Following the defenestration of Professor David Nutt, earlier in the month, from the Advisory Committee on the Misuse of Drugs for allegedly intruding on politics in making public his views on the relative risks of legal and illegal drugs, I was moved by simple exasperation to write something in response. This is part of what I wrote and tells the little-known and rather bizarre story of how cannabis came to be prohibited. It also discusses the relative toxicity of cannabis and alcohol and describes what I call the Avocado Theory of illicit drug use.

Many people will have heard of (or even seen) the hilariously alarmist 1930s American anti-drug film ‘Reefer Madness’ which implied that cannabis led inexorably to degradation, psychosis and homicide. Not many people seem to know how it was that cannabis came to be added to the rather limited ‘index prohibitorum’ (which initially covered only morphine and cocaine) several years after Prohibition became established around 1920. The story, told by the late Prof. Bob Kendall[1] would be merely amusing, had not cannabis Prohibition ruined quite a few lives by causing the imprisonment of people simply for preferring or preparing one vegetable-based intoxicant rather than another. It is also a very good example of the sort of arguments and tactics used by Prohibitionists both ancient and modern.

In 1925, the League of Nations Second Opium Conference convened in Geneva. Its purpose was to tighten the controls on opium and – less importantly, it would seem – on cocaine, that had first been negotiated rather unenthusiastically at The Hague in 1914 and then steam-rollered through the Treaty of Versailles by the US. Prohibition had always been a policy largely promoted by America and largely ignored by most other countries. After helping the Allies avoid defeat or stalemate in the First World War, America was riding high. Once it was clear that the US was not expecting the Allies, as the price of that help, to join it in prohibiting alcohol (Europe’s traditional intoxicant) the Allies seem to have been happy to go along with American proposals for prohibiting other peoples’ traditional intoxicants. Indeed, Prohibition in the West of drugs other than alcohol actually began in earnest, in the last quarter of the 19th century, as a campaign to restrict the trade in opium not to Europe or America (where laudanum was widely used) but to China and neighbouring countries. This was at least partly motivated by the hope that the Chinese would be more susceptible to the attention of the numerous Christian missionaries, mainly American, who were seeking converts in the region. Today, I suppose, we would regard it as pharmacological imperialism and would probably reject the whole idea as riddled with double standards, Eurocentrism, racism and other old-fashioned attitudes. However, in 1925, such attitudes were pretty routine in the corridors of Geneva.

Cannabis was not illegal or restricted when the 1925 conference began. It wasn’t even on the agenda and wasn’t mentioned at all until the fifth session, when the Egyptian delegate, Dr Salam el Guindy intervened. He said that cannabis was ‘at least as harmful as opium, if not more so’ and asked the conference to include it in the list of prohibited narcotics. He elaborated on this theme at subsequent meetings, claiming that hashish accounted for between ‘30 and 60% of the total number of cases [of insanity] in Egypt’ and insisting that prohibition of cannabis would be welcomed by every Egyptian ‘…from His Majesty King Fuad…down to the humblest fellah of the Nile valley’. This, as Kendall points out, was inconsistent with the large amounts of cannabis which, Dr el Guindy conceded, were evidently being grown by those same fellahin. The representatives of Greece and Brazil also claimed that cannabis was in the same league as opium or worse. Neither country can be said to have distinguished itself, then or later, for the quality of its psychiatric research.

The Chinese and American delegates supported these assertions, although Mr Sze, for China, admitted knowing ‘next to nothing’ about the subject and even Mr Porter, the American, conceded that his knowledge was ‘quite limited’. Porter is said to have been ‘bombastic’ and ‘a loose cannon’ but he was a moderate compared to the other American delegate, Bishop Brent, who had previously presided over the 1909 Shanghai commission and the 1912 Hague conference. Brent was ‘a man of evangelical fervour and righteousness’. He regarded any non-medical use of opium as ‘immoral’ and was, according to Kendall, an ‘extreme’ prohibitionist. Still, at least Brent wasn’t an odious hypocrite like one of his fellow ecclesiastics in the alcohol prohibition movement, Bishop James Cannon. In public, Cannon was a Puritan, who ‘had never been known to laugh’ and was opposed to dancing and theatricals and any other public activities that involved even transient exposure of female flesh. It eventually emerged that he had consorted with at least one prostitute (initially using a pseudonym) and had spent a night with her a few hours after his wife suffered a severe and ultimately terminal stroke.[2]

To their credit, several delegates were unhappy about the lack of opportunity before and during the conference to inform themselves adequately about cannabis. Nevertheless, the conference decided to add cannabis to the list of prohibited substances. The president believed they had ‘…struck a most powerful blow at the drug evil’ and ‘started on a road which eventually can lead only to success’. Even so, the conclusions were not firm enough for the US, which withdrew from the conference because the colonial powers could not commit themselves to eliminating opium from their oriental territories within 15 years. One reason for this was that 15 million kg. (ie about 15,000 tons) of opium were still being produced in rebellious Chinese provinces, and preventing smuggling was much easier said than done.

Reviewing the history of cannabis in Egypt, Kendell noted that attitudes to it had oscillated over the centuries following its introduction there around the 10th century. One school of Islamic law even refused to regard it a prohibited substance in the same class as alcohol. More importantly, the annual report of the larger of Egypt’s two psychiatric hospitals attributed only 2.7% of admissions in 1920 to hashish – barely a third of the proportion attributed to alcohol. Thirty years earlier, the Indian Hemp Commission had also looked into the psychiatric consequences of cannabis use in the jewel of Britain’s imperial crown. They concluded – correctly it would seem – that cannabis can be the sole cause of psychosis but not very often. Their own figure was 4.5% of admissions and they felt that prohibition was ‘neither necessary nor expedient’ even in a country like India where it was widely consumed.

Recent research suggests that although, like many other drugs that affect brain function, cannabis can exacerbate pre-existing schizophrenia, it increases the total number of cases by no more than about 8%.[3] This is hardly surprising given that the incidence of first episodes of schizophrenia has not altered much during a couple of generations when the smoking of cannabis in Western countries changed from being an eccentricity indulged in by a small number of jazz musicians and other ‘artistic’ people to something approaching a majority experience, at least during adolescence – even, as has been quite readily conceded, for many future British parliamentarians in government or opposition. (I was nearly 30 when I first tried the stuff myself. Unlike Bill Clinton, it wasn’t so much that I didn’t inhale as that – being a non-smoker – I found inhaling almost impossible. At the time, I was working in a Jamaican university hospital, where the patients’ families – many of them unable to afford a box of chocolates or a bottle of rum or whisky – would sometimes express their thanks to the doctors and nurses by offering us small bags of home-grown ganja.)

As well as annoying the British government by pointing out the relatively modest effect of cannabis on the incidence of schizophrenia, Prof Nutt has noted that if anything (and in contrast with official concerns that more potent types of cannabis might be more likely to cause psychosis) the incidence of schizophrenia is falling a little. If, despite widespread cannabis use, there really are consistently fewer new cases of schizophrenia, then one possible explanation may be found in some recent research about the genetics of cannabis-induced psychosis (CIP). It seems that the brain enzyme catechol ortho-methyl transferase (COMT) may be particularly important for this process and also that there are several variants of the gene that controls its expression.[4,5,6] These variants are not equally distributed in the British population (let alone in the planetary one) and the variant that makes people most vulnerable seems to be found disproportionately in those of African descent, though since Africans are at least as variable as Europeans, the variants are unlikely to be equally distributed there either. As British citizens of African descent increasingly intermarry with the white population and increasingly produce offspring of mixed race, it might be (and I stress, as someone who is not an expert in psychogenetics, that this is no more than a conjecture) that the vulnerability to CIP increasingly comes to resemble the relatively low one of the white population. That might also apply to certain cultural characteristics which, according to some black advocates, may have led to the over-diagnosis of schizophrenia among Afro-Caribbeans by white psychiatrists.

Simple acute intoxication with cannabis does not often lead to situations requiring medical attention. In contrast, a significant proportion of the work of any general hospital casualty department involves dealing with alcohol-related accidents, alcohol-related violence and alcohol-related suicide attempts, many of which conditions require at least a short admission. (By the last category, I mean people who make largely unplanned suicide attempts, while drunk, which they would not have made if they had been sober.) Some alcohol-abusers need admission for the treatment of alcohol withdrawal, a conditions that is considerably more dangerous to life than withdrawal from heroin and sometimes equally unpleasant. Some of them are admitted to general hospitals, others to alcoholism units in psychiatric hospitals. Many other alcohol-related psychiatric admissions are not for withdrawal but involve people whose excessive drinking has damaged or destroyed their marriage, their parenthood, their employment prospects, their friendships, their prosperity or their liberty and who are thus, in a very general sense, ‘depressed’. (If you think that ‘understandable misery’ would be at least as accurate a diagnosis in many cases, I wouldn’t strongly disagree, but that’s another article.) A much smaller number are admitted for alcohol-related psychoses, which can be as serious as anything produced by cannabis. Unlike cannabis, alcohol abuse can also cause devastating and irreversible brain damage that can amount to premature dementia.

Apart from alcohol-related brain damage, alcohol damages many other organs. In contrast, cannabis causes almost no obvious organ damage, apart from the damage that the process of smoking the stuff may cause to the lungs. The difference in toxicity may be because alcohol is actually a very weak drug. The average man needs to drink at least three or four units of alcohol over a relatively short period to become even moderately affected. That means the equivalent of 30 to 40 grams of pure alcohol in total. It also means an awful lot of alcohol molecules coursing through the body, representing quite a lot of calories if you make a habit of it. Cannabis is much more potent, with a typical intoxicating dose in the milligram range – ie at least 3-4000 times smaller. It is also a much larger and heavier molecule than alcohol Far fewer cannabis molecules, therefore, to damage your vital organs compared with alcohol – and it’s calorie-free to boot. Consequently, cannabis users do not trouble doctors in large numbers with perforated gastric ulcers, hypertension, various skin diseases and – of course – cirrhosis of the liver, all of them conditions that can be caused and/or aggravated by alcohol. It is thus difficult to argue convincingly that cannabis is so much more toxic a drug than alcohol that it requires special legislation that is not thought to be required for alcohol.

Finally, let me present my Avocado Theory of Illicit Drug Use.[3] In the 1950s, when I was a teenager, avocados were exotic and almost unknown, particularly outside London. Furthermore, such was the gastronomic conservatism and xenophobia of the average British teenager, and his or her parents, that if you had offered them an avocado, they would probably have refused even to try it. Yet within a decade, avocados had become less exotic and quite widely available. Many people had eaten them and for some, avocados became a normal part of their diet. By the 1970s, avocados were as ubiquitous as they were unremarkable. This embracing of the hitherto exotic didn’t stop at avocados and other foreign delicacies, of course. Young men started wearing clothes increasingly unlike their fathers’ blazers, suits, ties and sports jackets. The fathers themselves stopped taking their families on holiday to solid British resorts and started going instead to places with names so exotic that they sometimes found it difficult to pronounce them properly. All proper Englishmen knew that avocados (like garlic and Africa) began at Calais but they were increasingly disposed to explore and sample these various avocado-analogies in the fields of clothing, travel, music, sex and thought that burst upon a slightly nervous but receptive country in the 1960s. That disposition has persisted and these changes have generally been accepted and even encouraged by both governments and the media – especially the media. Indeed, significant sectors of the economies of developed countries depend on their continuation.

The odd thing is that people were somehow expected to ignore completely the other new idea that appeared in the 1960s. That just as there were alternatives to Blackpool for holidays, and to overcooked cabbage to have with your Sunday roast, so there were alternatives to alcohol and tobacco for adjusting – or temporarily abolishing – your feelings. That is one important reason why Prohibition has failed. In the next article, I will discuss some of the other reasons and – more importantly – what we might consider doing instead.

REFERENCES

[1] Kendell R. Cannabis condemned: the proscription of Indian hemp. Addiction 2003; 98: 143-51.

[2] Behr E. Prohibition: the 13 years that changed America. London. BBC Books. 1997. 228-9.

[3] Arsenault L, Cannon M, Witton J, Murray R. Causal association between cannabis and psychosis: examination of the evidence. Br J Psychiatry. 2004 Feb;184:110-7.

[4] Caspi A, Moffitt TE, Cannon M, McClay J, Murray R et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene x environment interaction. Biol Psychiatry. 2005 May 15;57(10):1117-27.

[5] Henquet C et al. COMT ValMet moderation of cannabis-induced psychosis: a momentary assessment study of ‘switching on’ hallucinations in the flow of daily life. Acta Psychiatr Scand. 2009 Feb;119(2):156-60.

[6] Henquet C et al.An experimental study of catechol-o-methyltransferase Val158Met moderation of delta-9-tetrahydrocannabinol-induced effects on psychosis and cognition. Neuropsychopharmacology, 2006 Dec;31(12):2748-57.

[7] Brewer C. The avocado principle. Nursing Times 1988; 84:22