marketing & Publications London. www.bma.org.uk

Coggans N, Shewan D, Henderson M and Davies JB ‘National Evaluation of Drug Education in Scotland’, ISDD 1991.

Paul Myles BSc Psychol (Hons) MSc Substance Misuse MBPsS

Paul is a Fellow of the Royal Society of Medicine and a Graduate member of the British Psychological Society. Contact: 01273 477723 pmyles@btclick.com 13 Hill Rd Lewes Sx BN7 1DB